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*USMLE* > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

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USMLE® Step 1 flashcards
1
Q

Pancreatic adenocarcinoma

Risk factors (3) + genetic predispositions (4)

A

Risks:
age >65
SMOKING
chronic pancreatitis

Genetic: 
hereditary pancreatitis
Peutz-Jeghers
MEN1
HNPCC (Lynch)
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2
Q

Pancreatic adenocarcinoma

s/s (lesion location-based)
paraneoplastic sign

A

weight loss, anorexia
epigastric/back pain (tail tumors > splanchnic plexus)
painless obstructive jaundice (head tumors > Courvoisier)
hepatomegaly / ascites in metastases

Migratory Thrombophlebitis (Trousseau sign)
maybe due to procoagulant factors from tumor
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3
Q

True Diverticula

what are they, examples, other characteristics of examples

A

contain ALL 3 layers of gut wall (mucosa/submucosa, muscularis and serosa)

embryological abnormalities such as:
CONGENITAL COLONIC DIVERTICULA (rare, single large lesion)
MECKEL DIVERTICULUM (heterotopic gastric or pancreatic mucosa; may bleed; located in SI not colon; pain nausea and vomiting in early childhood)

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4
Q

False Diverticula

what makes them “false”, cause + examples

A

only mucosa + submucosa herniate (NO MUSCULARIS) through areas of focal weakness in muscularis

exaggerated contractions in certain areas of colonic SM

ZENKER DIVERTICULUM - upper esophagus

DIVERTICULOSIS - sigmoid colon in pt over 60; painless hematochezia (vasa recta disruption); inflammation > LLQ pain, low fever, bowel habit change

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5
Q

Abetalipoproteinemia

genetic defect? presentation?

A

AR loss-of-function in MTP (microsomal triglyceride transfer protein) chaperone for ApoB folding and lipid loading onto chylos and VLDL

presents in first year with malabsorption sx

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6
Q

Abetalipoproteinemia

histo? labs? deficiencies?

A

histo - normal SI architecture with foamy/clear enterocytes at tips of villi due to lipid accumulation

labs - LOW triglycerides + cholesterol; absent chylomicrons, VLDL and apoB

deficiencies in VITAMIN E and essential fatty acids > acanthocyte RBCs, progressive ataxia and retinitis pigmentosa (other lipid-soluble vitamin defic. possible)

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7
Q

acute appendicitis

peak incidence? underlying cause?

A

all ages, but peaks at 6-10 years old

LUMINAL OBSTRUCTION - mostly fecaliths, sometimes lymph follicles, FBs, nematodes or carcinoids

retained mucus > wall distension > impaired venous outflow > ischemia > bacterial invasion (may rupture + cause peritonitis)

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8
Q

Pyloric Stenosis

epidem? presentation? tx?

A

mostly MALE INFANTS

recurrent projectile NON-BILIOUS vomiting with visible peristalsis and an olive-sized mass in distal stomach/pyloric area (hypertrophy of muscularis mucosae)

surgical splitting of muscle for tx

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9
Q

Zollinger-Ellison syndrome

s/s? differential dx?

A

gastrinoma in SI or pancreas; often malignant

cause parietal cell hyperplasia > peptic ulcer, heartburn and diarrhea (HCl impairs enterocytes)

ulcers are found in DISTAL DUODENUM; gastric rugae are thickened

  • “SECRETIN test” - normally increases HCO3 and INHIBITS GASTRIN release from G cells; paradoxically INCREASES GASTRINOMA GASTRIN release (abnormal adenylate cyclase activation)
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10
Q

3 yr old with abd pain, rectal bleeding. Blind pouch from ileum to umbilicus via fibrous band.

What is it? How does it form?

Its layers?

Rule of 2s?

A

Meckel’s diverticulum

failed obliteration of omphalomesenteric / vitelline duct
true diverticulum

all layers (mucosa, sub-, musc- and serosa) (ectopic gastric mucosa / pancreatic tissue common inside –> HCl –> bleeds)

2% population; 2 ft from IC valve; 2 inches long; 2% symptomtic; 2:1 male

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11
Q

2 types of gastric adenocarcinoma + general characteristics

A
  1. SIGNET RING CARCINOMA - cells don’t form glands; abundant mucin droplets marginalize nucleus (“signet ring” look); ILL-DEFINED, DIFFUSE wall involvement via E-CADHERIN LOSS; cause LINITIS PLASTICA

