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CONTENTS

A- X-ray.
1. Introduction to chest X-ray…………………………… … 1
2. Chest X-ray …………………………………………..…… 9
3. Heart X-ray …………………………………………..…... 14
4. Bone X-ray ..…………………………………………..…... 20
5. GIT X-ray ...…………………………………………..…... 22
6. Urinary tract X-ray ...………………………...…..………. 26

B- ECG.
1. Introduction…………………………………….……...….. 29
2. Leads, Axis………………………………………...……….. 32
3. Chamber enlargement ………….…………………...….... 34
4. Conduction disturbance ………………………………..… 36
5. Coronary heart disease……………………………….…… 40
6. Drug Effects, Electrolyte Abnormalities, and
Metabolic Factors………………………………………….. 47
7. Pericardial, Myocardial, and Pulmonary Syndromes….…51
8. Wolff-Parkinson-White Preexcitation Patterns ................ 53
9. Arrhythmias ………………………………………………...53
10. Scheme……………………………………………………… 62
11. Comment……………………................................................ 64
12. Examples……………………………………………………..65

C - CLINCAL PATHOLOGY.
1. Blood report (Haematology)……………………………… 74
2. Serology report (immunology)…………………………… 96
3. Hepatitis markers profile (immunology)……...…………. 103
4. Urine analysis (microbiology)………….............................. 107
5. CSF report (microbiology)…...………………………….... 113
6. Stool analysis (microbiology)……........................................ 116

D - CHEMICAL PATHOLOGY.
1. Liver function tests …………............................................ 119
2. Kidney function tests …………......................................... 125
3. Blood sugar profile …………….......................................... 129
4. Thyroid profile………………………….………....………. 132
5. Cardiac enzymes and proteins ............................................ 133
1
2
Normal structures’ opacity Normal structures
 Air = lung field is black Normal Posteroanterior view CXR is formed of
 Water = heart and mediastinum are white  Chest wall (ribs)  Lung field
 Bone is in between  Mediastinum including the heart
 Diaphragm

Bone
Chest wall

Normal posteroanterior & lateral view

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Position of the patient (centralization)

Both clavicles should be at same level and the midway between them should lie at the line of vertebral
spine.
Gender: female = breast shadow as the X-ray on the right.

Air Bronchogram
In a normal chest x-ray, the tracheobronchial tree is not visible
beyond 4th order. As the bronchial tree branches, the
cartilaginous rings become thinner and eventually disappears in
respiratory bronchioles. The lumen of bronchus contains air and
the surrounding alveoli contain air also. Thus there is no
contrast to visualize bronchi. The air column in bronchi beyond
4th order becomes recognizable if the surrounding alveoli is
filled, providing a contrast or if the bronchi get thickened.

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The term air bronchogram is used for the former state and
signifies alveolar disease. Note in the adjacent CXR
branching radiolucent columns of air corresponding to
bronchi which occurs in RUL consolidation & this helps to
differentiate consolidation from effusion.
Cardiothoracic ratio
Normal ratio of the heart to thorax is 1:2
Chest x-ray consists of
 Chest wall (ribs)  the heart
 Lung field (lobes)  Diaphragm
 Mediastinum
Mediastinum
It is formed of the tissues between the two lungs as heart, great vessels and LNs.
Deviation of the mediastinum is accessed by the position of the heart apex & trachea.

RIBS
First rib is the upper rib, highly curved than the
other ribs. It lies below the clavicle so it has a
common shadow with it. Ribs on the lt
hemithorax are counted from front the others on
the right hemithorax are counted from back
6th rib normally is the last rib crossing the
copula of the diaphragm. If the diaphragm
crosses at a lower ribs then there is
hyperinflation

The lungs Rt lung: 3lobes Lt lung: 2 lobes

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The hilum costophrenic angles
Contains the pulmonary vessels and pulmonary LNs

Heart
Heart borders
1. RT border:
a- SVC. b- RT atrium.
c- Ascending Aorta.
2. Front of the heart: RT ventricle.
3. LT border :
a- Aortic knuckle (1st space).
b- Pulmonary a. (2nd space).
c- LT auricule (3rd space).
d- Waist = constriction bet. PA & LA. e- LT ventricle forming the apex.
The cardiac contour

Chambers of the heart

Main chambers posteroanterior view Main chambers lateral view


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Right atrium Left atrium
Forms the right border of the heart It lies posteriorly

PA view: straightening of the left heart order. A discrete bulge on the left 3rd intercostal space,
immediately below the pulmonary bay. A double shadow (opacity) seen through the right side of
the heart = border of the right and left atria. Lateral view: Pressure on the oesophagus
Ventricular enlargements
Right ventricle
Left ventricle

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RVE LVE
Posteroanterior view
Increased cardiothoracic ratio
cardiac outline takes the triangular shape Elongation of the long axis of the left ventricle
Elevation of the apex Apex: rounding / displaced downward
Enlargement of the pulmonary artery Enlargement of the aorta
Lateral view
Obliteration of retrosternal space Obliteration of retrocardiac space
Ascending aorta Enlarged in volume overload (AR)

Aortic knob Enlarged in pressure overload (AS, HTN)

Pulmonary artery

 Enlargement of the heart chambers & vessels


A-In lateral view

LAE RVE LVE


Ba swallows Pressure on Plain X-ray Obliteration of Plain X-ray Obliteration of
oesophagus retrosternal space retrocardiac space 8
B-In post-anterior view

LAE
RAE RVE LVE
3rd space
- RT border bulge -↑↑cardiothoracic -↑↑cardiothoracic
Double contour
- Elevated apex - Apex: rounding /
- ++ PA displaced downward
-  shaped - ++ aorta

angle

Aortic P.A. Ascend. aorta


knuckle dilatation -
st
- 1 LT space - 2nd LT space

Lung X-rays
OPACITY HYPERTRANSLUCENCY CAVITY
COPD
Lung abscess
Pneumothorax
Homogenous
Heterogeneous

1. Pleural effusion (massive &


moderate) 1. Miliary shadows for D.D.
2. Collapse (massive & lobar) 2. Bronchopneumonia (Fluffy cotton
3. Hydro-pneumothorax appearance)
4. Lobar pneumonia 3. Polycystic lung (Soap bubble
5. Coin shadow for DD. appearance)
6. Apical homogenous opacity for 4. Honey comb appearance
DD. 5. Fibrosis
7. BHL for DD 6. multiple lung metastasis
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Which Lung & which zone ? If it is cavity you The most imp 3 items in
1. Upper zone should comment on the comment are
(From the apex to 2nd rib) 1. Site 1. Lesion description
2. Middle zone 2. Size (character ,site ,size)
(From the 2nd rib to the 4th rib) 3. Border 2. Mediastinum position
3. Lower zone 4. Content 3. Costophernic angle
(From the 4th rib to the base of 5. Uni or bilateral
the lung) 6. Multiple or single

Homogenous opacity
Massive pleural Effusion
 Homogenous opacity right hemithorax.
 Shift of mediastinum to the left.
 Obliterated right costophrenic angle.
 Absent bronchoalveolar markings in the lesion.

Mild pleural effusion


 Moderate homogenous opacity left lower zone of the
lung with its upper border rising to axilla.
 No shift of mediastinum.
 Obliterated left costophrenic angle
 Absent bronchoalveolar markings in the lesion.

Atelectasis (collapse) Right Lung


 Homogenous opacity right hemithorax
 Shift of mediastinum to the right.
 Obliterated right costophrenic angle

Atelectasis Left Lung


 Homogenous opacity left hemithorax.
 Shift of mediastinum to the left.
 Obliterated left costophrenic angle
 Compensatory emphysema Rt lung

Left Lower Lobe Atelectasis


 Homogenous opacity left lower zone of the lung
 Central mediastinum.
 Obliterated Lt costophernic angle

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Atelectasis Left Upper Lobe
 Homogenous opacity left lower zone of the lung
 Central mediastinum.
 Free both costophernic angles

Atelectasis Right Upper Lobe


 Homogenous opacity right upper lung zone
 Mediastinal shift to right
 Clear both costophernic angles
 Absent air bronchogram

RML Atelectasis

Vague opacity in right lower lung field (almost a normal film).


RML atelectasis in lateral view, not evident in PA view.

Consolidation Left Lower Lobe


 Homogenous opacity in left lower lung zone.
 Central mediastinum
 Obliterated Lt costophernic angle
 Air bronchogram is clear in the lesion.

Left Upper Lobe Consolidation


 Homogenous opacity in the left upper lung zone
 Loss of silhouette of left heart margin
 Clear both costophernic angles
 Air bronchogram is clear in the lesion.

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Right upper lobe consolidation
 Homogenous opacity in the right upper lung
zone.
 Central mediastinum
 Clear angles.
 Air bronchogram is clear in the lesion.
 Difference between consolidation and collapse is air
bronchogram

Hydropneumothorax
 The lesion occupies the Rt hemithorax with air /
fluid level and consists of 2 parts lower part
homogenous opacity & upper part Jet black
 Compensatory emphysema Rt side
 Shift of mediastinum to Rt side
 Obliterated Lt costophrenic angle

Coin shadow for D.D


 Right lower lung zone shows rounded
homogeneous opacity. Size 2x3 cm
 Central mediastinum
 Clear costophrenic angles
 Causes
 Bronchogenic carcinoma
 Bronchial adenoma
 Single metastasis neoplasms
 Tuberculoma ■ Calcified cyst

Apical homogenous opacity for D.D


 Apical homogenous opacity Lt upper lung zone
 Central mediastinum
 Clear costophrenic angles
 Causes
 Pancost tumour
 Apical T.B.
 Apical lung collapse
 Upper lobar pneumonia

Bilateral hilar LN enlargment


 (White arrows) Widened with increased opacity of
hilum on both sides with lobulated outline.
 Clear space between hilar nodes and mediastinum
(Dark arrow).
 Arrowhead: Paratracheal nodes
 DD: sarcoidosis, lymphoma.

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B. Heterogeneous opacity
Milary shadow for DD
 Bilateral diffuse nodules of uniform size of range
2-3 mm.
 Central mediastinum
 Clear costophrenic angles.
 Causes
 T.B. ▪ Alveolitis
 Sarciodosis ▪ Haemosederosis
 Pneumoconiosis

Bronchopneumonia
 Diffuse bilateral opacities of fluffy cotton
appearance
 Central mediastinum
 Clear costophrenic angles.

Metastasis
 Multiple bilateral rounded heterogeneous
opacities of different sizes largest is 3cm
diameter.
 Central mediastinum
 Clear costophrenic angles.

Diffuse lung fibrosis


 Small lungs
 Diffuse linear shadows
 Central mediastinum
 Crowded ribs
 5th rib crosses diaphragm

Localized bronchiectasis
 Shows dilated bronchi at lower zones
 Central mediastinum
 Clear costophrenic angles.

Polycystic lungs
 Diffuse soap bubble appearance
 Central mediastinum
 Clear costophrenic angles

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Honeycombing for DD
 (Seen in end stage lung disease)
 Bilateral multiple dilated tubular shadows + cystic
spaces with peribronchial fibrosis
 Central mediastinum
 Clear costophernic angles.
 Causes: bronchiectasis, cystic fibrosis.

HYPERTRANSLUCENCY
Bronchial asthma
CXR of an asthmatic during an episode of
bronchospasm. Lungs are hyperinflated due
to air trapping. This normalizes once
bronchospasm is controlled.

COPD Pneumothorax
Lesion Hyperinflated > 6th rib is seen crossing Hyperinflated > 6th rib is seen crossing
the diaphragm the diaphragm
Bilateral hypertranslucency Unilateral Rt hypertranslucency
with presence of bronchoalveolar (jet black) with absence of
markings bronchoalveolar markings
Mediastinum Central Shifted to opposite side
+ shadow of the collapsed lung
Bony cage Wide intercostals space Wide + /- fracture of ribs
Heart Ribbon-shaped (compressed bilateral)
Diaphragm Depressed bilaterally Depressed on the same side

Emphysematous
bullae
Multiple bilateral basal
hypertranslucency sacs
Ribbon-shaped
 Central mediastinum
Clear costophernic angles.

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Cavity = lung abscess
 Lesion : No. single
Shape rounded cavity
Size 5x6 cm
Site upper zone RT lung
Content upper part air----jet black lower part
fluid-opaque

Heart x-rays
Mitral stenosis (LAE)
 LAE The cardiac contour is abnormal with bulging on
the right giving a double right heart border (1 )
prominence of the left atrial appendage = 3rd Lt space
(2) elevation of the left main bronchus (3), indicating
left atrial enlargement

Mitral regurgetation (LAE+ LVE).


 LAE (a).the large bulge on the left heart border (left
atrium appendage = 3rd Lt space) (b) double shadow'
(border of the right and left atria) on the right side of
the heart.
 LVE ++ cardiothoracic ratio, apex displaced
downwards. (this is the diff. bet MS and MR there is
cardiomegaly in MR due to LVE.. in MS heart is
usually normal)

Fallout tetralogy (F4)Coeur en sabot


 Exaggerated waist ( pulmonary hypoplasia)
 RVE (Increased cardiothoracic ratio, Elevated apex)
 Enlarged ascending aorta
 Decreased pulmonary vascular markings(lung
oligaemia = dark field)

Aortic regurgitation
 Dilated ascending aorta
 Normal sized aortic arch
 LVE ++ cardiothoracic ratio, apex displaced
downwards.

Systemic Hypertension
 LVE ++ cardiothoracic ratio, apex displaced
downwards
 prominent aortic knuckle
 permanent pacemaker is seen.

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Pulmonary hypertension
 RVE ++ cardiothoracic ratio, elevated apex, triangular
shape of the heart.
 Prominent pulmonary artery (2nd left space).

Aortic aneurysm
The mediastinum is widened throughout
its length with increased lateral
convexity to the left.

Pericardial effusion
 Flask (onion) shaped heart
 Marked increased in cardiothoracic ratio
 Both borders are well defined (no angulations)
with bugle of both cardiac borders

Pulmonary venous congestion


 The heart is enlarged (due to failure. Where this
failure is not severe enough to cause pulmonary
oedema. However, the increased pulmonary
venous pressure about 15 to 20 mmHg has caused
upper zone blood diversion)
 The vessels above the hilum appear wider than
those below. (The mechanism of the blood
diversion is not fully understood.)
Interstitial oedema
 The escape of fluid into the interstitial tissue
occurs when the capillary pressure exceeds the
plasma osmotic pressure of 25 mmHg
 The heart is moderately enlarged.
 Fine, diffuse shadowing in the lung fields with
blurring of the vessel margins.
 Kerley 'B' lines,
Acute (alveolar) pulmonary oedema
 When the pulmonary venous pressure reaches 30
mmHg, oedema fluid will pass into the alveoli.
 Hilar haziness (bat's wing appearance), Kerley B lines,
upper lobe venous engorgement and fluid in the right
horizontal interlobar fissure.
 Basal pleural effusion..

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Heart failure

Left ventricular aneurysm


A cardiac silhouette with a 'bulge' (arrow) on the
left lateral border. A thin line of calcification can
be seen along the edge of this bulge. ++
Cardiothoracic ratio.

 The interstitial oedema is characterised by Kerley


'B' lines, which are oedematous interlobular septa.
They are best seen peripherally in the right
costophrenic angle (arrow), where they lie
horizontally, and are about 1 cm long. They
contain the engorged lymphatics, which were
originally thought by Kerley to be the sole cause of
the 'B' lines.

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1- LT atrial 2- LT ventricular 3- RT ventricular
enlargement enlargement enlargement
X-ray with contrast Plain X-ray Plain X-ray
(Ba swallow )
Lateral view
LAE with backward pressure on Obliteration of the retrocardiac Obliteration of the retrosternal
the oesophagus space space

Dextrocardia.
 Heart is roated with LV and apex on Rt side, RA on LT
side.
 Gastric air stomach on Lt side.

Situs inversus.
 Heart is roated with LV and apex on Rt side, RA on LT
side.
 Gastric air stomach on Rt side.

HEART & CHEST COMMENTS


1- Type of X-ray : Plain x-ray (no dye) or with contrast (mention the dye).
2- View: Postro-anterior or lateral.
3- Gender: Female (breast shadow) or male (no breast shadow).
4- Centralization: Well centralized (spine is at midway between both clavicles)
or not well centralized ( you shouldn't comment on mediastinum).
5- Mediastinum: Central (central trachea & heart) or shifted (mention side).
6- Bony cage: Free or fracture (of ribs, clavicle or sternum)
7- Diaphragm: Normal or depressed.
8- Costo-phernic angles: Clear both sides or obliterated (mention side(s)).
9- Heart or chest comment …..

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Examples
1. Plain CXR (chest X-rays).
2. Postro-anterior view.
3. Gender : male.
4. Well centralized.
5. Central mediastinum.
6. Free bony cage.
7. Normal diaphragm.
8. Clear costo-phernic angles.
9. The heart shows
 LAE (a). 3rd space bulge on the left heart border
(b) double shadow'on the right side of the heart.
Diagnosis: Mitralization (mitral stenosis)

1. Plain CXR (chest X-rays).


2. Postro-anterior view.
3. Gender : male.
4. Well centralized.
5. Central mediastinum.
6. Free bony cage.
7. Normal diaphragm.
8. Clear costo-phernic angles.
9. The heart shows
 LAE (a). 3rd space bulge on the left heart border
(b) double shadow on the right side of the heart.
 LVE ++ cardiothoracic ratio, apex displaced
downwards.
Diagnosis: Mitralization (mitral regurgitation)

1. Plain x-ray chest.


2. Postro-anterior view.
3. Gender: male.
4. Well centralized.
5. Central mediastinum.
6. Free bony cage.
7. Normal diaphragm.
8. Clear costo-phernic angles.
8. The LT lung shows a hialr mass.
9. The heart shows
 Marked increased cardiothoracic ratio.
 Both borders are well defined.
 Bilateral bugle of both cardiac borders.
Diagnosis : Pericardial effusion.

1. Plain x-ray chest.


2. postro-anterior view.
3. Gender : male. 4. well centralized.

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5. Central mediastinum. 6. Free bony cage.
6. Clear costo-phernic angles.
7. Normal diaphragm. .
9. The RT lung shows
 Single rounded homogeneous opacity.
 Lower zone.
 Size 2x3 cm.

Diagnosis : Coin shadow for D.D.


 Bronchogenic carcinoma.
 Bronchial adenoma.
 Single metastasis.
 Tuberculoma.
 Calcified cyst.

1. Plain x-ray chest. 3. Gender : male.


2. Postro-anterior view. 4. Well centralized.
5. Central mediastinum.
6. Free bony cage.
7. Clear costo-phernic angles.
8. Normal diaphragm .
9. Both lungs show
 Multiple bilateral heterogeneous opacities.
 Rounded in shape.
Diagnosis : Multiple lung metastasis.

1. Plain x-ray chest.


2. Postro-anterior view.
3. Gender : male.
4. well centralized.
5. Clear costo-phernic angles.
5. Central mediastinum.
7. Wide intercostals space (bony cage).
8. Depressed both copula of the diaphragm.
9. Ribbon-shaped heart.
10. Both lungs show
 Bilateral hypertranslucency with presence
of bronchoalveolar markings.
Diagnosis : COPD.

1. Plain x-ray chest. 3. Gender: male.


2. Postro-anterior view. 4. Well centralized.
5. Shifted mediastinum to the LT side.
6. Fracture of the 4th → 9th ribs.
7. Depressed RT copula of the diaphragm + widen
intercostal spaces on the right.
8. Clear costo-phernic angles.
9. The RT lung shows..

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 Unilateral hypertranslucency (jet black) with
absence of bronchoalveolar markings.
 Shadow of the collapsed RT lung.
Diagnosis : RT side pneumothorax

1. Plain x-ray chest.


2. postro-anterior view.
3. Gender : male. 4. Well centralized.
5. Central mediastinum. 6. Free bony cage.
7. Normal diaphragm.
8. Obliterated LT costo-phernic angle.
9. The LT lung shows..
 homogenous opacity.
 middle & lower zone.
 upper border rises laterally towards the axilla.
Diagnosis : LT side moderate pleural eff.
1. Plain x-ray chest.
2. Postro-anterior view.
3. Gender : male. 4. Well centralized.
5. Central mediastinum. 6. Free bony cage.
7. Normal diaphragm. 9. Free costo-phernic angles.
8. clear both costophernic angles.
9. Both lungs show
multiple miliary shadows heterogeneous opacities
of size between 1-2 mm
Diagnosis : Miliary shadow for DD.
 T.B. ▪ Alveolitis
 Sarcoidosis
 Hemosiderosis
 Pneumoconiosis

BONE X-rays
HANDS' X-rays
1. Acromegaly
 Plain X-ray of RT hand & wrist.
● Enlarged bones size & shadows.
● Increased soft tissues shadow.
● Mushroom shaped appearance of terminal phalanx
(white arrows).
2. Rheumatoid arthritis
 Plain X-ray of LT hand & wrist.
● Loss of bone density.
● Ulnar deviation at M-P
joints.
● Destruction of proximal I-P
joints.
● Z-shaped deformity of the
thumb.
● Amalgamated carpel bones.

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● Periarticular osteopenia.
3. Scleroderma
- Plain X-ray of LT hand & wrist.
● Tuft resorption.
● Soft tissue calcification.
4. Chronic haemolytic
anaemia.
 Plain X-ray of LT hand & wrist.
● Decreased bone density.
● Metacarpal bones show…
 Loss of waist (rectangular
shape).
 Thin cortex.
 expansion of medulla.

Skull X-rays
1. Acromegaly
 Plain X-ray of skull.
 Lateral view.
● Prognathism (prominent jaw).
● Enlargement of frontal air sinus.
● Prominent mastoids.
● Thick cortex.
● Saucerization ‫ صحن الفنجان‬of sella turcica
(black arrow).

2. Increased ICT before closure


of sutures (hydrocephalus).
 Plain X-ray of skull.
 Lateral view.
 Child.
● Increase size of cranial bones.
● Separated sutures
● Wide sella turcica.

3. Craniostenosis (increased ICT


after the closure of the sutures).
 Plain X-ray of skull.
 Lateral view.
● Increase skull convolutional markings
(the indentation of the sulci & gyri on the skull).
● No separation of sutures.
● Silver beaten appearance of the skull.

4. Chronic haemolytic anemia.


 Plain X-ray of skull.
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 Lateral view.
● Long striation of the skull (hair on end
appearance).
● Wide diploic space (medullary cavity).

5. Multiple osteolytic lesion for D.D.


Multiple metastases, myeloma,
lymphoma.
 Plain X-ray of skull.
 Lateral view.
● Multiple rounded hyperdense (osteolytic) shadows
of regular & equal size.

