BLOOD

CHEMISTRY

CARBOHYDRATES, LIPIDS,
ENDOCRINE, ENZYMES

OGTT for High risk women and Average

risk women with abnormal screening
result
100 g OGTT
75 g OGTT Plasma
Plasma glucose
Glucose

Fasting
1 hr
2 hr
3 hr

mg/dl
>95
>180
>155
>140

mmol/L
>5.3
>10
>8.6
>7.8

mg/dl
>95
>180
>155

GDM is diagnosed if >2 plasma glucose levels are exceeded

American Diabetes Association, 2004b

mmol/L
>5.3
>10
>8.6

LIPIDS

Total Cholesterol
HDL
Triglycerides
VLDL
LDL

Note: classification,transport and

metabolism

Blood sampling
Fasting 12-14 hrs
Chylomicrons increases plasma triglyceride
levels
LDL and HDL cholesterol decline after eating
due to CETP-mediated compositional changes
that occur in the catabolism of chylomicrons
Posture= 20 mins of recumbence decreases
plasma concentration of
Cholesterol,LDL,HDL,ApoA1, Apo B

Friedewald Formulas

LDL cholesterol =
Total cholesterol [ HDL cholesterol + VLDL cholesterol ]

VLDL-cholesterol =

in mmol/L = Plasma triglycerides

2.175 or 2.175

In mg/dL = Plasma triglycerides

5
LDL (mmol/L) = Total Cholesterol- (HDL + Triglycerides/2.2)
LDL (mg/dl)= Total cholesterol [ HDL-C + Triglycerides/5 ]

NCEP Adult Treatment Panel III

Classification of Serum Lipids
Lipid Test

Finding in mg/dL

Classification

Total Cholesterol

<200

Desirable

200-239
>240

Borderline high
High

LDL Cholesterol

<100
100-129
130-159
160-189
>190

Optimal
Near/above optimal
Borderline high
High
Very high

HDL Cholesterol

<40
40-59
>60

Low
Intermediate
High

Blood Lipoprotein Patterns in Hyperlipoproteinemia

(Frederickson Classification)
Type

Lipoprotein pattern after a 12-hour fast

Extremely elevated TG due to presence of chylomicrons

IIa

Elevated LDL

IIb

Elevated LDL and VLDL

III

Elevated cholesterol, TG; presence of B-VLDL; VLDLcholesterol/plasma TG ratio > 0.3

IV

Elevated VLDL

Elevated VLDL and presence of chylomicrons

EVALUATION OF ENDOCRINE
FUNCTION

ENDOCRINE signals
the secreted molecules, which are
frequently called hormones, act on target
cells that are distant from their site of
synthesis.
An endocrine hormone is frequently
carried by the blood from its site of
release to its target.
In response, the target tissue often
secretes factors that down-regulate the
activity of the gland that produces the
stimulating hormone, a process known
as feedback inhibition.

ANTERIOR PITUITARY

1. Somatotrophs, producing growth hormone (GH): These

acidophilic cells constitute half of all the hormone-producing
cells in the anterior pituitary.
2. Lactotrophs (mammotrophs), producing prolactin: These
acidophilic cells secrete prolactin, which is essential for
lactation.
3. Corticotrophs: These basophilic cells produce
adrenocorticotropic hormone (ACTH), pro-opiomelanocortin
(POMC), melanocyte-stimulating hormone (MSH), endorphins,
and lipotropin.
4. Thyrotrophs: These pale basophilic cells produce thyroidstimulating hormone (TSH).
5. Gonadotrophs: These basophilic cells produce both
follicle-stimulating hormone (FSH) and luteinizing hormone
(LH). FSH stimulates the formation of graafian follicles in the
ovary, and LH induces ovulation and the formation of corpora
lutea in the ovary. The same two hormones also regulate
spermatogenesis and testosterone production in males.

POSTERIOR PITUITARY
The two peptide hormones secreted from the
posterior pituitaryoxytocin and antidiuretic
hormone (ADH, also called vasopressin)
synthesized in the hypothalamus and stored within
the axon terminals residing in the posterior pituitary.
In response to appropriate stimuli, the pre-formed
hormones are released directly into the systemic
circulation through the venous channels of the
pituitary.

THYROID FUNCTION TESTS

THYROID FUNCTION TESTS

EUTHYROIDISM

FREQUENTLY requested tests:

TSH
T3
T4
FT3
FT4

tertiary

SECONDARY

Primary

TSH
T4
T3

What needs to be done

TSH
Keep the patient relaxed and recumbent for 30 mins
b4 the test
As ordered, withhold steroids, thyroid hormones,
aspirin and other drugs that may influence test
results. If must be continued, note down on lab
request.
Between 6 am and 8 am, perform venipuncture,
collect sample in 5 ml clot-activator tube, and send
immediately to the laboratory

WHAT NEEDS TO BE DONE

T3, T4
If test is performed to monitor thyroid
therapy, the patient continues to receive daily
thyroid supplements.
Collect the sample in a 7 ml clot activator
tube, send sample to laboratory immediately.

