Simple Notes - Paper I Physiology

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GENERAL PHYSIOLOGY
10 marks:
1. Explain all the passive transport processes across the membrane with suitable diagrams & examples
2. Explain all the active transport processes across the membrane and through cellular sheets with
suitable diagrams & examples
5 marks:
1. What are the functions of cell membrane proteins?
2. Give a short account of cell junctions
3. Differentiate between the following with examples:
-Passive & Active transport
-Simple & Facilitated diffusion
-Primary & secondary active transport
- Cotransport & countertransport
-Exocytosis & endocytosis
-Pinocytosis & Phagocytosis
4. Describe the structure, mechanism of action & functions of Na+-K+ ATPase pump
5. Explain the process of phagocytosis.
6. Define Homeostasis. Name any four systems involved in it. Explain the types of feedback mechanisms
with examples
7. What are starling’s forces? How they help in tissue fluid formation? Explain Starling’s hypothesis in
connection with the passage of fluid across a capillary wall
8. Classify the body fluid compartments & give their normal values. Name the substances used to
measure total body water, ECF & plasma volume. Explain the principle underlying the measurement of
body fluid compartments.
3 marks:
General
1. Describe the factors affecting the rate of diffusion across the membrane. What determines the rate of
facilitated diffusion?
2. What will be the total blood volume when the plasma volume is 3600ml & HT is 40%?
3. In a tabular form compare the composition of ICF & ECF. What is the importance of higher
intracellular concentration of protein anions?
4. Find the blood volume of the subject with the following values:
Evan’s blue (T 1824) dye dilution technique value – 2 lts
Hematocrit – 40%
5. Explain the usefulness of positive feedback mechanism
6. Sometimes positive feedback mechanism does not lead to stability but to instability. Explain
7. Briefly write the role of osmo-receptors in the regulation of body fluids.
8. Define the term ‘Biological thermostat’ and explain its role in thermal homeostasis.
9. Explain homeostasis with reference to body fluid volume
10. What are the functions of cell membrane?
11. What is the significance of lipid bilayer of cell membrane?
12. Explain the role of the following structures in cell functions:
- Golgi apparatus
- ribosomes
- Lysosomes
- Mitochondria
13. Describe the gap junctions & explain its role in normal cardiac functions.
14. Write the functions of tight junctions
15. Different types of gated channels - their mechanism of working & examples of sites where they are
Located
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Applied (General physiology)

Cell Physiology
1. What are G proteins? How does cholera toxin cause severe diarrhea?
2. Why ions though of smaller size cannot diffuse through lipid bilayer?
Body Fluid Compartments
1. A patient admitted in casualty with 60% burns. What change would you expect in his body fluid
compartment. Suggest a method to detect this change.
2. Why do red blood cells swell and eventually burst when they are placed in a solution of 0.3 % NaCl
solution?
3. Following diarrohea a patient develops dehydration and metabolic acidosis
a. In which compartment there is decrease in fluid volume
b. What is the course of metabolic acidosis?
4. Give the reason for generalized edema in hypoprotinemia
5. Which of the body fluid compartments gets expanded in generalized edema? List any two causes
of edema
6. Explain why in a dehydrated patient intravenous infusion of 5% glucose is better than 10% glucose
7. Explain the various forces that operate to prevent edema formation in tissue spaces
8. Intake of salty food is followed by feeling of thirst. What is the mechanism of stimulation of thirst
centre in this case?
Salty food - Hyperosmolarity of body fluids
↓
Stimulation of osmoreceptors
↓
Stimulation of thirst centre
9. What is edema? What are its causes?
10.Explain, why is dehydration common and usually fatal (if not treated immediately) in children.
11.A severely dehydrated child with diarrhea and vomiting was brought to the emergency. The
presenceof vibrio cholerae in the stool confirmed the diagnosis of cholera.
i. How does Vibrio cholerae cause diarrhea?
ii. Why dehydration is common and fatal in children?
12. What is normal saline? What is its clinical importance?
Transport AcrossThe Membrane
1. Name the sites where sodium and glucose are co transported. How is this principle used in oral
rehydration therapy.
2. How would having a fever affect body processes that involve diffusion?
3. Compare the ion transport in air way epithelium of a normal individual with a patient with cystic
Fibrosis
4. What would happen if Na+-K+ pump does not function?
5. Why the rate of diffusion for CO2 is 20 times more than that of O2?
6. Give any one example of secondary active transport across biological membrane. How is this
knowledge made use of clinically?
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GENERAL PHYSIOLOGY
1.Cell Membrane - Structure

Features:
Plasma membrane is a dynamic structure and its constituents are constantly renewed.
The thickness of membrane is about 7.5 nm
Semipermeable - allowing some substances to pass through while excluding others
Components:
Phospholipids
Cholesterol 40%
Proteins -------------- 55%
Carbohydrate -------- 5%
Arrangement of the components:
Explained by Fluid Mosaic Model proposed by Singer & Nicolson
- Phospholipids forms a fluid structure in which proteins and other components are
embedded to give a mosaic pattern.
- Fluidity helps the substances dissolved in lipid layer to move to different places in
the membrane
Lipid Bilayer:
- Made up of two layers of phospholipid molecules
- Each phospholipid molecule has a hydrophilic phosphate head and two hydrophobic
fatty acid chains
- These molecules are arranged in two layers in opposite direction
- The inner and outer surfaces of the lipid bilayer are hydrophilic and the interior of
the bilayer is hydrophobic
Proteins:
Two types of proteins: Peripheral & integral or transmembrane proteins
Peripheral proteins are attached to the outer and inner surfaces of membrane
Integral proteins extends through the membrane from outside to inside
Carbohydrates:
Oligosaccharide molecules are attached to the surface of membrane.
The molecules which are attached to membrane proteins are glycoproteins
The molecules which are attached to phospholipid molecules are glycolipids
These molecules form “Glycocalyx” surrounding the cell
Significance of each component:
Phospholipids - Maintains the membrane in fluid state & provides flexibility to the
membrane
Cholesterol – Provides rigidity (stiffness) to the membrane
Proteins – Critical components of membrane as it performs many functions
Glycocalyx – Helps in cell to cell recognition
Functions of cell membrane:
1. Forms a protective barrier surrounding the cells
2. Semipermeability of the membrane differentiates the concentration of ECF from ICF
3. which is responsible for development of biopotentials
4. Links adjacent cells together by intercellular connections
5. Provides anchoring sites for filaments of cytoskeleton
6. Allow cell to cell recognition – Glycocalyx
7. Provides a binding site for enzymes/hormones
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2. Cell membrane Proteins
Embedded in the fluid lipid bilayer
Peripheral proteins
Integral proteins
Types: Peripheral & integral or transmembrane proteins

1.Peripheral proteins :
 Loosely bound to the membrane
 Non-covalently bound to integral proteins
 Provides structural integrity to the cell membrane
Types
1. Intrinsic - anchored to cytoskeleton of the cell
2. Extrinsic - act as cell adhesion molecules (CAM)
2. Integral proteins (Transmembrane proteins ) :
 Covalently bond
 Penetrate lipid bilayer
Functions of integral proteins:
 Channels: Provide channels for the ions to diffuse in both directions e.g., Na+ Channels (allow
sodium ions to diffuse inside). Diffusion of ions through channels is simple diffusion
 Carriers: Transport the substances along the concentration gradient. Diffusion with the help of
carrier proteins is called facilitated diffusion. E.g., transport of glucose by a carrier protein GLUT
 Pumps: Transport the substances against the electrochemical gradient e.g., Na+-K+ ATPase
pump. The pumping of substances with the help of transport protein is called primary active
transport
 Receptors: Receive the chemical signals from outside e.g., Hormones & neurotransmitters
 Antigens: Differentiates the self from non-self e.g Human Leukocyte Antigen (HLA) & Blood
group Antigens
 Enzymes: Catalyze the reactions at surface of the membranes e.g Adenylate cyclase
 Cell Adhesion Molecules: Help to anchor the cells to neighboring cells and to the basal lamina
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3. Glycocalyx
Glycocalyx is a coat on the external surface of the plasma membrane. This coating consists of several
carbohydrate moieties (glycolipids and glycoproteins)
Functional significance:
contribute to cell-cell recognition, communication, and intracellular adhesion

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distinguish between own healthy cells and transplanted tissues, diseased cells, or invading organisms.
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Lipid Bilayer as semipermeable membrane::

The phospholipid bilayer structure with specific membrane proteins accounts for the selective
permeability of the membrane
Small molecules and larger hydrophobic molecules move through easily. e.g. O2, CO2, N2 and alcohol
Hydrophilic molecules have lower solubility to penetrate the membrane slowly. E.g. Ions, glucose and
urea ,
Importance of Semipermeability:
Semipermeability of plasma membrane determines the concentration difference between ECF & ICF
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Transport Across the Membrane
Membrane Transport
Passive Transport Active Transport

Passive transport mechanisms:
 Diffusion
 Facilitated Diffusion
 Osmosis
 Capillary filtration
 Bulk Flow / Solvent drag
DIFFUSION
Diffusion is the net movement of molecules (or ions) from a region of their high concentration to a
region of their lower concentration.
Characteristic features of diffusion
 The molecules move down a concentration gradient.
 Requires no energy
 Molecules move about randomly by kinetic energy
 As a result of diffusion, molecules reach equilibrium (no net movement of molecules from either
side).
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Factors Affecting Diffusion

 Cell membrane permeability
 Concentration Gradient
 Pressure gradient
 Electrical potential gradient
Cell membrane permeability depends upon:
 Solubility of the substance in the lipid bilayer
 Molecular size of the particle
 Charge of the particle
 Charge at the pore
 Surface area
 Thickness
 Number of protein channels
 Temperature
Fick’s law of Diffusion:
J = DA (C1-C2)
---------------
T
J = Rate of Diffusion T = Thickness of membrane
C1-C2 = concentration gradient D = Diffusion coefficient
A = Cross sectional area
Types of diffusion:
1. Simple diffusion
2. Facilitated diffusion
1. Simple Diffusion
Diffusion without the help of a carrier protein
Mode of Simple Diffusion
Through Lipid Bilayer Through Channels
Molecules that pass through the lipid bilayer by diffusion

 Gases (oxygen, carbon dioxide)
 Water molecules (rate is slow due to polarity)
 Lipids (steroid hormones)
 Lipid soluble molecules (hydrocarbons, alcohols, some vitamins)
 Small noncharged molecules (NH3)
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Molecules that pass through the Channels by diffusion

 Ions (Na+, K+, Cl-)
 Small water soluble molecules
 Water (faster rate)
Gating of Protein channels
Types of gated channels
1. Voltage gated channels – open when there is a change in the resting membrane potential
e.g., Na+ channels along the nerve fiber
2.Ligand gated channels – open when a chemical binds to the receptor which is attached
to the channel e.g., channels attached to the acetylcholine receptors in synapse or Neuro-
muscular junction
Mechanical gated channels – Open when there is a mechanical stretch

e.g Channels in the smooth muscle fiber
Drugs that block channels:
Sodium channels – Tetrodotoxin (TTX) & Saxitoxin
Potassium channels – TEA (Tetra Ethyl Ammonium)
Calcium channels – Verapramil (to treat hypertension)
2. Facilitated diffusion
Movement of solutes from high concentration to low concentration through the membrane
with the help of a carrier protein
Features of Facilitated Diffusion
 Occurs along the concentration gradient
 Does not require energy
 Involves carrier protein
 Carrier proteins are highly specific for molecules
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 Have saturation point. Diffusion increases with increase in concentration gradient in simple
diffusion whereas in facilitated diffusion, diffusion depends on availability of carrier proteins.
When the carrier proteins are saturated, facilitated diffusion stops
 Competitive inhibition occurs
Mechanism of Facilitated Diffusion
 Molecule binds to carrier
 Carrier changes conformation
 Molecule released on other side
 Purely passive process- stops when concentrations are equal
e.g., Glucose transport in to the cells with the help of a carrier protein GLUT (Glucose Transporter)
 Glucose molecule from interstitial fluid binds to GLUT
 GLUT changes its confirmation
 Glucose molecule is released in to the ICF
OSMOSIS
The diffusion of water from an area of high concentration of water molecules (high water potential) to an
area of low concentration of water (low water potential) across a partially permeable membrane.
Osmosis occurs through water channels called “Aquaporins”
Osmotic pressure
The minimum pressure which when applied on the side of higher solute concentration prevents osmosis
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Colloidal osmotic pressure

 The osmotic pressure exerted by colloidal substances in the body is colloidal osmotic pressure
 The colloidal osmotic pressure of blood due to plasma proteins is called ONCOTIC PRESSURE
 Oncotic pressure or colloidal osmotic pressure of blood is normally 25 – 30 mmHg
 80% of the oncotic pressure is determined by albumin
 colloidal osmotic pressure of blood is one of the factors influencing the capillary filtration
 colloidal osmotic pressure of blood opposes filtration and thereby prevents edema
 A decrease in colloidal osmotic pressure due to hypoproteinemia increases capillary filtration
and causes development of edema. E.g., Malnutrition, Liver cirrhosis and nephrotic syndrome
Osmolarity
 Number of osmotically active substances per Liter of a solution is called osmolarity
 Normal osmolarity of body fluid is 290 milliosmoles / liter
 Osmolarity of body fluid is mainly determined by sodium, Chloride and bicarbonate
 Osmolarity is also influenced to some extent by glucose, urea, plasma proteins etc.,
Tonicity
The effective osmotic pressure of a solution relative to the plasma is called tonicity
Isotonic solutions:
Solutions having same osmolarity as that of plasma ie., 290 milliosmoles/lt
Examples of isotonic solution:
 0.9% sodium chloride solution (isotonic saline)
 5% glucose solution
 20% urea solution
 10% mannitol solution
Significance of isotonic solution:
Isotonic solutions (0.9% NaCl / 5% glucose / 20% urea) can be infused in case of dehydration to
restore the body fluid volume without upsetting the osmotic equilibrium of the cells
Hypertonic solutions:
Fluids whose osmolarity is greater to that of plasma ie., > 290 milliosmoles/lt
Hypotonic solutions
Fluids whose osmolarity is lesser to that of plasma ie., < 290 milliosmoles/lt
CAPILLARY FILTRATION
 It is a process by which a fluid is forced through a membrane due to variation in the hydrostatic
pressure
 Major route of transport between blood and interstitial space.
 Filtration is determined by difference in various pressures of blood & interstitial space.
 The normal rate of net filtration in the entire body is only about 2ml/min.
 This fluid is drained by the lymphatics from the interstitial space.
Starling’s hypothesis:
 At any capillary bed the rate of filtration is determined by forces acting across the capillary
membrane.
 Any imbalance in these forces may lead to edema (accumulation of fluid in tissue spaces) or
dehydration (fluid loss from the body)
Starling’s Forces: The forces acting on the capillary membrane and influencing the rate of capillary
filtration are called Starling’s forces.
The forces are:
 Capillary hydrostatic pressure – favours filtration
 Capillary osmotic pressure – oppose filtration
 Interstitial fluid hydrostatic pressure – oppose filtration
 Interstitial fluid osmotic pressure – favours filtration
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At arterial end
Hydrostatic pressure of blood = 30 mmHg
Oncotic pressure of blood = 28 mmHg
Interstitial hydrostatic pressure = - 3 mmHg
Osmotic pressure of interstitial fluid = 8 mmHg
OUTWARD FORCES - INWARD FORCE = 30 + 8 – (-3) +28
= 30 + 8 + 3 – 28
= 13 mmHg (net filtration pressure)
At venous end
Hydrostatic pressure of blood = 10 mmHg
Oncotic pressure of blood = 28 mmHg
Interstitial hydrostatic pressure = - 3 mmHg
Osmotic pressure of interstitial fluid = 8 mmHg
OUTWARD FORCES = 10 + 8 + 3 = 21 mmHg
INWARD FORCE = 28 mmHg
28 – 21 = 7 mmHg (net absorption pressure)
SOLVENT DRAG
Transfer of solutes by being carried along with the water flow driven by osmotic gradients across cell
membranes.
Example: Transfer of fluid along with its constituents across the intestinal wall & Capillary
ACTIVE TRANSPORT
 Substances are transported against the chemical or electrical gradient (from the region of low
concentration to the region of high concentration)
 Utilizes energy from ATP
 Up-hill process
 Utilizes a transport protein (pump)
Pump
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Types of Active Transport

1) Primary
2) Secondary
3) Bulk/Vesicular Transport
a) Exocytosis
b) Endocytosis
i) Phagocytosis
ii) Pinocytosis
iii) Receptor-Mediated endocytosis
1.Primary active transport
The energy is derived directly from the breakdown of ATP or some high- energy phosphate compound.
Examples:
 Sodium-potassium ATPase pump
 Calcium ATPase pump
 Hydrogen ATPase pump
Sodium-potassium pump (a specific case of active transport)
Structure
α Subunit (100, 000 MW)
β Subunit (55000 MW)
3 Intracellular sites:
1. Sodium binding site
2. ATP binding site
3. Phosphorylation site
2 Extracellular sites
1. Potassium binding site
2. Ouabin binding site
Mechanism of the pump:

 Cytoplasmic Na+ binds to the sodium-potassium pump.
 Na+ binding stimulates phosphorylation by ATP.
 Phosphorylation causes the protein to change its shape. Na+ is expelled to the outside.
 K+ binds on the extracellular side and triggers release of the phosphate group
 Loss of the phosphate (dephosphorylation) restores the protein’s original shape.
 K+ is released, and the cycle repeats
 Three sodium ions are pumped outside where as two potassium ions are pumped inside
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Functions of Na+ -K+ Pump

1. Maintains Na+ & K+ gradients across the membrane essential for genesis of RMP (Resting
Membrane Potential).
2. Maintains Cell volume: If the pump is paralyzed, sodium ions which enter the cell remain
inside & water follows, causing swelling and rupture of cells.
3. Important role in secondary active transport.
4. Maintains high intracellular K+ which is important for protein synthesis
2. Secondary active transport
The energy is derived secondarily (indirectly) from the energy which has been stored in the form of
ionic concentration differences, created in by primary active transport. In other words the downhill
energy (energy of diffusion) of one substance is utilized for uphill movement (active transport) of
another substance
Types:
 Co-transport (symport)
 Counter transport (Antiport)
Co – transport: Both the substances are transported in the same direction
e.g., Sodium – Glucose Co-transport & Sodium-Amino acid Co-transport
Counter transport: Two substances are transported. One substance is transported in opposite
direction to the other substance
e.g., Sodium-Hydrogen counter transport & Sodium- Calcium counter transport
Sodium - Glucose co-transport:

 An example for secondary active transport
 Sodium and glucose are transported together from ECF to ICF through the cell membrane by a
transport protein
 The transport protein is SGLT (Sodium Dependent Glucose Transporter)
 This occurs secondary to Na+-K+ ATPase pump (secondary active transport) which maintains the
concentration gradient of sodium
 The diffusion energy of sodium is utilized by glucose for its active transport
 As this transport does not utilize energy directly, this is secondary active transport
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Sites of Sodium - Glucose co-transport

Absorption in Intestine
Reabsorption in Kidney
Clinical use of secondary active transport:
This is used in oral rehydration therapy which helps to restore the volume of body fluid which is lost
in dehydration
ORS (Oral Rehydration Solution)
 simple treatment for dehydration
 It consists of a solution of salts and sugars which is taken by mouth.
 As both substances are osmotically active particles, they increase the absorption of water. This
will restore the body fluid effectively
3.VESICULAR TRANSPORT
 Vesicular transport is an active process in which materials move into or out of the cell enclosed as
vesicles.
 Vesicles are small membrane sacs. They can form at the cell membrane or can fuse with the
membrane.
 Transports macromolecules like protein and even cells like bacteria
 There are two basic types of vesicular transport-endocytosis and exocytosis.
Exocytosis:
A process by which the contents of secretory vesicles move out of the cell and into the
extracellular space.
Mechanism of exocytosis:
intracellular vesicle moves to the plasma membrane
↓
fusion of the vesicular membrane and plasma membrane
↓
Rupture of membrane and release of contents outside
Examples
secretion of proteins like enzymes, peptide hormones and antibodies from cells, release of
neurotransmitter from presynaptic neurons
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Endocytosis
Process by which the macromolecules are transported in to the cells
Types:
1. Pinocytosis
2. Phagocytosis
3. Receptor mediated endocytosis
1. Pinocytosis
 Process in which the cell takes in surrounding fluids, including all solutes present.
 Pinocytosis is nonspecific in the substances that it transports.
 Also called as “cell drinking”
Mechanism of pinocytosis:
 Cell forms an invagination
 Vesicles are formed within the cell
 These pinocytic vesicles subsequently fuse with lysosomes to hydrolyze (break down) the
particles.
Example:
Absorption of antibodies in the intestine of baby from mother’s milk
2. Phagocytosis
Process by which microorganisms like bacteria and other particulate materials are engulfed in to the
Cell. Also called as “cell eating”
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Mechanism of Phagocytosis:
Example: Engulfing of bacteria by phagocytes (Neutrophils & Macrophages)
3. Receptor mediated endocytosis

This type of endocytosis is triggered by various ligands binding to the receptors on the cell surface
Mechanism:
 Binding of chemical molecules to the receptors in the clathrin-coated pits
 Contraction of clathrin
 The pit is then pinched off forming a coated vesicle
 The vesicle then becomes endosome
Example: Uptake of cholesterol
Transport of iron
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CELL JUNCTIONS
The cell membranes of adjoining cells are connected with one another through intercellular junctions.
Types
 Tight junctions
 Anchoring junction
- Desmosomes
- Hemidesmosomes
- Adherence junction
Focal adhesion
 Gap junction
1.Tight junctions (Zona Occludens or occluding zone):
 The cell membranes of two adjacent cells fuse with each other
 Obliteration of the space between them.
E.g: blood brain barrier, Intestinal epithelial cells
Functions:
 Form strong union between neighboring cells which provides strength & stability to the cells
 Barrier to the movement of ions and other solutes from one cell to other (Useful in Blood brain
barrier & Blood testis barrier)
 Prevents lateral movement of proteins  maintains polarity of cells
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2.Anchoring junction:
 Provide firm structural attachment between two cells or between a cell and the extracellular
matrix
 The attachment is provided by either actin or intermediate filaments
Desmosomes
 Cell membrane of adjacent cells is separated by 200A gap.
 A part of the gap is occupied by a solid structure which provides a strong union between the cells
 The proteins involved are Cadherins
 Seen in skin and neck of uterus
Hemidesmosomes:
 Appears like half desmosomes
 Anchor cells to the basement membrane
 The proteins involved are integrins
Adherence junctions
 Connect actin filaments of one cell to those of another cell
 The membranes of the adjacent cells are held together by transmembrane proteins called
cadherins
 Present at the basal regions of tight junction in cardiac muscle and epidermis of skin
Focal adhesions:
 Attach cells to basal lamina
 Also connect the actin filaments of the cell to the extracellular matrix
 The transmembrane proteins involved are integrins
 Seen in epithelia of various organs
3. Gap junction:
 Cell membrane of adjacent cells is separated by a gap of 2-3 nm
 The gap is connected by protein cannels
 One half of the protein cannel is contributed by one cell and the other half from the adjacent cell
 The protein channel contributed by each cell is called connexon and is made up of six subunits
enclosing a channel of about 2 nm
 Present in cardiac muscle, smooth muscle & astrocytes
Functions of Gap junctions
 Allow two way transmission of low molecular weight substances like glucose, aminoacids &
other ions
 Direct movement of ions between cells helps in rapid propagation (conduction) of impulses
 Synchronize the activity of neurons or muscle fibers in an all or none manner
 In astrocytes, play an active role in signaling in the brain through chemical messengers
Importance of gap junctions in cardiac muscle:
By synchronizing the activity of cardiac muscle fibers, make the heart to function as a syncytium
(single cell). Direct ionic movement and rapid propagation of electrical impulses through the fibers
play an important role in this
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What are Starling’s forces? How they help in tissue fluid formation? Explain Starling’s hypothesis
in connection with the passage of fluid across capillary wall
Starling’s hypothesis:
At any capillary bed, the filtration of fluid through the capillary membrane is determined by pressures
acting across the membrane.
Starling’s forces:
The forces that act across the capillary membrane are called starling’s forces. They influence the
filtration and absorption of fluid across the capillary. The Starling’s forces are:
1) Capillary hydrostatic pressure (Pc) – Favors filtration
2) Capillary colloidal osmotic pressure (c) – Opposes filtration & favors absorption
3) Interstitial fluid hydrostatic pressure (Pi) – Opposes filtration when it is positive (but
usually it is negative)
4) Interstitial fluid osmotic pressure (if) – Favors filtration (but the pressure is negligible)
Tissue fluid formation:

Tissue fluid or Interstitial fluid is formed by net filtration of fluid from capillary into interstitial
Space
Net Filtration= Kf X (Pc+ if) –(c +Pif)
Net filtration through the muscle capillary:

Arterial end of capillary:
Capillary hydrostatic pressure (Pc) = 30 mmHg
Capillary colloidal osmotic pressure/ oncotic pressure (c) = 28 mmHg
Interstitial fluid hydrostatic pressure (Pif) = 8 mmHg
(As the capillary hydrostatic pressure is higher than oncotic pressure, filtration occurs&
tissue fluid is formed)
Venous end of capillary:
(As the oncotic pressure is higher than capillary hydrostatic pressure, absorption of tissue
fluid occurs)
Excess tissue fluid is returned to the blood vessels via the lymphatic system.
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HOMEOSTASIS
Definition:
Maintenance of constant internal environment within certain physiological range inspite of changes in the
external environment. Internal environment refers to ECF especially interstitial fluid.
- The term ‘homeostasis’ was coined by Canon
- The term ‘Millieu interior’ which means internal environment was coined by Claude Bernard
Systems involved in enforcement of homeostasis:
- Nervous system
- Chemical system
Role of different body systems in homeostasis:
1. Supply of oxygen and nutrients – Respiratory, Digestive, circulatory & musculoskeletal
2. Removal of metabolic waste products – Renal, Respiratory & slin
3. Volume & composition – Renal, Respiratory, Digestive & skin
4. Temperature – CVS, nervous, Endocrine, Musculoskeletal & skin
5. pH – Renal, respiratory & blood buffers
Components of homeostatic system:
Sensors: Recognize any deviation from normal level and feed to control center.
Control center: Receives information from sensors and activate appropriate effector system
Effector: Corrects the deviation (corrects the deviation rapidly where as chemical systems take a
longer time)
Normal
Correction
Deviation
Sensors Effectors
Control
center
REGULATION OF HOMEOSTASIS (Feedback Mechanisms)

The deviation is corrected to normal by two types of mechanisms:
1. Feedback mechanisms
2. Adaptive control system (Feed forward signals)
Two types of feedback mechanisms:
1. Negative feedback
2. Positive feedback
Negative feedback mechanism:
- A stimulus(change in the environment) produces a response which inturn depresses or stop
the stimulus. This type of feedback mechanism is negative feedback mechanism.
- Stimulus and response are in opposite direction
- Consists of two variables. The first variable stimulates the second one which inturn inhibits
first one
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Examples:
a) Regulation of thyroxine secretion from thyroid gland
Increased TSH secretion from anterior pituitary will stimulate thyroid gland. The
response will be increased secretion of thyroxine from thyroid gland. Increased
concentration of thyroxine above the normal level in the blood depresses the
secretion of TSH from anterior pituitary.
Anterior pituitary ---
TSH
Thyroid gland
Thyroxine
b) Regulation of Blood Pressure:

Any deviation from normal blood pressure is sensed by Baroreceptors which feed the information
to cardiac and vasomotor centers in the brain. The centers will influence the activity of autonomic
nerves which will produce a response in opposite direction to stimulus.
Increase in Blood Pressure
Stimulation of Baroreceptors
Cardiovascular centers
Stimulation of Vagus & Inibition of sympathetic fibers
Decreased heart rate & vasodilation
Decrease in blood pressure.
(Opposite happens in condition of decrease in blood pressure)

Features of Negative feedback mechanisms:
1. Response decreases the strength of stimulus
2. Comprises most of regulating mechanisms (about 99%)
3. Participate only in physiological conditions
4. Occurs in conditions that need frequent monitoring & adjustment within physiological limits
Positive feedback mechanism:
- A stimulus(change in the environment) produces a response which inturn reinforces the
stimulus. This type of feedback mechanism positive feedback mechanism.
- Stimulus and response are in the same direction
- Consists of many variables. The first variable stimulates the second one which inturn
stimulates the next variable.
Examples:
a) Parturition:
Contraction of uterus push the foetus down Stimulation of uterine cervix  Nerve impulses to
hypothalamus  release of oxytocin  reinforces the strength of contraction of uterus. This goes on
till the baby is born
19
b) Blood clotting:
Activation of few clotting factors  activate other clotting factors in the coagulation cascade till the
blood clots.
Features of Positive feedback mechanisms:
1. Response increases the strength of stimulus
2. Comprises only 1% of regulatory mechanisms
3. Participate both in physiological & pathological conditions
4. Occurs in isolated conditions which do not require continuous monitoring
1
General physiology - Applied