Spinal X-rays
1. Extramedullary block. 2. Intramedullary block.
 X-ray with contrast myeloid (myelography).
● RT unilateral block. ● Complete block.
● Short tails. ● Long tails.
● Saddle shaped. ● Fusiform-shaped.
● Site: lumber (big vertebrae), cervical (small ● Site: lumber(big vertebrae),cervical
vertebrae), thoracic (ribs). (small vertebrae), thoracic(ribs)

3. Lumber Spondylosis.
 Plain X-ray of the spine.
● Variable intervertebral spaces.
● Loss of spinal lordosis.
● New bone formation (osteophytes, lipping).

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GIT X-rays
Oesophageal X-rays
1. Oesophageal varcies.
 X-ray with contrast Ba swallow.
● Multiple irregular filling defects (grape shaped).
● Site: all over the whole oesophagus but mainly at
the lower end of the oesophagus.

2.Achalsia of cardia.
 X-ray with contrast (Ba swallow).
● Body: dilated (sigmoid shaped).
● Lower end: narrow (pencil shaped).
● May shows air / fluid level.

3.Cancer oesophageus.
 X-ray with contrast (Ba swallow).
 Lesion.
● Shouldering + rate tail appearance = scirrhous tumour.
● Irregular filling defect = cauliflower ‫ قرنبيط‬mass.
(Mention site & size of the lesion).
Types of barium contrast radiology
Ba swallow shows oesophagus
Ba meal shows stomach and
duodenum
Ba follow through shows small
intestine
Currently all GIT radiology are
replaced by endoscope

Stomach X-rays
1. cancer stomach
 X-ray with contrast (Ba meal).
 Lesion.
● Irregular filling defect → cauliflower tumour.
● Large ulcer w/o notch → ulcerative tumour.
● Linitis plastica → diffuse tumour.
(mention site & size of the lesion)

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Linitis plastica Filling defect Malignant ulcer
2. Chronic gastric peptic ulcer.
 X-ray with contrast Ba meal.
 Lesion…
● Lesser curve → ulcer niche (funnel protrusion).
● Greater curve → ulcer notch (filling defect = fibrosis).
N.B.:
 There is also peptic ulcer occurring at the duodenum called duodenal
peptic ulcer.
 Healing gastric peptic ulcer forms "Ba flake" in post-evacuation
film.
 Healed one forms "hour glass stomach" due to fibrosis (also occurs
in gastric malignancy).
 Differences between malignant ulcer & peptic one is the following
the malignant ulcer has 2 menisci (edges) but the peptic one has a
niche & a notch.

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Biliary tract radiology
Plain x-rays X-ray with contrast

Oral Intravenous Tube


cholecystography cholecystography cholangiography ERCP PTC
Oral cholecystography: Endoscopic retrograde cholangio-
- Dye (Telepaque) is orally taken. pancreatography (ERCP):
- Visualize gall bladder. - Dye is injected through an
- Visualize radio-opaque stones & endoscope.
radio-lucent stones & neoplasm - Visualize CBD & pancreatic duct.
as a filling defect. - Visualize radio-opaque stones &
Intravenous cholecystography: radio-lucent stones as a filling
- Dye (Urografin) is parenterally defect.
injected. Percutaneous transhepatic
- Visualize gall bladder & biliary cholangiography (PTC):
Plain x-rays: ducts. - Dye is injected through a needle
- RT hypochondrium. - Visualize radio-opaque stones & through skin.
- Visualize only radio-opaque stones radio-lucent stones & neoplasm - Visualize intrabiliary hepatic
anywhere in the biliary tract. as a filling defect. duct.
- Lateral view is better than Tube cholangiography: - Visualize radio-opaque stones &
Postroanterior view as the former - Dye is injected through T-tube. radio-lucent stones & neoplasm
differentiate between renal & gall - Visualize CBD. as a filling defect.
- bladder stones, where renal stones - Visualize radio-opaque stones &
are posterior to vertebral column radio-lucent stones & neoplasm
while the gall stones are anteriorly as a filling defect.
located.
26
1. Gall bladder stones.
 Plain X-ray of the right hypochondrium.
 .Gall bladder is seen having
● Multiple radio-opaque stones.
2. Gall bladder stones.
 X-ray of the right hypochondrium with contrast =
oral cholecystography.
 Gall bladder is seen having.
● Multiple filling defects
= multiple radio-lucent stones.
3. Common bile duct stones.
 X-ray of the right hypochondrium with contrast =
Tube cholangiography.
 T tube is seen having.
 CBD is seen having
● Multiple radio-lucent stones at CBD.
4. Common bile duct stones.
 X-ray of the right hypochondrium with contrast = ERCP.
 An endoscope is seen.
 CBD, gall bladder are seen having
● Multiple radio-lucent stones at CBD.
5. Dilated intrabiliary system.
 X-ray of the right hypochondrium with contrast = PTC.
 A needle is seen.
 Intrabiliary system is seen having.
● Dilated intrabiliary system.
● A neoplasm is seen distal to the obstruction.

Intestinal X-rays
1. Crohn's disease.
 Terminal ileum on barium follow-through
 Lesion.
A long stricture is present (arrow A) and more
proximally there is ulceration with
characteristic 'rose thorn' ulcers (arrow B).

27
2. Ulcerative colitis.
 X-ray with contrast Ba enema (needle at anus).
Ba follow through (no needle).
 Lesion…
● Colonic shorting.
● Loss of haustrations (pipe stem rigid appearance).

Urinary X-rays
1. KUB: plain x-ray of kidneys, ureters & urinary bladder.
Contrast…
2. IVU: x-ray with contrast (Urografin) of whole urinary tract.
3. IVP: as IVU but shows only renal pelvis upper ureters.
4. Descending cystograpy: as IVU but shows only urinary bladder & lower ureters.
5. Ascending cystograpy: x-ray with contrast (Urografin) of urinary bladder, dye is injected
inside the urethra with a needle is seen done in renal failure to see the bladder.
6. Urethrography: x-ray with contrast (Urografin) of the urethra.
1. Stone.
 Plain X-ray = KUB.
 Both kidneys show multiple staghorn stones at renal pelvis.

2. LT kidney hydroureter & hydronephrosis.


 IVP (Urografin dye).
 Rt kidney is radiologically absent..
 Lt kidney shows..
● Dilation , thickening & tortuosity of both ureters.
● Dilation of renal pelvis.
● Distortion of pelvicalyceal system.
● Calyces (ballooning, loss of waist, clubbing).
3. RT RCC (hypernephroma).
 IVP (Urografin dye).
 The Rt kidney shows normal IVP appearance
 The Lt kidney shows
● Enlargement of the RT kidney.
● Soft tissue shadow (tumour) at the upper pole.
● Calyx = moth eaten (elongated, flatness, compressed
or amputated).
● Downwards displacement of the compressed pelvis.

28
4. Polycystic kidneys.
 IVP (Urografin dye).
 Lesion…
● Enlargement of the both kidneys.
● Smooth spider leg appearance.
● Elongation + attenuation & wide separation of
calyx (by the cysts in bet.).

5. RT incomplete double ureter.


 IVP (Urografin dye).
 Lesion…
● The RT kidney shows two independent ureters with
two separate collecting systems.
● Two ureters joins at lower part of their course.
● Rt kidney is not seen

29
Undergraduate syllabus
1. 1 degree heart block
st

2. LBBB, RBBB.
3. RVH, LVH, RAH, LAH.
4. Anterior, lateral, inferior MI (acute and old).
5. Anterior, lateral, inferior ischaemia.
6. AF, atrial flutter, extrasystoles, VT.
Usually one pathology is present.
Please study scheme P64

28
INTRODUCTION
ECG PAPER : The ECG is usually recorded on a graph divided into millimeter squares, with darker lines
marking 5-mm squares. Time is measured on the horizontal axis. With a paper speed of 25 mm/sec, each
small (1-mm) box side equals 0.04 second and each larger (5-mm) box side equals 0.2 second. The
amplitude of any wave is measured in millimeters on the vertical axis

‫مم =½ سم‬5 = ‫المربع الكبير = ُخمس ثانية‬


‫ مربعات كبيرة = ثانية = الشرطة الموجودة باألعلى‬5
‫ مربع كبير = ثالث ثوان‬55
‫ ثوان‬6 = ‫ شرط‬6
.‫ ثانية = دقيقة‬61 = 51 X ‫ ثوان‬6


A, The resting heart muscle cell is polarized; that is, it carries an electrical charge, with the outside of the
cell positively charged and the inside negatively charged. B, When the cell is stimulated (S), it begins to
depolarize (stippled area).C, The fully depolarized cell is positively charged on the inside and negatively
charged on the outside. D, Repolarization occurs when the stimulated cell returns to the resting state. The
direction of depolarization and repolarization is represented by arrows. Depolarization (stimulation) of
the atria produces the P wave on the ECG, whereas depolarization of the ventricles produces the QRS
complex. Repolarization of the ventricles produces the ST-T complex.

A, A positive complex is seen in any lead if the wave of depolarization spreads toward the positive pole
of that lead. B, A negative complex is seen if the depolarization wave spreads toward the negative pole
(away from the positive pole) of the lead.C, A biphasic (partly positive, partly negative) complex is seen
if the mean direction of the wave is at right angles (perpendicular) to the lead

These three basic laws apply to both the P wave (atrial depolarization) and the QRS complex (ventricular
depolarization).
 The P wave is positive (upward)

29
 T wave is negative (downward).
 The QRS complex is biphasic (partly positive,
partly negative)
 The ST segment is isoelectric (neither positive
nor negative).

First wave seen small rounded, upright


(positive) wave indicating atrial depolarization (and
contraction) The normal P wave is usually no more
than 2.5 mm in height and less than 0.12 sec in width
(2.5 x 2.5 small boxes).
Atrial depolarization (NORMAL P
WAVE)
With normal sinus rhythm, the atrial depolarization wave (arrow) spreads from the
right atrium downward toward the atrioventricular (AV) junction and left leg.
Atrial depolarization (ABNORMAL P WAVE)
When the atrioventricular (AV) junction (or an ectopic pacemaker in the low atrial
area) acts as the cardiac pacemaker (junctional or low atrial rhythm), the atria are
depolarized in a retrograde (backward) fashion. In this situation, an arrow
representing atrial depolarization points upward toward the right atrium. The opposite
of the pattern is seen with sinus rhythm.

: distance between beginning of


P wave and beginning of QRS complex.
Measures time during which a
depolarization wave travels from the atria to
the ventricles. the normal PR interval is
between 0.12 and 0.2 second (3to5 small
boxes)
Three deflections following P wave indicates ventricular depolarization (and contraction)

Q Wave: First negative deflection R Wave: First positive deflection


S Wave: First negative deflection after R wave

30
Notice that capital letters (QRS) are used to designate waves of relatively large amplitude and small
letters (qrs) label relatively small waves.
Ventricular depolarization (normal QRS complex)
The first phase of ventricular depolarization proceeds from the left wall of the septum to the right. A, An
arrow representing this phase points through the septum from the left to the right side. B, The second
phase involves depolarization of the main bulk of the ventricles. The arrow points through the left
ventricle because this ventricle is normally electrically predominant. The two phases produce an rS
complex in the right chest lead (V1) and a qR complex in the left chest lead (V6).

The QRS width, or interval, represents the time


required for a stimulus to spread through the ventricles
(ventricular depolarization) and is normally 0.1 second
or less If the spread of a stimulus through the ventricles
is slowed normal up to 3 small boxes
The is that portion of the ECG cycle from
the end of the QRS complex to the beginning of the T
wave. It represents the beginning of ventricular
repolarization. The normal ST segment is usually
isoelectric (i.e., flat on the baseline, neither positive nor
negative), The represents part of ventricular
repolarization. A normal T wave has an asymmetric
shape; that is, its peak is closer to the end of the wave
than to the beginning The is measured
from the beginning of the QRS complex to the end of
the T wave. It primarily represents the return of
stimulated ventricles to their resting state (ventricular
repolarization). It’s length varies with change of HR in
which if HR is 60- 150 (R-R 5 to 2 big boxes) the QT
will be normally from 2.5 to 1.5 big boxes.
Small rounded, upright wave following T
wave Most easily seen with a slow HR. Represents
repolarization of Purkinje fibers.
CALCULATION OF HEART RATE
Heart rate (beats per minute) can be measured by counting the number of large
boxes between two successive QRS complexes and dividing 300 by this number. In this example, the
heart rate is calculated as 300 ÷ 4 = 75 beats/min (choose a QRS on the side of a large box)
no. of QRS in 6 seconds x 10 (15 cm by a ruler) since 1 min = 60 sec = 10 x 6 sec

31
12 ECG Leads, AXIS
 Standard bipolar limb leads: I, II, III
 Bipolar limb leads aVR, aVL, aVF
 Chest (percordial, ventricular) leads: V1 to V6

Lead I records the difference in voltage


between the left arm (LA) and right arm (RA)
electrodes i.e. Lead I = LA – RA
Lead II records the difference between the left leg
(LL) and right arm (RA) electrodes i.e. Lead II = LL
– RA
Lead III records the difference between the left leg
(LL) and left arm (LA) electrodes i.e. Lead III = LL –
LA

The LA electrode detects the electrical voltages of the heart that are transmitted to the left arm.
The RA electrode detects the electrical voltages transmitted to the right arm.
The LL electrode detects the electrical voltages transmitted to the lower limb.
: "unipolar” leads in that they measure the voltage in any one location relative to about zero
potential.

32
High
Strict
High Low

Strict Low

The depolarization stimulus spreads through the ventricles in different directions from instant to instant.
For example, it may be directed toward lead I at one moment and toward lead III the next. The mean
direction of the QRS complex, or mean QRS electrical axis, can also be described. If you could draw an
arrow to represent the overall, or mean, direction in which the QRS complex is pointed in the frontal
plane of the body, you would be drawing the electrical axis of the QRS complex. The term mean QRS
axis therefore describes the general direction in the frontal plane toward which the QRS complex
is predominantly pointed. Each lead has a positive and negative pole. As a wave of depolarization
spreads toward the positive pole, an upward (positive) deflection occurs. As a wave spreads toward the
negative pole, a downward (negative) deflection is inscribed. The cardiac axis is at right angles (90") to
the lead in which the R and S waves are of equal size. It may +ve if the difference bet QRS (lead I – lead
II) is +ve and vice versa.

33
CHAMBER ENLARGEMENT

 Normal P wave < 2.5 small boxes. height & < 2.5 small boxes width. Ascending first part of P
wave is formed by RA since it contains the SAN so it is depolarized first followed by descending
part of late LA.LA is depolraized in opposite direction to lead V1 so it causes –ve deflection.
 P mitrale wide, notched P waves in any lead and/or wide biphasic P waves wave > 2.5 small
boxes width in lead V1.
 P pulmonale Tall narrow P waves (RAE/ RAH) wave > 2.5 small boxes height

34
The left ventricular hypertrophy exaggerates the normal pattern, causing deeper right precordial S
waves and taller left precordial R waves. By contrast, right ventricular hypertrophy shifts the QRS
vector to the right, causing increased right precordial R waves .

Big R in V1 ( R ≥ S) SV1+ RV5 or 6 ≥ 7 b. sq. Signs of LVE+


Depressed ST & inverted Depressed ST & inverted Tall R in V1 (RVE).
T wave in: Vl → V3 ( strain T wave in: V4 → V6 (strain OR
pattern ) pattern).
Right axis deviation. Left axis deviation. RAD (RVE)

 Big R inV1 R
≥S
 Depressed ST
& inverted T
wave in :Vl →
V3 ( strain
pattern(
 Right axis
deviation.

Strain pattern
May occur at the leads of hypertrophy due
relative ischaemia

35
CONDUCTION DISTURBANCES

Bundle branch block


One One Bifascicular Both Tri-
bundle fascicle bundles fascicular
RBBB LAHB RBBB + Complete heart Bifascicular
block + AV block
LBBB LPHB LAHB
(RBBB +LBBB)

Wide QRS < 3 small boxes (0.12 seconds).


rsR' complex RsR' complex (M - deep S in rsR' complex n V1 +deep S in deep S in
M – shaped + shaped, notched R ) inferior leads inferior leads esp. aVF lateral leads
big R in V1 in V6, I & aVL. esp. aVF
Deep QS complex NB: deep S wave is wave voltage (length) > 1
lead V1(notched S) big square.
Strain pattern Strain pattern V4
V1→V3 →V6
Normal axis LAD LAD LAD RAD

36
37
38
Atrioventricular (AV) Heart Block

First Second Third


First-degree Uniformly prolonged PR interval with conducted all P waves
)p
)present all P waves(
Second-degree block Intermittent conduction failure Absent P wave(s)
)absent some P waves(
Mobitz type I (Wenckebach (:
progressive PR interval until one sinus P wave is not
conducted at all
Mobitz type II :(
:(sudden conduction failure( sudden
unconducted P wave irrespective to PR changes
Third- (complete) block independent atrial (P) and ventricular (QRS complex) activity.
….. multiple Ps and variable PR intervals
, the PR interval is uniformly prolonged beyond 0.2 second (one big box) with
each beat.

(:The PR interval lengthens progressively with successive beats until one


sinus P wave is not conducted at all. Then the cycle repeats itself. Notice that the PR interval after the
nonconducted P wave is shorter than the PR interval of the beat just before it.

39
Abrupt nonconducted P waves without preceding changes in the PR
intervals sinus rhythm with 2:1 block alternating with 3:1 block (i.e., two consecutive nonconducted P
waves followed by a conducted one).

Type 2 heart block is simply seen as 2 succeeding Ps without QRS in between. Type I is preceded by
prolonged PR interval while it is not preceded by this change in type II.
independent atrial (P) and ventricular (QRS complex) activity. The
atrial rate is almost always faster than the ventricular rate. The PR intervals are completely variable.
Some sinus P waves fall on the T wave, distorting its shape. others may fall in the QRS and be “lost

Notice above that the QRS complexes are of normal width, indicating that the ventricles are being paced
from the atrioventricular junction.

Notice above that the QRS period may widen if it is paced by ventricular rhythm (idioventricular).

ISCHAEMIC (CORONARY) HEART DISEASE.


Ischaemic (coronary) heart disease.

Ischaemia Angina Infarction


Classic
ST segment Subendocardial Transmural
depression and/ NSTEMI Non-Q wave MI
or inverted T- Like ischaemia + ↑↑ cardiac
waves enzymes

Variant Recent (acute) Old


ST segment elevation + ST segment elevation patholgical Q waves
normal cardiac enzymes

40
 A With acute subendocardial ischaemia the electrical forces (arrows) responsible for the ST
segment are deviated toward the inner layer of the heart, causing ST depressions in lead V5,
which faces the outer surface of the heart.
 B, With acute transmural (epicardial) ischaemia, electrical forces (arrows) responsible for the ST
segment are deviated toward the outer layer of the heart, causing ST elevations in the overlying
lead.
Characteristics of the normal ST segment and
T wave. The junction (J) is the beginning of the
ST segment. To comment as elevated ST
segment the J point should be above baseline by
1 s. sq. in limb leads or 2 s. sq. at chest leads.

Elevated ST segment (elevated J point) high take off of ST segment (isoelectric J point)

Forms of ST depression Forms of ST elevation

Angina pectoris

Type Site
Classic (Stable( Variant

Stable Angina
 A, Baseline rhythm strip from the positive exercise
test of a patient with coronary artery disease.
 B, Notice the marked ST depressions with increased
heart rate.
Prinzmetal's (variant) Angina
 Prinzmetal's (variant) angina with transient ST elevations in a 30-year-old man with a history of
angina with exertion and at rest.
 A, The baseline resting ECG shows nonspecific inferior lead ST-T changes.
 B With chest pain, marked ST segment elevations occur in leads II, III, and aVF, and reciprocal
ST depressions are seen in leads I and aVL.
 C The ST segments return to baseline after the patient is given nitroglycerin. Cardiac
catheterization showed severe right coronary obstruction with intermittent spasm producing total
occlusion and transient ST elevations.

41
Lateral Low (V 5,6) I (high) high) aVL)
InFerior II , III aVF
Septal V1, 2
Anterior (strict) V 3, 4
Antroseptal V 1,2,3,4
Extensive anterior V 1→ 5, 6
Anterolateral ANY 2 succeeding I aVL
chest lead
Posterior V 1,2,3 (reciprocal) V8 Usually ass. Inf. MI Tall R, Depressed ST
(inferoposterior)) V9 Upright T
Right ventricle V1r V3r Usually ass. Inf. MI
2 leads at least should present in the wall.
Antrolateral ischaemia.

42
Myocardial infarction
Type Site
Transmural Subendocardial
Q-wave infarction Non-Q-wave infarction
NSTEMI
Acute (recent) Chronic (Old)

Pathological Q wave is>1 small square in duration (width) & >1/4 preceding R wave (length) or single Q
wave in any lead rather than aVR . the mechanism of formation of Q wave is that Q wave is septal wave
escapes through infracted area.
Examples of pathological Q-wave

Evolving Resolving
Hyperacute Acute
0 – 6 h rs ‫يتطور‬24 hr–3w Old > 3 weeks
6 - 24 hrs

 ST elevation  ST elevation  Inverted T wave  Path. Q

 inverted T wave  Path. Q

43
A, Acute phase of an inferior wall myocardial infarction: ST elevations and new Q waves.
B, Evolving phase: deep T wave inversions+ pathological Q waves.
C, Resolving phase: partial or complete regression of ST-T changes (and sometimes of Q waves). In A
and B, notice the reciprocal ST-T changes in the anterior leads (I, aVL, and V2).

A, Acute phase of an inferior wall myocardial infarction: ST elevations and new Q waves. B, Evolving phase:
deep T wave inversions. C, Resolving phase: partial or complete regression of ST-T changes (and sometimes
of Q waves). In A and B, notice the reciprocal ST-T changes in the anterior leads (I, aVL, and V2).
Inferior MI

Lateral MI

44
Persistent ST elevation in a patient with a history of MI.

45
 Tall R.
 ST depression Ant. leads
 Upright T.
 Ass. inferior MI.

Non–Q wave infarction in a patient who complained of severe chest pain. Subsequently, the
patient's cardiac enzyme levels were elevated. Notice the marked, diffuse ST depressions in leads I, II, III,
aVL, aVF, and V2 to V6, in conjunction with the ST elevation in lead aVR. These findings are consistent
with severe subendocardial ischemia. Other abnormalities include a prolonged PR interval (0.28 sec) and
left atrial abnormality.

46
we expect it if there is inferior infarction. Here there is elevated ST
segment inferior and right leads.

DRUG EFFECTS, ELECTROLYTE ABNORMALITIES, AND METABOLIC FACTORS

 Digitalis effect  Hypokalaemia


 Quinidine effect  Hypo & hypercalcaemia
 Hyperkalaemia
Digitalis effect (Not all patients taking digitalis exhibit these changes).
Scooping of the ST-T complex Shortened the QT interval
ST segment and T wave are fused together
Digitalis effect must be distinguished from digitalis toxicity, which refers to
arrhythmias, conduction disturbances (+digitalis effect).
Quinidine effect Prominent T-U waves, (QT) prolongation

Hyperkalaemia

47
 T waves peaking (“tenting” ‫)خيمة‬.  Prolonged PR interval
 P waves decrease in amplitude and may  A sine-wave )‫ )جيب الزاوية‬pattern leads to
disappear asystole
 QRS complexes widen and latter bizarre  ‫البوتاسيوم بتمط رسم القلب‬++
Hypokalaemia

Range from slight T wave flattening to the


appearance of prominent U waves
ST depressions or T wave inversions
Hypo & hypercalcaemia

Hypocalcemia prolongs the QT interval by stretching out the ST segment.


Hypercalcemia decreases the QT interval by shortening the ST segment so that the T wave seems to take
off directly from the end of the QRS complex.

50
PERICARDIAL, MYOCARDIAL, AND PULMONARY SYNDROMES
Acute pericarditis

Ventricular injury diffuse ST segment elevations in leads I, II, aVF, and V2 to V6, with reciprocal ST
depressions in lead aVR. A concomitant atrial injury PR segment elevations in lead aVR with reciprocal
PR depressions in the left chest leads and lead II.
Late pericarditis
 Notice the diffuse T wave inversions in leads I, II, III, aVL, aVF, and V2 to V6.
Difference between pericarditis and myocardial infarction
 No Q waves in percarditis.
 Diffuse affection of all leads by ST changes.
 PR change in acute pericarditis.

Pericardial effusion
Electrical alternans may develop in patients with pericardial effusion and cardiac tamponade. Notice the
beat-to-beat alternation in the P-QRS-T axis; this is caused by the periodic swinging motion of the heart
in a large pericardial effusion. Relatively low QRS voltage and sinus tachycardia are also present.

51
Pulmonary embolism

PE showers form Sinus tachycardia, Massive PE causes S waves in lead I with Q waves and T wave
inversions in lead III (SI, QIII, TIII pattern), Submassive PE makes slow R wave progression with T
wave inversions in chest leads especially V1 & V2 resulting from acute right ventricular overload
COPD

52
Notice the characteristic combination of relatively low voltages in the limb leads, right axis deviation, right atrial
overload pattern (“P pulmonale”), and slow R wave progression. The P wave axis is also more rightward than usual
(almost +90°). RVH may be also present.

Wolff-Parkinson-White Preexcitation Patterns

Notice the characteristic triad of the WPW pattern: wide QRS complexes, short PR
intervals, and delta waves (arrows) that are negative in some leads (e.g., II, III, and
aVR) and positive in others (aVL and V2 to V6). The Q waves in leads II, III, and aVF
are the result of abnormal ventricular conduction (negative delta waves) rather than an
inferior myocardial infarction. This pattern is consistent with a bypass tract inserting
into the posterior wall of the left ventricle

ARRHYTHMIAS
Arrhythmias
Arrhythmia is change in heart rate, rhythm or both. They are divided according the source of the pace
maker i.e. sinus, nodal (junctional), atrial and ventricular.

Bradycardia Nodal rhythm PSVT VT


Tachycardia Accelerated Junctional AF VF
tachycardia Atrial flutter Vent. flutter
AV nodal reentrant MAT idioventricular
tachycardia (AVRT) Escape beat rhythm
Escape beat APB (PAC) Escape beat
JPB (PJC) VPB (PVC)
Sinus rhythm
Sinus bradycardia :Pacemaker: SAN, regular & heart rate <60.




53
Sinus tachycardia: Pacemaker: SAN, regular & rapid rate >100.

Atrioventricular junctional (nodal) beats produce P


waves (atrial systole) that point upward in lead aVR
and downward in lead II; this is just the opposite of
what is seen with sinus rhythm. The P wave may just
precede the QRS complex (ventricular systole) (A),
follow it (B), or occur simultaneously with it
(Retrograde P waves) (buried in the QRS)
(C). In the last instance, no P wave is visible.
 All are regular arrhythmias
JUNCTIONAL ESCAPE RHYTHMS (Nodal rhythm)

 Pacemaker is AVN, P wave: Absent or inverted (retrograde), regular & slow rate.
Paroxysmal supra-ventricular tachycardia (PSVT) AV nodal reentrant tachycardia (AVRT)

 P wave absent, rapid regular heart rate.


ACCELERATED JUNCTIONAL RHYTHMS As nodal rhythm but rate 61 -100

JUNCTIONAL TACHYCARDIA As nodal rhythm but rate 101 – 108

Paroxysmal supraventricular tachycardia (PSVT), Paroxysmal atrial tachycardia (PAT)

Pacemaker: atrial ectopic foci (small P or superimposed on the preceding T waves).usually regular, any rate.
Atrial fibrillation

54
Pacemaker: multiple atrial foci. P wave is replaced by fibrillatory (f) waves which appears as rapid
oscillation of the baseline, irregular rapid (usually) heart rate. (if slow rate it is then called slow AF).
Atrial flutter

Usually regular. Rate: any. Pacemaker: reentrant atrial focus. P wave is replaced by flutter “F” waves it
appears as classic “saw tooth” waves. They (F) are multiple per QRS here it is 4:1. If atrial flutter with
irregular heart rate then it it is atrial flutter with variable block.
Wandering atrial pacemaker (WAP)

Pacemaker: Multiple atrial foci (one of them is SAN). More than three different P waves are present.
Regularity: irregular. Rate: usually slow.
Multifocal atrial tachycardia (MAT)

It is a type of WAP but rapid rate. (look like AF but with Ps).

Ventricular tachycardia
(VT)
Monomorphic…………

Polymorphic…………..

Torsades de pointes
(twisting of points)…….

Pacemaker: Ventricular ectopic foci. Regularity: irregular or regular. Rate: >150


Ventricular Fibrillation (VF)

Regularity: marked irregular. Rate: any. Pacemaker: multiple ventricular ectopic foci. Fibrillatory
waves are of variable shape, size and direction. QRS complex are lost
Ventricular Flutter
Pacemaker: Macro reentrant focus. Flutter waves. Regularity: regular. Rate: very rapid >300.

55
Escape idioventricular rhythm

Pacemaker: ventricular. Regularity: regular. Rate: slow < 40.Wide QRS duration.
Accelerated idioventricular rhythm

As escape idioventricular rhythm but rate is slow 60 - 100.

Escape beats: Sinus rhythm is interrupted by sinus pause followed by an ectopic beat
 Escape atrial beat
 Escape junctional beat
 Escape ventricular beat
Premature beats (premature contraction PC, extrasystole): Sinus rhythm is interrupted by
premature beat followed by a pause.
 Premature atrial beat  Premature junctional beat
 Premature ventricular beat
ESCAPE ATRIAL BEAT

JUNCTIONAL ESCAPE (JE) BEAT

VENTRICULAR ESCAPE BEAT

ATRIAL PREMATURE BEAT

56
JUNCTIONAL PREMATURE BEAT

Premature beat + compensatory pause periods less than periods of 2 beats

VENTRICULAR PREMATURE BEAT


Long and bizarre
No P wave Wide QRS complex

Pause
Premature beat + compensatory pause periods = periods of 2 beats i.e. full compensation.
PREMATURE BEAT WITH NON-CONDUCTED P

Premature beat occurring during ventricular contraction (QRS and/or T wave) only pause is left.
MONOFOCAL PREMATURE BEAT

Premature beats having the same SINGLE shape.


MULTIFOCAL PREMATURE BEAT

Premature beats having different shapes.


REGULAR PREMATURE BEAT
VENTRICULAR BIGEMINY

ATRIAL BIGEMINY Premature beat every other beat.

57
VENTRICULAR TRIGEMINY

Premature beat every third beat.


VENTRICULAR QUADRIGEMINY

Premature beat every fourth beat.


COUPLETS
VENTRICULAR COUPLETS

Two consecutive premature beats (couple) without a pause in between.


INTERPOLATED ‫ أقحم‬PREMATURE BEAT
INTERPOLATED VENTRICULAR

Premature beat (X) falls between two normal beats, in which case it is interpolated. No pause.

R WAVE PROGRESSION IN CHEST LEADS

Notice the
transition in lead
V3.

Somewhat
delayed R wave
progression, with
the transition in
lead V5.

Early transition
in lead V2.
R waves in the chest leads normally become relatively taller from lead V1 to the left
chest leads.

58
Early transition “poor” or preferably “slow” R wave progression
Anterior myocardial infarction (death of ventricle = R wave)
RVH LVH
RBBB LBBB
chronic lung disease

 Before taking an ECG, the operator must check to see that the machine is properly calibrated, so
that the 1-mV standardization mark is 10 mm tall.2 large boxes.
 A, Electrocardiograph set at normal standardization.
 B, One half standardization.
 C, Two times normal standardization.

59
DIFFERNTIAL DIAGNOSIS
lead II (= arrhythmias)
Sinus bradycardia: normal regular heart but slow.
 1st degree HB: like normal but slow rate + FIXED prolonged PR interval.
 2nd degree HB: 2 succeeding P waves with no QRS
 3rd degree HB: P waves everywhere.
 Nodal rhythm: absent P, inverted P:.
 Idioventricular rhythm: wide QRS, characteristic shape.
 Hypokalaemia: T wave flattening + u wave.
 Slow AF.
Tachycardia.
Supraventicular (sinus, atrial, nodal) …. Normal QRS
 Normal P waves… sinus
 Absent or inverted ….nodal
 Replaced: AF, atrial flutter.
Ventricular (abnormal QRS).
 VF, VT, ventricular flutter
Axis
Normal
LAD
 LVH: SV1+ RV5 or 6 ≥ 7 b. sq.
 LBBB: RsR' complex (M -shaped, notched R ) in V6, Deep QS complex lead V1(notched
S)
 LAHB: deep S in inferior leads esp. aVF.
 Bifasicular: LAHB + RBBB.
 Normal
RAD
 LPHB: deep S in lateral leads
 Normal
 PE, COPD, Lateral infarction
V1 Big R wave
 RVH: deep S in V6 + strain pattern in V1-V2
 RBBB: rSR' complex
 Posterior MI: associated inferior MI
VI deep S wave
 LVH: SV1+ RV5 or 6 ≥ 7 b. sq.
T wave inversion
 Subendocardial ischaemia: NO elevated cardiac enzymes
 Evolving transmural infarction: elevated cardiac enzymes
 Left or right ventricular hypertrophy (formerly called “strain” pattern)
 Secondary T wave alterations: bundle branch blocks, Wolff-Parkinson-White patterns
 Digitalis effect: Scooping of the ST-T complex ST segment and T wave are fused together
T wave hyperacute
 AMI
 Hyperkalaemia: long PR, lost P, wide QRS.
ST segment elevation
 Hyperacute MI: NO pathological q wave

60
 Acute MI: pathological q wave
 Both acute and hyperacute MI are associated with chest pain + enzyme elevation.
 Old MI + aneurysm: pathological q wave + ST elevation without chest pain or enzyme elevation
 Prinzimetal angina (vasospastic): NO pathological q wave no enzyme elevation anginal chest pain.
 Pericarditis: diffuse ST elevation.
 Hyperkalemia (usually localized to V1 and V2)
ST segment depression
 Subendocardial ischaemia: NO elevated cardiac enzymes
 Subendocaridal infarction: elevated cardiac enzymes
 Reciprocal change with acute transmural ischemia
 Left or right ventricular hypertrophy (formerly called “strain” pattern)
Pathological Q
 Myocardial infarction
 Myocarditis
QRS duration
 Intrinsic intraventricular delay (IVCD):Left bundle branch block and variants,
right bundle branch block and variants.
 Extrinsic (“toxic”) intraventricular delay: Hyperkalemia, drugs: class I antiarrhythmic drugs and
other sodium-channel blocking agents
 Ventricular beats: premature, escape, or paced
 Ventricular preexcitation: Wolff-Parkinson-White pattern and variants
Ectopic beats
 Escape beats (pause precedes the beat) or premature (beat precedes the pause).
 Atrial (upright P wave), junctional (inverted or absent P wave), ventricular (long, bizarre, wide
QRS).
 If regular…. bigeminy, trigeminy, qaudriqeminy.
 Same shape (monofocal), different shape (multifocal).

Scheme postgraduate
1. Lead II arrhythmias
2. LI / LIII axis
3. Limb leads
 Q wave … MI
 Deep S waves in inferior leads LAHB in lateral leads LPHB
 SIQIIITIII massive PE
 P wave atrial enlargement
4. V1: Big R wave: RVH, RBBB and Posterior MI.
5. V6: LBBB, LVH
6. All leads ST segment, T wave, pathological Qs

Arrhythmias
 Upright normal P waves: sinus arrhythmia
 Inverted , absent superimposed P waves: supraventricular arrhythmia
 Inverted , absent P waves: nodal arrhythmia
 superimposed P waves over T waves or replaced by F or f waves: atrial arrhythmia
 Wide + bizarre: ventricular arrhythmia.

61
SCHEME UNDERGRADUATE
comment diagnosis
Lead II
1. Rhythm  Sinus (+ve P wave) Bradycardia: 1st degree HB,
N: regular  Not sinus (–ve or absent) Nodal rhythm, Slow AF.
constant R-R  Irregular (variable R-R) Tachycardia:
2. Rate  If regular = 300/no of big sq bet Supraventicular (sinus,
N: HR 60-100 2R atrial, nodal) Normal QRS
> 100 = Tachy  If irregular = no QRS in (see P wave). Ventricular
< 60 = brady 6sec(15cm) x10 (abnormal QRS): VF, VT,
ventricular flutter
3. P-wave  Tall peaked (P-pulmonale > 2.5 ↑) right atrial enlargement
Normal +ve in  Broad ± Bifid (P-mitrale > 2.5 left atrial enlargement
L II size 2.5 x small boxes ↔ )
2.5 small boxes.  Absent P AF ,SVT ,VT ,nodal rhythm
 Inverted P nodal rhythm
 Flutter wave (absent P) Atrial flutter
 Fibrillatory waves Atrial fibrillation
4. P-R interval  Normal < 1 big box
AV conduction  Prolonged > 1 big box 1st degree heart block
Axis L I / L III or L I / L aVF
5. Axis  Extreme RAD ( both –ve )
Normal axis  RAD ( L I –ve , L III +ve ) RVH, Lat. infarction
both +ve  LAD ( L I +ve , L III –ve ) LVH, LBBB,
Chest leads … start with V1 & V6
6. QRS  Big R wave RVH, RBBB
voltage  SV1+ (RV5or6)≥35 s.sq (7 b. sq.) LVH
7. QRS Normal (<2.5 small boxes)
duration  Wide + rSR' (M-shaped V1) RBBB
 Wide + RsR' (M-shaped V6) LBBB
8. Path. Q  V 1,2 Septal infarction
is>1 s sq width or  V 3,4 Strict anterior infarction
>1/4 R wave or  V 1,2,3,4 Antroseptal infarction
single Q  V1→6 Extensive anterior infarction
 II , III , aVF InFerior infarction
 I, aVL(low) V 5,6 (high) Lateral infarction
9. ST Seg.  Raised Recent MI
Normal (iso-  Depressed VH , BBB(strain) ,
electric) ischaemia
10. T wave  Inverted (normal in lead aVR) Same causes of depressed
ST

62
Arrhythmia
Check QRS complex

Normal wide and bizarre


= supraventricular arrhythmia

Check P wave & HR ventricular arrhythmia

Normal Inverted / absent small / superimposed / replaced


AV node Ectopic atrial

 Sinus  Nodal rhythm  PSVT (AT): rapid atrial rhythm like


bradycardia  Accelerated nodal sinus tachycardia with superimposed
 Slow sinus rhythm: rapid beats.
rhythm nodal rhythm.  Atrial flutter: regular atrial tachycardia
 Sinus  AVRT: rapid nodal with F waves
tachycardia: rhythm w/o P  Atrial flutter with variable block: as
rapid sinus waves. atrial flutter but irregular
rhythm  Premature nodal  Atrial fibrillation: irregular AT with f
beat: early nodal waves = fibrillation of bases line
beat followed by  Slow AF: like AF but slow HR
pause  Fibrillatory flutter: P waves is replace
 Escape nodal by F and f waves
beat: pause  MAT: AF but with some P waves
followed by nodal  Premature atrial beat: early atrial beat
beat followed by pause
 Escape atrial beat: pause followed by
atrial beat

 Ventricular arrhythmia
 Accelerated idioventricular rhythm
 Escape idioventricular rhythm
 Ventricular ptachycardia (VT): wide
regular QRS complex.
 Ventricular Fibrillation (VF):
irregular wide QRS complex.
 Ventricular Flutter: as VTac.but HR>
300
 Premature atrial beat: early atrial beat
followed by pause
 Escape atrial beat: pause followed by
atrial beat
 Premature ventricular beat: early
ventricular beat followed by pause
 Escape ventricular beat: pause
followed by ventricular beat

63
COMMENT
regular or irregular.
: … beats per minute.

: normal (2.5 x 2.5 small squares), tall, wide. Upright, inverted, absent, replaced by flutter
or fibrillatory waves.
normal (1 big square), prolonged, short.

normal, RAD, LAD, Extreme axis.


(interval): normal (2 small squares), widen.
: normal , high voltage.
absent or present mention leads (ignore aVR).
in chest leads: normal V3 & V4, poor (V5 & V6), early transition (V1 &
V2).
: normal (don't comment) or big lead (RVH) or rSR' complex (RBBB) lead V1.
normal or deep S in inferior leads (LAHB) or lateral leads (LPHB), SI QIII TIII in
massive PE.

normal, elevated (1 small square limb leads or 2 small squares chest leads),
depressed (1 small square limb leads or 2 small squares chest leads).
upright, inverted, flat.
In hypokalaemia.

EXAMPLES

regular. left axis deviation.


: 150 beats per minute. normal.
: normal. : normal
normal. absent.
poor.

64
ST elevations are localized to leads V1, V2, V3, I, and aVL reciprocal ST
depressions in leads II, III, and aVF..
inverted II, III & aVF, hyperacute V2,V3.
.

regular. normal.
: 100 beats per minute. normal.
: normal.
wide in premature beats, normal.
leads II, III, aVR, aVL. aVF, V3. normal.
: high in premature normal, inverted leads II, III,
beats, leads II, III, aVF. aVF, V2.
absent.


65
irregular. : normal
: 75 beats per minute. absent.
: absent replaced by fibrillatory normal.
waves. downsloped leads I, II,
absent. V2- V6.
normal. normal.
normal.


regular. : normal
: 200 beats per minute. absent.
: absent (buried in QRS). normal.
absent. normal.
normal. normal.
normal.


66
regular. : normal
: 150 beats per minute. absent.
: normal. normal.
normal. depressed leads I, II, aVL,
left axis. V3-6.
normal. normal.
normal.


regular. absent.
: 75 beats per minute. normal.
: peaked especially lead II. : big R wave lead V1 &V2
normal. normal.
right. inverted leads II, II, aVF, V1-3
normal. (strain pattern).
: normal


67
irregular. : normal
: 80 beats per minute. absent.
: normal. normal.
normal. normal.
normal. normal.
normal.


regular. : high V4
: 150 beats per minute. absent.
: absent replaced by flutter waves. normal.
absent. normal.
normal. normal
normal.


68
regular. absent.
: 75 beats per minute. normal.
: normal. elevated II, II, aVF,
normal. depressed aVL, V2,3.
normal. normal.
normal.
: normal


regular. : normal
: 100 beats per minute. absent.
: normal. normal.
prolonged. normal.
normal. normal.
normal.


69
regular. absent.
: 100 beats per minute. : RsR' complex (M -shaped,
: normal. notched R ) in leads I, aVL, V5 & V6.
normal. Deep rS complex lead V1-3.
left. normal.
broad complex. inverted leads I, aVL, V6.
: insignificant


regular. : normal
: 60 beats per minute. absent.
: normal. : rSR' in lead V1-6.
normal. normal.
normal. inverted V1.
broad complex


70
regular. absent.
: 75 beats per minute. tall R leads V3-6.
: normal. deep s leads V, 2.
normal. depressed leads v3-v6 (strain
left. pattern).
normal. inverted leads I, II, aVL & V3-6.
: high in chest leads.


regular. : normal
: 50 beats per minute. leads II, II, aVF.
: normal. : peaked (hyperacute) leadsV2-3.
normal. normal.
left. inverted II, aVF & V6, hyperacute
normal. V2 &V3.


71
regular. : normal
: 90 beats per minute. absent.
: normal. normal.
normal. depressed I, II, V2-6.
normal. normal.
normal.
 

irregular.
: 90 beats per minute.

: absent replaced by fibrillatory.


absent.

normal.
: normal
absent.

absent buried in the fibrillatory wave.


absent buried in the fibrillatory wave..



72
VVV. imp. Clinical pathology exam is about lab. investigations ONLY

73
Blood report
Blood

Plasma Cells

Serum Plasma RBC WBC Platelets


protein

Nongranulocytes Granulocytes

Monocytes Lymphocytes Eosinophils Neutrophils Basophils

Complete blood picture (CBC) .


I-RBC's:
• Number: 5 million/cmm. ♀ 4- 5.5 millions/cmm. ♂ : 4.5 - 6.5 millions/cmm.
• Haemoglobin: 15 gm/dl ♀: 12 - 15 gm/dl. ♂ :13.5 - 17 gm/dl.
• Haematocrit or packed cell volume (PCV): 45% ♀: 42%. ♂ :46%.
• Colour index: HB% / RBC's = In normal person = 100 % /100% = 1
• Mean corpuscular haemoglobin (MCH): 27-33 pg
MCV, MCH
• Hb in grams x 10 / RBC's in millions. In normal person = 15 X 10 / 5 = 30 pg
& MCHC are
• Mean corpuscular Hb concentration (MCHC): 32-36 gm/dl collectively
• Hb in grams X 100 In normal person = 15 X 100 = 34. named RBC's
Packed cell volume 45 indices
• Mean corpuscular volume (MCV): 80-96 fl the average volume of RBC's.
• Mean corpuscular diameter (MCD): 6-8 p the average diameter of RBC's.
• Abnormal shapes of RBCs:
 Anisocytosis: is variability in the size of RBC's.
 Poikilocytosis: is variability in the shape of RBC's.
 Anisocytosis & poikilocytosis are present in anaemia mainly deficiency anaemias.
 Spherocytes: Hereditary spherocytosis, Post-splenectomy, Autoimmune haemolytic anaemia.
 Sickle cells: Sickle cell anaemia.
 Target cells central area of haemoglobinisation: Thalassaemia, Liver diseases, Post-splenectomy.
 Schistocytes: Traumatic haemolysis.
 Elliptocyte: Hereditary elliptocytosis.
 Bite cells, Blister cells & Heinz bodies: G6PD deficiency.
 Rouleaux formation: Red cells stack on each other (it causes a raised ESR; p356). Seen with
chronic inflammation, paraproteinaemia and myeloma..
 Howell-Jolly bodies (small round nuclear remnants): Megaloblastic anaemia,
Hyposplenism.

