Join @drdocstg

Join @drdocstg
 Join @drdocstg

Table Of Contents
SL No. Chapter Page No

VASCULAR PHYSIOLOGY

1 Mastering Edema 8
2 Blood Pressure Regulation 19
3 Micro circulation 30
4 Body Fluid Compartments 33
5 Hemodynamics 41
VASCULAR PATHOLOGY

6 Histology of CVS 52
7 Hypertension 71
8 Atherosclerosis 67
9 Aneurysms 73
10 Marfan Syndrome 76
11 Aortic Dissection 79
12 Vasculitis 82
13 Vascular Tumors 88
Join @drdocstg
 Join @drdocstg

We hope you enjoy using these notes

They have been hand-crafted with an obsessive attention

to details, with aim of capturing the course’s content in a
way that’s right for you.

Thank You

notespaedia

Join our official telegram handles to get all updates t.me/notespaedia

Join @drdocstg
Join @drdocstg
 Join @drdocstg

VASCULAR PHYSIOLOGY

1
 Join @drdocstg

Definition
accumulation
of excessive
fluid in body tissues extravascularly

Deemed Einstridkien
of Body fluids
considering a normal
young
adult individual of 70kg
Total Body weight 60 is contributed Total Body water i e
by 42L
d 40 28L
by lean Body mass ie

out of this 60 Of Total BodywaterCTBW

Interstitial space
6 I 10.5L
43rd 43rd is in extracellularspace
is in 14L
2
Intracellular Intravascular Space
space 3.5L
k
28L

NOTE The fluid present in blood cells of Intravascular compartment is

considered in 28L of Intracellular fluid henceIntravascular compartment
volume is considered as plasma Volume

Therefore Edema in a body tissue is classified as

Intracellular edema Extracellular edema

d
cellular Swelling e s
Interstitial Serous
Body
edema compartment edema
The minamount

exEifini
c

500mL HYDRO PERITONEUM

CASCITIS

2
 Join @drdocstg

Normal Distribution of Body Fluid

In 70 kg adult Individual
T t
PLASMA 3.5L

MKRO.cl tTONf
g t
10.5 Interstitial fluid

O r i r s
28L
Cell
Cavity boo
Intracellular
Extracellular L S L

If there is excessive fluid in vascular compartment

of an individual
it is called HYPEREMIA CONGESTION

HYPEREMIA VS CONGESTION
due to more Blood flow due to obstruction in venous
as
dilatation
a reason
of arteriolar outflow

alkla ERYTHEMA

3
 Join @drdocstg

In medical literature and everydayclinical practise edema usually means

INTERSTITIAL EDEMA

let's know about

Before we
go indetail into INTERSTITIAL EDEMA
INTRACELLULAR EDEMA

INTRACELLULAR EDEMA

alkla cellular
swelling

Excessive fluid in Intracellular compartment

Reason for Intracellular edema is due to increase in intracellular

osmolarity with relation to

extracellular
fluid

Some examples which increase intracellular

osmolarity are

1 HYPOXIA Normally for all cellular actions ATP is

necessary

In a cell ATP is utilisationof 02

prepared
by

If a cell receives less 02 HYPOXIA

ATP production decreases

eveunts

Cellular are deranged

notmalfunctioning Tha

One of Throws
the events is of Nat K ATPasechannel
fatpuo

3Nat out in exchange to 2K ions H eBUB

Deranged

As a result there is intracellular accumulation

ofNations pµa Nat

Nat Nat

Increase in Intracellular

osmolarity H2O 420

t t
TNat Nat

Nations are dive and pulls water in

osmotically Nat Nat

TN
µaqggg
ajaI

cellular

swelling

4
 Join @drdocstg

2 CELLMEMBRANE DAMAGE

Damage to cell membrane causes leak of extracellular Nat Gca

and H2O cellular

causing swelling

NOTE In a normal cell cellmembrane integrity

avoids free

movements of ions into cell

Normal concentration
of Nat in Extracellular Intravascular 135 l45mEq L
compartment compartment

this is because Nat

is freely permeable across

capillary membrane

EXTRACELLULAR EDEMA

Extracellular edema occurs in the extracellular Outside the cellsand

space ice

outside the vascular compartment also called Interstitial space edema

Forces that decide the movement of fluid bw Intravascular and

Interstitial space are called forces

Hydro dynamic a
Starting forces

Under normal conditions H2O along with Oz Glucose and otherminerals

also trace amountof proteins leak

and are absorbed back at the venous

through arterial end microcirculation
of

end microcirculation
of

Virtually the parenchymal cells are bathed in fluid of interstitialspace

5
 Join @drdocstg

FLOW OF FLUID THROUGH INTERSTITIAL SPACE

ARTERIOLE

VENULE taffeta E fi
aoot.AO e

a
L L L L L

THORACIC
LYMPHATIC DUCT INTERSTITIAL SPACE

att e

Normal flow of fluid in and out of Interstitial space depends upon

the
Normal Arterial Blood flow

8D Intact endothelium

BBC
capillary
Normal Venous Outflow

Normal Lymphatic Drianage

BORE
Normal plasma proteins

CONCEPT OF STARLING FORCES

In a healthy individual the heart produces a pressure on capillary

pumping

wall called as Hydrostatic pressure P 35mm

Hg

virtue proteins osmoticall active substances they produce

the
Bypressure in
of
Intravascular compartment called as osmotic
a
IT
pressure

Substances responsible for producing osmotic pressure

25mm
Hg

plasma proteins Albumin 3 5gm dl major component Determine IT

6 8gm dL Globulin 1.5 2 Sgm1dL

Fibrinogen 0.25 o 5gm1dl

Others

Hydrostatic pressure push fluid outof vascular compartment

osmotic pressure tend to hold fluid in vascular compartment

so the net movement of fluid across capillary membrane depends on

Difference Osmotic pressures

btw Hydrostatic
35 25

mmHg

NET FILTERATION 10mm

PRESSURE
Hg

6
 Join @drdocstg

NOTE osmotic pressure exerted

by plasma proteins is called

COLLOID OSMOTIC PRESSURE or ONCOTIC PRESSURE

NET FILTERATION PRESSURE is a pressure that forces out the

fluid along with the dissolved components compartment

throw semipermeable

capillary
membrane from the Intravascular to the

Interstitial space

NORMAL FLUID HOMEOSTASIS IN INTERSTITIAL SPACE

Endothelial

dagger
aBasemmentmbrane

T t

w i
l
e e

c e i e c

C C

a T venous end
of Arterial

Reabsorption

microcirculation
mainc x

O r i r o
o co O O

L n J la 1

Cells

NOTE

As blood moves from arterial end to venous end radius t.es G

Hydrostatic pressure t.es But Oncotic pressure remains same

7
 Join @drdocstg

Net Filteration pressure and exchange of fluid

Arterial end
of MICROCIRCULATION Venous end of MICROCIRCULATION

HYDROSTATIC PRESSURE 35mmHg HYDROSTATIC PRESSURE 15mmHg

ONCOTIC PRESSURE 25mmHg ONCOTIC PRESSURE 25

mmHg

NET FILTRATION PRESSURE 10mm NET FILTRATION PRESSURE 10

Hg mmHg

movement of fluid movement of fluid

Intravascular to Interstitial Interstitial to Intravascular

The small amount into Interstitial space is drained

into
very venous ofback
proteins leaking
Lymphatics

system through

So lymphatics drain protein Richfluid

If this protein is retained in interstitial space starts holding H2O causing

edema

MECHANISM OF EDEMA

in Hydrostatic pressure Increase arterial flow Decreased venous outflow

Any

Any 1 in oncotic pressure t plasma proteins

Obstruction to Lymphatics Surgical excision oflymphatics obstructionbyparasite

Damage to
membrane direct indirect LYMPHEDEMA

capillary injury

8
 Join @drdocstg

CONCEPT OF PITTING AND NON PITTING EDEMA

Case 1 Case 2

Venous obstruction of one limb Lymphatic obstruction ofotherlimb

accumulation of fluid accumulation of fluid

x x

Edema proteins are filtered Edema proteins arenot filtered

by lymphatics
1 by lymphatics

proteins hold the fluid in

space

on applying pressure on applying pressure

Displacement of Edema No Displacement of Edema

Transient pit produced forfewseconds No Transient pit produced

v v

PITTING TYPE OF EDEMA NON PITTING TYPE OF EDEMA

Canbe managed Diuretics Can't be managed

by by
Diuretics

Because Diuretics cause H2Oloss Because protein can't be reabsorbed

1 from Interstitial space

Hydrostatic pressure decreases

CONCEPT

OF DEPENDENT EDEMA

Dependentpart is theone wherethe effect ofgravitational force is more Eg Legswhilestanding

In normal condition the interstitial fluid present is held

a GLYCOPROTEINS

present in the interstitial space their BRUSH PILES

by

by

B S

s am

inay.mu
9
 Join @drdocstg

This arrangement of fluid space holds fluid to move freely andhence

fluid is not displaced in dependent part ofbody

Incase of
edema the excessive fluid causes freewater channels and

such water present in free wake channel can be displaced to dependent

part ofbody by the effect of gravitational forces

a FREE

F
WATER

oooo8 GLYCOPROTEIN BRUSH PILES

CHANNELS

Interstitial fluid heldin forms of

gg

pockets in Glycoprotein

Dependentedema is
usually seen in cases of pitting
edema edemadue to Fed fluid

alone

as seen in CHE

Dependent edema is rarely seen in cases of non

pitting
edema edema due to

protein in interstitialspace

as seen in hymphadema

IV ADMINISTRATION OF FLUIDS

Any
administration of IV fluids in aperson its distribution depends on
many things

