Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haematology > Thrombocytopenia > Flashcards

Thrombocytopenia Flashcards

1
Q

How is mild thrombocytopenia defined?

A

Platelet count 100,000 - 150,000

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

How is moderate thrombocytopenia defined?

A

Platelet count 50,000 - 100,000

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

How is severe thrombocytopenia defined?

A

Platelet count <50,000

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

What are the possible clinical features of thrombocytopenia?

A

Mucocutaneous bleeding - petechiae, epistaxis
Immediate bleeding after surgery
bleeding from mucocutaneous surfaces e.g. gingival, gastrointestinal, vaginal

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

What is pseudothrombocytopenia and how does this occur?

A

This is when the platelet count appears low due to a lab error.
EDTA in the sample tube can cause platelets in some people’s blood to clump together

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

What are the three main aetiologies of thrombocytopenia?

A

Failure of production of platelets
Shortened lifespan of platelets
Sequestration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Give examples of causes of thrombocytopenia which fall under the category of ‘failure of production’

A 
Drugs
Infection
Myelofibrosis
Malignant infiltration
Megaloblastic anaemia
Leukaemia
Myelodysplasia
Aplastic anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give examples of causes of thrombocytopenia which fall under the category of ‘non-immune mediated shortened lifespan’

A

Disseminated intravascular coagulation

Thrombotic thrombocytopenic purpura

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

Give examples of causes of thrombocytopenia which fall under the category of ‘immune mediated shortened lifespan’

A 
ITP
Connective tissue disorders
Antiphospholipid syndrome
Infection
Post-transfusion purpura
Neonatal alloimmune thrombocytopenia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Give examples of causes of thrombocytopenia which fall under the category of ‘sequestration’

A

Hypersplenism

Cardiopulmonary bypass surgery

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

What is immune thrombocytopenia purpura?

A

ITP is an autoimmune condition in which antibodies are produced against platelets

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

Describe the pathophysiology of immune thrombocytopenia purpura?

A

In ITP the spleen produces IgG antibodies which bind to the platelets receptor GPIIbIIIa. This targets the platelet-antibody complexes for destruction in the spleen. This lowers the platelet count and makes it harder for bleeding to stop.

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

What age group is typically affected by each of acute and chronic immune thrombocytopenia purpura?

A

Acute - children

Chronic - adults

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

What type of immune thrombocytopenic purpura usually follows viral illness?

A

Acute ITP

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

Compare and contrast acute and chronic immune thrombocytopenic purpura in terms of onset and duration of illness

A

Acute ITP has a sudden onset and last a few weeks - most cases resolve themselves within 2 months
Chronic ITP has an insidious onset and can last for years or be a lifelong illness. Spontaneous remission is rare.

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

What group of people are most susceptible to chronic immune thrombocytopenic purpura?

A

Females of reproductive age

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

Chronic immune thrombocytopenic purpura can be secondary to which conditions?

A

HIV
Hepatitis C
Lupus

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

What are purpura?

A

Red / purple spots on. the skin measuring 0.3-1cm in diameter

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

In severe cases of immune thrombocytopenic purpura, when platelet count is very low, frequent mucosal bleeding can occur. What is the most usual presentation of this?

A

Epistaxis (nosebleeds)

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

Immune thrombocytopenic purpura is often asymptomatic. T/F?

A

True

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

Immune thrombocytopenic purpura is associated with splenomegaly. T/F?

A

False

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

What would you expect from the FBC results of a patient with immune thrombocytopenic purpura?

A 
Isolated thrombocytopenia
(In some cases if there has been significant bleeding there may also be anaemia due to blood loss)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the management of acute immune thrombocytopenic purpura

A

Observation only

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

How are patients with immune thrombocytopenic purpura with an active bleed or platelet count <30,000 managed?

A

Corticosteroids - if patients don’t respond to steroids, splenectomy may be performed
IV immunoglobulins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How are patients with immune thrombocytopenic purpura with a platelet count <10,000 managed?

