Morphology Morphology: Gross: White, Chalky Fat Necrosis

GIT
Morphology Morphology
Gross: Gross Features:
- Red black hemorrhage with foci of yellow, - Sites:
white, chalky fat necrosis
• Head of pancreas (60%)
- Fat necrosis is also seen in, mesentery,
omentum etc. • Body (15%)
- Peritoneal cavity: serous, turbid, brown tinged • Tail (5%)

fluid and fat. • Diffuse (20%)
- Resolved lesion: fibrosis, calcification. - Hard, stellate, grey white.
Microscopy:
- Pancreatic duct is narrowed.
- Microvascular leakage: Edema
- Obstructs distal common bile duct
- Necrosis of fat by lipolytic enzymes
- Highly invasive even in early stage.
- Presence of polymorphs, necrosis, hemorrhage.
- Blood vessel destruction leading to interstitial - Elicits intense non-neoplastic host reaction
Hemorrhage. called as desmoplastic reaction.
- Released fatty acids with Ca++ → Bluish - May invade adrenal, spleen, vertebra, colon,
microscopic appearance of fat cells. stomach, peritoneum.
Complications Microscopy:
♦ Systemic organ failure: Shock, ARS, Acute renal - No difference based on sites.
failure. - Poorly formed glands in dense fibrotic stroma
♦ Pancreatic abscess, pseudocyst
Variants:
♦ Duodenal obstruction V
- Adenocarcinoma
♦ Disseminated intravascular coagulation.
- Acinar cell carcinoma
Note: Hypocalcemia may result from precipitation of
- Adenosquamos carcinoma
calcium soaps in necrotic fat.
- Colloid carcinoma
CARCINOMA OF PANCREAS - Hepatoid carcinoma
♦ Infiltrating ductal adenocarcinoma of the pancreas - Medullary carcinoma
more commonly known as "Pancreatic cancer"
- Signet ring cell carcinoma
♦ Is fourth leading cause of cancer death in US.
- Undifferentiated carcinoma
♦ One of the highest mortality rates of any cancer.
♦ Common in male
FAST TRACK BASIC SCIENCE MBBS -135-

Pathology
SPECIAL POINTS FOR MCQs

1. The presence of an esophageal web in association with glossitis and iron deficiency (i.e. Plummer
Vinson or Paterson Kelly syndrome) and congenital hyperkeratosis and pitting of the palms and
soles (i.e. tylosis Palmaris et plantaris) have each been linked with squamous cell esophageal
cancer.
2. Dietary deficiency of molybdenum, Zinc, and vita A is associated with esophageal cancer.
3. H. pylori colonization induces chronic superficial gastritis which includes both mononuclear and
polymorphonuclear cell infiltration of the mucosa.
- Progression to atrophy when H. pylori is present
4. Two major diseases associated H. pylori virulence factors are a vacuolating cytotoxin, VacA, and a
group of genes termed the “cag pathogenicity island” (cag pal)
5. H. pylori colonization diminishes the number of somatostatin producing cells, somatostatin -
mediated inhibition of gastrin release leads to hypergastrinemia.
6. Peutz - Jeghers syndrome is characterized by hemartomatous polyps; pigmentation around lips,
mouth.
7. Typhoid ulcer is longitudinal but Tuberculous are transverse
8. Typhoid ulcer is: ulceration of peyer's patches, longitudinal ulcer, may perforate, stricture is rare.
9. Pipe stem colon in ulcerative colitis is Barium enema.
V
10. String sign in Barium X - ray in chrons disease.
11. Colorectal carcinoma is associated with low fiber and high fat intake.
12. Ulcerative colitis, pigmentary cirrhosis, polyposis coli, crohns disease all are precancerous.
13. Destruction of fat in acute pancreatitis is due to lipase and trypsin.
14. "Adenocarcinoma" is commonest variety of carcinoma stomach.
15. Greater risk of carcinoma stomach is associated with "Intestinal metaplasia"
16. Transmural involvement of granuloma is seen in crohn's disease.
17. Malignant potential of colorectal polyps: Tubular adenoma = 5%, villous adenoma = 30%
tubulovillous adenoma = intermediate.
18. Erythrophagia and mononuclear cell infiltration ulcers are seen in typhoid ulcers.
19. Salmonella primarily affects the ileum and colon generating blunted villi, vascular congestion and
mononuclear inflammation on microscopic examination, macrophages containing bacteria RBC
(erythrophagocytosis) are visible.
20. Linitis plastica is seen in: Syphilis, Carcinoma stomach, sarcoidosis
21. Intestinal epithelium is rich in T - cells
22. Small intestinal stricture is not seen in typhoid.
-136- FAST TRACK BASIC SCIENCE MBBS

GIT
23. Chronic gastritis is caused by: H. pylori, pernicious anemia, and alcohol but not by overuse of
salicylates.
24. Barret's oesophagus is not associated with increased risk of squamous cell carcinoma of
esophagus.
25. Peptic ulcer common in Blood group 'O' carcinoma in Blood group 'A' @ P - O C-A
26. Commonest site of amoebiasis in gut: Caecum and ascending colon
27. Adenomatous polyp of large bowel are most often situated in: sigmoid colon
28. Macrophage, granuloma, erythrophagocytosis are found in Regional ileitis.
29. Yellowish exudates at multiple sites seen in colonoscopy indicates: Chrons disease.
30. Single most important prognostic factors of colorectal carcinoma: “Extent of tumor"
31. Gluten sensitive enteropathy is most strongly associated with HLA - DQZ.
32. Endoscopic biopsy from a case of H. Pylori relates duodenal ulcer is most likely to reveal: Antral
predominant gastritis.
33. When carcinoma of stomach develops secondary to pernicious anemia, it is usually situated to in
fundus.
34. Pneumatosis intestinalis is diagnostic of necrotizing enterocolitis.
- CD 1117 is specific marker for GI stromal tumors.
35. Sister mary joseph nodule usually seen in gastric carcinoma [Metastasis to periumbilical region]
36. Two hit theory in colorectal carcinogenesis includes: First hit by mutations of cancer suppressor V
genes and second by inactivation of normal alleles.
37. Risk of carcinoma is more in sessile villous adenoma than peduncular villous adenoma.
38. Peak incidence of colorectal carcinoma is seen in "60 - 79 yrs"
39. Elevation of carcinoembryonic antigen (CEA) level is particularly significant in: Metastatic
colorectal carcinoma.
40. Most common malignant tumor of small intestine is carcinoid tumor.
41. Among, gastric, Duodenal, tubercular and typhoid ulcer, malignant transformation is usually seen
in gastric ulcer.
42. Commonest site of diverticulosis is: sigmoid colon
43. Malignant potential of familial polyposis coli is very high. Colorectal cancer develops virtually in
100% of cases by age 50 yrs if not Rx with colectomy.
44. Carcinoma pancreas usually originates in duct epithelium.
45. Hallmark of inflammatory Bowel disease is chronic mucosal damage.
46. IBD causes: sclerosing cholangitis
47. CEA in colonic carcinoma, following surgery, if its level decreases, then it indicates clearance.

Pathology
48. Hour glass deformity is seen in peptic ulcer.

49. Duodenal ulcers are found most commonly at: First part, anterior surface.
50. Nature of whipple's disease is bacterial infection.
51. Most common gross growth pattern of gastric colloid carcinoma is ulcerative and its common
location is fundus of stomach.
51. Stress ulcers →most common in individuals with shock, sepsis or severe trauma.
Ulcers occurring in proximal duodenum and associated with severe burns of trauma are called
"Curling ulcers" (MCQ 2013)
52. Gastric, duodenal and esophageal ulcers arising in persons with intracranial disease are termed as
"Cushing ulcers" carry high incidence of perforation.

GIT
pharmacology
SYLLABUS
Therapy of Peptic Ulcer: (p. 141)
Introduction, pathogenesis, list of drugs- classification, mechanism of action, uses, adverse effects, and drug
interactions, nondrug measures.
Therapy of nausea and Vomiting (p. 144)
Classification, mechanism of action, uses, adverse effects and drug interactions
Therapy of Diarrhoea: (p. 147)
Oral rehydration solution –constituents, indications.
Non-specific antidiarrhoeals and antispasmodics- list.
Non-drugs treatment
Therapy of Constipation: (p. 149)
Commonly used drugs in constipation, clinical importance, adverse actions, non-drugs treatment
Therapy of Worm Infestation: (p. 149)
Antihelminthics list of drugs; its mechanism of action, uses, adverse effects, drug interactions, and
contraindications
Therapy of Amoebiasis: (p. 151)
V
Commonly used drugs- brief discussion
Therapy of Giardiasis: (p. 151)
Commonly used drugs-brief discussion
Hepatotoxicity of Drugs: (p. 152)
Brief discussion

Pharmacology

GIT
PHARMACOLOGY
THERAPY OF PEPTIC ULCER 3. Ulcer protectives:

Past Questions: - Sucralfate, colloidal bismuth subcitrate.
1. Short notes: 4. Anti H. Pylori drugs:
a. Proton Pump inhibitor [04 Dec] - Amoxicillin, clarithromycin, metronidazole,
b. Omeprazole [03 Dec, 04Dec] tinidazole, tetracycline.
c. H. pylori treatment regimen H2 Antihistaminics [10 Jan]
[09June, 07June, 04Dec] (Cimetidine, Ranitidine, famotidine, Roxatidine)
d. Treatment of H. pylori infection [07June] Action:
e. Omeprazole in peptic ulcer [07July] - H2 blockade and reduction of gastric secretion.
f. Sucralfate in peptic ulcer
MOA:
[11July,08 Jan, 08July]
- Acts by competitively blocking the binding of
g. Proton pump inhibitors in gastro-esophageal histamine to H2 receptors, these agents
reflux disease (GERD) [10 July] reduces intracellular concentrations of CAMP
h. H2 –receptor Antagonist [10Jan] and thereby secretion of gastric acid is
i. Triple regimen for H. pylori [3][13] decreased which is the aggressive factor for
♦ Introduction, pathogenesis: Refer pathology peptic ulcer.
Approach to treatment of PUD Acts by competitively blocking the binding of

Histamine to H2 receptors
♦ Acid suppression V
↓
♦ Eradication of H-pylori No activation of G - protein
♦ Neutralization of acid and peptic activity by ↓
antacid. No Conversion of ATP to CAMP
♦ Cytoprotective ↓
List of drugs: Classification Decreased acid secretion
1. Reduction of gastric acid secretion. Adverse Effects:
a. H2 antihistaminics: Cimetidine, Ranitidine, - Headache, dizziness, bowel upset, dry mouth,
famotidine, Roxatidine. rashes.
- CNS effects: Confusion state, restlessness,
b. Proton pumps inhibitors: Omeprazole,
convulsions and coma.
Lansoprazole, pantoprazole, Rabeprazole,
- Bolus injection can release histamine → can
esomeprazole.
cause bradycardia, arrhythmias, cardiac
c. Anticholinergics: Pirenzepine, propantheline, arrest.
oxyphenonium - Cimetidine causes: Gynaecomastia
d. Prostaglandin analogue: Misoprostol. - Loss of libido
2. Neutralization of gastric acid (Antacids) - Impotence (temporary decrease in sperm count)
a. Systemic: Sodium bicarbonate, sodium citrate - Transient elevation of plasma amino
b. Non-systemic: Magnesium hydroxide, transferases (but rarely hepatotoxic)
magnesium trisilicate, Aluminum hydroxide gel, Note: IV Ranitidines given slow infusion because of
magnesium hydroxide, calcium carbonate. above mentioned adverse effects with bolus dose.