74
 Leucoerythroblastic anaemia: Immature cells (myelocytes, promyelocytes, metamyelocytes,
normoblasts) seen in film. Due to marrow infiltration (eg malignancy) when these cells are
displaced; also seen in anorexia, sepsis, severe haemolysis.
 Blasts: Nucleated precursor cells. They are not normally in peripheral blood, but are seen in
myelofibrosis, leukaemia or malignant infiltration by carcinoma.
 Burr cells: Irregularly shaped cells occurring in uraemia.
 Howell-Jolly bodies: DNA nuclear remnants in RBCs, which are normally removed by the
spleen (fig 8). Seen post-splenectomy and in hyposplenism (eg sickle cell disease, coeliac
disease, congenital, UC/Crohn's, myeloproliferative disease, amyloid). Also in
dyserythropoietic states: myelodysplasia, megaloblastic anaemia.
 Leukaemoid reaction: A marked Leucocytosis (WCC>50,000/cmm). Seen in severe illness eg
with infection or burns, and also in leukaemia.
 Reticulocytes: 0.5-2% Young, larger RBCs (contain RNA) signifying active erythropoiesis.
Increased in haemolysis, haemorrhage, and if B12, iron or folate is given to marrow that lack these
• Reticulocytosis: indicates hyper-active BM as in
- Haemolytic anaemia. - Acute haemorrhage.
- Anaemia under specific treatment, especially megaloblastic, Fe def. anemia .
- Recovery from BM suppression.
• Absent reticulocytes: occurs in
- Aplastic anaemia ( B.M. failure ) - Dyshaemopoietic anaemia ( def. of Fe , B12 )
 Nucleated red blood cells (normoblasts)
 Marrow infiltration
 Severe haemolysis
 Myelofibrosis

 Acute haemorrhage II-White blood cells:


1. Total leucocytic count (TLC): 4,000 - 11,000 /cmm.
2. Differential leucocytic count:
• Neutrophils: 60-70 % .Staff (immature) : Segmented (mature) = 1 : 5 → 1 : 10. big segmented
cells are called polymorphinuclear PMN due to multiple segmentation of the nuclei. Left shift:
Immature neutrophils are sent out of the marrow, eg in infection.
• Basophils: 0-1 %
• Eosinophils: 3-5 %
• Lymphocytes: 20-30 %. Absolute count = 1,500 - 4,000/cmm.
• Monocytes: 3-8 % it may unite together with other cells forming large cells with high
phagocytic abilities called Macrophages.
III-Platelets: 150,000- 400,000/cmm
A normal
blood film,
with a
neutrophil,
normal red
cells, and
platelets
(arrows).

75
Stem cells and growth factors in haematopoietic cell development. (BFU-E = blast-forming unit-
erythroid; CFU-Meg = colony-forming unit-megakaryocyte; CFU-GM = colony-forming unit-
granulocyte, monocyte; CFU-E = colony-forming unit-erythroid; IL = interleukin; SCF = stem cell factor;
GM-CSF = granulocyte macrophage-colony stimulating factor; Epo = erythropoietin; Tpo =
thrombopoietin; G-CSF = granulocyte-colony stimulating factor; M-CSF = macrophage-colony
stimulating factor)

IV -Erythrocyte sedimentation rate (ESR).


-Def. : distance sedimented by RBCs in a vertical blood column at end of l & 2 hours
-Mechanism :
-Normally red cells are negatively charged and repel each other
-The increase in plasma globulin, fibrinogen causes a decrease in these negative charges, allowing
RBC to from rouleaux & increase their sedimentation.
-Normal value : (Westergren method)

1st hour 2nd hour


Male 5 8 mm
Female (♂x2) 10 16 mm
76
-Clinical significance: prognostic value (not diagnostic)
-Causes of change in ESR:
increased decreased
Physiological - females during menses - pregnancy
RBC's disease - anaemia - polycythaemia
Plasma's disease - Any infection (TB ) - afibrinogenemia
( acute phase - malignancy (multiple myeloma) - Heart failure
reactants ) - collagen diseases (Rh. Fever)
- Tissue damage (infarction – operation)
- Chronic liver or kidney diseases with
affection of plasma ptn (synthesis/loss).
ESR > 100 in autoimmune diseases, TB & malignancy.
Summary of CBC

• RBC's • WBC's
 HB 12- 16 o TLC 4000 – 11000/ cmm
 PCV 46 o Differential count Relative Absolute
 RBC's count 4.5-5.5m  Basophils 0-1% 10-100
 MCV 76-96  Eosinophils 1-6% 40-400
 MCHC  Neutrophils 40-75% 2500-7500
 MCH 34
 Lymphocytes 20-40% 1500-2500
27-32
 Reticulocytes  Monocytes
2-10% 200-800
0.5-2.5
• Platelets 150-450 • ESR ♂ ♀
thousand  1st hour 5 10
 2nd hour 8 16

 Causes of anaemia
RBC’s count

Increased Decreased

All blood RBC’s only Anaemia


Polycythemia Secondary
rubra Vera Polycythemia Normal indices ↓↓ indices ↑↑ indices
Normocytic rubra vera
normochromic Microcytic microchromic Macrocytic
- Acute hge
- Fe def. Folate def.
B12 def.
- All haemolytic an. except Thalassemia - Thalassemia
- Aplastic an. - An. of ch. disease e.g. CRF
- Hypersplenism Liver disease
B.M. dysplasia

o Anemia is reduction in RBC's count, HB conc. or PCV.


o Polycythaemia is increase in red cell mass > 36 ml/Kg in ♂ or 32 ml/Kg in ♀.
o Polycythaemia rubra vera (PRV) is 1ry polycythaemia which is myeloproleferative disorder
characterized by excessive proliferation of BM's erythroids→↑RBC's , myeloid→↑WBC's &
megakaryocytes→↑platelets .
o Secondary polycythaemia occurs secondary to a disease e.g. ch. Hypoxia , dehydration.
77
 Causes of normocytic normochromic anaemia? See above.
 Causes of macrocytic anaemia?
1- Megaloblastic BM: vit. B12 def. & folic acid deficiency.
2- Normoblastic BM: Alcohol, reticulocytosis, liver disease.
 Causes of haemolytic anaemia?

Corpuscular

membrane HB Enzyme
PNH  SCA
Spherocytosis Thalassemia G6PD def.

Extracorpuscular

infection Autoimmune physical chemical Liver spleen


inflammation (metabolic)

 Malaria  autoimmune  microangiopathy  drug  Wilson dis.  hypersplenism


Haemolytic an.  Lead
 prothetic cardiac valve

NB: haemolytic anaemia is also divided clinically into acquired, inherited and miscellaneous.
1- Hereditary.
a- Membrane defect (hereditary spherocytosis).
b- HGB defect (Thalassemia, SCA).
c- Metabolic (G6PD)
2- Acquired.
a-Immune: (autoimmune haemolytic an., incompatible blood transfusion, drug induced,
paroxysmal cold HGBuria).
b- Non immune: PNH, microangipathy, valve prosthesis, malaria).
3- Miscellaneous.
An approach to haemolytic anaemia
Haemolysis is the premature breakdown of RBCs, before their normal life span of ~120 d. It occurs in the
circulation (intravascular) or in the reticuloendothelial system i.e. macrophages of liver, spleen and bone
marrow (extravascular). In sickle-cell anaemia, lifespan may be as short as 5d. Haemolysis may be
asymptomatic, but if the bone marrow does not compensate sufficiently, a haemolytic anaemia results.
An approach is to first confirm haemolysis and then find the cause try to answer these 4 questions:
 Is there increased red cell breakdown?
o Anaemia with normal or ↑‘MCV.
o ↑‘Bilirubin: unconjugated, from haem breakdown (prehepatic jaundice).
o ↑‘Urinary urobilinogen (no urinary conjugated bilirubin).
o ↑‘Serum lactic dehydrogenase (LDH), as released from the RBC.
 Is there increased red cell production?
o ↑‘Reticulocytes, causing ↑‘MCV (reticulocytes are large immature RBCs) and
polychromasia.
 Is the haemolysis mainly extra- or intravascular?
Extravascular haemolysis may lead to splenic hypertrophy and splenomegaly. Features of
intravascular haemolysis are:
o ↑‘Free plasma haemoglobin: released from RBCs.

78
o Methaemalbuminaemia: some free Hb is broken down in the circulation to produce haem
and globin; haem combines with albumin to make methaemalbumin.
o ↑“Plasma haptoglobin: mops up free plasma Hb, then removed by the liver.
o Haemoglobinuria: causes red-brown urine, in absence of red blood cells.
o Haemosiderinuria: occurs when haptoglobin binding capacity is exceeded, causing free
Hb to be filtered by the renal glomeruli, absorption of free Hb via the renal tubules and
storage in the tubular cells as haemosiderin.
 Investigations of spherocytosis? See below
 Investigations of sickle cell anemia? See below.
 Investigations of G6PD? See below.
 Investigations of thalassemia?. See below.
U Investigations of haemolytic anemia
I. For diagnosis of hemolytic anemia:
1. CBC:
 Normocyte normochromic anemia with normal MCV & normal MCHC.
 Macrocytic anemia may occur in megaloblastic crisis or in severe reticulocytosis.
 Microcytic hypochromic anemia may occur in case of thalassemia.
 Reticulocyte count: High ......... this is the rule.
 Reticulocyte count: Low ......... in aplastic crisis.
 Blood film may reveal characteristic red cells, e.g. sickle cells, spherocytes.
 WBC's & platelets usually normal, BUT may t due to hyperactive BM.
2. Bone marrow examination:
 Hyperplastic BM: this is the rule. 3. Measure of life span of RBCs:
 Hypoplastic BM: in aplastic crisis. "using Cr - labeled red cells "
 Megaloblastic BM: in megaloblastic crisis.  Shortened life span of RBCs.
4. Bile pigments: 5. Increased serum LDH.
 Serum bilirubin: increased mainly the indirect
 Stools: increased stercobilinogen
 Urine: increased urobilinogen, absent bilirubin.
II. For diff. bet. Intravascular & Extravascular haemolysis:

Laboratory features of Intravascular hemolysis:


- Urine  ■ Hemoglobinuria ■ Hemosiderinuria.
- Plasma  ■ ↓Haptoglobin ■ ↓↓Hemopexin

III. For diagnosis of the cause:


 Investigations of hereditary spherocytosis
 General investigations of haemolytic anemia ( Normocyte normochromic anemia )
 Blood film→ microsherocytes
 Osmotic fragility test
 Investigations of thalassemia
 General investigations of haemolytic anemia (Microcytic hypochromic anemia )
 HB electrophoresis→ ++ HB F > 80% ( the most imp..)
 Serum iron→ ++Fe , ++ferritin(stores Fe+ptn),++transferrin Fe saturation,--TIBC .
 Blood film → characteristic target cells
 Investigations of sickle cell anaemia
 General investigations of haemolytic anemia ( Normocyte normochromic anemia )
 Blood film → characteristic sickle cells
 HB electrophoresis→ ++ HB S
 Investigations of G6PD
 General investigations of intravascular haemolysis of the haemolytic anemia
79
 Estimation of G6PD level
U Investigations of megaloblastic anemia
Vit B12 / folic acid  cell size  haemolysis
Vit B12
1- Schilling test
2- Serology 6- CBC
Folic acid 8- Blood chemistry
7- BM examination
3- Figlu test
Both
4- Serum level
5- Therapeutic test
1. Schilling test (Only In B12 Deficiency )
 Mechanism: Unlabeled B12 is given to saturate the body stores
then, Radiolabeled B12 is given orally then, The patient's urine is collected for 48 hours:
measure exreted Radiolabeled B12
 Results: If excretion is low → B12 malabsorption is diagnosed
o If pernicious anemia is the cause: excretion becomes normal after giving IF
orally.
o If bacterial overgrowth is the cause: excretion becomes normal after a course of
antibiotics.
o If pancreatic insufficiency is the cause: excretion becomes normal after giving
pancreatic enzymes.
2. Serology: (Only In Pernicious anemia)
 Antiparietal cell antibodies.  Anti-IF antibodies.
3. FIGLU test: (Only In Folic Deficiency)
 In folic acid deficiency: oral administration of HISTIDINE will lead to excessive excretion
of FIGLU in urine ( instead of glutamic acid ).
4. ↓↓Serum B12 & serum folic acid
5. Therapeutic tests: Ingestion of small doses of Vitamin B12 or Folic acid → Reticulocytosis.
6. CBC:
RBC's WBC's Platelets
count  Anemia  Leucopenia  Thrombocytopenia
--HB, count, PCV --count
 Reticulocytosis→ after giving ttt
 Aniscytosis & Poikilocytosis
size  Increased MCV (LARGE RBCS).  Large neutrophils  Large platelets
7. Bone marrow examination :
 Hypercellular megaloblastic bone marrow.
 Giant cells with abnormal morphology.
8. Blood chemistry : Increased serum indirect bilirubin , iron , LDH .

U Investigations of iron deficiency anemia

Investigations

to diagnose To know cause


1- CBC
- RBC :  decreased red cell count , HB level , PCV = ANAEMIA

80
 decreased red cell indices ( MCV , MCHC ) = Micro..Hypchromico
- WBC :  usually normal
 Eosinphilia if ancylostoma infection
- Platelets :  usually normal
2- Bone marrow examination
 Erythroid hyperplasia
 Decreased iron stores in the bm 's macrophages
3- Evidence of iron deficiency
 decreased ………...serum iron , stored iron (ferrtin) .
iron carrier ptn (transferring saturation )
 increased………....TIBC (total iron binding capacity)
FEP ( free erythrocyte protoporphyrin)
4- 5-
Test Result
Decreased 4- Achlorohydria - Stomach function test - ↓↓ HCl
absorption 5- Malabsorption - Stool -↑↑ fats (steatorrhoea)
syndrome - Urine (D-Xylose - Urine collecres after 5 hrs
test) show < 5gm D-xylose
- Malabsorption pattern
- Ba follow through - diagnostic
- Jeujenal biopsy
6-7-8
Test Result
Increased 6- Hge bl. disease Purpura Haemophilia
loss  Platelet count -- N
 Bleeding time ++ N
 Hiss test +ve -ve
 Clotting time N ++
 APTT N ++
7- GIT bleeding - Stool - occult blood / ancylostoma
- Endoscopy - oesophagoscopy ,
gasroduodnoscopy , colonscopy
- Ba follow Ba enema , Ba meal
through - arteriography , radioisotope scan
- Bleeding
8- Ancylostoma - Blood - eosinophilia , hypoalbuminaemia
- stool - ova
Most 2 important inv. in Fe def. an.
- decreased reticulocytes
- Iron profile
 Investigations of acute leukaemia?
Leukaemias are malignant disorders of the haematopoietic stem cell compartment, characteristically
associated with increased numbers of white cells in the bone marrow and/or peripheral blood. The
course of leukaemia may vary from a few days or weeks to many years, depending on the type.
NB: pluripotent stem cells Myeloid stem cells platelets, RBCs, granulocyts, monocyts.
Lymphoid stem cells T and B cells.
Investigations for acute leukaemia
1- CBC: -- HGB, -- platelets, ++ TLC with ++ blast cells (blast cells may be few in AML).
TLC usually 100,000 up to 500,000, AML's TLC count may be lower because it is mainly in
Bone marrow. Myeloblast should be differentiated from Lymphoblast by a) Auer bodies

81
present in myeloblast b) Ag myeloid are CD13, CD33 while lymphoid are CD10 (B cells)
c)karyotyping (chromosomal analysis)
2- BM aspirate or better biopsy (most vulnerable diagnosis): hypercellular BM + leukaemic
blast cells.
 Investigations of CLL?
This is a monoclonal proliferation of non-functional mature B lymphocytes (T cell CLL occurs
rarely). CLL constitutes 25% of all leukaemias♂:♀ 2:1. It is a disease of the elderly, median age at
diagnosis is ~65 years.
Investigations for CLL
1- CBC: Hb normal or low; WBC raised, and may be very high; platelets normal or low
Lymphocytes increased above 5000/cmm.
2- Bone marrow. Reflects peripheral blood, often very heavily infiltrated with lymphocytes.
3- Immunoglobulins. Low or normal.
4- Immunophenotyping shows mainly CD19/20 + CD5+ B cells. They may weakly express
surface immunoglobulin. Blood count. Hb normal or low; WBC raised, and may be very
high; platelets normal or low. Blood film. Lymphocytes increased above 5 × 109/L.
5- Later: autoimmune haemolysis (+ve Commb's test),
 Investigations of CML?
Chronic myeloid leukaemia is a myeloproliferative stem cell disorder resulting in proliferation of all
haematopoietic lineages but manifesting predominantly in the granulocytic series.
Investigations for CML
1- CBC: WBC ++ (often >100,000/ cmm) with whole spectrum of myeloid cells ie
neutrophils, myelocytes, basophils, eosinophils. Hb ++ or normal, platelets variable. Uric
acid ++, B12++. LDH ++.
2- BM aspirate or better biopsy: bone marrow is hypercellular. Ph found on cytogenetic
analysis of blood or bone marrow.
 Causes of polycythaemia?
Primary Polycythaemia Vera
Secondary
Due to an appropriate increase in erythropoietin
o High altitude
o Lung disease
o Cardiovascular disease (right-to-left shunt)
o Heavy smoking
o Mutant high oxygen affinity haemoglobin, e.g. congenital polycythaemia
Relative ('Apparent' polycythaemia) Dehydration, Burns
Due to an inappropriate increase in erythropoietin
o Congenital: Chuvasch polycythaemia
o Renal disease: tumours, cysts
o Liver disease: hepatocellular carcinoma, cirrhosis
o Endocrine: adrenal tumours
o Tumours: cerebellar haemangioblastoma, massive uterine fibroma, bronchial carcinoma
 Causes of aplastic anaemia?
 Most cases are autoimmune, triggered by drugs, (viruses eg Parvovirus, hepatitis) or
irradiation. May also be inherited eg Fanconi anaemia
 Pancytopenia is reduction in all the major cell lines: red cells, white cells and platelets.
Causes are due to
++ marrow production: aplastic anaemia, infiltration (eg acute leukaemia, myelodysplasia, 
myeloma, lymphoma, solid tumours, TB), megaloblastic anaemia, paroxysmal nocturnal
haemoglobinuria , myelofibrosis, SLE.
 ++ peripheral destruction: hypersplenism.
 Causes of haemophilia?
 Haemophilia A: Factor VIII deficiency
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 Haemophilia B (Christmas disease): Factor IX deficiency
 Causes of DIC?
 Disseminated intravascular coagulation (DIC): This is pathological widespread activation of
coagulation, due to release of procoagulant agents into the circulation. Clotting factors and
platelets are consumed, with ++ risk of bleeding. Fibrin strands fill small vessels, haemolysing
passing RBCs, and fibrinolysis is also activated.
 Causes: Malignancy, sepsis, trauma, obstetric: OHCS p88.
 laboratory investigations of DIC? –Platelets ++ PTT ++ APTT –fibrinogen (correlates
best with severity); ++ fibrin degradation products (D-dimers). Film: broken RBCs (schistocytes).
 Causes of thrombophilia? Thrombophilia is an inherited or acquired coagulopathy
predisposing to thrombosis, usually venous: DVT or PE (venous thromboembolism: VTE).
 Inherited
 Activated Protein c (APC) resistance/Factor V Leiden: Commonest cause of inherited
thrombophilia. Present in ~5% population, although most will not develop thrombosis. Usually
associated with a single point mutation in factor V (Factor V Leiden), so that this clotting factor is
not broken down by APC. Risk of venous thromboembolism (DVT or PE) is increased 5-fold in
patients who are heterozygous for the mutation, and 50-fold in homozygotes. Thrombotic risk is
increased in pregnancy and those on oestrogens.
 Prothrombin gene mutation: Leads to high prothrombin levels and increased thrombosis due to
down-regulation of fibrinolysis, by thrombin-activated fibrinolysis inhibitor.
 Protein C and Protein S deficiency: These vitamin K-dependent factors act together to cleave and
thus neutralize Factors V and VIII. Heterozygotes deficient for either protein risk thrombosis.
Skin necrosis also occurs, especially if on warfarin. Homozygous deficiency for either protein
causes neonatal purpura fulminans fatal, if untreated.
 Antithrombin deficiency: Antithrombin is a co-factor of heparin, and inhibits thrombin. Less
common, affects 1 : 500. Heterozygotes' thrombotic risk is greater than Protein C or S deficiency
by ~4-fold. Homozygosity is incompatible with life.
 Acquired
 Causes: newer 3rd generation progesterones in the oral contraceptive pill and the antiphospholipid
syndrome (APL) when serum antiphospholipid antibodies are found (lupus anticoagulant ‫آ‬±
anticardiolipin antibody) predisposing to venous and arterial thrombosis, thrombocytopenia, and
recurrent fetal loss in pregnant women. In most it is a primary disease, but it is also seen with
SLE.
 Causes of thrombocytosis Platelets >450,000/L may be a reactive phenomenon, seen with
many conditions including:
 Bleeding
 Infection
 Chronic inflammation, e.g. collagen disorders
 Malignancy
 Trauma
 Post-surgery
 Iron deficiency
 Causes of purpura? See latter.
 Causes of coagulopathy? See latter.
 Myelofibrosis
 There is hyperplasia of megakaryocytes which produce platelet derived growth factor, leading to
intense marrow fibrosis and myeloid metaplasia (haemopoiesis in the spleen and liver)→massive
hepatosplenomegaly.
 The myeloproliferative disorders
 These form a group of disorders caused by proliferation of a clone o
 f haematopoietic myeloid stem cells in the marrow. While the cells proliferate, they also retain the
ability to differentiate into RBCs, WBCs or platelets.
83
 Classification
 is by the cell type which is proliferating
RBC ++ Polycythaemia rubra vera (PRV).
WBC ++ Chronic myeloid leukaemia (CML).
Platelets ++ Essential thrombocythaemia.
Fibroblasts ++ Myelofibrosis.
 Philadelphia chromosome
 (Ph) Present in >80% of those with CML. It is a hybrid chromosome comprising reciprocal
translocation between the long arm of chromosome 9 and the long arm of chromosome 22 (9;22)
forming a fusion gene BCR/ABL on chromosome 22, which has tyrosine kinase activity. Those
without Ph have a worse prognosis. Some patients have a masked translocation cytogenetics do
not show the Ph, but the rearrangement is detectable by molecular techniques.

