liver problems

Question 1

major functions of the liver

Answer 1

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

Question 2

what is portal circulation

Answer 2

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

Question 3

what causes jaundice

Answer 3

increased level of bilirubin in the bloodstream

Question 4

hemolytic jaundice

Answer 4

caused by increased breakdown of RBCs

Question 5

hepatocellular jaundice

Answer 5

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

Question 6

obstructive jaundice

Answer 6

caused by decreased or obstructed flow of bile (gallstones)

Question 7

what is bilirubin

Answer 7

by product of heme breakdown –> mainly hemoglobin

Question 8

direct (conjugated) vs indirect (unconjugated) bilirubin

Answer 8

indirect elevations - bilirubin overproduction OR impaired liver functioning

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

Question 9

jaundice clinical manifestations

Answer 9

dark urine
liver enzymes elevated
normal/clay colored stool
pruritus

Question 10

what is viral hepatitis

Answer 10

systemic virus that mainly affects the liver - inflammation of liver

Question 11

hepatitis patho

Answer 11

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

Question 12

clinical manifestations of viral hepatitis

Answer 12

usually asymptomatic
abnormally elevated LFT

Question 13

explain prodromal stage

Answer 13

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

Question 14

icteric phase

Answer 14

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

Question 15

recovery phase

Answer 15

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

Question 16

hepatitis A

Answer 16

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

Question 17

hepatitis b

Answer 17

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

Question 18

hepatitis c

Answer 18

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

Question 19

Hep A vaccine

Answer 19

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

Question 20

Hep B vaccine

Answer 20

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

Question 21

hep c vaccine

Answer 21

there is no hep c vaccine

Question 22

who do you treat in hepatitis patients

Answer 22

high risk patients

increased AST levels
hepatic inflammation
advanced fibrosis

Question 23

what is cirrhosis

Answer 23

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

Question 24

common cirrhosis causes

Answer 24

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

Question 25

stages of alcoholism and liver disease

Answer 25

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

Question 26

cirrhosis patho

Answer 26

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

Question 27

cirrhosis early manifestations

Answer 27

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

Question 28

late cirrhosis manifestations

Answer 28

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)

Question 29

what is portal hypertension

Answer 29

resistant portal blood flow --> leads to varices and ascites

Question 30

causes of portal hypertension

Answer 30

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

Question 31

how to treat portal HTN

Answer 31

can not do anything to treat except liver transplant

Question 32

what is hepatic encephalopathy

Answer 32

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

Question 33

acute liver failure

Answer 33

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

Question 34

patho of acute liver failure

Answer 34

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

Question 35

2 drugs for hepatic encephalopathy

Answer 35

lactulose and rifaximin

Question 36

lactulose

Answer 36

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

Question 37

rifaximin

Answer 37

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