Approach to

Patients with

Anemia
Prof. Dr / Nabil Lymon
Blood Cells
and
Hemoglobin
structure
 :Definitions
- Anemia :
is defined as the lowering of hemoglobin
concentration below the established normal
levels:
In male < 13.5 gm/dl & In female < 11.5 gm / dl.
- Anemia is a clinical sign not a diagnostic
entity.

- Hematocrit (Hct):
is the proportion, by volume, of the blood
occupied by red blood cells. The hematocrit
(Hct) is expressed as a percentage, normal
levels are :
0.4 - 0.54 in Adult male & 0.37 - 0.47 in Adult
 :Definitions
Red Cell Indices
Are measurements that indicate the size
and hemoglobin content of red cells:
M.C.V (Mean Corpuscular Volume)

M.C.H (Mean Corpuscular

Hemoglobin)

M.C.H.C (Mean Corpuscular Hemoglobin

Concentration)
 M.C.V (Mean Corpuscular Volume):
Referred to the average volume of red cells , normally = 76 -
96 fl
It can be calculated from an independently-measured red
blood cell count and hematocrit:

MCV  (femtoliters) = 10 x HCT(percent) ÷ RBC

(millions/µL)

MICROCYTOSIS & MACROCYTOSIS : 

By definition, microcytosis is taken to mean the presence of
RBCs with a MCV less than normal, while macrocytosis
means the presence of RBCs with an MCV greater than
normal.
 M.C.H (Mean Corpuscular
Hemoglobin):

or "mean cell hemoglobin" (MCH), is a measure of the

mass of hemoglobin contained by a red blood cell.
It is diminished in microcytic anemias, and
increased in macrocytic anemias. It is calculated
by dividing the total mass of hemoglobin by the
RBC count :-
MCH=Hb/RBC
A normal value in humans is 27 to 32 picograms/cell
 M.C.H.C
(Mean Corpuscular Hemoglobin
Concentration):

is a measure of the concentration of hemoglobin in a

given volume of packed red blood cell.
It is diminished ("hypochromic") in microcytic
anemias, and normal ("normochromic") in
macrocytic anemias (due to larger cell size, though
the hemoglobin amount or MCH is high, the
concentration remains normal).
It is calculated by dividing the hemoglobin by the
hematocrit:
 Signs &Symptoms of
Anemia
- Cardiovascular :
Exertional Dyspnea Palpitations
Orthopnea
Tachycardia Angina
Claudications
Cardiomegally Bounding
peripheral Pulses
Murmurs Vascular bruits
Pedal edema

- Neurological :
Headache Tinnitus
Dizziness
 Signs &Symptoms of
Anemia
- Skin :
Pallor of skin , mucous membranes, nail beds and palms.
- Gastrointestinal :
Anorexia Nausea
Constipation
Diarrhea
- Respiratory :
Increased Respiratory Rates
- Genitourinary :
Menstrual irregularity Amenorrhea
Menorrhagia
Loss of libido or potency
- Fundus Examination :
Is the patient Anemic or
not ?
Anemic means single or
total decrease in :
- Hb
- Hct
- RBCscount
inBut …?
millions

What Type of Anemia..?

This depends on the RBCs
indices
 Red Cell Indices
According to MCV & MCH
Normal Decreased

Normocytic Microcytic
Normochro
mic Anemia Increased Hypochromi
c Anemia
Macrocytic

Anemia
 Anemia
It may be due to :
- Acute Blood Loss

- Aplastic Anemia
- Hemolytic Anemia ( Except
Thalasemia)
Which of Which ….? (Anemia Of Chronic
- A.O.C.D
(Diseases Do Reticulocytic
Count
Normal Low or High
A.O.C.D Absent - Acute Blood
e.g.: B.M.F Loss
TB, SLE, “Aplastic ( search for
Malignancy, Rh. evidence of
Arthritis Anemia”
the cause)

Note: BM biopsy or BM
- Evidence of the aspiration - Hemolytic
cause show :
 - low Hb &/or Hct & /or RBCs count
- Normal RBCs indices
- Reticulocytosis

Do Indirect Serum Billirubin

Unconjugated Hyper-
billirubinemia
“
jaundice”

Other Evidences of Hemolysis e.g.:-

- Hemoglobinuria - Hemoglobinemia
(increased free Hb)
- Decreased Haptoglobin.