Cell Physiology
1. What are G proteins? How does cholera toxin cause severe diarrhea?
‘G’ proteins are nucleotide regulatory proteins that bind with GTP. Mostly present in the cell
membrane. They help in translating extracellular chemical signals into biological effects inside the
cell.
‘Cholera toxin’ binds to G protein in the intestinal epithelial cells and causes formation of large
quantity of cAMP which activate chloride channels. Secretion of chloride into the intestine activate
sodium pump. Secretion of excess amount of sodium chloride causes osmosis of water into
intestine diarrhea
2. Why ions though of smaller size cannot diffuse through lipid bilayer?
The lipid bilayer of cell membrane is made of phospholipid molecules. The hydrophobic portion of
these molecules line up in the centre of the membrane .This layer is impermeable to water soluble
substances like ions, glucose and urea
Body Fluid Compartments
1. A patient admitted in casualty with 60% burns. What change would you expect in his body fluid
Compartment? Suggest a method to detect this change.
- Decrease in ECF compartment as plasma is lost from the capillaries in the damaged areas
- Estimation of hematocrit is a method to detect this change
2. Why do red blood cells swell and eventually burst when they are placed in a solution of 0.3 %
NaCl solution?
0.3 % NaCl solution is hypotonic to the cytoplasm of RBC. This may lead to osmosis of water into
the cell. So the RBCs swell and burst
3. Following diarrohea a patient develops dehydration and metabolic acidosis
a. In which compartment there is decrease in fluid volume
b. What is the course of metabolic acidosis?
a) Extracellular fluid compartment
b) In diarrhea there is excessive secretion of bicarbonates. This loss of bicarbonates leads to
metabolic acidosis
4. Give the reason for generalized edema in hypoprotinemia
Hypoproteinemia
↓
Less colloidal osmotic pressure
↓
Increased filtration of fluid from capillaries
↓
Accumulation of fluid in the interstitial spaces (edema)
5. Which of the body fluid compartments gets expanded in generalized edema? List any two causes
of edema
a) - interstitial fluid ( ECF)
b) -causes of edema
1) increase in capillary hydrostatic pressure Eg. Hypertension
2) decrease in colloidal osmotic pressure of blood Eg. Hypoproteinemia
in nephrotic syndrome
6. Explain why in a dehydrated patient intravenous infusion of 5% glucose is better than 10%
glucose
As 5% glucose is isotonic to body fluid it will not upset the osmotic equilibrium of the body where
as 10% glucose is hypertonic to body fluid which may cause shrinkage of cells
2
7. Explain the various forces that operate to prevent edema formation in tissue spaces
a) Low compliance of interstitium when the interstitial fluid pressure is in the negative pressure
range
b) The ability of lymph flow to increase 10-50 fold
c) Washdown of interstitial fluid protein concentration which reduces interstitial fluid colloidal
osmotic pressure
8. Intake of salty food is followed by feeling of thirst. What is the mechanism of stimulation of
thirst centre in this case?
Salty food - Hyperosmolarity of body fluids
↓
Stimulation of osmoreceptors
↓
Stimulation of thirst centre
9. What is edema? What are its causes?
Edema refers to the presence of excess fluid in the body tissues mainly in the extracellular fluid.
Causes:
1. Increased capillary pressure e.g Hypertension in acute or chronic kidney failure
2. Decreased plasma proteins E.g Protenuria in kidney disease (Nephrotic syndrome),
liver disease
3. Increased capillary permeability e.g Presence of toxins, bacterial infections, Vit . C
deficiency, prolonged ischemia & burns
4. Blockage of lymph return e,g Cancer, Filarial infection, surgery
10. Explain, why is dehydration common and usually fatal (if not treated immediately) in children.
The absolute volume of ECF is less in children compared to adults. So even a slight
decrease in ECF leads to drastic dehydration in children.
Moreover, dehydration is common & fatal in children for the following reasons:
- Body surface area of an infant is relatively greater than that of an adult which increases the
water loss significantly through the skin
- The breathing rate of an infant is higher (30-60 times/minute), which causes greater loss of
H2O from the lungs
- Kidneys of the newborn are only 50% efficient compared to adult kidneys.
- Hence the newborn & infants cannot conserve water by concentrating urine
11. A severely dehydrated child with diarrhea and vomiting was brought to the emergency. The
presenceof vibrio cholerae in the stool confirmed the diagnosis of cholera.
i. How does Vibrio cholerae cause diarrhea?
ii. Why dehydration is common and fatal in children?
Answer already discussed
12. What is normal saline? What is its clinical importance?
0.9 % sodium chloride solution is normal saline. It is isotonic to human blood plasma. So it can be
infused into the body in case of dehydration to restore the body fluid volume with out upsetting the
osmotic equilibrium of the body cells .
Transport AcrossThe Membrane
1. Name the sites where sodium and glucose are co transported. How is this principle used in oral
rehydration therapy.
Intestinal epithelial cells & renal tubular epithelial cells are the sites where sodium & glucose are
cotransported. As both substances are osmotically active particles, they increase the absorption of oral
rehydration fluid in the intestine. This will help to restore the body fluid volume effectively.
2. How would having a fever affect body processes that involve diffusion?
The body processes that involve diffusion will increase in fever as temperature increases the rate of
Diffusion
3
3. Compare the ion transport in air way epithelium of a normal individual with a patient with cystic
Fibrosis
- In normal individuals the sodium is not absorbed in the airway tract.
- In a patient with cystic fibrosis, a chloride channel is depressed which increases the absorption of
sodium & chloride in the air way tract.
4. What would happen if Na+-K+ pump does not function?
1. Failure of pumping back of sodium outside the cell accumulation of sodium inside the cell 
hypertonicity of cytoplasm  draws fluid from outside  increase in cell volume
2. Resting membrane potential will not be maintained
5. Why the rate of diffusion for CO2 is 20 times more than that of O2?
The rate of diffusion of CO2 is 20 times more than that of O2 as solubility of CO2 in lipid bilayer is
higher than that of O2
6. Give any one example of secondary active transport across biological membrane. How is this
knowledge made use of clinically?
Example for secondary active transport: Sodium – glucose co transport.
This is used in oral rehydration therapy which will increase the absorption in the intestine. This will
help to restore the volume of body fluid which is lost in dehydration
What are Starling’s forces? How they help in tissue fluid formation? Explain Starling’s hypothesis
in connection with the passage of fluid across capillary wall
Starling’s forces:
The forces that act across the capillary membrane are called starling’s forces. They influence the
filtration and absorption of fluid across the capillary. The Starling’s forces are:
1) Capillary hydrostatic pressure (Pc) – Favors filtration
2) Capillary colloidal osmotic pressure (c) – Opposes filtration & favors absorption
3) Interstitial fluid hydrostatic pressure (Pi) – Opposes filtration when it is positive (but
usually it is negative)
4) Interstitial fluid osmotic pressure (if) – Favors filtration (but the pressure is negligible)
Tissue fluid formation:

Tissue fluid or Interstitial fluid is formed by net filtration of fluid from capillary into interstitial
space
Net Filtration= Kf X (Pc+ if) –(c +Pif)
Net filtration through the muscle capillary:

4
Arterial end of capillary:

(As the capillary hydrostatic pressure is higher than oncotic pressure, filtration occurs&
tissue fluid is formed)
Venous end of capillary:

(As the oncotic pressure is higher than capillary hydrostatic pressure, absorption of tissue
fluid occurs)
Excess tissue fluid is returned to the blood vessels via the lymphatic system.
1
NERVE PHYSIOLOGY
10 Marks
1. What is action potential? Describe the phases of action potential with a proper diagram and
labeling. Write the properties of AP.
5 Marks:
1. What is Resting Membrane Potential? Describe the factors responsible for its genesis and
maintenance or causes for the resting membrane potential
2. Explain the mechanism of propagation of the action potential along a nerve fiber with a
suitable diagram
3. Classify nerve fibers
4. Describe the properties of nerves
5. Describe the degenerative & regenerative changes in a peripheral nerve after cut injury. Or
describe Wallerian degeneration Or describe briefly the structural and functional changes that
occur after sectioning of a nerve
6. Explain the structure of a synapse with suitable diagram and also the mechanism of
transmission of a nerve impulse across the synapse
7. Outline the properties of synapses
8. Describe synaptic inhibitions & facilitation
9. Differentiate the process of conduction of impulse in myelinated and in non- myelinated nerve
fibers. Give 2 advantages of conduction in myelinated nerve fibers
10. Define motor unit. What are the effects of denervation in a skeletal muscle. Explain what
happens in the inflammatory myopathy called ‘Poliomyelitis’
11. Explain the factors affecting conduction velocity in nerve fibers
12. Explain how the nerve conduction study, strength- duration curve and EMG are made use of
in assessing the function of nerve and muscle
3 Marks:
1. Outline the functions of various types of neuroglial cells
2. Explain the role of electrotonic potentials in saltatory conduction
3. With the help of a suitable diagram explain the compound action potential recorded from a
mixed nerve fiber or Give the Basis of Compound Action potential
4. Why regeneration does not occur in the central nervous system?
5. Define the terms All or none law and refractory period as applicable to different
excitable tissues
6. How do the absolute and relative refractory periods correlate in time with the various
phases of action potential? Why the excitability of a nerve is reduced during these
periods?
7. Give the physiological basis of Saturday night palsy where there is muscle weakness &
diminished sense of touch & pressure. Pain is not affected
8. Mention the intracellular concentration of Na+ & K+ and what happens to RMP when
extracellular concentration of K+ is increased from 5 to 10 meq/lt
9. In a tabular column give the susceptibility of different types of nerve fibers to hypoxia,
pressure & local anaesthesia.
NERVE PHYSIOLOGY 2013
1. ACTION POTENTIAL
Definition: Transient change in the resting membrane potential caused by electro chemical
changes across the membrane when the membrane is excited by a threshold stimulus
It is a property of excitable cells( nerve cells and muscle cells)
Resting membrane potential
• RMP is the electrical potential across living cell membranes at rest
• varies between –70mv to 100mv
Genesis of action potential
• depolarization – reversal of polarized state i.e., decrease in electronegativity of the interior of
the resting cell
• repolarization – return of RMP to negative value
• depolarization beyond threshold leads to action potential
• action potential is all or none principle
depolarization exceeds threshold
↓
sodium channels open
↓
sodium ions rush in
↓
membrane potential reverses
↓
shifts from -70 mv to +60 mv
↓
as membrane potential reaches +40mv , the
sodium channels close and are inactivated
↓
potassium channels open
↓
Potassium ions diffuse out
↓
membrane repolarizes
↓
Membrane potential returns to negative value (-70mv)
5 7
4 8
-55 mv
1 3
-70 mv 9
2
PHASES OF ACTION POTENTIAL
1. Stimulus artifact
2. Latent period
3. Slow depolarization
4. Firing level
5. Rapid depolarization
6. Spike potential
7. Rapid repolarisation
8. Slow repolarisation
9. Hyperpolarisation
IONIC BASIS OF ACTION POTENTIAL
Stimulus artifact – A brief irregular deflection of the baseline at the beginning of
recorded AP. It marks the point of stimulus
Latent period – the period between the application of stimulus and the beginning of
action potential. This is the time taken by the impulse to travel along the axon.
Slow depolarization – This is due to Na+ influx through the sodium leakage channels
Firing level – The point at which the rate of depolarization increases
Rapid depolarization – This is due to rapid entry of Na+ through voltage gated Na+
Channels
Spike potential – The sharp rise and rapid fall are the spike potential of the axon
Rapid repolarization – This is due to rapid exit of K+ through the voltage gated K+ channels
After depolarization – a slower fall of potential at the end of repolarisation. This is due
to slow exit of K+
After Hyperpolarization – Overshooting of tracing in the hyperpolarizing direction. This is
due to continuous efflux of K+ through slow K+ channels
5 MARKS
1. RESTING MEMBRANE POTENTIAL ( RMP)
Definition : The potential difference existing across the cell membrane when the cell is at rest is
called resting membrane potential
RMP of different cells:
Nerve fibers = -70 mv
Skeletal muscle fiber = -90 mv
Smooth muscle fiber = -50 mv
Cardiac muscle fiber = -90 mv
Genesis of RMP:
a) K+ Efflux: K+ is mainly responsible for the development of RMP. The membrane is
more permeable to K+ than Na+ (50 times). As a result a lot of K+ can
diffuse out creating negativity inside the cell (- 94 mv)
b) Na+ influx: Na+ that enters in to the cell may neutralize up to 8 mv
c) Cl- influx : Though membrane is more permeable to chloride ions its entry is
checked by electronegativity inside the cell
+ +
d) Na - K Pump:
Direct role – Pumps 3Na+ out and 2k+ in creating a negativity inside (- 4 mv)
Indirect role – Maintains the gradient for Na+ and K+ across the membrane so that
they can passively diffuse to the other side and cause RMP
Summary of net effect:
K+ diffusion to outside = - 94 mv
+
Na diffusion to inside = + 8 mv
Cl- diffusion to inside = 0 mv
Na+ - K+ Pump = - 4 mv
Net effect = +90 mv
Significance of intracellular proteins:
- Proteins carry negative charges
- Proteins are non diffusible anions
- Proteins remain inside the cell
Because of the above properties, intracellular proteins contribute to electronegativity inside the
cell (RMP) to some extent
2. CONDUCTION OF NERVE IMPULSE
• The action potential generated at the initial segment of the axon is conducted along the axon to
the nerve terminals
• Conduction of nerve impulse takes place in sequential depolarization of the adjacent area of the
nerve fiber
CONDUCTION IN UNMYELINATED FIBERS
• Explained by LOCAL CIRCUIT THEORY
• Conduction is by spread of +ve curent to adjacent area of membrane interiorly
• Exteriorly the circuit is completed
• This local circuit current reduces the membrane potential to firing level, increasing the sodium
permeability and the adjacent area becomes active(depolarized)
• When depolarisation reaches threshold, an action potential is produced
• Thus, by local circuit current flow, an active region stimulates the adjacent inactive regions to the
threshold.
• The impulse is conducted in both directions at constant speed
CONDUCTION IN MYELINATED NERVE FIBRES (SALTATORY CONDUCTION)

• The myelin sheath acts as an insulator. It does not allow passage of any ions through the
membrane. So the conduction of impulse is not continuous as in unmyelinated fiber
• The nerve impulse is conducted from one node of Ranvier to the next node of Ranvier
• The action potential “jumps” from one node to the next. Hence called saltatory conduction
• Local circuit current flows between active and inactive node
Advantages of saltatory conduction
• Conduction velocity in myelinated fibres is greater than conduction velocity in unmyelinated
fibres. This helps in faster conduction of impulses
• Energy is saved as sodium potassium pumps are only required at specific points along the axon.
3. CLASSIFICATION OF NERVE FIBRE
• Structure:
• Myelinated nerve fibre 8
• Non mylinated nerve fibre
• Distribution:
• Somatic-supply the muscles of the body
• Visceral or autonomic –supply varies internal organ.
• Origin:
• Cranial nerves – arise from the brain
• Spinal nerves – arise from the spinal cord
• Functional:
• Motor – carry motor impulses from the CNS
• Sensory – Carry sensory impulses towards higher centre.
Numerical classification
Number Origin
I–a Muscle spindle, annulospiral ending
I–b Golgi tendon organ
II Muscle spindle–flower spray ending

Touch, pressure
III Pain, temperature
IV Pain and other receptors

Erlanger gasser classification
Fibre type Function Diameter (µm) Conduction

velocity(m / s)
A-α Proprioception, 12 – 20 70 – 120
Somatomotor
A-β Touch, Pressure 5 – 12 30 – 70
A-γ Motor to spindle 3–6 15 – 30
A-δ Pain, temperature, touch 2–5 12 – 30
B Preganglionic autonomic 3 3–5
C Dorsol root pain 0.4 – 1.2 0.5 – 2
4. Describe the degenerative changes in a peripheral nerve after cut injury. Or describe Wallerian
degeneration
• When a peripheral nerve is cut, the part of the nerve separated from the cell body (i.e., distal part)
shows a series of chemical and physical degenerative changes called as Wallerian degeneration.
Early Phase(1st -7th day):
Functional changes:
– Changes in the enzymatic activity (choline acetylase & acetyl choline esterase)
– Decrease in the activity of ionic channels
– Decrease in the conduction velocity
– Failure in the conduction of nerve impulse
Late Phase (8th – 32nd day)
– Neurofibrils disappear
– Axis cylinder swells & breaks into fragments
– Debris collects in the axis cylinder place
– Myelin sheath slowly disintegrates into fat droplets
– Neurilemma remains intact
– Schwann cells proliferate rapidly
– Macrophages remove debris of axis cylinder
– Neurilemmal tube becomes empty (ghost tube)
– Schwann cell cytoplasm fills the neurilemmal tube
Changes in cell body:
– Starts after 48 hrs of nerve injury
– First nissle granules disintegrates into fragments - chromatolysis
– Golgi apparatus disintegrates
– Cell body swells due to accumulation of fluid and becomes round.
– Nucleus is pushed to the periphery.
Changes in the proximal part:
-- Same degenerative changes as in the distal part (anterograde degeneration)
Regenerative changes in nerve following injury.
- Sprouting of a large number of small branches from the cut fibers
- Entry of some of these branches into the peripheral stump
- Proliferation of Schwann cells & formation of continuous tubes. This bridges the gap
between proximal & distal stumps
- The growth of filaments is also guided towards the periphery
- When one branch grows in to the periphery, the other branches degenerate
- The growth towards denervated fibers is due to some chemical attraction called
neurotropism
- Myelin sheath begins to appear in about 15 days and proceeds peripherally
- Complete functional recovery takes 3 years
5.COMPOUND ACTION POTENTIAL
Compound action potential is a multipeak potential recorded from a nerve trunk.
Basis of compound action potential:
A nerve trunk is made up of different group of fibers.
Each group of nerve fibers has different conduction velocity. Hence the
impulses reach the recording electrode at different times. The first peak belongs to
fast conducting fibers & the last peak belongs to slow conducting fibers
excitable tissues
The excitable tissues are nerve and muscle.
All or none law states that the tissue is excited to maximum by a threshold stimulus & do
not respond at all to a subthreshold stimulus.
All or none is applicable to a single nerve fiber, a single skeletal muscle fiber & whole
cardiac muscle
Refractory period is the period of excitation during which the tissue does not respond to
a second stimulus.
For nerve fibers, the absolute refractory period is from firing level to 1/3 of repolarization
& for skeletal muscle fibers, the absolute refractory period is first half of latent period.
But for cardiac muscle fiber, the whole of contraction period is refractory period. This
long refractory period of cardiac muscle does not allow it to go for tetanic contraction
Neurolemma, the outermost layer surrounding the myelin sheath of an axon is found
only in peripheral nerve fibers, Presence of this layer is must for nerve regeneration.
Absence of this later in CNS does not allow regeneration in CNS
1
NERVE PHYSIOLOGY – 3 marks

1. Outline the functions of various types of neuroglial cells
Neuroglia are supporting cells of nervous system
Six types of supporting cells – 4 in CNS and 2 in the PNS
• Neuroglia in the CNS
• Astrocytes
• Microglia
• Ependymal Cells
• Oligodendrocytes
• Neuroglia in the PNS
• Satellite Cells
• Schwann Cells
Functions
• Provide support for neurons
• Produce myelin sheath which insulate neurons (oligodendrocytes &
Schwann cells)
• Produce chemicals that guide young neurons to the proper connections
• Promote health and growth of neurons
• Take part in forming blood brain barrier ( astrocytes)
• Act as phagocytes of brain ( microglia)
2. Explain the role of electrotonic potentials in saltatory conduction
Application of current through the electrodes (anode & cathode) produces
changes in the membrane potential.
- anodal current produces hyperpolarizing potential
- cathodal current produces depolarizing potential.
These potential changes are called Electrotonic potentials
Role of Electrotonic potentials in saltatory conduction:
The action potential at one node electrotonically depolarize the next node to firing
level. This is done by drawing off the positive charges from outside of the
membrane.
3. With the help of a suitable diagram explain the compound action potential recorded
from a mixed nerve fiber or Give the Basis of Compound Action potential
Compound action potential is a multipeak potential recorded from a nerve trunk.
Basis of compound action potential:
A nerve trunk is made up of different group of fibers. Each group of nerve fibers has
different conduction velocity. Hence the impulses reach the recording electrode at different
times. The first peak belongs to fast conducting fibers & the last peak belongs to slow
conducting fibers
Neurolemma, the outermost layer surrounding the myelin sheath of an axon is found only in
peripheral nerve fibers, Presence of this layer is must for nerve regeneration. Absence of this
later in CNS does not allow regeneration in CNS
excitable tissues
The excitable tissues are nerve and muscle.
All or none law states that the tissue is excited to maximum by a threshold stimulus &
do not respond at all to a subthreshold stimulus.
All or none is applicable to a single nerve fiber, a single skeletal muscle fiber &
Whole cardiac muscle
Refractory period is the period of excitation during which the tissue does not
respond to a second stimulus.
2
For nerve fibers, the absolute refractory period is from firing level to 1/3 of repolarization
& for skeletal muscle fibers, the absolute refractory period is first half of latent period.
But for cardiac muscle fiber, the whole of contraction period is refractory period. This
long refractory period of cardiac muscle does not allow it to go for tetanic contraction
6. How do the absolute and relative refractory periods correlate in time with the various
phases of action potential? Why the excitability of a nerve is reduced during these
periods?
Correlation of refractory period to the timing of Action potential:
Refractory period: The period of action potential during which the nerve fiber does
not respond to second stimulus is called refractory period.
Absolute Refractory period: Period during which even the strongest stimulus
fails to excite. Corresponds to the period from firing level to one third of
repolarization. This includes rapid depolarization & rapid repolarisation
Relative refractory period: Period during which a stronger second stimulus can
excite the nerve. Corresponds to the period from the end of absolute refractory
period to the start of after depolarization
Reason for reduced excitability during refractory period:
The sodium channels which are activated & opened during the excitation are not
deactivated until the repolarisation is partially completed.
7. Give the physiological basis of Saturday night palsy where there is muscle
weakness & diminished sense of touch & pressure. Pain is not affected
Saturday night palsy is due to the effect of mechanical pressure or compression on
Radial nerve. Type A fibers are more susceptible to pressure followed by type B
fibers. That is why there is muscle weakness (motor neuron – Type A) & diminished
sense of touch & pressure ( type B) . The least affected fibers are type C fibers which
carry pain sensation. So pain is not affected
8. Mention the intracellular concentration of Na+ & K+ and what happens to RMP when
extracellular concentration of K+ is increased from 5 to 10 meq/lt
- Intracellular concentration of Na+ -- 14 meq / lt. & K+ -- 142 meq/ lt
- When extracellular concentration of K+ is increased from 5 to 10 meq/lt, the
concentration gradient of K+ is reduced. So exit of K+ is stopped. This decreases the
RMP & excitability of nerve is reduced.
9. In a tabular column give the susceptibility of different types of nerve fibers to hypoxia,
pressure & local anesthesia.
Susceptibility Most Intermediate Least susceptible

for: susceptible
Hypoxia B A C
Pressure A B C
Local C A B
anesthetics
1
MUSCLE PHYSIOLOGY K.SENTHAMIL SELVI

10 marks
1. NEUROMUSCULAR JUNCTION
Neuro Muscular Junction is the junction between a motor nerve ending and a
muscle fiber
Physiologic Anatomy
- Terminal buttons(End Feet) – Divisions at the end of axon of motor neuron
- Synaptic gutter - the depression on the skeletal muscle fiber in which the
axon terminal lies
- Motor end plate - the thickened part of the muscle membrane (sarcolemma)
which makes a close contact with the axon terminal
- Junctional folds - folds of motor end plate
- Presynaptic membrane – membrane of the axonic terminal which is in
connection with the muscle fiber
- Postsynaptic membrane - muscle membrane
- Synaptic cleft - The space between the two membranes
- Synaptic vesicles – Vesicles containing the neurotransmitter Acetyl choline
at presynaptic nerve terminal
- Ach receptors – Receptors found on the post synaptic membrane)
Synaptic gutter
Motor End plate
Events in transmission
Arrival of nerve impulse (action potential) at the presynaptic nerve terminal

↓
Depolarisation of the presynaptic nerve terminal
↓
2
Opening up of the Ca++ channel and entry of calcium into the presynaptic membrane
↓
Release of the neurotransmitter (Ach) from vesicles into the synaptic cleft
↓
Fusion of the synaptic vesicle with the presynaptic membrane
↓
Rupture of vesicles & release of Ach into the synaptic cleft
↓
Binding of the Ach with the receptors on the post synaptic membrane
↓
Permeability of post synaptic membrane to Na+ increases
↓
Depolarisation of the post synaptic membrane-generation of a local potential - End Plate
Potential (non propagated)
↓
End Plate Potential reaches threshold & an action potential is produced which is
propagated.
DRUGS ACTING ON NMJ
1. Neuro Muscular Blockers
a) Inhibition of Ach release
Botulinum toxin –
A bacterial toxin which inhibits the synthesis or release of Ach
b) Antagonizing the action of Ach
Tubocurarine
By competitive inhibition. Both curare and Ach compete for the same
nicotinic receptor
c) By persistent Depolarisation
Suxamethonium(Succinyl choline)
Causes local energy exhaustion resulting in muscle relaxation
 Bungarotoxin
By irreversible combination with the receptor
2. Drugs that stimulate Transmission
a) By inactivating Anticholinesterase:
Neostigmine, Physostigmine- Prolonged depolarisation
Used in treating Myasthenia gravis
b) Di isopropyl flurophosphate-
Used in insecticides. Inactivates Anticholinesterase in an irreversible manner.
2.EXCITATION-CONTRACTION COUPLING
DEFINITION:
The process in which depolarization of the muscle fiber initiates its
contraction is called excitation-contraction coupling.
i.e electrical phenomenon is converted in to mechanical phenomenon.
Nerve Action Potential
↓ Neuromuscular transmission
Muscle Action Potential
3
↓ Excitation contraction coupling

Muscular contraction
EVENTS
• Release of Acetylcholine from nerve terminal

• Binding of acetylcholine to the receptors present on the motor end plate
• Increased Na+ and K+ conductance in end- plate membrane
• Generation of end plate potential
• When the end plate potential reaches the firing level  generation of action
potential in muscle fibers.
• Spread of depolarization along T tubules to interior of the musclefiber
• Change in configuration of DHP receptors in membrane of “T” tubule  opens
ryanodine receptors (Ca2+ channels) of cisternae release of calcium into the
cytosol
• Ca2+ diffuses to thick and thin filaments.
• Thin actin filaments slide over the thick myosin filaments
• Z lines come closure  Shortening of sarcomere Muscle contraction
Action potential
Motor end plate
Cisternae
3. MECHANISM OF MUSCULAR
CONTRACTION
EVENTS DURING MUSCULAR CONTRACTION
 Electrical events
 Mechanical events
4
 Chemical events
 Thermal events
ELECTRICAL EVENTS
• Transmission of nerve impulse to muscle across NMJ
• Excitation of muscle  development of muscle action potential
• Transmission of muscle action potential through “T” tubules to interior of muscle fiber
• Change in configuration of DHP receptors in membrane of “T” tubule  opens
ryanodine receptors (Ca2+ channels) of cisternae release of calcium into the cytosol
MECHANICAL CHANGES OR MOLECULAR EVENTS (FORMATION OF ACTO-
MYOSIN
COMPLEX)
• Explained by sliding filament theory-proposed by Huxley and Huxley in
1969. Most accepted theory
• States that muscular contraction is due to sliding of actin filaments over the
myosin filaments.
• The sliding reduces the length of sarcomere from its resting length of 2.2 µ to 1.5
µ
• Involves two important sequences:
• Exposure of myosin binding sites of actin molecules
• Cross bridge cycle
Exposure of myosin binding sites of actin molecules
• Binding of calcium to troponin C
• Conformational change of troponin C. (no longer can keep the tropomyosin on actin)
• Lateral movement of tropomyosin – troponin complex from actin filaments
Cross bridge cycle
1. Activation of myosin ATPase enzyme in the head of myosin molecule
2. Hydrolysis of an ATP molecule  release of energy  activation of myosin crossbridges
Hydrolysis
3. ATP ----------- ADP + P + Energy
4. Binding of crossbridges (myosin head) to the actin filaments
5. Bending of myosin head when ADP and P are released from the crossbridges  pulls the
actin filament towards the centre of sarcomere (powerstroke)
6. Binding of another ATP molecule  detachment of crossbridges from actin filaments
7. Binding of another ATP molecule  Attachment of crossbridge to another distal actin
molecule
CROSSBRIDGE CYCLE
Attachment – Swivel (power stroke) – detachment – attachment again.
RELAXATION OF MUSCLE
• Depends on reuptake of Ca2+ into sarcoplasmic reticulum (SR)
• Acetylcholinesterase breaks down ACh at neuromuscular junction
• Muscle fiber action potential stops
• When local action potential is no longer present, Ca2+ is pumped back into sarcoplasmic
reticulum
• Troponin-tropomyosin move back to their position and cover the active sites of actin
filaments.
 Interaction between the actin & myosin ceases

5
 The muscle relaxes

 The cycle repeats
 Actin filaments slide over the myosin
 Maximum contraction occurs when there is a maximum overlap between the actin
and the cross bridges of the myosin filament. This occurs at the normal resting
length of the muscle (2.2um)
CHEMICAL EVENTS (Energetics of muscle contraction)

• Energy is provided by hydrolysis of ATP & creatine phosphate
• Glycogen stores in the muscle are utilized for resynthesis of ATP
• Glucose and fatty acids are also utilized for energy production
Contraction-Relaxation Steps Requiring ATP
• For binding of myosin crossbridges to actin filaments
• Detachment of crossbridges from actin filaments
• Active transport (Pumping) of Ca2+ back into sarcoplasmic reticulum
THERMAL EVENTS DURING CONTRACTION
• Resting heat: Heat produced during resting state
• Initial heat:
– Activation heat:- Heat produced by chemical changes in the muscle before
the actual contraction
6
– Shortening heat:- Heat produced by shortening of muscle (mechanical

event during contraction)
• Recovery heat: Heat produced by chemical changes in the muscle during
recovery period (restoration to precontractile state)
• Relaxation heat: Heat produced by mechanical changes in the muscle during
relaxation
5 MARKS
MYASTHENIA GRAVIS – Discussed in applied
3 MARKS
1.SARCOMERE
Sarcomere is the contractile unit of the muscle fiber. It is the distance between two “Z”
lines. It consists of “A” band at the center and half of the “I” band at the sides. “A” band
is made up of thick myosin filaments and “I” band is made up of thin actin filaments.
The length of sarcomere at rest is about 2.5 µm. During muscle contraction the length of
sarcomere reduces to 1.5 µm. During stretching it increases in length to 3.5µm.
2. MOTOR UNIT
Definition: A single motor neuron with all its axonic terminals and the muscle fibers
supplied by it
Size principle:
The size of the type I motor unit is larger i.e., the number of muscle fibers supplied
by a single motor neuron is high. Type I motor unit controls the gross movements & the
muscle fibers involved are slow red muscle fibers.
7
The size of the type II motor unit is smaller i.e., the number of muscle fibers
supplied by a single motor neuron is low. Type II motor unit controls the fine skilled
movements & the muscle fibers involved are fast white muscle fibers.
3.SMOOTH MUSCLE CONTRACTION
Steps involved:
1. Depolarisation of smooth muscle fibers

2. Release of calcium from sarcoplasmic reticulum
3. Calcium bind to “Calmodulin”(calcium binding protein in smooth
muscle fibers)
4. This calcium- calmodulin complex activates myosin light chain
kinase
5. The enzyme light chain kinase causes phosphorylation of myosin
6. Sliding of actin over myosin
1
MUSCLE PHYSIOLOGY Applied

1. What is the physiological basis of administration of Neostigmine to a patient with
myasthenia gravis?
Neostigmine inhibits the action of acetylcholine esterase enzyme. So acetylcholine molecules
bind to the receptors for a long time. This increases the degree of contraction in Myasthenia
Gravis where there is weak contraction in muscles
2. Name the drugs that interfere with neuro-muscular transmission
Neuro Muscular Blockers
Botulinum toxin – a bacterial toxin
Tubocurarine & Gallamine(Flaxedil)
Suxamethonium(Succinyl choline) By irreversible combination with the receptor
 Bungarotoxin
Drugs that stimulate Transmission
• Neostigmine & Physostigmine
• Di isopropyl flurophosphate
3. What would happen if ATP were suddenly not available after the sarcomere had
started to shorten.
Muscle relaxation is also a energy consuming process .The non availability of ATP after the
muscle had started to shorten will not allow the muscle to relax. So the muscle will remain
rigid.
4. Explain the basis of the use of curare form of drugs as muscle relaxants and the
use of anticholinestrases in treatment of myasthenia gravis
- Curare form of drugs block the neuromuscular transmission by competitive inhibition
thus causing the muscle to relax
- Anticholinestrases inhibit the action of acetylcholine esterase enzyme. So acetylcholine
molecules bind to the receptors for a long time. This increases the degree of contraction in
Myasthenia Gravis where there is weak contraction in muscles
5. What is rigors mortis? What is its clinical significance?
Rigidity after death is called rigor mortis. Clinical significance – to find out the time
of death
6. A man after prolonged illness died. Several hours after death, his body becomes
rigid.
What is that phenomenon called?
Why rigidity occurs after death?
i) Rigor mortis
ii) Unavailability of ATP . The non availability of ATP after the muscle had started to
shorten will not allow the muscle to relax. So the muscle will remain rigid.
7. Atropine, a parasympatholytic, can inhibit the acetylcholine action at heart, not
at neuromuscular junction – Explain
Atropine binds to muscarinic receptor found on heart and inhibits the action of
parasympathetic where as the receptor found in neuromuscular junction is nicotinic
receptor. Atropine does not bind to nicotinic receptor
8. Explain the medicolegal importance of “Rigor Mortis”
Rigor mortis is development of rigidity of body after death. Rigidity develops 4-5
hours after death and disappears within 24 hours. This is useful in finding out the time of
death
9. Why tension is at maximal at a sarcomere length of 2.2 micro meter?
Maximum contraction occurs when there is a maximum overlap between the actin
and the cross bridges of the myosin filament. This occurs at the normal resting
length of the muscle (2.2um)
2
10. Explain the pathophysiology of myasthenia gravis

