Lab Med 3 Liver

Front 1

Liver fxn

Back 1

Store glycogen, release glucose, absorb fat, fat soluble vit, manufacture cholesterol, bile salts, clotting factor, detox (drug excretion, alcohol breakdown), proteins, ammonia --> urea

Front 2

Liver: Bile salt fxn

Back 2

Breakdown hemoglobin, dissolve dietary fat

Front 3

___ from protein metabolism ends up as ammonia --> converted to ____ in liver so kidneys can excrete

Back 3

Nitrogen; urea

Front 4

LFTs include
APPEBC

Back 4

Albumin
Protein
PT
Bilirubin
Enzymes

Front 5

Liver enzymes

Back 5

ALP
ALT
AST
GGT

Front 6

CMP = ___ + ___

Back 6

BMP + Liver enzymes

Front 7

General categories of liver problems

Back 7

Hepatcocellular dz
Cholestatic dz

Front 8

Disease of liver cells =

Back 8

Hepatocellular dz

Front 9

Hepatocellular dz e.g.

Back 9

Hepatitis
Mononucleosis
Cirrhosis
Liver tumor
Drug injury

Front 10

Fatigue, malaise, anorexia/nausea, jaundice, pruritis, bruising/bleeding, hematemesis, abd pain, swelling, confusion/coma, ammonia --> encephalopathy

Back 10

Hepatocellular dz

Front 11

Liver fxn

Back 11

Store glycogen, release glucose, absorb fat, fat soluble vit, manufacture cholesterol, bile salts, clotting factor, detox (drug excretion, alcohol breakdown), proteins, ammonia --> urea

Front 12

Liver: Bile salt fxn

Back 12

Breakdown hemoglobin, dissolve dietary fat

Front 13

___ from protein metabolism ends up as ammonia --> converted to ____ in liver so kidneys can excrete

Back 13

Nitrogen; urea

Front 14

LFTs include
APPEBC

Back 14

Albumin
Protein
PT
Bilirubin
Enzymes

Front 15

Liver enzymes

Back 15

ALP
ALT
AST
GGT

Front 16

CMP = ___ + ___

Back 16

BMP + Liver enzymes

Front 17

General categories of liver problems

Back 17

Hepatcocellular dz
Cholestatic dz

Front 18

Disease of liver cells =

Back 18

Hepatocellular dz

Front 19

Hepatocellular dz e.g.

Back 19

Hepatitis
Mononucleosis
Cirrhosis
Liver tumor
Drug injury

Front 20

Fatigue, malaise, anorexia/nausea, jaundice, pruritis, bruising/bleeding, hematemesis, abd pain, swelling, confusion/coma, ammonia --> encephalopathy

Back 20

Hepatocellular dz

Front 21

Fatigue, malaise, anorexia, nausea, jaundince, MAJOR pruritits, MAJOR abd pain & pancreatitis, gray or clay colored stool

Back 21

Cholestatic dz

Front 22

Cholestatic dz of?

Back 22

Dz of biliary tree

Front 23

PE signs of liver dz

Back 23

Nothing
Hepatic enlargement
Tender/nodular liver
Jaundice
Edema
Hypotension & tachycardia
Spider angiomata
Nail clubbing
Splenomeagly
Palmar erythema

Front 24

Albumin
-Half life
-___ levels indicate liver damage
-Function:

Back 24

-20 d
-Low
-Regulating amount of fluid in blood

Front 25

Low albumin causes fluid in blood vessels to:

Back 25

Leak out to surrounding tissues --> edema

Front 26

Asterixis

Back 26

An abnormal tremor consisting of involuntary jerking movements, especially in the hands, frequently occurring with impending hepatic coma and other forms of metabolic encephalopathy. Also called flapping tremor or liver flap.

Front 27

Bilirubin results from

Back 27

breakdown of RBC in spleen, marrow and liver

Front 28

Bilirubin synthesis pathway
1. RBC breakdown --> ___ release -->
2. converted to ____ -->
3. Bound to ___ & released into circulation -->
4. (Name) goes to liver & ___form (name)
5. Excreted into ___ via ____
6. Bacteria in GI break down to ___
7. Is _____ (color) until oxidized to ____ & is now ____ (color)

Back 28

1. Hemoglobin release
2. Heme
3. Albumin
4 Unconjugated (indirect) --> conjugated (direct)
5 intestine; hepatobiliary system
6 Urobilinogen
7 colorless; urobilin; brown

Front 29

How bilirubin is conjugated

Back 29

2 glcouronic acid added to unconjugated

Front 30

Urobilinogen --> feces steps

Back 30

Urobilinogen --> stercobilnogen --> stercobilin

Front 31

Urobilinogen --> pee

Back 31

Urobilinogen --> renter circulation --> kidneys --> urobilin

Front 32

___ & ___ can pass through kidneys, ___ cannot

Back 32

Urobilinogen, conjugated
Unconjucated

Front 33

Most times what bilirubin is reported?

