liver mod 4 Flashcards

1
Q

major liver functions

A
Metabolism &/or storage of:
 - Fat, CHO, PRO, vitamins and minerals
Blood volume reservoir
- Distends/compresses to alter circulating blood volume
Blood filter - kuppfer cells
- Helps purify blood - remove bilirubin
Blood clotting factors - thrombopoeisis
- Including prothrombin & fibrinogen
Drug metabolism and detoxification
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2
Q

jaundice manifestations

A

Urine - darker
Liver enzymes = elevated
Stools = Normal or clay colored
Pruritis - increased bilirubin

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3
Q

clinical manifestations hepatitis

A

Similar between all types
Many cases of ALL types of hepatitis are asymptomatic
But can range from none, mild, to liver failure
Causes abnormal elevated LFTs– but NOT consistent with cellular damage within the liver

must trend labs and see other s/s

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4
Q

complications viral hepatitis

A

Most patients with acute viral hepatitis recover completely with no complications
Overall mortality rate is less than 1%
Higher mortality in elderly and comorbidities

Complications include:
Chronic hepatitis
Liver cirrhosis (next section)
Liver cancer
Fulminant viral hepatitis – acute liver failure
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5
Q

hep a (HAV)

A
food borne
\Transmission - fecal-oral, parental, sexual 
Acute onset with fever
Usually mild severity 
Does NOT lead to chronic hepatitis 
Usually affects children and adult 
Hand hygiene, 

**Hep A vaccine

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6
Q

hep b (HBV)

A

Transmission - parental, sexual
Insidious onset - 60-180 days onset s/s
Severe disease, may be prolonged course or develop into chronic
Any age group affected

***HBV vaccine and safe sex and hygiene

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7
Q

hep c

**NO VACCINE

A

Transmission - parental, sexual, mother to child
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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8
Q

hepatitis vaccines

A
Hep A Series
2 doses 6 months apart
Recommendations
All children beginning at age 12 months
Special “high risk” populations

Hep B Series
3 doses at least 4 months apart
Recommendation: All infants beginning as newborns

Hep C = NO vaccine

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9
Q

HBV pharm

A

Two classes of drugs are used for chronic HBV:
Interferons
Nucleoside analogs

Treatment is only for high-risk patients:
↑ AST levels
Hepatic inflammation
Advanced fibrosis- able to see on CT scan

Disadvantages of treatment:
Prolonged therapy
Costs and adverse effects - tons drug interactions
High relapse

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10
Q

HCV pharm

CN TAKE TYLENOL, BUT <2 GRAMS

Now easily treatable and eliminated in most all patients
treat anyone with viral load, expensive

A

Treatment is only recommended for patients with CHRONIC DISEASE

However this thought process is changing with the introduction of newer, very effective drugs

Treated with direct-acting antiviral therapy and interferon-based regiments

Some require treatment along with a nucleoside analogue medication as well

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11
Q

HBV/HCV direct acting (not for drug matrix)

A
HBV:
Pegylated interferon-alpha
Ribavirin
Entecavir
Tenofovir alafenamide
Sofosbuvir
Daclatasvir (Daklinza)

HCV on attachment

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12
Q

clinical manifestations cirrhosis - EARLY

A

GI
- N/V, anorexia, flatulence, change bm habits

fever, weight loss, palpable liver

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13
Q

clinical manifestations cirrhosis -LATE

A

jaundice
peripheral edema - 3rd spacing
decreased albumin and protein
ascites - portal HTN
skin lesions - spider angiomata
hematologic problems - bleeding, anemia,
endocrine - stop menstruation, hypogonadism
esophageal and anorectal varices - distended veins
hepatic encephalopathy - due to toxin build up

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14
Q

portal HTN

A

Resistant portal blood flow - leads to varices & ascites

Causes: systemic hypotension, vascular underfilling, stimulation of vasoactive (RAAS system) systems, plasma volume expansion, increased cardiac output  ASCITES

Asymptomatic until complications
- Variceal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy

Treatment: prevent/treat complications
Can’t do anything for the portal hypertension except liver transplant

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15
Q

hepatic encephalopathy

not diagnosed off ammonia levels
liver unable to filter toxins
elevated ammonia = increase encephalopathy

