Liver 2 Flashcards

1
Q

HEP A

A

Transmission: Fecal-oral, parental (IVD), sexual

Acute onset of fever

Usually mild severity

Does NOT lead to chronic hepatitis

Usually affects children and adults

Hand hygiene, Hep A vaccine

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2
Q

HEP B

A

Transmission: parental or sexual

Insidious onset

-very long incubation

Severe disease, may be prolonged course or develop into chronic (10%)

Any age group affected

HBV vaccine and safe sex + hygiene

-all kids get vaccine

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3
Q

HEP C

A

Transmission: parental or sexual

Insidious onset

Mild to severe symptoms

Can develop into chronic hepatitis (80%)

Any age is affected

Screening blood, hygiene, NO vaccine

Leads to: hepatocellular carcinoma, liver transplant

-New treatment is developing and becoming more widely available

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4
Q

Hepatitis A vaccine

A

-2 doses 6 months apart

Recommendations:

-All children starting at 12 months

-Special “high risk” populations
(food handlers, hospital workers)

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5
Q

Hepatitis B vaccine

A

-3 doses at least 4 months apart

Recommendations:

-All infants beginning as newborns

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6
Q

2 Major classes of HEP B drugs

A
  1. Interferons

2. Nucleoside analogs

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7
Q

Treatment for B is only for

A

HIGH-RISK patients:

  • Elevated AST levels
  • Hepatic inflammation
  • Advanced fibrosis
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8
Q

Disadvantages of Hep B treatment

A
  • Prolonged therapy
  • Costs and adverse effects (interactions)
  • High relapse
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9
Q

Hep C is treated with

A

Direct-acting antiviral therapy and interferon-based regiments

-Some require treatment along with a nucleoside analogue medication as well

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10
Q

How much Tylenol can Hep C people take?

A

<2g/day

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11
Q

Common causes of cirrhosis

A
  1. Hepatitis B + C
  2. Excessive Alcohol Intake
  3. Idiopathic
  4. NASH + NAFLD (Non-alcoholic fatty liver disease)
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12
Q

Cirrhosis

A

Irreversible, inflammatory, fibrotic liver disease

Structural changes from injury (alcohol/virus) and fibrosis

Chaotic fibrosis leads to obstructive biliary channels and blood flow Jaundice + Portal hypertension

Regeneration is disrupted by hypoxia, necrosis, atrophy, and liver failure

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13
Q

Most common type of cirrhosis

A

Alcoholic cirrhosis most common type but still accounts for only 25% of all cirrhosis

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14
Q

3 stages of alcoholic liver disease

A
  1. Alcoholic fatty liver
  2. Alcoholic steatohepatitis
  3. Alcoholic cirrhosis
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15
Q
  1. Alcoholic fatty liver
A

-mildest, asymptomatic

reversible

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16
Q
  1. Alcoholic steatohepatitis
A
  • precursor to cirrhosis
  • inflammation (infiltration of WBC), degeneration of hepatocytes
  • Symptoms apparent

(Irreversible)

17
Q
  1. Alcoholic cirrhosis
A

-fibrosis and scarring alter liver structure

Irreversible

18
Q

Cirrhosis: pathogenesis

A
  1. Liver cells destroyed
  2. Cells try to regenerate
  3. Disorganized process
  4. Abnormal growth
  5. Poor blood flow and scar tissue
  6. Hypoxia
  7. Liver failure
19
Q

Cirrhosis: Early Manifestations

A

GI Disturbances

  • N/V
  • Anorexia
  • Flatulence
  • Change in bowel habits

Fever, Weight loss

Palpable Liver

20
Q

Cirrhosis Late Manifestations: Endocrine

A

Females:

  • Anovulation
  • Amenorrhea

Male:

  • Hypogonadism
  • Impotence
  • Infertility
21
Q

Cirrhosis Late Manifestations:

A
Jaundice 
Peripheral edema
Decreased albumin & PT
Ascites
Skin lesions
Hematologic Problems
-anemia + bleeding
Endocrine problems
Esophageal + anorectal varices
Encephalopathy
22
Q

Causes of Portal Vein Hypertension

A

-Systemic hypertension, vascular underfilling, stimulation of vasoactive (RAAS system), plasma volume expansion, increased CO&raquo_space;> ASCITES

23
Q

Complications of Portal Hypertension

A

Asymptomatic until complications:

-Variceal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy

24
Q

What leads to varices + ascites?

A

Resistant portal blood flow (portal hypertension)

25
Q

Primary factor of encephalopathy diagnosis

A

LOC + correlate with LIVER labs (ammonia)

26
Q

Acute Liver Failure: Fulminant liver failure: Most common cause

A

Acetaminophen OD

use acetylcysteine

27
Q

Acute Liver Failure (Fulminant Liver Failure): pathology

A

edematous hepatocytes and patchy areas of necrosis and inflammatory cells infiltrate and disrupt liver tissue

28
Q

Acute Liver Failure (Fulminant Liver Failure): When and how can it occur?

A

Can occur 6-8 weeks after viral hepatitis or metabolic liver disease

-5 days to 8 weeks after acetaminophen OD

29
Q

Lactulose

A

Class: hyperosmotic Laxitive

MOA: reduces blood ammonia levels by converting ammonia to ammonium

Given PO or enema/rectal

Can be given to titrate by number of stools or by ammonia levels

-Not just given for high ammonia levels though, MUST have signs/symptoms of encephalopathy

Make sure that patient is NOT hypokalemic

30
Q

Rifaximin

A

Second line if lactulose isn’t working

MOA: inhibits bacterial RNA synthesis by binding to bacterial DNA (initially used as an antibiotic for GI infections)

Can sometimes be given as preventative, depends on HCP

PO

SE: peripheral edema, nausea, ascites, dizziness, fatigue, pruritis, skin rash, abdominal pain, anemia

Has been associated with an increased risk of C. diff