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GI Flashcards

1
Q

Hormone responsible for gallbladder contraction? Where made?

A

Cholecystokinin (CKK), which is made in duodenum and jejunum in response to FA’s and AA’s

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2
Q

Dubin-Johnson syndrome

A

Defect of hepatic excretion of bilirubin glucuronides across canalicular membrane (MDR2 biliary transport protein); Chronic conjugated hyperbilirubinemia; black liver; histo with epi metabolites within lysosomes. Icterus, mostly asymtompatic; Benign = no tx

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3
Q

Extrahepatic biliary atresia

A

Obstruction of extra hepatic bile ducts. Jaundice by wk 3-4 w/ cholestatic picture (dark urine, echoic stools, and conjugated hyperbilirubinemia)
Liver bx = intrahepatic bile ductular proliferation, portal tract edema, fibrosis, parenchyma cholestasis

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4
Q

Whipple disease

A

Middle-aged Caucasian males - diarrhea, wt loss, arthropathy, polyarthritis, psych, cardiac
Tropheryma whippeli - Gram + actinomycete. Only proliferates in macrophages = no inflammatory.
Bx - Enlarged FOAMY macrophages w/ rod-shaped bacilli and PAS-positive diastase-resistant granules
Tx = abx

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5
Q

Bile acid-binding resin names?

A

Cholestyramine, colestipol, colesevelam

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6
Q

What agents increase cholesterol content of bile?

A

Bile acid resins and fibrates

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7
Q

Mallory-Weiss v. Boerhaave

A

Mucosal tear v. transmural tear (esophageal air + fluid leak)

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8
Q

Where do H. pylori biopsy?

A

Prepyloric region of gastric antrum has highest yield.

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9
Q

Porcelain gallbladder

A

Refers to abdominal radiograph with bluish, brittle, Ca-laden gallbladder wall that develops in some patients with chronic cholecystitis. 11-33%->gallbladder carcinoma = advise cholecystectomy

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10
Q

How does H. pylori lead to duodenal ulcers?

A

Chronic antral inflammation -> decrease in delta cells (somatostatin-producing cells) -> disinhibition of gastrin. High gastrin -> increased H+ secretion by parietal cells.

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11
Q

Pathogenesis of TPN-induced gallstones

A

Biliary stasis 2/2 to dec. cholecystokinin

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12
Q

Insulin secretion from pancreatic beta cells?

A

Glucose stimulates. Enters via GLUT-2 (fac.) then generates ATP. High ATP:ADP causes CLOSURE of K+ channels (KATP). Beta cells now depolarize b/c K+ not leaving the cell and building up inside –> opening of voltage dependent Ca2+ channel -> insulin release. Sulfonylureas bind to KATP –> channel closure -> insulin release.

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13
Q

Gilbert syndrome

A

Mild UDP glucuroyl transferase transferase defieincy. Uncojugated hyperbilirubinemia, usu. provoked by hemolysis, fasting, exertion, febrile illness, etc. No clinical consequence.

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14
Q

Bilirubin system

A

Bilirubin transported to liver w/ albumin. Uptaked. Conjugated by UDP-Glucuronyl transferase (absent in Crigler Najjar and low in Gilbert) -> Secreted (defetive in Rotor and Dubin-Johnson) as bilirubin glucuronide. Turned into urobilinogen in GI. Some go back thru portal system to liver/urine. Others go to feces (brown).

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15
Q

Portacaval anastomoses

A

Varices = left gastric vein to esophageal vein. Hemorrhoids = superior rectal vein to middle/inferior rectal veins. Caput medusae = paraumbilical veins to superficial and inferior epigastric veins

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16
Q

Chronic mesenteric ischemia

A

Pt with atherosclerotic risk factors has pain after meals not responding to antacids and nothing on EGD. Due to atherosclerotic narrowing of celiac, SMA, IMA - not able to dilate in response to digestion.

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17
Q

Celiac disease pathology?

A

Atrophy of villi, flattening of mucosa, chronic inflammation of laminal propria. All reversible w/ gluten-free diet.

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18
Q

Foregut and blood supply

A

Esophagus, stomach, liver, gallbladder, pancreas, upper duodenum. Celiac

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19
Q

Midgut and blood supply

A

Lower duodenum, small intestine, ascending colon, proximal 2/3 of transverse colon. SMA

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20
Q

Hindgut and blood supply

A

Distal third of transverse, descending, sigmoid. IMA.

