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M2 > GI > Flashcards

GI Flashcards

0
Q

What are stellate cells?

A 
Ito cells
Reside w/in Space of Disse
Store lipid and vitam A
Produce reticular fibers
Cirrhosis:  multiply and produce large amounts of ECM
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1
Q

What activities are carried out in Zone 1 vs Zone 3 of hepatic lopules?

A

Zone 1: adjacent to triad, O2 rich. gluconeogenesis, B-oxidation, AA metabolism, formation of urea

Zone 3: adjacent to central vein, O2 poor. P450 reactions, lipid synthesis, glycolysis

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2
Q

3 classifications of liver disease

A
  1. Hepatocellular: acute, fulminant, chronic
  2. Cholestatic: intrahepatic, extrahepatic
  3. Cirrhosis
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3
Q

What viruses are associated with hepatocellular injury?

A

Hepatotropic: Hepatitis A,B,C,D,E

Systemic: EBV, CMV, HSV, enterovirus

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4
Q

What are microscopic features of acute hepatitis?

A

lobular disarray - disruption of architecture
ballooning degeneration
apoptotic bodies (Councilman bodies)
inflammatory infiltrates, activated Kupffer cells
regeneration (with resolution)

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5
Q

What is fulminant hepatitis?

A

Rare variant of acute hepatitis. Rapid onset of liver failure over period of days - weeks.
Heralded by AMS and coagulopathy

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6
Q

Causes of fulminant hepatitis

A 
Drugs (acetaminophen overdose, antimycobacterial (rifampin, isoniazid), antidepressants (MAOi), halothane, mushroom poisoning)
Virus (HAV, HBV + HDV)
Autoimmune
Ischemia
Metabolic
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7
Q

What is chronic hepatitis?

A

Evidence of ongoing liver injury for >6mos

May be viral (HBV, HDV, HCV), autoimmune or metabolic

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8
Q

What is the predominant microscopic feature of chronic hepatitis?

A

inflammatory infiltrate surrounding portal tracts

fibrosis

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9
Q

What is “bridging” necrosis?

A

Seen in chronic hepatitis

fibrosis / necrosis stretching between portal tracts or from portal tract to central vein

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10
Q

What are microscopic indicators of HBV, HCV, and autoimmune hepatitis?

A

HBV: ground-glass cytoplasm
HCV: microvessicular fatty change and portal tract lymphoid aggregates
autoimmune: plasma cell infiltrates of portal triad

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11
Q

What is choledocholithiasis?

A

gall stones w/in the common bile duct

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12
Q

What are the characteristic lab findings assoc. with cholestasis?

A

Elevated alkaline phosphatase
elevated gamma-glutamyl transferase (GGT)
elevated 5’ nucleotidase

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13
Q

What hepatic condition presents with the highest aminotrasnferase elevations?

A 
ALT/AST elevation hallmark of hepatocellular necrosis: 
Acute Hepatitis 10-30x
Biliary obstruction 1-5x
Cirrhosis 1-3x
Hepatic metastases 1-2x
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14
Q

What defines acute liver failure?

A

Rapid onset of hepatic dysfunction with no underlying liver disease progressing to encephalopathy w/in 8-12 weeks

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15
Q

What are symptoms of acute liver failure?

A 
Mental status changes
Jaundice, dark urine, light stool
Seizure
Hypoglycemia
Coagulopathy
Hepatorenal syndrome
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16
Q

How is cholestasis diagnosed?

A 
Elevated alkaline phosphatase
Elevated GGT, 5' nucleosidase
Hypercholesterolemia
Hyperbilirubinemia (conjugated)
Prolonged prothrombin time (Vit K deficiency)
Anti-mitochondrial Ab (primary)

Imaging
Liver biopsy

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17
Q

What are the physical signs of portal hypertension?

A
  1. Ascites
  2. Splenomegaly
  3. Abdominal vasculature accentuation
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18
Q

3 classifications of portal HTN

A

Pre hepatic
Intrahepetic
Post hepatic

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19
Q

What does TIPS stand for?

A

Transjugular Intrahepatic Portosystemic Shunt

Performed by interventional radiologist - treatment for portal HTN

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20
Q

How do acute and chronic hepatic encephalopathy differ?

A

Acute: Type A: assoc. w/ acute disease. Delirium and convulsions progressing to coma. BBB and cerebral edema are common.

Chronic: Types B and C: chronic disease: pathogenesis unclear. Asterixis, Hyperreflexia, Mental disturbances, EEG changes
Production of toxic substances by gut bacteria implicated

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21
Q

What is therapy for chronic hepatic encephalitis?

A

Treat precipitating factor
Lactulose
Abx: Rifaximin, neomycin
Liver transplant

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22
Q

What does protein content of ascites fluid indicate?

A

Etiology of ascites
Serum albumin - ascites albumin
if > 1.1, portal HTN likely
Elevated ascites albumin: tumor or chronic infection

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23
Q

What are complications of ascites

A

Spontaneous Bacterial Peritonitis - esp. low protein fluid
Flood’s syndrome: ruptured umbilical hernia
Plural effusion
Drug dilution in “3rd space”

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24
Q

What is hepatorenal syndrome?

A 
Renal failure w/ accompanying advanced severe liver disease
No ATN (tubules intact - low urine Na+), but severe oliguria
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25
Q

How is hepatorenal syndrome diagnosed and treated?

A

Diagnosis: rule out pre-renal azotemia via trial of fluid expansion
Treatment: Often liver transplant. Dialysis.

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26
Q

Primary cause of unconjugated bilirubinemia

A

Hemolytic jaundice: production of bilirubin in excess of liver’s ability to process it.

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27
Q

What are the 2 leading causes for liver transplant?

A 
Hep C (45%)
Alcoholic cirrhosis (15%)
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28
Q

At what pressure within the hepatic portal vein is variceal bleeding likely?

A

> 12mmHg

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29
Q

5 factors that contribute to chronic ascites

A
  1. Portal HTN -> systemic vasodilation, decreased effective bv, SNS activation
  2. RAAS activation -> increased Na+
  3. ADH -> increased H2O
  4. Increased transsinusoidal filtration
  5. hypoalbuminemia -> decreased osm
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30
Q

What microscopic feature is associated with alcoholic hepatitis?

A

Mallory bodies or alcoholic hyalin: eosinophilic cytoplasmic inclusions

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31
Q

What are transaminase levels in alcoholic hepatitis?

A

Mild to moderate increase with AST > ALT

vs. viral where ALT > AST

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32
Q

Is alcoholic cirrhosis micro or macronodular?

A

typically micro

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33
Q

In what setting does Non-alcoholic Fatty Liver Disease typically present?

A

Obesity and Insulin resistance.

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34
Q

4 metabolic liver diseases

A

Non-alcoholic fatty liver disease
Hemochromatosis
a1 antitrypsin deficiency
Wilson’s disease

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35
Q

What mutation is often seen in hemochromatosis?

A 
HFE gene (6p) mutation
Autosomal Recessive
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36
Q

What organs are affected by hemochromatosis?

A

Liver - micronodular cirrhosis, hepatocellular carcinoma
Myocardium - dysfunction
Pancreas - fibrosis, cell loss -> diabetes mellitus
Joints - synovial tissue damage -> arthropathy
Endocrine glands - hypopituitarism -> hypogonadism

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37
Q

What is another name for Wilson disease?

A

Hepatolenticular degeneration

Lenticular = putamen and caudate = basal ganglia

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38
Q

What is Wilson’s disease?

A

Autosomal recessive defect in copper ATPase

defective transport in liver -> decreased incorporation into ceruloplasmin and decreased excretion in bile

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39
Q

Symptoms of Wilson’s disease

A

Hepatitis / cirrhosis
CNS injury (tremor, rigidity, dysarthria, depression, anxiety, psychosis)
Kaiser-Fleischer rings, sunflower cataracts
Hemolytic episodes

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40
Q

What gene is involved in a1-antitrypsin deficiency?

A

SERPINA-1
Autosomal codominant
chromosome 16: Pi locus: normal = MM, severe = ZZ

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41
Q

who should be screened for a1-antitrypsin deficiency?

A

All people w/ COPD, unexplained liver disease, and 1st degree family members of probands

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42
Q

How does a1-antitrypsin deficiency disease cause liver damage?

A

Accumulation of misfolded, polymerized a1-AT proteins in hepatocyte ER

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43
Q

Manifestations of a1-AT deficiency

A 
Panlobular emphysema (esp. basilar)
Hepatitis (neonatal hepatitis), cholestatic jaundice, cirrhosis, hepatocellular carcinoma
Eosinophilic inclusion bodies in hepatocytes
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44
Q

Pathology of primary biliary cirrhosis

A

Autoimmune, Tcell mediated destruction of small - medium bile ducts
Granulomatous destruction of bile ducts w/ chronic inflammatory infiltrate

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45
Q

Lab findings in Primary Biliary Cirrhosis

A

elevated hepatic alkaline phosphatase, GGT, cholesterol, conjugated bilirubin
elevated IgM, antimitochondrial Ab and lipoprotein X

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46
Q

What is treatment for PBC?

A

Urodeoxycholic Acid
Symptomatic treatment (pruritis, osteoporosis, portal HTN)
Liver transplant

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47
Q

What is Primary Sclerosing Cholangitis?

A

progressive destruction of large intra and extrahepatic bile ducts
autoimmune, ANCA assoc., close assoc. with ulcerative colitis
Mostly men <40
Produces alternating stricture and dilation in ducts

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48
Q

What are complications of Primary Sclerosing Colangitis?

A

Progressive biliary obstruction and portal fibrosis
Biliary cirrhosis
Increased risk of cholangeosarcoma

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49
Q

What is DILI?

A

Drug Induced Liver Injury

Most common reason for FDA removal of approved drugs

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50
Q

What part of the liver is initially affected by acetaminophen toxicity?

A

Zone 3 (P450 activity)

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51
Q

2 ways in which ETOH contribute to acetaminophen toxicity

A

Induction of P450 pathway

Depletion of GSH stores

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52
Q

First line treatment for acetaminophen OD?

A

N-acetylcysteine

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53
Q

Describe unpredictable / idiosyncratic DILI

A

Usually latent “sensitization” period before symptoms, more rapid on re-challenge
Associated fever, rash, eosinophilia

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54
Q

2 theories to explain unpredictable DILI

A
  1. Hypersensitivity: drug + carrier = macromolecule = neo-antigen -> Immune response -> hepatotoxicity
  2. Metabolic + genetic: drug + genetics -> novel metabolite -> liver injury
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55
Q

What drugs are associated w/ cholestasis?

A

Phenothiazines (Chlorpromazine)
Oral Contraceptives (estrogens)
Erythromycin Estolate
Amoxicillin / Clavulanate (augmentin)

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56
Q

What effect does Chlorpromazine (thorazine) have on the liver?

A

Assoc. with cholestasis + inflammation via unknown mechanism
3-5 weeks after initiation of therapy
Resolves w/ discontinuation
PBC-like

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57
Q

What effect does Methotrexate have on the liver?

A

Fatty change related to cumulative dose
Toxicity lower in RA, higher in psoriasis
Liver biopsy in follow up

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58
Q

Name some drugs assoc. w/ chronic hepatitis

A 
Acetaminophen
Amiodarone
Aspirin
Dantrolene
Ethanol
Isoniazid
a-methyldopa
Vit-a
nitrofurantoin
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59
Q

Name some drugs associated with granuloma formation

A 
Allopurinol
Hydralazine
Penicillin
Quinidine
Sulfonamides, sulfonylureas
a-methyldopa
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60
Q

3 drugs associated with “predictable” hepatotoxicity

A

Acetaminophen
CCl4
Amanita Phalloides

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61
Q

What is the cause of dental carries?

A

Dissolution of inorganic component of tooth by organic acids via microbial metabolism of carbohydrates

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62
Q

What microbes are primarily involved in the formation of dental carries?

A

S. mutans - crown

Lactobacillus - root

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63
Q

What is oral tori?

A

bony overgrowth of palate or lingual side of mandible.

No need for removal unless impedence of function or speech

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64
Q

What causes amalgam tattooing?

A

insoluble silver salt (from silver amalgam filling) deposited in collagen fibers of lamina propria

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65
Q

What are Fordyce Spots?

A

Occurrences of sebaceous glands in oral cavity
not apparent in children, activated at puberty
No clinical significance, found in 82% of population

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66
Q

Epulis fissuratum

A

“denture injury tumor” due to mechanical irritation of ill-fitting denture
Usually no pain or tenderness unless infection is involved

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67
Q

Papillomatosis

A

found on soft tissue of vault of hard palate

numerous papillary projections due to mechanical irritation and ill-fitting denture, food debris

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68
Q

Is oral papilloma cancerous?

A

NO - benign w/ stratified squamous epithelium

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69
Q

What is an aphthous ulcer?

A

Canker sore
Recurrent, superficial ulcer of non-keratinized epithelium
Persist 8-14 days
Causes: psychic, autoimmune, microbial, traumatic endocrine, hereditary
Treatment: tetracycline mouthwash, kenalog in orabase, analgesics

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70
Q

What is treatment for oral herpes?

A

Acyclovir ointment

Systemic acyclovir for immunocompromised patients.

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71
Q

What oral ulcers should be considered for biopsy?

A

Highly suspicious, slow healing ulcers in patients who are poor historians.

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72
Q

What is Moniliasis? Culture? treatment?

A

Oral thrush - Candida albicans
Culture: Sabouraud’s agar
Treatment: Nystatin, Ketoconazole, Fluconazole, saline baking soda rinse

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73
Q

Oral manifestation of Addison’s disease and treatment

A

Hyperpigmented spots due to pituitary stimulation of melanotrophic activity
treated w/ corticosteroids

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74
Q

What are oral manifestations of leukemia?

A

gingival hyperplasia, gingivitis, hemorrhage, petechia, mucosal ulceration

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75
Q

What is Paget’s disease, oral manifestations, treatment

A

Abnormal bone resorption and deposition
Oral: enlargement of maxilla / mandible, spacing of teeth
Treatment: NSAID, ASA, calcitoinin, diphosphonates, mithramycin

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76
Q

Oral presentation of Lichen Planus

A

Pruritic, Purple, Polygonal, Planar, Papules and Plaques
Oral: Wickham Striae: white, lace-like patterns on top of papules
may be erosive - low, but increased risk for malignancy
Yeast infection common
Treat with corticosteroids

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77
Q

Oral manifestations of HIV / AIDS

A

Hairy leukoplakia
Candidiasis
Herpes outbreaks
Kaposi’s sarcoma - most frequent malignancy of AIDS

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78
Q

What is the organism involved in cat scratch disease?

A

Bartonella henselae

Children w/ cervical lymphadenopathy referred for dental exam to exclude oral infection

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79
Q

In VZV outbreak, when should anti-virals be started?

A

w/in 72 hours of onset

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80
Q

What is leukoplakia?

A

white patch or plaque on oral mucosa that does not scrape off and cannot be otherwise classified.
Homogenous or Erythroleukoplakia (4-5x increased risk of malignant transformation)

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81
Q

Infrequent agents of viral hepatitis

A

CMV: children, anicteric, no chronicity. May be lethal in immunocompromised
EBV: self-limited mono. 40% have elevated transaminase. no chronicity
HSV: immunocompromised, high mortality. Liver biopsy shows viral inclusion bodies

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82
Q

HBV genome

A

incomplete dsDNA

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83
Q

HAV genome

A

ssRNA

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84
Q

How is HAV transmitted?

A

fecal-oral route - contaminated food and water

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85
Q

How is Hep A diagnosed?

A

IgM antibody: current infection

IgG antibody: previous infection

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86
Q

HAV therapy

A

Supportive

Infection spontaneously clears - no carrier state

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87
Q

How does Hep B result in death?

A

Cirrhosis w/ liver failure

Hepatocellular carcinoma

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88
Q

What is vertical transmission?

A

Mother to child

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89
Q

What is the gold standard for diagnosis of HBV?

A

Serum HBV DNA by PCR

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90
Q

If acute HBV infection is suspected, what test should be ordered to confirm?

A

IgM anti-HBVc

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91
Q

What marker is seen in patients immunized against HBV?

A

IgG anti-HBs

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92
Q

What is the earliest detectable Ab in HBV infection?

A

IgM anti-HBs

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93
Q

What does the presence of anti-HBcAg indicate?

A

Exposure to virus. will be positive for life.

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94
Q

What ethnicity has the highest rate of HBV carriage in USA?

A

Asian

95
Q

Most commonly used HBV medications

A

entecavir (guanosine analog)
tenofovir (adenosine analog)

both inhibit HBV RT

96
Q

Post-exposure treatment for HBV

A

HB immunoglobin

HB vaccine

97
Q

By age, what % of HBV infected patients will become chronic carriers?

A

Infant: 90%
1-5 yrs: 30%
Adult: 5-8%

98
Q

What does HDV require for replication?

A

HBsAg

99
Q

Which has a worse prognosis HBV + HDV co-infection of superinfection

A

superinfection: 90% develop chronic liver disease, 80% cirrhosis w/in 5 years

co-infection: 2% develop chronic disease. Co-infection is typically self-limited and resembles acute Hep B

100
Q

What is treatment of HDV?

A

HBV treatment!

101
Q

In HCV infection, what is assumed with symptoms of chronic liver disease?

A

End Stage Liver Disease has occurred.

Acute Hepatitis rare, usually asymptomatic until late in course

102
Q

What is Von Meyenberg Complex?

A

Bile duct hamartomas - non neoplastic - persistence of embryonic structure
Collection of small, irregular bile ducts in fibrous tissue
Multiple small, pale spots on liver

103
Q

3 non-neoplastic tumors of liver

A
  1. Von Meyenberg Complex
  2. Nodular Hyperplasia (oral contraceptives, anabolic steroids)
  3. Nodular Regenerative Hyperplasia: regenerative nodules w/o fibrosis
104
Q

Complication of Nodular regenerative hyperplasia of liver

A

Portal HTN

105
Q

What is the most common benign hepatic tumor?

A

Cavernous hemangioma

106
Q

What is hepatic cell adenoma associated with? appearance?

A

Young women taking contraceptives (long-term)

Solitary, well circumscribed, soft green mass lacking portal tracts

107
Q

Complication of hepatic adenoma?

A

Hemorrhage - acute onset of RUQ pain

108
Q

What is the risk of malignant transformation in hepatic adenoma?

A

Very small risk

B-catenin gene: elevated risk if present

109
Q

Malignancies that most frequently metastasize to the liver

A

Lung, GI (colon), pancreas, breast

110
Q

What lab abnormalities are found in tumors that have metastasized to the liver?

A

early: alkaline phosphatase and lactate dehydrogenase
Late: serum bilirubin and ALT / AST levels

111
Q

3 major risk factors for hepatocellular carcinoma

A

HBV carrier state (incorporation into cellular DNA -> oncogene activation and HBV X-protein expression)
Cirrhosis (repetitive regenerative cycles -> mutations (RAS, p53, etc))
Exposure to aflatoxin (p53 mutation)

112
Q

What is Budd-Chiari?

A

Occlusion of IVC or hepatic veins w/ centrilobular congestion and necrosis
Sudden liver enlargement, pain, and ascites
May occur w/ hepatocellular carcinoma

113
Q

What lab abnormalities may be seen in hepatocellular carcinoma?

A

a-fetoprotein: neither sensitive nor specific
ALP and LD elevation
Late: bilirubin and ALT/AST elevation

114
Q

What is an important variant of hepatocellular carcinoma?

A

Fibrolamellar variant
young adults, no predisposing factors, otherwise normal liver
well differentiated tumor cells in dense fibrous stroma w/ parallel collagen lamellae
Good prognosis

115
Q

Risk factors for cholangiocarcinoma

A

Primary sclerosing cholangitis
Congenital biliary tract structural abnormalities
Thorotrast exposure
Chronic parasitic biliary tract infection (Opisthorchis sinensis)

116
Q

What is angiosarcoma?

A

Endothelial tumor - hemorrhagic nodules and blood filled cysts
In liver associated with vinyl chloride, thorotrast, arsenic exposure

117
Q

What is hepatoblastoma?

A

tumor of young children
large, soft, hemorrhagic, necrotic mass
microscopic: small, round blue cells. epithelial mesenchymal differentiation

118
Q

What marker is elevated in hepatoblastoma?

A

a-fetoprotein

119
Q

2 functions of bile

A

absorption of fat via formation of micelles

rid body of cholesterol via bile salts and bilirubin

120
Q

What is a choledocal cyst?