What is the Further

?..………Step Coombs Test
 Coombs Test
Positive Negative
Immune Non-immune
Hemolytic Hemolytic
Anemia: Anemia:
May be due to :
- Membrane Defect e.g.
Spherocytosis (lab
- Iso immune show increased O.F.) &
P.N.H
- Auto immune - Enzyme Defect
e.g. G6PD (lab : Enz. assay)
- Hb Defect
(Hemoglobinopathy)
Red Cell Indices
According to MCV & MCH
Decreased

Microcytic

Increased Hypochromi
c Anemia
Macrocytic

Anemia
Microcytic Hypochromic
Anemia
- The Commonest Cause is:
Iron Deficiency Anemia
-Other Causes: - Thalasemias
- Sedroplastic Anemia
- Lead Poisoning
- A.O.C.D
Which of Which….?
:Do Iron Studies
- Serum Iron
- Serum Ferritin
- T.I.B.C (Total Iron Binding
Capacity)
- Transferrin Saturation
 According to Iron Studies
Iron Thalasse Sideropla A.C.O.D
Deficienc mia stic
y Anemia Anemia
Serum
Fe
Serum Normal N or
Ferritin
T.I.B.C Normal

Transferr
in
Saturatio
Iron Deficiency Anemia
Iron Deficiency Anemia
Iron Notes:
Studies - Search For The
Serum Fe Cause:
e.g.:
Serum Chronic Blood Loss
Ferritin
Ankylostoma
T.I.B.C
Cancer Colon
Nutritional causes
Transferri
n - Severe Aniso-cytosis
Saturatio and Poikilo-cytosis:
n Increased R.D.W(N ≤
13%)
Anisocytosis with
hypochromia and
(microcytes (IDA
Spoon Nails:
If nails look scooped out, like a
spoon, it could be a sign of iron-
.deficiency anemia
Plummer Vinson Syndrome
Left : Spoon shaped finger nails
Right :Showing angular cheilitis, and
dry skin
Plummer Vinson
Syndrome
Iron Deficiency Anemia
 Thalassemia
Iron Notes:
Studies - Hb Electrophoresis
Serum Fe will show:
Persistence of
Serum Hb[f]
Ferritin
- Specific Clinical
T.I.B.C Features of
Thalasemia:
Transferri
Huge Spleen
n
Saturatio Mongoloid Faces
n Hemosedrosis
Thalassemia minor
is an inherited form of hemolytic anemia that
is less severe than thalassemia major. This
blood smear from an individual with
thalassemia shows small (microcytic), pale
(hypochromic), variously-shaped
(poikilocytosis) red blood cells. These small
red blood cells (RBCs) are able to carry less
oxygen than normal RBCs
Thalassemia, being a genetic disease, runs in
a family. Most are silent carriers or suffer
mild anemia. Severe cases such as the
Hemoglobin H disease with enlarged spleen,
small body and malnourished look shows
more prominent symptoms.[Pic below:
[Enlargement of spleen, small body
 Sideroplastic Anemia
Iron Notes:
Studies Sedroplastic Anemia
Serum Fe is due to:
- B6 Deficiency
Serum Norma - Drugs e.g.: INH
Ferritin l - Inherited
T.I.B.C Norma
Blood film show:
l
Transferri RBCs contain Iron
n Granules
Saturatio Treated by:
n B6 supply
Many rounded sideroblasts are present
in this field. This is the hallmark
feature ofsideroblastic anemia
 Lead Poisoning
Notes:
- History is Suggestive.
- Elevated Serum Lead level.
- Purely Motor Neuropathy (foot and
wrist drop)
- Blood Film show:
Basophilic Stippling of RBCs
Basophilic Stippling of
RBCs
Basophilic stippling appears as round, dark-
blue granules in red blood cells on smears
stained with supra vital stains such as
brilliant cresyl blue.
They may be observed inlead poisoning,
exposure to some drugs, severe burns,
anemia, or septicemia. The granules are
precipitated ribosomes and mitochondria
Red Cell Indices
According to MCV & MCH

