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NUR 326 Exam 2 > Liver Problems > Flashcards

Liver Problems Flashcards

1
Q

major functions of the liver

A

–metabolism and/or storage of fat, CHO, proteins, vitamins, and minerals
–blood volume reservoir
–blood filter
–blood clotting factors
–drug metabolism and detox

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2
Q

blood volume reservoir

A

distends/compresses to alter circulating blood volume

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3
Q

blood clotting factors

A

prothrombin and fibrinogen

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4
Q

where is the liver located?

A

right epigastric region

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5
Q

liver cells

A

hepatocytes

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6
Q

portal circulatory system

A

brings blood to the liver from the stomach, intestines, spleen, and pancreas

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7
Q

how does portal circulation work?

A

–deoxygenated blood enters the liver through the portal vein
–absorbed products of digestion come directly to the liver and are sent to the lobules
–“first pass effect”

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8
Q

Liver Function Tests (LFTs)

A

–liver enymes (AST, ALT, Alk Phos)
–Bilirubin
–Serum Ammonia
–Serum protein
–Serum albumin
–Prothrombin Time

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9
Q

Liver enzymes with liver failure

A

> 150; not great indicator of severity

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10
Q

serum ammonia level with liver failure

A

increased

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11
Q

serum protein level with liver failure

A

decreased

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12
Q

serum albumin level with liver failure

A

decreased

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13
Q

prothrombin time with liver failure

A

increased

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14
Q

jaundice

A

–caused by increased levels of bilirubin in the bloodstream
–yellowish discoloration of skin and deep tissues

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15
Q

when is jaundice noticeable?

A

when bilirubin > 2-2.5 mg/dl

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16
Q

hemolytic jaundice

A

increased breakdown of RBCs

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17
Q

hepatocellular jaundice

A

liver unable to take up bilirubin from blood or unable to conjugate it

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18
Q

obstructive jaundice

A

decreased or obstructed flow of bile

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19
Q

example of cause of obstructive jaundice

A

gallstones

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20
Q

examples of hemolytic jaundice

A

bleeding, polycythemia, pathologic

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21
Q

direct jaundice

A

conjugated (30%)

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22
Q

indirect jaundice

A

unconjugated (70%)

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23
Q

elevations of indirect bilirubin

A

bilirubin overproduction OR impaired liver functioning

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24
Q

elevations of direct bilirubin

A

liver working, but can’t get the bilirubin out

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25
Q

examples of direct bilirubin

A

–bile duct obstruction
–gallstones

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26
Q

what is bilirubin?

A

byproduct of heme breakdown –> mainly hemoglobin

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27
Q

symptoms of jaundice

A

–darker urine
–elevated LFTs
–normal or clay colored stools
–pruritis

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28
Q

viral hepatitis

A

–inflammation of the liver
–hepatitis (not the infection) can occur from other causes (alcohol abuse, drugs, chemicals, and bacteria)

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29
Q

other viruses that cause hepatitis

A

–Epstein-Barr
–cytomegalovirus

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30
Q

pathogenesis of viral hepatitis

A

viral infection –> immune response from inflammatory mediators –> lysis of infected cells –> edema and swelling of tissue –> tissue hypoxia –> hepatocyte death

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31
Q

symptoms of viral hepatitis

A

–similar between all types
–asymptomatic
–abnormal elevated LFTs

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32
Q

when does the prodromal phase of viral hepatitis occur?

A

2 weeks after exposure

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33
Q

symptoms of prodromal phase of viral hepatitis

A

–fatigue
–anorexia
–malaise
–N/V
–HA
–hyperalgesia
–cough
–low-grade fever

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34
Q

hyperalgesia

A

increased pain response

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35
Q

when is viral hepatitis highly transmissible?

A

prodromal phase

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36
Q

what does the icteric phase of viral hepatitis begin with?

A

jaundice

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37
Q

symptoms of icteric phase of hepatitis

A

–jaundice
–dark urine
–clay colored stools
–enlarged liver potentially painful to palpation
–fatigue and abdominal pain

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38
Q

length of icteric phase of hepatitis

A

2-6 weeks

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39
Q

recovery phase of hepatitis

A

–resolution of jaundice
–6-8 weeks after exposure, symptoms diminish
–liver remains enlarged/tender

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40
Q

complications with viral hepatitis

A

–mostly recover completely with no complications
–low mortality rate
–chronic hepatitis
–liver cirrhosis
–liver cancer
–fulminant viral hepatitis

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41
Q

transmission of Hep A

A

fecal-oral, parental, sexual

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42
Q

specifics of Hep A

A

–acute onset with fever
–usually mild severity
–does NOT lead to chronic hepatitis
–usually affects children and adult
–food-borne illness

43
Q

prevention of Hep A

A

–hand hygiene
–vaccine

44
Q

routes of transmission of Hep B

A

–dirty needles (parental)
–unsafe sex (sexual)

45
Q

Hep B specifics

A

–severe disease
–may be prolonged course or develop into chronic
–any age group affected

46
Q

prevention of Hep B

A

–HBV vaccine
–safe sex
–hand hygiene

47
Q

routes of transmission of Hep C

A

–IV drugs (parental)
–unsafe sex (sexual)

48
Q

Hep C specifics

A

–insidious onset
–mild to severe symptoms
–can develop into chronic hepatitis (80%)
–any age is affected

49
Q

prevention of Hep C

A

–screening blood
–hygiene
–NO vaccine

50
Q

what can Hep C cause?