Thyroid Stimulating Hormone

It stimulates increase in
size, number, and secretory
activity of thyroid cells
Heightens iodine pump
activity commonly raising
the ratio of intracellular to
extracellular iodine as
much as 350:1
Stimulates the release of T3
and T4

TSH

Serum Thyrotropin Test

(Immunoassay)
Detects primary hypothyroidism
Determine whether it results from thyroid gland failure
or from pituitary or hypothalamic dysfunction
Helps in monitoring therapy for hypothyroidism
May not distinguish between low normal and subnormal
levels, especially in secondary hypothyroidism.
TRH challenge test evaluates thyroid function and can be
performed after a baseline TSH reading has been
obtained.

TSH
Normal values:
adult and children = undetectable to 15 mU/L

HIGH TSH
Primary hypothyroidism or endemic goiter:
>20 mU/L
Thyroid CA= slightly elevated
Decreased T3T4

Increased TSH

LOW TSH

Normal values:
adult and children = undetectable to 15 mU/L

Normal
Secondary hypothyroidism

Testing with TRH is necessary to confirm the

diagnosis

Hyperthyroidism (Graves Disease) or

thyroiditis
Increased T3T4

decreased TSH

Negative feedback mechanism

HYPOTHYROIDISM
Patients with unexplained increase in body weight or
hypercholesterolemia should be assessed for potential
hypothyroidism.
Measurement of the serum TSH level is the most sensitive
screening test for this disorder.
The TSH level is increased in primary hypothyroidism as a result of
a loss of feedback inhibition of TRH and TSH production by the
hypothalamus and pituitary, respectively.
The TSH level is not increased in persons with hypothyroidism due
to hypothalamic or pituitary disease.
T4 levels are decreased in individuals with hypothyroidism of any
origin.

T4 determination
Measures total circulating T4 when TBG is normal
100% is thyroidal in origin

T4 determination
Normal value: 5-13 ug/dl (SI, 60-165 nmol/L)
Normal T4 doesnt guarantee normal thyroid functioning ex in
T3 thyrotoxicosis
Elevated levels seen in primary and secondary hyperthyroidism
Subnormal levels in hypothyroidism or replacement levels of T3
Interferences:
1. Estrogens,progestins,levothyroxine,and methadone
increase T4 levels;
2. Free F.A.,
heparin,iodides,liothyronine,sodium,lithium,phenylbutazon
e,phenytoin,PTU,salicylates decrease T4
3. Clofibrate can increase/decrease T4

T3 (TRIIODOTHYRONINE)

More potent thyroid hormone

50-90% of T3 is thought to be derived from T4.
Remaining 10% is secreted directly by the thyroid gland.
Aids diagnosis of T3 toxicosis, helps diagnose hypothyroidism
and hyperthyroidism and helps monitor the course of thyroid
replacement therapy.
Although T3 is present in bloodstream in minute quantities,
its impact on body metabolism dominates over T4.
Binds less to T3, half life is 1 day

T3 DETERMINATION
NORMAL: 80-200 ng/dl (SI, 1.2 to 3 nmol/l)
May be higher than T4 in
Graves disease, toxic adenoma,or toxic nodular
goiter
Also in iodine-deficient areas T3 is higher than T4
in an effort to maintain euthyroid state.

Thyroxine binding globulin (TBG)

Measures serum TBG, the predominant carrier protein for
circulating T3 and T4
Test results for T3 and T4 are inaccurate in underlying T3
and T4 abnormality, however does not alter result if FT3
and FT4
Normal values: immunoassay:
16-32 ug/dl (SI, 120-180 mg/ml)
Elevated TBG indicate hypothyroidism and congenital
excess,some forms of hepatic disease, acute
intermittent porphyria
Decreased TBG in hyperthyroidism , congenital
deficiency, active acromegaly, nephrotic syndrome and
malnutrition with hypoproteinemia, acute illness or
surgical stress.

TBG
Estrogens and phenothiazines elevate TBG
levels
Androgens, prednisone, phenytoin and high
doses of salicylates depress TBG.

