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NUR326: exam 2 > liver disorders > Flashcards

liver disorders Flashcards

(61 cards)

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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
how is hepatitis C spread?
used or shared needles/syringes sex sharing care items (toothbrush, razor) born to a mom with hep C
26
S/S hepatitis C
asymptomatic stomach pain vomiting yellow eyes or skin
27
hepatitis A vaccine
2 doses, 6 months apart recommended for: all children beginning at 1 year special high risk populations
28
hepatitis B vaccine
3 doses, at least 4 months apart recommended for: all infants beginning as newborns
29
2 classes of drugs used for chronic HBV
interferons nucleoside analogs *usually used together
30
treatment of HBV- who is it for? disadvantages?
only for high-risk patients -increase in AST levels -hepatic inflammation -advanced fibrosis disadvantages: prolonged therapy cost and adverse effects high relapse
31
considerations for HCV pharm
-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
acetaminophen and HCV pharm
chronic hepatitis pt: <2g/day everyone else: <4g/day *in SERIOUS/advanced stage liver disease --> AVOID acetaminophen + NSAIDS
33
cirrhosis
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
fibrosis is a result of
infiltration of WBC that release inflammatory mediators in activation of this fibrotic process
35
chaotic fibrosis leads to
obstructive biliary channels and blood flow --> jaundice and portal HTN
36
common causes of cirrhosis
hepatitis B&C excess alc intake idiopathic non-alcoholic fatty liver disease
37
kupffer cells
cells responsible for removing toxins and other foreign substances from the blood
38
stages of alcoholic liver disease
1. alcoholic fatty liver 2. alcoholic steatohepatitis 3. alcoholic cirrhosis
39
alcoholic fatty liver
mildest asymptomatic reversible fat deposition is caused by increased lipogenesis r/t alcohol intake
40
alcoholic steatohepatitis
precursor to cirrhosis inflammation degeneration of hepatocytes with infiltration of WBC
41
alcoholic cirrhosis
fibrosis and scaring alter liver structure s/s: anorexia, nausea, jaundice, edema
42
patho of cirrhosis
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
stages of liver damage
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
early manifestations of cirrhosis
GI: N/V, anorexia, flatulence, change in bowel habits fever weight loss palpable liver *insidious
45
late manifestations of cirrhosis
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
portal HTN
resistant portal blood flow that leads to varices and ascites
47
causes of portal HTN
systemic hypotension vascular underfilling stimulation of vasoactive (RAAS system) systems plasma volume expansion increased cardiac output, ascites
48
complications of portal HTN
asymptomatic until complications vericeal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy
49
treatment of portal HTN
can do anything for portal HTN except LIVER TRANSPLANT *treat complications that occur
50
hepatic encephalopathy
30-45% cirrhosis patients LOC: primary determinant *graded by severity (minimal, 1, 2, 3, 4)
51
labs with hepatic encephalopathy
correlate with liver labs --> mainly ammonia which is primary chemical driver of LOC changes increase ammonia = increase risk for H.E.
52
ammonia
neurotoxic that crosses BBB marker of toxins built up in the brain
53
acute liver failure (fulminant)
SEPARATE liver failure NOT caused by cirrhosis most common cause: acetaminophen overdose *acetylcysteine (antidote)
54
patho of acute liver failure
edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrated and disrupts the liver tissue *can occur 6-8 weeks after OD
55
s/s acute liver failure and tx
similar to cirrhosis - late stage but do not see cellular changes in liver tx: not much - liver transplant
56
lactulose: class + MOA
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
lactulose: indications + routes
reduction of ammonia absorption in hepatic encephalopathy PO, enema/rectal
58
consideration of lactulose
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
rifaximin MOA
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
rifaximin SE
peripheral edema nausea ascites dizziness fatigue pruritus skin rash abd pain anemia
61
rifaximin route + consideration
PO **ASSOCIATED WITH INCREASED RISK OF C.DIFF

NUR326: exam 2 (12 decks)

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