Myasthenia gravis is an autoimmune disorder characterized by inability of
neuromuscular junction to transmit signals from nerve fiber to muscle
Cause: Antibodies against acetylcholine receptors on motor end plate
Features:
- Paralysis of skeletal muscles involved leading to extreme weakness
- Initially the muscles affected are eye, facial, pharyngeal & esophageal
muscles leading to ptosis, diplopia, toneless voice, chewing & swallowing
- Muscle strength is greatest in the morning and least in the evening
- EMG recorded on continuous effort shows a gradual decline in the
amplitude of potentials
Treatment:
a) Neostigmine & Physostigmine (anticholinesterase) – destroys acetylcholine
esterase & potentiates the effect of acetylcholine on the end plate
b) Edrophonium – a weak anticholinesterase enzyme
c) Steriods – destroy lymphocytes & there by reduce the antibody titre
d) Azathioprine – Immunosuppressive drug which reduces antibodies
e) Ambenonium - anticholinesterase
11. A female patient of 40 yrs. age complains of drooping of eye lid and general
weakness and fatigue that aggravates towards evening, but improves after
rest or sleep. What could be your provisional diagnosis and what is the
nature of dysfunction? Give the physiological basis of use of a drug in this
condition.
Diagnosis : Myasthenia gravis .
Drug: Neostigmine (anticholinesterase) – destroys acetylcholine esterase &
potentiates the effect of acetylcholine on the end plate
12. Two patients A & B, both with the muscle weakness, reported the ortho clinic.
On taking case history, however, A reported the weakness worsening as the
day pass on, while B revealed – in the morning it is worst and as the day
passes on he gets improvement.
Diagnose the two clinical conditions and the possible reason for patient A and
how it can be treated?
Diagnosis :
Patient A – Myasthenia gravis
Patient B – Lambert-Eaton syndrome
Reason & Treatment of myasthenia gravis already discussed
13. What will be the process of ‘Rigor mortis’ in a person who has undergone death
after a violent struggle. Why?
‘Rigor mortis’ develops very early. Because the ATP molecules are utilized during
struggle, the ATP availability will be very less. This causes the rapid development of
rigor mortis
BLOOD
10 marks :
1. Describe the stages of erythropoiesis with the help of suitable diagrams. Discuss about the factors
regulating it
2. Define and classify immunity. Discuss in detail about cell mediated and humoral immunity
3. Describe the structure of different types of leucocytes with suitable diagrams and list out their
functions. Add a note on the normal count of each type of cell and conditions in which their count
increase & decrease
4. Describe the role of platelets in hemostasis
5. What are the main clinically important blood groups? What is the physiological basis of blood
grouping? Discuss the applications of blood groups. What are the hazards of blood transfusion?
6. Define hemostasis. Discuss the events involved in it
7. Enumerate the clotting factors. Explain the mechanism of intrinsic and extrinsic mechanism of
coagulation
5 marks:
1. List out the functions of plasma proteins
2. List out any 5 anticoagulants used & explain their mechanism of action
3. Describe the neutrophil response during inflammation
4. What are the factors that prevent intravascular coagulation? Or describe anticlotting mechanisms inside
a blood vessel or describe the mechanisms that maintain the fluidity of the blood inside the blood
vessels or natural anticoagulants
5. Describe about E.S.R. (Erythrocyte Sedimentation Rate)
6. Briefly describe the composition and functions of lymph.
7. Fibrinolytic system and its therapeutic usefulness.
8. Give an account on the following:
- Complement system
- Cytokines
- Hypersensitivity
- Immunological tolerance
9. Hazards of whole blood & mismatched blood transfusion
10. Bleeding disorders
11. Name the substances present in the granules of platelets. What are the functions of those substances?
3 marks:
General:
1. Explain the mechanism of action of heparin.
2. Give in the tabular column form agglutinogen and agglutinin present in O, AB, Rh+ and Rh- groups
3. What is plasmapheresis?
4. What is passive immunity?
5. Autologous transfusion.
6. Oral anticoagulants and their mechanism of action
1
BLOOD
1. ERYTHROPOIESIS
* Refers to the process of production and maturation of Red Blood
Cells (erythrocytes)
* Site of production – Red bone marrow of all the bones upto 20
years of life. After 20 years, only flat bones produce RBCs.
Stages of Erythropoiesis :
1. Hemocytoblast
2. BFU –E, Blast Forming Unit – E
3. CFU-E, Colony Forming Unit – E
4. Proerythroblast
5. Early normoblast
6. Intermediate normoblast
7. Late normoblast
8. Recticulocyte
9. Mature erythrocyte
1. Hemocytoblast:
- 18 – 23 um in diameter
- Large Nucleus
- Thin rim of basophilic cytoplasm
- Pleuripotent stem cells
2. Blast Forming Unit – E:
- Unipotent progenitor cell.
- Less Sensitive to Erythropoietin
3. CFU (E) – Colony Forming Unit
- Matured unipotent progenitor cell
- Highly sensitive to erythropoietin
4. Proerythroblast:
- 14-19 µm in diameter.
- Large nucleus with distinct nucleoli
- Basophilic cytoplasm.
- Vit B12 & Folic acid are required for the conversion of this stage into next stage.
5. Early normoblast;
- Dense nucleus
- Basophilic cytoplasm.
6. Intermediate normoblast:
- 10-12 µm in diameter
- more condensed nucleus
- Hb (Hemoglobin) is formed
- Polychromatophilic cytoplasm.
7. Late normoblast:
- Dense nucleus (Pyknotic)
- Nucleus extrudes after this stage & disintegrates
- Acidophilic cytoplasm.
8. Reticulocyte:
- Almost of the same size of matured RBC
- A small reticulum is seen in the cytoplasm.
10. Mature Erythrocyte:
- About 7.2 um in diameter.
- No nucleus
- Acidophilic cytoplasm
2
Regulation of Erythropoiesis
1. Erythropoietin a hormone secreted by kidneys
- Stimulates the bone marrow tissue to produce more RBCs.
2. Hypoxia: Lack of O2 is the main condition which stimulates erythropoietin secretion.
Lack of O2 (Hypoxia)
Kidneys
Erythropoietin
Red Bone marrow
RBC Production
Restoration of O2 Supply
3
3. Nutrients:
a) Proteins for synthesis of Hb.
b) Minerals:
i) Iron : for synthesis of heme part of Hb.
ii) Copper: for synthesis of Hb.
4. Vitamins:
a) Vitamins B12 & Folic Acid: Required for synthesis of DNA. These factors are called
maturation factors.
b) Vitamin C is also required.
5. Hormones:
Thyroxine stimulate erythropoietin
Glucocorticoids
Testosterone
Growth hormone RBC Production
Normal Count of RBC:

- Male 5-6 million/cu mm of blood
- Female 4.5 – 5.5 millions/cu mm of blood.
---------------------------------------------------------------------------------------------------------------------
2.WBC – White Blood Cells
Leucocytes (anucleated, colourless)
Granulocytes Agranulocyte
Neutrophils (50 - 70%) Monocyte (2-8%)

Eosinophils (1-4%)
Basophils (0-1%) Lymphocyte (20-40)
Cell Type Size Nucleus Cytoplasm

Neutrophil 10-14 u Multilobed Fine granules
(1-5 lobed) Purple coloured
Eosinophil 10-14 u Bilobed, Spectacle, Coarse granules brick
shaped red coloured
Basophil 10-14 u Bilobed ‘S’ shaped Thick granules, Blue
coloured , obscure or
mask the nucleus
Monocyte 15-20 u Kidney shaped, Abundant cytoplasm,
eccentric (towards no granules
periphery)
Lymphocyte 7-10 u Round Nucleus filling A Thin rim of
(Small) the cells cytoplasm
Large 12-16 u Large Round Nucleus Abundant cytoplasm.

4
Functions of WBCs:
1. Neutrophils: Phagocytosis
Process of Phagocytosis:
a. Margination The neutrophils slow down in the circulation and get attached to
the wall of capillary endothelium.
b. Diapedesis - Neutrophils squeeze through the pores of capillary wall and

enter the tissue.
c. Chemotaxis – Neutrophils are attracted towards the infected site by the

chemicals released from the site.
d. Phagocytosis – Neutrophils, when comes in contact with bacteria ,the

membrane invaginates & enclose around the bacteria.
Then the enclosed vesicle is pinched off from the membrane. This forms a phagosome.
This combines with lysosomes. Lysosome releases lytic enzymes which digest the contents of
phagosome.
5
Examples:
- Phagocytosis of bacteria.
- Phagocytosis of dead cells.
- Phagocytosis of antigen - antibody complex
- Phagocytosis of foreign particles like carbon particles, sodium urate crystals.
2. Eosinophil:
a. Anti-allergic – Eosinophils contain anti – inflammatory histaminase which
inactivate histamine.
b. Anti-Parasitic – Eosinophils contain a basic protein which destroys larval

parasites.
c. clot lysis – Eosinophils produce prefibrinolysin when activated, lyse the clot.
d. Phagocytosis – Engulf antigen – antibody complexes.
e. Detoxification: Certain foreign proteins are detoxified.
3. Basophil:
a) Release histamine which takes part in allergic reactions.

b) Release heparin which takes part in prevention of intravascular clotting.
4. Monocyte:
a. Enter the tissues & form tissue macrophages.
b. The main function of monocytes in circulation & tissues is phagocytosis.
c. Macrophages also co operate with B & T cymphocytes in both hormonal &
cell mediated immunity.
5. Lymphocytes:
B- Lymphocytes and T- Lymphocytes
B Lymphocytes: Take part in humoral immunity on exposure to antigens

B- Lymphocytes.
Plasma cells.
6
Secretion of antibodies
T. Lymphocytes: Take part in cell-mediated immunity
i) Rejection of foreign grafts
ii) Destruction of cancer cells
iii) T helper cells take part in humoral immunity.
iv) T Suppressor cells prevent auto immunity.
v) Major defence against bacterial, Viral & fungal infections.
--------------------------------------------------------------------------------------------------------------------
3. IMMUNITY
Definition: The resistance of the body to the diseases caused by micro organisms (infectious
diseases) is called immunity.
Classification:
Immunity
Innate immunity (inherent) Acquired immunity

(Skin, mucous, membrane, (after exposure to micro-
GIT secretions, Micro & Macrophages, organisms.)
Natural killer cells etc.)
Natural Artificial
Passive Active Passive Active

Transfer of antibodies - Clinical Injection of Vaccination
Through placenta to fetus Disease activated
& through colostrums - Sub clinical lymphocytes
infection & Serum with
antibodies
Humoral immunity Cell-mediated

Activation of B Lymphocytes Activation of ‘T’ Lymphocyte
Plasma cells Formation of 4 Types of T cells
Antibodies a) Cytotoxic ‘T’ cells

b)T helper
c)T Suppressor
d)T Memory cells
7
HUMORAL IMMUNITY
- B Lymphocytes participate in humoral immunity.

- on exposure to antigens  activation of B- lymphocytes to plasma cells  produce
specific antibodies against foreign antigens.
Mechanism pf Humoral immunity
- Antigen is fragmented by macrophages.
- A fragment of antigen binds to MHC Class II protein in the cell membrane of macrophages
and forms a complex.
- this complex is presented to the B cell by macrophages ( Antigen Presenting cell).
- Macrophage also secretes interleukin 1 which activates both T-Helper cells and B-
Lymphocytes.
- ‘T’ helper cells secrete IL2, IL4, IL5, IL6 (cytokines).
- these cytokines act on ‘B’ lymphocytes.
- ‘B’ Lymphocytes undergo proliferation & differentiation
- ‘B’ lymphocytes form plasma cells.
- Plasma cells produce specific antibodies.
Antibodies: Types Ig G, Ig A, Ig M, Ig D, Ig E.
1. Ig G antibodies:
- 75% of the total antibodies in the body.
- can cross the placenta.
- secreted into colostrum
- role in immunity in the fetus & the new – born.
2. Ig A Antibodies:
- 20% of total antibodies.
- present in mucosal secretions.
- protect the mucosal surface from infections.
3. Ig M antibodies:
- Mostly intra vascular.
- Destroy the organisms that enter the circulation.
4. Ig D antibodies
- Present in the surface of immature B- lymphocytes.
- help in the functional maturation of B- Lymphocytes.
5. Ig E antibodies:
- Present mainly on the surface of mast cells and basophils.
- Responsible for hypersensitive immune reactions (Allergy)
Functions of Antibodies:
1. Neutralisation of Antigen : - Antibodies neutralise the toxic effect of some bacterial

toxins.
2. Immobilization of bacteria: Immobilise the cilia or flagella of motile bacteria.
This limits the spread of disease.
3. Enhancement of phagocytosis: (Opsonisation):
- Ig G antibodies form an attachment to the antigen and enhances the phagocytic
activity of neutrophils and macrophages.
4. Antibody dependant cellular cytotoxicity:
- Antibodies link the target cells with Natural killer cells which kill the targets
secreting toxic chemicals.
5. Agglutination & Precipitation of antigen:
By cross linking antibodies make the pathogens to clump together (agglutination) &
the soluble antigens to form precipitation. This helps in easy phagocytosis.
6. Activation of complement:
- Antibodies bound to antigens activate a group of proteins in the plasma called
complement proteins. They facilitate the exudation of phagocytes towards the site
of infection.
8
7. Provide fetal & newborn immunity:

- By the transfer of antibodies from mother through placenta & colostrums, the
fetus & newborn acquire immunity.
Cell – Mediated Immunity
- T Lymphocytes are involved in cell mediated immunity.
- They are produced in the bone marrow.
- They attain functional maturity in ‘Thymus’ under the influence of a hormone called
‘Thymopoietin” secreted from Thymus.
- They are 4 types of ‘T’ cells.
a) T helper cells (CD 4)
b) T Killer/Cytotoxic T Cells (CD 8)
c) T Suppressor cells.
d) T memory cells.
a) Activation of T Helper cells:
Antigen binds to MHC class II protein on the surface of Macrophage (Antigen presenting cell)
Forms a complex
secretion of IL-1
Presentation to “T” cell “
Activation of “T” Helper cells
B) Activation of cytotoxic ‘T’ Cells:
i) Antigen in virus infected cells, cancer cells & foreign grafts.
Processing of antigen to peptide fragments
Peptide fragments of processed antigen bind to MHC class I protein & forms a complex.
Presented to cytotoxic ‘T’ cells.
Activation of cytotoxic ‘T’ Cells.
-------------------------------------------------------------------------------------------------------------------
ii) Another way of activation of cytotoxic ‘T’ Cells
Antigen + MHC class II protein on the surface of macrophages (APC)
Interleukin – 1
Activation of ‘T’ helper cells.
Production of IL-2 by ‘T’ helper cells.

9
Activation of cytotoxic ‘T’ cells.
Function of Activated cytotoxic ‘T” Cells;
Activated cytotoxic ‘T’ Cells
Perforin lymphotoxin
Forms holes in the Activates damaging

Plasma membrane of enzymes in the target cell
Target cells - Entry of ECF-
Swelling & burst of cell Destruction of DNA
Cell death Cell death
Examples: Death of virus infected cells, Tumour cells & foreign graft cells.
a) Function of ‘T’ helper cells:

Take place in both humoral & cell mediated immunity
i) Role in humoral immunity:
T- helper cells(TH2)
Interleukin – 2,4,5 & 6 (cytokines)
Activation of B Cells
Plasma cell
Secretion of antibodies
(ii) Role in cell-mediated immunity:
T- helper cells (TH1)
Interleukin – 2
Activation of cytotoxic ‘T’ Cells
Release of perferins & lymphotoxins
Death of target cells

b) Function of cytotoxic ‘T’ Cells:
- Destruction of Virus infected cells.
- Destruction of cancer cells.
- Rejection of foreign grafts.
- Major defence against viral, fungal & bacterial infection.
c) Functions of ‘T’ Suppressor cells:
- Suppress the production of antibodies against the own tissue.
- this prevents the auto immune diseases like Rheumatoid arthritis etc.
d) Function of ‘T’ Memory cell:
- Facilitates the activation of ‘T’ lymphocytes faster during secondary response.
10
4.HEMOSTASIS
Definition:
Prevention of blood loss by arrest of bleeding
Stages:
Vasoconstriction
Platelet plug formation
Blood coagulation
Clot retraction
Fibrinolysis
Growth of fibrous tissue to repair the ruptured/damaged vessel permanently
a. Vasoconstriction:
Ruptured blood vessel
↓
Vasoconstriction
↓
Reduction in bleeding
-vasoconstriction due to Nervous reflexes, Local myogenic spasm & local humoral
factors (e.g Serotonin from platelets)
b. Platelet plug formation:
Platelets circulate in a resting, inactive state
↓
When blood vessel wall is injured
↓
Platelets adhere to collagen, laminin and von –
Willibrand factor in the vessel wall.
↓
Platelet activation
(Activated platelets change shape, release ADP & stick to each other platelet
aggregation.Platelet activating factor (PAF) secreted by neutrophil, monocytes &
platelets increase aggregation)
Thromboxane A2 increases platelet aggregation; helps in formation of temporary
hemostatic plug
c. Blood clotting or coagulation:
Damage to the tissues of Damage to the blood
blood vessel wall
EXTRINSIC INTRINSIC
PATHWAY PATHWAY
Formation of Prothrombin Activator Complex

↓
Prothrombin Thrombin
↓
Fibrinogen Fibrin (clot)
d. Clot retraction:
Definition:
Reduction in the size of clot
11
Mechanism:
Fibrin stabilizing factor & thrombosthenin produced by platelets cause
strong contraction of platelets which are attached to fibrin
↓
Reduction of clot into smaller mass
9.Fibrinolysis (lysis of clot):

Damaged vascular endothelium
↓
Releases Thrombomodulin
↓
Thrombomodulin + Thrombin complex
↓
Activates protein c
Inactivates factors V &VIII Inhibits the inhibitor of Tissue

Plasminogen Activator
↓
Activation of tPA ( Tissue Plasminogen Activator)
↓
Plasminogen  Plasmin(lysis of clot)
5. BLOOD COAGULATION/ CLOTTING

Introduction:
When blood comes out of the blood vessel, it looses its fluidity & becomes a
semisolid jelly. This process is called clotting.
Definition:
Defined as the sequence of events leading to the formation of fibrin from fibrinogen
Coagulation factors:
- these are substances required for coagulation
- all these substances are present in plasma in an inactive form
- these are activated and take part in coagulation when the blood vessel wall is
injured
I - Fibrinogen
ii - Prothrombin
iii - Tissue thromboplastin
iv - Calcium
v - Proaccelerin,labile factor
vi - Accelerin
vii - Proconvertin,stable factor
viii - Anti hemophilic factor A
ix - Plasma Thromboplastic Component(PTC), christmas factor, antihemophilic
factor b
x - Stuart-prower factor
xi - Plasma Thromboplastin antecedent(PTA),
Anti Hemophilic factor C
12
xii - Hageman factor,

xiii - Fibrin stabilizing factor
HMW- K - High Molecular Weight Kininogen,
pre-k - Prekallikrein
ka - kallikrein
PL - Platelet Phospholipid
Mechanism of coagulation:
3 main steps are involved
1. Damage to the blood vessel wall/ blood - Formation of Prothrombin Activator
Complex
2. Prothrombin Activator Complex activates prothrombin to thrombin
3. Thrombin converts fibrinogen to fibrin
Pathways of coagulation:
1. Extrinsic pathway
2. Intrinsic pathway
Extrinsic mechanism of clotting:

Triggered by tissue injury
Injured tissues release factor III (tissue factor)
VII VIIa
PF3
Ca2 + & III
X Xa
Va Prothrombin
Ca2+ Activator
tissue phospholipids Complex
Intrinsic mechanism of clotting:

Contact of blood with collagen, HMW kininogen, kallikrein
↓
Release of platelet phospholipids
&
activation of factor XII XIIa
↓
XI XI a
↓
IX IXa
PL
Ca2+
VIIIa
X Xa
Va Prothrombin
Ca2+ Activator
Platelet phospholipids Complex
13
common pathway:
Both intrinsic and extrinsic pathways activate
Factor X Xa
PF3
Ca2+
V
Prothrombin (II) thrombin
XIIIa
stabilization
fibrinogen(I) fibrin (clot)

Clot: A meshwork of fibrin threads entrapping the blood cells and a fluid called serum
6. BLOOD GROUPS
Discovered by Landsteiner
Awarded Nobel Prize
Blood group systems:
ABO system
Rh System
Lewis System
MN system
Luthern System
ABO system
Grouping depends on presence/absence of Antigens/Agglutinogens
Antigens –A & B
Blood groups are A(A1&A2), B, AB(A1B & A2B) & O
Antibodies/Agglutinins Are in plasma
Landsteiner’s Law:
- If an agglutinogen is present on the RBC, corresponding agglutinin will be
absent in the plasma
- If an agglutinogen is absent corresponding agglutinin will be present
[Exception to the 2nd part is Rh System - Rh-ve people will not have Rh
Antibodies]
Rh Blood Group:
Discovered by Landsteiner & Weiner
The Rh Antigens are C, D, E. The common antigen is D antigen
People having ‘D’ antigen are called Rh +ve (85%)
People not having ‘D’ antigen are called Rh-ve (15%)
There are no naturally occurring antibodies
Blood Group Agglutinogen and Agglutinin:
Genotype Blood Group Agglutinogen Agglutinin
(RBC) (plasma)
AA, AO A A Anti B
BB, BO B B Anti A
AB AB AB Nil
OO O Nil Anti A
Anti B
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Determination of Blood Group:
Cells (R.B.C)
Anti A serum Anti B serum
A + --
B -- +
AB + +
O -- --
+ Agglutination -- No Agglutination
Uses of Blood Grouping:
In Blood Transfusion
In Pregnancy
In Disputed Paternity
Infertility and Early Fetal loss
Disease Relation e.g O group have twice incidence of Duodenal ulcer than A or B
In forensic science
In Anthropological studies
Blood Transfusion:
Transferring blood from one person to another person
Cross matching :
Major cross matching
Recipient’s Serum + Donor’s RBC
Minor Cross matching
Recipient’s RBC + Donor’s Serum
Universal Donor - O group persons have no agglutinogen and so can give blood to
anyone.
Universal Recipient - AB group persons have no agglutinins and so can receive any
type of blood
The above are no longer valid as complications can be produced by Rh and other
sub groups. But in case of extreme emergency O-ve blood can be used
ABO incompatibility:
- ABO incompatibility rarely produces hemolytic disease of newborn
- Anti A & Anti B antibodies are of IgM
- Cannot cross the placenta
Rh Incompatibility:
When 2nd time Rh +ve blood is transfused into negative blood–severe reactions occur
In women – during pregnancy incompatibility leads to ERYTHROBLASTOSIS
FOETALIS – a hemolytic disease of new born
15
BLOOD – 5 MARKS
1.Functions of plasma proteins
Important plasma proteins are Albumin, Globulin & Fibrinogen
Normal Albumin/Globulin ratio = 1.7 : 1
a. Colloidal osmotic pressure: Albumin is mainly responsible for the development of
colloidal osmotic pressure. The normal colloidal osmotic pressure of blood is 25-30
mmHg. This is mainly responsible for the passage of fluid across the capillary
membrane
b. Viscosity of blood: Globulin maintains the viscosity of blood to some extent.
Viscosity is one of factors that influence blood pressure
c. Immunity: Antibodies (Immunoglobulins) belong to gammaglobulins. Antibodies
neutralize the antigen
d. Coagulation: Both prothrombin & fibrinogen take part in clotting process
Prothrombin activator
Prothrombin Thrombin
Fibrinogen Fibrin (clot)

e. Transport:
i) CO2 is transported by carbamino proteins
ii) Transferrin – transports iron
iii) Ceruloplasmin – transports copper
iv) TBG – Thyroxine Bound Globulin
v) CBG – Cortisol Bound Globulin
f. Acid-Base Balance – Plasma proteins act as buffers & neutralize any change in
blood pH
g. Protein reserve – Serve as storehouse of protein. Provides proteins to tissues during
starvation
h. ESR : Fibrinogen & Globulin increase the ESR. Albumin decreases the ESR
i. Haptoglobin: Forms the complex with hemoglobin & prevent its filtration into the
kidney
2. ANTICOAGULANTS
Anticoagulants are the substances that prevent clotting
a. Natural anticoagulants:
Heparin – produced by mast cells & basophils
Mechanism of action: facilitates antithrombin – III which inhibits the clotting
factors II, IX, XI & XII
b. Anticoagulants used in blood bank:
Acid Citrate Dextrose (ACD): Calcium chelating agent
Mechanism of action: forms a complex with calcium ions and decreases ionic
calcium level
c. Anticoagulants used in the laboratories:
Sodium citrate – Forms double salt with calcium ions
Double oxalate (Oxalates of K+ & NH4) - Precipitation of calcium
EDTA- Ethylene Diamine tetra acetate – Preparation of calcium ions
d. Therapeutic anti coagulants:
Dicoumarol – prevents the synthesis of blood clotting factors II, VII, IX, X by
competitive inhibition with vitamin .K.
------------------------------------------------------------------------------------------------------------
---------
16
3. PHAGOCYTOSIS (Neutrophil response during inflammation)

Definition: The process of engulfing of macromolecules like bacteria, dead cells & particulate
matter by neutrophils, monocytes & tissue macrophages is called phagocytosis.
Steps involved in the process
Margination: Neutrophils slow down in the circulation & get attached to the capillary wall. The
cell adhesion molecules adherin, Integrin & selectin are involved.
Diapedesis: Neutrophils squeeze through the pores in the capillary wall into the tissues.
Chemotaxis : Neutrophils are attracted towards the site of damage ( infection & inflammation)
by the chemicals released at the site of damage.
Engulfing :
Microbes are coated with complement & antibodies (opsonization)
↓
Neutrophil membrane invaginates enclosing the microbe
↓
Formation of vacuole
↓
Vacuole fusing with lysosome
↓
Lysosomes release hydrolyzing enzymes & bactericidal agents like hydrogen peroxide,
mycloperoxidase etc
↓
Killing & digestion of the microbe.
---------------------------------------------------------------------------------------------------------------------
4. ANTICLOTTING MECHANISMS (Factors that prevent intravascular

coagulation)
1. Physical characteristics of the endothelium (e.g) Smoothness of vascular endothelium
Atherosclerotic (deposit of fat) plague in the vascular endothelium gives a rough surface which
activates platelets & initiate clotting.
2. High blood flow rates: Increased velocity of blood flow prevents clotting.
3.Presence of natural anticoagulants: Anticoagulants like heparin, anti thrombin III & α2macro
globulin are some of the natural anti coagulants present in the circulation and prevent the intra
vascular clotting .
4. Fibrinolytic system: When small clots are formed in the vessels they are immediately lysed by
the system.
Tissue Plasminogen Activator (tPA)
↓
Plasminogen → Plasmin (digests the fibrin into soluble fragments dissolving the clot)
---------------------------------------------------------------------------------------------------------------
5. COMPOSITION & FUNCTIONS OF LYMPH
Composition of Lymph
Electrolytes – same as that of plasma
Minerals – Ca₂₊ & phosphorous are lower than plasma
Protein – lower than that of plasma
Aminoacids – same as that plasma
Urea & creatinine – same as that of plasma
Glucose & chlorides – more than that of plasma
Cells – Lymphocytes & plasma cells are present
Clotting factor and antibodies are present.
Functions of Lymph
 Returns protein, electrolytes and water to the blood from the tissue spaces
 Removes the bacteria and particulate matter
 Fat absorption in the intestine by the lacteals
17
 The lymphocytes and antibodies present in the lymph take part in body defence against
infectious diseases
 Helps in the redistribution of body water
 Transport antibiotics and other drugs injected intramuscularly
---------------------------------------------------------------------------------------------------------------------
6. FIBRINOLYTIC SYSTEM
Fibrinolysis refers to the process of dissolution of fibrin. Fibrinolytic system refers to the
substances taking part in fibrinolysis.
The important components of fibrinolytic system:
Protein C, tissue plasminogen activator & plasmin or fibrinolysin which is present in an inactive
form (plasminogen)
Protein C → Activated protein C
Inactivates clotting Inactivates inhibitor of tissue plasminogen activator

Factors V a & VIIIa ↓
Activation of tissue plasminogen activator
↓
Plasminogen Plasmin (fibrinolysis)
Fibrinolysin lyses fibrin into soluble fragments called as fibrin degradation products which inhibit
thrombin
Plasminogen Activaor system
Intrinsic: Factor XIIa and Kallikrein
Extrinsic: Tissue plasminogen activator, Streptokinase and staphylokinase
Physiological role of fibrinolytic system
 Cleans the minute clots of tiny vessels
 Promotes normal healing process
 Dissolution of menstrual clot
 Dissolution of sperms in the epididymis
Therapeutic role of fibrinolytic system
Streptokinase and staphylokinase are bacterial enzymes that activate plasminogen to
plasmin. So they are used in the treatment of early myocardial infarction.
---------------------------------------------------------------------------------------------------------------------
7.HAZARDS OF BLOOD TRANFUSION
Complications of whole blood transfusion
1. Hemolytic reaction due to red cell incompatibility
2. Transmission of certain diseases like hepatitis malaria, AIDS, Syphilis etc.,
3. Transient hyperkalemia followed by hypokalemia
4. Hypocalcemia
5. Volume overload
6. Bacterial contamination
7. Thrombophlebitis
8. Air embolismEffect of mismatched blood transfusion
Mismatching refers to transfusion of incompatible blood groups

a. Mild hemolytic reaction
Aggultination
↓
Hemolysis
↓
Bilirubin
↓
Jaundice
18
b. Severe immediate hemolytic reaction