Gold
penicillamine
Carbimazole
Captopril, enalapril,
nifedipine
Phenytoin, sodium
valproate,
carbamazepine
Sulphonamides,
penicillins,
cephalosporins
Ranitidine

84
Haemostatic
disorders
Purpura Coagulopathy

Platelet Vessel wall Herditary aquired


defect defect
1. Vasculitis: e.g. SLE , 1. Haemophilia 1. Liver failure (--synthesis)
PAN 2. Afibrinogenaemia 2. Renal failure (ptn loss)
2. Infection : SBE 3. Vit K def. (--synthesis)
3. Drugs : aspirin 4. DIC (consumption)
4. senile purpura 5. Drugs (heparin ,
5. purpura simplex oral anticoagulants)

Thrombocytopenia decreased platelets Thrombocytopathy diseased platelets

decreased production increased destruction Aquired hereditary

1. Bone marrow failure 1. Autoimmune: 1. Antiplatelet: e.g. aspirin e.g. glanzmann's disease
2. Bone marrow infilteration o 1ry → ITP 2. Autoimmune: SBE
3. Megaloblastic anemia o 2ry → SLE 3. Multipule myeloma
4. Myelodysplastic 2. Acute infection 4. uraemia
syndromes 3. Hypersplenism 5. Thrombocytosis

85
check RBCs

> 5.5 millions/mm3 4.5 - 5.5 millions / mm3 < 4.5 millions / mm3

Polycythemia Normal Anemia


check WBCs&platelets check WBCs&platelets

++ WBCs Normal WBCs -- WBCs ++ WBCs not >20,000


++ platelets ++ platelets check WBCs
Leucopenia Leucocytosis platelets &
primary secondary coagulation time
Check differential count
Polycythemia Polycythemia Relative lymphocytosis
If ++ lymphocytes neutrophilia lymphocytosis monocytosis

++ WBC's >20,000 --platelets --platelets & --WBC's all normal ++coagulation time
Leukaemia Thrombocytopenia Pancytopenia Haemophilia
Check MCV, MCH
check blast cells
low high normal
++blast no blast
Microcytic Macrocytic Normocytic
Acute Chronic
hypochromic (megaloblastic) normochromic
Leukaemia Leukaemia
anemia anemia anemia

if eosinophilia If reticylocytosis
++lymphocytes ++monocytes think of → haemolytic an.
CLL CML ancylostoma

86
U
I. Tests for purpura:
1. Bleeding time: Normally: 2-4 minutes.
• Measures platelet plug formation in vivo. Cuff of sphygmomanometer for 10 minutes is
inflated at pressure 40mmHg + small incision by a pin is made then count the time needed
for bleeding to stop.
• Depends on platelets & capillaries.
• It is prolonged in purpura.
2. Platelet count: Normally: 150,000-400,000/cmm
• Reduced in thrombocytopenic purpura if <40,000/cmm bleeding may occur.

II. Tests of coagulopathies:


1. Coagulation time: Normally: 4-8 minutes.
• Depends on coagulation factors.
2. Partial thromboplastin time (PTT): Normally: 30-50 seconds.
• Used to test the intrinsic system.
• Deficiencies of factors II, V, VIII, IX, X, XI, XII Heparin .Antibodies against clotting
factors Lupus anticoagulant
3. Prothrombin time (PT), concentration (PC) & International Normalized Ratio
(INR): Normal PT 12-15 seconds. PC > 75% INR: 1- 1.2.
• INR is the ratio of the patient' s PT to a normal control when using the international
reference preparation.
• Used to test the extrinsic system.
• Prolonged in deficient VII, X, V, II or I or usage of oral anticoagulants.
5. Plasma fibrinogen: in hypofibrinogenaemia & DIC.
6. Fibrin degradation products (FDP): present in DIC.
7. Assay of different coagulation factors. Haemophilia A -- factor VIII (normal PT, ++ PTT) ,
Haemophilia B -- factor IX, von Willebrand disease --factor (vWF)
DIC -- PC (consumed) ++ FDP.
Blood report mcq
Report 1
Haemoglobin 11.5 g/dl
PCV (haematocrit) 35 %
Red cell count 3,800,000 /cmm
Reticulocytic count 2 %
MCV 92 fl
MCH 30 Pg
MCHC 33 g/dl
TLC 35,000 /cmm

87
Basophils 0 %
Eosinophils 1 %
Staff 2 %
Segmented 15 %
Lymphocytes 80 %
Monocytes 2 %
Platelet count 250,000 /cmm
1.- Ineffective erythropoiesis is evident in all types of hemolytic anemia.
a. True b- false
2- In which of the following is the Philadelphia chromosome most likely to be found?
a. chronic lymphocytic leukemia c. acute lymphocytic leukemia
b. chronic myelogenous leukemia d. acute myelogenous leukemia
3- In which of the following situations would the platelet count be decreased:
a. in idiopathic thrombocytopenic purpura c. post splenectomy
b. in Essential Thrombocythemia d. in polycythemia rubra vera
4. Which of the following test results would most likely be seen in Hemophilia A:
a. an abnormal PT c. abnormal von Willebrand factor level
b. an abnormal Bleeding Time d. an abnormal APTT
5- What is the deficient coagulation factor in Hemophilia A:
a. F VII b. F VIII c. F I X d. F XII

Report 2
Haemoglobin 8.5 g/dl
PCV (haematocrit) 26 %
Red cell count 2,830,000 /cmn
Reticulocytic count 0.2 % -
MCV 92 fl
MCH 30 Pg
MCHC 33 g/dl
TLC 150,000 /cmn
Basophils 0 %
Eosinophils 0 %
Staff 2 %
Segmented 7 %
Lymphocytes 2 %
Monocytes 14 %
Myeloblasts 50 %
Promyelocytes 25 %
Platelet count 30,000 /cmm

1.-Which of the following is characteristic of pernicious anemia?


a. increased production of intrinsic factor c. antibodies to gastric HCI
b. decreased absorption of vit B 12 d. decreased absorption of folate
2-Which of the following would most likely lead to megaloblastic anemia?
a. vitamin E deficiency c. iron deficiency
b. vitamin B 6 deficiency d. folic acid deficiency
3-The peripheral blood of a patient with iron deficiency anemia will likely shows
a. Microcytic, hypochromic red cells c. macrocytic, hypochromic red cells
b. microcytic, normochromic red cells d. normocytic, hypochronic red cells
4.With hemolytic anemia all the following will occur except:

88
a. increased total bilirubin c. decreased haptoglobin
b. direct bilirubin levels will remain normal d. the reticulocyte count will decrease
5-All of the following occur in intravascular hemolysis except:
a. haptoglobin levels decrease c. hemopexin levels decrease
b. methemalburnin levels increase d. serum iron levels decrease

Report 3 Haemoglobin 10.0 g/dl


PCV (haematocrit) 29 %
Red cell count 3,300,000 /cmm
Reticulocytic count 1.0 %
MCV 87 fl
MCH 30 Pg
MCHC 34 g/dl
TLC 200,000 /cmm
Basophils 5 %
Eosinophils 2 %
Staff 10 %
Segmented 32 %
Lymphocytes 1 %
Monocytes 2 %
Myeloblasts 5 %
Promyelocytes 3 %
Myelocytes 25 %
Metamyelocytes 15 %
Platelet count 500,000 /cmm
1.- Osmotic fragility test is done to confirm the diagnosis of:
a. G6PD deficiency c. hereditary spherocytosis
b. pyruvate deficiency d. thalassemia
2- A patient with severe bacterial infection will likely shows the following
a. polymorph nuclear leukocytosis with shift c. lymphocytosis
to the left d. eosinophilia
b. leucopenia
3-A patient with severe allergic disease will most likely show
a. polymorph nuclear leukocytosis with shift c. lymphocytosis
to the left d. eosinophilia
b. leucopenia
4. A patient with a parasitic infestation will most likely show
a. polymorph nuclear leukocytosis with shift to the left
b. leucopenia c. lymphocytosis d. eosinophilia

5- All of the following are manifestations of bone marrow failure except:


a. Anemia c. Thrombocytopenia e. Jaundice
b. Neutropenia d. Pancytopenia

Report 4 Haemoglobin 8.8 g/dl


PCV (haematocrit) 27 %
Red cell count 2,800, 000 /cmm
Reticulocytic count 0.2 %
MCV 91 fl
MCH 30 Pg
MCHC 32 g/dl

89
TLC 96,000 /cmm
Basophils 0 %
Eosinophils 0 %
Staff 1 %
Segmented 5 %
Lymphocytes 0 %
Monocytes 1 %
Blasts 93 %
Peroxidase stain of blasts positive
Platelet count 28.000 /cmm
1.- Intrinsic factor is necessary for the absorption of:
a. folic acid b. iron c. vitamin B6 d. vitamin B12
2- Which of the following patients is most likely to have peroxidase positive blasts:
a. a child with Burkitt's leukemia/lymphoma
b. a child with acute myelogenous leukemia
c. a child with B acute lymphoblastic leukemia
d. a child with T acute lymphoblastic leukemia
3- hyperbilirubinemia is present in acute post-hemorrhagic anemia
a. true b. false
4. The red cell count is decreased in hemolytic anemia
a. true b. false
5- What is the deficient coagulation factor in Hemophilia B:
a. F VII b. F VIII c. F I X d. F X
Haemoglobin 14 g/dl
PCV (haematocrit) 44 %
Report Red cell count 4,500,000 /cm
5 Reticulocytic count 0.2 %
MCV 92 fl
MCH 30 Pg
MCHC 33 g/dl
TLC 24,000 /cmm
Basophils 0 %
Eosinophils 0 %
Neutrophils
-Band 20 %
-segmented 75 %
Lymphocytes 5 %
Monocytes 0 %
Platelet count 300,000 / cmm

1.- the reticulocyte count is increased in both acute post-hemorrhagic anemia & hemolytic anemia
a. true b. false
2- the red cell survival time is decreased in acute post-hemorrhagic anemia
a. true b. false
3-normal adult male reference range of HGB
a. 10 g/dl b. 12 g/dl c. 16 g/dl d. 20 g/dl
4-.Normocytic normochromic anemia is characterisd by
a. increase MCV b. decrease MCV c. normal MCV

5- Thalassemia causes:

90
a. Normocytic normochromic anemia c. Macrocytic hyperchromic anemia
b. Microcytic hypochromic anemia d. Aplastic anaemia

Report 6 Haemoglobin 9.0 g/dl


PCV (haematocrit) 28 %
Red cell count 3,000,000 /cmm
Reticulocytic count 0.2 %
MCV 92 fl
MCH 30 Pg
MCHC 33 g/dl
TLC 70,000 /cmm
Basophils 0 %
Eosinophils 0 %
Staff 1 %
Segmented 5 %
Lymphocytes 0 %
Monocytes 1 %
Blasts 93 %
Peroxidase stain of blasts negative
Platelet count 25.000 /cmm

1.-Haemolytic anemia is caused by all except


a. Splenomegaly c. Thalassemia e. BM depression
b. PNH d. G6PD
2-Blood transfusion is indicated in anemia if HGB is below
a. 7 g/dl c. 9 g/dl e. 11 g/dl
b. 8 g/dl d. 10 g/dl
3-Reticlocytosis occurs in following except
a. Haemolysis c. anemia under d. Aplastic
b. Acute hge TTT anemia
4.Small lymphocyte are found in the CBC of:
a. acute leukaemia b. CLL c. CML
5-ESR are increased by
a. polycythemia c. sickle cell d. All of the
b. DIC anaemia above

Report 7 Haemoglobin 7.5 g/dl


PCV (haematocrit) 25 %
Red cell count 2,400,000 /cmm
Reticulocytic count 3 %
MCV 92 fl
MCH 30 Pg
MCHC 33 g/dl
TLC 12,000 /cmm
Basophils 0 %
Eosinophils 1 %
Staff 19 %
Segmented 57 %

91
Lymphocytes 20 %
Monocytes 4 %
Platelet count 250,000 /cmm
Bleeding time 3 minutes
Coagulation time 15 minutes

1.- eosinophils are increased by all the following all except


a. Allergy b. parasite c. collagen d. Cushing
infestation disease syndrome
2- Normal neutrophil staff : segmented ratio is
a. 1 : 5-10 b. 1 : 10-20 c. 3 : 7-10 d. 5 : 1-10
3- Blast crises occurs in
a. AL c. CLL
b. CML d. All of the above
4. ESR is increased in
a. pregnancy c. Rh. fever e. all of the above
b. CML d. infarction
5-Prothrombin time increase in
a. Haemophillia b. purpra c. both
Haemoglobin 7.5 g/dl
Report 8
PCV (haematocrit) 25 %
Red cell count 2,400,000 /cmm
Reticulocytic count 3 %
MCV 92 fl
MCH 30 Pg
MCHC 33 g/dl
TLC 12,000 /cmm
Basophils 0 %
Eosinophils 1 %
Staff 19 %
Segmented 57 %
Lymphocytes 20 %
Monocytes 4 %
Platelet count 25,000 /cmm
Bleeding time 15 minutes
Coagulation time 3 minutes
1.-Neutorphils shift to the right is caused by
a. infection b. megaloblastic anemia c. acute hge d. malignancy
2-corticosteroids causes all the following all except
a. Neutropenia b. Eosinopenia c. Basopenia d. lymphopenia
3-Normal prothrombin time is 12-16 seconds
a. true b. false
4. In polycythaemia rubra vera there is increased
a. RBC c. platelets e. All of the above
b. WBC d. a+b

92
5- Philadelphia chromosome is
a. present in 60% of patients with CML c. presence denotes bad prognosis
b. found in the BM d. All of the above

Report 9
Haemoglobin 7.5 g/dl
PCV (haematocrit) 25 %
Red cell count 2,400,000 /cmm
Reticulocytic count 20 %
MCV 92 fl
MCH 30 Pg
MCHC 33 g/dl
TLC 18,000 /cmm
Basophils 1 %
Eosinophils 2 %
Staff 20 %
Segmented 60 %
Lymphocytes 13 %
Monocytes 4 %
Platelet count 150 000 /cmm

Bleeding time 3 minutes


Coagulation time 5 minutes

1.- ormal adult male reference range of eosinlphills


a. 1-5 % b. 5-10 % c. 10-15% d. 15-20%
2- Figlu test is done for
a. Vit B12 def. c. both
b. Folic acid def. d. none of the above
3- Bleeding time is increased in
a. haemophillia b. purpura c. both d. none of the above
4. Tests of coagulopathies are all of the following except
a. bleeding time c. Partial thromboplastin d. Prothrombin time (PT)
b. Coagulation time time (PTT): e. Plasma fibrinogen
5- Elevated anti-parietal antibodies occurs in
a. Haemolytic anaemia c. Haemoglobinuria
b. Aplastic anaemia d. None of the above

Report 10
Haemoglobin 19.0 g/dl
PCV (haematocrite) 60 %
Red cell count 7,800,000 /cmm
Reticulocytic count 2 %
MCV 92 fl
MCH 30 Pg

93
MCHC 33 g/dl
TLC 20,000 /cmm
Basophils 0 %
Eosinophils 2 %
Staff 10 %
Segmented 60 %
Lymphocytes 25 %
Monocytes 3 %
Platelet count 700,000 /cmm
ESR 1st Hour 1 mm
nd
2 Hour 3 mm
1.- normal adult male reference range of PCV
a. 25 % b. 35 % c. 45% d. 55%
2-Malaria causes …. haemolysis
a. Intracorpuscular b. Extracorpuscular
3-All of the following are causes of haemolytic anemia except
a. Thalassemia b. Sickle cell anemia c. PNH d. spherocytosis
4. In polycythaemia rubra vera there is increased
a. RBC c. platelets e. All of the above
b. WBC d. a+b
5- Philadelphia chromosome is
a. present in 60% of patients with CML c. presence denotes bad prognosis
b. found in the BM d. None of the above

Report 11
Haemoglobin 11.5 g/dl
PCV (haematocrit) 35 %
Red cell count 3,800,000 /cmm
Reticulocytic count 2 %
MCV 92 fl
MCH 30 Pg
MCHC 33 g/dl
TLC 35,000 /cmm
Basophils 0 %
Eosinophils 1 %
Staff 2 %
Segmented 15 %
Lymphocytes 80 %
Monocytes 2 %
Platelet count 250,000 /cmm
1.- In thalassemia the following occur except
a. Reticulocytic count is decreased c. Microcytic hypochromic anemia
b. HB electrophoresis is important d. BM aspirate is important
2- The red cell survival time is decreased in acute post-hemorrhagic anemia
a. true b. false
3- Normal adult male reference range of HGB
a. 10 g/dl b. 12 g/dl c. 16 g/dl d. 20 g/dl

94
4- Spherocytosis is caused by
a. Congenital b. Acquired c. Both
5- ESR > 100 is caused by
a. Malignancy b. TB c. SLE d. All of the above
Answers
1. 1- b 2- b 3- a 4- d 5- b 7. 1- d 2- a 3- d 4- e 5- a
2. 1- b 2- d 3- a 4- d 5- d 8. 1- b 2- a 3- a 4- e 5- b
3. 1- c 2- a 3- d 4- d 5- e 9. 1- a 2- a 3- b 4- a 5- d
4. 1- d 2- b 3- b 4- a 5- c 10. 1- c 2- b 3- c 4- b 5- b
5. 1- a 2- b 3- c 4- c 5- b 11. 1- a 2- b 3- c 4- c 5- d
6. 1- e 2- a 3- d 4- b 5- d

1. In thalassemia the following occur EXCEPT:


a) Extramedullary haemotapoiesis d) Basophilic stippling and normoblasts
b) TIBC increased in peripheral blood
c) Erthroid hyperplasia in bone marrow
2. Normoblasts are present in the preipheral blood in
a) Aplastic anaemia c) hypersplenism
b) thalassemia d) normal
3. Megaloblastic anaemia is characterised by
a) - - B12, folic acid c) Dx by bone marrow aspirate
b) Anti paraiteal cells antibodies d) All
4. Megaloblastic anaemia
a) Jaundice b) Pancytopenia c) Fever d) All of the above
5. ESR is
a) prognostic test c) used in follow up a case of SLE
b) decreased in polycythaemia d) All of the above
6. ESR is
a) increased in infarction c) decreased in acute infection
b) increased in Sickle cell anaemia d) the normal value in male is 25-30 mm
7. For routine investigations of case of haemolytic anaemia … is done
a) LDH c) Bone marrow aspirate and biopsy
b) B2 microglobulin d) Antiintrinsic factor antibody
8. All of the following conditions can cause haemolytic anaemia except
a) SLE c) Infectious mononucleosis
b) PNH d) Bone marrow infilteration by malignent cells
9. In sickle cell disease, which of the following will be seen on haemoglobin electrophoresis
a) only haemoglobin S c) haemoglobin S & F
b) haemoglobin A & S d) haemoglobin H
10. Ineffective erythropoiesis is evident in all types of haemolytic anaemia
a) True b) false
11. The red cell count is decreased in haemolytic anaemia a) True b) false
12. The reticulocyte count is increased in both acute post-haemorrhagic anaemia & haemolytic
anaemia a) True b) false
13. The red cell survival tome is decreased in acute post-haemorrhagic anaemia
a) True b) false
14. Paroxysmal nocturnal haemoglobinuria (PNH) is associated with abnormal Ham's test
a) True b) false
15. Paroxysmal cold haemoglobinuria is cold autoimmune haemolytic anaemia
a) True b) false
16. Paroxysmal nocturnal haemoglobinuria (PNH) may develops an aplastic anaemia

95
a) True b) false
17. Blast cells that are myeloperoxidase positive and contain Auer rods most likely belong to
which cell
a) lymphoid b) AML c) ALL d) myeloma
18. Which FAB type of myelodysplastic syndrome shows less than 1% blasts in the peripheral
blood, less than 5% blasts in the bone marrow, and ringed sideroblasts in at least 15% of the
nucleated RIBC in the bone marrow
a) refractory anaemia
b) refractory anaemia with ring sideroblasts
c) refractory anaemia with excess blasts
d) refractory anaemia with excess blasts in transformation
19. All of the following are characteristic of M3 leukaemia EXCEPT:
a) the myeloperoxidase and sudan black stain are positive
b) patients may develop DIC
c) a translocation between chromosomes 15 and 17 is common
d) the predominate cell on the peripheral smear is monocyte
20. In which of the following situations the platelet count could be decreased
a) ITP c) postsplenectomy
b) essential thrombocythaemia d) polycythaemia rubra vera
21. Hyperbilirubinaemia is present in acute post-haemorrhagic anaemia
a) True b) false
22. Oral anticoagulant is monitored by
a) PT b) PC c) APTT d) INR
23. Bleeding time is prolonged in
a) Purpura c) Patient on oral anticoagulants
b) Haemophilia d) anaemias
24. ESR> 100 mm in the first hour occurs in … EXCEPT
a) breast abscess c) pulmonary TB
b) breast cancer d) lupus nephritis
25. Unfractionated heparin is monitored by
a) PT b) PC c) APTT d) INR
26. Low molecular weight heparin is monitored by
a) PTT b) INR c) both d) none
27. Evidence of intravascular haemolysis are all… EXCEPT
a) ++ free HB c) ++ metHB
b) ++ haptoglobin d) haemosiderinuria.
Answers
1) d 8) d 15) a 22) d
2) a 9) c 16) a 23) a
3) d 10) b 17) b 24) a
4) d 11) a 18) b 25) c
5) d 12) a 19) d 26) d
6) a 13) b 20) a 27) b
7) a 14) a 21) b

SEROLOGY report
I-Widal test:
 Value :
 Salmonella agglutination test in enteric (typhoid) fever

96
 Measures body's Abs causing agglutination of Salmonella Abs .
 Ag are H (flagellar) , O (somatic) , Vi ( capsular) .
 Interpretation :
 Positive from the second week (to detect salmonella before that do blood culture)
 Positive when the titer > 180 or rising titer
 Recent infection = rising Anti O or Anti Vi Ab.
 Type of infection = AntiH Ab
 False positive test = previous vaccination or infection
 Amanasetic reaction = nonspecific reaction in fever causing rise of all types
of Anti H abs
 The salmonella are detected in blood from the first week by blood culture , second week
antibodies in blood by Widal test, third week by stool and urine culture.
 Drawbacks of Widal test :
 Needs 2 weeks to be positive
 Needs a rising titre ( not only positive)
 Affected by antibiotics

Widal test
check Anti O

> 1/180 (increased) 1/40 (normal)


check Anti H check Anti H

Rise of Rise of all Rise of Rise of all


ONE type ONE type
Amnesetic Vaccination
Old
reaction
infection
II-Brucella agglutination test :
 Measures body's IgM against brucella ( i.e. done for acute brucella)
 Positive from the second week
 Positive when the titre > 1/ 180 or rising titre 4 times over a week
 Agglutination is done over latex
III-Monospot test & Paul – Bunnell test :
 Serum contain heterophil Ab (Ig M) agglutinating sheep's RBCs.
 Positive in infectious mononucleosis IMN (EBV).
IV- Antistreptolysin O test ( ASOT) :
 Measures body's Abs against streptolysin enzyme of streptococci.
 +ve in recent streptococcal infection (better rising titer)
 Normally < 250 Todd's units, in rheumatic fever> 400 units.
V- C- reactive protein ( CRP ) :
 Normally absent
 it is graded from +1 to +4
■■:
 +ve in tissue damage (acute phase reactant) especially Rh.fever
VI- Comb's test :
 for autoimmune haemolytic anemia

97
 Direct : detect fixed RBCs Ab
 Indirect : detect free RBCs Ab in serum (severe cases)
VII- Antibodies:
IgM (Produced first in immune response)
The antibody is confined mainly to the intravascular pool. It is a large pentameric molecule, bound
together by the joining 'J' chain. It does not cross the placenta, and is not normally produced in the child
until after birth. Therefore, if present in the newborn infant, antigen-specific IgM is a good marker for
intrauterine infection. It is usually a sign of acute infections.
IgG (Dominant class of antibody)
This is the most abundant immunoglobulin in serum, present as a monomer. IgG is the antibody of
secondary response, and has high antigen affinity. It is the only antibody to cross the placenta in
significant quantities. IgG antibody is involved in resistance to infection, as patients who are lacking in
IgG suffer with recurrent, even life-threatening bacterial infections. Those with isolated IgA or IgM
deficiency have much less severe problems.
IgA (Found in mucous membrane secretions)
This is mainly the antibody of secretions, being present in the respiratory, gastrointestinal and urinary
tracts. IgA is mainly monomeric in the serum, but dimeric in secretions, the two molecules being
complexed by a joining (J) chain. For IgA responses, localized antigen exposure gives rise to generalized
mucosal immunity, which is of importance in vaccination. This is because after encountering antigen, IgA
precursor B cells in the mucosal lymphoid follicles journey to regional lymph nodes. After clonal
expansion the cells return to the systemic circulation via the thoracic duct and circulate to settle widely in
the mucosa-associated lymphoid tissue (MALT, not just the area where antigen exposure occurred.
IgD (Found almost solely on lymphocyte membrane)
Serum levels are very low and its function at this site is uncertain.
IgE (Responsible for symptoms of allergy; used in defence against nematode)
IgE is a monomer that is normally present in very low levels in serum, as most is membrane-bound to the
high-affinity receptors on mast cells and basophils. Its main physiological role is its antinematode
(parasites) activity, but its most common clinical relevance is in the pathogenesis of type 1
hypersensitivity (atopic or allergic) disease.
VIII- autoimmune profile:
Plasma autoantibodies (Abs): disease associations. Always interpret in the context of clinical findings:
Rheumatological
 ANA antinucleic antibody in most of autoimmune disease.
 Rheumatoid Factor (RhF): +ve in (%)
Sjogren's syndrome 100% Mixed connective tissue disease 50%
Felty's syndrome 100% SLE 40%
RA 70% Systemic sclerosis 30%
Infection (endocarditis, Hepatitis)50% Normal 2-10%
Rheumatoid factor measured by Rose-Waaler , Bentonite ,Latex test. It is an antibody against
immunoglobulin
 Anti-histone Ab: Drug-induced SLE (~100%).
 Anti-double stranded DNA (dsDNA): SLE (60%, more specific than ANA).
 Anti-phospholipid Ab (eg anti-cardiolipin Ab): antiphospholipid syndrome, SLE.
 Anti-centromere Ab: limited systemic sclerosis.
 Anti-extractable nuclear antigen (ENA) antibodies (usually with +ve ANA)
 Anti-Ro (SSA): SLE, Sjogren's syndrome, systemic sclerosis. Associated with congenital heart
block. Associated with congenital heart block
 Anti-La (SSB): Sjogren's syndrome, SLE (15%).
 Anti-Sm: SLE (20-30%)
 Anti-RNP: SLE, mixed connective tissue disease.
 Anti Jo-1; Anti-Mi-2: Polymyositis, dermatomyositis.

98
 Anti-Scl70: Diffuse systemic sclerosis.
GastroIntestinal
 Anti-mitochondrial Ab (AMA): Primary biliary cirrhosis (PBC: >95%). Also: autoimmune
hepatitis (30%), idiopathic cirrhosis (25-30%).
 Anti-smooth muscle Ab (SMA): Autoimmune hepatitis (70%), PBC (50%), idiopathic cirrhosis
(25-30%).
 Gastric parietal cell Ab: Pernicious anaemia (>90%), atrophic gastritis (40%). Also: autoimmune
thyroid disease (40%), normal controls (10-15%).
 Intrinsic factor Ab: Pernicious anaemia (50%).
 gliadin Ab, anti-tissue transglutaminase, anti-endomysial Ab: Coeliac disease.
Endocrine
 Thyroid peroxidase Ab (TPO): Hashimoto's thyroiditis (80-95%), Graves' (50-80%).
 Islet cell Ab (ICA), glutamic acid decarboxylase (GAD) Ab: Type 1 DM (75%).
Renal
 Glomerular basement membrane Ab (GBM): Goodpasture's syndrome.
 Anti-neutrophil cytoplasmic Ab (ANCA): vasculitis
Neuromuscular
 Acetylcholine receptor (ACR) Ab: Myasthenia gravis (90%).
Consumed C3 and C4 and ESR > 100 also indicate autoimmune activity.
Typhus are tested by Weil-Felix test.
Report 1
Anti-O : 1/80. Anti-H para-A : 1/80.
Anti-H typhoid: 1/80. Anti-H para-B : 1/80
1-Normal Anti O titre is 1/80 d. Non of the above
a. true 4-Increased Anti O Ab titre means
b. False. a. Recent infection
2.- Widal test is positive from the b. Amenestic reaction
a. Frist week c. both
b. Second week d. none of the above
c. Third week 5-The diagnosis is
d. Fourth week a. Recent typhoid infection.
3- The H antigen is b. Recent para-typhi A infection.
a. flagellar antigen c. Old para-typhi B infection
b. Somatic antigen d. Vaccinated person
c. Capsular antigen
Report 2
Anti-O : 1/240. Anti-H para-A : 1 / 80.
Anti-H typhoid: 1/240. Anti-H para-B : 1 / 80
1- Normal Anti H typhoid titre is d. droplet
1/80 4- Blood culture for salmonella is positive
a. True . during the
b. False. a. Frist 2 week
2.- False positive Widal test occurs in b. Second 2 week
a. Previous infection c. Third 2 week
b. Past vaccination d. Fourth 2week
c. Both 5-The diagnosis is
d. none of the above a. Recent typhoid infection.
3- Typhoid is transmitted by b. Recent para-typhi A infection.
a. injection c. Old para-typhi B infection
b. sexual
c. feco-oral
d. Vaccinated person
Report 3
99
Anti-O : 1/240. Anti-H para-A : 1/240.
Anti-H para-B : 1 / 80
Anti-H typhoid: 1 / 40.
1- Normal Anti H paratyphoid A titre is 4- Which type of theses Abs rise frist during
1/80 an immune reaction
a. True . a. Ig A
b. False. b. Ig G
2.- positive Widal if c. Ig M
a. Rising titre
b. Titre>1/80
d. Ig D
c. Titre>1>160 e. Ig E
d. All of the above 5-The diagnosis is
3.- Stool culture is positive during a. Recent typhoid infection.
a. Frist - Second week b. Recent para-typhi A infection.
b. Second - Fourth week c. Old para-typhi B infection
c. Fourth -Fifth week d. Vaccinated person
Report 4
Anti-O : 1 / 80. Anti-H para-A : 1/160.
Anti-H typhoid: 1/160. Anti-H para-B : 1/160
1- Normal Anti H paratyphoid B titre is d. Hydate disease
1/80 4- Increased Anti O Ab titre means
a. True . a. Recent infection
b. False. b. Amenestic reaction
2.- Widal test is positive from the c. a or b
a. Frist week
b. Second week
d. none of the above
5- The diagnosis is
c. Third week
d. Fourth week a. Recent typhoid infection.
3. Casoni test is done for b. Recent para-typhi A infection.
a. Salmonella c. Old para-typhi B infection
b. TB d. Vaccinated person
c. Taenia saginata
Questions
1- Recent vaccination elevates c) 1 samples 10 days apart from first week
a) Anti-O d) 1 samples 10 days apart from second
b) Anti-H week
c) both 4- Widal antibodies
d) none a) Anti-H rises early and disappears late
2- Recent infection increases b) Anti-O rises early and disappears late
a) Anti-O c) Anti-O rises early and disappears late
b) Anti-H d) None of the above
c) Both 5- Detection of salmonella in the first week
d) none a) Blood culture
3- Ideal method of Widal sampling b) Stool culture
a) 2 samples 10 days apart from first week c) Widal test
b) 2 samples 10 days apart from second d) None of the above
week
ANSWERS
1 2 3 4 5
Report 1
Report 2
Report 3
Report 4

100
1- To which of the following classes of immunoglobulins do the allergy-mediated antibodies
belong
a) IgA c) IgM e) IgE
b) Ig G d) IgD
2- Which of the following antibody classes is the frist to be produce in an immune response to a
given antigen?
a) IgA c) IgM e) IgE
b) Ig G d) IgD
3- In the most of normal persons; what is the percentage of IgG in the whole
immunoglobulins?
a) 10% c) 50% e) Over 70%
b) 25% d) 60%
4- Which one of the following immunoglobulins is the principle immunoglobulin exocrine
secretion?
a) IgA c) IgM e) IgE
b) Ig G d) IgD
5- Which of the following statements about IgM is true?
a) it is reaginic antibody
b) it is important in the first few days of the primary immune response
c) it increases in serum concentration after IgG has reached its peak serum concentration
d) it is the smallest of the immunoglobulin molecules
e) it is involved in allergic reactions
6- Actively acquired immunity can be caused by all of the following EXCEPT?
a) The specific disease.
b) Exposure to subclinical doses of the disease causing organism
c) Vaccination with appropriate antigen.
d) Injection with immune serum containing appropriate antibodies.
7- Which of the following substances may be passively transferred from the mother to the fetus
during the third trimester
a) IgG c) Anti-Rh antibody
b) IgM d) Natural isohaemagglutinis
Answers
1) e 3) e 5) b 7) a
2) c 4) a 6) d

Report 1
Widal test
 Anti-H para-A: negative.  Anti-O: negative.
 Anti-H para-B: negative  Anti-H typhoid: 1/40.
Monospot test: negative Brucella (latex):positive
1- Titer of brucella agg. > 1/160 indicates a. acute brucellosis
chronic brucellosis b. chronic brucellosis
a. True . c. both
b. False. d. None of the above
2.- Brucella is characterized by 4- Dick test is done for
a. Aplastic anemia a. Salmonella
b. polycythaemia b. Scarlet fever
c. leucocytosis c. Taenia saginata
d. leucopenia d. Hydate disease
3- Elisa test is done for

101
5- Which of the following is passively b. IgM
transmitted from a mother to her foetus during c. Anti-Rh antibodies
pregnancy d. Natural isohaemoagglutinins
a. IgG
Report 2
ESR:
1sthour 54 mm
nd
2 hour 82 mm
Rheumatoid Factor:
Latex Positive
Rose Waaler 64 DAT (up to 16) up to 16)
ASO: 125 Todd Units (up to 250) up to 166)
CRP: Positive

1- This is a case of 4- Casoni test is done for


a. Rh arthritis a. Salmonella
b. Rh fever b. Scarlet fever
2.- Rheumatoid factor is increased in c. Taenia saginata
a. Rh arthritis d. Hydate disease
b. Rh fever 5- Rh factor may be present in he following
c. Infection except
d. All of the above a. Rh arthritis
3- The following is a serological test for Rh b. Rh fever
factor c. SLE
a. Weil-Flexi
b. ASOT
d. Normal people
c. CRP e. Spondylosis
d. Bentonite
Report 3

ESR Increased
ASO 100 Todd,s units
ANA Positive

1- ANA is good … for SLE d. Ig E


a. positive. 4- allergy-mediating antibodies
b. negative. a. Ig A
2.- Coomb's test is done for b. Ig G
a. Autoimmune haemolytic anemia c. Ig M
b. polycythaemia d. Ig E
c. leukocytosis 5- Which clinical feature is commonly found in
d. leucopenia patients with systemic lupus erythematosus
3- Principal immunoglobulin in exocrine a. Vasculitis is a basic lesion.
secretions b. A linear deposition of immunoglobulin in
a. Ig A their glomerular bm
b. Ig G c. Thyroid receptor antibody is present
c. Ig M d. Rh. factor is rarely present
Questions
1. Al the following is correct about ASOT except
a) Better rising titer. b) It is antibody against haemolysin of
streptococci
102
c) Value of 200 Todd's units is diagnostic. c) Anti-La
2. Dick test is done for d) Anti-mitochondrial
a) IBV 5. RF is antibody against antibodies
b) CMV secreted by the body
c) SLE a) True
d) Scarlet fever b) false
3. If blood picture is suggestive of EBV 6. Which of the following statements
with monspot test what further describes the rheumatoid factor?
investigation is done? a) it is the antigen initiating the
a) Serology rheumatoid inflammatory process
b) Blood culture b) it is an antibody against cellular DNA
c) Repeat monspot test c) it consists primly of DNA
4. The following antibodies may be d) it is an antibody against
elevated in Sjogren disease EXCEPT immunoglobulin
a) ANA
b) Anti-Ro
1 2 3 4 5
ANSWERS
Report 1
Report 2
Report 3

Hepatitis marker report


 Introduction :
 Viral hepatitis has markers which are the antigens of the viri and the antibodies against them also;
the viral DNA & RNA can be detected and is considered as a marker.
 PCR is a new technology done for HBV, HCV & HDV.
 IgM Ab is indicative of a recent infection while , IgG is indicative of a old infection
 HBV has three antigens core (C) ,surface (S) & envelope (E).
 All viral hepatitis are RNA viri except HBV is DNA virus .
 HDV infection occurs only on top of chronic HBV infection .
 HBV & HCV only have chronic sequels
# Markers :
A. Hepatitis " A " Markers ( 1 marker ) :
1- HAVAb: IgM denotes recent infection, IgG denotes old infection.

B. Hepatitis " B " Markers ( 7 markers ) :


1. HBsAg (Hepatitis B surface antigen):
■ Appears 6 weeks after infection & disappears after 3 months
■ Persistence more than 6 months indicates either carrier state OR chronic state.
2. HBsAb (Anti - HBs antibodies):
■ Appear after 3 months & persist.
■ They indicate either: recovery or immunity.
3. HBcAg (Hepatitis B core antigen):
■ It is not detected in the blood, it is only detected in a liver biopsy.
4. HBcAb (Anti - HBc antibodies):
■ IgM: Chronic active B hepatitis.
■ IgG: carrier OR old infection.
5. HBeAg (Hepatitis B envelope antigen):

103
■ Its presence indicates high infectivity.
■ Its persistence more than 3 months indicates chronicity
6 .HBeAb (Anti - HBe antibodies):
■ Its presence indicates low infectivity
7. PCR for HBV DNA:
■ It is the most sensitive index for viral replication.
Summary
 Incubational period: HBsAg, HBcAb IgM.
 Acute hepatitis: as incubational period + HBcAb IgG.
 Post-infection immunization: HBsAb + HBcAb IgG
 Postvaccination immunization: HBsAb only.
 Chronic infection: HBsAg + HBcAb IgG.
 Follow up viral ttt therapy: HBV DNA PCR + HBVeAg + liver enzymes.
 Window phase HBcAb are positive and the rest are negative

C. Hepatitis " C " Markers ( 2 markers ) :


1. HCVAb (Anti - HCV antibodies: by ELISA
■ Detected after 6 weeks of infection.
2. PCR for HCV RNA:
■ Detected after 2 weeks of infection.

D. Hepatitis " D " Markers ( 3 markers ) :


1. HDVAb(Anti - HDV antibodies):
■ IgM: recent infection. ■ IgG: old infection.
2. PCR for HDV RNA.
3. HBsAg is positive.

E. Hepatitis " E " Markers ( 1 marker ) :


1. HEVAb (Anti - HEV antibodies):
■ IgM: recent infection. ■ IgG: old infection.

104
Acute hepatitis

Hepatitis A Hepatitis C

Acute Old Acute Chronic


infection infection hepatitis hepatitis

Positive  Positive  High viral load Positive 


HAV Ab IgM HAV Ab IgG  HCV Ab
Hepatitis B HCV RNA PCR
check HBsAg

Only positive Positive + other marker Negative


check HBsAb
Carrier for HBV
Only positive Positive Negative
+ HBcIgM + HBcIgM + HBcIgG + HBeAb Check HBcAb IgM
+ HBeAg If positive 
Vaccination Early recovery
Acute HBV Acute HBV Inf.+ Chronic HBV
infection High infectivity infection + +ve AntiHBc IgG Window phase

Early recovery

105
Report 1

HbsAg Negative d. cholangiocarcioma


HbsAb Positive 3. Pre HBV vaccination marker is
HbcAb IgG Negative a. HBeAb
HbcAbIgM Negative b. HBeAg
HbeAg Negative c. HBsAb
HbeAb Negative
HCVAb Positive
d. HBsAg
4- This is acase of
1- PCR is done for
a. HAV a. Chronic HCV infection
b. HBV b. Acute HCV infection
c. HDV 5- A HBV carrier has … in his blood
d. B+C a. HBeAb
2.- HCV may be followed by…. except b. HBeAg
a. Ch.hepatitis c. HBsAb
b. Glomerulonephritis d. HBsAg
c. Aplastic an.
Report 2
HbsAg Positive b. HBeAg
HbsAb Negative c. HBsAb
HbcAb IgG Negative d. HBsAg
HbcAb IgM Positive 4- This is a case of
HbcAb IgM
HbeAg Positive a. Acute HBV infection
HbeAb Negative b. Window phase of HBV infection.
1- prevaccination hepatitis marker done is c. Immunity after recovering from HBV
a) HbsAg infection
b) HbsAb d. Carrier for HBV.
c) HbcAb IgG
e. Immunity after HBV vaccination
d) HbeAg 5- All are correct about HBsAg except
2.- HBV is a …. virus
a. RNA a. It’s the HBV surface Ag
b. DNA b. Appears after one month
3. Window phase the following …is positive c. Disappears after 3 months
a. HBcAb IgM d. Its persistence indicates a carrier state
Report 3
HbsAg Positive b. HBeAg
HbsAb Negative c. HBcAb
HbcAb IgG Negative d. HBsAg
HbcAb IgM Negative 3. HEV is a …. virus
HbeAg Negative a. RNA
HbeAb Negative b. DNA
1- This is a case of 4- A chronic HBV pt. has … in his blood
a. Acute HBV infection a. HBeAb IgG
b. Window phase of HBV infection. b. HBeAg
c. Immunity after recovering from HBV c. HBcAb IgG
infection d. HBcAg
d. Carrier for HBV. 5- HBV may be followed by…. except
2.- Which of the following markers is not a. Ch. hepatitis
detected in peripheral blood b. Glomerulonephritis
c. Aplastic an.
a. HBeAb d. cholangiocarcinoma
106
1- Postvaccination hepatitis marker done is
a) HbsAg b) HbsAb c) HbcAb IgG d) HbeAg
2- HCV viraemia can be found in patients with
a) Abnormal liver function tests c) Normal & abnormal liver function test
b) Normal liver function test d) None of the above
3- During the early phase of primary HCV infection
a) HCV RNA is the only marker of the infection
b) HCV antibodies are the only markers of the infection
c) Elevated liver enzymes are the only markers of infection
d) None of the above
4- Absent HCV Ab means absent HCV infection
a) True b) False
5- Follow up HBV viral ttt therapy:
a) HBV DNA PCR d) All of the above
b) HBeAg e) A+B
c) Liver enzymes
ANSWERS 1 2 3 4 5
Report 1 D A C A D
Report 2 B B A B B
Report 3 A C A C D
B A A B D

Urine analysis
NORMAL VALUES
1-Volume 500 - 1500 cc /day
2-Colour - aspect: amber yellow , clear
3-Specific gravity: 1015 - 1025
4-Reaction "pH" : acidic - 5.5 - 6.5
5-Chemical contents :
a-Nitrogenous: urea, creatinine, uric ammonium.
b-Non nitrogenous : ketone & glucose are absent
c-Enzymes & small MW proteins
6-Microscopic examination :
a-Cells : RBCs : N: 0 - 4 / HPF -Pus cells : N: 0 - 4 / HPF
b-Bacteria - parasites - ova : absent
c-Casts
d-Crystals : - Acidic urine : ca oxalate, uric acid.
- Alkaline urine : phosphate
a) Volume of urine:
 Polyuria: ++ urine volume more than 1500 CC / 24h: ++ fluid intake, DM, DI.
 Oliguria: -- urine volume less than 400 CC / 24h.
Causes:
Prerenal causes as shock, dehydration
Renal causes as ARF, CRF, Acute GN.
Postrenal cause: obstructive uropathy
b) Aspect: Turbid in infection or phosphate or urate deposits.
c) Colour:
 pale yellow if diluted
 Red in bleeding, Rifampicin.
 pigments as vitamin B complex … dark yellow
 Green yellow in infection.
107
 Black in metastatic melanoma or phenol derivatives.
 Milky urine due to rupture of lymphatics, sever infection, phosphate.
d) Specific gravity:
 It depends on amount of solute and volume of urine.
e) Urinary casts: coagulated protein cast formed in tubular lumen
 Red casts in nephritic syndrome.
 Fatty casts in nephrotic syndrome.
f) Sterile pyuria: no culture on ordinary culture media despite the presence of pus cells in urine >
10/HPF (high power field).
Causes:
 Renal TB  Recent antimicrobial therapy
 Female genital tract infection  Prostatitis
 Non-gonnocal urtheritis  Renal neoplasms, calculi.
 Infection by anaerobic bacteria
.

