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USMLE Step 1 > Gastroenterology > Flashcards

Gastroenterology Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the embryology defect in duodenal atresia?

A

failure to recanalize, double bubble on Xray

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2
Q

What is the embryological defect for jejunal/ileal atresia?

A

disruption of the mesenteric vessels

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3
Q

what is the metabolic abnormality for pyloric stenosis?

A

hypokalemic, hypochloremic metabolic alkalosis from vomiting HCl

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4
Q

How does the pancreas develop?

A

from the foregut. ventral buds-uncinate process and main pancreatic duct. Dorsal bud -body, tail,isthmus and accessory duct. both dorsal and ventral contribute to the head
annular pancreas-when it wraps around duodenum (abnormal rotation of ventral bud)
pancreatic divisum-when ventral and dorsal don’t fuse at 8 weeks

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5
Q

What type of cells are in the esophagus?

A

nonkeratinized stratified squamous epithelium

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6
Q

what are peyer patches and where are they?

A

ileum-lymphoid aggregates in lamina propria and submucosa

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7
Q

where do posterior duodenal ulcers perforate?

A

gastroduodenal artery leading to potential hemorrhage

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8
Q

Are internal hemorrhoids painful?

A

No-visceral innervation (above pectinate line). Below the pectinate line are external hemorrhoids- painful because somatic innervation (inferior rectal branch of the pudenal nerve)

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9
Q

What is Courvoisier sign?

A

enlarged gallbladder and painless jaundice

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10
Q

what is the difference between a direct and indirect inguinal hernia?

A

Direct-directly through parietal peritoneum (through hesselbach triangle) external inguinal ring only and medical to the inferior epigastric vessels. Lateral to rectus abominis (old)
Indirect- goes through external and internal inguinal ring because of patent processus vaginalis, follows testes into scrotum and lateral to inferior epigastric vessels (young)

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11
Q

what is a femoral hernia?

A

below inguinal ligament, through femoral canal (more common in females)

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12
Q

what are the borders of hesselbachs triangle?

A

inguinal ligament on the bottom, lateral is the inferior epigastric vessels and slope medial is rectus abdominis

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13
Q

What does secretin do?

A

decreases acid, increases bile secretion and increases bicarb so that pancreatic enz can work (inc by fatty acids in the duodenum)

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14
Q

What does GIP do?

A

glucose dependent insulinotropic peptide (glucose inhibitory peptide- decreases acid and increases insulin

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15
Q

what does vasoactive intestinal peptide do?

A

increases intestinal water and electrolyte secretion- VIPoma watery diarrhea, hypokalemia and achlorhydria

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16
Q

What does pepsin do and where is it secreted from?

A

chief cells in the stomach- digests protein

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17
Q

What are zymogens?

A

proenzymes of proteases (proteases are for protein digestion)

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18
Q

what are the monosaccharides and how are they absorbed?

A

by enterocytes- glucose, galactose and fructose, glucose and galactose are taken up by SGLT1 and fructose is taken up by facilitated diffusion through GLUT5. All tyransported to blood by GLUT2

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19
Q

What is the most common salivary gland tumour? whats the most common malignant tumour?

A 
pleomorphic adenoma (chondromyxoid stroma) and epithelium (benign mixed tumour)
malignant-mucoepidermoid carcinoma-mucinous and squamous components
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20
Q

whats a warthrin tumour

A

salivary gland tumour in smokers (papillary cystadeoma lymphomatosum)- benign cystic tumour with germinal centers

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21
Q

What is achalasia?

A

failure of relaxation of LES (no auerbach plexus in muscosa externa) so no postganglionic inhib neurons (no NO or VIP) so you get progressive dysphagia to liquids and solids, birds beak on X ray because dilation of esophagus then stenosis

22
Q

What is the difference between HSV and CMV esophagitis?

A

HSV1 is punched out lesions CMV is linear lesions

23
Q

What can cause pill esophagitis?

A

bisphosphonates, NSAIDS, tetracycline, iron and potassium chloride

24
Q

Where is a Mallory Weiss tear and what is the thickness?

