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Boards Final Review > GI > Flashcards

GI Flashcards

1
Q

Which amino acids are the most potent products of protein digestion that stimulate gastrin secretion?

A

Phenylalanine

Tryptophan

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2
Q

What is the cause of steatorrhea in Zollinger-Ellison syndrome?

A

Elevated gastrin levels —> increased H+ in the lumen of the stomach —> increased H+ in the lumen of the intestines —> elevated acid in the intestines inactivates pancreatic lipase (enzyme necessary for fat digestion) —> lack of fat digestion or absorption —> fat is excreted in the stool (steatorrhea)

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3
Q

Where is CCK secreted from?

A

I cells of the duodenum and jejunum in response to MONOGLYCERIDES AND FATTY ACIDS (not TAGs) and small peptides and AA [pretty much almost basic units]

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4
Q

What are the 5 actions of CCK?

A
  1. gallbladder contraction
  2. pancreatic enzyme secretion
  3. Bicarb secretion from pancreas
  4. exocrine pancreas and gallbladder growth (makes sense if the main actions of CCK are on the gallbladder and pancreas)
  5. inhibition of gastric emptying (slows gastric emptying time to allow time in the intestines for proper absorption)
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5
Q

What is the optimum pH for pancreatic lipase function?

A

pH b/t 6-8

enzymes are inactivated and denatured when the pH is less than 3, so as soon as the gastric juices enter the intestines, secretin and other hormones need to be released to increase pH

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6
Q

What is the only hormone to be secreted in response to all types of nutrients: glucose, amino acids, fatty acids?

A

GIP (glucose-dependent insulinotropic peptide) secreted by the K cells in the duodenum and jejunym

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7
Q

What is the composition of saliva?

A

high K+
high bicarb
low sodium
Hypotonic (compared to plasma)

  • *acinar cells secrete an isotonic solution
  • *ductal cells secrete K+ and bicarb and reabsorb Na+ and Cl- [Na+-H+ antiporter, Cl-bicarb antiporter, H+-K+ antiporter]

Higher saliva flow rates = more similar to acinar secretion
Slower saliva flow rates = more similar to ductal cell modification (more time!)

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8
Q

How does pancreatic juice flow rate effect electrolyte composition?

A

low flow rate: high Na+, high Cl-, low bicarb, low K+
high flow rate: high Na+, low Cl-, high bicarb, low K+
**this relationship is somewhat different compared to what you see in the saliva – higher the flow rate the more active the Cl- reabsorption and bicarb secretion exchanger works, the slower the flow rate the less active the exchanger is

acinar cells – mediated by CCK and Ach
ductal cells – mediated by secretin (wants high bicarb)

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9
Q

What are the primary and secondary bile acids?

A

Primary bile acids – cholic acid, chenodeoxycholic acid

Secondary bile acids – Lithocholic acid, deoxycholic acid

Although the intestinal bacteria produces secondary bile acids from primary bile acids, there are actually still a higher concentration of primary bile acids compared to secondary

[liver conjugates bile acids with glycine and taurine to produce bile acids increasing water solubility]

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10
Q

What is the rate limiting step of bile acid synthesis?

A

cholesterol 7a-hydroxylase

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11
Q

What transporters help with GI absorption of AA and dipeptides/tripeptides?

A

Na+-AA cotransporter

H+-dipeptide/tripeptide cotransporter

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12
Q

What are the difference b/t pancreatic lipase and phospholipase A2?

A

Pancreatic lipase (requires assistance from colipase by preventing inactivation by bile salts) - hydrolyzes TAG molecules to one molecule of monoglyceride and two molecules of fatty acid.

Phospholipase A2 hydrolyzes phospholipids to lysolecithin and fatty acids.

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13
Q

What are aphthous ulcers? What syndrome is it associated with?

A

Painful, superficial ulcerations on the oral mucosa commonly due to stress. It is characterized by a grayish base (granulation tissue) surrounded by erythema.

These ulcers are commonly associated with Behcet syndrome where you have recurrent aphthous ulcers PLUS genital ulcers and uveitis. It is though that this is due to IMMUNE COMPLEX VASCULITIS involving small vessels.

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14
Q

What type of meningitis is seen with the mumps virus?

A

Aseptic meningitis

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15
Q

Why is there a high risk of reoccurrence of pleomorphic adenomas?

A

Irregular margins within the parotid gland, so some surgeons may not resect the entire tumor allowing it to grow back.

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16
Q

Describe the histology of a Warthin Tumor.

A

Cystic tumor with lymph node tissue (abundant lymphocytes and germinal centers).

**2nd most common benign tumor of the parotid gland

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17
Q

Describe Zenker diverticulum.

A

False diverticulum (mucosal outpouching) created by a weakening of the muscular wall b/t the esophagus and pharynx

18
Q

What is the most common cause of death in a pt with cirrhosis?

A

Rupture of esophageal varices

19
Q

What GI pathology should you think about with adult-onset asthma?

A

GERD – shooting of acid into esophagus where it can irritate it leading to a cough

20
Q

What lymph nodes drain the upper, middle and lower 1/3 of the esophagus?

