Clinical Chemistry

VLDL =

 [TG] : 5 in mg/dL or [TG] : 2.2 in mmol/dL

 not valid if: 1.[TG] > 400mg/dL 2.Chylomicrons present

 3. b-VLDL –> Type III dyslipidemia (rare)

 

Fridewald equation

 

LDL =

LDL= Total Cholesterol – HDL – TG/5

 not valid if: TG > 400mg/dL,Chylomicrons present,

 Type III dyslipidemia

 

Lipid Disorders

 Phenotypes  and Lipoproteins increased

 I

 IIa and IIb

 

Chylomicrons

 b- region (II) LDL (II L’s) + VLDL (IIb)

;

;

;

LDL and VLDL –> major apolipoprotein?

 

HDL –> major apolipoprotein?

Apo B (bad cholesterol)

 Apo A1 –> ( a-region)

Total Cholesterol mg/dL

 – desirable

 – high

< 200

 

> 240

LDL mg/dL

– optimal

 – borderline

 – high

 

< 100

 130 -159

 160 – 189

HDL mg/dL

 Low

 High

 < 40

 > 60

LDL Targets – Risk groups

 – CHD or equivalents

 – 2 or >2 major risk factors

 – < 2 major risk factors

< 100 mg/dL

 < 130 mg/dL

 < 160 mg/dL

Method of TG/Cholesterol measurement

Enzymatic reactions–> dye product

–> spectrophotometry

Lipid Disorders: Phenotypes  and Lipoproteins increased

III, IV, V

IDL ( intermediate – 1-5 = 3)

 VLDL (IV)  pre b-region

 V = I + IV  = VLDL + Chylomicrons

 

Chylomicrons

-Electrophoretic mobility

-Major lipid / Protein %

-Apolipoprotein

Origin

TG / 1%

B-48, A-1,C, E

VLDL

-Electrophoretic mobility

-Major lipid / Protein %

-Apolipoprotein

 

pre-b (“V for beta”)

TG / 8%

B-100, C, E

IDL

-Electrophoretic mobility

-Major lipid / Protein %

– Apolipoprotein

pre-b/b

Cholesterol / 15%

B-100, E

LDL

-Electrophoretic mobility

-Major lipid / Protein %

– Apolipoprotein

b

Cholesterol / 20%

B-100

 

HDL

-Electrophoretic mobility

-Major lipid / Protein %

– Apolipoprotein

a

Cholesterol / 50%

A-1, C, E (“ACE”)

Eruptive xanthomas, pancreatitis

Cholesterol +, TG +++

DDx

Familial LPL deficiency – Phenotype I

Familial hypertriglyceridemias IV / V

 

Pancreatitis

Cholesterol +, TG +++

Dx

Familial apo C-II deficiency

Phenotype I / V

Tendinous xanthomas, premature atherosclerosis

Cholesterol +++, TG nml/ +

Familial hypercholesterolemia (IIa) –> most common 1ocause of hypercholesterolemia <– LDL Rc deficiency

autosomal dominant

 

Eruptive xanthomas, premature atherosclerosis

Cholesterol +++, TG +++

DDx

Apolipoprotein E deficiency – Phenotype IIb

Familial dysbetalipoproteinemia – III

Premature atherosclerosis

Cholesterol + , TG +

Familial combined hyperlipidemia

II or IV

Predominant hypertriglyceridemia

–> most common 2o cause

heavy EtOH consumption

Low Cholesterol, TG nml – increased, absent HDL & A-1

Tonsils, lymph nodes, vasculature, spleen –> cholesterol esters

Dx?

Tangier disease

Pregnancy: Relative Gluc intolerance

Cause?

HPL (somatomammotropin) –> anti-insulin

Measurement of Insulin

Assay? Endogenous vs exogenous Insulin

Immunometric: C-peptide : Insulin = 5-15: 1 <– rapid metabolization of C-peptide (endogenous)

Gluc measurement

Assay?

Enzymatic: glucose oxidase / hexokinase –> G6PD

–> plasma

Point of care testing

Un-calibrated whole blood Gluc compare with Glucplasma

10-15% lower depending –> Hematocrit

HgbA1c reflects Gluc control in the past—–?

why?

nonenzymatic: Gluc + HgbA –> HgbA1c ~ RBC-t1/2

= 60d –> younger RBCs little > 50%

=>HgbA1c ~ Gluc control in past 1 month

Normal HgbA1c level-causes of false decrease Alternative test?

< 6% Shortened Red cell survival – hemolytic anemias,

Hemoglobinopathies

fructosamine –> 2-3wks

Moderade and gradual drop in Glucserum 

Altered mental status

Dx:

“fasting” hypoglycemia

Sweating,palpitations,tachycardia,nervousness

Dx

“Reactive” hypoglycemia –> profound and rapid

<–hormonal response

Hypoglycemic symptoms, [Gluc]plasma< 45mg/dL, relief of symptoms with Gluc, [Insulin]absolute=nml

Dx?

Insulinoma/Nesidioblastosis

Insulin: Gluc > 180

Cause of false elevation of c-peptide

Renal impairement

–> cleared by the Kidney

“c=child=kid”

Hypoinsulinemic hypoglycemia

– low [beta-OH-butyrate]

causes?

nonketotic=> insulin-like activity

Autoimmune, liver failure, stavation

Patient with insulinoma

What other test should be ordered?

[Ca++]serum –> MEN I
Post mortem test for hypoglycemia?

c-peptide

proinsulin

Type I DM – frequency

Antibodies?

10% common in childhood

Auto-Ab–> anti-GAD65, anti-ICA512, anti-IAA

 

Fasting Glucplasma

– DM

– Impaired fasting Gluc (pre-diabetes)

>125 mg/dL

99 – 126 mg/dL

Criteria for + 100gram OGTT in pregnancy

 

Any 2 of: >95mg/dL fasting, >180 @1hr, > 155 @2hr

>140 @ 3hr

Goal of therapy in diabetic patients?

What test?

HgbA1c < 7%

–> should not be used in pregnancy

DM Patient: difficulty to maintain glycemic control

What other test?

Magnesium

–> hypomagnesemia–> complicate glycemic control

DM I Pt with polyuria,polydipsia, nauseaa and abdominal pain, hyperglycemia, metabolic acidosis.

Dx?

early DKA

late–> altered breathing (Kussmaul resp) –> altered mental status –>coma

Major serom ketones?

Measurement technique?

1Acetone, 2acetoacetic acid, 3b-hydroxybutyrate

Nitroprusside, semi-quantitative method

DKA: [1+2] ~ 20%, [3] ~ 80%

DKA : [Na+]serum and [K+]serum

[Na+]serum = initially low <– urinary losses

[K+]serum = initial elevated –> transcellular shifts and urinary losses => [K+]total decreased

Pt: Altered mental status, hyperglycemia > 600mg/dL, hemiplegia, hyperosmolarity, dehydration, pH, ketones, bicarbonate =nml — Dx?

Hyperglycemic hyperosmolar nonketotic coma

DM II

Pt: Insulin resistance, central obesity, dyslipidemia, hypertension, increased CRP, PAI-1.

Dx?

Metabolic syndrome (syndrome X)

–> accelerated atherosclerosis

PAI-1 =plasminogen activator inhibitor -1

Factors that interfere with test results of fructosamine test
high levels of VitC, lipedemia, hemolysis, hyperthyroidism
x

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