Increased

Macrocytic

Anemia
Macrocytic
Anemia
- In Which :
- low Hb &/or Hct & /or RBCs count
- Increased RBCs indices
- Causes :
# Folic Acid Deficiency # B12 Deficiency

- Search For The Cause:

# Pregnancy # Mal-absorption
Syndrome
# Chronic Gastritis # Atrophic Gastritis
# Cancer Stomach # Iliac Resection
# Drugs: Methotrexate / Metformin / Epanutin

- To be sure do the following tests:

Serum Folic Acid / Serum B12 /
Schilling test / FIGLU test
Schilling
Test
The Schilling test is
performed to evaluate
vitamin B12 absorption.
B12 helps in the
formation of red blood
cells, the maintenance of
the central nervous
system, and is important
for metabolism.
Normally, ingested
vitamin B12 combines
with intrinsic factor,
which is produced by
cells in the stomach.
Intrinsic factor is
necessary for vitamin
B12 to be absorbed in
the small intestine.
Certain diseases, such as
pernicious anemia, can
result when absorption
of vitamin B12 is
FIGLU test
a test of vitamin b12 deficiency,
folic acid deficiency, liver disease,
or genetic deficiency of glutamate
formimino-transferase, based on
urinary excretion offormimino-
glutamic acid (figlu), an
intermediate metabolite in
histidine catabolism in the
conversion of histidine to glutamic
acid, with the formimino group
being transferred to
.tetrahydrofolic acid
(commentary) -1
 A healthy 52-year-old man presents to the
doctor’s office complaining of increasing
fatigue for the past 4-5 months. He
exercise every day but lately he has
noticed becoming short of breath while
jogging.
 He denies orthopnea. Paroxysmal
nocturnal (PND), or swelling in his ankles.
The patient reports occasional joint pain
for which he uses over the counter
ibuprofen.
 He denies bowel changes, melena or
bright red blood per rectum, but reports
vague left side abdominal pain for a few
months off and on, not related to food
intake. The patient denies fever, chills,
.Cont
 On examination, his weight is 90kg and he
is aferbrile. There is slight pallor of
conjunctiva, skin and palms.
 No lymphadenopathy is noted chest is
clear to auscultation bilaterally.
 Cardiovascular system: regular rate and
rhythm, with no rub or gallop.
 There is a II/IV systolic ejection murmur.
 His abdomen is soft, nontender and
without hepato-splenomegaly.
 Bowel sounds are present. He has no
extremity edema, cyanosis or clubbing.
 His peripheral pulses are palpable and
symmetric. A hemoglobin level is 9.2g/dl,
MCV 75µ3
 What is the differential diagnosis
such case?
 Investigations of insulin
malabsorption
 Comprehension
Questions
1- A 25year-old man with a history of a
duodenal ulcer is noted to have a
hemoglobin level of 10g/dl. Which of
the following is most likely to be seen
on laboratory investigation?
a- Reticulocyte count of 4%.
b- Elevated total iron-binding capacity
(TIBC).
c- Normal serum ferritin.
2- A 22-years-old Woman is pregnant and 14 weeks
gestation. Her hemoglobin level is 9g/dl. She
asks why she could have iron deficiency when
she is no longer menstruating. Which of the
following is the best explanation:

a- Occult gastrointestinal blood loss.

b- Expanded blood volume and transport to

the fetus

c- Hemolysis
3- A 35-year-old man has undertaken a self
imposed diet for 3 months previously, he
has been healthy, but now complains of
fatigue. His hemoglobin level is 10g/dL
and his MCV is 105fL. Which of the
following is the most likely etiology of his
anemia?
a- Iron deficiency
b- Folate deficiency
c- Vitamin B12 deficiency
d- Thalassemia
e- Sideroblastic anemia
 Match the following laboratory
parameters (a to e ) to the clinical
(picture (4 to 6
MCV Ferritin TIBC RDW
a- Elevated Decreased Elevated Decreased

b- Decreased Elevated Increased

Decreased
c- Normal Elevated Normal Normal

d- Increased Normal Normal

Decreased
e- Elevated Increased Decreased Increased

4- A 20 year-old woman with heavy menses.

