P3 Therapeutics Test 2 Liver Therapeutics

Front 1

what is unique about the livers blood supply

Back 1

it gets blood via the portal vein and hepatic artery

Front 2

what is unique about the liver as an organ

Back 2

it can regenerate and has a huge reserve capacity (can take a lot of damage before you see S/S)

Front 3

what are the hepatocytes in contact with

Back 3

bile canaliculus (canals that run blood throughout liver)
blood

Front 4

what alterations to hepatocytes can cause liver complications

Back 4

death of hepatocytes - no longer able to carry out functions

or alteration of hepatocyte blood supply (ex cirrhosis causes scarring and the new tissue will be fibrous and have a decreased amount of blood reaching the hepatocytes)

HEPATOCYTE DEATH AND DECREASED BLOOD SUPPLY ARE THE MAIN COMPLICATIONS

Front 5

how can cirrhosis lead to portal HTN

Back 5

when cirrhosis occurs the liver regnerates but the new tissue is fibrotic/scarred so this changes the blood flow to the liver what results is blood backing up into the portal vein causing an increase in pressure therefore leading to portal HTN

Front 6

when would you classify someone as having ESLD

Back 6

when they display S/S b/c it takes substantial amount of damage for these S/S to occur therefore disease is very severe

Front 7

what are the functions of the liver

Back 7

synthesis
biotransformation/metabolism
storage

Front 8

what does the livery synthesize

Back 8

proteins, clotting factors
cholesterol and lipoproteins

Front 9

what does the liver biotransform/metabolize

Back 9

lipids into lipoproteins
ammonia > urea
amino acids > urea
Hemoglobin > bilirubin
drugs/hormones/carbs/AA

Front 10

what does the liver store

Back 10

glycogen
copper
vit B12

Front 11

what is the most common cause of liver disease

Back 11

chronic hep C

Front 12

how many alcoholic drinks a day does it take for CLD to begin to develop

Back 12

4

Front 13

what metabolic diseases can cause CLD

Back 13

alpha 1 antitrypsin deficiency - detoxifies things
hereditary hemochromatosis - increase RBC/iron (iron toxicity)
wilson's disease - copper buildup in liver

Front 14

what cholestatic diseases cause CLD

Back 14

primary or secondary biliary cirrhosis - bile backs up and kills hepatocytes

primary sclerosing cholongitis - autoimmune disease

Front 15

what are causes of CLD

Back 15

chronic viral hepatitis ( C>B>D)
metabolic diseases
cholestatic diseases
alcohol abuse
drugs

Front 16

what are the main causes of CLD in america

Back 16

hep C
alcohol abuse

Front 17

what is the pathophysiology of CLD

Back 17

necrosis of hepatocytes leads to fibrotic changes

resistance of blood flow - leading to increase pressure in portal vein

decrease synthesis - proteins/clotting factors

decrease metabolic capacity

Front 18

how are most of the problems in liver disease noted and why

Back 18

via labs b/c S/S don't develop until disease is fairly advanced

Front 19

what are some things you may see in the history/physical of someone with CLD

Back 19

jaundice - seen later in disease
right upper quadrant pain
dark urine - due to bilirubin breakdown

splenomegaly - spleen normally not palpable

hepatomegaly - seen early in disease due to inflammation but once scar tissue is formed liver shinks and is no longer palpable

spider angiomata
palmar erythema - estrogen
gynecomastia - estrogen

Front 20

would you see an increase or decrease in estrogen in CLD pt and why

Back 20

increase due to decrease metabolism of estrogen precurssors and increase testosterone binding by sex binding globulin

Front 21

what are some things you can do to prevent CLD

Back 21

moderate alcohol intake
Hep B vaccination (Hep A if already have liver disease)
decrease exposure to Hep C (Transmitted like HIV)
avoid/minimize hepatotoxic drugs

Front 22

why is it recommended that pt get Hep A vaccination if they already have liver disease

Back 22

if you have cirrhosis and get Hep A you have a worse outcome

Front 23

what is the recommended amount of drinks for a man and women to prevent CLD

Back 23

<= 2 men
<= 1 women

if you have liver disease, hep C, or on hepatotoxic drugs NO ALCOHOL

Front 24

what are the downfalls of LFT tests

Back 24

most access damage NOT FUNCTION
don't truly reflect severity

Front 25

what can liver disease be broken in to

Back 25

hepatocellular disease - death of hepatocytes
cholestatic disease - back up of bile

these can overlap since bile is very irritating and can lead to death of hepatocytes therefore making a hepatocellular disease as well

Front 26

what are the tests for hepatocellular injury

Back 26

aminotransferases (AST/ALT)
lactate dehydrogenase (LDH)

Front 27

what does Aminotransferases (AST/ALT) tell us and what are the properties of these enzymes

Back 27

intracellular enzymes that get released into circullation when hepatocytes die

indicate hepatic inflammation and necrosis (doesn't tell you severity or if irreversible)

Front 28

do AST/ALT represent long term damage, why or why not and what are they good markers for

Back 28

they don't represent long term damage b/c hepatocytes die and regenerate

they are good markers of liver damage and injury BUT NOT FUNCTION

Front 29

what lab is most specefic for liver disease

Back 29

isoenzyme LDH5

Front 30

what are the properties of Lactate Dehydrogenase (LDH)

Back 30

less specefic than aminotransferases

Front 31

why must you use caution when looking at AST/ALT/LDH in pts with severe disease

Back 31

this is because pt with severe disease are no longer actively killing off their hepatocytes so they will have NORMAL AST/ALT

Front 32

what are the tests for cholestatic disease

Back 32

Alkaline phosphatase (ALP)
GAMMA glutamyl transpeptidase (GGTP)

Front 33

what is the major draw back of Alkaline phosphatase

Back 33

it isn't only found in the liver but also in the bone so increased levels may be indicator of bile back up but may be an indicator of bone turn over therefore HAVE TO CHECK GGTP

Front 34

what is the purpose of checking GAMMA glutamyl transpeptidase (GGTP)

Back 34

helps determine the cause of the elevated ALP (cholestatic disease or increased bone turnover)

Front 35

what are the tests for metabolic capacity

Back 35

Bilirubin

check total bilirubin
-increase in total bilirubin shows that the liver not processing bilirubin properly and is a good marker of liver disease

Front 36

is bilirubin relevant for drug dosing

Back 36

no

Front 37

what are the tests for synthetic capacity

Back 37

albumin
Prothombin time/INR

Front 38

what do albumin levels tell you

Back 38

livers synthetic capacity

decrease synthesis seen in late stages of liver disease when the liver is unlikely to bounce back

Front 39

what are the most useful markers of advanced disease

Back 39

albumin
INR/PT

Front 40

what is the issue with albumin levels

Back 40

also affected by malnutrition and chronic illness

Front 41

what is a good overall marker of health

Back 41

albumin

decrease albumin = increased mortality

Front 42

what does prothombin time/INR tell us

Back 42

livers synthetic capacity
elevation is an indicator of severe disease

Front 43

what is the issue with prothombin time/INR

Back 43

also affected by malnutrition and vit K intake

Front 44

what is the purpose of giving a pt with an elevated INR vit K

Back 44

if pt responds to vit K then increased INR due to vit K deficiency

if pt doesn't respond to vit K then increased INR due to inability to make clot factors therefore giving them vit K will do nothing

Front 45

what are the most useful tests in determining significant advanced liver disease

Back 45

albumin
INR

Front 46

what are some of the complications of chronic liver disease

Back 46

esophageal varicies
ascites
encephalopathy
hepatorenal syndrome
bleeding disorders
hepatocellular carcinoma
spontaneous bacterial peritonitis (SBP)

Front 47

what does high E

Back 47

means a lot of drug will be extracted via 1st pass

THIS IS BAD

Front 48

what BZD can we give

Back 48

temazepam
oxazapam
lorazepam

mainly phase 2