Pharmacology
Uses: Adverse effects On long term

- Duodenal ulcer - Nausea - Hypergastrinemia
- Gastric ulcer.
- Loose stools - Achlorhydria
- Stress ulcer and gastritis.
- Zollinger-Ellison syndrome. - Headache - Carcinoid tumor
- Gastroesophageal reflux disease - Abdominal pain @ ACH
- Prophylaxis of aspiration pneumonia - Muscleand joint pain
- Preanesthetic medication. - Dizziness
Interactions:
- Hepatic dysfunction
Cimetidine inhibits cytochrome P450 isoenzymes and
@ H MANDAL
reduces hepatic blood flow.
↓ Uses:
Many drugs accumulate to toxic levels 1. Peptic ulcer
Example: 2. NSAID induced gastric /duodenal ulcer
- Theophylline, phenytoin, carbamazepine, 3. Stress ulcer
phenobarbitone, sulfonylurea, metronidazole,
4. Gastroesophageal reflux disease (GERD)
warfarin, lidocaine etc.
- Antacids reduce absorption of all H2 blockers. 5. Zollinger Ellison syndrome
6. Treatment of PUD resistant to H2 blocker.
Note: On concurrent use of antacids and H2 blocker a
gap of 2hr should be allowed. Interactions:
Proton pump inhibitors [04, 10] 1. Omeprazole inhibits oxidation of certain drugs;
V Diazepam, phenytoin, and warfarin levels may be
Note: Omeprazole is a prototype drug of this group. increased.
MOA: 2. Clarithromycin inhibits omeprazole metabolism
Drug taken by oral route and increases its plasma concentration.
↓
Note:
Prodrug released in alkaline medium of duodenum
Esomeprazole is the s - enantiomer of omeprazole:
↓
Absorbed in duodenum and transported to parietal - Have higher oral bioavailability
cell canaliculus via blood - Produce better control of GERD
↓ - Have longer T1/2
Converted into active from (suphonamide and Lansoprazole:
sulphenic acid) - More potent than omeprazole
Reacts with - SH group of proton pump
- High oral bioavailability, long T1/2 than omeprazole
↓
Pantoprazole:
Forming a stable covalent compound
- Similar in potency and clinical efficacy to
↓
Irreversibly inactivate the proton pump (H+/K+ omeprazole.
ATPase) - High oral bioavailability.
↓ - Only PPI available as I.V. administration
Decreased HCL secretion
GIT
Ulcer protective Mechanism of action:

(Sucralfate, colloidal bismuth subcitrate) - Increases secretion of mucus and bicarbonate
Sucralfate: through stimulation of mucosal PGE2
production.
- Complex polyaluminum hydroxide salt of
sucrose sulphate. - CBS and mucus forms glycoprotein-Bismuth
complex which coats the ulcer and acts as
Mechanism of action:
diffusion barrier to HCL.
Basic aluminum salt of sulphated sucrose
- Detaches H. Pylori form surface of mucosa and
↓ directly kills the organisms in causation of ulcer
Polymerizes at PH < 4 by cross linking of molecules and relapses.
↓ Adverse effects:
Formation of sticky gel - Diarrhea, Headache, dizziness.
↓ - Osteodystrophy and encephalopathy due to
Precipitation of surface proteins at ulcer base causing Bismuth toxicity
their deposition. - Black stool, black discoloration of tongue, oral
↓ mucosa, metallic taste.
Creates physical barrier preventing acid, pepsin and Uses:
bile coming in contact with ulcer base - Gastritis and non ulcer dyspepsia associated
↓ with H.Pylori
Addition of dietary protein forms another layer Antacids
↓ ♦ Basic substance; neutralize gastric acid and raise
Ulcer protection pH of gastric contents.
- Also stimulates PG release and mucus/HCO3– ♦ Peptic activity reduces if pH rises above 4 V
output. (optimum peptic activity at pH 2-4)
Uses Note: They don't decrease acid production rather
1. Peptic ulcer evoke reflex gastrin release → more acid is secreted
2. Bile reflux called "Acid rebound"
3. Gastritis MOA
4. Prophylaxis of stress ulcer - Neutralization of HCL
Adverse Effects - Inhibits pepsin at pH > 4
1. Constipation in 2% patients - No effects on underlying cause of ulceration.
2. Hypophosphatemia
Antacids Properties
3. Dry mouth
Non- - Not absorbed systemically
4. Nausea
systemic - Insoluble
Note: It requires acidic PH, so not administered with - No acid base abnormality
antacids - Diarrhea, constipation is common A/E
Colloidal Bismuth subcitrate/CBS Systemic - Absorbed systemically
- Colloidal water is soluble compound but - Soluble
precipitates at PH less than 5. - Produce acid base abnormality
- Not an antacid, but heals the ulcers. - Quick onset of Action.

Pharmacology
Antacid combinations (Aluminium and Triple therapy: USFDA approved regimen. [13]
magnesium hydroxide) 1. Omeprazole (20 mg) or Lansoprazole (30 mg) × BD
- Combination of two or more antacids is 2. Amoxycillin 1000mg or metronidazole 400mg × BD
frequently used. 3. Clarithromycin 500mg BD
- No single antacid is satisfactory so, - The drugs in triple therapy is used twice
daily for 14 days/7 days.
combination is preferred.
Advantages of combination: Note: 2 week regimen is preferable because high
relapse rate after 1 week regimen indicates
a. Fast (Mag. hydroxide) and slow (Alum. incomplete eradication leading to recrudescence.
hydroxide acting components yield prompt as
Quadruple therapy:
well as sustained effect.
1. Bismuth subsalicylate 625 mg QID.
b. Magnesium Salts are laxative, while
2. Metronidazole 400 mg 3 times a day/
aluminium, salts are constipating: Combination Tinidazole 500 mg BD.
may annual each other's action and bowel
3. Tetracycline 500 mg four times a day.
movement may be least affected.
4. Omeprazole (20 mg) or lansoprazole (30 mg) × BD
c. Gastric emptying is least affected, because - Quadruple therapy gives 95% H. pylori
aluminum salts tend to delay it, magnesium eradication in 14 days regimen.
salts tend to hasten it. Non drug measures:
d. Dose of individual components is reduced; - Avoid Hurry, worry, spicy and chilly foods.
systemic toxicity (dependent on fractional - Maintain proper routine of food intake.
absorption) is minimized. - Avoid stress.
Note:
THERAPY OF NAUSEA & VOMITING
- Magnesium salts ⇒ Diarrhea
V Past Questions:
- Aluminum salts ⇒ Constipation @ M -D. A-C
1. Short notes on:
Treatment for eradication of H. pylori a. Hyoscine in motion sickness (3) [10 July]
[04, 07, 09] b. Ondansetron in therapy (3) [8 Jan]
- H. pylori are now accepted as an important c. Metoclopramide (3)[10 July]
contributor to the causation of chronic d. Ondansteron as antiemetic (3)[10 Jan]
gastritis, dyspepsia, peptic ulcer, gastric Antiemetics
lymphoma and gastric carcinoma
Classification:
- Up to 90% patients of duodenal and gastric 1. Anticholinergics:
ulcer have tested positive for H. Pylori. - Hyoscine, Dicyclomine
Drugs used in management are: 2. H1 antihistaminics:
- Clarithromycin - Promethazine, Diphenhydramine, Dimenhydrinate,
- Amoxicillin Doxylamine, cyclizine, meclizine, cinnarizine.
3. Neuroleptics: Chlorpromazine, Prochlorperazine,
- Metronidazole
Haloperidol
- PPI 4. Prokinetics: Metoclopromide, Domperidone,
- Bismuth compound Cisapride, Mosapride, Tegaserod
- Tetracycline 5. 5HT3 antagonists: Ondansetron, Granisetron
- H2 antagonist 6. Adjuvant Antiemetics: Dexamethasone,
Benzodiazepines, Cannabinoids

GIT
Mechanism of vomiting
NTS-Nucleus tractus solitarius; VC- Vomiting centre; CTZ-Chemoreceptor trigger zone; 5-HT3 -5–HT3 receptor; H1 - Histamine H1 receptor;
D2 - Dopamine 2 receptor; M–Muscarinic receptor; NK1–Neurokinin1 receptor; CB1 - Cannabinoid 1 receptor
Anticholinergics MOA:
♦ Hyoscine, Dicyclomine - Antiemetic effects are due to:
Hyoscine: • Anticholinergic
- Most effective for motion sickness.
• Antihistaminic
MOA:
- Blocks conductions of nerve impulses across a • Sedative properties.
cholinergic link in the pathway leading to Note: Anticholinergics, Antihistaminics, are first
vestibular apparatus to vomiting centre. choice drugs for motion sickness.
- S/E is sedation and other Anticholinergic S/Es
H1 Antihistaminics - All motion sickness drugs act better when
- Promethazine, Diphenhydramine, dimenhydrinate taken 0.5 - 1 hr before commencing journey.
etc. • Once sickness is started, it is difficult to
- Useful in motion sickness, morning sickness, control
post operative vomiting.
Pharmacology
Neuroleptics 2. 5HT4 agonism:

MOA: - 5HT4 receptor activation on primary afferent
neuron of ENS via excitatory inter neurons
- Act by blocking D2 receptors in CTZ
↓
- Have addition antimuscarinic as well as H1
Enhanced Ach release from myenteric motor neuron
antihistaminic property.
↓
- Less effective in motion sickness because the
Gastric hurrying and LES tonic effects
vestibular pathway doesn't involve
3. 5HT3 antagonism:
dopaminergic link
At high concentrations
Uses:
↓
1. Drug induced and postanaesthetic nausea and
Metoclopramide block 5HT3 receptors in inhibitory
vomiting. myenteric interneurons
2. Disease induced (gastroenteritis, uraemia, liver ↓
disease, migraine) vomiting. Gastric hurrying
3. Malignancy associated and cancer Note: D2 antagonism action is secondary to that
chemotherapy induced vomiting. exerted through 5HT4 receptors.
4. Radiation sickness vomiting (less effective) Adverse effects:
5. Morning sickness: Should not be used except - Generally well tolerated.
in hyperemesis gravidarum. - Sedation, dizziness, loose stools, muscle
Adverse Effects: dystrophies.
1. Sedation - Long term use causes: Parkinsonism,
V galactorrhoea and gynaecomastia
2. Muscle dystonia
Uses:
Prokinetic drugs 1. Antiemetic
♦ Metoclopramide, Domperidone 2. Gastrokinetic
Metoclopramide: 3. Dyspepsia
MOA: 4. GERD
- Acts through both dopaminergic and Note:

serotonergic receptors. - Domperidone has less extra pyramidal side effects
1. D2 antagonism: - Has less antiemetic efficacy than metoclopramide
- Based only on D2 - receptor blockade in upper GIT
- Dopamine (acting through D2 receptors) is an
- Used also to treat L-dopa induced vomiting in
inhibitory transmitter in the gastrointestinal
Parkinsonism patients.
system.
- Normally acts to delay gastric emptying. 5HT3 Antagonists
- Also causes gastric dilatation and esophageal ♦ Ondansetron, Granisetron
sphincter relaxation. Ondansetron:
- Metoclopramide blocks D2 receptors and has MOA:
opposite effect. - Cytotoxic drugs/ radiation causes cellular
damage → release of mediators, including 5HT

GIT
from intestinal mucosa → Activation of vagus THERAPY OF DIARRHEA

afferents in the gut → emetogenic impulses to
Oral rehydration solution [06]
NTS and CTZ.
- Ondansetron blocks emetogenic impulses both at Past Questions:
their peripheral origin and their central relay.
1. Short notes on oral rehydration solution in
Uses: diarrhoea. (3) [6 June]
1. Cancer chemotherapy/radiotherapy induced
vomiting Constituents
2. Post operative nausea and vomiting. New formula WHO - ORS
Adverse Effects: Content Concentrations
- Headache Nacl 2.6 g Na+ - 75 mM
- Mild constipation or diarrhea
Kcl 1.5 g k+ - 20 mM
- Abdominal discomfort
–
- Rashes and allergic responses. Trisodium citrate 2.9 g Cl - 65 mM
Comparison of Metoclopramide and Glucose 13.5 g Citrate - 10 mM
Domperidone Water 1L Glucose 75 mM
Metoclopramide Domperidone Total osmolarity: 245mosm/L
MOA: MOA: Indication:
1. 5HT4 agonism Block D2 receptor in upper 1. Diarrhea
2. D2 antagonism GIT 2. Non diarrheal uses:
3. 5HT3 antagonism ↓ a. Postsurgical, postburn, and posttrauma
↑ed release of Ach maintenance of hydration
↓ b. Heat stroke V
↑ed peristalsis, ↑ed tone c. During change over from parenteral to enteral
of LES and stomach alimentation
↓ Rational of ORS composition/Principle for
↑ gastric emptying composition
↓ - ORS is not designed to stop diarrhea but to
↓vomiting restore and maintain hydration, electrolyte and
Efficiency: Efficiency: pH balance until diarrhea ceases, almost
- More efficacious - Less efficacy than spontaneously
metoclopramide - Is best and not the second choice approach to
IV hydration.
Adverse Effects: Adverse Effects:
1. It should be isotonic or somewhat hypotonic, i.e.
- Has extrapyramidal S/E's - Less extrapyramidal
S/E's total osmolarity should be 200-310 m.osm/l (diarrhea
- Crosses BBB
fluids) are approximately isotonic with plasma.
- Other Adverse Effects: - Don't cross BBB
2. The molar ratio of glucose should be equal to or
are similar
somewhat higher than Na+ (excess glucose will be
Uses: Uses: utilized in absorbing Na+ present in intestinal
- Can't be used in L - - Used in L-dopa induced secretions in addition to that present in ORS itself).
dopa, bromocriptine vomiting in parkinsonism 3. Enough K+ and bicarbonate/citrate should be
induced vomiting in patients. provided to make up the losses in stool.
parkinsonism patient

