Goljan inflammatory and infectious disorders of liver Flashcards

1
Q

pathogen for ascending cholangitis

A

E. coli

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2
Q

pathogen for liver abscess

A

E. coli;
Bacteroides fragilis;
streptococcus faecalis

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3
Q

pathogen for granulomatous hepatitis

A

mycobacterium Tb;

histoplasma capsulatum

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4
Q

pathogen for spontaneous peritonitis

A

E. coli in adults;

strept pneumoniae in children

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5
Q

pathogen for leptospirosis

A

leptospira interrogans

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6
Q

pathogen for amebiasis

A

entamoeba histolytica

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7
Q

pathogen for clonorchiasis

A

clonorchis sinensis (chinese liver fluke)

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8
Q

pathogen for schistosomiasis

A

schistosoma mansoni

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9
Q

pathogen for echinococcosis

A

echinococcus granulosus (sheepherder’s disease)

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10
Q

Define ascending cholangitis

A

inflammation of bile ducts (cholangitis) from concurrent biliary infection and duct obstruction (stone);
life threatening disease

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11
Q

clinical findings of ascending cholangitis

A

fever, jaundice, RUQ pain

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12
Q

What is ascending cholangitis likely to cause?

A

MC cause of multiple liver abscesses

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13
Q

Tx for ascending cholangitis

A

decompression and drainage;

piperacillin-tazobactam

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14
Q

Epidemiology for autoimmune hepatitis

A

type 1 is predominant form in US and worldwide (80%);
type 2 is uncommon in US;
young women

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15
Q

what are the range of autoimmune presentations?

A

symptomatic w/ increased transaminases;
fulminant hepatitis;
cirrhosis

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16
Q

Genetic associations w/ autoimmune hepatitis

A

HLA-D3 and DR4 association

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17
Q

What are autoimmune associations w/ AI hepatitis?

A

Hashimoto’s thyroiditis;

Graves’ disease

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18
Q

clinical findings of AI hepatitis

A

fever;
jaundice;
hepatosplenomegaly

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19
Q

lab findings for type I AI hepatitis

A

positive ANA (>60%);
anti-smooth muscle Ab (>85%);
increased serum transaminases;
decreased serum albumin in severe disease;
prolonged prothrombin time in severe disease

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20
Q

Tx for AI hepatitis

A

initial Tx w/ corticosteroids + azathioprine;

liver transplantation if resistant to Tx

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21
Q

where do a majority of liver abscess occur?

A

right lobe w/ majority being solitary

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22
Q

What are causes of liver abscess?

A
ASCENDING CHOLANGITIS (MC);
INTRA-ABDOMINAL INFECTION (pathogen spread via portal vein, diverticulitis, bowel perforation);
DIRECT EXTENSION (empyema of gallbladder, subphrenic abscess);
HEMATOGENOUS SPREAD (bacterial endocarditis)
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23
Q

Clinical findings of liver abscess

A

spiking, intermittent fever;
RUQ or right CVA tenderness;
jaundice is uncommon

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24
Q

How is liver abscess diagnosed?

A

ultrasound (least expensive);

CT scan

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25
Q

Tx for liver abscess

A

percutaneous drainage;

metronidazole + ceftriaxone

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26
Q

What does granulomatous hepatitis indicate?

A

sign of miliary spread

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27
Q

When will spontaneous peritonitis occur?

A

develops in ascities => cirrhosis, nephrotic syndrome

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28
Q

Tx for spontaneous peritonitis

A

cefotaxime

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29
Q

Describe the pathogen that causes leptospirosis

A

G-; tightly wound spirochetes;

crook at end resembles shepherd’s staff

30
Q

what are the reservoirs for leptospira interrogans and how it is transmitted?

A

dogs (MC), rats; spirochetes excreted in urine

transmitted by swimming in contaminated water (ponds on farms);
farmers, miners, people who work w/ sewage

31
Q

What type of disease is leptospirosis

A

biphasic disease => Weil’s disease

32
Q

Describe the septicemic phase of leptospirosis

A

fever, jaundice, hemorrhagic diathesis;
renal failure (interstitial nephritis);
conjunctivitis and photophobia, meningitis;
phase terminated by appearance of Ab

33
Q

describe immune phase of leptospirosis

A

presence of numerous organisms in urine => darkfield micro to confirm

34
Q

Tx of leptospirosis

A

pen G

35
Q

What is the most common cause of liver abscess worldwide?

A

amebiasis => entamoeba histolytica

36
Q

What is the common location for amebiasis?

A

usually produces a right lobe abscess

37
Q

Tx for amebiasis

A

metronidazole followed by paromomycin

38
Q

What is the life cycle of the pathogen that causes Clonorchiasis?

A

nonschistosomal=> egg (human) =>
ciliated miracidial larva =>
infects snail (1st intermed host) =>
produces fork-tailed cercarial larvae =>
infect 2nd intermed host (fish) =>
form infective metacercariae =>
man ingests 2nd intermed host => gets disease

39
Q

How is clonorchiasis contracted?

