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Peds Patho > Liver > Flashcards

Liver Flashcards

1
Q

7 functions of liver:

A

1) Biliary
2) Infectious
3) Oncotic Pressure
4) Lipid Metabolism
5) Glucose Homeostasis
6) Coagulation
7) Detoxification

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2
Q

biliary function of liver:

A

1) bile secretion

2) bile excretion

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3
Q

infectious function of liver:

A

1) globulins

2) complement

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4
Q

function of liver in regards to oncotic pressure:

A

1) Albumin

2) Transferrin

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5
Q

lipid metabolism function of liver:

A

1) digestion

2) absorption

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6
Q

glucose homeostasis function of liver:

A

1) glycogenesis
2) glycogenolysis
3) gluconeogenesis

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7
Q

oncotic pressure

A

keeps fluid in your blood vessels

–when it drops –> seep fluid into your abdomen, legs, etc.

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8
Q

detoxification function of liver:

A

1) conjugation
2) degradation
3) NH3 –> urea

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9
Q

should you be able to palpate the liver in the toddler years?

A

is normal to feel the liver from neonatal period up until age 2

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10
Q

can the liver regenerate?

A

yes! can regenerate in 4-6 weeks

also: shrinks, depending on metabolic need

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11
Q

what happens if nh3 can’t be converted into urea?

A

encephalopathy

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12
Q

liver disease can be characterized in 4 general ways:

A

1) duration: acute vs. chronic
2) extent: mild, moderate, severe
3) patho:
- -> hepatocellular
- -> cholestatic
4) Etiology (infectious, toxic, metabolic errors, immune-mediated, vascular)

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13
Q

hepatocellular disease is caused by:

A

AST/ALT levels

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14
Q

primary liver #s

A

AST/ALT

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15
Q

are AST/ALT ever zero?

A

no: bc liver is constantly regenerating itself

- -if #s go up –> indicates a problem

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16
Q

cholestatic liver disease is caused by:

A

a biliary issue:

–PSC, PBC, bile duct injuries

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17
Q

example of infection that causes liver disease:

A

viral hepatitis

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18
Q

ex. of toxins that cause liver disease:

A
  • -Tylenol

- -Alcohol

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19
Q

metabolic errors that cause liver disease:

A
  • -A1, AT deficiency
  • -tyrosinemia
  • -Wilson’s
  • -cystic fibrosis
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20
Q

immune-mediated causes of liver disease:

A
  • -AIH
  • -PBC
  • -PSC
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21
Q

PBC

A

primary biliary cirrhosis

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22
Q

PSC

A

primary sclerosing cholangitis

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23
Q

vascular cause of liver disease?

A

Budd Chiari Syndrome

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24
Q

acute liver failure

A

–rapid onset of synthetic dysfunction:
jaundice, coagulopathy
–encephalopathy
–no prior liver disease

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25
Q

synthetic dysfunction is indicated by what lab values?

A
  • -Albumin decreased

- -INR increased

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26
Q

what determines course of acute liver failure?

A

–interval b/t jaundice & encephalopathy:
< 2 weeks: Fulminant hepatic failure w/ rapid recovery as virus clears, or death/transplant
2 weeks to 3 mos: Subfulminant hepatic failure w/ slow course proceeding to death w/out transplant

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27
Q

what causes encephalopathy in acute liver failure?

A

liver can’t convert NH3 to urea

–> ammonia builds up on brain

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28
Q

signs of encephalopathy in babies:

A

non-specific:

–sleepy, irritable, not feeding well

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29
Q

3 components make up clinical features of liver failure:

A

1) history
2) labs
3) physical exam

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30
Q

history + for liver failure:

A
  • -lethargy/confusion
  • -nausea/vomiting
  • -bleeding
  • -jaundice
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31
Q

labs that can indicate liver failure:

A

1) Hyperbilirubinemia
2) Hypoalbuminemia
3) Coagulopathy (incr. INR)
4) Raised plasma ammonia
5) Hypoglycemia
6) +/- elevated transaminases

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32
Q

plasma ammonia levels are only accurate if:

A

–arterial stick, on ice, processed w/in 20 min

venous stick NOT accurate

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33
Q

physical exam signs + for liver failure:

A

1) jaundice
2) +/- hepatomegaly
3) bruises (Vit. K)
4) asterix
5) clonus

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34
Q

asterixis

A

–hold hands up –> hands flap
(a tremor of the hand when the wrist is extended)
–indicates ammonia is built up on the brain

