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Advanced Haematology > Week 6 > Flashcards

Week 6 Flashcards

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1
Q

List 3 contents of a platelet?

A

lysosomes, granules and membrane,

microtubules

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2
Q

Granules are key in primary hemostasis; list some things that they contain (6)

A
  • ADP
  • Thromboxane
  • Platelet factor 4
  • Adhesive and aggregation glycoproteins
  • Coagulation factors
  • Fibrinolytic inhibitors
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3
Q

What stage in hemostasis does platelet aggregation initiate?

A

Secondary hemostasis through the coagulation cascade

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4
Q

Coagulation system needs to be regulated

or it would continually produce what?

A

thrombi.

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5
Q

Clotting factors have antagonists what are they?

A

Anti-coag agents that can cleave them.

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6
Q

Define thrombosis

A

inappropriate formation of platelet or fibrin clots that

obstruct blood vessels.

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7
Q

List two resulting risks of thrombosis

A

ISCHEMIA i.e loss of blood flow,

NECROSIS i.e. tissue death.

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8
Q

List some contributors to thrombosis

A
  • Blood flow e.g. stasis
  • Coagulation system
  • Platelet function
  • Leucocyte activation molecules
  • Blood vessel walls
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9
Q

EMBOLI = fragments of thrombi - how can this cause ischemia?

A

move to right chamber of heart

  • lodge in arterial pulmonary vasculature
  • cause ischaemia & death of lung tissue
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10
Q

What are 3 types of arterial thrombosis?

A

Myocardial infarction
Cerebrovascular accidents
Transient ischaemic attacks (TIA)

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11
Q

Atherosclerosis is fatty plaque with what 3 things?

A
  • Activated platelets
  • Monocytes
  • Macrophages
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12
Q

Atherosclerosis suppresses the release of ___________ molecules like Nitric oxide and Exposes __________ substances like Tissue factors

A

anti-thrombotic, prothrombotic

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13
Q

In atherosclerosis unstable plaques rupture, releasing what?

A

thrombotic mediators - platelets + vWF, minimal fibrin

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14
Q

List 3 risk factors for atherosclerosis.

A
  • Total cholesterol
  • LDL-cholesterol
  • HDL-cholesterol
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15
Q

Factor V Leiden, Prothrombin G20210A are common genetic mutations relating to what?

A

CONGENITAL thrombosis

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16
Q

APC acts as an anticoagulant by proteolytically inactivating which 2 factors? and which protein enhances this anticoag activity

A

FVa & FVIIa

Protein S

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17
Q

WARFARIN impacts which proteins?

A

Prot C, S & Z

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18
Q

Antithrombin is a serine protease inhibitor (serpin) which binds an neutralises all serine proteases except which factor?

A

FVIIa

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19
Q

What is prothrombin G20210A

A

Mutation at base 20210 in the

prothrombin (FII) gene.

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20
Q

Mildly increased prothrombin levels leads to increased risk of what?

A

increased risk of thrombosis

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21
Q

Factor V Leiden is most common inherited cause of increased risk of venous thrombosis. T-F

A

T

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22
Q

Normally APC breaks down which factor?

A

FVa

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23
Q

Factor V Leiden is a variant of which factor?

A

V

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24
Q

Factor V Leiden is a mutation because of a _____ ______ substitution. Factor V Leiden is also a mutation that makes FV resistant to ______ cleavage