A

Upper 1/3 – cervical

Middle 1/3 – mediastinal or tracheobronchial nodes

Lower 1/3 – celiac and gastric nodes

21
Q

What is the difference b/t the defect that causes omphalocele and gastroschisis?

A

Omphalocele – failure of herniated intestines to return to the body cavity during development

Gastroschisis – congenital malformation of anterior abdominal wall leading to exposure of abdominal contents

22
Q

When does pyloric stenosis present?

A

About 2 weeks after birth – the baby IS NOT born with pyloric stenosis, rather it takes some time for the fibrosis to develop which is why there is a delayed onset compared to when the child is born

23
Q

What is the pathogenesis of chronic autoimmune gastritis of gastric parietal cells

A

Type IV HSN mediated by T cells

*also associated with antibodies against parietal cells and/or intrinsic factor - which can be useful for diagnosis

There will be atrophy of the mucosa due to cell mediated damage, achlorhydria due to destruction of parietal cells, elevated gastrin levels in antrum due to G-cell hyperplasia (lack of H+ negative feedback).

Chronic inflammation within the stomach induces intestinal metaplasia – gastric adenocarcinoma.

24
Q

Where is the most common location of H. pylori?

A

Lesser curvature of the Antrum [think pyloric antrum, so it is right before the pyloric sphincter]

**increased risk of ulceration, gastric adenocarcinoma (especially at the lesser curvature of the antrum), and MALT lymphoma [germinal center formation from chronic inflammation]

25
Q

Where is the most common site of duodenal ulcers? What are complications are posterior ulcers?

A

Anterior wall - most common site

Posterior wall - watch out for rupture of gastroduodenal artery or acute pancreatitis

26
Q

Describe the diffuse type of gastric cancer.

A

Signet ring cells that diffusely infiltrate the gastric wall leading to cancer as well as a reaction to the cancer (Desmoplasia). Desmoplasia (fibrosis and blood cells) results in thickening of the stomach wall (linitis plastica).

27
Q

What are the two types of stomach cancer?

A

Intestinal type - Ulcer

Diffuse type - thickening of stomach wall and presents with signet ring cells [more commonly presents with early satiety]

28
Q

What two skin manifestations are seen with gastric cancer?

A
  1. Acanthosis nigricans

2. Leser-Trelat sign [seborrehic keratosis all over the body]

29
Q

What type of gastric cancer presents with Sister Mary Joseph nodules?

A

Intestinal type – Periumbilical region of LN

30
Q

Where is the most common location of a volvulus in the elderly vs young adult?

A

Elderly - sigmoid colon

Young adult - cecum

31
Q

What is the primary cause of the leading edge of intussusception in children vs adults?

A

Children - lymphoid hyperplasia at the terminal ileum (ex. peyers patch hyperplasia in rotavirus)

Adults - tumor

32
Q

What is the pathology behind celiac disease?

A

Immune-mediated damage of small bowel villi due to gluten exposure.

Gliadan (most pathogenic component of gluten) is deaminated by tTG. The deaminated gliadin is presented by APCs via MHC II. This leads to activation of helper T cells which mediate tissue damage.

IgA antibodies against endomysium, tTG, or gliadin.

**some celiac pts are IgA deficient, so look for IgG antibodies

33
Q

Where does celiac disease most frequently destroy?

A

Duodenum

**This is different from tropical sprue where the jejunum and ileum is where the damage is most commonly located

34
Q

What AE are seen in refractory celiac disease despite good dietary control?

A

Increased risk of small bowel carcinoma and T-CELL LYMPHOMA (EATL)

35
Q

Where is the classic site of involvement of Whipple disease?

A

Lamina propria of the small bowel

36
Q

What is the histological hallmark of ulcerative colitis?

A

crypt abscess with neutrophils

37
Q

What is the result of high stress in the right and left colon?

A

High stress in left colon - diverticula

High stress in right colon - angiodysplasia

**both present with hematochezia

38
Q

What is a juvenile polyp?

A

Sporadic HAMARTOMATOUS (benign) polyp that arises in children less than 5 yo. It is generally a solitary rectal polyp that may prolapse and bleed.

If the pt has multiple juvenile polyps this is juvenile polyposis syndrome – the polyps will be in the stomach and colon and there is an increased risk of progression to carcinoma.

39
Q

What are the two types of necrosis seen in pancreatitis?

A
  1. liquefactive necrosis of the pancreas itself occurs 1st as the digestive enzymes are activated
  2. fat necrosis of the adipose tissue surrounding pancreas (peripancreatic fat) – leads to saponification uses up calcium possibly resulting in hypocalcemia (bad prognosis b/c it would mean there is a massive amount of necrosis)
40
Q

What is the cause pf pancreatic abscess?

A

Complication of pancreatitis, most commonly due to E. coli, presenting with abdominal pain, high fever and persistent elevated amylase levels.

41
Q

What are the two major risk factors of pancreatic carcinoma?

A

Smoking and chronic pancreatitis

**cancer arising from pancreatic ducts (NOT acini) and commonly seen in the elderly

42
Q

Thin, elderly, female, who all of a sudden presents with diabetes??

A

THINK pancreatic carcinoma

Boards Final Review (7 decks)

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