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21
Q

Midgut rotation

A

Midgut herniates through umbilical ring at wk 6 b/c slower growth of abdominal cavity. Return at wk 10 and completes 270 deg turn CCW around the SMA.

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22
Q

Pancreas divisum

A

Failure of ventral and dorsal buds to fuse at wk 8. Asymptomatic.

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23
Q

How does pregnancy predispose to gallstone formation?

A

Estrogen-induced HMG-CoA reductase activity = cholesterol hypersecretion. Progesterone induces gallbladder hypomotility

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24
Q

Hirschsprung disease path

A

RECTAL biopsy. Failure of neural crest cells to migrate to intestinal wall. Submucosa will demonstrate absence of ganglionic cells (Meissner). Rectum always involved (wk 12), sigmoid 75%. Present will failure to pass meconium within 48 hrs, intestinal obstruction.

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25
Q

Final pathway of pancreatitis pathogenesis following acinar cell injury

A

Intra-acinar conversion of trypsinogen to active trypsin! This leads to other activation (elastase, chymotrypsin, phospholipase)). Proteases auto digest. Elastase leads to vascular dmg and hemorrhage. Lipase/phospholipase -> fast necrosis

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26
Q

Reflux esophagitis patho

A

Elongation of papillae, basal cell hypertrophy, intraepithelial eosinophils

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27
Q

Primary Biliary Cirrhosis

A

Chronic. Autoimmune destruction of INTRAhepatic bile ducts and CHOLESTASIS. Middle-aged women, insidious. PRURITIS (esp. night), fatigue. Hepatosplenomegaly, xanthomatous lesions. Jaundice, steatorrhea, portal HTN. Labs - elevated alkPhos, cholesterol, and serum IgM. Dx = anti-mitochondrial antibodies. Associated w/ Sjogren’s, Raynaud’s scleroderma, autoimmune thyroid, hypothyroidism, and celiac disease

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28
Q

Hereditary pancreatitis

A

Mutations in trypsinogen or SPINK1 (trypsin inhibitor). Mot common mut -> abnl trypsin that is not susceptible to inactivating cleavage by trypsin.

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29
Q

True vs. pseudodiverticulum

A

True diverticula contain mucosa, submucosa, AND muscular layers. e.g. Meckel’s is failure of obliteration of vitelline duct (usu. wk 7). 2% of pop, 2 feet from ileocecal valve, 2 inches in length, 2% symptomatic, males 2x more affected. False diverticula DON’T contain muscularis (e.g. colonic and Zenker’s)

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30
Q

Ballooning degeneration of liver?

A

Hepatocyte swelling found along with mononuclear infiltrates and Councilman bodies histologically during acute viral hepatitis. Regeneration nodules found in chronic hepatitis.

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31
Q

Peptic ulcer disease ulcer sites?

A

First portion of duodenum within 3 cm of pylorus. Distal ulcers are not common (think Zollinger-Ellison)

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32
Q

Zenker diverticulum

A

Oftentimes, cricopharyngeal dysfunction leads to increased pharyngeal contractions required for swallowing b/c of diminished relaxation. (Traction diverticulum contains ALL layers).

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33
Q

How does HBV induce HCC?

A

Thought to be triggered by integration of viral DNA into genome. Synthesis of insulin-like growth factors, suppresses p53, chronic inflammation and regeneration.

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34
Q

Pernicious anemia pathology?

A

Parietal cell damage. Appear pale pink, round, plate-like in the upper gland layers. Loss of intrinsic factor-secreting parietal cells, marked infiltration by lymphocytes and plasma cells, and megaloblastic changes. (Chief cells that secrete pepsinogen are found in deeper glandular layers - small basophilic)

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35
Q

Brown pigment gallstones?

A

Usu. secondary to infection of biliary tract (E. coli, Ascarin, Opisthorchis sinuses). Injured hepatocytes and bacteria release Beta-glucuronidase -> hydrolysis of bilirubin glucoronides -> inc. unconjugated bilirubin in bile.

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36
Q

Schilling test

A

Used to ID cause of B12 deficiency. (1) Oral radio B12 w/ IM non-B12 (to ensure excretion) and check urine. If lots of urine radio B12 = good absorption and poor diet. If low radio B12 = poor absorption. Phase II = radio labeled B12 w/ intrinsic factor. If still high radio B12, then still poor absorption not corrected by IF (e.g. pancreatic insufficiency, ileal disease, intestinal bacterial overgrowth)

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37
Q

How does octreotide work?

