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USMLE 1 > Gastrointestinal- Phatology (2) > Flashcards

Gastrointestinal- Phatology (2) Flashcards

1
Q

Acute mesenteric ischemia

A

Critical blockage of intestinal blood flow (often embolic occlusion of SMA) Ž small bowel necrosis Ž abdominal pain out of proportion to physical findings. May see red “currant jelly” stools.

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2
Q

Chronic mesenteric ischemia

A

“Intestinal angina”: atherosclerosis of celiac artery, SMA, or IMA Ž intestinal hypoperfusion Ž postprandial epigastric pain Ž food aversion and weight loss.

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3
Q

Colonic ischemia

A

Crampy abdominal pain followed by hematochezia.

Commonly occurs at watershed areas (splenic flexure, distal colon). Typically affects elderly.

Thumbprint sign on imaging due to mucosal edema/hemorrhage.

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4
Q

Angiodysplasia

A

Tortuous dilation of vessels Ž hematochezia. Most often found in the right-sided colon. More common in older patients.

Confirmed by angiography. Associated with aortic stenosis and von Willebrand disease

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5
Q

Adhesion

A

Fibrous band of scar tissue; commonly forms after surgery.

Most common cause of small bowel obstruction, demonstrated by multiple dilated small bowel loops on x-ray

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6
Q

Ileus

A

Intestinal hypomotility without obstruction Ž constipation and decrease flatus; distended/tympanic abdomen with decrease bowel sounds.

Associated with abdominal surgeries, opiates, hypokalemia, sepsis.

Treatment: bowel rest, electrolyte correction, cholinergic drugs (stimulate intestinal motility).

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7
Q

Meconium ileus

A

In cystic fibrosis, meconium plug obstructs intestine, preventing stool passage at birth.

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8
Q

Necrotizing enterocolitis

A

Seen in premature, formula-fed infants with immature immune system.

Necrosis of intestinal mucosa (primarily colonic) with possible perforation, which can lead to pneumatosis intestinalis, free air in abdomen, portal venous gas.

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9
Q

Colonic polyps

- Non-neoplastic

A

Hamartomatous polyps (Peutz-Jeghers syndrome and juvenile polyposis)

Mucosal polyps

Inflammatory pseudopolyps (inflammatory bowel disease)

Submucosal polyps (lipomas, leiomyomas, fibromas)

Hyperplastic polyps (Most common; in rectosigmoid)

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10
Q

Colonic polyps

- neoplastic

A

Adenomatous polyps: with mutations in APC and KRAS. Tubular histology has less malignant potential than villous.

Serrated polyps: Characterized by CpG island methylator phenotype (CIMP). Defect may silence MMR gene (DNA mismatch repair) expression. Mutations lead to microsatellite instability and mutations in BRAF. “Sawtooth” pattern of crypts on biopsy. Up to 20% of cases of sporadic CRC

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11
Q

Polyposis syndromes

- Familial adenomatous polyposis

A

Autosomal dominant mutation of APC 5q21.

Thousands of polyps arise starting after puberty; pancolonic; always involves rectum.

Prophylactic colectomy or else 100% progress to CRC

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12
Q

Polyposis syndromes

- Gardner syndrome

A

FAP + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium,
impacted/supernumerary teeth.

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13
Q

Polyposis syndromes

- Turcot syndrome

A

FAP/Lynch syndrome + malignant CNS tumor (eg, medulloblastoma, glioma). Turcot = Turban

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14
Q

Polyposis syndromes

- Peutz-Jeghers syndrome

A

Autosomal dominant syndrome.

Numerous hamartomas throughout GI tract, along with
hyperpigmented mouth, lips, hands, genitalia.

Associated with risk of breast and GI cancers (eg,
colorectal, stomach, small bowel, pancreatic).

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15
Q

Polyposis syndromes

- Juvenile polyposis syndrome

A

Autosomal dominant syndrome in children (typically < 5 years old).

Featuring numerous hamartomatous polyps in the colon, stomach, small bowel. Associated with  risk of CRC.

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16
Q

Polyposis syndromes

- Lynch syndrome

A

hereditary nonpolyposis colorectal cancer (HNPCC).

Autosomal dominant mutation of DNA mismatch repair genes with subsequent microsatellite instability.

∼ 80% progress to CRC. Proximal colon is always involved. Associated with endometrial, ovarian, and
skin cancers.

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17
Q

Colorectal cancer

  • Epidemiology
  • Risk factors
A

Most patients are > 50 years old. ~ 25% have a family history.

Adenomatous and serrated polyps, familial cancer syndromes, IBD, tobacco use, diet of processed meat with low fiber.

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18
Q

Colorectal cancer

  • Ascending
  • Descending
A
  • Rectosigmoid > ascending > descending.

Exophytic mass, iron deficiency anemia, weight loss.

Infiltrating mass, partial obstruction, colicky pain, hematochezia.

*Rarely, presents with S bovis (gallolyticus) bacteremia.