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35
Q

5 causes of acute liver failure in neonates:

A

1) Infection
2) Poisoning
3) Hematologic
4) Metabolic
5) Vascular

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36
Q

infectious causes of liver failure in neonates:

A

1) bacterial
2) viral
- -herpes
- -adenoviruses
- -enteroviruses (echovirus, coxsackie b)

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37
Q

poison that can cause acute liver failure in neonates:

A

Tylenol

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38
Q

hematologic cause of acute liver failure in neonates:

A

HLH (hemophagocytic lymphohistiocytosis)

–build-up of WBCs –> damages liver

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39
Q

metabolic causes of acute liver failure in neonates:

A
  • -hereditary (fructose intolerance)
  • -galactosemia
  • -tyrosinemia
  • -hemochromatosis
  • -fatty acid oxidation defects
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40
Q

hemochromatosis

A

too much iron in the body

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41
Q

galactosemia

A

a condition in which the body is unable to use (metabolize) the simple sugar galactose

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42
Q

vascular causes of acute liver failure in neonates:

A

1) heart failure

2) asphyxia

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43
Q

6 causes of acute liver failure in children >6 mos:

A

1) Infection
2) Poisoning
3) Autoimmune
4) Oncologic
5) Metabolic
6) Vascular

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44
Q

we really worry about which type of cause of acute liver failure in neonates?

A
  • -really worry about metabolic causes

- -but in NY state: all of these are on Newborn Screen

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45
Q

infectious causes of acute liver failure in children > 6 mos:

A

1) Bacterial
2) Viral
- -Adenovirus
- -Echovirus
- -Hepatitis B
- -Hepatitis A, C, E, non A-G
- -EBV/CMV/HIV
- -Parvovirus B19

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46
Q

oncologic causes of acute liver failure in children > 6 mos:

A

1) hepatoblastoma (often @ 6-9 mos)
2) ALL, lymphoma
3) neuroblastoma

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47
Q

metabolic causes of acute liver failure in children > 6 mos:

A
  • -hereditary fructose intolerance
  • -galactosemia
  • -tyrosinemia
  • -hemochromatosis
  • -fatty acid oxidation effects
  • -Alpers disease
  • -Wilson’s disease
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48
Q

vascular causes of acute liver failure in children > 6 mos:

A
  • -heart failure
  • -asphyxia
  • -Budd-Chiari
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49
Q

Budd-Chiari

A

autoimmune syndrome: clot off little venules, blood can’t leave liver –> engorged & inflamed

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50
Q

how does acetaminophen cause liver toxicity?

A
  • -interruption of p450 system/glutathione p’way
  • -glutathione is depleted
  • -NAPQI induces necrosis
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51
Q

glutathione

A

usually converts metabolite

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52
Q

what induces necrosis w/tylenol poisoning?

A

NAPQI

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53
Q

2 exacerbating conditions for acetaminophen toxicity:

A

1) pre-existing glutathione depletion

2) enhanced cytochrome p-450 system activity

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54
Q

acetaminophen toxicity: presentation

A
  • -nausea, vomiting, RUQ tenderness
  • -12-24 hrs. post-ingestion:
    • -> ALT, AST increase & peak at 72 hrs
    • -> PT (INR) increases
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55
Q

what indicates poor prognosis w/acetaminophen toxicity?

A

if PT is elevated >72 hrs

not enough liver to regenerate itself

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56
Q

severe effects of acetaminophen overdose

A

1) oliguric failure w/ATN (acute tubular necrosis)
- -d/t not peeing! damage to kidney
2) Rhabdomyolysis, hypophosphatemia, & metabolic acidosis may be assoc.

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57
Q

rhabdomyolysis

A

kidney damage

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58
Q

tx for acetaminophen toxicity

A

N-acetyl cysteine, IV or PO (precursor of glutathione)
dose:
140mg/kg load (all ages)
70 mg/kg q 6 hrs x 17 doses

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59
Q

overall mortality rate of acetaminophen toxicity?