One them is distributionof solute present in the N fluid administered into

among

different compartments of
body

administered the dextrose moves into cell along c water

eg HenceIf

For 5T Dextrose is

it is not a fluid used for Resustication

10
 Join @drdocstg

ROLEOF HYDROSTATIC PRESSURE IN GENERATION OF EDEMA

It is generated the pumping heart that produces

of
Genesis Hydrostatic pressure
by

pressure on
capillary bed

Suppose there is transientincrease in Blood pressure pressure rises in arterial

circulation But that doesn't increase Hydrostatic pressure in capillaries

This is due to presence of pre capillary Sphinter present on arterialside of

microcirculationthat regulates bloodflow to capillaries

If4

Ptecapillaya

Sphinter of
Consists smooth muscle cells

If there is increase in BP

I can c

CON

a
Can

x a of
constriction
stretched dueto

Normal smooth

of
opening
Ca channel contraction of precapillarysphinter

muscle TinBP Smooth muscle

But there is no such sphinter mechanism at venousend of microcirculation

Hence Increase in venous pressure causes tin Hydrostatic pressure and

edema

may cause

In mild T in Hydrostatic pressure development of edema depends on how efficient

local lymphatic drianage

lymphatics are

Under Increased fluid retention can function 5 to times to

drain thefluid from

Lymphatics
interstitial space
by

when there is so much of fluid that even lymphatics fail to drain

their edema develops

11
 Join @drdocstg

CAUSES OF INCREASE IN HYDROSTATIC PRESSURE

Failure of precapillary sphinter as seen in case of local applicationofheat

Neutohumoral dysfunction sympathetic innervation

like by

Drugs Hydralazine

i SIE ofHydralazine is Ankleedema

Increased pressure on venous side of Microcirculation

Local systemic

External pressure on vein

Right heart failure
as seen in prolonged immobilisation Venous
a

pregnancy

thrombosis of vein pooling

seen in DVT

Some important terms

Platelet adhesion adhesion of platelets to damaged endothelial wall

Platelet aggregation platelets adhering toeach other

toplatelet plug lotsof platelets adhering to form a plug

Coagulation The series ofevents happening near 10plateletplug c final step

involving soluble fibrinogen to insoluble fibrin

Thrombus 10 platelet
plug
c fibrin deposition on them

Emboli Detached part of thrombus

12
 Join @drdocstg

REGULATION OF BLOOD PRESSURE BP

Normal Bloodpressure of an healthy adult individual

i20mmHg

120 Systolic BP

80 DiastolicBP

NORMAL ARTERIAL CIRCULATION

_T

mitral

major Arteries AORTA

value

ARTERIOLE q

Aortic

smooth muscle cells valve left

ventricle

DURING SYSTOLE

T t

mm

t mitral

i I
aortaf t I p zo
valve
close

e
distends v y

aortic T

valve Leftventricle

Opens contracts

DURING DIASTOLE

systolic Bl

mommy

mitral
I valve

1 opens
Aortarecoils

Aortic

Diastolic BP valve 1 1

closes LeftVentricle

Relaxes

13
 Join @drdocstg

DETERMINANTS OF BLOOD PRESSURE

to ventricle

Systolic BP is due contraction

of left

Diastolic BP is due to
diastole
Recoil of aorta
Interventricular is not related to

During pressure

aortic pressure

BP Cardiac Output X Total peripheral Resistance

If Arterioles dilate Decreased total peripheral Resistance Decreased BP

If Arterioles constrict Increased total peripheral Resistance Increased BP

CONCEPT OF MEAN ARTERIAL PRESSURE

mean arterial pressure Diastolic BP

MAP 31 Systolic BP

Mean arterial pressure is usually around loommHg

Mean systemic pressure s mean Pressure of arterial and venous circulation

MSP

6.5

mmHg

MAP MSP

Ii It

II t

Capillaries capillaries

14
 Join @drdocstg

COMPONENTS OF BLOOD PRESSURE

L S

Cardiac Output Total Peripheral Resistance

s x

Stroke Heart Rate Arteriolar tone

volume

Afterload

Contractility

Preload

EndDiastolicvolume

Total peripheralResistance

Bloodvolume

VenousReturn Venomotortone

Diastolic Interval

Blood in arterial system is High pressure so called stressed volume

Blood in venous system is Low pressure so called Unstressed volume

Venoconstriction causes Blood to move from Unstressed to stressedvolume

Venodilationcauses Blood to move from stressed to Unstressed volume

MAP CO x TPR

NOTE

If there is excessive increase of TPR MAP doesn't increase

proportionately because excessive increase in TPR causes slight

decrease of cardiac output so as to compensate severe increase

in TPR and MAP slightly increase

of BP is mediated Neurohumoral mechanism short term

Regulation
by

Renin Angiotensin Aldosterone System

Gongterm

15
 Join @drdocstg

NEUROLOGICAL REGULATION OF BLOOD PRESSURE SHORT TERM

Blood pressure
sensing receptors are called BARORECEPTORS

Baroreceptors are present Bifurcation of Common Carotid

Artery and

Arch of Aorta

The afferents from Carotid Baroreceptors are carried CranialNerve

by
The afferents from Aortic carried
by I CranialNerve

Baroreceptors are

Carotid Baroreceptors are sensitive to both increase and decrease in Blood pressure

