Lab Medicine

Front 1

how do liver enzymes tell you whether liver dysfunction is due to cell necrosis or obstruction?

Back 1

obstruction - increased ap, increased direct bilirubin, increased ggt

necrosis (hepatitis or something) - increased ast and alt

enzymes being induced vs enzymes leaking from dead cells

Front 2

what are some biliary obstruciton markers?

Back 2

alkaline phosphatase - production increased in response to extrahepatic obstruction of the biliary tree

bilirubin

ggt (synthesis is increased by cholestasis, alcohol, and drugs like phenobarbitol)

Front 3

difference b/t direct and indirect bilirubin?

Back 3

conjugated bilirubin can be measured directly

unconjugated bilirubin is measured indirectly

Front 4

what do high levels of indirect bilirubin indicate?

Back 4

hemolytic disease

Front 5

what increases ggt?

Back 5

cholestasis
alcohol
drugs (phenobarbitol)

Front 6

what kind of increase in ap would an extrahepatic vs intrahepatic block cause?

Back 6

intrahepatic - 2-3 fold increase
extrahepatic - >3 and up to 10-11 fold worse, a greater increase!

Front 7

what do incresed alt and ast tell you about the liver?

Back 7

cell necrosis

Front 8

how can you tell where elevated AP came from?

Back 8

liver lives, bone burns

liver is heat resistant isoform

now you can do electrophoresis

Front 9

what does albumin tell you about liver disease?

Back 9

acute - increased albumin
chronic - decreased albumin

Front 10

how would you differentiate b/t obstructive and hepatocellular liver disease just using AST and AP

Back 10

AST > 3x
AP < 2x
hepatocellular

AST <3x
AP >2x
obstructive

Front 11

4 Fs predisposing to gallstones

Back 11

fat female fertile forty

Front 12

what is wilson's disease?

Back 12

copper overload

Front 13

which is worse, hepatitis A or B

Back 13

B is much worse

A always resolves in 6 weeks
B can be acute and self limiting, resolving in 6 months. it can also become chronic

Front 14

how is hepatitis b usually diagnosed

Back 14

HepB surpresence of these denotes recoveryface Ag

Front 15

what test can tell you if you are going to recover from hepatitis B?

Back 15

IgG to the surface antigen (vs IgM)

Front 16

how does HepB kill you?

Back 16

all the liver functions get screwed up

gluconeogenesisis
plasma protein synthesis

Front 17

are AST, ALT, and LDH sensitive or specific markers for hepatocellular liver disease?

Back 17

they are sensitive but not specific. good for screening. catch true positives but also give false positives

Front 18

what 2 antibodies do a sandwich assay use?

Back 18

capture antibody and detection antibody

Front 19

how can albumin be used to follow progression of nephropathy

Back 19

micro albumin in urine

Front 20

when would you measure glycosylated albumin?

Back 20

in a diabetic patient with an unstable form of hemoglobin where glycosylated hemoglobin cannot be measured

Front 21

formula and use for sensitivity

Back 21

sensitivity is used to rule out

sens = TP / (TP + FN)

Front 22

formula and use for specificity

Back 22

specificity is used to rule in

spec = TN / (TN + FP)

Front 23

fasting glucose level for DM

Back 23

126

Front 24

OGTT level for DM

Back 24

200

Front 25

why does someone in DKA have hyponatremia?

Back 25

sodium goes down 1.6 mmol/L for every 100 glucose because it is diluted by the increased plasma volume

Front 26

why does someone in DKA have hyperkalemia?

Back 26

acid exchanges for K

Front 27

does someone in DKA have high or low intracellular potassium?

Back 27

low because H+ exchanges for it!

Front 28

what is Cl level of someone in DKA?

Back 28

HCO3 is decreased
Cl is decreased too because it shifts into cells in exchange for HCO3 (AE)

Front 29

why is BUN elevated in DM type I?

Back 29

they are breaking down protein!

Front 30

what is osmolar gap?

Back 30

difference between measured and calculated osmolyte level
measured - (2NA + urea + glucose)
greater than 10 is abnormal

Front 31

what can elevate osmolar gap

Back 31

acetoacetate, acetate, and BHBA
ethanol
greater than 10 is abnormal

Front 32

what is anion gap

Back 32

diff b/t levels of major anions and cations.

indicates presence of mystery anions
such as ketones

Front 33

difference b/t isoenzymes and isoforms?

Back 33

isozymes are from different loci

isoforms are with different post trans mods

Front 34

3 types of CK?

Back 34

CK MM
CK MB - heart isoenzyme
CK BB

Front 35

where is CK MB

Back 35

heart

Front 36

where is CK MM

Back 36

muscle

Front 37

what is CKMB/CK

Back 37

a ratio which is better to use because there is some CKMB in muscle

Front 38

what is the cutoff point for normal CKMB/CK

Back 38

2.5%

Front 39

what is CKM+B+ CKM+B- CKM-B+ and CKM-B-

Back 39

+ and - are isoforms. - has an amino acid cleaved.

Front 40

what is a macro enzyme?

Back 40

enzymes aggregated to circulating IGs. this keeps them from being cleared and they elevated measured nzm levels (false psitives)

Front 41

what can increase myoglobin

Back 41

skel muscle injury (even minor - lifting weights)
MI
renal failure

Front 42

is troponin I elevated by renal failure?

Back 42

NO

Front 43

how many hours after a heart attack will troponin I be detectable?

Back 43

8-48 hours after
elevated up to a week or so

Front 44

which LDH isozyme is concentrated in the heart?

Back 44

LDH-1

Front 45

what is the temporal change for CKMB like? vs troponin I

Back 45

up and down in 48 hours
troponin stays high for about a week

Front 46

when should you order cardiac markers

Back 46

on admission
2-4 hours
6-9 hours (troponin should be elevated by now even if not at admission!!!)

Front 47

why does a normal cardiac marker not rule out MI?

Back 47

serial measurement (temporal) must be done@!@@@@

Front 48

wTf are heterophile antibodies?

Back 48

they bind to all sorts of animal antibodies and can form a bridge in a sandwich assay between the detection and the capture antibody!!!