A

<5%
cerebral edema: 30%
renal failure: 50%
metabolic acidosis: 90%

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60
Q

liver lab values:

A

1) Ammonia
2) Serum & Urine Bile Acids
3) Trace elements abnormalities
4) vitamin abnormalities (phos, mg, etc)
5) alpha feto-protein
6) alpha 1-antitrypsin
7) iron & ferritin
8) thyroid function (hypothyroid –> abnorm. liver #s)

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61
Q

alpha feto-protein

A

marker of immature cell generation

  • *normally high in infants, but should drop in a few weeks
  • -> w/ Tyrosinemia, it stays up
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62
Q

alpha 1-antitrypsin

A

indicates genetic d/o that causes liver disease

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63
Q

where to start w/lab eval:

A

divide into patterns; is it:

1) Cholestatic or obstructive bile duct injury
2) Hepatocellular/liver cell injury

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64
Q

cholestatic

A

obstructive bile duct injury

–look at: Alk. phos, GGTP, bilirubin, urinalysis

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65
Q

hepatocelluar injury

A

liver cell injury

–look at: ALT, AST, PT, albumin

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66
Q

GGTP

A

gamma-glutamyl-transpeptidase (liver enzyme)

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67
Q

4 key questions in evaluating liver function tests:

A

1) hepatocellular vs. cholestatic?
2) acute vs. chronic?
3) obstruction?
4) immunosuppressed?

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68
Q

characteristics of hepatocellular injury

A
  • -increased AST, ALT (released on cell death)
  • -when hepatocyte necrosis is severe & liver function is impaired:
    • -> PT & Albumin will increase
    • -> glucose will fall
69
Q

characteristics of cholestatic injury

A
  • -increased alkaline phosphatase & bilirubin
    (alk. phos. synthesized by bile duct cells)
  • -prutitus can be present, in the absence of jaundice d/t increased bile salts
70
Q

alkaline phosphatase is synthesized by:

A
  • -bile duct cells
  • -bone
  • -intestine
  • -liver
71
Q

can children have abnormal alk. phos. #s?

A

yes, bc they’re growing!
300/340 –> normal!
–released normally from bone & intestines

72
Q

hepatocellular causes of acute liver disease:

A
  • -viral
  • -toxin
  • -alcohol
  • -meds
  • -ischemia
  • -sepsis
73
Q

cholestatic causes of acute liver disease:

A
  • -stones (uncommon except for sickle cell kids)
  • -meds
  • -pancreatitis
  • -common bile duct compression (us. r/t cancers)
74
Q

hepatocellular causes of chronic liver disease:

A
  • -viral
  • -alcohol
  • -meds
  • -ischemia
  • -metabolic
  • -neoplastic
75
Q

cholestatic causes of chronic liver disease:

A
  • -idiopathic (PBC/PSC: autoimmune diseases)
  • -meds
  • -chronic pancreatitis
  • -secondary biliary cirrhosis (us. r/t clipping of bile duct)
  • -neoplastic (cancers)
76
Q

what cause of chronic liver disease is us. r/t a surgical mishap?

A

secondary biliary cirrhosis

clipping of bile duct

77
Q

+ hx for liver problems:

A
  • -risk factors (transfusion, alcohol, drugs)
  • -meds (esp. OTCs: tylenol, motrin)
  • -pain
  • -comorbidity (AIDs, diabetes, cardiac, autoimmune)
  • -family hx
  • -surgical hx
  • -sx (B sx, pruritus)
78
Q

why is pruritus assoc. w/ liver disease?

A

bile salts –> pruritus

79
Q

B symptoms

A

fever, night sweats, and weight loss

–can be associated with both Hodgkin’s lymphoma and non-Hodgkin’s lymphoma

80
Q

is it ever normal to feel the spleen?

A

NO

81
Q

signs of liver disease upon physical exam:

A
  • -stigmata of portal hypertension
  • -liver size & shape
  • -xanthelasma
  • -excorciation, hyperpigmentation
  • -petechiae, hematomas
  • -Kaiser-Fleischer rings
  • -signs of comorbid illness
82
Q

xanthelasma

A

fatty deposits: see little white/yellow bumps around the eyes, folds of arms in obese pts

83
Q

Kaiser-Fleischer rings

A

copper ring seen in eye

–> send to optho!

84
Q

lab tests for chronic liver disease:

A
  • -HBsAG, HBc IgG, HCV
  • -Ferritin, iron studies
  • -ANA, AMA, ASMA, ceruloplasmin, alpha 1-antitrypsin when appropriate
85
Q

ceruloplasmin

A

marker for Wilson’s disease

86
Q

alpha 1-antitrypsin

A

marker for Alpha 1-antitrypsin deficiency (genetic d/o)

87
Q

HBsAG

A

hepatitis B surface antigen

–indicates active infection

88
Q

alpha HBc IgM

A

indicates acute infection

IgM: you’re miserable. active infection

89
Q

alpha HBc IgG

A

indicates prior or chronic infection

–prior, resolving infection

90
Q

alpha Hbs

A

indicates immunity

  • -get thru vaccine
  • -or had disease & cleared it
91
Q

acholic stools

A
  • -pale, clay or putty-colored

- -may be d/t prob. in biliary sys.

