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BLOOD GLUCOSE TEST

Mainly tested for diagnosis and management of diabetes mellitus

What are the Normal ranges for blood glucose?

Adults
– Fasting (plasma) 3.6–6.4 mmol/l
– Random (plasma) 3.3–7.4 mmol/l
Children
– Fasting (plasma) 2.4–5.3 mmol/l
Newborn values are slightly lower, i.e. 1.1–4.4

Causes of raised blood glucose levels

Hyperglycaemia (Raised blood glucose levels) may accompany pancreatic disease
and some endocrine disorders such as thyrotoxicosis and Cushings syndrome. Steroid therapy may also cause hyperglycaemia. Transient hyperglycaemia
often occurs following severe stress, e.g. after surgery, injury, shock, infections, or severe burns.

Causes of low blood glucose levels

A low blood glucose level is called hypoglycaemia.
Persistent occurrences of hypoglycaemia with glucose levels less than 2.2 mmol/l accompanied by symptoms such as fainting, fits, sweating, hunger, pallor, confusion, or violence, should be investigated.
Causes of hypoglycaemia include severe malnutrition, kwashiorkor, severe liver disease, alcoholic excess, insulin secreting tumours, Addison’s disease,
and certain drugs. Commonly, however, markedly reduced blood glucose levels occur following the overtreatment of diabetes.

Neonatal hypoglycaemia: Newborn infants may suffer hypoglycaemia when blood glucose levels fall below 1.1 mmol/l. Infants particularly at risk are
underweight poorly nourished babies, twins, premature infants, and babies born of diabetic mothers. It is important to detect hypoglycaemia of the newborn because without treatment brain damage may
occur.
Malaria associated hypoglycaemia: In severe malaria, hypoglycaemia is a common finding and can increase mortality particularly in young children.
Hypoglycaemia can also occur in those being treated with quinine and quinidine.

HAIR SAMPLE FOR FUNGAL DETECTION

• A Wood’s light, if available, may be helpful in selecting specimens.

• Pluck broken or lustreless hairs from periphery of lesion. Scrape scalp from edge of hair loss area.

• Do not cut hair.

• If hair are broken off (endothrix), it often may be necessary to scrape the coiled hair stubble from the scalp with a sterile blade or slide edge, rather than plucking with tweezers.

• Submit specimen to laboratory in sterile petri dish.

See also:

TYPES OF ANAEMIA

Anemia classified as follows based mechanisms described here

Iron deficiency
Microcytic hypochromic RBCs
● MCHC: ↓ Below 320 g/l
● MCV: ↓ Below 78 fl
● Reticulocytes: Normal or Low
– cells with ‘pencil’ appearance

Macrocytic anaemia
Folate deficiency(megaloblastic)
-MCV: ↑ More than 100 fl
– Macrocytes mostly oval, occasional megaloblast, pancytopenia
– Reticulocytes: Normal or ↓
-(late stages), hypersegmented neutrophils. -WBC and platelets: ↓
-MCHC: Normal
Liver disease: Non-megaloblastic Macrocytes (mainly round with target cells)

Sickle cell disease – Sickle cells, polychromasia,
● HbS: Positive
poikilocytosis, nucleated red cells,
● Reticulocytes: ↑ (blue stippling in
HbS thalassaemia target cells. Macrocytes due to folate background of thick film)
deficiency (when patient not receiving
folate)
Further test: Hb electrophoresis.

MECHANISM OF ANEMIA

BLOOD LOSS
● Acute bleeding, e.g. from wounds, surgical, ectopic pregnancy, placenta praevia
● Chronic blood loss, e.g. hookworm infection, schistosomiasis, gastrointestinal bleeding, menorrhagia

DECREASED RED CELL PRODUCTION
● Lack of essential nutrients, e.g. deficiencies of iron,
folate, vitamin B12, protein
● Depressed bone marrow activity, e.g. anaemias associated with chronic disease such as tuberculosis, HIV disease, chronic nephritis, chronic hepatitis,
connective tissue disorders, malignant disease, leukaemias
● Due to drugs, chemicals, ionizing radiation, some viruses
● Thalassaemia syndromes

