SECTIONS OF THE LABORATORY
CLINICAL
PATHOLOGY
1. Clinical Chemistry
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BUN
Cholesterol
FBS
2. Clinical Microscopy
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Analysis of body fluids
Urin analysis
Fecal anaysis
Semen analysis
3. Microbiology
Cultures (sputum,
blood, urine)
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4. Hematology
Biggest section
Includes CBC,coagulation,
PT, PTT
BLOOD BANK
Very critical section
Serology/Immunology
Bec. May have errors

Blood typing

Cross match

AB

Identification
Goes hand in hand with serology
and immunology
Tests done for

MALARIA

SYPHILIS

HIV

Cardiac and thyroid fxntest
II. ANATOMY PATHOLOGY
Histopathology
Submission of tissues for tests
NATURE OF REQUEST
STAT
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Performed immediately
and by itself.
Run control and
standard
20-50% More expensive
TAT is shortened
Request is needed
Today
 Confusing
 Performed as soon as
possible, given
priority
 Based on “running
time”
Routine
 Done with the batch
 Wait for TAT stated
by laboratory
VALUES
REFERENCE VALUES
 Better term than
“normal value”
 Pulled value, usually
95%of population
 Vary in diff. hospitals
but not that far
SIGNIFICANT
VALUES
 Clinical decision should
be made if higher
or lower than reference
value
 Usually when 2x to 3x
CRITICAL VALUES
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


Needs immediate attention
“panic values”
Should call physician
Patient is at risk
REFERENCE VALUES
Not fixed for all
Should consider:
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Age
Sex
Pregnancy
Diurnal Variation
Race
Blood type
ROUTINE EXAMINATIONS
ROUTINE ADMISSION TESTS
CBC, Urinalysis, Fecalysis
ROUTINE CHEMISTRIES
BUN, Creatinine, Glucose, Uric Acid, Cholesterol
Sometimes triglycerides
BASIC LAB EQUIPMENTS

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The Light Microscope.
Colorimeters and photometers
Water bath
Laboratory centrifuge
Balance
Cold incubators refrigerators
pH meters
Mixers
Ovens
De-ionizers
Safety cabinets.
Glassware and plasticware
SAMPLING
Pathologist should try to answer the question
which is imposed by the clinician.
 Correct specimen for requested test with
necessary information so that right test is carried
out And result is delivered to the requesting
clinician with the minimum of delay.
 Patient identification must be correct.

SPECIMEN TYPES
Venous blood serum or plasma.
 Arterial blood.
 Capillary blood
 Urine
 Feces
 Cerebrospinal fluid
 Sputum and sliva
 Tissue and cells
 Aspirates (pleural fluid, ascites, joint fluid,
intestinal (duodenal) fluid, pancreatic
pseudocysts.
 Calculi

BLOOD SPECIMENS


Serum
Plasma
Urine specimen
 Preservative may be added to prevent bacterial
growth or acid may be added to stabilize metabolites.
Other specimen types
Dangerous specimen
 Labelled as “dangerous specimen” yellow sticker.
 Similar label should be attached on the request form.
 HBV and HIV
SAMPLING ERRORS
Blood sampling techniques
 Prolonged stasis during venepuncture
 Insufficient specimen
 Errors in timing
 Incorrect specimen container
 In appropriate sampling site
 Incorrect sample storage.

LIPID CHEMISTRY AND
CARDIOVASCULAR PROFILE
Main lipids in the blood are the triglycerides and
cholesterol.(phospholipids, FFA)
 These are insoluble in the water.
 Transport in the blood is via
lipoproteins.(protein)
 4 major classes of lipoproteins.

Chylomicrons
 Very low density lipoproteins (VLDL)
 Low density lipoproteins (LDL)
 High density lipoproteins (HDL)

LIPOPROTEINS COMPOSITIONS
COMPOSITION OF LIPOPROTEINS
Class
Diamete
r (nm)
%
triacylglyc
%
%
erol
% protein
phospholipi
cholesterol
&
d
cholesterol
ester
HDL
5–15
33
30
29
4
LDL
18–28
25
50
21
8
IDL
25–50
18
29
22
31
VLDL
30–80
10
22
18
50
8
7
84
Chylomicr
100-1000 <2
ons
LIPOPROTEINS