A

by ingesting encysted larvae in fish;

larvae enter CBD and become adults

40
Q

What is a risk for clonorchiasis?

A

may produce cholangiocarcioma

41
Q

Tx for clonorchiasis

A

praziquantel

42
Q

Describe the life cycle of the pathogen causing schistosomiasis

A
egg (human) => 
ciliated miracidial larva=>
infects snail (1st intermed host)=>
produces fork-tailed cercarial larvae =>
penetrate skin in human => gets disease
43
Q

How does Schistosoma mansoni cause schistosomiasis in the human? (not the life cycle)

A

larvae in SMV enter into portal vein =>
develop into adult worms that deposit eggs=>
host develops immune response w/ concentric fibrosis in a “pipestem cirrhosis) in the vessel wall

44
Q

Complications of schistosomiasis

A

portal HTN;
ascites;
esophageal varices

45
Q

Tx for schistosomiasis

A

praziquantel

46
Q

Where is echinococcosis likely to be found?

A

single or multiple cysts containing larval forms => may be in liver (MC), lungs, brain

47
Q

Life cycle of echinococcus granulosus

A

eggs develop into larval form only;

larval form only develops into adult that can lay eggs

48
Q

How does echinococcosis pathogen get to the point of infection in human?

A
infected sheep (intermed host w/ larva in liver cyst)
dog eats sheep liver (definitive host & larva develops into adult to lay eggs);
human eats eggs from dog is intermed host (eggs develop into larvae that penetrate bowel and enter liver => hydatid cyst
49
Q

What is a likely way a child may contract echinococcosis?

A

eating grass contaminated w/ dog excreta

50
Q

What leads to the ultimate infection of echinococcosis?

A

inner germinal layer of hydatid cysts has protoscolices (larva) in brood capsules => rupture of cysts can produce anaphylaxis

51
Q

Tx of echinococcosis

A

percutaneous drainage + albendazole

52
Q

Epidemiology of neonatal hepatitis

A

idiopathic;
congenital infections like CMV;
inborn errors of metabolism=>a1-antitrypsin def

53
Q

What does biopsy show in neonatal hepatitis?

A

multinucleated giant cells => “giant cell” hepatitis

54
Q

Triad associated w/ Reye syndrome?

A

encephalopathy;
microvesicular fatty change;
transaminase elevation

55
Q

What is the typical cause of Reye syndrome?

A

aspirin given to young child w/ infection

56
Q

Pathogenesis of reye syndrome

A
mitochondrial damage (virus, salicylates);
disruption of urea cycle (increase serum ammonia);
defective Beta-oxidation of fatty acids
57
Q

What may be the effect of salicylates in Reye syndrome? How is it viewed on micro?

A

microvesicular fatty change => small cytoplasmic globules w/o nuclear displacement;

no inflammatory infiltrate

58
Q

Initial Clinical findings in Reye syndrome

A

afebrile, quiet, lethargic sleepy, and vomiting => hepatomegaly and liver dysfxn present

59
Q

Clinical findings as Reye syndrome progresses

A

Signs & Sx related to cerebral edema & pressure increase;

1) sleepy but respond; vomit
2) stuporous, seizures, decorticate rigidity, intact papillary reflexes
3) deepening coma, decerebrate rigidity, fixed pupils
4) coma, loss of deep tendon reflex, fixed dilated pupils, flaccidity/decerebrate
5) death

60
Q

lab findings w/ Reye syndrome

A

transaminasemia;
normal to slight increase in total bilirubin;
increased serum ammonia and PT (levels give severity);
hypoglycemia;
CSF usually normal

61
Q

Tx for Reye syndrome

A

supportive;

mannitol, glycerol, hyperventilation to reduce cerebral edema

62
Q

mortality rate for Reye syndrome

A

25-50% mortality rate

63
Q

Pathogenesis of acute fatty liver of pregnancy? risks?

A

abnormality in Beta-oxidation of fatty acids;

FATAL TO MOTHER AND FETUS UNLESS DELIVERED

64
Q

Define preeclampsia

A

HTN, proteinuria, dependent pitting edema in 3rd trimester

65
Q

How does preeclampsia damage the liver? what lab will be elevated?

A

liver cell necrosis around portal triads (zone 1);

increased serum transaminases

66
Q

Define HELLP syndrome

A

Hemolytic anemia w/ schistocytes;
Elevated Liver enzymes
Low Platelets (DIC)

67
Q

Define fulminant hepatic failure

A

acute liver failure w/ encephalopathy w/in 8wks of hepatic dysfxn

68
Q

causes of fulminant hepatic failure

A

Viral hepatitis (MC overall cause);
drugs (acetaminophen MC);
Reye syndrome

69
Q

gross and micro findings of fulminant hepatic failure

A

wrinkled capsular surface due to loss of hepatic parenchyma;

dull red-yellow necrotic parenchyma w/ blotches of green (bile)

70
Q

clinical findings in fulminant hepatic failure

A

hepatic encephalopathy;

jaundice

71
Q

Lab findings w/ fulminant hepatic failure

A
DECREASE transaminases (liver parenchyma destroyed);
INCREASE in PT and ammonia