Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Haematology > Haematology Conditions > Flashcards

Haematology Conditions Flashcards

(83 cards)

Start Studying
1
Q

Which drugs can commonly cause platelet dysfunction?

A

NSAIDs
Aspirin
Clopidogrel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How can you differentiate between platelet disorders caused by destruction of platelets and those caused by deficiencies of platelets?

A

Look at megakaryocytes (platelet precursors) on bone marrow examination - they will be high in destruction and low in deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the causes of platelet dysfunction?

A

Drugs - NSAIDs, aspirin
Uraemia e.g. in end stage renal failure
Myeloproliferative disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is immune thrombocytopenia purpura?

A

Destruction of platelets caused by autoantibody to antigen on the platelet surface.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the differences in clinical presentation of immune thrombocytopenic purport (ITP) in adults and in children?

A

Adults: Slow onset, no identified infective cause, requires treatment, chronic / relapsing

Children: Acute onset usually of bruising, usually follows viral infection, usually self-limiting and not requiring treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What treatment is used for ITP (immune thrombocytopenic purpura)?

A
  • Oral corticosteroids e.g. prednisolone (produces response in 60-80% of patients)
  • Immunoglobulin infusion e.g. IV IgG
  • Splenectomy (because platelets are destroyed in the spleen)
  • Thrombopoeitin agonist
  • Rituximab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 5 key features of thrombotic thrombocytopenic purpura?

A
  • Thrombocytopenia
  • Microangiopathic haemolytic anaemia
  • Neurological disturbance
  • Fever
  • Renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the pathophysiology of thrombotic thrombocytopenic purpura?

A

Deficiency in ADAMTS 13 - a protease which is normally responsible for degredation of vWF. Results in thrombus formation in the smallest vessels, profound thrombocytopenia and end-organ ischaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes thrombotic thrombocytopenic purpura?

A

Congenital
Sporadic e.g. pregnancy
Autoimmune e.g. SLE
Drug induced e.g. clopidogrel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the treatment of thrombotic thrombocytopenic purpura?

A

Plasma exchange - removes the ADAMTS 13 autoantibody
Steroids e.g. methylprednisolone
Rituximab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is disseminated intravascular coagulation (DIC) and what causes it?

A

Massive activation of the clotting cascade usually due to traumatic processes to the vascular endothelium. Causes include sepsis, burns, advanced cancer, obstetric complication, major trauma, acute promyelocytic leukaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When would you suspect a patient is suffering from post-transfusion purpura?

A

Thrombocytopenia occuring 10 days after transfusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the pathophysiology which causes post-transfusion purpura?

A

Affects patients who lack the HPA-1a antigen on their platelet surface (about 98% of the population DO have this antigen). When transfused with HPA-1a positive platelets, the recipient develops an antibody to them and their own platelets will cross react with the new ones, causing thrombocytopenia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the treatment of post-transfusion purpura?

A

Intravenous immunoglobulin

Avoid HPA-1a positive platelet transfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do aspirin and NSAIDs affect platelet function?

A

Inhibit cyclo-oxygenase 1 enzyme and thus prevent thromboxane synthesis which consequently decreases platelet aggregation (because thromboxane causes platelet aggregation)

Aspirin does this irreversibly, while the mechanism in NSAIDs is reversible.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why is recombinant Factor VIII preferable in patients with Haemophilia A than plasma-derived Factor VIII?

A

Hep C and HIV infections have historically been associated with plasma-derived Factor VIII so recombinant is much safer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What might cause Vitamin K deficiency?

A

Malnutrition
Malabsorption e.g. in obstructive jaundice
Warfarin treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is a thrombus?

A

A mass in the lumen of a vessel, made up of fibrin and blood components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

True or false - Thrombus formation can only occur in the venous system

A

False. Thrombus formation can occur in either venous or arterial vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is Virchow’s Triad?

A

Describes 3 prerequisites for thrombus formation:

1) Stasis e.g. in venous obstruction due to tumour, bed rest, long plane/car journey, plaster cast
2) Damage to vessel wall e.g. atheroma, trauma, invasion by malignancy
3) Hypercoagulability e.g. pregnancy, oestrogen therapies, thrombophilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

List some rick factors for venous thromboembolism

A

Age >60, obesity (BMI > 30), immobility, high oestrogen (e.g. pregnancy, postpartum, contraceptive pill, HRT), trauma and surgery, ITU admission, history of VTE, FHx of VTE, thrombophilic disorders, varicose veins with phlebitis, dehydration, medical comorbidities (e.g. heart disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Define the term ‘thrombophilia’

A

Patients with an increased tendency towards thrombus formation (usually venous), due to an inherited or acquired cause.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Give 4 inherited disorders of thrombophilia

A

Factor V Leiden
Prothrombin 20210A Mutation
Protein C and Protein S Deficiency
Antithrombin Deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