Wide spread agglutination leads to development of following signs and symptoms.
1. Chill and rigors
2. Fever and headache
3. Breathlessness
4. Chest pain and abdominal pain
5. Nausea and vomiting
6. Joint pain
7. Circulatory shock (due to release of histamine and other vasodilators)
Feathers of post shock phase
8. Hemolysis of agglutinated cells
9. Release of hemoglobin and its excretion into the urine
10. Jaundice
11. Anemia
12. Renal shut down due to precipitation of Hb in the renal tubules
13. Hyperkalemia and uraemia
c. Delayed hemolytic reaction:
1. Occurs 3days to 3weeks after transfusion only as 1 in 3200 transfusions
2. Antibodies that develop against donor cells cause agglutination and hemolysis
3. Symptoms are often mild or absent.
--------------------------------------------------------------------------------------------------------------------------------
8. FUNCTIONS OF PLATELETS
Platelets/Thrombocytes are biconvex discs produced by bone marrow
Size: 2 to 4μ
Normal count: 1.5 to 4 lakhs/cumm of blood
Granules of platelets: α granules and dense granules
α granules : consists of factor V, Fibrinogen, Von williebrand Factor, Platelet
factor IV, PGDF
Dense granules: Consists of ADP, Calcium, serotonin
Functions of Platelets
1. Primary hemostasis – Arrest of bleeding by temporary platelet plug formation is
referred as primary hemostasis.
Injury to wall of blood vessel
↓
Exposure of collagen
↓
Platelet adherence to damaged vessel wall

↓
Release of ADP and Thromboxane A2

↓
Activation of more platelets
↓
Aggregation and adherence of platelets (enhanced by platelet activation
factor produced by platelets and macrophages)
19
↓
Temporary platelet plug
2. Secondary Hemostasis: Arrest of bleeding by the definite clot formation is called

secondary hemostasis
Platelet phospholipids and platelet activation factor III are the factors which are
involved in clotting.
3. Clot retraction: Contraction of contractile proteins (actin, myosin and
thrombosthenin) present in the platelets play an important role in clot retraction
4. Repair of capillary endothelium: Platelets adhere to the von – willebrand factor in
the wall of damaged blood vessels and release platelet derived growth factor
(PDGF). This factor plays an role in the repair of endothelium
5. Vasoconstriction: Platelets release serotonin which is a vasoconstrictor.
6. Defense /Phagocytosis: Platelets are helpful in phagocytosis of carbon particles,
viruses and immune complexes
--------------------------------------------------------------------------------------------------------------------------------
9.Oral Anticoagulants
Refers to anticoagulants which are used as drugs. These substances are given through
mouth to prevent clotting.
The substances which are used as oral anticoagulants - coumarin derivatives (Dicoumarol
and warfarin)
Dicoumarol
- It is a synthetic product
- It resembles vitamin K in structure
Mechanism of action
- Vitamin K is required for synthesis of clotting factors II, VII, IX, X protein C and
Protein S
- By competitive inhibition with Vitamin K, dicoumarol inhibits the synthesis of the
above factors from liver
Other Vitamin K antagonists

Warfarin, Phenindione, Nicoumalone
Therapeutic use:
Patient with hypercoagulability (increased tendency of blood to clot) are given
these oral anticoagulants for preventing the formation of thrombus
Oral anticoagulants are not effective invitro as they are vitamin K competitive
inhibitor and can act only inside the body
1
BLOOD - Applied
1. A 14 year old boy, under therapy for epilepsy develops reddish spots all over the body.
His platelet count was found to be below normal.
a) Give the normal platelet count.
b) What are the other tests of haemostatic functions that should be done on this
patient and what could be the observations?
a) Normal platelet count – 1.5 lakhs to 4 lakhs / cu mm of blood
b) Tests for purpura
1. Bleeding time (more than 6 minutes )
2. Platelet count (less than 50 thousands /cu mm)
3. Clot retraction (less than 50% at the end of 1 hour)
4. Capillary resistance test (more than 20 petitchae- hemorrhagic spots)
5. Platelet aggregation/ adhesiveness test (less adhesiveness)
2. Differentiate between Purpura and Hemophilia in all respects
Purpura Hemophilia
1. Bleeding disorder 1.Clotting disorder
2. Caused by deficiency of 2.Caused by deficiency of
Platelets clotting factors
3. Normal clotting time 3.Prolonged clotting time
4. Prolonged bleeding time 4.Normal bleeding time
5. Characterized by purplish blotches 5.Characterized by profused bleeding
Under the skin even for minor injury
6. Spontaneous bleeding 6. Trauma induced bleeding
7. Types- thrombocytopenic and 7.Types- Hemophilia A, B & C
Thrombosthenic
3. Mention any two clinical conditions where Albumin – Globulin ratio is reversed
Nephrotic syndrome (due to loss of albumin)
Hepatic cirrhosis (due to failure of production of albumin)
4. Briefly describe the hemolytic disease of newborn
Erythroblastosis foetalis is a hemolytic disease of newborn due to Rh incompatibility between
Rh negative mother & Rh positive foetus.
Physiological basis:
When a Rh negative female conceives a Rh positive foetus for the first time, the baby is born
safely without any complication as the antigen D from foetus does not enter into maternal
circulation during pregnancy. But during delivery, the shearing of placenta causes entry of foetal
blood into maternal circulation. Antibodies are produced against Rh antigens entered & remain in
maternal circulation. When the Rh negative female conceives for the second time, the antiRh
antibodies from maternal circulation enter into the foetal circulation through placenta and
agglutinate the foetal RBCs.
Features:
- Hemolytic anemia
- Erythroblastosis ( release of blast cells into the circulation)
- Kernicterus ( basal ganglia damage due to excess bilirubin)
- Hydrops fetalis – edema of fetus
Prevention:
- Rh typing before marriage
- Anti D injection at 28th & 34th weeks of pregnancy
- Anti D injection within 48 hours after first delivery
- Avoiding transfusion of Rh positive blood to Rh negative female
Treatment:
- Exchange transfusion of the fetus with Rh –ve cells
2
5. Enlist the conditions producing hypochromic microcytic anemia, normocytic

normochromic anemia and macrocytic normochromic anemia
Microcytic Hypochromic anemia – Iron deficiency
Normocytic Normochromic anemia – Acute blood loss
Macrocytic Normochromic anemia – Vitamin B12 & Folic acid deficiency
6. Which is the commonest anemia encountered in India? What is the reason?
Iron deficiency anemia. Due to nutritional deficiency
7. When the mother is B group & the child is O group, can the father be of A group?
Explain
The genotype for B group is BB or BO. The genotype for A group is AA or AO.
The chances of children blood group are A, B, O & AB. So there is a chance for the father to
be of A blood group
8. Generally myocardial infarcted patients are advised to take aspirin regularly along with
other drugs. How it may help him?
Aspirin – Aspirin reduces clot formation by the following mechanism.
Arachidonic acid
↓ Cyclooxygenase (inhibited by low doses of aspirin)
Prostaglandins
↓
Platelet aggregation & consequent clot formation
9. Give a note on the physiological basis of graft rejection.
Graft rejection refers to rejection of transplanted tissue.
Physiological basis of graft rejection:
- T lymphocyte system is responsible for rejection of transplanted tissue.
- Due to incompatibility of the MHC (HLA system) proteins between donor & recipient
tissues, activation of cytotoxic T cells occurs. This leads to development of immune
response against graft tissue in recipient which causes graft rejection
Prevention: Tissue matching before grafting
Treatment:
1. Cyclosporin – A – inhibits cell mediated immune response.
2. Azathioprine – kills T lymphocytes
3. Corticosteroids – suppress T cell production
10. Radiotherapy in a person leads to which type of anemia. What is the pathophysiology in
it?
Aplastic or hypoplastic anemia. Radiation from frequent radiotherapy destroys
the bonemarrow. Bonemarrow failure leads to less production of RBCs.
11. A child after 5 days of high grade fever develops purpuric spots over the skin. Discuss
the pathophysiology
The fever is Dengue fever in which platelets are destroyed. Deficiency of platelets leads to
spontaneous hemorrhage under the skin which are seen as purpuric spots over the skin. This
condition is called is called purpura.
12. A 3 yr old anemic boy, with decreased ESR value, but hemolysis getting started
very late (at 0.32% saline). Diagnose the clinical picture and explain how it is produced
Diagnosis: Sickle cell anemia . Decreased ESR value is due to change in the shape of the cell
which opposes rouleaux formation. Diminished fragility is due to the cells being flat.
13. Match the following
1. Vit. B12 deficiency anemia - a) Valine replaces glutamic acid in the ß chain
2. Aplastic anemia - b) Microcytic hypochromic and most common
3. Blood loss anemia - c) Macrocytic, Normochromic, with
neurological symptoms.
4. Iron deficiency anemia - d) Normocytic, normochromic with increased
3
reticulocyte count.
- e) RBC count less, MCV normal, Reticulocyte
Less
- f) Macrocytic normochromic with out
neurological symptoms
1. Vit B12 deficiency anemia – C
2. Aplastic anemia – E
3. Blood loss anemia – D
4. Iron deficiency anemia – B
a) Valine replaces – Sickle cell anemia
f) Macro-----without neurological symptoms – Folic acid defeciency
14. Oral intake of Vit. B12 may not cure Vit. B12 deficiency, in most of the time- Explain.
As Vit. B12 deficiency is mainly due to intrinsic factor deficiency in most of the time, oral
intake of Vit.B12 may not cure. Because absorption of Vit. B12 cannot occur. So Vit.B12 can
be given intravenously
15. Does the clotting occur in a blood sample treated with oral anti coagulant (dicumarol) –
give reasons?
No. Clotting does not occur as oral anticoagulant dicoumarol is not effective outside the body
Because dicoumarol acts as a vitamin- K antagonist & inhibits the activity of clotting factors
II, VII, IX & X. This can occur only inside the body
16. Why ABO incompatibility does not give rise to hemolytic disease of newborn, the way
Rh incombatibility does?
- ABO system antigens are not expressed properly on fetal RBC
- Anti A & Anti B antibodies are of Ig M type which do not cross the placenta easily
17. What are the normal values of MCV, MCH, MCHC and how they are altered in iron
deficiency anemia, blood loss anemia and pernicious anemia using a tabular column?
Normal values :
MCV – 78 – 96 fl
MCH – 27- 33 pg
MCHC - 30 – 37 %
MCV MCH MCHC
Iron deficiency anemia ↓ ↓ ↓
Blood loss anemia normal normal normal
Pernicious anemia ↑ normal normal

18. In case of Rh incompatibility, why does anti-D (passive immunization) given during
pregnancy not damage the fetal red cells, the way normally induced antibodies may do?
Antibodies given through passive immunization are not sufficient enough to damage all foetal
red blood cells whereas antibodies which are normally produced (active immunity) by entry
of foetal RBCs into maternal circulation are sufficient enough to damage the foetal RBCs
19. A new born baby delivered by a Rh negative mother had severe anemia, jaundice,
generalized swelling of the body and some degree of motor deficits. What is the probable
condition and what could be the possible cause of the dysfunctions? Briefly mention the
physiological basis of treatment of the dysfunction. How will you prevent this
dysfunction from occurring in subsequent pregnancy of the same mother?
Refer erythroblastosis foetalis/hemolytic disease of newborn
20. Pernicious anemia – its cause, hematological picture, clinical picture and treatment.
Cause – Deficiency of intrinsic factor which causes malabsorption of Vit.B12
Hematological picture –
- MCV is above normal – Macrocytic
4
- low RBC count

- Relative leucopenia & thrombocytopenia
Clinical picture –
o Glossitis (inflammation of tongue)
o Peripheral neuropathy which causes paraesthesia, tingling & numbness
o Subacute combined degeneration of the spinal cord
21. Mention the abnormal shape of RBC. What are the physiological effects of it?
Sickle shape & spherical shape
Physiological effects –
-Sickle shape & spherical shape oppose rouleaux formation. So ESR is decreased
-Sickle shaped cell, being flat show diminished osmotic fragility
-Spherical cells show increased osmotic fragility
22. What is physiological jaundice? When will it occur? How do you treat? What is the
physiological basis?
Jaundice in newborn infants is called physiological jaundice. It occurs during first week after
birth.
Cause:
by excessive hemolysis or immaturity of the hepatic conjugating enzyme system
(glucuronyl transferase)
Treatment:
1. Phototherapy (exposure of the skin to light) – light converts bilirubin to lumirubin which
has a shorter life span than bilirubin.
2. Administering the drug Phenobarbitone – increases the glucuronyl transferase activity
23. Briefly describe the neutrophil responses during inflammation.
Inflammation refers to sequence of events that occur when there is tissue damage.
Neutrophil invasion of the inflamed area is the second line of defense.
Neutrophil responses during inflammation:
- Margination – attachement of neutrophils to the vascular endothelium in nearby
capillaries
- Diapedesis – squeezing of neutrophils through the openings of capillary wall
- Chemotaxis – attraction of neutrophils toward the injured tissues
All the above processes are due to chemicals released from the inflamed tissues
Phagocytosis – Engulfing of microorganisms mainly bacteria which cause the
Inflammation (explain the phagocytosis process in short)
24. What is cross matching? Why it is done before blood transfusion? Can Rh
incompatibility be detected by cross matching of blood – Give reason?
Cross matching is mixing the donor RBCs with recipient plasma & checking for
agglutination. It is done before blood transfusion to find out the compatibility
between donor & recipient blood groups.
No., the Rh incompatibility cannot be detected by cross matching as the
antiRh antibodies are not present naturally. So both the persons will not have
antibodies
25. Why is the life of RBC in stored blood shortened?
In cold storage, metabolism is decreased Decrease in ATP  Decrease in the
action of Na+ - K+ ATPase pump  accumulation of Na+ inside the cells drawing
of fluid into the cells cells bulge & become spherical fragility increases
26. How do you differentiate Vitamin B12 deficiency from that of Folate deficiency?
Folic acid deficiency produces only hematological disturbances. But Vit B12 deficiency
5
produces both hematological & neurological disorders.

27. What is reticulocytosis? Give two conditions that cause reticulocytosis.
Reticulocytosis means increase in the count. Conditions which cause reticulocytosis are high
altitude, acute hemorrhage, hemolytic anemia, treatment of deficiency of anemia
28. What is the role of calcium in clotting?
Calcium acts as a cofactor in the activation of clotting factors. Except the first two steps in
intrinsic mechanism of coagulation all the steps of both intrinsic & extrinsic mechanisms of
coagulation require the presence of calcium ions.
29. What is the critical count of platelets?
The minimum count of platelets below which produces purpura is called critical count of
platelets. It is 50000(fifty thousands) / cumm of blood
30. What is thrombocytopenic purpura? How do you treat this condition?
A bleeding disorder caused by low platelet count is called thrombocytopenic purpura.
It is treated by platelet transfusion
31. What is Von- Williebrand disease?
A bleeding disorder characterized by prolonged clotting time & bleeding time. This is caused
by deficiency of Von- Williebrand factor which is a component of clotting factor VIII. This
factor is produced by endothelial cells and platelets
32. Chronic blood loss due to worm infestation will produce what type of anemia?
What investigation to be done to substantiate the diagnosis?
Microcytic hypochromic anemia. Investigation to substantiate the diagnosis –
determination of blood indices (MCV, MCH & MCHC) & analyzing the peripheral
blood smear.
33. A patient having C/O fever, loss of appetite and loose stools of 8 days duration. O/E
shows coating of the tongue and hepatosplenomegaly, blood picture shows neutropenia.
What is the propable diagnosis.
Typhoid fever
34. A man complaints of small, purplish blotches in the skin, and when his blood is tested,
his blood fails to retract.
i) What is the disorder called?
ii) What is the cause of failure of retraction?
iii) What treatment should be given?
Disorder – Thrombocytopenic Purpura
Cause for failure to retract – deficiency of platelets
Treatment – Platelet transfusion
35. What type of anemia will occur in patients who have intestinal sprue? What is the cause
of anemia? What treatment is advised?
Anemia in patients with intestinal sprue – Megaloblastic anemia
Cause – Folic acid deficiency
Treatment – Administering antibiotics like tetracyclin
36. A patient with recurrent attacks of vaso occlusive phenomenon called “painful crises” in
various parts of body like abdomen, chest & back is found to be suffering from anemia
also.
i) What may be your diagnosis
ii) Write the cause for anemia
iii) Why pain develops in various parts of the body?
i) Sickle cell anemia
ii) Sickling & hemolysis
iii) Vasoocclusion leads to ischaemic pain
37. What will happen in RBCs which are small and spherical in shape?
Small RBCS can take up more fluid inside before they rupture. So osmotic fragility
6
is decreased. Spherical cells rupture easily when fluid enters inside. So the osmotic
fragility is increased.
38. What type of anemia will occur in hook worm infestation? What is the cause of
anemia? What treatment to be given?
Microcytic hypochromic anemia. Caused by iron deficiency due to chronic blood
loss. Treated by administering antihelminthic drugs
39. A patient who took a course of Chloroquinine & Aspirin (antimalarial & analgesic
respectively) developed hemoglobinemia, hemoglobinuria and anemia. On history
taking, this kind of drug reaction existed in his family members also.
i) What is the reason for hemolysis & hemoglobinuria on exposure to drugs?
ii) Which deficiency leads to such a condition?
iii) Why it appears genetically controlled?
i) As RBCs become fragile, hemolysis occurs. Hemoglobin which comes out of
the cells is excreted through urine(Hemoglobinuria). This reduces the amount of
hemoglobin in the blood (Hemoglobinemia)
ii) Deficiency of Glucose-6-Phosphate Dehydrogenase
iii) As the condition exists in family members also, it appears genetically controlled. This
defect is inherited as X-linked recessive trait
40. In a patient both clotting time and bleeding time are prolonged. On investigation, all
clotting factors and platelet count seems to be normal.
i) What may be the diagnosis?
ii) How it affects both primary (prolonged bleeding time) and secondary (Prolonged
clotting time) hemostasis?
i) Diagnosis – VonWilliebrand disease
ii) It is caused by deficiency of VonWilliebrand factor (VIII-R) - a protein essential for the
integrity of the capillary and platelet adhesion at the endothelium. So bleeding time is
prolonged.
- It is a component of VIII clotting factor. So deficiency causes prolonged clotting time
41. A patient who is bed ridden quiet for a long time after a surgery, had symptoms of MI.
i) What may be the cause?
ii) Explain the pathophysiology of it
i) Cause – Stasis of blood
ii) Pathophysiology – Stasis of blood leads to thrombosis which may block
the coronary blood vessels. This causes MI
1
DIGESTION
10 Marks:
1. Describe the mechanism of HCl secretion by the gastric parietal cells with suitable
diagram. Describe the various phases of gastric secretion and their regulation.
2. Describe the Various phases of deglutition & disturbances associated with each stage. What is
the effect of deglutition on respiration?
3. Give the composition & functions of saliva. Draw a reflex pathway for salivary secretion on
placing food in the oral cavity. Explain the process of reflex salivation.
4. Describe the composition, functions & regulation of secretion of pancreatic juice.
5. Describe the movements observed in small intestine
5 Marks:
1. Describe the protective mechanisms during second stage of deglutition.
2. Name the bile salts & write their functions
3. Explain gastric emptying & the control mechanism.
4. Explain the mechanism & purpose of peristalsis in oesophagus & small intestine
5. With the help of a labeled diagram briefly describe defecation reflex
6. Describe the process of digestion & absorption of carbohydrates
7. What is the mechanism of glucose absorption in intestine?
8. Describe the process of digestion & absorption of protein
9. With the help of a schematic diagram, illustrate the mechanism of absorption of fat in the
small intestine
10. Explain the proteolytic enzymes of GIT with respect to their sites of production and actions.
11. Explain the role of dietary fibers
3 Marks:
General:
1. Describe the role of bile in digestion & absorption
2. What is Secretin? What are its physiological actions?
3. Describe briefly about ‘Micelle’
4. Explain – gastrocolic reflex
5. What are hunger pangs?
6. What are the functions of liver?
7. List out the functions of large intestine
1
1
Digestive System
10 Marks
1. Deglutition
The process of passage of food from mouth into the stomach is called swallowing or deglutition. This
process is divided into three stages
1. Oral phase
2. Pharyngeal phase
3. Oesophageal phase
ORAL PHASE PHARYNGEAL OESOPHAGEAL

PHASE PHASE
1) Oral phase: Passage of food from mouth to pharynx. It is a voluntary process

- the tongue is elevated and pressed against the hard palate
- the soft palate is also elevated
- the bolus is propelled into pharynx
- myolohyoid, styloglossus & intrinsic tongue muscles help this stage
2) Pharyngeal phase: Passage of food from pharynx into oesophagus. It is a reflex process. This
reflex is called swallowing reflex
Receptors: Stretch receptors in the anterior and posterior pillars of fauces and tonsils
Stimulus: Presence of bolus
Afferent: Sensory fibers of trigeminal, vagal & glossopharyngeal (V, IX & X cranial nerves)
Center: Swallowing center in medulla
Efferent: Motor fibers of 5th , 9th , 10th & 12th cranial nerves
Events during the second stage of following:
 Elevation of soft palate  closure of nasopharynx  prevents the reflux of food into
nasal cavities
 The vocal cords of the larynx are closely approximated & epiglottis close the glottis
(opening of larynx). Both the above events prevent the entry of food into the larynx
 Larynx is pulled upwards & forwards  stretches the opening of esophagus
 Upper esophageal sphincter relaxes  allows the food to pass into esophagus
 Superior pharyngeal constrictor muscle contracts  produces a rapid peristaltic wave
(primary peristaltic wave)  propels the food downwards (into esophagus)
2
 Persistent elevation of the tongue maintains the high pressure gradient. This prevents the
entry of bolus again into the oral cavity
All the above events are the protective mechanisms during second stage of deglutition
3) Esophageal stage of swallowing: The passage of food from pharynx to stomach through
esophagus is the third phase of swallowing
Events:
 Upper esophageal sphincter relaxes allowing the food from pharynx into esophagus
 Three types of peristaltic waves are seen in the body of esophagus.
A) primary peristaltic wave – continuation of the peristaltic wave produced
in the pharynx by superior constrictor muscle
B) Secondary peristaltic wave – produced in the esophagus by the distension
of esophagus by retained food
C) Tertiary peristaltic wave – occurs irregularly & locally in the esophagus
 Lower esophageal sphincter relaxes & allows the food to pass into the stomach
Applied – Disorders of swallowing
1. Achalasia
2. Gastroesophageal Reflux Diseases – GERD/Heart bur n
3. Dysphagia
1. Achalasia:- Failure of lower esophageal sphincter (LES) to relax. So food is not emptied into
the stomach
Cause: Degeneration of the myenteric plexus in the lower part of the esophagus
Features: Dilation of esophagus due to accumulation of the food – called as
megaesophagus
Treatment
A) Antispasmodic drugs to relax – to relax LES
B) Botulinium toxin – to inhibit the release of acetylcholine  relaxation of
LES
C) Surgery – to open the LES
2.GERD/ heart burn – Reflux of gastric contents into the esophagus due to failure of
closure of LES. Also called as hiatus hernia.
Features: Heart burn – due to regurgitation of acid containing meals into the lower part
of esophagus. Chest pain, feeling of lump in the throat are other features.
Treatment: Antacids, H2 – blockers, Proton pump blockers
3. Dysphagia - Difficulty in swallowing due to disorders in any stage
2. GASTRIC SECRETION
Gastric juice is secreted from the gastric gland of stomach. Gastric glands are made up of six
types of cells
Type of cell Secretion
1. Parietal or oxyntic cell HCl, Intrinsic factor
2. Chief cells Pepsinogen
3. Mucous cell Mucus
4. Enterochromaffin Like Cell (ECL cell) Histamine
5. “D” cells Somatostatin
6. “G” cells Gastrin
3
Composition of Gastric juice

- 1 to 1.5 lt of gastric juice is secreted/day
- Secretion is maximum during meals & minimum during sleep
Gastric juice
Water (99.45%) Organic & Inorganic substances
Inorganic:- HCl, Na+, K+, Cl- & HCO3-

Organic:-
1. Soluble & Insoluble mucus – Protects the gastric mucosa from HCl
2. Intrinsic factor – Regulates erythropoiesis by facilitating the absorption of Vit. B12 at illeum
3. Enzymes:
a. Pepsinogen: activated to pepsin by HCl
b. Renin: Acts on milk in the presence of Ca2+ & cause precipitation  curdling of
milk
c. Lipase: Acts chiefly on tributyrin & loe molecular weight triglycerides
d. Gelatinase: Digestion of gelatin
Mechanism Of HCl secretion:
HCl is secreted by parietal or oxyntic cells of gastric glands
2 components of secretion:
a) Secretion of H+ ions into the lumen
b) Secretion of Cl- ions into the lumen
Secretion of H+ ions:
i) By hydration of CO2, H2CO3 is formed in the parietal cell
CO2 + H2O  H2CO3
ii) Carbonic acid splits into H+ and HCO3-
H2CO3  H+ + HCO3-
iii) HCO3 is transported into the blood by antiport with Cl- (active transport)
-
iv) H+ combines with OH- to form H2O

H+ + OH-  H2O
v) H2O (water) dissociates into H+ & OH-
vi) Hydrogen ions are actively secreted into the lumen in exchange for one K+ ion
Secretion of Chloride ions:
i) For each HCO3- ion transported into the blood, one chloride is transported into the
cell by antiport
ii) This chloride ion diffuses into the lumen passively
iii) For each H+ ion secreted into the lumen, one chloride ion is secreted
iv) H+ combines with Cl- to form HCl
4
Stimulants of HCl secretion:

Vagal stimulation, Acetylcholine, Histamine, Gastrin, Caffeine, Protein & protein digested
Products
Inibitors of HCl secretion:
Somatostatin, H2 blockers, Atropine
Regulation of Gastric secretion
Gastric secretion occurs in four phases:
a) Cephalic phase
b) Gastric phase
c) Intestinal phase
d) Interdigestive phase
a) Cephalic phase – Secretion of gastric juice even before food enters the stomach. This phase is
regulated by vagus nerve. This involves two reflexes
i) Unconditioned reflex
ii) Conditioned reflex
Food in the oral cavity ------ Unconditioned reflex ---------- NTS
Smell, sight & thought of food –Conditioned reflex ----- cortex, -- vagus
hypothalamus
Limbic system
Acetylcholine Direct effect
Vagus Chief cell & Parietal cell HCl & enzyme
GRP  G cell -- Gastrin
b) Gastric phase: Secretion of gastric juice when food enters the stomach. This phase is regulated
by both neural & hormonal mechanisms
i) Neural regulation:
Presence of food in stomach
↓
Stretching of gastric mucosa
Long vagovagal reflex Local reflex

(vagal stimulation) (Intrinsic nerve plexus)
Enhance gastric secretion

Mecanism:
Food in the stomach
↓
Ach release  Direct
Distension of
Gastric mucosa Local & vagal - GRP ------- Gastrin Gastric juice
secretion
ECL cells ------- Histamine  Direct
Release
ii) Hormones:
Gastrin
Acetylcholine
Histamine
5
Mechanism:
1. “G” cells ----- Gastrin-- Gastrin receptor ↑ in intracellular
Ca2+
2. ECL cells ----- Histamine H2 receptor --- cyclic AMP  Gastric juice
secretion
3. Vagus ----- Ach ------- Ach receptor -↑ in intracellular
Ca2+
c) Intestinal phase : Secretion of gastric juice when food enters the intestine. This phase is mainly
regulated by hormones. Depending upon the type of food entering into the
intestine, there may be secretion or inhibition of secretion
i) Protein digested products in the duodenum
(Peptides, Peptones & aminoacids)
Stimulate the intestinal “G” cells
Release of gastrin
Stimulation of gastric secretion
ii) Acid, fat & hyperosmolar solution in the duodenum
Release of secrtin, CCK-PZ, bulbogastone
Inhibition of gastrin release & gastic juice secretion

\
iii) Enterogastric reflex: (Neural mechanism)
Presence of food in duodenum
Stretching of duodenal wall
Activation of locale nerve plexus
Activation of sympathetic fibers
Inhibition of gastric secretion & motility

d) Interdigestive phase: Minimal secretion of gastric juice when there is no food in GI tract. This
represents basal acid secretion
3. MOVEMENTS OF SMALL INTESTINE
Types of movements:
1. Mixing movements
a. Segmentation
b. Pendular
2. Propulsive movements
a. Peristalsis
b. Peristaltic rush
c. Interdigestive peristalsis
3. Movements of villi
SEGMENTATION:
- Ring like contractions at regular intervals divide the loop of intestine into a
number of segments of equal size
6
- Each of the segments quickly divide again & reunite to form new segments
- Enhanced by vagus & hormones gastrin, CCK & motilin
Functions:
- Agitation of intestinal contents
- Subdivision of food particles
- Mixing of food with digestive enzymes
- Facilitates absorption of food
PENDULAR:
- Side to side swaying movements accompanied by lengthening and shortening of the
intestine
- Causes to and fro movement of the intestinal contents
PERISTALSIS:
-
A wave of contraction preceded by a wave of relaxation which always travel in
aboral direction.
- Mechanism:
- Presence of food in GI tract
- ↓
- Stretching of GI wall
- ↓
- Local myenteric plexus
- ↓ ↓
- Ach NO , VIP
- ↓ ↓
- Contraction Relaxation
- - 0.5 – 2 m/s
- - always move towards the aboral direction(Law of intestine)
- - helps in proper propulsion & digestion of food in intestine
- Factors influencing peristalsis:
- After meals – increases
- vagal stimulation – increases
- Sympathetic stimulation – decreases
- Injury of GI tract – decreases
- Gastrin & CCK – increases
INTERDIGESTIVE PERISTALSIS:
- - peristalsis during fasting i.e., when there is no food in the intestine
- - takes origin in duodenum & spreads to ileum
- - helps to clear any food residue that remains after previous meal
PERISTALTIC RUSH:
- - peristaltic waves sweeping over long segments of intestine in
- response to powerful irritation of intestinal mucosa
- - helps to relieve intestine from irritants
- - results in diarrhea
ANTIPERISTALSIS:
- - movement of peristalsis towards oral (mouth) direction
- - results in vomiting (expulsion of food through mouth)
MOVEMENTS OF VILLI:
- Initiated by presence of local nervous reflexes in response to chyme in the
intestine
- Two types of movements – Lashing & Lengthening – shortening
- Facilitates absorption by increasing the blood flow
7
4. PANCREATIC JUICE
Phases of Secretion
Cephalic Phase
Gastric phase
Intestinal Phase
a) Cephalic Phase:
Contributes to about 15-20% of secretion
Sight, smell, thought secretion of pancreatic juice (conditioned reflex)
Presence of food in mouth  secretion of pancreatic juice (Unconditioned reflex)
Nervous Regulation:
Vagal stimulation  Acetylcholine  Pancreatic secretion rich in enzymes.
b) Gastric Phase
Contributes to about 5-10% of secretion
Both neural & hormonal regulation
Neural Mechanism
Presence of food in the stomach (distension)

Vagal stimulation (Gastropancreatic reflex)

Secretion of pancreatic juice
Hormonal Mechanism
Food in the stomach

Release of Gastrin from gastric mucosa

Secretion of pancreatic juice rich in fluids and bicarbonate
c) Intestinal Phase
Contributes to about 75% of secretion
Mainly hormonal regulation
i) Acid food in the duodenum
↓
Release of secretin

Secretion of pancreatic juice rich in fluids and bicarbonate
ii) Partially digested proteins & fatty acids in the duodenum

↓
Release of CCK-PZ (Cholesystokinin)

