GI Diseases Flashcards

1
Q

fatigue, nausea, anorexia, fever, arthralgia, mylagia, h/a, RUQ pain

A

All Hepatitis: Symptoms

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2
Q

jaundice, scleral icterus, coca-cola urine, hepatomegaly

A

All Hepatitis: Signs

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3
Q

very high ALT/AST, high TP+AP, bilirubin in urine, increase IgM

A

All Hepatits: Labs

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4
Q

diffuse periportal lymphocytic inflammation, hepatocellular ballooning

A

All Hepatitis: Biopsy

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5
Q

Oral-fecal, asympotomatic in children

A

Hepatitis A: MOI

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6
Q

ALT and symptoms peak in 1 month, IgM peaks 3 months post-infxn

A

Hep A

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7
Q

Nonenveloped ssRNA virus; @2wks - excreted in stool; @4wks - increased ALT, Sx begin; @8wks - resolution

A

Hepatitis A: Pathophysiology

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8
Q

Never chronic, no tx but gamma-globulin vaccine available (passive)

A

Hepatitis A: Treatment/Notes

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9
Q

Horizontal (IVDU, sex) in US

A

Hepatitis B: Epi/MOI

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10
Q

The only enveloped, partially double-stranded DNA virus; 6-8wk incubation, 20% serum sickness prodrome

A

Hepatitis B: Pathophysiology

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11
Q

Progresses to chronic in 4%, Tx and vaccine (passive + active)

A

Hepatitis B: Treatment/Notes

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12
Q

Epi: HepB coinfection/hx

A

Hepatitis D: Epi/MOI

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13
Q

Delta agent, uses HBsAg protein coat, HepB must be present

A

Hepatitis D: Pathophysiology

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14
Q

Pigs

A

Hepatitis E: Epi/MOI

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15
Q

~HepA, waterborne, endemic in Asia, N. Africa, Mexico

A

Hepatitis E: Pathophysiology

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16
Q

350M; 1M in US

A

Chronic Hepatitis B: Epi/MOI

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17
Q

Labs: increased ALT+AST >6mo, (+)HBsAg, (+)HBcAb IgG; Biopsy: Ground glass

A

Chronic Hepatitis B: Signs/Symptoms/Findings

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18
Q

Vertical transmission predominant in most parts of the world; can lead to HCC; see charts on Chronic Hepatitis B

A

Chronic Hepatitis B: Pathophysiology

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19
Q

PEG-interferon, tenofovir / entecavir to decrease HBV DNA levels; not curative

A

Chronic Hepatitis B: Treatment/Notes

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20
Q

170M; 3M in US;

A

Chronic Hepatitis C: Epi/MOI

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21
Q

Labs: increased ALT+AST >6mo, (+)anti-HCV, (+)HCV RNA; Biopsy: Portal lymphoid aggregates, interface hepatitis

A

Chronic Hepatitis C: Signs/Symptoms/Findings

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22
Q

Unlike chronic HepB, anti-HCV doesn’t kill virus; but also unlike HBV, HepC can be cured (in ~75%), since no virus in nucleus

A

Chronic Hepatitis C: Pathophysiology

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23
Q

PEG-interferon, ribavirin, (+boceprevir/telaprevir in genotype 1); SNP encoding interferon(IFN lamba 3) = 2x change in response

A

Chronic Hepatitis C: Treatment/Notes

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24
Q

Decades of alcohol use

A

Alcoholic Hepatitis / ASH (Alcoholic Steatohepatitis : Epi/MOI

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25
Q

Acute jaundice, liver failure, hepatomegaly, ascites, encephalopathy; increased AST+ALT, AST:ALT >2:1; PMNs, ballooned hepatocytes, Mallory bodies, centrilobular macrosteatosis, chicken-wire fibrosis

A

Alcoholic Hepatitis / ASH (Alcoholic Steatohepatitis : Signs/Symptoms/Findings

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26
Q

Acetaldehyde (toxic metabolite of alcohol) damages central hepatocytes, leads to production of TGs; some degree of fibrosis but generally not cirrhotic; can see portal HTN from hepatic swelling

A

Alcoholic Hepatitis / ASH (Alcoholic Steatohepatitis : Pathophysiology

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27
Q

Tx: Abstinence, banana bag, steroids (esp. if discriminant fxn >32, which = poor prognosis), pentoxifylline (anti-TNF), need 6 mo abstinence for xplant

A

Alcoholic Hepatitis / ASH (Alcoholic Steatohepatitis : Treatment/Notes

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28
Q

Metabolic syndrome, M>F, 40-60 yo

A

NAFL (Non-Alcoholic Fatty Liver)& NASH: Epi/MOI

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29
Q

Same as ASH except mixed PMNs + lymphos, AST:ALT <1; also see perivenular and sinusoidal fibrosis

A

NAFL (Non-Alcoholic Fatty Liver) & NASH: Signs/Symptoms/Findings

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30
Q

1st hit: increased TG’s, FFA; 2nd hit: oxidative stress leads to lipid peroxidation, cytokine release, damage to cell membranes + mitos

A

NAFL (Non-Alcoholic Fatty Liver) & NASH: Pathophysiology

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31
Q

Less cirrhosis risk than ASH; Tx: wt loss, exercise, glycemic/lipid control, pioglitazone, vitamin E

A

NAFL (Non-Alcoholic Fatty Liver)& NASH: Treatment/Notes

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32
Q

Rare Steatosis

A

Small Droplet Steatosis: Epi/MOI

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33
Q

Small fat vacuoles, nucleus at center

A

Small Droplet Steatosis: Signs/Symptoms/Findings

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34
Q

Severe mitochondrial injury leads to decrease beta-FA oxidation

A

Small Droplet Steatosis: Pathophysiology AND Treatment/Notes

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35
Q

Normal blood bilirubin

A

<17microM, 1 mg/dL

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36
Q

In real life, unconjugated serum bilirubin percent

A

96%

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37
Q

Lab overestimates conjugated bili by up to

A

30%

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38
Q

bilirubin level leading to jaudince

A

> 35 microM

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39
Q

conjugated hyperbilirubinemia always caused by

A

impaired secretion of BDG from hepatocytes OR biliary obstruction

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40
Q

heptocellular causes of conjugated hyperbilirubinemia

A

cirrhosis, acute hepatitis (drugs, viral, alcohol)

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41
Q

biliary obstruction causes of cinjugated hyperbilirubinemia

A

gallstones, tumors, primary biliary cirrhosis

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42
Q

Dubin-Johnson syndrome (ABCC2) & Rotor syndrome (SLCO1B1/IB3)

A

genetic conjugated hyperbilirubinemia

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43
Q

unconjugated hyperbilirubinemia: overproduction causes

A

hemolysis, bad erythropoesis

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44
Q

unconjugated hyperbilirubinemia: impaired uptake causes

A

fast, sepsis, drugs (probenicid)

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45
Q

unconjugated hyperbilirubinemia: impaired conjugation causes

A

inherited mutations/polymorphisms

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46
Q

Crigler-Najjar (UGT1 mut) & Gilbert sydrome (polymorphism)

A

cause impaired conjugation unconjugated hyperbilirubinemia

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47
Q

less H bonding in E diastereoisomers, makes unconj. Bili more water soluble

A

phototherapy in neonates with jaudice

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48
Q

metabolism produces a hepten that binds to cells, triggers T-cells and eosinophils

A

drug-induced hepatitis

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49
Q

M>F (due to .’s), N. Euros. Variable penetrance

A

Hemachromatosis: Epi/MOI

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50
Q

Bronzing diabetes, HCC, cirrhosis, cardiomyopathy; transferrin saturation (TIBC) >50% in F, >60% in M

A

Hemachromatosis: Signs/Symptoms/Findings

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51
Q

HFE mutation (C282Y +/+ or H63D/C282Y) results in decrease hepcidin, which is usually inhibitor of iron absorption, recycling, storage

