Haematological disease

8 Haematological disease



Questions




Question 1


What is favism?



Question 2


What is the haemoglobin content of reticulocytes and how can this be measured or determined?



Question 3


We are told that an erythrocyte sedimentation rate (ESR) above 100mm/h has a limited differential diagnosis, mainly vasculitis, malignancy and granulomatous diseases. Could you explain whether that applies to an ESR after one hour or two?



Question 4


What causes a raised erythrocyte sedimentation rate (ESR)?



Question 5


What are the causes of very raised erythrocyte sedimentation rate (ESR)? I mean an ESR < 100mm/h. Is this test diagnostic in any disease besides polymyalgia rheumatica and giant cell arteritis?



Question 6



1. Does the erythrocyte sedimentation rate (ESR) rise with age?

2. Can an ESR of 50mm/h in an 80-year-old female with no evidence of systemic disease be considered normal?


Question 7



1. What is a ‘normal’ erythrocyte sedimentation rate (ESR)? Is the equation of a normal ESR = age – 10, correct?

2. Would a normal ESR exclude a vasculitic cause in the case of stroke?


Question 8


In which conditions is C-reactive protein (CRP) more informative than the erythrocyte sedimentation rate (ESR)?



Question 9


What is the management of an isolated high ferritin (without any signs, symptoms or changes in the other blood investigations)?



Question 10


Is the mean corpuscular volume (MCV) useful? What is the RDW and when is it used?



Question 11


What is the significance of renal disease with respect to anaemia, if any?



Question 12


Can anaemia be a differentiating point between muscle wasting and cachexia owing to another systemic disorder?



Question 13


Anaemia of chronic disease does not respond to iron therapy, but there are trials studying the use of iron and erythropoietin (EPO). Could you tell me where to find more detailed information about these trials, and whether there have since been any further developments?



Question 14


Is the deoxyuridine test helpful?



Question 15


The Schilling test is very rarely performed. Why is this?



Question 16


There is no extramedullary haematopoiesis in aplastic anaemia, why?



Question 17


Why is the anaemia in aplastic anaemia, macrocytic?



Question 18


Is vitamin B12 absorbed passively from the jejunum?



Question 19


What role does ‘R’ binder play in the absorption of vitamin B12?



Question 20


In pernicious anaemia, investigation of the serum shows an elevated level of gastrin. Why is it so?



Question 21



1. Please explain the term Coombs’ positive (direct and indirect) and negative haemolytic anaemia.

2. What are the principles of the Coombs’ test?


Question 22


How often is Aldomet (alpha methyldopa) associated with autoimmune haemolytic anaemia or hepatitis? Is a normal person, with a positive Coombs’ test owing to previous treatment with this drug, safe to donate blood?



Question 23


What is the mechanism of priapism in sickle-cell anaemia?



Question 24


Is sickle-cell disease associated with any of the glomerular disorders?



Question 25


What is the acute chest syndrome?



Question 26


Patients with thalassaemia intermedia have recurrent leg ulcers and recurrent infections. What is the mechanism of this?



Question 27


What is the mechanism of iron absorption from iron polymaltose complex and carbonyl iron?



Question 28


Iron overload in patients with thalassaemia major should be checked by measuring the serum ferritin and hepatic iron stores. How are the hepatic iron stores measured? By liver biopsy? And does not the measurement of serum ferritin suffice?



Question 29


In the investigation for paroxysmal nocturnal haemoglobinuria (PNH), are the sucrose haemolysis test and Ham’s acid serum test commonly done? What are the principles behind these tests?



Question 30


Why isn’t the blood of polycythaemia vera patients, after repeated phlebotomies, used for transfusion purposes? Although it is a premalignant condition, the red cells do not contain a nucleus and thus transfusion of only pure red blood cells (RBCs) would be a great benefit.



Question 31


What investigations are necessary to exclude secondary polycythaemia?



Question 32


What is the management plan in a patient with secondary polycythaemia presenting with transient ischaemic attacks (TIA)?



Question 33


Why do patients with polycythaemia vera have a tendency to bleed, even though 50% of them have an elevated platelet count?



Question 34


In hyposplenic patients, what precautions are necessary for patients who intend to travel to Saudi Arabia for the Haj?



Question 35


What is the mechanism of development of splenomegaly in chronic leukaemia?



Question 36


In idiopathic thrombocytopenic purpura (ITP), thrombocytes are mainly destroyed in the spleen owing to an immune mechanism. Why, therefore, is there no splenic enlargement as there is with other diseases?



Question 37


Where exactly is the Traub’s space? How exact is the percussion of the Traub’s space as a sign indicating the size of the spleen?



Question 38


Can you please tell me the indications and complications of blood transfusion.



Question 39


Several times I have read the phrase ‘white blood cells elevated with a left shift’. I am wondering what ‘left shift’ or ‘left deviation’ stands for.



Question 40


What is the clear definition of ‘bleeding time’ and ‘clotting time’? And what are the applied differences between them?



Question 41


What is the meaning of the international normalized ratio (INR) blood test?



Question 42


What is the cause of moderate thrombocytopenia in Bernard-Soulier syndrome? It is a qualitative defect not a quantitative platelet disorder.



Question 43


What is new about thrombopoietin?



Question 44


What is the rationale behind the use of desmopressin in bleeding disorders?



Question 45


What effect does the contraceptive pill have on the blood fibrinogen level and on blood coagulability?



Question 46


Does standard (unfractionated) heparin in doses of 10000-15000 units/day need monitoring?



Question 47


Is there an antidote for low-molecular-weight heparin (LMWH)? Can Enoxaprin be used?



Question 48



1. What is the mechanism of the action of aprotinin?

2. What is the therapeutic window for aprotinin?

3. In a case of haemorrhagic stroke, how many days should aprotinin be prescribed for and what is the recommended dosage?


Question 49


My question is, what are thrombophilia scan tests? Can we use these in patients on anticoagulant therapy?



Question 50


In thromboembolic disorders, how is clopidogrel superior to aspirin?

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Dec 4, 2016 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Haematological disease

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