A

Platelet transfusions

26
Q

Give examples of drugs associated with thrombocytopenia

A 
Heparin
Diazepam
Sulphonamides
Cephalosporins
Penicillin
Gold salts
Aspirin
Rifampicin
Quinine
Tolbutamide
Thiazides
Ranitidine
27
Q

Describe the pathophysiology of how heparin can cause thrombocytopenia

A

Heparin binds to a protein on the surface of inactivated platelets called paltelet factor 4 (PF4). Together they form the heparin-PF4 complex which is immunogenic in some people, meaning they have circulating IgG antibodies which recognise the complex as foreign pathogens. Thus, these antibodies bind to the heparin-PF4 complex and mark it for destruction in the spleen

28
Q

Describe the pathophysiology of how heparin induced thrombocytopenia leads to an increased risk of thromboembolism

A

The immune response against heparin causes the activation of platelets which release procoagulants that result in further platelet activation. The original platelet also releases more PF4 sp. that antibodies bind to keep it activation. This causes clot formation throughout the body in which platelets are consumed and this furthers thrombocytopenia

29
Q

How long after the administration of heparin does it usually take for heparin induced thrombocytopenia to develop?

A

1-2 weeks

30
Q

How soon can heparin induced thrombocytopenia develop in a patient who has previously been treated with heparin?

A

A day

31
Q

What is the gold standard test for the diagnosis of heparin induced thrombocytopenia?

A

Serotonin release assay

32
Q

The widespread formation of abnormal clots can lead to life-threatening thrombotic events. How does these most commonly present?

A

Venous thrombosis e.g. DVT and PE

33
Q

How is heparin-induced thrombocytopenia managed?

A

Immediately stop heparin and start anticoagulation with a non-heparin anticoagulant
Anticoagulation continues until the platelet count normalises or, if a thrombotic event occurs, for 3-6 months

34
Q

What is disseminated intravascular coagulation?

A

DIC is a complex clinical syndrome in which there is simultaneously too much and too little clotting.

35
Q

List some common causes of disseminated intravascular coagulation?

A 
Infections - particularly sepsis
Obstetric emergencies - septic abortion, abruptio placentae
Shock - surgical trauma, burns
Severe haemolytic transfusion reaction
Liver disease
36
Q

Describe the pathophysiology of disseminated intravascular coagulation

A

DIC starts with a trigger which causes the release of a procoagulant which causes the coagulation cascade to go into overdrive. This results in widespread clot formation, causing blockage of medium and small vessels. This leads to ischaemia and necrosis which particularly effects the kidneys, liver, lungs and brain. The massive formation of clots throughout the body depletes the supply of platelets and clotting factors. Additionally as clots are broken down through fibrinolysis, fibrin graduation products are released into the circulation which interfere with platelet aggregation and clot formation. Thus bleeding occurs.

37
Q

How does disseminated intravascular coagulation usually present?

A

Widespread bleeding in an ill patient

Oozing of blood from cannulation sites is characteristic

38
Q

What are the typical laboratory findings in DIC?

A 
Reduced platelet count
Prolonged PT and APTT
Prolonged thrombin time
Reduced fibrinogen level
Elevated d-dimers
39
Q

In what patients is it more common for DIC to occur as a more chronic process?

A

Patients with certain solid tumours of aortic aneurysms

40
Q

How is DIC managed?

A

By treating the underlying cause and using supportive measures such as transfusions

41
Q

What are the three characteristic features of haemolytic uraemic syndrome?

A

Microangiopathic haemolytic anaemia
Thrombocytopenia
Acute renal failure

42
Q

What is the typical trigger of haemolytic uraemic syndrome?

A

E.coli 0157 infection causing bloody diarrhoea

43
Q

Typical haemolytic uraemic syndrome typically occurs in what age group?

A

Children

44
Q

Describe the pathophysiology of how e.coli 0157 infection causes haemolytic uraemic syndrome?

A

E.coli o157 attaches to the intestinal wall and secretes a toxin (shiga-like toxin). This toxin is absorbed and taken up by immune cells which transport the toxin on their surface to the site of blood filtration - the glomerular capillaries of the kidneys. The glomerular capillaries express the Gb3 receptor which has a strong affinity for the shiga-like toxin. Thus the toxin binds and becomes engulfed by endothelial cells and acts to cause apoptosis of these cells. This disruption of the endothelial cell lining leads to the formation of many small blood clots in the kidneys. These clots cause the characteristic features of HUS: microangiopathic haemolytic anaemia, thrombocytopenia and acute renal failure

45
Q

Describe how the formation of clots in the kidneys results in microangiopathic haemolytic anaemia as occurs in haemolytic uraemic syndrome?

A

The clots that. form in these vessels act as boulders in a river, making it difficult for RBCs to flow through without becoming damaged. Thus the blood clots result in the formation fo schistocytes (cell fragments). This cell destruction causes microangiopathic haemolytic anaemia

46
Q

Atypical HUS is caused by rare abnormal clots forming in the kidneys which is not associated with preceding diarrhoea illness. T/F?

A

True

47
Q

What are the symptoms fo haemolytic uraemic syndrome?

A

Symptoms of anaemia - fatigue, weakness, lethargy
Pre-hepatic jaundice
Symptoms of thrombocytopenia - easy bruising and purpura
Signs of renal failure - proteinuria, haematuria

48
Q

What would you expect to see on blood tests in haemolytic uraemic syndrome?

A

Elevated. kidney waste products - urea and creatinine
Anaemia
Thrombocytopenia

49
Q

What would you expect to see on blood film in haemolytic uraemic syndrome?

A

Evidence of schistocytes

50
Q

How is typical haemolytic uraemic syndrome treated?

A

Supportive treatment as the shiga-like toxin will clear from the body within days - weeks. Antibiotics are not recommended as this can cause lysis of bacteria and further toxin release which furthers disease

51
Q

How is atypical haemolytic uraemic syndrome treated?

A

By managing the underlying cause

52
Q

What is thrombotic thrombocytopenic purpura?

A

TTP is a disorder which. results in clot formation in small blood vessels throughout the body, resulting in thrombocytopenia, haemolytic anaemia and often kidney, heart and brain dysfunction

53
Q

Give examples of common triggers of thrombotic thrombocytopenic purpura?

A

Bacterial infections
Medications
Autoimmune diseases (e.g. SLE)
Pregnancy

54
Q

What is the name of the condition in which individuals have inherited thrombotic thrombocytopenic purpura?

A

Upshaw-Schilman syndrome

55
Q

Describe the pathophysiology of thrombotic thrombocytopenic purpura

A

In TTP, the ADAMTS13 enzyme which normally acts to break down Von Willebrand factor, is not active. Thus there is excess vWF in the blood which leads to inappropriate clot formation which consumes platelets causing thrombocytopenia. In most cases, the underlying mechanism involves antibody inhibition of the ADAMTS13 enzyme.

56
Q

What is the classical presentation of thrombotic thrombocytopenic purpura?

A 
Fever
Changes in mental status
Thrombocytopenia
Reduced kidney function
Microangiopathic haemolytic anaemia
(although the classic presentation occurs in <10% of cases)
57
Q

What neurological symptoms might occur in thrombotic thrombocytopenic purpura?

A 
Tiredness
Confusion
Headaches
Seizures
Stroke
58
Q

How can thrombotic thrombocytopenic purpura and haemolytic uraemic syndrome be differentiated?

A

By checking ADAMTS13 and shiva-like toxin levels

Neurological symptoms are more commonly associated with TTP

59
Q

The treatment of choice for thrombotic thrombocytopenic purpura is plasmapheresis. What is plasmapheresis?

A

This is an exchange transfusion involving removal of the person’s blood plasma via aphaeresis and replacement with donor plasma

60
Q

Other than plasmapheresis, how is thrombotic thrombocytopenic purpura treated?

A

Infusion of fresh frozen plasma
Corticosteroids
Immunosuppressive therapy

Haematology (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions