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GI/Endo/Repro > Assessment 3 > Flashcards

Assessment 3 Flashcards

1
Q

Cystinuria

A

Defect in transport of cystine, lysine, arginine, ornithine

Poor absorption in kidneys/intstines

Cystine accumulates in urine (least soluble)

Treat w/ lots of water

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2
Q

Hartnup disease

A

Defect in transport of neutral AA (Ile, Leu, phe, Thr, Trp, Val)

Intestine and kidneys

D173N mutation

Lack of tryptophan, treat with try and niacin supplements

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3
Q

Cystinosis

A

Cannot transport cystine out of lysosome

Autosomal recessive, ESRD by 7-10yrs

Treat with cysteamine - reacts with cystine and end products leave lysosome

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4
Q

Pyruvate TA

A

Pyruvate –> Alanine

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5
Q

OAA TA

A

OAA –> Asp

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6
Q

a-KG TA

A

a-KG –> Glutamate

Alanine to Pyruvate

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7
Q

Transaminations all require…

A

Vitamin B6

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8
Q

Biosynthesis of Serine

A

3PG –> Phosphopyruvate –> phosphoserine –> Serine

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9
Q

Glycine synthesis

A

Serine –> Glycine

Serine hydroxymethyl transferase, creates N5/N10 methylene THF

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10
Q

Most stable THF?

A

N5 Methyl THF

All THF forms go towards that

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11
Q

Degradative reactions involving THF: Serine

A

Serine comes from 3PG which comes from Glucose

Glucose carbons —–> end up in THF compound

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12
Q

Degradative reactions involving THF: Formate

A

Make N10 formyl THF

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13
Q

Degradative reactions involving THF: Histidine degradation

A

Make N5-formimino THF

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14
Q

Biosynthetic reactions with THF

A

dUMP to TMP (N5/N10 methylene THF)

Glycine to Serine

Homocysteine –> methionine (N5 Methyl THF)

Purine biosynthesis (N10 formyl THF)

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15
Q

S Adenosylmethionine

A

Used in all methyl transferase reactions except homocysteine –> methionine

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16
Q

Phe –> Tyr

A

Enzyme: Phenylalanine hydroxylase

Cofactor: Tetrahydrobiopterin

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17
Q

AA degraded into which 7 families

A 
Acetoacetyl-CoA
Acetyl CoA
Pyruvate
a-KG
Succinyl CoA
Fumarate
Oxaloacetate
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18
Q

Leucine degraded into…

A

Acetyl CoA

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19
Q

Leucine/Lysine degraded into…

A

Acetoacetyl-CoA –> Acetyle CoA

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20
Q

AA degradation cycle

A

Pyruvate –> Acetyl CoA + OAA –> Citrate –> aKG –> Succinyl CoA –> Fumarate –> Oxaloacetate

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21
Q

Ketogenic AA

A

Leucine

Lysine

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22
Q

Phenylalanine degradation

A

Phe –> Tyr –> x –> Homogentisic acid –> Fumorylacetoacetate –> Fumarate + Acetoacetate

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23
Q

Alcaptonuria

A

Buildup of homogentisic acid in urine

Black urine

Arthritis

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24
Q

Phenylketonuria

A

Cannot breakdown Phe:

Classical - no enzyme
Other - lack of THB

Buildup of TA product phenylpyruvate, phe, phenyllactate

Restrict Phe diet

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25
Q

Tyrosinemia Type I and II

A

Type I: Lack of fumarylacetoacetate hydrolase
Early death

Type II: Defect in tyrosineaminotransferase, buildup of Tyr

Treat both with low Phe and Tyr diet

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26
Q

Nitisinone

A

Treatment for Type 1 tyrosinemia

Blocks homogentisic acid production

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27
Q

Bilirubin production

A

Heme degraded –> biliverdin –> bilirubin –> Attached to albumin –> Carried in blood to liver

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28
Q

Bilirubin in hepatocytes

A

Albumin released, bilirubin enters hepatocytes –> Conjugated with glucoronic acid, water soluble –> excreted to bile and deconjugated by bacteria in intestines –> most leaves in feces

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29
Q

Hemochromatosis

A

Defect in HFE gene - excessive iron absorption

Excessive iron accumulation, especially in liver

Autosomal recessive

Hemosiderin (iron storage) deposition = damage to liver, pancreas, heart

Micronodular cirrhosis, diabetes, brown skin

Phlebotomy can be useful treatment

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30
Q

Wilson Disease

A

Copper accumulation - liver, brain, eye

ATP7B gene mutation (copper transporting ATPase) - Failure to incorporate copper into ceruloplasmin which takes copper to bile

Rare disease

Kayser Fleischer rings (copper in cornea)

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31
Q

Alpha-1 antitrypsin deficiency

A

Inhibitor of proteases, when not there –> tissue damage

Increase risk for hepatocellular carcinoma

Cirrhosis

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32
Q

Acute fatty liver of pregnancy

A

Very rare

Microvesicular steatosis

Fetus causes inherited metabolic disorder in mother

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33
Q

Adult Polycystic kidney disease

A

Mutation in gene encodinc polycystin-1 (transmembrane glycoprotein)

Loss of function of stress response on ciliary membranes = abnormal fluid filled cysts

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34
Q

Familial hypercholesterolemia

A

Mutation in gene encoding LDL receptor on hepatocytes

Increased blood cholesterol

Heterozygotes have 1/2 LDL receptors, homozygotes have none

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35
Q

Gilbert syndrome

A

Fluctuating hyperbilirubinemia in response to stress, fasting, exercise

UGT1A1 mutation

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36
Q

Bilirubin conjugator

A

UGT1A1

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37
Q

Bilirubin transport proteins

A

Albumin/bilirubin transporter: OATP2

Conjugated bilirubin tranporter: MRP2

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38
Q

Control points for bilirubin clearance

A
  1. Uptake
  2. Conjugation
  3. Secretion
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39
Q

CAR agonist

A

Increases bilirubin metabolism and clearance

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40
Q

Unconjugated hyperbilirubinemia

A

Increased production - hemolysis
Decreased uptake - OATP2
Impaired conjugation

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41
Q

Crigler-Najjar type I vs type II

A

Type 1: No UGT1A1 activity, high levels of bilirubinemia
Kernicterus

Type II: Reduced UGT1A1 activity, usually benign

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42
Q

Indinavir and UGT1A1

A

Huge increase in bilirubinemia with Gilbert syndrome

Inhibits UGT1A1

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43
Q

Kernicterus treatment

A

Expose to light, photoisomerization of Bilirubin

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44
Q

Dubin Johnson Syndrome

A

MRP2 mutation

Cannot excrete conjugated bilirubin

Black livers - lipofuscin melanin complex

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45
Q

Rotor syndrome

A

Conjugated bilirubin secreted back into blood (MRP3) cannot be taken back into hepatocyte

OARP1B1/3 defect

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46
Q

Bilirubin and inflammation

A

Heme oxygenase suppresses inflammation

Activated leukocytes upregulate HO = increased bilirubin = slow inflammation

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47
Q

Neurotransmitters developed from tyrosine

A

Dopamine

Norepinephrine

Epinephrine

Need B6 and THB

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48
Q

Serotonin

A

Derived from tryptophan

B6 and THB

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49
Q

GABA

A

Derived from glutamate

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50
Q

Histamine

A

Derived from histidine

B6

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51
Q

Homocystinemia/uria

A

Buildup of homocysteine

Optic lens issues, osteoporosis, mental retardation

B6 can lower levels in 50% of cases (lower affinity of B6 by enzyme)

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52
Q

Defective enzymes that can lead to homocystinemia

A
  1. Cystathionine beta synthase (Homocysteine –> Cystathionine)
  2. N5/N10 methylene THF reductase (N5/N10 methylene THF –> N5 methyl THF)
  3. Methionine synthase (N5 methyl THF –> THF and Homocysteine –> Methionine)
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53
Q