A

–hepatocellular carcinoma
–liver transplant

51
Q

Hep A vaccine series

A

–2 doses, 6 months apart
–all children beginning at 12 months
–special “high risk” populations (traveling, HC, food handlers)

52
Q

Hep B vaccine series

A

–3 doses at least 4 months apart
–all infants beginning as newborns

53
Q

two classes of drugs used for chronic HBV

A

–interferons
–nucleoside analogs

54
Q

treatment indications for HBV pharm

A

–increased AST levels
–hepatic inflammation
–advanced fibrosis

55
Q

disadvantages of HBV pharm

A

–prolonged therapy
–costs and adverse effects
–high relapse

56
Q

who is HCV treatment recommended for?

A

patients with chronic disease

57
Q

HCV treatment regimen

A

direct-acting antiviral therapy and interferon-based

58
Q

Tylenol and hepatitis

A

active hepatitis can only take <2g of Tylenol per day

59
Q

examples of hepatitis meds

A

–entecavir
–tenofovir

60
Q

cirrhosis

A

–irreversible
–inflammatory
–fibrotic

61
Q

effect of fibrosis in liver

A

–leads to obstructive biliary channels and blood flow

62
Q

what do obstructive biliary channels and blood flow lead to?

A

–jaundice
–portal HTN

63
Q

effect of removal of toxin with cirrhosis

A

removal can slow progression, but won’t stop it

64
Q

what is liver regeneration interrupted by with cirrhosis?

A

hypoxia, necrosis, atrophy, and liver failure

65
Q

common cause of cirrhosis

A

–Hep B and C
–excessive alcohol intake
–idiopathic
–non-alcoholic fatty liver disease

66
Q

alcoholic fatty liver

A

–mildest
–asymptomatic
–increased lipogenesis
–reversible if stop drinking

67
Q

alcoholic steatohepatitis

A

–precursor to cirrhosis
–inflammation
–degeneration of hepatocytes
–becomes irreversible

68
Q

alcoholic cirrhosis

A

–fibrosis and scarring alter liver structure
–irreversible

69
Q

symptoms of alcoholic steatohepatitis

A

–jaundice
–anorexia
–edema
–nausea

70
Q

how does alcoholism cause cirrhosis?

A

increased acetylhyde = altered hepatocyte function –> hepatic stellate cells

71
Q

hepatic stellate cells

A

primary cell in liver fibrosis

72
Q

patho of cirrhosis

A

liver cells destroyed –> cells try to regenerate –> disorganized process –> abnormal growth –> poor blood flow and scar tissue –> hypoxia –> liver failure

73
Q

early manifestations of cirrhosis

A

–N/V
–anorexia
–flatulence
–change in bowel habits
–fever
–weight loss
–palpable liver

74
Q

late manifestations of cirrhosis

A

–jaundice
–peripheral edema
–decreased albumin and PT
–ascites
–skin lesions
–hematologic problems
–endocrine problems
–esophageal and anorectal varices
–encephalopathy

75
Q

portal hypertension

A

–resistant portal blood flow = varices and ascites

76
Q

causes of portal hypertension

A

–systemic hypotension
–vascular underfilling
–stimulation of vasoactive systems
–plasma volume expansion
–increased CO

77
Q

complications of portal HTN

A

–variceal hemorrhage
–ascites
–peritonitis
–hepatorenal syndrome
–cardiomyopathy

78
Q

treatment of portal HTN

A

–prevent/treat complications
–no treatment except liver transplant

79
Q

hepatic encephalopathy

A

–liver isn’t filtering out toxins
–increased toxins in brain

80
Q

diagnosis of hepatic encephalopathy

A

LOC = primary driver of diagnosis

81
Q

minimal severity hepatic encephalopathy

A

abnormal results on psychometric or neurophysiological testing without clinical manifestations

82
Q

Grade I hepatic encephalopathy

A

changes in behavior, mild confusion, slurred speech, disordered sleep

83
Q

Grade II hepatic encephalopathy

A

lethargy, moderate confusion

84
Q

Grade III hepatic encephalopathy

A

marked confusion, incoherent speech, sleeping but arousable

85
Q

Grade IV hepatic encephalopathy

A

coma, unresponsive to pain

86
Q

labs and hepatic encephalopathy

A

–correlate with liver labs
–mainly ammonia = LOC changes
–ammonia crosses BBB

87
Q

acute liver failure

A

separate liver failure not caused by cirrhosis or other types of liver disease

88
Q

most common cause of acute liver failure

A

acetaminophen overdose
–treated with acetylcysteine

89
Q

patho of acute liver failure

A

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

90
Q

timing of acute liver failure

A

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

91
Q

symptoms of acute liver failure

A

similar to cirrhosis symptoms

92
Q

treatment of acute liver failure

A

liver transplant

93
Q

class of lactulose

A

hyperosmotic laxative

94
Q

indication of lactulose

A

reduction of ammonia absorption in hepatic encephalopathy

95
Q

where does lactulose work?

A

colon and large intestines

96
Q

MOA of lactulose

A

reduces blood ammonia levels by converting ammonia to ammonium

97
Q

route for lactulose

A

PO or enema/rectal

98
Q

when is lactulose given?

A

–titrated by number of stools or by ammonia levels
–not just high ammonia levels…must have s/s of encephalopathy

99
Q

nursing consideration for giving lactulose

A

make sure patient is not hypokalemic

100
Q

when is rifaximin given?

A

second line of defense if lactulose isn’t working

101
Q

MOA of rifaximin

A

inhibits bacterial RNA synthesis by binding to bacterial DNA

102
Q

route of rifaximin

A

PO

103
Q

side effects of rifaximin

A

–peripheral edema
–nausea
–ascites
–dizziness
–fatigue
–pruritis
–skin rash
–abdominal pain
–anemia

104
Q

specifics of rifaximin

A

–can sometimes be given preventatively
–has been associated with increased risk of c. diff

NUR 326 Exam 2 (7 decks)

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