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Gastrointestinal > FA 2 > Flashcards

FA 2 Flashcards

1
Q

Diverticulisis - complications/treatment of complications

A
  1. abscess
  2. fistula (colovesical –> pneumaturia)
  3. obstruction (inflammatory stenosis)
  4. perforation (–> peritonitis)
    treatment: percutaneous drainage or surgery
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2
Q

Acute mesenteric ischemia - presentation

A
  1. abdominal pain out of proportion of physical findings
  2. red currant jelly stools
  3. decreased sounds
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3
Q

Angiodysplasia - definition, presetation, location

A

acquired torturous dilation of vessels –> hematoscezia

MC often in cecum, terminal ileum, ascenidng colon

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4
Q

Colonic polyps - histological types (neoplastic or not?)

A
  1. hyperplastic - nonneoplastic
  2. hamartomatous - non-neoplastic
  3. adenomatous - neoplastic
  4. serrated - premalignant
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5
Q

Colonic polyps - Adenomatous - types and malignancy

A

tubular –> less malignant potential
villous –> more malignant potential
tubulovirous –> intermediate malignant potential

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6
Q

Serrated - mechanism/biopsy

A

premalignant, via CpG hypermethylation phenotype pathway with microsatellite instability
biopsy: saw-tooth pattern of crypts

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7
Q

Polyposis syndromes - types

A
  1. familiar adenomatous polyposis (FAP)
  2. Gardner syndrome
  3. Turcot syndrome
  4. Peutz-Jeghers syndrome
  5. Juvenile polyposis syndrome
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8
Q

Gardner syndrome?

A

FAP + osseus and sot tissue tumors, congenital hypertrophy of retinal pigment epithelium, impacted/supernumerary teeth

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9
Q

Turcot syndrome

A

FAP + malignant CNS tumor

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10
Q

Peutz-Jeghers syndrome - definition/mode of inheritance/presentation

A

AD syndrome featuring with numerous hamartomas throughout GI tract, along with hyperpigmented mounth, lips hands, genitalia

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11
Q

Peutz-Jeghers syndrome - cancer

A

increased risk of breast and GI cancers (eg. CR, stoma, small, panceas)

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12
Q

Juveniles polyposis syndrome - definition/mode of inheritance/presentation

A

AD syndrome in children (typically under 5) featuring with numerous hamartomatous polyps in large and small intestine, stomach

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13
Q

Lynch syndrome - cancers?

A
  1. Colorectal (de novo, not drom adenomatous polyp_
  2. ovarian
  3. endometrial
  4. skin
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14
Q

Colorectal cancer (CRC) - risk factors

A
  1. adenomatous polys
  2. serrated polys
  3. familiar cancer syndromes
  4. Inflammatory bowel disease
  5. tobacco use
  6. diet of processed meat with low fiber
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15
Q

Colorectal cancer (CRC) - location (in order)

A

rectosigmoid>ascending>descending

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16
Q

Colorectal Cancer - barium enema x-ray

A

“Apple core” lesion

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17
Q

Colorectal Cancer - markers/characteristics

A

CEA tumor marker –> food for monitoring recurrence, should not used for screening

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18
Q

γ-Glutamyl transpeptidase (γ-GT) - increased in

A
  • increased in various liver and biliary disease (just as ALP but not in bone disease
  • associated with alcohol use
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19
Q

Functional liver markers

A
  1. Bilirubin
  2. Albumin
  3. Prothrombin
  4. platelets
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20
Q

Functional liver markers - platelets (and mechanism)

A
  1. decreased in advanced liver disease (low thrombopoietin, liver sequestration)
  2. decreased in portal hypertension (splenomegaly/splenic sequestration)
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21
Q

hepatic steatosis?