A

It is a somatostatin analog. Inhibits glucagon and VIP —> reduced vasodilation –> splanchnic vasoconstriction w/o systemic vasoconstriction. Helpful for esophageal varices.

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38
Q

Palpable but NONtender gallbladder, wt loss, obstructive jaundice (pruritus, dark urine, pale stool)

A

Adenocarcinoma of the head of the pancreas compressing the common bile duct

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39
Q

Annular pancreas

A

Abnormal encirclement of the duodenum by the ventral pancreatic bud -> duodenal narrowing

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40
Q

What parts of the GI are retroperitoneal?

A

Lower 2/3 of esophagus. 2-4th part of the duodenum. Ascending and descending colon. Part of the rectum.

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41
Q

Retroperitoneal structure acronym

A

SAD PUCKER = Suprarenal glands, Aorta + IVC, Duodenum (2-4), Pancreas (except tail), Ureter, Colon (Des. and asc.), Kidneys, Esophagus (lower 2/3), Rectum

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42
Q

Falciform ligament

A

Connects liver to ant. abdominal wall. Contains ligamentum teres hepatic (fetal umbilical vein.).

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43
Q

Hepatoduodenual ligament

A

Contains the portal triad. Therefore, the Pringle maneuver (compressing ligament w/ one finger in lesser sac via omental foramen) controls bleeding.

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44
Q

Gastrohepatic ligament

A

Liver to LESSER curvature. Contains the gastric arteries.

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45
Q

Gastrosplenic ligament

A

Greater curvature to spleen. Contains the SHORT gastrics and L gastroepiploic vessels.

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46
Q

Splenorenal ligament

A

Contains splenic artery and vein. Tail of pancreas.

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47
Q

Where are Peyer’s patches found?

A

In the lamina propria and submucosa of the Ileum

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48
Q

Crypts of Lieberkuhn found where in GI?

A

Small and large intestine. NOT stomach (it has gastric glands).

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49
Q

Where are villi found in the GI?

A

Small intestine but NOT colon.

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50
Q

What GI regions does the vagus nerve and pelvic nerve innervate?

A

Pelvic nerve innervates hindgut (distal 1/3 of transverse colon to upper portion of rectum). Rest in vagus.

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51
Q

Three main branches of the celiac trunk?

A

Common hepatic, splenic, and left gastric.

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52
Q

Superior and inferior epigastric arteries anastomose what major systems?

A

Internal thoracic/mammary with external iliac.

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53
Q

Superior and inferior pancreaticoduodenal arteries anastomose what major systems?

A

Celiac and SMA

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54
Q

Middle colic and left colic arteries anastomose what major systems?

A

SMA and IMA

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55
Q

Superior rectal and middle/inferior rectal arteries anastomose what major systems?

A

IMA and the internal iliac.

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56
Q

Pectinate line - above & below arterial and venous

A

Above - superior rectal a. from IMA. Venous from superior rectal v. to IMV to portal system. Below - Inferior rectal a. from internal pudendal a. Inferior rectal vein to internal pudendal vein to internal iliac to IVC

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57
Q

Flow of bile and blood in the liver?

A

Blood flows from the portal triad (portal a. and vein) into the central vein (to hepatic veins and systemic circulation). Bile flows into the bold ductule.

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58
Q

Zones of the liver

A

Zone 1 = periportal and is first affected by viral hepatitis and ingested toxins. Zone 3 = (Centrilobular) pericentral vein zone and is affected 1st by ischemia = acetaminophen tox. Site of alcoholic hepatitis, CYP-450 system.

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59
Q

Femoral vessel organizatoin?

A

NAVEL is lateral to medial. Nerve, artery, vein, empty space, lymphatics.

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60
Q

Indirect vs. direct inguinal hernia

A

Lateral to epigastric vessels vs. medial to (in Hesselbach). Into the scrotum vs. only through external/superficial ring.. Infants/young ppl vs. older men.

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61
Q

Gastrin - action and regulation

A

Increases parietal cell H+ secretion, hypertrophies the gastric mucosa, (and increases gastric motility). Activated by stomach distention/alkalinzation, aa’s, peptides, and vagal stimulation. Repressed by a stomach pH < 1.5. Phenylalanine and tryptophan are particularly potent stimulators.

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62
Q

Gastrin produced where?

