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GI 2 Final > Diseases of Liver - McGowan > Flashcards

Diseases of Liver - McGowan Flashcards

1
Q

Common cause of ascites

A

Portal HTN from chronic liver disease

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2
Q

Risk factor for chronic liver disease

A

ETOH, transfusion, tattoos, IVDU, viral hepatitis

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3
Q

Non-portal HTN causes of ascites

A

infections, malignancy, inflammatory disorders, ductal disruption

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4
Q

Factors that which produces SAAG of greater or equal to 1.1g/dL

A
  1. Hepatic congestion (HF, constriction pericardidtis, Budd-CHiari, etc)
  2. Liver disease (cirrhosis, haptitis, fibrosis etc)
  3. Portal vein occlusion
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5
Q

Complications of NAFLD/NASH

A
  • CV diseases
  • Cirrhosis
  • Colorectal cancer
  • CKD
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6
Q

How’s serum albumin ascites gradient (SAAG) calculated?

A

SAAG = (serum albumin) - (ascitic fluid albumin)

if > 1.1 ascites due to portal HTN
if < 1.1 ascites not associated with increased portal pressure

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7
Q

Etiologies of fatty liver aka hepatic steatosis

A
  • Alcohol related fatty liver disease
  • NAFLD (<20 g of Etoh/day in women and <30 in men allows diagnosis of NAFLD)
  • Steatosis
  • Other: amiodarone, corticosteroids, vinyl chloride, carbon tetracholirde and yellow phosphorus
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8
Q

How do NAFLD pt usually present?

A

Usually asymptomatic or mild RUQ discomfort, hepatomegaly

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9
Q

Etiology of NAFLD

A
  • obesity
  • DM
  • Hypertriglycerdemia
  • Metabolic syndrome (insulin resistance)
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10
Q

On histology what is a characteristic finding of NAFLD?

A
  • macrovaseicular steatosis and focal infiltration by PMNs and Mallory hyaline –> NASH (nonalcoholic steatohepatitis)
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11
Q

What is spontaneous bacterial peritonitis (SBP)

A
  • ascitic fluid infection w/o apparent source: translocation of gut bacteria (commonly ecoli, klebsiella; strep pneumo or viridans)
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12
Q

If a patient with spontaneous bacterial peritinitis presents with decompensation (worsening encephalopathy, fever, abd pain, worsening renal function), what other underlying disease does he MOST likely have?

A

cirrhosis

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13
Q

what lab test is common important to obtain in pts suspected of spontaneous bacterial peritonitis?

A
  • WBC w/diff

PMN >250 with >75% of all WBC = highly suggestive of SBP and abx should be started

If elevated WBC with lymphocyte predominance think TB

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14
Q

Common PE and S/s of SBP

A
  • altered mental status, abd pain, diarrhea

- fever, diffuse abd tenderness, flank dullness, shifting dullness and fluid wave

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15
Q

what’s the SAAG measurement in pts with SBP

A

> 1.1

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16
Q

which Hep Virus has no chronic carrier state, self limited, transmitted fecal orally, diagnosed by IgM anti-Hep_V, and vaccination can prevent it

A

HAV

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17
Q

How is does HAV present?

A

anorexia, malaise, N/V, aversion to smoking, mild RUQ pain

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18
Q

How HAV acquired?

A

fish or seafood –> gastroenteritis

- fecal-oral (international travel is a risk factor)

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19
Q

Lab findings of someone who’s had HAV but no longer has it

A

Anti-HAV IgG

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20
Q

Lab findings of someone who’s had HCV but has cleared it

A

Anti-HCV with negative HCV-RNA

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21
Q

what’s considered the window period for HBV infection and is very important when screening for blood donatiosn?

A

Between HBsAg disappeariang and HBsAg appearing,whic may be several weeks, and pt is still considered to have ACUTE HBV and is only detectable with HBcAb IgM

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22
Q

how is HBV transmitted?

A
  • inoculation of infectedblood or blood products, sexual contact (present in saliva, semen, vaginal secretions), mom to baby at delivery
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23
Q

what lab findings are seen in the window period of HBV?

A

All negative except anti-HBc IgM (aka HBcAb) positive

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24
Q

Lab findings of prior infection of HBV

A

negative: HBsAg, anti-HBc IgM, HBeAg,
Positive: Anti-HBs, Anti-HBc IgG,

-/+ anti-HBe (depending on when you check it, early it’ll be -, but later it’ll be positive)

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25
Q

Lab findings of someoen with acute infection of HBV

A

Positive: HBsAg, Anti-HBc IgM, HBeAg

Negative: Anti-HBs, AntiHBc, AntiHBe

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26
Q

lab findings of chronic infection w/o active infection (inactive carrier)

A

Positive: HBsAg, anti-HBc IgG, anti-HBe

Negative: Anti-HBs, Anti-HBc IgM, HBeAg,

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27
Q

Lab findings of chronic infection with active infection and replication

A

Negative: AntiHBs, antiHBe

Positive: HBsAg, Anti-HBcIgM and IgG, HbeAg

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28
Q

Lab findings of chronic infection with active infection than is transforming into inactive carrier

A

negative: AntiHBs
Positive: HBsAg, AntiHBc IgM, IgG,

-/+ HBeAg and anti-HBe (depending on when you check it)

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29
Q

lab findings of immunized against HBV

A

Positive AntiHBs, all other negatives

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30
Q

HDV is only able to cause hepatitis in the presence of which HBV antigen?

A

HBsAg

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31
Q

Presence of anti-HCV in serum but negative HCV RNA indicates what

A

recovery from past infection

32
Q

HCV puts pts at increased risk of what neoplasm?

A

non-Hodgkin lymphoma

33
Q

Mixed cryoglobulinemia is a complication of which Hep virus?

A

HCV

34
Q

membranoproliferative GN is a complication of which hep virus?

A

HCV

35
Q

Lichen planus, autoimmune thryoiditis, lymphocytic sialodenotis, idiopathic pulm fibrosis porphyria cutaneous tarda, monoclonal gammapathies are all complications of which hep virus?

A

HCV

36
Q

HEV usually causes acute hepatitis, but chronic with rapid progression to cirrhosis has been documented in what patient population/

A
  • Transplant recipients particularly those treated with tacrolimus rather than cyslosporine for immunosuppression
37
Q

Two most common cause of acute liver failure

A
  1. Acetoaminophen

2. idiosyncratic drug reaction

38
Q

in patients with acute liver failure what is the leading cause of death?

A

cerebral edema and sepsis

39
Q

with acetaminophen toxicity AST/ALT is elevated by how much

A

> 5000

40
Q

ammonia elevated by how much is sign of encephalopathy and intracranial HTN?

A

> 200

41
Q

How is acute liver failure treated?

A

supportive, stress gastropathy prophylaxis, N-acetylcysteine (NAC) in tylenol OD, liver transplant

42
Q

Tylenol OD is treated with NAC if int he toxicity area. the critical ingestion-treatment interval for max protecion against severe hepatic injury is between _ hours

A

0-8

43
Q

what is the Rumack-Mathew monogram?

A

graphs probablity of hepatic toxicity based on hours after ingestion and acetaminophen plasma concentration.

44
Q

what is the workflow of tylenol OD

A
  • estimate time of acetiminophen ingestion
  • If < 24hrs obtain serum acetamiinphen level at 4hrs post ingestion and plot level on monogram
  • If time of ingestion is unknown consider starting acetylcystine empirically
  • If plasma level BELOW treatment line –> stop acetylcysteien
  • If plasma level ABOVE treatment line –> give acetylcystien
45
Q

Autoimmune hepatitis in most common in what patient population/

A
  • young-mid age women with other autoimmune diseases
46
Q

What antibodies are checked for autoimmune hepatitis?

A
  • ANA and/or smooth muscle AB

- Anti-LKM1

47
Q

how is autoimmune hepatitis treated?

A
  • steroids +/- azathioprine
48
Q

Pts with autoimmune haptitis are at increased risk of

A

cirrhosis and HCC

49
Q

when treating alcoholic liver disease in anorectic patients, glucose administration requires coadministration of _ to avoid what CNS issues?

A

Coadminister thiamine. glucose adminstration increase the need for thiamine and can precipitate Wernicke-Korsakoff syndrome if thiamine is not given

50
Q

Alcoholic liver disease pt may require liver transplant, but given they can be considered for liver transplant, they must abstain from alcohol for how long?

A

6 months

51
Q

consumption of how much alcohol for how long is a risk of alcoholic cirrhosis?

A

> 50g daily for over 10 years

52
Q

what is the Maddrey discriminant function (DF)

A

DF estimates disease severity and mortality risk in pts with alcoholic hepatitis

DF gr or equal to 32 = high short-term mortality and may benefit from treatment with glucocorticoids

lower scores have low short-term mortality and do not benefit glucocorticoids

53
Q

what measurement tool predicts mortality in alcoholic hepatitis based on multivariable model that takes into account age, serum bili, BUN, PT, peripheral WBC

A

Glasgow alcoholic hepatitis score (GAH)

54
Q

GAH score of what receiving glucocorticoids have higher survival rates

A

> /=9

those with score under 9 has no survival benefit with glucocorticoids

55
Q

Common signs of cirrhosis include fatigue, disturbed sleep, msucle cramps, weight loss. What are other possible signs/symptoms

A
  • reduced muscle strenght, amenorrhea, ED, loss of libido, sterility, gynecomastic, spider telangiectasis, palmer erythema, dupuytren contractures, glossits, wasting, jaundice, ecchymosis, encephalopathy, asterixis, tremor
  • Portal HTN
56
Q

hepatic encephalopathy grading

A
  1. lack of awareness, short attention span, impaired performance or anxiety
  2. lethargy or pathy, disoreintation of time and place, personality changes, imappropriate behavior
  3. Somnolence to semistupor, responsive to verbal stimuli; confusion, gross disorientation, bizarre bahavior
  4. Coma
57
Q

Lab findings in person with cirrhosis

A
  • macrocytic anemia (folic acid def, GIB, hemolysis)
  • dec WBC (hypersplenism)
  • inc infection
  • Thrombocytopenia
  • Prolongation of PT
  • Modest elevation of AST (ALT) and alk phos and T bili
  • dec albumin
  • vit D def
58
Q

What is Child-Pugh and Model used for?

A

End-Stage liver disease (MELD) scoring system for cirrhosis.

Grade 1-3 of severity of: ascites, encephalopathy, bili, albumin, prothrombin time.

Numerical score of 1-3 and then those are added to get Class A, B or C

5-6 = A; 7-9 = B; 10-15 = C

C would require liver transplant

59
Q

sjogren Pt with isolated elevated alk phos, with antimitochondiral ab, increased IgM, and h/o UTI, think what disease?

A

PBC

60
Q

Which HLA are associatd with PBC

A

HLA DRb1 08 and DQB1

61
Q

What are the risk factors for PBC

A
  • Risk factors: H/O UTI, smoking, HRT, hair dye;

- infection with novosphincgobium aromaticovorans and chlamydophila pneumonia may trigger or cause it

62
Q

Treatment option for PBC

A

Ursodeoxycholic acid

63
Q

what part of GI is iron absorbed

A

Duodenum

64
Q

in Hemochromotosis iron is deposited in what organs?

A
  • Liver,
  • Pancreas
  • adrenals
  • Testes
  • Pituitary
  • Kidney
  • heart
65
Q

Gene mutation of hemochoromatosis

A

HFE on chromosome 6; particulalry C282Y homozygous mutation –> increased iron absorption from duodenum

66
Q

Pt with hemochromatosis are at increased risk of infection with

A

vibriovulnificus, listeria monocytogenes, Yersinia enterocolitica and othe rsiderophilic organism

67
Q

how is hemochromotosis treated?

A
  • avoid food rich in iron (red meat), alcohol, vit C, raw shellfish, and supplemental iron
  • phlebotomy to get iron sat >50% and ferritin level 50-100
  • PPI
  • deferoxamine - chelating agent
68
Q

Gene mutation of wilson’s disease

A

ATP7B (compound heterozygotes H1069Q) most common

69
Q

In wilsons disease, excess copper is deposited where

A

brain, cornea, kidney, liver

- absorbed from small intestine

70
Q

increased urinary copper excretion, low serum ceruloplasmin, Kayser-Fleischer rings. Treatment option

A
  • Oral penicillamine (chelating agent)

- liver transplant

71
Q

Presenting symptoms of Budd-Chiari

A

Pt present with RUQ pain and tenderness, ascites, HSM, juandice,

72
Q

Budd-Chiari is due to occlusion of flow to

A

hepatic vein or IVC –> back of blood into the liver –> centrilobular congestion and necrosis

73
Q

Causes of Budd-Chiari

A
  • Polycythemia vera
  • CHF
  • hepatocellular carcinoma
  • Post partum state
  • Hypercoaguable state
74
Q

How is Budd-Chiari diagnosed?

A

Imaging showing prominent caudate lobe

  • contrast-enahced, color, or pulsed doppler US
  • MRI with spin-echo
  • Direct venography showing spider web pattern
  • Bx: Centrilobular congestion with likely fibrosis and multiple regenerative nodules “nutmag liver”
75
Q 
Alpha1-antitrypsin deficiency:
A. Normal function
B. mutation
C. Consequence
D. Biopsy finding
E. treatment
F. risk for
A 
A. inhibits elastase
B. AD (codomiant) inheritance of PiZZ
C. Accumulation of misfolded ATT in liver --> cirrhosis
D. PAS+ globules in hepatocytes
E. IV AAT for lung/ Liver transplant 
F. HCC

GI 2 Final (11 decks)

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