GI Flashcards

1
Q

Retroperitoneal struc’s?

A
SAD PUCKER
Suprarenal (ad) gl
Ao and IVC
Duo (2nd and 3rd parts)
Panc
Ureters
Colon (descending and ascending)
Kidneys
Eso (lower 2/3)
Rectum (lower 2/3)
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2
Q

Hepatoduodenal lig contains? is btwn?

- name of mech to stop bl’ing from it?

A

Portal triad; liver to duo (connects greater and lesser sacs)
- Pringle maneuver

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3
Q

Gastrohepatic lig contains?
Gastrocolic lig?
Gastrosplenic lig?
Splenorenal lig?

A
  • gastric a’s (sep’s greater/less sacs on R)
  • gastroepiploic a’s (part of greater omentum)
  • short gastrics, L gastroepiploic (sep’s greater and lesser sacs on L)
  • splenic a/v, tail of panc
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4
Q

Layers of the gut wall from inside out:

A

Mucosa: epi, LP (support), muscularis mucosa (motil)
Submucosa: w/ Meissner’s n. plexus
Muscularis externa: outer longitudinal, inner circular, w/ myenteric n. plexus
Serosa (intraperitoneal) vs. Adventitia (retroperitoneal)

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5
Q

Erosions are in?

Ulcers are in?

A

Mucosa only

into submucosa

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6
Q

Where are these:

  • Brenner’s gl’s?
  • Crypts of Lieberkuhn?
  • Peyer’s patches?
  • plicae circulares
  • the most amt of goblet cells
A
  • duo
  • duo, jej and ileum
  • ileum
  • jej and prox ileum
  • ileum, colon also has a lot
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7
Q

SC level for:

  • Celiac trunk
  • SMA
  • L renal a.
  • IMA
  • Bifurcation of Ao
A
  • T12
  • L1
  • L1
  • L3
  • L4
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8
Q

SMA synd =

A

When transverse (3rd) part of duo is entrapped btwn SMA and Ao -> intestinal obstruction

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9
Q

Parasymp innervation to foregut -> hindgut?

A

Foregut (inc’ing liver, GB, spleen, panc): X
Midgut: X
Hindgut (distal 1/3 transv. colon to upper rectum): Pelvic

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10
Q

Portal HTN -> see varices where?

A

Gut (esophaGUS), butt (rectal, aka int hemorrhoids), and caput (medusae)

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11
Q

Space of Disse =

A

lymphatic draining in liver

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12
Q

Apical and basolat sides of hep’s face what?

A

Apical faces bile canaliculi

Basolat fases sinusoids (which drain to central v.)

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13
Q

Organization of femoral region?

- Femoral triangle contains? bounded by?

A

“Go from lat to medial to find your NAVeL”
Femoral nerve, art, vein (empty), lymphatics
- Femoral NAV
- “SAIL” = Sartorius m. (lat), Adductor longus (med), Inguinal Lig (sup)

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14
Q

Layers of the spermatic cord:

A

Ext spermatic fascia (ext oblique)
Cremasteric m/fascia (int oblique)
Int spermatic fascia (transversalis fascia)

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15
Q

Layers of ab wall near inguinal cavity and their corresponding layers in spermatic cord:

A

Aponeurosis of ext oblique m. (ext spermatic fascia)
Int oblique m. (cremasteric m and fascia)
Transversus abdominis m. (deep inguinal ring thr it)
Transversalis fascia (int spermatic fascia)
Extraperitoneal tissue
Parietal peritoneum w/ int inguinal ring

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16
Q

2 types of diaphragmatic hernia?

- usu occur in who?

A

Sliding hiatal hernia where gastroeso jxn is displace up
Paraesophageal hernia where GE jxn is nl but fundus protrudes into thorax
- infants from defective develop of pleuroperitoneal mem

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17
Q

Indirect inguinal hernia =

- usu occurs in who?