Pharmacology
Non specific Anti diarrhoeal

Class Drug Use
Ispaghula Irritable bowel syndrome (IBS)
Absorbants Psylium Ileostomy/colostomy diarrhoea
Methyl cellulose
Antisecretory Sulfasalazine Ulcerative colitis, other inflammatory bowel diseases (IBD)
Bismuth subsalicylate Traveller's diarrhoea
Atropine Nervous, drug induced diarrhoea
Octreotide Carcinoid, VIP secreting tumour, diarrhoea in AIDS
Rececadotril Acute secretory diarrhoea
Antimotility Codeine Noninfective or mild travellers' diarrhoea
(Opioids) Diphenoxylate atropine Idiopathic diarrhoea in AIDS
(also antisecretory) Loperamide After anal surgery, colostomy
Note: Anti motility drugs are contraindicated in acute Note: Loperamide is contraindicated in infective
infective diarrheas. But why? diarrhoea because it increases the risk of bacterial
- Because they delay clearance of pathogen from proliferation due to retention of fecal matter
the intestine. containing bacteria.
- If invasive organisms (Shigella, EPEC, EH etc) are Sulfasalazine
present, anti motility drugs can be disastrous.
- It is a compound of 5-aminosalicylic acid (5-ASA)
V Loperamide: with sulfapyridine linked through an azo bond.
- Opiate analogue - Specific therapeutic effect in inflammatory
bowel disease (IBDs) like ulcerative colitis and
- Major peripheral µ opioid and additional weak
crohn's disease.
anticholinergic property.
- Additional use: Disease modifying drug in
- More potent than codeine. rheumatoid arthritis.
- CNS effects are rare. MOA:
MOA: - The azo bond is split by colonic bacteria to
1. Opiate analogue with anticholinergic property release 5-ASA and sulfapyridine. The former
2. Also inhibits secretion exerts a local antiinflammatory effect.
• By directly interacting with calmodulin Adverse effects:
- Rashes, fever, joint pain, haemolysis and blood
Adverse effects:
dyscrasias.
- Abdominal cramps
- Rashes
Non - Pharmacological Management
♦ In case ORS not available:
In young children's:
- Alternative method:
- Paralytic ileus • Preparation at home
- Toxic megacolon a. Requires salt, sugar and clean water
- Abdominal distension b. Place 6 level tea spoons of sugar and half
Contra Indications: a level teaspoon of salt into 1 liter of
1. Acute infective diarrhea clean water.
2. Ulcerative colitis and diverticulosis ⇒ because c. Allow salt and sugar to dissolve
they ↑es intraluminal pressure. ♦ Maintain Nutrition, safe water, personal hygiene

GIT
THERAPY OF CONSTIPATION: MOA: Lactulose in hepatic encephalopathy

- Causes reduction of blood NH3 concentration
Past Questions:
by 25 - 50% in patients with hepatic
1. Short notes on Lactulose in therapy (3)[07 July] encephalopathy.
Commonly used drugs in constipation: - The break down products of lactulose is acidic
1. Bulk forming: ↓
- Dietary fiber: Bran, Psyllium (plantago), Reduces pH of stools
Isphaghula, Methylcellulose ↓
2. Stool softener: Ammonia produced by bacteria in colon
- Docusates, liquid paraffin ↓
3. Stimulant purgatives converted to ionized NH4+ salt and is not absorbed.
a. Diphenyl methanes: Adverse Effects:
• Phenolpthalein, Bisacodyl, Sodium picosul fate - Flatulence, Nausea
b. Anthraquinones Nonpharmacological management of
• Senna, Cascara sagrada constipation
c. 5HT4 agonist ♦ Increase fibers in diet, Avoid refined and fast
• Prucalopride foods.
d. Fixed Oil: ♦ Increase fluid intake
• Caster oil ♦ Exercise
4. Osmotic purgatives: THERAPY OF WORM INFESTATION

- Magnesium salt: Sulfate, hydroxide V
Past Questions:
- Sodium salts: Sulfate, phosphate, sodium pot.
1. Write short notes on:
tartrate, lactulose
a. Drugs used in Ascariasis (3)[04 Dec]
Note:
b. Albendazole (3) [10 Jan, 09Jan, 07June]
- Laxative: Milder action, elimination of soft but
c. Albendazole in therapy (3) [07 July]
formed stools
- Purgative: stronger action resulting in more fluid Worm First choice Alternatives
evacuation 1. Ascaris Mebendazole, Piperazine,
Lumbricoides Albendazole, Levamisole,
Lactulose [07] Ivermectin
Pyrantel
MOA: As purgative
2. Wuchereria DEC Albendazole
- Osmotic purgative
bancrofti
- Semisynthetic disaccharide of fructose and
lactose. 3. Taenia solium Praziquantel Niclosamide
- Neither digested nor absorbed in small 4. Ancylostoma Pyrantel, Levamisole
intestine, retains water. duodenale Mebendazole,
- Further, it is broken down in colon by bacteria Albendazole
to osmotically more active products.

Pharmacology
Drugs MOA Adverse Effects

Mebendazole 1. Blocking glucose uptake, depletion of glycogen stores in - Diarrhea
parasite. - Nausea
2. Intracellular microtubules are gradually lost - Abdominal pain
3. Binds to β - tubulin of worms and inhibits its polymerization - Allergic reactions
4. Hatching of Nematode eggs and their larvae are also - Loss of hair
inhibited, Ascaris ova are killed - Granulocytopenia
Albendazole - Similar as mebendazole, has advantage of single dose - Similar as mebendazole
administration
- More effective than mebendazole
Pyrantel - Activation of nicotinic cholinergic receptors in worms - Remarkably free of S/E's
resulting in persistent depolarization → Slowly developing - Occasional GI symptoms
contracture and spastic paralysis → Worms expelled - Headache
- Dizziness.
Piperazine Hyperpolarization of ascaris muscle by GABA Agonistic action - Nausea, vomiting, abdominal
opening Cl– channels→relaxation and ↓es responsiveness to discomfort and urticaria
contractile action of Ach.
↓
Flaccid paralysis
V
↓
Worms expelled alive
Levamisole Ganglia in worms are stimulated causing tonic paralysis and - Nausea,
expulsion of live worms. - Abdominal pain
- Giddiness
- Fatigue, drowsiness.
Nicolsamide Inhibits oxidative phosphorylation in mitochondria - Minor abdominal symptoms
↓ - Malaise, pruritus, light
Interferes with anaerobic generation of ATP by tapeworm. headedness.
Praziquantel Causes leakage of intracellular calcium from membrane - Tastes bitter

↓ - Can produce nausea and
Paralysis abdominal pain.
↓ - Headache, dizziness, sedation.
Tapeworm lose the grip of intestinal mucosa
↓
Expelled.

GIT
Note: MOA:
- Oral administration of drug (Aldendazole) with After entering the cell by diffusion, its nitro group is
fatty meal causes enhanced absorption. So, we reduced by certain redox proteins (operative only in
advice albendazole with fatty meal in anaerobes)
neurocysticercosis. ↓
- Fraction absorbed is converted by first pass Reduced to highly reactive nitroradical
metabolism to its sulfoxide metabolite which is
↓
active form.
Exerts cytotoxicity by damaging DNA (DNA helix
THERAPY OF AMOEBIASIS AND stabilization and strand breaking)
GIARDIASIS Nitro radical of metronidazole causes disruption of
Past Questions: energy metabolism of aerobes
1. List the antiamoebic drugs. Give the mechanism Adverse Effects:
of action and adverse effect of metronidazole. 1. Anorexia, nausea, metallic taste, abdominal
(2+3+2=7, 3+2+2=7) [10 July, 08 July] cramps.
2. Mention one regimen commonly prescribe for 2. Less frequent: headache, glossitis, dry mouth,
chronic amoebic dysentery. (3)[07 Dec] dizziness, rash
3. Uses and adverse effects of metronidazole 3. Prolonged administration: Peripheral
(3) [11 July] neurophathy, seizures.
Anti protozoals 4. Thrombophlebitis of injected vein if solution is
Classification: not well diluted
[10] V
1. Tissue amoebicides: Contraindications:
a. For both intestinal and extra intestinal 1. Neurological disease
amoebiasis:
2. Blood dyscrasia
Nitroimidazoles: Metronidazole, Tinidazole,
secnidazole, ornidazole, satranidazole 3. 1st trimester of pregnancy
Alkaloids: Emetine, dehydroemetine 4. Chronic alcoholism.
b. For extraintestinal amoebiasis only: Interactions:
chloroquine. 1. Disulfuram like intolerance to alcohol
2. Luminal amoebicides:
2. Enzyme inducers (phenobarbitone, rifampin)
a. Amide: Diloxanide furoate, nitazoxanide
may reduce its therapeutic effect.
b. B-Hydroxy quinolines: quiniodochlor,
3. Cimetidine reduces metronidazole metabolism;
diiodohydroxyquin
dose may need to be decreased.
c. Antibiotics: Tetracyclines
4. Metronidazole enhances warfarin action.
Metronidazole [08]
Uses:
♦ Prototype nitroimidazole
1. Ameobiasis
♦ Doesn't affect aerobic bacteria
2. Giardiasis
♦ Selectively toxic to anaerobic microorganisms.
3. Trichomonas vaginalis

Pharmacology
4. Anaerobic bacterial infections ♦ Metronidazole is almost completely absorbed

5. Pseudomembrane enterocolitis from small intestine
6. Ulcerative gingivitis ↓
7. H.pylori gastritis/peptic ulcer. Little unabsorbed metronidazole reaches colon.
8. Guinea worm infestation. ↓
Diloxanide furoate So trophozoites which have already reached
colonic mucosa are less susceptible to destruction
♦ Highly effective luminal amoebicide
by metronidazole
♦ Directly kills trophozoites responsible for
♦ Diloxanide furoate is a strong luminal amoebicide
production of cysts.
thus kills the trophozoite responsible for
♦ Furoate ester is hydrolysed in the intestine the
formation of cysts.
released diloxanide is largely absorbed.
♦ Thus helps in elimination of cyst passer stage.
♦ Diloxanide is weaker amoebicide than furoate
ester. Note: Metronidazole is less effective than many
luminal amoebicides in eradicating amoebic cysts
♦ No systemic antiamoebic activity is evident
from colon because it is nearly completely absorbed
despite absorption.
from Upper bowel.
♦ Less effective in invasive amoebic dysentery
because of poor tissue amoebicidal action. Drugs for giardiasis
♦ Single dose produces high cure rate in mild 1. Metronidazole
intestinal amoebiasis and asymptomatic cyst • 200 mg TDS for 2 days.
passers. 2. Nitazoxanide
V Uses: • Prodrug of Tizoxanide
1. Mild intestinal amoebiasis 3. Quiniodochlor
2. Asymptomatic cyst passers • 250 mg TDS for 7 days.
Adverse Effects: 4. Furazolidone:
1. Flatulence • 100 mg TDS for 5 - 7 days.
2. Occasional nausea (Inferior to metronidazole or tinidazole)
3. Itching
HEPATOTOXICITY OF DRUGS
4. Urticaria
Past Questions:
5. Constipation.
1. Name the drug to be avoided in this case. Give
Rationale of combination of
reasons. (Case was Hepatitis) [3](PBQs 2013 KU)
metronidazole and Diloxanide furoate
Drugs induced liver damage:
♦ Helps in eradication of every stage of organism
from body. Include:
♦ Site of action: 1. Type A (Augmented)
- Metrodinazole → extraluminal (mainly) 2. Type B (bizarre or idiosyncratic)
- Diloxanide furoate → intraluminal 3. Type C (Continued use, cumulative effect)