Aortic Baroreceptors are sensitive to mainly increase in Blood pressure

The centre for Baroreceptor is Nucleus Tractus solitarius in medulla

MECHANISM OF BARORECEPTOR ACTION

Baroreceptor

Carotid Sinus

when there is increase in Blood pressure TBP

Carotid Baroreceptor stretch

Opens touch sensitive Nat Channel Etna

mechanoreceptors Nat

Nat influx

oepoiaisneaiionenfesmeamdbrane.it

Action potential Firing carried IX G X cranial N

by afferents

16
 Join @drdocstg

BARORECEPTOR CIRCUIT

Nucleustractussolitatius

ED

it

f she

XEN

Medulla

Sympathetic

outflow

TBP

O Vasoconstriction

T catecholamines THR TBP

Adrenal

medulla

Sympathetic outflow increases Heart rate increases BP

parasympathetic outflow through vagus

decreases HR O Decreases BP

Afferents from Baroreceptors Stimulate NTS

NTS stimulates cardio inhibitory centre 9 inhibits cardioaccelatorycentre

cardio
inhibitory
centre act on SA node to t.HR through vagus

Cardio accelerator centre act on SA node outflow to

through sympathetic

Heart Vessels and adrenal medulla

17
 Join @drdocstg

IBP IBP

t t

increased firing by baroreceptor Decreased firing by baroreceptor

Stimulation
Stimulation

of NTS Less
of NTS

I 1 thocardio

0
cardiostimulatory cardio cardiostimulatory

inhibitory inhibitory

t t

1ed Sympathetic TVagal tone Ted Sympathetic bedvagal tone

outflow

1 outflow
f

t t

tied HR IHR Ted HR THR

ed Catecholamines Ted Catecholamines

edVenomotortone TedVenomotortone

t TPR TedTPR

v v v

Reduced Blood pressure IncreasedBlood pressure

Baroreceptor are more sensitive to Rate of change of Blood pressure

In HTN Baroreceptor set the MAP to high pressure so not useful

SUMMARY

T BP Tafferents TPNs 65ns t.HR IBP

to BP f afferents LPNs 95ns THR TBP

Carotid occlusion d afferents LPNs 95ns THR TBP

Carotid
massage
Tafferents Tpns t.SNSI.HR IBP

Afferents are cut d afferents d DNS TSNS THR TBP

volume overload Tafferents TPNs d SNS t.HR IBP

Sudden 1 afferents LPNs TSNS THR TBP

standing

PNS parasympathetic Nervous system SNS Sympathetic Nervous System

18
 Join @drdocstg

If on sudden standing sympathetic system fails to activate or even if

activated is able able to maintain BP due to history of massive fluidloss

the person feels dizziness and called as ORTHOSTATIC HYPOTENSION

Vertigo

RENIN ANGIOTENSIN ALDOSTERONE AXIS LONG TERM

RAAS

99

Angiotensin

convertingenzyme

angiotensin

Lungs 4 9

µe

angiotensin 1 a

t.it no8enO

Rennin

v I ago

gqqqzgyq.aggggyqe.gg my y.m.a.g.ea m amm

I 00 Lasix cells

Macula Densa

19
 Join @drdocstg

Hemorrhage Bloodloss

Dereased Blood pressure

Reduced Renal perfusion

Sympathetic

outflow L s

t Afferent arterioles Reduced GFR

JGA less stretched

stimulated

Baroreceptors activated
in
slowmovement
1
of Glomerularfiltrate

IGA
TNat resorption in PCT
t

TGA stimulated Reduced Nat in luminal fluidwhile

passing through DCT

1
Sensed Macula Densa cells

e t
by

SECRETERENINC

Stimulate TGA

Renin secreted in

kidney

Liver Angiotensinogen Angiotensin

I

synthesize Renin

Angiotensin converting

ungegn3yme

I Angiotensin.ec

t
A
84

that 17 pg
Fonagbmentosa

Hypothalamus

muscleendothelium 1 7 stimulate
thirstcentre

f l d

venous Arteriole NE I

t t fee Tedsecretion ofaldosterone

constriction constriction 7 from adrenalcortex

t t

venous Return Ted TPR Tsympatheticnerve

I t ending
stimulation Nat and H2O Retention

TEDV TCO tDiastolic BP t t

t Ted Norepinephrine TBP

T systolicBP Epinephrine

20
 Join @drdocstg

ACTIONS OF ALDOSTERONE

Luminal 00 00 Aldosterone Aldosterone

receptor

fluid Na Nat

e
Nucleus

Kt 0 K Nat
0

00 00

Collecting P cell

duct

Aldosterone acts on intracellular receptor in Principle cells of collectingduct

and signals nucleus to produce more

NatK ATPase Nat channel Kt channel on

on basolateral on luminal terminal membrane

membrane

membrane

Throws Nat outside

and K
cell
inside cell
Resorption
Nat
of
c
Excretion
Kt
of

H2O

Retention of Nat G H2O

Tin Blood pressure

UPDATE

Angiotensin I also actson cells of PCT to increase absorption of

Nat G tho through Nat Ht cotransporter andusing Luminal carbonic

anhydrase

Angiotensin I also acts on efferent arterioles Constriction TIGER

21
 Join @drdocstg

DRUGS ACTING ON RAAS

ACE inhibitors Inhibit Angiotensin Converting enzyme

and prevents

formation of angiotensin I
CAPTOPRIL

eg

ENALAPRIL

USINOPRIL

SIE s
Hyperkalaemia

Contraindicated in Renal Artery Stenosis Causes serene reduction in GFR

Angiotensin II receptor Blocker Blocks action of Angiotensin I Reduces BP

Losartan

Aldosterone receptor Blocker Blocksaction of aldosterone and causes

excretion
of Nat GH2O Retention
of Kt

alkla potassium sparing

diuretics

SPIRONOLACTONE

eg

CHEMICAL REGULATION OF BLOOD PRESSURE CHEMORECEPTOR

chemoreceptors canbe central or peripheral

Peripheral chemoreceptors present on carotid bodyand aortic Body

carried
by II G E Cranial Nerves respectively

Sensitive to poz poor pH

Reduced
pcs stimulates peripheral chemoreceptors and causes Tedsympathetic

outflow

Result THR TBP

Central chemoreceptors present in floor of fourth ventricles

sensitivity to pca pH

TedCO2 in CNS cause CO2 1 H2O Hzcoz Htt HC05

accumulation
of Htions Reduced
pH stimulating chemoreceptors

That causes TPNS outflow G TSNS outflow So

Result t.HR T BP CUSHING'S REFLEX Intracerebral

seen in

Hemorrhage Ispaceoccupying
lesions
22
 Join @drdocstg

CUSHING'S REFLEX

TICP Ncp
t

t TCSFpressure

1 02 accumulation t

t obliteration of

Central Chemoreceptor ophthalmic Vein

stimulation I

TPNS TSNS pappiledema

edema opticdisc

1 of

projectile t.HR THR TBP option of

vomiting
counter
t u
3

balanced

t.HR

others i

r k f Bp TBP

W i Tin atrialpressure

a
t
qq.tvasggess.in

1 Secretion
of ANP

act v2receptor on kidney 1

Retention
Nat excretion

ofHao GHuo

IBP stabilised

NOTE Higher concentration of ADH

Higher concentration of

causes vasoconstriction ANP causes vasodilation

23
 Join @drdocstg

SALIENT FEATURES OF MICROCIRCULATION

Endothelial

dagger

nBasemmentmbrane

T t

w i
l
e

c c c c

C C

a T venousend of Reabsorption Arterial

microcirculation
maintain i

r i r

t o co
o o O
o
co O

L L L

MICROCIRCULATION

Input arteriole

output venous drianage G lymphatics

Fn of Microcirculation

Nutrition to cells

collect waste metabolites fromcells

leaked proteins

Drainage of by
lymphatics

24
 Join @drdocstg

1BASEMENT MEMBRANE

CAPILLARY ENOTHELIAL LAYER

than
capillary endothelium

Basement membrane is more porous

TYPES OF CAPILLARIES

cells are porous

Endothelial

Space b w two endothelialcells

f f PDX is nonporous

Fenestrated capillaries found in Glomerulus

e
Tt It space b w two endothelial

cells

y X

SINUSOIDS found in Liver

EX WIFE space b w

two endothelial
cells is compact

by

tight junctions

seen in cerebral Microcirculation

TRANSPORT OF SUBSTANCES ACROSS MICROCIRCULATION

Transcellularly paracellularly

Lipid soluble substances proteins

Gases cells

Glucose Antibodies

Ions others

peptide Hormones

25
 Join @drdocstg

ARTERIOLE

VENULE FEHRINGER
p Hathi.PL c

thecapillary
THORACIC

LYMPHATIC Duct Tif Pif sphinter

me afghan

INTERSTITIAL SPACE

Direction
of fluid flow

Pc Hydrostatic pressure in capillaries

Tic Oncotic pressure in capillaries

Pif Hydrostatic pressure in interstitial space

Oncotic pressure in interstitial space

Iif

Forces that push fluid into interstitial space Pc Aif

Forces that oppose fluid into interstitial space Pif t Ac

Net movement of fluid Pct A if Pif Ac

26
 Join @drdocstg

BODY FLUID COMPARTMENTS

Most abundant component in body is water

ICF

Cells

Non Circulatory Circulating Extra

Extra cellular cellular fluid

fluid plasma

Interstitial fluid

Capillary wall is porous through capillary membrane fluid constantly leaksout

to interstitial fluid

Interstitial fluid is ultrafiltrate of plasma fluid

Simplified

Capillary membrane porous

Total Body water u

at Na 8
K mg y

Na a

ATP A Hoz O
proteins ADP

Hoz
Amp

g plasmaproteins

Interstitial plasma

Intracellular 40 Extracellular 20

Young females have lessbody water because

generally females have more adipose

tissue and adipose tissue has less water content

Normally a standard person will be having 60s water of total Body weight

Major cations of Intracellular fluid K G Mg

Major onions of Intracellular fluid negatively charged proteins

Intracellular
organic phosphates g ATP ADP AMP negatively charged

major ions in interstitial fluid Nat Ct Hc05

are

Major ions in plasma are Nat Ct Hoz and negativelycharged plasmaproteins

27
 Join @drdocstg

capillary membrane allows Nat Gct to move freely hence Nat Gct

concentration is same in both Interstitial fluid and plasma

Nat a cannot move freely from interstitial fluid to intracellular fluid

The amounts of water in compartment

anypresent
is directly proportionate to no of

osmotically active substances in it

Osmolarity of a compartment

X no of solutes in that compartment

In an equilibrium intracellular and extracellular osmolarity is equal

Increase in solutes extracellularspace can pull water

in from cell and

the cell shrinks and there is extracellular fluid expansion

Normal osmolarity of Body fluid compartments is 287 mosm IL

a 300 mosm L

osmolarityof distilled water is Oosmk

In case of dehydration or prolonged fever extracellular fluid is lost and

extracellular osmolarity increases and water from intracellular space

moves into extracellular Space to attain equilibrium

osmolarity as of plasma

fluid Isoosmotic 30Omosmll is called

Anyisotonic having same

fluid

Isotonic Saline

osmolarity as of plasma
fluid having less 30Omosmll is called

Any

Hypotonicfluid

eg Half Saline

osmolarity as of plasma
fluid having more 30Omosmll is called

Any

Hypertonicfluid

Double Saline

28
 Join @drdocstg

EFFECT OF IV ADMINISTRATION OF DIFFERENT TYPES OF FLUIDS

Hypotonic Isotonic Hypertonic

A B C

150

mosmL
300 600
mosmk mosmk

ooo

8 oooo

ooo

300mosm L 0 I

Intracellular Extracellular

A compartment A is connected to intravascular space Hypotonic solution

1 eg Half normalsaline

osmolarity of Extracellular space reduces

H2O from Extracellular space moves to intracellularspace

1 Fluid solute

osmolarity of Intracellular space decreases

Osm 05mm

t t t t t t t

O c

ICF ECF c ICF

ICF ECF

ECF

X
volume volume voluhemme volume

RBC swell

H2Omoves also in RBC hematocrit remains same and

volume of plasma also increase plasma protein concentrationDecreases

Addition of Hypotonic solution Volume expansion Both ECFG ICF

of

to extracellular fluidspace Decrease in osmolarity ofboth ECF G ICF

B compartment B is connected to intravascular space Isotonic solution

isotonic saline

osmolarity of Extracellular space remain same

No H2O from Extracellular space moves to intracellular space

osmolarity G
volume
of Intracellular space remain same

volume expansion of Extracellular space Isoosmoticvolume expansion

29
 Join @drdocstg

Osm 05mm
n n

O O s

ICF ECF ICF

ICF ECF

ECF
c

volume volume volume vowmme

RBC volume remains same and Hematocrit decreases

Addition of Isotonic solution volume expansion

ofECF

to extracellular fluidspace osmolarity ofboth ECF G ICFremain same

C compartment Ca is connected to intravascular space Hypertonic solution

1 leg mannitol

osmolarity G volume of Extracellular space increases

H2O from intracellularspace moves to Extracellular space

Osmolarity of Intracellular space increases

nosm

Osm

T T T T T T T

D Q
ICF ECE p

ICF
ICF E

ECF

volume volume volume vowmme

RBC shrinks as H2O from RBC moves out

osmotic volume

Hematocrit decreases Dilutional anemia Hyper

expansion

plasma protein concentration decreases

Addition of Hypertonic solution volume expansion

