D & M Ii: Hepatology

Front 1

liver function tests

Back 1

1. ALT (SGPT): amino alanine transferase, formerly alled serum glutamic-pyruvic transaminase

2. AST (SGOT): asparate amino transferase, formerly called serum glutamic oxalaceric transaminase, measure cellular integrity

3. prothrombin time and albumin reflext the liver's synthetic capacity

4. bilirubin, gamma-glutamyl transpeptidase (GGT), and alkaline phophatase measure hepatic excretory function

Front 2

evaluation of cellular integrity

1. AST

2. ALT

3. AST/ALT ratio

4. GTT

Back 2

1. alcohol intake most common reason to elevate AST, could also be due to MI and MSK injury

2. ALT highest in toxin or drug induced, viral or ischemic hepatitis

3. ALT > AST: hepatitis

AST > ALT: alcohol ratio > 2:1

4. elevated GTT confirms hepatic origin

Front 3

evaluation of cellular integrity

1. Alkaline phosphatas elevated, GGT elevated

- ALP elevated and GTT is normal

Back 3

1. bilarysource, obstruction, infiltration, congestion

2. isoenzymes liver, bone, intestinal, regan's or placental/carinoplacental- some kind of growth turn over, ie could be cancer

Front 4

evaluation of excretory function

1. ALP

2. elevated bilirubin

3. GTT

Back 4

1, ALP has origin in multiple tissues

- may be normally elevated in late pregnancy, childhood/adolescence

- elevation correlates with cholestatic injury

2. elevated bilirubin: cholestasis or liver damage, things are sitting there and not moving which is why bili is elevated

3. sensitive indicator of hepatic disease, particularly caused by drugs, chemicals or alcohol

Front 5

evaluation of protein synthesis

1. what can impact albumin synthesis?

2. what does elevated PT mean?

how do you differentiate between problems?

Back 5

1. albumin synthesis can be affected by liver disease, dietary protein, alcohol, trauma, and corticosteroids-- all impact albumin synthesis

2. elevated PT may be due to one of these factors or due to Vit K deficit

- administer vit K 10 mg IM and check PT 24 hours later to differentiate liver disease or Vit K deficiency

- if PT improves by at least 30% then synthesis is intact and it's not a liver problem

- know that there are ways to piece out where the problem is coming from

Front 6

causes of chronic liver disease

1. what's the number one issue?

2. other causes (2)

3. immunological

4. genetic/metabolic

Back 6

1. alcohol

2. viral, non-alcoholic fatty liver disease, chronic changes in the liver

3. immunological

- autoimmune hepatitis

- primary sclerosing cholangitis

- primary biliary cirrhosis

4. genetic/metabolic

- hereditary hemochromatosis: cannot get rid of iron, sits in the liver

- WIlson's disease-- copper overload, sits in the liver and cannot be removed from the body

- alpha 1: antitrypsin deficiency: genetic problem where cannot produce certain proteins that protect the liver

Front 7

history for abnormal LFTs

what should you ask?

Back 7

patient may be asymptomatic or if they do have symptoms: anorexia, malaise, weight loss, puritis

- ask for a detailed medication history

- PMH: hepatitis (or symptoms of), abdominal surgery, blood transfusions (before 1992 before blood was screened for Hep B)

- alcohol intake

- sexual history

- household/work exposure to chemicals

- family history of liver disease

Front 8

physical exam

Back 8

sclera for icterus

- skin exam: spinder angioma (increased portal hypertension), palmar erythema (red palms), jaundice

- abdominal exam: ascites, RUQ tenderness, hepatomegaly- measure liver, splenomegaly

- neuro exam: asterixis neurological sign of hepatic insuffiency

Front 9

investigation of abnormal LFT

1. history

2. viral markers

3. cause of hep B outbreak

4. cause of hep C outbreak

Back 9

1. history: alcohol, drugs, sex, blood, travel, PMH, FH

2. viral makers

- HCV antibody (HCV Ab)

- hepatitis B surface antigen (HBsAg)