A

Dilation or outpouching of common bile duct

121
Q

2 causes of biliary atresia

A
  1. Hypoplasia or aplasia (rare)

2. Idiopathic neonatal bile duct destruction (several weeks after birth)

122
Q

What is the most common type of gallstone in US?

A

Cholesterol

123
Q

How are cholesterol gallstones formed?

A

supersaturation of bile with cholesterol + bile stasis -> crystal nucleation

124
Q

Risk factors for cholesterol gallstones

A

Due to excess cholesterol secretion (+/- decreased bile salt secretion)

  • Estrogens (contraceptive use)
  • Age
  • Obesity / rapid weight loss
  • Inherited metabolic disorders
125
Q

How do cholesterol gallstones appear on xray?

A

radiolucent

126
Q

2 types of pigment gallstones and causes.

A
  1. black stones: chronic hemolysis. Unconjugated bilirubin precipitates with Ca++
  2. brown stones: assoc. with biliary tract infections (Flukes)
127
Q

2 causes of acute cholecystitis

A
  1. calculus: stone obstructs neck of gallbladder or cystic duct -> distention and vascular compression
  2. acalculus: critically ill patients - biliary sludge obstructs cystic duct -> poor biliary perfusion, possibility of infection
128
Q

What is seen on CBC in acute cholecystitis?

A

elevated WBC, esp. neutrophils

129
Q

What are Rokitansky-Aschoff sinuses?

A

Feature of chronic cholecystitis

mucosal diverticula w/in gallbladder wall

130
Q

What is a significant risk factor for cancer of the gallbladder?

A

Porcelain gallbladder : dystrophic calcification

131
Q

Prognosis for carcinoma of the gallbladder?

A

very poor - diagnosis frequently incidental
Frequent local invasion of liver, and adjacent viscera
Metastasis to lymph nodes, peritoneum, lungs

132
Q

What is a Klatskin tumor?

A

tumor at origin of common bile duct- slowly progressive

Subtype of carcinoma of extrahepatic bile duct

133
Q

3 regulators of pancreatic exocrine function

A

Vagus nerve
CCK: HCO3- secretion
Secretin: zymogen secretion

134
Q

How is trypsin activated?

A

Trypsin (from pancreas) activated by enterokinase on brush border of duodenum

135
Q

Systemic and local complications of acute pancreatitis

A

Systemic:

  • DIC
  • ARDS
  • ARF (shock -> ATN -> ARF)
  • metabolic hypocalcemia, hypoalbuminemia, hyperglycemia, acidosis)

Local:
-pseudocyst, abscess, biliary / duodenal obstruction

136
Q

What defines chronic pancreatitis and what are symptoms?

A

Frequently relapsing inflammation -> progressive pancreatic injury
Usually alcohol related
May be CF, obstruction, idiopathic
Symptoms: pain, loss of function (malabsorption, DM), biliary / duodenal obstruction

137
Q

Differentiate true pancreatic cysts from pseudocysts

A

true cysts: lined with epithelium, associated with ADPKD, VHL

pseudocysts: complications of pancreatitis - no epithelial lining

138
Q

What are risk factors for pancreatic adenocarcinoma?

A

Smoker, male, black, Native American, high fat diet, nitrosamine exposure, diabetes mellitus

139
Q

What part of the pancreas is most frequently involved in adenocarcinoma?

A

Head > body > tail

140
Q

How does pancreatic cancer usually spread?

A 
Local:
Head:  duodenum, common bile duct
Body and Tail: vertebrae, retroperitoneal and abdominal organs
Metastasis:
lymph nodes, liver
141
Q

What causes hereditary pancreatitis?

A

Autosomal Dominant
Mutation of trypsinogen on chromosome 7
Trypsin is resistant to lysis -> prolonged activity

142
Q

What are lab findings in acute pancreatitis?

A 
Lipase and amylase 3x normal (lipase more specific for pancreas)
AST 2x (gallstone)
143
Q

What imaging studies are preferred in diagnosis of acute pancreatitis?

A

Initial: ultrasound
Prognosis: CT - specific and indicates extent of necrosis -> complication / mortality risk

144
Q

According to Ranson’s criteria, what features on admission are suggestive of gallstone pancreatitis?

A

Age >70
WBC/mm^3 >18,000
Glucose (blood) >220
LDH >400

145
Q

What organisms are most frequently involved in necrotizing pancreatisis?

A

E. coli
Klebsiella
Enterococcus

146
Q

How is infected pancreatic necrosis treated?

A

surgical debridement

Abx use is controversial

147
Q

Should pancreatic pseudocysts be treated?

A

Only if symptomatic

148
Q

What is a Bentiromide test?

A

Test of pancreatic function. Oral dose given (Bentiromide has PABA linked) chymotrypsin cleaves, frees PABA for absorption and renal excretion.
Low PABA in urine indicates decreased pancreatic function

149
Q

How is a secretin stimulation test performed?

A

IV secretin given
Tube placed in pancreatic duct, timed periodic collections measuring for HCO3- levels: low indicates chronic pancreatitis
Cumbersome, unpleasant, rarely done

150
Q

What is the role of the Schilling test in pancreatitis diagnosis / treatment?