Elevated homocysteine effects

A

Decrease endothelial growth

Increase smooth muscle cell proliferation - can exacerbate atherosclerosis

Block coagulation cascade –> clots/thrombosis

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54
Q

Homocysteinemia treatment

A

Vit supplements: B6, folic acid, B12

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55
Q

Neural tube defects and homocysteine

A

Does not have direct effect

But can monitor levels of functional folate by checking homocysteine levels

Increased homocysteine = decreased functional folate

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56
Q

Vit B12

A

Obtain from milk/meat, absorbed via intrinsic factor

Methyl cobalamin: Used Methionine synthase reaction

Adenosyl cobalamin: Methly malonyl coa –> succinyl coa

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57
Q

B12 deficiency - neurological problems

A

Lack of B12 = lack of methionine = lack of SAM

SAM needed for DNA methylation

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58
Q

Betaine pathway

A

Choline –> Betaine –> Dimethylglycine

Homocystein –> methionine in final step

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59
Q

Branched chain amino acid metabolism, step 1 and 2

A
  1. Transamination, B6 required

2. Branched chain alpha keto acid DH

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60
Q

Isoleucine metabolism final product

A

Succinyl CoA + Acetyl CoA

Ketogenic and Glucogenic

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61
Q

Leucine metabolism final products

A

Acetyl CoA

Ketogenic only

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62
Q

Valine metabolism final products

A

Succinyl CoA

Glucogenic

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63
Q

Maple syrup urine disease

A

Defect in branched chain alpha keto acid DH

Buildup of branched chain amino acids

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64
Q

Glycine metabolism pathways

A
  1. Glycine Serine
  2. Glycine cleavage enzyme = CO2, N5/N10, NH4
  3. Oxidase to Glyoxylate, transaminate back to Glycine
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65
Q

Primary Oxaluria type 1

A

Lack of glycine transaminase

Buildup of Glyoxylate and subsequently oxalate kidney stones

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66
Q

Non ketotic hyperglycinemia

A

Glycine cleavage enzyme defect

Elevated glycine in CSF and plasma –> Neurological defects because glycine is inhibitory neurotransmitter

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67
Q

Heme synthesis

A

Succinyl CoA + Glycine –> delta aminolivulenic acid –> x2 –> Porphobiliniogen –> Heme

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68
Q

Lead poisoning

A

Inhibits heme synthesis

Affects Aminolevulinic acid Dehydratase

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69
Q

Porphyria

A

Class of defects in heme biosynthesis

Photophobia, eat rare meats

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70
Q

AST/ALT ratio in NAFLD

A

AST/ALT less than 1

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71
Q

AST/ALT ratio in alcoholic liver disease

A

AST/ALT >1

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72
Q

NASH vs hepatic steatosis

A

NASH has fibrosis, not to extent of cirrhosis

Hepatic steatosis has fatty droplets only

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73
Q

Ballooning degeneration

A

NASH

Cells swell and fill with fluid, nuclei in center

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74
Q

Cirrhosis

A

Extensive fibrosis around regenerating nodules

Large web of fibrosis and noticeable cell damage

Collagen deposition in Space of Disse = blockage of hepatocytes to blood

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75
Q

Mechanisms of death in cirrhosis

A

Liver failure

Portal hypertension

Hepatocellular carcinoma

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76
Q

Alcoholic liver disease

A

Cirrhosis preceded by hepatic steatosis and alcoholic hepatitis

Mallory bodies surrounding hepatocytes

Alcohol metabolizing enzymes create more NADH and H = more lipid synthesis = fatty droplets

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77
Q

Hyperdynamic circulation

A

Portal hypertension = body response to dilate arteries = BP Drop = more salt/water retained = even more edema

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78
Q

Ascites

A

Fluid in peritoneal cavity

Hypoalbuminemia, hyperdynamic circulation

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79
Q

NAFLD

A

Due to hyperlipidemia, obesity etc

Steatosis more common than NASH

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80
Q

NAFLD lab findings

A

AST/ALT

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81
Q

NAFLD guidelines

A

Weight loss reduced hepatic steatosis

Loss of body weight helps steatosis but need more for necroinflammation improvement

Exercise may help

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82
Q

NASH treatment?

A

Vitamin E

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83
Q

Intrahepatic cholestasis vs extrahepatic

A

Intrahepatic: Defective bile secretion or intrahepatic bile duct disease

Extrahepatic: Mechanical obstruction or injury of large bile ducts outside of liver

