Gi Part 2

Front 1

3 features of Hep A:

Back 1

1. rare in US

2. ONLY acute

3. mild course of flu-like illness and jaundice

Front 2

HAV IgM indicates:

Back 2

ACUTE infection

Front 3

HAV IgG indicates:

Back 3

prior exposure

OR

vaccination

Front 4

HBV can be acute AND chronic; severity ranges from:

Back 4

asymp to mild illness to acute LF

Front 5

95% of those exposed to HBV will:

Back 5

have the acute version

=> will clear it on their own and become immune

Front 6

4% of those exposed to HBV will develop:

Back 6

the chronic version

Front 7

1% of those exposed to HBV will develop:

Back 7

fulminant HBV, ~~ ALF

Front 8

perinatal (vertical) transmission of HBV is most common in:

Back 8

Asia, Africa

~~ **higher risk of CHRONIC HBV**

(West ~ sexual, IV)

Front 9

HBV is a MAJOR cause of:

Back 9

cirrhosis/HCC

Front 10

a positive HB sAg means:

Back 10

ACTIVELY infected

Front 11

a positive cAB means:

Back 11

you've seen it before (prior exposure)

(NOT vaccination)

Front 12

a positive HB sAB means:

Back 12

IMMUNE to Hep B

Front 13

a negative HB sAg means:

Back 13

NOT actively infected

- should get vaccinated if all are negative

Front 14

a negative HB cAB means:

Back 14

you've NEVER SEEN Hep B before

Front 15

negative sAg, negative cAB, and positive sAB means:

Back 15

you've been vaccinated

Front 16

if both cAB and sAB are positive, you're immune due to:

Back 16

INFECTION,

not vaccination

Front 17

if sAg and cAB are positive, you need to figure out if you're infected _____________ or _______________

Back 17

acutely

OR

chronically

Front 18

to figure out if you're infected with Hep B acutely or chronically, use:

(2)

Back 18

IgM and sAB

Front 19

if IgM is positive but sAB is negative, your Hep B infection is:

Back 19

ACUTE

Front 20

if both IgM and sAB are negative (keeping in mind that sAg and cAB are positive), your Hep B infection is:

Back 20

CHRONIC

Front 21

4 phases of chronic Hep B:

Back 21

1. immune tolerance

2. immune clearance

3. inactive carrier state

4. reactivation

Front 22

immune tolerance of HBV ~~

(4)

Back 22

1. occurs in first 10-30 years following perinatal exposure

2. HIGH HBV DNA

3. + eAg

4. but nl ALT, biopsy; no symptoms

=> immune system is ignoring HBV

Front 23

eAg is a sign of:

Back 23

rapid viral replication

Front 24

eAB is a sign of:

Back 24

indolent HBV

Front 25

immune clearance of HBV ~~

(4)

Back 25

1. immune system starts waking up to high eAg

2. inflam cells in liver => hepatocellular injury => spikes in ALT

3. **WIDE range of HBV DNA, depending on how successful the immune system is at clearing HBV

4. body is trying to commit HBV to the indolent kind

Front 26

in the immune clearance phase of HBV, you might see:

Back 26

IgM

- **might misdiagnose it as ACUTE HBV**

Front 27

inactive carrier phase of HBV ~~

(5)

Back 27

1. IS has succeeded in turning HBV inf. into an indolent disease

2. eAg is NEGATIVE

3. eAB is positive

4. HBV DNA might be undetectable

5. but liver biopsy might be abnl

Front 28

reactivation phase of HBV ~~

(4)

Back 28

1. suppression of the IS +

2. older pts with advanced liver disease

3. => threshold to treat is LOWER => treat sooner

4. eAg remains negative - can't make the envelope again - called a precore mutant

Front 29

precore mutants can't make eAg, but they are still:

Back 29

dangerous

~~ *higher* risk for cirrhosis

Front 30

resolution of chronic HBV is _________

Back 30

RARE

- but clearance of HBV sAg is a good prognosis

Front 31

after clearance of HBV sAg, HBV remains in hepatocytes as:

Back 31

HBV cccDNA

~~ you're immune

Front 32

Hep D:

(3)

Back 32

1. cannot occur unless you have Hep B

2. an RNA virus

3. dialysis, IVDA

Front 33

in Hep C, a _________ is much more common than an _____________

Back 33

a chronic infection is much more common than an acute

Front 34

Hep C is the leading cause of:

Back 34

liver-related death in the U.S.

Front 35

**acute HCV is ___________**

Back 35

*asymp*

- but can lead to development of chronic Hep C

Front 36

G1 Hep C ~~

Back 36

the U.S.

G2/G3 ~ Europe,

G4 to Egypt/ME

Front 37

3 symptoms of chronic HCV:

Back 37

1. fatigue/nonspecific symps

2. usually asymp

3. until you develop cirrhosis => decompensation

Front 38

which kind of pts should you screen for chronic Hep C?