2 INTESTINAL-TYPE ADC - resemble colon cancers > glands of columnar/cuboidal cells; nodular, polypoid, WELL-DEFINED and RAPIDLY EXPAND into lumen; often ulcerate + bleed

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12
Q

2 sites of gastric adc metastases

A

Virchow node - left supraclavicular

Sister Mary Joseph nodule - periumbilical nodes

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13
Q

Menetrier disease

histo + functional changes

A

rugal hypertrophy with PARIETAL CELL ATROPHY

decreased acid secretion

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14
Q

Ulcerative Colitis biopsy

A

diffuse inflammatory infiltrates with NEUTROPHILIC MICROABSCESSES in crypts

(intermittent bloody d and abd. pain)

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15
Q

Whipple disease biopsy

A

distended macrophages in intestinal lamina propria

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16
Q

GI MALT lymphoma biopsy

A

ATYPICAL LYMPHOCYTES in the lamina propria

assoc. with H. pylori in stomach

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17
Q

Mesenteric Adenitis

age? cause? s/s?

A

mostly age 5-14; Yersinia enterocolitica (dog poop)

fever, RLQ pain, nausea/vomiting

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18
Q

Colitis-associated vs. sporadic colorectal cancer

Age? Origin of dysplasia?
Location? # of tumors?
Histo? Mutations?

A

COLITIS-ASSOCIATED:
younger (40-55)
flat, nonpolypoid lesions
proximal > distal (especially in Crohn’s)
multifocal
mucinous / signet ring cell; poorer differentiation
early p53, late APC mutation

SPORADIC:
older (>60)
polypoid lesions
distal > proximal
single lesion
rarely mucinous; better differentiation
early APC, late p53 mutation
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19
Q

Acalculous Cholecystitis

in whom? s/s? special sign? dx?

A

in CRITICALLY ILL pts (sepsis, severe burn, trauma, immunosuppression) via GB stasis and ischemia

can be hard to notice if pt intubated/sedated

fever, RUQ pain, leukocytosis, mild LFT elevation

Murphy sign positive - pt breathes in while doc has hand below ribs, R midclavicular. pt will wince + stop inhaling when GB hits doc’s hand

dx by US > large GB with edema and no stones

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20
Q

Choledochal cyst

what is it? in whom? sx?

A

congenital dilation of common bile duct

present in kids <10

recurrent abdominal pain + jaundice

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21
Q

US in chronic cholecystitis

A

shrunken, fibrosed GB via repeated mild attacks of acute cholecystitis

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22
Q

incidental GB finding on abdominal XRAY

what? cause? increases risk of?

A

porcelain gallbladder

rim of calcium deposits visible on xray

caused by chronic cholecystitis

incr. risk of GB carcinoma

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23
Q

Esophageal SCC

histo?

A

nests of squamous cells with abundant pink cytoplasm
KERATIN PEARLS
INTERCELLULAR BRIDGES

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24
Q

Esophageal SCC

epidem? s/s? progno?

A

man > 50 with smoking/drinking history

solid food dysphagia (may progress to liquid)
retrosternal burning / discomfort
weight loss
IDA + fatigue via blood loss

poor progno (locally advanced/metastatic common)

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25
Q

gag reflex

efferent + afferent limbs

A

afferent - glossopharyngeal n. (CN IX)

efferent - vagus (CN X)

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26
Q

Pancreas development

2 buds: which gives what?
how is it different in pancreas divisum?

A

ventral bud - gives UNCINATE proc. and PROXIMAL MAIN DUCT (Wirsung)

dorsal bud - gives rest of head, body + tail plus ACCESSORY DUCT and distal main duct

in divisum, 2 buds don’t fuse fully > dorsal duct (Santorini) is dominant, ventral duct is accessory

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27
Q

Locating appendix during appendectomy

how?

A

Follow TAENIA COLI to their origin at the end of the cecum

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28
Q

Psoas sign

what is it?

A

abdominal pain elicited by thigh extension

positive in acute appendicitis when pt has RETROCECAL appendix > can irritate psoas and any stretching of it causes pain (pt generally sits/lays with hips flexed)

not specific for appendicitis; positive in other retroperitoneal conditions

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29
Q

Meckel diverticulum

what is it and how does it form?

A

ILEAL outgrowth due to FAILED VITELLINE DUCT OBLITERATION (aka omphalomesenteric duct)

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30
Q

Meckel diverticulum

s/s?