5- A 34 year-old man of Mediterranean
descent with a family history of anemia.
6- A 50 year-old man with severe
rheumatoid arthritis.
 Conclusions
 Anemia is a clinical finding, not a
diagnosis and requires some
investigation to determine the
underlying etiology.
 Iron deficiency anemia in men or
postmenopausal women is primarily
a result of gastrointestinal blood
losses; therefore, finding iron
deficiency anemia in this patient
population warrants a through GI
workup.
.Cont
 The fecal occult blood testing (FOBT)
is negative in about 50% of patients
with GI cancer. Therefore, a negative
FOBT in the presence of iron
deficiency anemia should not
discourage you from pursuing a
through GI workup.
 The mean corpuscular volume, RDW
and the reticulocyte index are
important parameters in the
evaluation of anemia.
Polycythaemia
 Polycythaemia refers to an increase
in red cell count, haematocrit and
usually haemoglobin.
 There are two main types of
polycythaemia, the classification
depending on the results of
measurement of red cell mass and
plasma volume:
 Relative (pseudo) polycuthaemia: due
to decrease in plasma volume.
 True polycythaemia: the red cell mass in
increased.
 Primary true
polycythaemia
In the meloproliferative disorder
polythaemia rubra vera (PRV), there is
uncontrolled production of red cells by the
marrow, even though erythropoietin is
switched off.
 Clinical features: hypertension,
splenomegaly, arterial and venous
thrombosis, pruitus, plethoric features,
peptic ulceration, gout.
 Laboratory features: there is high red
cell count, haemoglobin, haematovril,
whole blood viscosity and uric acid. The
white cell count, platelete count and
 Secondary true
polycythaemia
 This condition is associated
with increased levels of
erythropoietin, which is
produced by other the kidney
or an ectopic tumor.
 Cause of secondary
polycythaemia
Increased renal erythrpoietin
production due to hypoxia
• Physiological
Adaptation to altitude in neonates (eg pyonephrosis, renal cysts,
• Congential cyanotic heart
disease
(eg Fallot’s tertragoly,
Eisenmenger’s complex)
• Respiratory related
Smoking
COPD
•High- affinity haemoglobins
(eg haemoglobin M)
Inappropriate erythropoietin
production
• From the kidney
renal artery stenosis after renal
transplantation)
• From a tumor (ectopic
erythropoietin secreted in an
uncontrolled fashion)
(eg carcinoma of the kideny,
giant uterine fibroids, hepatoma,
cerberallar haemangioma)
Relative polycythaemia
 A reduction in circulating plasma volume
can be to pyrexia, diarrhoea, vomiting and
diuretic therapy.
Gaisbok’s polycythaemia
 Refers to a from of stress polycythaemia;
this has been noticed in middle-aged men
who have stressful occupations, a
chronically reduced plasma volume of
uncertain cause.
Treatment of polycythaemia
 Treatment is indicated for polycythaemia
as high blood viscosity leads to an
 Venesction to a great haematocril: the
packed cell volume is more closely related
to the blood viscosity than is the
haemoglobin (as repeated vensection may
result in iron-deficient red cells with a low
haemoglobin content). Venesection may
be traditional or isovolamic (with saline
replaement). The latter is used in patients
with cardiovascualr risk factors (eg angina
or hypertension), in those who are taking
drugs that may impair physiological
response to vensection (ACE inhibitors,
beta blockers), or in patients with relative
 Cytotoxic agent (particularly
hydroxyurea): this presuppose
erythropoiesis ad cause a
macrocytosis which is not related to
vitamin B12 or folate deficiency.
