Hepatitis and Cirrhosis Flashcards
1
Q
LFTs?
A
Enzymes
- aminotransferases: ALT & AST
- AP
- GGT
synthetic fxn:
- serum albumin
- PT
Bili
2
Q
What are impt hx ?s to ask if you are concerned about liver disease?
A
- exposure to chemicals, meds, herbs
- accompanying sxs
- parenteral exposure
- IV and intranasal drug use
- tattoos and piercings
- sexual activity
- travel and exposure hx
- ETOH hx
3
Q
PE findings that suggest liver disease?
A
- cachexia: malnourishment (drinks a lot, drug user)
- stigmata of longstanding liver disease
- signs of alcoholic liver disease: acutely - large, if cirrhotic - small
- enlarged L supraclavicular node - HCC
- JVP suggests RHF secondary portal HTN
- R pleural effusion in absence of advanced ascited can be seen in cirrhosis (this can cause portal HTN)
4
Q
What is autoimmune hepatitis? Type 1 and type 2?
A
- chronic hepatitis: pp isn’t well understood
type 1 (classic): occurs in women of all age groups
type 2 (ALKM-1): occurs in girls and young women - characterized by circulating autoabs (not thought to be part of pp)
- high levels of serum globulin concentrations
5
Q
Clinical manifestations of autoimmune hepatitis?
A
- can be asx
- subclinical and those presenting with advanced cirrhosis
- fulminant hepatitis
- labs:
presence of serological markers
generally aminotransferases more elev than bili and AP
6
Q
Extrahepatic manifestations of autoimmune hepatitis?
A
- hemolytic anemia
- thyroiditis
- celiac sprue
- ITP
- DM I
- UC
(all of these are autoimmune)
7
Q
Tx of autoimmune hepatitis?
A
- corticosteroids for sx disease
risks/complications of steroids: - short term: HTN, high glucose, psychosis, insomnia, gastric irritation
- long term: osteoporosis, cataracts, PUD, immunosuppression
- azathioprine - 2nd line agent
8
Q
What is hemachromatosis?
A
- genetic disease due to autosomal recessive
- identified gene: HFE
- most common single gene disorder:
10% caucasians heterozygous
0.5% caucasians homozygous
very rare in other pops
9
Q
PP of hemochromatosis?
A
- gene defect results in increased iron absorption in the intestinal tract from the diet
- iron overload in the body
- eventual fibrosis and organ failure:
cirrhosis
cardiomyopathy
diabetes
hypogonadism
10
Q
Hematochromatosis - iron overload in the body? Why do females have delayed sxs?
A
- normal Fe: 3-4 mg/day
- normally Fe storage is controlled so there is no excess accumulation
- accum of 500-1000 mg/yr occurs in hemochromatosis
- sxs usually occur around age 40 or when Fe stores reach 15-40 g
- females have delayed sxs b/c of menstruation and breast feeding
11
Q
Clinical manifestations are influenced by what factors?
Classic presentation?
A
influenced by:
- age
- sex
- alcohol use
- dietary iron
- menstruation and breast feeding
- unkown factors
- alcohol abuse and hep C accelerate the process
- classic presentation: cutaneous hyperpigmentation w/ diabetes and cirrhosis
12
Q
Reversible manifestations of hemochromatosis?
A
- CV:
infections - cardiomyopathy (vibrio vulnificus)
conduction of disturbances
(monocytogenes)
- Liver: pastcuerlla pseudotubercullosis: abdominal pain, elevated LFTs, hepatosplenomegaly - skin: bronzing (melanin deposition) grayness (Fe deposition)
- listeria
13
Q
Irreversible manifestations of hemochromatosis?
A
- liver: cirrhosis, HCC
- anterior pituitary gland: gonadotropin insufficiency- hypogonadism
- pancreas: DM (30-60%)
- thyroid: hypothyroidism
- genitalia: primary hypogonadism
- jts: pseudogout
14
Q
Dx hemochromatosis?
A
- combo of:
clinical
lab: elevated serum transferrin sat of more than 45%, elevated serum ferritin (this is pathologic) - confirmation = gold std = liver bx (also defines extent of disease)
15
Q
Tx hemochromatosis?
A
- education for evidence of iron overload/complications: avoid red meat, Fe supps avoid ETOH avoid handling or eating raw seafood (increased risk of infections) receive vaccinations for Hep A and B - mainstay of tx: phlebotomy: removing 500 ml of blood removes 250 mg iron - do weekly until iron depletion: Hgb = 10-12 gm/dl ferritin less than 50 transferritin sat is less than 50% - maintenance: phlebotomy q 2-4 months
16
Q
Genetic testing for hemochromatosis?
A
- screen 1st degree relatives, unless under 18
- likely to uncover homozygotes who are asx
- screening test cost: $200, done on whole blood sample
17
Q
What is Wilson’s disease?
A
- hepatolenticular degeneration
- autosomal recessive
- affects copper metabolism
- organ damage due to copper build up in liver and brain
- easily tx if dx early
- difficult to dx
18
Q
Epidemiology and pathogenesis of Wilson’s disease?
A
- occurs worldwide: prevalence - 1/30,000 live births
- 1/90 persons carry the abnormal gene ATP7B
- pathogenesis:
gene affects the carrier protein of copper which is primarily in hepatocytes - it also impairs the excretion of copper via bile
19
Q
Clinical manifestations of Wilson’s?