A

G-cells in the antrum of the stomach. (Zollinger-Elilson syndrome - gastrinoma)

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63
Q

CCK’s 5 major effects; How is it activated?

A

Contraction of gallbladder + relaxation of Oddi, secretion of pancreatic enzymes, secretion of HCO3 from pancreas, trophic effects on pancreas and gallbladder, inhibition of gastric emptying. Activated by FA’s and AA’s. Actions via neural muscarinic pathways.

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64
Q

CCK source

A

I cells of the duodenum and jejunum.

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65
Q

D, I, G, K, S cells are where and produce what?

A

D is pancreatic islets and GI mucosa; somatostatin. I cells are duodenum/jejunum and CCK. G is antrum of stomach and gastrin. K is duodenum and jejunum and GIP. S is duodenum and secretin.

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66
Q

Secretin’s actions and stimulation?

A

Stimulated by acid, FA’s in lumen of duodenum. Increases pancreatic bicarb, bile secretion, and DECREASED gastrin effects (H+). All for a better pH for pancreatic enzymes.

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67
Q

GIP’s actions and stimulation

A

Exocrine function is DEC. gastric H+ secretion while endocrine function is INC. insulin release. Stimulated by FA’s, aa’s, oral glucose.

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68
Q

Motilin function and activation

A

Increases in fasting state and produces migrating motor complexes. Made in small intestinee.

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69
Q

Somatostatin function and activation.

A

Activated by acid and inhibited by vagal stimulation. It is the INHIBITORY and anti-growth hormone. Decreased gastric acid and pepsinogen, pancreatic and small intestine fluid sections, dec. gallbladder contraction, dec. insulin and glucagon release

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70
Q

VIP source?

A

Parasympathetic ganglia in sphincters, gallbladder, small intestine. Or VIPoma - non-alpha, non-beta islet cell pancreatic tumor.

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71
Q

VIP function and activation?

A

Increases intestinal water and electrolyte secretion while relaxing intestinal smooth muscles and sphincters. Activated by distention and vagal stimulation. Inhibited by adrenergic input.

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72
Q

VIPoma symptoms?

A

WDHA syndrome. Watery Diarrhea, Hypokalemia, Achlorhydria.

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73
Q

Intrinsic factor f(x) and made where?

A

Made by parietal cells and is the vitamin-B12 binding protein for uptake in terminal ileum

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74
Q

Pepsin’s function and regulation?

A

Protein digestion. Activated by vagal stimulation and local acid (secreted by CHIEF cells in stomach). Pepsinogen to pepsin via H+.

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75
Q

What produces HCO3 in the GI tract?

A

Mucosal cells of the stomach, duodenum, salivary glands, and pancreas. As well as Brunner glands in the duodenum. Pancreatic and biliary secretion of HCO3 with secretin.

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76
Q

Gq acting substances on the gastric parietal cell?

A

Vagus nerve via Ach-M3 and GRP to G-cell -> Gastrin onto CCKb receptor.

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77
Q

cAMP acting substances on gastric parietal cell

A

Gs - Histamine from ECL cells. Gi - Prostaglandin/misoprostol and somatostatin.

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78
Q

Trypsinogen is activated how?

A

By enterokinase/enteropeptidase, which is located on the brush-border in the duodenal and jejunal mucosa. Some tripsinogen is activated by trypsin itself.

79
Q

D-xylose test

A

A monosaccharide that can be absorbed w/o the help of any enzymes. Test for urine excretion in 5 hours. Solely dependent on the health of the GI mucosa (e.g. Celiac, Whipple disease, small intestine bacterial overgrowth)

80
Q

How are carbs absorbed in intestine?

A

Glucose and galactose by Na+ dependent SGLT1. Fructose by facilitated diffusion via GLUT-5. On basolateral side, GLUT-2 transports these monosacharrides into the blood stream.

81
Q

Vitamin/mineral absorption?

A

Iron Fist, Baby. Duodenum for iron. Jejunum and ileum for folate. Terminal ileum for B12.

82
Q

M cells?

A

Sampling cells of the Peyer’s patches.

83
Q

Rate limiting step of bile synthesis?

A

Cholesterol 7alpha-hydroxylase, which is inhibited by bile salts.

84
Q

Composition of bile?

A

Bile salts, phospholipids, cholesterol, bilirubin, water, and ions.

85
Q

Function of bile

A

Emulsify lipids and vitamins. Cholesterol excretion. Membrane disrupt microbes.

86
Q

What enzyme conjugates bilirubin?