Back 38

ANYONE with an ablnl ALT

- it should be at the top of your differential always

Front 39

diagnosis of Hep C:

(2)

Back 39

1. positive HCV AB
(positive means pt has been exposed)

2... with confirmatory pos. HCV *RNA*

Front 40

every viral hepatitis shows:

Back 40

a spike in ALT

Front 41

Hep B, C, and D are transmitted by:

Back 41

blood

A and E by fecal-oral/food and water

Front 42

pos. HCV AB with pos. HCV RNA =

Back 42

you HAVE CHRONIC HCV

Front 43

pos HCV AB with negative HCV RNA means =

Back 43

you've CLEARED the infection

Front 44

2 other tests for Hep C pts:

Back 44

1. genotyping

2. check immunization against Hep A and B

Front 45

factors promoting progression and inc. severity of Hep C:

(6)

Back 45

1. alcohol (gasoline onto a smoldering fire)

2. age >40

3. steatosis

4. HIV co-infection

5. other chronic liver disease

6. men

Front 46

HCV affects not only the liver but can also affect:

Back 46

renal, bone joints

- most commonly renal

Front 47

features of Hep E:

(3)

Back 47

1. Mexico, India

2. DOES show animal transimission (undercooked meat)

3. pregnant women are more likely to have a fulminant version

Front 48

**treatment for fulminant Hep B:**

Back 48

Lamivudine

(an oral nucleoside that inhibits DNA replication)

Front 49

decision to treat fulminant Hep B depends on:

Back 49

*synthesis* function and encephalopathy,

NOT ALT

Front 50

when you commit someone to treatment for HBV, you're signing them up for:

Back 50

60+ years appts and followups

Front 51

**why is the threshold for HBV DNA so much lower in eAg-NEG pts?**

Back 51

b/c they probably have the precore mutant, which means they've had the disease for decades,

which means they may already have fibrosis and thus can't handle an HBV flairup

=> lower threshold for treatment

Front 52

for HBV WITH cirrhosis, whether eAg is present or not, check:

Back 52

DNA

- if DNA is >2,000, TREAT

Front 53

what do you use to treat cirrhotic HBV with DNA >2,000?

(2)

Back 53

1. Entecavir

2. Tenofivir

Front 54

both Entecavir and Tenofivir are:

Back 54

oral nucleosides that inhibit DNA replication

Front 55

if cirrhotic HBV shows LESS than 2,000 DNA (via PCR), you may choose to:

Back 55

treat or observe

Front 56

***with DECOMPENSATED (cirrhotic) HBV, the first step is to:***

Back 56

measure DNA

Front 57

if DNA is NOT detectable with decompensated HBV:

(2)

Back 57

1. observe

2. put on wait list for transplant

Front 58

if DNA in decompensated HBV *IS* detectable,

(3)

Back 58

1. monotherapy with oral agents like Entecavir or Tenofivir

2. wait list for transplant

3. IFN will KILL the pt- don't use it

Front 59

Entecavir and Tenofivir are NEVER:

Back 59

used together

- use one or the other

Front 60

treatment for HBV with concurrent HIV:

(2)

Back 60

1. Entecavir, Tenofivir, or Emtricitabine (active against BOTH)

2. IFN

Front 61

Trurada =

Back 61

Emtricitabine + Tenofivir

Front 62

ALL oral nucleosides may cause:

Back 62

lactic acidosis

Front 63

on followups for HBV, ALWAYS check:

(3)

Back 63

1. HBV DNA

2. eAg

3. eAB

Front 64

HCV - whom to treat:

(5)

Back 64

1. >18 y.o.

2. detectable HCV RNA in serum

3. *compensated* cirrhosis ONLY

4. willing to adhere

5. no other contra (e.g. renal failure)

Front 65

why does HCV treatment require that pt have *conpensated* liver disease?

Back 65

IFN cannot be used on someone with decompensated cirrhosis

Front 66

SVR =

Back 66

sustained virologic response

= **cured of HCV**

Front 67

RVR =

Back 67

rapid virologic response

= HCV RNA is *undetectable* 4 weeks after therapy

Front 68

eRVR =

Back 68

extended RVR

= HCV RNA undetectable 12 weeks after therapy

Front 69

relapser =

Back 69

s/o who was Hep C RNA-negative on therapy, but the virus came back

Front 70

**treatment for Genotype 1 of HCV = **

(3)

Back 70

triple therapy -

PEG-IFN + Ribaviron + protease inhibitor

Front 71

2 protease inhibitors:

Back 71

1. telaprivir

2. boceprivir

- NEVER used alone

Front 72

2 results of triple therapy:

Back 72

1. decreases duration of treatment by half in 50% of pts,

2. increases SVR (cure) rates

Front 73

treatment for G2-G4 HCV:

Back 73

PEG-IFN + RBV

Front 74

SE's of INF:

(4)

Back 74

1. depression

2. blood dyscrasias

3. irreversible thyroid disorders

4. flu-like symptoms

Front 75

1 SE of RBV:

Back 75

anemia

Front 76

SE's of Telaprivir:

(3)

Back 76

1. rash

2. anemia

3. burning butt (diarrhea, hemorrhoids)

Front 77

SE's of Boceprivir:

(2)

Back 77

1. anemia

2. dysgeusia (metallic taste)

Front 78

2 COMMON SE's in HCV treatment:

Back 78

1. depression
- may need to discontinue therapy

2. fatigue
- due to IFN side Effect, anemia

Front 79

fatigue is also HIGH in HCV treatment, due to:

Back 79

IFN side Effect, anemia

Front 80

in HCV treatment, flu-like symptoms appear:

Back 80

early,

while depression and fatigue inc. over time

Front 81

anemia in HCV treatment:

(2)

Back 81

1. most common SE

2. => dose-reduce RBV, give EPO

Front 82

Asians are sensitive to:

Back 82

INF,

Africans are R

=> different SVR rates

Front 83

2 kinds of liver failure:

Back 83

1. cirrhotic (75%)

2. non-cirrhotic

Front 84

cirrhotic liver failure is by FAR:

Back 84

the most common kind of chronic LF

Front 85

by FAR the most common cause of ALF =

Back 85

drugs

- followed by toxins

Front 86

hepatotoxic drugs come in two types:

Back 86

1. intrinsic

2. idiosyncratic

Front 87

intrinsic hepatotoxic drugs are:

(2)

Back 87

1. predictable (e/o exposed will be injured)

2. dose-dependent


(idiosyncratic are the inverse)

Front 88

best example of intrinsic hepatotoxic drug =

Back 88

acetaminophen

Front 89

best examples of idiosyncratic hepatotoxic drugs =

Back 89

meds,

antibiotics

Front 90

NAPQI =

(3)

Back 90

1. minute, INCREDIBLY toxic metabolite of acetaminophen following glucuronidation/sulfation metabolism

2. conjugated to glutathione via Cyto P450

3. excreted by kidneys when bound to glutathione

Front 91

OD of acetaminophen =>

(3)

Back 91

1. saturation of glucuronidation/sulfation pathways

2. depletion of glutathione stores

3. => NAPQI binds and inactivates hepatocyte prots, causing them to die

Front 92

elevated bili ~~

Back 92

dec'd ability of the liver to excrete it into bile

Front 93

in acetaminophen toxicity, you should see:

Back 93

hepatocyte necrosis

Front 94

***histo features of hepatocyte necrosis:***

(3)

Back 94

1. condensed nuclei

2. ghostly nuclear shadows

3. bright pink necrosis

Front 95

elevated creatinine ~~

Back 95

kidney failure, always

Front 96

**treatment for aceta OD = **

Back 96

N-acetylcysteine (NAC)

**increases glutathione stores**

Front 97

chronic liver injury ~~ mild but persistent injury =>

Back 97

attempts to repair

=> fibrosis

=> cirrhosis

Front 98

fibrosis can be reversible, but cirrhosis

Back 98

is not

Front 99

5 causes of chronic liver injury:

Back 99

1. viral hepatitis

2. cholestasis

3. metabolic dz

4. fatty liver

5. alcohol

Front 100

cirrhosis =

Back 100

thick fibrous septa alternating with regenerative nodules

Front 101

3 categories of causes of NON-cirrhotic LF and/or portal HTN:

Back 101

1. pre-hepatic

2. post-hepatic

3. intrahepatic

Front 102

best example of prehepatic non-cirrhotic cause of portal HTN =

Back 102

thrombotic occlusion of the portal vein

=> portal HTN ONLY

=> splenomegaly ONLY; NOT a surgical disease

Front 103

b/c occlusion of the portal vein does NOT cause CLF, there is NO:

Back 103

dec. in liver func.

=> completely nl biopsy

Front 104

best example of POSThepatic non-cirrhotic cause of CLF/portal HTN =

Back 104

thrombotic occlusion of the HEPATIC vein

=> CLF due to venous back P

=> cirrhosis CAN develop

Front 105

posthepatic CLF can also be caused by:

Back 105

severe RHF

increased venous back P => congestion of central vein

=>=> RBC's pushed into hepatocyte trabeculae

=> RBC's replace hepatocytes entirely

(called RBC-trabecular lesion - seen in Budd-Chiari

=> pain, ascites, hepatomegaly)

Front 106

best example of Intrahepatic non-cirrhotic cause of CLF/portal HTN =

Back 106

amyloidosis

= accumulation of abnl prots in one OR MORE organs

=> HSM

- liver dysfunction occurs late

Front 107

amyloidosis can be visualized by the _________ stain

Back 107

Congo Red