A

amino acid, APC

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25
T-F; FV Leiden mutation also known as APC resistance
T
26
List some Acute causes of DIC | Hint: Deficiencies of multiple haemostasis components.
Obstetric emergencies, Septicaemia, viraemia | Burns, Acute inflammation, Crush injuries, Aortic aneurysm, Cardiac disorders
27
List some Chronic causes of DIC
Liver disease, Renal disease, Chronic inflammation, Prosthetic devices, Vascular tumors
28
DIC is characterised by loss of normal ______ control | in response to sustained systematic injury
haemostatic
29
In thrombocytopenia what happens to the production, destruction, and distribution of platelets?
Decreased production, increased destruction and abnormal distribution
30
What are the 2 categories of abnormalities in platelet PRODUCTION?
Megakaryocyte hypoplasia, Ineffective thromobopoiesis
31
Is Acute ITP (idiopathic thrombocytopenia purpura) primarily seen in children or adults?
children
32
Acute ITP Usually manifest 1 to 3 weeks after an __________
infection
33
In Chronic ITP _________ coated platelets are destroyed in RE system
Antibody | Autoantibodies in 50% of cases
34
ITP patient blood film morphology • RBC and leucocytes _______ • Platelets _____________ • MPV
RBC and WBC - normal Platelets - reduced in number, may be large MPV may be increase
35
In ITP Coagulation studies what would the results be for tests that rely on platelet function
* Abnormal | * Bleeding time, clot retraction time
36
Immune mediated thrombocytopaenia can be secondary to what conditions?
* Chronic lymphocytic leukaemia * System lupus erythematosus * Parasitic infection e.g. Malaria
37
The mechanism of _________ is to bind to antithrombin, enhance inhibition of FIIa, FXa. Used for prophylaxis against thrombosis
Heparin
38
What is the mechanism in Heparin induced thrombocytopenia (HIT)?
develop IgG Antibody to heparin – Platelet Factor 4 complex
39
Heparin induced thrombocytopenia leads to what 3 things?
Platelet activation Decreased platelet count Formation of microvascular thrombi
40
HELLP syndrome stands for .....
Haemolysis, Elevated Liver enzymes, Low Platelet count
41
Thrombotic thrombocytopaenic purpura caused by a RARE inherited mutation of which gene?
ADAMTS13
42
What cleaves vWF into smaller fragments?
ADAMTS13
43
Cleaved fragments of vWF bind to what?
exposed collagen
44
Platelets some receptors bind to vWF, others | to what?
fibrinogen
45
In TTP the ADAMTS13 enzyme is deficient or blocked | by an __________, cleaving of large multimeric vWF chains is inhibited
autoantibody
46
Large chains of multimeric vWF bind to areas of endothelial damage, and initiate recruitment of large numbers of _______ into large aggregates
platelets
47
Large numbers of sites with large platelet | aggregations cause what 3 potential things?
* Thrombocytopaenia * Microangiopathic haemolytic anaemia * Organ ischaemia
48
Large numbers of sites with large platelet | aggregations cause what 3 potential things?
• Thrombocytopaenia • Microangiopathic haemolytic anaemia • Organ ischaemia TAI
49
Is TTP intravascular or extravascular | haemolysis?
Intravascular
50
What would you expect to find on a blood film of a patient with TTP?
Schistocytes, low platelets, polychromasia
51
What would you expect the PT, APTT and fibrinogen test results be for a patient with TTP
Normal PT, APTT, fibrinogen - note these results differentiate TTP from DIC.
52
What form of therapy would restore the presence of ADAMTS13 enzyme, reduces platelet aggregation in small vessels.
Plasma infusion
53
What would dilute the autoantibodies to ADAMST13?
Plasma exchange
54
What is the name of the CD20 binding | monoclonal antibody that binds to the B-cells that are producing the autoantibody, mediating their destruction
Rituximab
55
Haemolytic uraemic syndrome (HUS) resembles what other disorder?
TTP | HUS is seen mainly in children 6 mths to 4 years
56
90% of cases of haemolytic uraemic syndrome relate to presence of bacteria in GI tract. Which bacteria?
* Shigella dysenteriae → Shiga toxin | * Eschericia coli
57
In HUS and TTP which features predominantly renal and which features predominantly neurological?
HUS - Renal | TTP - Neurological
58
Give 2 examples of a qualitative disorder of adhesion receptors. (tip) both are - Rare, autosomal recessive disorders
1. Bernard-Soulier Syndrome (BSS) or Giant platelet syndrome | 2. Glanzmann Thromboasthenia
59
What would be the treatment for bernand-soulier syndrome, and Glanzmann Thromboasthenia?
Platelet transfusions → Develop allo-antibodies
60
What would the results of aggregation studies for Bernard-Soulier Syndrome (BSS) be for ADP, epinephrine, collagen & AA, Ristocetin
Normal to ADP, epinephrine, collagen & AA NO response to Ristocetin (instab of P :VWF binding) ↓ response to thrombin
61
What would the lab findings be for Glanzmann Thromboasthenia? FBC, Platelet count, Bleeding time, Platelet aggregation studies
``` FBC: Normal Platelet count : Normal Bleeding time: prolonged Platelet aggregation: Risto – normal Others NO response ```

Advanced Haematology (13 decks)

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