Gi Part 3

Front 1

a NON-infectious cause of hepatitis can result in:

Back 1

a similar biopsy as viral hepatitis

Front 2

in addition to the liver, other organs may be affected by:

Back 2

viral hepatitis

Front 3

liver biopsies are performed only when:

(2)

Back 3

1. a diagnosis is uncertain or

2. severity needs to measured

Front 4

** histo of acute hepatitis = **

(2)

Back 4

1. lobular inflammation

2. Acidophils

Front 5

Acidophil =

Back 5

single, necrosed hepatocyte

Front 6

***histo features of Acidophils:***

(4)

Back 6

1. cytoplasm is condensed and deeply eosinophilic (red)

2. retraction halo

3. condensed, darker nucleus

OR

4. nuc. might fragment or disappear entirely

Front 7

the lymphocytes of lobular inflammation are:

(color)

Back 7

dark blue

Front 8

**histo features of chronic hepatitis = **

(3)

Back 8

lobular inflam + Acidophils + interface hepatitis

Front 9

***interface hepatitis = ***

(2)

Back 9

1. infiltration of PA's by lymphocytes

AND

2. destruction of limiting plate

Front 10

late-stage cirrhosis no longer has:

Back 10

PA's

Front 11

****histo of Hep B = ***

Back 11

ground glass hepatocytes

- accum. of pale, hazy sAg, which pushes nucleus to the edge

Front 12

****histo of Hep C = ***

Back 12

well-formed lymphocytic nodules, esp. in PA's

Front 13

NAFLD is a spectrum of disease:

(3)

Back 13

1. simple steatosis

2. non-alcoholic steatohepatitis (NASH)

3. cirrhosis

Front 14

**risk factors for NAFLD = **

(4)

Back 14

obesity,

DM

HTN

hyperlipidemia

Front 15

simple steatosis =

Back 15

fat in hepatocytes, but NO inflammation/injury

Front 16

NASH ~~ fat accum. in hepatocytes +

Back 16

inflammation of hepatocytes

Front 17

histo of simple steatosis =

Back 17

macrovascular fatty liver

Front 18

macrovascular fatty liver =

Back 18

large bubbles of fat displace the nucleus to the edge of the cell

Front 19

in EITHER theory of NAFLD etiology, the common factor =

Back 19

free O2 radicals causing inflam. in the liver

Front 20

histo of steatohepatitis, either NASH or ASH (indistinguishable by histo) shows:

(3)

Back 20

1. macrovesicular steatosis

2. mallory bodies

3. scattered lobular inflam

Front 21

mallory bodies =

Back 21

eosinophilic concentrations within ballooned hepatocytes

Front 22

diagnosis of NAFLD comes via these (3):

Back 22

1. ALT > AST,
though not extremely high (~200)

2. neglible (<20g/day) alcohol consumption

3. absence of other causes of liver disease

Front 23

liver biopsy = gold standard of FLD diagnosis, but may not be necessary; instead, __________________________________ may suffice

Back 23

an image showing fatty infiltrate

[in the right clinical presentation)]

Front 24

the NAFLD fibrosis score is based upon:

Back 24

routine clinical data

- age, BMI, CBC

Front 25

the NAFLD fibrosis score is good for:

Back 25

advanced fibrosis,

but might miss mild disease

Front 26

4 pot. targets for NAFLD therapy:

Back 26

1. obesity

2. insulin

3. hyperlipidemia

4. oxidative stresss

Front 27

Vit E. might be a good therapy for oxidative stress, but

Back 27

CAN'T be used with smokers

also, might cause cancer

Front 28

**best therapy for NAFLD = **

Back 28

diet and exercise

Front 29

alcohol-related liver disease ~~

(3)

Back 29

1. AST to ALT = 2 or 3:1

2. elevated GGT

3. others: macrocytosis, dec. folate/B12, low BUN

Front 30

if the liver disease is alcohol-related, assess extent of use with CAGE:

Back 30

feel like you need to CUT down?

Annoyed about ppl asking you?