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84
Q

Cholestasis clinical features

A

Jaundice

Pruritis

Malabsorption

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85
Q

Cholestasis lab findings

A

Elevated ALP, GGT, 5NT

Elevated conjugated bilirubin

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86
Q

Secondary biliary cirrhosis

A

Prolonged obstruction of extrahepatic biliary tree

Fibrosis of liver –> cirrhosis

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87
Q

Intrahepatic cholestasis histology

A

Centrilolobular

Intracellular and canalicular

Hepatocyte necrosis

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88
Q

Extrahepatic cholestasis histology

A

Bile duct/bile plugs

Edema and acute inflammation of portal tracts

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89
Q

Cholelithiasis

A

Gall stones

Can be asymptomatic

Cholesterol (80%) and pigment stones

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90
Q

4 F’s of gall stones

A

Female
Forties
Fat
Fertile

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91
Q

Biliary colic

A

Severe RUQ pain post prandial

Fatty food intolerance

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92
Q

Acute cholesytitis

A

Murphys sign

Palpable gall bladder

Elevated ALP and leukocytosis

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93
Q

Acute cholecystitis complications

A

Gangrenous cholecystitis

Emphysematous

Stone in bile duct

Gall bladder hydrops

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94
Q

Acute cholecystitis treatment

A

Early cholestectomy

Intraoperative cholangiogram to rule out common bile duct stones

Electrolytes/fluid

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95
Q

Choledocolithiasis

A

Stones in biliary tree

Obstruction can lead to ascending cholangitis - bacterial infection of bile ducts

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96
Q

Acute Cholangitis

A

Bacterial infection of biliary tree

Inflammation aggravated

E. coli, Clostriidium, Enterobacter

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97
Q

Charcot triad

A

Abdominal pain, fever, jaundice

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98
Q

Reynolds Pentad

A

Charcot triad + hypotension, altered menta status

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99
Q

Clinical features of acute cholangitis

A

Charcot triad

Reynolds Pentad

Elevated WBC

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100
Q

Acute pancreatitis

A

Can be caused by stone in Ampulla of Vater, occlusion of pancreatic duct

101
Q

Acute pancreatitis clinical

A

Elevated amylase/lipase

Hypocalcemia

Leukocytosis

102
Q

Biliary atresia

A

Luminal obstruction of biliary tree

Congenital

103
Q

Biliary atresia treatment

A

Kasai portoenterostomy

Liver transplant

104
Q

Primary sclerosing cholangitis

A

Cholestatic liver with fibrosis and inflammation

Narrowing/obstruction of larger bile ducts –> cirrhosis

Males>females

70-75% coexisting IBD

105
Q

PSC ERCP

A

segmental constrictions

String of beads

106
Q

PSC clinical/lab features

A

Fatigue, pruritis, jaundice

Antinuclear antiboy
Anti smooth muscle anti body

p-ANCA

107
Q

PSC cirrhotic stage

A

Biliary cirrhosis

3-6 years after presentation

108
Q

Cholangiocarcinoma

A

Rare

PSC is risk factor

Poor prognosis

Painless jaundice, clay stool, cola urine

Obstructive jaundice labs (GGT, ALP, Bilirubin increase)

109
Q

Courvoisier Sign

A

Jaundice + Palpable gall bladder

Painless jaundice

110
Q

Primary biliary cirrhosis

A

Granulomatous destruction of intrahepatic bile ducts

Female>Male

Hepatocellular carcinoma risk

Pruritis, fatigue, jaundice (late)

Can be asymptomatic

111
Q

PBC treatment

A

Ursodeoxycholic acid

Cholestyramine - bind bile salts in intestines to enhance excretion

Immunosuppressants

liver transplant

112
Q

Autoimmune hepatitis

A

Female predominance

Immune system attacks hepatocytes

High IgG and gama globulin

Liver biopsy

Prednisone, azathioprine

113
Q

Autoimmune hepatitis Type 1

A

More common, all ages

Antinuclear antibody

Anti smooth muscle antibody

Anti actin antibody

114
Q

Autoimmune hepatitis type 2

A

Girls and women, children 2-14

Anti livery kidney microssome

Anti liver cytosol-1

115
Q

Most common HIV transmission

A

Male to male sexual contact

116
Q

5 body fluids that transmit HIV

A 
Blood
Semen/pre semen
Rectal secretions
Vaginal secretions
Breast milk
117
Q

HIV Transmission types (3)

A

Sexual (horizontal transmission)

Blood exposure: Needles, IV drug use, transfusions

Vertical transmission: Fetus in birth canal or in utero, breast milk

118
Q

Postive male/Negative female prevention

A

Donor insemination
Sperm washing
IVF w/intracytoplasmic sperm injection

119
Q

Positive female/Negative male prevention

A

Intra-uterine insemination

IVF

120
Q

HIV risk by type of exposure: Sexual

A 
Least risk
Insertive vaginal
Receptive vaginal
Insertive anal
Receptive anal
Highest risk
121
Q

HIV risk by type of exposure: Blood exposure

A 
Least risk
Needle share
Needle stick
Mucous membrane exposure
Transfusion
Most risk
122
Q