Unlike other cytotoxic agents (eg
busslfan) it is unlikely to be
leukaemogenic.
 Aspirin and anticoagulants: if the
patient presents with thrombosis.
Multiple
myeloma
 Myeloma
 In myeloma there is a clonal proliferation
of plasma cells and the clinical
manifestations of disease "= are -Mated to
substances secreted by the plasma cells
as much as to the effects of marrow infil­
tration. Clonality (all diseased cells
originating from one parent plasma cell)
may be confirmed by: 
 the presence of a paraprotein (monoclonal)
band on serum electrophoresis, or by
 Immunopheno typing the increased numbers of
plasma cells in the bone marrow, and finding,.
that they all express either kappa or
 Paraprotein sub-types
 The normal immunoglobulin
concentrations in serum
parallel the relative frequency
of the three main sub-classes
of myeloma paraprotein.
Hence, IgG is the most
common form of myeloma,
followed by IgA, with IgM
being the least common type.
 Plasma hyperviscosity syndrome may
be found This: consists of confusion,
capillary bleeding, oedema and renal
impairment. The incidence of
hyperviscosity syndrome relates to
the size of the immunoglobulin
molecule as well as its concentration.
As IgM is the largest molecule (750,
000 daltons) this syndrome is seen
relalatively frequently in IgM
myeloma, less frequently in IgA
myeloma and rarely in IgG myeloma:.
Transfusion should be avoided in
 Cryoglobulin: rarely, the
paraprotein may be a
cryoglobulin, so that the protein
precipitates from plasma in the
cold. This may be a cause of
vasculitis. Some myeloma
paraproteins precipitate within
 Bence-Jones protein
 Sometimes, the malignant plasma
cells are so defective that they
cannot make a complete
immunoglobulin molecule and are
only able to make light chains. The
latter are small enough to he filtered
within the glomerulus and to appear
in the urine as Bence-Jones
proteinurias. They may obstruct the
renal tubules and contribute to the
renal failure which is often found in
Role of cytokines in myeloma
 Osteoclast-activating factors
stimulate the normal osteoclasts
to dissolve bone and lead to
bone pain, hypercalcaemia and
pathological fractures in
myeloma. In other myeloma
cases, IL -6 may be produced in
excess by bone marrow stromal
cells infected with human herpes
virus (HHVB).
Treatment of myeloma
 Inn younger patients, most centers are
moving away from single-agent melphalan
therapy towards continuous low-dose
combination chemotherapy such as VAD
(Vincristine, Adriamycin and
Dexamethasone) or ZDex (oral idarubicin
and dexamethasone). Malignant cells are
most sensitive to the action of
chemotherapy when they are dividing; as
plasma cells divide relatively infrequently,
it is necessary to administer the
chemotherapy over several days in order
 Thalidomide has a proven role in
myeloma treatment although its
mechanism of action remains
uncertain. It is likely to inhibit
cytokine release, but an anti-
angiogenesis activity has not been
ruled out.
 Bisphosphonates, such as monthly
intravenous pamidronate, have an
important role in the prevention off
pathological fractures and in the
 Monoclonal gammopathy of
undetermined significance (MGUS)
 A common clinical problem is the
differentiation between myeloma and
MGUS (benign monoclonal
gammopathy) in patients found to
have a paraprotein. Ten per cent of
patients with MGUS develop
myeloma at 5 years, and 50% at 15
years. It is probable that most
patients would eventually develop
myeloma but many die of other
 Differentiation of myeloma from
MGUS