A

Sometime asymptomatic

Sometimes painless spontaneous lower GI bleed

Can cause INTUSSUSCEPTION > colicky pain and “CURRANT JELLY” poop

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31
Q

Meckel diverticulum

cell types in diverticulum? consequences of this?

specific imaging for Meckel’s?

A

Can have GASTRIC MUCOSA > acid causes ULCERS + BLEEDING

Can have PANCREATIC TISSUE

99Tc-Pertechnetate (with parietal cell affinity) goes to diverticulum > increased uptake in periumbilical or RLQ is characteristic

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32
Q

2 Ventral wall defects?

Cause?

A

Gastroschisis - loose herniated bowel loop to right of umbilicus

Omphalocele - sac-enclosed herniated bowel through umbilicus

failed LATERAL BODY FOLD CLOSURE

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33
Q

Imperforate anus

embryological cause

A

Hindgut (distal 1/3 of transverse colon onward) descends along the inferior mesenteric artery normally

FAILED HINDGUT DESCENT causes imperforate anus

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34
Q

Other than Meckel’s diverticulum…

what are 3 vitelline duct abnormalities?

A

Persistent vitelline duct - goes all the way to umbilicus from ileum

Vitelline sinus - fibrous band from ileum to umbilicus; deep fibrous sinus inward from umbilicus

Vitelline / entero-cyst - cyst suspended from 2 fibrous bands btwn ileum + umbilicus

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35
Q

“Pancreatic cholera”

what is the main hormone involved? weird syndrome name?

symptomatic tx?

A

VIPoma (pancreatic islet cell tumor) causes…

“WDHA” syndrome…
Watery D
Hypokalemia
Achlorhydria - low gastric acid

VIP stimulates pancreatic chloride/bicarb, plus it binds enterocytes > cAMP > Na, Cl and water secretion

Tx is SOMATOSTATIN (Octreotide) to inhibit GI hormone production (VIP, gastrin, glucagon and CCK)

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36
Q

TWO things involved in solubilization of cholesterol in GB

would be low in case of cholesterol stones

A

bile salts and PHOSPHATIDYLCHOLINE

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37
Q

best examination for general screening for the presence of malabsorption due to ANY etiology

A

fecal fat testing (stool microscopy with Sudan III stain)

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38
Q

Crohn’s complications

3 (+ their consequent complications)

plus ONE SPECIAL HISTO FEATURE of Crohn’s (a type of inflammation seen in many other diseases)

A
  1. STRICTURES - wall edema, fibrosis + muscularis mucosae hypertrophy narrows lumen > obstructive ileus
  2. FISTULAS - ulcer penetrates bowel wall and forms a “sinus tract” to another organ (enterovesicular, -vaginal, -enteric)
  3. ABSCESS - form when sinus tracts become walled off; may perforate > diffuse peritonitis

CD histo shows NON-CASEATING GRANULOMATOUS inflammation

39
Q

Esophageal SCC risk factors (5)

A
  1. Alcohol
  2. Tobacco
  3. N-nitroso foods
  4. Underlying esophageal disease (achalasia, etc.)
  5. Hot liquids
40
Q

Esophageal ADC risk factors (4)

A
  1. Barrett esophagus
  2. GERD
  3. Obesity
  4. Tobacco
41
Q

Primary Biliary Cirrhosis/Cholangitis

in whom? initial presentation (2 sx)?

A

middle-aged women

fatigue, NIGHT PRURITUS at first

42
Q

Primary Biliary Cirrhosis/Cholangitis

later s/s? (after pruritus + fatigue)

A
  • HSmegaly + cholestasis (jaundice, pale poo, dark pee)
  • fat malabsorption (A, D, E, K defic.)
  • impaired cholesterol excretion - HIGH LIPIDS and XANTHELASMA
  • very late = cirrhosis and portal htn
43
Q

Primary Biliary Cirrhosis/Cholangitis

main auto-Ab?

