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GI Flashcards

1
Q

Retroperitoneal structures

A 
SAD PUCKER
Suprarenal (Adrenals)
Aorta and IVC
Duodenum (2nd and 3rd parts)
Pancreas (except tail)
Ureters
Colon (descending/ascending)
Kidneys
Esophagus (lower 2/3)
Rectum (lower 2/3)
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2
Q

Gastrin (source, action, regulation, notes)

A
  • G cells (antrum of stomach)
  • inc acid secretion, growth of mucosa, motility. Acts on ECL cells –> hist –> incr HCl from parietal cells
  • inc secretion by stomach distension/alkalinization, amino acids (esp phenylalanine and tryptophan), peptides, vagal tone. Decr secrretion by pH <1.5
  • inc in ZES and by chronic PPI use.
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3
Q

Cholecystokinin (source, action, regulation, notes)

A
  • I cells (duodenum, jejunum)
  • inc pancreatic secretion, gallbladder contraction. Dec gastric emptying. Relaxes sphincter of Oddi
  • incr by fatty acids, amino acids
  • CCK acts on neural muscarinic pathways to cause pancreatic secretion
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4
Q

Secretin (source, action, regulation, notes)

A
  • S cells (duodenum)
  • inc pancreatic bicarb, decrease gastric acid, inc bile secretion.
  • incr secretion with acid, fatty acids in duodenum
  • incr bicarb neurtralizes acids, allowing panc enzymes to fxn
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5
Q

Somatostatin (source, action, regulation, notes)

A
  • D cells (pancreatic islets, GI mucosa)
  • decrease gastric acid, pepsinogen, pancreatic/small intestin fluid secretion. Decr gallbaldder contration, decr insulin and glucagon release
  • incr by acid, decr by vagal stimulation
  • inhibitory and antigrowth hormone (inhibits absorption of anabolic substances.)
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6
Q

Glucose-dependent insulinotropic peptide (source, action, regulation, notes)

A
  • K cells (duodenum, jejunum)
  • Exocrine: decr gastric H+. Endocrine: incr insulin
  • incr by fatty acids, amino acids, oral glucose
  • AKA GIP (gastric inhibitory peptide). Oral glucose load is used more rapidly than IV due to GIP
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7
Q

Vasoactive intestinal polypeptide (VIP) (source, action, regulation, notes)

A
  • Parasympathetic ganglia in sphincters, gallbladder, small intestine
  • Incr intestinal water and electrolyte secretion, relaxation of smooth muscle and sphincters
  • incr by distention and vagal stimulation. Decr by adrenal output
  • VIPoma - non-alpha/beta islet cell tumor. Watery Diarrhea, Hypokalemia, Achlorhydria (WDHA sydrome)
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8
Q

Nitric oxide

A
  • increased smooth muscle relaxation, including LES

- loss of NO is implicated in achalasia (incr tone)

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9
Q

Motilin (source, action, regulation, notes)

A
  • Small intestine
  • produces MMCs (migrating motor complexes)
  • incr in fasting state
  • motilin receptor agonists (e.g. erythromycin) stimulate intestinal parastalsis
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10
Q

intrinsic factor (source, action, notes)

A
  • parietal cells (stomach)
  • Binds vit B12 (required for uptake)
  • autoimmune destruction of parietal cells –> chronic gastritis/pernicious anemia
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11
Q

Gastric acid (source, action, regulation, notes)

A
  • parietal cells (stomach)
  • decreased pH
  • incr secretion by histamine, ACh, gastrin. Decr by somatostatin, GIP, prostaglandins, secretin
  • gastrinoma: gastrin-secreting tumor that causes continuous high acid secretion and ulcers.
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12
Q

Pepsin (source, action, regulation, notes)

A
  • Chief cells (stomach)
  • decreases protein
  • incr by vagal stimulation, local acid
  • inactive pepsinogen is activated to pepsin by H+
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13
Q

HCO3- (source, action, regulation, notes)

A
  • Mucosal cells (stomach, duodenum, salivary glands, pancreas) and Brunner’s glands (duodenum)
  • neutralizes acid
  • incr by pancreatic and biliary secretion with secretin
  • HCO3- is trapped in mucus that covers gastric epithelium
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14
Q

channel for absorption of glucose/galactose

A

SGLT1 (Na dependent)

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15
Q

fructose absorption channel

A

GLUT-5

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16
Q

Monosaccharide transport to blood

A

GLUT-2

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17
Q

Test for distinguishing GI mucosal damage from other causes of malabsorption

A

D-xylose test

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18
Q

rate limiting step of bile salt formation

A

cholesterol 7alpha hydroxylase

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19
Q

bile conjugation enzyme

A

UDP-glucuronosyl transferase

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20
Q

Pleomorphic ademoa

A

benign mixed tumor, most common salivary gland tumor. Painless, mobile. cartilage and epithelium, recurs frequently

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21
Q

Warthin’s tumor

A

papillary cystadenoma lymphomatosum

benign cystic tumor of salivary gland with germinal centers

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22
Q

Mucoepidermoid carcinoma

A

malignant tumor of salivary gland. mucinous and squamous. painful mass; often involves facial nerve

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23
Q

DDx Achalasia

A 
primary = loss of myenteric plexus
secondary = Chagas, scleroderma (CREST)
24
Q

Whipple’s dz

A

infxn with tropheryma whipplei (gram+).
malabsorption, cardiac, arthralgias, neuro sx. older men
path: PAS-positive foamy macrophages in intestinal lamina propria.

