COURSE OUTLINE: PASSAGEWAY OF FOOD

1. Gastrointestinal System Mouth

a. Mouth/Oral Cavity ↓
b. Stomach Throat
c. Small Intestines
↓
d. Passage of food
e. Large Intestines Esophagus
2. Gastrointestinal Disorders ↓
a. GERD LES → Going down, one way only! [Tighten]
b. Hiatal Hernia ↓
c. Peptic Ulcer Disease Stomach
d. Dumping Syndrome Upper portion: Fundus
e. Diverticulosis & Diverticulitis
Lower portion: Antrum
f. Appendicitis
g. Liver Cirrhosis ↓
h. Cholecystitis Pyloric sphincter → Will close when there is food
i. Cholethiasis present
j. Acute Pancreatitis ↓
k. Chronic Pancreatitis Small Intestines [DJI]
REFERENCE ↓
Toprank – Keith Garino Large Intestine
↓
Anus
GASTROINTESTINAL SYSTEM
MOUTH/ORAL CAVITY LARGE INTESTINES
MECHANICAL DIGESTION ● Terminal ileum
● Chewing ● Defecation
● Inversely proportional with chemical digestion ● Absorption of large amount of water
● Appendicitis
STOMACH ● Transverse, Descending, sigmoid, rectum, anus
CHEMICAL DIGESTION
● Pain in the colon – Crampy
● Enzymes → Amylase
○ Given antispasmodics and
○ Breaks down the starch
anticholinergics
● Hydrochloric Acid – pH = 1.2-3.5
● What is the movement of the colon? Peristalsis
● Pepsin → Proteins
○ Increase Peristalsis = Decreased
● Intrinsic Factor = Absorption of Vitamin B12
absorption → Diarrhea
○ Gastrectomy → Pernicious Anemia
○ Decreased peristalsis = Increased
● Gastric Emptying [1-2 hrs after meal]
absorption of water → Constipation
○ Which is fastest? (In order of fastest) →
■ Exercise → Increased peristalsis
Carbohydrate, Protein and Fats
■ Rest → Decreased peristalsis
● When there is a severe pain in the abdomen?
SMALL INTESTINES
● Longest What will happen? – the bowel sound will be
absent or decreased!
DUODENUM ○ If this an irritation? – then increased bowel
● Hepatobiliary sounds!
1. Pancreas → Amylase, Lipase
2. Liver → Produces bile
■ Bile = Breakdown of fats
3. Gallbladder → Storage of bile

JEJUNUM
● Absorption of nutrients

ILEUM
● Absorption of bile salts, vitamin b12
● What will happen when the ileum is cut?
○ Steatorrhea
○ Dec Vit B12 → P. Anemia ● Assessment of the abdomen – IAPePa

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 TOPRANK INTENSIVE PHASE – GASTROINTESTINAL

GASTROINTESTINAL DISORDERS
GASTROESOPHAGEAL REFLUX DISEASE
● Weak LESS → Open causing backflow
● Reflux = regurgitation/backflow of gastric contents
(HCl)

QUESTIONS
1. Which of the ff is a priority intervention for
esophageal disease?
○ Lie down
○ High fat
SIGNS & SYMPTOMS ○ High protein
● Pyrosis /Heartburn → Common Complaint ○ Elevate HOB
● Dyspepsia [Indigestion]
● Nausea & Vomiting
● Dysphagia HIATAL HERNIA
● Injury – Odynophagia [Painful swallowing] ● Hernia = Abnormal Protrusion of fundus
● AKA Diaphragmatic Hernia
CAUSES ○ Hiatus tightens
● Coffee
● Cigarette Smoking
Chocolate
● Citrus Fruits
● Carbonated drinks
● Alcohol
● High Fat
● Peppermint
● Spicy

MANAGEMENT
“Food should go down!” CAUSES
● High carbohydrate ● Increased Intra-abdominal Pressure
● Decreased protein & fats ○ Pregnant
● High fiber diet! (Always remember!) ○ Obese
○ When you eat a lot of fiber, the feeling of ○ Heavy Lifting → When your upper body
fullness increases → Increase satiety! muscles cannot lift the weight, other
○ Prevent overeating! muscles try to contract which causes
● Small frequent feedings herniation
● Position: Elevate HOB & turned to left
○ Left because the esophagus in nasa taas TYPES