A

Path of spermatic cord:
Thr int (deep) inguinal ring LAT to inf epigastric a. -> ext (superficial) inguinal ring -> into scrotum
- infants from failure of processus vaginalis to close, usu M

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18
Q

Direct inguinal hernia =

  • covered by?
  • usu occurs in who?
A

Thr inguinal (Hesselbach’s) triangle -> thr ab wall MEDIAL to inf epigastric art. -> ext inguinal ring (ONLY)

  • ext spermatic fascia (from ext oblique aponeurosis)
  • older men
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19
Q

Femoral hernia =

  • usu occurs in who?
  • leading cause of?
A

Below inguinal lig thr femoral canal and lat to pubic tubercle

  • F
  • bowel incarceration
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20
Q

Hesselbach’s triangle =

-what goes thr it?

A

Inf epigastric vessels, lat border of rectus abdominis, inguinal lig
- Direct hernia

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21
Q

VIPoma =

- sx

A

non-a, non-b islet cell panc tumor, secretes VIP

- WDHA synd: tons of Watery D, HypoK, and Achlorhydria

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22
Q

Gastrin

- source, action, reg’n

A
  • G cells in antrum of stomach
  • incr gastric H+, growth of mucosa and motility
  • incr’d by stomach distension/alk/AAs/ peptides/vagal stim’n (via GRP, not ACh); decr’d by pH<1.5
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23
Q

Cholecystokinin

- source, action, reg’n

A
  • I cells in duo/jej
  • incr panc secretions, GB contrac, decr gastric emptying, incr Oddi relax
  • incr’d by FA/AA
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24
Q

Secretion

- source, action, reg’n

A
  • S cells in duo
  • incr panc bicarb, decr acid, incr bile secretion
  • incr’d by acid/FA in duo
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25
Q

Somatostatin

- source, action, reg’n

A
  • D cells in panc islets/GI mucosa
  • decr acid and pepsinogen secretion, decr panc/smI fluid secretion, decr GB contrac, decr insulin/glucagon release
  • incr’d by acid, decr’d by vagal stim’n
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26
Q

Glc-dep insulinotropic peptide (GIP)

- source, action, reg’n

A
  • K cells in duo/jej
  • exocrine: decr gastric H+ secretion; endo: incr insulin release
  • incr’d by FA/AA/Glc
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27
Q

Vasoactive intestinal polypeptide (VIP)

- source, action, reg’n

A
  • parasymp gang in sphincters/GB/smI
  • incr GI water/electrolyte secretion, incr relax of SmM and sphincters
  • incr’d by distension and vagal stim’n, decr’d by adrenergic input
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28
Q

Nitric oxide

- action

A

incr SmM relax, inc: LES

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29
Q

Motilin

- source, action, reg’n

A
  • smI
  • makes MMCs (migrating motor complexes)
  • incr’d in fasting state
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30
Q

Intrinsic factor

- source, action

A
  • parietal cells in stomach

- VitB12 binding pr for uptake in term ileum

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31
Q

Gastric acid

- source, action, reg’n

A
  • parietal cells in stomach
  • decr stomach pH
  • incr’d by Hist/ACh/gastrin, decr’d by somatostatin/GIP/PGE/secretin
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32
Q

Pepsin

- source, action, reg’n

A
  • chief cells (stomach)
  • pr digestion (needs H+ to be act’d from pepsinogen)
  • incr’d by vagal stim’n, local acid
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33
Q

HCO3-

- source, action, reg’n

A
  • mucosal cells (stomach, duo, salivary gl’s, panc) and Brunner’s gl’s (duo)
  • neutralizes acid
  • incr’d by panc/biliary secretion w/ secretin
34
Q

3 components of saliva:

- usu is hypo/isotonic?

A

amylase (digest starch), HCO3- (neutralize bac acids), mucins (lubricate food)
- hypo, but more isotonic w/ higher flow rates bc less time for ab’n

35
Q

What is the main mech that gastric parietal cells secrete H+?

