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1
Q

Colorectal cancer

A

most all arise from adenomas
liver is most common site of distant spread
most common cause of large bowel obstruction in adults

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2
Q

Colorectal staging

A
Duke's staging
A- muscularis mucosa only (90% 5 yr)
B- past muscularis mucosa, no nodes (70%)
C- positive regional nodes (40%)
D- distant mets (5%)
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3
Q

Colorectal cancer risk factors

A
age (>50)
Adenomatous polyps (villous)
Prior CRC
Inflammatory bowel disease (UC > Chron's)
Family hx
Dietary
Polyposis syndromes
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4
Q

Familial adenomatous polyposis

A

autosomal dominant
colon always involved, duodenum (90%)
CRC risk 100% by 20’s-30’s
prophylactic colectomy

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5
Q

Gardner’s syndrome

A

Polyps + osteomas, dental abnormalities, benign soft tissue tumors, desmoid tumors, sebaceous cysts
CRC risk 100% by 40

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6
Q

Turcot’s syndrome

A

autosomal recessive

polyps + neuro tumor (medulloblastoma, glioblastoma multiforme)

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7
Q

Peutz-Jaghers

A

single or multiple hamartomas throughout GI tract
pigmented spots around lips, oral mucusa, face
intussusception or GI bleeding may occur

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8
Q

Familial juvenile polyposis coli

A

presents in childhood, small risk CRC

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9
Q

Hereditary non-polyposis CRC

A

Lynch syndrome I- early onset CRC, absent multiple polyposis

Lynch synd II- as above + other cancers

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10
Q

Diverticulosis

A

caused by increased intraluminal pressure
most commonly in sigmoid colon
LLQ discomfort, bloating, constipation/diarrhea

Dx: barium enema
Complications: painless rectal bleeding (40%)

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11
Q

Diverticulitis

A

impacted feces in diverticulum
fever, LLQ pain, leukocytosis

Dx: CT scan with contrast
Tx: initial- IV abx, bowel rest, iV fluids
Multiple episodes- surgery

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12
Q

Abx with frequent association to pseudomembranous colitis

A

clindamycin
ampicillin
cephalosporins

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13
Q

Child’s classification

A

A- no ascites, bili < 2, no enceph, good nutrition, albu > 3.5
B- controlled ascites, bili 2-2.5, minimal enecph, good nutrition, albu 3-3.5
C- uncontrolled ascites, billi >3, sever enceph, poor nutrition, albu < 3

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14
Q

Wilson’s disease

A

deficiency of ceruloplasmin, can’t excrete copper

Tx: D-penicillamine, chelating agent

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15
Q

asymptomatic elevation of LFTs

A
Autoimmune hepatitis
hep B
hep C
Drugs or toxins
Ethanol
Fatty liver (triglyceridemia)
Growths (tumors)
Hemodynamic disorders (CHF)
Iron (hemochromatosis), copper (wilsons), AAT deficiency
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16
Q

Boa’s sign

A

referred right subscapular pain of biliary colic

17
Q

Charcot’s triad

A

RUQ pain
jaundice
fever

cholangitis- only in 50-70% pts

18
Q

Reynolds’ pentad

A

Charcot’s triad + septic shock and altered mental status

19
Q

antimitochondrial antibodies (AMAs)

A

positive in 90-95% of primary biliary cirrhosis

98% specificity

20
Q

Ranson’s criteria

A

Assess acute pancreatitis

Glucose > 200
Age > 55
LDH > 350
AST > 250
WBC > 16,000
21
Q

Small bowel obstruction

A

Dehydration is key
Intestinal distention causes reflex vomiting, increased secretions proximal to obs, decreased absorption -> hypochloremia, hypokalemia, metabolic alkalosis

22
Q

Extraintestinal manifestations of IBD

A
Eye- Episcleritis, Anterior uveitis
Skin- Erythema nodosum (CD), Pyoderma gangrenosum (UC)
Arthritis- Migratory monoarticular arthritis, Ankylosing spondylitis, Sacroiliitis
Thromboembolic-hypercoagulable
Idiopathic thrombocytopenic purpura
Osteoporosis
Gallstones (CD, ileal involvement)
Sclerosing cholangitis (UC)
23
Q

Sulfasalazine

A

main treatment for IBD (UC, CD)

Mesalamine (5-ASA) is active component (metabolite from intestinal bacteria breakdown)