(several others)

A

antimitochondrial - against pyr DH complex

ANA
anti-glycoprotein-210
anti-centromere

44
Q

Primary Biliary Cirrhosis/Cholangitis

histo

A

dense infiltrate in PORTAL TRACTS of macros, lymphos, PLASMA cells and EOSINOPHILS

GRANULOMATOUS destruction of interlobular bile ducts

45
Q

Primary Sclerosing Cholangitis

in whom? presentation? (sx, lab)

A

pt with long history of ULCERATIVE COLITIS

fatigue
cholestasis sx
HIGH ALP

(p-ANCA can be seen in many cases; ANA and anti-smooth muscle can be seen in cases with overlapping AI hepatitis)

46
Q

Primary Sclerosing Cholangitis

histo

A

diffuse inflammation/fibrosis of LARGE INTRA- AND EXTRAHEPATIC bile ducts

“ONION SKIN” fibrosis around ducts with obstruction

47
Q

Most specific dx test for ACUTE CHOLECYSTITIS

A

Radionuclide biliary scan

radiotracer given IV accumulates in liver + bile; if it is only seen excreted into the duodenum and not the GB then positive for acute cholecystitis

(US is the initial test and would show thick wall, fluid around GB and positive sonographic Murphy sign, but IS LESS SPECIFIC; radionuclide used if US is inconclusive)

48
Q

Lymphatic drainage of colon (cecum to anus) by segment

A

Cecum + Asc. + 2/3 transverse - SUPERIOR MESENTERIC nodes

1/3 transverse to superior 1/3 rectum - INFERIOR MESENTERIC nodes

middle 1/3 rectum - INFERIOR MESENTERIC + INTERNAL ILIAC nodes

distal 1/3 rectum - INGUINAL nodes (some to inf. mes. and int. iliac)

49
Q

Type I: familial chylomicronemia syndrome

defect, what’s elevated, s/s

A

defect in LPL or ApoC-II

high chylomicrons

acute pancreatitis
lipemia retinalis
eruptive xanthomas
HSmegaly

50
Q

Type IIA: Familial Hypercholesterolemia

defect, what’s elevated, s/s

A

defect in LDL-R or ApoB-100

high LDL

premature CAD
corneal arcus
tendon xanthomas, xanthelasma

51
Q

Type III: Familial Dysbetalipoproteinemia

defect, what’s elevated, s/s

A

defect in ApoE

high chylomicron + VLDL remnants

premature CAD and PVD
tuboeruptive + palmar xanthomas

52
Q

Type IV: Familial Hypertriglyceridemia

defect, what’s elevated, s/s

A

defect in ApoA-V (but also polygenic)

high VLDL

increased pancreatitis risk
assoc. with obesity, insulin resistance, and CAD

53
Q

What are the 2 MCCs of acute pancreatitis?

A

gallstones - middle-age or older; mostly women; if young then prob due to hemolysis (sickle cell, etc.)

alcoholism

54
Q

After gallstones + alcoholism…

what are some less common causes of acute pancreatitis?

procedures? drugs? microbes? structural issues etc.?

A

ERCP or surgery (gastric, biliary or after cardiac surgery)

azathioprine, sulfasalazine, furosemide, valproate

mumps, Coxsackie, Mycoplasma

high triglycerides or hypercalcemia

pancreas abnormalities (stricture, cancer, divisum) or Vater ampulla (Oddi stenosis, choledochal cyst)

55
Q

Simple mnemonic for remembering the defects in the 4 important familial hyperlipidemia disorders

A

CBET

Type I = ApoC-2 (or LPL)
Type II = ApoB-100 (or LDL-R)
Type III = ApoE
Type IV = Triglycerides (polygenic)

(If you know the functions of these, you’ll know what’s elevated:

  1. C-2 activales LPL > no chylo breakdown > high chylos + TGs > pancreatitis
  2. B-100 binds LDL-R for hepatic uptake > hi LDL
  3. E binds liver for chylo/VLDL remnant uptake
  4. Just remember it…)
56
Q

What does ApoA-1 do?

Deficiency of it or a related molecule results in what?

A

activates LCAT > esterifies free cholesterol in HDL

ApoA-1 or LCAT defic. leads to low HDL and hi free cholesterol

57
Q

Diffuse Esophageal Spasm

how do contractions look on manometry?

radiological sign?

A

periodic SIMULTANEOUS contraction along whole length of esophagus

instead of contractions appearing in sequence down the length of the esoph

radio = “CORKSCREW” esophagus on barium esophogram

58
Q

Diffuse Esophageal Spasm

pathogenesis

A

impaired inhibitory neurotransmission in the myenteric plexus

59
Q

Collagenous (microscopic) colitis

in whom? histo?

A

older women with frequent diarrhea

thickening of subepithelial collagen band

60
Q

Colorectal adenocarcinomas:

Right-sided vs. left-sided vs. rectal

S/S?

