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Nursing Semester 2 > Monica - Exam 5: Chronic Liver Failure > Flashcards

Monica - Exam 5: Chronic Liver Failure Flashcards

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1
Q

The liver is the largest internal organ and has the greatest regenerative capacity.

A

True dat

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2
Q

functional liver cells are called:

A

hepatocytes

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3
Q

Functions of the liver (brief):

A
  1. endocrine: angiotensinogen (RAAS)
  2. bile synthesis (excretory): clearance of bilirubin; fat digestion in small intestine
  3. metabolism:
    - protein: albumin (colloidal osmotic pressure)
    - fat: cholesterol, lipoproteins
    - carbohydrate: glycogenolysis, gluconeogenesis based on energy needs
  4. hematologic: vit k storage; synthesis of clotting factors (2, 7, 9, 10)
  5. detoxification: medications, ammonia
  6. vitamin/mineral storage: vit k, B12, folate, ferritin (Hgb formation), calcifidiol (intermediate vit D)
  7. immunity: Kupffer cells (macrophages) phagocytize bacter, debri, old RBCs
    8.
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4
Q

liver fx:

protein metabolism

A
  • sythesis and breakdown of proteins

- colloidal osmotic pressure maintains fluid balance in the intravascular space

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5
Q

liver disease r/t protein metabolism

A
  1. decreased albumin levels - decreased oncotic pressure - third-spacing - acsites and edema
  2. muscle wasting, malnutrition
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6
Q

normal range for albumin

A

3.5 - 5.0 g/dL

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7
Q

liver fx:

fat metabolism

A
  • formation of fatty acids, lipoproteins, cholesterol

- cholesterol fx: hormones, bile salts, myelin sheath

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8
Q

liver fx:

carbohydrate metabolism

A

the liver stores glycogen and breaks it down depending on energy needs.

  • glycogenesis
  • gluconeogenesis: new glucose made from fatty acids and amino acids
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9
Q

How does liver disease lead to unstable glucose levels?

A

Inability of liver to store or breakdown glycogen based on energy needs.

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10
Q

Inability to synthesize clotting factors leads to:

A
  • increased Prothrombin time

- increased risk of bleeding

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11
Q

Blockage of bile flow in the cannaliculi to the bile duct and small intestine leads to:

A
  • lack of fat digestion in small intestine (steatorrhea)
  • accumulation of bilirubin in blood stream (jaundice, light/clay-colored stool)
  • accumulation of bile salts in blood stream and seeping through skin (pruritis)
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12
Q

Bile consists of:

A

cholesterol, bile salts, bilirubin, water, body salts

*yellow-green alkaline fluid

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13
Q

bilirubin: normal range

A

0.1 - 1.2 mg/dL

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14
Q

life of bilirubin: from formation to elimination

A
  • formed by the breakdown Hgb to heme
  • insoluble in water; fat-soluble
    1. bilirubin binds to albumin for transport (unconjugated/indirect)
    2. conjugates to glucorinic acid to become water-soluble (conjugated/direct)
    3. able to enter bile and pass to small intestine for elimation in stool
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15
Q

The second most common cause of cirrhosis is:

A

alcoholism.

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16
Q

Chronic hepatitis __ infection increases the risk of liver disease.

A

Hep C

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17
Q

How is Hep C spread?

A

contact with infected blood - inj. drug use, surgery, hospitals, blood products before 1992

18
Q

Liver Function Tests Panel

A
  • Liver enzymes: ALT, AST, ALP
  • direct/indirect bilirubin

May also include: ammonia, albumin, total protein, prothrombin time (PT)

19
Q

ALT - alanine aminotransferase

A
  • *specific to liver function
  • found primarily in liver
  • damaged hepatocytes release ALT: diagnoses hepatocyte destruction
  • rises before other signs of liver damage
20
Q

ALT: normal range

A

10 - 35 U/L

21
Q

Which lab value rises before other signs of liver damage?

A

ALT - alanine aminotransferase

22
Q

In end-stage liver disease which LFT values may be normal? Why?