A

UDP-glucuronosyl transferase (liver)

87
Q

What are the fates of conjugated bilirubin in the gut?

A

First turned into urobilinogen by gut bacteria. 20% is reabsorbed into the enterohepatic system (of which a small 10% goes via kidney into the urine as urobilin). The other 80% of urobilinogen is excreted into feces as sterobilin.

88
Q

Diagnosis Meckel’s divericulum?

A

Meckel scan = 99mmTc-pertechnetate scan showing accumulation. Highly specific for gastric mucosa. Will find ectopic mucosa.

89
Q

Meckel diverticulum ectopic tissue?

A

Mostly gastric (–> acid and ulceration). Often pancreatic, colonic, small intestine, or endometrial.

90
Q

Cholecystenteric fistula

A

A large gallstone causes formation of fistula between gallbladder and small intestine leading to passage of stone but air in the gallbladder and biliary tree. Ileocecal valve catches gallstones -> gallstone ileus. Pain.

91
Q

Pathogenesis of hepatic encephalopathy

A

Increased lvls of ammonia, which depletes glutamate and alpha-ketoglutarate and increased osmolarity that causes astrocytic swelling and impairment. Also decreased brain glutamate stores -> impaired neurotransmission.

92
Q

Most common salivary gland tumor - histo

A

Pleomorphic adenoma. Painless, mobile mass. Histo - chondromyxoid stroma and epithelium

93
Q

Warthin tumor

A

Benign cystic tumor with germinal centers

94
Q

Most common malignant salivary gland tumor

A

Mucoepidermoid carcinoma. Mucinous and squamous. Painless, slow-growing mass.

95
Q

Etio of achalasia?

A

Failure of LES relaxation 2/2 loss of myenteric plexus. Secondary cause is Chagas disease.

96
Q

Lye ingestion—>

A

Esophageal strictures. Also associated with acid reflux

97
Q

Eosinophilic esophagitis

A

Atopic patients eating food allergens can lead to dysphagia, heartburn, strictures. Eos seen on histo

98
Q

Increased risk of what cancer 2/2 Barrett esophagus?

A

Esophageal adenocarcinoma

99
Q

Barrett esophagus histo?

A

Metaplasia from nonkeratinized stratified squamous epithelium to non-ciliated columnar epithelium with goblet cells. Moved up squamocolumnar junction (“Z” line).

100
Q

Areas of esophagus where you’d find squamous vs. adenocarcinoma?

A

Squamous in upper 2/3. Adeno in lower 1/3

101
Q

RF’s for esophageal squamous cell carcinoma?

A

Alcohol, Cigarettes, Zenker, esophageal web, hot liquids

102
Q

RF’s for esophageal adenocarcinoma?

A

Barrett, cigarettes, obesity, GERD

103
Q

RF’s overall for esophageal cancer?

A

AABCDEFFGH - Alcohol, Achalasia, Barrett, Cigarettes, Diverticula, Esophageal web, Familial, Fat, GERD, Hot liquids

104
Q

Etios of acute gastritis

A

Stress, NSAID, alcohol, uremia, burns (-> Curling ulcer where ischemia leads to gastric mucosa sloughing), brain injure (Cushing ulcer - inc. vagal tone -> H+ production)

105
Q

Type A vs. Type B chronic gastritis?

A

A is autoimmune [parietal cells, pernicious anemia, achlorhydria) and first part of stomach (funds). B is bacteria (H. pylori) and is second part of stomach (antrum)

106
Q

Menetrier disease

A

Precancerous lesion of stomach. Gastric hypertrophy (“brain gyri”-like) -> protein dolls, parietal cell atrophy. Increased mucous cells.

107
Q

Intestinal vs. diffuse stomach cancer?

A

Intestinal is associated with H. pylori vs. NOT. Lesser curvatures looking like ulcer vs. gross thickening and leathery (linitis plastic) w/ Signet ring cells. Intestinal is also associated with dietary nitrosamines (smoked food), tobacco, achlorhydia, chronic gastritis

108
Q

Krukenberg tumor

A

b/l metastases of stomach cancer to the ovaries. SIGNET ring cells.

109
Q

Sister Mary Joseph nodule

A

SQ periumbilical metastases 2/2 stomach cancer

110
Q

Gastric ulcer vs. Duodenal ulcer

A

Pain greater with meals vs. decreases with meals. Increased risk of carcinoma in GASTRIC ulcer. Zollinger-Ellison associated with duodenal. 70% of gastric ulcers with H. pylori whereas 100% of duodenal ulcers with H. pylori. NSAIDs gastric.

