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My Notes > GI > Flashcards

GI Flashcards

1
Q

How can you use BUN/Cr ratio to help differentiate b/w upper and lower GI bleed?

A

It may be elevated in upper GI bleed because proteins in blood digested and reabsorbed → elevates BUN

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2
Q

What are angiodysplasias?

A

They are like AVMs that occur with aortic stenosis or ESRD (or heriditary hemorrhagic telangiectasia?). Can cause bleeding in bowel esp. on blood thinners.

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3
Q

What is the main risk with an annular pancreas?

A

duodenal obstruction

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4
Q

What are the 2 most common causes of acute pancreatitis?

A

Alcohol (b/c it creates a contraction at sphincter of otti) Gallstones (obstructs ampula of vader)
decreased drainage → ↑ risk for premature activation of enzymes

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5
Q

What does the pancreatic ventral bud develop into?

A 
uncinate process (portion of the head)
main pancreatic duct (of Wirsung)
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6
Q

Where is a true diverticulum usually located in the esophagus? What is the cause?

A

mid-portion: mediastinal lymphadenitis (TB, fungal infections) → scaring and traction of the esophagus → outpouching

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7
Q

What causes Mallory Weiss syndrome?

A

↑ intraluminal P in the stomach during vomiting, retching (dry heaving), hiccups, repeated abdominal trauma → longitudinal tears at GE junction

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8
Q

What are two main manifestations of malrotation of the midgut?

A
  1. adhesion bands → obstruction

2. midgut volvulus → ischemia

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9
Q

What 2 patient populations get Mallory Weiss syndrome?

A
  1. alcoholics

2. bulimics

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10
Q

An absorption test with what substance can be used to distinguish b/w pancreatic and mucosal etiology of malabsorption?

A

D-xylose

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11
Q

What 3 important structures lie posteriorly to the duodenal bulb? Which structure lies inferiorly?

A
  1. gastroduodenal artery
  2. common biliary duct
  3. portal vein
    The head of the pancreas lies inferiorly
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12
Q

Which parts of the duodenum and pancreas does the inferior pancreaticoduodenal artery supply?

A

lower duodenum and head of the pancreas

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13
Q

What does the gastroduodenal artery supply?

A

the pylorus and the proximal duodenum

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14
Q

How does the urease breath test work? What might lead to a false negative?

A
  1. pt consumes 13C labeled urea
  2. H. pylori has urease which breaks the urea to CO2 and ammonia
  3. CO2 is absorbed into blood
  4. about 30 min later breath is monitored for 13C labeled CO2
    FN: antibiotic or PPI use during 2-4 wks prior
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15
Q

Where is vitamin C absorbed? Actively or passively?

A

distal small bowel; active transport

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16
Q

Where is pyridoxine absorbed? Actively or passively?

A

Jejunum and ileum - passive diffusion

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17
Q

Where are biotin and pantothenic acid absorbed? What is the mechanism?

A

small and large intestine via Na+-dependent multivitamin transporter

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18
Q

Malabsorption of which vitamins is associated with gastrojejunostomy?

A

Iron, B12, folate, fat-soluble vitamins (especially D), Ca2+

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19
Q

What are the GI symptoms of lead poisoning?

A

“Lead colic” (colicky abdominal pain), constipation

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20
Q

What are the GI symptoms of iron poisoning (in 4 stages)?

A

stage I: nausea, diarrhea, abdominal pain
stage II: GI symptoms improve
stage III: metabolic acidosis, hepatic dysfunction, hypoglycemia
stage IV: scarring of the recovering GI tract

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21
Q

What are the 3 causes of lactose intolerance, and which is most common?

A
  1. Congenital lactase deficiency - very rare
  2. Acquired lactase deficiency - common (80-95% of Native Americans, 90% of some Asians, 60-75% of Africans/Af. Ams, 50% of Hispanics)
  3. Lactose malabsorption secondary to bacterial overgrowth or GI mucosal injury
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22
Q

What is the mode of inheritance of congenital lactase deficiency, what gene is affected, and how does this condition present?

A
  1. Autosomal recessive
  2. a gene near, but separate from the lactase gene
  3. explosive, watery diarrhea
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23
Q

When does acquired lactase deficiency usually present?

A

Run out of lactase by mid-childhood

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24
Q

What does lactase do?

A

breaks the disaccharide lactose into glucose and galactose

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25
Q

Why is there diarrhea in lactose deficiency?

A

undigested lactose → osmotic diarrhea

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26
Q

How do you test for lactose intolerance?

A
  1. Give 50 g lactose
  2. measure blood glucose at 0, 60, and 120 min
  3. if blood glucose increase is < 20 mg/dL and symptoms (bloating, pain, vomiting, flatulence, diarrhea, etc..) present → lactose intolerant
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27
Q

What happens to breath H+ content in lactose deficient patients?