MEDICATIONS
● Avoid Anticholinergic → Muscle relaxant (LES
should not relax more)
○ Irritants: ASA, NSAIDS, Steroids
■ Taken with meals!
● H2 receptor blocker = Decreased HCL
● Proton Pump Inhibitor = Decreased HCL
● Antacids = Neutralizes Acid ● Hernia has same symptoms of GERD because
● Prokinetics = Increases Gastric Emptying when the fundus is protruded, HCL is pushed
back up presenting symptoms of GERD
SURGICAL
● Fundoplication [Nissen & Toupet] PEPTIC ULCER DISEASE
● The LES will be tighten again CAUSES
● Most common causative agent: H.Pylori
○ From raw meat → Will go to the lining of
the stomach
● Increased HCL and Increased Pepsin → Why is
the stomach not damaged despite being very
potent?

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 TOPRANK INTENSIVE PHASE – GASTROINTESTINAL

○ Because normal stomach has increased 4. OCTREOTIDE

mucus production for protection ● Mimics Stomastasin
● Has decreased mucus → Dec protection Example: HCL and Alkaline are neutral in the stomach.
● Burn Injury → Fluid shifting happens → causing When you vomit and lose HCL, the alkaline is dominant
edema → decreased blood volume → decrease causing Metabolic Alkalosis.
blood supply to the stomach → decreased
production of mucus → CURLING’S ULCER RISK FACTORS
○ Burn victims are given PPI because they ● Stress → Parasympathetic → Inc Acetylcholine →
may develop ulcer Inc HC
● Cigarette smoking
PATHOPHYSIOLOGY
● Alcohol
Food intake/smell
● Caffeine
↓
● Aspirin and NSAID
Vagus nerve (CN X) [Acetylcholine = Cholinergic]
○ All increase HCL
(Parasympathetic)
● zollinger-Eisom Syndrome → Pituitary tumor →
↓
Inc Gastrin → Inc HCL
Stimulates the G-Cell
● Irregular and hurried meals → decreased chewing
↓
→ Inc HCL
Produces Gastrin → Stimulate chief cell [release
● Type A personality → Workaholic → stress inc
Pepsinogen]
● Type O blood → Inc Pepsin
↓
● Genetics → High level of parietal cell → Inc HCL
Stimulates ECL (Enterochromaphil Light Cell)
↓
Produce Histamine 2
↓
Stimulate Parietal Cell
↓ ↓
Proton Pump Alkaline tide
↓ ↓
HCL Increase blood pH
(Alkaline)
↓ ↓
Stimulate Pepsinogen (Pepsin)
↓
GASTRIC ULCER DUODENAL ULCER
(Pepsin & HCL in) Small intestine
↓ ● Poor man’s or ● Executive ulcer
Pancreas release enzyme → Somatostatin [Stops on laboror’s ulcer (stress)
Gastrin] ● 20% incidence ● 80% incidence
↓ ● Common in (most common)
people 50yrs old ● Common in
and above people 25-50 yrs
○ Decrease old
MANAGEMENT d interest ○ Career
1. VAGOTOMY in food stage
● Malnourished ● Well nourished
● Decreased Acetylcholine, Gastrin, histamin 2, (Weight loss) ● Pain – 2-3 hrs
Proton Pump, & HCL ● Pain – ½ -1hr after meal (empty)
after meal (w/ ● Pain relieved by
food) food intake
○ #1 ● Pain is common at
symptom! night (empty
● Pain is triggered stomach)
by food intake ● Melena (Old
● Pain relieved by blood)
vomiting
● N&V&
hematemesis
(Vomit w/ blood)

QUESTION
*Question has both gastric and duodenal symptoms →
2. H2 RECEPTOR BLOCKER Should answer by tagging!
● Histamine 2 is shutdown which causes proton ● Weight loss → G
pump to decrease ● Pain common at night → D
● 25-50 yrs → D
3. PROTON PUMP INHIBITOR ● Poor man's ulcer → G
● PPI is removed which decreased HCL ● Stress related → D
● N&V→G
● Pain triggered by food intake → G
● Melena → D