A
  1. Right-sided - EXOPHYTIC mass in large lumen > no obstruction (stool more liquid here); have IRON-DEF ANEMIA via occult loss plus WEIGHT LOSS, anorexia + fatigue
  2. Left-sided - INFILTRATIVE mass ENCIRCLES lumen > obstruction with CONSTIPATION, pain, DISTENSION and VOMITING
  3. Rectal - TENESMUS and SMALL-CALIBER stool
61
Q

what is superior mesenteric artery syndrome?

presentation?

A

compression of 3rd part (inferior transverse) of duodenum between SMA and aorta

intermittent intestinal obstruction with POSTPRANDIAL PAIN in person with little mesenteric fat (LOW WEIGHT or MALNUTRITION)

62
Q

gastric chief cells release what? 2

A

pepsinogen and gastric lipase

(Chief cells are basophilic, lots of RER, deep in pits)

HCl from parietals converts to pepsin

63
Q

After gastric surgery (Whipple), what can be cut to decrease gastric acid output and resulting jejunal ulcers?

A

vagal trunks

64
Q

How is PERISTALSIS and LES TONE affected in esophageal dysmotility of scleroderma?

A

BOTH are decreased

65
Q

gastric acid suppressing drug with POTENT CYP450 INHIBITION

what other sfx does it have? (one of which is shared by another drug in its class)

A

Cimetidine - H2 blocker

anti-androgenic effects - high PRL, gynecomastia, impotence and low libido

crosses BBB > dizziness, HA

cimetidine and RANITIDINE both DECREASE CREATININE CLEARANCE (incr. serum levels)

66
Q

if a patient has a first degree relative with colon cancer, HOW AND WHEN SHOULD THEY BE SCREENED?

what other method should not be used for screening and why?

A

start at AGE FORTY (normal low-risk population screening starts at 50) via COLONOSCOPY

or start TEN YEARS BEFORE RELATIVE’S presentation

should not use occult blood screening, due to LOW SENSITIVITY

67
Q

Gastric vs. Duodenal ulcer

how do meals affect the pain

A

Gastric - pain is Greater with meals

Duodenal - pain is Decreased with meals

68
Q

Gastric vs. Duodenal ulcer

Relation to H. pylori?
General pathophys?
Other cause (1 for each)?

A

Gastric - 70% H pylori; via decreased mucosal protection; other cause is NSAID

Duodenal - 90% H pylori; via low mucosal protection OR increased HCl; other cause is Zollinger-Ellison

69
Q

How are gastric and duodenal ulcers related to cancer?

Histo considerations?

A

Gastric - risk of CARCINOMA increases! must BIOPSY MARGINS to rule it out

Duodenal - generally benign, no risk increase; biopsy shows BRUNNER GLAND HYPERTROPHY

70
Q

1 complication of gastric + duodenal ulcers?

site of ulcer with predilection for this complication?

A

Hemorrhage - posterior ulcers > anterior

gastric - lesser curvature bleeding from left gastric a. common

duodenal - posterior wall bleeding from gastroduodenal artery common

71
Q

Complication… more commonly of duodenal ulcers… that may be visible on x-ray?

Predilection site for this?
Related sign?

A

Perforation - anterior > posterior (opposite of hemorrhage)

may have referred shoulder pain via phrenic irritation

72
Q

Musculoskeletal complication of IBD, especially when treated with corticosteroids

A

Aseptic necrosis

common in femoral head; x-ray shows collapse of head with preservation of articular cartilage

73
Q

A heavy-drinking, heavy-smoking Japanese man who eats mostly traditional Japanese food

what is his main risk for gastric cancer?

A

the Japanese food

due to smoking of fish + preservation with nitrites

74
Q

what two things are produced by bacterial overgrowth in SIBO and elevated in serum?

A

vitamin K and folate

75
Q

Other than distended bowel loops with air-fluid levels…

what is a MORE SPECIFIC sign of gallstone ileus?

A

“pneumobilia” - air in the biliary tree

gallstone ileus happens when a large stone enters the GI tract via a CHOLECYSTOENTERIC FISTULA formed btwn the GB and duodenum; air from the GI tract can travel backward into the biliary tree through this fistula

76
Q

How does Celiac disease affect calcium homeostasis?

A

malabsorption of fats > low vitamin D

results in low Ca, low Pi and increased PTH > increased ALP due to bone turnover

77
Q

Cholecystokinin

produced by what in response to what?

effects (3)?

