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1. DIC;
Gram negative septicaemia known to cause DIC
D-dimers elevated
Target cells are characteristics
Heparin is usually given

a) T severe sepsis of both gram + & -. Commonly meningococcal and other
gram ve bacteria due to their procoagulant endotoxins
b) T increased fibrin degradation products due to plasmin
c) F target cells in liver disease, iron deficiency anaemia, thalassaemia,
hyposplenism, sickle cell disease
d) T if predominantly thrombosis Eg. Solid tumour
e) T excess platelet and fibrin deposition forming clots

2. ABO incompatibility;
Is an aetiology agent of DIC
Is known to cause HDN
Can be detected in patients serum by direct Coombs test
AB blood given to O patient wont cause it

a) T activation of coagulation cascade
b) T
c) T positive direct Coombs
d) F definitely cause since IgM antibodies against A & B antigens are already
present in O patient : O can be transfused only with O

3. The coagulation screening test
Has high specificity & sensitivity
Is not affected by the anticoagulant: blood proportion in collecting tubes
Doesnt need a control
Is helpful in the diagnosis of DIC
Should be performed on family members of patients with ITP

a) F low specifity and sensitivity in normal screen (PT,APTT,TT). Correction
studies, factor assays are more specific and sensitive
b) F need correct ratio blood : citrate 1.8 ml : 0.2 ml
c) F since additional substances are added
d) T all tests prolonged
e) F Autoimmune disease causing peripheral destruction of platelets

4. TOF regarding laboratory features in DIC;
Raised PT
Raised TT
Fragmented RBC are less seen in peripheral blood
Can be diagnosed by blood picture

a) F platelet & fibrin deposition in vessels leads to thrombocytopenia
b) T
c) T
d) F seen due to mechanical damage to RBC when passing through obliterated
e) F can only suspect, needs further investigations like coagulation profile,
platelet counts & D-dimers

5. TOF regarding bleeding disorders
Family history is important
Bleeding into mucus membranes occurs commonly in platelet defects
vW disease is due to factor viii deficiency
less than 2% factor viii severe haemophilia
replacement with cryoprecipitate is better than with factor viii concentrates in haemophilia A

a) T common ones have familial inheritance
b) T vascular and platelet defects cause mucocutaneous bleeding
c) F qualititative/ quantitative deficiency of vWF. This prevents early clearance
of factor VIII by binding to it : thus vWF deficiency leads to factor VIII deficiency
d) F less than 1% severe, 1-5 % moderate , 5-40% mild
e) F factor VIII concentrate is first choice, if not cryoprecipitate which contains
factor VIII, vWF, XIII & fibrinogen

6. TOF
Warfarin inhibits vitamin K dependent coagulation factor formation
PT is a better indicator for warfarin than INR
Heparin is given orally
Platelet aggregation causing thrombosis is a known complication of heparin therapy
Warfarin is contraindicated in 1

a) T Vit K needed for carboxylation of clotting factor II, VII, IX, X. Vit K
undergoes oxidation into Vit K epoxide during this process. Vit K epoxide
reductase enzyme reduces the epoxide to active Vit K. This enzyme is inhibited
by warfarin
b) F INR since it is standardized & does not depend on tissue factor used
c) F IV or SC. Warfarin given orally
d) T autoantibodies (IgG) against heparin platelet factor 4 complex binds to
platelets thus activating them & aggregation leading to thrombosis &
thrombocytopenia - HIT
e) T teratogenic, Can also cause placental & fetal haemorrhage at term.
Contraindicated in pregnancy

7. TOF regarding DIC;
Caused by gram negative bacteria
HELLP syndrome is a cause
Blister cells are found
PT is normal in acute DIC

a) T sepsis is a main cause
b) T usually in third trimester of pregnancy, associated with pre-eclampsia,
Hemolytic anaemia, elevated liver enzymes, low platelets
c) T RBC in which Hb is concentrated to one half with other half almost empty
: due to damage / change in shape due to removal of RBC inclusions (Heinz
bodies) DD are TTP, DIC, G6PD deficiency, Thalassaemia
d) F prolonged. Also APTT,TT prolonged