A

↑ by more than 20 ppm (measured by gas chromatography)

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28
Q

Is D-xylose absorption affected in lactose intolerance?

A

no - think of conditions that lead to more general malabsorption like celiac sprue (remember, it’s not affected by pancreatic insufficiency either)

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29
Q

What muscle between the pharynx and esophagus pushes food downward into the esophagus?

A

cricopharyngeus

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30
Q

What are the symptoms of diffuse esophageal spasm (DES)? How would you test for it?

A

severe non-cardiac chest pain (can mimic angina pectoralis); uncoordinated contractions can been seen on esophageal manometry of the middle and lower esophagus; could also see “corkscrew” esophagus on barium esophagogram due to disorganized simultaneous contractions

31
Q

What vitamin must be supplemented lifelong in patients with gastrectomy?

A

B12 (due to IF deficiency)

32
Q

What are the two actions of leptin? Where does it act?

A

Acts in the arcuate nucleus of the hypothalamus to:

  1. inhibit neuropeptide YY production→ ↓ appetite
  2. simulate production of α-MSH → ↑ satiety
33
Q

How does leptin relate to obesity?

A

↑ fat stores → ↑ leptin release → desensitization to effects (leptin resistance) → ↑ appetite and ↓ satiety

34
Q

What is the most common location of intussusception? Which population most often gets this condition? How is it diagnosed and treated?

A

Iliocolic junction; children 2 y.o. look for a lead point); barium enema is diagnostic and may be therapeutic w/ surgery as a backup

35
Q

Chronic gastritis with antral sparring suggests what etiology?

A

Autoimmune (antibodies to parietal cells)

36
Q

What does antral-predominant gastritis suggest?

A

H. pylori infection

37
Q

What type of gastric cancer has signet ring cells?

A

Diffuse gastric adenocarcinoma

38
Q

What tumor is the result of gastric adenoma metastasizing to the ovaries bilaterally? What characterizes it histologically?

A

Krukenberg tumor - signet ring cells and abundant mucus

39
Q

What gives a pancreatic pseudocyst its name?

A

The walls aren’t lined by epithelium like other cysts, they are lined by f granulation tissue that result from enzyme-induced inflammation of surrounding tissue. The walls become fibrotic 4-6 wks after the episode of acute pancreatitis.

40
Q

What kind of polyp is considered precancerous? What other kinds are there?

A

Adenomatous = precancerous, especially if villous

Other types: hyperplastic, juvenile/lymphoid, hamartomatous, inflammatory

41
Q

What is the pathophys of appendicitis?

A

appendix obstructed (most commonly by fecalith) → mucus retention → distention of appendicular wall → impaired venous outflow → hypoxia, ischemia and bacterial invasion → inflammation/edema → further distention → necrosis (→ inflammatory fluid and bacteria spill in to peritoneum → peritonitis)

42
Q

Which opioids can be used in low doses as antidiarrheal drugs?

A

loperamide and diphenoxylate (combined with atropine to prevent addiction = lomotil)

43
Q

What is the most severe complication of ulcerative colitis?

A

toxic megacolon

44
Q

Which two structures make up the lesser omentum?

A 
hepatoduodenal ligament (spans the first part of the duodenum)
hepatogastric ligament (runs along the entire lesser curvature of the stomach
45
Q

What structure connects the liver to the anterior body wall? What does it contain?

A

the falciform ligament, contains the round ligament (aka ligamentum teres hepatis; derivative of the fetal umbilical vein); derived from ventral mesentery

46
Q

What ligament stretches from the greater curvature of the stomach to the transverse colon? What structures would you divide this ligament to access?

A

gastrocolic ligament; anterior pancreas and posterior wall of stomach

47
Q

What does the splenorenal ligament connect? What structures does it contain?

A

left kidney and spleen; contains the splenic vessels and tail of the pancreas

48
Q

What cells are seen on histology in Whipple’s disease?

A

distended macrophages in the intestinal lamina propria

49
Q

What cells are seen on histology in ulcerative colitis?

A

collections of neutrophils within the crypt lumina

50
Q

What disease is characterized by intestinal inflammation with scattered noncaseating granulomas?

A

Crohn disease

51
Q

In pancreas divusum, in which week do the dorsal and ventral buds fail to fuse? What papilla would each duct drain into?

A 
dominant dorsal duct (of Santorini; aka accessory duct) → minor papilla
ventral duct (of Wirsung) → major papilla
52
Q

What do you see histologically in HSV-1 ulcers of esophagitis? How would this differ from CMV ulcers histologically?

A

Eosinophilic intranuclear inclusions (Cowdry type A) in multinuclear squamous cells at the margins of ulcers; CMV would have both intranuclear and cytoplasmic inclusions

53
Q

Which of the 3 causes of esophagitis is most common?

A

candida albicans (the other two causes are HSV-1 and CMV)

54
Q

What is another name for ectopy?