A

Hemachromatosis: Pathophysiology

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52
Q

Tx: phlebotomy; liver xplant if bad; can also see iron overload due to causes other than HFE mutation. Can halt symptoms, but cannot reverse damage

A

Hemachromatosis: Treatment/Notes

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53
Q

AR, 1/30K, 2-40 yo

A

Wilson’s Disease: Epi/MOI

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54
Q

Kayser-Fleischer rings, decrease ceruloplasmin, urinary Cu high, stool low (25% direct, 50% as metallothionin),low AlkP, AST+ALT > 2.2, renal dz

A

Wilson’s Disease: Signs/Symptoms/Findings

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55
Q

ATP7B on chr17 encodes metal-transporting ATPase, mutation results in excessive copper in liver and brain

A

Wilson’s Disease: Pathophysiology

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56
Q

Chelation (penicillamine), zinc (prevents absorbtion), transplant if bad (always fatal without tx)

A

Wilson’s Disease: Treatment/Notes

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57
Q

Biopsy: (+)PAS granules; Labs: decrease alpha 1AT;Chronic hepatitis, cirrhosis

A

Alpha-1-Antitrypsin Deficiency: Signs/Symptoms/Findings

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58
Q

SERPINA ZZ, some ZS, rarely SS leads to alpha 1AT getting trapped within ER of hepatocytes, leads to fibrosis, cirrhosis, HCC

A

Alpha-1-Antitrypsin Deficiency: Pathophysiology

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59
Q

Serpina Pi null-null

A

no a1t, severe lung disease, no liver dz

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60
Q

Tx: smoking cessation, abstinence, pneumovax, alpha 1AT, manage chronic liver dz, augementum for lungs, only xplant cures liver

A

Alpha-1-Antitrypsin Deficiency: Treatment/Notes

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61
Q

F>M 4:1, dx by exclusion, biopsy

A

Autoimmune Hepatitis (AIH), overlap syndromes: Epi/MOI

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62
Q

Acute hepatitis (30%), occ fulminant, 34% asympt; increased ALT + AST, IgG, gamma-globulin ; plasma cell infiltrate + interface hepatitis

A

Autoimmune Hepatitis (AIH), overlap syndromes: Signs/Symptoms/Findings

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63
Q

97% are Type 1: anti-smooth muscle Ab (SMA) and/or ANA, age 16-30; Type 2: anti-ILKM1, affects kids 2-14yo; type III looks like one, adults 30-50

A

Autoimmune Hepatitis (AIH): Pathophysiology

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64
Q

Tx: Prednisone + azathioprine, 10yr survival 90% but 3yr relapse 90%; long-term Tx usually necessary; xplant

A

Autoimmune Hepatitis (AIH), overlap syndromes: Treatment/Notes

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65
Q

AIH + (PBC or PSC)

A

Overlap Syndromes: Pathophysiology

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66
Q

F>M, other AI diseases

A

Primary Biliary Cirrhosis (PBC): Epi/MOI

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67
Q

(+)AMA, increased AlkP and gamma-globulin, fatigue, pruritus, cirrhotic Sx, chronic cholangitis

A

Primary Biliary Cirrhosis (PBC): Signs/Symptoms/Findings

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68
Q

AMA (anti-mitochondrial Ab) vs. small intrahepatic bile ducts

A

Primary Biliary Cirrhosis (PBC): Pathophysiology

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69
Q

Tx: Ursodeoxycholic acid; cholestyramine for pruritus

A

Primary Biliary Cirrhosis (PBC): Treatment/Notes

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70
Q

M>F 3:1, 20s-30s, 80% IBD (mostly UC)

A

Primary Sclerosing Cholangitis (PSC): Epi/MOI

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71
Q

increased increased AlkPhos+TB, increased ALT+AST, gamma-globulin, (+)pANCA, ANA, SMA, (-)AMA; Onion-skin fibrosis on biopsy, Beads-on-a-string on ERCP

A

Primary Sclerosing Cholangitis (PSC): Signs/Symptoms/Findings

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72
Q

ANCA>ANA>SMA vs. both intrahepatic and extrahepatic bile ducts

A

Primary Sclerosing Cholangitis (PSC): Pathophysiology

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73
Q

Median survival 12 yrs; transplant is only way to improve; watch for colon cancer, cholangiocarcinoma, gallbladder dz, IBD, metabolic bone disorder

A

Primary Sclerosing Cholangitis (PSC): Treatment/Notes

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74
Q

Cholestasis: increased direct bili, pruritus, jaundice, xanthomas, fibrosis, ADEK deficiency, fat malabsorption, hepatocellular injury, acholic stool (grey/white)

A

Infectious Hepatitis, TPN-associated cholestasis, galactosemia, tyrosemia, idiopathic neonate hepatitis: Signs/Symptoms/Findings

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75
Q

ToRCHeS - Toxo, Rubella, CMV, HSV, Syphilis; Coxsackie; Echovirus

A

Infectious Hepatitis: Pathophysiology AND Treatment/Notes

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76
Q

Premies

A

TPN-Associated Cholestasis: Epi/MOI

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77
Q

Lipids in TPN worsens underlying dz

A

TPN-Associated Cholestasis: Pathophysiology

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78
Q

Tx: feed, cycle or stop TPN

A

TPN-Associated Cholestasis: Treatment/Notes

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79
Q

AR pediatric liver diseases

A

Galactosemia, Tyrosemia, PFIC, Congential Hepatic fibrosis: Epi/MOI

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80
Q

Galactose-1-phosphate-uridyl transferase mutation leads to fatty liver

A

Galactosemia: Pathophysiology

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81
Q

Tx: galactose/lactose-free formula

A

Galactosemia: Treatment/Notes

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82
Q

Fumaryl acetoacetate hydrolase deficiencylead to increased succinyl acetone

A

Tyrosinemia: Pathophysiology

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83
Q

Dx: urinary succinyl acetone; Tx: transplant curative

A

Tyrosinemia: Treatment/Notes

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84
Q

Jaundice in 1st week of life, fulminant in 30% (giant cell hepatitis, necrosis)

A

Idiopathic Neonatal Hepatitis: Pathophysiology

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85
Q

Also increased indirect bili; 30-40% of neonatal cholestasis;

A

Idiopathic Neonatal Hepatitis: Treatment/Notes

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86
Q

1/10K, 1wk old, acholic stools,

A

Biliary Atresia : Epi/MOI

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87
Q

Biopsy: swirly, neuron-like ductule cells with bile plugs
Dx: abd USG to r/o other causes, HIDA w/ phenobarb, increased direct bili

A

Biliary Atresia : Signs/Symptoms/Findings

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88
Q

Idiopathic proliferation of bile ductules with bile plugs leading to blockage of bile ducts; cause of 50-60% of liver transplants in kids

A

Biliary Atresia : Pathophysiology

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89
Q

Kasai hepatic porto-enterostomy to delay progression to biliary cirrhosis and transplant

A

Biliary Atresia : Treatment/Notes

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90
Q

Abdominal ultrasound shows cysts, dilation (in children)

A

Choledochal Cyst: Signs/Symptoms/Findings

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91
Q

Congenital weakness in wall of common bile ductlead to dilation, cyst

A

Choledochal Cyst: Pathophysiology

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92
Q

Resection due to malignancy potential

A

Choledochal Cyst: Treatment/Notes

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93
Q

AD, variable penet. Pediatric liver dz

A

Alagille Syndrome: Epi/MOI

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94
Q

Triangular facies, ocular / CV / vertebral anomalies, decrease growth, pruritus, xanthomas

A

Alagille Syndrome: Signs/Symptoms/Findings

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95
Q

JAG1 mutation results in dysfunctional Notch signaling, malformation and paucity of intrahepatic bile ducts, arteriohepatic dysplasia

