lab Flashcards by Angela Maestre

diagnose a patient w/ High GGT (& normal ALP, AST, ALT)

Alcoholism & drugs

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diagnose a patient w/ High GGT & High ALP

cholestasis

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diagnose a patient w/ High GGT, Hi ALT & Hi AST (& normal ALP)

Hepatocellular disease

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diagnose a patient w/ High ALP (& normal GGT)

Skeletal bone disease (occur in pregnant females)

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State where in&direct biliruben can appear whther in plasma or urine

In: plasma (bc insoluble in water)
Direct: plasma & urine (bc water soluble)

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Equation to finding [ ] of test =

[ Abs(test) / Abs(Std) ] x C(std)
*NOTE: equ. comes from 
A(test)     C(test)
\_\_\_\_\_ = \_\_\_\_\_
A(Std)     C(Std)

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3 isoenzymes of CK & location in the body

CKBB: brain
CKMB: cardiac muscle
CKMM: skeletal muscle

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Equation to finding CK-MB activity =

*Significance of results if >5 or <5

(CK-MB / CK) x 100
* >5 = myocardial infarction
<5 = damage in skeletal muscles

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Ideal marker for diagnosing AMI & drawback

a) cTroponin (cardiac troponin)

b) Re-infarcture

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2 Drawbacks for using CK-MB as a marker for diagnosing AMI

CK-MB won’t rise till 4-8hrs after chest pain begins

2. rise in CK-MB may be masked by a rise in CK-MM => %CK activity < 5% = F.neg. result

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CK-MB is calculated by measuring CK-_ & multiplying its [ ] by _ (bc CK-_ is inactivated by an Ab)

a) B
b) 2
c) M (inactivated by Anti-CKMM Ab)

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Where can you find ALT, AST, ALP & GGT

ALT: hepatocyte
AST: hepatocyte, RBC, skeletal muscles
ALP: bone, hepatic, placenta
GGT: liver

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Enzyme that converts unconjugate to conjugate bilirubin

UDP / glucurunosyl-transferase

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GIlbert’s syndrome causes _ due to reduced activity of _

a) hyperbilirubinameia

b) glucurunosyl-transferase

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What liver function does bilirubin & Albumin look into?

Albumin: Liver synthesis

- BIlirubin: Liver excretion

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Frieldwald formula: ie Total cholesterol =

*what situation would make formula in valid?

HDL + LDL + VLDL

*TG >4.5mM = Invalid

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LDL equ. (in mM) =

Tc - HDL - Trig/2.17

*bc VLDL = Trig/2.17 (mM)

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LDL equ. (in mg/dL) =

Tc - HDL - Trig/5

*bc VLDL = Trig/5 (mg/dL)

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Describe the condition: familial hypercholesterolaemia

primary disorder of lipoprotein metabolism (hyperlipidaemia)
Inc. LDLc in blood
*defects in LDL receptor (bc mutations) = not absorb LDL
OR excess production of LDL
OR ApoB100 is faulty

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Describe the condition: Hyperlipidemia

Inc. TG OR Inc. Chol.

- elevated lipoproteins OR lipids (Both = combined/familial hyperlipidemia/Hyperlipoproteinemia)

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Cockcroft–Gault equation “Body weight – Age - Sex” to give Creatinineclearance(mL/min)

[140 - age(yrs)] x weight(kg)

815 (OR 0.85 fem.) x serum creatinine (mmol)

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In the lab how was creatinine separated from other plasma proteins?

precipitate plasma proteins w/ tungstic acid & separate from supernatant (has creatinine)
react supernatant w/ picrcic acid => red (Jaffe’s Rxn) => measure absorbance

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What molecule interfered w/ creatinine in Jaffe’s reaction & how it effects results? A way to increase specificity on creatinine?

a) acetoacetate = falsely increased results

b) Aluminum silicate (Lloyd’s reagent) - bind to & isolate creatinie ONLY

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risk factors for atherosclerosis

> 5 mM LDL c
> 4.5 mM TG
Obese
diabetes mellitus
smoking
hypertension

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Characteristics of hyperkalemia

- Hyperglycemia (low insulin) - acidosis - Hyponatremia - Addison's syndrome (low aldosterone) - Low GFR (Inc. K+ reabsorption & retention) [bc heart can undergo cardiac arrest = dec. blood flow]

Characteristics of hypokalemia

- Hypoglycemia (High insulin) - Alkalosis - Hypernatremia - Conn syndrome (High aldosterone) - renal tubular acidosis (Dec. K+ reabsorption)

hypokalemia can be caused by

- GI tract poor intake - Excess GI loss (feces) - Excess renal loss (diuretic) bc aldosterone & cortisol secretions - Transmembrane redistribution

Plasma creatinine [inc. OR dec.] as GFR decrease

increase

Equation for GFR when doing the creatinine clearance test

[urine creatinine] x urine vol. (x1000*) ---------------------------------------------------- [plasma creatinine] x 24 x 60 min *in lab: convert mM to uM

Smith line-Gardner formula to calulate osmolality =

2[Na] + [Glu] + [Urea]

decreased GFR may be due to

- pre-renal factors: decreased blood flow - kidney or renal disease: dec. functioning nephron - post-renal: obstruction by renal stones / enlarged prostate

Find abs. Beer's equation

Abs = E x C x l

De-ritis equation & significance of results

a) AST÷ALT | b) >2.0 = alcoholic liver disease

Purpose of the De ritis equation

> differentiate between causes of hepatocellular damage or hepatotoxicity (e.g. alcoholic)

Which marker for liver synthetic capacity declines the earliest?