A

partial thickness mucosal tear secondary to vomiting at the GE junction

25
Q

What is Plummer-Vinson syndrome?

A

dysphagia, iron deficiency, anemia and esophageal webs, can have glossitis, high risk of esophageal squamous cell carcinoma

26
Q

What is the pathology change in Barretts esophagus?

A

nonkeratinized squamous cell epithelium to intestinal (nonciliated columnar cells with goblet cells)- risk of esophageal adenocarcinoma

27
Q

H pylori can give you what type of lymphoma?

A

MALT

28
Q

What is Virchows node?

A

L supraclavicular related to mets in stomach

29
Q

What is the difference in symptoms between a gastric ulcer and duodenal ulcer?

A

gastric can have pain with meals, but duodenal often improves with meals
duodenal- 90% H pylori, can be inc acid or decreased mucosal protection, Zollinger-Ellison association, generally benign in terms of cancer risk, hypertrophy of brunner gland

30
Q

What kind of diarrhea do you see with lactase deficiency?

A

osmotic with low stool ph because colonic bacteria ferment the lactose. Should have normal villi though

31
Q

what happens in pancreatic insufficiency?

A

can’t absorb fat soluble vitamins adeK and b12

32
Q

what is the microscopic morphology of crohns?

A

noncauseating granulomas with lymphoid appregates. Th1 mediated

33
Q

What is the major difference between Zenkers diverticulum and meckels?

A

z= false

m-true

34
Q

what is malrotation?

A

anomaly of midgut rotation, you get small bowel clumped on right side with ladd fibrous bands between liver and colon

35
Q

What is a finding of colonic ischemia on imaging?

A

thumbprint sign due to mucosal edema and hemorrhage

36
Q

What is Lynch syndrome?

A

hereditary nonpolyposis colorectal cancer (HNPCC)- AD (mutation in DNA mismatch repair genes) , can get ovarian, endometrial and skin cancers

37
Q

Which marker is used for colorectal cancer monitoring, but not screening?

A

CEA

38
Q

Which enzyme is higher in alcoholic liver disease?

A

AST>ALT

39
Q

What is Reye syndrome?

A

hepatic encephalopathy in children caused by aspirin in viral infection (VZV, influenza), aspirin metabolites decrease beta oxidation of mitochondrial enz and you get hypoglycemia, steatosis SHINE-steatosis, hypoglycemina, infection, not awak (coma) and encephalopathy

40
Q

What are mallory bodies?

A

seen in hepatic cirrhosis- intracytoplasmic inclusions of eosinophils with damaged keratin filaments

41
Q

what causes nutmeg liver?

A

mottled appearance- budd chiari- obstruction of hepatic veins (hypercoagulable states)

42
Q

what do you see in liver of alpha 1 antitrypsin deficiency?

A

PAS + globules

-young people with liver damage and dyspnea (inc elastase in lungs so you get decrease elastin and panacinar emphysema)

43
Q

what is a gallstone ileus?

A

fistula between gallbladder and GI tract so you get gallstone causing GI obstruction, can see air in biliary tree (pneumobilia)

44
Q

What is Charcot’s triad for acute ascending cholangitis?

A

jaundice, fever and RUQ pain

45
Q

what are the antacids?

A

aluminum hydroxide
calcium carbonate
magnesium hydroxide

46
Q

how does misoprostol work?

A

prostaglandin analog, builds up mucosal layer, decreases acid secretion

47
Q

How does sulfasalazine work?

A

antiinflammatory and antibacterial in the colon

48
Q

How does loperamide work?

A

agonist of u opoid receptors, slows gut motility

49
Q

how does ondansetron work?

A

5HT3 antagonist, dec vagal stim

50
Q

how does metoclopramide work?

A

D2 receptor antagonist, increases gut motility. Can have parkinsonian effects, tardive dyskinesia

51
Q

how does orlisat work?

A

inhibits gastric and pancreatic lipase, can’t break down dietary fats

USMLE Step 1 (20 decks)

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