92
Q

1 cause of jaundice in babies?

A

high bilirubin from breastfeeding

93
Q

high direct bilirubin indicates?

A

pathologic cause!

  • -st seriously wrong w/liver
  • -must be seen by specialist same day
94
Q

tx for liver blockage?

A

blockage requires surg. repair:
Kasai
–must be done before 12 weeks of age
–surg. bypass

95
Q

w/jaundiced infant w/acholic stools…what do you do next?

A

fractionated serum bilirubin

  • -> elevated direct bilirubin
    • -> abdominal ultrasound
      • -> choledochal cyst?
96
Q

if jaundiced infant is + for choledochal cyst after abdom. us, what do we do?

A

surgery!

–w/out surg, can –> cirrhosis

97
Q

choledochal cyst

A

ballooning of bile duct

98
Q

if jaundiced infant has abdom. us and shows no choledochal cyst, what do we do?

A

1) DISIDA scan (nuclear medicine test)
- -give phenobarb 1st; increases p450 sys; helps to excrete
2) Liver Biopsy
- -> if + for biliary atresia, do Kasai
- -> if no biliary atresia, medical management

99
Q

diseases causing jaundice in infants:

A
  • -infections
  • -metabolic d/o’s
  • -neonatal hepatitis, PFIC
  • -atresia/paucity
  • -cystic malformations
100
Q

paucity

A

scarcity; common w/consanguinity

–ask if parents are related by blood!

101
Q

PFIC

A

progressive familial intrahepatic cholestasis

–begins in infancy, progresses –> cirrhosis w/in 1st decade of life

102
Q

diseases causing jaundice in children & adolescents:

A
  • -acute viral hepatitis
  • -interited d/o’s
  • -malignancies
  • -parasitic infection
  • -IBD, chronic hepatitis
103
Q

rates of biliary atresia

A

1 in 12,000 live births

104
Q

biliary atresia

A
  • -idiopathic inflammatory process that affects intra & extra hepatic bile ducts
  • -> leads to fibrosis & obliteration of the biliary tract
  • -> eventual development of biliary cirrhosis
  • *child is born normally, then w/in 1 weeks, common bile duct solidifies itself
105
Q

how can we ensure prompt surgical correction w/biliary atresia?

A
  • -early differentiation of biliary atresia from idiopathic neonatal hepatitis
  • -> allows for prompt surgical correction! (Kasai)
106
Q

dx of biliary atresia?

A
  • -no excretion on DISIDA

- -liver biopsy

107
Q

when is Kasai most effective?

A

prior to 12 weeks of life

108
Q

physical findings of biliary atresia:

A
  • -hepatomegaly
  • -enlarged spleen
  • -pain
  • -ascites
  • -assoc/ features/dysmorphic features (Gargoyle)
109
Q

when might you see Gargoyle-like features?

A

w/biliary atresia

110
Q

5 diseases causing hepatomegaly:

A

1) storage disorders
2) nutritional problems
3) infiltrative disorders
4) congential hepatic fibrosis
5) tumors

111
Q

encephalopathy

A
  • -blood is shunted around the liver & not through it, allowing toxins from the GI tract to circulate freely to the brain
  • -made worse w/blood loss into the GI tract
112
Q

most hazardous substance, in r/t encephalopathy?

A

Ammonia! builds up on the brain

113
Q

s&s of encephalopathy

A
  • -subtle changes in personality
  • -memory loss
  • -irritability
  • -lethargy & sleep disturbances
  • -confusion
  • -flapping tremor (asterixis)
  • -stupor
  • -coma (leads –> death bc of cerebral edema)
114
Q

ascites

A 
excess accumulation of:
--salt
--water
--protein
in the peritoneal cavity
115
Q

hx, phys exam, & radiology clues to ascites:

A

1) Hx: increasing abdominal girth
2) Phys. Ex:
- -shifting dullness upon percussion
- -fluid wave
(v. poor in detecting sm. amts of ascites)
3) Radiology:
- -ultrasound, CT scan very sensitive