25
Q

Abetalipoproteinemia

A

decreased synthesis of apo B –> inability to form chylomycrons –> fat accumulation in enterocytes.
Early childhood: malabsorption and neuro manifestations

26
Q

Curling’s ulcer

A

acute gastritis in burns (due to reduced plasma volume)

27
Q

cushing’s ulcer

A

acute gastritis in TBI (due to increased vagal tone –> H+)

28
Q

Chronic gastritis types

A

Type A = pernicious anemia = fundus/body

Type B = H pylori = antrum

29
Q

menetriers’ dz

A

gastric hypertrophy with protein loss, parietal atrophy and inc mucous cells. Hypertrophied rugae. Precancerous

30
Q

Stomach cancer (two types)

A

Adenocarcinoma almost always. aggressive. Acanthosis nigricans
Intestinal – h pylori, smoked foods, achlorhydria, chronic gastritis, type A blood. Less curvature. ulcer with raised margins
Diffuse – not h pylori. Signet ring cells. linitis plastica (grossly thickened/leathery wall)

31
Q

Krukenberg’s tumor

A

b/l signet ring gastric cancer mets to ovaries

32
Q

Sister mary joseph nodules

A

subQ gastric mets periumbilical

33
Q

adenomatous polyps

A 
precancer
more villous (vs tubular) = more malignant.
34
Q

Hyperplastic polyp

A

most common non-neoplastic polyp

35
Q

Juvenile polyp

A

sporadic lesions in children <5. mostly rectum. If single, not malignant
Juvenile polyposis = multiple polyps , inc risk of adenocarcinoma

36
Q

Putz-jeghers

A

AD syndrome with multiple hamartomas (non-malignant) throughout GIT, hyperpigmented lips, hands, genitalia. incr risk of CRC and other cancers

37
Q

Molecular pathogenesis of CRC

A

2 pathways:
chromosomal instability: APC (AD mutx in FAP–involves rectum!) loss –> incr proliferation –> K-RAS mutx –> dysregulated signal transduction –> Adenoma –> p53 mutx –> carcinoma

microsatellite instability: DNA mismatch mutx: sporadic and HNPCC (proximal colon!)

38
Q

Turcot’s syndrome

A

FAP + malignant CNS tumor

39
Q

Gardner’s syndrome

A

FAP + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium

40
Q

Carcinoid tumor

A

Most common cancer of small bowel
path: “dense core bodies” on EM
5-HT –> wheezing, right sided murmurs, diarrhea, flushing (Sx only after mets, since liver metabolizes 5-ht).
Tx: resection, octreotide, somatostatin.

41
Q

cavernous hemangioma

A

common benign liver tumor 30-50yrs. Bx contraindicated b/c of hemorrhage risk

42
Q

hepatic adenoma

A

benign liver tumor 2/2 OCP or steroid use. can regress spontaneously

43
Q

angiosarcoma

A

malignant liver tumor of endothelial origin. Arsenic, polyvinyl chloride

44
Q

alpha-1-antitrypsin deficiency (inheritance, mechanism)

A
  • codominant
  • in liver: misfolded gene product accumulates in ER –> cirrhosis with PAS-positive granules)
  • in lungs: lack of functioning enzyme –> decr elastic tissue –> panacinar emphysema
45
Q

Gilbert’s

A

mild decr in UDP-glucouronyl transferase or dec bilirubin uptake. Asymptomatic. Elevated unconjugated bili, incr with fasting and stress

46
Q

Crigler-Najjar syndrome

A

Absent UDP glyucoronyl transferase.
Presents early in life.
Jaundice, kerncterus, incr unconjugated bili
Type 1: fatal. Tx plasmaphersis and phototherapy
Type 2: less severe. Responds to phenobarbital (incr liver enzyme synthesis)

47
Q

Dubin-Johnson

A

Defective liver excretion –> conjugated hyperbili and black liver. benign. Rotor’s is milder and no black liver

48
Q

hemochromatosis

A

Sx: cirrhosis, diabetes, pigmentation, CHF, testicular atrophy, HCC
primary: AR mutx in HFE gene. HLA-A3 association
secondary: chronic transfusions
Tx: phlebotomy, deferasirox, deferoxamine

49
Q

PBC (path, serology, association

A
  • lymphocytic/granulomatous
  • anti-mitochondrial Abs
  • assoc with other autoimmune conditions
50
Q

PSC (path, serology, association)

A
  • onion skin fibrosis, “beading” of intra and extrahepatic ducts
  • hyper-IgM
  • UC
51
Q

Acute pancreatitis (DDx, complications)

A

GET SMASHED – gallstones, EtOH, trauma, steroids, mumps, autoimmune, scorpion, hypercalcemia/hyperTG, ERP, Drugs (sulfa)
- DIC, ARDS, hypocalcemia (pancreatic soap deposites), pseudocyst (lined by granulation tissue) –> rupture/hemorrhage

52
Q

Trousseau’s syndrome

A

migratory thrombophelbitis associated with pancreatic adeno

53
Q

LPL deficiency

A

Type I
Apo C-II
elevated chylomicrons
pancreatitis, lipemia retinalis, eruptive skin xanthomas, HSM

54
Q

LDL R deficiency

A

Type IIA
ApoB-100
elevated LDL
premature CAD, corneal arcus, tendon xanthoma, xanthelasma

55
Q

ApoE deficiency

A

Type II
elevated chylomicrons and VLDL remnants
premature CAD/PVD
tuberoeruptive and palmar xanthoma

56
Q

ApoA-V deficiency

A

Type IV
elevated VLDL
Obesity, insulin resistance, risk of pancreatitis

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