A

Alagille Syndrome: Pathophysiology

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96
Q

Prolonged survival good but defective spermatogenesis

A

Alagille Syndrome: Treatment/Notes

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97
Q

increased AlkPhos, pruritus, normal GGT; biliary paucity, giant cells

A

Progressive Familial Intrahepatic Cholestasis (PFIC): Signs/Symptoms/Findings

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98
Q

Defect in ATP8B1 (type 1: ATPase) or BSEP (2: salt pump) leads to bile transport problems

A

Progressive Familial Intrahepatic Cholestasis (PFIC): Pathophysiology

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99
Q

External biliary diversion, esp. in type 1; transplant

A

Progressive Familial Intrahepatic Cholestasis (PFIC): Treatment/Notes

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100
Q

Abd pain, cholangitis, varices; ductular cells, no cirrhosis (in children)

A

Congenital Hepatic Fibrosis: Signs/Symptoms/Findings

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101
Q

Malformation of embryonic ductal plate leads to fibrosis, ARPKD

A

Congenital Hepatic Fibrosis: Pathophysiology

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102
Q

Comorbid with Caroli’s

A

Congenital Hepatic Fibrosis: Treatment/Notes

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103
Q

75% M

A

Caroli’s Disease: Epi/MOI

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104
Q

Abd pain, hepatomegaly, Gm- sepsis, CBD normal

A

Caroli’s Disease: Signs/Symptoms/Findings

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105
Q

Multiple saccular dilatations of intrahepatic ducts (~choledochal cyst)

A

Caroli’s Disease: Pathophysiology

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106
Q

Stenting, Abx, pain meds, transplant curative

A

Caroli’s Disease: Treatment/Notes

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107
Q

CT: lumpy-bumpy, enlarged liver; Biopsy: collagen; increased TB (Tx: see PBC), increased PT/INR

A

Cirrhosis: Epi/MOI AND Signs/Symptoms/Findings

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108
Q

Chronic inflammationlead to fibrosis from stellate cells, regenerative nodules, distortion of liver parenchyma; etiologies = HepB/C, EtOH, autoimmune, congenital, toxins

A

Cirrhosis: Pathophysiology

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109
Q

Pro-oncogenic environment (1-5% / yr progress to cancer); prognosis: compensated 8.9 yrs, decompensated 1.6 yrs

A

Cirrhosis: Treatment/Notes

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110
Q

Other sequelae include hepatic hydrothorax (Tx: ~ascites), hyponatremia (Tx: decrease fluids, vaptans), hepatoencephalopathy, varices, portopulmonary syndrome

A

Portal Hypertension: Epi/MOI AND Signs/Symptoms/Findings

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111
Q

Portal pressure increased >7mm Hg (>10 is “significant”) from increased outflow resistance (fibrosis or vasoconstriction) + increased inflow; Tx: beta blockers, octreotide

A

Portal Hypertension: Pathophysiology AND Treatment/Notes

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112
Q

SAAG >1.1, nl glucose, low LDH, low protein+amylase

A

Ascites: Signs/Symptoms/Findings

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113
Q

> 10mmHglead to fluid in peritoneal cavity from lymphatic backflow

A

Ascites: Pathophysiology

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114
Q

Tx: Low Na+ diet, diuretics, LVP, TIPS

A

Ascites: Treatment/Notes

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115
Q

increased WBC (>500, or >250 with more than half polys), (+)culture (klebsiella, e.coli, entercoccus, pneumococcus)

A

Spontaneous Bacterial Peritonitis (SBP): Signs/Symptoms/Findings

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116
Q

Ascites fluid infected by bacteria or fungi w/o gut perforation

A

Spontaneous Bacterial Peritonitis (SBP): Pathophysiology

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117
Q

Tx: 3G cephalosporin x 5d

A

Spontaneous Bacterial Peritonitis (SBP): Treatment/Notes

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118
Q

Serum Cr >1.5, despite volume expansion, d/c diuretics

A

Hepatorenal Syndrome: Signs/Symptoms/Findings

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119
Q

Renal insufficiency with cirrhosis and ascites; Type 1 worse than Type 2

A

Hepatorenal Syndrome: Pathophysiology

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120
Q

Tx: Albumin, midodrine, octreotide, TIPS, liver xplant

A

Hepatorenal Syndrome: Treatment/Notes

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121
Q

Platypnea-orthodeoxia, clubbing, cyanosis

A

Hepatopulmonary Syndrome: Signs/Symptoms/Findings

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122
Q

V-Q mismatch from vasodilation in lung due to NO from portal HTN

A

Hepatopulmonary Syndrome: Pathophysiology

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123
Q

Tx: O2, liver transplant

A

Hepatopulmonary Syndrome: Treatment/Notes

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124
Q

Gross: “Nutmeg liver” Biopsy: congestion near central vein

A

Centrilobular Congestion: Signs/Symptoms/Findings

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125
Q

Right-sided heart failure (or biventricular heart failure)

A

Centrilobular Congestion: Pathophysiology AND Treatment/Notes

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126
Q

Biopsy: necrosis near central vein

A

Centrilobular Necrosis: Signs/Symptoms/Findings

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127
Q

Left-sided heart failure

A

Centrilobular Necrosis: Pathophysiology

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128
Q

Ascites & increased coag state

A

Budd-Chiari Syndrome: Signs/Symptoms/Findings

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129
Q

Liver (cont’d)

A

Budd-Chiari Syndrome: Cat

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130
Q

Thrombi/tumor invade hepatic vein/IVC; liver blocked, congested

A

Budd-Chiari Syndrome: Pathophysiology

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131
Q

50% due to Tylenol

A

Acute Liver Failure (ALF): Epi/MOI

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132
Q

Acute, change MS, coagulopathy (increased INR), no cirrhosis; coagulative necrosis

A

Acute Liver Failure (ALF): Signs/Symptoms/Findings

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133
Q

Drugs, viruses, toxins, metabolic dz, ischemia, etc. leads to liver damage; can lead to encephalopathy, infection, cerebral edema, renal failure, SIRS

A

Acute Liver Failure (ALF): Pathophysiology

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134
Q

ICU, IV N-acetylcysteine if acetaminophen, early liver transplantation (other organs usually recover)

A

Acute Liver Failure (ALF): Treatment/Notes

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135
Q

28% Tylenol, 52% indeterminate (probably viral)

A

Pediatric Acute Liver Failure: Epi/MOI AND Signs/Symptoms/Findings

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136
Q

Acetaminophen better prognosis than viral/indeterminant

A

Pediatric Acute Liver Failure: Pathophysiology

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137
Q

OLT (King’s college criteria)

A

Pediatric Acute Liver Failure: Treatment/Notes

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138
Q

Asterixis, stupor, coma, change LOC

A

Hepatic Encephalopathy: Signs/Symptoms/Findings

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139
Q

Gut neurotoxin (e.g. NH3) bypass liver due to portal-systemic shunt

A

Hepatic Encephalopathy: Pathophysiology AND Treatment/Notes

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140
Q

1M die / yr

A

Hepatocellular Carcinoma: Epi/MOI

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141
Q

Screen with liver USG q6mo in at-risk pts, vaccinate for HBV

A

Hepatocellular Carcinoma: Signs/Symptoms/Findings

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142
Q

Screen ALF pts every 6 mos

A

for Hepatocellular Carcinoma

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143
Q

Chemo, RF ablation

A

Hepatocellular Carcinoma: Treatment/Notes

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144
Q

hepatic failure + iron deposition

A

gestational alloimmune liver disease

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145
Q

complement cascade activates, intrauterine onset. Anti-human C5B9 complex

A

gestational alloimmune liver disease

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146
Q

IVIg, exchange transfusion, OLT

A

gestational alloimmune liver disease

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147
Q

PT prolongs within

A

one day of liver dysfunction

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148
Q

marked ALT/AST elevation

A

hepatocellular

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149
Q

marked AlkP, TB elevation

A

cholestatic

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150
Q

marked AlkP only

A

infiltrative

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151
Q

normal albumin

A

3.5-5.3

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152
Q

normal AST

A

six-40

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153
Q

normal Alk-P

A

30-120

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154
Q

normal TB

A

0.1-1

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155
Q

normal direct B

A

0.1-0.4

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156
Q

normal GGT

A

0-42

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157
Q

normal INR (PT ratio)