8. TOF regarding ITP
Small platelets can be seen
Coombs test is positive
Bone marrow biopsy is mandatory for diagnosis
Splenectomy is indicated if no response to corticosteroids

a) F increased peripheral destruction is compensated sometimes by making
abnormally large platelets
b) F detects antibodies against RBC
c) F not mandatory (only when there is no response to treatment , over 60
years of age, diagnosis in doubt). Shows normal or increased megakaryocytes
d) F symptomatic and platelets below 30,000 after 3 months of steroids /
needing unacceptably high steroid doses to maintain platelets above 30,000

9. TOF regarding coagulation factors
Active proteins in circulation
Reduced in liver disease
Consumed in DIC
Antibodies are formed against them in pregnancy
Platelets are required to form a fibrin clot

a) F inactivated, Activated by vessel wall injury or other stimuli
b) T all clotting factors except a majority of factor VIII
c) T
d) T in antiphospholipid antibody syndrome
e) T platelet plug is converted to a definitive clot

10. Regarding thrombocytopenia
Thrombocytopenia due to ineffective megakaryopoiesis occurs in Wiskott-Aldrich syndrome
In HIV infection thrombocytopenia results from immune-complex mediated injury
Massive blood transfusion is known to cause dilutional thrombocytopenia
Formation of antibodies against platelets occurs in ITP
vWF is reduced in thrombocytopenia

a) T
b) T also due to marrow dysfunction
c) T
d) T
e) F vWD can lead to thrombocytopenia : but vWF levels are normal
(qualitative defect)

11. TOF regarding heparin
When unfractionated heparin is given in low doses subcutaneously it doesnt inhibit thrombin
IV heparin is used in pulmonary embolism to dissolve the emboli
LMW heparin is recommended to be used in pregnancy
Routine monitoring of therapy is not required
Heparin is used in treatment of unstable angina to improve survival

a) T only inhibits factor X : prevents thrombosis. Inhibits thrombin when given
in IV form
b) T
c) T
d) F only with LMWH. Unfractionated heparin monitored with APTT
e) T

12. The following drugs interact with warfarin & shouldnt be used concurrently

a) T GI irritation, bleeding due to antiplatelet action, displaces warfarin from
b) F paracetamol is better than NSAIDS
c) T accelerates metabolism : reduced anticoagulation (Carbamazepine,
d) T inhibit metabolism : increased anticoagulation (other antibiotics like
sulphonamides, ciprofloxacin)
e) T synthesis of vitamin K depedndant factors increased, USE POP

Also Amiodarone, Cimetidine (liver enzyme inhibition), Anti convulsants and
anti depressants like MAO inhibitors

13. Regarding Heparin
Limits Vit K dependant coagulation factors
Known to induce immune mediated thrombocytopenia
LMEH usually is administered as continuous IV infusions
HMWS therapy is monitored by APTT
used to treat unstable angina

a) F warfarin. Heparin combines with anti thrombin III and inhibits IXa, Xa, Xia,
XIIa and IIa
b) T - HIT
c) F heparin. LMWH as subcutaneous injections
d) T LMWH therapy is not routinely monitored
e) T also LMWH

14. Prolonged PT, APTT, and TT are seen in
Thrombotic thrombocytopenic purpura
Patients on warfarin therapy
factor vii deficiency
Vit K deficiency

a) F only platelets affected, coagulation factors not consumed
b) F TT normal
c) T
d) F only prolongs PT
e) F Similar to B with only PT, APTT prolonged

15. A woman with DVT presents to the hospital. Initial management would be
a) IV unfractionated heparin
b) Subcutaneous unfractionated heparin
c) Subcutaneous LMW heparin
d) Warfarin starting from a low dose and increase
e) Warfarin starting from a high dose and decrease

a) T
b) F
c) T now preferred option (out of A & C)
d) F
e) T high doses started, heparin continued for at least 5 days, warfarin dose
adjusted with INR (2 to 2.5)

