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Haematology Flashcards

(51 cards)

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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?

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

What would cause a failure in the production of platelets?

Study These Flashcards
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?

Study These Flashcards
A

Immune/autoimmune
Drug induced (heparin)
Infections
DIC

24
Q

What would cause dilutional thrombocytonpenia?

Study These Flashcards
A

Massive blood transfusion

25
What do you treat congenital disorders if platelet function with?
Tranexamic acid, platelet transfusion | Avoid antiplatelet drugs
26
Give 2 examples of congenital disorders of platelet function
Bernard-Soulier | Glanzmann's
27
What would cause an acquired disorder of platelet function?
``` Antiplatelet agents (aspirin, NSAIDs) Renal failure Gammaglobulins Cardiopulmonary bypass Myeloproliferative disorders ```
28
Name 4 congenital coagulation disorders
Haemophilia A, Hameophilia B, vWF disease, Factor XI deficiency
29
What is tranexamic acid?
Blocks fibrinolysis | Used in haemophila and platelet function disorders
30
What stimulates red blood cell production?
Decreased O2 supply | Erythropoetin produced by the kidneys
31
What can iron be stored as?
Ferritin, haemosiderin
32
Name 4 symptoms of anaemia
SOB Lethargy Headache Angina
33
Name 2 haemaglobinopathies
Sickle cell | Thalassaemia
34
What is pancytopenia?
White cell, red cell and platelet deficiency
35
What can caused pancytopenia?
Bone marrow failure Bone marrow infiltration (Myelofibrosis, lymphoma, leukaemia, carcinoma) Peripheral consumption/destruction (septicaemia, splenomegaly, immune mediated destruction)
36
What is aplastic anaemia?
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
What anticoagulant is used in a FBC bottle?
EDTA (purple bottle)
38
What is a blood film used for?
Assess red cell size and shape White cell appearances Platelet size and morphology Parasites
39
What does iron deficiency anaemia look like?
Low Hb Hypochromic microcytic red cells Pencil and target cells Low ferritin
40
What does haemolytic anaemia look like?
Low Hb Increased platelets and reticulocytes increased bilirubin Serum haptoglobins low/absent
41
Types of acute leukaemia
Myeloid (AML) | Lymphoblastic (ALL)
42
Pathogenesis of acute leukaemia
Alteration of leukaemia stem cells Development arrested at level of blast Lack of functionally useful and differentiated cells
43
What can cause leukaemia?
``` Ionising radiation Viruses Chemicals Congenital factors (eg Down's) Acquired haematological disorders ```
44
Which acute leukaemia occurs in younger patients?
ALL
45
Signs and symptoms of ALL and AML
``` Bone marrow failure Anaemia (SOB, tired) Neutropenia (sepsis?) Thrombocytopenia (decreased clotting) Infiltration of gums, skin, retina ```
46
What is CML?
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
Signs and symptoms of CML?
``` Fatigue, malaise Anorexia, abdo discomfort Gouty arthritis Priapism (persistent painful erection of the penis) Splenomegaly Pallor ```
48
What is CLL?
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
Why infection common in advanced CLL?
Neutropenia Hypogammaglobulinaemia Impaired immunity
50
CLL can progress into:
Diffuse lymphoma | Prolymphocytic leukaemia
51
Treatment of CLL?
Supportive blood products Treatment of infection (antibiotic, antifungals, antivirals) Specific combination chemo Marrow cell transplant

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