of ECF Evolume contractionof ICF

to extracellular fluidspace osmolarity ofboth ECF G ICF increases

moles

osmolarity ofsolutes

L ofsolutions

moles solutes

osmolality of

kgof solvent

For practical methods 1L of Hao 1kgof H2O

If a solvent Solution is H2Othen Osmolarity Osmolality

30
 Join @drdocstg

STEADY STATE

Is equilibrium state b w Intracellular and Extracellular with same

osmolarity

and no net fluid movement b w two spaces

VOLUME CONTRACTION In medical literature contraction

of ECF is referred as

volume contraction

VOLUME EXPANSION In medical literature Expansion of ECF is referredas

volume expansion

Isotonic fluid loss Diarrhoea

vomiting ECF volume Decreases G

Isotonic Urinaryloss ECF osmolarity remainssame

Hemorrhage

No change in ICFvolume a osmolarity

i there is isoosmotic volume contraction

Iso osmotic fluid gain Isoosmotic ECF volume expansion

Iso osmotic fluid loss Isoosmotic ECF volume contraction

Osm 05mm
A

ICF ECF ICF

O
ECF c

ICF ECF
e s

volume volume volume vowemme

RBC volume remains same

Hematocrit increases

BP reduces

31
 Join @drdocstg

Hypertonic fluid loss solutes are lost fluid Caddinson's disease

ECF ECF osmolarity volume decreases

Hypoosmotic volume contraction

fluid from ECF to ICF

Osmolarity of ICE decreases

nosm

Osm

t t t t t t.tt

ICF ECF ICF

ICF E

ECF

volume c
volume volume volume

RBC swell up 9 Hematocrit increases

BP reduces

Hypotonic fluid loss H2o is lost more than solute

Seenin excessive

tiffins

Ime medicteniasis

Hyperosmotic fluid contraction Highgradefeverfor

1 Longtime

Fluid shifts from ICF to ECF

Intracellular Osmolarity increases

nosm

Osm

T T T T TT

O to

ICF ECF ICF

ICF
Ifk
E
ECF c
c

e s

volume volume volume volume

RBCshrink ECF volume decreases Hematocrit Remains same

plasma protein concentration increases

32
 Join @drdocstg

SUMMARY

c s c

ISO OSMOTIC VOLUME EXPANSION ISO OSMOTIC VOLUME CONTRACTION

Isotonic fluid infusion Diarrhoea

vomiting

Isotonic Urinaryloss

Hemorrhage

c s c

HYPERTONIC VOLUME EXPANSION HYPERTONIC VOLUME CONTRACTION

Hypertonic saline mannitol infusion

or

c s c

HYPOTONIC VOLUME EXPANSION HYPERTONIC VOLUME CONTRACTION

Hypotonic fluid infusion Halfsaline Seenin excessive

SIADH Sweating

Diabetes Insipidus

HighgradefeverforLongtime

33
 Join @drdocstg

HYPOTONIC VOLUMECONTRACTION

Aldosterone
deficiency

34
 Join @drdocstg

HEMODYNAMICS CIRCUITRY OF CARDIOVASCULAR SYSTEM

Fn Supply nutrients toperipheral tissues and remove waste products from

the tissues

carry hormones from endocrine glands

pulmonary.Art

vascularbed

PYm Y aortic valve

RA pulmonaryveins

LA

µ tricuspid
aorta

RV
mitral

Lv

CORONARY KKK

venawa.s.ua

main.es

Renal KKK

Arterioles

CNS can

IIIjg.es yteprecapinaryT

majorveins
capillary we

sphinter

venues

iii i

GIT W

Skin M

35
 Join @drdocstg

CIRCULATORY SYSTEM

Systemic Pulmonary

Left Ventricle Pump Left ventricle

High pressure Pressure High pressure

carry Oxygenatedblood Arteries Carry Deoxygenatedblood

carry Deoxygenatedblood veins carry Oxygenatedblood

All vascular beds are arranged in parallel so that every

vascular bed receives

fraction of cardiac output

pulmonary
vascular bed receives whole of cardiac output from Right Ventricle

Fractional Distribution of Cardiac Output

Total Cardiacoutput

I 5h1min gy

5.1 C

Coronary Cutaneous

15 zgy

v v
cerebral

25.1 25 Musculoskeletal

GIT Renal

These blood flow canbe regulated by arterioles

Pressure in systemic Circulation

leftatrium

Normal BP systolic T G8mmHg

Diastolic

SBP is the pressure in systemic systole Diastole

arterial tree when Leftventricle GrommHg 8ommHg

is peakof systole

LeftVentricle

Systole Diastole

120
mmHg CommHg

36
 Join @drdocstg

Diastolic is the pressure which

Mean ArterialPressure t
Yg pulsepressure

Bloodpressure blood is pushed into

arterioles

pulse pressure SystolicBP Diastolic BP The pressure forwhich baroreceptors

are sensitive to

Normal valueof Pp 120 80mmHg

40mm

Hg

Normal MAP 80 1 a 93mmHg

During systole the elastic arteries stretch and accommodate

systemic blood

During diastole the stretched elastic arteries recoil and maintain MAP

Arterioles have maximum smooth muscle and can constrict vasoconstriction

and dilate vasodilation and regulate blood flow to the tissues

During steady state arterioles are tonically semiconstricted and offer maximum

resistance to the bloodflow

innervated sympathetic Nerve endings leg RenalGsplanchnic

Arterioles are richly by

Sympatheic stimulation Stimulate A receptor and cause vasoconstriction

stimulate 132 receptor and cause vasodilation

During stress

FLIGHT FIGHT

sympathetic RESPONSE

stimulation

L v

Li 132

GITRenal skeletalmuscle

Vasoconstriction

vasodilation Blood flow to skeletal muscle increased

Blood Redistributed to

skeletal muscle

37
 Join @drdocstg

PRESSURES IN VENOUS SYSTEM

All capillaries have pressure

of 3ommHg except glomerular capillary 50mmHg

venous diameter is larger than arterial diameter

Hence veins are called reservoir vessels Got of total Blood volume is in veins

a Kla capacitance vessels

pulmonarycapillary 8mm
Hg

systolic 25mm Hgp

PulmonaryA

Diastolic 8mmHg T

htatrium ommHg Mustang

IgY

RightVentricle 25mmHg

majorveins 4mmHg

Venules bmmHg

IN

Capillaries zommHg

VELOCITY OF BLOOD FLOW v

Defn Rate of linear displacement of blood unit time within circulatorysystem

Blood flow volume of blood passing through a area

of circulatory systemhfumit

V L Blood flow Q

v L 1

Radius Crosssectional area

V a

Tt2

Radius
of aorta radiusof all arteries Radius of all

put together capillariesputtogether

velocity in aorta 7 velocity in arteries velocity in capillaries

38
 Join @drdocstg

Total Cross sectional area and velocity

capillarieshave maximum cross sectionalarea

when put together

agiosgreqorwadienbtewiseenmewd
ivingg.vencepoY.nfshe

me

Resistance isthe impedance to bloodflow

Max resistance is arterioles veins venules Arterioles

major Aorta

given by
arterioles constrict Resistance increases
capillaries
Arteries

If

If arterioles dilate Resistance decreases

Blood flow 2
y

pressure gradient DP

L 1

Resistance Velocity in a blood vessel

Blood flow DP_

Blood fiobusrouguinra.esatuanafeorgan

D PCArterial PCvenous

Resistance

Total cross sectional area ofvessel

Also total Peripheral Resistance DP_ MAP

Resistance of whole Blood flow co

systemic
circulation Q

I Resistance DI

39
 Join @drdocstg

HEMODYNAMIC's

Velocity v Blood flow cardiac output

Area

Total amount of blood flowing through the system is cardiac output

total Cross sectional area of

aorta

F Ifine mpaiteiges.ae adf.aiaiogei.se

velocity in

Hence

capillaries arterioles majorvessels aotta

also

Blood flow 1 arterioles offer maximum Resistance to bloodflow

POISEUILLE EQUATION

RESISTANCE 8 R density viscosity of Blood InternalResistance tobloodflow

IT 4
ye l length of vessel

r radius of vessel

Resistance L viscocity Cz

T viscosity TResistance eg polycythemiaVera

multiple myeloma

Walderstorms Macrogammaglobuilinaemia

t viscocity 4 Resistance
eg
Severe Anemia

Also Resistance L I EEing

t
radius Fok

t t

If in acase of atherosclerosis thrombus if radius is halvedthen Resistance increase

by 16 times

If radius is doubled Resistance decreases

by 16times

This resistance is controlled arterioles

mainly by

40
 Join @drdocstg

Laminar flow and Turbulant flow

The flow ofblood in a normal conditions is in multiple layers i e laminar

The layer near the vessel wall has maximum Resistance and least velocity

away from the

The subsequent layers vessel wall has less Resistanceand velocity

increases

the velocity makes a parabolic shape

The central has maximum velocity

layer

Normally the whole CVS exceptat valves has

laminar flow

velocity ofdiff layers

If there is acase of obstruction orstenosis the laminar flowof blood is disturbed

and flow becomes

radially and axially called as Turbulant flow

ffji.cl

In a turbulent flow parabolic arrangement islost

The turbulant flow produce audible sounds in Heart meetings and in vessels

called as Bruits

The tendency of flow to get turbulant is measured by Raynaud's number

F densityof fluid

RAYNAUD'S NUMBER DVD V velocity offluid

if D Diameter

of viscosity of fluid

If RN 72000 the flow has higher tendency to become turbulent

In acase of
severe anemia
µ Cviscocity T and due to hypoxia cardiac

Output increases and also velocity thus RN increases and the flow becomes

turbulant and produces a manner

during ejection blood called asof

FUNCTIONAL EJECTION MURMER nd

Blood flow in a normal the flow ofblood is turbulent at thebranches

41
 Join @drdocstg

Concept of Compliance

Veins Arteries

If equal amount of volume is added to veins and arteries

veins are more stretchable and accomodate

larger volume of blood at low

pressures and hence veins are said to be more compliant thanarteries

Dueto such property ofveins 701 of blood volume is held in veins at

less pressure and veins are called capacitance vessels

same amount ofblood Higher pressure and theblood in

Arteries hold

arteries is called stressed volume and in veins is called unstressed

r n 9
at a volume

Veins Atteties
given of blood v

volume vessels in veins hold the blood lowpressure

D aged people
Arterieshold the blood high pressure

vessels in old people are more

stiff and less compliant

Pressure

42
 Join @drdocstg

ARRANGEMENT VESSELS
OF

SERIES PARALLEL

urn

Bc mm mm Bc mm A
R3 R2 R

mm

R 122.123 are the vessels offering R 122.123 are the vessels offering

resistance inseries resistance in parallel

of
Total Resistance Sum all resistors TotalResistance

RT R Rz1123

Blood flow through all theresistors Each vessel receives afraction

of

is same from
blood flow
the total blood

Pressure of blood decreases as it of

Pressure blood is same as it

passes through resistors passes through diff resistors

adding a extra vessel c resistanceRa adding a extra vessel c resistorR

increases total Resistance decreases the total resistance

parallely arranged vascularbed

vessels

g passing through single eg

organ in systemic circulation

BLOOD PRESSURES IN CVS

120 There is sharp decrease in pressure in

MXN

arterioles

systole and

Oscillations in pressure dueto

80 diastole are called pulsations

Pressure Pulsepressure SBP DBP

120 80

40mmHg

pulsepressure in majorarteries is

slightly higher than aorta

Aotta major small ArteriolesCapi venues

veins

arteriesarteries Haties

This is because whenblood is propelled

intomajor arteries the pressure wave moves faster

than column of blood

the pressure on arterioles is reflected back

43
 Join @drdocstg

Systolic Blood pressure DiastolicBlood pressure

due to contraction of LeftVentricle Due to recoil of aorta

Max pressure in aorta and Pressure in aorta diastole

major during

arteries
during peak of systole

Depends on stroke volume Depends on total peripheral

Resistance

Compliance L l Compliance DBP

SBP

Graphical Representation of Pressure changes

SBP

map

DBP

Dicrotic Notch is due to closure of aortic wall at the beginning ofDiastole

SBP Increased

map creased

pulse pressure Increased

DBP

In old age less competent vessels

44
 Join @drdocstg

VASCULAR PATHOLOGY

45
 Join @drdocstg

f
cardiovascular.eswteam.onsisdwiuiofedinfogemetuofirmmaainhiinsn
µ
Homeostasis
body pomonaiyaite'T
Left
atrium
A Atrium

image.mg gfbloroadwesfromattiabventrides
µ
n
kffentn.de
et Pulmonary
ventricle

Differences between
pulmonary Circulation
and systemic circulation

PULMONARY SYSTEMIC aAlveoli

Emf
S
c

i
Mati add
Lowpressure
F
Highpressure 71
L
Pulmonary
catty deoxy
arteries
blood
Systemic arteries
carry Oxy
blood

