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Clinical biochem. > lab > Flashcards

lab Flashcards

1
Q

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

A

Alcoholism & drugs

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2
Q

diagnose a patient w/ High GGT & High ALP

A

cholestasis

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3
Q

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

A

Hepatocellular disease

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4
Q

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

A

Skeletal bone disease (occur in pregnant females)

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5
Q

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

A

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

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6
Q

Equation to finding [ ] of test =

A 
[ Abs(test) / Abs(Std) ] x C(std)
*NOTE: equ. comes from 
A(test)     C(test)
\_\_\_\_\_ = \_\_\_\_\_
A(Std)     C(Std)
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7
Q

3 isoenzymes of CK & location in the body

A
  1. CKBB: brain
  2. CKMB: cardiac muscle
  3. CKMM: skeletal muscle
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8
Q

Equation to finding CK-MB activity =

*Significance of results if >5 or <5

A

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

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9
Q

Ideal marker for diagnosing AMI & drawback

A

a) cTroponin (cardiac troponin)

b) Re-infarcture

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10
Q

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

A
  1. 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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11
Q

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

A

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

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12
Q

Where can you find ALT, AST, ALP & GGT

A
  • ALT: hepatocyte
  • AST: hepatocyte, RBC, skeletal muscles
  • ALP: bone, hepatic, placenta
  • GGT: liver
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13
Q

Enzyme that converts unconjugate to conjugate bilirubin

A

UDP / glucurunosyl-transferase

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14
Q

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

A

a) hyperbilirubinameia

b) glucurunosyl-transferase

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15
Q

What liver function does bilirubin & Albumin look into?

A
  • Albumin: Liver synthesis

- BIlirubin: Liver excretion

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16
Q

Frieldwald formula: ie Total cholesterol =

*what situation would make formula in valid?

A

HDL + LDL + VLDL

*TG >4.5mM = Invalid

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17
Q

LDL equ. (in mM) =

A

Tc - HDL - Trig/2.17

*bc VLDL = Trig/2.17 (mM)

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18
Q

LDL equ. (in mg/dL) =

A

Tc - HDL - Trig/5

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

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19
Q

Describe the condition: familial hypercholesterolaemia

A
  • 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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20
Q

Describe the condition: Hyperlipidemia

A
  • Inc. TG OR Inc. Chol.

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

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21
Q

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

A

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

  1. 815 (OR 0.85 fem.) x serum creatinine (mmol)
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22
Q

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

A
  1. precipitate plasma proteins w/ tungstic acid & separate from supernatant (has creatinine)
  2. react supernatant w/ picrcic acid => red (Jaffe’s Rxn) => measure absorbance
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23
Q

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

A

a) acetoacetate = falsely increased results

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

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24
Q

risk factors for atherosclerosis

A
  • > 5 mM LDL c
  • > 4.5 mM TG
  • Obese
  • diabetes mellitus
  • smoking
  • hypertension
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25
Q

Characteristics of hyperkalemia

A
  • 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]
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26
Q

Characteristics of hypokalemia

A
  • Hypoglycemia (High insulin)
  • Alkalosis
  • Hypernatremia
  • Conn syndrome (High aldosterone)
  • renal tubular acidosis (Dec. K+ reabsorption)
27
Q

hypokalemia can be caused by

A
  • GI tract poor intake
  • Excess GI loss (feces)
  • Excess renal loss (diuretic) bc aldosterone & cortisol secretions
  • Transmembrane redistribution
28
Q

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

A

increase

29
Q

Equation for GFR when doing the creatinine clearance test

A

[plasma creatinine] x 24 x 60 min
*in lab: convert mM to uM

30
Q

Smith line-Gardner formula to calulate osmolality =

A

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

31
Q

decreased GFR may be due to

A
  • pre-renal factors: decreased blood flow
  • kidney or renal disease: dec. functioning nephron
  • post-renal: obstruction by renal stones / enlarged prostate
32
Q

Find abs. Beer’s equation

A

Abs = E x C x l

33
Q

De-ritis equation & significance of results

A

a) AST÷ALT

b) >2.0 = alcoholic liver disease

34
Q

Purpose of the De ritis equation

A

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

35
Q

Which marker for liver synthetic capacity declines the earliest?

A

Prothrombin time

36
Q

Describe Wilson’s disease

A

excess copper in tissues due to a lack of serum ceruloplasmin

37
Q

Difference b/w regenerative & regurgitative/obstructive jaundice

A
  • regenerative: excess haemolysis

- regurgitative: bc of cholestasis

38
Q

markers for hepatocellular damage

A

ALP, AST, ALT, GGT

39
Q

markers for liver excretory function

A

bilirubin

40
Q

Markers for liver synthetic function

A

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

41
Q

Substrate, product, activator, pH of alkaline phosphatase

A
  • substrate: p-nitrophenol phosphate
  • product: p-nitrophenol
  • Activator: magnesium sulfate
  • pH: ~10
42
Q

diuretics results in __ potassium excretion in kidney

A

inc

43
Q

excretion of potassium by the kidney _ in acidosis

A

decreases

44
Q

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

A

low

45
Q

creatinine is from the break down of….

A

creatinie phosphate in the muscle

46
Q

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

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

47
Q

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

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

48
Q

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

A
  • LDL: Apo-B100
  • IDL: Apo-B100
  • VLDL: Apo-B100
49
Q

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

A
  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)
50
Q

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

A

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

51
Q

Normal range of K & Na in the blood

A

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

52
Q

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

A

normal: 3.5 - 5.5 mM
DM: 7

53
Q

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

A

lipoprotiens

  1. chylomicrons
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
54
Q

describe the exogenous cycle: chylomicron metabolism

(eating)

A
  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
55
Q

Describe the endogenous lipid transport cycle (fasting)

A
  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
56
Q

enzyme that converts cholesterol to cholesteryl - ester

A

LCAT: lethicin/cholesterol acyl transferase

57
Q

Describe the condition: LDL receptor defect

A

inc. LDL

58
Q

types of enzyme classes

A
  • 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.
59
Q

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

A
  1. glucose oxidase breaks down glucose => gluconic acid + H2O2
  2. H2O2 + phenol + 4-aminophenazone => pink complex
60
Q

Describe metabolic acidosis & metabolic alkalosis

A
  • M. acid: a dec. in plasma HCO3-

- M. base: excess intake of HCO3-

61
Q

describe respiratory acidosis & respiratory alkalosis

A
  • R. acid: in CO2 retention: Hi [CO2] => Hi HCO3- + H+ = pH Lo
  • R. base: in hyperventilation: Lo [CO2] => Lo HCO3- + H+ = pH Hi
62
Q

describe hypertriglyceridaemia & cause

A
  • inc. TG, VLDL (not LDL)

- bc deficiency of LPL or over production of VLDL

63
Q

Diagnosis of dyslipidemia is dependent upon the measurement of:

A

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

Clinical biochem. (12 decks)

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