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SBOMs > Haematology > Flashcards

Haematology Flashcards

1
Q

What is APTT?

A

Activated partial thromboplasmin time

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2
Q

What is haemostasis?

A

Process whereby haemorrhage following vascular injury is arrested
Tightly regulated by vascular endothelium, platelets, coagulation factors and fibrinolysis

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3
Q

What is activated in injury of the vascular wall?

A

Tissue factor-> coagulation cascade
Collagen exposure and vWF-> platelet activation
Vasoconstriction-> stable plug

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4
Q

How does the endothelium usually act as an anticoagulant?

A

Prostacyclin, NO, heparin sulphate

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5
Q

What are platelets derived from?

A

Megakaryocyte shards

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6
Q

What stimulates platelet production?

A

Thrombopoetin

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7
Q

How long do platelets circulate for before being destroyed?

A

6-8 days

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8
Q

Describe the extrinsic pathway in the coagulation cascade

A 
Tissue injury-> tissue factor and phospholipids
F7->F7a
F8-> F10->F10A
Prothrombin-> thrombin
Fibrinogen-> fibrin
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9
Q

Describe the extrinsic pathway in the coagulation cascade

A 
-ve surface (collagen/plastic)
F12-F12A
F11-F11A
F9->F9A
F10-> F10A
Prothrombin-> Thrombin
Fibrinogen-> Fibrin
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10
Q

What initiates fibrinolysis?

A

Coagulation cascade
tPA (tissue plasminogen activator)
urokinase-like plasminogen activator

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11
Q

Plasminogen does what?

A

Turns into plasmin, degrades factor 5&7

Fibrin-> soluble products

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12
Q

What does a blood count and film show?

A

Number and morphology of platelets

May show leukaemia

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13
Q

When is PT (prothrombin time) extended?

A 
Abnormal factor II, V, VII, X
Liver disease
Warfarin
Vitamin K deficiency
DIC
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14
Q

What is DIC?

A

Disseminated intravascular coagulation

Seen in septicaemia and post partum haemorrhage

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15
Q

When is APTT prolonged?

A

Deficiency/inhibition of II, V, VII, IX, X, XI, XII
Unfractionated heparin therapy
Vitamin K deficiency
DIC

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16
Q

What is a correction test?

A

Add normal plasma to patient’s plasma so its 50:50
See if clotting time corrects
If it does it is a deficiency not an inhibitor

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17
Q

What do you look for in a bleeding disorder examination?

A

Signs of systemic diseases
Skin, mouth, fundi, joints
Easy bruising?
Purpura, bruising, petechiae

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18
Q

What is scurvy?

A

Vitamin C deficiency

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19
Q

What are Henoch-Schönlein purpura?

A

Small vessel vasculitis
Purple nodules that do not disappear on pressing
Intradermal bleeding
Seen in young males
+glomerulonephritis, joint pain, abdo pain

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20
Q

What is haemorrhagic telangiectasia?

A

Small red/purple clusters if dilated capillaries on skin or surface of organs

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21
Q

What is thrombocytopenia?

A 
Low platelet count
Failure of production?
Increased consumption?
Dilutional?
Abnormal distribution?
22
Q

What would cause a failure in the production of platelets?

A 
Selective megakaryocyte depression
Dugs/chemicals/viral infections
Part of generalised bone marrow failure
Leukaemia, lymphoma, cancer
Aplastic anaemia
HIV
23
Q

What would cause an increased consumption of platelets?

A

Immune/autoimmune
Drug induced (heparin)
Infections
DIC

24
Q

What would cause dilutional thrombocytonpenia?

A

Massive blood transfusion

25
Q

What do you treat congenital disorders if platelet function with?

A

Tranexamic acid, platelet transfusion

Avoid antiplatelet drugs

26
Q

Give 2 examples of congenital disorders of platelet function

A

Bernard-Soulier

Glanzmann’s

27
Q

What would cause an acquired disorder of platelet function?

A 
Antiplatelet agents (aspirin, NSAIDs)
Renal failure
Gammaglobulins
Cardiopulmonary bypass
Myeloproliferative disorders
28
Q

Name 4 congenital coagulation disorders

A

Haemophilia A, Hameophilia B, vWF disease, Factor XI deficiency

29
Q

What is tranexamic acid?

A

Blocks fibrinolysis

Used in haemophila and platelet function disorders

30
Q

What stimulates red blood cell production?

A

Decreased O2 supply

Erythropoetin produced by the kidneys

31
Q

What can iron be stored as?

A

Ferritin, haemosiderin

32
Q

Name 4 symptoms of anaemia

A

SOB
Lethargy
Headache
Angina

33
Q

Name 2 haemaglobinopathies

A

Sickle cell

Thalassaemia

34
Q

What is pancytopenia?

A

White cell, red cell and platelet deficiency

35
Q

What can caused pancytopenia?

A

Bone marrow failure
Bone marrow infiltration (Myelofibrosis, lymphoma, leukaemia, carcinoma)
Peripheral consumption/destruction (septicaemia, splenomegaly, immune mediated destruction)

36
Q

What is aplastic anaemia?

A

Anaemia caused by bone marrow failure/stem cell defect/growth factor defect
Bone marrow is ‘empty’
A version of pancytopenia, defined by a bone marrow biopsy

37
Q

What anticoagulant is used in a FBC bottle?

A

EDTA (purple bottle)

38
Q

What is a blood film used for?

A

Assess red cell size and shape
White cell appearances
Platelet size and morphology
Parasites

39
Q

What does iron deficiency anaemia look like?

A

Low Hb
Hypochromic microcytic red cells
Pencil and target cells
Low ferritin

40
Q

What does haemolytic anaemia look like?

A

Low Hb
Increased platelets and reticulocytes
increased bilirubin
Serum haptoglobins low/absent

41
Q

Types of acute leukaemia

A

Myeloid (AML)

Lymphoblastic (ALL)

42
Q

Pathogenesis of acute leukaemia

A

Alteration of leukaemia stem cells
Development arrested at level of blast
Lack of functionally useful and differentiated cells

43
Q

What can cause leukaemia?

A 
Ionising radiation
Viruses
Chemicals
Congenital factors (eg Down's)
Acquired haematological disorders
44
Q

Which acute leukaemia occurs in younger patients?

A

ALL

45
Q

Signs and symptoms of ALL and AML

A 
Bone marrow failure
Anaemia (SOB, tired)
Neutropenia (sepsis?)
Thrombocytopenia (decreased clotting)
Infiltration of gums, skin, retina
46
Q

What is CML?

A

Chronic myeloid leukaemia
Clonal proliferation of primitive haematopoietic stem cells
Characterised by chromosomal marker ‘philadelphia chromosome’ translocation (9; 22)
Leads to increased tyrosine kinase activity

47
Q

Signs and symptoms of CML?

A 
Fatigue, malaise
Anorexia, abdo discomfort
Gouty arthritis
Priapism (persistent painful erection of the penis)
Splenomegaly
Pallor
48
Q

What is CLL?

A

Chronic lymphoblastic leukaemia
Clonal proliferation and accumulation of immune incompetent B-lymphocytes
Insidious onset
Infiltration of spleen, lymph nodes, liver
Most patients are over 50yrs old

49
Q

Why infection common in advanced CLL?

A

Neutropenia
Hypogammaglobulinaemia
Impaired immunity

50
Q

CLL can progress into:

A

Diffuse lymphoma

Prolymphocytic leukaemia

51
Q

Treatment of CLL?

A

Supportive blood products
Treatment of infection (antibiotic, antifungals, antivirals)
Specific combination chemo
Marrow cell transplant

SBOMs (18 decks)

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