INCREASED RED CELL DESTRUCTION
(HAEMOLYSIS)
● Inherited haemolytic anaemias:
– Haemoglobinopathies, e.g. sickle cell diseases,
thalassaemia syndromes
– Red cell enzyme deficiencies, e.g. G6PD
deficiency, pyruvate kinase deficiency
– Red cell membrane defects e.g. hereditary
spherocytosis
● Non-immune acquired haemolytic anaemias:
– Infections, e.g. malaria, African trypanosomiasis, meningococcal septicaemia, C. perfringens
infection, bartonellosis
– Pre-eclampsia and HELLP syndrome (haemolysis, elevated liver enzymes, low platelet count)
– Conditions which cause disseminated intravascular coagulation (DIC)
– Haemolytic uraemic syndrome
– Hypersplenism and splenomegaly, e.g. visceral
leishmaniasis, hyper-reactive malaria, splenomegaly, myelofibrosis
– Burns
– Venomous snake and spider bites
– Chemicals, oxidant drugs, local herbal remedies
– Paroxysmal nocturnal haemoglobinuria
● Immune acquired haemolytic anaemias (DAT positive):
– Haemolytic disease of the newborn
– Haemolytic blood transfusion reaction
– Warm reactive autoantibody, e.g. drug-induced chronic lymphatic leukaemia, lymphoma, systemic lupus erythematosus
– Cold reactive autoantibody, e.g. M. pneumonia infection, lymphoma
– Paroxysmal cold haemoglobinuria

HAEMOGLOBIN MEASUREMENT

Haemoglobin is measured to detect Anaemia and its severity and to monitor an patient’s response to treatment. Monitoring the haemoglobin level (or PCV) is also required when patients with HIV disease are being treated with drugs such as AZT. The test is also performed to check the haemoglobin level of a blood donor prior to donating blood.

What are normal ranges for Haemoglobin?

Children at birth . . . . . . . . . 135–195 g/l
Children 2 y–5 y . . .. . . . . . 110–140 g/l
Children 6 y–12 y . . . . . . . .. . . 115–155 g/l
Adult men. . . . . . . . . . . . . . . 130–180 g/l
Adult women . . . . . . . . . . . 120–150 g/l
(Pregnant women) . . . . . . . . . . 110–138 g/l

As stated, Hb measurement along with other parameters can be used to identify different types of anaemia as described here

Hb 12 g/dl Not anaemic
Hb 10–11 g/dl Mild anaemia
Hb 8–9 g/dl Moderate anaemia
Hb 6–7 g/dl Marked anaemia
Hb 4–5 g/dl Severe anaemia
Hb 4 g/dl Critical

URINE APPEARANCE AND VOLUME

Urine changes in disease
Production and composition of urine depend on glomerular filtration, tubular reabsorption and tubular secretion.
Changes that can occur in the volume, appearance, constituents, and mass density (specific gravity) of
urine in disease are as follows:
Volume

What is the normal volume of urine in 24hrs?

The volume of urine excreted daily depends on fluid intake, diet, climate, and other physiological factors. It is usually between 1–2 litres per 24 hours.

What causes increase in urine volume?

An increase in the volume of urine is called
polyuria. It occurs in diabetes mellitus due to an increase in the osmolality of the filtrate preventing the normal reabsorption of water (osmotic diuresis).
Polyuria also occurs when the secretion of the antidiuretic hormone is reduced, e.g. in diabetes

What causes decrease in urine volume?

A decrease in the volume of urine excreted is called oliguria. It occurs when the renal blood flow and, or, glomerular filtration rate are reduced. One of the causes of a reduced renal blood flow is low
blood pressure (hypotension) caused for example by severe dehydration or cardiac failure. A fall in glomerular filtration rate occurs in acute glomerulonephritis (inflammation of the kidney glomeruli) and also in the early stages of acute tubular necrosis.

If severe, oliguria progresses to a complete cessation of urine flow, this is called anuria and is usually due to severe damage to the renal tubules (acute tubular necrosis). Acute tubular necrosis may
follow any of the conditions which cause severe hypotension or may be due to a direct toxic effect on
the tubules by drugs or following an incompatible
blood transfusion.

Interpretation of urine appearance

Normal freshly passed urine is clear and amber in colour. A dilute urine appears pale in colour and a concentrated one has a dark yellow appearance. The yellow colour is due to the pigments
urochrome, urobilin, and porphyrins.
When normal urine has been allowed to stand for some time, a white phosphate deposit may form
if the urine is alkaline (dissolved by adding a drop of acetic acid) or a pink uric acid deposit may form if the urine is highly acidic or concentrated (disappears
on warming). A ‘mucus’ cloud may also form if normal urine is left to stand.