GIT
Type A Mechanism Example

- Liver injury occurs as 1. Interference with bilirubin - Estrogen, rifampicin, fusidic acid
dose of some drugs is metabolism and excretion - Paracetamol in over dose
increased 2. Centrilobular necrosis - Carbon tetrachloride, salicylate
3. Hepatocellular necrosis - Tetracyclines
4. Fatty change
Type B Mechanism Example

- Drugs can cause hepatic 1. Acute hepatocellular necrosis - General anesthetics (halothane)
damage at therapeutic - Antiepileptics: Carbamazepine, Phenytoin Sodiu
doses - Antidepressants: MAO inhibitors
- Antiinflammatory: Indomethacin, Ibuprofen
- Antimicrobials: Isoniazide, Sulphonamides,
Nitrofurantoin
- Methyldopa, hydralazine
2. Cholestatic hepatitis - Anti diabetics (tolbutamide, Glibenclamide)
- Carbimazole
- Chlorpropamide
Type C Mechanism Example

Liver damage at 1. Chronic active hepatitis - Methyldopa, V
continuous dose, - Isoniazid
cumulative effect - Dantrolene
- Nitrofurantoin
2. Hepatic fibrosis or cirrhosis - Methotrexate
- Amiodarone

Pharmacology

1. The primary use of prostaglandin analogue like misoprostol is in prevention and treatment of
NSAID associated GI injury and blood loss. However, PPI are more effective, convenient, better
tolerated and cheaper.
2. Antacids interfere with absorption of:
(1) Tetracyclines (2) Iron salts (3) All-fluoroquinolones (4) Ketoconazole (5) H2 - blockers (5)
Diazepam (6) Phenothiazines (7) Indomethacin (8) Phenytoin (9) Isoniazide (10) Ethambutol (11)
Nitrofurantion
@ IT INDIA KHEP
3. Cimetidine has antiandrogenic action so, causes gynaecomastia
4. H2 receptor antagonist which has little or no effect on acid secretion but can antagonize the effects
of histamine in CNS is "Zolentidine"
5. H2 receptor antagonist which has maximum oral bioavailability is "Nizatidine"
6. PGE2 and PGI2 is produced in gastric mucosa and appears to serve protective role by inhibiting
acid secretion and promoting mucus +HCO3– secretion.
7. Prostaglandins also inhibit gastrin production and increase mucosal blood flow, prostaglandin
analogues (miso prostol, Arboprostil, emprostil, Trimoprostil) are thus used in peptic ulcer.
V 8. Misoprostol causes: Diarrhea, Abdominal cramps, uterine bleeding and abortion.
9. Misoprostol can be used also in abortion in addition to NSAID induced peptic ulcer.
10. Aluminum hydroxide relaxes smooth muscles and has mucosal Astringent action so causes
constipation.
11. Constipating antacid: Aluminum hydroxide, calcium carbonate.
12. Action of cimetidine is not affected by food.
13. Drug of choice for treating idiopathic diarrhea in AIDS patients is "Octreotide"
14. "Erythromycin" is the antibiotic which acts as a prokinetic agent by stimulating motilin receptors.
15. Loperamide is most effective and most suitable antimotility drug.
16. Drugs effective in:
Morning sickness: Promethazine
Mountain sickness: Acetazolamide
Motion sickness: Hyoscine → Preparation (transdermal scopolamine)
Sea sickness: Meclizine
17. PPI with enzyme inhibiting activity is: Omeprazole.
18. Dexlansoprazole is newly developed PPI with novel delivery system for GERD.
19. Drug with highest emetogenic potential: Cisplatinum

GIT
20. Prokinetic drug without D2 blockade is cisapride

21. 5HT3 receptor blocker with highest receptor affinity is: "Palonosetron".
22. Super ORS is improvement in ORS by adding certain actively transported Amino acids
(Alanine, glycine which cotransport Na+)
23. Chloroquine is not cystcidal for entamoeba.
24. Diodohydroxyquinoline causes
(a) Eye defects
(b) Iodism (furunculosis, inflammation of mucus membranes)
(c) Prolonged use ⇒ Neuropathic syndrome called as: "Subacute myelo - optic neuropathy"
25. DOC for cutaneous larva migrans: thiabendazole
26. Drugs of choice for cysticercosis: Praziquantel"
27. For Rx of ascariasis during pregnancy and in children under 2 yrs of age the drug of choice is
"Piperazine"
28. Emetics: Drugs used to evoke vomiting:
a. Act on CTZ: Apomorphine
b. Act reflexly and on CTZ: Ipecacuanha
29. Sucralfate + omeprazole⇒ defect is: sucralfate needs low pH for it sactivation so anatacids should
not be given.
Sucralfate + Ranitidine ⇒ defect is: sucralfate inhibits absorption of ranitidine.
30. DOC for intractable hicups is: Chlorpromazine. V
31. "Veratrum alkaloids" is the emetic agent which stimulate nodose ganglion of the vagus.
32. Cisapride when taken with CYP3A4 inhibitors like azole, antifungals, macrolide antibiotics,
antidepressants, HIV protease inhibitors can cause: Serious ventricular arrhythmia and death. So,
patient on:
Cisapride for GERD if prescribed erythromycin for his upper respiratory tract infection can
develop: fatal ventricular arrhythmias"
33. Average fecal sodium excretion in rota virus diarrhea is: 30 meq/l
34. In diarrhea:
Antimicrobials of no value in Useful only in severe case of Regularly useful in
diarrhea caused by
- IBS (irritable bowel syndrome) - Travellers diarrhea - Cholera
- Coeliac disease - EPEC - Campylobacter
- Pancreatic enzymes deficiency - Shigella - Clostridium
- Tropical sprue - Salmonella typhimurium - Ameobiasis
- Yersinia enterocolitica - Giardiasis

Pharmacology
35. Cathartic are those which cause emptying of bowels. Lactulose are cathartics inhibits absorption
of Ammonia + causes bacteria to utilize ammonia but doesn't inhibit absorption of aminoacids.
36.
Prokinetic drugs MOA
1. Metoclopromide → D2 antagonism, 5HT3 antagonism, 5HT4 agonism
2. Domperidone → D2 antagonism
3. Cisapride → 5HT4 agonism mainly
4. Mosapride → 5HT4 agonism (major) 5HT3 Antagonism
5. Tegaserod → Selective 5HT4 Partial agonist
37. Cisapride is DOC in treatment of gastroparesis.

38. Methylpolysiloxane is defoaming agent.
39. Gall stones are due to ↑ saturation of cholesterol bile acid like chenodeoxycholic acid is used in
dissolving gallbladder stone. Other drugs are: Ursodeoxycholic acid.
40. "Bisacodyl" causes hypokalemia.

GIT
physiology
SYLLABUS
Introduction to Gastrointestinal system: (p. 159)
Functions of GI system, Enteric nervous system, Innervation of gut
Oral Cavity: (p. 161)
salivary secretion- mechanism of formation, composition, regulations, functions, mastication, digestion in
mouth
Physiology of Deglutition: (p. 162)
Definition, stages, neural control
Stomach: (p. 163)
Overview of functions, Physiology of gastric secretion- mechanism, compositions, functions, control
Experimental procedures to elucidate phases of gastric secretion.
Gastric motility- characteristics, control, gastric emptying, antral pump mechanism, gastric mucosal barrier,
Digestion and absorption in stomach
Pancreatic Secretions (Exocrine): (p. 167)
Composition, Functions, control.
Small Intestine: (p. 168) V
Exocrine and endocrine Secretions, regulations and functions, movements, functions and their control
Large Intestine: (p. 170)
Movements, functions and their control
Gastrointestinal Hormones: (p. 171)
Role in secretomotor functions of the gut
Physiology of Vomiting: (p. 171)
The reflex mechanism involved
Defecation: (p. 172)
Mechanism, control

Physiology

GIT
PHYSIOLOGY
INTRODUCTION TO GI PHYSIOLOGY ♦ Lies entirely in the wall of the gut, beginning in the
Function of Gastrointestinal system: esophagus & extending all to way to anus.
1. Digestion & absorption of food ♦ Number of neurons in enteric nervous system is
about 100 million, almost exactly equal to no. in
2. Excretion of waste materials
entire spinal cord.
3. Fluid & electrolyte levels balance
♦ Composed of mainly 2 plexuses.
4. Immunity
1. Myenteric plexus or Auerbach plexus: Outer
5. Intestinal bacterial flora
plexus lying between longitudinal and circular
Enteric Nervous system muscle layer.
♦ Although it can function independently of extrinsic 2. Submucosal plexus or meissner’s plexus: Lies
nerves stimulation by sympathetic and in the submucosa.
parasympathetic systems can greatly enhance or Functions:
inhibit GI functions.
- Myenteric plexus controls GI movements
♦ Helps in Neural control of Gastrointestinal - Submucosal plexus controls GI secretions
function.
Difference between Myenteric and Submucosal plexuses:
Myenteric plexus/Auerbach plexus Submucosal plexus/meissner's plexus
1. Linear chain of many interconnecting neurons, Extends 1. Concerned with controlling functions within the
the entire length. Concerned with controlling muscle inner wall of each minute segment of intestine.
V
activity along the length of gut.
2. Lies between Longitudinal & circular muscle layers of 2. Lies in submucosa
small intestine
3. Principle Effects on stimulation : 3. Helps to control:
a. ↑ed tone of gut wall a. Local intestinal secretion
b. ↑ed intensity of rhythmical contraction b. Local Absorption
c. Slightly increased rate of the rhythm of contraction c. Local contraction of submucosal muscle
d. ↑ed velocity of conduction of excitatory waves along causing various degrees of infolding of GI
Gut wall mucosa.
e. Inhibiting some of intestinal sphincter muscles like
pyloric sphincter, sphincter of ileoceal valve.
Gastrointestinal Reflexes ii. Reflexes from gut to prevertebral
- Supported by a Anatomical arrangement of sympathetic ganglia & then back to GI tract.
enteric Nervous system & its connection with Example:
sympathetic and parasympathetic system. 1. Gastrocolic reflex
i. Reflexes integrated entirely within gut wall 2. Enterogastric reflex
Eg. Enteric nervous system 3. Colonoileal reflex.

Physiology
iii. Reflexes from gut to spinal cord or brain spontaneous rhythmic fluctuations in membrane
stem & then back to GI tract. potential ranging between -55 to -40mv.
Example: ♦ The slow waves which oscillate significantly are
1. Reflexes from stomach & duodenum to called Basal Electrical rhythm (BER).
brain stem & back to stomach. ♦ BER is present in all part of GIT Except esophagus.
2. Pain reflexes that causes general ♦ Precise cause of slow waves is not completely
inhibition of entire GI tract. understood although they appear to be caused by
3. Defecation reflex. complex interactions among smooth muscle cells
& specialized cells called “Interstitial cells of
Innervation of the gut cajal”
♦ Sympathetic innervation: ♦ These specialized cells are believed to act as
- Is Via nor adrenergic fibers having cell bodies in “Electrical pace makers” for smooth muscle cells.
prevertebral & paravertebral chain ganglia ♦ These cells undergo cyclic changes in RMP which
- Post ganglionic fibers mainly originate from helps in generating slow waves activity.
celiac, superior mesenteric & inferior
♦ Slow waves don’t themselves causes muscle
mesenteric ganglion.
contraction Except in stomach.
- Sympathetic stimulation results in:
♦ Frequency of slow waves:
1. Inhibition of motor activity resulting in
relaxation of GI smooth muscles. - 3 in body of stomach [MCQ 2013 KU]
2. Stimulation or contraction of sphincters. - 12 in duodenum
3. Inhibition of GI secretions. - 8 in ileum
♦ Parasympathetic Innervation: Spike potentials:
- Is Via ♦ True action potentials
i. Vagus nerve → Innervates GI tract from oral ♦ Occur automatically when RMP of GI smooth
V cavity up to transverse colon muscle becomes more positive than about – 40mv
ii. Remaining parts Via pelvic nerves. ♦ Higher the slow wave potential rises, greater the
frequency of spike potentials.
- Parasympathetic stimulation results in:
♦ These spike potential are due to entry of Na+ &
- Increased motility and exocrine secretions Ca++ ions (large Vo of ca2+ Ions) therefore called
of GI Tract. calcium sodium channels (contrast: Na+ ions entry
♦ Enteric Nervous system: Described above in nerve fibers)
CNS
Sympathetic system Parasympthetic