Back 33

Total & direct (calc indirect= total - direct)

Front 34

Urine tests for what type of bilirubin?

Back 34

Urobilinogen & conjugated

Front 35

How Jaundice occurs

Back 35

LIver damage --> bilirubin leaks into blood stream --> build up

Front 36

Signs of leaked/built up bilirubin besides yellow skin

Back 36

Dark urine (all being sent back to kidney from circulation), light feces (none making it to intestine)

Front 37

Causes of abnl bilirubin

Back 37

Viral hepatitis
Biliary obstruction
Other liver dz
Cirrhosis
Hemolysis (including hematomas)

Front 38

level of bilirubin required for jaundice of eyes

Back 38

3 mg

Front 39

level of bilirubin required for jaundice of face

Back 39

5 mg

Front 40

level of bilirubin required for jaundice of head to mid abd

Back 40

15 mg

Front 41

level of bilirubin required for jaundice of feet

Back 41

20 mg

Front 42

If bile blocked before enters intestines/bacteria, what happens?

Back 42

still have conjugated but not made into urobili ---> clay stool & clear urine
--Conjugated shows in urine & blood stream b/c things backed up, white stool

Front 43

Bilirubin > __ in newborns leads to complications

Back 43

25

Front 44

Complications of neonate jaundice

Back 44

Hearing loss
Mental retardation
Death

Front 45

When (level) to tx neonate jaundice
-Age < 48 hr & Bili >__
-Age < 72 hr & Bili >__
-Tx bili >__ anytime

Back 45

>15
>18
>20

Front 46

____ jaundice occurs after 1st week of life

Back 46

Breast milk

Front 47

-Cz of Breast milk jaundice
-Tx

Back 47

-Breast milk contains enzymes that deactivate baby's enzymes
-Switch to formula 24-48 h, more frequent feedings

Front 48

How bili lights tx jaundice

Back 48

Photolysis of unconjugated bili to water soluble product

Front 49

-TP or serum total protein measures
-2 major
-Help dx:
-NL level

Back 49

-Amount of protein in blood stream; albumin & globulin
-Kidney/liver dz, blood CA, malnutrition, anl body swelling
-6.5-8.2

Front 50

PT or prothrombin time or INR

Back 50

Increases in liver dz
**Most sensitive indicator of liver dz

Front 51

-Liver enzyme: Alkaline Phosphatase (ALP) fxn
-If elevated --> next step?

Back 51

-Hydrolyze phosphate esters
-Find out source!!

Front 52

Sources of ALP

Back 52

Liver
Biliary tree
Bone
Placenta

Front 53

Cholestatic liver enzymes =

Back 53

GGT
ALP

Front 54

Cholestasis =

Back 54

partial or full blockage of bile duct; GGT & ALP get backed up & spill into blood

Front 55

ALP fxn

Back 55

Metabolize phosphorus & brings energy to body

Front 56

GGP fxn

Back 56

Brings oxygen to tissues

Front 57

If ALP is elevated, first step is?

Back 57

Confirm it's from liver by getting GGP!
Alcohol Loving People ---> Go Get Trashed

Front 58

NL range GGT
Causes of increased GGT

Back 58

5-80
**HEAVY DRINKING**
Obesity
Fatty liver
Meds toxic to liver

Front 59

Causes of elevated ALP & GGP

Back 59

Primary biliary cirrhosis
Fatty liver (statosis)
Alcohol liver dz
Liver inflammation d/t meds herbs
LIver tumors
Gall stones/gall bladder probs

Front 60

If ALP is elevated but not GGT what's the cause?

Back 60

-Bone d/t increased ostoblastic activity
-Metastatic tumor
-pagets
-Fracture
-Nl bone growth

Front 61

ALP sources besides liver

Back 61

Biliary tree
Bone
Placenta (ALP ^ in 3rd trimester)

Front 62

If ALP >5 x NL =

Back 62

Obstruction (extrahepatic)

Front 63

If ALP <3 x NL =

Back 63

(Intrahepatic) hepatitis, cirrhosis, mono, liver tumor, drug injury

Front 64

2 enzymes made in liver to metabolize acids & make proteins

Back 64

ALT
AST

Front 65

-AST AKA
-Fxn

Back 65

SGOT
Catalyze transfer or amino group of apartic acid to alpha ketoglutaric acid

Front 66

If AST is elevated, first step?

