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1

Common cause of ascites

Portal HTN from chronic liver disease

2

Risk factor for chronic liver disease

ETOH, transfusion, tattoos, IVDU, viral hepatitis

3

Non-portal HTN causes of ascites

infections, malignancy, inflammatory disorders, ductal disruption

4

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

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

5

Complications of NAFLD/NASH

- CV diseases
- Cirrhosis
- Colorectal cancer
- CKD

6

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

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

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

7

Etiologies of fatty liver aka hepatic steatosis

- 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

8

How do NAFLD pt usually present?

Usually asymptomatic or mild RUQ discomfort, hepatomegaly

9

Etiology of NAFLD

- obesity
- DM
- Hypertriglycerdemia
- Metabolic syndrome (insulin resistance)

10

On histology what is a characteristic finding of NAFLD?

- macrovaseicular steatosis and focal infiltration by PMNs and Mallory hyaline --> NASH (nonalcoholic steatohepatitis)

11

What is spontaneous bacterial peritonitis (SBP)

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

12

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?

cirrhosis

13

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

- 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

14

Common PE and S/s of SBP

- altered mental status, abd pain, diarrhea
- fever, diffuse abd tenderness, flank dullness, shifting dullness and fluid wave

15

what's the SAAG measurement in pts with SBP

>1.1

16

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

HAV

17

How is does HAV present?

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

18

How HAV acquired?

fish or seafood --> gastroenteritis
- fecal-oral (international travel is a risk factor)

19

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

Anti-HAV IgG

20

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

Anti-HCV with negative HCV-RNA

21

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

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

22

how is HBV transmitted?

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

23

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

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

24

Lab findings of prior infection of HBV

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)

25

Lab findings of someoen with acute infection of HBV

Positive: HBsAg, Anti-HBc IgM, HBeAg

Negative: Anti-HBs, AntiHBc, AntiHBe

26

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

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

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

27

Lab findings of chronic infection with active infection and replication

Negative: AntiHBs, antiHBe

Positive: HBsAg, Anti-HBcIgM and IgG, HbeAg

28

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

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

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

29

lab findings of immunized against HBV

Positive AntiHBs, all other negatives

30

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

HBsAg

31

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

recovery from past infection

32

HCV puts pts at increased risk of what neoplasm?

non-Hodgkin lymphoma

33

Mixed cryoglobulinemia is a complication of which Hep virus?

HCV

34

membranoproliferative GN is a complication of which hep virus?

HCV

35

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

HCV

36

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

- Transplant recipients particularly those treated with tacrolimus rather than cyslosporine for immunosuppression

37

Two most common cause of acute liver failure

1. Acetoaminophen
2. idiosyncratic drug reaction

38

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

cerebral edema and sepsis

39

with acetaminophen toxicity AST/ALT is elevated by how much

> 5000

40

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

> 200

41

How is acute liver failure treated?

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

42

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

0-8

43

what is the Rumack-Mathew monogram?

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

44

what is the workflow of tylenol OD

- 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

Autoimmune hepatitis in most common in what patient population/

- young-mid age women with other autoimmune diseases

46

What antibodies are checked for autoimmune hepatitis?

- ANA and/or smooth muscle AB
- Anti-LKM1

47

how is autoimmune hepatitis treated?

- steroids +/- azathioprine

48

Pts with autoimmune haptitis are at increased risk of

cirrhosis and HCC

49

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

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

50

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?

6 months

51

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

>50g daily for over 10 years

52

what is the Maddrey discriminant function (DF)

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

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

Glasgow alcoholic hepatitis score (GAH)

54

GAH score of what receiving glucocorticoids have higher survival rates

>/=9

those with score under 9 has no survival benefit with glucocorticoids

55

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

- 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

hepatic encephalopathy grading

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

Lab findings in person with cirrhosis

- 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

What is Child-Pugh and Model used for?

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

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

PBC

60

Which HLA are associatd with PBC

HLA DRb1 08 and DQB1

61

What are the risk factors for PBC

- Risk factors: H/O UTI, smoking, HRT, hair dye;
- infection with novosphincgobium aromaticovorans and chlamydophila pneumonia may trigger or cause it

62

Treatment option for PBC

Ursodeoxycholic acid

63

what part of GI is iron absorbed

Duodenum

64

in Hemochromotosis iron is deposited in what organs?

- Liver,
- Pancreas
- adrenals
- Testes
- Pituitary
- Kidney
- heart

65

Gene mutation of hemochoromatosis

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

66

Pt with hemochromatosis are at increased risk of infection with

vibriovulnificus, listeria monocytogenes, Yersinia enterocolitica and othe rsiderophilic organism

67

how is hemochromotosis treated?

- 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

Gene mutation of wilson's disease

ATP7B (compound heterozygotes H1069Q) most common

69

In wilsons disease, excess copper is deposited where

brain, cornea, kidney, liver
- absorbed from small intestine

70

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

- Oral penicillamine (chelating agent)
- liver transplant

71

Presenting symptoms of Budd-Chiari

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

72

Budd-Chiari is due to occlusion of flow to

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

73

Causes of Budd-Chiari

- Polycythemia vera
- CHF
- hepatocellular carcinoma
- Post partum state
- Hypercoaguable state

74

How is Budd-Chiari diagnosed?

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

Alpha1-antitrypsin deficiency:
A. Normal function
B. mutation
C. Consequence
D. Biopsy finding
E. treatment
F. risk for

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