Best HIV diagnosis

A

HIV Ag/Ab test + Ab differentiation test

Earlier diagnosis

123
Q

Newborn HIV test

A

Newborns carry maternal Ab

HIV RNA quantitation at different time frames

AZT for 6weeks

124
Q

Acute HIV infection

A

2-6 weeks after exposure

  1. Mono like illness, adenopathy and pharyngitis
  2. Rash on trunk
  3. Neurological symptoms
125
Q

HIV infection: first 3 months

A

Huge rise in viral count, decline in CD4 count

HIV immune response occurs and viral load decreased to steady state level

126
Q

HIV monitoring

A

Viral load

CD4 cell count

127
Q

Steps of HIV progression

A
  1. Binding/Fusion
  2. Uncoating
  3. Reverse transcription
  4. Integration
  5. Proviral transcription
  6. Translation
  7. Cleavage
  8. Assembly, maturation, release
128
Q

Binding and Fusion drugs

A

CCR5 antagonist

Fusion inhibitor: Enfuviritide - side effect, injected, no bueno

129
Q

Uncoating

A

Virus fused with CD4 membrane, viral RNA released into cytoplasm

130
Q

Reverse Transcription

A

Viral RNA transcribed into DNA

131
Q

Reverse transcription drug classes

A

NNRTI: Prevents binding of RT to HIV RNA

NRTI: Allows RT and HIV RNA binding, chain terminator, eventually DNA degrades

132
Q

NNRTI drugs

A

Efavirenz - dreams

Rilpivirine - Need food

Entravirine: CYP450

133
Q

NRTI drugs

A

Zidovudine - AZT, children born to HIV+ mothers

Lamivudine (3TC) - Hep B

Emtricitabine (FTC) - Hep B

Abacavir - Hypersensitivity, HLAB5701

Tenofovir (TDF/TAF) - decreased bone density, renal toxicity

134
Q

Integration drugs

A

-tegravir

Raltegravir - Rash, myopathy

Elvitegravir

Dolutegravir - hypersensitivity

135
Q

Proviral transcription

A

Viral DNA reprograms CD4 machinery to produce Viral RNA and viral mRNA

136
Q

Translation

A

Ribosomes use viral mRNA to create proteins/enzymes in polyprotein

137
Q

Cleavage

A

Proteases cut polyprotein and release enzymes/proteins needed for creation of new HIV virus

138
Q

Protease inhibitors

A

Ritonavir (RTV): First PI, used as booster

Lopinavir (LPV): Increase cholesterol/TG

Darunavir (DRV): Hypersensitivity

Atazanavir (ATV): Kidney stones, UGT1A1 inhibitor

139
Q

HIV clearance evasion

A

Rapid replication

Mutagenesis

Latency

Down regulation of MHC on infected cells

Structure

Infection of sanctuary sites

140
Q

Chronic HIV infection

A

Latency phase, generally asymptomatic

Immune system able to limit replication, virus lays dormant

Avg 8-10 years

141
Q

Immune defects in HIV+

A

Low CD4

Dysregulation: altered cytokines, impaired response to antigens, hypergammaglobulinemia

142
Q

When to start ART

A

All HIV patients, differs based on baseline CD4 levels

143
Q

Absolute indications for ART

A 
Hep B/C
HIV associated neuropathy
HIV associated neurocognitive disorders
Pregnancy
Malignancy
AIDS defining disease
144
Q

ART start: 3 medications

A

2 NRTI + integrase inhibitor OR protease inhibitor

145
Q

Morphological changes with ART

A

Lipodystrophy
Lipohypertrophy
Lipoatrophy

146
Q

HIV mutagenesis

A

Mutation rate of 1/10,000

Mutation occurs during Reverse Transcription

147
Q

CD4 response after ART

A 
Increased numbers 
Response to non HIV antigens
Decreased inflammatory cytokines
No response to HIV antigens
Response to new antigens
148
Q