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 TOPRANK INTENSIVE PHASE – GASTROINTESTINAL

MANAGEMENT ○ Total
● Monitor signs of bleeding → melena and ○ Subtotal/Antrectomy
hematemesis 3. ANASTOMOSIS
● Diet: ○ Reconnection
○ Milk → Avoid, especially HIGH amount ○ Billroth 1 [Gastroduodenostomy]→ First
■ Milk may be alkaline but what it part ng small intestine
will do is increase the pH of ○ Billroth 2 [Gastrojejunostomy] → Second
stomach (Stomach is naturally part ng small Intestine
acidic)
■ High Alkaline will make the
stomach come back to its natural
level which is acidic
■ 200mL max only
■ Meron ring milk na acidic →
Increase HCL
○ Feeding → small frequent feedings →
Less food, less HCL
○ Chew → Thoroughly
○ Food → As tolerated
● Avoid factors → Mod and Non-mod factors DUMPING SYNDROME
● Stress reduction → Rest and relaxation ● When stomach is cut, the gastric capacity is
decreased (lumiit ang stomach) → gastric
MEDICATIONS emptying is rapid → the food bolus is being
1. ANTACIDS DUMPED into the small intestine → the food is
○ 1-2 hours after meals diluted highly concentrated (Hyperosmolar) →
○ Neutralizes acids Small intestine has b.v. surrounding it for
○ Aluminum Hydroxide → SE: Constipation absorption, the fluid shifts to the highly
○ Magnesium Hydroxide → SE: Diarrhea concentrated cell(Blood is attracted to intestine –
○ Aluminum Magnesium Hydroxide Osmosis) → Blood volume decreases as it
○ Maalox transfers to s.m. → SHOCK-LIKE s/sx (30 mins
○ Calcium Carbonate after meals)
○ Sodium Bicarbonate [WOF Metabolic ● Concentrated food will have hyperglycemia →
Alkalosis] increase insulin → postprandial hypoglycemia (2
2. HISTAMINE 2 RECEPTOR BLOCKERS hrs after meal)!
[RANITIDINE] ● Hypo tachy
○ At bedtime because drowsy effects ● Dizziness
○ Decrease HCL
3. PROTON PUMP INHIBITORS [OMEPRAZOLE] MANAGEMENT
○ Onset before meals DIET [“Food should stay in the stomach]
○ Decrease HCL ● Protein [High]
○ zole - ● Fat [High]
4. CYTOPROTECTIVE DRUGS [SUCRALFATE] ● Carbohydrate [Low]
○ Before meals ● Meals [Small Frequent]
○ Protects/Coats the stomach ● Fluids [Avoid during meals]
5. PROSTAGLANDINS [MISOPROSTOL / CYTOTEC] ○ In between meals!!!
○ Decreases HCL ● Salt, sugar & Milk [Avoid]
○ Increases Mucus ○ Will increase the concentration
○ Inflammation
○ Causes Uterine Contraction POSITION
6. HORMONE [OCTREOTIDE] ● Lie down → So food will stay
○ Mimics Somatostatin → Decreases Gastrin → ● Turn to the left side!
Decreases HCL
DIVERTICULOSIS & DIVERTICULITIS
SURGERY DIVERTICULOSIS
1. VAGOTOMY ● Outpouching of intestinal mucosa
○ Decreases stimulus of vagal nerve → For ● Common site: at the sigmoid colon
HCL production ● Cause: Fiber Diet [Low]
2. GASTRECTOMY ○ Constipation
○ Increase amount of stool → Increased
pressure → Weakens the wall of the colon
→ Outpouching
● Asymptomatic

DIVERTICULITIS
● Inflammation of 1 or more diverticula
● Cause: Accumulation of fecal material
● With infection & inflammation

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 TOPRANK INTENSIVE PHASE – GASTROINTESTINAL

○ Increase amount of stool → Increased SIGNS & SYMPTOMS

pressure → Weakens the wall of the colon ● Pain
→ Outpouching → Stool will enter the ● Mcburney’s point
diverticula → Obstruction → Infection & ○ RLQ
Inflammation

