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GI 2 > Hepatitis Cirrhosis > Flashcards

Hepatitis Cirrhosis Flashcards

1
Q

Liver Function Tests:

  • what are the enzyme tests?
  • test for synthetic function?
A

Enzymes:

  • ALT, AST
  • ALP
  • Gamma glutamyl transpeptidase (GGT)

Synthetic Function:

  • serum albumin
  • PT

Bilirubin

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2
Q

Autoimmune Hepatitis

  • what are the types? MC in which gender and age?
  • Characterized by?
  • clinical manifestations
  • labs
A

Chronic Autoimmune Hepatitis:
Types:
-Type 1 (Classic): occurs in women of all age groups
-Type 2 (ALKM-1): occurs in girls and young women

Characterized by circulating autoantibodies (not part of pathophys) & high levels of serum globulin concentrations

Clinical Manifestations:

  • asymptomatic
  • fulminant hepatitis

Labs:

  • serological markers
  • aminotransferases (ALT AST) more elevated than bilirubin and ALP.
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3
Q

Autoimmune Hepatitis

  • extraheptaic manifestations
  • Tx
A

Extrahepatic manifestations:

  • hemolytic anemia
  • thyroiditis
  • celiac sprue
  • ITP
  • T1DM
  • UC

Tx:

  • corticosteroids for symptomatic dz
  • azathioprine 2nd line agent (immunosuppressant)
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4
Q

Short term SE of corticosteroids?

A

HTN, Hyperglycemia, psychosis, insomnia, upset stomach.

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5
Q

Hemachromatosis:

  • cause
  • pathophysiology
  • late manifestations
A

Cause: genetic; autosomal recessive, gene HFE

Pathophys:
-gene defect results in increased iron absorption in the intestinal tract from the diet. (Iron overload in the body)

Late manifestations:

  • eventual fibrosis and organ failure
  • cirrhosis
  • cardiomyopathy
  • DM
  • Hypogonadism
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6
Q

What is normal iron content in the body?

How much iron accumulation occurs in hemochromatosis?

What level of Fe in the body when sx occur?

A

Normal iron content in the body is 3-4mg/day ‘

Accumulation of 500-1000 mg/yr of iron occurs in hemochromatosis

Sx usually occur around age 40 or when iron stores reach 15-40g
*females may have delayed sx b/c of menstruation & breast feeding

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7
Q

Hemochromatosis:

  • clinical manifestations
  • reversible manifestations
  • IRREVERSIBLE manifestations
A

Clinical manifestations:
-cutaneous hyperpigmentation w/ diabetes & cirrhosis

Reversible manifestations:
-CV: cardiomyopathy, vibrio vulnificus, Listeria monocytogenes, conduction disturbances

  • Liver: pastcuerlla pseudotubercullosis
  • Skin: bronzing (melanin deposition) , grayness (iron deposition)

IRREVERSIBLE manifestations:

  • Liver: cirrhosis, hepatocellular CA***
  • Pancreas: DM
  • Thyroid: hypothyroidism
  • Genitalia: hypogonadism
  • Joints: pseudogout
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8
Q

Hemachromatosis:

  • dx
  • tx
A

Dx:

  • combo of: clinical and labs
  • -elevated serum transferrin saturation greater than 45%***
  • -elevated serum ferritin* (pathologic)

-Liver Bx (GOLD STANDARD!!!)

Tx:

  • education for evidence of iron overload/complications:
  • -avoid red meat, iron supplememnts, avoid alcohol, recieve Hep A and B Vaccine
  • MAINSTAY is phlebotomy!!!!!
  • -removal of 500nl of blood (removes 250 mg iron)
  • -do weekly until iron depletion; Hgb 10-12, Ferritin less than 50%, transferritin sat less than 50%
  • –maintenance: phlebotomy every 2-4mo
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9
Q

Hemochromatosis:

-screening

A

Screening:

-screen 1st degree relatives unless under 18YO

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10
Q

Wilsons Dz

  • aka
  • cause
  • pathophys
  • clinical manifestations
A

AKA: hepatolenticular degeneration

Cause: Genetic: ATP7B autosomal recessive inheritance.

Pathophys:
-gene affects the carrier protein of copper which is primarily in hepatocytes. organ damage d/t copper build up in the liver and brain.

Clinical manifestations

  • generally presents between 0-20YO.
  • liver dz
  • neurologic sx
  • kayser-fleischer Ring (brownish ring around iris)
  • psychiatric sx
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11
Q

WIlson Dx

  • dx
  • tx
A

Dx:

  • ceruoplasmin level
  • 24hr urine for copper excretion
  • look for kayser-fleischer rings in eyes

Tx:

  • fatal if untreated
  • lifelong chelation therapy w/ D-penicillamine
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12
Q

Alcoholic Liver Dz:

-stages

A

Stage:

  • fatty liver (steatosis)
  • alcoholic hepatitis
  • alcoholic fibrosis and cirrhosis
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13
Q

Fatty Liver:

  • sx
  • onset
  • cause
  • reversible or nah?
A

Sx: most are asymptomatic, may have tender hepatomegaly

Onset: can occur within hours of a large alcoholic binge.

Cause: alcoholic binge, obese, pregnancy

Reversible!!!!

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14
Q

Alcoholic Hepatitis

  • sx
  • PE
  • lab findings
A

Sx:

  • asymptomatic to extremely ill
  • anorexia, N/V, weight loss, abd pain, poor nutrition
  • hepatosplenomegaly
  • jaundice
  • fever is common.
  • PE:
  • -spider angiomas
  • -palmar erythema
  • -gynecomastia
  • -parotid enlargement
  • -testicular atrophy
  • -ascites
  • -encephalopathy

Labs:

  • leukocytosis w/ left shift
  • anemia (macrocytic)
  • AST:ALT ration greater than 2:0
  • increased ALP
  • hyperbilirubinemia
  • hypoalbuminemia (severe dz)
  • coagulopathy (severe dz)
  • elevated ammonia levels (severe dz)
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15
Q

What are the Complications of alcoholic Liver dz?

-reversible or nah?

A

Complications:

  • fibrosis and death
  • cirrhosis
  • GI bleeds
  • esophageal varices
  • gastritis/PUD

usually reversible.

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16
Q

What might you find on histology in severe liver dz?

WHat is the most common cause of liver failure in the US?

A

-mallory bodies

MC cause of liver failure in US is drug-induced liver injury.

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17
Q

Alcoholic Liver Dz

-tx

A

Tx:

  • cessation of alcohol
  • supportive tx:
  • -nutrition
  • -B12 and Folate
  • Fluids
  • glucocorticosteroids for severe hepatitis
  • liver transplan in appropriate pts
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18
Q

Drug Induced Liver Injury (DILI)

  • sx
  • tx
  • medications causing injury
A

Sx: may be asymptomatic

Tx: discontinuation of the agent

MC drugs causing this:

  • acetaminophen
  • abx
19
Q

Tx of acetaminophen overdose?

A
  • activated charcoal within 2-3hrs of ingestion

- N-acetylcysteine

20
Q

Chronic Acetaminophen Intoxication:

  • signs and sx
  • patients who are at greater risk for developing hepatoxicity
  • tx
A

Signs and Sx:

  • nonspecific
  • often confused with viral dx

Greater risk for hepatotoxicity:
-ingestion of greater than 7.5 - 10g over 24hrs

  • ingestion of less than 4 g w/ increased susceptibility
  • liver tenderness, jaundice, or ill-appearing
  • supretherapeutic acteminophen concentrations ( greater than 20mcg/mL)

Tx:

  • N-acetylcysteine if:
  • -liver tenderness
  • -elevated aminotransferases
  • serum acetaminophen conc greater than 10mcg/mL
  • toxic by the nomogram.
21
Q

Hepatitis A, B, C, E symptoms

  • general signs on exam?
  • labs
A

many cases can be asymptomatic especially in children

Usually PRODROME* after exposure:

  • malaise and fatigue
  • anorexia, N/V
  • Myalgias
  • Pale stools, dark urine
  • Jaundice

Signs:

  • jaundice
  • RUQ pain
  • +/- hepatomegaly

Labs:

  • transaminases elevated; ALT greater than AST
  • hyperbilirubinemia
  • bilirubinuria
  • alkaline phosphatase mildly elevated
  • WBC normal to low
  • may have prolonged PT
22
Q

Acute viral hepatitis management?

A

supportive care!!!

  • manage the sx
  • avoid, acetaminophen, alcohol, exposure to hepatitis viruses
  • vaccination!!!
23
Q

Hepatitis A:

  • what type of virus?
  • acute, chronic or both?
  • Route of transmission
  • serology findings
A

RNA Virus

Acute ONLY!!!!