A

1

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158
Q

dx biliary obstruction

A

MRCP (costly)

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159
Q

test to access cirrhosis

A

liver-spleen scan (medium)

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160
Q

will not evaluate liver function, can’t detect fibrosis, rarely reveals etiology

A

CT, MRI/MRCP

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161
Q

mild elevation

A

<5x normal

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162
Q

severe elevation

A

> 15x normal

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163
Q

decreases UGT1 activity, increased bili production, bad erthropoesis and decreased RBC survival

A

why babies be jaundiced

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164
Q

female, advanced age, DM, obese, chronic viral disease, alcohol, decreased renal fxn, nutritional deprivation

A

factors associated with drug-related liver damage

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165
Q

acetominophen, after P450, produced

A

toxic NAPQ1

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166
Q

tylenol and beer both

A

deplete glutathione, leading to mercapturic acid conjugates and mitochondrial dysfunction

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167
Q

picornaviridal hepatovirus

A

hep A

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168
Q

hepandaviridae

A

hepB

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169
Q

flaviveridal hepacivirus

A

hep C

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170
Q

unclassified viroid, delta virus

A

hep D

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171
Q

unclassified, toga- and alphavirus-like

A

hep E

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172
Q

mono, lymphadenopathy, splenomegaly and hepatitis

A

EBV

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173
Q

immunocompromised with hepatitis

A

CMV?

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174
Q

HBsAg

A

acute or chronic hep B

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175
Q

Anti-HBc IgM

A

acute hep B

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176
Q

HBeAg

A

increased infectivity hep B

177
Q

Anti-HBe

A

decreased infectivity hep B

178
Q

Anti-HBs

A

hep B immunity

179
Q

Anti-HBc IgG + HBsAg

A

hep B chronic infxn

180
Q

Anti-HBc IgG + Anti-HBs

A

hep B resolved infxn

181
Q

Hep C incubates for

A

6-8 weeks

182
Q

Hep C becomes chronic for

A

80%

183
Q

Hep C becomes cirrhotic for

A

20%

184
Q

HCV RNA positive at

A

2 weeks post-infxn

185
Q

Anti-HCV appears

A

12-24 weeks post infxn

186
Q

AST:ALT in alcoholic hep

A

> 2:1

187
Q

three effects of alcohol ingestion

A

aldehyde adducts, increased ROS, increase NADH:NAD+ ratio

188
Q

required abstinence for xplant

A

six months

189
Q

predict progression in NAFLD

A

DM, high initial fibrosis, obesity

190
Q

portal hepatic pressure gradient PV-HV

A

7 is normal, 10 is significant, balloon is in the HV

191
Q

NO increases in PHTN because

A

shear stress activates eNOS in splanchnic beds, increased TNF and VEGF

192
Q

spontaneous bacterial peritonitis, refractory ascites, dilutional hyponatremia, hepatorenal syndrome

A

prognosis in PHTN, worst to best

193
Q

GI bleed/hypotension, advanced liver disease, prior Hx

A

risk factors for spontaneous bacterial perotinitis

194
Q

All tx for end-stage liver dz, except OLT

A

supportive not curative

195
Q

INR in ALF

A

> 1.5

196
Q

barbituates, mannitol, hyperventilation, head elevation

A

may prevent encephalopathy in fulminant liver failure

197
Q

discrimination function equation

A

4.6*(patient’s PT-control PT) + total bili

198
Q

DF>32

A

alcoholic hepatitis, treat with steroids

199
Q

pH100 and creatinine>3.5, in III/IV coma

A

King’s College OLT criteria in acetominophen poisoning

200
Q

PT>100, or three of these:PT>50, younger than 10 or older than 40, jaundice 7 days prior to encephalopathy, bili>17, not hep A or B

A

Kings College OLT criteria (not ACM)

201
Q

associated with polysplenia, heterotaxia, intraabdominal vascular abnormalities

A

biliary atresis

202
Q

alaguille’s prognosis is good except defective sperms and

A

CNS aneurysms

203
Q

percent of HCC due to HBV

A

80%!

204
Q

HBV, HCV, alcoholic cirrhosis, NAFLD, metabolic syndrome, aflatoxin (from corn, soy, nuts), dirty water

A

HCC risk factors

205
Q

Lymphocytes in islets lead to

A

Type I Diabetes Mellitus: Signs/Symptoms/Findings

206
Q

Autoimmune vs. beta cells

A

Type I Diabetes Mellitus: Pathophysiology

207
Q

Amyloid buildup in pancreas

A

Type II Diabetes Mellitus: Signs/Symptoms/Findings

208
Q

Insulin resistance in beta cells

A

Type II Diabetes Mellitus: Pathophysiology

209
Q

Hypoglycemia

A

Islet Cell Adenoma (Insulinoma): Signs/Symptoms/Findings

210
Q

Benign but functional encapsulated tumor of islet cell origin

A

Islet Cell Adenoma (Insulinoma): Pathophysiology

211
Q

Complete (IPF1 single nucleotide deletion) or partial lack of pancreas

A

Pancreatic Agenesis: Pathophysiology

212
Q

Partial still has full function

A

Pancreatic Agenesis: Treatment/Notes

213
Q

Obstructed pancreatic fluid flow, canlead to chronic pancreatitis

A

Pancreas Divisum: Signs/Symptoms/Findings

214
Q

10% of the people

A

Pancreas Divisum: Epi/MOI

215
Q

dx w/Ultrasound, ECRP. Think of in patients with recurrent pancreatitis

A

Pancreas Divisum

216
Q

Pancreas separated, not fused together

A

Pancreas Divisum: Pathophysiology

217
Q

Completely separated pancreas strangulates duodenum

A

Annular Pancreas: Pathophysiology

218
Q

Surgical resection

A

Annular Pancreas: Treatment/Notes

219
Q

35% alcohol use, 45% gallstones

A

Acute Pancreatitis: Epi/MOI

220
Q

Epigastric abd pain rad to back, rapid onset, N/V, may have Cullen’s/Grey-Turner’s signs; increased Serum lipase + amylase (3x nl), liquefactive necrosis, elastase destruction of blood vesselslead to

A

Acute Pancreatitis: Signs/Symptoms/Findings

221
Q

No initial abx if severe. ERCP for stones

A

Acute Pancreatitis

222
Q

Dx requires 2 of: imaging, characteristic pain, amylase/lipase 3x normal

A

Acute Pancreatitis

223
Q

Intracellular enzymes released, digest pancreatic fat, lobules, blood vessels; most common cause is gallstones, followed by alcohol, post-ERCP, drugs (E2, valproate, thiazide diuretics, PIs)

A

Acute Pancreatitis: Pathophysiology

224
Q

Tx: IV fluids, NPO; can lead to fat necrosis, hemorrhage, ARDS, hypovolemia, hypocalcemia, coagulopathy, hyperglycemia,

A

Acute Pancreatitis: Treatment/Notes

225
Q

Alcohol #1 cause

A

Chronic Pancreatitis: Epi/MOI

226
Q

Calcified pancreas on XR/CT; exocrine insufficiency; large duct disease (more common in males, alcohol) vs. small duct (females, idiopathic); pain

A

Chronic Pancreatitis: Signs/Symptoms/Findings

227
Q

Episodes of repeated acute pancreatitis and resultant fibrosis; EtOH increased mRNA production of degradation enzymes, blocks apical migration of lysosomes