  • Another stimulator?
  • 2 inhibitors?
A

Gastrin from G cells (stim’d by GRP from CN X) stim’s ECL cells to secrete hist -> binds H2 R on parietal cells -> incr cAMP -> H/K ATPase secretes more H+ into lumen

  • ACh (CN X) on M3 R (via Gq -> IP3/Ca)
  • PGEs/misoprostol and somatostatin
36
Q

How is trypsinogen act’d to trypsin?

A

First by enterokinase/enteropeptidase (NZ from duo mucosa), later by active trypsin peptides

37
Q

Carb digestion:

  • Salivary amylase does what?
  • Panc amylase does what?
  • Oligosaccharide hydrolases do what?
A
  • hydrolyzes a1.4 links -> disacch’s (maltose and a-limit dextrins)
  • duo; hydrolyzes starch to oligo/di-sacch’s
  • BB; RL step, makes monosacch’s form oligo/disacch’s
38
Q

How are the 3 monosaccharides ab’d by enterocytes?

A

Glc and galac by SGLT1 (Na+ dep)
Fruc by GLUT-5 facilitated diffusion
All into bl by GLUT-2

39
Q

D-xylose ab’n test =

A

distinguishes GI mucosal damage from other causes of malab’n

40
Q

Where are these ab’d:

- Fe2+, folate, B12, bile acids

A

duo, jej, term ileum, term ileum

41
Q

What are Peyer’s patches?
Where are they?
Why type of cell do they contain?

A

Unencap’d lymphoid tissue (make secretory IgA)
LP and submucosa of ileum
M cells that take up Ag

42
Q

Bile salts are made of?

RL step?

A

Bile acids conj’d to Gly or Taurine -> water soluble

- Choles 7a-hydroxylase

43
Q

Bilirubin:

  • made from?
  • NZ that conj’s it in liver? to what?
  • excreted how?
  • name in feces? in urine?
A

Heme

  • UDP-glucuronosyl-transferase; to glucuronate
  • as conj’d bilirubin in bile (urobilinogen)
  • stercobilin, urobilin
44
Q

Salivary gl tumors:

  • Benign mixed tissue tumor?
  • Benign cystic tumor?
  • Malignant mixed tissue tumor?
A
  • Pleomorphic adenoma (cart and epi), recurs, painless mobile mass
  • Warthin’s tumor (pap cystadenoma lymphomatosum), salivary gl tissue in LN
  • Mucoepidermoid ca (mucinous and sq), painful mass bc involves CN VII
45
Q

Esophagitis infectious causes (vs. reflex):

  • white pseudomem?
  • punched-out ulcers
  • linear ulcers
A
  • Candida
  • HSV-1
  • CMV
    (usu a complication of AIDS)
46
Q

Plummer-Vinson synd

- triad of?

A

dysphagia (eso webs), glossitis, Fe defic anemia

47
Q

Risk factors for eso ca:

A
"AABCDEFFGH"
Achalasia, Alcohol (sq)
Barrett's (adeno)
Cigarettes (also corrosive esophagitis)
Diverticula (sq)
Eso web (sq)
Familial, Fat (adeno)
GERD (adeno)
Hot liquids (sq)
48
Q

Curling’s ulcer =

Cushing’s ulcer =

A
  • from burns: decr’d pl vol -> sloughing of gastric mucosa (burned by the curling iron)
  • from brain injury: incr’d vagal stim’n -> incr’d ACh and H+ production (always cushion the brain)
49
Q

Menetrier’s disease =

- risk of?

A

gastric hypertrophy w/ pr loss, parietal cell atrophy, and incr mucus cells (rugae of stomach look like brain gyri)
- adenoca

50
Q

Stomach adenoca, intestinal vs. diffuse types:

  • assoc’d w/ H.pylori?
  • location?
  • looks like?
A
  • YES, vs. no
  • pylorus/antrum lesser curvature vs. diffuse stomach wall
  • ulcer w/ raised margins vs. wall is thickened and leathery (linitis plastica)
51
Q

Stomach adenoca:

  • 2 sx it can present w/?
  • Virchow’s node =
  • Krukenberg tumor =
  • Sister Mary Joseph’s nodule =
A
  • Acanthosis nigricans OR seborrheic keratoses (Leser-Trelat sign)
  • mets to L supraclavicular node
  • bilat mets to ovaries (mucus, signet ring cells)
  • subcut perium met’s
52
Q

PUD: Gastric vs. Duo ulcer:

  • pain w/ food?
  • H.pylori?
  • causes?
  • risk of ca?
A
  • YES (wt loss), vs. decr’d pain (wt gain)
  • most vs. all
  • decr’d mucosal protection against acid vs. incr’d acid production and decr’d protection
  • incr’d vs. none (benign)
53
Q

Topical sprue

- affects? trtmt?

A
  • entire smI

- Abx

54
Q

Whipple’s dz

  • caused by?
  • dx’ic test?
  • assoc’d sx?
  • usu affects who?
A
  • Tropheryma whipplei (Gm+)
  • PAS(+) foamy Mphage (in LP and LNs)
  • “Foamy Whipped cream in a CAN”: Cardiac sx, Arthralgias, Neuro sx
  • older men
55
Q

Celiac sprue

  • 3 Abs?
  • HLA assoc’n?
  • location?
  • assoc’d w/?
A
  • anti-endomysial, tissue transglutaminase, gliadin
  • DQ2/8
  • distal duo and prox jej
  • dermatitis herpetiformis, and other autoimm dz’s
56
Q

The 5 2s of Meckel’s diverticulum:

- bl’ing from it caused by?

A

2” long, 2’ from ileocecal valve, 2% of pop, presents in first 2yrs of life, may have 2 types of epi (gastric/panc), males are 2x more likely to be affected
- gastric acid from ectopic tissue -> ulceration of adjacent tissue and lower GI bl’ing

57
Q

Zenker’s diverticulum is due to herniation of?

A

mucosal tissue at Killian’s triangle btwn thyropharyngeal and cricopharyngeal parts of inf pharyngeal constrictor

58
Q

Carcinoid synd =

- need tumor to be where to see synd?

A

wheezing, R sided heart murmurs, D, flushing

- outside GI system bc liver metab’s 5-HT to 5-HIAA (out in urine)

59
Q

Pain after eating -> wt loss, due to?

A

Ischemic colitis

60
Q

Colonic polyps, benign or malig?

  • adenomatous
  • hyperplastic
  • juvenile
  • Peutz-Jeghers
A
  • preca (more so as more villous) (CRC)
  • benign (rectosigmoid colon)
  • benign if single; mult is juvenile polyposis synd and has incr’d risk of adenoca
  • benign if single; have benign hamartomas in GI, but incr’d risk of CRC, br/gyn ca’s
61
Q

Colon ca: L-sided tend to? R-sided tend to?

A

L sided obstruc (smaller diam)

R sided bleed (bl mixed in w/ stool, Fe defic)

62
Q

FAP =

- what is always involved?

A

AD mutation in APC gene on chr5q

100% get CRC, always involves rectum

63
Q

Gardner’s synd =

A

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

64
Q

Turcot’s synd =

A

FAP + malig CNS tumor

“Turcot = Turban”

65
Q

HNPCC/Lynch synd =

- what is always involved?

A

AD mutation of DNA mismatch repair gene, 80% get CRC, prox colon always involved

66
Q

2 molec pthwys to CRC?

A

1) microsatellite instability pthwy: DNA mismatch repair gene mutations -> sporadic and HNPCC synd
2) APC/b-catenin (chr instability) pthwy: lose APC -> K-RAS mutation -> lose p53

67
Q

Reye’s synd

  • triad of?
  • usu occurs post?
  • mech?
A
  • encephalopathy, fatty change in liver, incr’d transaminases
  • viral infec (VZV/influenza) trted w/ aspirin
  • aspirin metabolites decr b-ox’n by inhib’ing mito NZ -> mito abnl’ities
68
Q

What type of jaundice?

  • incr’d direct, incr’d urine bili, decr’d urine UBG
  • incr’d mixed bili, incr’d urine bili, incr’d urine UBG
  • incr’d indirect, no urine bili, incr’d urine UBG
A
  • obstructive
  • hepatocellular
  • hemolytic
69
Q

Gilbert’s synd =

- sx incr w/?

A

mildly decr’d UDP-glucuronyl transferase activity and problems w/ UCB uptake -> incr’d UCB but asymp
- fasting, stress, EtOH, phenobarbital

70
Q

Crigler-Najjar synd, type I =

  • presents when?
  • type II is?
A

no UDP-glucuronyl transferase -> high UCB

  • early in life w/ jaundice, kerticterus -> death
  • less severe, responds to phenobarbital which incr’d liver NZ syn
71
Q

Dubin-Johnson synd =

A

defective liver excretion of CB -> high CB and blk liver, benign

72
Q

Rotor synd =

A

milder defect in liver excretion of CB than Dubin-Johnson, liver is not blk

73
Q

Wilson’s dz

  • defect in?
  • serum levels are?
  • neuro sx?
A

AR chr13 -> can’t excrete hep Cu nor put Cu into ceruloplasmin to enter circ

  • decr’d total serum Cu (decr’d ceruloplasmin) but incr’d serum/urine FREE Cu
  • Yes bc BG degen and tox to brain -> parkinsonian sx, dementia, dyskinesia, dysarthria, asterixis
74
Q

Hemochromatosis

  • defect in?
  • classic triad of?
  • results in?
A
  • HFE gene, chr6 -> max ab’n of Fe (max conj to transferrin)
  • Cirrhosis, DM and skin pigmentation (bronze diabetes)
  • CHF, testic atrophy is males, incr’d risk HCC
75
Q

Mallory bodies =

- seen in?

A

intracytoplasmic Eo’ic inclusions in hepatocytes, are damaged cytokeratin
- alcoholic hepatitis

76
Q

PBS (1* biliary cirrhosis) =

  • assoc’d Ab?
  • assoc’d w/?
A

autoimm granulomatous txn to mito mem that destroys bile ducts in portal triads, done by CD8 T cells

  • anti-mito Ab
  • other autoimm dz’s: CREST synd, RA, celiac dz
77
Q

PSC (1* sclerosing cholangitis) =

  • on ERCP see?
  • assoc’d w/?
  • can lead to?
A

concentric “onion skin” bile duct fibrosis

  • alt’ing stricture and dilation w/ “beading” of intra/extra hep bile ducts
  • hypergammaglobulinemia (IgM), UC
  • PBC
78
Q

Secondary biliary cirrhosis =

- complicated by?

A

extrahep biliary obstruction -> incr’d P in intarhep ducts -> injury/fibrosis and bile stasis
- ascending cholangitis

79
Q

Who gets gall stones?

  • Charcot’s triad of cholangitis?
  • which sign is pos?
A

Female, fat, fertile (preg), forty (use of OCPs, bc incr’d E incr’s choles to liver and into bile)

  • jaundice, F, RUQ pain
  • Murphy’s sign: insp arrest on deep RUQ palpation due to pain
80
Q

Gallstones: choles vs. pigment

  • on XR are?
  • due to?
  • assoc’d w/?
A
  • radiolucent VS. radiopaque
  • high choles oversat’ing bile salts VS. extravasc hemolysis (blk stones) or CBD infec (brown stones)
  • fat, CD, CF, age, clofibrate, E, maltiparity, wt loss, Native Am VS. chronic hemolysis, alcoholic cirrhosis, age, biliary infec
81
Q

Causes of pancreatitis?

A

GET SMASHED:
Gallstones, EtOH, Trauma, Steroids, Mumps, Autoimm dz, Scorpion sting, HyperCa/HyperTG (>1000), ERCP, Drugs (sulfa drugs)

82
Q

RFs for panc adenoca?

A

Tobacco use (not EtOH), chronic pancreatitis (>20yrs), age >50yo, Jewish/AfAm M