Hepatitis B assicated with infection control breaks during assisted monitoring of blood glucose

4. Hep C outbreak in hemodialysis setting

Front 10

investigation of abnormal LFT

5. immunoglobulins, if elevated then these are most common causes

6. auto antibodies - just know these exist

Back 10

5. immunoglobulins, if elevated then these are the common cause s

- IgG: auto immune hepatitis (AIH)

- IgM- primary bilary cirrhosis (PBC)

- IgA alcohol

all 3: cirrhosis but doesn't help us diffentiate the cause

6. autoantibodies

- ANA: autoimmune hepatitis (AIH), primary sclerosing cholangitis (PSC), PBC

- A-SM anti smooth muscle that's positive, AIH, PSC

- A-LKM anti liver kidney muscle antibody AIH

- AMA: antimitochondrial-- PBC

- P ANCA (used for UC)- PSC (link with PSC and UC)

Front 11

investigation of abnormal LFT

7. hemochromatosis

8. Alpha 1 anti trypsin deficiency

9. Wilson's diease

10. Imaging

Back 11

7. iron overload

- ferritin

- consider HFE genotype, transferrin saturation levels to find them elevated, elevated LFT

8. Alpha 1 anti-trypsin deficiency

- A1AT level

9. copper check the caeruloplasmin

10. ultrasound to see if there's liver inflammation, any kind of other structural issues with the liver

Front 12

chronic liver disease screen (7)

Back 12

1. HbsAg: hepatitis surface antigen is positive says you're immune to Hep B

2. HCV Ab: hep C antibodies

3. Igs and auto antibodies to r/o on someone with chronic liver disease

4. ferritin

5. A1AT

6. AFP alpha feto protein to check liver tumors for liver cancer

7. +- caeruloplasmin/copper

Front 13

liver disease severity

1. biochemical - what are you thinking about (3)?

2. Clinical- what does the patient look like (3)?

Back 13

1. biochemical

a. albumin

b. PT: make sure they're making vit K

c. bilirubin

2. clinical

a. ascities

b. hepatic encephalopathy

c. nutritional status

Front 14

radiology

1. why?

2. what tests (5)?

Back 14

1. to see structural changes

2.

abdominal ultrasound (not the best): could detect obstruction but not fully reliable bc the patient could have a contracted gallbladder, bile duct stones

HIDA (hepatobiliary iminodiacetic acid scan)

CT: shows structure

magnetic resonance cholangiopanreatography (MRCP) shows structure

other: endoscopic retrograde cholangiopancreatography (ERCP) refer to specialist: shows structure

Front 15

child pugh score for cirrhosis severity

Back 15

draw it

child's A 6 or less

child's B 7-9

child's C 10+

Front 16

pros/conts with child pugh score

Back 16

pros:

- simple

- easily calculated

- good predictor

cons:

- subjective measure

- "ceiling" effect - if bili > 300, alb 19 scores the same as bili 65, alb 26

Front 17

other liver severity score

1. when is it used?

2. list two

Back 17

1. used in transplant listing decisions

2. a. MELD: model for end stage liver disease to determine if the patient needs transplant

b. INR / bilirubin/ creatinine

Front 18

caveats

Back 18

- abnormal LFTs do not always indicate liver disease

- normal LFTs do not always exclude liver disease

- HCV- 1 out of 6 patients with persistently normal ALT will have significant pathology on liver biopsy

- clear link between ALT elevation and liver mortality, even for values within normal range as their LFTs go their mortality goes up rapidly

- in a community setting >70% with abnormal imaging (fibrosis on US) had normal LFTs, very patient specific and make sure to watch their numbers

Front 19

differential diagnosis

1. elevated ALT and AST (3)

2. elevated Alkaline Phosphatase (3)

3. elevated bilirubin (1)

Back 19

1. a. alcoholic or viral hepatitis; \

b. cytotoxic drugs,

c. NASH/NAFLD (non-alcoholic steatohepatitis- fatty liver disease)

2. a. obstruction of biliary system

b. intrahepatic: medications or infiltrative

c. extrahepatic: gallstones

3. may be elevated in hepatitis

Front 20

plan

1. what's the first step?