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19
Q

Colorectal cancer

- Diagnosis

A

Screen low-risk patients starting at age 50 with
colonoscopy. alternatives include flexible sigmoidoscopy, fecal occult blood testing (FOBT), fecal immunochemical testing (FIT), and CT colonography.

“Apple core” lesion seen on barium enema x-ray.

CEA tumor marker: good for monitoring recurrence.

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20
Q

Molecular pathogenesis of colorectal cancer

A

Chromosomal instability pathway: mutations in APC cause FAP and most sporadic CRC (via adenoma-carcinoma sequence AK-53) APC Ž KRAS Ž P53

Microsatellite instability pathway: mutations or methylation of mismatch repair genes (eg, MLH1) cause Lynch syndrome and some sporadic CRC (via serrated polyp pathway).

*Overexpression of COX-2 has been linked to colorectal cancer

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21
Q

Cirrhosis

- Etiologies

A

alcohol, nonalcoholic steatohepatitis, chronic viral hepatitis, autoimmune hepatitis, biliary disease, genetic/metabolic disorders.

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22
Q

Portal hypertension

- Etiologies

A

cirrhosis, vascular obstruction (eg, portal vein thrombosis, Budd- Chiari syndrome), schistosomiasis.

23
Q

Spontaneous bacterial peritonitis

  • Physiopatology
  • Clinical features
  • Etiology
A

bacterial infection in patients with cirrhosis and ascites.

Often asymptomatic, but can cause fevers, chills, abdominal pain, ileus, or worsening encephalopathy.

Commonly caused by aerobic gram ⊝ organisms (eg, E coli, Klebsiella) or less commonly Streptococcus.

24
Q

Spontaneous bacterial peritonitis

  • Diagnosis
  • Treatment
A

Diagnosis: paracentesis with ascitic fluid absolute neutrophil count (ANC) > 250 cells/mm3.

Empiric first-line treatment is 3rd generation cephalosporin (eg, cefotaxime).

25
Q

Serum markers of liver pathology

A

Pag. 384

26
Q

Reye syndrome

A

Reye of sunSHINE:

Steatosis of liver/hepatocytes
Hypoglycemia/Hepatomegaly
Infection (VZV, influenza)
Not awake (coma)
Encephalopathy

*Avoid aspirin in children, except in those with Kawasaki disease.

27
Q

Alcoholic liver disease

- Phases

A
  1. Hepatic steatosis
  2. Hepatic steatosis (Mallory bodies, AST > ALT)
  3. Alcoholic cirrhosis (Sclerosisaround central vein)
28
Q

Nonalcoholic fatty liver disease

A

Metabolic syndrome (insulin resistance); obesity Ž fatty infiltration of hepatocytes A Ž cellular “ballooning” and eventual necrosis.

ALT > AST

29
Q

Hepatic encephalopathy

A

Cirrhosis Ž portosystemic shunts Ž low NH3 metabolism Ž neuropsychiatric dysfunction.

Treatment: lactulose ( NH4 + generation) and rifaximin or neomycin (NH3 producing gut bacteria).

30
Q

Hepatocellular carcinoma/hepatoma

- Associations

A

Associated with HBV (+/− cirrhosis) and all other causes of cirrhosis, and specific carcinogens (eg, aflatoxin from Aspergillus). May lead to Budd-Chiari syndrome.

31
Q

Hepatocellular carcinoma/hepatoma

  • Findings
  • Diagnosis
A

Findings: jaundice, tender hepatomegaly, ascites, polycythemia, anorexia. Spreads hematogenously.

Diagnosis: α-fetoprotein; ultrasound or contrast CT/MRI, biopsy.

32
Q

Other liver tumors

A

Cavernous hemangioma (Most common benign liver tumor, biopsy is contraindicated).

Hepatic adenoma: often related to oral contraceptive or anabolic steroid use. may regress spontaneously or rupture

Angiosarcoma: associated with exposure to arsenic, vinyl chloride

33
Q

Budd-Chiari syndrome

A

Thrombosis or compression of hepatic veins with centrilobular congestion and necrosis Ž congestive liver disease.

Absence of JVD. Associated with hypercoagulable states, polycythemia vera, postpartum state, HCC.

May cause nutmeg liver

34
Q

α1-antitrypsin deficiency

A

cirrhosis withcPAS ⊕ globules in liver. Codominant trait.

Often presents in young patients with liver damage and dyspnea without a history of smoking.

*panacinar emphysema

35
Q

Jaundice

- Etiologies

A

HOT Liver—common causes of high bilirubin level:

Hemolysis
Obstruction
Tumor
Liver disease

36
Q

Unconjugated (indirect) hyperbilirubinemia

- etiologies

A

Hemolytic, physiologic (newborns), Crigler-Najjar, Gilbert syndrome.

37
Q

Conjugated (direct) hyperbilirubinemia

- Etiologies

A

Biliary tract obstruction

Biliary tract disease: 1° sclerosing cholangitis, 1° biliary cholangitis

Excretion defect: Dubin-Johnson syndrome, Rotor syndrome.