A

30-45% of cirrhosis patients
LOC is the primary driver of diagnosis

Graded by severity:
Minimal: Abnormal results on psychometric or neurophysiological testing without clinical manifestations (see ‘Psychometric tests’ below)

Grade I: Changes in behavior, mild confusion, slurred speech, disordered sleep

Grade II: Lethargy, moderate confusion

Grade III: Marked confusion (stupor), incoherent speech, sleeping but arousable

Grade IV: Coma, unresponsive to pain

Correlate with liver labs- mainly ammonia which is primary chemical driver of LOC changes

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16
Q

acute liver failure (fulminant liver failure)

A

Separate liver failure NOT caused by cirrhosis or other type of liver disease

Most common cause: acetaminophen overdose
Can be treated with N-acetylcysteine

Patho: edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates and disrupts the liver tissue

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

5 days to 8 weeks after an acetaminophen overdose
Signs are similar to cirrhosis symptoms

Treatment: not much, liver transplant

17
Q

pharm cirrhosis/liver disease

***hepatic encephalopathy

A

lactulose

rifaximin

18
Q

lactulose

**begin with this drug
induces acidic environment

A

Class: Hyperosmotic laxative
Indication: reduction of ammonia absorption in hepatic encephalopathy

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 hypokalemia

hypok = increased ammonia levels

19
Q

rifaximin

increased risk c-diff

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 preventive, just depends on HCP
Given PO

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

Has been associated with an increased risk of C diff

20
Q

portal circulation

“first pass effect”

A

The portal circulatory system brings blood to the liver from the stomach, intestines, spleen, and pancreas
The blood enters the liver through the portal vein
The absorbed products of digestion come directly to the liver, and are sent to the lobules

21
Q

liver function tests (lft)

A

everything increased except total protein and albumin

22
Q

jaundice

A

Caused by increased level of bilirubin in the bloodstream

Usually causes problems and is noticeable with total bilirubin is greater than 2-2.5mg/dl

Yellowish discoloration of skin and deep tissues
3 classifications:
Hemolytic - increased breakdown of RBCs
Hepatocellular - liver unable to take up bilirubin from blood or unable to conjugate it
Obstructive - decreased or obstructed flow of bile

23
Q

bilirubin

A

By product of heme breakdown - mainly hemoglobin

DIRECT: Conjugated INDIRECT: unconjugated

Elevations of INDIRECT bilirubin = bilirubin overproduction OR impaired liver functioning

Elevations of DIRECT bilirubin = liver working, but can’t get the bilirubin out
Bile duct obstruction, gall stones

24
Q

viral hepatitis

A

Systemic virus that mainly affects the livers
Inflammation of the liver
Various strains cause the different types of hepatitis
HAV, HBV, HCV
Other viruses that can cause hepatitis  Epstein-Barr, cytomegalovirus
Know that hepatitis (not the infection) can occur from other causes
Alcohol abuse, drugs, chemicals, and bacteria

25
Q

viral hepatitis: prodromal phase

A

2 weeks after exposure
Fatigue, anorexia, malaise, nausea, vomiting, HA hyperalgesia, cough, low-grade fever
HIGHLY transmissible

26
Q

viral hep: icteric

A

Begins with jaundice
Jaundice, dark urine, clay-colored stools
Liver enlarged and may be painful to palpation
Fatigue abdominal pain persists or increases in severity

27
Q

viral hep: recovery phase

A

Resolution of jaundice
6-8 weeks after exposure, symptoms diminish
Liver remains enlarged/tender

28
Q

cirrhosis

hepatocytes can regenerate

severity depends of amount slow

A

Irreversible, inflammatory, fibrotic liver disease
Structural changes from injury (alcohol/viruses) and fibrosis
Chaotic fibrosis leads to obstructive biliary channels and blood flow  jaundice and portal hypertension
Regeneration is disrupted by hypoxia, necrosis, atrophy, and liver failure

29
Q

common causes cirrhosis

A

hep B and C
excessive etoh
idiopathic
non-alcohol fatty liver disease (NASH, NAFLD)

30
Q

stages of alcoholic liver disease (3)

A

alcohol fatty liver

alcoholic steatohepatitis

alcoholic cirrhosis