116
Q

4 essential fluids for ascites fluid analysis:

A

1) total & differential cell counts
2) culture & sensitivity
3) amylase levels
4) ambumin level

117
Q

3 useful fluids for ascites fluid analysis:

A

1) glucose level
2) pH analysis
3) gram stain

118
Q

3 fluids that may need evaluated in special circumstances of ascites:

A

1) cytologic exam (> or equal to 50ml of fluid preferred)
2) lactate level
3) triglyceride level

119
Q

Ascites: Serum-Ascites-Albumin Gradient

A

–sensitive & specific for transudate
–has replaced total protein & LDH measurements
Ratio:
>1.1 –> indicates portal hypertension
< 1.1 –> indicates exudative process

120
Q

transudate

A

fluid substance that has passed through a membrane

121
Q

Serum-Ascites-Albumin ratio that indicates portal hypertension?

A

> 1.1

122
Q

Serum-Ascites-Albumin ratio that indicates exudative process?

A

< 1.1

123
Q

chylous ascites

A
  • -milky ascites

- -high in lipid content w/triglyceride content >200mg/dl

124
Q

cause of chylous ascites?

A
  • -83% of adults have malignancies (lymphomas most common)
  • -congenital anomalies most common in children
  • -can occur w/cirrhosis
125
Q

tx for chylous ascites?

A
  • -children respond to low-fat diets

- -w/adults, tx aimed at underlying cause

126
Q

tx for ascites

A
  • -Na restriction, fluid restriction
  • -Diuretics: spironolactone, amiloride, furosemide, HCTZ, metolazone
  • -large-volume paracentesis
  • -surgery: LaVeen shunt, side-to-side portocaval shunt; liver transplantation
  • -TIPS: transjugular intrahepatic portosystemic shunt
127
Q

hepatic hydrothorax

A
  • -ascites is under pressure & leaks through vents in the diaphragm
  • -dx: fluid should have characteristics similar to ascites
128
Q

tx for hepatic hydrothorax:

A

AVOID chest tubes!!

  • -surg. repair us. not effective (complications!)
  • -liver transplantation = T.O.C. for diuretic-refractory causes
  • -TIPS works if renal function okay
129
Q

hepatorenal syndrome

A

–etiology unclear, but likely an exaggeration of mechanisms involved in salt & water retention in cirrhosis
(usually end-stage)

130
Q

dx of hepatorenal syndrome:

A

1) urine output < 10 mEq/l

3) absence of intravascular depletion

131
Q

tx for hepatorenal syndrome:

A

–Dopamine
–large-volume paracentesis
–LeVeen shunt
–TIPS
–liver transplantation
(st need liver & kidney transplant both)

132
Q

which type of liver/biliary tract imaging is diagnostic?

A

liver biopsy: often get v. definitive answer

BUT v. invasive, requires GA

133
Q

5 methods of imaging liver/biliary tract:

A

1) ultrasound
2) DISIDA (nuclear med, looks @ biliary tree)
3) C.T.
4) MRI (but need GA to put child to sleep –> avoid)
5) liver biopsy (v. invasive, requires GA)

134
Q

Acute Hep C

A
  • -blood & body fluid route
  • -acute state but 70% become chronic
  • -can –> cirrhosis & cancer
135
Q

what percentage of acute hep c cases become chronic?

A

70%

136
Q

leading cause of cirrhosis in US?

A

viral Hep C (OR: alcoholism?)

137
Q

is there a med that can cure Hep C?

A

yes: in adults, 95% effective (oral med)

* * still in trials for kids

138
Q

Hep D route of transmission?

A
  • -blood & body fluid route

* *must have Hep B to get it

139
Q

you must have hep b to get what other form of hepatitis?

A

Hep D

140
Q

Hep E

A

v. similar to Hep A: oral-fecal route

141
Q

chronic hepatitis

A
  • -hepatitis lasting > 6 mos
  • -may be viral, autoimmune, drug exposure, cardiac, or metabolic disorders
  • -may –> cirrhosis, hepatocellular cancer
142
Q

autoimmune hepatitis

A
  • -caused by antibodies

- -often coexists w/other disease (Lupus, IBD…)

143
Q

2 types of autoimmune hepatitis:

A 
Type 1:
--positive ANA (anti-nuclear antibodies)
--more common in females
Type 2:
--mostly affects young women
144
Q

6 less common diseases that affect the liver:

A

1) sclerosing choangitis assoc. w/IBD
2) secondary cholangitis assoc. w/stones or surgical bil duct injury
3) Wilson’s Disease
4) Icshemic hepatitis d/t CHF, shock, asphyxia, seizure (see more in ICU)
5) infiltrative d/o’s: leukemia, lymphoma, neuroblastoma
6) hepatocarcinoma, hepatoblastoma (v. tx’able types of cancers if found early enough!)