A

Chronic Pancreatitis: Pathophysiology

228
Q

Tx: abstinence, analgesics, octreotide, enzyme replacement, ERCP/neurolysis for pain, Puestow procedure. Can cause DM by destroying islets

A

Chronic Pancreatitis: Treatment/Notes

229
Q

AD, 80% with mutation develop inflammation

A

Hereditary Pancreatitis: Epi/MOI

230
Q

PRSS1 mutation results in increased intracellular enzymes

A

Hereditary Pancreatitis: Pathophysiology

231
Q

High risk for pancreatic cancer (>40%)

A

Hereditary Pancreatitis: Treatment/Notes

232
Q

Other AI disorders, plus pancreatitis

A

Autoimmune Pancreatitis: Epi/MOI

233
Q

IgG deposits, especially IgG4

A

Autoimmune Pancreatitis: Signs/Symptoms/Findings

234
Q

Autoantibodies results in narrowing of main pancreatic duct

A

Autoimmune Pancreatitis: Pathophysiology

235
Q

Tx: steroids

A

Autoimmune Pancreatitis: Treatment/Notes

236
Q

Fat, Forty, Fertile Female; 10-15% of adults, hispanic>white>black

A

Gallstones (Cholelithiasis): Epi/MOI

237
Q

USG: hyperechoic with shadow

A

Gallstones (Cholelithiasis): Signs/Symptoms/Findings

238
Q

Cholesterol stones (85%, radiolucent), black pigment stones (radiodense, from hemolysis), or brown pigment stones (infectious)

A

Gallstones (Cholelithiasis): Pathophysiology

239
Q

Cholecystectomy

A

Gallstones (Cholelithiasis): Treatment/Notes

240
Q

Steady epigastric/RUQ pain, rad to back/R shoulder

A

Biliary Colic: Signs/Symptoms/Findings

241
Q

Most common complication; = pain from GB stones or CBD stones

A

Biliary Colic: Pathophysiology

242
Q

Onset of pain >1hr after meals and at night

A

Biliary Colic: Treatment/Notes

243
Q

Fever, leukocytosis, mild LFTs in 25%, N/V, RUQ pain rad to back, worse with movement or cough, HIDA scan, Murphy’s sign, stones + thick wall on USG

A

Acute Cholecystitis: Signs/Symptoms/Findings

244
Q

Inflammation of gallbladder itself; can be calculous (impaction of stone at GB necklead to inflammation, bacteria) or acalculous (immunocompromised)

A

Acute Cholecystitis: Pathophysiology

245
Q

Tx: NPO, supportive care, antibiotics, surgery, cholecystectomy, endo-scopic cystic duct stenting, meperedine for pain

A

Acute Cholecystitis: Treatment/Notes

246
Q

Biliary colic, obstructive jaundice, cholangitis, pancreatitis; Dx: intraductal or radial endoscopic USG

A

Choledocholithiasis: Signs/Symptoms/Findings

247
Q

CBD blocked by stones (any type)

A

Choledocholithiasis: Pathophysiology

248
Q

Tx: ERCP w/ cannulation, sphincterotomy, or stone retrieval; surgical biliary bypass, cholecystectomy

A

Choledocholithiasis: Treatment/Notes

249
Q

Charcot’s triad in 60-70% (fever, jaundice, RUQ pain); infected bile, frank pus, increased LFTs, less severe tenderness

A

Acute Cholangitis: Signs/Symptoms/Findings

250
Q

stents, tumors, congenital cysts, pancreatitis, ascaris lumbroides, HIV

A

Acute Cholangitis: Associated Conditions

251
Q

BD stone results in bacterial (usually Gm-, multiple agents) infection of bile ducts, usually with partial or complete cholestasis

A

Acute Cholangitis: Pathophysiology

252
Q

Tx: broad spectrum antibiotics (cypro, zocin), NPO, hydration, ERCP if emergent(better than surgery)

A

Acute Cholangitis: Treatment/Notes

253
Q

acini cells (84%), then ducts (5) then islets (1)

A

by mass, pancreas is mostly

254
Q

cues acinar enzyme secretion

A

CCK via IP3

255
Q

cues ducts to secrete water, Na and bicarb

A

secretin via cAMP

256
Q

Cough, aspiration; more problems with liquids

A

Oropharyngeal Dysphagia: Signs/Symptoms/Findings

257
Q

Difficulty transferring bolus out of mouth

A

Oropharyngeal Dysphagia: Pathophysiology

258
Q

Caused by Zenker’s diverticulum, stroke, ACS, parkinson’s MS, muscular dystrophy

A

Oropharyngeal Dysphagia

259
Q

Sense of bolus “sticking”

A

Esophageal Dysphagia: Signs/Symptoms/Findings

260
Q

Bolus trapped in esophagus

A

Esophageal Dysphagia: Pathophysiology

261
Q

Only solid food impaction (with forced regurgitation), often progressive (especially malig.)

A

Mechanical, Schatzki Ring, Esophageal Stricture, Esophageal Carcinoma: Signs/Symptoms/Findings

262
Q

Can also be caused by Barrett’s

A

Mechanical: Pathophysiology

263
Q

Ring at squamo-columnar junction, dysphagia with large boluses of food

A

Schatzki Ring: Pathophysiology

264
Q

Steakhouse syndrome

A

Schatzki Ring: Treatment/Notes

265
Q

Can be asymptomatic, usually caused by acid reflux

A

Esophageal Stricture: Pathophysiology

266
Q

Tx: with esophageal dilators

A

Esophageal Stricture: Treatment/Notes

267
Q

Irregular stricture with lots of ulcers

A

Esophageal Carcinoma: Pathophysiology

268
Q

Tx: chemotherapy, resection, radiation, stents

A

Esophageal Carcinoma: Treatment/Notes

269
Q

Liquid impaction, nocturnal

A

Motor: Signs/Symptoms/Findings

270
Q

Aperistalsis, LES HTN and incomplete relaxationlead to distal narrowing

A

Achalasia: Signs/Symptoms/Findings

271
Q

Idiopathic or Chagas results in esophageal denervation/dilation, failure of smooth muscle relaxation

A

Achalasia: Pathophysiology

272
Q

Tx: laparoscopic myotomy, Botox, pneumatic dilation

A

Achalasia: Treatment/Notes

273
Q

Esophageal dysmotility, weak LES, weak contraction, LES hypotension, GERD

A

Scleroderma: Signs/Symptoms/Findings

274
Q

Aka CREST syndrome, where smooth muscle becomes fibrotic

A

Scleroderma: Pathophysiology

275
Q

Tx: immunosuppression

A

Scleroderma: Treatment/Notes

276
Q

Heartburn, atypical sx: chest pain, ENT problems, vocal changes, asthma, cough; Biopsy: basal cell hyperplasia, mixed inflammatory cells, erosions

A

Gastroesophageal Reflux Disease (GERD): Signs/Symptoms/Findings

277
Q

LES transiently relaxes, leading to esophagitis due to acid, can lead to strictures

A

Gastroesophageal Reflux Disease (GERD): Pathophysiology

278
Q

Dx: 24hr pH monitoring, Bravo capsule study, etc. Tx: avoid precipitants, wt loss, PPI > H2RA

A

Gastroesophageal Reflux Disease (GERD): Treatment/Notes

279
Q

most common GI referral, late complication: Barretts

A

GERD

280
Q

no fatty food, alcohol, caffeine, small meals, raise bed, antacids

A

Mild GERD tx

281
Q

histimine 2 receptor antagonist: Cimetidine

A

severe GERD tx

282
Q

Junctional: mucinous glands; Gastric fundic: parietal cells; normal cells, just abnormal location

A

Barrett’s Esophagus (Columnar Metaplasia): Signs/Symptoms/Findings

283
Q

Intestinal metaplasia (i.e. esophagus looks like small intestine) due to injury to squamous mucosa and subsequent stem cell repair