2. then what?

Back 20

1. diagnostic testing

2. no underlying cause is found and patient is asymptomatic, observe 1-3 months for progressive symptoms and liver dysfunction

- do further lab testing, if abnormal refer to specialist

Front 21

therapeutic recommendations

Back 21

1. maintain caloric intake 2000-3000 cal/day

2. prohibit the use of alcohol or hepatotoxic agents

3. avoid sedatives

4. monitor PT, serum albumin, and bilirubin esp for synthetic function

5. daily weights, regular hemoccult testing

6. check for signs of encephalopathy at each visit

7. check abdomen for signs of ascites

Front 22

jaundice

1. define

2. common causes

3. newborns (who cares?)

4, infant/child

5. elderly

Back 22

1. yellowish staining of the skin, sclera and mucous membranes by bilirubin, yellow-orange bile pigment (bili >2.5-3)

2. obstruction, intrahepatic cholestasis, hepatocellular injury

3. indirect or unconjugated hyperbilirubinemia (physiologic jaundice)

4. hepatitis

6. stones or tumor

Front 23

jaundice

prehepatic

1. finding

2. cause

Back 23

1. increased levels of unconjugated (indirect) bili

2. bilirubin hemolysis and hematoma resorption

Front 24

jaundice intrahepatic

1. finding

2. cause

Back 24

1. increased unconjugated or conjugated bili

2. alcohol, infectious hepatitis, drug reactions, and autoimmune disorders

Front 25

jaundice posthepatic

1. finding

2. cause

Back 25

1. increased conjugated bili

2. gallstone formation is most common

differential diagnosis also includes serious conditions such as biliary tract infection

- pancreatitis

- malignancies

Front 26

jaundice differential diagnosis

Back 26

hepatitis, infectious

hepatitis, autoimmune

drug reaction

hemolytic anemia

hereditary syndromes

cirrhosis

cholestasis

postoperative

cholestatic jaundice secondary to pregnancy

infectious mononucleosis

sarcoidosis

lymphoma

toxins

cholangitis

tumor

pancreatitis

hepatobiliary tuberculosis

Front 27

jaundice management

1. main goal

2. when to give liver biopsy?

3. cholangitis

4. diet

Back 27

1. treat underlying disease process

2. if LFTs fail to return to normal after 6 months

3. antibiotics, ERCP with dilation

4. high protein (vegetable proteins), low sodium, no alcohol

Front 28

jaundice management

5. supplement

6. what should you avoid?

7. puritis

8. others

Back 28

5. MVI, folic acid

6. barbituates and sedatives

7. laculose (to reduce blood ammonia levels 20-30 g

rifaziman if encephalopathy worsening on lactulose

8. bile acid sequestrants- cholestyramine TID, anti-hystamines, mild soaps, emollients

Front 29

inflammation of the liver

causes

Back 29

1. alcohol

2. medications

3. viruses

4. autoimmune diseases

5. metabolic diseases

Front 30

common medications that cause hepatitis

Back 30

acteaminophen

allopurinol

high dose aspirin

captopril

carbamazepine

isonazid

ketaconazole

methyldopa

NSAIDs

procainamide

sulfonamides

Front 31

viral hepatitis stages

I

II

III

IV

Back 31

I: incubation: no subjective or objective signs of disease

II: prodromal- anorexia, n/v, malaise, upper respiratory infection symptoms, myalgia, arthralgia, fatigue, abdominal pain

III: icteric: jaundice, dark urine, pale stools

IV: convalescent: improved well being

Front 32

prevention of hepatitis - general

Back 32

vaccines can prevent against hep A &

Hep A for kids 12-23 months and adults that travel or work in locations with higher prevalence of hep A infection

vaccination for hep A should be given to people with hep B & C

no vaccine for hep C

Front 33

prevention of hepatitis - pregnant

Back 33

if a pregnant woman has chronic hep B then the infant should get hep B vaccine and hep B immune globulin to prevent the development of chronic hep B

Front 34

patient presentation with viral hep

Back 34

most are asymptomatic

- anorexia, fatigue, myalgias, n/v, fever, headache, arthralgia, abd pain

- jaundice with hep B

- hep B & D are clinically indistinguishable

Front 35

hep A

1. what kind of virus?