108
Check urine volume ( N: 800 - 1500 ml / day )

Increased > 1500/day Decreased < 800 / day


check specific gravity ( N : 1 0 1 5 - 1 025 ) check specific gravity ( N : 1 0 1 5 - 1 025 )

Increased Low fixed


Increased Low fixed Very low
> 1025 1010
> 1025 1010 1003
Check RBC ARF
DM CRF D. Insipidus
Check pus cells
D. nephropathy
Normal Increased +
N: 0-4 increased smoky urine
if proteinuria
CRF on top of CRF on top of Acute normal
glomerulonephritis pyelonephritis glomerulonephritis concentrated urine

Normal ( N: 800 - 1500 ml / day )


Check ptn

Normal  Check colour/aspect marked proteinuria > 3.5 gm / 24 hour

Nephrotic
Turbid (aspect) Reddish (colour) Brown or dark red (colour) syndrome
Acute
Haematuria Jaundice Obstructive Bilirubin Urobilinogen
pyelonephritis
Examples
+  pus cells Haemolytic Bilirubin Urobilinogen
Jaundice
Hepatocellular
Jaundice Bilirubin Urobilinogen
109
Jaundice
Jaundice
# Answers of urine analysis reports
Report 1: Urinary infection in diabetic patient.
Report 2: Urinary infection.
Volume 100 ml 200 ml 4000 2500 3500 500 ml/24h
101 (Random 201 (Random ml/24h ml/24h ml/241
Colour Amber yellowsam Amber yellowamp Pale yellow Pale yellow Pale Smoky
Reaction Alkaline ple) Acidic le) Alkaline Acidic Acidic Acidic
Specific Gravity 1030 1025 1002 1040 1010 1035
Aspect Turbid Turbid Clear Clear Clear Clear
Protein + ++ Nil + + +
Sugar + Nil Nil ++++ Nil Nil
Acetone Nil Nil Nil Nil Nil Nil
Bile Pigment Nil Nil Nil Nil Nil Nil
Urobilinogen Normal trace Normal trace Normal trace Normal trace Normal trace Normal trace
Epithelial Cells + ++ Nil + Nil +
Pus Cells 15-20 > 100 0-1 1-3 0-1 1-5
RBC's 8-10
/HPF 2-3
/HPF 0-1
/HPF 0-1
/HPF 0-1
/HPF 10-20
Crystals Amorphous Nil /HPF
Nil Nil Nil Nil
phosphate
Triple phosphate
Casts Nil Nil Nil Hyaline Hyaline & Red Casts
Ova Nil Nil Nil Nil granular
Nil Nil
Report 3: Diabetes insipidus or functional polyurea.
Report 4: Diabetic proteinuria.
Report 5: Chronic renal failure or, Diuretic stage of acute renal failure.
Report 6: Nephritic syndrome.

110
Examples
Volume 1000 1400 2500 500 ml/24 600 3500
ml/24h ml/24 hours ml/24 hours hours ml/24 hours ml/24 hours
Colour Amber yellow Brown Pale yellow Amber yellow Smoky Watery
Reaction Alkaline Alkaline Alkaline Acidic Alkaline Alkaline
Specific Gravity 1025 1018 1040 1035 1010 1010
Aspect Turbid Clear Clear Clear Clear Clear
Protein + + +++ Nil + +
Sugar Nil Nil ++++ Nil Nil Nil
Acetone Nil Nil Nil Nil Nil Nil
Bile Pigment Nil ++ Nil Nil Nil Nil
Urobilinogen Normal trace Normal trace Normal trace Normal trace Normal trace Normal trace
Epithelial Cells + + Nil NIL + Nil
Pus Cells 15-20 /HPF 0-1 /HPF 1-3 1-3 3-5 35-40
RBC's 3-5
/HPF /HPF 0-1 /HPF 1-3
/HPF 1-3
/HPF 25-30
/HPF 5-7
/HPF
Crystals Nil Nil Nil /HPF
Nil Nil /HPF
Nil

Casts Hyaline & White Hyaline Hyaline & Fatty Nil Hyaline, Red cell Hyaline, White
Ova cell
Nil Nil Casts
Nil Nil & Granular Casts Nil
Nil cell & granular
Casts
Bile salts
# Answers of urine analysis reports
Report 1:Pyelonephritis.
Report 2:Cholestasis..
Report 3:Diabetic nephrosis (KW
syndrome)..
Report 4:Pre-renal uraemia or functional
oliguria.
Report 5: Acute renal failure (Acute tubular necrosis).
Report 6:Chronic pyelonephritis & chronic renal failure.
111
Report 1
Volume 1000 ml/24h
Colour Amber yellow
Reaction Alkaline
Specific Gravity 1025
Aspect Turbid
Protein +
Sugar Nil
Acetone Nil
Bile Pigment Nil
Urobilinogen Normal trace
Epithelial Cells +
Pus Cells 15-20 /HPF /HPF
RBCs 3-5 /HPF
Crystals Nil
Casts Hyaline & White cell
Ova Nil
1-What is your diagnosis:
a) Acute nephritic syndrome. c) nephrotic syndrome
b) Chronic renal failure d) pyelonephritis
2- increased urine volume occurs in all …. except:
a) D.M. c) Chronic renal failure.
b) D. insipidus d) acute Renal failure
3- haematuria occurs in …except
a- Acute nephritic syndrome. c- bilharsiasis
b- Crystals d- Nephrotic syndrome
4- Turbid urine indicates
a- Acute nephritic syndrome. c- nephrotic syndrome
b- pyelonephritis d- All of the above.
5- proteinuria occurs in
a- Nephrotic syndrome c- Acute pyelonephritis
b- Chronic G.N. d- All of the above
Report 2 Volume 4000 ml/24h
Colour Pale yellow
Reaction Alkaline
Specific Gravity 1002
Aspect Clear
Protein Nil
Sugar Nil
Acetone Nil
Bile Pigment Nil
Urobilinogen Normal trace
Epithelial Cells Nil
Pus Cells 0-1 /HPF
RBCs 0-1 /HPF

112
Crystals Nil
Casts Nil
Ova Nil
1-What is your diagnosis:
a-- Acute nephritic syndrome. c- Diabetes iinsipidus
b- Chronic renal failure d- pyelonephritis
2- The cause is in :
a-- Pituitary gland. b- Kidney c- both d- none
3- investigation needed is
a- serum ADH. c- both
b- serum insulin level d- none
4- Very low specific gravity occurs in
a-- D.M. c- ch. Renal failure
b- D. insipidus d- acute Renal failure
5- Anuria characterized by all except
a- means complete absence of urine output for more than 12-24 hours
b- occurs in bilateral ureteric obstruction
c- occurs in renal failure d- occurs in nephotic syndrome
1- d 2- d 3- d 4- b 5- d 1- c 2- c 3- c 4- b 5- d

CSF profile
The pressure: (N: 80-120 mm CSF)
1. Causes of high pressure:
- Meningitis. - Brain tumour & abscess.
- Haemorrhage. - Idiopathic increased ICT
2. Causes of low pressure:
- Subarachnoid block. - Excessive CSF aspiration.
The colour & aspect (N: clear & colourless):
1. Red: in haemorrhage.
2. Yellow:
- After subarachnoid haemorrhage. - Subarachnoid block.
3. Turbid: in meningitis.
The proteins (N:20-40 mg/dl):
1. High with excessive WBCs: in meningitis.
2. High with excessive RBCs: in haemorrhage.
3. High with normal cells: in "cyto-albuminous dissociation":
- Subarachnoid block. - Multiple sclerosis.
- Infective polyneuritis. - Some brain tumours as acoustic neuroma.
The cells (N: no cells):
1. Neutrophils: in septic meningitis. meningitis.
2. Lymphocytes: in tuberculous & viral 3. RBCs in haemorrhage.
The sugar (N: 40-80 mg/dl):
1. It is low in meningitis especially septic type.
2. It is high in diabetes and haemorrhage.
The chlorides (N: 115-130 mmol/L).
1. It is low in meningitis especially tuberculous.
2. It may be high in uraemia.
Froin tirade (Occurs in extramedullary block in paraplegia)
1) Spontaneous coagulation
2) Xanthochromia
3) Cytoalbuminous diss. ( ++ ptn , N. cell count )

113
T.B Septic Viral Extrmed. Intramed.
- pressure Increased Normal decreased increased
- Colour Turbid Clear Yellow Clear red
/ aspect (xanthoch.)
- ptn ++ ++++ ++ ++
- chloride -- N N N
- sugar -- N N N
- cells Lymph. PMN Lymph. N RBC
- Culture +ve +ve -ve No organism
Septic = pyogenic meningitis is caused by meningococcal.

Check colour/aspect

Turbid Yellow Clear Red


Meningitis Extramedullary Subarachinoid
block hge

Check sugar/cells
Normal sugar
-- Sugar -- Sugar ++ Lymphocytes
++ Lymphocytes ++ PMN
Intramedullary Viral
T.B. Septic block meningitis
meningitis meningitis
Examples
 Septic (pyogenic) meningitis
Aspect Turbid
Colour Colourless
Protein 150 mg/dl (15-45mg/dl)
Sugar 5 mg/dl (45-80 mg/dl)
Chloride 115 mmol/1 (115-130 mmol/1)
Cells 300 Cell/ul (Polymorph nuclear)
 Viral meningitis
Aspect Clear
Colour Colourless
Protein 40 mg/dl (15-45 mg/dl)
Sugar 60 mg/dl (45-80 mg/dl)
Chloride 125 mmol/1 (115-130 mmol/I)
Cells 90 Cell/ul (Lymphocytes)

114
 Extramedullary block
Aspect Clear
Colour Xanthochromic
Protein 200 mg/dl (15-45 mg/dl)
Sugar 65 mg/dl (45-80 mg/dl)
Chloride 120 mmol/1 (115-130 mmol/I)
Cells 5 Cell/ul (mononuclear)
1- In septic meningitis the CSF shows:
a- Decreased chloride. b- Increased sugar. c- Increased lymphocyte.
d- Increased PMN (polymorph nuclear leucocytes).
2- The following precutions must be done during CSF aspirate procedure except:
a- The procedure is done under complete aseptic conditions.
b- The sample must be put in sterile tube and taken immediately to the lab and not leave it in the
fridge.
c- The sample must be put in the three sterile tubes.
3- Increased lymphocytes in
a- Septic meningitis meningitis d- A+B.
b- Tuberculous c- Viral meningitis. e- B+C.
4- In viral meningitis the CSF shows:
a- Decreased chloride. b- Increased sugar. c- Increased lymphocyte.
d- Increased PMN (polymorph nuclear leucocytes).
5- Decreased pressure occurs in
a- Septic meningitis c- Viral meningitis.
b- Tuberculous meningitis d- Paraplegia.
6- Pyogenic meningitis differ from TB meningitis in
a- pressure c- colour of CSF e- amount of sugar
b- cellular type d- amount of ptn
7- Viral meningitis shows increased ptn and decreased chloride
a- True b- False
8- Negative culture of CSF occurs in
a- Septic meningitis b- Tuberculous meningitis c- Viral meningitis.
9- Clear CSF occurs in
a- Septic meningitis b- Tuberculous meningitis c- Viral meningitis.

1- d 2- c 3- e 4- d 5- d 6- b 7- b 8- c 9- c

115
stool analysis
1- Volume :
- < 200 gm / day ( unless excess dietary fibers are ingested )
-Diarrhea = loose stool, frequent motion > 4 times / d. or both
-Constipation = infrequent bowel evacuation (> 48 hr.) + passage of hard small stools
2- Consistency : soft, well formed
3- Colour : light to dark down
4- Odour : fecal (not offensive)
5- Reaction : alkaline
6- Contents : - mucus , pus , RBC : absent
- fat < 6 gm / day

check fat content ( 6 gm / day )

Normal Increased
> 6 gm / day or > 25 % of total weight
Check mucus & pus cells
Malabsorption
syndrome
check split/unsplit fats

mainly split fat mainly unsplit > 25%

Intestinal Maldigestion
Malabsorption (pancreatic -
syndrome hepatobiliary
)

Excess mucus Excess pus

Amebic dysentry Bacillary dysentry


(amebic cysts (gm -ve bacilli)
or vegetative
forms)

116
Stool Report
Diagnosis Normal Amebic Bacillary
dysentery dysentery Malabsorption Maldigestion
(intestinal) (pancreatic - hepatobiliary)

Volume 200 gm/day 180 300 350 330


Consistency soft, well formed loose loose (watery ) loose

Colour brown brown

Odour fecal offensive offensive offensive alkaline offensive

Reaction alkaline acidic alkaline alkaline

Contents
-Mucus - excess slight + slight + slight +

-Pus cells - ++ +++ - -


-RBCs - +++ +++ - -
-Food residues - + + ++ ++ (meat fibers )
-Others - ameba cyst gm -ve bacilli

Fat contents < 6 gm / day - -


10 gm/day
11 gm / day
-Split fat - - -
90% 50 %
-Unsplit fat - - - 50%
10%

117
LIVER FUNCTION TESTS
1- Bile pigments & salts tests
Bile pigments & salts

Serum Urine Stools


- Bilirubin - Bilirubin - Stercobilinogen
- Urobilinogen
- Bile salts
I. Serum Bilirubin:
Direct (conjugated) Indirect (unconjugated) Total Bilirubin
- Normal 20% of total 80% of total 0.2-1 mg / dl
- Increased in Obstructive jaundice Haemolytic jaundice All types of jaundice
II. Bilirubin in urine:
• Normally: bilirubin is absent in urine.
• Present if obstructive or hepatocellular jaundice.
III.Urobilinogen in urine: (N: 0.5-2 mg / day)
• Increases in: haemolytic & Hepatocellular jaundice
• Decreases in: obstructive jaundice.
IV. Bile salts in urine:
• Normally: absent in urine.
• Present in urine: Obstructive jaundice.
V. Stercobilinogen in stools: (N: 50-200 mg / day)
• It increases in: haemolytic jaundice.
• It decreases in: obstructive & hepatocellular jaundice
Liver
» Normally indirect bilirubin (blood)  direct bilirubin (blood) absorbed
Bile Stercobilinogen (stools) Urobilin.(urine)
» Haemolytic jaundice is exaggeration of normal
» Obstructive jaundice there is obstruction at biliary system   stercobilinogen
(stools) & Urobilinogen (urine) +  escape of direct bilirubin to the blood
» Hepatocellular jaundice as obstructive + indirect bilirubin (decreased conjugation
due to diseased liver )
2-SERUM ENZYMES

Transaminases Alkaline  -Glutamyl Serum 5-


- AST phosphatse Transpeptidas nucleotidase
- ALT e
I. Transaminases:
- Serum Glutamic Oxalacetic Transaminase (SGOT) = Aspartate Transaminase (AST).
- Serum glutamic Pyruvic Transaminase (SGPT) = Alanine Transaminase (ALT).
- AST increase in acute diseases (damage) of Liver, heart, kidney& skeletal muscles.
- ALT increase in acute diseases (damage) of Liver ONLY so it is more specific for liver.
II. Alkaline Phosphatase (ALP) : (N: 40- 117 units).
- Formed in liver (normally excreted in bile) & bone
- ALP increases markedly in obstructive jaundice (liver) & bone diseases .
moderately in hepatitis & cirrhosis (liver), pregnancy.
III. Gamma Glutamyl Transpeptidase( GGT ) : (N: ♀7- 35 ♂10-60 U/L).
119
- It increases in:
1. Obstructive jaundice (it helps differentiating elevated ALP due to liver or bone diseases).
2. Hepatocellular diseases (esp. Alcoholic hepatitis more important in alcoholics less important in
Egypt).
IV. Serum 5-nucleotidase: It increases in biliary obstruction.
N.B. How to differentiate between an increased ALP due to LIVER DISEASE and due to BONE
DISEASE ? » Associated increase in liver enzymes GGT & 5-nucleotidase
» Abdominal ultrasonography
3-tests for Proteins
I. Chemical Separation of Plasma proteins:
Normal Chronic liver dis. Acute liver dis.
 Total proteins 6- 8 gm/dl. Decreased Normal
 Albumin 3.5 -5.5 gm/dl. Decreases Normal
 Globulin 2 gm/dl. Increases Mild increases
 A/G ratio >1 Reversed Normal
N.B.: - Albumin has a long half life time so , it isn't decreased in acute liver disease.
- HYPOALBUMINEMIA is a marker of a chronic liver disease
4-tests for Fats
- Normally: fasting blood cholesterol is 150 - 200 mg %.
- In Obstructive jaundice: Hypercholesterolemia.
- In Liver failure: Normal cholesterol level, with decreased esterification
5-tests for Carbohydrates
Glucose Tolerance Test: of limited value in assessment of liver diseases
- In acute liver failure: hypoglycemia.
- In chronic liver failure: impaired glucose tolerance & rarely DM.
6-PROTHROMBIN TIME
- Normally Prothrombin time (PT): 12-14 sec. Prothrombin concentration (PC): 100 %.
- PT is prolonged & PC is decreased in:
1. Obstructive jaundice (-- fat and fat soluble vitamins absorption) & other causes of Vitamin
K deficiency. Vitamin K will correct the PT & PC.
2. Liver cell failure (acute & chronic …… decrease synthesis of prothrombin and other
coagulation factors) + obstruction of biliary system by oedema + cirrhosis (abnormal
biliary architecture) Vitamin K will correct the obstructive part causing mild improvement
of the PT & PC..
7-ALPHA FETOPROTEIN
- Normally: It is absent in the serum, or very low in the serum: < 10 ng / ml.
- In disease: It is present in the serum in the following conditions:
Marked elevation Moderate elevation
 Liver Hepatocellular carcinoma (HCC) Hepatitis & Cirrhosis
 other Pancreatitis.
Malignancy of GIT , Ovary ,testis
- It is useful in the following conditions:
1. Follow up of cirrhotic patients for early detection of HCC.
2. Suspected cases of HCC: e.g. focal hepatic lesion.
3. After tumour resection:
■ Early: to confirm successful resection.
■ Late: to detect recurrence of the tumour.

120
SUMMARY of LIVER FUNCTION TESTS

Normal Haemolytic Obstructive Acute liver Chronic liver


jaundice Jaundice disease disease
1.Bile a) Bilirubin- Serum 0.2 - 1 mg / dl. ++ indirect +++++ direct ++ Both ++ Both
pigment b) Bilirubin- urine Absent Absent Present Present Present
c) Urobilinogen-urine 0.5 - 2 mg / day ++ -- ++ --
d) Stercobilinogen stool 50-200 mg / day ++ -- -- --
e) Bile salts- urine absent absent Present absent absent
2. Serum a) SGOT (AST) 0- 37 U/L Normal +++++ +
enzymes b) SGPT (ALT) 0- 40 U/L +++++ +
c) ALP 40- 117 U/L +++++ ++ +
d) GGT ♀7- 35 ♂10-60 ++ ++ +
U/L ++
e) 5-nucleotidase 3.5- 5.5 U/L
3. proteins a) Albumin 4-5 gm/dl Normal Normal Normal --
b) Globulin 2-3 gm/dl. ++ ++
c) A/G ratio 2/1. Not affected >1 Reversed <1
4. FATs T. Cholesterol 150 - 200 mg/dl ++ (--excertion -- (-- synthesis)
in bile)
TGs 100- 160 mg/dl
5. CHO Glucose hypoglycemia IGT
6. Prothromb PT 12-14 sec -- corrected -- not corrected Partially
in corrected
7.  feto ptn < 10 ng / ml < 100 ng / ml < 100 ng / ml < 100 ng / ml
An acute liver disease is like acute hepatitis
A chronic liver disease is like liver cirrhosis
Jaundice
Increased total bilirubin > 1
Check direct bilirubin

Increased > 0.3 (usually > 1). Normal 0-.25


Check AST & ALT ± ALP Haemolytic
jaundice
Elevated AST & ALT with normal Normal AST & ALT with elevated + Normal liver enzymes
ALP ALP

Hepatocellular Obstructive In acute hepatitis there is marked


jaundice jaundice increased AST & ALT (above 100
iu) where in chronic liver disease
+ marked increase in total and direct their mild increase around 60 iu.
Check albumin bilirubin In obstructive jaundice the is
marked increase in both total and
Normal (3.5-5.5) Decreased <3.5 direct bilirubin more than
hepatocellular jaundice.
Acute liver disease Chronic liver disease
e.g. Acute hepatitis e.g. Cirrhosis

A/G ratio > 1 A/G ratio < 1

122
Total Bilirubin 0.85 mg/dl (N: 0.1-1.0)
Direct Bilirubin 0.35 mg/dl (N: 0.0-0.25)
AST 95 U/L (N: 0-37)
ALT 5 U/L (N:0-40)
ALP 140 U/L (N: 40-117)
Total Protein 7.4 g/dl (N: 7-9)
Albumin 2.9 g/dl (N: 3.5-5.5)

1-What is your diagnosis:


a- Obstructive jaundice c- Acute hepatocellular jaundice
b- Haemolytic jaundice d- Chronic liver disease
2-The following is correct for unconjugated bilirubin:
a- It is mainly increased in obstructive c- It is the minor form of bilirubin in
jaundice normal serum.
b- It is absent in normal serum d- It is increased in haemolytic jaundice
3-The following syndromes are associated with hyperbilirubinaemia:
a- Gilbert's syndrome c- Criggler-Najjar syndrome
b- Dubin-Johnson's syndrome d- All of the above
4-Increased serum direct bilirubin occurs in:
a- Thalassemia c- Obstructive jaundice
b- Renal failure d- Myocardial infarction
5-liver enzymes AST & ALT show maximum increase in:
a- Haemolytic jaundice c- Acute hepatitis
b- Myocardial infarction d- Obstructive jaundice

Total Bilirubin 5.1 mg/dl (N: 0.1-1.0)


Direct Bilirubin 0.3 mg/dl (N: 0.0-0.25)
AST 25 U/L (N: 0-37)
ALT 18 U/L (N:0-40)
ALP 40 U/L (N: 40-117)
Total Protein 7.5 g/dl (N: 7-9)
Albumin 5.0 g/dl (N: 3.5-5.5)

1-What is your diagnosis:


a- Obstructive jaundice c- Acute hepatocellular jaundice
b- Haemolytic jaundice d- Chronic liver disease
2-The following is correct for conjugated bilirubin:
a- It is mainly increased in haemolytic jaundice
b- It is absent in normal serum
c- It is the minor form of bilirubin in normal serum.
d- It is increased in obstructive jaundice
3-Reversed A/G ratio ocurrs in:
a- Gilbert's syndrome c- Obstructive jaundice
b- Dubin-Johnson's syndrome d- Liver cirrhosis
4-Increased serum 5-nucleotidase occurs in:
a- Thalassemia c- Obstructive jaundice
b- Renal failure d- Myocardial infarction
5-liver enzymes ALP show maximum increase in:
a- Haemolytic jaundice c- Acute hepatitis
b- Myocardial infarction d- Obstructive jaundice

123
Total Bilirubin 0.88 mg/dl (N: 0.1-1.0)
Direct Bilirubin 0.35 mg/dl (N: 0.0-0.25)
AST 95 U/L (N: 0-37)
ALT 57 U/L (N:0-40)
ALP 140 U/L (N: 40-117)
Total Protein 7.4 g/dl (N: 7-9)
Albumin 2.9 g/dl (N: 3.5-5.5)

