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liver (W4) Flashcards

1
Q

what does the liver do?

A

so much stuff!
1. metabolism/storage
2. blood volume reservoir
3. blood filter
4. blood clotting factors
5. drug metabolism and detoxification

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2
Q

liver metabolism

A

fat, cholesterol, protein, vitamins, minerals

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3
Q

blood reservoir

A

distends and compresses to alter circulating blood volume

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4
Q

blood filter

A

helps purify blood

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5
Q

blood clotting factors

A

includes prothrombin and fibrinogen

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6
Q

drug metabolism and detoxification

A

metabolizes drugs and removes toxins

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7
Q

when liver isn’t working…

A

effects all of these things:
1. metabolism/storage
2. blood volume reservoir
3. blood filter
4. blood clotting factors
5. drug metabolism and detoxification

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8
Q

portal circulation

A

brings blood to liver, stomach, intestine, spleen, pancreas

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9
Q

where does blood enter the liver?

A

portal vein

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10
Q

where are absorbed products of digestion sent?

A

directly to liver and sent to lobules

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11
Q

first pass effect

A

liver responsible for first past effect, oral drugs have hight mg, liver takes a portion

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12
Q

what is a LFT

A

liver function test

AST
ALT
Alk phos

not a great indicator of disease severity

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13
Q

LFT

A

LFE, increase
bilirubin
serum ammonia, increase
serum protein, decrease
serum albumin, decrease
PT, increase

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14
Q

jaundice AKA icterus

A

increase levels of bilirubin in blood
visible at 2-2.5
yellow

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15
Q

classifications of jaundice

A
  1. hemolytic, increased 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
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16
Q

bilirubin

A

by productive of heme breakdown
unconjugated versus conjugated

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17
Q

conjugated/direct bilirubin

A

30%
the liver isn’t working, bilirubin can’t get out
obstruction/gallstones

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18
Q

unconjugated/indirect bilirubin

A

70%
elevations when overproduction or impaired liver function

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19
Q

where to look for jaundice

A

sclera of eyes
palms/soles of feet
mucus membranes

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20
Q

jaundice manifestations

A

darker urine
liver enzymes, elevated
stools, normal/clay-colored
pruritis

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21
Q

viral hepatitis

A

systemic virus
liver
inflammation
A/B/C

other types of viruses that can cause inflammation of liver: epsetin barr/cytomegalovirus

inflammation of the liver can occur from: ETOH abuse, certain drugs, bacteria, chemicals

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22
Q

most common types of hepatitis

A

a and b

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23
Q

hepatitis e

A

very dangerous in pregnancy

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24
Q

pathogenesis of hepatitis

A

viral infection
immune response: inflammatory mediators
lysis of infected cells
edema/swelling
tissue hypoxia
hepatocyte death- can lead to LT liver failure

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25
Q

clinical manifestations of hepatitis

A

similar between all types

many times asymptomatic

can range from none, mild, liver failure

causes abnormal LFTs but not consistent with cellular damage within the liver- trend data

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26
Q

3 stages of hepatitis a/b/c

A

prodromal, icteric, recovery

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27
Q

prodromal

A

2 weeks after exposure
fatique, anorexia, malaise, nausea, vommitting, HA, hyperalgesia, cough, low grade fever
HIGHLY TRANSMISSIBLE

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28
Q

icteric (active)

A

begins with jaundice
jaundice, dark urine, clay-colored stools
enlarged liver, painful upon palpation
fatigue, abdominal pain persists or increases in severeity

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29
Q

recovery

A

resolution of jaundice
6-8 weeks after exposure
symptoms diminish
liver remains enlarged/tender

30
Q

viral hepatitis complaints

A

most require with no complications
higher mortality in older/comorbidities

complications include: chronic hepatitis, liver cirrhosis, liver cancer, fulminant viral hepatitis (acute liver failure)

31
Q

hepatitis a

A

foodborne illness
transmissible via fecal oral, parental, sexual
acute onset with fever
usually mild severity
does not lead to chronic hepatitis
affects children/adults
prevent with: hand hygiene, vaccine (get if high risk, traveling to areas with poor sanitation)

32
Q

hepatitis b

A

iv drug use, sexual contact
dirty needles/unsafe sex
insidious
reallllyyyyy long incubation period
can lead to chronic
any age group
vaccine

33
Q

hepatitis c

A

iv drug use/sexual contact/mother to fetal/medical mishaps
insidious
mild to severe symptoms
80% converts to chronic hepatitis
any age is affected
sceening blood, hygiene
no vaccine
leads to hepatocellular carcinoma- transplant
new treatment available! can be cured

34
Q

which hepatitis conditions have vaccines?