List some clinical features of DVT

A 
Pain and swelling of affected limb
Calf tenderness
Local increase in temperature
Unilateral oedema
Accentuation of venous pattern
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is the use of the Well's Score?
Assesses a patient's pre-test probability of having a DVT and directs further investigation and management. If score 1 or less, DVT is unlikely (Perform D-dimer: If -ve exclude DVT, if +ve perform ultrasound)...If score 2 or more, DVT is likely (Perform D-dimer and ultrasound and only exclude DVT if both negative)
26
What is the treatment for DVT?
LMWH e.g. enoxaparin 1.5mg/kg/24hrs or fondaparinux. Continue this for at least 5 days, until INR stable at 2-3 for 2 days Start warfarin simultaneously...most treated for 3 months (longer if unprovoked DVT or high risk of recurrence)
27
List the 4 types of leukaemia
Acute myeloid leukaemia Acute lymphoblastic leukaemia Chronic myeloid leukaemia Chronic lymphocytic leukaemia
28
What is the commonest malignancy in childhood?
Acute lymphoblastic leukaemia
29
What is occurring in acute lymphoblastic leukaemia?
Malignancy involving the lymphoid tissue, responsible for production of T and B lymphocytes. There is arrested maturation and rapid proliferation of immature blast cells, with bone marrow failure and tissue infiltration.
30
List 5 clinical features of tissue infiltration in acute leukaemia
``` Lymphadenopathy Gum hypertrophy Hepatosplenomegaly Rash CNS involvement ```
31
List some clinical features of acute lymphoblastic leukaemia
Signs of bone marrow failure: anaemia, infection, bleeding Signs of tissue infiltration: hepatosplenomegaly, lymphadenopathy, orchidomegaly, CNS involvement (meningism, cranial nerve palsies)
32
CNS involvement is more common in which type of acute leukaemia?
Acute lymphoblastic leukaemia. It is rare in acute myeloid leukaemia.
33
What is the key treatment for chronic myeloid leukaemia...and why?
Imatinib It's a BCR/ABL tyrosine kinase inhibitor which targets the specific Philadelphia mutation involved in CML
34
Which is the most common leukaemia?
CLL
35
Which cell is characteristic of Hodgkin's lymphoma?
Reed-Sternberg cell. It has a mirror-image nuclei.
36
What is the peak incidence of Hodgkin's lymphoma?
2 peaks - one in young adults and one in elderly people
37
How is lymphoma diagnosed?
Tissue biopsy of lymph nodes
38
How is Hodgkin's lymphoma classified?
``` I = One nodal region affected II = Involvement of 2 or more nodal regions on the same side of the diaphragm III = Nodal involvement on both sides of the diaphragm IV = Spread beyond the lymph nodes e.g. to liver, bone marrow ``` Each stage is either 'A' or 'B' defined by the absence or presence of B symptoms.
39
What are 'B' symptoms?
>10% weight loss in 6 months Night sweats Unexplained fever >38 degrees
40
What are the 4 drugs involved with the treatment of Hodgkin's lymphoma?
ABVD Adriamycin Bleomycin Vanblastine Dacarbazine
41
Give 2 low-grade and 2 high-grade Non-Hodgkin's Lymphomas
Low grade: Follicular NHL, marginal zone lymphoma | High grade: Diffuse large B-cell lymphoma, Burkitt's lymphoma
42
What is polycythaemia?
Increase in red cell mass - this may be relative (due to normal red cell mass but decreased plasma volume e.g. in dehydration) or absolute (i.e. actual rise in red cell mass)
43
List some causes of absolute polycythaemia
Primary - polycythaemia rubra vera Secondary - due to hypoxia (high altitude, chronic lung disease, cyanotic congenital heart disease etc.), or inappropriate EPO production
44
What mutation is present in >90% of patients with polycythaemia rubra vera?
Mutation in JAK2
45
How might a patient with polycythaemia rubra vera present?
- May be asymptomatic and only picked up via FBC - Non specific signs of hyper viscosity: headache, dizziness, tinnitus, visual disturbance - Itching after a hot bath - Erythromelalgia (burning in hands and feet) - Facial plethora - Signs of arterial or venous thrombosis
46
What might you see on the blood count of someone with polycythaemia rubra vera?
Raised RCC, Hb, HCT, PCV, WCC and platelets | Raised B12
47
What is essential thrombocythaemia?
Malignant proliferation of megakaryocytes causing persistently raised platelets
48
What is the treatment for essential thrombocythaemia?
Aspirin 75mg daily Or Hydroxycarbamide if over 60 years old or previous thrombosis
49
Give some causes of neutropenia
Drugs: Carbimazole, colchicine, chemotherapy, clonazepine, carbamazepine Radiotherapy Bone marrow failure Sequestration in spleen e.g. Felty's Syndrome Viral infections Benign Ethnic Neutropenia Autoimmune conditions
50
What is thalassaemia?
A haemoglobinopathy - Abnormal production of one or more types of haemoglobin 'globin' chains. There is precipitation of globin chains within red cells, resulting in cell damage, ineffective erythropoiesis, and haemolysis.
51