2. transmission (3)?

3. symptoms

4. when is it infectious?

5. CDC recommendations

Back 35

1. RNA virus

2. transmission

a) fecal oral

b) person to person

c) ingestion of contaminated food or water

3. fever, jaundice, anorexia, nausea, malaise, myalgia, could be asymptomatic

4. infectious 2 weeks before symptoms and 1 week after, no carrier state or chronic illness

5. travel advisories that identify countries with outbreaks or endemic hepatitis A

eating raw or uncooked food increases risk for hep A

Front 36

hepatitis A testing

Hep A Ab IgM

Hep A Ab IgG

does the virus go away?

stats for remission and progression

Back 36

IgM for acute illness

IgG for past infection or immunity

virus does not remain in the body after the infection has gone away

over 85% of people with Hep A recover within 3 months, 99% of patients get better within 6 months

there are usually no complications. 1/1000 become fulminant hepatitis which can be life threatening

Front 37

hepatitis A treatment

Back 37

- supportive care

- LFTs every 2 weeks until normalize

Front 38

hep B

1. what kind of virus

2. transmission in:

a) asia and africa

b) north america and europe

3. outbreaks

Back 38

1. DNA virus

2. a) vertical

b) percutaneous tranmission

3. 82% associated with infection control breaks during assisted monitoring of blood glucose

Front 39

risk factors for hep B

Back 39

1. unprotected sex with more than one partner

2. unprotected sex with someone who is infected with HBV

3. shares needles during IV drug use

4. share a household with someone who has chronic HBV infection

5. have a job w/ exposure to human blood related needle sticks

6. hemodialysis for end stage kidney disease

7. travel to regions with high infection rates of HBV ( africa, central and southeast asia, and eastern europe)

Front 40

vaccination recommendations for Hep B

Back 40

- kids younger than 18, including newborns esp those born to mothers with HBV

- health care and public safety workers who may be exposed to bloody people, have hemophilia or other blood clotting disorders and receive transfusions of human clotting factors

- people who require hemodilaysis for kidney disease

- travelers to countries where HBV infection is common

- inmates

- people who live in residential facilities for developmentally disabled persons

- IV drug users

- people with chronic liver disease like hep C

- people who have multiple sex partners or ever had a STI

Front 41

candidates for screening for HBV

Back 41

- all pregnant women

- patients with high endemic areas (asia and africa)

- household and sexual contacts of HBsAg positive patients.

- IV drug users

- multiple sex partners, history of STI

- inmates of correctional facilities

- individuals with chronically elevated ALT/AST

- individuals infected with HIV or HCV

- patients undergoing dialysis

Front 42

concentration of HBC in various body fluids

1) high

2) moderate

3) low/ not detectable

Back 42

1) blood, serum, wound exudates

2) semen, vaginal fluid, saliva

3) urine, feces, sweat, breast milk, tears

Front 43

hep B immune globulin

1. names and who to give it to (5)

2. why give immune globulin and vaccine together?

Back 43

1. Hep B immune globulin (BayHep B, Nabi-HB) is given with hep B vaccine to unvaccinated people who have been exposed to Hep B.

- includes close contacts of people with HBV infection

- health care workers exposed to HBV contaminated blood

- infants born to mothers infected with HBV

- people who have finished only part of 3 shot vaccination series

2. prevents transmission of the disease in 80-90% of cases

Front 44

hep B treatment

1. when is treatment recommended?

2. first line agents

3. time period

Back 44

1. treatment is recommended when HBeAG + and HBV DNA viral level >20,000 IU / mL (if <20,000 IU/ mL monitor every 6-12 months)

2. tenofovir, entecavir, and peginterferon are preferred first line agents

3. tx should continue for 12 months after HbeAG seroconverts to negative and HBV DNA undetectable

Front 45

Hep C

1. kind of virus

2. how many genotypes

3. transmission?

