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NUR326: exam 2 > liver disorders > Flashcards

liver disorders Flashcards

1
Q

functions of the liver

A

-metabolism/storage of fat, PRO, CHO, vitamins and minerals
-blood volume reservoir –> distends and compresses to alter circulating blood volume
-blood filter - purifies by removing bilirubin
-blood clotting factors (prothrombin and fibrinogen)
-drug metabolism and detoxification

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2
Q

portal circulation

A

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

blood enters liver through portal vein

absorbed products from digestion go directly to liver and sent to lobules

“first pass effect”

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3
Q

liver function tests

A

liver enzymes - ALT, AST, Alk Phos: INCREASE
ammonia: INCREASE
protein + albumin: DECREASE
prothrombin time: INCREASE

bilirubin - conjugated (direct) and unconjugated (indirect)

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4
Q

icterus is caused by

A

jaundice - yellowish tint to skin

increased level of bilirubin in blood
> 2-2.5 mg/dL

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5
Q

3 classifications of jaundice

A
  1. hemolytic: increase breakdown of RBC
  2. hepatocellular: liver unable to take up bilirubin from blood or unable to conjugate it
  3. obstructive: decreased/obstructed flow of bile (r/t gallstones)
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6
Q

where can you see jaundice?

A

scelera (whites of eyes)
mucous membranes
palms of hands
soles of feet

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7
Q

bilirubin

A

by product of heme breakdown - mainly Hgb

direct: conjugated
indirect: unconjugated

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8
Q

elevations of INDIRECT bilirubin

A

bilirubin overproduction OR impaired liver fxn

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9
Q

elevations of DIRECT bilirubin

A

liver working, but cannot get bilirubin out
(bile duct obstruction, gall stones)

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10
Q

clinical manifestations of jaundice

A

*darker urine
*elevated liver enzymes
*stools –> normal or clay colored (liver releases bile salts - make poop brown OR liver infection decreases bile production/bile flow is blocked keeps stool clay colored)
*pruritus (d/t bilirubin build up)

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11
Q

viral hepatitis

A

inflammation of liver
A, B, C

can be caused by EBV, CMV + alcohol abuse, drugs, chemicals, bacteria

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12
Q

viral hepatitis: PATHO

A
  1. viral infection
  2. immune response: inflammatory mediators
  3. lysis of infected cells
  4. edema and swelling of tissue
  5. tissue hypoxia
  6. hepatocyte death
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13
Q

clinical manifestations of viral hepatitis

A

typically asymptomatic –> can range from none to mild to liver failure

abnormal elevated LFTs but NOT consistent with cellular damage within liver

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14
Q

3 stages of hepatitis

A
  1. prodromal
  2. icteric
  3. recovery
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15
Q

prodromal stage

A

2 weeks after exposure and HIGHLY contagious

S/S: fatigue, anorexia, malaise, N/V, HA, cough, low-grade fever, hyperalgesia (increased sensitivity to pain)

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16
Q

icteric stage

A

begins with jaundice –> dark colored urine, clay stools
liver is enlarges and painful to palpate
fatigue and abd pain persist or increase

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17
Q

recovery stage

A

6-8 weeks after exposure
symptoms diminish and jaundice resolved
liver still enlarged/tender

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18
Q

complications of viral hepatitis

A

chronic hepatitis
liver cirrhosis
liver cancer
fulminant viral hepatitis –> acute liver failure

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19
Q

hepatitis A

A

transmission: FOOD/WATER contamination, parental, sex

acute onset
fever
mild severity
affects children + adults

prevention: hand hygiene and hep A vaccine

does NOT progress to chronic hepatits

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20
Q

S/S of hep A

A

fatigue
fever
N/V/D
stomach pain
dark pee
pale poop
no appetite
jaundice

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21
Q

where is HAV most common?

A

underdeveloped countries

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22
Q

hepatitis B

A

transmission: parental, sex
insidious onset
severe disease —> 10% develop chronic
all age groups affected

prevention: safe sex, HBV vaccine

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23
Q

hepatitis C

A

transmission: parental, sex
insidious onset
mild-severe symptoms
can develop into chronic (80%)
all age groups affected

treatment: screen blood
*NO VACCINE

~new tx makes it almost completely curable

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24
Q

what does hepatitis C lead to?

A

chronic hep (80%)

hepatocellular carcinoma (liver cancer)
liver transplant

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25
Q

how is hepatitis C spread?

A

used or shared needles/syringes
sex
sharing care items (toothbrush, razor)
born to a mom with hep C

26
Q

S/S hepatitis C

A

asymptomatic

stomach pain
vomiting
yellow eyes or skin

27
Q

hepatitis A vaccine

A

2 doses, 6 months apart

recommended for:
all children beginning at 1 year
special high risk populations

28
Q

hepatitis B vaccine

A

3 doses, at least 4 months apart

recommended for:
all infants beginning as newborns

29
Q

2 classes of drugs used for chronic HBV

A

interferons
nucleoside analogs

*usually used together

30
Q

treatment of HBV- who is it for? disadvantages?

A

only for high-risk patients
-increase in AST levels
-hepatic inflammation
-advanced fibrosis

disadvantages:
prolonged therapy
cost and adverse effects
high relapse

31
Q

considerations for HCV pharm

A

-treatment only recommended for pt with chronic disease
-easily treatable and eliminated in almost all patients
-treat w/ direct acting antiviral therapy and interferon based regiments (+some require nucleoside analog)

32
Q

acetaminophen and HCV pharm

A

chronic hepatitis pt: <2g/day
everyone else: <4g/day

*in SERIOUS/advanced stage liver disease –> AVOID acetaminophen + NSAIDS

33
Q

cirrhosis

A

irreversible, inflammatory, fibrotic liver disease
develops SLOWLY, over many years
*structural changes from injury (alc/virus) and fibrosis

regeneration is disrupted by hypoxia, necrosis, atrophy, liver failure

34
Q

fibrosis is a result of

A

infiltration of WBC that release inflammatory mediators in activation of this fibrotic process

35
Q

chaotic fibrosis leads to

A

obstructive biliary channels and blood flow –> jaundice and portal HTN

36
Q

common causes of cirrhosis

A

hepatitis B&C
excess alc intake
idiopathic
non-alcoholic fatty liver disease

37
Q

kupffer cells

A

cells responsible for removing toxins and other foreign substances from the blood

38
Q

stages of alcoholic liver disease

A
  1. alcoholic fatty liver
  2. alcoholic steatohepatitis
  3. alcoholic cirrhosis
39
Q

alcoholic fatty liver

A

mildest
asymptomatic
reversible

fat deposition is caused by increased lipogenesis r/t alcohol intake

40
Q

alcoholic steatohepatitis

A

precursor to cirrhosis
inflammation
degeneration of hepatocytes with infiltration of WBC

41
Q

alcoholic cirrhosis

A

fibrosis and scaring alter liver structure

s/s: anorexia, nausea, jaundice, edema

42
Q

patho of cirrhosis

A
  1. liver cells destroyed
  2. cells try to regenerate
  3. disorganized process
  4. abnormal growth
  5. poor blood flow and scar tissue
  6. hypoxia
  7. liver failure
43
Q

stages of liver damage

A
  1. healthy liver
  2. fatty liver (deposits of fat lead to enlargement of liver)
  3. liver fibrosis (scar tissue forms)
  4. cirrhosis (growth of connective tissue destroys liver cells
44
Q

early manifestations of cirrhosis

A

GI: N/V, anorexia, flatulence, change in bowel habits
fever
weight loss
palpable liver

*insidious

45
Q

late manifestations of cirrhosis

A

jaundice
peripheral edema
decrease albumin and prothrombin
ascites
skin lesions
hematologic problems (anemia, bleeding)
endocrine problems (amenorrhea)
esophageal and anorectal varies (distended veins r/t portal HTN)
encephalopathy

46
Q

portal HTN

A

resistant portal blood flow that leads to varices and ascites

47
Q

causes of portal HTN

A

systemic hypotension
vascular underfilling
stimulation of vasoactive (RAAS system) systems
plasma volume expansion
increased cardiac output, ascites

48
Q

complications of portal HTN

A

asymptomatic until complications

vericeal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy

49
Q

treatment of portal HTN

A

can do anything for portal HTN except LIVER TRANSPLANT

*treat complications that occur

50
Q

hepatic encephalopathy

A

30-45% cirrhosis patients
LOC: primary determinant
*graded by severity (minimal, 1, 2, 3, 4)

51
Q

labs with hepatic encephalopathy

A

correlate with liver labs –> mainly ammonia which is primary chemical driver of LOC changes

increase ammonia = increase risk for H.E.

52
Q

ammonia

A

neurotoxic that crosses BBB
marker of toxins built up in the brain

53
Q

acute liver failure (fulminant)

A

SEPARATE liver failure NOT caused by cirrhosis

most common cause: acetaminophen overdose
*acetylcysteine (antidote)

54
Q

patho of acute liver failure

A

edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrated and disrupts the liver tissue
*can occur 6-8 weeks after OD

55
Q

s/s acute liver failure and tx

A

similar to cirrhosis - late stage
but do not see cellular changes in liver

tx: not much - liver transplant

56
Q

lactulose: class + MOA

A

class: hyperosmotic laxative

MOA: reduces blood ammonia levels by converting ammonia to ammonium

metabolized in large intestine and induces an acidic environment to reduce ammonia levels

draw water into colon and make poop

57
Q

lactulose: indications + routes

A

reduction of ammonia absorption in hepatic encephalopathy

PO, enema/rectal

58
Q

consideration of lactulose

A

make sure pt NOT hypokalemic

can be given to titrate by # of stools or by ammonia levels
*NOT given just for high ammonia - MUST have S/S of encephalopathy

59
Q

rifaximin MOA

A

second line in lactulose isn’t working
MOA: inhibits bacterial RNA synthesis by binding to bacterial DNA

*initially used as an antibiotic for GI infections

60
Q

rifaximin SE

A

peripheral edema
nausea
ascites
dizziness
fatigue
pruritus
skin rash
abd pain
anemia

61
Q

rifaximin route + consideration

A

PO
**ASSOCIATED WITH INCREASED RISK OF C.DIFF

NUR326: exam 2 (12 decks)

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