AIDS definition

A

CD4

149
Q

Candidiasis

A

Oral thrush

CD4

150
Q

PCP/PJP

A

Pneumocystits iroveci (carinii) Pneumonia

CD4

151
Q

Cryptococcal Meningitis

A

CD4100 for 3mo, undetectable, start ART

152
Q

Toxoplasmosis

A

CD4

153
Q

Mycobacterium Avium

A

CD4

154
Q

AIDS defining cancers

A

Kaposi Sarcoma
Non hodgkins lymphoma: EBV
Cancer of cervix/anus/rectum: HPV

155
Q

Biochemical nutritional evaluation

A

Albumin
Transferrin
Prealbumin
Retinol binding protein

156
Q

Pregnancy nutrition

A

Energy: +340 2nd tri, +450 3rd tri

Protein +25

Carbs

Iron +50%

Folate +50%, B12

157
Q

Food to avoid during pregnancy

A

Vit/mineral mega doses

Fish w/mercury

Soft cheeses/food poisoning risks

158
Q

Lactation nutrient needs

A

+500 kcal energy

All more than during pregnancy, nutrient dense foods

Inadequate diet = reduced milk quantity and deprives mother of nutrient stores

159
Q

Infancy nutrients

A

Energy and protein highest/kg in infancy

30g fat

Vit/minerals highest than during adulthood

160
Q

Infancy food guidelines

A

Solid foods @4-6 months

Introduce foods singly at intervals, 3-5 days

Iron rich/vit C

161
Q

Childhood nutrients

A

Energy need increases, but per kg decreases

Carb: Fiber = age +5

High quality protein

Fat: 30-40% 1-3yrs
25-35% 4-18

162
Q

Nutrient concerns in childhood

A

Iron
Vit D: Fortified milk/cereal
Fluoride: Water

163
Q

Adolescence

A

Puberty/growth spurt

Tanner staging

Energy, protein, vit/mineral increase

164
Q

Acute Liver Failure Definition

A

Coagulation abnormality, mental alteration

No preexisting cirrhosis

Illness less than 26 weeks

165
Q

Acute liver failure stats

A

2000 cases anually

33% mortality, 40% survival without transplant

> 65% survival with transplant

166
Q

ALF etiology

A

Mainly drugs, esp acetaminophen

Hep A/B

Unknown

167
Q

ALF classification

A

Hyperacute: 7d

Acute: 8-28d

Subacute: 29-60d

168
Q

ALF type and cause

A

Subacute: Drug
Acute: Acetaminophen, Hep A
Acute: Hep B

169
Q

Acetaminophen toxicity

A

Enhanced P450 –> NAPQI toxicity

Doses >15g

Hepatic dysfunction at day 3

170
Q

Acetaminophen overdose treatment

A

Glutathione precursors

171
Q

Hep B ALF

A

1% pt with Hep B, 8% ALF is HBV

.4% mortality

172
Q

Hep A ALF

A

Less than 1% Hep A pts

Elevated creatinine

173
Q

ALF complications

A 
Jaundice
Infection
Hepatic encephalopathy
Coagulopathy
Metabolism issue
Renal failure
174
Q

Hepatic encephalopathy treatment

A

Airway protection

Lactulose - meh

Sedation

175
Q

Coagulopathy

A

Decreased synthesis of clotting factors

Decreased platelets

176
Q

Infection and ALF

A

80-90%

Sepsis is leading cause of death

G+

177
Q

Phase I enzymes

A

Minor structural changes, oxidation

CYP

178
Q

Phase II enzymes

A

Large molecular additions

Transferases: UGT

179
Q

CYP3A4

A

Most common CYP used by many drugs

180
Q

CYP2D6

A

Neurological drugs

Genetic polymorphism

181
Q

Rifampicin

A

Most important CYP3A4 inducer

Results in other drug concentration reduction

182
Q

Most powerful CYP competitive inhibitor

A

Ketoconazole

Huge increase for other drug

183
Q

Hepatitis A Virus

A

Single serotype

Acute disease, no chronic infection

Usually asymptomatic

Lifelong immunity after immune response

184
Q

Hep A transmission

A

Fecal oral

Personal contact

Blood exposure (RARE)

185
Q

Hep A pathogenesis

A

Survives in stomach and enters blood –> liver

Replicates in hepatocytes, not cytotoxic

Excreted in stool before jaundice

Immune mediated damage to liver

186
Q

Hep A clinical features: Incubation, symptoms

A

Avg incubation: 28-30 days

Cholestasis, dark urine, clay stool, jaundice

Jaundice more likely as age increases

187
Q

Hep A antibody history

A

IgM detectable 5-10 days before symptoms

IgG 4 weeks post infection then mass rise

188
Q

Hep A diagnosis

A

Serum HAV IgM antibody

189
Q

Hep A prevention

A

Hygiene
Sanitation
Vaccination: Recombinant (pre), Immune globulin (post)