(thoracolumbar system (vagal and
outflow) sacral outflow)
Myenteric and auerbach plexuses in gut wall
Smooth muscle Secretory cells or Epithelial

glands (exocrine cells
and endocrine)
Basal Electrical Rhythm & slow waves

♦ Resting membrane potential (RMP) of smooth
muscle or GI tract exhibit wide range of
fluctuation. The Electrical slow waves are wide
GIT
Note: Mechanism of formation

- RMP of smooth muscle can be changed by ♦ It is formed by 3-major glands:
following factors: - Parotid, submaxillary, sublingual
- Depolarization by:
• Stretching of the muscle
• Stimulation by Ach released from nerve endings
of parasympathetic Nerves.
• Stimulation by various GI- hormones
- Hyperpolarization by:
• Effect of Norepinephrine & Epinephrine
• Stimulation of sympathetic Nerves
- Depolarization of RMP makes smooth muscles
more excitable.
- Hyperpolarization makes smooth muscles less
excitable.
ORAL CAVITY
Past Questions:
1. Functions of saliva (2) [08 July]
Composition of saliva ♦ Salivary secretion occurs in two stages:
♦ Contains mainly water (99.5%) & some solids 1. Secretion in acinus:
(0.5%) V
- Produces an initial saliva with a composition
♦ Solids are organic & inorganic similar to plasma.
♦ Organic solids: - This initial saliva is isotonic & has same Na+,
1. Enzymes: Ptyalin, lysozyme, lactoperoxide, K+, Cl- & HCO3- concentration as plasma.
carbonic anhydrase, Lingual lipase, RNAse & 2. Secretion in ducts:
DNAse. - Modify the initial saliva by following processes:
2. Kallikrein i. The ducts reabsorbs Na+& Cl-; therefore
the concentration of these ions are
3. Secretory immunoglobulin (IgA)
lower than their plasma concentrations.
4. Nerve growth factor
ii. The ducts secrete K+ & HCO3- ; therefore
♦ Inorganic Solids: concentrations of these ions are higher
1. Cations: Sodium, calcium, potassium & than their plasma concentrations.
Magnesium ions. iii. Aldosterone acts on ductal cells to
2. Anions: Chloride, bicarbonate, phosphate, increase the reabsorption of Na+&
sulphate & bromide ions secretion of K+.
♦ Saliva is always Hypotonic to plasma. iv. Saliva becomes hypotonic in ducts
because ducts are relatively impermeable
♦ Concentration of sodium & chloride ions in saliva
to water. Because more solute than water
is less than that of plasma.
is reabsorbed by ducts, saliva becomes
♦ Tonicity of saliva is about 70% of that of plasma. dilute relative to plasma.

Physiology
Regulation of saliva production 4. Excretory function: Excretes urea, Heavy metals (Pb,
♦ Saliva production is controlled by the Bis, As), thiocynates, I2, morphine, penicillin etc.
parasympathetic & sympathetic nervous system. 5. Saliva helps in water balance.
♦ Parasympathetic activity is more important. 6. Buffering function:
A. Parasympathetic stimulation: 7. Bacteriolytic function.
- Facial (Submaxillary & submandibular) & Digestion in mouth:
Glossopharyngeal nerve ( parotid) & Refer biochemistry
- Profuse secretion rich in water.
- Increases saliva production by Increasing PHYSIOLOGY OF DEGLUTITION
transport processes in acinar & ductal cells ♦ Receptors for Deglutition reflex are present near
& by causing vasodilation. the opening of pharynx.
- Anticholinergic drugs (Eg: Atropine inhibits ♦ Afferent impulses are transmitted to deglutition
the production of saliva & causes dry mouth) centers in medulla & pons.
B. Sympathetic stimulation: ♦ The efferent impulses are directed to muscles of
- Less saliva, rich in organic constituents. pharynx & upper esophagus via cranial verves.
- Increased production of saliva & the growth of Stages of deglutition
salivary glands, although the effects smaller
♦ Divided into 3- steps
than those of parasympathetic stimulation.
1. Oral phase / Buccal phase:
Note: Both sympathetic and parasypathetic - Voluntary phase of swallowing
stimulation increases secretion.
- Food is voluntarily squeezed or rolled
C. Reflex secretion: posteriorly into pharynx by pressure of tongue
- Saliva is secreted reflexly by contact of food upward & backward against palate.
V with the mouth cavity. - Once food bolus touches receptors at pharyngeal
- This reflex secretion is unconditioned as opening, swallowing reflex is initiated.
this is present since birth. - Nasopharynx closes, breathing is inhibited.
- However, salivary secretion due to smell, 2. Pharyngeal phase:
thought of food is conditioned reflex. - Involuntary
- Salivary secretion exclusively occurs in - Reflex pathway:
cephalic phase & secretion is nil in gastric & • Receptors:
intestinal phase of digestion of food.
→ Receptors present around the pharyngeal
Function of saliva: [08 July] opening .
1. Mechanical function: • Afferent:
- Keeps the mouth moist & helps in speech. → Impulses from pharyngeal receptors are
- Facilitates swallowing transmitted to centers through trigeminal,
glossopharyngeal, & vagus nerve.
- Help in preparing food stuffs into a bolus
• Centers:
suitable for digestion.
→ Nucleus tractus solitarius & nucleus
- Dilutes hot & irritant food, thus prevents injury
Ambiguous in medulla.
to mucosa.
• Efferent:
- Acts as lubricant
→ Effector organs are muscles of pharynx &
2. Helps in taste by dissolving foodstuffs. tongue that are innervated by
3. Digestive function: Breaks down starch into trigeminal, glossopharyngeal, vagus &
maltose in presence of ptyalin. hypoglossal nerves.

GIT
• Events: 4. Describe how HCl is secreted by cells in the

→ Soft palate pulled upward, palatopharyngeal gastric mucosa and the factors that influence it.
folds inward (3 +2 = 5) [05 June]
→ Laryngeal opening is closed by vocal 5. Describe how acid is secreted by the cells of the
cords pulled together. gastric mucosa and explain the mechanism of
Esophageal phase: regulation of gastric juice. (2 +5 = 7) [03 Dec]
- Once food enters Esophagus, facilitated by 6. Describe briefly regulation of HCl secretion from
relaxation of upper esophageal sphincter the gastric mucosa. (4) [06 June]
(UES), the peristaltic wave (primary 7. Pathophysiology of gastric ulcer (2.5) [08 Jan]
peristalsis) is initiated just below the UES. Functions:
- If primary peristalsis is ineffective, a second 1. Storage of food
peristaltic wave is initiated to push the food bolus. 2. Grinding & mixing of food
Note: Primary peristaltic wave is simply continuation 3. Secretion of HCL
of peristaltic wave that begins in pharynx & spreads 4. Secretion of intrinsic factors
to Esophagus during pharyngeal stage of swallowing. 5. Absorption of water & lipid soluble substances
such as Alcohol & few drugs.
STOMACH
Past Questions:
Mechanism of HCL secretion [11,06,05,03]
♦ Cl- is actively transported from Cytoplasm of
1. State the composition and functions of gastric
parietal cell to lumen of canaliculus & Na+ ions –
juice. (2+2=4)
are actively transported out of lumen.
2. Write the composition of gastric juice. State the
♦ These two effects together create a negative
mechanism of secretion of HCl (6) [11 July]
potential of -40 to -70 mV in the canaliculus
3. Briefly describe the Mechanism of gastric acid
♦ Which inturn causes passive diffusion of K+ ions &
secretion. (6) [07 July] V
a small number of Na+ ions from cell cytoplasm to
canaliculus.

Physiology
♦ H2O becomes disassociated into H+ and OH- in cell contains HCL (150-160 meq/l ), KCL ( 15 meq/l), &
cytoplasm. H+ is then actively secreted into the a small amount of NaCl.
canaliculus in exchange of K+ ions; this active ♦ Finally CO2 combines OH- under the influence of
exchange process is catalyzed by H+K+ ATPase. carbonic anhydrase to from HCO3- .
Most of K+ & Na+ ions that have diffused into ♦ This then diffuses out of cell into ECF in exchange
canaliculus are reabsorbed. of Cl- that enter the cell & later will be secreted
♦ H2O passes into the canaliculus by osmosis thus into the canaliculus.
the final secretion entering the canaliculus
Factors influencing HCL- Secretion [06, 03]
A. Factor that increase HCL secretion: Composition of Gastric Juice [08, 11]
V Luminal: ♦ Daily secretion: 1.2-1.5 L/day
1. Distension of stomach ♦ PH = 1-2
2. Products of protein digestion ♦ Constituents:
Hormonal: 1. Water (99.5%)
1. Acetylcholine 2. Solids (0.5%)
2. Gastrin - Inorganic constituents: Anions are :Cl-, Po43-,
3. Histamine So42-& HCO3-, & Cations are Mg2+ , Na+, K+, H+
Neural: [Mujhe Na KaHo]
- Vagal stimulation (cholinergic & non cholinergic) - Organic constituents: pepsinogen, intrinsic
Blood borne: factor, mucin, rennin, gastric lipase,
gelatinase, carbonic anhydrase & lysozyme.
- Epinephrine
B. Factors that decrease HCL secretion note: normal gastric juice doesn't contain Ca2+ ions.
Luminal: Phases of gastric secretion
- Increased acid content (Highly acidic chyme) Cephalic phase:
Hormonal: - Occurs even before food enters stomach.
- Somatostatin - Results from sight, smell, thought or taste.
Blood borne: - Neurogenic signals that cause cephalic phase of
- Secretin, GIP, Gulcagon gastric secretion originate in cerebral cortex up in
appetite centers or amygdala & hypothalamus.
GIT
- They are transmitted through dorsal Motor 3. Helps in killing ingested bacteria.
nuclei of vagus & then through vagus nerve to 4. Helps in iron Absorption by converting ferric to ferrous
stomach. from of iron; the form in which iron can be absorbed.
- Accounts for 30% of gastric secretion 5. Stimulates bile & pancreatic juice secretion.
associated with eating a meal. Function of pepsinogen:
Gastric Phase: - Pepsinogen is secreted as an inactive protein
- Once, the food enters stomach, it excites: which is converted by HCL at PH =2, to active
• Long vagovagal reflexes from stomach to proteolytic enzyme pepsin.
brain & brain to stomach. • It digests proteins to polypeptides (Peptones &
• Local enteric reflexes Proteases)
• The gastrin mechanism • Curdles milk.
- Accounts for 60% of gastric secretion.
Functions of Gastrin
Intestinal phase : 1. Stimulates gastric acid & pepsin
- Accounts for 10% gastric secretion 2. Stimulates growth of mucosa of stomach.
Gastric phase Brain limbic Cephalic
system phase 3. Stimulates gastric motility
Stimuli
Stimuli 4. Has feeble influence on contraction of bladder.
Hypo- sight, smell,
5. Stimulates insulin & glucagon secretion after
Peptides & Distension thalamus taste, emotion
proteins in of protein meal.
stomach stomach Vagus nerve
Vago
Experimental procedures to elucidate
vagal
Local
reflex
reflex phases of gastric secretion
G-cell Enteric neurons
1. To study cephalic phase:
- Sham feeding: V
Gastrin ECL Parietal cell
• Dog is taken as experimental animal
Histamine HCL secretion
• Fistula is made in esophagus of dog
Intestinal phase • When animal eats the food, comes out of
Entry of chyme into duodenum neck through fistula (food is not allowed to
reach stomach)
Distention of Stimulation of Activation of Release of • Simultaneously gastric juice is collected
duodenum duodenal oxyntic enterogastri GI hormones from stomach by placing canula into it
cells c reflex
2. To study Gastric phase:
Secretion, GIP, VIP,
Vago vagal Secretion of enteroglucagon - By making 5 different types of pouches:
reflex enterooxyntin Pavlov pouch, Heidenhain pouch, Bickel pouch,
Inhibition of HCl secretion
farrell pouch & Ivy pouch.
Stimulation of HCl secretion from G-cells of stomach.
from G-cells of stomach (in (In later phase) A. Pavolv pouch:
initial phase) • Is small pouch separated from the main
body of stomach by double layer of mucus
Functions of Gastric Juice membrane.
Functions of HCl [08 July] • This pouch of mucus membrane has intact
+
1. It provides H concentration necessary for nerve & Blood supply.
optimum pepsin activity. • Therefore helps to study both neural &
2. Activates “pepsinogen” to “Pepsin” chemical factors of gastric acid secretion.
Physiology
B. Heidenhain pouch: 3. Migrating Motor complex (MMC):