I Systemic I
µ
Pulmonaryveins systemicveins
blood blood
carry Oxy carry deoxy

considering ventricles

Right Ventricle Input valves Tricuspidvalve

outputvalves pulmonaryvalve

LeftVentricle Inputvalves Bicuspid Initial

Outputvalves Aortic

46
 Join @drdocstg

Normal Circuitof Systemic Circulation

Arteries capillaries Veins

variations in systemic circulations

Renal portohepatic

Arteries Arteries
x x
Afferent arteriole
capillaries in GIT

9107kWh capillaries PAID veins

efferent arteriole capillariesagain in
Liver
peritubularcapillaries v
Hepatic vein
4
venules
x

veins Ivc

Histology of vessels

TUNICA MEDIA

smoothimayuserdecell
external engoatyheefialcell

Thy
Elasticlamina
Basalmembrane TUNICA
TUNICAADVENTITIA subendothelial

I
INTIMA
f
fEfI I
s.m.in i
EEEEEEIqeEEg
f

iassa.mn
REED
lymphatics
Meg

47
 Join @drdocstg

Composition of Media
ELASTIC ARTERY
Alternate layers of elastic lamina and smooth muscle cell layer

X I

4
a
X TUNICA MEDIA
Is 4
l za g
A f y f 1
TUNICA ADVENTITIA

it g
i f f fitil t
f f f f Endothelial layer
l TUNICA
f ftd T ftp Basement membrane INTIMA
Y v Tiff
1yd I Itf
a
f

Large
arteries can accommodate
incoming
blood during systole and recoil to pushthe
blood into circulation diastole
during
Media contains 40 70 fenestrated elastic lamina fenestrations provide passage of
nutrients to all the layers of media

Endothelial lager cells secrete which can be identified with antiVWF

VWF
antibodies to detectvascular tumors of endothelial cell
origin
In 30 SYPHILIS the chronic inflammation disrupts vasavasot.am Blood
vessels
supplying
Blood vessels and cause disruption of tunica media
that causes abnormal dilatation vessel wall of leading to aneurysms knownas
SYPHILITIC ANEURYSMS

Scarring of tunica media causes wrinkling of intimal layer referred to as

TREE BARK APPEARANCE

congenital connective tissue diseases leads to weak elastic lamina

progressive
intimal leads to accumulation ofblood in Tunicamedia called as
injury
Dissection ofvessel
Egfor elastic artery Aorta

48
 Join @drdocstg

muscular
Artery

a
r j TUNICA MEDIA
AA f i
gyp A
ftp.fff
t IH i
fi Hlf HI INTERNAL ELASTIC LAMINA
f Add
it EXTERNALELASTIC LAMINA

Kang iii go.lk

HII f.EE
E
iuo E
a

Media of smooth muscle mainly consists of smooth muscle cell layer

and less elastin

Eg Medium sized arteries Brachial

artery coronary artery

Arterioles

Arterioles are around 10 100 and contains minimal smooth muscle

and offer max
µ resistance tothe blood flow and hence are
layer
called RESISTANCE VESSELS

F
eye
minimal smoothmusaecenayer

r No internal Elastic lamina

MetaArterioles

less smooth muscle cell

Very layer
End of systemic arterial circulation
P Yf.me aat
precapillary sphinter

49
 Join @drdocstg

HISTOLOGY OF HEART

Layersof
Heart Inner Endocardium
Middle myocardium
outet pericardium

Myocardium is
attached to fibrous skeletonof Heart Fibrous Rim madeofdense
irregular connective tissue

Ii
amo.mg
imIg
pericardium

g
IH

Fibrous rim with fourapertures Pattern of attachment of myocardium to fibrous rim

annulus
ring
leftatrium
T
i
H
iitifiAH

Left atrium is mounted on annulus

ringof mitralvalve
tingof
Left ventricle is
mounted annulus on aortic valve

Any disease with left ventricular dilatation stretch the annulus

ring and
stretches the valve apart
of
Function fibrous Septa

Attachment of valve leaflets

Attachment of Atrial and ventricular myocardium
Attachment of major vessels pulmonary artery and Aorta
Electrical insulator between atria and ventricle

50
 Join @drdocstg

Y H Y cardiac
Syntitium
Gap junctions

All myocardial cells are connected with gapjunction toform a single syntitium

SA node generates electrical signal and both atria contracts

Atria should contract first to pump blood and then ventricle should contract

Signals from Atria are passed toventricle through AV node which is the only
electrical window b w Atria and ventricle

AV node holds the current for 0.1 seconds for ventricles to accomodate blood

ENDOCARDIUM

a
Endothelial a
a

endothelial
sub
connective tissue
a
x a
consistsof veins and
nerves

layerof endocardium iscontinuous with layerofvessels

Endothelial cell endothelial

CARDIAC VALVES

Valves aremade upof dense layerof aponeurosis from

loose connective tissue
atinbdwsenotiontheufundf.in
ngted by

qY t
i iF uea Ee.ttbInsgaiosaDeIEoseGIeIeaustieesngthibraiions
i iii
the

raw I diseases name

inyµ vasculatisation of valves along with vegetation

51
 Join @drdocstg

At the peak of ventricular systole the fallback of valve into attia is prevented
by
tendon like structures attached to cusps of valve called chorda tendinae

Choida Tendinae are attached to ventricular myocardium through papillary muscle

long
Choida tendinae or papillary muscle paralysis leads to prolapse ofvalues
causing regurgitation

Seen in Infective Endocarditis 9 Myocardial infarction

MYOCARDIUM

Myocardial cells areof threetype General present in atria and ventricle

specialised conduction ofelectricalsignal
myocardialendocrinecells secrete ANP

AND is secreted by atrial cells in response to volume load in

systemic
circulation and causes H2oand Nat loss to maintain back the
volume in vascular compartment

Specialised myocardial cells are concerned with generation and propagation

of electrical signal and include SA node AVnode and BundleofHis

000
sanode
at
Avnode c fIf af
IEi
Fibrous e e in
Septa

HAHN
l l ll
t

52
 Join @drdocstg

CAPILLARIES

Usually 8 lope length C 1mm

a a a Pericytes
Temne

Endothelialcell
layer
Ti3asal lamina

capillary membrane are semipermeable tonutrients andgases

Intermediate filaments found in endothelial cells are Desminand Vimentin

TYPES OF CAPILLARIES

1 Continuous capillaries posess pinacocytic vesicles that helps in trans

cellulartransport
of substances

j xI EH
gapjunctions120haoccludens
Contains
inb w two endothelialcells
Too.IO o.oooooo.ooooXoo.ooooo

Seen in muscles exocrine glands lungs GCNS

pinacocytic vescicles are not seen in CNS

2 Fenestrated capillaries

46 46 00

M 04070 x
Fenestrations size 7ohm and are regulated
byfascia
diaphragms
Adjacent endothelial cells are connected
by occludens
seen in kidneys GIT endocrine glands and pancreas

3
Sinusoidal capillaries
T E E E g
TE

AT a a a a

Discontinuous Basal lamina

widely spaced endothelial cells
seen in Bone marrow Liver Spleen Lymph node

53
 Join @drdocstg

Permiability of capillaries

simple diffusion Gases

Activetransport Aminoacid Glucose
Interendothelialgaps WBC
Capillaryfenestrations Largerprotein
pinocytic vescicles Largerprotein

Functions of Endothelial
layer
Lungs production of Angiotensin converting enzyme ACE
catabolic function to destroy Bradykinin NE prostaglandins
convert lipoproteins into Triglycerides
production of prostacyclins No endothelin and factors that inhibit platelet
aggregation and coagulation

THOROPHASE

venule
Arteriole

THOROPHASE

µ T AE i
metaarterioles
PreEapillarysphintet

When there is reduced demand for blood pre capillary sphinter of capillaries close
and blood isdirectly drained into venules through thorophase vessels

VEINS

accomodate 70 1 of circulatory Blood capacitance vessels

consists of intima media and adventitia
adventitia of veins is thickest and contain longitudinal smooth muscle cell
veinshave large lumen and are thinwalled
layer
Venules do not have tunica media
Blood flow in veins is regulated valves
by
Nonfunctioning of valves cause poolingof blood dueto gravity called varicose
veins

54
 Join @drdocstg

Blood pressure in a population is distributed under a gaussian curve like heightand weight

Elevation of systolic Blood pressure 7140mmHg or Diastolic Blood pressure 790mmHg

is the criteria for Hypertension
sustained elevation causes risk for cardiovascular complications

Elevation of systolic Blood pressure is more dangerous than Diastolic BP as itcauses

left ventricular Hypertrophy

considering above criteria 251 of population in us is Hypertensive

In USA 50 million people are hypertensive and 301 among them are not aware of
disease

Only 251 people have good compliance for treatment

GRADING OF HTN

SYSTOLIC DIASTOLIC mmHg

mmHg

Pre HTN 120 139 80 89

HTNGradeI 140 159 go 99
HTNGrade2 3160 3100

Rx for HTN most important is lifestyle modification

MALIGNANTHYPERTENSION

alkla accelerated HTN is sustained elevation of SBP 200mmHg or DBP 120mmHg

with severe end organ damage

Has 90 mortality without treatment in 1

year
q 301mortality with treatment in 1
year

55
 Join @drdocstg

Determinants of Blood Pressure

BP Cox TPR

contractility and determines systolic BP

cardiac output is dependent on myocardial

Total peripheral Resistance is due to toneof arteriolar smooth muscle and determines
Diastolic BP

TBlood volume dueto cause due to exogenous administration

any NatG H2O Retention
ofvenousReturn T Mineralocorticoid
Renal impairment
TEnddiastolicvolume
Factors that determine CO
TCardiac Output
COL HR COLContractility

Tin SystolicBlood pressure

Factors
determining TPR
1
Humoral Neuronal
1 h
constrictors Dilators A stimulation TTPR
t t 132 stimulation 41792
Angiotensin II Prostaglandin
Catechlomines
Bradykinin
Thromboxane As Histamine
Variations in Normal physiological mechanisms that cause HTN

Renin producing tumors

Renal Disease with decreased perfusion or ImpairedNat balance

0C pills Increased Angiotensin fromLiver

ogen

Tumors ofadrenal medulla

congenital adrenal hyperplasia Deficient enzymes

GITTLEMAN'S SYNDROME abnormal

gainof function of THIAZIDE's
sensitive NatChannel
LIDDLE'S SYNDROME abnormal
gain of function of AMILORIDE
sensitive NatChannel
If eRfffftion