A

Barrett’s Esophagus (Columnar Metaplasia): Pathophysiology

284
Q

Cancer risk (adenocarcinoma)

A

Barrett’s Esophagus (Columnar Metaplasia): Treatment/Notes

285
Q

Vomiting, reflux symptoms; >20 eos per HPF, rings, strictures, white papules, linear furrows

A

Eosinophilic Esophagitis (Allergic): Signs/Symptoms/Findings

286
Q

Children/YA, M>F

A

Eosinophilic Esophagitis (Allergic): Epi

287
Q

Hypersensitivity to dietary or airborne allergens

A

Eosinophilic Esophagitis (Allergic): Pathophysiology

288
Q

Tx: corticosteroids, diet, avoid allergens, AA formulas. Anti-reflux drugs ineffective

A

Eosinophilic Esophagitis (Allergic): Treatment/Notes

289
Q

Red inclusion bodies, multiple nuclei per cell, molded cells, ground glass nuclei, affects squamous cells

A

HSV Esophagitis: Signs/Symptoms/Findings

290
Q

Fairly common, self-limited, peripheral ulcers secondary to infxn. Relapse frequent

A

HSV Esophagitis: Pathophysiology

291
Q

Cytomegaly, intranuclear inclusions, granules and pale zone, epithelium spared

A

CMV Esophagitis: Signs/Symptoms/Findings

292
Q

In immunocompromised patients, enlarged stromal cells (endos, histiocytes, nerve, muscle). Dx w/ulcer base biopsy

A

CMV Esophagitis: Pathophysiology

293
Q

AIDS/DM

A

Candida Esophagitis: Epi/MOI

294
Q

White pseudomembranes grossly, pseudohyphae and yeasts on silver stain

A

Candida Esophagitis: Signs/Symptoms/Findings

295
Q

Indicator of AIDS, must see tissue invasion

A

Candida Esophagitis: Pathophysiology

296
Q

NSAIDs, tetracycline, bisphosphonates, potassium, vitamin C, iron

A

Pill Esophagitis

297
Q

dx: clinic pathology, or biopsy (iron)

A

pill Esophagitis

298
Q

2-3 weeks post, self-limiting, esophageal ulcers

A

radiation esophagitis: acute

299
Q

3-6 months post, fibrosis, treat with stents and dilation

A

radiation esophagitis: chronic

300
Q

10% lifetime prevalence, 50% have H. pylori

A

Peptic Ulcer Disease: Epi/MOI

301
Q

Dyspepsia, relieved (DU) or worsened (GU) by food; majority asymptomatic; can result in upper GI bleeding; DU (right), GU (left)

A

Peptic Ulcer Disease: Signs/Symptoms/Findings

302
Q

Recurrent ulcers in upper GI tract, especially near mucosal junctions; due to increased acid+pepsin and decrease PGE-related protective factors (HCO3, mucus, etc.)

A

Peptic Ulcer Disease: Pathophysiology

303
Q

H. pylori classical cause, NSAIDs becoming more common (decrease PGE2 from decrease COX-1);dx: upper endoscope and biopsy; Tx: PPI + amox

A

Peptic Ulcer Disease: Treatment/Notes

304
Q

Parietal cell/IF antibodies, loss of parietal and chief cells, intestinal metaplasia

A

Autoimmune (Type A) Chronic Atrophic Gastritis: Signs/Symptoms/Findings

305
Q

Rarest form, associated with pernicious anemia (B12 malabsorption)

A

Autoimmune (Type A) Chronic Atrophic Gastritis: Pathophysiology

306
Q

Can result in gastrin cell tumors; mostly affect body / fundus

A

Autoimmune (Type A) Chronic Atrophic Gastritis: Treatment/Notes

307
Q

H. pylori seen outside cells; Dx: urea breath test / stool test

A

H. Pylori (Type B) Chronic Atrophic Gastritis: Signs/Symptoms/Findings

308
Q

children with multifocal gastritis, gastric ulcer, gastric cancer

A

H. Pylori (Type B) Chronic Atrophic Gastritis: Signs/Symptoms/Findings

309
Q

adults with chronic gastritis, duodenal ulceers

A

H. Pylori (Type B) Chronic Atrophic Gastritis: Signs/Symptoms/Findings

310
Q

H. pylori produces urease, leading to increased ammonia; can lead to gastric adenocarcinoma

A

H. Pylori (Type B) Chronic Atrophic Gastritis: Pathophysiology

311
Q

Usually affects antrum / pylorus, but can be corpus (elderly) or pangastric

A

H. Pylori (Type B) Chronic Atrophic Gastritis: Treatment/Notes

312
Q

Foveolar hyperplasia, mucosal edema and fibrosis, mild chronic inflammation

A

Reactive Gastritis (Type C): Epi/MOI AND Signs/Symptoms/Findings

313
Q

aka Chemical; NSAIDs (decrease COX, decrease prostaglandins, low protection and platelet inhibition), reflux, EtOH

A

Reactive Gastritis (Type C): Pathophysiology

314
Q

Rare, 25% hereditary

A

Zollinger Ellison Epi

315
Q

Very thick mucosa, increased gastrin, acid, PUD

A

Zollinger-Ellison (Gastrinoma) Syndrome : Signs/Symptoms/Findings

316
Q

Parietal and chief cells hyperplastic, hypersecreting, due to MEN1 (25%) or islet cell tumor

A

Zollinger-Ellison (Gastrinoma) Syndrome : Pathophysiology

317
Q

Surgical resection, high dose PPIs. Only cure is surgery

A

Zollinger-Ellison (Gastrinoma) Syndrome : Treatment/Notes

318
Q

Large hyperplastic folds, antrum-sparing

A

Menetrier’s Disease : Signs/Symptoms/Findings

319
Q

Mucus cells hyperplastic

A

Menetrier’s Disease : Pathophysiology

320
Q

Watermelon stomach in GAVE (gastric antral vascular ectasia)

A

Vascular Lesions: Signs/Symptoms/Findings

321
Q

Gastric varices, gastric hypertensive gastropathy, or GAVE

A

Vascular Lesions: Pathophysiology

322
Q

Usually a complication of portal HTN

A

Vascular Lesions: Treatment/Notes

323
Q

Fundic most common

A

Gastric Polyps: Epi/MOI

324
Q

Hyperplastic = oddly shaped, fundic = cystically dilated

A

Gastric Polyps: Signs/Symptoms/Findings

325
Q

Hyperplastic, fundic gland, adenomatous, or fibroid polyps

A

Gastric Polyps: Pathophysiology

326
Q

Adenomatous has malignancy potential

A

Gastric Polyps: Treatment/Notes

327
Q

C-section, early or late gluten exposure

A

Celiac Disease (Gluten-Sensitive Enteropathy): Epi/MOI

328
Q

Steatorrhea, malabsorption, weight loss; Biopsy: CD3+ IELs, Inflammation, villous atrophy (<4:1 V:C ratio) Labs: anti-tTG, EMA, and gliadin

A

Celiac Disease (Gluten-Sensitive Enteropathy): Signs/Symptoms/Findings

329
Q

Gliadin gets activated by tTG, presented to APCs because of HLA DQ2/8, cross-reaction with small bowel tissue; can be comorbid with lymphocytic gastritis/colitis

A

Celiac Disease (Gluten-Sensitive Enteropathy): Pathophysiology

330
Q

Response to gluten-free diet is both diagnostic and primary treatment; rule out other causes of villous atrophy

A

Celiac Disease (Gluten-Sensitive Enteropathy): Treatment/Notes

331
Q

common (1% prevalence) only 17% dx in US, twins is 70%

A

Celiac

332
Q

H. pylori protects, best tests are tTG IgA and DGP

A

Celiac

333
Q

Diarrhea in <2 yo, growth issues at all ages

A

Pediatric Celiac Disease: Epi/MOI AND Signs/Symptoms/Findings

334
Q

No diarrhea, IBS, incidental, decrease Fe anemia, dermatitis herpetiformis

A

Silent Celiac Disease: Signs/Symptoms/Findings

335
Q

Non-diarrheal presentations of celiac disease; oral lesions is from interaction with tTG in skin

A

Silent Celiac Disease: Pathophysiology

336
Q

Can also get enamel abnormalities (dental applications!)