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Chylomicrons carry triglycerides ( dietary fat) from
the intestines to the liver, to skeletal muscle, and to adipose
tissue.
Very-low-density lipoproteins (VLDL) carry (newly synthesised
or endogenous) triglycerides from the liver to adipose tissue
and metabolized to LDL through IDL.
Intermediate-density lipoproteins (IDL) are intermediate
between VLDL and LDL. They are not usually detectable in
the blood.
Low-density lipoproteins (LDL) carry cholesterol from the liver
to cells of the body. LDLs are sometimes referred to as the "bad
cholesterol" lipoprotein.
High-density lipoproteins (HDL) collect cholesterol from the
body's tissues, and take it back to the liver. HDLs are
sometimes referred to as the "good cholesterol" lipoprotein.
LIPOPROTEIN METABOLISM
60% of plasma cholesterol is present in LDL, 25%
in HDL and small quantity in VLDL.
 Lipoprotein metabolism is controlled by their
protein component apolipoproteins.
 Apo A-1 in HDL and Apo B-100 in LDL are very
important ones.
 Lipoprotein (a) in also present in human
plasma. It is synthesized in the liver.
 Smaller but denser than LDL.
 Cholesterol esters are major lipids and it is an
independent risk factor for IHD.

LDL and VLDL are associated with premature
atherosclerosis.
 HDL high levels are negative risk factors for
IHD.
 HYPERLIPIDEMIA
 Coronary heart disease
 Acute pancreatitis
 Failure to thrive and weakness
 Cataract

Endothelial dysfunction
 Lpid accumulation.
 Migration of inflammatory cells into the arterial
wall.

Atherosclerosis and plaque formation
Plaque stability
SCAD (asymptomatic)
Chest pain at rest
(angina, non ST elevation MI, STEMI)
PATHOPHYSIOLOGY
Atherosclerotic plaque, rupture and thrombus
formation.
 Obstruction of coronary circulation.
 Necrosis of the heart tissue.
 Irreversible cardiac injury if occlusion is complete
for 15-20 mins.
 Starts from endocardium and spreads towards
epicardium.
 If full thickness of myocardium is involved then it
is transmural infarct.

DIAGNOSIS OF MI
Detection of rise and fall of cardiac biomarker
troponinT/I with one of the following:
 Symptoms of ischemia
 ECG changes
 Q wave

ECG CHANGES
LACTATE DEHYDROGENASE (LDH)
Catalyzes the reversible oxidation of lactate to
pyruvate
 Used to indicate AMI
 Is a cytoplasmic enzyme found in most cells of
the body, including the heart
 Not specific for the diagnosis of cardiac disease

DISTRIBUTION OF LD ISOENZYMES

LD1 and LD2 (HHHH, HHHM)
Fast moving fractions and are heat-stable
 Found mostly in the myocardium and erythrocytes
 Also found in the renal cortex


LD3 (HHMM)
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Found in a number of tissues, predominantly in the white
blood cells and brain
LD4 and LD5 (HMMM, MMMM)
Slow moving and are heat labile
 Found mostly in the liver and skeletal muscle

CONSIDERATIONS IN LD ASSAYS
Red cells contain 150 times more LDH than
serum, therefore hemolysis must be avoided
 LDH has its poorest stability at 0°C

Clinical Significance
 In myocardial infarction, LD increases
3-12
hours after the onset of pain
 Peaks at 48-60 hours and remain elevated for 1014 days
 In MI, LD1 is higher than LD2, thus called
“flipped” LD pattern
FLIPPED
LDH
An inversion of the ratio of LD isoenzymes
LD1 and LD2; LD1 is a tetramer of 4 H–heart
subunits, and is the predominant cardiac LD
isoenzyme;
Normally the LD1 peak is less than that of the
LD2, a ratio that is inverted–flipped in 80% of
MIs within the first 48 hrs DiffDx. LD flips also
occur in renal infarcts, hemolysis,
hypothyroidism, and gastric CA
CREATINE KINASE (CK)
Is a cytosolic enzyme involved in the transfer of
energy in muscle metabolism
 Catalyzes the reversible phosphorylation of
creatine by ATP
 -Is a dimer comprised of two subunits, resulting
in three CK isoenzymes

The B, or brain form
 The M, or muscle form

Three isoenzymes isolated after
electrophoresis:



CK-BB (CK1) isoenzyme
 Is of brain origin and only found in the blood if the bloodbrain barrier has been breached
CK-MM (CK3) isoenzyme
 Accounts for most of the CK activity in skeletal muscle
CK-MB (CK2) isoenzyme
 Has the most specificity for cardiac muscle
 It accounts for only 3-20% of total CK activity in the heart
 Is a valuable tool for the diagnosis of AMI because of its
relatively high specificity for cardiac injury
 Established as the benchmark and gold standard for other
cardiac markers
Clinical Significance
-In myocardial infarction, CK will rise 4-6 hours
after the onset of pain
 -Peaks at 18-30 hours and returns to normal on
the third day
 -CK is the most specific indicator for myocardial
infarction (MI)

CHOLESTEROL
Normal values: range varies according to age
 Total Cholesterol: 150-250mg%
 Cholesterol esters: 60-75% of the total cholesterol

CHOLESTEROL IS ADVISED IF YOU
 have been diagnosed with coronary heart disease,
stroke or mini-stroke (TIA) or peripheral arterial
disease (PAD)
 are over 40
 have a family history of early cardiovascular disease
 have a close family member with cholesterol-related
condition
 are overweight
 have high blood pressure, diabetes or a health
condition that can increase cholesterol levels, such as an
underactive thyroid
FACTORS LEADING TO RAISED
CHOLESTEROL
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an unhealthy diet: some foods already contain
cholesterol (known as dietary cholesterol) but it is the
amount of saturated fat in your diet which is more
important
smoking: a chemical found in cigarettes called
acrolein stops HDL from transporting LDL to the
liver, leading to narrowing of the arteries
(atherosclerosis)
having diabetes or high blood pressure(hypertension)
having a family history of stroke or heart disease
There is also an inherited condition known as familial
hypercholesterolaemia (FH). This can cause high
cholesterol even in someone who eats healthy diet.
TRIGLYCERIDES
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Ester derived from glycerol and three fatty acids.
Main lipids in the blood and important energy substrate.
Insoluble in water.
Hypertriglyceridemia
Not an important risk facotr for coronary artery disease.
 It can cause pancreatitis when severe.

Both hypertriglyceridemia and hypercholesterolemia are
associated with various types of cutaneous fat deposition and
xanthomatas.
Hypertension
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
Very common clinical problem. Usually essential type
meaning that have no identifiable cause.
Investigations for treatable causes like endocrine is
necessary.
HYPERLIPIDEMIAS
LIVER
Anatomy of liver
I.
TESTS BASED ON EXCRETORY
FUNCTIONS
LABORATORY RESULTS
II.
TESTS DUE TO DETOXIFICATION
TESTS B/O SYNTHETIC FUNCTION
Liver is the main source of synthesis of
 Plasma proteins

Albumin
 Globulin
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Blood clotting factors
Prothrombin
 Factors V, VII, and X

SERUM ALBUMIN *

3.5- 5.5 gm/dl
SERUM GLOBULIN

2 -3.5 gm/dl
TOTAL PROTEINS*

6-8 gm/dl
Albumin/ Globulin ratio
 1.2:1 – 2.5: 1
Prothrombin time
TESTS B/O METABOLIC FUNCTIONS
SERUM TRANSAMINASES
SERUM ALKALINE PHOSPHATASES
REFERENCE RANGE
ALT ( upto 42 U/L)
 AST (0-37 U/L)
 ALP (65-306 U/L) raised in obstructive jaundice.

OTHER ENZYMES
GGT (11-60 u/l)
 5- NUCLEOTIDASE (2-17u/L)
 LDH (180-360 u/l)

GGT (OR GGTP)
Gamma Glutamyl Transpeptidase. This enzyme
level is elevated in case of liver disorders. In
contrast to the alkaline phosphatase, the GGT
tends not to be elevated in diseases of bone,
placenta, or intestine
PROTHROMBIN TIME
good correlation between abnormalities in
prothrombin time and the degree of liver dysfunction.
 Expressed in seconds and compared to a normal
control patient's blood
SPECIALIZED TESTS
 serum iron,
 the percent of iron saturated in blood,
 the storage protein ferritin for hemochromatosis.
 accumulation of copper in the liver in wilson disease.
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