Guilty a/b drinking?

Eye-opener?

Front 31

alcoholic hepatitis shows:

(4)

Back 31

fever, leukocytosis, hepatomegaly

- **may have portal HTN in absence of cirrhosis**

Front 32

if alcoholic hepatitis is severe, pts may benefit from:

Back 32

steroid treatment

Prednisone, Pentoxi

Front 33

drug-induced liver injury can occur from:

Back 33

ANY drug, including herbal

Front 34

most notorious injury-inducing drugs =

(3)

Back 34

Tylenol,

MTX,

statins

Front 35

most common injury-inducing drugs =

(2)

Back 35

NSAID's,

antibiotics

Front 36

DILI is often subclinical; shows:

(2)

Back 36

1. asymp elevations in transaminases

2. which normalize when drug is withdrawn

Front 37

acute liver injury is caused by _____________(3 drugs)

and you could see ____________________ on LFT's

Back 37

Tylenol, amoxicillin, clavulanic acid

- could see elevated transaminases OR cholestatic appearance.

Front 38

"cholestatic" abnl LFT's =

(3)

Back 38

inc. GGT, AP, and tBili

Front 39

chronic liver injury is usually caused by _____ (drug)

Back 39

MTX

also amiadarone and tamoxifin, which mimic NAFLD

Front 40

PBC =

Back 40

cholestasis due to destruction of intrahepatic bile ducts

(some components of bile are toxic to hepatocytes)

=> progressive liver disease => cirrhosis

***doesn't necessarily have to cause cirrhosis***

Front 41

what does ursodiol do?

Back 41

thins out the thick, stuck bile

Front 42

what treats pruritis?

Back 42

cholestyramine

Front 43

in PBC, these 2 therapies are NOT effective:

Back 43

1. steroids - will worsen bone disease

2. liver transplants are RARE

Front 44

PSC = inflammation/sclerosis that leads to:

Back 44

obliteration of medium and large bile ducts

=> cholestasis

(intra- OR extrahepatic ducts)

Front 45

diagnosis for PSC is more invasive than for PBC;

Back 45

need to use cholioangiogram

Front 46

complications of PCS:

(5)

Back 46

1. cirrhosis

2. cholangitis (recurrent bacteremia)

3. cholelithiasis (gallstones)

4. choledocholithiasis (obstruction of CBD)

5. cholangiocarcinoma

Front 47

if PSC and Ulcerative Colitis occur together, you have a greater risk of:

Back 47

colon cancer

Front 48

treatment of PSC does NOT:

Back 48

stop progression

- meds might even be harmful

- treat only if symptomatic

Front 49

AI hepatitis: unlike PBC and PSC, it produces:

Back 49

hepatoCELLULAR injury

(not bile ducts)

- linked to HLA

Front 50

ALT lvl of AI hepatitis ~~

Back 50

alcoholic/NAFLD ~~ 200,


400

viral hep, tylenol OD ~~ 10,000

Front 51

liver biopsy of AI Hepatitis shows:

(2)

Back 51

plasma cell infiltrates and interface hepatitis

Front 52

Type I AIH is more common - lab features =

(2)

Back 52

1. ANA+

2. ASMA+

(anti-SM AB)

Front 53

Type II AIH is NOT ANA+, but:

Back 53

ALKM+

(liver/kidney/muscle AB)

Front 54

even after transplant, AIH can still:

Back 54

occur in the pt

Front 55

HHC is a primary cause of:

Back 55

hemochromatosis (inc. iron in the blood)

Front 56

4 secondary causes of iron overload:

Back 56

1. EtOH

2. HCV

3. NAFLD

4. transfusions

Front 57

primary and secondary causes of iron overload are distinguished by:

Back 57

blood work

Front 58

2 HHC genetic features:

(2)

Back 58

1. AR disorder

2. probably with HFE gene

Front 59

abnl HFE gene => abnl HFE protein, which is:

Back 59

necessary for crypt cells of the duodenum to take up iron from the gut

when abnl, => excessive absorption of Fe and low lvls of hepcidin production

Front 60

hepcidin normally prevents:

Back 60

iron storage

- when HFE prots are abnl, hepcidin lvls are low

=> iron overstorage

Front 61

2 main missense mut's of HHC:

Back 61

1. major = C282Y

2. minor = H63D

Front 62

ONLY there 2 phenotypes cause HHC:

Back 62

1. C282Y/C282Y

2. C282Y/H63D (cmpd heterozygote)

Front 63

consider HHC even if pt is asymp, to prevent:

Back 63

progression

=> risk for cirrhosis/HCC

Front 64

***a/o who is either over 50 y.o. or has ferritin >1000 MUST:***

Back 64

get a biopsy

- need to see if they're cirrhotic

Front 65

goal of HHC treatment is to get ferritin down to:

Back 65

<50,

Hb <11

Front 66

Wilson's Disease =

Back 66

failure of hepatocytes to excrete Cu into bile canaliculi => gets backed up into blood

Front 67

low AP and high tBili =

Back 67

Wilson's

Front 68

what does ceruloplasmin do?

Back 68

transplants Cu from the liver

- low in Wilson's

Front 69

which drugs get Cu out of blood quickly?

which drug prevent reaccumulation?

Back 69

D-penicillinmine and Trientine

- Zinc

Front 70

a1AT deficiency =

Back 70

failure to secrete a1AT from hepatocytes

Front 71

biopsy of a1AT def. shows:

(2)

Back 71

PAS+ hepatocytes (big, pinkish) and R to washout (diphasic)

Front 72

a1AT def. => liver disease due to:

Back 72

intrahepatic accumulation of a1AT,

lung disease due to unchecked elastase

Front 73

what's the only thing you need to diagnose steatosis?

Back 73

imaging

(U/S, CT)

Front 74

steatohepatitis MAY have:

Back 74

fibrosis

Front 75

differentiating NASH vs. ASH:

(2)

Back 75

NASH ~~

AST to ALT = 1:1,
mallory bodies are unrecognized

AHS = 2:1, organized

Front 76

***on CT a nl liver is _________ than the spleen; if it's ___________, it's a ___________ ____________***

Back 76

BRIGHTER than spleen;

if liver is darker, it's a *fatty* liver

Front 77

deposition of fat in steatosis tends to be near:

Back 77

CENTRAL venules,

but late-stage, it's near central AND PA's

Front 78

as steatohepatitis progresses, fat droplets:

Back 78

decrease, and eventually disappear

Front 79

NAFLD is the result of:

(2)

Back 79

1. oxidative stress

2. pro-inflammatory cytokines

Front 80

which combo of liver diseases is the WORST risk for cirrhosis/HCC?

Back 80

Hep C + FLD

Front 81

mallory bodies are seen in ASH, but also in:

Back 81

Wilson's, PBC, and chronic cholestatic conditions

Front 82

eosinophilic infiltrates are the result of:

(2 possible)

Back 82

1. drug-induced toxicity,

2. a1AT (within hepatocytes)

Front 83

**when LARGE bile ducts are blocked, **

(2)

Back 83

1. PA's expand

2. small bile ductules proliferate within PA's, adjacent to the limiting plate
(called ductule rxn)

Front 84

when large biles ducts are blocked, the centrilobular zones see:

(3)

Back 84

1. tiny bile canaliculi become distended due to thick bile retained

2. hepatocytes become brownish-green due to retention of bile pigments

3. toxicity of bile injures/kills hepatocytes

Front 85

pancreatic cancer can compress:

Back 85

the CBD

Front 86

choledocholithiasis =>

(5)

Back 86

1. ascending cholangitis

2. RUQ

3. jaundice

4. **PMN's in the walls/lumens of interlobular bile ducts**

5. s/ts, reflux of bile into pancreatic duct => severe pancreatitis

Front 87

nl liver: PA's are small, light purple;

Back 87

centrilobular areas are large and dark purple

Front 88

***histology of PBC = ***

(4)

Back 88

1. distorted intrahepatic ductules

2. with lymphocytes inside

3. granulomas may be present

4. ***bizarre, jigsaw-like cirrhosis***
(compared to round nodules of regular cirrhosis)

Front 89

3 features to distinguish AI hepatitis from viral hepatitis:

Back 89

1. plasma cells

and

2. acidophils (late)

3. ...near venules (portal OR central)

Front 90

why do women usually present with HHC LATER in life?