● Rovsing’s sign
○ Palpate at L then pain is felt on R

SIGNS & SYMPTOMS

1. Inflammation
○ Abdominal pain [Cramping] at the Left Lower
Quadrant
2. Infection
○ Fever
3. Injury ● Dunphy’s sign → Pain triggered by coughing
○ Blood in stool – Fecal Occult ● Blumberg’s sign → Rebound tenderness
4. Obstruction [Increased Gas] ○ Pain upon release
○ Bloating & flatulence ● WBC → Increased – Infection
○ Chronic constipation [low fiber] with episodes ● Bowel sound [Decreased]
of diarrhea [irritation] ● Psoas Sign → Turn to left then flex the hip →
Pain
MANAGEMENT ○ Psoas muscles will touch the pancreas
1. Fiber Diet → Increase causing pain
2. Fluid Intake → Increase
3. Medications → Laxative

ACUTE PHASE [PAINFUL EPISODES]

● Target is to rest the bowel → Decrease peristalsis
● Fiber Intake → Decrease
● Oral intake → None! NPO
○ Will increase peristalsis
● Activity → Bed Rest
● Medication → Antispasmodic [Propantilin] ● Obturator Sign → 90º → Pain
Anticholinergic
● Monitor for perforation

*Remember → Any disorder that can cause

perforation & rupture → Can lead to Peritonitis [Rigid
hard board like abdomen]

APPENDICITIS
● Ascending colon [Cecum and under it is the
appendix]
● Fecalith → Stool entered the appendix
○ It can cause obstruction → Decreasing
blood flow → Causing injury to the MANAGEMENT
appendix → Infection and Inflammation ● Decrease peristalsis
● Complication = Rupture [Peritonitis] ● NPO
○ Anything that increases peristalsis ● Bed Rest
○ If sudden disappearance of pain = ● IV Fluids
Rupture → Nawala na yung inflammation ● Avoid anything that will increase peristalsis
→ Sumakit na buong abdomen → ○ No enema
Peritonitis ○ No laxatives
● Goal: Decrease Peristalsis ○ Always clarify with the doctor
● Caused by: Ficaleth ○ No heat application → Dilation