38
Q

Hereditary hyperbilirubinemias

  • Gilbert syndrome
  • Crigler-Najjar syndrome, type I
A

Mildly decrease UDP glucuronosyltransferase. Asymptomatic/benign

Absent UDP-glucuronosyltransferase. kernicterus. plasmapheresis and phototherapy.

39
Q

Hereditary hyperbilirubinemias

  • Dubin-Johnson syndrome
  • Rotor syndrome
A

Defective liver excretion. Grossly black (Dark) liver. Benign.

Is similar, but milder in presentation without black liver.

40
Q

Wilson disease (hepatolenticular degeneration)

  • Etiology
  • affected organs
A

Autosomal recessive (ATP7B gene; chromosome 13).

Copper accumulates, especially in liver, brain, cornea, kidneys; High urine copper.

41
Q

Wilson disease (hepatolenticular degeneration)

  • Clinical presentation
  • Treatment
A

Presents before age 40 with liver disease, neurologic
disease, psychiatric disease, Kayser-Fleischer rings, hemolytic anemia, renal disease (eg, Fanconi syndrome).

Treatment: chelation with penicillamine or trientine, oral zinc.

42
Q

Hemochromatosis

  • Etiology
  • Affected organs und diagnosis
A

Autosomal recessive. C282Y mutation > H63D mutation on HFE gene, located on chromosome 6;
associated with HLA-A3.

Iron accumulates, especially in liver, pancreas, skin, heart, pituitary, joints. Hemosiderin (iron) can be identified on liver MRI or biopsy with Prussian blue stain.

43
Q

Hemochromatosis

  • Clinical presentation
  • Treatment
A

Presents after age 40 when total body iron > 20 g; Classic triad of cirrhosis, diabetes mellitus, skin pigmentation (“bronze diabetes”). Also cardiomyopathy, hypogonadism, arthropathy.

Treatment: repeated phlebotomy, chelation with deferasirox, deferoxamine, oral deferiprone.

44
Q

Primary sclerosing cholangitis

  • Phatology
  • Epidemiology
  • Associations
A

concentric “onion skin” bile duct fibrosis Ž alternating
strictures and dilation with “beading” of intra- and
extrahepatic bile ducts on ERCP, magnetic resonance
cholangiopancreatography (MRCP).

Classically in middle-aged men with IBD.

Associated with ulcerative colitis. p-ANCA ⊕. High IgM.

45
Q

Primary biliary cholangitis

  • Phatology
  • Epidemiology
  • Associations
A

Autoimmune reaction Ž lymphocytic infiltrate + granulomas Ž destruction of lobular bile ducts.

Classically in middle-aged women.

Anti-mitochondrial antibody ⊕, high IgM. Associated with other autoimmune conditions.

46
Q

Secondary biliary cholangitis

  • Phatology
  • Epidemiology
  • Associations
A

Extrahepatic biliary obstruction Ž pressure in intrahepatic ducts Ž injury/ fibrosis and bile stasis.

Patients with known obstructive lesions

May be complicated by ascending cholangitis.

47
Q

Porcelain gallbladder

A

Calcified gallbladder due to chronic cholecystitis; High rate of gallbladder cancer.

48
Q

Ascending cholangitis

A

Charcot triad of cholangitis includes jaundice, fever, RUQ pain.

Reynolds pentad is Charcot triad plus altered mental status and shock (hypotension).

49
Q

Acute pancreatitis

- Etiologies

A

I GET SMASHED:

Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia/Hypertriglyceridemia (> 1000 mg/dL), ERCP, Drugs (eg, sulfa drugs, NRTIs, protease inhibitors).

50
Q

Acute pancreatitis

- Diagnosis

A

By 2 of 3 criteria: acute epigastric pain often radiating to the back, high serum amylase or lipase (more specific) to 3× upper limit of normal, or characteristic imaging findings.

51
Q

Chronic pancreatitis

A

Chronic inflammation, atrophy, calcification of the pancreas. Major causes include alcohol abuse and genetic predisposition

Pancreatic insufficiency (typically when <10% pancreatic function) may manifest with steatorrhea, fat-soluble vitamin deficiency, diabetes mellitus.

52
Q

Pancreatic adenocarcinoma

- Phatology

A

arising from pancreatic ducts. Tumors more common in pancreatic head. Associated with CA 19-9 (also CEA, less specific).

53
Q

Pancreatic adenocarcinoma

- Risk factors:

A 
ƒƒ Tobacco use
ƒƒ Chronic pancreatitis (especially > 20 years)
ƒƒDiabetes
ƒƒ Age > 50 years
ƒƒ Jewish and African-American males
54
Q

Pancreatic adenocarcinoma

- Clinical presentation

A

Abdominal pain radiating to back

Weight loss

Trousseau syndrome

Courvoisier sign

USMLE 1 (73 decks)

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