Back 45

1. single stranded RNA

2. 6 major types which are indicated numerically and multiple subtypes

3. blood to blood contact, mother- to - child transmission (vertical transmission) of HCV ~6 out of 100

no documented transfusion related case of HCV in US for over a decade

Front 46

Hep C (acute)

1. what does it refer to?

2. symptoms

3. what percentage of patients clear the virus without treatment and do not develop chronic infection?

Back 46

1. first 6 months after infection with HCV. 60-70% of people infected have no symptoms during the acute phase

2. symptoms of acute hepatitis C include decreased appetite, fatigue, abdominal pain, jaundice, itching, flu-like symptoms

3. 15-25% , reasons not well known

Front 47

Hep C (chronic)

1. when is hep C detectable?

2. definition

3. which test do you need and why?

4. risk factors for HCV

Back 47

1. 1-3 weeks after infection by PCR and antibodies are detectable within 3-15 weeks

2. chronic hep C is defined as infection persisting for more than 6 months, clinically, it's often asymptomatic

3. liver biopsy will show the rate of progression of fibrosis or scarring.

1/3 pts progress to cirhosis (stage 4 fibrosis) in less than 20 years

another 1/3 progress within 30 years

4. increasing age, male gender, alcohol consumption, HIV and co-infection and NAFLD

Front 48

Hep C treatment

1. list meds (6)

2. which one is an injection?

3. what should you know about treatment?

Back 48

1. Interferon, ribavirin (rebetol, copegus) and beceprevir (or telaprevir)

2. interferon is IM while all the rest are pills

3. combination of these drugs (all 3) can cure all but a small proportion of patients however serious side effects of treatment can occur

Front 49

Hepatitis D

1. kind of virus, what kind of genotypes

2. when transmitted

3. why has it decreased?

4. where is it endemic?

Back 49

1. RNA virus that requires co-infection with HBV for replication, 8 genotypes

2. transmitted with HBV or super-infected in a patient with HBV

3. in the past 20 years HDV transmission has decreased because of the HBV vaccine

4. Endemic in Asia, North East Africa, Middle East, and Mexico ~70% prevalence

Front 50

Hepatitis E

1. what kind of virus and with how many genotypes?

2. cause of?

3. how long does it last?

4. how is it spread?

5. pregnancy considerations

Back 50

1. RNA virus w/ 4 known genotypes

2. common cause of acute hepatitis in adults in Central and South Eastern Asia

3. self limited disease

4. enterically spread, most commonly in contaminated water

5. infection during pregnancy with HEV leads to liver failure and death, esp in 3rd trimester

Front 51

Alcoholic Hepatitis

1. cause

women:

men:

2. percentage of heavy drinkers that develop alcoholic hepatitis

3. additional risk factors

Back 51

1. chronic consumption of excessive alcohol

women: 10-20 g daily (3-6 oz wine, 10-20 oz beer, 1-2 oz hard liquor)

men: 20-40g daily (6-12 oz wine, 20-40 oz beer, 2-4 oz hard liquor)

2. 10-35% of heavy drinkers develop

3. additional factors that increase risk of alcoholic hepatitis

- genetics

- environment

- age

- BMI: men >27, women >25

Front 52

non-alcoholic fatty liver disease

Back 52

- spectrum of chronic liver diseases assocaited with metabolic syndrome

- most common chronic liver disease

- most serious NAFLD: non-alcoholic steatohepatitis (NASH)

NASH can lead to cirrhosis

Front 53

drug induced liver injury

1. common with?

2. 1/2 of all acute liver failure is caused by?

Back 53

1. NSAIDs and antimicrobials

2. 1/2 of all acute liver failure is caused by hepatotoxicity

possibly genetic predispodition

- more than 800 therapeutic agents have been implicated in drug induced liver injury

- prescriptions, over the counter meds, nutritional supplements, herbal remedies

Front 54

drug induced liver injury

what are the two patterns of drug induced liver injury?