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 TOPRANK INTENSIVE PHASE – GASTROINTESTINAL

SURGERY ● Liver produces lipoprotein → Produces lipids &

APPENDECTOMY protein [albumin -- most abundant] → oncotic
● Surgery in the abdomen pressure [usually at the end of the arteries or
● Dehiscence → Bumuka yung sugat capillaries] → Papasok
● Evisceration → Lumabas ang mga colon ○ If nasira si liver → Promotes hydrostatic
● Position: Should never stretch the abdomen! pressure → Fluid shifting → Edema &
○ Semi-fowlers. If not in choices then dorsal Ascites
recumbent ● Blood supply to heart going to the liver [Portal
Circulation]
LIVER CIRRHOSIS ○ Heart → Blood supply to kidneys through
● Injury to liver → healing and scarring → leading to renal arteries and the GIT through
a nonfunctional liver mesenteric artery → Liver will filter the
blood → Blood will return to the heart
LIVER ○ If there is an obstruction in the liver, there
1. Kupffer cells → clean blood through phagocytosis will be alterations in blood flow →
→ is an immune response increase blood in liver → hepatomegaly
a. This will be injured and decreased → Blood will search for a collateral
immunity → Inc infection ciculation → backflow of blood → High
2. Excretion pressure → Portal Hypertension [Ascites,
● Glucocorticoid, mineralocorticoid, and Caput Medusa, Rectal
adrgen will all increase→ increase in Varices/Hemorrhoids, Esophageal
cortisol, glucose, aldosterone, Na, H2o Varices] → Decrease blood flow going
(Edema and ascites), and decrease in K back to the heart → Decrease blood going
a. Liver has something do do with secretion to kidney → Hepatorenal syndrome
of hormones → glucocorticoids → cortisol [Renal failure]
→ increases blood glucose level
b. Mineralocorticoids → aldosterone → LAENNEC’S CIRRHOSIS
affects sodium, water, and potassium → ● Most common
increases Na, H2o, ad K decreases ● Caused by alcoholism
c. Androgen → testosterone & estrogen
baba na kooo (vasodilator) POST NECROTIC
i. Increase testosterone in female ● Caused by hepatitis B & C (Hepatotoxins)
→ hirsutism ○ Oro fecal - A/E
ii. Increased estrogen → side
rangiora (Spider veins) BILIARY CIRRHOSIS
1. In male → gynecomastia ● Obstruction in gallbladder
● Ammonia ● Cholethiasis
○ Protein → Amino acid → ammonia →
move to the liver and convert this into CARDIAC CIRRHOSIS
urea → when it goes to the blood → blood ● Systemic → Right sided heart failure
urea nitrogen (BUN) → and will be
excreted by kidneys and out into the urine LABORATORY TESTS
○ Causes neurotoxic → hepatic 1. ALBUMIN [3.5-5g/dL]
encephalopathy → asterixis (flapping a. Decreased
hand tremors) 2. PARTIAL THROMBOPLASTIN OR PROTHROMBIN
■ Construction; apraxia TIME/INR [25-35 SEC/ 11-14 SEC/ 8-12 SEC]
■ Dec LOC a. Prolonged
■ Fetorhepaticus (bad breath amoy 3. SERUM BILIRUBIN [0.3-1.9mg/dL]
ammonia) a. Increase
4. ASPARTATE AMINOTRANSFERASE [AST/SGOT]
SIGNS & SYMPTOMS [10-40]
● Hemoglobin a. Increase
○ Heme → iron that can turn into bilirubin 5. ALANINE AMINOTRANSFERASE [ALT/SGPT
that goes to liver → mix into bile (for [7-56U/L]
emulsification of fats) → absorption of vit a. Increase
ADEK: K is for bleeding clotting→ bile will 6. BUN
go to GIT → Urobilin → kidney (reason a. Decrease
why urine is straw colored) → urine
○ GIT → stercobilin → stool MANAGEMENT
● Hyperbilirubinemia → Jaundice 1. CALORIE
○ Accompanied by pruritus ○ Increase
○ Enters kidneys → dark urine 2. PROTEIN
○ No bile → No emulsification → ○ Low
Steatorrhea → No absorption of Vit ADEK ○ Pag tinaasan → tataas ammonia
→ High risk for bleeding 3. FAT
○ No urobilin and stercobilin → Pale/Clay ○ Low fat because wala ng bile
colored stool

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 TOPRANK INTENSIVE PHASE – GASTROINTESTINAL

4. SODIUM CHOLECYSTITIS
○ Decreased ● Inflamed gallbladder
5. FLUID INTAKE
○ Decreased CALCULOUS
6. HEPATIC ENCEPHALOPATHY ● Gallstone
○ Asterixis – Extend hands [flapping
ACALCULOUS
motion/tremors]
● Direct trauma to the gallbladder
○ Constructional apraxia [inability to copy
shapes]
CHOLELITHIASIS
○ LOC – Decreased ● Caused by supersaturation → cholesterol [fat],
○ Fetor Hepaticus – Check the breath [Amoy bilirubin [hemolytic reactions → Will be stones →
patay] Obstruction → Injury → Inflammation → Pain →
7. ESOPHAGEAL VARICES Bile will be trapped → Indigestion of fat]
○ Prevention of rupture!
○ Avoid anything that can increase the pressure RISK FACTORS
inside the esophagus [no coughing] ● Fair skin
○ Ruptured → Bleed → Balloon Tamponade ● Fat diet / Obesity
[Sengstaken Blakemore tube] ● Female
■ Balloon lumen → Apply pressure at the ● Fertile / Multigravid
bleeding site ● Forty
■ Gastric Balloon → Anchor’s the
esophageal balloon SIGNS & SYMPTOMS
■ Gastric → For Drainage 1. INFLAMMATION
■ Should be closely monitored because a. Biliary Colic → From tube like structure
there is an increase incidence that the i. Severe Pain
gastric balloon deflates → Dislodges b. Murphy’s Sign → Hand at hepatic margin
→ Airway obstruction [dyspnea] → Inhale → Diaphragm will Contract →
● Always have scissors on hand Inflamed Gallbladder → Pain @ RUQ
to cut the balloon lumens
[yellow & red] = To
immediately deflate → Airway
clearance