111
Q

Common hemorrhage site from gastroduodenal ulcers?

A

Lesser curvature gastric ulcer = L gastric artery. Posterior duodenal ulcer = gastroduodenal artery.

112
Q

Tropical spure

A

Unknown etiology, but responds to antibiotics. Recent travel to the tropics.

113
Q

Celiac sprue lab findings

A

Anti-endomysial, anti-tissue transglutaminase (diagnostic test), anti-gliadin Ab’s. HLA-DQ2 and DQ8 (Dairy Queen)

114
Q

Abetalipoproteinemia

A

Presents as FTT, steatorrhea, acanthocytosis, ataxia, night blindness. Due to decreased apoB synthesis = less CHYLo’s = less VLDLS = ACCUMULATION of fat in enterocytes. Histo shows foamy cells at GI mucosa. Smear shows ACANTHOCYTES 2/2 poor membrane production.

115
Q

Skip lesions

A

Crohn’s. Spares the rectum whereas UC is continuous always with rectal involvement.

116
Q

Lead pipe

A

UC. Loss of hausfrau.

117
Q

IBD with noncaseating granulomas?

A

Crohn’s disease. UC has crypt abscesses with NEUTrophils and ulcer but NO granulomas.

118
Q

Cobblestone mucosa

A

CD.

119
Q

How deep is the inflammation in Crohn’s vs. UC?

A

Crohn’s is TRANsmural. UC is mucosa and submucosa only.

120
Q

Extraintestinal manifestations of IBD

A

Both have pyoderma gangrenous, erythema nodosum, anklyosing spodylitis, apthous ulcers, uveitis.

121
Q

Tx for UC

A

sulfasalazine, 6-MP, infliximab, colectomy

122
Q

Tx for CD

A

Corticosteroids, azathioprine, methotrexate, infliximab, adalimumab (TNF-alpha)

123
Q

Complications of UC vs. CD

A

UC has sclerosing cholangitis, toxic megacolon. CD has strictures, fistulas, perianal disease. Both have colon cancer.

124
Q

Irritable bowel syndrome

A

Recurrent abdominal pain w/ 2+: relief on defecation, change in consistency, change in frequency.

125
Q

Appendicitis etios

A

Fecalith in adults but lymphoid hyperplasia in children

126
Q

Diverticulosis presentation

A

Often asymptomatic or with vague discomfort. May cause hematochezia.

127
Q

Diverticulitis presentation

A

Classically a LLQ pain, fever, leukocytosis. FOBT w/ +/0 hematochezia. If colovesical fistula, pneumaturia

128
Q

Where is Zenker’s diverticulum usu. location?

A

Killian triangle - between thyropharyngeal and cricopharyngeal parts of inferior pharyngeal constrictor.

129
Q

Meckel’s diverticulum presentation?

A

RLQ pain, melena, intussusception, volvulus, or obstruction.

130
Q

Intussusception

A

Telescoping. Commonly at ILEO-CECAL junction. Pain and currant jelly stool 2/2 compromised blood supply. Usu. children (might be associated with enteric or URI). If patient is older than 2, consider Meckel, foreign body, or intestinal tumor as the lead point.

131
Q

Volvulus

A

Midgut volvulus in children and sigmoid volvulus in elderly. Gut twists around own mesentery.

132
Q

GI pathology associations with Down’s

A

Hirschsprung’s, duodenal atresia (double bubble; failure to re-canalize)

133
Q

Ischemic colitis presentation

A

Pain after eating -> weight loss. often older people

134
Q

Peutz-Jegher’s

A

AD. Serine/threonine kinase gene 11 on ch. 19. Nonmalignant Hamartomas throughout GI. Hyperpigmented MOUTH, lips, hands, genitalia. Increased risk of colorectal cancer and other visceral malignancies.

135
Q

What type of polyps are recancerous?

A

Adenomatous. More villous, the more villainous.

136
Q

Juvenile polyps

A

Sporadic. < 5 y/o. Rectm.

137
Q

FAP vs. HNPCC etio

A

FAP is APC gene on 5q (20hit). HNPCC is AD mutation of DNA mismatch repair genes. 100% progress in FAP but only 80% in HNPCC do.