Back 66

Confirm w/ elevated ALT

Front 67

Why is ALT used to confirm AST?
(Mnemonic?)

Back 67

Absolute LIver Test b/c it's only in the liver

Front 68

ALT AKA
High levels mean
Predictive of amount of damage?

Back 68

SGPT; alanin aminotransferase
Liver inflammation or damge
NO

Front 69

ALT levels rise and fall over time with ___ dz

Back 69

hep c virus

Front 70

Remembering ALP vs ALT
-P =
-ALT=

Back 70

p = parenchyma
alp = absolute liver test

Front 71

If AST > 10 tx NL hink

Back 71

Viral hepatitis

Front 72

AST < 10 x NL think

Back 72

Extra hepatic obstruction, cirrhosis, tumor, mono

Front 73

AST/ALT **RATIO**
>1 think

Back 73

Cirrhosis
Tumor
Extra hepatic obstruction

Front 74

AST/ALT **RATIO**
<1 think

Back 74

Hepatitis
Mononucleosis

Front 75

Marker for alcohol?

Back 75

GGT

Front 76

If pt is acting strange, get a ___ level

Back 76

Ammonia

Front 77

AST & ALT are ______ (category of enzyme)

Back 77

Transaminases

Front 78

-LDH fxn
-Found:

Back 78

-Catalyze pyruvate to L lactate
-Heart, liver, skeletal m, kidney, lung, eyrhtrocytes

Front 79

If could only give one test for liver if would be?

Back 79

PT

Front 80

AST >10-20
ALT <3

Back 80

Acute hepatitis

Front 81

AST <10
ALP <3

Back 81

Chronic hepatitis, tumor, cirrhosis

Front 82

AST <10
ALP >3

Back 82

Obstruction

Front 83

AST/ALP ratio >1

Back 83

Obstruction, tumor, cirrhosis

Front 84

AST/ALP ratio <1

Back 84

Acute hepatitis, mono

Front 85

E.g.
AST > 20
ALP <3
ALT > 5

Back 85

Acute hepatitis

Front 86

AST <10
ALP >4
ALT <10

Back 86

Obstruction

Front 87

AST <10
ALP <4
ALT <10

Back 87

Cirrhosis

Front 88

-Sickle cell, RUQ pain, chills, fever, vomiting, light stool
-WBC 16K
-Total bili incr
-Direct bili incr
-ALP >10
-AST <3

Back 88

Common duct stone

Front 89

-Total bili incr
-Direct bili incr

Probably ---?

Back 89

obstruction

Front 90

ALP incr suggests?

Back 90

Obstruction!

Front 91

-Enzyme findings in liver CA
-Screening tool

Back 91

-Can be NL or ABNL
-screening with a tumor marker (alpha-fetoprotein)

Front 92

Hep C exposure vs infxn
-Early infection level of ant HCV & why
-Pos antiHCV differentiates:
--Active/passive?
--Acute/chronic?
--Past infx/immunity?
-Follow up:

Back 92

-may be negative, as antibodies may not develop until 4-6 weeks after exposure.
-doesn't distinguish acute from chronic disease or active from past infection nor is it a sign of immunity or protection.
-confirmatory viral load testing. (HCV RNA)

Front 93

Common laboratory abnormality seen in chronic hepatitis C infection

Back 93

Isolated, elevated alanine aminotransferase (ALT)

Front 94

Liver dz & clotting
1. Increased ___ risk
2. Increased ___ risk

Back 94

Increased bleeding risk —
Increased thrombotic risk —

Front 95

Why is there incr thrombitic risk w/ liver dz?
(3 decr in anticoagulants; 2 incr thrombosis)

Back 95

1. Decr liver-synthesized natural anticoagulant proteins C and S
2. Decr antithrombin levels
3. Decr plasminogen
1. Elevated levels of endothelial cell-derived factor VIII and
2. von Willebrand factor (vWF) favor thrombosis formation

Front 96

Why is there increased bleeding risk w/ liver dz?
-Factors t n t f s e th

Back 96

Decr production of non-endothelial cell-derived coagulation factors (eg, factors II, V, VII, IX, X, XI, XIII)

Front 97

Plasmin

Back 97

destroys blood clots by attacking fibrin.

Front 98

How long before a change in albumin levels are seen in liver dz?

Back 98

several Weeks