Free T3 and Free T4 (FT3 & FT4)

The best indicator of thyroid function
Minute portions of T3 and T4 not bound to
TBG
These unbound hormones enter the target
cells and are responsible for the thyroids
effect
Normal range:
FT3 = 0.2 to 0.6 ng/dl (SI, 0.003-0.009 nmol/L)
FT4 = 0.9 to 2.3 ng/dl (SI, 10-30 nmol/L)

Enzymes
Mechanism of blood enzyme activity increase

Change due to destruction of organs/tissues

Excess production in the organ (induction)
Excretion disorder (obstruction)
Increased enzyme half-life (enzyme-binding
immunoglobulin)
Ectopic production due to malignancy (ex. amylase)

Enzymes
Enzyme activity is given in international units
(IU)
1 IU = one micromole of substrate converted/minute
If the enzyme activity is in IU, the volume will be 1L
(IU/L).
If the activity is in mIU, it is expressed in mIU/mL.

Isoenzymes are measured via electro-phoresis

Enzymes
Enzyme activity is commonly measured by
rate of change of the product formed,
substrate depleted, or NAD coenzyme
converted
Coupled enzyme reactions
Those that do not utilize NAD or NADH as a
coenzyme and does not form a convenient
colored endpoint can be coupled to >1
enzymatic reaction

Enzymes
Alanine aminotransferase (ALT)
Increased in liver parenchymal diseases
(hepatitis, Reyes syndrome, cholestasis)
Also increased in CHF and AMI

Alkaline phosphatase (ALP)

Increased in bone diseases, hepatobiliary
diseases
Also increased in hyperparathyroidism, sprue

Enzymes
ALP isoenzymes
Liver, bone, intestinal, placental, Regan

Amylase and Lipase

Increased in pancreatic and salivary gland
inflammation
Decreased in pancreatic insufficiency

Amylase isoenzymes
P type and S type

Enzymes
Aspartate aminotransferase (AST)
Increased in heart, skeletal muscle, and liver
diseases
Decreased in uremia

Creatinine Kinase (CK)

Increased in heart, skeletal muscle, and CNS
diseases
Depressed in hyperthyroidism and decreased
muscle mass

Enzymes
CK Isoenzymes
Electrophoresis
CK1 or CK-BB (0% or trace)
CK2 or CK-MB (<4 6%)
CK3 or CK-MM (>94 96%)

Gamma glutamyl transferase (GGT)

Increased in liver diseases, alcohol abuse,
antiepileptic drug administration

Enzymes
Lactate Dehydrogenase (LD)
Increased in cardiac and skeletal muscle diseases,
liver diseases

LD isoenzymes
Electrophoresis

LD1 HHHH: heart muscle , RBC, kidney

LD2 HHHM: heart muscle , RBC, kidney
LD3 HHMM: spleen, lungs, RBC, kidney
LD4 HMMM: spleen, lungs, kidney
LD5 MMMM: liver, skeletal muscle

Cardiac Function

LD1-to-LD2 Ratio

Ratio of LD1-to-LD2 is less than 1.00.

LD1/LD2 "flip" resulting in the ratio being greater
than 1.00 is seen more often in AMI
Time course after AMI:

Earliest rise: 12-24 hours after the injury

Peak: 55-60 hours after injury.
Return to normal: 10-14 days.

Limitations

not useful for early recognition of AMI

troponin useful for late diagnosis of myocardial injury

Cardiac
Marker

Principal
Source

Diagnostic Window

Comments

AST

liver, skeletal, Rise: 6-8 hr

& cardiac
Peak: 18-24 hr
muscle
Normal: 4-5 days

AMI

Total CK

skeletal, & Rise: 6-8 hr

cardiac
Peak: 24-36 hr
muscle, brain Normal: 3-4 days

Limited
diagnostic
value

CK MB

skeletal, &
cardiac
muscle

Myoglobin

skeletal, &
cardiac
muscle

Rise: 4-6 hr
Peak: 12-24 hr
Normal: >48 hr
Rise: 2-3 hr
Peak: 6-9 hr
Normal: 24-36 hr

AMI

Non-specific
early marker of
AMI

Cardiac
Marker
LDH

Principal
Diagnostic
Source
Window
skeletal, &
Rise: 8-12 hr
cardiac muscle, Peak: 24-48 hr
RBC, liver
Normal: 7-12 days

Comments

Cardiac
Troponin I

cardiac muscle Rise: 4-8 hr

Peak:14-18 hr
Normal: 5-9 days

Highly specific
for AMI

AMI

Cardiac
cardiac muscle Rise: 4-8 hr
Highly specific
Troponin T
for AMI
Peak: 14-18 hr
Normal: > 14 days
Relative Index = evaluates INCREASED total CK activity only
= CK-MB in ug/L x 100
Total CK in U/L
= > 6% indicates cardiac damage; < 6%
indicates skeletal muscle damage