Secretion of pancreatic juice rich in enzymes
5MARKS
1. GASTRIC EMPTYING
The emptying of food from stomach into duodenum is called gastric emptying.
Mechanism:
The antrum, pylorum of stomach & the upper part of duodenum act as a unit in emptying of stomach
Antrum – peristaltic waves grind the food into chyme
8
Pylorum – act like a sphincter & does not allow the food to pass into duodenum
until food becomes fluid
Duodenum – gives a feedback effect on gastric emptying
Factors influencing gastric emptying:
Gastric factors :
i) Increased food volume in the stomach
↓
Stretching of stomach wall
↓
Local myentric plexus
↓
Increase in gastric emptying
ii) Presence of protein digestion products

↓
Release of gastrin
↓
Promotes gastric emptying
Duodenal factors:
i)Enterogastric nervous reflex
Presence of protein digestion products,distension,acid & hypotonic or hypertonic fluid
in duodenum
↓
Through myenteric nerve plexus
↓
Inhibition of gastric emptying
ii) Hormonal feed back
Presence of Fat in duodenum
↓
Secretion of CCK
↓
Inhibition of gastric emptying
2. PERISTALSIS
Definition:
A wave of contraction preceded by a wave of relaxation which always travel in aboral
(opposite to mouth ) direction.
Mechanism:
Presence of food in GI tract
↓
Stretching of GI wall
↓
Local myenteric plexus
↓ ↓
Ach NO , VIP
↓ ↓
Contraction Relaxation
Rate of movement:
0.5 – 2 m/s
Peristalsis in Esophagus:
Primary peristaltic wave
9
Secondary peristaltic wave

Tertiary peristaltic wave
Primary peristalsis –
- continuation of the peristaltic wave produced in the pharynx
- function is to propel food through the oesophagus to the stomach.
Secondary peristalsis -
- initiated by local stimulation of by food in oesophagus
- serves to reinforce the primary peristalsis
Tertiary peristalsis –
- occurs irregularly, significance not clear.
Peristalsis in stomach:
- called as digestive peristalsis
- occurs at a rate of 3/ m
- takes origin from a pacemaker zone
- helps in mixing & propelling the food through stomach
Peristalsis in small intestine:
- same mechanism of production of peristaltic wave
- rate of movement—o.5 to 2 m/s
- always move towards the aboral direction(Law of intestine)
- helps in proper propulsion & digestion of food in intestine
Factors influencing peristalsis:
After meals – increases
vagal stimulation – increases
Sympathetic stimulation – decreases
Injury of GI tract – decreases
Gastrin & CCK – increases
Interdigestive Peristalsis:
- peristalsis during fasting i.e., when there is no food in the intestine
- takes origin in duodenum & spreads to ileum
- helps to clear any food residue that remains after previous meal
Peristaltic rush:
- peristaltic waves sweeping over long segments of intestine in
response to powerful irritation of intestinal mucosa
- helps to relieve intestine from irritants
- results in diarrhea
Antiperistalsis:
- movement of peristalsis towards oral (mouth) direction
- results in vomiting (expulsion of food through mouth)
3. DEFAECATION
Definition:
-The process of removal of unwanted food residues or faeces from rectum at
regular intervals
Mechanism of defaecation reflex:
Stimulus – Presence of faeces in rectum increasing the rectal pressure to 20 – 25 cm
of water
Receptors – stretch receptors
Afferent fibers – sensory fibers in pelvic nerve
Centre – sacral segments of spinal cord (S2, S3 & S4 )
Efferent fibers – motor fibers in pelvic nerve
Effect or Response – contraction of rectum & relaxation of internal anal sphincter)
Other events during defecation:
10
relaxation of external anal sphincter(controlled by pudendal nerve)

contraction of abdominal muscles
straightening of anorectal muscles
4. DIETARY FIBERS
Dietary fiber is the indigestible portion of food derived from plants. The main dietary fibers are
cellulose, hemicelluloses and lignin components of the vegetable products.
Physiological role ofdietary fibers
1.The ingested dietary fibers reach the large intestine in an essentially unchanged state
and thus add bulk to the feces. This play a role in defecation reflex by distending the
colon.
2.Speeds the passage of foods through the digestive system, which facilitates regular
defecation. This prevents constipation
Role of dietary fibers in prevention of diseases
1.Dietary fibers bind to bile acids in the small intestine, making them to get excreted in
the feces; this in turn lowers cholesterol levels in the blood.[3] Lowers total and LDL
cholesterol, which may reduce the risk of hypercholestremia, atherosclerosis and
cardiovascular disease
2.Dietary fibers increase food volume without increasing caloric content, providing
satiety which may reduce appetite. This helps to reduce obesity
3.Reduce the absorption of digested food stuffs. Delayed absorption of glucose regulates
blood sugar. This may lower risk of diabetes[63]
4.Insoluble fiber increases the rate at which wastes are removed from the body. This
means the body may have less exposure to toxic substances produced during digestion.
This gives protection against colorectal cancer
Therapeutic role of dietary fibers
The daily recommended intake of dietary fibers is about 25 to 35 gm/day
High fiber supplements have therapeutic role in following conditions:
In constipation
In spastic colon and diverticular disease
In diabetes and high cholesterol levels
3 MARKS
Describe the role of bile in digestion and absorption.

Role of bile in digestion:
Takes part in digestion of fat. The bile salts emulisify the fat i.e., reduce the
surface tension of fat there by breaking the fat globules into small size so that
water soluble enzymes (lipase) can act on it to digest.
Role of bile in absorption:
Takes part in absorption of fat. Bile salts form ‘Micelles’ in the centre of
11
which the fat digested products are dissolved. Fat is carried in this form to the
intestinal villi through the chyme. The ‘ferrying’ action of bile salts plays an
important role in absorption of fat & fat soluble vitamins
Laxative role:
By increasing the motility of intestine, bile salts increase the passage of food through intestine
Bacteriostatic role:
Bile salts inhibit the growth of bacteria in the intestinal lumen
Choleretic action:
Bile salts stimulate the secretion of bile from the liver
Cholagogue action:
Bile salts stimulate the secretion of CCK which increases the expulsion of bile from gall bladder
Bile salts prevent gall stone formation by excreting cholesterol
-----------------------------------------------------------------------------------------------------------------------
1
DIGESTIVE SYSTEM Applied

1. Mention the clinical condition resulting from the absence of bile in the digestive
tract
Steatorrhea – presence of fat in the stools due to failure of digestion & absorption of
fat as bile salts are absent
2. Why totals biliary obstruction leads to bleeding disorder?
Total biliary obstruction absence of bile in the digestive tract  failure of absorption of fat
& fat soluble vitamins  deficiency of vitamin K  failure of production of clotting factors
from liver  bleeding disorder
3. The intake of creamy milk before consuming alcohol prevents the alcoholic
intoxication. Explain the physiologic basis
Fat (creamy milk) inhibit gastric emptying  keeps the alcohol in the stomach for a long
time  Absorption of alcohol is slower in stomach than in intestine Prevents the sudden
rise of the blood alcohol to a high level and the consequent intoxication
4. Explain why excessive amounts of fat are excreted in faeces, in pancreatic insufficiency
and in obstructive jaundice
In pancreatic insufficiency, the availability of pancreatic lipase enzyme is less.In obstructive
jaundice, the bile salts are not delivered to GI tract. Both the conditions lead to failure of
digestion & reabsorption of fat. So it is excreted in the faeces
5. You feel heaviness in the stomach for a long time after a fatty meal. Give the reason.
Fat inhibits the gastric emptying and keeps the food in the stomach for a long time.That is
why heaviness is felt in the stomach for a long time after a fatty meal
6. A new born baby has persistent diarrhea and dehydration on breast feeding.
What is the reason, how will you treat the baby?
This is due to deficiency of Lactase enzyme in the GI tract. This makes the baby to become
intolerant to milk (Lactose intolerance). Either by administering commercial lactase
preparations or providing lactose free cow’s milk
7. Why is vitaminB complex is given to a patient treated with broad spectrum
antibiotics?
Broad spectrum antibiotics may destroy the intestinal flora (bacteria) which synthesize
Vitamin B complex .
8. Why partial or total gastrectomy leads to pernicious anemia?
Intrinsic factor which is required for the absorption of Vitamin B12 is produced from
gastric mucosa.. Partial or total gastrectomy  Absence or deficiency of intrinsic factor 
failure of absorption of vit. B12  Failure of maturation of RBC (pernicious anemia – a type
of megaloblastic anemia)
9. Why a patient with duodenal ulcer is advised to take frequent but small meals
and parasympatholytics?
Distension of GI tract will increase the gastric secretion thus aggravating the ulcer. Small
meals prevent distension. The deficiency in meeting the daily energy requirement can be
compensated by taking frequent meals.
Parasympathetic nerve stimulates gastric secretion. Parasympatholytic drugs
inhibit the parasympathetic activity there by reducing the gastric secretion.
10. A patient passes large bulky stool and also has intolerance for diet with high fat content.
Explain the physiological basis of these signs & symptoms.
The condition is called Steatorrhea. The large bulky stool is due to presence of fat in the
stools. This defect is due to defect in fat digestion & absorption. This may be due to either
pancreatic insufficiency or absence of bile salts .
11. A patient after gastrectomy has a following blood picture of MCV=120 μ3 and MCH 45
pgm. Make the most probable diagnosis and explain the cause
The condition is called pernicious anemia.
2
Cause:
Partial or total gastrectomy  Absence or deficiency of intrinsic factor  failure of
absorption of vit. B12  Failure of maturation of RBC pernicious anemia – a type of
megaloblastic anemia
12. Explain the purpose of using H2 – blockers in the treatment of peptic ulcer
Histamine stimulates gastric secretion . It acts through H2 receptors on gasric wall
Blocking the H2 receptors with drugs such as cimetidine or ranitidine suppress the
acid secretion.
13. What is Achalasia cardia? Describe its effect & treatment?
Achalasia is a condition in which the lower oesophageal sphincter fails to relax.
Effect:
The esophagus can not empty the food into stomach for many hours. The esophagus
becomes tremendously enlarged and may also get infected. The infection may lead to
ulceration of esophageal mucosa sometimes leading to severe substernal pain or even
rupture & death
Treatment:
Pneumatic dilation of the sphincter
Incision of the esophageal muscle (Myotomy)
Injection of botulinium toxin to inhibit Ach release
Administration of antispasmodic drugs to relax LOS
14. Give the physiological basis for alkaline urine immediately after meals.
Meals
↓
Elevation of gastric juice secretion
↓
Increased secretion of H+ ions
↓
Decrease in H+ ion concentration of blood
↓
Blood alkalosis
↓
Corrected by excretion of alkaline urine
This is called as postprandial alkaline tide.
15. Why a patient with duodenal ulcer is advised to take up
i. frequent and small meals
ii. yoga
iii. atropine
iv. omeprazole
v. Cimetidine
Frequent & small meals – already discussed
Yoga – to relieve mental anxiety which is one of the reasons for acidity
Atropine – parasympatholytic drug which reduces vagal stimulation of acid
Secretion
Omeprazole – blocks the H+ -K+ pump
Cimetidine – H2 blocker – blocks the H2 receptors of histamine
16. Why jaundice occurs in hepatic failure?
Jaundice is yellowish discolouration of the skin, sclera and mucous membranes
due to accumulation of free or conjugated bilirubin in the blood.
This may be due to
- decreased uptake of bilirubin into hepatic cells
- disturbance in the conjugation of bilirubin with glucronic acid in the liver
3
- disturbance in the secretion of conjugated bilirubin from hepatic cells into the bile
canaliculi.
Role of liver in bilirubin metabolism:
The bilirubin formed by hemolysis of RBC is taken into hepatic cells &
conjugated with glucronic acid by the enzyme glucronyl transferase. The conjugated
bilirubin (bilirubin glucuronide) is secreted into the bile which reach the intestine
through bile duct. Thus hepatic failure as in the cases Cirrohosis, drug toxicity,
hepatitis etc., leads to jaundice
17. A person with obstructive jaundice has prolonged clotting time – Explain.
Obstructive jaundice is mainly due to obstruction of bile ducts which leads to
unavailability of bile salts for absorption of fat & fat soluble vitamins. As vitamin K
absorption is reduced, synthesis of clotting factors by liver is disturbed. This causes
prolonged clotting time
18. What is heart burn? Discuss its pathophysiology and ways it might be treated?
Heart burn
It is otherwise called chalasia or GERD (Gastroesophageal reflux disease). This
condition is characterized by reflux of acid gastric contents into the esophagus due to
incompetency of LES (Lower Esophageal Sphincter) – inability to contract properly
Causes heartburn and esophagitis and leads to ulceration and stricture of the
esophagus due to scarring.
Treatment –
- Inhibiting the acid secretion with H2 blockers or Omeprazole
- Fundoplication ( wrapping the LOS with a portion of the fundus of the stomach)
19. What is dumping syndrome? List out the symptoms & describe the cause for
each symptom .
Dumping syndrome refers to a group of symptoms that occurs in patients with
gastrojejunostomy or total or partial gastrectomy. These symptoms appear about
hours after meals
Symptoms Cause
1. Weakness - Due to hypoglycemia

(Rapid absorption of glucose
↓
Insulin secretion
↓
Hypoglycemia)
2.Dizziness - fall in BP
(Rapid entry of hypertonic meals

into the intestine
↓
Osmosis of water into the gut
↓
↓plasma volume
↓
↓cardiac output
↓
Fall in BP)
3. Sweating - stimulation of autonomic reflexes
4
(secondary to distension of small intestine & also by hormones

released from the gut due to rapid entry of gastric contents into
the duodenum & jejunum)
Treatment:
- Small & dry meals
- Meals with some dietary fibers
- Avoiding milk & carbohydrate meals
- Daily and regular supplement of iron & Vit B complex (to prevent anemia)
20. A person’s ileum has been removed because of tumour. What is its long term effect?
Absorption of bile acids is prevented which leads to deficient fat absorption. This
may cause steatorrhea. Moreover entryof unabsorbed bile acids into the colon
increase the adenyl cyclase activity which inturn leads to intestinal secretion of water.
This may cause diarrhea.
21. “Proteins get absorbed as such from GI tract without getting digested’ – write such an
instance in case of infants. Give its significance
The protein antibodies in the maternal colostrum are undigested proteins absorbed by
endocytosis. They are largely secretory immunoglobulins & provide passive
immunity against infections
22. What is paralytic illeus?
A condition in which there is a diffuse decrease in intestinal motility in the small
intestine is called paralytic (adynamic) illeus. This occurs mainly after abdominal
operations. Characterized by irregular distensions in small intestine by pockets of gas
& fluid due to failure of propulsion of intestinal contents into colon.
Causes: Intestinal trauma in surgery or infection
Basis :
- activation of opiod receptors which directly inhibits intestinal
smooth muscles
- irritation of peritoneum causes reflex inhibition due to increased
discharge of sympathetic fibers in splanchnic nerves.
Treatment:Aspirating the gas & fluid till peristalsis returns (Intestinal peristalsis
returns in 6-8 hours, followed by gastric peristalsis, but colonic activity takes 2-3
days to return)
23. A patient with the history of chronic gastritis developed severe anemia. What
are the possible pathophysiological basis of anemia in this condition and what is
the possible physiological basis of management?
In chronic gastritis, there is damage of intrinsic factor secreting parietal cells of
gastric mucosa. Deficiency of intrinsic factor leads to malabsorption of vitamin B12
which causes pernicious anemia.
Management: Intramuscular injection of Vitamin B12
24. What is Hirshprung’s disease? What are the two main complaints of this
patient?
This is a condition characterized by infrequent defecation (once every 3 weeks) in
children which leads to abdominal distension, anorexia & lassitude. Also called as
aganglionic megacolon.
Causes:
Congenital absence of ganglionic cells in both the myenteric & submucosal
plexuses of a segment of distal colon. It may be probably due to failure of the
normal cranial to caudal migration of neuroblasts during development.
Basis:
Absence of peristalsis causes feces to pass the aganglionic region with
difficulty. This leads to infrequent defecation.
5
Treatment:
Surgical removal of the aganglionic region of the colon & anastomising the
portion of colon above it to the rectum
25. What type of metabolic disturbance will occur for a child who is having severe
diarrhea? What could be the cause? What treatment to be given?
Metabolic acidosis occurs due to loss of alkaline (sodium bicarbonate) fluid into the
stools. There is also loss of water & other electrolytes which leads to hypovolemia
dehydration & hypokalemia.
Treatment: Administration of ORS (oral rehydration solution)
26. Describe the pathophysiological aspects of vomiting
Vomiting refers to forceful expulsion of gastric & duodenal contents through the mouth.
It is a reflex process.
Cause:
Stimulation of vasomotor center either directly or through Chemotrigger Zone (CTZ)
Vomiting center:
Located in the reticular formation of medulla near nucleus tractus solitarius
Chemotrigger Zone:
Located in the area postrema
Activation of vomiting center:
Direct activation - ↑intracranial pressure & Meningitis
Afferent impulses – from upper GIT (Distension or irritation)
from higher centers (emotional stimuli)
from vestibular nuclei (motion sickness)
Activation of CTZ:
- Uraemia & radiation sickness
- Amorphine, digitalis & glucosides
Events during vomiting:
1. Nausea
2. Antiperistalsis in the upper GIT
3. Contraction of diaphragm
4. Arrest of respiration
5. Contraction of abdominal muscles
6. Relaxation of the esophagus & opening of UOS & LOS
27. A woman complaints of pain in her upper abdomen and the pain is worse
between meals & often she wakes up with severe pain. The antacids relieve the
pain.
a) What is the cause for her pain?
b) Why is the pain worse between meals?
c) How do antacids work?
a) Cause: Peptic ulcer
b) Worsening of pain between meals is due to increased basal acid secretion
c) Antacids neutralize the HCl by forming a complex
28. What type of anemia will occur in patients who have intestinal sprue/ What is
the cause of anemia? What treatment is advised?
Anemia in patients with intestinal sprue – Pernicious anemia
Cause – Folic acid deficiency
Treatment – Administering antibiotics like tetracyclin
29. What are the different agents used to control the stimuli of HCl secretion in ulcer
patients? Explain the physiological basis for the treatment of peptic ulcer.
Stimuli for HCl secretion Agent to control Basis
Acetylcholine Atropine Acetylcholine blocker
6
Histamine Ranitidine, Cimetidine H2 blocker

Helicobacter pylori Ampicillin Antibiotic
Gastrin Proglumide ↓gastrin secretion
H+- K+ pump Omeprazole Proton pump blocker
Anxiety Yoga & Anxiolytic drugs Anxiolytic
30. A lady about 30 years complains of pallor of conjunctiva, Stomatitis and spoon shaped
nails. What is the condition & How will you treat her?
Condition – Iron deficiency anemia
Treatment – Administration of iron supplementation & iron rich food
31. The bacteria on the colon exist in a symbiotic relationship with the host. How does the
host benefit from this relationship and what harmful effect may occur to the host?
Benefit: The colonic bacteria synthesize Vitamin B complex and also help to breakdown the
unabsorbed food residue.
Harmful effect: The host becomes susceptible to radiation poisioning & sepsis.
32. A patient with chronic abdominal pain has H/O loss of weight and passing large
quantitity of clay coloured stool for past few months. What is the condition called and
describe the pathophysiology of this condition.
Condition:
Steatorrhea (presence of fat in the stools due to failure of digestion &absorption of fat).
Pathophysiology:
- This may be due to either pancreatic insufficiency (absence of pancreatic
Lipase) or absence of bile salts
- In pancreatic insufficiency, the availability of pancreatic lipase enzyme is less.
- In obstructive jaundice, the bile salts are not delivered to GI tract.
- Both the conditions lead to failure of digestion & reabsorption of fat
33. A 28 year old man is admitted to hospital with complaints of difficulty in swallowing.
The investigations revealed the esophagus is greatly dilated and food accumulates in it,
tricking only slowly into the stomach.
i) What is this disorder called?
ii) What is it due to?
iii) What treatment is advised?
i) Disorder - Achalasia cardia
ii) Cause - lower oesophageal sphincter fails to relax
iii) Treatment:
Pneumatic dilation of the sphincter
Incision of the esophageal muscle (Myotomy)
Injection of botulinium toxin to inhibit Ach release
Administration of antispasmodic drugs to relax LOS
34. A 40 year old male complaints of fatty, bulky, clay coloured stools.
i) What is the condition called?
ii) What are the causes for the above condition?
iii) Which treatment is advised?
i) Condition - Steatorrhea
ii) Causes - due to failure of digestion & absorption of fat. This may be due to either
pancreatic insufficiency (absence of pancreatic Lipase) or absence of bile salts
iii) Treatment - Avoidance of fatty food & treatment for the cause
EXCRETION K.SENTHAMIL SELVI
10 MARKS
1. PROCESS OF URINE FORMATION

Every day kidney produces 1 – 2 liters of urine.
The mechanism of urine formation involves three processes:
a) Glomerular filtration
b) Tubular reabsorption
c) Tubular secretion
a) Glomerular filtration:
- Process by which the fluid along with the substances dissolved in it passes from the
glomerular capillaries in to the Bowman’s capsule is called glomerular filtration
- Blood cells and plasma proteins are not filtered
- Filtration occurs through filtering membrane which is made up of 3 layers – Fenestrated
capillary endothelium, basement membrane & podocytes (epithelial cells of Bowman’s
capsule) with filtration slits
- The fluid which gets collected in the capsule is called filtrate
- The amount of filtrate formed per minute (GFR – Glomerular Filtration Rate) is 125ml.
- This is mainly determined by net filtration pressure which depends upon the Starling forces
acting across the filtering membrane – Glomerular capillary hydrostatic & colloidal osmotic pressure,
Bowman’s capsule hydrostatic pressure
b) Tubular reabsorption:
- Passage of water and solutes from the filtered fluid in the kidney tubule into the blood is called
tubular reabsorption
- Solutes which are reabsorbed are nutrients (glucose & aminoacids), electrolytes (sodium,
potassium & chloride) & ions such as bicarbonates.
- Ihe modes of transport are both passive & active transport mechanisms
Reabsorption At Proximal Convoluted Tubule:
- Majority of reabsorption takes place at PCT as the surface area is increased due to presence
of brush border microvilli
- 65% of filtered water, sodium, chloride, potassium and other solutes
- 100% of glucose and aminoacids
- Sodium is reabsorbed by secondary active transport along with substances like glucose and
aminoacids
- This is followed by osmosis of water into the blood. The reabsorption of water at PCT is
called obligatory reabsorption of water
- The reabsorption of water and sodium are exactly proportional. So the fluid which leaves
the PCT is isotonic
Reabsorption At Loop of Henle:
- Loop of Henle consists of three segments - Descending limb, thin ascending limb &
thick ascending limb
- About 20% of filtered sodium and chloride, 15% of filtered water and cations such as K+,
Ca2+ and Mg2+ are reabsorbed in the Loop of Henle
- In the descending limb, water absorption occurs passively because of hypertonic
interstitial fluid in this part
- The thin ascending limb is impermeable to water. Limited passive absorption of sodium
and chloride occurs
- Thick ascending limb is impermeable to water. 20% of filtered sodium and chloride and
other cations are reabsorbed here by the following mechanisms:
- Sodium, potassium – 2 chloride symporter mediated active transport of sodium
- Na+ - H+ antiporter mediated active reabsorption
- Paracellular passive reabsorption of Na+, K+, Ca2+ & Mg+
- Sodium reabsorbed here is the main driving force behind the countercurrent multiplier
system which concentrates sodium and urea in medullary interstitium
- As the reabsorption of solutes is not followed by water reabsorption, the fluid that leaves
this segment is hypotonic compared to plasma. Hence this segment is called diluting
segment
Reabsorption At Distal Convoluted Tubule (DCT) & Collecting Duct (CD)
- Approximately 7% of filtered NaCl & 8 to 17% of water is resbsorbed
- Late DCT & CD have two cell types - “P” (Principal) cells & “I” (Intercalated) cells
- Principal cells reabsorb Na+, Cl- & H2O
-
Intercalated cells reabsorb K+
- H2O reabsorption by principal cells is influenced by the hormone ‘ADH’-Anti Diuretic
Hormone. The reabsorption of water at this segment is called facultative reabsorption of
water.
-
Na+ reabsorption by principal cells is influenced by the hormone aldosterone which is
secreted from the adrenal cortex
c)Tubular Secretion:
The substances which escape filtration are transported from peritubular capillary in to the tubular fluid.
This transport is called tubular secretion.
Substances secreted:
-
H+ ions, K+, NH3-
-
Drugs
-
Pencillin
-
Creatinine
Secretion at PCT:
-
Organic anions & cations
-
Exogenous organic compounds
-
Certain drugs
-
H+ & NH3- are secreted. H+ is secreted in exchange with Na+ absorption. This is mainly
utilized for the absorption of HCO3-
Secretion at DCT & CD:
- K+ secretion by principal cells takes place. This is increased by hormone aldosterone
- H+ & NH3- are secreted. H+ secretion by intercalated cells is mainly responsible for
acidification of urine
2. GFR (GLOMERULAR FILTRATION RATE) & ITS REGULATION

Definition: The amount of filtrate that is formed by both the kidneys per minute is called
glomerular filtration rate
Normal value:
125 ml / minute
180 lt / minute
Factors regulating GFR:
GFR = Kf X EFP ( Kf – Filtration coefficient, EFP – Effective Filtration Pressure)
1. Kf = Filtration coefficient which denotes the efficiency of the filtering membrane to filter
the plasmaThis depends upon the following factors:
A. Thickness of filtering membrane: Inversely proportional to Kf . Increase in thickness
reduces Kf and thereby reduces GFR also
B. Surface area of the membrane: Directly proportional to Kf & GFR
– the normal surface area is about 0.8 m2
– Contraction of the messangial cells compresses the glomerulus & reduces the area
of the membrane
C. Permeability of the membrane:
– Glomerular capillaries are 50 times more permeable than capillaries of skeletal
muscle.
– Permeability of the membrane is influenced by
– size of the particles filtered
– charge of the particles filtered
– Charge of the pores in the filtering membrane
- Particles below 4 nm size (both negative & positive charged) are filtered easily
- Particles above 8 nm size ( both negative & positive charged) are not filtered
- Particles of 4-8 nm size are filtered with difficulty (Positively charged particles
are filtered in this size range where as negatively charged particles are not
filtered)
Reason: The negative charge of the pores in the filtering membrane repel the
negatively charged particles
E.g – Albumin which is about 6 nm size is not filtered as it is negatively charged
particle
2. Effective Filtration Pressure: It is the net outward pressure which determined by forces
acting across the filtering membrane. These forces are called Starling forces.
Starling Forces acting across the filtering membrane:
1. Glomerular capillary hydrostatic pressure (PGC) = 45 mmHg (favors filtration)
2. Glomerular capillary osmotic pressure (πGC) = 25 mmHg (oppose filtration)
3. Bowmans capsular hydrostatic pressure (PBS) = 10 mmHg (oppose filtration)
4. Bowmans capsular osmotic pressure (πBS) = 0 (no effect on filtration)
EFP = Forces favoring filtration – Forces opposing filtration
EFP = PGC + πBS – PBS + πGC
= (45+0) – (10 + 25)
= 10 mmHg
Thus GFR = Kf X EFP
= 12.5 X 10
= 125 ml / minute
Conditions which alter Starling’s forces:
Glomerular Hydrostatic pressure (PGC):
i) Change in systemic blood pressure – drectly proportional to PGC

ii) Constriction of afferent arteriole – decreases PGC
iii) Constriction of efferent arteriole - increases PGC
Glomerular osmotic pressure (πGC):
i) Dehydration - increases πGC

ii) Malnutrition - decreases πGC
Bowman’s capsular Hydrostatic pressure (PBS):
i) Ureteral obstruction – increases PBS

ii) Edema of the kiney inside the tight renal capsule – increases PBS
C) Renal blood flow:
- directly proportional to GFR. Renal bood flow is influenced by nerves, hormones like
catecholamines, angiotensin, dopamine & ANP
D) Sympathetic stmulation:
-strong acute sympathetic stimulation  constriction of both afferent and efferent
arterioles decrease in renal blood flow  decrease in GFR
-------------------------------------------------------------------------------------------------------------------------------
3. COUNTERCURRET MECHANISM OF CONCENTRATING THE URINE
Normal osmolarity of urine: 300 mosm/lt
Osmolarity of diluted urine: Upto 50mosm/lt
Osmolarity of concentrated urine: Upto 1200mosm/lt
Requirements for concentrating the urine:

1. ADH
2. Hyperosmolar medullary interstitium
Factors contributing to hyperosmolarity of medullary interstitium:

1. Countercurrent system
2. Reabsorption at DCT & CD
3. Urea recirculation
1. Countercurrent system: A system in which the inflow runs in parallel, in opposite direction
& in close proximity to the outflow
Components of countercurrent system in kidney:
a) Loop of Henle (contercurrent multiplier)
b) Vasarecta (countercurrent exchanger)
Role of Loop of Henle as countercurret multiplier in countercurrent mechanism:
To generate osmotic gradient & hyperosmolarity of medullary interstitium
Mechanism –
- Diffusion of water out of thin descending limb of LOH (This makes the fluid in the
tip of the loop to become more concentrated than the surrounding interstitum)
- Passive reabsorption of solutes from the hypertonic fluid in the tin ascending limb
(This helps in multiplication of interstitial osmolarity)
- Active reabsorption of sodium & chloride in the thick ascending limb of Loop of
Henle (This helps in building up of a higher interstitial osmolarity)
Role of vasa recta as countercurrent exchanger in countercurrent mechanism:
To maintain the osmotic gradient & hyperosmolarity of medullary interstitium
Mechanism –
Descending limb of vasa recta :
- Solutes diffuse into the lumen
- Water diffuses out
- The osmolarity of blood increases from 300 milliosmoles to 1200 milliosmoles towards
the tip of vasarecta
Ascending limb of vasa recta:
- Solutes move out
- Water diffuses in
- The osmolarity of the blood decreases from 1200 milliosmoles to 300 milliosmoles from
the tip upwards
So the solutes are exchanged for water between the ascending and the descending limbs
of vasarecta. This maintains the hypertonicity of medulla
Loop of Henle & Collecting duct
2. Reabsorption in the DCT & Collecting duct:

 Sodium ions are actively absorbed from distal tubule and collecting duct under the
influence of aldosterone.
 Sodium ions are accompanied passively by chloride ions.
 This also increases the medullary osmotic gradient
3. Urea recirculation:
 Large amounts of urea is reabsorbed in the medullary collecting duct.
 The urea which moves into the interstitium is secreted in to the descending &
ascending limb of LOH.
 Again it is reabsorbed in the medullary collecting duct.
 This recirculation of urea before it is excreted in the urine helps to generate medullary
osmotic gradient
 Urea recirculation contributes 40% to hyperosmolarity of medullary interstitium
ADH: Increases urea reabsorption (This increases the interstitial osmolarity)
Increases water reabsorption (This makes the urine concentrated)
Renal blood flow: Slow rate of blood flow through the medulla causes retention of sodium in
the medullary interstitium
5 marks & 3 marks