A

Pancreatitis -> reduced absorption of fat soluble vitamins (B)
Schilling test will be abnormal
Administration of pancreatic enzymes will normalize Schilling test, suggesting chronic pancreatitis

151
Q

At what point in pancreatic disease is steatorrhea usually apparent? How is it treated?

A

90% loss of lipase activity

Supplement pancreatic enzymes w/ 30,000 IU lipase activity at each meal
Acid suppression and low-fat diet

152
Q

Pancreatic adenocarcinoma 5 year survival rate

A

<5%

153
Q

What are some indications for cholecystectomy?

A

Symptomatic gallstones, hemolytic anemia, gastric bypass, porcelain bladder, gallbladder adenoma >1-2cm

154
Q

What is a drug that can be used to treat cholesterol gallstones

A

Ursodeoxycholic acid
Inhibits HMG coA reductase -> reduced cholesterol production
Reduces hepatic cholesterol secretion in bile

155
Q

What is cholangitis?

A

Infection of the common bile duct
Usually gram neg organisms. can spread to liver and blood.
Charcot’s triad: pain, fever, jaundice

156
Q

3 risk factors for carcinoma of the extrahepatic biliary ducts

A

In Asia: parasites - Chloronorchis sinensis, infections, IBD, sclerosing cholangitis

157
Q

What is sudan black staining used for?

A

Sudan black stain of stool: shows excess fat in stool (steatorrhea) chronic pancreatitis

158
Q

Describe venous drainage of esophagus

A

Upper 1/3: SVC
Mid 1/3: Azygos
Lower 1/3: Hepatic portal vein via L. gastric (coronary) vein

159
Q

What is the muscular distribution of the esophagus?

A

Upper 1/3: Skeletal
Mid 1/3: Mixed
Lower 1/3: Smooth

160
Q

What are Auerbach and Meisner’s plexuses?

A

Auerbach: peristalsis
Meisner: sensory

161
Q

What is EGD used for?

A

Esophagogastroduodenoscopy: used to visualized epithelium of esophagus, stomach, duodenum. Allows biopsy capability.

162
Q

3 components of swallowing (esophageal phase

A

Primary: swallow-initiated
Secondary: stretch-initiated
Tertiary: uncoordinated, non-propulsive

163
Q

What factors can trigger diffuse esophageal spasm?

A

Stress, very hot or very cold liquids

164
Q

What happens with the lower esophageal sphincter in Diffuse Esophageal Spasm?

A

Normal function is preserved.

165
Q

How does scleroderma affect the esophagus?

A

Collagen deposition in smooth muscle -> aperistalsis in distal esophagus
Incompetent LES

166
Q

How are strictures and obstructive ring lesions of the esophagus usually treated?

A

Dilation - usually balloon or bougie

Surgery - uncommon

167
Q

What are possible pharmacological treatments for GERD

A 
Acid suppressors (H2RA, PPI, antacid)
Prokinetics  (metoclopramide, domperidone, cisapride)
168
Q

Where are Meissner and Auerbach plexuses located in esophagus?

A

Meissner: within the submucosa
Auerbach: between layers of muscularis propria

169
Q

What are pulsion diverticula and 2 examples

A

Outpouchings of esophagus due to high pressure

  1. Zenker: hypopharynx: between inferior pharyngeal constrictor and cricopharyngeus
  2. Epiphrenic: just above LES: associated w/ motility disorders (achalasia, hiatal hernia)
170
Q

What causes an esophageal traction diverticulum?

A

Continuous external traction - mediastinal inflammation / fibrosis
Located mid-esophagus

171
Q

Who is most at risk for esophageal webs?

A

Middle aged women

172
Q

Plummer-Vinson

A

Esophageal webs, iron-deficiency anemia, glossitis, cheilosis, koilonchia (spoon nails)
Increased risk for pharyngeal and esophageal carcinoma

173
Q

2 examples of esophageal rings

A

A ring: proximal to GE junction

B ring: located at squamo-columnar GE junction. Almost always associated w/ hiatal hernia

174
Q

2 subtypes of hiatal hernias

A
  1. Sliding: GE junction and portion of stomach slide through esophageal hiatus
  2. Paraesophageal: “rolling” portion of fundus prolapses into thorax adjacent to esophagus. GE junction stays in abdomen.
175
Q

2 esophageal lacerations

A
  1. Mallory-Weiss: after prolonged vomiting / retching as w/ ETOH intox. superficial longitudinal tears at GE junction
  2. Boerhaave: distal esophageal rupture -> mediastinitis - catastrophic event
176
Q

3 types of esophagitis

A
  1. Iatrogenic: (radiation, GVHD)
  2. Infectious: immunocompromise: candida, HSV
  3. Reflux: GERD
177
Q

Complications of Barret’s Esophagus

A

Epithelial dysplasia

Adenocarcinoma

178
Q

How many layers of muscle surround the stomach?

A

3 layers of smooth muscle: innermost oblique, inner circular, outer longitudinal

Note: Auerbach’s plexus between circular and longitudinal

179
Q

3 etiologies of gastric ulceration

A
  1. NSAID use
  2. Intracranial trauma: vagal stimulus -> increased gastric H+ secretion
  3. Physiologic stress (shock, sepsis, burns): decreased perfusion of gastric mucosa, systemic acidosis (-> decreased HCO3-)
180
Q

What are Cushing and Curling ulcers?