• Is denervated pouch, which helps to study - During interdigestive period, Antrum of
the influence of neural factors on gastric stomach remains silent for about 75-
secretion. 90mins.
Gastric Motility - After which a burst of electrical & motor
activities Occurs.
♦ Stomach has 3 layers of smooth muscle, Outer
longitudinal, circular & oblique layer. - Causes intense antral contraction with
relaxation of pylorus.
♦ Has 3 Anatomic divisions: Fundus, Body & Antrum
- Wave of contraction progresses from
♦ Antrum and distal body are responsible for
stomach to terminal ileum.
contractions that mixes food and propel it into
- Helps in cleaning the stomach & intestine &
duodenum.
keeps GI tract ready for next meal.
Types:
- Usually, it is repeated every 90mins during
1. Gastric Relaxations:
interdigestive period.
a. Receptive relaxation:
- “Motilin” is mediator of these contractions.
- Relaxation of fundus and body of
4. Hunger contraction:
stomach in response to chewing &
- Gastric contractions in between meals, felt
swallowing of food.
as mild pain
- Stomach prepares itself to receive food.
- Associated with MMC
- Because of Receptive relaxation, the
intragastric pressure doesn’t rise inspite Has 3 phases:
of accumulation of large volume of food. 1. Quiescent phase: With no spikes
- It is mediated by vagus nerve & 2. Irregular electrical & mechanical activity
V Neurotransmitters released are VIP & 3. Burst of regular activity.
NO (Noncholinerigic fibers) Gastric emptying
b. Adaptive & feedback relaxation:
- Adaptive: Occurs in response to
stretching of stomach wall, Mediated by
vagovagal reflex .
- Feedback relaxation: Is reflexive
relaxation – due to presence of food in
proximal segment of small intestine.
2. Peristalsis:
- After about half an hour following gastric
filling gastric peristalsis starts. ♦ Occurs by 3 – mechanisms:
- Are initiated by gastric slow waves. a. Peristaltic contraction
- Pacemaker for gastric peristalsis is located b. Antral contraction
in middle of stomach close towards greater
c. Retropulsion
curvature.
- Start as ring of contractions that progress a. Peristaltic Contraction:
slowly towards antrum - Begin in middle of stomach & proceeds in
- Occurs at rate of 3/min ring like fashion towards pylorus.
- Helps in propelling food into antrum & - These contractions push the food into
mixing of food with gastric juice. antral part of stomach.

GIT
- As contraction are weak in fundus & body of ♦ Mucus gel layer is 0.2 mm thick & effectively
stomach the proximal portion of stomach separates the bicarbonate rich secretion of
mainly serves the reservoir function. epithelial cells from the acidic content of stomach.
b. Antral contraction: ♦ This allows the pH of epithelial cells to remain
- Help thorough mixing of food with gastric Alkaline despite acidic pH of gastric content.
juice ♦ It protects mucosal epithelium from injury caused
- Forceful contractions of Antrum forces by acidic chyme.
gastric contents towards the pylorus. ♦ However, when secretion of mucus is impaired, or
- But, as the pyloric sphincter remains closed, bicarbonate production is decreased, or when the
peristaltic wave fails to push food into mucosal coat is mechanically damaged, Acid &
duodenum, rather food returns back into pepsin causes ulcer formation.
body of stomach. ♦ Such damage is usually produced by use of aspirin
- After few such contractions, pylorus opens & NSAIDs that inhibit secretion of mucus &
partially with a narrow opening at the bicarbonate.
center. ♦ Catecholamines also inhibit mucus secretion.
- Therefore, stomach empties in small squirts ♦ In chronic stress, ulcer is produced (stress ulcer)
with each peristaltic wave. by chronically elevated level of catecholamines in
c. Retropulsion: blood
- Terminal part of antrum exhibit rapid & Digestion & absorption in stomach
forceful contraction that forces the chyme
& Refer Biochemistry
to be propelled back towards the proximal
part of antrum & body of stomach;
PANCREATIC SECRETIONS
movement called as retropulsion
(EXOCRINE) V
- Effective in mixing & grinding larger food
Past Questions:
particles into small ones.
1. Composition of pancreatic juice (2) [08 July]
Physiological significance:
- As the muscle layers in the fundus & body are 2. Describe briefly the composition of pancreatic
thin, contractions in these parts of stomach are juice and outline the mechanism that regulates
weak. the secretion. (2 +3 = 5) [08 Jan]
- Therefore, gastric content in body of stomach 3. Write the composition of pancreatic juice what is
settles into different layers based on their density. the role of pancreatic juice in protein digestion?
- Fat content of food forms an oily layer on top (2 +2 = 4) [06 Dec]

of other gastric contents.
Composition [08, 06]
- This is why fat is emptied slower than the
carbohydrate & protein.
Aqueous components (98%)
- Contain mainly water & ions.
Gastric mucosal barriers:
Cations: Na+, K+ , Ca2+, Mg2+, Zn2+
♦ The defense barrier of the stomach is the mucous
Anions: HCO3- , Cl-, Po43-, SO42-
coat on the gastric epithelium. This is called
mucosal defense barrier. Enzyme component (2%)
♦ Mucus is secreted by mucous cells. - Enzymes for lipid digestion:
♦ Mucus is viscous gel that contains mucin, • Lipase, colipase, phospholipase, cholesterol
phospholipid, electrolytes (mainly HCO3-) & water. hydrolase.

Physiology
- Enzymes for protein digestion: CCK:

• Trypsin, chymotrypsin, carboxypeptidase, - Secreted by I cells located in upper small
elastase, Ribonuclease, Deoxyribonuclease, intestine in response of fatty foods.
- Enzymes for carbohydrate digestion: - Has 2 receptors; located in gallbladder,
pancreas, GI tract etc. are CCK A receptors
• Amylase
but CCK B receptors present in Brain areas.
Function - CCK increase pancreatic secretion rich in
1. Pancreatic secretion contains enzymes that help in enzyme
digestion of fat, protein, and carbohydrate. - “Ecbolic type” of secretion.
2. Pancreatic secretion contains Bicarbonate & water Secretin:
that neutralizes “acidic chyme” entering intestine
- Secreted from 5-cells of upper small
from stomach. intestine in response to acidic chyme.
Factor that influences the secretion [08] - Increases pancreatic secretion rich in
Hormonal factors: bicarbonate & water.
1. CCK: CCK – A & CCK- B Receptors. - Hydrolytic type of secretion
2. Secretin
SMALL INTESTINE
3. Gastrin: Gastrin receptors, CCK ‘B’
Past Questions:
receptors.
1. Describe the briefly the movements of small
4. GRP.
intestine with diagrams. [03, 06, 09 July,013]
5. GIP 2. Name the types of movement seen in the small
6. VIP intestine and describe the functions of each.
V
(6) [10 Jan]
Gastrin VIP
GRP Ach CCK Secretin 3. Movements of small intestine (6) [05 Dec]
R R
R R 4. Briefly describe the movements of small
intestines. [2] [013 KU]
CAMP Exocrine secretions

Ca2+
Enzymes Substrate Products
Acinar
cell Enterokinase Trypsinogen Trypsin
Enzyme synthesis
& secretion d-dextrinase d- dextrins Glucose
Maltase maltose Glucose
Acinar Lumen Enzyme Sucrase Sucrose Glucose & fructose
Neural factors: Lactase Lactose Glucose & glactose
- Parasympathetic : stimulates secretion Peptidases Terminal AA Peptides &
- Sympathetic: inhibits secretion. aminoacids at amino
end of peptides
CCK & secretin
Nucleotidases Nucleotides Nitrogenous base,
♦ Natural primary regulation of pancreatic pentoses &
secretion. phosphates

GIT
Regulation ♦ Vagal stimulation ↑es secretions

♦ Controlled by GI hormones & vagus nerve ♦ Dietary factors in intestine.
Endocrine secretion and regulation:
Hormone Stimuli for secretion Site of secretion Actions
Stimulates
G-cells of the antrum,
Gastrin Protein - Gastric and secretion
duodenum, and jejunum
- Mucosal growth
i. Stimulates
- Pancreatic enzyme secretion
I-cells of the duodenum, - Pancreatic bicarbonate secretion
Cholecystokinin Protein, Fat, Acid
jejunum, and ileum - Gallbladder contraction
- Growth of exocrine pancreas
ii. Inhibits Gastric emptying
i. Stimulates
- Pepsin secretion
- Pancreatic bicarbonate secretion
S-cells of the duodenum,
Secretin Acid, Fat - Biliary bicarbonate secretion
jejunum, and ileum
- Growth of exocrine pancreas
ii. Inhibits
- Gastric acid secretion V
Gastric Stimulates insulin release
Protein, Fat, K-cells of the duodenum and
inhibitory Inhibits
Carbohydrate jejunum
peptide Gastric acid secretion
Stimulates
M-cells of the duodenum
Motilin Fat, Acid, Nerve Gastric motility
and jejunum
Intestinal motility
Movement of small intestine (09, 013) ↓

As one set of segmentation contraction relaxes
♦ Mixing contraction
a new set begins but contraction this time
♦ Propulsive contraction occurs at new points between previous
1. Mixing contraction/ segmentation contractions.
contractions: - Causes segmentation of small intestine.
When a portion of small intestine becomes - No net forward movement of chyme.
distended with chyme Functions:
- Segmentation contraction chops the chyme
↓
two to three times per minute.
Stretching of the intestinal wall elicits localized - Promotes progressive mixing of food with
concentric contraction, spaced at intervals secretions of small intestine
& lasting fraction of a minute. - Digestion & absorption of nutrients
Physiology
Factors affecting peristalsis

♦ Increased by: parasympathetic, Gastrin, CCK-PZ,
secretin, high chyme delivery.
♦ Decreased by: sympathetic , secretin, Glucagon
♦ Gastro ileal reflex :
- Mediated by extrinsic ANS & possibly by gastrin
- The presence of food in stomach triggers
increased peristalsis in ileum & relaxation of
ileocecal sphincter.
LARGE INTESTINE
Movements
2. Propulsive contraction: ♦ Mixing movement
- Chyme→ stretches intestinal wall→ Local ♦ Propulsive movement
stimulation of mesenteric plexus → 1. Mixing movement/Haustrations:
contraction behind the chyme & relaxation Larger circular constrictions occurs in the large
infront→ food moves forwards into relaxed intestine
part → new position &New cycle. ↓
- This reflex is coordinated by enteric nervous At each of this constriction, 2.5 cm of circular
system. muscle contract
- In fact, peristalsis wave spreads in both ↓
direction however waves towards oral cavity At the same time, longitudinal muscle of colon;
tenia coli contract
V dies out after a short spread & waves towards
colon continues progressively, called as law of ↓
intestine. This combined contraction of circular &
longitudinal strips of muscle causes the
unstimulated portion of large intestine to bulge
outward into bag like sacs called haustrations.
Function:
1. Especially in cecum & ascending colon, they
provide minor amount of forward
propulsion of colonic contents.
2. All fecal material is gradually exposed to
mucosal surface of large intestine & fluid &
dissolved substances are progressively
absorbed.
Functions :
2. Propulsive movement: “mass movement”
- Propel the chyme in forward direction
- Much of propulsion in cecum & ascending
- Forward movement aids absorption. colon result from slow but persistent haustra
- Prevents bacterial growth due to contractions.
continuous movements. - From cecum or sigmoid, mass movements take
- Increases blood & lymph flow → increases over propulsive role.
absorption. - They occur 1-3 times each day in many people.