List some clinical features of beta thalassaemia major
``` Presents in 1st year of life Severe anaemia Failure to thrive Recurrent infections Skull bossing Hepatosplenomegaly ```
52
List some clinical features of beta thalassaemia trait
Asymptomatic carrier state | Anaemia is mild and usually well tolerated (reduced Hb, MCV and MCH)
53
How would you treat beta thalassaemia?
Regular blood transfusions (every 2-4 weeks) Iron chelators Ascorbic acid to increase urinary excretion of iron
54
Give 2 causes of relative polycythaemia
Dehydration | Diuretics
55
What is the treatment for absolute polycythaemia?
Regular venesections to keep haematocrit
56
What is the inheritance pattern of sickle cell anaemia?
Autosomal recessive
57
What is the pathophysiology of sickle cell anaemia?
Deoxygenated HbS polymerises, causing abnormal 'sickle' red blood cells. These sickle cells are fragile and can undergo haemolysis. They also cause occlusion in small vessels.
58
What is the character of the anaemia in sickle cell anaemia?
Hb 60-90g/L | Raised reticulocytes
59
What does the blood film show in sickle cell anaemia?
Sickle cells | Target cells
60
How long can erythrocytes for transfusion be kept?
Up to about 35 days They are stored at 4 degrees
61
True / False: Platelets are stored at 4 degrees
False Platelets are stored at room temperature. Red blood cells are stored at 4 degrees.
62
When might someone be given fresh frozen plasma (FFP)?
When a patient is actively bleeding and has abnormalities in their clotting tests. Also warfarin reversal e.g. in urgent surgery
63
What type of antibodies are the A, B and O antibodies?
IgM
64
What is the mechanism of action of [unfractionated] heparin?
Binds to and activates antithrombin. This inhibits thrombin and other proteases (especially Factor Xa) which are involved in clotting.
65
Give 3 example of low molecular weight heparins
Dalteparin Enoxaparin Tinzaparin
66
What is the difference in mechanism between unfractioned heparin and LMWH?
Unfractionated heparin binds to antithrombin to increase it's ability to inactivate thrombin. LMWH just inactivates Factor Xa
67
What is the method of administration of LMWH?
subcutaneous injection
68
What might be some advantages of using unfractionated heparin?
In patients with high bleeding risk - can be stopped quickly as has a very short half life Also consider in renal failure patients where LMWH might be inappropriate due to accumulation
69
List some side effects of using heparin
Bleeding Thrombocytopenia (heparin-induced thrombocytopenia) Hyperkalaemia Osteoporosis (with long-term use)
70
What is the mechanism of action of warfarin?
Inhibits a reductase enzyme responsible for regenerating active Vitamin K, thus leaving Vitamin K 'deficient'
71
What is the target INR for a patient with DVT or PE on warfarin?
2-3 or 3.5 if recurrent
72
What is the target INR for a patient with a prosthetic heart valve?
3-4
73
What is the target INR for a patient with AF who is on warfarin?
2-3
74
What is the treatment durations for a patient on warfarin with DVT / PE?
If provoked below knee DVT = 6 weeks If provoked above knee DVT or PE = 3 months If unprovoked = 6 months
75
How would you measure the effect of unfractionated heparin?
Measure the APTT
76
Give 2 examples of Factor Xa inhibitors
Rivaroxaban | Apixaban
77
Give an example of a direct thrombin inhibitor
Dabigatran
78
What is Bence-Jones protein and when is it relevant?
Free immunoglobulin light chains (kappa and lambda type) which are filtered by the kidney into the urine in 2/3 of cases of myeloma.
79
List some clinical features of myeloma
``` Bone pain/pathological fractures Anaemia, neutropenia, thrombocytopenia Renal failure Recurrent infections (due to increased levels of IgG and/or IgA but low levels of all other immunoglobulins) Hypercalcaemia ```
80
What might you see on blood film of a patient with myeloma?
Rouleaux
81
What is the diagnostic criteria for myeloma?
Monoclonal band on urine or serum electrophoresis Raised plasma cells on bone marrow biopsy Signs of end-organ damage from myeloma e.g. hypercalcaemia, anaemia, renal impairment Bone lesions
82
What investigations would you carry out for suspected myeloma and what would they show?
FBC - Normochromic, normocytic anaemia ESR raised due to hyperviscosity Blood film - Rouleaux formation Urine test - Bence Jones protein Serum immunoglobulins - Certain types will be raised U+Es - Raised urea, creatinine (due to renal failure) and calcium (due to increased osteoclast activity) Bone marrow sample - Raised plasma cells X-ray - Lytic bone lesions, collapse fractures
83
What is the treatment for myeloma?
``` Required if there are symptoms: Bisphosphonates Analgesia Blood transfusion or EPO for anaemia Chemotherapy: Steroids, cytotoxic IVIg for infections if necessary ```

Haematology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions