Sush Unity Haemotology-1700

HAEM-System
Wise 1700-by Sush and Team. 2016

Susmita, Asad, Manu, Saima, Zohaib, Savia, Shanu, Mona, Manisha, Sitara, Samreena, Sami and Komal

Dear Plabber,

• This first ever System Wise 1700 document was created thanks to 3 months of daily hard
work by the PLAB Skype group ‘Unity’ which was brought together by Dr Susmita
Chowdhury.

The team members were:

& Susmita (Lead/most ignorant as she is working full time in public health for 13 years)
& Asad (Invaluable in IT and all types of support/the heart of the group)
& Manu (Volunteered to solve more questions/pathologist/amazing genuine person)
& Saima (Most concise clear notes/ photographic memory)
& Zohaib (Great research/a surgeon)
& Savia (Great research/multi-tasker with two little ones)
& Shanu (Very helpful after her March exam for those appearing in June)
& Mona (Great contributor in discussions)
& Manisha (Gyne/great discussion contributor)
& Sitara (Good discussion contributor)
& Samreena (Stayed a shorter time but great)
& Sami (Contributed the most early on but too brilliant for the group/still great friends)
& Komal (Knowledgeable sweet supportive girl)

• The main purpose was to break down the 1700 Q Bank System wise.

• We did our own reliable research for the options (OHCM/Patient info etc.) and concluded
these keys below on skype. This can save you 100s of hours of research. But I suggest you
also do your own.

• 90% of the document consists of Unity research. We also added information from other
circulating documents and they are referenced as Dr Khalid/Dr Rabia (and her Team).

• However, several keys may be ‘incorrect’ and so please use your own judgment as we take
no responsibility. I suggest cross checking with Dr Khalid’s latest keys (a few of which are still
debatable). Finally decide on your own key.

• Sorry if some members failed to make their answers thorough. The highlights are mostly as
per what the team members wanted to highlight. Blank tables to be ignored.

• Note that some 1700 Questions are missing from here (when members did not do their
share). Questions may not be in order due to merging of documents and there is excess
information than required. Read as much as needed.

• This has been circulated by our team as a generous contribution to the Plabbers’ success and
must not be ‘sold’.

1
HAEM-System Wise 1700-by Sush and Team. 2016

Q: 114 A 37yo woman presents with fatigue. Exam: angular stomatitis, no koilonychia.
Choose the single cell type you will find on the blood film.
a. Macrocytes
b. Microcytes
c. Granulocytes wthout blast cells
d. Blast cells

Clincher(s) Fatigue, angular stomatitis, no koilonychea
A Correct answer
B Common IDA also koilonychia present
C CML
D AML
E
KEY A Vit B12 / Folate deficiency
Additional
Information
2

3

Reference OHCM and GP Notebook
Dr Khalid/Rabia Q. 1. What is the key?
Q. 2. What is the cause here?
Q. 3. What are the points in favour of mentioned cause?
Ans. 1. The given key is A. Macrocytes.
Ans. 2. The cause here is VIT. B12 or folate deficiency.
Ans. 3. Points in favour of Vit. B12 or folate deficiency: i) fatigue (anaemia) ii)
angular stomatitis (can be seen in Vit. B12 or folate deficiency) iii) absence of
koilonychea is against IDA.

SIGNS in ANEMIA:
Koilocychia (spoon shaped nails) iron deificiency anemia
atrophic glossitis in iron def.
post cricoid webs (plummer vinson syndrome)
Angular stomatitis (cheilosis) in both vit B12 and iron def.
glossitis (beefy-red sore tongue) Vit. B12 def.

Q: 118 A term baby born to a 30yo woman of blood group A-ve develops severe
jaundice within the first 24h of birth. What is the most likely dx?
a. Hereditary spherocytosis
b. G6PD
c. ABO incompatibility
d. Rh incompatibility
e. Physiological jaundice

Clincher(s) Jaundice with first 24hr of birth
A
B
C
D Correct answer
E
KEY D Rhesus disease ! hemolysis ! jaundice/anaemia
Additional
Information

4

5

Reference Passmedicine & GP Notebook
Dr Khalid/Rabia As mentioned in the Q116 neonatal jaundice within 24hrs of birth could be
either because of sepsis or Rh incompatibility.
Mother is always Rh- and the baby is Rh +. Fetal antigen crosses the placenta
and the mother produces the antibodies against the antigen. Which cross the
placenta in subsequent pregnancies as a result of secondary response (greater
in magnitude) and cause hemolysis of the fetal blood.
ABO incompatibility: (mother O; baby A or B, or mother A and baby B, or vice
versa) DCT +ve in 4%; indirect Coombs +ve in 8%. Maternal IgG anti-A or anti-
B haemolysin is ‘always’ present

Q: 146 A 55yo male presents with malaise and tiredness. Exam: spleen approaching
RIF (right iliac fossa), no lymphadenopathy. Choose the single cell type?
a. Helmet shaped cell
b. Sickle cell
c. Granulocyte without blast cells
d. Blast cells

Clincher(s) Spleenomegaly, tiredness and malaise
A AKA Schistocyte ! Disseminated Intravascular Coagulation, Thrombotic
Thrombocytopenic Purpura, Heart Valve Hemolysis and Haemolytic-Uremic
Syndrome
B Disorder of RBC
C CML " granulocyte cells. Spleenomegaly. HUGE
D Blast cells in AML/ALL
E
KEY C
6

Additional
Information
7

Reference OHCM 352 & 606 and DOK Notes
Dr Khalid/Rabia Ans. 1. The key is C. Granulocyte without blast cells.
Ans. 2. The diagnosis is CML.
Ans. 3. Diagnostic features are i) increased number of mature granulocytes ii)
huge splenomegaly.

Causes of Splenomegaly: If massive, think of: chronic myeloid leukaemia,
myelofibrosis, malaria (or leishmaniasis)
Splenomegaly with fever Infection (malaria, SBE/IE • hepatitis, EBV,TB, CMV,
HIV)
With lymphadenopathy Glandular fever, leukemia/lymphoma, Sjogrens
syndrome
With purpura Septicemia, typhus, DIC, amyloid, meningococcemia
CML: It is a myeloproliferative disorder, common ge of occurence is 40-60
years.
Philadelphia chromosome (Ph) Present in >80% of those with CML t(9:22)
Symptoms Mostly chronic and insidious: weightloss, tiredness, fever, sweats.
There
may be features of gout (due to purine breakdown), bleeding (platelet
dysfunction),
and abdominal discomfort (splenic enlargement). ~30% are detected by
chance.
Signs Splenomegaly (>75%)—often massive. Hepatomegaly, anaemia, bruising
(fi g 2).
Tests WBC increased (often >100≈109/L) with whole spectrum of myeloid
8

cells, ie increased neutrophils, myelocytes, basophils, eosinophils. Hb dec or
normal, platelets variable. Urate increased B12increased. Bone marrow
hypercellular.
Treatment: is by chemotherapy or stem cell transplantation.

Q: 151 A 6yo boy is brought to the hospital for a 3rd episode of sore throat in 1 month.
He is found bleeding from gums and nose and has pale conjunctiva. What’s the
single cell type?
a. Clumped platelets
b. Microcytes
c. Granulocyte without blast cells
d. Blast cells
e. Mature lymphocytes

Clincher(s) 6yo, recurrent sore-throat, bleeding from gums/nose and has pale
conjunctiva
A
B
C
D ALL … correct answer because : recurrent infection due to neutropenia and
abnormal lymphoblast’s, age 6 yrs, thrombocytopenia (gum and nose
bleeding), pale conjunctiva ! anaemia.
E
KEY D
Additional ALL matches with the above scenario. Can be aplastic anaemia but risk factor is
Information not mentioned for this patient. Unless bone marrow aspiration is done we
cannot exactly say.

9

10

Aplastic Anaemia
11

Reference
Dr Khalid/Rabia Ans. 1. The key is D. Blast cells.
Ans. 2. The diagnosis is ALL
Ans. 3. Points in favour: i) Age-6yrs ii) recurrent infection (sorethroat) due to
neutrpenia and abnormal lymphoblasts which cannot protect from infection iii)
thrombocytopenia causing gum and nose bleeding. Iii) anaemia (pale
conjunctiva) due to reduced red cell production from marrow occupation by
blast cells. [Here debate came why it is not aplastic anaemia? There is no risk
factor mentioned for this patient for aplastic anaemia. There may be
congenital aplastic anaemia but again it would present earlier in life. So it goes
more with leukaemia but it cannot be confirmed unless we do bone marrow
aspiration.]

ALL: This is a malignancy of lymphoid cells, affecting B or T lymphocyte cell
lines, arresting
maturation and promoting uncontrolled proliferation of immature blast
cells, with marrow failure and tissue infiltration.
Causes: Genetic susceptibility, environmental factors (ionizing radiations)
Down’s syndrome.
Commonest cancer of childhood.
Signs and symptoms:
• Marrow failure: Anaemia (Hb), infection (WCC), and bleeding (platelets).
• Infiltration: Hepatosplenomegaly, lymphadenopathy—superficial or
mediastinal, orchidomegaly, CNS involvement—eg cranial nerve palsies,
meningism.
INVESTIGATIONS: Characteristic blast cells on blood film and bone marrow
CXR and CT scan to look for mediastinal and abdominal lymphadenopathy.
Lumbar puncture should be performed to look for CNS involvement.
TREATMENT: Blood transfusions, prophylactic antibiotics, IV antibiotics in case
of infection. Main stay of treatment is chemotherapy.
Prognosis Cure rates for children are 70–90%; for adults only 40%

12

Q: 178 A middle aged Asian presents with episodes of fever with rigors and chills for
last 1y. Blood film: ring form plasmodium with schuffners dots in RBCs. What is
the drug to eradicate this infection?
a. Doxycycline
b. Mefloquine
c. Proguanil
d. Quinine
e. Artesonate

Clincher(s) Schuffners dots in RBC
A used to treat bacterial infections like urinary tract infections, acne and
chlamydia
B Malaria treatment ! alternative for uncomplicated chloroquine-resistant
Plasmodium falc malaria
C prophylactic antimalarial drug
D prevent and treat malaria due to plasmodium falciparum
E Treatment of malaria but given as second antimalarial to Mefloquine
KEY B is wrong; Answer will be D
Additional Schüffner's dots refers to a hematological finding that is associated with
Information malaria, exclusively found in Plasmodium ovale and Plasmodium vivax.

Reference
Dr Khalid/Rabia MALARIA:
Plasmodium vivax and ovale: cyclical fever every 48 hours.
P.malariae: Cyclical fever every 72 hours. Can cause glomerulonephritis. Rarely
fatal.
P. falciparum: fevr 36-48hrs cyclical. Fulminant disease.
Presentation: 3 phases:
1 Shivering (1h): “I feel so cold.”
2 Hot stage (2–6h): T ≈ 41°C, flushed, dry skin; nausea/vomiting; headache.
3 Sweats (~3h) as T° falls
Also malaise, fatigue, anorexia, myalgias...
13

Signs: Anaemia, jaundice, and hepatosplenomegaly. No rash or
lymphadenopathy
Protective factors: G6PD lack; sickle- cell trait; melanesian ovalocytosis;
Complications: Hemolytic anemia can occur.
5 grim signs: 1 dec Consciousness/coma (cerebral malaria) 2 Convulsions 3
Coexisting chronic illness 4 Acidosis (eg esp bad if HCO3 – <15mmol/L) 5 Renal
failure
Diagnosis: Serial thin & thick blood films.
P. vivax ring forms partly hidden by Schuffner’s dots. P. malariae: ring and
band forms
P. falciparum: sausage-like gametocytes in RBC ghosts.

Treatment: If the patient has taken prophylaxis, don’t use the same drug for
treatment.
If species unknown or mixed infection, treat as P. falciparum. Nearly all P.
falciparum is resistant to chloroquine and in many areas also to Fansidar
(pyrimethamine + sulfadoxine).
Chloroquine is 1st choice for benign malarias in most parts of the world. Never
rely on chloroquine if used singly for prophylaxis.
Treating uncomplicated P. ovale, P. vivax, & P. malariae: Chloroquine base:
10mg/
kg, then 5mg/kg at 6h, 24h and 48h. In resistant cases, try Malarone®
(atovaquone and proguanil) ,quinine, or Riamet®. Primaquine dose in P. vivax:
500μg/kg (max.30mg) daily for 14d; P. ovale: 250μg/kg (max. 15mg) daily for
14d—given after chloroquine to treat liver stage and prevent relapse. Screen
for G6PD deficiency first. CI: pregnancy. P. malariae does not need primaquine.
Treating uncomplicated P.falciparum malaria:
Artemether-lumefantrine—if >35kg: 4 tabs stat, then 4 tablets at 8, 24, 36, 48
and 60h. • Artesunate-amodiaquine; if a fixed combination pill is available.
Dihydroartemisinin-naphthoquine • Dihydroartemisinin piperaquine. •
Atovaquone-proguanil. can be used.
In pregnancy: Artemisinins are OK in children and pregnancy from 13 weeks;
(use quinine + clindamycin in 1st trimester).
In addition give symptomatic treatment for fever, blood transfusion if
required.
Prophylaxis:
If little/no chloroquine resistance: Proguanil 200mg/24h+chloroquine base
300mg/wk.
If chloroquine-resistant P. falciparum: Mefloquine 250mg/wk (18d before to
4wks after trip) or doxycycline 100mg/d (1d before to 4wks after) or
atovaquone 250mg + proguanil 100mg (Malarone®) 1 tab/d (1d before travel
to 7d after).

Q: 236 A 60 yo man has a pathological rib fx. He also complains of recurrent infection.
BMA is done. Labs: Ca2+ = 3.9mmol/L and ALP = 127u/L. what type of cell
14

would be found in abundance in the marrow smear?
a. Plasma cell
b. Myeloid cell
c. Bence-jones protein
d. Megakaryocytes
e. Reticulocytes

Calcium serum ! 2.25 – 2.5mmol/L, ALP ! 30–150iU/L
Clincher(s) Pathological Rib Fx, Recurrent Infection. Ca2+ increased.
A Dx = Multiple Myeloma ! PLASMA Cell
B
C
D
E
KEY A (rx- plasma paresis- read others)
15

Additional
Information

16


Reference
Dr Khalid/Rabia Points in favour: i) age 60 yrs ii) pathological rib fracture (from metastases) iii)
recurrent infection (due to B cell dysfunction (manifested as
hypogammaglobulinemia), numerical and functional abnormalities of T cells,
and dysfunction of natural killer cells), iv) raised calcium level.

Multiple Myeloma: PCDs are due to an abnormal proliferation of a single clone
of plasma or lymphoplasmacytic cells leading to secretion of immunoglobulin
occuring as monoclonal bands or paraprotein in urine or serum
electrophoresis.
IgG in ~ ⅔; IgA in ~ ⅓; A very few are IgM or IgD. Other Ig levels are low
(‘immunoparesis’, causing susceptibility to infection). In ~ ⅔, urine contains
Bence Jones proteins.
Symptoms:
Osteolytic bone lesions causing backache, pathological fractures (eg long
bones
or ribs) and vertebral collapse. Hypercalcaemia may be symptomatic.
• Anaemia, neutropenia, or thrombocytopenia may result from marrow
infiltration
by plasma cells, leading to symptoms of anaemia, infection and bleeding.
• Recurrent bacterial infections due to immunoparesis, and also because of
neutropenia
due to the disease and from chemotherapy.
• Renal impairment due to light chain deposition.
Diagnostic criteria:
1 Monoclonal protein band in serum or urine electrophoresis.
2 Plasma cells on marrow biopsy
3 Evidence of end-organ damagefrom myeloma:
• Hypercalcaemia • Renal insufficiency • Anaemia
4 Bone lesions: a skeletal survey afterdiagnosis detects bone disease: Xraysof
chest; all of spine; skull; pelvis.

Tests: Rouleaux formation, persistently inc ESR or Polycythemia Vera, inc urea
and creatinine, inc Ca2+ (in ~40%), alk phos usually normal unless healing
fracture.
Screening test: Serum and urine electrophoresis. Beta2-microglobulin (as a
prognostic test).
Imaging: X-rays: lytic ‘punched-out’ lesions, eg pepper-pot skull, vertebral
collapse, fractures or osteoporosis.
CT or MRI may be useful to detect lesions not seen on XR.
Treatment: Symptomatic. For bones give bisphosphonates. For anemia
transfusion or erythropoietin. Keep hydrated to prevent renal failure, dialysis
may be needed. Treat infections.
Chemotherapy: If unsuitable for intensive , melphalan + prednisolone is used.

Complications: Hypercalcemia, Renal injury, cord compression, hyperviscosity.
17

Q:456 456. A 35yo lady is admitted with pyrexia, weight loss, diarrhea and her skin is
lemon yellow in color.
CBC = high MCV. What is the most probably dx?
a. Aplastic anemia
b. Pernicious anemia
c. Leukemia
d. ITP
e. Lymphoma

Clincher(s) Fever, weight loss, diarrhea, lemon skin, high mcv
A Aplastic Anemia- all cell lines show low count, no h/o jaundice
B Pernicious Anemia- high MCV, increased rbc destruction and jaundice, diarrhea
C Leukemia- wbc high
D ITP- platelets low
E Lymphoma- high lymphocytes? Possible diagnosis.
KEY B
Additional
Information
Reference
Dr Khalid/Rabia Clincher- High MCV. It may be graves with pernicious anemia. Lemon yellow
pallor occurs in pernicious anemia. Hyperthyroidism may cause persistently
raised body temperature

Q:513 513. A 30yo lady has epistaxis for 30mins. Her Hgb is normal, MCV normal,
WBC normal,PT/APTT/Bleeding time are normal. Where is the defect?
a. Plts
b. Coagulation factor
c. Sepsis
d. Anatomical
e. RBC

Clincher(s)
A PLATELETS-
B COAGULATION FACTOR- PT /APTT/BT NORMAL
C SEPSIS- NO SIGNS OF INFECTIONS
D ANATOMICAL- POSSIBLE
E RBC- NORMAL
KEY
Additional
Information
Reference
Dr Khalid/Rabia d. Anatomical
18

All labs normal

Q:531 531. A 5yo child was admitted with hx of feeling tired and lethargic all the
time, bleeding gums and sore throat since the last 3months. Exam:
hepatosplenomegaly. What is the most probable dx?
a. ALL
b. AML
c. CML
d. CLL
e. Lymphoma

Clincher(s)
A ALL- (WBC)
B AML (more hx of bleeding gum) (WBC)
C CML (much higher WBC)
D CLL (WBC but lymphocutes more than 11K)
E LYMPHOMA (no bleeding gums)
KEY A
Additional
Information
Reference
Dr Khalid/Rabia ALL
Acute lymphoblastic leukaemia (ALL) is the most common type in children,
primarily affecting 2 to 8 year-olds.
Approximately 2/3s of AML patients are over 60.
hepatosplenomegaly in both. lymphadenopathy in ALL.
AML presents with bleeding gums, but bleeding tendency in ALL too. ALL also
has gum hypertrophy.

ALL
Symptoms
• Fatigue, dizziness and palpitations
• bone and joint pain
• Recurrent and severe infections (oral, throat, skin, perianal infections
commonly)
• Fever
• Left upper quadrant fullness and early satiety due to splenomegaly (10-
20%)
• Haemorrhagic or thrombotic complications due to thrombocytopenia
or disseminated intravascular coagulopathy (DIC) - for example,
menorrhagia, frequent nosebleeds, spontaneous bruising
Signs
• Pallor
• Tachycardia and a flow murmur
• Nonspecific signs of infection
19

• Petechiae,purpura or ecchymoses
• hepatosplenomegaly
• Lymphadenopathy
• Gum hypertrophy
• Cranial nerve palsy (especially III, IV, VI and VIII) in mature B-cell ALL

Q:892 892. A 55yo male after gastrectomy developed anemia. His MCV=106fl. Exam:
loss of proprioception and vibration sense. What is the most likely dx?
a. IDA
b. Folate def
c. Vit B12 def
d. Anemia of chronic disease

Clincher(s)
A IDA- MCV LOW
B FOLATE DEF- ISOLATED FOLATE ?
C VIT B 12 DEF- MCV HIGH WITH NEUROPATHY
D ANEMIA OF CHRONIC DISEASE- MCV NORMAL
E
KEY C
Additional
Information
Reference
Dr Khalid/Rabia Key : c
Clincher : gastrectomy, anemia, mcv, loss of proprioception and vibration
sense

IDA ... mcv is decreased
Anemia of ch. Disease ... mcv is decreased
Folate def. Anemia ... mcv is increased but it doesn't affect proprioception and
vibration sense

VITAMIN B12 DEFICIENCY ANEMIA (source : patient.co.uk)

Vitamin B12 is present in meat and animal protein foods. Absorption occurs in
the terminal ileum and requires intrinsic factor (IF), a secretion of gastric
mucosal (parietal) cells, for transport across the intestinal mucosa. In
pernicious anaemia, IF production is deficient. It is believed to be an
autoimmune disease.Helicobacter pylori infection has been mooted to be an
initiating factor, with subsequent autoimmune changes affecting the gastric
mucosa. Genetic susceptibility to this process has been suspected.[1]

Causes
Pernicious anaemia accounts for 80% of cases of megaloblastic anaemia due to
20

impaired absorption of vitamin B12.
Other causes of vitamin B12 deficiency include:
Gastric causes: gastrectomy, gastric resection, atrophic gastritis, H. pylori
infection or congenital IF deficiency or abnormality.I
Inadequate dietary intake of vitamin B12 - eg, a vegan diet.
Intestinal causes - eg, malabsorption, ileal resection, Crohn's disease affecting
the ileum, chronic tropical sprue, HIV and any radiotherapy causing irradiation
of the ileum.
Drugs - eg, colchicine, neomycin, metformin, anticonvulsants.
Long-term use of drugs that affect gastric acid production (eg, H2 receptor
antagonists, proton pump inhibitors) can worsen deficiency because gastric
acid is needed to release vitamin B12 bound to proteins in food.

Presentation
Symptoms of anaemia may include fatigue and lethargy, dyspnoea, faintness,
palpitations and headache. Vitamin B12 deficiency may present with
unexplained neurological symptoms - eg, paraesthesia, numbness, cognitive
changes or visual disturbance.

Peripheral loss of vibratory sense and position are early indications of central
nervous system (CNS) involvement, accompanied by reflex loss and mild-to-
moderate weakness. Later stages may be characterised by spasticity, Babinski's
responses and ataxia.

Management
For patients with neurological involvement, referral to a haematologist is
recommended. Initial treatment is with hydroxocobalamin 1 mg on alternate
days until there is no further improvement, after which 1 mg should be given
every two months for life.

Q:961 961. A 4yo boy presents with recurrent episodes of self limiting spontaneous
bleeding. Coag test: PT normal, bleeding time normal, APTT prolonged, Factor
VIII decreased. His father and uncle suffer from a similar illness. What is the
most likely dx?
a. Hemophilia A
b. Hemophilia B
c. Von WilleBrand’s disease
d. ITP
e. TTP

Clincher(s)
A Haemophilia A- Factor VIII, XLR, APTT increased, Factor VIII decreased
B Hemophilia B- Factor IX, XLR
C Von Willebrand’s disease-
21

D ITP
E TTP (autoimmune)
KEY A
Additional
Information

Haemophilia A Factor VIII defi ciency; inherited in an X-linked recessive pattern
in 1 : 10,000 male births—usually due to a ‘fl ip tip’ inversion in the factor VIII
gene in the X chromosome. There is a high rate of new mutations (30% have
no family history).
Presentation depends on severity and is often early in life or after surgery/
trauma—with bleeds into joints leading to crippling arthropathy, and into
muscles causing haematomas ( pressure can lead to nerve palsies and
compartment syndrome).
Diagnose by increased APTT and decreased factor VIII assay. Management:
Seek expert advice.
Avoid NSAIDS and IM injections (fi g 2). Minor bleeding: pressure and elevation
of the part. Desmopressin (0 . 3μg/kg/12h IVI over 20min) raises factor VIII
levels, and may be suffi cient. Major bleeds (eg haemarthrosis): factor VIII
levels to 50% of normal. Life-threatening bleeds (eg obstructing airway) need
levels of 100%, eg with recombinant factor VIII. Genetic counselling: OHCS
p154.

Haemophilia B (Christmas disease) Factor IX defi ciency (inherited, X-linked
recessive);
behaves clinically like haemophilia A.

Acquired haemophilia is a bleeding diathesis causing big mucosal bleeds in
males
and females caused by suddenly appearing autoantibodies that interfere with
factor
22

VIII. 51 Tests: APPTincreased; VIII autoantibody increased; factor VIII activity
<50%. : Steroids.

Liver disease produces a complicated bleeding disorder with synthesis of
clotting factors, absorption of vitamin K, and abnormalities of platelet
function.

Malabsorption leads to less uptake of vitamin K (needed for synthesis of
factors II, VII, IX, and X). Treatment is IV vitamin K (10mg) or FFP for acute
haemorrhage
Reference
Dr Khalid/Rabia Reason It is a bleeding disorder which presents with the deficiency of factor
VIII, there are three forms,

Severe which usually presents in infancy ( time of circumcision or as
intracranial hemorrhage )factor activity <1%
Moderate which presents with bleeding following venepuncture (age Before 2
years) Factor Activity 1-5 %.
Mild. Only bleed after major trauma or surgery.Age >2 years, Factor Activity
>5%

INvestigations : PT,BT,fibrinogen and Von willebrand Normal
APTT) - usually prolonged, Factor VIII:C - is reduced

Treatment:
Children with severe haemophilia (ONce weekly prophylaxis with FActor VIII)
Recombinant factor VIII preferred. Fresh frozen plasma and cryoprecipitate
should only be used in an emergency when the concentrates are not available
Desmopressin boosts Factor VIII activity.

Q:1026 A 45yo man has developed an annular rash with a scaly edge on his thigh. The
rash has been spreading over the last 3wks. He has some general aches and
pains. What is the single most useful investigation?
a. ANA
b. Biopsy lesion
c. Lyme antibodies
d. Skin scrap for mycology
e. Skin swab for bacteria

Clincher(s)
A ANA
B BIOPSY LESION
C LYME ANTIBODIES
D SKIN SCRAP FOR MYCOLOGY
23

E SKIN SWAB FOR BACTERIA
KEY C
Additional Erythema migrans (fi g 3 p587) We all need
Information to be good at this rash as it’s the best way to
diagnosis Lyme disease, as serology is diffi cult

<50% give history of a tick
bite. City and rural people have similar risk. A papule becomes a spreading red
ring, lasting weeks to months. : 3wks PO doxycycline 100mg/12h, amoxicillin
500mg/8h, or cefuroxime.
Reference
Dr Khalid/Rabia Annular spreading rash points towards erythema migrans, which is
characterisitic of Lyme disease. Also accociated with general aches and
myalgia.
Lyme disease caused by bacteria borrelia burgdorferi, spirochaete.
Humans may have it if bitten by tics infected by bacteria.
Presententation depends on stage of disease.
Stage 1, early/localized: characteristic is erythema migrans. (spreading annular
rash over 3-36 days, central clearing, target like appearance, bull’s eye lesion)
associated flu like symptoms.
Stage 2, disseminated: occurs days to months later. Flu like symptoms.
Neurological involvement. Unilateral, bilateral facial nerve palsy, meningitis,
encephalitis, peripheral mononeuritis. Lymphocytic meningo rediculitis. Cardio
vascular problems: myo/pericarditis, heart block. Lymphocytoma. Cutaneous
lesion.
Stage 3/late: arthritis in knee. Acrodermatitis chronic. Late neurological
disorders.
Post lyme syndrome: similar to chronic fatigue syndrome.
Investigations: clinical diagnosis. Serology: antibodies. PCR.
Rx: Doxycycline 100mg/day. Or amoxicillin

Q:1162 A 36yo woman presented with massive bleeding from multiple sites. Lab: fibrin
degradation products: +++, plt=30, bleeding time=prolonged, PT=prolonged,
APTT=prolonged. What is the most likely dx?
a. Hemophilia
b. DIC
c. ITP
d. Factor V leiden

Clincher(s)
A HEMOPHILIA- factr viii, or ix
B DIC- FDP – Low Fibrin, platelets, Increased FDP, Clotting time- increases (
decreased factors
II, V, VII)
C ITP- low platelets
D FACTOR V LEIDEN- CAN CAUSE THROMBOPHILIA- APCR
24

E
KEY B
Additional
Information
Reference
Dr Khalid/Rabia key : B
cause : lab criteria ( decreased fibrinogen and platelets +increased PTT,PT )

Q:1414 An 18yo girl presents with rash on her trunk, abdominal pain, arthritis,
proteinuria and hematuria. What is the most probable dx?
a. TTP
b. ITP
c. HSP
d. HUS
e. Measles

Clincher(s)
A TTP-
B ITP
C HSP
D HUS
E Measles
KEY C
Additional Thrombotic thrombocytopenic purpura (TTP fi g 2) There is an overlap
Information between
TTP and HUS, and many physicians consider them a spectrum of disease. All
patients
have MAHA (severe, often with jaundice) and low platelets. Other features
can include AKI, fl uctuating CNS signs (eg seizures, hemiparesis,
consciousness,
vision) and fever. The classic description included the full ‘pentad’ of features,
but with the advent of plasma exchange this is rarely seen. Mortality is higher
than childhood HUS and can be >90% if untreated, though reduced to ~20%
with
plasma exchange.

Pathophysiology: There is a genetic or acquired defi ciency of
a protease (ADAMTS13) that normally cleaves multimers of von Willebrand
factor
(VWF). Large VWF multimers form, causing platelet aggregation and fi brin
deposition
in small vessels, leading to microthrombi.
25

Causes: Idiopathic (40%), autoimmunity
(eg SLE), cancer, pregnancy, drug associated (eg quinine), bloody diarrhoea
prodrome (as childhood HUS), haematopoietic stem cell transplant. It is a
haematological emergency: get expert help.

Tests: As HUS. : Urgent plasma exchange
may be life-saving. Steroids are the mainstay for non-responders, although
new
therapies such as eculizumab (monoclonal antibody targeting terminal
complement
pathway C5) have shown promising results in case reports,45 though seem to
be more eff ective in children than adults.46 Trials are ongoing. Because
thrombotic
thrombocytopenic purpura is uncommon, a high index of suspicion is required
for
rapid diagnosis and prompt initiation of plasma-exchange treatment. The
unexplained
occurrence of thrombocytopaenia and anaemia should prompt immediate
consideration of the diagnosis and evaluation of a peripheral blood smear for
evidence
of microangiopathic haemolytic anaemia.

Haemolytic uraemic syndrome (HUS) HUS is characterized by microangiopathic
haemolytic anaemia (MAHA): intravascular haemolysis + red cell
fragmentation.
Endothelial damage triggers thrombosis, platelet consumption and fi brin
strand
deposition, mainly in renal microvasculature. The strands cause mechanical
destruction
of passing RBCS. Thrombocytopenia and AKI result. Causes: 90% are from
E. coli strain O157 (‘O’ denotes the somatic antigen, as opposed to H, the fl
agellar
antigen). This produces a verotoxin that attacks endothelial cells. This typically
aff ects young children in outbreaks (more common than sporadically) after
eating
undercooked contaminated meat. Signs: Abdominal pain, bloody diarrhoea,
and AKI. Tests: Haematuria/proteinuria. Blood fi lm: fragmented RBC
(schistocytes,
p330); platelets, Hb. Clotting tests are normal. : Seek expert advice. Dialysis
for
AKI may be needed. Plasma exchange is used in severe persistent disease.
Prognosis:
Worse in non-E. coli cases. Mortality 3–5%, good prognosis if caught early

Henoch–Schonlein purpura (HSP) (fi g 2) A small vessel vasculitis, presenting
26

with
purpura (non-blanching purple papules due to intradermal bleeding), often
over buttocks
and extensor surfaces, typically aff ecting young . There may be
glomerulonephritis
(p300), arthritis, and abdominal pain ( } intussusception), which may mimic an
‘acute abdomen’. : Mostly supportive

Reference
Dr Khalid/Rabia Answer= C. HSP. Henoch-Schönlein purpura (HSP) is an IgA-mediated,
autoimmune hypersensitivity vasculitis of childhood.

The main clinical features are skin purpura, arthritis, abdominal pain,
gastrointestinal bleeding, orchitis and nephritis. In classic cases palpable
purpuric rash (with localized oedema) over buttocks and other sites are
extensor surfaces of arms and legs and trunk. Features of IgA nephropathy
may occur e.g. haematuria, renal failure.

exclusion of other causes:

HUS=Haemolytic uraemic syndrome is generally seen in young children and
produces a triad of:acute renal failure, microangiopathic haemolytic anaemia
and
thrombocytopenia.

Typical (or infection-induced) HUS is most commonly associated with
Escherichia coli with somatic (O) antigen 157 and flagella (H) antigen 7 - hence
the designation O157:H7.The classical presenting feature is profuse diarrhoea
that turns bloody 1 to 3 days later.

Henoch-Schönlein purpura (HSP) is an IgA-mediated, autoimmune
hypersensitivity vasculitis of childhood.
The main clinical features are skin purpura, arthritis, abdominal pain,
gastrointestinal bleeding, orchitis and nephritis. In classic cases palpable
purpuric rash (with localized oedema) over buttocks and other sites are
extensor surfaces of arms and legs and trunk. Features of IgA nephropathy
may occur e.g. haematuria, renal failure.
Treatment:
analgesia for arthralgia
treatment of nephropathy is generally supportive. There is inconsistent
evidence for the use of steroids and immunosuppressants
27

Prognosis:
usually excellent, HSP is a self-limiting condition, especially in children without
renal involvement
around 1/3rd of patients have a relapse
HSP = 10 P's
PALPABLE
PURPURA
PLATELETS OK -- DDx from ITP
PRURITUS -- URTICARIA
PAIN -- ABDOMEN and LEGS
POSITIVE +guaiac (occult blood test in stools) -- FECES
PRESSURE -- increased blood pressure
PROTEINURIA
PREDNISONE = Tx

Q:1450 A 40yo woman presented with generalized itching (also in IDA) and tiredness
for few months. She gave a hx of heavy menstrual periods. Exam: pallor. What
is the single most likely causative factor?
a. IDA
b. Lichen planus
c. Dermatitis herpitiformis
d. Eczema
e. Uremia

Clincher(s)
A
B
C
D
E
KEY A
Additional Confusion if uremia or not as all s/s match, but for plab stick to IDA
Information
Reference
Dr Khalid/Rabia Answer= A. IDA (iron deficiency anemia). features of anemia like tiredness and
pallor due to the menorrhagia points towards the diagnosis

Iron Deficiency Anemia
28

it is microcytic hypochromic anemia. most common cause of anemia. (seen in
up to 14% of menstruating women).
Causes:
Blood loss, eg menorrhagia or GI bleeding
• Poor diet may cause IDA in babies or children (but rarely in adults), those on
special
diets, or wherever there is poverty.
• Malabsorption (eg coeliac disease) is a cause of refractory IDA.
• In the Tropics, hookworm (GI blood loss) is the most common cause.

Presentation:
koilonychia, atrophic glossitis, angular cheilosis and rarely, post-cricoid webs
(Plummer-Vinson syndrome).
Tests:
Microcytic, hypochromic anaemia with anisocytosis and poikilocytosis
↓ MCV,↓ MCH and ↓MCHC. Confi rmed by ferritin↓ (also serum iron↓ with
↑total iron-binding capacity—TIBC, but these are less reliable).

Diagnostic test: Bone marrow iron. Perl’s stain.

Management:
Treat the cause.
Oral iron, eg ferrous sulfate 200mg/8h PO.( SE: nausea,
abdominal discomfort, diarrhoea or constipation, black stools).
Continue until Hb is normal and for at least 3 months, to replenish stores.

Q:1453 A 25yo man presented with painless cervical lymphadenopathy with lethargy,
night sweats and itching. What is the single most likely causative factor?
a. Lymphoma
b. Polycythemia
c. IDA
d. Uremia
e. Drug induced

Clincher(s)
A itching
B
C
D
E
KEY
Additional
Information
Reference Answer= A. Lymphoma. painless cervical lymphadenopathy with lethargy,
29

itching and night sweats are the features of hodgkin's lymphoma

Hodgkin’s lymphoma: Lymphomas are disorders caused by malignant
proliferations of lymphocytes. These accumulate in the lymph nodes causing
lymphadenopathy.In Hodgkin’s lymphoma,characteristic cells with mirror-
image nuclei are found, called Reed–Sternberg cells

Cause: 2 peaks of incidence: young adults and elderly. EBV has a role in causing
it.

Symptoms Often presents with enlarged, painless, non-tender, ‘rubbery’
superficial lymph nodes, typically cervical (60–70%), also axillary or inguinal
nodes. Nodes may become matted. 25% have constitutional symptoms.
Mediastinal lymph node involvement can cause features due to mass effect, eg
bronchial or SVC obstruction or direct extension, eg causing pleural effusions.

Signs Lymph node enlargement. Also, cachexia, anaemia, spleno- or
hepatomegaly.

Types:

Tests Tissue diagnosis: Lymph node excision biopsy if possible. Inc ESR or dec
Hb show worse prognosis.
Staging is by Ann-Arbor system.
Treatment: Depends on chemotherapy and radiotherapy
Dr Khalid/Rabia
30

Q:1558 Pt with low Hgb, MCV=76, angular stomatitis, red tongue, and koilonichea.
What is the most probable dx?
a. Folate def
b. B12 def
c. Iron def
d. Vit E def
e. Hemolytic anemia

Clincher(s)
A
B
C
D
E
KEY C
Additional
Information
Reference
Dr Khalid/Rabia Key: Iron Deficiency Anemia (C)
Reason: Folate and B12 are automatically ruled out with the low MCV. Vitamin
E deficiency hasn’t been shown to cause anemia. This is probably a fore-runner
of Plummer-Vinson syndrome which is related to Iron Deficiency Anemia in
this case. The treatment is oral Iron (Ferrous Sulphate 200mg PO x 8 hourly).
Continue until Hb normal and for atleast 3 months to replenish stores.

Q:1450

Clincher(s)
A
B
C
D
E
KEY
Additional
Information
Reference
Dr Khalid/Rabia

Q: 388 A 7yo girl has been treated with penicillin after sore throat, fever and cough.
Then she
develops skin rash and itching. What is the most probable dx?
a. Erythema nodosum
b. Erythema multiforme
c. SJS
31

d. Erythema marginatum
e. Erythema gangernosum

Clincher(s)
A Painful, blue-red raised lesions on shin fronts mostly.
B Target lesions ; symetrical with or without central blister, on palms, soles,
limbs, and elsewhere
C Rare severe variant of erythema multiform, with fever and mucosal
involvement…mouth, genital, and eye ulcers…associated with hypersensitivity
reaction to drugs (salicylates, sulfonamides, penicillin, barbiturates,
carbamazepine, phenytoin) or infections or cancer.
D Pink coalescent rings on trunk which come and go, seen in rhematic fever
E Recyurring nodulo-pustular ulcers, about 10cm wide, with tender red/blue
overhanging necrotic edge, purulent surface, and healing with cribriform scars
on leg, abdomen, or face. Associtions….ibd, autoimmune hepatitis, myeloma,
neoplasia
KEY The key is B. Erythema multiforme.

Additional
Information Medication
Medication can sometimes trigger the more severe type of erythema
multiforme. Possible medications include:
• antibiotics such as sulfonamides, tetracyclines, amoxicillin and
ampicillin
• anticonvulsants (used to treat epilepsy) such as
phenytoin and barbiturates
• non-steroidal anti-inflammatory drugs (NSAIDs)

Reference Ohcm 564, nhs uk
Dr Khalid/Rabia Common drugs causing erythma multiforme are: antibiotics (including,
sulphonamides, penicillin), anticonvulsants (phenytoin,barbiturates), aspirin,
antituberculoids, and allopurinol.
CLOSELY related option is SJS which would have muco cutaneous rash but in
here we hav only cutaneous rash.
Nodosum is in diseases like Tb, sarcoidosis, IBD
Marginatum is the rash of acute rheumatic fever

Q: 416 A 16yo boy presents with rash on his buttocks and extensor surface following a
sore throat.
What is the most probable dx?
a. Measles
32

b. Bullous-pemphigoid
c. Rubella
d. ITP
e. HSP

Clincher(s)
A • Measles rash is made up of small red-brown, flat or slightly raised spots
that may join together into larger blotchy patches
• usually first appears on the head or neck, before spreading outwards to
the rest of the body

B Bullous pemphigoid is a blistering skin disease that tends to affect the elderly.
It's caused by a problem with the immune system, but usually goes away on its
own within a few years. In the meantime, blisters can be controlled with
medication.
C The rubella rash is typically a red-pink colour. It consists of a number of small
spots, which may be slightly itchy.
The rash usually starts behind the ears before spreading around the head and
neck. It may then spread to the chest and tummy (the trunk), and legs and
arms. In most cases, the rash disappears by itself within three to five days.

D ITP caused by anti platelet antibodies. It is acute usually in children, 2 weeks
after infection, with sudden self limitng purpura, or chronic mainly seen in
women.
E Systemic variant of igA nephropathy, causing small vessel vasculitis, featuring
purpuric rash on extensor surfaces typically on legs, flitting poilyarthritis,
scrotal and scalp swelling, abdominal pain and bleeding. igA and C3 in skin and
renal biopsy.
The exact cause of HSP is not known. The body's immune system is believed to
play a role in targeting the blood vessels involved. An abnormal immune
response to an infection may be a factor in many cases. Approximately two-
thirds of the cases of HSP occur days after symptoms of an upper respiratory
tract infection develop.
KEY it's a wrong key
right ans is E

Additional
Information
Reference Ohcm 294 and 338, nhs
Dr Khalid/Rabia In HSP rash typically found in buttocks, legs and feets and may also appear on
the arms, face and trunk.
in ITP it mostly occurs in lower legs. #HSP usually follow a sore throat and ITP
follow viral infection like flue or URTI.
33

# HSP is a vasculitis while ITP is deficiency of platelets from more destruction in
spleen which is immune mediated].

Q: 575 A 33yo lady with Hodgkin’s lymphoma presents with temp=40C, left sided
abdominal pain and lymphadenitis. Blood was taken for test. What will you do
next?
a. Wait for blood test
b. Start broad spectrum IV antibiotics
c. Oral antibiotics
d. CBC
e. Monitor pyrexia

Clincher(s)
A
B
C
D
E
KEY b. Start broad spectrum IV antibiotics

Additional
Information
Reference
Dr Khalid/Rabia the patient has an immune compromising disease ,you cant wait until you get
lab results or give oral antibiotics, you shuld give systemic antibiotic to treat
any possible infectons
Chemotherapy causes imunosuppresion so increased chance of infections,as in
this case temp 40,and lymphadenitis so broad spectrum antibiotics

Q: 584 A 15yo girl was admitted with anemia, chest infection and thrombocytopenia.
She was treated and her symptoms had regressed. She was brought again with
fever and the same symptoms a few days later. She also seems to have
features of meningitis. What is the most likely dx?
a. AML
b. ALL
c. Aplastic anemia
d. CML
e. CLL

34

Clincher(s)
A
B Cns involvement is common
C
D
E
KEY B
Additional Only meningitis here differentiates it from AML, Aplastic
Information
CSF- Blast cells in ALL
Reference
Dr Khalid/Rabia Young, anemia, thrombocytopenia, recurrent infectionswith/without cns
involvement and testicular swelling... always go for All..if not treated
completed can appear again...in aplastic anemia the cell count of all cell types
is low with a mention of some predisposing factor..like drugs, radiation or a
dry tap of bone marrow.
Patients with ALL frequently have meningeal leukaemia at the time of
relapse (50-75% at one year in the absence of CNS prophylaxis) and a few
have meningeal disease at diagnosis (<10%).

ALL
Symptoms
• Fatigue, dizziness and palpitations
• bone and joint pain
• Recurrent and severe infections (oral, throat, skin, perianal infections
commonly)
• Fever
• Left upper quadrant fullness and early satiety due to splenomegaly (10-
20%)
• Haemorrhagic or thrombotic complications due to thrombocytopenia
or disseminated intravascular coagulopathy (DIC) - for example,
menorrhagia, frequent nosebleeds, spontaneous bruising
Signs
• Pallor
• Tachycardia and a flow murmur
• Nonspecific signs of infection
• Petechiae,purpura or ecchymoses
• hepatosplenomegaly
• Lymphadenopathy
• Gum hypertrophy
• Cranial nerve palsy (especially III, IV, VI and VIII) in mature B-cell ALL

35

Q: 839 A 45yo man presented with pruritic purple papules on the flexor surface of his
wrist and some white lacy markings on his buccal mucosa. What is the single
most likely causative factor?
a. ALL
b. Lymphoma
c. Polycythemia
d. IDA
e. Lichen planus

Clincher(s) Purple papules on flexor surface of wrists and white lacy markings on buccal
mucosa
A
B
C Post bath pruritus
D
E
KEY E
Additional Lichen planus, non infectious itchy rash
Information
Reference
Dr Khalid/Rabia Lichen planus
Presentation
Onset is usually acute, affecting the flexor surfaces of the wrists,
forearms and legs.
The typical lesion is an intensely itchy 2-5 mm red or violet shiny flat-
topped papule with white streaks ('Wickham's striae').
Mucous membranes are commonly affected >>> Classically, white slightly
raised lesions with a trabecular, lacy appearance on the inside of the cheeks

Q: 847 847. A young man who has no PMH presented with jaundice, low Hgb, retics
(RBC with nuclear material) 8% and other indices WNL but occasional
spherocytes were seen on blood film. What is the single most appropriate inv?
a. G6PD enzyme assay
b. Direct coombs test
c. Repeat blood film
d. Indirect coombs test
e. BMA (Bone marrow asp)

Clincher(s)
A
B The direct antiglobulin test (DAT) is used primarily to help determine if the
36

cause of haemolytic anaemia, a condition in which red blood cells (RBCs) are
being destroyed more quickly than they can be replaced, is due
to antibodies attached to RBCs.
C
D The indirect Coombs test is used in prenatal testing of pregnant women and
in testing blood prior to a blood transfusion. It detects antibodies against RBCs
that are present unbound in the patient's serum. In this case, serum is
extracted from the blood sample taken from the patient.
E
KEY B
Additional
Information
Reference
Dr Khalid/Rabia

Q:

Clincher(s)
A
B
C
D
E
KEY
Additional
Information
Reference
Dr Khalid/Rabia

Q:

Clincher(s)
A
B
C
D
E
KEY
Additional
Information
Reference
Dr Khalid/Rabia

37

Q:

Clincher(s)
A
B
C
D
E
KEY
Additional
Information
Reference
Dr Khalid/Rabia

Q: 1628 A previously well 15yo girl had an acute onset of fever, sweating, bruising and
petechiae. A blood count showed: Hgb=63g/L, WBC=1.1mg/L, Neutrophils=0.1,
plt=14. No abnormal white cells were seen on the blood film. She was
transfused and given IV antibiotics and her condition improved. 3wks later her
blood count has returned to a similar picture. What is the SINGLE most likely
underlying dx?
a. ALL
b. AML
c. Aplastic anemia
d. CML
e. Pernicious anemia

Clincher(s) Young teenage girl with blood count showing Hb 63g/L, WBC 1.1mg/L,
neutrophils 0.1 and platelets 14. No abnormal white cells were found. After
transfusion and antibiotics her condition got better for 3 wk only before
going back to similar picture as before
A Blast cells should be present with lymphadenopathy.
B Mainly affect adults and Aeur rods cells presents.
C All three white cells, RBC and platelets will be low.
D Again affect ppl age 40-60 with make predominance and rare in children.
WBCs are normally very high. Philadelphia chromosome present in >80% of
those with CML.
E Pernicious anemia will present with megaloblastic anemia features.
KEY C
Additional
Information
Reference
Dr Khalid/Rabia The age of the patient and pancytopenic picture give us a clinical diagnosis of
Aplastic anemia. Normal WBC morphology rules out ALL, AML and pernicious
anaemia
while the age rules out CML as a diagnosis.
38

Q:1641 A 72yo man being investigated for anaemia is booked for a colonoscopy in 24
hours. What is the SINGLE most appropriate management the night before the
procedure?
a. Bisacodyl tablets
b. Glycerine suppository
c. Lactulose syrup
d. Magnesium citrate (orally)
e. Senna tablets

Clincher(s) Elderly pt booked for colposcopy for investigation of anemia
A Stimulant laxative
B Rectal stimulant.
C Produces osmotic diarrhoea
D It's used for rapid bowel evacuation. (Na picosulphate is given usually)
E Stimulant laxative. Not all uses for senna have been approved by the FDA.
KEY D
Additional Osmotic laxatives usually start to work after about 2 or 3 days, while
Information stimulant laxatives usually have an effect within 6 to 12 hours.
Reference
Dr Khalid/Rabia Colonoscopy is a test to assess your colon (large intestine).
What preparation do I need to do?
The colon needs to be empty so that the operator can obtain a clear view.
You will be instructed on how to take a special diet for a few days before
the test. You will also be given some laxatives to take.(magnesium citrate is
the least harmful)
·
YOh will need somebody to accompany you home, as you will be drowsy
with the sedative

Q:1661 An anemic young man is found to have a macrocytosis of 90%. The most likely
cause is?
a. Zieve’s syndrome
b. Thalassemia minor
c. Chronic renal disease
d. IDA
e. Folate def
f. Chronic liver disease
g. HUS
h. Cytotoxic chemotherapy
i. Phenytoin
39

Clincher(s) Macrocytosis in young man (most others are microcytic..)
A Zieve's syndrome is an acute metabolic condition that can occur during
withdrawal from prolonged alcohol abuse. It is defined by hemolytic anemia
(with spur cells and acanthocytes), hyperlipoproteinaemia (excessive blood
lipoprotein), jaundice, and abdominal pain
B Gives microcytic anemia picture
C Normalcytic anemia.
D Microcytic anemia
E Macrocytic anemia.
KEY E
Additional Anti folate drugs: phenytoin, valproate, co trimaxazole, alcohol and
Information methotrexate.
Conditions which shows megaloblastic picture are B12 def, folic acid def and
anti folate drugs and cytotoxic drugs such as hydroxycarbamide.
Reference Ohcm page :326
Dr Khalid/Rabia

Q:1672 A pt presented with the following blood film, , MCV: Decreased Serum ferritin:
Decreased Total iron binding capacity: Increased Serum iron: Decreased
Marrow iron: Absent. What is your dx?
a. Thalassemia trait
b. Hypoparathyroidism
c. Hereditary sideroblastic anemia
d. Protein energy malnutrition
e. Chronic renal failure
f. Anemia of chronic disease
g. Acute blood loss
h. IDA
i. Oral contraceptives
j. Megaloblastic anemia

Clincher(s) MCV decreased, TIBC increased, ferritin decreased and marrow shows iron is
absent
A Although similar picture clinically to IDA but marrow picture will show reduce
or abnormal B chain Hg. (bone marrow iron will be increased)
B
C Iron is usually high, ferritin is high but TIBC is normal.
D
E
KEY H
Additional
Information
40

Reference Ohcm page 321
Dr Khalid/Rabia Reason: S/S pallor, koilonychia,angular cheilitis, atrophic glossitis, IN marked
Anemia ( Cardiac enlargemnet,Flow Murmurs,ankle oedema and heart failure)
Inv: FBC : shows microcytic hypochromic anemia
Serum ferrtitin Level reduced, normal 12-15 mcg/L, ( serum ferritin is falsely
raised during infections)
Anisocytosis and poikilocytosis , Total iron binding capacity is increased

Q:1684 INR:Normal, APTT:Elevated, Thrombin time:Elevated, Plt count:Normal,
Bleeding time: Normal. A likely aetiology is?
a. Waldenström's
macroglobulinaemia
b. Heparin
c. Sézary cell leukaemia
d. Pelger-Hüet anomaly
e. von Willebrand's disease
f. Haemophilia
g. HIV infection
h. DIC
i. Acanthocytosis
j. Vit K deficiency

Clincher(s) APTT and Thor bin time elevated with normal INR and bleeding time.
A Waldenström macroglobulinaemia (WM) is a rare type of slow growing non-
Hodgkin lymphoma. It develops when a type of white blood cells, called
plasma cells, become abnormal and grow out of contro
B
C Sézary syndrome and mycosis fungoides are T-cell lymphomas whose primary
manifestation is in the skin
D
E
KEY B
Additional
Information
Reference Pls check the chart on OHCM page 341 and detailed description on 340.
Dr Khalid/Rabia PT-test for extrinsic system
INR- 0.9-1.2 (PT Control), Increased INR in warfarin, Vitamin K and liver
disease
APTT- intrinsic system, increased PTT (Heparin,Haemophillia (Factor 8
affected))
THrombin Time- 10-15 seconds, increased in heparin, increasedd in DIC
Bledding Time (normal 7 min) - commonest ccause Von willlbrand disease

41

Q:1686 A 4yo boy has the sudden onset of bone pain. He begins experiencing bleeding
of his gums and frequent bloody noses. His mother takes him to his
pediatrician. Exam: he is pale and has numerous petechiae over his body, with
lymphadenopathy and hepatosplenomegaly. He has WBC=100,000mm and
numerous circulating blast cells. He is admitted to the hospital. A bone marrow
biopsy=35% blast cells. Which of the following is most likely?
a. Mantle cell lymphoma
b. Infectious lymphocytosis
c. Waldenstrom’s
macroglobulinemia
d. CML
e. CLL
f. Burkitt lymphoma
g. ALL
h. Mycosis fungoides
i. Hairy cell leukemia
j. AML

Clincher(s) Young boy with complaints of bleeding from noise and gums. On
examination petechia were found all over the body with lymphadenopathy
and hepatospleenomegaly. Blast cells on marrow.
A
B
C
D
E
KEY G
Additional Burkitt’s lymphoma is a rare and aggressive form of non-Hodgkin lymphoma.
Information Common in children.
Reference
Dr Khalid/Rabia

Q:1688 A 2m baby develops a life-threatening anemia. Blood tests show a normal
serum iron, ferritin and TIBC. Hemoglobin electrophoresis reveals a markedly
decreased Hemoglobin A content and an increased hemoglobin F content. This
baby's anemia is likely to be secondary to?
a. Failure of alpha chain production
b. Failure of beta chain production
c. Deficiency of B12
d. Lead poisoning
e. IDA
f. Presence of hemoglobin S
g. Presence of hemoglobin M
h. Deficiency of folate
i. Bone marrow failure
42

j. Inability to manufacture heme

Clincher(s) Normal serum iron, TIBC, ferritin and HB F and Dec HB A and life threatening
anemia.
A
B
C
D
E
KEY B
Additional B thalasemia major or cooleys anemia denotes the abnormality in both
Information b globin genes and present in the first ur with severe anemia and failure to
thrive.
Extra medullary erythropoeisis occur in response to anemia which gives rise to
typical head shap called skull bossing.
Lifelong transfusions are needed with chelation to avoid iron overload.
Reference
Dr Khalid/Rabia

Q:

Clincher(s)
A
B
C
D
E
KEY
Additional
Information
Reference
Dr Khalid/Rabia

Q:

Clincher(s)
A
B
C
D
E
KEY
43

Additional
Information
Reference
Dr Khalid/Rabia

Q:

Clincher(s)
A
B
C
D
E
KEY
Additional
Information
Reference
Dr Khalid/Rabia

Q: 38 A 73yo woman has lymphadenopathy and splenomegaly. She feels well but has
had recurrent chest infections recently. Choose the single most likely blood
film findings?
a. Atypical lymphocytes
b. Excess of mature lymphocytes
c. Plasma cells
d. Multiple immature granulocytes with blast cells
e. Numerous blast cells

Clincher(s) 73yo, woman, lymphadenopathy and splenomegaly, recurrent chest
infections >> CLL
A
B
C
D
E
KEY: B Excess of mature lymphocytes
Age of patient (usually above 50 yrs), lymphadenopathy and splenomegaly,
appearance of lymphocytes (mature lymphocytes – but functionally not
normal). Repeated chest infection points towards abnormal function of
lymphocytes against infection.
Additional
Information
44

Reference
Dr Khalid/Rabia Q. 1. What is the key?
Q. 2. What is the diagnosis?
Q. 3. Points in favour of your answer?
Ans. 1. B.
Ans. 2. CLL
Ans. 3.
It's CLL because in CML the risk age is 40-60 years, and in CBC there should be
increased myeloid cells(which is absent in options). If I exclude these factors,
then the possible DX would be CLL and film finding is B.

1. Acute lymphoblastic leukemia- abnormal immature lymphocytes, (can be
immature B or T lymphocytes) called lymphoblasts.

2. Chronic lymphocytic leuaemia- Excess of mature lymphocytes.

3. Acute myeloid leukaemia- blast cells (abnormal immature white cells)
derived from myeloid stem cells.

4. Chronic myeloid leukaemia- near normal granulocytes developed from
abnormal stem cells (these are mature cells). Also age is a factor ALL in any age
but common in child, AML- age over 50, CLL common over age 60, CML- in
adults and commoner with increasing age.

Q: 194 The dx cells of Hodgkin disease are:
a. T-cells
b. R-S cells
c. B-cells
d. Macrophages
e. Auer rods

Clincher(s)
A
B
C
D
E
KEY: B Reed Sternberg cells
Additional
Information
Reference
Dr Khalid/Rabia Hodgkin’s lymphoma: Lymphomas are disorders caused by malignant
proliferations of lymphocytes. These accumulate in the lymph nodes causing
lymphadenopathy.In Hodgkin’s lymphoma,characteristic cells with mirror-
image nuclei are found, called Reed–Sternberg cells
45

Cause: 2 peaks of incidence: young adults and elderly. EBV has a role in causing
it.
Symptoms Often presents with enlarged, painless, non-tender, ‘rubbery’
superficial lymph nodes, typically cervical (60–70%), also axillary or inguinal
nodes. Nodes may become matted. 25% have constitutional symptoms.
Mediastinal lymph node involvement can cause features due to mass effect, eg
bronchial or SVC obstruction or direct extension, eg causing pleural effusions.
Signs Lymph node enlargement. Also, cachexia, anaemia, spleno- or
hepatomegaly.
Types:

Tests Tissue diagnosis: Lymph node excision biopsy if possible. Inc ESR or dec
Hb show worse prognosis.
Staging is by Ann-Arbor system.
Treatment: Depends on chemotherapy and radiotherapy.

Q: 243 A 56yo woman is known case of pernicious anemia. She refuses to take
hydroxycobalamin IM as she is needle shy. She asks for oral medication. Why
will oral meds be not effective?
a. Intrinsic factor def
b. Malabsorption
c. Irritated gastric mucosa
d. Lack of gastric acidity

Clincher(s) pernicious anemia
A

B
C
D
E
KEY A. Intrinsic factor def.
46

Additional Pernicious Anemia (type of megaloblastic anemia) : This is caused by an
Information autoimmune atrophic gastritis (loss of gastric parietal cells), leading to
achlorhydria and lack of gastric intrinsic factor secretion which is essential for
subsequent absorption of vitamin B12 in the ileum.

Associations Other autoimmune diseases: thyroid disease (~25%), vitiligo,
Addison’s disease, hypoparathyroidism. Carcinoma of stomach is ~3-fold more
common in pernicious anaemia

Investigations: • Hb (30–110g/L) •Raised MCV • Decreased WCC and platelets
if severe • Decreased Serum B12 • Reticulocytes reduced or normal as
production impaired •Hypersegmented polymorphs • Megaloblasts in the
marrow •

Specific tests: 1.Parietal cell antibodies: found in 90% with PA, 2 Intrinsic factor
(IF) antibodies:
specific for pernicious anaemia, but lower sensitivity.

Treatment Treat the cause if possible. If a low B12 is due to malabsorption,
injections are required. Replenish stores with hydroxocobalamin (B12) 1mg IM
alternate days, for 2wks Maintenance: 1mg IM every 3 months for life.
If the cause is dietary, then oral B12 can be given after the initial acute course.
Reference
Dr Khalid/Rabia

Q: 250 A 61yo man underwent a surgery in which ileal resection had been done. He
complains of fatigue, headache, and heart racing. Labs: MCV=108fL,
Hgb=8.9g/dL. What is the most likely dx?
a. Vit B12 def
b. Iron def
c. Folate def
d. Hemolytic anemia
e. Anemia of chronic disease

Clincher(s) ileal resection
A Vit B12 is absorbed mostly in ileum. Megaloblastic anaemia.
B
C
D
E
KEY The key is Vit. B12 deficiency
47

Additional
Information

Reference
Dr Khalid/Rabia

Q: 260 A 57yo man presents with weight loss, tiredness, fever and abdominal
discomfort. Exam: spleen palpable up to the umbilicus. Labs: WBC=127,
Hgb=8.7, Plt=138. What is the most likely dx?
a. CML
b. AML
c. CLL
d. AML
e. Polycythemia

Clincher(s) Palpable spleen, thombocytocis
A Splenomegaly and raised WBC along with typical signs and symptoms.
48

B
C
D
E
KEY Key = A (CML)

Additional
Information

Reference
Dr Khalid/Rabia

Q: 265 A 65yo woman presents with headache. She also complains of dizziness and
tinnitus. He has recently realized she has visual problems. There is hx of
burning sensation in fingers and toes.
On exam: splenomegaly, itchy after hot bath. Labs: RBC=87, Hgb=31.9,
Plt=796. What is the dx?
a. CML
b. CLL
c. Polycythemia vera
d. Myelofibrosis
e. NHL (Non hodgkins Lym)

Clincher(s)
49

A
B
C Points in favour = Headache, burning finger along with visual problems. High
hb
D
E
KEY Key = C (Polycythemia vera)

Additional
Information

Reference
Dr Khalid/Rabia

Q: 280 A woman has pernicious anemia. She has been prescribed parenteral vitamin
B12 tx but she is needle phobic. Why is oral tx not preferred for this pt?
a. IM B12 is absorbed more
b. Intrinsic factor deficiency affects oral B12 utilization
c. IM B12 acts faster
d. IM B12 needs lower dosage
e. Pernicious anemia has swallowing difficulties

Clincher(s)
A
B Points in favour = There is def of intrinsic factor dt autoimmune causes in
50

pernicious anemia.

VitB12 can not be absorbed without binding to intrinsic factor.
C
D
E
KEY Key = B

Additional
Information
Reference
Dr Khalid/Rabia

Q: 318 A 53yo man presents complaining of weight loss, lethargy, increasing
abdominal discomfort and gout for the pat yr. Exam: spleen palpated 5cm
below left costal margin, no fluid wave. CBC:
Hgb=10.5g/dL, WBC=200 – 85% neutrophils, plts=100, Na+=140mmol/L, K+
4mmol/L, create=151umol/L, urea=7mmol/L. Serum B12 increased.
Philadelphia chromosome +ve. What is the most likely dx?
a. CML
b. CLL
c. AML
d. ALL
e. Lymphoma

Clincher(s) Philadelphia chromosome +ve.
A Points in favour: i) wt loss ii) lethargy iii) abdominal discomfort iv)
splenomegaly v) gout [may be secondary to cytotoxic treatment], Also blood
picture is suggestive and +ve Philadelphia chromosome is diagnostic.
B
C
D
E
KEY The key is A. CML.
Additional
Information
Reference
Dr Khalid/Rabia

51

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cause : lab criteria ( decreased fibrinogen and platelets +increased PTT,PT )

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