A

Silent Celiac Disease: Treatment/Notes

337
Q

Type I: CD8+, responds to immunosuppression; Type II: refractory to immunosuppression, malignancy risk (T-cell lymphoma)

A

Refractory Sprue: Epi/MOI AND Signs/Symptoms/Findings

338
Q

Celiac that doesn’t respond to gluten-free diet; can be from noncompliance, wrong diagnosis

A

Refractory Sprue: Pathophysiology AND Treatment/Notes

339
Q

Increased collagen in subepithelial area

A

Collagenous Sprue: Signs/Symptoms/Findings

340
Q

Travel

A

Tropical Sprue: Epi/MOI

341
Q

Vs. celiac: distal bowel affected more than proximal, macrocytic anemia from B12 malabsorption

A

Tropical Sprue: Signs/Symptoms/Findings

342
Q

Post-infectious (e. coli, heterophilus) sprue that doesn’t respond to gluten-free diet

A

Tropical Sprue: Pathophysiology

343
Q

Tx: doxycycline, B vitamins

A

Tropical Sprue: Treatment/Notes

344
Q

Vs. celiac: other Crohn’s Sx AND No hematochezia, RLQ pain, aphthous ulcers Gross: skip areas, crypt malformation, giant cells, granulomas, pyloric metaplasia

A

Crohn’s Disease: Signs/Symptoms/Findings

345
Q

Vs. celiac: gastric heterotopia (duodenum looks like stomach)

A

Peptic Duodenitis: Signs/Symptoms/Findings

346
Q

H. pylori infection in duodenum, gastric metaplasia

A

Peptic Duodenitis: Pathophysiology

347
Q

Vs. celiac: much more eosinophils

A

Eosinophilic Gastroenteritis: Signs/Symptoms/Findings

348
Q

Mucosal dominant: most common, see diarrhea, bleeding; mural: abd pain, obstruction, N/V; serosal: eosinophilic ascites

A

Eosinophilic Gastroenteritis: Pathophysiology AND Treatment/Notes

349
Q

Vs. celiac: anti-enterocyte/anti-goblet cell Abs

A

Autoimmune Enteritis: Signs/Symptoms/Findings

350
Q

Can affect entire gut, see virtually no goblet or Paneth cells on biopsy

A

Autoimmune Enteritis: Pathophysiology

351
Q

Vs. celiac: reduced plasma cells, chronic giardiasis

A

Common Variable Immunodeficiency: Signs/Symptoms/Findings

352
Q

Hypogammaglobulinemia, B lymphocytes fail to mature

A

Common Variable Immunodeficiency: Pathophysiology

353
Q

Responds to steroids (not curative)

A

Common Variable Immunodeficiency: Treatment/Notes

354
Q

Vs. celiac: metaphase mitoses (colchicine), increased apoptosis (mycophenolate)

A

Drug-Related Enteritis: Signs/Symptoms/Findings

355
Q

NSAIDs, mycophenolate, colchicine, chemo, radiation

A

Drug-Related Enteritis: Pathophysiology

356
Q

Vs. celiac: histiocytes (Whipple’s), (+)acid fast (MAI), (+)silver (Histo), worms+cysts (strongy)

A

Infectious Enteritis: Epi/MOI AND Signs/Symptoms/Findings

357
Q

Can be from adenovirus, CMV, calicivirus, Whipple’s disease, MAI, histoplasmosis, strongyloides, AIDS

A

Infectious Enteritis: Pathophysiology AND Treatment/Notes

358
Q

Rule of 2s: 2% of people, 2ft from ileocecal valve, 2cm, 1/2 heterotopic mucosa (gastric or pancreatic)

A

Meckel’s Diverticulum: Epi/MOI AND Signs/Symptoms/Findings

359
Q

True diverticulum from persistence of vitelline duct leads to an appendix-like lesion in terminal ileum

A

Meckel’s Diverticulum: Pathophysiology

360
Q

Complications: inflammation, bleeding ulcer, obstruction

A

Meckel’s Diverticulum: Treatment/Notes

361
Q

Intussusception (2nd to masses in adults), volvulus, herniation, adhesions

A

Intestinal Obstruction: Pathophysiology AND Treatment/Notes

362
Q

reduced risk in smokers

A

Ulcerative Colitis

363
Q

increased risk in smokers

A

Crohns

364
Q

15-25, 50-65; M=F, Jews, FMHx, White>Black

A

Ulcerative Colitis: Epi/MOI

365
Q

Bloody diarrhea, 6+ BMs/day, LLQ pain, anemia Gross: red friable mucosa, pseudopolyps Biopsy: flat ulcers, overhanging mucosa, crypt abscesses, Paneth metaplasia, crypt irregularity

A

Ulcerative Colitis: Signs/Symptoms/Findings

366
Q

Environmental triggers (smoking, diet, NSAIDs, stress, etc.) + genetic predisposition + increased immune response (TNF- alpha , alpha 4beta7); complications include toxic megacolon, low-grade or high-grade dysplasia, carcinoma

A

Ulcerative Colitis: Pathophysiology

367
Q

Tx: 5-ASA (mesalamine) formulation depending on location (e.g. Asacol or Lialda for ileocolitis), oral/IV steroids, infliximab (anti-TNF), 6-mercaptopurine / azathiprine, cyclosporins / tacrolimus, biologics

A

Ulcerative Colitis: Treatment/Notes

368
Q

no blood in stool, RLQ pain, apthous ulcers, skip areas, cobblestoning Biopsy: fissures, transmural dz, pyloric metaplasia, non-caseating granulomas

A

Crohn’s

369
Q

Smoldering disease with chronic inflammation of terminal ileum, ileum+colon, colon, or upper GI tract; complications: strictures, perianal fistulae, dysplasia, colon cancer (4-20x greater risk)

A

Crohn’s Disease: Pathophysiology

370
Q

Tx: 5-ASA (mesalamine) formulation depending on location (e.g. Asacol or Lialda for ileocolitis), oral/IV steroids, infliximab (anti-TNF), 6-mercaptopurine / azathiprine, cyclosporins / tacrolimus, biologics

A

Crohn’s Disease: Treatment/Notes

371
Q

Travel, c.diff

A

Infectious Colitis: Epi/MOI

372
Q

(-) stool culture in 70%, PMNs in lamina propria, crypts intact

A

Infectious Colitis: Signs/Symptoms/Findings

373
Q

Acute, self-limited

A

Infectious Colitis: Pathophysiology

374
Q

Resolved by Abx

A

Infectious Colitis: Treatment/Notes

375
Q

Volcano lesions, membranous white plaques, PMNs in lamina propria

A

Pseudomembranous Colitis: Epi/MOI AND Signs/Symptoms/Findings

376
Q

C. diff overgrowth destroys epithelium

A

Pseudomembranous Colitis: Pathophysiology AND Treatment/Notes

377
Q

> 70 yo, increased coag state

A

Ischemic Colitis: Epi/MOI

378
Q

LLQ pain, hematochezia, urgency; crypt atrophy, fibrotic lamina propria

A

Ischemic Colitis: Signs/Symptoms/Findings

379
Q

Slowly progressing, affects crypts (most O2 demand); can result in hemorrhage, ulcer, stricture, infarct

