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GIT Flashcards

1
Q

Enzyme present in saliva

A

Ptyalin

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2
Q

Defecation observed immediately after a meal in children is

A

Gastrocolic reflex

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3
Q

Digestion of proteins occur in

A

Dudodenum, jejunum

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4
Q

Functions of bile

A

*Digestion and absorption of fats
*bile pigments - major excretory products of bile
*bile salts acts as laxative
*Inhibits growth of cholerectic and cholagogue bacteria
*maintenance of pH
*lubricates chyme in intestine
* prevents gall stone formation

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5
Q

Steatorrheod

A

*Bulky , foul smelling, pale greasy stools
*FAT CONTENT INCREASED
*deficiency of pancreatic digestive enzymes affecting fat metabolism seen in chronic pancreatitis

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6
Q

Jaundice define

A

Raised levels of bilirubin
Yellow discoloration of skin and mucous membrane

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7
Q

Types and causes of jaundice

A

Hemolytic jaundice (pre-hepatic)
Hepatocellular jaundice (hepatic jaundice )
Obstructive jaundice (post-hepatic )

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8
Q

Causes of pre hepatic jaundice ( flowchart )

A

*Increased breakdown of RBCs
*Hemolytic disease of newborn
*hereditary spherocytosis
*malaria
*sickle cell anemia
*snake bite
*Mismatched blood transfusion

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9
Q

Symptoms and signs of hemolytic jaundice

A

*Unconjugated bilirubinemia
Hemolytic anemia
*Fecal stercobilinogen^( dark brown stools )
*urinary urobilinogen ^
*urine bilirubin normally absent
* vandenberg’s test - indirect positive
* liver function test is normal

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10
Q

Symptoms and signs of hepatocellular jaundice

A
  • conjugated , unconjugated bilirubinemia
    *fecal stercobilinogen v
    *Urinary urobilinogen v
    *Urine bilirubin present
    *liver function test impaired
  • vandenberg’s test biphasic ( direct and indirect positive)
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11
Q

Signs and symptoms of obstructive jaundice

A

*Conjugated bilirubinemia ^
* fecal stercobilinogen- absent (clay stools )
Urinary urobilinogen
*urine bilirubin increases ( dark urine )
*vandenberg’s test - positive
* normal liver func test
Impaired in later stages
*fecal fat content ^

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12
Q

Causes of hepatic jaundice

A

Liver cannot conjugate bilirubin efficiently
*infective ( bacteria / viral hepatitis)
*toxic liver damage
* cirrhosis

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13
Q

Cause of obstructive jaundice

A

Conjugated bilirubin cannot flow thro the biliary tract freely
*cholestasis
* biliary cirrhosis
* gall stones
* carcinoma head of pancreas

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14
Q

Enterohepatic circulation

A

(Diagram )
* recirculating of bile salts from the liver to the small intestine and back again

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15
Q

Advantages of enterohepatic circulation

A
  • limited pool of bile salts available for fat digestion& absorption, enterohepatic circulation is necessary
    *total circulating pool of bile salts 3.6gm
    *required bile salts during each meal 4-8gm
  • bile salts circulate twice during digestion of each meal
    *approx 6-8 times per day
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16
Q

Clinical significance of entero hepatic circulation

A

Conditions that interrupt entero hepatic circulation (ileal resection , Crohn’s disease )leads to malabsorption of fats

17
Q

Define peptic ulcer

A

Excoriated area of stomach or intestinal mucosa caused by the digestive action of gastric juice or upper small intestinal secretion .

18
Q

Where the ulcer frequently occur

A

Lesser curvature of the antra, end
Peptic ulcer in stomach +gastric ulcer
In duodenum- duodenal ulcer

19
Q

The auto digestion of the mucosa is prevented by .
Mucosal protective mechanism

A
  1. Mucosal barrier

2.bicarbonate secretion
3. Epithelial barrier
4.Trifoil peptides
5.PGE2

20
Q

What is PGE 2

A

Can help in the synthesis of mucus and formation of new mucosal cells . Of there is injury in the gastric mucosa , dead cells can be speed.y replaced

21
Q

Trifoil peptides in mucosal protective mechanism

A

TP in the mucosa of stomach are acid resistant and protect stomach

22
Q

Epithelial barrier in MPM

A

Intercellular tight junction provide barrier to back diffusion of H+

23
Q

Bicarbonate secretion in MPM

A

Between the mucus and epithelium some bicarbonate rich fluid is present .
Within lumen pH is low (2.5) , pepsin very active digest proteins easily .
Near epithelium bicarbonates present , increases pH , lesser activity of Pepsin.
This hco3- cannot ,I’ve towards lumen because of unstirred layer

24
Q

Why can’t Pepsin and other gastric glands come in contact with the musosal epithelium