Back 54

1. allergic reaction

- occurs within 6 weeks of starting a drug

example: dilantin

2. metabolic reaction

- can manifest after a year of continued usage

example: isoniazid

Front 55

autoimmune hepatitis

1. frequency

2. sex and racial prevalence

3. type 1 AIH

4. common with?

Back 55

1. rare

2. female > male, all ages and ethnicies

3. adolescence or young adults, ~70 of cases

4. common with other auto immune diseases

Front 56

AIH symptoms

Back 56

- fatigue

- joint pain

- nausea

- anorexia

- RUQ pain

- skin rashes

- dark urine

- light stools

- jaundice

Front 57

AIH diagnostics

1. autoantibodies (4)

which indicates most severe disease?

2. procedure

Back 57

1. a. ANA

b. anti-smooth muscle antibody (SMA)

c. anti-liver kidney muscle (LKM)- LKM 1 indicates most severe disease

d. anti soluble liver antibody (SLA)

- 20% of cases no antibodies present

2. liver biopsy

Front 58

AIH treatment (3)

Back 58

1. corticosteroids

2. immune system suppressors (azathioprine)

3. transplant

Front 59

primary sclerosing chlangitis (PSC)

1. define

2. what does it lead to

Back 59

1. disease of bile ducts, inflammation and obstruction both intra and extra hepatic

2. leads to cirrhosis, liver failure, and hepatocellular carcinoma

~80% of patients with PSC have ulcerative colitis

Front 60

primary sclerosing chlangitis (PSC)

diagnostics

list the tests

Back 60

80% of patients will have perinuclear anti neutrophil cytoplasmic antibodies (P-ANCA)

ANA & ASMA + 20-50% of cases

ERCP

MRCP

Front 61

primary sclerosing chlangitis (PSC)

symptoms

Back 61

- fatigue

- jaundice

- pruritus

- malabsorption

- heaptomegaly

- cholangitis

- hepatic encephalopathy

Front 62

primary sclerosing chlangitis (PSC)

treatment

Back 62

- ursodiol- a bile acid reduces LFTs but has not been shown to improve survival

- pruritus bile acid sequesterants- cholestyramine

- antibiotics for episodes of cholangitis

- vitamin supplements: A, D, E, and K

- ERCP with dilation

- liver transplant

Front 63

primary biliary cirrhosis (PBC)

Back 63

- autoimmune disease

- slow, progressive destruction of small bile ducts in the liver, leads to cholestasis, scarring, fibrosis and cirrhosis

1 in 3,000

9: 1 female to male ratio

Front 64

PBC symptoms

Back 64

- fatigue

- jaundice

- pruritus

- xanthoma

- xanthelasma

- ascites

- splenomegaly

- esophageal varices

- hepatic encephalopathy

Front 65

PBC diagnostics

Back 65

> 90% + anti-mitochondial antibodies (AMA)

- ANA

- US

- CT scan

- ERCP

Front 66

PBC

treatment

Back 66

- ursodiol

- cholestyramine

- alcohol contraindicated

Front 67

cirrhosis

1. define

2. treatment

3. what can it lead to?

Back 67

1. irreversible state of chronic liver injury (Stage IV scarring)

2. best treatment is prevention

3. address causes that lead to it:

chronic hepatitis

chronic alcohol abuse

hemochromatosis

primary bilary cirrhosis

Front 68

cirrhosis

complications

Back 68

- ascites

- peripheral edema

- encephalopathy infection

- bleeding

- renal dysfunction

- electrolyte imbalances

Front 69

cirrhosis: clinical presentation

subjective (4)

Back 69

- fatigue

- easy bruising

- abdominal swelling

- ankle edema

Front 70

cirrhosis: clinical presentation

objective (2)

Back 70

1. portal hypertension

- splenomegal

- abdominal distension- shifting dullness

- prominent abdominal venous pattern

2. chronic failure

- palmar erythema

- spider angiomas

- parotid hypertrophy

- loss of pubic or axillary hair

- clubbing

- gynecomastia