138
Q

Gardner syndrome

A

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

139
Q

Turcot syndrome

A

FAP + malignant CNS tumor

140
Q

Order of mutation events in colorectal cancer?

A

APC/Beta-catenin (sporadic, 80%), K-RAS, p53/DCC OR Microsatellite instability (~15%) in DNAN mismatch repair gene

141
Q

Manifestations of cirrhosis that are 2/2 to estrogen?

A

Spider angioma, palmar erythema, gynecomastia, testicular atrophy, decreased body hair, Dupuytren’s contractores. 2/2 to decreased metabolism of estrogen by failing living.

142
Q

Most specific lab for acute pancretitis?

A

Lipase

143
Q

Reye syndrome

A

Rare, often fatal childhood hepatoencephalopathy. Fatty liver, mitochondrial problems, hypoglycemia, vomiting. Aspirin metabolites decreased Beta-oxidation. Microvesicular steatosis on path.

144
Q

Alcoholic hepatitis vs. cirrhosis pathology?

A

Hepatitis has swollen, necrotic cells with Mallory bodies (intracytoplasmic eosinophilic inclusions). Cirrhosis has central vein sclerosis, shrunken liver.

145
Q

Treatment for hepatic encephalopathy?

A

Lactulose (ammonia ion generation, low0protein diet, rifaximin)

146
Q

HCC associations?

A

HBV, HCV, Wilson, hemochromatosis, alpha-1-antitrypsin, alcoholic cirrhosis, alfatoxin.

147
Q

HCC diagnosis?

A

alpha-fetoprotein; US or CT.

148
Q

Nutmeg liver?

A

Etio - Right-sided HF, Budd-Chiari. Leads to back up of blood. Can lead to centrilobular congestion and necrosis.

149
Q

Budd-Chiari syndrome

A

Occlusion of IVC or hepatic veins. Associated with hyper coagulable states, polycythemia vera, pregnancy, HCC.

150
Q

In what liver tumor is biopsy contraindicated?

A

Cavernous hemangioma (NOT angiosarcoma) b/c of risk of hemorrhage.

151
Q

Histopath for alpha-antitrypsin deficiency in the liver?

A

PAS+ globules in the liver

152
Q

How does urine urobilinogen change with unconjugated vs. conjugated hyperbilirubinemia?

A

Urine urobilinogen is HIGH in unconjugated hyperbilirubinemia. LOW in conjugated hyperbilirubinemia.

153
Q

Etios of conjugated hyperbilirubinemia?

A

Biliary tract obstruction. Biliary tract disease (primary sclerosing cholangitis, pBC). Excretion defect (Dubin-Johnson, Rotor)

154
Q

Etio of physiologic neonatal jaundice?

A

Immature UDP-glucuronylsyltransferase -> unconjugated hyperbilirubinemia. Tx = phototherapy.

155
Q

Rotor syndrome

A

Milder Dubin-Johnson. NO black liver.

156
Q

Crigler-Najjar syndrome.

A

ABSENT UDP-glucuronosyltransferase. EARLY in life. Patients die in couple of years. Jaundice, kernicterus, UNconjugated bilirubinemia. Type I is more severe than type II, which responds to phenobarbital to increase liver enzyme synthesis.

157
Q

Wilson disease specific brain findings

A

Basal ganglia degeneration. And sooo Parkinsonism. Dyskinesia, Dysarthria, Dementia. Asterixis.

158
Q

Treatment for Wilson’s disease

A

Penicillamine, trientine (Cu chelators)

159
Q

Gene defect in hemochromatosis

A

HFE gene - C282Y or H63D. Associated with HLA-A3.

160
Q

Treatment of hereditary hemochromatosis

A

Repeated phlebotomy, deferasirox, deferoxamine (these are Fe chelators)

161
Q

Classic Hemochromatosis triad?

A

CHF, Bronze diabetes, cirrhosis

162
Q

Labs in primary sclerosing cholangitis vs. primary biliary cirrhosis?

A

PBC has increased serum mitochondrial antibodies (IgM). PSC has hypergammaglobulinemia.

163
Q

Etiology of PBC vs. PSC?

A

PBC - autoimmune reaction of lymphocytes and granulomas of interlobular ducts. PSC - unknown onion-skin fibrosis of bile ducts that alternate into “beads” in the intra AND extra-hepatic bile ducts (Seen on ERCP)

164
Q

Radioopaque gallstones?

A

BLACK pigment stones - hemolysis.

165
Q

Radiolucent gallstones?