A

Macrovesicular fatty change, heavy greasy liver, that may be reversible with alcohol cessation

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22
Q

alcoholic hepatitis - histology

A
  1. Swollen and necrotic hepatocytes with neutrophilic infiltration
  2. Mallory bodies
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23
Q

Mallory bodies - appearance

A

intracytoplasmic eosniphhiic inclusions of damaged keratin filaments

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24
Q

Hepatic encephalopathy - triggers example

A
  1. increased NH3 production and absorption –> dietary protein, GI bleed, constipation, infection
  2. decreased NH3 removal –> renal failire, diuretics, bypassed hepatic flow post-TIPS
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25
Q

Hepatic encephalopathy - treamtnet (and mechanism)

A
  1. lactulose –> increases NH4+ generation

2. rifamixn or neomycin –> decreases NH4+ producing gut bacteria

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26
Q

GI bleeding increases ammonia - mechanism

A

RBCs contain proteins Significant bleeding (esp upper GI) –> increases the protein load in the intestine and the production of ammonia

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27
Q

Diuretic therapy ammonia

A

Decreased serum potassium levels and alkalosis may facilitate the conversion of ammonium (NH4) to ammonia (+NH3).

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28
Q

Constipation - ammonia

A

Constipation increases intestinal production and absorption of ammonia

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29
Q

Liver tumors - types (and MC)

A
  1. Hepatocellular Carcinoma (hepatoma)
  2. Cavrnous hemangioma
  3. Hepatic adenoma
  4. Angiosarcoma
  5. Metastases (MC)
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30
Q

cancers that give metastasis to liver

A
  1. GI malignancies (Collon»stomach>pancreas)
  2. breast
  3. lung
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31
Q

A complication of Hepatocellular carcinoma (may lead to..)

Hepatocellular carcinoma spreads ….

A
  • Budd-Chiari syndrome

- hematogenously

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32
Q

Hepatocellular carcinoma - diagnosis

A
  1. increased a-fetoprotein
  2. US or contrast CT/MRI
  3. biopsy
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33
Q

Cavrnous hemangioma - frequency/behavior/epidimiology

A

common, benign liver tumor
typically occurs at 30 - 50
(NO BIOPSY–> hemorrhage)

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34
Q

Liver angiosarcoma - definition/risk factors

A

Malignant tumor of endothelial origin

associated with arsenic, vinyl chloride

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35
Q

Hepatic adenoma - definition/risk factors

A

Rare, benign liver tumor, often related to oral contraceptive or anabolic steroid use
- may regress spontaneously or rupture (abdominal pain and shock)

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36
Q

α1-antitrypsin deficiency causes (and mechanism

A
  1. misfolded gene product protein aggregates in hepatocellular ER –> Cirrhosis with PAS+ globules in liver
  2. lings –> low α1-antitrypsin –> uninhibited elastase in alveoli –> low elastic tissue –> panacinar emphysema
    (CONDOMINANT TRAIT)
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37
Q

bilirubin - levels

A

total: 0.1 - 1 mg/dL
direct: 0 - 0.3 mg/dL
indirect: 0.2 - 0.7 mg/dL
jaundice: more than 2.5 mg/dL

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38
Q

Causes of mixed (direct and inderect) hyperbilirubinemia

A
  1. Hepatitis

2. Cirrhosis

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39
Q

Wislon disease (hepalenticular degeneration) - mechanism

A

AR mutation in hepatocyte copper transporting ATPase (ATP7B gene, ch13) –> inadequate copper excretion into bile and blood (low serum ceruloplasmin, low serum copper, high urine copper) –> accumulates in liver, brain, kidneys, joints, cornea

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40
Q

Wislon disease (hepalenticular degeneration) - copper accumulates in (organs)

A
  1. liver 2. brain
  2. kidneys 4. joints
  3. cornea
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41
Q

Wislon disease (hepalenticular degeneration) - presentation

A

before 40 with

  1. liver disease (eg. hepatitis, acute liver failure, cirrhosis),
  2. neurologic disease (dysarthria, dystonia, tremor, parkinsonism
  3. psychiatric disease
  4. Kayser-Fleisher rings
  5. Hemolytic anemia
  6. renal disease (eg. Fanconi syndrome)
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42
Q

Hemochromatosis - iron accumulation especially in

A
  1. liver 2. pancreas 3. skin

4. heart 5. pituitary 6. joints

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43
Q

Hemochromatosis - lab/diangosis

A
  1. increased ferritin and iron, decreased TIBC –> increased transferrin saturation
  2. Liver MRI
  3. biopsy with Prussian blue stain
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44
Q