MGUS Myeloma
Low level of paraprotein (< 20 High level of
g/I for an IgG paraprotein) paraprotein
Paraprotein level remains Level rises
stable over a period of Other
observation depressed immunoglobulin
(months or years) levels are depressed
Other immunoglobulin levels Clinical evidence of
are normal myeloma
No clinical evidence of
myeloma
(bone disease, renal disease)
 Summary
 It is a malignancy of B-lymphocytes.
 The malignant plasma cells and their
lymphocytes precursor are present in
the bone marrow. Sometimes they
are detected in the peripheral blood
and in soft tissue.
 The tumor cells secrete factors
which:
 Activate osceoclasts which destroy the
bone.
 Suppress bone marrow function.
Laboratory findings
 CBC: Anemia (normocytic and
normochromic)
 ESR: Increased
 Renal function:
 Decreased
 Blood urea sr. creatinine increased
 Serum calcium: Increased
 Serum alkaline phosphatase: Normal.
 Serum total proteins:
 Elevated
 Protein electrophoresis +
immunoelectrophoresis  monoclonal band.
 Immunoglobulin level:
 Increase of the type affected

 B.M
 Infiltration with malignant plasma cells.

 Urine analysis:
 Bone jones proteins may be presents.

 B2- microglobulin: Increased

Diagnosis
 Two of the following criteria should
be present:
 Bone marrow infiltration by more than
30% of malignant plasma cells.
 Osteolytic bone lesions.
 Presence of monoclonal Ig in blood
and/or urine, as a whole molecule or as
light chains.
Commentary
 A healthy 52-year-old man presents to the
doctor’s office complaining of increasing
fatigue for the past 4-5 months. He
exercises every day but lately he has
noticed becoming short of breath while
jogging, he denies orthopnea, paroxysmal
nocturnal (PND), or swelling in his ankles.
The patient reports occasional joint pain
for which he uses over the counter (OTC)
ibuprofen, he denies bowel changes,
melena or bright red blood per rectum, but
reports vague left side abdominal pain for
 The patient denies fever, chills, nausea or
vomiting, he has lost a few pounds intentionally
with diet and exercise. On examination, his
weight is 90kg and he is aferbrile. There is slight
pallor of conjunctiva, skin and palms. No
lymphadenopathy is noted chest, is clear to
auscultation bilaterally, regular rate and rhythm
of pluse with no rub or gallop, There is a grade
II/IV systolic ejection murmur, his abdomen is
soft, nontender and without hepato-
splenomegaly, bowel sounds are present. He has
no extremity edema, cyanosis or clubbing, his
peripheral pulses are palpable and symmetric. A
hemoglobin level is 9.2g/dl, MCV 75µ3, MCH 25
Pgm.
 The typical features of acute hepatic failure
include, except:
 Onset within 8 weeks of the initial illness.
 Hepatoplenomegaly and ascitis.
 Encephalopathy and fetor hepaticus.
 Nausea, vomiting and renal failure.
 Cerebral oedema without papilloedema.

 The typical feature of primary biliary

cirrhosis include:
 Xanthomata of the palmar creases and eyelids.
 Poor prognosis even in asymptomatic patients.
 Hepatomegaly without splenomegaly.
 Dilated bile ducts on ultrasonography.
 Improved survival rate without immunosuppressant
therapy.
 The clinical features of acromegaly include, except:
 Arthropathy and myopathy.

 Hypertension and impaired glucose tolerance.

 Goiter and cardiomegaly.

 Increased sweating and headache.

 Skin atrophy and decreased sebum secretion.

 Causes of short stature in childhood include, except;

 Klinefelter's syndrome.

 Turner's syndrome.

 Emotional deprivation.

 Cushing's syndrome.

 Primary hypothyroidism.
 Which of the following studies is most
sensitive for detecting diabetic
nephropathy:
 Serum creatinine level
 Creatinine clearance
 Urine albumin
 Glucose tolerance test
 Ultrasonography

 Haematocrit value of 45% means that:

 45% of the Hb in the plasma.
 45% of the total blood volume is made up of plasma.
 45% of the total blood volume is made up of blood cells.
 45% of the Hb is in the red blood cell.
 An anaemic subject has R.B.Cs count
3.5millom/mm3, PCV42% & Hb 14gm%, by
using the blood indices this subject most
probably has?
 Aplastic anaemia.
 Macrocyric hyperhormic anaemia.
 Normocytic normochromic anaemia.
 Microcytic hypochromic anaemia.

 If a man's plasma agglutinates both A and B

red cells, he is group:
 B
 A
 AB
 O
 Clinical features suggesting severe aortic
stenosis include, except:
 Early systolic ejection click.
 Pulsus bisferiens.
 Heaving displaced apex beat.
 Syncope associated with angina.

 Which of these is not a peripheral sign of

infective endocarditis?
 Osler's nodes.
 Splinter haemorrhages.
 Janeway lesions.
 Clubbing.
 Palmar erythema.
 Thrombin is required for activation of all the
following except:
 Plasminogen
 Fibrinogen
 Clot retraction
 Factor III

 All the following drugs for the treatment of

peptic ulcer disease alter gastric acid pH
except:
 Calcium carbonate
 Cimmetidine
 Omeprazole
 Pirenzepine
 Sucralfate
 Characteristic feature of cholestatic
jaundice include, except:
 Dark green stool.
 Dark brown urine.
 Conjugated hyperbilirubinaemia.
 Serum alkaline phosphatase concentration increased
>2.5 normal.
 Increased serum bile acid concentrations.

