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NUR 326 > Liver > Flashcards

Liver Flashcards

1
Q

major functions of the liver

A
  • metabolism and/or storage of fat, CHO, PRO, vitamins, minerals
  • blood volume reservoir: distends/compresses to alter circulating blood volumes
  • blood filter: helps purify blood
  • blood clotting factor: includes prothrombin and fibrinogen
  • drug metabolism and detoxification
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2
Q

liver cells are called

A

hepatocytes

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3
Q

what is the functional unit of the liver

A

lobules

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4
Q

where is the liver located

A

R epigastric region

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5
Q

what are kupfford cells

A

line the inner liver capillaries and are responsible for removing bacteria and toxins from blood

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6
Q

what is portal circulation

A

the circulatory system that brings blood to the liver from the stomach, spleen, pancrease

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7
Q

where does the blood enter the liver

A

portal vein

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8
Q

absorbed products of the digestion…

A

come directly to the liver and are sent to the lobules

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9
Q

abnormal LFT trends

A

LFT: inc
bilirubin: inc
NH3: inc
serum protein: dec
serum albumin: dec
prothrombin time: inc

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10
Q

jaundice cause

A

inc levels of bilirubin in bloodstream

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11
Q

what level of bilirubin does jaundice become noticeable

A

2-2.5 mg/dl greater

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12
Q

what is jaundice

A

yellowish discoloration of skin and deep tissues

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13
Q

three classifications of jaundice

A

hemolytic –> inc breakdown of RBCs
hepatocellular –> liver unable to take up bilirubin from blood or unable to conjugate it
obstructive –> dec or obstructed flow of bile

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14
Q

what is bilirubin

A

byproduct of heme breakdown

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15
Q

what is conjugated bilirubin

A

aka direct
result from a obstruction, liver working but cant get bile out

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16
Q

what is unconjugated bilirubin

A

aka indirect
bilirubin overproduction or impaired liver functioning

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17
Q

jaundice clinical manifestations

A
  • urine darker
  • liver enzymes elevated
  • stool will be normal or clay colored
  • pruritis due to build up of bilirubin
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18
Q

viral hepatitis causes

A

inflammation of the liver

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19
Q

what are the strains of hepatitis

A

HAV, HBV, HCV
other viruses like epstein barr, CMV
alc abuse, drugs, chemicals, bacteria

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20
Q

viral hepatitis pathogenesis

A

viral infection
immune response: inflammatory mediators
lysis of infected cells
edema and swelling of tissues
tissue hypoxia
hepatocyte death

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21
Q

clinical manifestations of viral hepatitis

A

none, mild to liver failure
elevated LFTs –> not consistent with cellular damage within the liver

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22
Q

stages of hepatitis

A

prodromal
icteric
recovery

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23
Q

prodromal stage

A
  • 2 wks after exposure
  • fatigue, anorexia, malaise, NV, HA, hyperalgesia, cough, low grade fever
  • highly transmissible
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24
Q