A

heterotopy

55
Q

Where is a Meckel diverticulum usually located? What is the most common type of heterotopic tissue found here and why is this important?

A

connected to the ileum 2 feet proximal to the IC junction; ectopic gastric tissue is usually found here → produces acid → ulceration of nearby tissue

56
Q

What lab values can be used to indicate acute pancreatitis and the severity?

A
  1. ↑ amylase (also ↑ if salivary gland damage)
  2. ↑ lipase (more specific to pancreas)
  3. degree of hypocalcemia indicates severity (fat necrosis binds calcium)
  4. degree of hyperglycemia indicates severity (destruction of acinar cells)
57
Q

How do you perform a direct tissue diagnosis of H. pylori?

A

Rapid urease test (instead of time-intensive culture):

  1. take gastric biopsy
  2. place it in a urea containing solution with a pH indicator (phenol red)
  3. urease will break down urea into ammonia (NH3, weak base) and CO2 → pH ↑ → turns phenol red indicator pink
  4. give 24 hours before ruling negative (but usually color change in 30 min)
58
Q

Describe the surrounding structures around the 4 parts of the duodenum:

A

1st part - horizontal at L1 (1 &1)
2nd part - wraps around head of pancreas, where ampula of Vater empties
3rd part - horizontal at L3 (3&3) - courses over abdominal aorta and IVC; close to uncinate process, and superior mesenteric vessels
4th part - ascends to the left of L2/L3 and turns in to the jejunum at the ligament of Treitz;

59
Q

What causes Hirschprung disease?

A

mutation in RET gene → failure of neural crest cells to migrate to intestinal wall → no ganglion cells of the Auerbach and Meissner plexuses → narrowed rectum (always involved b/c the cells migrate caudally) → megacolon

60
Q

What causes Hirschprung disease?

A

mutation in RET gene → failure of neural crest cells to migrate to intestinal wall → no ganglion cells of the Auerbach and Meissner plexuses → narrowed rectum (always involved b/c the cells migrate caudally) → megacolon

61
Q

What is the string sign on x-ray in Chron’s?

A

wall thickening → narrowing of lumen → thin string of contrast gets through affected area of gut

62
Q

What part of the GI tract can Chron’s disease affect?

A

any part from mouth → anus

63
Q

What would be the GI manifestation of abetalipoproteinemia?

A

lipids accumulate in enterocytes → foamy cytoplasm; steatorrhea → deficiency of fat soluble vitamins

64
Q

What would be the GI manifestation of abetalipoproteinemia?

A

lipids accumulate in enterocytes → foamy cytoplasm

65
Q

How might asprin ↓ incidence of polyps?

A

inhibition of COX-2 which has been implicated in some polyp formation

66
Q

What happens when conjugated billirubin builds up in the blood? How about unconjugated bilirubin?

A

conjugated is water soluble and excreted in urine; unconjugated binds tightly to albumin so not excreted and builds up in tissues including the brain → kernicterus (e.g. in Crigler Najjar syndrome in which UDP glururonosyl transferase is deficient)

67
Q

What test is necessary for a definitive diagnosis of acute calculous cholecystitis? Why isn’t ultrasound visualization of gallstones sufficient?

A

a HIDA scan (Hepatobiliary Iminodiacetic Acid; aka radionucleotide biliary scan) - this visualizes obstruction as absence of gallbladder due to obstruction preventing contrast entry; ultrasound can show gallstones, but lots of people have them and don’t have disease (note: more specific ultrasounds signs include gallbladder wall thickening, pericholecystic fluid, and positive sonographic Murphy sign)

68
Q

Distinguish b/w risk factors for the two main types of gallstones:

A 
cholesterol stones: ♀ , fat, fertile, 40
pigment stones (black): chronic extravascular hemolysis (sickle cell, β thalassemia, hereditary spherocytosis)
69
Q

What is a precipitate of unconjugated billirubin called? Are these visible on x-ray?

A

calcium bilirubinate; yes

70
Q

What GI disease can cause Parkinson-like symptoms, ataxia, slurred speech and liver damage? What is the gold standard for diagnosis, and the more common method?

A

Wilson’s; gold standard = liver biopsy w/ copper level > 250 mcg/gram dry weight; more common method: low serum ceruplasmin (< 20 mg/dL) + ↑ copper excretion or Kayser-Fleischer rings

71
Q

Why does aldolase B deficiency cause hypoglycemia following fructose ingestion?

A

phosphate trapping in F-6-P

72
Q

Distinguish between serum albumin and PT time as indicators of liver damage

A

serum albumin - half life of 20 days, so cannot be used to indicate acute injury, unlike PT time

73
Q

What is a test that can be used to detect the presence of gastric mucosa? (e.g. to detect a Meckel diverticulum)

A

99mmTc-pertechnetate scan

My Notes (23 decks)

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