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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
Q

recovery stage

A
  • resolution of jaundice
  • 6-8 wks after exposure, sx diminish
  • liver remains enlarged/tender
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26
Q

complications of viral hep

A

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

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27
Q

hep a

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

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28
Q

hep b

A

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

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29
Q

hep c

A

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
Q

hep a vaccine series

A

2 doses 6 months apart
- begin at 12 months
- high risk populations

31
Q

hep b vaccine series

A

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

32
Q

two classes for HBV

A

interferons
nucleoside analogs

33
Q

treatment of HBV

A

used for high risk pts only
- inc AST levels
- hepatic inflammation
- advanced fibrosis

34
Q

disadvantages for HBV treatment

A
  • prolonged therapy
  • costs and adverse effects
  • high relapse bc all the cost and se
35
Q

considerations of HCV

A

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
Q

cirrhosis

A

irreversible, inflammatory, fibrotic liver disease
- structural changes that occur from injury
- infiltration of leukocytes that release chemical mediators and activate the fibrotic process

37
Q

what can chaotic fibrosis lead to

A

obstructive biliary channels and blood flow
- jaundice and portal HTN

38
Q

can the liver regenerate

A

liver cells can regenerate but can be dirupted by hypoxia, necrosis, atrophy, and liver failure

39
Q

common causes of cirrhosis

A

Hep B and C
excessive alc intake
idiopathic
NASH, NAFLD

40
Q

what is alc broken down into

A

acetaldehyde

41
Q

what does acetaldehyde do

A

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
Q

what are kupffer cells

A
  • attracts neutrophils which promote inflammation
  • causes toxins to accumulate from translocation bacteria
  • causes cellular mediated immunity to be suppressed
43
Q

most common type of cirrhosis

A

alcoholic

44
Q

stages of alc liver disease

A

alcoholic fatty liver
alcoholic statohepatitis
alcoholic cirrhosis

45
Q

stage: alc fatty liver

A

mild, asymptomatic

46
Q

stage: alc steatohepatitis

A

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
Q

stage: alc cirrhosis

A

fibrosis and scarring alter liver structure
- inflammation, oxidative stress, cellular damage
- cause cellular necrosis

48
Q

pathogenesis of cirrhosis

A

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

49
Q

early manifestations of cirrhosis

A

GI: NV, anorexia, flatulence, change in bowel habits
fever, wt loss
palpable liver
*insidious so hard to diagnosis

50
Q

late manifestations of cirrhosis

A

jaundice
peripheral edema
dec albumin and PT
ascites
skin lesions
hematologic problems (anemia, bleeding)
endocrine problems
esophageal and anorectal varices
encephalopathy

51
Q

Portal HTN

A

Resistant portal blood blood flow due to fibrotic liver
- leads to varies and ascites

52
Q

portal HTN causes

A
  • systemic HypoTN
  • vascular under filling
  • stimulation of vasoactive systems
  • plasma volume expansion
  • inc CO
53
Q

Portal HTN is asymptomatic until

A

Complications like
- variceal hemorrhage
- ascites
- peritonitis
- hepatorenal syndrome
- cardiomyopathy

54
Q

Treatment of portal HTN

A

Prevent
Treat complications
- nothing for portal HTN except transplant

55
Q

Hepatic encephalopathy

A

Alterations in LOC due to ammonia build up in the brain
~30-45% of pts

56
Q

Acute liver failure is also known as

A

Fulminant liver failure

57
Q

What is acute liver failure caused by

A

Acetaminophen overdose
- not cirrhosis

58
Q

Antidote for acetaminophen

A

Acetylcysteine

59
Q

Pathogenesis of acute liver failure

A

Edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrate and disrupts the liver tissue

60
Q

When does acute liver failure occur

A

6-8 weeks after a viral hepatitis or metabolic liver disease
5 days to 8 weeks after an acetaminophen od

61
Q

Signs of acute liver failure

A

Same as cirrhosis

62
Q

Treatment of acute liver failure

A

Liver transplant

63
Q

Lactulose class

A

Hyper osmotic laxative

64
Q

Lactulose indication

A

Reduction of ammonia absorption in hepatic encephalopathy

65
Q

Lactulose MOA

A

Reduces blood ammonia levels by converting ammonia to ammonium

66
Q

Lactulose is given

A

PO, rectal enema
Given by number of stools or by ammonia levels

67
Q

When is Lactulose given

A

When the pt has symptoms of encephalopathy

68
Q

Nursing considerations for Lactulose

A

Make sure the patient is not hypokalemic

69
Q

Rifaximin MOA

A

Inhibits bacterial RNA synthesis by binding to bacterial DNA

70
Q

How is rifaximin given

A

PO

71
Q

Side effects of rifaximin

A

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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