icteric stage

A
  • begins with jaundice
  • dark urine, clay colored stools
  • liver enlarged and may be painful to palpation
  • fatigue, abdominal pain, persists or inc in severity
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25
recovery stage
- resolution of jaundice - 6-8 wks after exposure, sx diminish - liver remains enlarged/tender
26
complications of viral hep
most make full recovery with no complications but - higher mortality with elderly and comorbidities - chronic hep, liver cirrhosis, liver cancer, fulminant viral hep --> acute liver failure
27
hep a
transmission via food borne illnesses --> fecal oral, parental, sexual - acute, onset w fever, mild severity - does not lead to chronic hep - affects children and adults - hand hygiene and vaccine
28
hep b
transmission via parental, sexual (IV rugs and unsafe sex) - insidious onset - severe disease and may be prolonged course or develop into chronic - any ages - hand hygiene, vaccine, safe sex
29
hep c
transmission via parental, sexual - insidious onset - mild to severe sx - can develop into severe hepatitis (80%) - any age - leads to hepatocellular carcinoma, liver transplant - hygiene, no vaccine, screening blood
30
hep a vaccine series
2 doses 6 months apart - begin at 12 months - high risk populations
31
hep b vaccine series
3 doses at least 4 months apart - all infants beginning as newborns
32
two classes for HBV
interferons nucleoside analogs
33
treatment of HBV
used for high risk pts only - inc AST levels - hepatic inflammation - advanced fibrosis
34
disadvantages for HBV treatment
- prolonged therapy - costs and adverse effects - high relapse bc all the cost and se
35
considerations of HCV
treatment only for chronic disease - treat when viral load is detectable - treat with direct acting antiviral therapy and interferon based regiments - work very well but very expensive - not more then 2 g of acetaminophen
36
cirrhosis
irreversible, inflammatory, fibrotic liver disease - structural changes that occur from injury - infiltration of leukocytes that release chemical mediators and activate the fibrotic process
37
what can chaotic fibrosis lead to
obstructive biliary channels and blood flow - jaundice and portal HTN
38
can the liver regenerate
liver cells can regenerate but can be dirupted by hypoxia, necrosis, atrophy, and liver failure
39
common causes of cirrhosis
Hep B and C excessive alc intake idiopathic NASH, NAFLD
40
what is alc broken down into
acetaldehyde
41
what does acetaldehyde do
inhibits the export of protein from liver - alters metabolism of vit/min and induces malnutrition alters hepatocyte function and activates stelate cells which are involved in fibrosis
42
what are kupffer cells
- attracts neutrophils which promote inflammation - causes toxins to accumulate from translocation bacteria - causes cellular mediated immunity to be suppressed
43
most common type of cirrhosis
alcoholic
44
stages of alc liver disease
alcoholic fatty liver alcoholic statohepatitis alcoholic cirrhosis
45
stage: alc fatty liver
mild, asymptomatic
46
stage: alc steatohepatitis
precursor to cirrhosis - inc hepatic fat storage, inflammation, degeneration and occurance of hepatocytes w infiltration of WBC inflammation and degradation of hepatocytes - causes edema, N, jaundice, anorexia *stimulating irreversible fibrosis*
47
stage: alc cirrhosis
fibrosis and scarring alter liver structure - inflammation, oxidative stress, cellular damage - cause cellular necrosis
48
pathogenesis of cirrhosis
liver cell destroyed cells try to regenerate disorganized process abnormal growth poor blood flow and scar tissue hypoxia liver failure
49
early manifestations of cirrhosis
GI: NV, anorexia, flatulence, change in bowel habits fever, wt loss palpable liver *insidious so hard to diagnosis
50
late manifestations of cirrhosis
jaundice peripheral edema dec albumin and PT ascites skin lesions hematologic problems (anemia, bleeding) endocrine problems esophageal and anorectal varices encephalopathy
51
Portal HTN
Resistant portal blood blood flow due to fibrotic liver - leads to varies and ascites
52
portal HTN causes
- systemic HypoTN - vascular under filling - stimulation of vasoactive systems - plasma volume expansion - inc CO
53
Portal HTN is asymptomatic until
Complications like - variceal hemorrhage - ascites - peritonitis - hepatorenal syndrome - cardiomyopathy
54
Treatment of portal HTN
Prevent Treat complications - nothing for portal HTN except transplant
55
Hepatic encephalopathy
Alterations in LOC due to ammonia build up in the brain ~30-45% of pts
56
Acute liver failure is also known as
Fulminant liver failure
57
What is acute liver failure caused by
Acetaminophen overdose - not cirrhosis
58
Antidote for acetaminophen
Acetylcysteine
59
Pathogenesis of acute liver failure
Edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrate and disrupts the liver tissue
60
When does acute liver failure occur
6-8 weeks after a viral hepatitis or metabolic liver disease 5 days to 8 weeks after an acetaminophen od
61
Signs of acute liver failure
Same as cirrhosis
62
Treatment of acute liver failure
Liver transplant
63
Lactulose class
Hyper osmotic laxative
64
Lactulose indication
Reduction of ammonia absorption in hepatic encephalopathy
65
Lactulose MOA
Reduces blood ammonia levels by converting ammonia to ammonium
66
Lactulose is given
PO, rectal enema Given by number of stools or by ammonia levels
67
When is Lactulose given
When the pt has symptoms of encephalopathy
68
Nursing considerations for Lactulose
Make sure the patient is not hypokalemic
69
Rifaximin MOA
Inhibits bacterial RNA synthesis by binding to bacterial DNA
70
How is rifaximin given
PO
71
Side effects of rifaximin
Peripheral edema N Ascites Dizzy Fatigue Pruritus Skin rash Abdominal pain Anemia Inc risk of c diff

NUR 326 (20 decks)

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