56
 Join @drdocstg

RELATION B W SBP G DBP

SYSTOLIC BLOOD PRESSURE DIASTOLIC 1310013PRESSURE

Increase in Body volume Increase in TPR ofanycause
v r
sustained increase in co BBP Increased workload onHeart
r
Arteriolesprotectthetissues compensatory myocardial
from Hyperperfusion Hypertrophy
r
Arteriolarsmoothmuscleconstrict Increased cardiac output
r
Reactive Hypertrophy 9Hyperplasia Increase in systolic Blood
of arteriolarsmooth muscle pressure

and also connective tissue

proliferation ofarterioles
thick arteriole

Increase in total peripheral

Resistance

Increase In DiastolicBP

10 HYPERTENSION

Onset 25 45years
MK than 20 HTN
90 95 1 population of HTNpeople
Can be treated and managed
cannot becured completely

GeneticPredisposition Essential HTN

F
en 1onmental
factors

57
 Join @drdocstg

Environmental factors
for 10 HTN

Sympathetic Nervous system overactivity

overactive Renin Angiotensin Aldosterone system
NatGHQ excretion
Defects in
Increase in Intracellular Nat GCa't due to failure of Nat 1kt ATPase
Obesity
Excess Nat intake r
Alcohol
BNS activity f
smoking if daily intakeof ethanol exceeds 4Ogm I
Sedentary life style
polycythemia
NSAID's
low Kt intake

HYPERTENSION

Secondary to underlying disease

curable stages
early
5 lot of total HTN pt's
occurs extreme ofages
causes of 20 Hypertension
Renovascular causes
Atherosclerosis MK in male smokers 50
yrs
Renal Artery stenosis
fibro
musculardysplasia mkin female
young

Glomerulonephritis
pyelonephritis
Adult polycystic kidney disease Autosomal Dominant
Renal vasculitis PAN and Renin producing tumors
eg

Endocrine causes

d Pitutary Acromegaly TGH

Thyroid Hyperthyroidism more adrenergic drive

Hypothyroidism
Retention of Nat
Parathyroid Hyperparathyroidism Tca

58
 Join @drdocstg

ancreas Diabetes mellitus

Adrenal medulla PHEOCHROMOCYTOMA

cortex CONN's syndrome TAldosterone
Cushing's syndrome
congenital adrenal hyperplasia
Licorice Injection Ted activity of mineralocorticoid receptors
Exogenous hormones
steroids 0Cpills

induced HTN Ot
Pregnancy p eecegfgmmppssi.ge

vs causes Neurologic causes

psychosis severe anxiety

I
rotation of Aorta
f Coa TantraCranialtension

PAN or
any
disease causing
Tedco or TedTPR
SHIITE Afffeesas

µ
TARGET ORGAN DAMAGE IN HTN

CNS Transcient ischaemic Attack

Neurologicdeficitlasting
lessthan24hrsdue tovascular
abnormalities and are completely reversible

stroke Neurologic deficit lasting more than24hr5 rapidly developing dueto

vascular phenomenon andare not completely reversed

Hypertensive encephalopathy

Miaoaneurysms and rupture

multiinfarct dementia

Renal Hypertensive nephropathy

RETINA Hypertensive Retinopathy

59
 Join @drdocstg

GRADING OF HYPERTENSIVE RETINOPATHY

I n
Normal X

Grade I Arteriolar
thinning
Arteriolarattenuation

silver wiring on 9
fundoscopy
Grade I AV nipping
f AVnipping

Grade II cottonwool spots 1

and Hemorrhages my Flame

flame hemorrhage
egg Hemorrhages

Grade II pappiledema pappiedema

741

Cvs complications

supplyand
Left ventricular Hypertrophy
Mismatch bw Blood demand
coronary
1
LHD
Arrhythmias GSudden Cardiac Death

Aortic Dissection

ARTERIOSCLEROSIS

Hardening of arteries with lossof elasticity

Monckeberg medialCalcificSclerosis Atherosclerosis Arteriosclerosis

Hyaline arteriosclerosis
Mlctype andinvolvestunicamedia Diseaseof intima causeof senile essential
hypertension
affectsmediumsizedarteries fibro T
like characterised
by fatty seen in f
d'effosinies

radialandUlnarA plaques Dmf gg

do

doesn'tcompress thelumen affectselasticandmedium

sized musculararteries plastic arteriosclerosis
Hyper
Aorta 9coronaryarteries
Eg
q0
in g calcifications seen in
malignant HTN
660 ofmedia Fibrinoid necrosis
qfff.EE
IMJf8jiEIe
d
Neaotisingarteriolitis

IE
8088k
55 fEfzaggoEEEEIoE
Fibrinoid
necrosis
J
60
 Join @drdocstg

Disease of Intima characterised

by
formation of
fibrofatty plaques in intima
leading
to
luminal obstruction and changes in tunica media

Principle Response to injury Hypothesis

Causes of Injury
Hemodynamic stress HTN BothSBP 9 DBP
Lipid abnormalities Hypertipidaemia
TLDL TVLDL I HDL
smoking H
DM seen in familial hypercholesterolemia
Homocysteinutia DM
Toxins endotoxin Nephrotic Syndrome
microbes CMV Chlamydia Hypothyroidism
Alcoholism

Healthy endothelium releases No thatprevents aggregation of platelets

Damaged endothelium produces freeradicals that neutralises No and causeplatelet
aggregation

Damaged
endothelium exhibits adhesion moleculesfor WBC macrophages andmonocytes V CAM

Damaged endothelium increases permeability to lipids lipidsentertunica intima

LDLgets oxidised and helps in formation of Atheroma

HDL mobilises TG to liver fromtissues and prevents atherosclerosis

PATHOGENESIS
Injury maacrophages
platelet aggregation
vcam

LDL 000 000

I
femonocytes
Tunicaintima
IEL
musclecells
Smooth

EEL
c l c e c c e c

Inflammatory mediatorsreleased by
macrophages 1L 1 Lymphocytes INF 8 stimulate macrophages
TNF
Mcp 1

61
 Join @drdocstg

Steps in formation of atheroma

Endothelial cellinjury

Increased permeability adhesionof WBC and thrombogenicstate

macrophages and monocyte infiltration

Release of inflammatory mediators and Growth factors

Attracts smooth muscle cell into Tunica intima

De differentiationof smooth muscle cells

oxidation of LDL andthen phagocytosed macrophages monocytes and

smoothmuscle cells
by
Oxidised LDL is cytotoxic leading to apoptosis of cells leading toformation
oflipid core
Aggregated platelets release growthfactors that leads to subendothelial
smooth muscle cells

Smooth muscle cells secrete extracellular matrix collagen9 proteoglycan

that forms fibrous cap of atheroma

some macrophages are also present in fibrous cap along with lymphocytes

At the shoulder oflesion growth factors stimulate vasavasotum to form

neovasculatisation

hth 3
you end ut z
no µ
980889090
888
Sto E EE oo
e E
T.ee
laden
tw.X
wFaf Lipidcore
macrophages Angiogenesis
foamcells

Riskof arteries for Atherosclerosis

Abdominal Aorta
coronaryartery poplitealartery carotidartery Circle of Willis
62
 Join @drdocstg

EPIDEMIOLOGY AND RISKFACTORS OF ATHEROSLEROSIS

Mlc in industrialised countries

studies have shownthat lifestyle modification and better drugs along with better
management of complications have
advances for
healthcare
significantly reduced
riskof stroke 70 t and Mt 50 post 19605 in US
by by during

cases

I 5
1963
Riskfactors

Age 40 60 years

Sex E f estrogen have protectiverole

the Risk in post menopausal female is same thatof males
Genetics HTN
DM increase Riskof atherosclerosis
Hypercholesterolemia
Hypertipidaemia

Diet containing PUFA

excess alcohol intake
obesity
DM
Smoking
minorfactors

Type A personality
sedentary life style
Homocysteinuria
DVD CAD coronary artery disease
Chronically
elevated plasminogen activatorinhibitor GCRP

63
 Join @drdocstg

CLASSIFICATION OF ATHEROSCLEROTIC LESIONS

American Heart Association
By
Type I Initial lesions Fattydots

veryfew lipid
laden macrophages
about Imm size yellow colourplaque
onto
080 080

occur very early

age
mostof them
occur in abdominal
have suchlesion
aorta by10years ofage

Type I

dueto fusionof fattydots

linear lesions fattystreaks
macrophages with lipid and lymphocytes
about 1cm oflength
also occur in coronary arteries
precursor of mature atherosclerotic plaques
convert
only some into atherosclerotic plaques

Type111 Intermediate lesions

fat laden smooth muscle cells

fat is also present extracellulary o o
00800 o

type true lesions

afoenngtrdwimcore.ee
lipid o Ooooooo

aka atheromatouslesion
touscap
Type fibro
atheromalesions

Fibrous for atherosclerosis OooDOO 00 or

cap patrognomic
Neovascularisation shoulders

Surface
feels
Type complicated plaques 8o8o8OFTf.de
Thrombosis_gq
Thrombosis on surface
surface defects 000008 00 on
Hemorrhage intoplaquefromnewressels or F
from intravascular compartment
produces severe obstruction to bloodflow TIntraplaquehemorrhage

64
 Join @drdocstg

Growth of plague
TypeI Type 3
accumulation of fat
Type 4 Type
5 proliferation of smoothmuscle

Type6 Depends on thrombus formation

plaques inlarger vessel cause abnormal dilatation

plaques insmaller vessel cause obstructive complications

COMPLICATIONS OF ATHEROMATOUS LESIONS

Aneurysmal lesions

e
k

08

a
rooftops qigong

j
ta
ffBG EYmqy
meetly
Fibrosis or surface defects
calcification Erosion Intraplaque hemorrhage
ulcerations
Rupture
H
Platelet aggregates Thrombogenesis
with fibrincap
partial obstruction

65
 Join @drdocstg

COMPLICATIONS OF ATHEROSCLEROSIS

AbdominalAorta CoronaryArtery popliteal

artery
carotid
artery of Willis
Circle

IHD
D
lowerlimb Stroke Stroke
Pectoris
Angina ischaemia TIA TIA
Dq Myocardial Ischaemic Ischaemic
g
Infarction Encephalopathy Encephalopathy
Suddencardiac
death
CCF
lowerlimb
ischaemia
Rupture ofaorta

Artery ostium
Mesenteric

Ischaemiaofgut

Renal Artery ostium

TTRAAS HTN

Leiiche syndrome

atherosclerotic lesion in abdominal aortaand Iliac

artery
present c impotencyand calf claudication
Atropy of calf muscles

CONCEPT OF P G20 PREVENTION

Pprevention prevention of disease with no hlo atherosclerosis or associated complication

