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liver (W4) Flashcards

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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
clinical manifestations of hepatitis
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
26
3 stages of hepatitis a/b/c
prodromal, icteric, recovery
27
prodromal
2 weeks after exposure fatique, anorexia, malaise, nausea, vommitting, HA, hyperalgesia, cough, low grade fever HIGHLY TRANSMISSIBLE
28
icteric (active)
begins with jaundice jaundice, dark urine, clay-colored stools enlarged liver, painful upon palpation fatigue, abdominal pain persists or increases in severeity
29
recovery
resolution of jaundice 6-8 weeks after exposure symptoms diminish liver remains enlarged/tender
30
viral hepatitis complaints
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
hepatitis 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
hepatitis b
iv drug use, sexual contact dirty needles/unsafe sex insidious reallllyyyyy long incubation period can lead to chronic any age group vaccine
33
hepatitis c
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
which hepatitis conditions have vaccines?
a and b
35
hep a series
2 doses, 6 months apart recommended for all children beginning at 12 months special high risk population
36
hep b series
3 doses, 4 months apart recommended for all infants as newborns
37
hep c series
kidding! no vaccine
38
HBV pharm considerations
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
HCV pharm considerations
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
hepatitis and tylenol
2 gram max, avoid if serious advanced liver disease
41
cirrhosis
irriversible inflammatory fibrotic liver disease
42
what happens to the liver during cirrhosis
structural changes from injury, either alcohol or virus, and fibrosis
43
what is chaotic fibrosis?
leads to obstructive biliary channels and blood flow, causes jaundice and portal hypertension
44
what disrupts the regeneration of liver during cirrhosis?
hypoxia, necrosis, atrophy, and liver failure
45
removal of toxin
can stop porgression, not reversible
46
cirrhosis common cause
hepatitis B and C excessive alcohol intake idiopathic NASH
47
most common type of cirrhosis
alcoholic cirrhosis
48
stages of alcoholic liver disease
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
pathogenesis of cirrhosis
liver cells destroyed cells try to regenerate disorganized process abnormal growth poor blood flow and scar tissue hypoxia liver failure
50
stages of liver damage
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
early manifestations of cirrhosis
slow, insidious process GI disturbances fever, weight loss palpable liver
52
late manifestation of cirrhosis
jaundice peripheral edema decreased albumin and protein ascites skin lesions hematologic problems endocrine problems- amenorrhea esophageal and anorectal varices encephalopathy
53
portal hypertension
resistant portal blood flow, leads to varices and ascites
54
what causes portal hypertension
systemic hypotension, vascular underfilling, stimulation of RASS system, plasma volume expansion, increased CO- all lead to ascites
55
portal hypertension is asymp until
complications occur- variceal hemmorhage, ascites, peritonitis, heptorenal syndrome, cardiomyopathy
56
portal hypertension is asymp until
complications occur- variceal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy
57
fibrosis of the liver
irreversible, prevent/treat complications and wait for liver transplant
58
vascular lesions
common in end-stage liver failure
59
hepatic encephalopathy
LOC is primary driver of diagnosis
60
encephalopathy is graded by severity
minimal to grade 4
61
liver not filtering out toxins, toxins enter the brain, impact LOC- confusion (abnormal psychometric test) to coma (unresponsive)
encephalopathy
62
encephalopathy
high ammonia levels, neurotoxin, crosses BBB
63
never diagnose encephalopathy based on
ammonia level
64
acute liver failure- fulminant liver failure
separate liver failure, not caused by cirrhosis of liver
65
most common cause of acute liver failure
acetaminophen OD
66
patho of acute liver failure
edematous heptocytes and patchy areas of necrosis and inflammatory cell infiltrates and disrupts the liver tissue
67
when does acute liver failure occur
6-8 weeks after viral hepatitis or metabolic liver disease 5-8 weeks after acetaminophen OD
68
s/s of acute liver failure
similar to cirrhosis
69
treatment for acute liver failure
not much, liver transplant
70
lactulose
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
rifaximin
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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