GIT
- Occurs especially for about 15mins during first GI HORMONES

hour after eating breakfast.
Past Questions:
Sequences of Events:
1. Gastrin (3) [06 Dec]
First, a constrictive ring occurs in response to a
distended or irritated point in colon 2. CCK- PZ (3) [06 Dec]
↓ 3. What is the role of CCK - PZ? [1][KU 2013]
Then rapidly, 20 or more cm of colon distal to
& Refer exocrine secretions of small intestine
constrictive ring lose their haustration &
instead contracts as unit (Already discussed)
↓
PHYSIOLOGY OF VOMITING
Propels fecal material in this segment further
down the colon Past Questions:
Note: 1. Physiology of vomiting (2) [08 July]

2. Write briefly the act of vomiting. (3) [06 June]
- Appearance of Mass movements after meals is
facilitated by: Gastrocolic & duodenocolic reflexes. 3. Briefly describe the physiological mechanism of
vomiting (4) [11 July]
- They occur hardly or not at all when extrinsic
autonomic nerves to colon have been removed. 4. What are important factors that cause vomiting?
Write a note on CTZ. [3][2013 KU PBQs]
Function: It propels the feces from colon towards anus.
NTS-Nucleus tractus solitarius; VC- Vomiting centre; CTZ-Chemoreceptor trigger zone; 5-HT3 -5–HT3 receptor; H1 - Histamine H1 receptor;
D2 - Dopamine 2 receptor; M–Muscarinic receptor; NK1–Neurokinin1, receptor; CB1 - Cannabinoid 1 receptor

Physiology
♦ Vomiting is expulsion of Gastroduodenal content 3. Forced inspiration occurs against closed

from GIT to external environment Via mouth. glottis, lowering the diaphragm → ↑es intra-
abdominal pressure
♦ Stimuli: [PBQ 2013 KU]
1. Distention of stomach 4. Vigorous contraction of abdominal muscles →
further ↑ed intra-abdominal pressure forces
2. Tickling the back of throat
gastric content to enter esophagus.
3. Painful injury of genitourinary tract
5. Relaxation of lower esophageal sphincter
4. Many chemicals or drugs
6. With stronger retching & sharp rise in intra-
5. Unpleasant sensory stimuli such as bad odor,
abdominal pressure → upper esophageal
fear
sphincter relaxes
6. When equilibrium is disturbed or body rotated.
7. Expulsion from mouth (Vomiting)
- Stimuli Originates in pharynx, esophagus,
stomach, S.I. \DEFECATION
- from pharynx, impulses are transmitted by Defection Reflexes
glossopharyngeal nerve.
- Nerve impulses are transmitted by both vagal
& sympathetic afferent Nerve fibers to multiple
distributed nuclei in brain stem that all
together called as “Vomiting center”
- Chemoreceptor trigger zone located in area
postrema & Nucleus tractus solitarius(outside
V blood brain barrier) are most important relay
areas for afferent impulses arising in GIT,
throat & other viscera. [PBQ 2013 KU]
♦ From, vomiting center, motor impulses are transmitted
- Via 5th, 7th, 9th, 10th and 12th Cranial Nerves to
upper GI tract.
- Via vagal & sympathetic verves to lower tract
- Through, spinal nerves to diaphragm &
abdominal muscles.
Act of vomiting: [ 06 ] ♦ Ordinarily defecation is inhibited by defecation
reflexes.
- Vomiting reflex is executed in a sequence of Events:
1. Intrinsic reflex:
1. Antiperistalsis, the prelude to vomiting:
- Mediated by the local enteric Nervous
Sweeps the content of intestine & duodenum system in rectal wall.
into stomach.
- When feces enters the rectum → distention
2. Relaxation of pyloric sphincter: Allows of rectal wall imitates afferent signals that
intestinal content to enter the stomach. spread through the myenteric plexus to
initiate peristaltic waves in the descending

GIT
colon, sigmoid & rectum → forces feces into the spinal cord & then reflexly back to
towards the anus. descending colon, sigmoid, rectum &anus
- As peristaltic waves approaches the anus by the way of parasympathetic Nerve fibers
→ the internal anal sphincter is relaxed by in pelvic nerve.
inhibitory signals from the myenteric - These parasympathetic signals greatly
plexus. intensify the peristaltic waves as well as
- If the external anal sphincter is also relax the internal anal sphincter → thus
consciously, voluntarily relaxed at the same convert the intrinsic myenteric defecation
time →defecation occurs. reflex from a weak effort into a powerful
process of defecation that is sometimes
- However, the intrinsic myenteric defecation
effective in emptying the large bowel all the
reflex functioning by itself is relatively weak.
way from splenic flexure of colon to anus.
- To be effective in causing defecation, it
3. Also, the afferent defecation signal entering
usually must be fortified by another type of
the spinal cord initiate other effects such as,
defecation reflex; a parasympathetic
taking deep breath, closure of glottis &
defecation reflex.
contraction of abdominal muscles to force
2. Parasympathetic defecation reflex:
contents of colon downward. At the same
- It involves sacral segment of the spinal cord. time, this causes the pelvic floor to relax
- When Nerve endings in the rectum are downward & pull outward in the anal ring to
stimulated → signals are transmitted first evaginate the faeces.

Physiology

1. Substance Site of absorption
Vit C Iron Duodenum @ C I D
Calcium JeJunum @ Ca.Je
Folate, fat Jejunum @ fo -Je
Vit. B12 Terminal Ileum (MCQ 2013 KU)
Bile salts Terminal Ileum
Electolytes, short chain fatty acids produced by Colon

bacteria
- Maximum absorption or reabsorption of water from gastrointestinal tract occurs in jejunum.

- Ca2+, Cl–,Fe2+,SO42–, long chain fatty acids and vitamins (except B12) are mainly absorbed in
upper small intestine (i.e. jejunum & duodenum)
- Sodium (Na+) is mainly absorbed in upper and lower small intestine (jejunum, illeum) and
colon. and K+ in upper mid & lower small intestine.
- Sugars and amino acids are mainly absorbed in mid small intestine where as bile salts, and
V vitamin B12 in lower small intestine (ileum).
- Oxyntic cells of Gastric glands contain receptors for: PGE2, N2, H2, Somatostatin
3. Somatostatin antagonizes insulin secretion
4. Chief cell / zymogen cells secrete “Pepsinogen”
5. Parietal cells / Oxyntic secrete Intrinsic factor & HCl. ( @ POX→ Hint)
6. Gastric Intrinsic Factor :
- Necessary for Vit. B12 absorption from ileum.
- Absence of this factor results in Vit B12 deficiency & Consequent development of pernicious anemia.
- Because liver stores high quantities of Vit B12, a deficiency of this vitamin may take several
months to develop after production of gastric intrinsic factor ceases.
7. Somatostatin:
a. GH inhibitory property, Also inhibits basal & stimulated TSH secretion.
b. Via, paracrine & Endocrine actions:
- It suppresses secretion of Insulin, Glucagon, CCK, Gastrin, secretin, VIP & other GI
hormones as well as some functions as Gastric acid secretion, Gastric emptying, gall
bladder contraction & splanchnic blood flow.

GIT
8. Gastric emptying:
- Stimulated by gastrin & distension of stomach.
- Decreased by CCK, fatty meal, Hyperosmolarity in duodenum.
9. Motilin is polypeptide → secreted by Enterochromaffin cells,
- Secreted by Endocrine M cells (not same as m cells in peyers patches)
- M- cells found in duodenum & Jejunum
- Because of Ability to stimulate gastric activity, Named as “ Motilin”.
- Circulating level Increases at approximately 100 min. in inter digestive state & is “major
regulator of MMC”.
- “Erythromycin” binds to these motilin receptors & is used for treating “gastric hypomotility”.
10. Pacemaker of small intestine is “Second part of duodenum”
- Pace maker of GIT is located in “fundus of stomach”.
11. Cephalic phase of gastric secretion is mediated by “Parasympathetics”.
Gastric phase mediate by “hormones “& “Neural factor”.
12. Intestinal motility is stimulated by:
- Distension, Ach, Cholecystokinin
13. Gastrocolic reflex is a mass reflex.
- Enterogastric reflex:
a. “Chyme entering intestine inhibits gastric motility” V
b. Stimulated by :
- Duodenal distension, protein/ fat breakdown products
- Acidity, osmolarity of duodenal chyme
14. Factors decreasing gastric motility are:
- GIP, CCK, - Vagotomy, - fear.
15. Dietary fibers:
- Increases bulk of stools
- ↑es metabolism of sugar in GIT.
- ↑es stool transit time
- Prevent against colonic cancer
Eg: Pectin, cellulose, Hemicellulose.
16. Major force in vomiting is provided by: “Abdominal muscles”.
17. Normal acid level in stomach is: 20-40 meq.
18. Chymotrypsinogen is activated into chymotrypsin by : “Trypsin”

Physiology
19. Gastrin is polypeptide produced by:

a. Gastric antral cells
b. Pancreas
c. Pituitary
20. Pepsinogen is activated by low PH/ Gastric HCl.
21. Normal basal acid output is = 1-2 mmol/ hr.
22. Final sugars in intestinal chyme: Glucose & Fructose.
23. CCK causes Gallbladder contraction but secretin doesn’t cause GB contraction.
24. Longest transit time is seen in colon.
25. Salivary amylase is activated by Cl- ion.
26. When stomach contains foods, weak peristaltic constrictor wave called mixing wave begin in mid-
portion of stomach wall & move towards antrum along the stomach wall about once every 15-20
sec.
- Mixing waves of stomach originates in body of stomach,
27. Mass movement of colon will be abolished by “Destruction of aeurbach plexus”
28. Migrating motility complex occurs at the rate of 5cms per minute from stomach.
29. Paneth cells in mucosa of small intestine secrete “lysozyme”
30. Micelles is formed by “Amphipathic lipids in water”
V 31. Upper esophageal sphincter is “physiological not anatomical”.

32. In stomach H+ ions. Are secreted in Exchange for K +.
33. Intestinal motility:
a. ↑ed by distension.
b. ↑ed by Ach
c. ↑ed by CCK
d. Depends on Gastric motility
34. Gastric inhibitory peptide inhibits only Gastric acid secretion but not gastric motility but
somatostatin inhibits both Secretion & motility
35. In infants, defecation often follows a meal, the cause of colonic contraction in this situation is:
Gastrocolic reflex.
36. Maximum postprandial motility is seen in:
- “Descending colon”
37. Maximum potassium ions secretion is seen in “Saliva”
- Highest concentration of potassium is seen in “Rectum”
38. Effect of flow rate on saliva composition is explained by change in the contact time available for
reabsorption & secretion processes to occur in ducts
GIT
- At high flow rate:

i. Mostly like initial secretion from acinus
ii. Closest to that of plasma
iii. Highest Na+& cl- & lowest K+ Concn
39. Maximum water reabsorption in GI tract occurs in “Jejunum”
40. Primary action of ‘NO’ in GI tract is :
- “GI stomach muscle relaxation”
41. Myenteric plexus receives preganglionic parasympathetic type of innervation.
42. GIT structure, up to Junction between proximal 2/3 & distal 1/3 of transverse colon is supplied by
vagus.
43. PH of saliva is around ‘6-7’, PH of gastric juice = 1-2
44. Lysozymes, IgA & lactoferrin minimizes risk of buccal infection & dental caries, these components
are found in saliva.
45. Vagal stimulation following intake of food doesn’t affect secretion of “Parotid”.
46. Secretion of saliva increases when:
a. Sympathetic nerves to gland are stimulated
b. When touch receptors in mouth are stimulated
c. Just before vomiting.
47. Deglutition reflex triggered during oral phase. V
- Deglution center is in medulla.
48. Principle functions of lower esophageal sphincter is: To prevent reflux of stomach contents.
49. Achalasia cardia is characterized by:
- Accumulationof food in esophagus.
50. Gas present in fundus of stomach is mostly due to: swallowing
- Gastric juice secreting glands are present in all parts of body of stomach, except “lesser
curvature”
51. Pepsin doesn’t have bactericidal effect but helps in:
a. Conversion of pepsinogen to pepsin
b. Proteolysis
c. Curdling of milk.
52. Atrophy of gastric mucosa produces: “Pernicious anaemia”
53. Raised gastrin levels without associated ↑in gastric acid level secretion is seen in: pernicious
anaemia.