Transmission:

  • fecal-oral route**
  • sexual contact
  • contaminated food, water
  • blood

Serology:

  • IgG anti-HAV = they have had the infection or have been vaccinated for it, wont know which one unless you get hx.
  • IgM anti-HAV, fecal HAV, & elevated ALT = active acute infection.
24
Q

Hepatitis A Vaccine:

  • active or inactivated?
  • SE
  • regimen
  • postexposure prophylaxis
A

inactivated vaccine

SE: fever, injection site rxn, rash, HA

Regimen: two doses 6-12mo apart

Postexposure prophylaxis:
Hep A vaccine AND IMIG

25
Q

Hepatitis B Virus:

  • what type of virus?
  • routes of transmission
  • prevention
  • postexposure prophylaxis
A

DNA virus

Transmission:

  • sexual contact*
  • perinatal (@ or near birth) (vertical)
  • horizontal: via minor breaks in the skin or mucous membranes (HBV can survive outside the hospital for prolonged periods)
  • percutaneous:
  • -IVDU
  • -body piercings
  • -nosocomial
  • organ transplantation
  • Transfusions (oh so rare)

Prevention:
-Hepaitis B vaccine

Prophylaxis:
-Hep B vaccine AND HBIG concurrently.

26
Q

Hepatitis B VIrus

  • acute, chronic, or both?
  • sx
  • complications
A

Acute (90%) Chronic (10%)…BOTH!!!

Sx:

  • many are asymptomatic
  • fever, rash, athralgias, arthritis, polyarteritis nodosa
  • glomerular dz

Complications:

  • cirrhosis
  • hepatic cell carcinoma
27
Q

Hepatitis B virus:

-serology

A

Serology:
-HbsAg = first Ag to be seen, if this Ag is present greater than 6mo post infection you know its chronic.

-IgM anti-HbcAg = indicates an acute infection.

  • Anti-HBsAg = indicates they’ve had the infection or that they have been immunized. Usually follows disappearance of HBsAg, persists for life.
  • when HBsAg and anti-HBsAg coexist the persons are carriers of HBV.

HbeAg; marker of HBV replication and infectivity

Anti-HBe = occurs when the HBeAg goes away (seroconversion means remission of their dz)

HBV DNA = disappearance of HBV DNA = recovery
*major role is to monitor need for tx and response to tx.

28
Q

HBV infection :

  • tx
  • who should not receive tx?
A

interferon or peginterferon is DOC*!

  • pts who show evidence of virus replication are candidates of therapy:
  • -HBeAg +
  • -high serum HBV DNA level
  • -Active liver dz or elevated LFTs

***Pts who have decompensated cirrhosis or are carriers SHOULD NOT receive tx, its too late for them.

29
Q

SE of Peginterferon

A

flu-like sx

immunosuppression

abd pain

N/V

dry mouth

hair loss

blurred vision

depression

anemia

*on these meds 9mo

30
Q

Hepatitis C

  • type of virus?
  • transmission
  • acute, chronic, both?
  • sx
  • serology
A

Type of Virus: RNA

Transmission:

  • IVDU/sex w/ IVDU*
  • jail greater than 3 days
  • blood transfusion
  • stuck or cut with bloody object
  • pierced ears or body parts
  • immunoglobulin injection
  • perinatal transmission
  • solid organ transplant

Acute (20%) Chronic (80%).. so both!

Sx:
-fatigue

Serology:
HCV RNA = active infection, if persists longer than 6mo it is chronic.

Anti-HCV = positive 12wks after exposure

Both HCV and anti-HCV are present in both acute and chronic infection.

*look at ALT, if elevated after 6mo then chronic.

31
Q

Hepatitis C Virus

  • tx
  • how do you determine cure?
A

Tx:

  • dont drink, do drugs, no tylenol
  • vaccinate for Hep A and B
  • Peginterferon + ribavirin, protease inhibitors (harvoni)
  • transplant (one already infected with HCV)

Cure:
-sustained response HCV RNA negativity 6mo after tx is stopped.

32
Q

SE of Peginterferon/Ribavirin

A

bone marrow suppression

myalgias, HA, low grade fevers

irritability

ischemic retinopathy, retinal hemorrhage

Thyroid dysfunction

Rash, hair loss, hearing loss, insomnia.

non-productive cough andd dyspnea

33
Q

Hepatitis D Virus

  • whats required for replication?
  • what type of virus
  • pathophys
  • MC genotype found in western world?
  • transmission
A

HBV required for replication

Single Stranded RNA rod-lik structure

Pathophys:
-HDAg activates replication of HDV RNA in hepatocyte, large HDAg directs packaging HD virion into HBsAg.