A

Because mucus of the unstirred layer acts as a barrier

25
Q

What is mucus and stirred layer

A

Gastric mucosal epithelium covered by mucus .
Primarily thick insoluble variety and does not flow or move easily . This is called the stirred layer
Soluble mucus is also present

26
Q

Causes of peptic ulcer

A

1.Usual cause of peptic ulcer = imbalance between the rate of secretion of gastric juice and degree of protection offered by the *gastroduodenal mucosal barrier
*The neutralization of the gastric acid by bicarbonate
2. Helicobacter pylori breaks down mucous barrier
3. Long term use of nonsteroidal anti inflammatory drugs (NSAIDs) like aspirin ( decrease mucus and bicarbonate secretion, inhibit production of prostaglandins
4. Smoking , alcohol etc . Disrupt the mucosal barrier
5. Reflux of gastric content into the esophagus &
Duodenal content into the stomach
6.excess secretion of gastric juices due to
* increase parietal cell mass
*increased sensitivity for secretory stimuli
*zollinger - Ellison syndrome- seen in patients with gastrinomas (tumours secreting gastrin). These tumors in stomach , duodenum and mostly in pancreas .
Gastrin causes prolonged hyper secretion of acid and severe ulcers
7. Poor blood supply

27
Q

Differences between duodenal and gastric ulcer

A
28
Q

Complications of ulcer

A
  1. Perforations - burrows through all coats of the stomach —> gastric and duodenal lumen now communicate thro perforations with peritoneal cavity
  2. Hemorrhage from the ulcer
29
Q

Physiology of treatment of ulcers

A
  1. Antacids (Gelusil) neutralize the acid.
  2. Use of antibiotics along with other agents to kill infectious
    bacteria.
  3. Administration of an acid-suppressant drug such as cime-
    tidine, ranitidine (both block H2 histamine receptors on
    parietal cell), omeprazole (inhibits H+- K+ ATPase).
  4. NSAIDs induced ulcers can be treated by stopping the use of NSAIDs or by treatment with prostaglandin agonist
    misoprostol.
  5. Gastrinomas can be removed surgically.
  6. Vagectomy, partial gastrectomy. 7. Coating agents—sucralfate.
  7. Atropine—anticholinergic.
30
Q

Passes of gastric secretion and their regulation

A

Cephalic - before entry of food into the stomach
Taste , smell , thought, sight
20% total secretion
Under neural control , mediated by vagus nerve

Gastric - 70%
Of gastric secretion , occurs when food enters stomach
Mediated by neural and hormonal mech

a. Neural: Distension of stomach by food stimulates gastric juice secretion (through local myentric and vagovagal reflex). b. Chemical/Hormonal: Products of partial digestion stimu- late the secretion of gastrin. Gastrin enters the circulation
and stimulates gastric glands.

Intestinal (10%) -begins as the chyme begins to empty from the stomach into duodenum
Initiatly (during the early intestinal phase) the secretion is increased and later it is inhib- ited. This inhibition results from the following influences.
a. Enterogastric reflex: It is a reflex mechanism mediated through myentric nervous system as well as through extrinsic sympathetic system and vagus nerve. It is initiated by distension of small intestine in the presence of acids or protein breakdown products in the upper intestine and irritation of mucosa.
b. Hormonal mechanism: Presence of acid, fat, protein break down products, hypo-osmotic or hyperosmotic fluids and any irritating factors in the upper small intestine causes release of hormones like CCK, GIP, VIP and somatostatin which inhibit gastric secretion.

31
Q

Role of gastrin in chemical control of gastric secretion

A

1.Chemical regulation of secretion of gastric juice
2. GI hormone produced by G cells (pyloric glands )
3. ,most known powerful stimulantof HCl secretion
4. Presence of products of protein digestion in the stomach acts on G cells =release gastrin.
5. stimulates secretory activity of parietal cell and chief cells.

32
Q

The actions of gastrin in chemical regulation

A

a. Gastrin stimulates the secretion of histamine from ECL cells. Histamine stimulates HCl secretion and this is the principal way by which gastrin stimulates acid secretion.
b. Gastrin also stimulate HCl secretion by acting on the gastrin receptors in the parietal cell. This increases intra- cellular Ca2+.
c. To a lesser extent it stimulates chief cells to secrete pep- sin.

33
Q

What are chemical regulators of secretion of gastric juice

A
  1. Gastrin
  2. Histamine
  3. Somatostatin
  4. PGE2
  5. Low pH (<3)
34
Q

Steatorrhea in acute pancreatitis or after pancreatectomy

A
35
Q

Phases of deglutition

A
36
Q

Mechanism of HCl secretion by parietal cells

A
37
Q

Deglutition aponea

A
38
Q

Deglutition

A

Passage food from oral cavity to the stomach .

Systems (4 decks)

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