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NUR 326 Exam 2 > liver problems > Flashcards

liver problems Flashcards

1
Q

major functions of the liver

A

located in right upper gastric
metabolism and/or storage of fat, carbohydrates, protein, vitamins, minerals
blood volume reservoir - distends/compresses to alter circulating blood volume
blood filter
blood clotting factors
drug metabolism and detoxification

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2
Q

what is portal circulation

A

portal circulatory system brings blood to the liver from the stomach, intestines, spleen, and pancreas
–> 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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3
Q

what causes jaundice

A

increased level of bilirubin in the bloodstream

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4
Q

hemolytic jaundice

A

caused by increased breakdown of RBCs

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5
Q

hepatocellular jaundice

A

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

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6
Q

obstructive jaundice

A

caused by decreased or obstructed flow of bile (gallstones)

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7
Q

what is bilirubin

A

by product of heme breakdown –> mainly hemoglobin

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8
Q

direct (conjugated) vs indirect (unconjugated) bilirubin

A

indirect elevations - bilirubin overproduction OR impaired liver functioning

direct elevations - liver working but can’t get the bilirubin out
-bile duct obstruction gallstones

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9
Q

jaundice clinical manifestations

A

dark urine
liver enzymes elevated
normal/clay colored stool
pruritus

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10
Q

what is viral hepatitis

A

systemic virus that mainly affects the liver - inflammation of liver

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11
Q

hepatitis patho

A

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

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12
Q

clinical manifestations of viral hepatitis

A

usually asymptomatic
abnormally elevated LFT

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13
Q

explain prodromal stage

A

2 weeks after exposure
fatigue, anorexia, malaise, n/v, h/a, hyperalgesia (increase pain response), cough, low grade fever
highly transmissible

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14
Q

icteric phase

A

active phase; 1-2 weeks after prodromal
begins with jaundice
dark urine, clay colored stools
liver enlarged and may be painful to palpation
fatigue abdominal pain persists or increases in severity

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15
Q

recovery phase

A

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

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16
Q

hepatitis A

A

food-borne
transmission - fecal-oral, parental, sexual
acute onset with fever
does NOT lead to chronic hepatitis
hand hygiene, hep A vaccine

17
Q

hepatitis b

A

transmission: IV drug use and sexual
insidious onset - really long incubation –> maybe 60-100 days before symptoms
severe disease, may be prolonged course or develop into chronic
HBV vaccine and safe sex and hygiene

18
Q

hepatitis c

A

transmission: parental, sexual, mother to fetus
higher chance of chronic
screening blood, hygiene, NO VACCINE

19
Q

Hep A vaccine

A

2 doses 6 months apart
recommended for children beginning at 12 months
special high risk populations

20
Q

Hep B vaccine

A

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

21
Q

hep c vaccine

A

there is no hep c vaccine

22
Q

who do you treat in hepatitis patients

A

high risk patients

increased AST levels
hepatic inflammation
advanced fibrosis

23
Q

what is cirrhosis

A

scarring
irreversible inflammatory fibrotic liver disease
structural changes from injury (alcohol/virus)
leads to obstructive biliary channels and blood flow –> jaundice and portal hypertension

24
Q

common cirrhosis causes

A

hep b and c
excessive alcohol intake
idiopathic
NASH (non alcoholic fatty liver disease)

25
Q

stages of alcoholism and liver disease

A

alcoholic fatty liver (first stage) - mildest, asymptomatic –> reversible if drinking stops

alcoholic steatohepatitis - increased hepatic fat storage –> precursor to cirrhosis; inflammation and degeneration

alcoholic cirrhosis - fibrosis and scarring alter liver structure - cellular damage

26
Q

cirrhosis patho

A

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

27
Q

cirrhosis early manifestations

A

Gi disturbances : n/v, anorexia, flatulence, change in bowel habits
fever, weight loss
palpable liver

28
Q

late cirrhosis manifestations

A

jaundice, peripheral edema, decreased albumin and PT, ascites, skin lesions, hematologic problems (anemia, bleeding), endocrine problems, esophageal and anorectal varices (distended veins),encephalopathy (toxins build up)

29
Q

what is portal hypertension

A

resistant portal blood flow –> leads to varices and ascites

30
Q

causes of portal hypertension

A

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

31
Q

how to treat portal HTN

A

can not do anything to treat except liver transplant

32
Q

what is hepatic encephalopathy

A

liver is not filtering toxins –> toxins build up in brain –> cause confusion –> lead to coma

33
Q

acute liver failure

A

separate liver failure not caused by cirrhosis or other type of liver disease
most common cause is acetaminophen overdose –> can be treated with acetylcysteine

34
Q

patho of acute liver failure

A

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

35
Q

2 drugs for hepatic encephalopathy

A

lactulose and rifaximin

36
Q

lactulose

A

hyperosmotic laxative
MOA: reduces blood ammonia levels by converting ammonia to ammonium (drawing water into colon to make them poop)
make sure pt is not hypokalemic –> monitor potassium

37
Q

rifaximin

A

second line if lactulose isnt working
MOA: inhibits bacterial RNA synthesis by binding to bacterial DNA
SE: peripheral edema, nausea, ascites, dizziness, fatigue, pruritus, skin rash, abdominal pain, anemia

associated with increased risk of C. diff

NUR 326 Exam 2 (7 decks)

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