Physiology
54. VIP: ↑es intestinal secretion rich in electrolytes & water

a. ↓ es gastric motility, relax GI smooth muscle including sphincters.
b. Potentiates the action of acetylcholine on salivary glands.
c. Causes vasodilatation.
VIP secreting cell tumor is called VIPoma.
55. Post- prandial alkaline tide is cause by: “Rise in HCO3- in systemic blood PH following a meal”
56. Mechanism which causes maximum Gastric acid secretion is “ H2 receptor stimulation”
57. Gastric motility can be inhibited by:
Enterogasterone, Ca++, Epinephrine.
58 Major stimulus for receptive relaxation of stomach is: Food in the stomach.
59. “Chyme” is food mixed with Gastric secretions.
60. Vagotomy doesn’t prevent the ↑ in gastric secretions which normally occur in response to
“Injection of histamine”
61. Total Gastrectomy may lead to:
a. Severe anemia
b. Giddiness
c. Dizziness, pallor & sweating after meals called as “Dumping syndrome”
62. Duodenal mucosa is protected from action of acid & pepsin by: “ Secretion of brunners gland”
V 63. True vomiting center is –“CTZ”
64. PH of pancreatic juice is : alkaline
65. Salivary Amylase Acts: Only on boiled starch but pancreatic Amylase Acts: on both boiled &
unboiled starch
Pancreatic Amylase is stable in PH range of 4-11.
66. Normal Amylase level in serum is: 50- 1200µg/l
67. Coeliac disease is characterized by: “congenital absence of Enzyme gluten hydrolase”
68. Peristalsis movement of small intestine occurs at rate of 20cm/sec. : Are also called vermicular
movements & can occur in either direction from stimulated points.
69. Small intestinal peristalsis is dependent upon the integrity of “Myenteric nerve plexus.”
70. First part of test meal reaches cecum in about 4 hours, hepatic flexure in 6 hrs, splenic flexure in 9
hrs & sigmoid colon in 12 hrs.
71. Following test meal, total recovery of substance in stool requires more than 7 days.
72. Congenital absence of myenteric plexus in distal colon results in Aganglionic megacolon
(Hirschsprug’s diseases)
73. Characteristic odour of feaces is due to : “Indole”
74. Malabsorption of sucrose results in fermentive diarrhoea.

GIT
75. Digestion of carbohydrates is maximum in: Jejunum & proximal ileum.

76. Glucose & Galactose are absorbed against concentration gradient.
77. Steatorrhoea is of severe intensity if it is due to: “Destruction of exocrine portion of pancreas”
78. Enzyme responsible for final release of aminoacids from parent polypeptide is : “polypeptidase &
Dipeptidases”
79. End product of Nucleoprotein digestion is : “purine & pyrimidimes”
80. Iron absorption is ↑ ed by: Vit. C
- Is ↓ ed by: Phytates, phosphate,Taurine etc.
81. Lipase is not present in : “colon secretions”
- Succusentericus is intestinal juice, It also contains lipase.
82. Daily secretion of Intestinal juices:
Daily volume ( ml) PH. K+ ion conc. (meq/L)
Saliva 1000 6-7 25-30 (low flow)

15-20 (high flow)
Gastric secretion 1500 1-3.5 10 (may be upto 32)
Pacreatic secretion 1000 8-8.3 4.5 (same as plasma)
Bile 1000 7-8 5-6 (in liver bile)

12 (in gall bladder bile) V
Small intestine secretion 1800 (maximum) 7.5-8 10-12 (in ileum)
Brunner’s gland secretion 200 8-8.9
Large intestine secretion 200 7.5-8 75 (rectum)
Total 6700ml.
- Maximum concentration of K+ ion is seen in colonic secretions (or stool) but this accounts
for only a small amount of Potassium because of only 100 - 200 ml quantity of large intestinal
secretion per day.
- Where as saliva has 2nd highest concentration of K+ ions but this accounts for overall
maximum potassium ion secretion because of high turnover.
- Therefore maximum amount of potassium is secreted in saliva.
83. Iron absorption:
- ↑ by:
• Acids
• Ascorbic acid (Vit C)
• Amino acids containing SH group

Physiology
- ↓ by:
• Alkalies
• Phosphates
• Phytates (in maize, wheat)
• Tetracyclin
• Presence of other food in stomach
84. After meal rich in carbohydrate, insulin secretion is stimulated by:
GLP – 1> Gastric Inhibitory peptide > gastrin > CCK > secretin & gulcagon
85. Transit time in small intestine & colon
- The first part of a test meal reaches the caecum in about 4 hours, all of the undigested portions
have entered the colon in 8–9 hours.
- On average, the first remnants of the meal reach the hepatic flexure in 6 hours, the splenic
flexure in 9 hours & the pelvic colon in 12 hours.
- From the pelvic colon to the anus, transport in much slower.
- As much as 25% of the residue of a test meal still be in the rectum in 72 hours.
So, the transit time of colon is the longest.
86. Lignin is a dietary fibre that is neither digested nor fermented
Digestion/Hydrolysis by Digestion/ Fermentation

Type of fibre
V enzymes in small intestine by colonic bacteria
Soluble Pectin Not digested Fermented

@ PAG Alginates
Gums
Insoluble Hemicellulose Not digested Fermented

@HCL Cellulose
Lignin Not digested Not fermented

Hepat
ANATOMY
SYLLABUS
Liver, Gallbladder, Bile duct and Hepatoportal system: (p. 185)
Gross features, Applied anatomy,
Microscopic structure: (p. 190)
Liver and Gall bladder

Hepatobiliary Apparatus: (p. 191)
Parts, Gross anatomy, Development, Congenital anomalies of hepatobiliary system

Anat

Hepat
ANATOMY
LIVER Gross features [09, 10]

Past Questions: ♦ The liver is the largest gland of the body and
1. Mention different lobes of liver. Draw a neat consist of both (I) exocrine and (II) endocrine
labeled diagram to explain histological features parts.
of liver. (1 +4 = 5) [09 July] I. Exocrine part: Secrets bile, which is conveyed
2. List the vascular segments of liver. Draw a by biliary passages.
labeled diagram to describe its microscopic II. Endocrine part: Liberates glucose from
anatomy. (2 +3 =5) [08 Dec] glycogen, most of plasma protein except
3. Draw a labeled diagram to show the microscopic (immunoglobulin) and heparin.
structure of liver. Name two clinical conditions ♦ Highly vascular organ, reddish brown in colour,
related to this organ (5) [11 July] soft, solid and friable to the touch
4. Give shape, situation of the organ which secretes ♦ Shape: Wedge–shaped, with the broad base
bile. Name the surface and lobes. Name two directed to right.
organs related to its inferior surface. ♦ Situation: Occupies whole of right
(2 +2 +1 =5) [10, 08 July] hypochondrium, upper part of epigastrium and
5. a. Draw a labelled diagram to show the part of the left hypochondrium upto left lateral
histological structure of liver (no description plane.
required) (3) [06 Dec] ♦ Weight:
b. Mention the formation and termination of the In adult male → 1400gm to 1800 gm V
bile duct. (2) [06 Dec] In adult female → 1200 gm to 1400 gm
6. Give an account of the inferior (visceral) surface At birth → 150 gm
of the liver with a suitable labelled diagram. Parts
(5) [10 July, 04 Nov] a. Five surfaces
10.Describe briefly the course with relations of the I. Anterior surface
common bile duct. Add a note on its applied II. Posterior surface
anatomy. (4)[06 June] III. Superior surface
11.Write short notes on: (1+2+2=5) [03 Nov] IV. Inferior surface
a. Hepato-renal pouch of Morison V. Right surface
b. Lobes [O9]
b. Source of nutrition of liver
I. Anatomical right and left lobes.
c. Sphincters of oddi at the termination of bile
II. Physiological right and left lobes
duct.
c. Borders
12.Write short notes on:
I. Inferior border (Prominent border):
a. Intrahepatic circulation of blood (2) [06 June] - Separates inferior surface from anterior
and right lateral surface.
II. Posterior – Inferior border:
- Separates the inferior surface from
posterior surface.

Anat
III. Posterior – superior border: - Bare areas:

- Separates posterior surface from I. A triangular bare area: on the posterior
superior surface. surface of right lobe, limited by the upper and
d. Fissures: non peritoneal, 'H' shaped lower layers of coronary ligament and by the
I. Right limb of fissure: Includes groove for right triangular ligament.
IVC and fossa for Gallbladder. II. The groove for the IVC: On the posterior
II. Left limb of fissure: Includes fissures for surface of right lobe of liver.
ligamentum venosum and ligamentum III. The fossa for the Gall bladder: Lies on inferior
teres. surface of right lobe to the right of quadrate
lobe.
Relation:
IV. The coronary ligament
1. Peritoneal relation of liver and bare areas
V. The lesser omentum
Bare area of liver:
- The area of liver which is devoid of peritoneal VI. Portahepatis: Is false gate way.
covering are called bare areas
2. Visceral relation of liver: II. Posterior surface

I. Anterior surface - Triangular and middle part shows deep
- Triangular and slightly convex concavity for vertebral column.
- Possess bare area: Related to diaphragm and
- Related to: right suprarenal gland.
• Xiphoid process - Possess groove for IVC
• Anterior wall in median plane - Caudate lobe lies superior recess of this lesser
Sac, which is related to
• Diaphragm on each side
• Crura of diaphragm above aortic opening
• 6th – 10th costal cartilage on the right • Right inferior phrenic artery
side, 6th – 8th on left side. • Coeliac trunk

Morphology Morphology: Gross: White, Chalky Fat Necrosis

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Morphology Morphology: Gross: White, Chalky Fat Necrosis

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GIT

- Peritoneal cavity: serous, turbid, brown tinged • Tail (5%)

FAST TRACK BASIC SCIENCE MBBS -135-

SPECIAL POINTS FOR MCQs

-136- FAST TRACK BASIC SCIENCE MBBS

FAST TRACK BASIC SCIENCE MBBS -137-

48. Hour glass deformity is seen in peptic ulcer.

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FAST TRACK BASIC SCIENCE MBBS -139-

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THERAPY OF PEPTIC ULCER 3. Ulcer protectives:

Approach to treatment of PUD Acts by competitively blocking the binding of

FAST TRACK BASIC SCIENCE MBBS -141-

Uses: Adverse effects On long term

Ulcer protective Mechanism of action:

FAST TRACK BASIC SCIENCE MBBS -143-

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Neuroleptics 2. 5HT4 agonism:

- Acts through both dopaminergic and Note:

-146- FAST TRACK BASIC SCIENCE MBBS

from intestinal mucosa → Activation of vagus THERAPY OF DIARRHEA

FAST TRACK BASIC SCIENCE MBBS -147-

Non specific Anti diarrhoeal

-148- FAST TRACK BASIC SCIENCE MBBS

THERAPY OF CONSTIPATION: MOA: Lactulose in hepatic encephalopathy

• Caster oil ♦ Exercise

4. Osmotic purgatives: THERAPY OF WORM INFESTATION

FAST TRACK BASIC SCIENCE MBBS -149-

Drugs MOA Adverse Effects

Praziquantel Causes leakage of intracellular calcium from membrane - Tastes bitter

-150- FAST TRACK BASIC SCIENCE MBBS

FAST TRACK BASIC SCIENCE MBBS -151-

4. Anaerobic bacterial infections ♦ Metronidazole is almost completely absorbed

- Metrodinazole → extraluminal (mainly) 2. Type B (bizarre or idiosyncratic)

- Diloxanide furoate → intraluminal 3. Type C (Continued use, cumulative effect)

-152- FAST TRACK BASIC SCIENCE MBBS

Type A Mechanism Example

Type B Mechanism Example

Type C Mechanism Example

FAST TRACK BASIC SCIENCE MBBS -153-

SPECIAL POINTS FOR MCQs

-154- FAST TRACK BASIC SCIENCE MBBS

20. Prokinetic drug without D2 blockade is cisapride

FAST TRACK BASIC SCIENCE MBBS -155-

Prokinetic drugs MOA

1. Metoclopromide → D2 antagonism, 5HT3 antagonism, 5HT4 agonism

3. Cisapride → 5HT4 agonism mainly

4. Mosapride → 5HT4 agonism (major) 5HT3 Antagonism

5. Tegaserod → Selective 5HT4 Partial agonist

37. Cisapride is DOC in treatment of gastroparesis.

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FAST TRACK BASIC SCIENCE MBBS -157-

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FAST TRACK BASIC SCIENCE MBBS -159-

Sympathetic system Parasympthetic

Myenteric and auerbach plexuses in gut wall

Smooth muscle Secretory cells or Epithelial

Basal Electrical Rhythm & slow waves

Note: Mechanism of formation

FAST TRACK BASIC SCIENCE MBBS -161-

-162- FAST TRACK BASIC SCIENCE MBBS

• Events: 4. Describe how HCl is secreted by cells in the