Changes of urine appearance in difference condition

The appearance of urine may be altered in many
conditions including:
● Urinary tract infections in which the urine appears cloudy because it contains pus cells and bacteria.
● Urinary schistosomiasis in which the urine often appears red and cloudy because it contains blood (haematuria).
● Malaria haemoglobinuria (blackwater fever) and other conditions causing intravascular haemolysis in which the urine appears brown and cloudy
because it contains free haemoglobin (haemoglobinuria).
● Jaundice in which the urine may appear yellowbrown or green-brown because it contains bile pigments or increased amounts of urobilin (oxidized urobilinogen).
● Bancroftian filariasis in which the urine may appear milky-white because it contains chyle.

MEASURING C.S.F PROTEINS

Total protein in c.s.f. can be measured by the following methods:
Colorimetrically using a trichloroacetic acid method.
Visual comparative semiquantitative method when a colorimeter is not available

What are normal ranges for C.S.F proteins?

0.15–0.40 g/l

What Causes increase in C.S.F Proteins?

An increase in total protein and a positive
Pandy’s test occurs in all forms of meningitis, in amoebic and trypanosomiasis meningoencephalitis,
cerebral malaria, brain tumours, cerebral injury, spinal cord compression, poliomyelitis, the GuillainBarré syndrome (often the only abnormality), and polyneuritis.

Increases in c.s.f. protein also occur in diseases which cause changes in plasma proteins such as multiple myeloma.
When the total protein exceeds 2.0 g/l (200mg%), the fibrinogen level is usually increased sufficiently to cause the c.s.f. to clot. This may occur in severe pyogenic meningitis, spinal block, or following haemorrhage.

OCCULT BLOOD TEST

Bleeding into the gastrointestinal tract may be rapid with the vomiting of blood (haematemesis) or the passage of blood through the rectum (melaena).
When the bleeding is chronic with only small amounts of blood being passed in the faeces, the blood (or its breakdown products) is not recognized in the faeces and is referred to as occult (hidden)
blood.

When is Occult blood requested

Requests for occult blood testing are usually made to investigate the cause of iron deficiency anaemia or to assist in the diagnosis of bleeding lesions of the gastrointestinal tract, e.g. peptic ulcer,
carcinoma, or diverticulosis.

Methods applied in Occult blood Test

Chemically using guaiac based reagents prepared in the laboratory, e.g. aminophenazone test, or ready-made reagent in kit tests, e.g. Hema-Screen.
Immunologically using a haemoglobin specific cassette or strip test such as the Instant-View
Immunological tests are more expensive

Evaluation of Occult blood test

Specificity of occult blood tests:

Chemical tests are not specific for haemoglobin. They are based on the principle that haemoglobin and its derivatives react in a similar way to peroxidase
enzymes, i.e. they catalyze the transfer of an oxygen atom from a peroxide such as hydrogen peroxide to a chromogen
such as guaiacum, 2,6-dichlorophenolindophenol or aminophenazone. Oxidation of the chromogen is shown by the production of a blue, blue-green, or pink colour.

In chemical tests, non-haemoglobin substances with peroxidase activity can therefore cause false positive reactions.
Other substances can interfere with peroxidase activity resulting in false negative results. The specificity of chemical tests can be improved by dietary restriction.
Immunological occult blood tests are specific for the detection of human haemoglobin in faeces. A monoclonal antibody directed against human haemoglobin is used. This
selectively binds to human haemoglobin present in the faeces.

Sensitivity of occult blood tests:

Considerable variation of
sensitivity is shown by both chemical and immunological occult blood tests. Highly sensitive tests can be misleading because they detect trace amounts of blood which can be found in normal faeces. Highly sensitive chemical tests can give false positive reactions when faeces contain dietary substances which have peroxidase-like activity. Tests of low sensitivity can also be misleading because they may fail to detect small
amounts of blood which are pathological.

SERUM ELECTROLYTES TEST

The measurement of sodium, potassium, or both electrolytes is usually requested in the assessment of renal function, to assist in the management of a patient that is unconscious or confused or a diabetic
patient with ketoacidosis, to assess and monitor states of dehydration (particularly an infant losing fluid), to monitor diuretic therapy and to assist in fluid replacement therapy.

What are the Normal ranges for sodium and potassium?

Sodium:
134–146 mmol/l (134–146 mEq/l)
Potassium:
Adults: 3.6–5.0 mmol/l (3.6–5.0 mEq/l)
Newborns: 4.0–5.9 mmol/l (4.0–5.9 mEq/l)
Values are highest immediately after birth

What are causes of increase in Sodium levels?