 The typical clinical features of diabetic

ketoacidosis include, except:
 Abdominal pain and air hunger.
 Rapid weak pulse and hypotension.
 Dry skin and polyuria.
 Vomiting and constipation.
 Coma with extensor plantar response.
 Cause of polyuria include, except:
 Chronic hyperglycaemia.
 Chronic renal failure.
 Hypercalcaemia.
 Hypothyroidism.
 Lithium toxicity.

 All the following drugs are associated with

an increased risk of osteoporosis in adults
except:
 Cyclosporine
 Dilantin
 Herparin
 Presnisone
 Ranitidine
 Hypercyanotic spell of Tetralogy of fallot is
treated with all of the following except:
 Knee chest position.
 Morphine.
 Digoxin.
 Propranolol.
 Sodium bicarbonate.
 Which of the following symptoms lists of
rheumatic fever are in the correct order of
most common least common?
 Erythema Marginatum, subcutaneous nodules, carditis,
fever.
 Arthritis, carditis, chorea, erythema Marginatum.
 Chorea, Erythema Marginatum, subcutaneous nodules.
 Arthritis, chorea, fever, Carditis,, subcutaneous nodules
 Fever, chorea, carditis, erythema Marginatum
 All of the following are included in the
revised Jones major criteria Except:
 New significant murmur indicative of carditis.
 Migrating polyarthitis.
 Chorea.
 Erythema multiforme.
 Subcutaneous nodules.
 Laboratory finding in a case of thalassemia
include all of the following except:
 High serum ferritin
 Recticulocytosis
 Decreased osmotic fragility
 Normocytic hypochromic anaemia
 hyperbilirubinaemia
 The following are essential for diagnosis of
primary nephrotic syndrome except:
 Severe edema
 Massive albuminuria
 Renal failure
 Hypoalbuminemia
 Hypercholesterolaemia
 The following are features of acute
glomerulonephritis except:
 Haematuria
 Ascities & pleural effusion
 Hypertension
 Proteinuria
 Oliguria
 In Tetralogy of Fallot, all are true except:
 Pulmonary congestion in chest X-ray
 Central cyanosis and clubbing
 Basal ejection systolic murmur and single 2nd heart
sound.
 Cyanotic spells due to infundibular pulmonary spasm
and decrease blood flow.
 Heart failure rarely occurs.
 Anaphylactoid purpura may be associated
with all except:
 Urticarial maculopapular rash distributed manily on
extensor surface of limbs.
 Hepatosplenomeglay
 Microscopic haematuria and mild notenuria
 Abdominal pain with occult blood in stool.
 Joint pains
 All of the following are normocytic
normochromic anemia except:
 Sickle cell anemia
 A plastic anemia
 Juvenile pernicious anemia
 Immune hemolytic anemia
 Treatment of thalassemia includes all the
following except:
 Repeated blood transfusion.
 Iron therapy
 Splenectomy
 Bone marrow transplantions
 Gene therapy.
 One of the following is a not a minor
manifestation in the diagnosis of initial
attack of rheumatic fever:
 Fever
 Arthralgia
 High ESR
 Elevated or rising antistreptococcal antibody titer.
 Prolonged P-R interval on ECG.
 Causes of huge splenomegaly include all of
the following except:
 Bilharzial splenomegly
 Chronic myeloid leukemia
 Chronic malaria
 Thalassemia major
 E.B virus infection
 Which of the following is a cause of
microcytic hypochromic anemia:
 Iron deficiency anemia
 Thalssemia
 Lead poisoning
 Anemia of chronic infection
 All of the above
 The following are essential for diagnosis of
primary nephrotic syndrome except:
 Severe edema.
 Massive albuminuria
 Low C3
 Hypoalbuminemia
 Hypercholesterolemia.
 Which of the following statements
concerning infectious mononucleosis
is incorrect:
 Rash appears in 10-20% of cases, discrete
macular, petichial, morbilliform or
scarlentiform appearance.
 Triad of membranous tonsillitis,
lymphadenopathy and splenomegaly.
 Causative organism is Enterovirus
 Incubation period: 5-15 days.
 Prodromal period: fever, fatigue, headache,
myalgia, abdominal pain.
Thank You