1. SPECIAL FEATURES OF RENAL CIRCULATION
a. Renal Blood Flow (RBF): The normal blood flow to kidney is about 1200 ml. This
forms about 25% of cardiac output. Kidney receives the maximum blood flow next to
liver.
b. Portal circulation: An arteriole is interposed between two capillaries. Glomerulus
(capillary tuft) – Efferent arteriole – Peritubular capillary
c. High pressure system: The pressure in the glomerular capillaries is 45 mmHg. This is
much higher compared to the pressure in the systemic capillaries which is 30 mmHg.
This high pressure is the main driving force for glomerular filtration
d. Vasa recta: Longest capillaries in the form of hairpins. It runs parallel to LOH of
juxtamedullary nephron. It acts as countercurrent exchanger and maintains the osmotic
gradient from the cortex towards the inner medulla of kidney
e. Autoregulation: The ability of kidney to regulate its own blood flow is called
autoregulation. This helps the kidney to maintain the blood flow constant between a
systemic pressure of 90 – 220 mmHg. Autoregulation is achieved by myogenic principle
and tubuloglomerular feedback mechanism
f. Regional blood flow: Cortex receives the maximum blood flow whereas the inner
medulla receives the minimum blood flow
g. Arterio-venous difference of oxygen is minimal compared to the other organs
h. Renal O2 consumption is high
2. JUXTAGLOMERULAR APPARATUS
Juxta Glomerular Apparatus refers to the collection of specialized cells located very near to the
glomerulus
Components:
a) Juxtaglomerular cells
b) Macula densa cells
c) Mesangial cells
Juxtaglomerular cells:
- Modified smooth muscle cells of afferent arteriole
- Secrete renin
Macula densa Cells:
- Specialized tubular epithelial cells at DCT
- Act as chemoreceptors ( detect the changes in the concentration of sodium and chloride in
tubular fluid)
Messangial cells:
- Supporting cells present around glomerulus
- Contractile in nature
Functions of JG Apparatus:
1. JG cells secrete renin that activates Renin- Angiotensin system which takes part in
regulation of blood volume and pressure
2. Macula densa cells act as sensor in Tubuloglomerular feedback which takes part in
autoregulation of renal blood flow and GFR
3. JG apparatus helps to regulate the volume and osmolarity of ECF
4. It secretes erythropoietin which influences erythropoiesis
3. TUBULOGLOMERULAR FEEDBACK
Tubuloglomerular feedback refers to a mechanism which maintains a constant renal blood flow
& GFR inspite of the changes in mean arterial pressure.
It involves the feedback signals from DCT when there is a change in the concentration of sodium
chloride in the tubular fluid
Increased renal arterial pressure Decreased renal arterial pressure
↓ ↓
Increased RBF & GFR -- Decreased RBF & GFR +
↓ ↓
Increased NaCl concentration Decreased NaCl concentration
In the tubular fluid in the tubular fluid
↓ ↓
Sensed by macula densa cells Sensed by macula densa cells
↓ ↓
Feedback effect Feedback effect
(Release of adenosine) (Less release of adenosine)
↓ ↓
Constriction of afferent arteriole Dilation of afferent arteriole
4. MICTURITION & CYSTOMETROGRAM
Micturition
Definition: The periodic complete voluntary emptying of the bladder is called micturition
Events involved:
- Micturition is basically a spinal reflex
- Influenced by higher centers
a) Micturition reflex
b) Voluntary control of micturition
c) Role of other muscles in micturition
a) Micturition reflex:
Stimulus: Filling of bladder by 300 to 400 ml of urine
Receptors: Stretch receptors in the detrussor muscle
Afferent: Sensory fibers in pelvic nerve
Center: S2, S3 & S4 of sacral segments
Efferent: Motor fibers in pelvic nerve
Effector organ: Detrussor muscle of urinary bladder & internal urethral sphincter
Response: Contraction of detrussor muscle of the bladder & relaxation of the urethral
Sphincter
(Excitation of parasympathetic afferent fibers causes inhibition of pudendal nerve 
relaxation of external urethral sphincter)
b) Voluntary control of micturition: (Role of supraspinal centers)
Supraspinal centers involved
Pons – Facilitate
Mid brain – Inhibits
Posterior hypothalamus – Facilitate
Limbic system -- Facilitate
Basal ganglia – Inhibits
Cerebral cortex – Inhibits
c) Role of other muscles:
Perineal & abdominal muscles help the emptying of bladder
Cystometrogram
Definition: Cystometrogram is a graphical record showing the relationship between the
intravesicular volume and pressure of urine in the urinary bladder
Phases of normal cystometrogram:
a) Phase Ia
b) Phase Ib
c) Phase II
a) Phase Ia : Initial rise in intravesicular pressure
- Rise in intravesicular pressure when about 50 ml of urine is collected in the
bladder
Basis: Filling of bladder with urine  stretching of bladder wall  contraction of
muscles of bladder wall  increase in pressure from 0-10 cm of H2O
b) Phase Ib: (Pleateau phase)
- No rise in the pressure (remains at 10 cm of H2O) till the bladder volume is
400 ml
Basis: Can be explained by Laplace Law (Laplace law: P = 2T / R where ‘P’ is the
pressure, ‘T’ is the tension in the wall & ‘R’ is the radius of the bladder
Explanation:
Urine accumulation  increase in tension of the bladder wall, but there is
increase in radius of the bladder too (called as plasticity of the smooth muscle). The
effects of these two factors get neutralized & the pressure remains same.
c) Phase II: Steep rise in intravesicular pressure:
- Starts beyond 400 ml
- Tension of wall increases due to contraction of detrussor muscle, but
radius is not increased. So, the pressure increases (20 cm to 40 cm of
H2O)
-This stimulates voiding sensation (triggering the micturition reflex)
5. ACIDIFICATION OF URINE
- Normally the urine is acidic with a pH range from 4.5 to 6.0.
- Acidification of urine is brought about by H+ secretion in to the tubular fluid
- H+ secretion takes place throughout nephron.
- H+ secreted at PCT & LH is utilized for absorption of HCO3-. Does not contribute to
acidification of urine.
- H+ secreted in small amounts in the DCT & CD is responsible for the acidification of
urine
Mechanism Of H+ secretion:
BLOOD Tubular Epithelial Cell LUMEN
H2O + CO2
↓
H2CO3
HCO3- HCO3- H+ ATP H+ (In DCT)
H+
+
K K+ (In CD)
Fate of H+ ion in the lumen:
1. Reaction with HCO3-:
BLOOD TUBULAR CELL LUMEN
H2O + CO2 CO2 H2O
H2CO3 H2CO3
HCO3 - HCO3- H+ H+ + HCO3-
2. Reaction with Ammonia (NH3)
Blood Cell Lumen

Na Na + Cl
CO2 + H2O
H2CO3
HCO3- H+
H+ + Cl
Glutamine NH3 NH4Cl
NH3
3. Reaction with Na2HPO4 (Titratable acidity)
CELL
Blood Lumen
Na2HPO4
Na + NaHPO4
HCO3- +
H
H+ + NaHPO4
H2CO3
NaH2PO4
CO2 + H2O
6.PLASMA CLEARANCE
Definition – Defined as the volume of plasma that is cleared of a substance in one minute by
excretion of that substance in urine
Clearance tests used to measure
GFR – Inulin clearance, Creatinine clearance & Urea clearance
RBF (Renal Blood Flow) – PAH clearance
Plasma clearance of Inulin :
- Inulin is freely filtered in the glomerulus
- neither reabsorbed nor secreted in the tubules
- so used to determine GFR
The formula used to calculate Inulin clearance:
UxV
---------- (U- Inulin concentration in urine(mg/ml), V- Volume of urine
P excreted(ml/mt), P- Plasma concentration of Inulin mg/ml)
Normal value – 125ml/min
Urea clearance:
Two types: Maximum & Standard urea clearance
Maximum urea clearance: Uu X V
----------- when the urine output is more than 2ml/m
Pu
Normal value = > 75 ml / minute
Standard urea clearance: Uu X√V
----------- when the urine output is less than 2ml/m
Pu
Normal value = 57 ml / minute
Plasma clearance of PAH:
- 90% cleared from plasma
- used to determine renal plasma flow
Formula to calculate RPF:
Clearance of PAH
--------------------------
PAH extraction ratio
Clearance of PAH: UxV

--------
P
Normal Value – 630 ml / minute
6. DIURETICS
Diuretics are the substances which cause diuresis (increase in urine volume). They either inhibit
the reabsorption of water or inhibit the reabsorption of solutes. Unreabsorbed solutes hold the
water in the tubules and cause osmotic dieresis
CLASSIFICATION SUBSTANCE SITE OF MECHANISM OF ACTION
ACTION
WATER DIURETIC Water - Inhibits ADH secretion

Alcohol - Inhibits ADH secretion
Coffee & Tea - Increase GFR & decrease reabsorption

of Na+
Lithium ADH antagonists
& Democlocycline -
OSMOTIC
DIURETIC
1. Carbonic Acetazolamide PCT Inhibit the enzyme – carbonic anhydrase

anhydrase inhibitor Methazolamide Inhibit the reabsorption of Na+ & HCO3-
2. Loop Diuretic Furosemide (Lasix) Thick Ascending Inhibit the Na+ - K+ - 2Cl- Cotransporter
Bumetanide Limb of LH Inhibit the reabsorption of Na+
Ethacrynic acid
3. Thiazide Hydrochlorothiazide Early DCT Inhibit Na+- Cl- symport

Chlorothiazide
Trichlormethiazide
Metolazone
4. K+ sparing Spironolactone Collecting duct Aldosterone antagonist

diuretics Amiloride Block the epithelial Na+ channels
Triamterene
1. CORTICAL & JUXTAMEDULLARY NEPHRON
CORTICAL NEPHRON JUXTAMEDULLARY NEPHRON

Location of Glomerulus Cortex Near junction of cortex and medulla
Number 85% 15%
Loop of Henle Short Long
Vasarecta Absent Present
Fluid flow Faster Slow
Major Function Excretion of waste Concentration of urine by
products countercurrent system
2. FILTERING MEMBRANE COMPLEX
- Filtration membrane is otherwise called as filtration barrier or glomerulo-capillary
membrane
- It is the membrane through which the fluid from the plasma of glomerular capillaries pass
in to the Bowman’s Capsule.
Components:
1. Capillary endothelium:
– Fenestrated (contains pores of 70-90 nm diameter)
– Freely permeable to water, small solutes & small proteins
2. Basal lamina:
– Union of glomerular capillary basement membrane & Bowman’s capsule
basement membrane
– Consists of glycoproteins & mucopolysaccharides
– Prevents filtration of proteins as strong negative charges are associated with

proteoglycans in the basal lamina
3. Bowman’s Capsule Visceral Epithelium:
– Formed by special cells called podocytes
– Podocytes have finger like processes called pedicels
– The pedicels interdigitate to cover the basement membrane & they are separated
by gaps called filtration slits (25 nm diameter)
3. INNERVATION OF URINARY BLADDER

Sympathetic nerve supply (Hypogastric nerve) – T12 to L2
Site of supply: Trigone of bladder & internal urethral sphincter
Functions:
a) Carry pain sensation from bladder
b) On stimulation, causes relaxation of bladder & contraction of internal
urethral sphincter (called as nerve of filling)
Parasympathetic nerve supply (Pelvic nerve) – S2, S3 & S4
Site of supply: Trigone of bladder & internal urethral sphincter
Functions:
a) Carry stretch and pain sensation from bladder
b) On stimulation, causes contraction of bladder & relaxation of internal
urethral sphincter (called as nerve of emptying)
Somatic nerve supply (Pudendal nerve) – S2, S3 & S4
Site of supply: External urethral sphincter
Function:
On stimulation, causes contraction of external urethral sphincter (voluntary
control of micturition)
WATER REABSORPTION
Amount of filtrate formed = 125 ml/minute or 180 lt/day
Amount of filtrate reabsorbed = 124 ml / minute or 178.5 lt/day
Amount of fluid excreted in urine = 1.5 lt /day
Reabsorption at PCT (65% of filtered fluid)
Mechanism: Pumping of sodium out of tubular epithelial cells by Na+-K+ ATPase pump
↓
Passive diffusion of Na+ along with other solutes
↓
Hypoosmolarity of tubular fluid
↓
Osmosis of water into the cells
(through water cannels called “aquaporins”)
This type of osmosis of water in PCT is called “obligatory water reabsorption”
Reabsorption at LH: About 15% of filtered fluid is absorbed at the thick ascending limb of
Loop of Henle
Mechanism: Diffusion independent of solute reabsorption
Reabsorption at DCT & CD: (5% at DCT & 14.7% at CD)
Mechanism: Osmosis of water through aquaporins is influenced by the hormone ADH (Anti
Diuretic Hormone) secreted from posterior pituitary. This type of water
reabsorption at DCT & CD under the influence of ADH is called
“ facultative water reabsorption”.
4. PROTEINURIA
Presence of protein in urine more than the usual amount (100 mg/dl) is called proteinuria
Most common protein found is albumin. So the defect is commonly called albuminuria
Cause:
- Usually the proteins are not filtered. As they are negatively charged, they are repelled by
negative charges at the pores of glomerular capillary wall
- In cases of renal diseases like nephritis, the negative charges are dissipated.
- The permeability of the glomerulus to protein is increased.
Effects:
- Loss of protein from plasma leads to hypoproteinemia
- Hypoproteinemia leads to decreased colloidal osmotic pressure
- Decreased colloidal osmotic pressure  decreased plasma volume & edema
Orthostatic proteinuria:
Proteinuria in standing position
5. AUTOREGULATION
Definition: Ability of the kidneys to regulate their own blood flow inspite of the changes in
systemic blood pressure is called autoregulation
- Seen between a pressure range of 90 – 120 mmHg
- Seen even after cutting of renal nerves & in an isolated kidney perfused with isotonic saline
Mechanisms:
a) Myogenic theory
b) Tubuloglomerular feedback
Myogenic theory:
Increase in blood pressure  stretching of smooth muscle of afferent arteriole 
contraction of smooth muscle  vasoconstriction  decrease in blood flow
Tubuloglomerular feedback (also called as chloride feedback theory):
Mechanism: Increase in blood pressure  Increased renal blood flow  Increased GFR
 increased chloride concentration at macula densa  increased
absorption of chloride at macula densa  increased absorption of chloride
at macula densa  release of adenosine by JG apparatus  constriction of
afferent arteriole & contraction of messangial cells  decrease in RBF &
GFR
Decrease in in blood pressure  Decreased renal blood flow  Decreased
GFR  decreased chloride concentration at macula densa
Vasoconstrictor mechanism Vasodilator mechanism

(production of angiotensin II & activation of (Release of dopamine & NO
Sympathetic fibers) Less release of adenosine)
(The opposing effect of the above mechanisms maintains the constant blood flow to the
kidney)
1
EXCRETION - applied
1. Why albumin is absent in normal individual’s urine?
Albumin is negatively charged particle. It is repelled by negatively charged pores in
the glomerulo – capillary membrane. So it is not filtered by glomerulus and it remains
in the plasma itself. That is why albumin does not appear in the urine
2. Explain the pathophysiology of glycosuria and polyuria in Diabetes mellitus.
Glycosuria in DM – The plasma glucose level exceeds the renal threshold value
(180 – 200 mg %), So glucose starts appearing in the urine.
Polyuria in DM – Glucose is an osmotically active particle. Presence of glucose in
the urine causes osmotic diuresis that leads to polyuria
3. Compare osmotic diuresis with water diuresis
Osmotic diuresis Water diuresis
1. Diuresis caused by presence of 1. Diuresis caused by failure of
osmotically active particles in the reabsorption of water.
tubular fluid
2. Solutes hold water in the tubule 2. Capacity of the kidney tubule to
& prevents reabsorption of water reabsorb water is impaired
3. Occurs in diabetes mellitus due to 3. occurs in diabetes insipidus due to
presence of glucose in the urine deficiency of ADH
4. The kidneys play an important role in bringing the blood pressure after
a bout of haemmorhage. Explain
Haemmorhage leads to decrease in blood flow through renal artery  Release of renin
from Juxtaglomerular cells of kidney  Activation of angiotensinogen to Angiotensin
I  Conversion of angiotensin I to Angiotensin II  Vasoconstriction  increase in
blood pressure
5. An elderly patient with chronic renal failure develops anemia. What is the cause
for anemia? How will you manage this condition?
Erythropoietin – a hormone that stimulates erythropoiesis is produced from
Juxtaglomerular cells of kidney. That is why in chronic renal failure where there is
extensive damage of kidney tissues , the erythropoietin production is decreased. This
leads to anemia.
Treated by administration of Erythropoietin
6. What is glycosuria? Mention two causes for Glycosuria
The presence of glucose in the urine is called as Glycosuria
Causes:
1. Hyperglycemia (when plasma glucose level exceeds renal threshold value)
2. Renal Glycosuria (Plasma glucose level is normal, but the threshold value
decreases)
7. Apply the ‘Law of Laplace’ in the micturition reflex of urinary bladder
Laplace Law: P = 2T
--- Where P is pressure, T is tension & R is radius
R
When bladder is filled with urine the pressure remains same for certain range of
volume of urine in the bladder.( 100 – 400 ml). This is because the bladder radius
also increases along with tension. Thus the bladder is filled properly before
micturition starts
1
2
8. Give the reasons of overflow incontinence in spinal cord transection.

The first stage of spinal transection is spinal shock. During this period, there is no
tone in the muscles of bladder. The bladder becomes flaccid & unresponsive. So the
bladder becomes overfilled & urine dribbles through the sphincters (overflow
incontinence)
9. Briefly explain how kidney compensates metabolic alkalosis
Kidney stops reabsorbing the bicarbonates which are filtered from plasma in the
glomerulus. So the bicarbonate is excreted in the urine in a large amount making the
urine alkaline. Thus the metabolic alkalosis is compensated by kidney
10. Briefly explain the diuretic action of carbonic anhydrase inhibitors
Carbonic anhydrase inhibitors like Acetazolamide inhibits the enzyme ‘ Carbonic
anhydrase’ which catalyzes the formation of carbonic acid. As carbonic acid is not
available, the formation of H+ ions from that is also reduced. So Na+ - H+ counter
transport is less. This less secretion of H+ leads to less reabsorption of Na+ which is
now excreted in the urine in a large amount. This leads to osmotic diuresis.
11. Explain the mechanism of formation of hypertonic urine
By reabsorbing water as much as possible, the kidneys form hypertonic urine (1200
mOsm/lt.) This requires two conditions:
1. Increased levels of ADH (increases the permeability of tubules to water)
2. Hyperosmolarity of medullary interstitial fluid (provides the osmotic gradient
for reabsorption of water)
Hyperosmolarity of medullary interstitial fluid involves the countercurrent system
which includes Henle’s loop & vasarecta.
The mechanisms involved:
a) Active reabsorption of solutes in the ascending limb of Henle’s loop
b) Passive diffusion of urea from the medullary collecting ducts into the
interstitium
c) Very less reabsorption of water
d) Minimized washout of solutes from the interstitium due to the countercurrent
exchanger (vasarecta)
12. Explain briefly why Inulin is used to determine GFR
Advantages of using Inulin in determining GFR:
- it is freely filtered in the glomerulus
- it is neither reabsorbed nor secreted in the tubules
13. Briefly explain renal plasma clearance for Inulin & PAH indicating their
significance
Plasma clearance of Inulin :
- Inulin is freely filtered in the glomerulus
- neither reabsorbed nor secreted in the tubules
So used to determine GFR
The formula used to calculate Inulin clearance:
UxV
---------- (U- Inulin concentration in urine(mg/ml), V- Volume of urine
P excreted(ml/mt), P- Plasma concentration of Inulin mg/ml)
Normal value – 125ml/min
Plasma clearance of PAH:
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3
- 90% cleared from plasma

- used to determine renal plasma flow
Formula to calculate RPF:
Clearance of PAH
--------------------------
PAH extraction ratio
Clearance of PAH:
UxV
--------
P
14. What are ‘loop diuretics’? How do they act?
Loop diuretics such as flurosemide (Lasix) inhibit the Na- K – 2 Cl co transporter
in the thick ascending limb of loop of Henle. As sodium absorption is inhibited, it is
excreted in the urine. This causes osmotic diuresis.
15. Presence of albumin in urine suggests renal dysfunction. Explain why
Albumin is normally absent in the urine as it is not filtered in the glomerulo capillary
membrane due to its negative charges. But in renal dysfunction like nephritis or
nephrosis, the negative charges of pores in the membrane are abolished. So albumin
is filtered & excreted in the urine
16. Explain briefly the effect of acute complete transection of spinal cord
The first stage of spinal transection is spinal shock. During this period, there is no
tone in the muscles of bladder. The bladder becomes flaccid & unresponsive. So the
bladder becomes overfilled & urine dribbles through the sphincters (overflow
Incontinence)
The second stage is stage of reflex activity. During this stage the Micturition reflex
returns, but there is no voluntary control & no inhibition or facilitation from higher
centres. The bladder capacity is reduced & the bladder becomes hypertrophied. The
reflex becomes hyperactive. This type of bladder is called Spastic neurogenic bladder
17. Briefly explain the effects of denervation (destruction of both afferent &
efferent nerves) on bladder function
In the beginning, the bladder is flaccid & distended .Then gradually the bladder
becomes active, shrunken (reduced in size) & the wall of the bladder becomes
hypertrophied. The hyperactivity may be due to denervation hypersensitivity
18. Explain the principle of ‘Dialysis’
The blood is made to pass through the minute channels bounded by a thin membrane.
On the other side of the membrane is a dialyzing fluid into which unwanted
substances in blood pass by diffusion.
19. What is the effect of increased arterial pressure on urinary output?
Increase in arterial pressure leads to increase in glomerular hydrostatic pressure. This
causes increase in GFR. So urinary output increases.
20. A patient complaints of loss of control on his micturition following recovery
from a spinal injury. What could be the nature of bladder dysfunction and what
is the cause of dysfunction? What investigation you would like to perform to
confirm the nature of dysfunction.
The bladder capacity is reduced & the bladder becomes hypertrophied. The reflex
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becomes hyperactive. This type of bladder is called Spastic neurogenic bladder.

Cause: There is no voluntary control & no inhibition or facilitation from higher
centres.
20. A child who is infected with Streptococcal sore throat, after 1-3 weeks the child
develops anuria.
a) What is the cause of anuria?
The child develops glomerulonephritis, a kidney disorder in which there is damage
of nephrons. So anuria occurs
b) What are the other causes of anuria?
Poisioning, snake bite & anaphylaxis
c) What is the treatment?
Since it is a bacterial infection, antibiotics are given to treat the condition
21. How Starling forces play a role in the process of filtration and how they get
changed in urinary tract obstruction & nephritic syndrome?
Starling forces acting on the process of Glomerular filtration are:
Glomerular hydrostatic pressure (GCP) - (45 mmHg)
Glomerular osmotic pressure (GOP) - (20 mmHg)
Bowman’s capsular hydrostatic pressure (BCP) - (10 mmHg)
GCP favors filtration. GOP & BCP oppose filtration
In nephritic syndrome : Albuminuria  decrease in GOP  increase in GFR
In urinary tract obstruction: Increase in BCP  decrease in GFR
22. Investigation of a patient with history of polydipsia & polyuria with 15 lts of
Urine output/day, revealed a colourless, sugarless & albumin free urine with
1.002 to 1.004 specific gravity. Give your diagnosis with explanation
Diagnosis: Diabetes insipidus.
Explanation: The urine is sugarless & albumin free. So the high urinary output
must be due to water dieresis. Moreover the low specific gravity indicates that the
urine is diluted. This type of urinary output occurs in diabetes insipidus caused by
deficiency of ADH
23. In a patient with blood glucose concentration of 200 mg% and a GFR of 125
ml/minute, how much is the tubular load of glucose? He passes glucose in the
urine. This contradicts Tm value of glucose reabsorption (375 mg/minute).
Explain the contradiction
Tubular load = blood glucose concentration X GFR
= 200/100 X 125 = 250 mg/ minute
The contradiction between the theoretical value & practical value is called renal splay.
Reason : learn the reason for splay from the book
24. Aldosterone produces alkalosis. How?
Aldosterone increases Na+ reabsorption from the kidney tubules. This leads to
increased secretion of H+ in exchange of Na+ absorbed. Loss of H+ from the body
leads to alkalosis
26. After heavy meals urine becomes alkaline – explain
Heavy meal stimulates gastric secretion through which H+ is lost. This leads to
alkalosis. To correct this condition kidney starts excreting HCO3- in to the urine. This
makes the urine alkaline
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5
27. Patients suffering from nephrotic syndrome shows the signs of pitting edema in
the extremities . Explain
In nephrotic syndrome, the negative charges of pores in the filtering membrane are
abolished. This leads to filtration of albumin which inturn leads to albuminuria. Loss
of albumin from blood  Low colloidal osmotic pressure increased filtration at
capillary bed Accumulation of fluid in tissue spaces (edema)
28. Find out the urea clearance of the patient whose blood urea concentration is 50
mg%,urine flow = 2 ml, & urine urea concentration – 5 mg/ml. Give your
comments about renal functions
Urea clearance = U X V
-------
P
=5X2
------
50/100
= 50 ml/mt
Urea clearance normal value = 75 ml/mt. So the calculated value indicates impaired
kidney function
29. Why loop diuretic is considered to be more powerful than all other diuretics?
Loop diuretics block the active sodium-chloride-potassium cotransport in the
ascending limb of Henle’s loop. This impairs the ability of kidneys to concentrate or
dilute the urine. As reabsorption is inhibited, the solutes are excreted more through
the urine. This impairs the dilution of urine. Renal medullary osmolarity is reduced.
This reduces the aborption of water from the collecting duct. This impairs the
production of concentrated urine. This makes a increase in urinary output to 25 times
normal
30. Compression of renal artery in an experimental animal shows rise in BP.
Explain the finding.
Compression of renal artery  Renal ischaemia  release of renin from
juxtaglomerular cells formation of angiotensin & aldosterone  vasoconstriction
& retention of salt & water  increase in blood pressure
31. Give the physiological basis of:
- alkaline urine in high altitude
- acidosis in renal failure
High altitude : Hypoxia  hyperventilation  Washout of CO2  alkalosis of blood
renal correction by excreting HCO3- in the urine (alkaline urine)
Renal failure: As acid metabolites are not removed from the body, their accumulation
leads to acidosis. Impairment is in renal tubular HCO3- reabsorption or renal tubular
H+ secretion
32. Describe the two major techniques of dialysis used clinically & explain the
physiological basis of it
Two major techniques of dialysis:
- Hemodialysis
- Peritoneal dialysis
Hemodialysis:
Heparinized blood is pumped from one of the arteries of the patient
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through cellophone tubings which is surrounded by a large volume of dialyzing fluid.