An elevated sodium level is known as hypernatraemia. It is nearly always due to dehydration with the rise in sodium (also chloride and urea) being due
to a concentrating effect. It is usually brought about by a reduction of body water content by fluid loss without compensatory reduction in sodium content, rather than a dietary overload, although excessive IV saline is a potential factor.
Typical causes of hypernatraemia are:
– Severe vomiting
– Prolonged diarrhoea
– Profuse sweating, fever
– Polyuria, as in diabetes
– Hyperaldosteroidism
– Cushing’s syndrome
– Inadequate water intake
– Accidental ingestion of sea water.

Note: A high sodium level must be reported as soon as possible. Severe hypernatraemia (sodium level that has reached 155 mmol/ is a serious finding .

What are causes of low sodium levels?

A low sodium level is known as hyponatraemia. It is a common finding than hypernatraemia. A greatly
reduced level (as low as 125 mmol/l) indicates a dangerous condition and must be reported as soon as possible.
A low sodium level may accompany any severe illness including viral and bacterial infections, malaria, heart attacks, heart failure, strokes, and tumours of the brain and lung.

Other causes of hyponatraemia
– Surgery or severe accident.
– Treatment with diuretics.
– Side effect of some drugs.
– When loss of salt and water (e.g. by vomiting,
diarrhoea or excessive sweating) is replaced by
water only.
– Loss of sodium in the urine as in severe renal impairment and salt-losing nephritis.
– Hypoadrenalism (Addison’s disease). In tropical countries hypoadrenalism can be caused by tuberculosis of the adrenal glands.

What are causes of high Potassium levels?

A raised potassium level is known as hyperkalaemia.
Levels above 6.5 mmol/l are particularly dangerous and must be reported immediately because fatal
disorders of heart rhythm can occur suddenly.

Typical causes of hyperkalaemia are:
– Excessive IV infusion, or increased ingestion of
potassium.
– Reduced renal excretion, renal failure with oliguria, anuria, acidosis.
– Addison’s disease.
– Hypoaldosteronaemia.
– Leakage of cellular potassium following: acute starvation, gross haemolysis, diabetic ketoacidosis, dehydration, severe tissue injury.

Falsely high potassium result: This can occur if a blood sample is haemolyzed due to poor venepuncture technique, a sample is left for a long time (e.g.
overnight) without the plasma or serum being removed or if whole blood is refrigerated before it is centrifuged. Red cells contain a high concentration
of potassium.

What are causes of low Potassium levels?

A low potassium level is called hypokalemia. The depletion of potassium can be masked by topping up of the plasma levels from intracellular sources and clinical symptoms may present in the
face of apparently normal values. These include:
weakness, tetany, polyuria and ECG changes.
Causes of hypokalaemia include:
– Inadequate intake of potassium in the diet and long term starvation.
– Increased loss of potassium due to prolonged vomiting or diarrhoea, renal tubular failure, diuretics, hyperaldosteroidism.
– Redistribution from plasma into cells; insulin therapy, metabolic or respiratory alkalosis.

Note: In the management of patients with salt and water depletion a simple test for urine chloride may be of value when facilities are not available for measuring serum or plasma electrolytes.

ACUTE PANCREATITIS

Very high concentrations of serum or plasma amylase (over 1850 U/l) are virtually diagnostic of acute
pancreatitis or acute episodes of chronic relapsing pancreatitis.

When chronic pancreatitis has reached
the stage of scarring and calcification, the serum amylase level is usually normal.
With acute pancreatitis, the rise in serum or plasma amylase is often very brief with the enzyme reaching its highest level within 12–24 hours and returning to normal within 3–5 days.

Slight to moderate increases of serum amylase must be interpreted carefully. They are not diagnostic of acute pancreatitis unless the blood has been
collected too late to catch the peak level.

Other laboratory findings in pancreatitis
In acute pancreatitis the white cell count is raised. A serious condition is indicated if the serum or plasma albumin and calcium and blood haematocrit levels fall and the serum or plasma bilirubin and urea
levels rise.

Falsely elevated amylase levels may result if the serum is markedly turbid or the sample has been contaminated with amylase during analysis

Note: It is useful to measure amylase both in serum and in urine. Amylase is quickly filtered into the urine, therefore a person suffering from acute pancreatitis may have normal serum amylase levels but
high enzyme activity in the urine.