190
Q

Hep E

A

Acute asymptomatic in developing countries

Enteric zoonotic transmission

Very rare in developed countries

191
Q

HEV pathogenesis

A

15-60 day incubation

Replication in hepatocytes, feces excretion

Ab pain, anorexia, fever, hepatomegaly, jaundice

192
Q

HEV natural history (Ig and enzymes)

A

Large ALT rise at around 6 weeks post infection

IgM rise faster than IgG

193
Q

HEV mortality

A

Relatively low but 20% in pregnant women

194
Q

HEV diagnosis/prevention

A

Antibody assays available but inconsistent

anti HEV IgG/IgM
HEV RNA detection

No antivirals

195
Q

HEP B

A

DNA virus with RNA intermediate

350mil infected

Multiple genotypes with differing progression/response rates

196
Q

HBV transmission

A

Blood, semen, vaginal

197
Q

HBV pathogenesis

A

Multiple viral proteins: Surface, core, E, Polymerase, X

Detectable protein is HBsAG (surface)

Not cytotoxic, immune mediated damage

198
Q

HBV pathogenesis

A

2-3 month incubation
Jaundice
Low acute case mortality
15-25% chronic case fatality

199
Q

HBV diagnosis

A

Choestasis
AST/ALT elevation
IgM anti HBsAg = acute infection

HBsAg+ = infectious
HBeAg correlates with infectiousness

200
Q

Acute HBV natural history: Virus, enzymes, Ag, Ig

A

Large rise of virus within weeks = large rise in antigen, decline at 3mo

IgM anti HBc at clinical onset then declines @6months

Anti HBsAg = resolution of disease, viral load/Ag undetectable

201
Q

Chronic HBV natural history

A

Large rise in DNA/HBsAg

Antigen persists = chronic

IgG HBc rises and persists

IgM anti HBc decrease = chronic

202
Q

Immunity with HBV vaccination serology

A 
HBsAg = negative
anti-HBc = negative
anti-HBs = positive
203
Q

Immunity with HBV infection serology

A

HBsAg = negative
anti HBc = positive
anti HBs = positive

204
Q

Chronic HBV infection serology

A

HBsAg = positive
Anti HBc = positive
Anti HBs = negative
IgM anti HBc = negative

205
Q

Acute HBV infection serology

A

HBsAg = positive
Anti HBc = positive
anti HBs = positive
IgM anti HBs = negative, rises after resolution of disease

206
Q

HBV prevention/treatment

A

Vaccine: HepB IG, Recombinant

Treatment: IFN
Polymerase inhibitors - Lamivudine, Tenofivir, Emtricitabine

207
Q

Hep C

A

Leading cause of liver transplant

RNA virus

208
Q

Hep C transmission

A

IV drugs

Transfusion/transplantation

Sexual and perinatal but much lower than HBV

209
Q

HCV natural history

A

Exposure (20% resolved)

Chronic (Some stable/variable progression)

Cirrhosis (Some slowly progressive)

HCC/Transplant/Death - 25yrs

210
Q

HCV diagnosis

A

HCV antibody - Not good early/acute

HCV RNA - Better

Abnormal liver enzymes

211
Q

Acute HCV natural history

A

Large ALT rise with HCV RNA detection

Huge anti HCV after a few months

212
Q

Chronic HCV progression

A

HCV RNA detection
Large initial ALT rise, then decline, then variable spikes

Anti HCV increase like in acute

213
Q

HCV vaccine

A

NONE

214
Q

Sofosbuvir

A

2014: NS5B polymerase inhibitor

215
Q

Boceprevir/Telaprevir

A

NS3/4A protease inhibitors

216
Q

Hep D

A

HBV coinfection

Derived from HBV

Cytotoxic effect on hepatocytes

No bueno

217
Q

Hep D detection

A

Anti HD Ab detected via ELISA

HBV vaccination protects from HDV

HBV antivirals DO NOT reduce HDV

218
Q

ALF and urea

A

Liver can’t create urea so ammonia leaves and goes to brain

Ammonia becomes glutamate, osmotic pressure increase –> increase intra cranial pressure

219
Q

NAS scoring system categories

A

Steatosis
Lobular inflammation
Ballooning degeneration
Fibrosis

220
Q

ALF liver transplant contraindications

A

Uncontrolled intracranial hypertension

Prolonged systemic hypotension

Sepsis/ARDS

221
Q

Lab parameters for liver transplant

A

Creatinine

INR

Total Bilirubin

222
Q

Achilles heel of liver transplantation

A

Biliary complication

Bile leaks/obstruction/strictures

223
Q

Porcelain gall bladder

A

Wall thickening and calcium deposition

Increased risk of gall bladder carcinoma

224
Q

PSC treatment

A

Endoscopic balloon dilation

Endoscopic stent

Liver transplant

225
Q

PSC histology (Stain and presentation)