A

Brown pigment (infection) OR Cholesterol stones.

166
Q

Cholangitis symptom?

A

Charcot triad = fever, jaundice, and RUQ pain

167
Q

RF’s for gallstones?

A

4 F’s - Female, fertile, fat, forty

168
Q

Murphy sign?

A

Inspiratory arrest on RUQ palpation. Cholecystitis.

169
Q

Diagnosis cholecystitis how?

A

US or HIDA

170
Q

Complications of acute pancreatitis?

A

DIC, ARDS, diffuse fat necrosis, hypocalcemia, pseudocyst, hemorrhage, infection, multi organ failure.

171
Q

Etios of acute pancreatitis?

A

GET SMASHED = Gallstone, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion sting, Hypercalcemia/HyperTG, ERCP, Drug (sulfa), idiopathic.

172
Q

Trousseau syndrome

A

Migratory thrombophlebitis associated with pancreatic adenocarcinoma

173
Q

CA 19-9

A

Tumor marker for pancreatic adenocarcinoma

174
Q

Bismuth, sucralate f(x)?

A

Ulcer healing and traveler’s diarrhea. Binds to ulcer base for protection!

175
Q

Cimetidine side effects

A

P450 inhibitor. Antiandrogenic (gynecomastia, impotence, decreased libido), cross BBB (confusion, dizziness, HA), decrease renal excretion of Cr

176
Q

Misoprostol

A

PGE1 analog used to increased mucous barrier and decrease acid production. SE - diarrhea. Also an abortifacient.

177
Q

3 antacids

A

Aluminum hydroxide, calcium carbonate, magnesium hydroxide

178
Q

Major side effects of antaacids

A

Affect absorption of other drugs. Hypokalemia.

179
Q

Aluminum hydroxide

A

Constipation, hypophosphatemia. Proximal m. weakness, osteodystrophy, sz.

180
Q

Ca Carbonate side effects

A

Hypercalcemia, rebound acid increase. Decrease effectiveness of other drugs

181
Q

MgOH side effects

A

Diarrhea. Hyporeflexia, hypotension, cardiac arrest.

182
Q

Sulfasalazine

A

Combination of sulfapyridine and 5-aminosalicylic acid. Activated by COLONIC bacteria. Used for IBD. fox - malaise, nausea, sul fox, reversible oligospermia.

183
Q

Metoclopramide mech and usage

A

D2 receptor antagonist used to increase resting tone, contractility, LES tone, and motility. Anti-emetic. Used to treat gastroparesis.

184
Q

Metoclopramide tox

A

Increased parkinsonian effects. Contra’d in small bowel obstruction and parkinson disease.

185
Q

Ondansetron mech

A

5-HT3 antagonist. Decreased vagal stimulation decreases central-acting emesis.

186
Q

Corkscrew esophagus?

A

Diffuse esophageal spasm. Non-peristaltic, periodic contractions

187
Q

Incretins

A

Hormones secreted by gut mucosa in response to sugary meals to induce insulin response. GIP and GLP (glucagon-like peptide).

188
Q

Path for acetaminophen overdose?

A

Centrilobular necrosis that may include entire lobule.

189
Q

Pathogenesis of alcoholic liver disease?

A

Excess NADH production (using up NAD+) b/c of alcohol and aldehyde dehydrogenase -> decrease free FA oxidation (Can’t break down lipids!!!). Also have impaired lipoprotein assembly and increased peripheral fat catabolism -> fatty liver.

190
Q

Pathogenesis of colitis-associated colorectal carcinoma?

A

More likely to come from NON-polyploid dysplastic lesions, be multifocal, develop EARLY p53 and LATE APC, and HIGHER histological grade.

191
Q

Screen for malabsorption?

A

Sudan III stain of stool to identify fecal fat.

192
Q

How is free cholesterol converted into bile acid?

A

In the liver, cholesterol turned into cholic and chenodeoxycholic acid (7-alpha-hydroxylase). Then, bile acids conjugated to glycine and taurine -> bile salts, which are secreted into bile canaliculi.

193
Q

Left-sided vs. right-sided colon cancer?

A

Left-sided tends to have infiltrated the wall and encircled the lumen = dec. stool caliber, constipation, cramps, abdominal distention, n/v. Right-sided are exophytic masses = Fe-deficiency anemia (fatigue, pallor), anorexia, malaise, wt-loss. Right-sided is MORE INSIDIOUS.

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