Hemochromatosis - clinical manigestation

A

classic triad: 1. cirrhosis 2. DM 3. Skin pigmentation (bronze diabetes). ALSO: 4. reversible dilated cardiomyopathy 5. hypogonadism 6. arthropathy 7. HCC

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45
Q

hemochromatosis - mechanism of arthropathy

A

calcium pyrophosphate deposition –> esp in metacarpophalangeal joints

46
Q

common cause of death in hemochromatosis

A

HCC

47
Q

wilson vs hemochromatosis according to age of presentation

A

wilson –> before 40
hemochromatosis –> after age of 40 when total body iron > 20g (iron loss through menstruation slows progression in women)

48
Q

wilson vs hemochromatosis according to treatment

A

hemochromatosis –> 1. repeated phlebotomy 2. chelation with deferasirox 3. deferoxamine
4. oral deferiprone
Wilson –> 1. chelation with penicillamine or trientine
2. oral zinc

49
Q

Hepatocellular carcinoma - paraneoplastic

A

EPO

50
Q

Biliary tract disease - clinical presentation

A
  1. pruritus
  2. jaundice
  3. dark urine
  4. light-colored stool
  5. hepatosplenomegaly
51
Q

Biliary tract disease - labs

A

cholestatic pattern of LFTs:

  1. increased CB
  2. increased cholersterol
  3. increased ALP
52
Q

Biliary tract diseases - types and epidemiology (what type of patients

A
  1. Priamary sclerosing cholangitis –> middle-aged men with IBD (UC)
  2. Primary billiary cirrhosis –> middle aged women
  3. Secondary biliary cirrhosis –> Patients with known pbstructive lesions (gallstone, biliary strictures, pancreatic carcnoma)
53
Q

Priamary sclerosing cholangitis - appearance (histology and gross)

A

histology –> concentric “onion skin” bile duct fibrosis (intrahepatic and extrahepatic ducts) –> alternating strictures and dilation “beading” on ERCP and MRCP

54
Q

Primary sclerosing cholangitis is associated with

A
  1. ulcerative colitis
  2. p-ANCA
  3. high IgM
55
Q

Primary sclerosing cholangitis can lead secondaty to

A
  1. biliary cirrhosis
  2. cholangiocarcinoma
  3. gallbpaladder cancer
56
Q

Primary biliary cirrhosis - mechanism

A

anti - mitochondrial antibodies –> autoimmune reaction –> lymphocytic infiltrate + granulomas –> destraction of intralobular bile ducts

57
Q

Primary biliary cirrhosis - associated with

A
  1. anti - mitochondrial antibodies
  2. increased IgM
  3. other autoimmune conditions (eg. Sjogren, CREST, Hashimoto, RA, celiac disease)
58
Q

Secondary biliary cirrhosis - mechanism

A

extrahepatic biliary obstruction (gallstones,, biliary structures, pancreatic Ca) –> high pressure in intrahepatic ducts –> injury/fibrosis and bile stasis

59
Q

Gallstones (cholelithiasis) - types (MC)

A
  1. Cholesterol stones (MC - 80%)

2. Pigment stones

60
Q

cholelithiasis - definition and types and radiolucent of radiopaque

A

cholelithiasis: solide round stone in gallbladder
1. Cholesterol stones –> radiolucent with 10-20% radiopaque due to calcifications
2. Pigment stones –> if black –> radiopaque (Ca2+ bilirubinate, hemlyisis), if brown (infection) –> radiolucent

61
Q

cholelithiasis - cholesterol stones are associated with

A
  1. estrogen (female, obesity, multiparity, estrogen therapy)
  2. Crohn
  3. advanced age
  4. rapid weight loss
  5. Native american origin
  6. Fibrates
62
Q

cholelithiasis - pigment stones are associated with

A
  1. Crohn
  2. chronic hemolysis
  3. Alcoholic cirrhosis
  4. advanced age
  5. biliary infections (Ascaris lumbricoides, Clonarchis sinensis)
  6. total partental nutrition
63
Q