Risk factor is modified

20 prevention factors in patient in

Modifying Risk apt 5h10 one or more
atherosclerosis associated complication

66
 Join @drdocstg

Abnormal irreversibledilatation of cardiovascularsystem inn

True aneurysm when dilatation involves all layersof vessel

Pseudo
aneurysm f
whenaneurysm doesnt involves all partsof Eff
Falseaneurysm vessels

General complications of Aneurysm

Infectionof compression of adjacent structures

aneurysm
Thrombus

f ke Rupture of aneurysm
a
Thrombo
embolism
GRODD

HEMODYNAMICS OF ANEURYSMS

wall stretchout due topressure in intravascular space

pathologic

ate P dt and maintain Ysdmilsa

Tension Pressure X Radius

1
Causes of dilatationof vessel wall

Atherosclerosis disease of intima

medial
Cystic degeneration
Trauma
vasculitis PAN
egdiseases
Congenital BerryAneurysms found within the circle of Willis in CNS
Postcommunicating A Ant communicatingA
Infections ofvessel wall Mycotic aneurysm

67
 Join @drdocstg

CLASSIFICATION

IE a e
sm

Types of Ascending Aorta aneurysm

Syphilitic AneurysmILeutic aneurysm

tertiary stage of syphilis

less common due
nowadays to early diagnosis and treatment

Gk
soooooo
On Oo O of
collection Release
of growthfactors abnormalproliferation of intimaof
0Oo 800 lymphocyte 9 vasa
ooo
0 plasmacells vasone.mg
of Compression
peducted

supply to
Vasarasotum blood
media of Abdominalaorta

1
Dilatation Damaged Degenerative changes in mediaGadventitia
datingsystole vesselwall of abdominal aorta

COMPLICATIONS

ya g coronary ostealstenosisdue to

iiii i
structures
geodescompressing
tfitifiniiiifiiigifiifeiffifiifii
i iii
Ii ii
MM TREEBARK
ii ii
Bonypain
us iii a disease

i'µµµ
APPEARANCE Stidot Dyespnoea

68
 Join @drdocstg

Overstretched aorticvalve Aortic Regurgitation

I
volume overload in
left ventricle
y.jp ifffFE
4
i
it Dilated

k
cardiomyopathy c Lv Hypertrophy

yYyg
CORBOVINUM sizeofheart resemblesheartofcow

hi
Hill

Types of abdominal Aorta aneurysm Inflammatory variant

mycotic aneurysm
variant

i i
J R 2cm
73cm aorticaneurysm

i i
i
i
Abdominal
aneurysm Mk cause atherosclerotic plaques
i
Hypertension
i Abnormal turnover ofconnectivetissue
i in tunica mediaandadventitia
I
tend
µmaY
eighths
Imbalance b w matrixMetalloproteinases
9 Tissue inhibitorsof metalloproteinases
mk inmales active smokers

In inflammatory variant aortic fibrosis is seen

Dense pen

In mycotic variant inf from Salmonella staphaureus Streptococcus leads to

aneurysm

Diagnosis

On Xray curvilinear deposition ofCa on aneurysmal wall Incidental

found in Routine USG

Incidentally

41
asymptomatic
40 abdominal mass that is pulsatile and expansile
40 Symptoms arising from aneurysmal compression Ureters Hydronephrosis
Vertebral Backache
Body
Thromboembolic complications lowerlimb
compression of mesenteric artery abdominalpain ischaemia
compression of Iliac Artery 9 vertebral artery
sudden rupture Severe shock or death
69
 Join @drdocstg

an autosomal dominant genetic disorder due to mutationof FBN 1 gene on Ch15

FBN 1 codesfor Fibrillin that acts as a scaffolding protein for tropoelastin

gene

mutant FBN 1 abnormal fibrillin that combines with normal fibrillin

gene produces
other gene and inhibits its function
produced
by
This phenomenon is called Negative dominant phenomenon

Occurs in 1 5000 individuals

among
8 9 No gender predominance

Mutations seen in Marfan's disease

Missense mutation most common

Nonsense Mutation
FrameshiftMutation

Clinicalfeatures

familyHo in 80t cases For Dsis 2 outof 4 system is

eye
necessary
skin
MARFAN
Musculo
skeletal Cvs

musculoskeletal

Tall individual
Aimspan Body Height
cylindrical and long fingers andtoes Arachnodactyly
Lax joints
Elongation ofskull Doliocephalic

IHighpfnfhedabnpo.almaatfih.es
kyphosis or scoliosis

chest compression Rectusexcavations 17

Ot protrusion Pigeon chest

Frontal Bossing and prominent supraorbital Ridges

70
 Join @drdocstg

Cvs
valvularabnormalities mitral valve prolapse
Aorticvalve Aortic Regurgitation

In Tunica Media

unmanning
mmmm FEET
man medialcysticdegenerations
immune m
immune Inman
unmmunn
composed of amorphous
Normalarrangementof Abnormal separation connective tissue
elastic lamina ofelastinfibres
Aortic Dissection

Dsis Echocardiography

Eye

oflens
superiordislocation
suspensoryligaments of DOJ
Zinn
f µ
Normal Holdlens in place Diseased
eyes

Bk Ectopia lentis
myopia
large eyeball
Retinal detachment
may occur
other complications

Spontaneous pneumothorax
Ductal Atresia
Increased tendencies forHernia
Rx
13Blocker to prevent aortic dissection
Antibiotics to prevent endocarditis before dental procedures
any

71
 Join @drdocstg

MARFAN'S HOMOCYSTEINURIA

Autosomal Dominant Autosomal recessive

FBN 1 gene mutation Defect in

enzyme
p
Cystathione synthetase

Lens dislocated upwards Lensdislocateddownwards

Aortic Regurgitation

Skeletal abnormalities

Nomental Retardation mental Retardation

Urine cyanideNitroprusside
test

Respond positively to
Pyridoxine

72
 Join @drdocstg

alkla dissecting hematoma

ufofehaa
aan.fm
nndaeatedinwallofaoitadueto
jj Ifg
in aidissaeapsiuamoinani.nu
in
If the ptis lucky enough theremaybe
another intimal leat distal to yiffiftyititigiifU
initialteat and thus creating a pseudochannel forthe bloodto flow
y
µ
RISK FACTORS

aseinomeyuo.gg nd 9du.aiswfthoyhgwtiYFEteENnsa FeisD

my
Hi
ing systemic many
of connective tissue Foi Eg Marfan's Syndrome
Ehler Danlos syndrome

ooo ooo ooo

k
ii tiiii iii
i Tiki
k
4,4444
ooo ooo
I
ifooo im

dissecting ntffnf.ca
Namal vesselwall Marfan's 0ffssa
syndrome
ectionCoisiupledadlagen
IPtegnanY due to catheter induced trauma in aorta
Iatrogenic cause
coaretation of aorta

a
i
Eiiiiifiifigiiiggi

Iii
73
 Join @drdocstg

Clinical features

sudden cutting typeof pain radiating toback

Abdominal pain
features of coronary A compression Ml
Rupture into pericardial peritoneal pleural cavities
Dueto rapid Bloodloss pt may present c acute severe shock

Diagnosis

BEST Transesophagial Echocardiography

other
DynamicCTScan
Dynamic MRI

eatin in.AM IfE

YIaintgif.gl
ggdideptessute

ivEsmo1oL
iv Labeten

J µµ Y
r.n.in
pericardium
I
hfig
f v i di
severeacute
o.se

0
I
it i
i 4

i
Bp
BECK'S
TRIANGLE
iiiiiiiiiIUii
Distant
1

HeartSounds

74
 Join @drdocstg

Classification
of Aortic Dissection

g
i
g
AH
I tf p g
iifiififiigiifiggid tittiifiififiigiifive tititifiififgitifiive
Intimaltear f i k
innit
11111N
I inn
11111N
I iiiIt III
11111N

T T
Type A aortic Type13 Aortic Dissection
dissection

Origin Root ofaorta OriginDistal tott SubclavianA

Extent Ascendingaorta I Extent Descending aorta
Descendingaorta E
TypeA 501 Mortality ein t
day

75
 Join @drdocstg

Inflammation ofwall ofvessels Systemic effects manifested

only inseverecases
General clinical featuresof vasculitis
localeffects
0
systemic
effects
of inflammatory condition TESR TCRP

fever wt loss anorexia easyfatigue

hh i
If vasculitis involves elastic arteries like aortaandits branches
Manifestation depend on size and location vessel of CRP Nolag
cinflammation
Inflammation of can leadto thrombosis andinfaction
muscular arteries
Inflammation of arterioles and capillaries canlead to rupture and microhemorrhages and
manifest as purpura
Dysfunctional platelets
Causes of Purpura fragile capillaries Cvitcdeficiency
Vasculitis ofmicrovessels

General mechanisms involved in vasculitis lesions

Direct Infection Neisserial infections

Rickettsia infections Ceg
Rocky mountain spottedfever
spirochete 20 Stage
eg syphilis
Fungal infections mucormycosis in Diabetic ketoacidosis pt's
Viral infections Herpes Zooster varicella

Immunemediated Circulating Antigenantibody complexes HbsAg

Type111 HypersensitivityReaction HCV
Henoch Schonlein
purpura
ANCA mediatedvasculitis SLE
antinuclear
9cytoplasmic Antibodies Rheumatoid Arthritis
Serum sickness
Direct Antibody Toxicity seenin GoodPasteur's syndrome

cell mediated immunity

physical injury
Chemical
injury
others

76
 Join @drdocstg

VASCULITIS

Large cell vasculitis mediumsized vasculitis Small vesselvasculitis

GaintCell Temporal arteritis Kawasaki vasculitis Polyangitis

vasculitis polyarteritis Nodosa Wegener's disease
Takayasu's
PAN ChurgStraussyndrome
Buerger's disease
Thromboangitisobliterans

TAKAYASU'S VASCULITIS

vasculatic inflammation oflarge arteries aorta andits branches

Agegroup 440years
involves Asian females
usually
The starts from adventitia ofaorta and spreads to media
inflammation
progressive fibrosis of
vessels produces stenosis
Blood supply to head and upper limbs is reduced
vasavasorum are surrounded
by inflammatory cells