16. PT, APTT prolonged but TT normal
a) VwF factor deficiency
b) DIC
c) warfarin therapy
d) heparin therapy
e) fibrinogen deficiency

a) F only APTT prolonged
b) F all prolonged
c) T possible (2,7,9,10)
d) F all prolonged (inhibition of thrombin)
e) F all prolonged
TT is only sensitive for fibrinogen abnormalities, impaired fibrin formation and
thrombin inhibitory effects

17. In collecting blood for coagulation investigation, what is the ratio of blood: anticoagulant?
a) 4:1
b) 9:1
c) 5:1
d) 7:1
e) 16:1

B - Blood : Anticoagulant 1.8ml : 0.2 ml
In ESR, it is 4:1

18. Facts favouring inherited DVT
>60 years
Increased HCT
Factor eight deficiency
Protein C deficiency
Increased CRP

a) F in young patients
b) F acquired cause
c) F leads to bleeding
d) T
Hereditary - Factor V Leiden, Protein C,S deficiency, Antithrombin deficiency,
Dysfibrinogenaemia, Prothrombin G20210A variant, ABO blood group

Hereditary or acquired Raised levels of factor VIII, fibrinogen, homocysteine
e) F acquired cause

19. Which of the following will give rise to a defect in clotting profile?
Collecting from drip arm
Delay in specimen transport
Prolonged use of tourniquet

a) F
b) T anticoagulant should be adjusted for HCT > 55%
c) T
d) T
e) T

20. 62 year old man presented with peripheral venous thrombosis diagnosed as having pancytopenia. Reticulocyte
index is 2. Increase levels of LDH. BM biopsy showed hyperplastic marrow and erythroplasia. Most likely diagnosis?
a. Macrocytic anaemia
b. Multiple myeloma
c. Aplastic anemia
d. Myelodysplasia
e. PNH

a) F marrow should show megaloblasts
b) F should show hyperplastic marrow with increased plasma cells
c) F marrow is acellular
d) F hypercelluar marrow with dysplastic cells
e) T intravascular hemolysis and thrombosis support this
Best Choice - E

21. A blood sample of an ICU patient was sent for an APTT. What anti-coagulant should be used
a. Na citrate
b. Heparin
c. Na Oxalate
e. Na fluoride

A Trisodium Citrate
EDTA used for full blood count

22. 60 year old man with advanced metastatic ca presented with easy bruising gum bleeding and haematuria,
suspected of DIC, which of the following Ix exclusively supports the above diagnosis
a. red cell fragmentation in blood
b. prolonged PT
c. prolonged APTT
d. prolonged TT
e. low plasma fibrinogen

All true, but best choice is E or elevated D-dimers

23. A 12 year old boy presented with haemochromatosis. Initial investigations are APTT 56 s, PT 12 s, bleeding time 5
min. What is the next most suitable Ix?
Question has to be on haemophilia.
If so, the next investigation should be a mixing study to determine, whether
haemophilia A or B

24. 2 day old baby, normal vaginal delivery had purpura on the skin and bullae. No family hx of thrombosis.
Diagnosed as neonatal purpuric fulminance. What is the likely cause?
a. Factor V leiden gene mutation analysis

Most likely protein C or S deficiency

25. WOTF shows correct bond of a clot
c. fibrinogen platelet-fibrinogn
d. platelet fibrinogen-collagen
e. fibrinogen vWF-platelet

A is correct
Fibrinogen platelet vWF - collagen

26. A 10 year old boy diagnosed as having haemophillia B and had severe bleeding following a laceration of his lower
lip. Which of the following product most likely arrest his bleeding
a) Packed RBC
c) Cryoprecipitate

Factor IX deficiency
Have to give Factor IX concentrate

If Haemophilia A , Factor VIII concentrate / cryoprecipitate can be given