1-What is your diagnosis:


a- Obstructive jaundice c- Acute hepatocellular jaundice
b- Haemolytic jaundice d- Chronic liver disease
2-The following is correct for cholesterol except:
a- It is mainly increased in obstructive c- Decreased in liver cell failure
jaundice d- Decreased esterification in liver
b- Normal level is 200 mg% cell failure
3-The following syndromes are associated with hyperbilirubinaemia:
a- Gilbert's syndrome c- Criggler-Najjar syndrome
b- Dubin-Johnson's syndrome d- All of the above
4-Increased prothrombin time occurs in .... except:
a- viral hepatitis c- Obstructive jaundice
b- Liver cell failure d- amebic liver abscess
5-liver enzyme ALT increase in:
a- Liver disease c- kidney
b- Heart d- All of the above
Total Bilirubin 4.5 mg/dl (N: 0.1-1.0)
Direct Bilirubin 3.0 mg/dl (N: 0.0-0.25)
AST 90 U/L (N: 0-37)
ALT 160 U/L (N:0-40)
ALP 50 U/L (N: 40-117)
Total Protein 7.5 g/dl (N: 7-9)
Albumin 5.0 g/dl (N: 3.5-5.5)

1-What is your diagnosis:


a- Obstructive jaundice c- Acute hepatocellular jaundice
b- Acute hepatitis d- Chronic liver disease
2-Alpha feto-ptn shows maximum increase in:
a- Haemolytic jaundice c- Acute hepatitis
b- Hepatocellular carcinoma d- Obstructive jaundice
3- Stercobilinogen in stool increase in:
a- Obstructive jaundice c- Acute hepatocellular jaundice
b- Haemolytic jaundice d- Chronic liver disease
4-Increased serum 5-nucleotidase occurs in:
a- Thalassemia c- Obstructive jaundice
b- Renal failure d- Myocardial infarction
5-liver enzyme AST increase in:
a- Liver disease c- kidney
b- Heart d- All of the above
1-In haemolytic jaundice the following increase EXCEPT:
a- direct bilirubin c- LDH
b- total bilirubin d- heptoglobin
2- Chronic liver disease causes bleeding tendency due to:
a- decreased prothrombin synthesis b- decreased Vit K absorption
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c- increased platelet dysfunction d- All of the above
3- Alkaline phosphatase enzyme increase in:
a- Obstructive jaundice c- Chronic liver disease
b- bone diseases d- all of the above.
4-Alpha feto protein increases in the following EXCEPT:
a- Hepatocellulcar carcinoma c- cirrhosis
b- hepatitis d- haemolytic jaundice
5-serum amylase increases in:
a- Liver disease c- renal failure
b- chronic pancreatitis d- non of the above
1. 1- d 2- d 3- d 4- c 5- c 4. 1- b 2- b 3- d 4- c 5- d
2. 1- b 2- d 3- d 4- c 5- d 5. 1- d 2- d 3- d 4- d 5- b
3. 1- d 2- c 3- b 4- d 5- a

KIDNEY FUNCTION TESTS


 Non-Protein Nitrogenous Compounds (NPN)
They are the products of catabolism of proteins & nucleic acids; they include ammonia, urea,
creatine, creatinine & uric acid.
 Serum urea (N: 20-40 mg/dl)
 Major NPN of protein catabolism.  Formed from ammonia in the liver
 Rate of synthesis depends on exogenous intake of protein & endogenous catabolism of protein.
 Excreted mainly through the kidneys.
 Blood urea level increases due to:
I. Renal causes (  excretion of urea ) e.g. renal impairment and failure.
II. Non-renal causes ( synthesis of urea):
- High protein diet. - Muscle wasting (starvation).
- Digestion of protein after GI bleeding. - Dehydration (sweating,  intake).
- Increased protein catabolism.
- Blood urea level decreases due to excess hydration, -- intake of ptn, ATN (-- reabsorption).
 Serum creatinine (N: 0.5-1.5 mg/dl )
 Creatinine is a waste product of creatine produced from muscles; where the amount of creatinine
produced is related to muscle mass.
 Creatinine is excreted by the kidneys.
 It is used as an indicator for glomerular function since it is of nearly main endogenous origin not
affected by nutrition; also its amount is little compared to urea so not affected by hydration or
dehydration, also in the kidney it is minimally excreted in the tubules which means that all
filtrated creatinine are almost excreted, while urea undergoes excretion and reabsorption so
creatinine is better indicative to GFR than urea..
 Creatinine clearance (N: 90-120 ml/min )
 It is an indicator of glomerular function.
 Clearance = UXV/P. U = Urine creatinine (mg/dl) V = Volume of urine (ml/min)
P = plasma (Serum) creatinine (mg/dl)
N.B.:
 Urea measuring is not a good test  Creatinine clearance is the best sensitive
because urea is affected by many causes test as it is not affected by other causes
e.g. exogenous intake, hydration. and also it detects early decrease in
 Creatinine measuring is not a good test kidney function.
because Creatinine is affected by many  In renal failure there is increased serum
causes e.g. muscular built of the person. creatinine with decreased creatinine
clearance.

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Normal Nephrotic syndrome CRF
 Blood urea 10-50 mg/dl Normal  250 
 Serum creatinine 0.5-1.5 mg/dl Normal  10 
 Serum uric acid 3.5-7 mg/dl Normal 
 Serum phosphorus 2.5-5.0 mg/dl Normal 
 Serum calcium 8.5-10.5 mg/dl Normal 
 Serum Na 135-145 mmol/L Normal 
 Serum K 3.5-5.2 mmol/L Normal 
 Serum Glucose 70-110 mg/d1 Normal 
 Serum total protein 6.6-8.6 mg/d1 Normal normal
 Serum albumin 3.5-5.6 mg/d1  2.3  normal
 Serum cholesterol 100-250 mg/dl  350  

Kidney profile

Nephrotic Chronic
syndrome renal failure
- Serum albumin < 2.3 - Blood urea > 250
- Serum cholesterol > 350 - Serum creatinine > 10

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Nephritic syndrome Nephrotic syndrome Acute renal failure Chronic renal failure
1-Urine analysis
- Gross
1) Volume Oliguria Normal Oliguria<400ml/day, upto Polyuria3-4L/day,then
2) Aspect, colour Smoky/dark/haematuria Frothy, amber yellow anuria oliguria
3) Sp. Gravity Increased Increased Dark ‫بول غامق مركز‬ Pale ‫بول فاتح مخفف‬
4) pH Acidic Low+fixed 1010 in ATN Low+fixed 1010 in ATN
5) ptn ptnuria < 3.5 gm/day Heavy ptnuria >3.5
- Microscopic gm/day Mild ptnuria Mild ptnuria
6) cells RBC most imp.
7) casts Red cell most imp. Epith. + RBC
Lipid v. specific to it. Granular v. specific to it Broad casts specific to it
2-Kidney funct. IMPAIRED
- urea, creatinine ,  urea , creatinine  normal unless renal 
uric acid may  . failure occurs
- creat. clearance  ( -- GFR ) ,, ,, ,, ,, 
3-Biopsy. If prolonged case To see the pathology If persistent ARF > 4 weeks Reveals pathology
4-Radiology Normal Normal PUT , U/S in postrenal obst.
5-C&S if pus Normal Normal Normal Normal
cells
6-Bl. Electrolyte
- K
+
, H+ N -- K+ ++ K+ & ++ H+ As ARF but
+
- Na , HCO
-
O -- Na+ -- Na+ & - - HCO- Variable Na+
2+
- Ca , P
3+
R -- Ca2+ -- Ca2+ & ++ P3+ & hyperlipidaemia
- ptn M -- mainly albumin
- lipids AL ++Chlolest. / TGA
7-CBC Anemia(--ptn) ,++ESR Anemia(--ptn) Anemia Anemia(--erythropoetin)
Nephritic syndrome = 1) oliguria 2) nephritic oedema 3) HTN 4) haematuria
Nephrotic syndrome = 1) heavy ptnuria 2) hypoalbuminaemia 3) generalized oedema 4) hyperlipidaemia

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Report 1
Blood urea 250 mg/dl N 10-50mg/dl
Serum creatinine 10.5 mg/dl N 0.4-1.4 mg/dl
Serum uric acid 9.0 mg/dl N 3.2-7mg/dl
Serum phosphorus 7.0 mg/dl N 2.5-5.0 mg/dl
Serum calcium 7.1 mg/dl N 8.5-10.5 mg/dl
Serum Na 139 mmol/1 N 135-145 mmol/1
Serum K 5.8 mmol/1 N 3.5-5.2 mmol/1
Serum Glucose 96 mmol/1 N 70-110 mmol/1
Serum total protein 7 mmol/1 N 6.6-8.6 mmol/1
Serum albumin 4.6 mmol/1 N 3.5-5.6 mmol/1
Serum cholesterol 150 mg/dl N 100-250 mg/dl

1-Serum creatinine
a- Is affected by liver disease c- Always elevated in nephrotic syndrome
b- Mainly endogenous in origin d- Not related to muscle mass
2- What is your diagnosis:
a-- Acute nephritic syndrome. b- Chronic renal failure
c- Nephrotic syndrome d- Chronic active hepatitis
3-In chronic renal failure:
a- Serum creatinine and uric acid are increases hypophosphataemia
b-There is metabolic alkalosis d-Serum AST and ALT are always elevated.
c-There is hypocalcemia and
4- Serum urea:
a- Is mainly excreted through GIT d-Its rate of synthesis does not depend on
b- Increases in chronic renal failure exogenous intake of nitrogen
c- Is higher in females than males
5- In nephrotic syndrome:
a- There is hypoalbuminaemia and proteinuria Less than 3 g/day
b- There is hypoalbuminaemia and hypocholesterolaemia
c- There is heavy proteinuria and hypoalbuminaemia
d- Increased urea and creatinine is a constant feature

Blood urea 140 mg/dl N 10-50mg/dl


Serum creatinine 3.1 mg/dl N 0.4-1.4 mg/dl
Serum uric acid 9.0 mg/dl N 3.2-7mg/dl
Serum phosphorus 7.0 mg/dl N 2.5-5.0 mg/dl
Serum calcium 7.1 mg/dl N 8.5-10.5 mg/dl
Serum Na 139 mmol/1 N 135-145 mmol/1
Serum K 5.8 mmol/1 N 3.5-5.2 mmol/1
Serum Glucose 96 mmol/1 N 70-110 mmol/1
Serum total protein 7 mmol/1 N 6.6-8.6 mmol/1
Serum albumin 4.6 mmol/1 N 3.5-5.6 mmol/1
Serum cholesterol 150 mg/dl N 100-250 mg/dl

128
1- In nephrotic syndrome:
a- Cholesterol is usually increased c- urea and creatinine are affected early
b- Heavy proteinuria is a cardinal symptom d- All of the above
2- What is your diagnosis:
a- Acute nephritic syndrome. c- Nephrotic syndrome
b- Chronic renal failure d- Chronic active hepatitis
3-In acute nephritic syndrome:
a- Serum creatinine and uric acid are increased glomerulonephritis
b- ASO titre may be elevated d- All of the above.
c- RBC casts are highly suggestive of
4- Serum urea:
a- Is mainly excreted through GIT d-Its rate of synthesis does not depend on
b- Increases in chronic renal failure exogenous intake of nitrogen
c- Is higher in females than males
5- In nephrotic syndrome:
a- There is hypoalbuminaemia and proteinuria Less than 3 g/day
b- There is hypoalbuminaemia and hypocholesterolaemia
c- There is heavy proteinuria and hypoalbuminaemia
d- Increased urea and creatinine is a constant feature
1. 1- b 2- b 3- a 4- b 5- c 2. 1- d 2- b 3- d 4- b 5- c

Blood sugar profile


U

Normal Renal Hyperglycaemia Diabetes


glycosuria IFG IGT Melitus
 Plasma
- FPG 70-110 110-126 <126 >126
- Peak I hr <160 >200
- 2 hrs 70-140 140-200 >200
 Urine Absent present Absent Absent May be
Diagnosis of DM
WHO diagnostic criteria - 1999 are:
 Fasting plasma glucose > 7.0 mmol/L (126 mg/dL)
 Random plasma glucose > 11.1 mmol/L (200 mg/dL)
 One abnormal laboratory value is diagnostic in symptomatic individuals; two values are needed in
asymptomatic people.
U
 Indications:
The glucose tolerance test is only required for borderline cases and for diagnosis of gestational
diabetes.
 Procedure:
 Adult: 75 g glucose in 300 mL water.
 Only a fasting and a 2 hrs sample are needed.
Results are 4 venous plasma samples (every half an hour for 2 hours) and 2 urine samples at 1 and 2
hour.
 Types:
1-Normal curve: see the table.
2-Diabetic curve: see the table
3-Flat curve:
Blood glucose rises very little. Causes …
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Malabsorption.,Myxoedema, Addison's disease & hypopituitarism.
4-Lag curve:
There is rapid rise of blood glucose and the peak is higher than normal, but the curve returns
to normal in less than 2 hours. Causes:
1. Gastrectomy or gastroenterostomy (rapid absorption).
2. Hyperthyroidism (rapid metabolism ).
3. Chronic severe liver disease (delayed storage of glucose).
5-Renal glycosuria:
Normal curve associated with glucose in urine indicating decreased renal threshold for glucose.
Normal renal threshold is 180 mg/dl. Renal glycosuria is presence of glucose in urine at lower
plasma glucose level i.e. decreased renal threshold.

Check FPG
check FPG

70-110 >126
>126 >200
check 1 hrs PPG check 2 hrs PPG
(peak) D.M.
70- 140 140-200
<160 160 >160
IFG IGT
Flat Lag
curve curve

check urine

glucose absent

Renal Normal
glycosuria
130
Examples
Blood sugar Urine Sugar Acetone
IGT Fasting: 130 mg/dl Nil Nil
30 min: 180 mg/dl Nil Nil
60 min: 170 mg/dl Nil Nil
90 min: 170 mg/dl Nil Nil
120 min: 150 mg/dl Nil Nil

Renal glycosuria Blood sugar Urine Sugar Acetone


Fasting 90 mg/dl Nil Nil
30 min: 110 mg/dl + Nil
60 min: 160 mg/dl + Nil
90 min: 140 mg/dl + Nil
120 min: 100 mg/dl + Nil

Flat curve Blood sugar Urine Sugar Acetone


Fasting 90 mg/dl Nil Nil
30 min: 100 mg/dl Nil Nil
60 min: 120 mg/dl Nil Nil
90 min: 95 mg/dl Nil Nil
120 min: 80 mg/dl Nil Nil
Lag curve
Blood sugar Urine Sugar Acetone
Fasting: 145 mg/dl Nil Nil
30 min: 180mg/dl Nil Nil
60 min: 230 mg/dl Nil Nil
90 min: 280 mg/dl Nil Nil
120 min: 210m2/dl Nil Nil
normal Blood sugar Urine Sugar Acetone
Fasting: 80 mg/dl Nil Nil
30 min: 200 mg/dl + Nil
60 min: 80 mg/dl Nil Nil
90 min: 50 mg/dl Nil Nil
120 min: 90 mg/dl Nil Nil

D.M. with ketoacidosis


Blood sugar Urine Sugar Acetone
Fasting 200 mg/dl + Nil
30 min: 280 mg/dl ++ Nil
60 min: 310 mg/dl +++ +
90 min: 450 mg/dl +++ +
120 min: 500 mg/dl ++++ +

131
thyroid profile

Primary Primary secondary


Normal hyperthyroidism hypothyroidism hypothyroidism
FT3 1.3-5.0 pg/dl   
FT4 0.8-2.0 pg/dl   
TSH 0.3-5.0 IU/ml   

 Primary means the cause is in the thyroid gland


 Secondary means the cause is in not in thyroid gland usually pituitary or hypothalamus
 In primary hyperthyroidism the thyroid gland secrets excess thyroxine causing a
negative feedback on the pituitary gland leading to decreased TSH secretion.
 Free thyroxin (FT3, FT4) is not bounded to plasma ptn; so it isn't affected by ptn metabolism.

Check FT3

Increased Decreased
+ low TSH
Check TSH
Primary
hyperthyroidism Increased Decreased

Primary Secondary
hypothyroidism hypothyroidism
Examples
1. Primary hypothyroidism. 3. Hyperthyroidism (primary).
FT3 0.4pg/dl (N: 1.3-5.0) . FT3 6.7 pg/dl (N: 1.3-5.0).
FT4 0.2 pg/dl (N: 0.8-2.0).
FT4 4.9 pg/dl (N: 0.8-2.0).
TSH 85 IU/ml (N: 0.3-5.0).
TSH 0.01 IU/ml (N: 0.3-5.0).
2. Pituitary hypothyroidism.

FT3 0.4 pg/dl (N: 1.3-5.0).


FT4 0.2 pg/dl (N: 0.8-2.0).
TSH 0.05 IU/ml (N: 0.3-5.0).

FT3 6.7 pg /dl (N: 1.3-5.0).


FT4 4.9 pg /dl (N: 0.8-2.0).
TSH 0.01 IU/ml (N: 0.3-5.0).

1- What is your diagnosis ?


a- Primary hypothyroidism c- Primary Hyperthyroidism.
b- Secondary hypothyroidism d- Secondary hyperthyroidism

132
2- Increased serum T3 & T4 with increased serum TSH is a charecteristic of
a- Primary hypothyroidism c- Primary Hyperthyroidism.
b- Secondary hypothyroidism d- Secondary hyperthyroidism
3- To differntiate Primary from Secondary hypothyroidism the following test is
done
a- Fee T3 b- Free T4 c- TSH d- PTH
4- FT4 is better than total T4 beacause it is affected by
a- Fasting c- Blood glucose level
b- Plasma ptn d- Muscle mass
5- In thyrotxicosis oral glucose tolerance test is
a- Flat curve c- Lag curve
b- Diabetic curve d- Normal curve

ANSWERS 1- c 2- a 3- c 4- b 5- c

Cardiac enzymes & proteins


U Blood Levels of cardiac enzymes
Normal Recent MI Old MI
o CK-MB 0-25 U/L  40 20
o CK 0 -170 U/L  300 140
o AST 0- 36 U/L 23 30
o LDH 240- 480 U/L 360 790
U onset & duration of cardiac enzymes elevations
Onset (hrs) Duration (days)
Back to normal in
- CK-MB 3 (3 x 1) 3
- CK 6 (3x2) 4
- AST 12 (3 x 4) 5
- LDH 24 (1 day) 15 (2 w)
1- Troponin T & I:
- It is a specific cardiac protein .i.e. raised in myocardial damage only .
- Rises after 2 hours, peak in 12 hours & normalizes in 2 days.
2- Creatine kinase (CK & CK-MB):
- CK: raised in myocardial & skeletal muscle damage.
- CK-MB: raised only in myocardial damage so more specific than CK.
the first enzyme to rise and the first to normalize.
CK-MB is cardiac isoenzyme of CK .
3- Aspartate aminotransferase (AST):
- Rises in myocardial & skeletal muscle & liver damage (non-specific).
4- Lactic dehydrogenase (LDH& LDH1):
- LDH: rises in myocardial & lung damage and haemolysis.
- LDH1: rises only in myocardial damage.
- LDH is the last enzyme to rise and the last to normalize

133
check CK-MB

 > 40 N : 20

Check AST
AMI
Within 3 days  <23 Decreased

AMI check LDH


Within 6 days
360  > 790

AMI OMI
Within 2 weeks Within 2 weeks
U diagnosis of ami
1- TYPICAL chest pain of infarction U importance of enzymes
2- ECG 1- Confirm diagnosis
3- Cardiac enzymes 2- Timing of infarction
3- Detect the efficacy of the ttt
Changes in plasma enzyme
concentrations after myocardial
infarction. Creatine kinase (CK) and
troponin T (TnT) are the first to rise,
followed by aspartate
aminotransferase (AST) and then
lactate (hydroxybutyrate)
dehydrogenase (LDH). In patients
treated with a thrombolytic agent,
reperfusion is usually accompanied
by a rapid rise in plasma creatine
kinase (curve CK (R)) due to a
washout effect; if there is no
reperfusion, the rise is less rapid but
the area under the curve is often
greater (curve CK (N)).

o CK-MB 60 U/I N: 0-24 U/L


o CK 500 U/I N: 0 -170 U/L
o AST 30 U/I N: 0-32 U/L
o LDH 180 U/I N: 240-480 U/L

1- In acute myocardial infarction:


a- estimation of CK, CK-MB , AST are useful
b- AST is specific to the myocardium.
c- Serum enzymes start to rise 1 hour after the onset of the pain.
d- CK is mote specific than CK-MB.

134
2- One of the following plasma enzymes is frequently abnormal in acute myocardial
infarction:
a- Alkaline phosphatase c- LDH
b- Amylase d- Glucose-6-phosphate dehydrogenase.
3- In patients with acute myocardial infarction:
a- AST is the first enzyme to return to normal
b- After one week LDH is still elevated.
c- CK-MB reaches its peak after one week.
d- CK starts to rise 3 days after the pain.
4- This cardiac profile probably belongs to a case of :
a- Angina pectoris c- Recent myocardial infarction
b- Unstable angina d- Acute myocardial infarction > two WEEKS
5- CK:
a- Its estimation is only useful in cases of muscle dystrophy.
b- It is of great value in diagnosis old myocardial infarction
c- Returns to normal in about 3 days following onset of pain.
d- Is not a useful marker of myocardial infarction .
o CK-MB 5 U/I N: 0-24 U/L
o CK 80 U/I N: 0 -170 U/L
o AST 30 U/I N: 0-32 U/L
o LDH 500 U/I N: 240-480 U/L
1- CK-MB:
a- Peaks 30 min after the onset of pain
b- Is the last of the cardiac enzymes lo return in normal.
c- ls cardiac isoenzyme of CK
d- Its determination is useful in the second week , following the infarction
2- LDH
a- Reaches its peak 6 hours after the onset of pain.
b- Is the last of the cardiac enzymes lo return to normal.
c- Is specific to the myocardium.
d- Returns to normal levels 2 days after the onset of pain
3- AST:
a- Is the first of the cardiac enzymes to rise and to return to normal.
b- Is elevated only in cases of acute myocardial infarction.
c- elevated in patients suffering from acute viral hepatilis.
d- Returns to normal 48 hours following the onset of pain.
4- The diagnosis of this case may be:
a- Acute pancreatitis.
b- Recent myocardial infarction.
c- Angina pectoris.
d- Myocardial infarction occurring more than 5 days ago.
5- One of the following plasma enzymes is frequently normal in acute myocardial infarction:
a- Alkaline phosphatase
b- Amylase
c- LDH
d- Glucose-6-phosphale dehydrogenase.
1- a 2- c 3- b 4- c 5- c 1- c 2- b 3- c 4- d 5- c

135
Oral questions in clinical pathology
U Laboratory investigations of …….
 Blood: Anaemias , Leukaemia , Purpura.
 GIT: Jaundice, Liver functions, hepatitis markers.
 Infection: Widal test, Brucella, IBV.
 Cardiology: Cardiac enzymes.
 Nephrology: Laboratory investigations ARF, CRF.
 Neurology: Differentiation bet. CSF.
 Rheumatology: SLE, Rheumatoid arthritis.
 Endocrine : DM

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benefit for the future students. nassefintouch@hotmail.com
NB: the exact words of the MCQ are not totally required at least the idea in the question given to you.

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