A

Trichrome stain

Onion skin fibrosis

226
Q

Klatskin Tumor

A

Cholangiocarcinoma arising at hepatic hilum

No gall bladder distention

227
Q

PBC Lab findings

A

Antimitochondrial antibodies

Increased IgM

Elevated ALP but NORMAL total bilirubin

228
Q

Cirrhosis - 3 morphological characteristics

A
  1. Bridging fibrous septa
  2. Regenerative parenchymal nodules
  3. Architectural disruption throughout entire liver
229
Q

Hepatic stellate cells

A

When activated, deposit collagen into Space of Disse

230
Q

Intra/pre/post hepatic portal hypertension

A

Intra: Cirrhosis

Pre: Portal vein thrombosis

Post: Hepatic vein thrombosis

231
Q

Clinical consequences of Portal Hypertension

A

Congestive Splenomegaly

Hepatic Encephalopathy

Portosystemic venous shunts with risk of bleeds

Ascites

232
Q

Chronic liver disease signs

A

Caput medusae (PH)

Jaundice/Scleral icterus (Hyperbilirubinemia)

Asterixis (flapping tremor)

Encephalopathy (Ammonia)

Gynecomastia/spider angiomas (Androgen/estrogen metabolic dysfunction)

Palmar erythema (Red palms)

233
Q

Ultrasound benefits

A

Bile duct dilation
Gall bladder
Hepatic vasculature

Obese patients ruin everything

234
Q

CT benefits

A

Optimal with contrast

Visualize ductal dilation

Better assessment of pancreas and level of obstruction

Gall stones can’t be seen though

235
Q

MRI benefits and contraindications

A

Evaluate hepatic parenchyma

Level and etiology of obstruction

Biliary and pancreatic ducts via MRCP

Contraindications: Pacemakers, obesity

236
Q

Nuclear Medicine

A

Functional assessment of biliary system

Sensitive to diagnosis of acute cholecystitis

237
Q

Iminodiactetic acid analogues

A

Nuclear medicine technique

Uptake by hepatocyte, transport into bile canaliculi, excreted into biliary system

Flows into gall bladder

238
Q

Endoscopy

A

ERCP: Direct access to papillae, can extract stones or place stents

239
Q

PTC

A

Percutaneous Transhepatic Cholangiography

Access biliary system through skin/liver

Dilate/stent strictures

240
Q

Neonatal jaundice TORCH

A

Etiologies

Toxoplasmosis
Other
Rubella
CMV
Herpes
241
Q

Ascending Cholangitis bacteria

A

E Coli
Enterococcus faecalis
Klebsiella Pneumoniae

Ascending because bacteria starts in intestines then moves up bile duct to liver

242
Q

Entamoeba Histolytica

A

Ingest cysts, trophozoites burrow into intestines, can get into liver

Anchovy paste nastiness

Liver abscesses

Treat with Metronidazole

243
Q

Physiological jaundice of newborn

A

Takes time for baby to start conjugating bilirubin

High levels dangerous, goes to brain = kernicterus

244
Q

Simple cyst

A

Thought to be congenital

Common - 5%

245
Q

Liver abscess - pyogenic

A

Induce pus formation

E. Coli
Klebisella pneumoniae
Strep
Bacteroides

Drain
Metronidazole, clindamycin

3rd gen cephalosporin

246
Q

Hydatid Cyst

A

Echinococcus granulosis - tapeworm (cestode)

Live in intestinal lumen (definitive host), Tissue cysts (intermediate hosts)

Humans are accidental hosts

Liver and lungs

Surgery, albendazole (blok glu uptake)

247
Q

Ascariasis

A

Nematode - roundworm

Common infestation

Travel up lungs and into GI tract and grows –> to liver causing abscesses

Mebendazole

248
Q

Fasciolasis

A

Liver flukes - flatworms

Watercress salad

249
Q

Schistosoma

A

Swimmers itch

Katayama fever

Eggs in liver = granulomatous reaction, fibrosis, portal hypertension

Eosinophilia
Risk of hepatocellular carcinoma

GI/Endo/Repro (8 decks)

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