Genotype I

Transmission:

  • parenteral
  • close personal contact
  • multiple transfusions
34
Q

Hepatitis D Virus

  • types of infection?
  • prevention?
  • postexposure prophylaxis
  • tx
A

coinfection w/ HBV; severe acute disease B + D; usually self limited, low risk of chronic infection

Superinfection on top of chronic Hep B: high risk of severe progressive chronic liver dz

Prevention:
Hep B vaccine

postexposure prophylaxis:
-Hep B vaccine and HBIG

Tx:
Peginterferon

35
Q

Hepatitis E Virus

  • type of virus?
  • transmission
  • acute chronic or both?
A

RNA virus

Transmission:

  • enterically transmitted
  • waterborne
  • fecally contaminated water
  • blood transfusion
  • vertical mom-newborn

Acute only!

36
Q

HGV

  • aka
  • type of virus?
  • transmission
  • protective if you have what other dz?
A

aka: GB virus type C

Flavivirus

Transmission: contaminated blood and sexual contact

Protective if you are coinfected w/ HIV.

doesnt cause hepatitis in humans.

37
Q

Which types of hepatitis can be:

  • chronic
  • raging fulminant hepatitis
  • cholestatic hepatitis
A

Chronic: B,C,D

Raging fulminant: ABCDE

Cholestatic: ABCDE

38
Q

Chronic Hepatitis Typical progression

A

Chronic inflammation in portal areas

Necrosis/inflammation

Fibrosis

Cirrhosis

39
Q

Cirrhosis

  • definition
  • dx
  • etiologies
  • pathophys
A

def: development of fibrosis of liver with formation of regerative nodules; results in impairment of synthetic, metabolic, and hemodynamic functions of the liver.

Dx:

  • US, CT, MRI = suggest dx
  • Bx is GOLD STANDARD

Etiologies:
-alcohol and chronic HCV

Pathophys:
chronic insult to liver, collagen production increases and ECM becomes stiffer and normal functions of liver are compromised.

*early fibrotic changes are reversible, as progression occurs the changes become irreversible.

40
Q

Cirrhosis:

-lab abnormalities

A

Labs:

  • AST/ALT moderately elevated
  • Alkaline phosphatase; elevated
  • bilirubin rises as cirrhosis progresses
  • albumin: levels fall
  • PT: increases
  • serum Na: hyponatremia seen w/ ascities, high levels of ADH.

(Portal HTN and ascities, acities takes fluid from intravaascular space, leading to decreased volume in intravascular space. Body thinks you don’t have enough fluid in the intravascular space so body secretes ADH to hold more fluid, thereby diluting leading to hyponatremia)

Hematologic:

  • thrombocytopenia
  • leukopenia
  • anemia
41
Q

Portal HTN may result in what other manifestations?

Management of Portal HTN?

A

esophageal varices

enlarged abd wall vessels (caput medusa)

hemorrhoids

splenomegaly

ascites

Hepatic encephalopathy

Management:
-temporarily; remove ascitic fluid

  • portal shunts
  • treat liverr dz /liver transplant
42
Q

Hepatic Encephalopathy:

  • what is this?
  • causes
A

WHat:
spectrum of potentially reversible neuropsychiatric abnormalities:
–cognitive abilities
–psychiatric state
–motor impairment, focal neurological findings

Causes:

  • portal HTN
  • hypovolemia
  • GI bleed
  • hypokalemia/metabolic alkalosis
  • hypoxia
  • sedatives
  • hypoglycemia
  • infection
  • hepatoma or vascular occlusion
43
Q

Hepatic Encephalopathy

  • grading
  • dx
  • tx
A

Dx:
-West-haven classification system grades stages 0-4;
0-1 = overt encephalopathy
2-4 = more severe

-Glasgow Coma Scale

Dx:

  • ammonia and manganese
  • serial ammonia levels are inferior to clinical assessment in gauging improvement or deterioration in pts who is being treated for HE.

Tx:

  • Lactulose to lower ammonia levels (3-4soft stools/day)
  • Correct hypokalemia if present
  • low protein diet
  • rifampin orally effects the metabolic function of the gut microbiota and is as effective as lactulose with less SE.

GI 2 (9 decks)

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