A

I cells of small intestine via FAs and AAs

  1. increases panc. enzymes + bicarb
  2. GB contraction
  3. Inhibit gastric emptying

(so basic effect is to get food in duodenum digesting well + inhibit more food coming in until current food is dealt with)

78
Q

Hormone that decreases secretion of many GI hormones

made by what + decreases what

A

Somatostatin

Delta cells in islets, duodenum, pyloric antrum

decr. VIP, gastrin, glucagon, CCK

79
Q

Mechanism of ANTRAL H pylori infection pathogenesis

which cells are affected?
where is the ulcer?

A

DELTA cell depletion > decreased SOMATOSTATIN > elevated gastrin > more HCl release

(cytotoxins also decrease duodenal bicarbonate)

acid into unprotected duodenum > DUODENAL ulcers

80
Q

Mechanism of GASTRIC BODY H pylori infection pathogenesis

which cells are affected?
where is the ulcer?
associated risks?

A

multifocal atrophic gastritis > PARIETAL CELL loss > acid is low or normal

GASTRIC ulcers form via direct mucosal damage (ammonia, toxins) and inflammation

assoc. with metaplasia + malignancy (MALT lymphoma and ADC), whereas antral infection is not

81
Q

two mechanisms by which gastrin increases HCl release

A
  1. Direct - via CCK-B receptors on parietals

2. Indirect - via acting on on ECL cells > histamine release

82
Q

What parts of the LIVER and COLON are most susceptible to ischemic injury?

A

Liver - area around CENTRAL VEIN (“zone III”)

Colon - splenic flexure + rectum

83
Q

2 main types of HIATAL HERNIAS

which is more common? which part protrudes?

A
  1. SLIDING - more common; GE junction displaced upwards and cardia slides into hiatus; “hourglass” imaging
  2. PARAESOPHAGEAL - in this case the FUNDUS protrudes into the thorax; less common
84
Q

Through what muscle (general + two specific parts) does a Zenker diverticulum protrude?

A

inferior pharyngeal constrictor

thyropharyngeus + cricopharyngeus portions

85
Q

What nerve innervates the INFERIOR PHARYNGEAL CONSTRICTOR muscles?

A

vagus nerve

86
Q

2 types of gastroesophageal mural injury + main feature

cause of both (same)

A
  1. Mallory-Weiss tear - MUCOSAL tear (bleeding only)
  2. Boerhaave syndrome - TRANSMURAL tear (air/fluid leakage into mediastinum + pleura

(both via forceful vomiting)

87
Q

Mallory-Weiss tear vs. Boerhaave syndrome

Presentation similarities (1) and differences (2)

A

same - vomiting + retching

M-W tear - hematemesis and EPIGASTRIC pain

BS - CHEST + UPPER ABD. pain and FEVER, DYSPNEA + SEPTIC SHOCK

(because BS has leakage of fluid + air into mediastinum and pleura)

88
Q

Difference in acid-base balance between excessive VOMITING vs. DIARRHEA

A

vomiting = HCl loss = metabolic ALKALOSIS

diarrhea = HCO3 loss = metabolic ACIDOSIS

89
Q

First genetic change in colon cancer?

Later 3 changes (1 activation, 2 inactivations)

A

First is APC inactivation

Then KRAS activation and p53 / DCC inactivations

90
Q

What side do a cerebellar lesion’s symptoms manifest on?

A

IPSILATERAL side

91
Q

What 3 symptoms can arise from cerebellar HEMISPHERE lesions?

(cerebellar, not cerebral!)

A
  1. Dysdiadochokinesia - impaired rapid alternating movements
  2. Limb dysmetria - over/undershoot
  3. Intention tremor - during targeted movement

(all are IPSILATERAL!)

92
Q

Lesions to cerebellar VERMIS cause what sx?

A

TRUNCAL ATAXIA

wide, unsteady gait

(vermis controls the “medial descending” motor systems - ant. corticospinal, reticulospinal, vestibulospinal, tectospinal)

93
Q

Lesions to the FLOCCULONODULAR LOBE of the cerebellum cause what?

(bonus: this lobe plus the inferior vermis make up the “_____cerebellum”)

A

vertigo and nystagmus

“vestibulocerebellum”

94
Q

Secretin

made by what cells? in response to what? causes what?

A

by duodenal S cells

in response to H+ in duodenum

pancreatic HCO3 secretion

(NOT enzyme secretion… CCK and cholinergic stimulation stimulates enzymes)

*USMLE* (28 decks)

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