Liver Failure Flashcards

1
Q

Ramble off some roles of the liver in Metabolism

A
  • Metabolizes Carbs, Proteins and fats
  • Converts glucose to glycogen for storage
  • Provides bile for fat breakdown
  • converts ammonia to urea for excretion (byproduct of protein metabolism)
  • Breaks down fatty acids to Ketones (when glucose is in short supply)
  • Vit storage and Metabolism
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2
Q

Role of the liver in maintaining blood

A
  • “detoxifies” blood.
  • Metabolizes OH and drugs
  • Excretes bilirubin (in bile) which is a byproduct of hemoglobin breakdown
  • Uses Vit K to synthesis prothrombin and other clotting factors
  • Synthesizing plasma proteins, nonessential amino acids, Vit A and essential nutrients such as iron, Vit D, B12
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3
Q

Factors that affect liver risk assessment

A

Exposure to hepatotoxic chemicals or infectious agents
High risk sex practices
OH or drug abuse
Occupational and travel history

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4
Q

What’s the most common cause of liver disease in Canada? 2nd?

More common in men or women

A

Non-Alcoholic Fatty Liver Disease leading cause of liver disease in Canada.

…Hepatitis C next leading cause but decreasing

…Men

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5
Q

What is Cirrhosis?

A

Cirrhosis is common end result of many chronic liver disorders.

Diffuse scarring of liver – follows hepatocellular necrosis of hepatitis.

Inflammation – healing with fibrosis - Regeneration of remaining hepatocytes from regenerating nodules.

Loss of normal architecture & function.

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6
Q

What is the initial treatment of non viral hepatitis

A

Effective treatment aims to remove the causative agent by lavage, catharsis, or hyperventilation

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7
Q

Types VIral Hepatitis

Spread and severity

A

• Hep A
o Water or food or membrane contact, no carrier state, not chronic, short incubation
• Hep B
o STD/ spread through serum / body fluids, 10% chronic, can be carrier state, inc risk of liver complications
• Hep C
o Direct blood contact, chronic carrier state, chronic liver disease
• Hep D
o Must already have B
• Hep x
o Unknown virus

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8
Q

Diet for hepatitis

A

Small meals high in calories and protein. (even though ammonia may be high r/t protein breakdown) (May need to get NH3 under control and avoid protein initially)

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9
Q

What Diagnostics might tell us about liver function

A
  • ALT, AST (not liver specific), GGT (OH)
  • Albumin
  • PT-INR (ability to meta. Vit K test)
  • Liver biopsy
  • CT, MRI US
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10
Q

What is the relationship between cirrhosis and protein loss/synthesis

A

Trade off between high ammonia levels and Malnutrition

The cirrhotic liver causes the body to breakdown proteins at a fast rate, quickly depleting stores and increasing body needs. While protein breakdown is elevated with cirrhosis, synthesis is decreased, which causes muscle wasting and a decrease in blood protein. Malnutrition is a major concern, so protein in diet is required.

However, some people with cirrhosis have high levels of ammonia, a by-product of protein metabolism, in their blood and may need to restrict protein intake to prevent adverse effects.

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11
Q

Changes seen in Alcoholic liver disease.

Reversible vs Permanent

A

Alcoholic Liver disease - Patterns

REVERSIBLE:
Fatty change,
Acute hepatitis
Chronic hepatitis with Portal fibrosis

PERMANENT
Cirrhosis, Chronic Liver failure

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12
Q

Neuro S and S of Liver failure

A
Asterixis				
Paraesthesias
Dec LOC				
Sensory disturbances
Behavorial changes		
Cognitive changes
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13
Q

Integument S and S of Liver Failure

A
Spider angiomas		
Palmar erythma
Jaundice	
Pruritis
Hair production		
Caput medusa
Pigmentation			
Bruising
White Nails
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14
Q

What are the possible causes of liver disease?

End and irreversible result?

A
Viral Hepatitis
Autoimmune Hepatis
OH
non alcoholic fatty liver disease
Non viral (Hepatotoxins/Chemicals)

Cirrhosis (scarring of the liver)

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15
Q

Possible Meds r/t to liver damage/failure

A
Abx- Bact in GI produce ammonia
H2 Rec. Blocker- GI bleeding 
Ativan- withdrawal from alcohol
Beta blockers- Dec POrtal Hypertension
Lactulose- Bind to Ammonia 
Spironolactone- K sparring/Aldo blocking    Diuretic
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16
Q

Hepatic Encephalopathy… Why?

S and S ?

A

Ammonia (urea) accumulation in blood stream effects neurotransmitters in brain.

Portal HTN and shunting leading to blood not being processed by liver.

Confusion, motor disturbances, mood, altered LOC, cannot copy simple figures (constructional apraxia)
Asterixis (flapping tremor of the hands)

17
Q

Causative factors of NAFLD

A
Obesity
High Blood Cholesterol
Type Two Diabetes
Malnutrition
Rapid Weight Gain
Medication: steroids, exposure to toxins and
chemicals
18
Q

What Age groups experience NAFLD

A

ALL- including pediatrics. Becoming more common in kids with a higher rate of mortality

19
Q

IS there treatment for NAFLD

A

Not really. Life style changes (physical activity, low fat/healthy diet, loss weight, deal with Diabetes, easy on the liver) and catch it early.

FROM PP:
Liver Transplant
No Medication available to treat
Antioxidant vitamins? Studies inconclusive
Ongoing studies with meds designed to increase sensitivity to insulin

20
Q

Three types of jaundice?

A

Pre-Hepatic- Hemolytic (unconjucated)

Hepatocellular- VIral, OH, toxin (prevent conjugation or obstruction in liver itself)

Post hepatic- Conjugated, Obstructive

Hereditary hyperbillirunemia

(Pruritus, yellow sclera (bilirubin deposits)

21
Q

Liver disease and fluid retention/edema??

A

Reduced albumin production ((hypoalbuminemia) leading to loss of fluid to extravascular space) (Also stimulating RAAS)

Damaged liver can’t metabolize aldosterone, leading increased plasma level and mention of Na and water. (More fluid available to go into extravascular space)

(Cycle puts albumin rich fluid in Abd Space)

22
Q

Connection between liver dysfunction and thiamine.

A

Liver can’t metabolize certain vitamins (like thiamine Vit B-1) which leads to deficiency.

Korsakoff Syndrome (memory disorder r/t low thiamine) often associated with OH abuse or nutritional deficit.

23
Q

Marasmus?

Kwashiorkor?

A

1) Universal starvation (nutritional defecit)
2) Protein deficiency

Both cause deficit in growth, plasma proteins and immune response. Ascites and edema

24
Q

4 stages of OH liver disease

A

fatty change, acute hep, chronic hep, cirrhosis