A

a and b

35
Q

hep a series

A

2 doses, 6 months apart
recommended for all children beginning at 12 months
special high risk population

36
Q

hep b series

A

3 doses, 4 months apart
recommended for all infants as newborns

37
Q

hep c series

A

kidding! no vaccine

38
Q

HBV pharm considerations

A

chronic disease

  1. interferons
  2. nucleoside analogs

treatment only for high risk patients:
increased AST levels
hepatic inflammation
advanced fibrosis

disadvantages:
prolonged therapy
costly
AE- drug interactions/etc.
high relapse

39
Q

HCV pharm considerations

A

treatment only recommended for chronic disease

treatable and eliminated in most patients

treated with direct anti-viral therapy and interferon based regiments

some require treatment along with nucleoside analogue medication as well

40
Q

hepatitis and tylenol

A

2 gram max, avoid if serious advanced liver disease

41
Q

cirrhosis

A

irriversible inflammatory fibrotic liver disease

42
Q

what happens to the liver during cirrhosis

A

structural changes from injury, either alcohol or virus, and fibrosis

43
Q

what is chaotic fibrosis?

A

leads to obstructive biliary channels and blood flow, causes jaundice and portal hypertension

44
Q

what disrupts the regeneration of liver during cirrhosis?

A

hypoxia, necrosis, atrophy, and liver failure

45
Q

removal of toxin

A

can stop porgression, not reversible

46
Q

cirrhosis common cause

A

hepatitis B and C
excessive alcohol intake
idiopathic
NASH

47
Q

most common type of cirrhosis

A

alcoholic cirrhosis

48
Q

stages of alcoholic liver disease

A

alcohol fatty liver- mildest asymp (reversible)
alcoholic steatohepatitis- the precursor to cirrhosis, inflammation, degeneration of hepatocytes
alcoholic cirrhosis- fibrosis and scarring alter the liver structure

49
Q

pathogenesis of cirrhosis

A

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

50
Q

stages of liver damage

A

healthy liver
fatty liver- deposits of fat lead to liver enlargement
liver fibrosis- scar tissue forms
cirrhosis- growth of connective tissue destroys liver cells

51
Q

early manifestations of cirrhosis

A

slow, insidious process
GI disturbances
fever, weight loss
palpable liver

52
Q

late manifestation of cirrhosis

A

jaundice
peripheral edema
decreased albumin and protein
ascites
skin lesions
hematologic problems
endocrine problems- amenorrhea
esophageal and anorectal varices
encephalopathy

53
Q

portal hypertension

A

resistant portal blood flow, leads to varices and ascites

54
Q

what causes portal hypertension

A

systemic hypotension, vascular underfilling, stimulation of RASS system, plasma volume expansion, increased CO- all lead to ascites

55
Q

portal hypertension is asymp until

A

complications occur- variceal hemmorhage, ascites, peritonitis, heptorenal syndrome, cardiomyopathy

56
Q

portal hypertension is asymp until

A

complications occur- variceal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy

57
Q

fibrosis of the liver

A

irreversible, prevent/treat complications
and wait for liver transplant

58
Q

vascular lesions

A

common in end-stage liver failure

59
Q

hepatic encephalopathy

A

LOC is primary driver of diagnosis

60
Q

encephalopathy is graded by severity

A

minimal to grade 4

61
Q

liver not filtering out toxins, toxins enter the brain, impact LOC- confusion (abnormal psychometric test) to coma (unresponsive)

A

encephalopathy

62
Q

encephalopathy

A

high ammonia levels, neurotoxin, crosses BBB

63
Q

never diagnose encephalopathy based on

A

ammonia level

64
Q

acute liver failure- fulminant liver failure

A

separate liver failure, not caused by cirrhosis of liver

65
Q

most common cause of acute liver failure

A

acetaminophen OD

66
Q

patho of acute liver failure

A

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

67
Q

when does acute liver failure occur

A

6-8 weeks after viral hepatitis or metabolic liver disease

5-8 weeks after acetaminophen OD

68
Q

s/s of acute liver failure

A

similar to cirrhosis

69
Q

treatment for acute liver failure

A

not much, liver transplant

70
Q

lactulose

A

hepatic encephalopathy
hyperosmotic
indication: reduce ammonia absorption in hepatic encephalopathy
MOA: reduces blood ammonia levels by converting ammonia to ammonium
given PO/enema aka recetal
can be given to titrate by number of stools or by ammonia levels
not just given for high ammonia levels- must have s/s of encephalopathy
make sure patient is not hypokalemic

71
Q

rifaximin

A

hepatic encephalopathy
second line if lactulose isn’t working
moa: inhibits bacterial RNA synthesis by binding to bacterial DNA (usually used as an AB for GI infections)
can be given preventative- HCP preference
given PO
SE: peripheral edema, nausea, ascites, dizziness, fatigue, pruritis, skin rash, abdominal pain, anemia
associated with increased risk of c diff

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