Mirizzi’s syndrome is a rare complication in which

A

gallstone in cystic duct of gallbladder –> compression of the common bile duct common hepatic duct –> obstruction and jaundice

64
Q

acute pancreatitis - diagnosis

A

2 of 3 critera

  1. acute peigastric pain (often radiating to the back)
  2. high serum amylase or lipase (more specific) to 3x upper limit of normal
  3. characteristic imaging findings
65
Q

pancreatic pseudocyst risk for

A

rupture –> enzymes in the abnominal cavity and hemorrhage

66
Q

Pancreatic abscess - due to, presents with

A

due to E. Coli

presents with abdominal pain, high fever, persistently elevated amylase

67
Q

special clinical presentation in necrotic pancreatitis

A

Periublical (Cullen’s sign) and flank (Grey Turner) hemorrhage

68
Q

Chronic pancreatitis - serum enzymes

A

amilase and lipase may or may not be elevated

69
Q

pancreatic adenocarcinoma - Risk factors

A
  1. Tobacco 2. chronic pancreatitis (esp >20 years)

3. Diabetes 4. >50 age 5. Jewish and African amerinan males

70
Q

pancreatic adenocarcinoma - clinical presentation

A
  1. abdominal pain radiating to back
  2. Weigh loss (malabsrorption and anorexia)
  3. Migratory thrombophlibitis (Trousseau syndrome)
  4. Obstrctive jaundice (and pale stool) with Courvoisier sign (if at head)
  5. secondary DM (if at body or tail)
71
Q

pancreatic adenocarcinoma - markers

A
  1. CA 19-9,

2. CEA (not specific)

72
Q

pancreatic adenocarcinoma - Courvoisier sign?

A

presence of a palpably enlarged gallbladder which is nontender and accompanied with mild painless jaundice, the cause is unlikely to be gallstones

73
Q

CEA as a marker

A

not specific

  1. colorectal ca (70%)
  2. pancreatic ca (70%)
  3. gastric ca
  4. breast ca
  5. medullary thyroid ca
74
Q
  1. primary biliary cirrhosis - antibodies
  2. antoimmue hepatitis type 1 - antibodies
  3. Biliary tract disease associated with ulcerative colitis
A
  1. antimitochondrial
  2. anti smooth muscle
  3. primary sclerosing cholangitis
75
Q

H2 blockers - drugs

A
  • TIDINE

1. Cimetidine 2. Ranitidine 3. Famotidine 4. Nizatidine

76
Q

H2 blockers - clinical use

A
  1. Peptic ulcer
  2. gastritis
  3. mild esophageal reflux
77
Q

H2 blockers - adverse effect

A
  1. cimetidine inhibits p-450
  2. cimetidine has antiandrogenic effects (prolactin release, gynecomastia, impotence, low libido in males)
  3. cimetidine can cross BBB (confusion, dizziness, headache) and placenta
  4. Cimetidine and ranitidine –> decrease renal excretion of creatinine
    other H2 blockers are relatively free ok all these effects
78
Q

proton pump inhibitors (PPIs) - adverse effects

A
  1. high risk for C. difficile infection
  2. high risk for pneumonia
  3. low serum Mg2+ with long-term use
79
Q

Antiacid affect on other drugs - mechansim

A

Can affect asbsorption, biovailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastrinc emptying

80
Q

Antiacids - drugs

A
  1. Aluminium hydroxide
  2. calcium carbonate
  3. Magnesium hydroxide
81
Q

Aluminium hydroxide - toxicity

A
  • all antiacids can cause hypokalemia

- constipation and hypophosphatemia, proximal muscle weakness, osteodystrophy, seizures

82
Q

calcium carbonate - toxicity

A
  • all antiacids can cause hypokalemia
  • hypercalcemia (milk-alkali syndrome
  • rebound acid increasing
83
Q

Magnesium hydroxide - toxicity

A
  • all antiacids can cause hypokalemia
  • diarrhea
  • hyporeflexia
  • hypotension
  • cardiac arrest
84
Q