A

Ischemic Colitis: Pathophysiology

380
Q

Middle age

A

Microscopic Colitis: Epi/MOI

381
Q

Watery (secretory) diarrhea, grossly normal on colono/endoscopy

A

Microscopic Colitis: Signs/Symptoms/Findings

382
Q

Lymphocytic or collagenous colitis, only microscopically inflamed

A

Microscopic Colitis: Pathophysiology

383
Q

Not improved with fasting, osmotic gap 1L, maybe blood, happens in the night

A

Secretory Diarrhea: Signs/Symptoms/Findings

384
Q

Iso-osmotic fluid secreted; caused by toxins, function hormone tumors, etc. (E.coli, cholera, inflammation)

A

Secretory Diarrhea: Pathophysiology

385
Q

Tx: ORS, ribosylates Gsalpha

A

Cholera: Signs/Symptoms/Findings

386
Q

Vibrio cholerae toxin increased Na+ export

A

Cholera: Pathophysiology

387
Q

Resolves with fasting, watery, osmotic gap >50 mOsm/kg, <1L

A

Osmotic Diarrhea: Signs/Symptoms/Findings

388
Q

sorbitol, fructose intolerance, sprue, celiac

A

Osmotic Diarrhea causes

389
Q

Osmotically active substance in lumen; often lactase deficiency

A

Osmotic Diarrhea: Pathophysiology

390
Q

Foul-smelling, floaters, multiple flushes, increased w/ fat ingestion

A

Fatty Diarrhea: Signs/Symptoms/Findings

391
Q

Fat malabsorption

A

Fatty Diarrhea: Pathophysiology

392
Q

make illness 1-2 days shorter, increase salmonella populations, make c. dif and ecoli worse

A

Abx in Diarrhea

393
Q

Can result in nephrolithiasis (FAs out-compete oxalate for Ca+)

A

Short Bowel Syndrome: Signs/Symptoms/Findings

394
Q

After resection, <200cm SB

A

Short Bowel Syndrome: Pathophysiology

395
Q

Bloody, mucus, tenesmus

A

Inflammatory Diarrhea: Signs/Symptoms/Findings

396
Q

Invasive infectious result in bloody, proteinaceous, exudative diarrhea with decrease serum protein + albumin

A

Inflammatory Diarrhea: Pathophysiology

397
Q

AIDS

A

Cryptosporidiosis: Epi/MOI

398
Q

Blue dots on Giemsa stain

A

Cryptosporidiosis: Signs/Symptoms/Findings

399
Q

Invasive infectious result in bloody, proteinaceous, exudative diarrhea with decrease serum protein + albumin

A

Cryptosporidiosis: Pathophysiology

400
Q

AIDS

A

CMV Colitis: Epi/MOI

401
Q

Owl’s eye epithelial nucleus

A

CMV Colitis: Signs/Symptoms/Findings

402
Q

Invasive infectious result in bloody, proteinaceous, exudative diarrhea with decrease serum protein + albumin

A

CMV Colitis: Pathophysiology

403
Q

22%, F>M (3:1), >40yo

A

Irritable Bowel Syndrome: Epi/MOI

404
Q

Abdominal pain (3d/mo for 3+ mos) relieved by defecation, change stool freq/form

A

Irritable Bowel Syndrome: Signs/Symptoms/Findings

405
Q

increased Permeability leads to inflammation, activation of mast cells leads to ENS hyper-sensitivitylead to symptoms

A

Irritable Bowel Syndrome: Pathophysiology

406
Q

IBS-D = diarrhea, IBS-C = constipation; 5HT and IL-10 both implicated; Tx: chart

A

Irritable Bowel Syndrome: Treatment/Notes

407
Q

50% of >60, 2/3 of >80, more men than women only if 20-30

A

Diverticular Bleeding (Diverticulosis): Epi/MOI

408
Q

Diverticulae common in L colon but bleeding often from R; bleeding sudden, often painless

A

Diverticular Bleeding (Diverticulosis): Signs/Symptoms/Findings

409
Q

Low fiber dietlead to decrease stool volumelead to herniations of colonic mucosa through muscularis (pseudodiverticulae)

A

Diverticular Bleeding (Diverticulosis): Pathophysiology

410
Q

NSAIDs or aspirin worsens risk; Tx: resuscitation, vasopressin, embolization

A

Diverticular Bleeding (Diverticulosis): Treatment/Notes

411
Q

> 50%

A

Hemorrhoidal Bleeding: Epi/MOI

412
Q

Scant hematochezia; most common cause of LGIB

A

Hemorrhoidal Bleeding: Signs/Symptoms/Findings

413
Q

Tx:increased fiber, topical anti-inflammatory, ligation, etc.

A

Hemorrhoidal Bleeding: Pathophysiology AND Treatment/Notes

414
Q

Lifetime 7%, usually young adults

A

Appendicitis: Epi/MOI

415
Q

Periumbilicallead to RLQ pain, nausea, Rovsing’s sign, fever, increased WBC; abd CT most diagnostic

A

Appendicitis: Signs/Symptoms/Findings

416
Q

Obstruction of appendiceal lumenlead to polymicrobial (e. coli, b. fragilis, etc.) bacterial overgrowth, inflammation

A

Appendicitis: Pathophysiology

417
Q

Tx: appendectomy, earlier surgery = better prognosis, Abx prophylaxis

A

Appendicitis: Treatment/Notes

418
Q

Self-limited and mild in some cases

A

Clostridium Difficile: Epi/MOI

419
Q

Fever, diarrhea, toxicity, increased WBC, pain; Dx: tissue culture assay for cytotoxin

A

Clostridium Difficile: Signs/Symptoms/Findings

420
Q

Antibiotics, esp. clindamycin; complications include toxic megacolon, colonic perforation

A

Clostridium Difficile: Pathophysiology

421
Q

Tx: d/c antibiotic if possible, oral ABx or IV metronidazole (+rifampin if relapse)

A

Clostridium Difficile: Treatment/Notes

422
Q

10% of diverticuli pts

A

Diverticulitis Epi

423
Q

LLQ pain, change in bowel habits, fever, increased WBC, bladder fistula, peritonitis, CT with IV contrast

A

Diverticulitis: Signs/Symptoms/Findings

424
Q

Gm- infect diverticulum (sigmoid) after fecalith impacts;lead to perforations; occurs in 10-25% of diverticulosis, mostly sigmoid

A

Diverticulitis: Pathophysiology

425
Q

Tx: metronidazole + other Abx, colonoscopy 4-6wk later, surg after 3rd episode

A

Diverticulitis: Treatment/Notes

426
Q

Abx that cover enterobacter, bacteroids, (less: pseudomonas and enterococci), 4-6 weeks, follow up with colonoscopy

A

Diverticulitis

427
Q

relapse rate 10-30%

A

diverticulitis

428
Q

M>F 3:1

A

Sigmoid Volvulus: Epi/MOI

429
Q

Distended abd, plain films

A

Sigmoid Volvulus: Signs/Symptoms/Findings

430
Q

Lengthened sigmoid gets twisted

A

Sigmoid Volvulus: Pathophysiology

431
Q

Tx: Non-op decompression + surgery, resection if relapse

A

Sigmoid Volvulus: Treatment/Notes

432
Q

bird’s peak deformity

A

Sigmoid Volvulus

433
Q

3rd world, high plant fiber diet

A

Sigmoid Volvulus

434
Q

Obstipation, abd pain, distention

A

Large Bowel Obstruction: Signs/Symptoms/Findings

435
Q

Any mechanic obstruction

A

Large Bowel Obstruction: Pathophysiology

436
Q

Tx: surgery, enteral stents

A

Large Bowel Obstruction: Treatment/Notes

437
Q

decrease BS or high-pitched; abd pain; Dx: barium enema

A

Ileus: Signs/Symptoms/Findings

438
Q

Failure of peristalsis

A

Ileus: Pathophysiology

439
Q

Tx: neostigmine, supportive

A

Ileus: Treatment/Notes