A
- presentation varies widely and is often non-specific
- generally presents b/t 1st-3rd decade:
liver disease (usually presenting sx in young kids)
neuro sxs
psych sxs
20
Q
Dx and prognosis of Wilson’s
A
- dx:
ceruoplasmin level
24 hr urine for copper excretion
look for kayser fleischer rings in eyes - prognosis:
universally fatal if left untx
once dx chelation therapy with D-penicillamine is toc (lifelong)
21
Q
What are the 3 stages of alcoholic liver disease?
A
- fatty liver (steatosis)
- alcoholic hepatitis
- alcoholic fibrosis and cirrhosis
22
Q
Fatty liver - etiology, presentation, labs?
A
- most pts are asx
- can occur w/in hours of large alcohol binge and if continues to drink - it can progress
- may have tender hepatomegaly
- transaminases mildly elevated
- can also occur in obese individuals and pregnancy
23
Q
alcoholic hepatitis presentation?
A
- asx to extremely ill
- anorexia, N/V, wt loss, abdominal pain, poor nutritional status
- HSM
- jaundice
fever is common
24
Q
PE of alcoholic hepatitis?
A
- spider angiomas
- palmar erythema
- gynecomastia
- parotid enlargement
- testicular atrophy
- ascites
- encephalopathy
25
Q
Lab findings in alcholic hepatitis?
A
- leukocytosis w/ left shift (in severe disease)
- anemia: most likely be macrocytic from B12 and folate deficiency, may have microcytic from GI blood loss
- transaminases elevated: AST:ALT ratio usually greater than 2:0 (ratio rarely seen in other forms of liver disease)
- increased AP (less than 3x the normal)
- hyperbilirubinemia (60-90%) - jaundice
- hypoalbunemia (severe disease)
- coagulopathy (severe)
- elevated ammnonia level (severe)
26
Q
Complications of alcoholic LD?
A
- alcoholic fatty liver is reversible
- alcoholic hepatitis: is usually reversible, but may run a fulminant course progressing to fibrosis and death
- long standing alcoholic liver disease can lead to cirrhosis
- others:
GI bleeds
esophageal varices
gastritis/PUD
27
Q
When do you see mallory bodies?
A
- when protein filaments are damaged in hepatocytes, appear pink on stain
- primarily seen with alcholic LD and wilsons
- will also see in HCC, even morbid obesity, assoc with severe liver disease
28
Q
Tx of alcoholic LD?
A
- cessation of alcohol!!
- supportive tx:
nutrition
B12 and folate
fluids
R/O other causes for fever, liver disease such as Hep C, hemochromatosis, neoplasms
glucocorticosteroids for severe hepatitis - liver transplant in approp pts
29
Q
What are factors influencing toxicity in toxic hepatitis?
A
- excessive intake
- excessive cytoP450 activity
- decrease metabolism pathways in liver
- depletion of glutathione stores
- concomitant use of alcohol or other drugs
- comorbid illness
- advancing age
- nutritional status
30
Q
Prevalence of drug-induce liver injury (DILI)?
A
- annual incidence w/ prescription meds 1/10,000
- DILI accounts for 10% of all adverse drug rxns
- **DILI most common cause of liver failure in the US
- over 1000 meds and herbal products have been implicated in development of DILI
31
Q
Level of injury of DILI?
A
- many drugs induce asx elevations in liver enzymes w/o causing disease
- DILI most common liver injury caused by drugs and accounts for 10% of all cases of acute hepatitis
- may be cholestasis, cytotoxic or mixed, less likely steatosis
- usually d/c of agent results in complete recovery
32
Q
Most common drugs implicated in DILI in US?
A
- acetaminophen
- abx
33
Q
Tx for acetaminophen overdose?
A
- get an acetaminophen level
- activated charcoal if ingested w/in 2-3 hrs
- N-acetylcysteine for severe overdose
34
Q
Signs and sxs of chronic acetaminophen intoxication? What pts are at the greatest risk for developing hepatotoxicity?
A
- signs and sxs are nonspecifc: confused w/ viral dx
- ask about acetaminophen usage, dosing
pts who are at greater risk for developing hepatotoxicity:
- ingestion of more than 7.5-10g over 24 hrs
- ingestion of less than 4 g with increased susceptibility
- liver tenderness, jaundice or ill-appearing
- supratherapeutic acetaminophen concentrations (over 20 mcg/mL)
35
Q
Tx with NAC is recommended for which pts?
A
- all pts with liver tenderness and
- elevated aminotransferases and
- serum acetaminophen concentrations over 10 mcg/mL
- if serum acetaminophen concentrations are potentially toxic by the nomogram
36
Q
General presentation of HAV, HBV, HCV, HEV?
A
- many cases can be asx especially in kids
- usually prodrome after exposure:
malaise and fatigue
anorexia, N/V
myalgias
pale stools, dark urine
jaundice
37
Q
General signs of Hepatitis infection on exam?
A
- jaundice
- RUQ pain
- +/- hepatomegaly
38
Q
Labs in Hepatitis infection?
A
- transaminases elevated, usually in 1000s with ALT more increased than AST
- hyperbilirubinemia
- bilirubinuria
- AP mildly elevated
- WBC normal to low
- may have prolonged PT