145
Q

cholangitis

A

an infection of the common bile duct

the tube that carries bile from the liver to the gallbladder and intestines

146
Q

Wilson’s Disease

A

autosomal recessive; copper excretion defect

  • -> too much copper in the body’s tissues
  • -> the excess copper damages the liver and nervous system
  • -present in adolesence, 1st as mood behaviors/ “acting out” etc, d/t copper build-up on the brain
  • -if find early enough, can chelate to remove copper (binds copper, & is then excreted in the urine)
  • *Kayser-Fleischer rings**
147
Q

liver disease tx options (7)

A

1) replacement of deficient abnormal end products–bile acids
2) depletion of the stored substance (NTBC= Nitisinone, a new drug)
3) induction of enzymes
4) dietary restriction
5) gene therapy
6) hepatocyte transplantation
7) liver transplantation

148
Q

liver transplantation

A
  • -can last a long time!
  • -v., v. successful
  • -96% 1-year survival; 92% 3-year survival
  • -can take just 1 med daily
149
Q

NAFLD

A

non-alcoholic fatty liver disease

150
Q

clinical definition of NAFLD

A

1) Macrovesicular fat in >5% of hepatocytes
2) lack of:
- -significant ethanol ingestion
- -other drugs or toxins
- -viral hepatitis
- -TPN
- -inborn metabolic errors
- -autoimmune hepatitis
- -cystic fibrosis
- -Wilson’s disease

151
Q

steatosis

A

intracellular deposition of fat in the liver

–liver looks yellow

152
Q

how does steatosis progress to hepatocellular carcinoma?

A

steatosis–> steatohepatitis

  • -> inflammation can cause scarring, fibrosis, or cancer
    • -> cirrhosis
      • -> hepatocellular carcinoma
153
Q

steatohepatitis

A

–fat deposits
–inflammation on biopsy
–fibrosis w/necrosis
…really attacking the liver

154
Q

rates of steatosis?

A

varies by ethnicity: 45% hispanics, 33%whites, 24%blacks

–in whites only, more males than females

155
Q

how to dx steatosis in children?

A
  • -us. asymptomatic & no screening guidelines

* *biopsy is only definitive test**

156
Q

NASH

A

non-alcoholic steatohepatitis

157
Q

surrogates for dx in steatosis:

A
  • -surrogates insensitive & nonspecific
  • -ALT used mostly
  • -can distinguish b/t NASH & not NASH
  • -underestimate prevalence
158
Q

prevalence of steatosis in children:

A
  • -elevated ALT in 8-11% of population

- -assoc w/: male sex, waist circumference, Mexican ethnicity, high insulin levels, older age

159
Q

tx for steatosis:

A
  • -primary therapy = diet & exercise, if overwt.
  • -gradual wt. loss correlated w/NAFLD improvement in adult studies
  • -studies show decrease in LFTs & liver echogenicity w/lifestyle interventions
  • -BUT lack of standardization in dietary/exercise interventions & outcome measures
  • -bariatric surg. effective in adults but data lacking in adolescents
160
Q

most common liver disease in USA in adults & children?

A

NAFLD

161
Q

NAFLD can progress to …?

A

cirrhosis/HCC (hepatocellular carcinoma)

162
Q

NAFLD

A
  • -hepatic manifestation of metabolic syndrome
  • -influences CV outcomes
  • -no biomarker or bioimaging currently replaces biopsy for trial or tx purposes
163
Q

negative HBSAg means:

A

susceptible

164
Q

negative Anti-Hbs means:

A

susceptible

165
Q

positive Anti-Hbc means:

A

immune

166
Q

labs showing synthetic dysfunction:

A

increased INR
decreased Albumin
( could be drug overdose!!)

167
Q

why might you see increased bilirubin?

A

something going on in biliary system–hemolysis

–maybe r/t chemo

168
Q

T. bili and D. bili both high; indicates?

A

typical biliary atresia

Peds Patho (8 decks)

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