c. Abdominal Pain
d. Rebound Tenderness → Pain upon
release
e. Radiating → At right shoulder
f. Usually after a heavy meal or high fat
meal
i. Fat → Signals GB → Contract
[Pain] → Release Bile
MEDICATION 2. INDIGESTION
1. SPIRONOLACTONE [POTASSIUM SPARING a. Fats
DIURETIC] b. Nausea & Vomiting
a. Hypokalemia c. Belching
b. D/t Edema & Ascites d. Flatulence
2. IV ALBUMIN 3. OBSTRUCTION
a. To increase oncotic pressure a. Skin → Jaundice
3. LACTULOSE b. Stool → pale or clay colored
a. Laxative = Increase Defecation → c. Urine → Dark
Ammonia will bind to stool [decreases d. Vitamin ADEK deficiency
ammonia levels] 4. INFECTION
4. NEOMYCIN a. Fever
a. Antibiotic → Decrease bacteria in the GIT b. Dehydration
→ Waste product of bacteria is protein → 5. DIET
Decrease bacteria → Decrease protein → a. Low fat diet
decrease Ammonia b. Small frequent feeding
c. Gas forming foods → AVOID

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 TOPRANK INTENSIVE PHASE – GASTROINTESTINAL

MEDICATIONS ● TPN
1. Ursodeoxycholic Acid [dissolves] ● NGT → Lavage (Suction out) to remove HCL
2. Chenodeoxycholic acid [dissolves]
3. Antispasmodics/Anticholinergics MEDICATIONS
1. H2 RECEPTOR BLOCKER
ACUTE PANCREATITIS a. Decreases HCL → Decreases P. Enzyme
INFLAMMATION 2. PROTON PUMP INHIBITOR
● Can usually be caused by a obstruction → a. Decreases HCL → Decreases P. Enzyme
pancreatic enzyme is trapped → pancreatic 3. MORPHINE
enzymes assist with digestion → If it cannot be a. Bawal na opioid → Demerol
released → Autodigestion→ Injury --< i. Contains a metabolite that
Inflammation and bleeding produces Seizure
● Pain → LUQ radiating at back (pancreas locate at b. Taken with Atropine {Anticholinergic]
back of stomach) i. No spasms
● Aggravated by
○ Diet → fatty CHRONIC PANCREATITIS
○ Beverage → alcohol INFLAMMATION
○ Position → Flat on bed (Because when ● Repeated injury → healing → when we heal,
flat the upper organ or the body ay calcium is increased in usage → and lead to
dadaagan sa ilaim na organs) fibrosis (scarring) → non functional
● Bowel sound → Decrease ○ Exocrine → Decreased P. Enzyme
● N&V (Malnourished)
○ Endocrine → Decreased Insulin (Can
BLEEDING cause DM)
● Dehydration ● Abdominal pain → LUQ
● Weight loss
● Cullen’s & Grey turner’s sign FIBROSIS
○ Cullen → Bluish discoloration at ● Mass → LUQ
periumbilical area ● Calcium → Decreased (Hypocalcemia)
○ Turner → Turn your back
LOSS OF FUNCTION
● Weight → Low (Malnourished)
● Bilirubin → High
● Stool → Fasts wont get digested (Steatorrhea)
● Glucose → High

MANAGEMENT
DIET
● Food → Bland (Nonstimulant), no more smoking,
spicy food
● Meals → SFF
● Fats → Low
● Protein → Low
LABORATORY FINDINGS
MEDICATION
1. WBC
1. Pancreatin → Use synthetic P. Enzymes. Found
a. Increase
effective when steatorrhea is gone
2. GLUCOSE
2. Pancrelipase → Use synthetic P. Enzymes. Found
a. Increase – insulin dysfunction
effective when steatorrhea is gone
3. BILIRUBIN
3. Insulin & OHA → Endocrine
a. increase
4. ALKALINE PHOSPHATASE
a. Increase
5. SERUM AND URINARY AMYLASE
a. Increase → will leak towards the blood
b. Best indicator of recovery
6. SERUM LIPASE
a. Increase
b. Best indicator for recovery

MANAGEMENT
ACUTE PHASE
● NPO → Food → HCL -- P. enzyme
○ No smell of food → lalabas HCL →
Stimulate pancreatic enzymes
○ Until when is pt NPO? → Normal serum
amylase and lipase