A

ALT and AST - nonfunctioning hepatocytes are unable to release those enzymes

23
Q

AST - aspartate aminotransferase

A
  • nonspecific: found in liver, heart, skeletal muscle, blood
  • rises 10x+ in liver disease ( 100+)
  • AST/ALT need for evaluation
  • *rises higher and more prolonged elevation than ALT
24
Q

AST: normal range

A

8 - 35 U/L

25
Q

ALP - alkaline phosphatase

A
  • nonspecific: found primarily in liver, bone, and kidneys
  • higher in kids/teens because growing bones
  • levels increase w/ liver cirrhosis, liver cancer, or obstruction in the biliary tract
26
Q

ALP - alkaline phosphatase: normal range

A

42 - 136 U/L

27
Q

Ammonia is a waste product of ____ digestion that is converted to _____ in the liver and excreted by the _____.

A

protein digestion
urea
kidneys

28
Q

In cirrhosis or hepatitis, if the liver is unable to metabolize ammonia:

A

it accumulates in the bloodstream and passes into the brain causing hepatic encephalopathy.

29
Q

ammonia: normal range

A

15 - 60 mcg/dL

30
Q

sxs of hepatic encephalopathy

A

mental and neurological changes leading to: confusion, disorientation, restlessness, asterixis (flapping hand reflex)

eventually: coma, death

31
Q

pharmacological tx of hepatic encephalopathy

A

lactulose, neomycin

32
Q

neomycin:

classification, action, indication, AEs

A
  • aminoglycoside antibiotic
    A: decrease amonnia-producing bacteria in the gut
    I: management of HE
    AEs: diarrhea, n/v, ototoxicity, nephrotoxicity*
    *monitor kidney function b/c >90% metabolized and excreted by kidneys
33
Q

lactulose:

classification/route, action, indication, AEs

A
  • laxative (PO, PR)
    A: inhibits ammonia from diffusing into blood
    I: adjunct therapy for HE
    AEs: belching, cramps, distention, flatulence, diarrhea, hyperglycemia
  • DO NOT quit w/o consultation even if experiencing side effects
34
Q

cirrhosis

A
  • collagen and fibrous connective tissue (scar tissue) grows in disorganized manner slowing or obstructing blood flow through the liver (and flow of bile to bile ducts)
  • chronic and insidious disease leading to end-stage liver disease and failure
35
Q

early symptom of cirrhosis

A

fatigue

36
Q

later manifestations of cirrhosis

A

jaundice, itching, weight loss, edema, bleeding issues

37
Q

complications of cirrhosis

A

portal hypertension, ascites, encephalopathy, varices (esphagus, stomach, rectal)

38
Q

portal hypertension

A

Structural changes of the liver compress the portal/hepatic veins and increase resistance to blood flow in liver = increased portal vein pressure as cirrhosis worsens

39
Q

How does portal hypertension lead to varices and increased risk of bleeding?

A

Collateral vessels form to bypass obstructed blood flow and relieve pressure. Blood backs up into GI tract and spleen. Veins of the esophagus, stomach, and rectum dilate and engorge with blood (varices). Fragile, tortuous varices and decreased synthesis of clotting factors leas to an increased risk of bleeding.

40
Q

ascites: sxs

A

abdominal distention, anorexia, difficulty breathing, dehydration, dry mucous membranes, decreased urine output

41
Q

cirrhosis:

nursing considerations

A

ASESS:

  • jaundice, itching
  • hematologic: bruising, bleeding, PT
  • abdominal girth, edema, daily weight, I&O
  • mental status, ammonia levels
  • urine and stool color
  • appetite and dietary intake
  • respiratory effort
  • skin integrity
  • Labs: LFTs, ammonia, protein, BUN/Cr
42
Q

cirrhosis:

collaborative care and lifestyle modifications

A
  • alcohol abstinence, avoid or lower doses of hepatotoxic drugs, no aspirin
  • plant-based foods: avoid protein (ammonia) and fat (bile malfx)
  • small, frequent meals: reserve energy
  • soft foods: prevent rupture of fragile varices
  • low sodium (1500-2000mg): third-spacing/edema
  • decrease bleeding risks: avoid straining (stool softeners), soft toothbrush, no harsh blowing, humidified O2, electric razor

Nursing Semester 2 (7 decks)

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