CLINICAL FEATURES
ummm ummm

systemic features feed features

wt loss anorexia fever

by fibrosis
elastic tissue isreplaced
Night sweats malaise H
pulse is notformed and popogated
I
Blood flow
mu
to
w
CNS
un
reduced
mum
No pulse pulseless disease
Numbness offingersdue to ischemia
Dizziness
Syncope Fibrotic aorta stretches
mm
deficits
Neurologic I
ocular abnormalities Aortic Regurgitation

Fibrosis of coronary ostium Duetofibrosis Intimal wrinkling

mm arterymm ummm
H
coronary ostial stenosis

rticosteroids

77
 Join @drdocstg

TEMPORAL ARTERITIS Gaint cell arteritis

Mlc systemic vasculitis in adults

occurs usually in 50 years
seen in population
of NORDIC
origin
Granulomatous inflammation in media of temporal Artery
presence ofgaint cells
o
Oo
Langham o 0 ooo ForeignBody type
Gaintcell o o faint cell

Involves different segments ofvessels so minimumof 2 3cmof artery isneeded

for Biopsy
Granuloma destroying Internal elastic lamina
301 cases don't show granuloma

4f
pain and along the course of temporal artery
tenderness
be nodular on palpation
Artery may
Involvement of ophthalmic Artery BLINDNESS so treated withhighdosesteroids

Lab findings show Raised ESR

40 jaw claudication due to involvement of maxillary artery

40 facial pain
If vessels
supplying nerves are involved Neuronal
injury
MononentitisMultiplex

faintcell arteritis canbe associated with polymyalgia Rheumatica Gotcases

pain in proximal muscles

periarticular inflammation
Difficulty in mobilisation

Rx
Highdose steroids

78
 Join @drdocstg

KAWASAKI's DISEASE

off
Conjuctivitis
8Th s
cardiac Complications Transmutedinflammation ofcoronaryA

µ KAWASAKI
if
BIKE 5
I
maylead to M1 aneurysmsG
Suddencardiacdeath
5
commonly seen in babies 44years
conjuctivitis
cardiac complications Inflammation of coronary artery
mucocutaneous
lymph node syndrome
palms and soles be edematous
G etythematous
epidemic in Japan may

Cause of disease is unknown but believed to be autoimmune disease

with antibodies directed against endothelial cells

Rx
Aspirin reduces cardiac complications

POLYARTERITIS NODOSA
Fibrinoid necrosis
inflammation of medium sized arteries 006.029098
Transmuted inflammation of visceral arteries
Doesn't effect pulmonary arterial tree
Fibrinoid necrosis in the wall of artery
301pt's are HbsAg positive
Not associated with ANCA

Theweakening of artery may cause thrombosis aneurysm or obstruction

Thrombosis can cause ischaemia to partof tissue and cause ulceration
may
also cause infarction or rupture of vessel leads to hemorrhage intissue

4f systemic Localm

Fever malaise Mesenteric Abdominal

artery pain
anorexiaGwtloss Renal artery Renal injury or HTN
Mononeutti's Multiplex
TCRPTESR

Rx
Immunosupression E corticosteroids and cyclophosphamide
79
 Join @drdocstg

BUERGER'S DISEASE

alkla Thrombo angitis obliterans

severe inflammation of medium sized peripheral arteries UlnarA Radial A
the veins and nerves
may spread upto thrombosis
Inflammation leads to and obliteration of arteries
with smoking
associated
i strongly
Usually occurs in 740years and more in males than females

vein
Inflammation Granuloma microabscess
Neutrophils
i

Ulna'T
A UlnarNerve
Thrombus

Hypensitivity Reaction to
Tobacco products
The classically involves nerve too
disease
episodic attacks segmental

Clf
pale cyanotic cold periphery
altered sensation pain on Rest
Advanced
Stage Reduced sensation
Hypoasthesia
Ulcers due to extreme ischaemia
Auto amputation of fingers

Rx
Stop smoking

WEGENER's GRANULOMATOSIS

4f Respiratory manifestations
Paranasal Sinusitis Pathology Nectolising Granulomas
saddle 4 otitis media in mucousmembrane

nainseth D mastoiditis

congestion
epiglottitis
Stridor
fff Laryngitis

lesion in
Pulmonary symptoms

vituantogjy
of 1 Bloodvessel

WAGON Glomerulonephritis

Pt may present c cough hemoptosis g

dyspnea
80
 Join @drdocstg

Lab finding shows C ANCA

focalsegmental Necrotising GN
Renal manifestations Glomerulonephritis y
cresentGN severe form

symptoms proteinuria hematuria

Rx
Steroids cyclophosphamide

MICROSCOPIC POLYANGITIS

Inflammation of small vessels

seen in

Henoch Schonlein
purpura

seen in younger children

usually a respiratory infection
after
deposition underskin glomerular basement membrane Sinovial membrane
IGA
and GITmucosa
Complement aginst deposited Antibodies cause destruction and symptoms
like palpable purpura glomerulonephritis arthritis and abdominal pain

Gyoglobulinaemia

formation
of antibodies in cold environment

Connective tissue disorder like SLE

CHURGE STRAUSS SYNDROME

ptmay already have 40 allergic Rhinitis asthmalanyother allergy

and presents with allergic Granulomatous

angitis

Lab findings show Eosinophilia and Biopsy shows eosinophils in Granuloma

Sof of cases are associated with P ANCApositive

81
 Join @drdocstg

uarO
EEETiasieadeinaugn.sn iaasi

Etiquette
x x x
Glomangiomas vascular ectasia
Hemangiomas Lymphangiomas BacillaryAngiomatosis
Glomustumors
Developmentally
endothelialcell endothelialcell Abnormallocalised Reactiveproliferation
abnormalcapillaries lined channels linedchannels dilatation ofcapillaries reactive
usuallybybirth to bacilli
to Li I
f
acini

ii ii sublingual
a
very painful Dilation
i i
Tumormarkets
lymphfluid
Contains massofcapillaries
9331,9334VWF in
Commonlyseen
HNpt's caused
containsBlood by
BartonellaHenselae
cells BartonellaQuintana

Hemangiomas

a Capillary hemangiomas STRAWBERRY Hemangiomas

endothelium lined loops

of capillaries

Xf
fullof blood
presentat birth growforsometime andregress ontheir own

b Cavernous
Hemangiomas
1 2cm sometimes
conttains
calcified
interconnecting
endotheliumlined capillaries
fullofBlood
mange.si 9ideausydesEcm nadneeeeIo datgeeesi
sseage
i
If present in CNS produce deficits dueto pressure a
may
also rupture

VON HIPPLE LINDAU SYNDROME

Multiple cavernous hemangiomas in CNS retina kidney pancreasetc

82
 Join @drdocstg

c Lobular Capillary Pyogenic granuloma

Hemangiomas
edgematous fluid
posttraumatic condition development ofmultiple loopsof capillaries
Rapid growing exophytic nodule with stalk attached toskin or
mucous membrane

Easily bleeds on minor trauma

t.tt
h.g.y
Infiltration

by cells
inflammatory
alsoseen in It pregnant women Regress after delivery

Lymph
angiomas

a
Capillary Lymph
angiomas

endothelial lined capillary like lesions

contains clear fluid
fluid filled blisters blebs off
b cavernousLymphangiomas

Seenunder baseof head axilla i

Massively dilated large cystic masses
atKla cystic Hygromas
are associated E Glomus tumors

GLOMUSTUMORS

Bacillary Angiomatosis

Bartonella Henselae
In immunocompetent causes Catscratch disease
Reservoir Domestic Cat
vector Cat flea

In immunocompromised causes Bacillary angiomatosis

Bartonella Quintana
In immunocompetent Trenchfever
Vector Human Body Lice

83
 Join @drdocstg

Vascular Ectasia

localised dilation
of preexisting vessels

Telengectasias small focal mucocutaneous lesions made of arterioles venules or

capillaries

a NEVUS FLAMMEUS b SPIDERTELENGECTASIAS c HERIDITARY HEMORRHAGIC

mk ARTERIAL SPIDERS 0 TELENGECTASIA
J OD
Birthmarks Osler WeberRenda
consistofmacularlesions mlc in females syndrome
e autosomal dominant
Dennis
i Clf presenton skin mucous
mm
Ryong
i membranes
I Bleeds easily
fade c
11
away age arteriole
presents as epistaxis
PORTWINE
spidal branchingof arteriole
hemoptysis Othematamesis
STAINSN and or hematuria
seenin Hyperestrinism
Grow cage
Yirrhosis
thickened pregnancies
ofliver
present in distribution of
TRIGEMINALN area ill
alsopresent in leptomeninges
duetoabnormaldevelopment
I MAYSHOW
CH Mental Retardation
Seizures
Radioopaqueopacities
Hemiplegia

STURGEWEBERSYNDROME

IntermediateGradeNeoplasia KAPOSI'S SARCOMA

Borderline vasculartumors
lowgrade malignanttumors HEMANGIO ENDOTHELIOMA

84
 Join @drdocstg

KAPOSI'S SARCOMA

Neoplyasticgrowthdestroyed

monocompetent

p.no

enesyNffaPlngasqYcmafionHy.yuasntieiPes
I
ion
ifeng.ee nIotgeans If Immunocompromised
1111111
Tumors upressorgenes
Neoplasm Persists

HHV 8 produces proteins that stimulate protooncogenes andinhibit 1053 function

Neoplastic transformation happens the if
is immunocompromised
pt
4f
Firstlesion patch like lesions
If immunocompromised transforms into papularstage then to Nodulatstage
KAPOSI'S SARCOMA TYPES

Sporadic

C
ss

gI gtyi4DIaapnossiHasntsgaate
t.si191
tepideamsscociated
endemic
variety
Seen inoldermales localisedand transplant recipients are
90 have lesions generalisedspread immunocompromised
onskin throughlymph
lot have visceral nodes involves mucousmembrane
involvement nodes andvisceral
lymph
organs
Rx
local Resection Rx Reduce immunosupression
local Radiation
Chemotherapy

85
 Join @drdocstg

MALIGNANT VASCULAR TUMORS

L J
ANGIOSARCOMA HEMANGIOPERICYTOMA

Highly malignant Aggressive originate from pericytes

seen in skin breast
seen in LIVER are associatedwith
ARSENIC TOXICITY A
EXPOSURE TO THOROTRAST CT
POLYVINYL CHLORIDE P

Tumormarkets
1
CD31 CD34 VWF

86