The solutes of the plasma (except proteins) tends to reach diffusion equilibrium with that
of the solutes in the dialyzing fluid. The purified blood is conducted back in to the
patient’s body through a vein. Dialysate flowing out of the machine is collected outside
in a bottle and discarded.
Peritoneal dialysis:
Dialyzing fluid is injected via a needle into the abdominal cavity through the
abdominal wall. The lining of the patient’s abdominal cavity (peritoneum) acts as a
dialyzing membrane. The dialyzing fluid is allowed to remain there for hours, during
which solutes diffuse into fluid from patient’s blood. The dialyzing fluid is then removed
and replaced with new fluid
33. A 30 year old male passes 6-7 liters of urine/day. The urine specific gravity is
1.002. He drinks large quantities of water.
What is the disorder he is having?
What are the causes for his disorder?
What treatment is advised?
Disorder – Diabetes insipidus
Causes – deficiency of ADH (neurogenic DI) / insensitivity of nephron to ADH
(nephrogenic DI)
Treatment –
Desmopressin – High antidiuretic activity
Clofibrate – increases ADH secretion.
Chlorpropamide – increases renal response to ADH
34. Define renal clearance. Name the clearance tests used to measure GFR and renal
blood flow. Give their normal values
Definition – Defined as the volume of plasma that is cleared of a substance in one
minute by excretion of that substance in urine
Clearance tests used to measure
GFR – Inulin clearance, Creatinine clearance & Urea clearance
RBF (Renal Blood Flow) – PAH clearance
35. What are the causes and its features of a atonic bladder?
Causes of atonic bladder:
Deafferentiation (Destruction of parasympathetic afferent nerve fibers from
bladder to spinal cord)
Features:
- Loss of tone in the bladder muscle
- Bladder becomes thin & distended
- Overflow dribbling of urine
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ENDOCRINE QUESTIONS
10 marks
1. Describe the synthesis and secretion of thyroxine. Discuss the mechanism of
actions and regulation of secretion of thyroxine. List out the actions of thyroxine.
Add a note on Grave’s disease / hyperthrodism/hypothyroidism in adult/cretinism
2. Name the hormones from adrenal cortex & explain the physiological actions of
Glucocorticoids/Cortisol. Explain the mechanism of action and regulation of
secretion of Cortisol
3. Depict diagrammatically calcium distribution in the body & enumerate the
functions of calcium. Briefly describe how calcium homeostasis is maintained in
the body
4. Name four hormones concerned with the glucose metabolism. Explain their
effects on blood glucose / Name the hormones secreted from islets of
Langerhans. Describe the synthesis and their physiological actions
5. Mention the normal level of Na+ & K+ in the ECF. Explain the hormonal
influence in the sodium and potassium homeostasis / regulation of K+ & Na+
level in the body/ Discuss the role of Aldosterone on sodium and potassium
homeostasis
6. Discuss the physiological actions of growth hormone & the regulation of
secretion of it
7. Name the hormones secreted from posterior pituitary. Describe their physiological
Actions. Discuss the regulation of secretion of ADH
5 marks
1. Briefly describe the hypothalamo-hypophyseal portal system & tract with suitable
diagram
2. What are the anterior pituitary hormones? List out their actions
3. Write shortly about the actions of oxytocin in the pregnant & non pregnant uterus.
Describe the actions of ADH/Vasopressin on kidney and blood vessels
4. Explain the cause, features, lab investigations(diagnosis) & treatment of acromegaly
& dwarfism
5. Explain the cause, features, lab investigations(diagnosis) & treatment of “Diabetes
insipidus”
6. Explain the cause, features, lab investigations(diagnosis) & treatment of cretinism
7. Explain the cause, features, lab investigations(diagnosis) & treatment of Myxoedema
8. Explain the cause, features, lab investigations(diagnosis) & treatment of Exopthalmic
goitre.
9. Explain the cause, features, lab investigations(diagnosis) & treatment of Tetany
10. Explain the cause, features, lab investigations(diagnosis) & treatment of Addison’s
disease
11. Explain the cause, features, lab investigations(diagnosis) & treatment of Cushing
syndrome
12. Explain the causes, features, lab investigations(diagnosis) & treatment of
Adrenogenital syndrome
13. Explain the causes, features, lab investigations(diagnosis) & treatment of primary and
secondary hyperaldosteronism
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14. Explain the cause, features, lab investigations(diagnosis) & treatment of “Diabetes
mellitus”
15. Discuss the manifestations of hypoglycemia
16. Describe the thyroid function tests.
17. Second messangers (especially cAMP)
18. Mechanism of action & regulation of secretion of growth hormone, ADH, thyroxine,
Aldosterone & cortisol
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ENDOCRINE K.SENTHAMIL SELVI

10 marks
1. THYROXINE
Synthesis:
1. Synthesis of thyroglobulin by follicular cells
2. Trapping of iodide by Na+ - I symport
3. Oxidation of iodide to iodine
Peroxidase
Iodide Iodine
4. Iodination of tyrosine --- MIT - Monoiodotyrosine (iodine at 3rd position) &
DIT - Diiodotyrosine (iodine at 3rd & 5th position)
5. Oxidative Condensation:
MIT + DIT T3 (Triiodothyronine)
DIT + DIT T4 (Thyroxine)
Secretion:
Thyroglobulin molecule (with MIT, DIT, T3 & T4) in the lumen of follicle
Endocytosis
Follicular cell
Fuse with lysosome
Lysis of thyroglobulin & release of MIT, DIT, T3 & T4 in the cytoplasm
T3 & T4 diffuse into the blood stream and reach the target organs
Mechanism of action:
T3 & T4 diffuse into the cell
Bind with receptors in the nucleus
Forms hormone –receptor complex
Binding of complex to DNA
Transcription of mRNA
Diffusion of mRNA to cytoplasm
Synthesis of new proteins (structural & functional)

(Also increase the number & size of mitochondria, rate of ATP synthesis &
activity of Na-K ATPase)
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Actions:
I. Effect on metabolism:
1. General metabolism
2. Carbohydrate metabolism
3. Protein metabolism
4. Fat metabolism
II. Effect on growth
1. Body growth
2. Growth differentiation
3. Neural growth
III. Effect on systems
Effect on metabolism:
1. General metabolism :
– stimulates metabolism of the tissues (maintains the BMR)
– increases O2 consumption
– increases heat production (Thermogenic effect)
Hypothyrodism – Low BMR & intolerance to cold
Hyperthyrodism – High BMR & intolerance to heat
2. Carbohydrate metabolism: Causes hyperglycemia by
- increasing glucose absorption in the intestine
- increasing glycogenolysis
- increasing gluconeogenesis
- Increasing insulin breakdown
Hypothyrodism – Hyperglycemia
Hyperthyrodism – Hypoglycemia
3. Protein metabolism:
Normal doses – Protein synthesis
Large doses - Proteolysis
Hyperthyrodism – Thin muscles & loss of weight
4. Fat metabolism:
- Increases cholesterol synthesis as well as breakdown & excretion
- As the breakdown is greater than the synthesis, thyroxine lowers the blood
cholesterol level
- Also causes lipolysis & increases free fatty acids & its oxidation
Effect on Growth
a. Body growth: Stimulates body growth directly by stimulating metabolism
and indirectly by increasing the production of GH (Growth Hormone) & IGF
(Insulin like Growth Factor)
b. Growth differentiation: Stimulates tissue differentiation and maturation
c. Neural growth : Thyroxine stimulates the growth of brain
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3
Effect on Systems:
a. CNS:
- Thyroxine maintains the normal growth & activity of CNS
- stimulates the growth of brain in fetus & newborn (mainly cerebral cortex, basal
ganglia & cochlea)
- increases the branching of dendrites, number of synapses & myelination
Hypothyroidism: slow mental activity, low memory power, slow
reflexes & excessive sleep
Hyperthyroidism: Increased nervous excitability  irritability,
emotional, restlessness & anxiety
b. CVS:
Thyroxine acts on SA Node and cardiac muscle & maintains normal heart
rate, cardiac output & blood pressure
Hyperthyroidism – Tachycardia & hypertension
Hypothyroidism – low heart rate & blood pressure
c. Blood: Stimulates erythropoiesis
d. Muscle: Maintains normal muscle mass & strength.
Hypothyroidism – Muscular weakness – due to depression of BMR
Hyperthyroidism - Muscular weakness – due to breakdown of muscle
proteins
e. Bones: Facilitates excretion of Ca2+ & PO4- in to the urine.
Hyperthyroidism – mobilization of calcium & Phosphate from bone 
osteoporosis
f. Skin: Maintains the normal texture.
Hypothyroidism – Dry & scaly skin
Hyperthyroidism – Soft , warm & wet skin
g. GIT: Stimulates a) Appetite & food intake b) Motility & secretions
Hyperthyroidism – Diarrhea
Hypothyroidism – constipation
h. Vitamins: Thyroxine converts β carotene into vitamin A. It is also required for
activation of B complex vitamins
i. Excretion: Maintains the normal renal blood flow of, GFR & function of
nephron
j. Endocrine: Increases the sensitivity of the tissues to catecholamines. Acts with
catecholamines to stimulate thermogenesis, lipolysis,
glycogenolysis & gluconeogenesis.
k. Reproduction: Thyroxine is required for normal sexual development &
gonadal function.
Hypothyroidism:
Children – Hypogonadism & absence of secondary sexual characteristics
Women – Reduced fertility, loss of libido & menstrual abnormalities
Men – Oligospermia, impotency and sterility
l. Respiration: Stimulates respiration & maintains normal ventilation
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2. GLUCOCORTICOIDS (CORTISOL)
Adrenal cortex:
Layer - Hormone
1. Zona glomerulosa - Mineralocorticoid (e.g Aldosterone)
2. Zona fasciculata - Glucocorticoid (e.g Cortisol)
3. Zona reticularis - Androgens (e.g Androstenedione)
Actions Of Cortisol:
1. Effect on Metabolism:
a. Carbohydrate metabolism:
Increases blood glucose level by
- Stimulating gluconeogenesis in liver
- Inhibiting glucose uptake & utilization by the tissues
b. Protein metabolism:
Decreases tissue protein & increases plasma amino acids
- Reduces protein synthesis in all tissues except liver
- Facilitates breakdown of tissue proteins
c. Lipid metabolism:
Increases the free fatty acid level in the blood & also increases the oxidation
of fatty acids
d. Mineral metabolism: Promotes retention of K+, Ca2+ & PO4-
e. Water metabolism: Facilitates water excretion in to the urine
2. Effect on immunity:
a. Anti-inflammatory effect: Cortisol prevents inflammation by
-
Stabilizing the lysosomal membrane
-
Decreasing the permeability of the capillaries
-
Preventing the synthesis of vasoactive substances like histamine
-
Inhibiting the migration of leucocytes to the affected area
b. Antiallergic effect: Cortisol prevents allergic reactions by
-
Inhibiting the formation of histamine from histidine
-
Reducing the number of basophils and mast cells
c. Immunosuppressive effect: Cortisol suppresses the immune system by
-
Decreasing the number of lymphocytes
-
Suppressing the activity of lymphoid tissue
d. Autoimmunity: Cortisol suppresses the production of autoantibodies
3. Effect on stress: Cortisol avoids the harmful effects of stress by
-
Releasing fatty acids for providing energy
-
Increasing blood flow to the tissues to provide O2 supply and remove the
metabolic products
-
Minimizing the effect of stress on tissues
4. Effect on systems:
a. Blood:
- Decreases the number of circulating eosinophils, lymphocytes & basophils
- Increases the number of RBCs, platelets & neutrophils
- Inhibits the proliferation of lymphoid tissue
- Maintains the normal blood volume
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b. Muscle:
- Causes destruction of muscle proteins releasing amino acids
c. Bones:
- Inhibits bone formation & enhances bone resorption
- Inhibits absorption of calcium & phosphate in intestine by opposing the effect of
vitamin D
d. GIT:
- Stimulates HCl and enzyme secretion from the gastric mucosa
- Cortisol produces peptic ulcers when given in excess
e. CVS:
- Positive ionotropic effect on heart and increases cardiac output
- Enhances the vasoconstrictor effect of catecholamines and increases BP
f. CNS:
- Maintains the normal functioning of nervous system
- Influences the sleep pattern, mood, cognition and reception of sensory input
5. Effect on Fetus:
- Stimulates the secretion of surfactant
- Helps in maturation of pancreatic beta cells & enzymes in the liver
- Play a role in the change from foetal Hb to adult Hb
6. Permissive role:
- Enhances the calorigenic, lipolytic, broncodilatory and vasoconstrictor effects of
catecholamines
- Enhances the effect of growth hormone on growth
CLINICAL USES OF GLUCOCORTICOIDS:
Glucocorticoids are used as drugs:
- To suppress rejection in organ transplantation
- To suppress the antibody formation in autoimmune diseases
- To suppress inflammatory reactions in conditions like Rheumatoid arthritis
- To suppress allergic reactions
----------------------------------------------------------------------------------------------------------
3. CALCIUM HOMEOSTASIS
Calcium Distribution in the body
1000 mg (0.1%)
ECF
1 Kg (99%)
g
BONE
11 gm (0.9%)
TISSUES
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Total content of calcium in the body: 1200 g

Bones & teeth - 1000 gm (99%)
Extracellular fluid – 1 gm (0.1%)
Intracellular fluid – 11gm (0.9%)
Normal Plasma calcium level in the body – 9 to 11 mg / 100 ml of blood
Hormones regulating plasma calcium level:

1. Parathormone from parathyroid gland Influence blood calcium
2. Calcitonin from thyroid gland and phosphorous by
3. Vitamin D (1, 25 – dihydrocholecalciferol) acting on bone, kidney
& GIT
ACTIONS OF PARATHORMONE:
Increases blood calcium level and decreases blood phosphate levels
On Bones: PTH causes resorption of bones in two phases:
Rapid phase: PTH binds to receptors on the membrane of osteocytes &
increases the cyclic AMP. This causes entry of calcium in to
the cell. The accumulated calcium activates the calcium pump
allowing the calcium to diffuse out of osteocytes into the
interstitial fluid.
Slow phase: PTH stimulates osteoclasts which release proteolytic, lysosomal
enzymes and acids. The enzymes digest organic matrix and
the acids dissolve bone salts. All dissolved substances
including Calcium enter ECF. Phosphate is also released
On Kidney: PTH facilitates the reabsorption of calcium from the thick ascending
limb of Loop of Henle & distal nephron and inhibits the absorption of
Phosphate from PCT
On GIT: PTH increases absorption of calcium and Phosphate from the gut. This
effect is mediated through 1, 25 (OH)2 cholecalciferol
On lactating mammary glands: PTH decreases the calcium content of milk,
sweat and GIT fluids and thus conserves Ca2+ in the body fluids.
ACTIONS OF CALCITONIN:
- Secreted from parafollicular or “C” cells of thyroid gland.
- Calcitonin decreases calcium as well as phosphate in plasma
1. On Bone:
a) Calcitonin antagonizes the effect of PTH on bone
b) It increases the calcium deposition to bone
c) It increases osteoblastic activity and decreases the osteoclastic activity
2. On Kidney:
a) Facilitates excretion of calcium and phosphate.
b) Decreases the formation of 1,25 Di Hydroxy Cholecalciferol
3. On GIT:
- Inhibits absorption of calcium & phosphate.
Clinical uses of Calcitonin:
- Given for relieving bone pain and maintaining normal bone structure
- Protects the bones of the mother from excess calcium loss during pregnancy and
lactation
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ACTIONS OF VITAMIN D:
- Vitamin D increases blood Calcium & Phosphate levels
1. On GIT:
- Vitamin D binds to a cytoplasmic receptor in the intestinal epithelial cells and
reaches the nucleus. Acting on DNA it increases the production of calcium-
binding protein (calbindin).This protein increases the absorption of both calcium
and phosphate, Thus 1,25 dihydroxy cholecalciferol (vitamin D) increases the
serum levels of both calcium and phosphate
2. On Bones:
- Acting on DNA it increases the production of calcium-binding protein. This
inturn increases the entry of calcium in to the osteocytes. The increased
intracellular calcium leads to accumulation of lactic acid and citric acid. These
acids dissolve the bone salts and calcium is released (bone resorption). But
Vitamin D also increases the calcium deposition in the bones.
3. On kidney:
- Vitamin D increases the reabsorption of calcium and phosphate in the kidney
tubules
OTHER HORMONES:
Estrogen:
- Elevate plasma calcium and phosphate levels
- Stimulates osteoblastic activity and inhibits osteoclastic activity
- Causes calcification and ossification of bones
- Favours bone formation and bone growth especially at the time of puberty
Cortisol:
- Depresses bone formation by inhibiting the synthesis of protein matrix
- Increases osteoclasts formation
- Causes destruction of protein matrix
- Decreases calcium absorption from the gut and reabsorption from the kidney
tubules
4. GLUCOSE HOMEOSTASIS
- The normal fasting blood glucose level is 70-100 mg/100 ml of blood
- This is mainly regulated by hormones secreted from Islet tissue of pancreas
Pancreatic hormones which regulate blood glucose level are:
1) Insulin from β cells
2) Glucagon from α cells
ACTIONS OF INSULIN:
Effect on membrane:
1) Facilitates the entry of glucose in to all the cells except the brain, liver & RBC
there by increases the utilization of glucose by the tissues
2) Promotes the entry of aminoacids and fatty acids into the cells
3) Also facilitates the entry of K+ into the cells.
Effect on Metabolism:
1) Carbohydrate metabolism:
- Insulin increases peripheral utilization of glucose by the tissues by stimulating the
enzymes of glycolysis
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- Promotes entry of glucose into adipose tissue and muscle

- Promotes glycogenesis (synthesis of glycogen from glucose)
- Inhibits glycogenolysis (breakdown of glycogen to glucose0
- Inhibits gluconeogenesis by inhibiting the enzymes participating in it.
2) Protein metabolism:
- Insulin promotes entry of aminoacids into the cells
- Facilitates protein synthesis
- Inhibits proteolysis
3) Fat metabolism:
- Insulin facilitates the entry of free fatty acids into adipose cells.
- Incorporates FFA into neutral fat (triglycerides) in adipose tissue
- Promotes lipogenesis
- Inhibits lipolysis
(In diabetes mellitus, there is increased lipolysis & FFA in the blood. The FFA are
converted into ketone bodies)
ACTIONS OF GLUCAGON:
1. Stimulates glycogenolysis through cAMP. The enzymes involved in the process
are stimulated
2. Stimulates gluconeogenesis by stimulating the enzymes participating in it
3. Stimulates the hormone sensitive lipase enzyme which causes lipolysis and
increases the plasma free fatty acids
4. Glucagon has calorigenic action. It may be due to increased hepatic deamination
of aminoacids
OTHER HORMONES:
1. EPINEPHRINE AND NOREPINEPHRINE: Increase blood glucose by
- Stimulating glycogenolysis in liver and muscle. This increases blood glucose and
lactate levels.
- These hormones activate the enzyme phosphorylase which participates in
glycogenolysis
2. GLUCOCORTICOIDS: Increase blood glucose level by
- Stimulating gluconeogenesis. Glucocorticoids cause breakdown of proteins and
make the aminoacids available for gluconeogenesis
- Decrease the uptake of glucose by the tissues
5.GROWTH HORMONE
• A polypeptide containing 188 aminoacids
• Secreted from somatotropes (acidophilic cells ) of anterior pituitary
ACTIONS OF GROWTH HORMONE
Direct effects - growth hormone binding its receptor on target cells
Indirect effects - through Somatomedin a polypeptide secreted from the liver in
response to growth hormone.
Somatomedins are Insulin – like Growth Factor I & II ( IGF I & II)
• Effect on growth
• Effect on metabolism
• Effect on milk production
• Effect on erythropoiesis & lymphopoiesis
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Effect on growth
on cartilage
stimulates proliferation of chondrocytes (cartilage cells), resulting in bone
growth
on bone
stimulates osteoblastic activity (conversion of chondrocyte into osteocytes)
on muscle
increases the skeletal muscle mass by stimulating both the differentiation and
proliferation of myoblasts. It also stimulates amino acid uptake and protein
synthesis in muscle.
on other organs
stimulates the growth of visceral organs like kidney, liver, heart etc.,
Effect on metabolism
On carbohydrate metabolism
Hyperglycemic hormone (anti insulin effect)- increases blood glucose by
- decreasing peripheral utilization of glucose
- increasing formation of glucose (gluconeogenesis)
So GH is a diabetogenic hormone
Proof: Pancreatectomy in an animal diabetes
Hypophysectomy in that animal  diabetes comes under control
(Houssay animal)
On protein metabolism
Protein anabolic hormone – increases protein synthesis by
- increasing the rate of aminoacid uptake into the cells
- Stimulating mRNA transcription from DNA
- increasing protein synthesis in ribosomes
On fat metabolism:
- stimulates lipolysis & increases free fatty acids
On mineral metabolism
- increases renal absorption of Ca2+, PO4- & Na+.
- promotes the retention of Na+, K+ & Cl-
(By increasing Ca2+, GH promotes bone mineralization in growing children)
Effect On lactation:
enhances milk production in mammary gland
Efect On erythropoiesis:
stimulates erythropoiesis by increasing the secretion of erythropoietin from
kidney
Effect On lymphopoiesis:
stimulates the growth of lymphoid tissue & also proliferation of lymphocytes
Effect On gonads
stimulates the growth of gonads
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6.Anterior Pituitary Hormones & their functions

1) GH (growth hormone)/STH (somatotropic hormone)
Stimulates cell division & differentiation & there by influences physical growth
2) TSH (thyroid stimulating hormone) / Thyrotropin
Stimulates the growth of thyroid gland & secretion of thyroid hormones
3) ACTH (adrenocorticotropic hormone)/ corticotropin
stimulates adrenal cortex to secrete hormones
4) FSH (follicle stimulating hormone)
Stimulates development of ovarian follicles, secretion of ovarian sex hormones,, and sperm
production (spermatogenesis)
5) LH (luteinizing hormone)
stimulates ovulation, stimulates corpus luteum to secrete progesterone, stimulates testes to
secrete testosterone
6) PRL (prolactin)
stimulates mammary gland development, synthesis and secretion of milk
7.Posterior pituitary Hormones

1. Antidiuretic hormone (ADH) or vasopressin (SUPRAOPTIC NUCLEUS)
2. Oxytocin (PARAVENTRICULAR NUCLEUS)
1. ADH (vasopressin)
A polypeptide containing 9 aminoacids is produced mainly in SupraOpticNucleus of
hypothalamus.
ADH activates (2) second messenger systems:
1. cAMP
2. IP3/Ca2+
Action of ADH
1.  water re-absorption (retention) by distal tubules & collecting ducts of the kidneys .
This effect is regulated by V2 receptors, through the action of cAMP
2. In large doses, acts on blood vessels and causes vasoconstriction
This effect is regulated by V1 receptors, through the action of IP3/Ca2+.
Regulation of ADH secretion
-  in osmolarity of the ECF as in dehydration shrinkage of osmoreceptors in the
hypothalamus  stimulation of osmoreceptors   ADH secretion from SON of
hypothalamus
-  blood volume (Hypovolemia)   stimulation of mechanoreceptors in the great
arteries (aorta & carotids) & right atrium   ADH secretion from SON of
hypothalamus
2. Action of oxytocin
1.Contraction of smooth muscles of the uterus during parturition  enhance labor.
2.Ejection of milk from mammary glands as a reflex in lactating women.
3.Act on non pregnant uterus to facilitate sperm transport in the female genital tract upto
fallopian tube where fertilization takes place
4. Men   at the time of ejaculation (causes contraction of smooth muscles of vas deferens
propelling sperm towards urethra)
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11
5 marks
1. Hypothalamic control of pituitary /
hypothalamo-hypophyseal portal system & tract
Control of anterior pituitary
Hypothalamus (Arcuate nucleus)
Releasing hormones & Inhibitory hormones

Through
Stimulates Inhibits Hypothalamo - hypophyseal
portal system
Anterior pituitary
Hypothalamo - hypophyseal portal system
- Releasing & Inhibiting hormones are secreted into the median eminence
region of hypothalmus
- Hormones enter into the capillary plexus of superior hypophyseal artery

- Transported through long portal veins to anterior pituitary
- Exit of hormones from the secondary capillary plexus in the anterior pituitary
- Regulation of secretion of anterior pituitary hormones
Releasing & Inhibiting hormones
Growth hormone releasing hormone
Growth hormone inhibiting hormone
Thyrotropin releasing hormone
Corticotropin releasing hormone
Gonadotropin releasing hormone
Prolactin releasing hormone
Prolactin inhibiting hormone
Control of posterior pituitary
Supraoptic nucleus & Paraventricular nucleus (Hypothalamus)
Hypothalamo- hypophyseal tract
Posterior pituitary
Hypothalamo- hypophyseal tract
Cellbodies of neurosecretory cells of supraoptic & Paraveentricular nuclei of
hypothalamus
Secrete oxytocin & vasopressin which travel down the axons in neuro secretory granules
Axons pass through the infundibular stem & form a series of dilated nerve endings in
neurohypophysis called as “Herringbodies”
Hormones are stored in the nerve terminals in the posterior pituitary & released by
exocytosis on stimulation of cell bodies
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2.Aldosterone functions
• A mineralocorticoid secreted by zona glomerulosa
1. REGULATION OF PLASMA ELECTROLYTES
SODIUM:
a. Increases the reabsorption of sodium in the DCT & CD of kidney tubules (by
activating Na+-K+ ATPase pump & increasing the number of epithelial sodium
channels)
b. Increases the absorption of sodium in the colon
POTASSIUM:
 Increases excretion of potassium into the urine. So the plasma potassium
level decreases
2. REGULATION OF ECF VOLUME:

a. Increases sodium absorption. This is followed by water absorption  Increase in
ECF volume
3. REGULATION OF BLOOD VOLUME & PRESSURE:
Renin-angiotensin system:
4. HYDROGEN ION SECRETION:

By increasing Na+ reabsorption, it causes H+ secretion
5. Mild glucocorticoid activity and influences Carbohydrate metabolism
6. Takes part in stressful conditions
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3. Acromegaly
Clinical condition caused by hypersecretion of GH in adults after the closure of epiphysis
Features:
- Acral (peripheral) – hands & feet & Megaly – large. So large hands & feet
- Acromegalic face (coarse facial features) –due to overgrowth of malar, frontal & facial
bones
• Thick lips
• Macroglossia ( large tongue)
• Broad & thick nose
• Prominent eyebrows
• Thickened skin
• Prognathism (protrusion of mandible)
- gorilla like appearance with kyphosis (forward bending due to improper growth of
vertebrae)
- increased amount of body hair
- enlargement of visceral organs
• Cardiomegaly
• Hepatomegaly
• Splenomegaly
• Renomegaly
- bitemporal hemianopia (inability to see objects in temporal fields of both the eyes) due to
damage of binasal fibers of optic chiasma caused by compression of pituitary tumor
over optic chiasma
- Hyperglycemia (about 25% of acromegalic patients are diabetic)
Reason - Hyperglycemia excess insulin secretion  over activity of beta
cells of pancreas  exhaustive degeneration of beta cells 
deficiency of insulin  diabetes mellitus
- Gynacomastia (development of breast in males)
- Excessive sweating & hypertension due to increased sympathetic activity
Treatment :
- Surgical removal of pituitary tumour
- Administration of somatostatin
4. Diabetes insipidus.
A clinical condition caused by inadequate secretion / action of ADH
a. Neurogenic (central, or cranial) – Inadequate secretion of ADH
Problem in Hypothalamus or Post pituitary gland
Treatment: ADH
b. Nephrogenic
Resistance of V2 receptors in collecting ducts of the kidneys.
Symptoms:
Polyurea  20 L/day (N  1.5 L/d)
Polydipsia,
Dehydration
 specific gravity of urine
Treatment:
Drugs – Desmopressin, Clofibrate ( increases ADH secretion) &
Chlorpropamide (increases renal response to vasopressin)
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5.CRETINISM
A clinical condition caused by hypo secretion of thyroxine from thyroid glands in
children
Features:
- Physical & mental retardation
- Short stature
- Protruded tongue
- Macro-glossia (enlargement of tongue)
- Pot belly
- Lethargic attitude
- Puffy face
- Dry coarse & scaly skin
- Scanty hair
- Delayed developmental milestones
- Infantile facial features
- Obese & stocky
- Flat nose
- Hypogonadism
Lab findings-
- Low BMR(less than 50%)
- Radio-active iodine uptake low
Treatment:
- Administration of iodine or thyroxine
6.MYXOEDEMA
A clinical condition caused by hypo secretion of thyroxine from thyroid glands in adults
Features:
- Puffiness of the face
- Obesity and weight gain
- Lethargy (tiredness)
- Slow mentation
- Intolerance to cold
- Skin – dry & coarse
- Non-pitting edema
- Hoarse voice
- Hypoglycemia
- Anemia
- Hypotension
- Low BMR
- High cholesterol
- Menstrual disorders
- Excessive sleep (somnolence)
Tests to confirm the diagnosis: (Thyroid Function Tests)
1) Radioactive iodine uptake (Low)
2) Estimation of total serum thyroid hormones level (T3 & T4) - Low
3) TSH level – High
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4) Determination of BMR – Low

Treatment:
- Levothyroxine (oral thyroxine) – Life long
7.HYPERTHYRODISM / THYROTOXICOSIS
A clinical condition caused by hypersecretion of thyroxine from thyroid glands
Features:
- Inability to sleep (insomnia)
- Frequent bowel movements
- Excessive sweating and heat intolerance
- Loss of weight inspite of good appetite
- Increased pulse rate
- Hypertension
- Fine tremors visible in outstretched hands
- Voracious appetite
- Thirst
- Palpitations
- Nervousness
- Anxiety
- Muscle weakness
- Soft, warm & wet skin
- Polycythemia
- Hyperglycemia
- Low cholesterol
Tests to confirm the diagnosis: (Thyroid Function Tests)
1) Radioactive iodine uptake (high)
2) Estimation of total serum thyroid hormones level (T3 & T4) - High
3) TSH level - low
4) Determination of BMR - High
EXOPHTHALMIC GOITRE: Above features + Following features
- Goitre : Warm swelling in the neck that moves with deglutition
- Exophthalmos – Protrusion of eyeball (due to swelling of extraocular muscles &
increase in retrobulbar pressure. This is caused by accumulation of
glycosaminoglycans at retrobulbar region of the orbit. Glycosaminoglycans are
produced by infiltrated fibroblasts)
- Retraction of upper eyelids
8.TETANY
A clinical condition caused by hypocalcemia
Causes:
1. Hypoparathyrodism
2. Vitamin D deficiency
3. Alkalosis
Features:
- Numbness and tingling sensation especially in face and extremities.
- Stiffness of hands
- Muscular cramps
- Accoucher’s hand or carpopedal spasm: There is flexion at elbow, wrist &
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metacarpophalangeal joints & extension at interphalangeal joints .

- Laryngeal stridor: Loud noisy sound during inspiration
Latent Tetany (features that develop on examination)
Trousseau’s sign: Development of carpopedal spasm when BP cuff is applied over
the arm and arresting the blood flow temporarily
Chvostek’s sign: quick contraction of the ipsilateral facial muscles by tapping over
the facial nerve at the angle of the jaw.
Erb’s sign: Contraction of hand muscles on applying galvanic current
Diagnosis: Estimation of plasma calcium level
Treatment: Providing calcium rich food & Injection of calcium gluconate
9.ADDISON’S DISEASE
Addison’s disease is due to adreno cortical insufficiency (chronic deficiency of
both mineralocorticoids & glucocorticoids)
Features:
- Hyponatremia
- Hyperkalemia
- Inability to withstand any stress
- Marked pigmentation on the skin
- Chronic hypotension (low BP)
- Anemia
- Muscle weakness & easy fatiguability (due to hyperkalemia & hypoglycemia)
- Hypotension
- Hypovolemia
- Less resistance to stress and infection
- Anorexia, nausea, vomiting and weight loss
Diagnosis:
serum Cortisol, urinary 17-OHCS, plasma K, Na & serum glucose
Treatment:
Hormone replacement therapy (Administration of mineralocorticoid &
Glucocorticoid)
10. CUSHING SYNDROME
Excess secretion of glucocorticoids leads to Cushing syndrome.
Features:
- centripetal distribution of fat – truncal obesity with thin arms & legs but excess of
fat accumulates on the face, abdomen, buttocks & back of the neck
- Moon face
- Buffalo hump
- Obese but poor muscular development (feeling very weak)
- Poor wound healing capacity
- Pendululous abdomen
- Reddish striae on the skin of abdomen & upper thigh
- Hyperglycemia
- Hirsutism (excess growth of hair over the face)
- Polycythemia, lymphocytopenia & eosinopenia
- Muscular wasting
- Hyperglycemia
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- Hypertension
- Peptic ulcer
- Mental disturbances
Diagnosis:
– ACTH stimulation test
– Dexamethasone suppression test
– Estimation of 17-hydroxy corticosteroids
Treatment: Removal of pituitary or adrenal gland in respective tumour.
11. ADRENOGENITAL SYNDROME / VIRILISM
Increased secretion of adrenal androgens with concomitant decreased secretion of
glucocorticoids & mineralocorticoids
Features in females:
- Change in voice (masculine)
- Growth of hair in the face (Hirsutism)
- Baldness
- Masculine distribution of hair
- Growth of clitoris
- Amenorrhea
- Heavy limbs with increased muscle mass
- Increased pigmentation
- Smaller breast glands
Features in Males:
After puberty- Exaggeration of existing masculine characters
Prepuberty – Precocious puberty
Diagnosis:
 Low Cortisol
 Elevated plasma ACTH levels
 Low Aldosterone
 High androgens
 Serum electrolytes & glucose
 Low Sodium & high potassium
 Fasting hypoglycemia
 Urinary steroid profile
 Chromosomes
12. Diabetes Mellitus

Characterized by hyperglycemia
Two types:
1. Primary (related to insulin)
2. Secondary
Primary DM:
1. Insulin - dependant DM (due to deficiency of insulin)
2. Non-insulin dependant DM (Due to insulin resistance of tissues)
Features:
1. Hyperglycemia
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2. Glycosuria
3. Polyuria (↑ urine formation)
4. Polyphagia (↑ food intake)
5. Polydipsia (↑ thirst)
6. Hyperlipidemia
7. Hypercholesteraemia
8. Acidosis
9. Fatigue
Complications:
1. Nephropathy
2. Retinopathy
3. Neuropathy
4. Ketoacidosis
5. Coma
Diagnosis:
1. Oral glucose tolerance test
2. Estimation of blood Hb A1C
3. Urine and blood glucose estimation
Treatment:
1. Insulin injection
2. Oral hypoglycemic drugs
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1
REPRODUCTIVE SYSTEM
10 marks
1. MENSTRUAL CYCLE
- Refers to cyclical changes that takes place in the women
- Preparatory step for fertilization and Pregnancy
Duration - 25 – 35 Days
Average – 28 Days
Changes include:
Ovarian Cycle
Uterine Cycle
Cervical Cycle
Vaginal Cycle
Ovarian Cycle
Follicular Phase
Ovulation
Luteal Phase
1. Follicular Phase
-Involves the development of a follicle
- One follicle matures each month
- During the lifetime of a female only 400 follicles mature
Stages of follicular development:
Primordial follicle  Primary Follicle  Secondary follicle  Tertiary follicle
(Involves addition of granulosa cells surrounding the oocyte & also formation
of theca cells)Antral follicle(Having fluid filled space)  Matured
Graafian follicle
2. Ovulatory Phase
The process of expulsion of secondary oocyte from ovary into peritonial cavity
following rupture of mature graffian follicle
Timing:
14th day of sexual cycle
Events of Ovulation
- Rapid swelling of follicle
- Formation of stigma
- Release of proteolytic enzymes
- Dissolution of capsular wall
- Rupture of graffian follicle
3. Luteal Phase ( 15th - 28th Day)
Events :
- Formation of corpus hemorrhagicum (ruptured follicle filled with blood)
- Formation of corpus luteum (clotted blood replaced with yellow colored
lipid rich luteal cells)
- Formation of corpus albicans ( regression of corpus luteum)
2
Uterine (Endometrial) Cycle

Menstrual (Bleeding) Phase
Proliferative phase
Secretory phase
1.Menstrual Phase
The lining of the uterus (endometrium) breaks down and is lost from the body. This is
called menstruation or a period
Duration - Days 1-5
Components:
- 30 – 50 ml blood (75% Arterial)
- Ovum - unfertilized
- Mucus
- Endometrial debris – damaged endometrial tissue, serous fluid, a large amount
of prostaglandins & fibrinolysin
Mechanism of menstruation
1. steroid production declines.
2. shrinking of endometrial tissue
3. reduction in blood flow to superficial layers – ischemic hypoxia & damage to
the epithelial and stroma cells & constriction of spiral arteries
4. Individual arteries re-open  tearing and rupturing the ischemic tissues.
5. Bleeding into the cavity
- About 50% of degenerating tissues is resorbed and 50% is lost as 'menstrual
bleeding'.
2. Proliferative Phase
- Days 6-13
- increase in estrogen causing the endometrium to thicken (from 1mm to 4 mm)
- angiogenesis
- stimulation of endometrial glands to grow
3. Secretory Phase
Days 15-28 :
increase in progesterone causes
- endometrial thickness
- increased vascularity
- secretion of endometrial glands
(in preparation for the developing embryo)
Cervical Cycle
1. Preovulatory Phase - Estrogen is predominant hormone
- Cervical mucus - Thin, Watery & Alkaline
2. Postovulatory Phase - Progesterone
- Cervical mucus - Thick & Tenacious
Vaginal Cycle
1. Preovulatory Phase - Estrogen predominance
Thick & Cornified Epithelium
2. Postovulatory Phase - Progesterone predominance
Thick & viscid secretion
Infiltrated with Leucocytes
3
Hormonal Control of Sexual Cycle

Gonadotropins from Anterior pituitary
FSH - development of follicles (follicular phase)
LH - triggers ovulation
Ovarian Hormones
Estrogen – influences proliferative phase of endometrial cycle
Progesterone – influences secretory phase of endometrial cycle
Menstrual Disorders
Premenstrual Syndrome
Amenorrhoea - Absent
- Primary
- Secondary – Pregnancy
Menorrhagia – Excess bleeeding
Metorrhagia – intermenstrual bleeding
Oligomenorrhoea – decreased frequency
Dysmenorrhoea – painful menstruation
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2. CONTRACEPTION
- Refers to prevention of Conception
Methods of Contraception
Temporary Permanent
1. Barrier Methods 1. Vasectomy
2. Natural Methods 2. Tubectomy
3. Intrauterine Devices
4. Hormonal Contraception (Oral pills)
1. Barrier Methods
- Prevention of deposition of sperms in vagina
Mechanical Methods
Males - Nirodh (Condoms)
Females - Pouch (Female condom)
Diaphragm
Cervical Cap
Chemical Methods
Spermicides - Kill the Sperms
Jelly
Cream
Sponge
Combined (Mechanical & Chemical) - More Effective
2. Natural Methods
Rhythm Method – Following safe period
Coitus Interruptus
Complete abstinence
SafePeriod
Definition – the period of least fertility during menstrual cycle
Duration - 5-6 days after menstruation & 5-6 days before next cycle
Significance – rhythm method of contraception
3. Intrauterine Devices
Lippe’s Loop
Cu T 200
Multiload Cu T-250
Progestasert
Mechanism of Action
Increase tubal motility
Prevent implantation
Spermicidal activity
4.Hormonal /Oral Contraceptives
Sex Hormones - Oral Pills
Mechanism of Action
Negative feedback mechanism
Suppress FSH & LH secretion
Pills
Combined Pill - Progesterone & Oestrogen
21 Days - From the day bleeding stops
5
Withdrawal bleeding occurs

Sequential Pill - 15 days Oestrogen + Combination
Mini pill - Low dose estrogen
Postcoital pill – within 72 hours after sexual intercourse
Complications of oral contraceptives
Thromboembolic phenomenon
Increase in weight
Jaundice
Avoid in Diabetics
Fibroid Uterus
Permanent Contraceptive Methods
Vasectomy
Tubectomy
Medical Termination of Pregnancy (MTP) or Abortion
Dilatation & curettage (D&C)
Vacuum aspiration
Administration of prostaglandins
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5 MARKS
1. SERTOLI CELLS
Sertoli cells are the supportive cells found in the seminiferous tubules of testis.
Functions:
1. Play a role in the maturation of sperms
2. Provide nutrition to the developing spermatozoa
3. Play a part in the mechanism of blood testis barrier
4. Phagocytize damaged germ cells.
5. Takes part in aromatization of testosterone into estrogen
6. Secretes the following substances:
- MIS (Mullerian Inhibiting substance)
- Inhibins
- Androgen binding protein
7. Influence Leydig cell secretion through activins & inhibins
2. SPERMATOGENESIS
Definition: The development and maturation of spermatozoa (male gametes) is called
spermatogenesis.
Stages:
I.Spermatocytogenesis: Development of spermatogonia into spermatids
1. Spermatogonium A: Primitive germ cells which are diploid (44+XY) and
divide by mitosis to spermatogonium B cells
2.Spermatogonium B: These are also Primitive germ cells which are
diploid (44+XY) and divide by mitosis. These cells
give rise to primary spermatocyte
3. Primary spermatocyte: Diploid cells which divide by meiosis to form
secondary spermatocyte.
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4. Secondary spermatocyte: These are haploid cells (22+X or Y). They

undergo second meiotic division to form spermatids
5. Spermatids: Haploid cells which transform into motile spermatozoa.
II.Spermiogenesis: Transformation of spermatids into tailed, motile spermatozoa
(sperms)
Spermatozoa: Matured male gamates, haploid and posses a head, middle
piece and a tail. About 512 spermatozoa develop from a single
spermatogonium
Spermatocytogenesis
Spermiogenesis
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Regulation of Spermatogenesis:
A.Hormones:
1. Testosterone: Secreted from Leydig cells of testis. Acts on seminiferous
tubules and stimulates the proliferation of spermatogonia into
primary spermatocyte
2. FSH: Stimulates proliferation as well as maturation of spermatozoa. Trophic to
Sertoli cells which play an important role in maturation.
3.LH: Stimulates the Leydig cells to produce testosterone which is required for
Spermatogenesis
4. Other hormones which are required for spermatogenesis: Thyroxine, Growth
hormone & Insulin
B.General factors:
1. Temperature: Speramatogenesis requires 2 to 3oc less than the core temperature
of the body
2. Irradiation: Exposure to harmful radiation causes degeneration of seminiferous
tubules and leads to sterility
3. Toxins: Bacterial and viral toxins may cause selective destruction of
seminiferous ubules. E.g. Mumps
4. Vitamins: Vitamins A, C & E are required for spermatogenesis
3. TESTOSTERONE.
Secreted from Leydig cells of testis. About 4-9 mg is secreted per day.
Mechanism of Action:
It combines with cytoplasmic receptor and reaches DNA. It acts on DNA and
stimulates mRNA and protein synthesis
Functions:
1. In Fetus:
a) Sex differentiation: Stimulates the development of Wolffian duct into
male accessory sex organs. Development of male external genitalia
requires dihydrotestosterone which is derived from testosterone
b) Descent of testes: Along with MIS, testosterone stimulates the descent of
testes from abdominal cavity into scrotum through inguinal canal
2.During Puberty:
a) On accessory sex organs: Stimulates the development and growth of the
male accessory organs like vas deference, seminal vesicles,
prostate, scrotum & penis
b) On distribution of body hair: General body hair increases. Moustache &
beard appear.Pubic hair appear & attains male pattern
c) On voice: Becomes deeper and low pitched due to growth of vocal cords &
larynx
d) On skin: Thick with more sebaceous secretion. Acne appears on face
e) Mental behavior: More aggressive
3. Spermatogenesis: Stimulates the proliferation of spermatogonia into primary
spermatocyte in seminiferous tubules.
4. On growth: Stimulates skeletal growth. But finally it causes fusion of

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epiphyseal plates and arrest growth

5. On muscle mass: Testosterone is a protein anabolic hormone. It increases
protein synthesis.This increases the muscle mass and muscle power in
males.
6. On erythropoiesis: Stimulates the production of erytropoietin there by
increases RBC count. Hence males have higher RBC count than females
4. PLACENTA
Nutritive Function
-Transport of Glucose, Amino acids , Fatty acids & Vitamins from maternal blood
to foetal blood
- Storage of Glycogen, Lipids, Fructose
Respiratory Function
-Diffusion of O2 from maternal blood to foetal blood
-Diffusion of CO2 from foetal blood to maternal blood
Double Bohr effect
- Increased affinity of Foetal Hb (Hb F) shifts the ODC of foetal blood to left
- Increased Level of CO2 shifts the ODC of maternal blood to right
(Both the effects increase the O2 content of foetal blood)
Excretory function: Transport of metabolic waste products like urea, uric acid,
creatinine from foetal blood to maternal blood
Endocrine function
Placental Hormones
-Human Chorionic Gonadotrophin (HCG)
- Human Placental Lactogen (HPL, HCS - Human Chorionic
Somatomammotrophin)
-Human Chorionic Thyrotrophin (HCT)
-Oestrogen , Progesterone
-Relaxin
Human Chorionic Gonadotrophin (HCG)
Growth of Corpus Luteum
Presence in Serum & Urine - Diagnostic of Pregnancy
Growth of Testis / Ovarian Follicles in Fetus
Human Placental Lactogen
- Maternal Growth Hormone of Pregnancy
- Growth of Breast glands
- Retention of Nitrogen, Calcium , Sodium
- Makes Glucose & Fats available to the Fetus
Oestrogen
- Growth of ducts of Breast glands
- Increases the sensitivity of uterus to Oxytocin
Progesterone
- Growth of alveoli of Breast glands
- Maintenance of Pregnancy
-
Relaxin - Relaxes Pelvic joints & Pubic symphysis
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Softens and dilates the uterine cervix Facilitates delivery
6. INDICATORS OF OVULATION
1. Basal Body Temperature- A rise of 0.50C after ovulation
2. Billings Method -
Cervical Mucus :
Before ovulation- Elastic, Stretchable upto 10 cms (Spinnbarkeit effect)
After ovulation – Thick and can not be stretched
3. Fern Test
Before Ovulation –cervical mucus produce a fern pattern when dried on a glass
slide
After Ovulation – Fern pattern disappears
4. Biopsy of the endometrium – checking for the secretory phase
5. Endoscopy
6. Blood Gonadotrophins Level
7. Ultrasound Abdomen
7. NEUROENDOCRINE REFLEXES
Partiturition/Ferguson Reflex
Uterine contraction
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Milk let down or suckling reflex

Suckling of breast by the baby
↓
Stimulation of mechanoreceptors on nipple & areola
↓
Afferents (somatic nerve)
spinal cord
↓
Hypothalamus
Anterior pituitary Posterior pituitary

(Lactotrops) (Paraventricular nucleus)
↓ ↓
Prolactin Oxytocin
8. FETO_PLACENTAL UNIT
- Fetus & Placenta function as a unit in synthesising estrogen & progesterone
- Helps to maintain the level of steroids which inturn maintain the pregnancy
Maternal blood Placenta Foetal Adrenal
Progesterone Progesterone Cortisol, Corticosterone
Acetate
Pregnenolone DHEAS
16 – OH DHEAS 16 – OH DHEAS
Estrogen Estrogen
9. HCG
-Secreted by syncytiotrophoblast of placenta
-Reaches its maximum level at 60th -70th day of pregnancy
Functions:
- Growth of corpus luteum
- Secretion of progesterone & estrogen from Corpus Luteum
- Growth of testes & testosterone secretion in male foetus
- Androgen production from fetal adrenal cortex
- Formation of primordial follicle in fetal ovary
- Growth of breast
- High level in urine – diagnosis of pregnancy
1
REPRODUCTIVE SYSTEM (Applied)
1. What is the cause of Amenorrhea during the first sixth months of

lactation?
High levels of prolactin in the blood blocks the action of gonadotropins (FSH & LH)
on ovary. No follicular development & no ovulation  amennorhea
2. What is the effect of hypophysectomy on the uterus?
Hypophysectomy : Removal of pituitary
(No FSH & LH secretion . No estrogen & progesterone secretion from ovary.)
Hypophysectomy before puberty -
- Uterus remain infantile (Child like)
- Menstrual cycle does not appear (primary amenorrhea)
Hypophysectomy after puberty –
- Uterus gets reduced in size
- Menstrual cycle disappear
3. Mention the condition resulting from excess androgen exposure in a
female fetus
Female pseudohermaphroditism (genetic females with male external genitalia)
4. Briefly describe the characteristic feature of a young boy having defective leydig’s
cell functions
The clinical picture is that of a enuchoidism. The person grow tall with narrow
shoulders having a body configuration of an adult female. The genitalia remain
small, female pattern of pubic hair development & voice is high pitched
5. What could be the cause for the infertility in a diabetic man who is having a
normal healthy sperm count?
Diabetic neuropathy may lead to erectile dysfunction which causes impotency. This
inturn may lead to infertility
6. While investigating a male patient complaining of infertility showed evidence of
testis in the abdomen? Give the physiological reasons for his infertility and name
this condition
The condition is called Cryptorchidism.
Reason for infertility –
The temperature required for spermatogenesis is 2-3 degrees less than body
temperature. In cryptorchidism the testis remains in the abdomen. So the
spermatogenesis is affected in the body temperature. This leads to infertility
7. How can you determine the genetic sex of an individual by examining the cell
from buccal mucosa?
In the female cell, the inactive X chromosome is seen as Barr body or sex chromatin
near the nuclear membrane.
8. A child is born with undescended testis. How will you correct this abnormality?
The condition is called cryptorchidism. This is corrected by treatment with
gonadotrophins or surgical implantation of testis in the scrotum
9. A twenty five years old female present with two months amenorrhea and morning
sickness. How will you investigate her? What is the cause for morning sickness?
By making her to undergo reliable pregnancy test, the pregnancy can be confirmed.
Cause for morning sickness- high amounts of estrogen, progesterone & the chemicals
2
released due to the effect of these hormones act on the vomiting centre & cause
morning sickness
10. A couple married for five years did not have any children. On examination of
the husband his sperm count was found to be less than 16 millions / ml of semen.
What is the normal sperm count? Explain other investigations that may have to be
carried out in his wife to rule out infertility?
The normal sperm count is 35 to 200 million / ml of semen.
Investigations to rule out female infertility
Testing the time of ovulation
Testing the ovarian disorders (polycystic ovary etc.,)
Testing the uterus
Testing for the presence of endometriosis, Salpingitis etc.,
11. When does ovulation occur in the woman with menstrual cycle duration of 35
days. Explain two tests for confirmation of ovulations?
On 21st day (35 – 14).
Tests to confirm ovulation:
a) Determination of Basal Body Temperature
b) Estimation of estrogen levels in the plasma & urine
12. What are the consequences of Vasectomy and Orchidectomy?
Vasectomy is a surgical procedure in which the vas deference of both sides are cut &
Ligated. It has no effect on libido & hormonal production . Sperm get lysed in the
epididymis & the fluid is absorbed. Sometimes granulomas develop.
Orchidectomy is removal of testis. Otherwise called as castration
Effect before puberty:
No pubertal changes
No spermatogenesis
No development of secondary sexual characteristics
No sexual desire
Taller, feminine & Voice high pitched
Feminine pattern of hair & fat distribution
Effect after puberty:
Spermatogenesis stops
Seminal vesicle & prostate degenerate
Other genitalia remains unaltered
Secondary sexual characters remain intact
Muscle becomes soft & skin becomes smooth
13. A small girl aged 5 years developed a pubic hair and started having menstrual
cycle at the age of 45 weeks onwards. She had shown signs of development of
breast tissues also. Identify the above case and give suitable reasons. Explain the
mechanism of onset of menarche in females.
a) True precocious puberty
Reasons:
- constitutional
- tumour & infection of posterior hypothalamus
- developmental abnormalities
3
b) Mechanism of onset of menarche: (menarche- onset of menstruation)

When a female reaches the age of puberty, an unknown signal (may be
neural signal from limbic system or chemical signal like a hormone called leptin
from fat cells) causes pulsatile secretion of GnRH (Gonadotropin Releasing
Hormone) from hypothalamus. This in turn stimulates anterior pituitary to secrete
Gonadotrophins (FSH & LH ) which act on ovary and lead to menstruation
14. What is the normal sperm count and what is Oligospermia?
Normal sperm count – 16 to 120 million / ml of semen.
Oligospermia – reduction in sperm count
15. What is the effect of the removal of the corpus leuteum during second month of
pregnancy?
As corpus luteum secretes large amounts of progesterone & estrogen , it is needed for
the maintenance of pregnancy till 8th week (second month ) .Removal of corpus
luteum during the second month causes expulsion of foetus from the uterus
(abortion).
After the 2nd month, the estrogen & progesterone are secreted by placenta. So
removal of corpus luteum will not affect the pregnancy
16. Why does testosterone rightly deserve the name ‘male sex hormone’?
Testosterone is mainly responsible for growth and development of all male sex
organs , male internal & external genitalia & secondary sexual characters. All
masculine characters of male depend upon the secretion of testosterone
17. Explain why lactation begins after delivery.
During pregnancy, the placenta secretes estrogen which inhibits the milk producing
effect of prolactin on the breast. During delivery the placenta is expelled out. The
estrogen level decreases in the blood.. This initiates lactation
18. Mention any two defects due to non-disjunction of the sex chromosomes at the
time of meiosis
1. Turner’s syndrome (XO chromosomal pattern)
2. Klinefelter’s syndrome (XXY chromosomal pattern)
19. What could be the probable cause for ammenorhea in a girl aged 10 years, a
young married woman , a lactating woman, and a woman aged 50 years?
Reason for amenorrhea:
Girl aged 10 years – Has not attained the puberty
A young married woman – Pregnancy
A woman aged 50 years – menopause
20. What is the physiological basis for the use of Intra Uterine Contraceptive
Device (IUCD) as contraceptives?
Intrauterine Contraceptive devices prevent implantation of zygote by altering the
endometrial functions
21. Explain the functions of corpus luteum of menstrual cycle & Pregnancy.
Functions of corpus luteum :
During menstrual cycle – corpus luteum secretes progesterone which influences
the endometrial changes during secretory phase of menstrual cycle.
During pregnancy – Secretes progesterone & estrogen which influence the
changes in uterus, mammary glands & other structures during pregnancy
& also responsible for maintenance of pregnancy
4
22. Explain the physiological basis for pregnancy tests and describe one highly
reliable test:
Physiological basis of pregnancy tests:
During pregnancy,human chorionic gonadotrophin (HCG) is secreted by the
placenta. HCG level peaks between 60-70 th day of pregnancy. Detection of this
hormone in the urine confirms pregnancy.
IMMUNOLOGICAL TESTS
Principle:
The HCG in the urine of pregnant female is made to react with antisera which
contains antibodies against HCG & checked for agglutination
a. Haemagglutination test.
2 steps.
1st step:
Urine containing HCG+antiserum- antibodies are used up (agglutination not
2nd step: visible)
Above mixture + sheep RBC coated with HCG no agglutination (negative test)
indicates pregnancy.
23. Explain briefly the physiological basis of oral contraceptive pills
Physiological basis of oral contraceptive pills:
-consists of progesterone & estrogen which prevent the conception by the
following ways:
1. Prevent ovulation by inhibiting the release of LH & FSH
2. Prevent implantation by causing endometrial hypoplasia
3. Prevent entry of sperm in to the uterus by altering cervical mucus
24. Mention effects of bilateral vasectomy on the semen quantity and Composition
Effect on semen quantity:
10 to 20 % of the quantity is reduced
Effect on composition :
Sperms will be absent
25. A young couple is advised to follow ‘safe period’ to delay the birth of their first
baby. What is the physiology behind the advice?
Safe period is the period during which there is no ovum in the fallopian tube. When
sperms enter in to the fallopian tube during this period ,there is no chance for
fertilization
26. Why does milk secretion stop, when a stranger suddenly intrudes while mother
is feeding her baby?
Psychogenic factors have got a inhibitory influence over the secretion of Oxytocin
from hypothalamus. The milk secretion stops.
27. What are sertoli cells? Give their functions
Sertoli cells are the supportive cells found in the seminiferous tubules of testis.
Functions:
1. Play a role in the maturation of sperms
2. Provide nutrition to the developing spermatozoa
3. Play a part in the mechanism of blood testis barrier
4. Phagocytize damaged germ cells.
5
5. Takes part in aromatization of testosterone into estrogen

6. Secretes the following substances:
- MIS (Mullerian Inhibitig substance)
- Inhibins
- Androgen binding protein
7. Influence leydig cell secretion through activins & inhibins
28. Explain the mechanism of milk ejection reflex
MILK EJECTION REFLEX (NEURO ENDOCRINE REFLEX)
Suckling of the baby at mother’s breast

↓
Transmission of sensory impulses to the mother’s hypothalamus
↓
Oxytocin
↓
Contraction of myoepithelial cells
↓
Milk Ejection
29. What are the stages of spermatogenesis? What is the normal sperm count?
Stages of spermatogenesis:
Spermatogonia, Primary spermatocyte, Secondary spermatocyte, Spermatid &
Spermatozoa
Normal sperm count : 16 – 120 millions/ml
30. What is Turner’s syndrome?
Complications that arise in a individual having XO chromosomal pattern.
Also called as gonadal dysgenesis/ ovarian agenesis
Cause: Non disjunction of one of the X chromosome during oogenesis
Features : - Gonads are rudimentary or absent
 Development of female external genitalia
 Short stature
 No maturation at puberty
34. What advice you would like to give to a newly married couple not desirous of
children for two years? Briefly explain the mechanism of action of this
contraceptive method
Oral contraceptive pills.
Mechanism of action:
Physiological basis of oral contraceptive pills:
-consists of progesterone & estrogen which prevent the conception by the
following ways:
1. Prevent ovulation by inhibiting the release of LH & FSH
2. Prevent implantation by causing endometrial hypoplasia
3. Prevent entry of sperm in to the uterus by altering cervical mucus
35. An individual has female external genitalia in genetic male.
What is that developmental disorder?
What are the causes for that disorder?
Disorder – Male pseudohermaphroditism
6
Causes:
 Defective embryonic testis
 Androgen resistance (5α-reductase deficiency/ defects in receptor
function)
36. What is the normal amount of blood loss during menstrual cycle? If the duration
of menstrual cycle is 40 days, on which day there is ovulation?
Average amount of blood loss during menstrual cycle - 30 ml.
Day of ovulation : 40-14 = 26th day
37. What is the effect of temperature and antigenic stimulus on spermatogenesis?
Temperature – Spermatogenesis requires a temperature considerably lower
than that of interior of the body. The testes are normally
maintained at a temperature of about 320C.
Antigens- Bacterial & viral toxins may cause selective destruction of
seminiferous tubules. This may inhibit spermatogenesis
E.g. Mumps
38. A 26 year old married female presented with amenorrhea for 45 days.
i) Which hormonal test would you like to prefer?
ii) What is the cause for amenorrhea?
i) HCG (Human Chorionic Gonadotropin)
ii) Corpus luteum persists and secretes progesterone & estrogen. The high
level of ovarian hormones in the blood inhibits the secretion of FSH & LH
from anterior pituitary. So no menstruation occurs
39. What is menarche? Name the hormones involved in it
Onset of menstruation is called menarche.
Hormones involved:
FSH & LH (Gonadotropins) from anterior pituitary
Estrogen & Progesterone from ovary
40. What is the normal sperm count? When is a person marked sterile?
Normal sperm count : 16 – 120 millions/ml
A person is marked sterile when the sperm count is less than16 million cells/ml
41. What determines the sex of the fetus?
Presence of SRY (Sex determining region of Y chromosome)
42. What is precocious pseudopuberty?
Early development of secondary sexual characters without gametogenesis mainly
caused by abnormal exposure of males to androgens and females to estrogen
43. What is the name given for the following conditions?
i) Excessive bleeding during a menstrual period
ii) Bleeding from the vagina in between menstrual period
iii) Scanty menstruation
iv) Painful menstruation
i) Excessive bleeding during a menstrual period - Menorrhagia
ii) Bleeding from the vagina in between menstrual period – Metrorrhagia
iii) Scanty menstruation- Hypomennorrhea
iv) Painful menstruation - Dysmenorrhea
44. A male child showing sexual development of an adult even at the age of 4 or 5
years with enlarged penis and scrotum, hair on the face, chest and pubis with
7
precocious sex desire and increased muscular development

i) What is this disorder called?
ii) What is it due to?
iii) What test should be done to diagnose it?
i) Disorder: Precocious puberty
ii) Cause:
 Tumour or infection of posterior hypothalamus
iii) Diagnosis:
 Assay of GnRH in the blood
45. A 28 year female who got delivered 5 months ago and regularly breast feeding
her child, has no menstruation since her delivery
i) What is that condition called?
ii) Why no menstruation?
i) Condition: Lactation amennorhea
ii) High prolactin level in the blood blocks the effect of gonadotropins on
ovaries. So no menstruation
46. Explain LH surge and its significance
At 36-48 hours before ovulation the estrogen feedback effect on LH secretion from
anterior pituitary becomes positive and there is a burst of LH secretion. This is called
LH Surge.
Significance : Produces ovulation
47. Outline the effect of castration in male before puberty.
Castration: Removal of testicles in male
Effect of castration before puberty:
Leads to a clinical condition called Enuchoidism
Features:
 Permanent sterility
 Underdevelopment of external genitalia
 Underdevelopment of secondary sexual characters
 Abnormal bone growth (Tall with narrow shoulders)
 Presence of feminine characters (small muscles, high pitched voice &
feminine pattern of pubic hair distribution)
48. What are the tests for ovulation?
1. Basal Body Temperature- A rise of 0.50C after ovulation
2. Billings Method -
Cervical Mucus :
Before ovulation- Elastic, Stretchable upto 10 cms (Spinnbarkeit effect)
After ovulation – Thick and can not be stretched
3. Fern Test
Before Ovulation –cervical mucus produce a fern pattern when dried on a glass
slide
After Ovulation – Fern pattern disappears
4. Biopsy of the endometrium – checking for the secretory phase
5. Endoscopy
6. Blood Gonadotrophins Level
7. Ultrasound Abdomen
8
49. Name some female contraceptive devices

Intrauterine Devices
Lippe’s Loop
Copper T 200
Multiload Cu T-250
Progestasert
Mechanical Barriers:
Vaginal Pouch - Female condom
Diaphragm
Cervical Cap
50. What are the causes for female infertility?
• Decreased hormonal levels
• Absence or damaged ovaries - PCOD
• Absence of ovulation
• Blockage of fallopian tubes- Salpingitis
• Endometriosis
51. What is capacitation of the spermatozoa?
52. What are the causes for male infertility?

• Low sperm count
• Low sperm motility
• Impotence including erectile dysfunction
• Aspermia
53. Women who nurse their babies regularly have lactation amenorrhea for 25-30
weeks.Consequently nursing as been an important and partly effective method
of birth control. Explain the mechanism
High prolactin level in the blood during lactation blocks the effect of
gonadotropins on ovaries.So no ovulation & menstruation. This prevents
conception
54. Semen analysis of a male aged 30 years reveals tail-less sperms, many non
motile sperms and a sperm count of 10 million/ml. Comment on these findings
and what impact are these findings likely to have on his reproductive life?
Presence of tail-less and non motile sperms indicate some pathology. More over a
sperm count of below 20 millions/ml is considered to be Oligospermia(low count).
All the above conditions will result in sterility(infertility)
55. A couple in their mid thirties have two healthy children and decided to have no
more children. They seek advice on contraception from a doctor. What method
is the doctor likely to suggest? Give reason for the doctors choice.
Vasectomy in males or tubectomy in females. It is a permanent and reliable method.
Recanalization can be performed later whenever needed.
9
56. Fusion of one sperm with the membrane of the ovum in the fallopian tube
prevents polyspermy. What is the mechanism?
57. A newly married couple approach a doctor for advice on a method of

contraception which will have the least effect on the normal physiological
activity in the body. What method is the doctor likely to suggest? What are the
practical difficulties in following this method?
58. What are the functions of HCG (Human Chorionic Gonadotropin)?

59. Some lactating women undergo milk eection in response to cry to their babies.
Explain its physiological basis
60. Mechanism of action of IUCD in females.

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1

Applied (General physiology)

1.Cell Membrane - Structure

2. Cell membrane Proteins

Embedded in the fluid lipid bilayer

Types: Peripheral & integral or transmembrane proteins

contribute to cell-cell recognition, communication, and intracellular adhesion

Lipid Bilayer as semipermeable membrane::

Passive Transport Active Transport

Factors Affecting Diffusion

Through Lipid Bilayer Through Channels

Molecules that pass through the lipid bilayer by diffusion

Molecules that pass through the Channels by diffusion

Mechanical gated channels – Open when there is a mechanical stretch

Colloidal osmotic pressure

Types of Active Transport

Mechanism of the pump:

Functions of Na+ -K+ Pump

Sodium - Glucose co-transport:

Sites of Sodium - Glucose co-transport

Example: Engulfing of bacteria by phagocytes (Neutrophils & Macrophages)

3. Receptor mediated endocytosis

Tissue fluid formation:

Net Filtration= Kf X (Pc+ if) –(c +Pif)

Net filtration through the muscle capillary:

REGULATION OF HOMEOSTASIS (Feedback Mechanisms)

b) Regulation of Blood Pressure:

Increase in Blood Pressure

Stimulation of Vagus & Inibition of sympathetic fibers

Decreased heart rate & vasodilation

Decrease in blood pressure.

(Opposite happens in condition of decrease in blood pressure)

General physiology - Applied

Tissue fluid formation:

Net Filtration= Kf X (Pc+ if) –(c +Pif)

Net filtration through the muscle capillary:

Arterial end of capillary:

Venous end of capillary:

CONDUCTION IN MYELINATED NERVE FIBRES (SALTATORY CONDUCTION)

I–a Muscle spindle, annulospiral ending

I–b Golgi tendon organ

II Muscle spindle–flower spray ending

III Pain, temperature

IV Pain and other receptors

Fibre type Function Diameter (µm) Conduction

A-γ Motor to spindle 3–6 15 – 30

A-δ Pain, temperature, touch 2–5 12 – 30

B Preganglionic autonomic 3 3–5

C Dorsol root pain 0.4 – 1.2 0.5 – 2

NERVE PHYSIOLOGY – 3 marks

Susceptibility Most Intermediate Least susceptible

MUSCLE PHYSIOLOGY K.SENTHAMIL SELVI

Motor End plate

Arrival of nerve impulse (action potential) at the presynaptic nerve terminal

↓ Excitation contraction coupling

• Release of Acetylcholine from nerve terminal

Motor end plate

 Interaction between the actin & myosin ceases

 The muscle relaxes