A

Cushing: gastric ulceration due to intracranial injury
Curling: gastric ulceration assoc. with burns

181
Q

What is the most common cause of chronic gastritis?

A

H. pylori infection (90% of cases)

182
Q

H.pylori virulence factors

A

flagella
urease (urea -> NH3 -> neutralization of acid)
Lewis antigens: allow adherence to gastric foveolar epithelium
toxins

183
Q

3 diagnostic tests for H.pylori

A
  1. H. pylori fecal Ag test
  2. Carbon labeled Urea breath test (detects exhaled labeled CO2)
  3. H. pylori serology: not helpful for post-treatment follow up
184
Q

What happens in autoimmune gastritis?

A

Uncommon
CD4+ cells lose tolerance for parietal cell antigens -> anti parietal cell and anti-IF antibodies
Hyperplasia of G cells -> increased gastrin production
B12 deficiency

185
Q

How is the spinal cord affected by autoimmune gastritis?

A

B12 deficiency -> demyelination of neurons

Posterior and lateral columns most effected -> loss of position and vibratory sensation (leg > arms) w/ sensory ataxia

186
Q

What are the most common locations for gastric ulcers

A

proximal duodenum > antrum > elsewhere

187
Q

Clinical presentation of gastric ulcer

A

Recurrent epigastric pain - worse at night and few hours post-meal
-relieved w/ food and alkalai

188
Q

Describe Menetrier disease

A

Excessive productin of TNF-a -> hyperplasia of foveolar mucous epithelium and atrophy of parietal and chief cells
Protein loss
increased risk of gastric adenocarcinoma

189
Q

What is Zollinger-Ellison Syndrome?

A

Gastrin secreting tumor -> intractible peptic ulcer disease and mucosal hyperplasia (esp. parietal cells)

190
Q

How is peptic ulcer disease diagnosed?

A

History and physical
EGD
Upper GI series (75% sensitivity)

191
Q

What patients can be tested and treated for H. pylori w/o undergoing endoscopy?

A

Patient <45 w/ ulcer symptoms and no alarm signs or complications

192
Q

What NSAIDS are “high risk” for Ulcer development?

A

Indomethacin
Ketorolac
Piroxicam

193
Q

Who is a candidate for co-administration of NSAID and acid suppressive agent?

A

Patient requiring chronic NSAID use and having at least 1 risk factor for development of gastric ulcer (>60 yoa, multiple NSAID, corticosteroid or anticoagulant use, Hx of PUD or GI complications)

194
Q

2 prokinetic agents that can be used to treat gastroparesis

A
  1. Dopamine antagonist: DA has anti-motility action on GI

2. 5-HT agonist: Serotonin stimulates motility

195
Q

What is the preferred drug for hospitalized patients w/ gastroparesis?

A

Eythromycin: motilin receptor agonist

196
Q

What is the MOA of Metoclopramide?

A

D2 antagonist
5-HT4 agonist
Accelerates gastric emptying in treatment of gastroparesis

197
Q

What is the treatment of choice for variceal bleeding?

A

Endoscopic sclerotherapy

Endoscopic ligation is also acceptable

198
Q

In a patient with an active GI bleed, when should PPI be given?

A

Post-endoscopy. No value to Pre-endoscopy admin.

199
Q

Drugs used to treat ulcerative colitis

A

5-aminosalicylates: oral - active management, maintain remission
rectal - most effective for patients w/ proctitis
corticosteroids: suppress migration of PMNs. Used for management of acute / extensive disease.
Immunomodulators (6MP, Azathioprine): if corticosteroid unresponsive

200
Q

What receptors are found in high density in the emesis center of the medulla?

A

5-HT3
M1
H1

201
Q

Treatment for hypertrophic pyloric stenosis

A

pyloromyotomy

202
Q

What is Meckel diverticulum? complication?

A

Failure of embryonic vitelline duct to involute

Often contains heterotropic foci (gastric mucosa) -> gastric acid production -> GI bleeding, pain, perforation

203
Q

What serology can be used to diagnose Celiac Disease?

A

Anti-gliadin Ab

Anti-tissue transglutaminase Ab

204
Q

What is the dermatologic presentation of celiac sprue? Cause?

A

Dermatitis Herpetiformis: Pruritic vessicles that form on back and extensor surfaces of extremities
Caused by anti-gliadin IgA

205
Q

What is Abetalipoproteinemia?

A

Autosomal recessive
Deficient apoprotein B -> defective lipid transport -> lipid accumulation in enterocytes
Vacuolization of enterocytes, acanthocytes

206
Q

Is celiac sprue associates w/ malignancy risk?

A

Yes
Non-Hodgkin’s Lymphoma
Sm. intestinal adenocarcinoma
Sq. cell carcinoma of esophagus

207
Q

What is Whipple Disease?

A

bacterial infection affecting middle-aged white men
Tropheryma whippelli
PAS+ macrophages (foamy) fill lamina propria of sm. intestine
also affects joints, brain, heart valves
-> chronic malabsorption, arthropathy, lymphadenopathy, hyperpigmentation, psychiatric complaints, cardiac dysfunction

208
Q

Where are GI carcinoid tumors usually found?

A

Appendix, ileum, rectum

209
Q

Where do MALT lymphomas generally develop? What is a common associated disorder?