Bismuth - similar drug/mechanism of action

A

Similar drug: sucralfate
Binds to ulcer base, providing physical protection and allowing HCO-3 secretion to reestablish pH gradient in the moucous layer

85
Q

Bismuth, sucralfate - clinical use

A
  1. increases ulcer healing

2. travelers diarrhea

86
Q

Misoprostol - mechanism of action

A

A PGE1 analog –> 1. increases production and secretion of gastric mucous barrier
2. decreases acid production

87
Q

Misoprostol - clinical use

A
  1. Prevention of NSAID-induced peptic ulcers (NSAID block PDE1 production)
  2. maintenance of PDA
  3. off label for induction of labor (ripens cervix)
88
Q

Misoprostol - adverse effect

A
  1. Diarrhea

2. contraindicated in women of childbearing potential (abortifacient)

89
Q

Octreotide - mechanism

A
  • Long acting somatostatin analog

- Inhibits secretion of various splanchnic vasodilatory hormones

90
Q

Octreotide - clinical use

A
  1. acute variceal bleeds
  2. acromegaly
  3. VIPoma
  4. carcinoid tumors
  5. gastrinoma
  6. glucagonoma
91
Q

Octreotide - adverse effects

A
  1. nausea
  2. cramps
  3. steatorrhea
  4. increased risk for cholelithiasis (inhibition of CCK)
92
Q

Sulfasalazine - mechanism

A

A combination of sulfapyridine (antibacterial) and 5- aminosalicylic acid (anti-inflammatory) –> activated by colonic bacteria

93
Q

Sulfasalazine - clinal use

A
  1. Ulcerative colitis
  2. Crohn disease
    (colitis component)
94
Q

Sulfasalazine - adverse effect

A
  1. malaise 2. nausea 3. sulfonamide toxicity

4. reversible oligospermia

95
Q

Osmotic lexatives - drugs

A
  1. Magnesium hydroxide
  2. magnesium citrate
  3. polyethlene glycol
  4. lactulose
96
Q

Loperamide - mechanism of action

A

agonist at μ-opiodi receptor –> slows gut motility

POOR CNS penetration –> low addictive potential

97
Q

Loperamide - clinical use / SE

A

Diarrhea

SE: 1. constipation 2. nausea

98
Q

Ondansetron - mechanism of action

A

5-HT3 agonists –>a. decreases vagal stimualtion

b. central acting antiemetic

99
Q

Ondansetron - clinical use

A

control vomiting:

a. postoperatively
a. in cancer chemotherapy

100
Q

Ondansetron - adverse effect

A
  1. Headache
  2. constipation
  3. QT interval prolongation
101
Q

Metoclopramide - mechanism

A

D2 receptor agonists –> increased resting tone, conractility, LES tone, motility (does not influence colon transport time)

102
Q

Metoclopramide - clinical use

A
  1. Diabetic and postsurgery gatroparesis

2. antiemetic

103
Q

Metoclopramide - adverse effects

A
  1. increased parkinsonian effects, tardtive dyskenisia
  2. restlessness/fatique 3. drawsiness 4. depression
  3. diarrhea 6. Interaxt with digoxin and diabetic agents
104
Q

Metoclopramide - drug interactions

A
  1. digoxin

2. diabetic agents

105
Q

Metoclopramide - Contraindicated in

A

patients with small bowel obstruction or Parkinson disease

106
Q

Orlistat - mechanism

A

inhibits gastric and pancreatic lipase –> decreases breakdown and absorption of dietary fats

107
Q

Orlistat - clinical use

A

weight loss

108
Q

Orlistat - adverse effects

A
  1. steatorrhea

2. decreased absorption of fat-soluble vitamins

109
Q

Ursodiol (ursodeoxycholic acid) - mechanism

A

nontoxic bile acid –> increases bile acid secretion and decreases cholesterol secretion and reabsorption

110
Q

Ursodiol (ursodeoxycholic acid) - clinical use

A
  1. primary biliary cirrhosis

2. gallostone prevention or dissolution

Gastrointestinal (4 decks)

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