Prothrombin time

Describe Wilson's disease

excess copper in tissues due to a lack of serum ceruloplasmin

Difference b/w regenerative & regurgitative/obstructive jaundice

- regenerative: excess haemolysis | - regurgitative: bc of cholestasis

markers for hepatocellular damage

ALP, AST, ALT, GGT

markers for liver excretory function

bilirubin

Markers for liver synthetic function

Albumin, prothrombin, Glucose, ammonia, LDH, 5' nucleotidase

Substrate, product, activator, pH of alkaline phosphatase

- substrate: p-nitrophenol phosphate - product: p-nitrophenol - Activator: magnesium sulfate - pH: ~10

diuretics results in __ potassium excretion in kidney

inc

excretion of potassium by the kidney _ in acidosis

decreases

elevated urea & creatinine => [hi / lo / normal]

low

creatinine is from the break down of....

creatinie phosphate in the muscle

HDL from cells travels in blood w/ Apo-_ (apolipoprotein) to the _ where it is taken up by cells when it's recognised by _ (receptor)

a. Apo-A1 b. Liver c. ABCA1 (HDL receptor)*

LDL from cholesterol travels in blood w/ Apo-_ (apolipoprotein) to the _ where it is taken up by cells when it's recognised by a (receptor)*

a. Apo B-100 b. cells c. LDL receptor*

Apolipoprotein (Apo) is like a belt for cholesterol. What is the Apo of LDL, IDL, VLDL?

- LDL: Apo-B100 - IDL: Apo-B100 - VLDL: Apo-B100

Describe the reverse direct pathway when there is a lot of cholesterol in tissues (need to be excreted)

1. Cholesterol in tissue taken up by HDL 2. LCAT converts cholesterol to cholesteryl ester 3. liver uptakes cholesteryl ester in via SR-BI (reverse scavenger)

Describe the reverse indirect pathway which is mediated by _ & function

a. cholesteryl ester transfer protein (CETP) > exchanges TG in VLDL for cholesteryl esters in HDL b. 1. VLDL processed to LDL => removed from circulation by LDL receptor pathway 2. TG in HDL degraded by hepatic lipase => small HDL particles => uptake of cholesterol from cells

Normal range of K & Na in the blood

K: 3.5 - 4.5 mM Na: 135 - 145 mM

Glucose range of normal & diabetes mellitus (DM) in fasting state

normal: 3.5 - 5.5 mM DM: 7

The name of cholesterol transporters. & the types from biggest to smallest (& dec. fat; inc. protein & inc density)

lipoprotiens 1. chylomicrons 2. VLDL 3. IDL 4. LDL 5. HDL

describe the exogenous cycle: chylomicron metabolism | (eating)

1. TG & chol. from broken-down food is absorbed in the small intestine 2. lipids are transported in chylomicron 3. LPL breaks down chylomicron to VLDL & FFA -> goes to muscles & adipocytes 4. VLDL goes to the liver

Describe the endogenous lipid transport cycle (fasting)

1. liver produces VLDL 2. VLDL (carry TG, Chol.) is broken down by LPL from tiss. => remove FFA &TG (to muscle, adipocytes) 3. this reduces the size of VLDL -> IDL -> LDL

enzyme that converts cholesterol to cholesteryl - ester

LCAT: lethicin/cholesterol acyl transferase

Describe the condition: LDL receptor defect

inc. LDL

types of enzyme classes

- oxidoreductase: +O = oxidation; +H = reduction - transferase: part moved to other molecule - hydrolase: add water - lyase/synthase: breakdown/make - isomerase: move particle around in same molecule - ligase: binds tog.

Describe how plasma glucose is prepared for spectro. w/ Trinder reaction

1. glucose oxidase breaks down glucose => gluconic acid + H2O2 2. H2O2 + phenol + 4-aminophenazone => pink complex

Describe metabolic acidosis & metabolic alkalosis

- M. acid: a dec. in plasma HCO3- | - M. base: excess intake of HCO3-

describe respiratory acidosis & respiratory alkalosis

- R. acid: in CO2 retention: Hi [CO2] => Hi HCO3- + H+ = pH Lo - R. base: in hyperventilation: Lo [CO2] => Lo HCO3- + H+ = pH Hi

describe hypertriglyceridaemia & cause

- inc. TG, VLDL (not LDL) | - bc deficiency of LPL or over production of VLDL

Diagnosis of dyslipidemia is dependent upon the measurement of:

1- Total cholesterol (Tc) 2- Triglycerides (TG) 3- HDL cholesterol (HDL-c) 4- LDL cholesterol (LDL-c)