A

stomach > sm. intestine > colon

Very often associated w/ H. pylori infection

210
Q

What are important factors that go with Burkitt’s Lymphoma?

genetics, infections

A

c-myc gene translocation (t[8;14])
latent EBV infection
HIV associated

211
Q

What is GIST and what is it associated with (origin, genetics)?

A

Gastrointestinal stromal tumor - from interstitial cells of Cajal
Varying malignant potential
mutations: c-KIT, PDGFRA: tyrosine kinase receptors

212
Q

How does steatorrhea -> renal stones?

A

Malabsorbed FAs bind Ca++ which would normally bind oxalate in the colon
Oxalate is then available for colonic reabsorption -> renal oxalate stones

213
Q

How does smoking effect the risk of developing either of the 2 forms of IBD?

A

Crohn’s: current and former smokers - increased risk of developing
Ulcerative Colitis: former and non-smokers have increased risk

214
Q

What serum markers are found in Crohn’s and UC?

A

Ulcerative Colitis: p-ANCA (60-80%)

Crohn’s: ASCA: (70%)

215
Q

What is recommended for colon cancer surveillance in UC and Crohn’s?

A

Colonoscopy every 2 years w/ multiple biopsy after 8-10 yrs. of diagnosis

216
Q

What are some causes of sm. bowel obstruction?

A 
#1:  adhesions from prior surgery
Other: hernia, crohn's, volvulus, neoplasm, foreign body
217
Q

What is open loop vs. closed loop bowel obstruction?

A

Open loop: Intestinal flow blocked, but decompression possible via vomiting

Closed loop: Inflow and outflow blocked -> gas and secretion accumulation w/ no means of decompression

218
Q

what is obstipation?

A

inability to pass flatus or feces

sign of obstruction along w/ pain, vomiting and distension

219
Q

What organisms tend to flourish in sm. bowel obstrution?

A

E.coli
Klebsiella
S.faecalis
Normally sm. intestine is nearly sterile

220
Q

Outline treatment for intestinal obstruction

A

IV fluids (NaCl, lactated ringer’s) - monitor electrolytes
Add KCl if needed after adequate urine formed
NG tube - decompression, avoid aspiration of stomach contents
Imaging - monitor - surgery if no resolution

221
Q

What cancers are associated with Peutz-Jeghers?

A

colon, pancreas, breast, testicular, ovarian, cervical

222
Q

What ovarian cells do LH and FSH work on respectively and what is the effect?

A

Rising FSH (folicular phase) induces increase in LH receptors in Theca
LH works on Theca cells -> androgen production (Prog, Androstenedione, T) Theca lacks aromatase
FSH works on granulosa cells -> Estradiol from androgens Granulosa cells lack 17a-hydroxylase

223
Q

What causes the LH surge and what is its effect?

A

increasing estradiol levels -> pos. feedback @ hypothalamus -> LH surge -> ovulation
Ovulation 36 hrs. after surge

224
Q

What genes are involved in migration of GnRH secreting neurons? What is the route of migration?

A

Genes: Kal-1 (encodes for Anosmin), Kal-2, Prox-2

Migration from olfactory placode to Arcuate Nucleus of medial basal hypothalamus

225
Q

Primary amenorrhea

A

Absence of menses by 16 regardless of growth / pubertal dev
-or-
Absence of menses by 13 w/o dev. of 2ndary sex characteristics

226
Q

Secondary amenorrhea

A

lack of menses for 3 cycles

227
Q

What is idiopathic hypogonadotrophic hypogonadism? subtype?

A

Functional congenital absence of GnRH secretion

Kallman: defective migration of GnRH cells and formation of olfactory bulb: IHH + anosmia and other defects

228
Q

What is the cause of Functional Hypothalamic Amenorrhea? How is it diagnosed?

A

No pathologic disease found
Eating disorders, weight loss, exercise, stress
Low leptin levels believed to be involved - neg. impact on GnRH secretion
Diagnosis: Estrogen <50pg/mL; no withdrawal bleeding on Progesterone challenge

229
Q

Female Athletic Triad

A

Disordered eating
Menstrual dysfunction
Osteoporosis

230
Q

What are treatments for hyperprolactinemia?

A

DA agonists: bromocriptine, cabergoline

Surgery if adenoma

231
Q

What is the most common cause of gonadal dysgenesis in women?

A

Turner syndrome (X0)
Accelerated postnatal follicular atresia -> primary amenorrhea
High LH and FSH, but low estrogen

232
Q

With what disease is Premature Ovarian Failure associated?

A

Fragile X Syndrome: CGG repeat amplification (usually >500)

Also: autoimmune oophoritis (polyglandular autoimmune disease)

233
Q

Describe the pathogenesis of Polycystic Ovary Syndrome

A

Elevated LH production -> excess androgen production by theca cells
Depressed FSH production -> low estrogen level, depressed follicle maturation
Insulin intolerance contributes to androgen production by theca cells
Obesity -> increased adipose -> aromatization of androgen -> estrone -> promotes high LH, low FSH

234
Q

Rotterdam criteria for PCOD

A

2+ of the following:

1) Menstrual irregularity (amen or oligo (<9/yr))
2) Hyperandrogenism / -emia
3) 12+ follicles 2-9mm / ovary

Other causes of hyperandrogen ruled out

M2 (19 decks)

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