Back 90

b/c menstruation is a natural phlebotomy to prevent iron over-storage

Front 91

the spleen DOESN'T store:

Back 91

iron

=> on MRI, compare its color to liver, heart, pancreas to evaluate iron deposition

Front 92

grossly, HHC ~~

Back 92

dark brown/red discoloration of liver, pancreas

Front 93

**histo of HHC = **

Back 93

yellow-brown pigment WITHIN hepatocytes

Front 94

HHC => cirrhosis => HCC, which:

Back 94

won't show iron deposition at first

Front 95

when age and sex are counter to HHC, think:

Back 95

transfusion overload

~~ sickled RBC's

Front 96

Wilson's Cu accumulation begins at childhood;

- in teenage years, becomes:

(3)

Back 96

1. acute LF

2. chronic hepatitis

3. cirrhosis

Front 97

a1AT stain = brown; will see:

(2)

Back 97

1. eosinophilic hepatocytes

2. on PAS stain, AT granules at PURPLE

Front 98

the liver converts ammonia into:

Back 98

urea

Front 99

steatorrhea =

Back 99

abnl amount of fat in stool

Front 100

bilirubin is not itself a:

Back 100

bile acid

Front 101

90% of pts with cirrhosis will develop:

Back 101

varices

Front 102

a complete shunt bypasses:

Back 102

gastro-esophageal varices

Front 103

selective shunt = a not-complete shunt =>

Back 103

SOME flow through the portal vein is maintained

- you can shunt flow around collaterals too

Front 104

a transplant cures both:

Back 104

cirrhosis AND portal HTN

Front 105

portal veins are HUGE compared to:

Back 105

hepatic artery and bile duct

Front 106

at first, Hep B and C are:

Back 106

asymp

Front 107

In almost all cases of Hep B and C, liver enzymes can be:

Back 107

NORMAL

Front 108

Hep A and E are NOT:

Back 108

asymp

– they have flu-like, mild illness

Front 109

in liver disease, plat’s tend to get sequestered in:

Back 109

the spleen

=> splenomegaly

Front 110

2 major categories of injury from liver disease:

Back 110

Hepatitis/hepatocellular or cholestatic

Front 111

hepatitis injury IS:

Back 111

hepatocellular injury

Front 112

before Prussian blue staining, Iron deposition is:

(color)

Back 112

golden brown

Front 113

Acute hepatitis is RARELY __________

Back 113

biopsied

Front 114

Normal hepatocytes ~~

Back 114

GRANULAR/ROUGH cytoplasm edges

Front 115

Remember, well-formed *lymphocyte nodules * on histology ~~

Back 115

Hep C

Front 116

Sarcoidosis => elevated:

Back 116

ACE

Front 117

Sickled cells in sinusoids on histology ~~

Back 117

transfusion iron overload, not HHC

=> Chelation, reduce transfusion frequency

Front 118

2 features of Steatosis:

Back 118

1. NORMAL LFT’s

2. reversible

Front 119

Complications of PBC are the same as for:

Back 119

PSC

Front 120

Chicken-wire perisinusoidal fibrosis ~~

Back 120

steatohepatitis

Front 121

Cirrhosis is DIFFUSE – there won’t be completely normal parts of the liver in cirrhosis.

therefore, think:

Back 121

Focal nodular hyperplasia

Front 122

Hemangiomas ~~ significant bleeding =>

Back 122

DON’T biopsy

Front 123

other features of Hemangiomas:

(3)

Back 123

1. TONS of blood on biopsy/histology

2. NOT a primary liver

3. BENIGN