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Clinical Biomedicine > W7: Assessing Haemostasis :((((( > Flashcards

W7: Assessing Haemostasis :((((( Flashcards

1
Q

5 steps of haemostasis

A

vessel spasm
platelet plug formation
coag
clot retraction
clot dissolution

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2
Q

define coag

A

fluid blood converted into a gelatinous clot.
converts platelet plug into a more stable clot.

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3
Q

how is thrombin generated?

A

from prothrombin at sites of tissue injury

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4
Q

what does thrombin catalyse?

A

conversion of fibrinogen to fibrin

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5
Q

diff btwn intrinsic and extrinsic

A

E - need molecules from tissue
I - molecules already in blood

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6
Q

what does plasmin do?

A

plasmin cleavage of crosslinked fibrin creates d-dimers (fibrin degradation prods)

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7
Q

what might cause bleeding disorders (insufficient haemostasis)?

A

defs of platelet no or function, or defs in coag factors

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8
Q

what might cause thrombosis (inapprop haemostasis)?

A

arterial - inapprop stim of platelets (rupture of atherosclerotic plaques)
venous - defs in inhibitors of coag factors

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9
Q

S&S of thrombotic disorders (depending on location of thrombus)

A

coronary arteries: chest pain
carotids arteries: FAST
deep veins of legs: unilateral leg pain

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10
Q

S&S of bleeding defects: pts present w/

A

easy bruising (purpura/petechiae/ecchymoses)
mucosal bleeding (epistaxes, menorrhagia, GI, GU)
haemarthrosis
complications w surgery/trauma/venepuncture

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11
Q

what is a bruise?

A

micro or macroscopic tearing
leaked blood cell are phagocytosed & degraded -> colour changes:
red-blue: Hb
green: biliverdien
yellow: bilirubin
golden: hemosiderin

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12
Q

sizes of haematomas

A

Petechiae - <3mm
Purpura – 3mm – 1cm
Ecchymoses - >1cm

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13
Q

issues w/ platelet plug formation are what type of disorders?

A

primary haemostatic

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14
Q

abnormal bleeding may result from 4 causes…

A

vascular defects (weak vessels – leak)
decr platelet number (thrombocytopenia)
decr platelet function (disorders of platelet function)
decr coagulation

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15
Q

primary haemostatic disorders vs coag disorders: e.g.

A

thrombocytopenia, VWD
haemophilia

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16
Q

primary haemostatic disorders vs coag disorders: bleeding

A

immediate
delayed

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17
Q

primary haemostatic disorders vs coag disorders: petechiae

A

yes
no

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18
Q

primary haemostatic disorders vs coag disorders: epistaxes

A

common
uncommon

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19
Q

primary haemostatic disorders vs coag disorders: menorrhagia

A

common uncommon

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20
Q

primary haemostatic disorders vs coag disorders: haemarthroses

A

no
yes

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21
Q

primary haemostatic disorders vs coag disorders: intramuscular haematomas

A

uncommon
common

22
Q

primary haemostatic disorders vs coag disorders: gender

A

equal
>80% male

23
Q

haemostatic investigations: blood film/smear

A

morphology
clumping platelets

24
Q

haemostatic investigations: FBC

A

EDTA removes Ca - so clotting can’t occur
thrombocytosis vs thrombocytopenia

25
Q

haemostatic investigations (platelet tests): bleeding time

A

normal = 3-8 min

26
Q

haemostatic investigations (platelet tests): PFA-100

A

replaced bleeding time
mem coated w/ molecules that would activate platelets, aggreg would decr flow, if platelets not activated, no effect on flow

27
Q

haemostatic investigations (platelet tests): platelet aggregation studies

A

aggreg of platelets, gaps btwn clumps, so light can pass thru
see how diff activators affect aggreg

28
Q

haemostatic investigations (platelet tests): flow cytometry

A
29
Q

haemostatic investigations (platelet tests): aspirin-specific tests

A

serum thromboxane & aspirinworks
5-40% of ppl don’t respond to aspirin (don’t want to be taking it & experiencing side effects, if it doesn’t work for you)
Test if they do respond by measuring thromboxane levels
Need to know before surgery if someone’s taking aspirin (bc aspirin reduces clotting)

30
Q

haemostatic investigations (coag tests): PT

A

assesses extrinsic pathway. Many clotting factors in extrinsic pathway require vit K for their synthesis, therefore, the prothrombin time can be used to assess pts on warfarin. (warfarin use ↓).

Warfarin blocks vit K cycling, so less CFs prod

31
Q

normal value for PT

A

11-16 sec

32
Q

haemostatic investigations (coag tests): aPTT

A

assesses intrinsic pathway, which is initiated by exposure of collagen (due to vessel damage)

33
Q

normal value for aPTT

A

30-40 sec

34
Q

haemostatic investigations (coag tests): TT

A

assesses final stages of common pathway
no ca needed (ca independent)

35
Q

normal values for TT

A

15-19 sec

36
Q

normal platelet count
normal PT
normal aPTT
normal TT

A
  • Disorder of platelet function
  • Factor XIII deficiency
  • Disorder of vascular haemostasis
  • Severe bleeding w/ normal haemostasis
37
Q

normal platelet count
long PT
normal aPTT
normal TT

A
  • Deficiency or defect of the extrinsic pathway.
  • Rare FVII deficiency
  • Start of oral anti-coagulant therapy (Warfarin)
38
Q

normal platelet count
normal PT
long aPTT
normal TT

A

Deficiencies or defects of intrinsic pathway
FVIII / IX (Haemophilia A / B), FXI, FXII, prekallikrein, HMWK.
- Von Willebrands Disease
- Anti-coagulants

39
Q

normal platelet count
long PT
long aPTT
normal TT

A

Vit K deficiency
- Oral anti-coags (Warfarin)
- Deficiencies in FV, VII, X and II

40
Q

normal platelet count
long PT
long aPTT
long TT

A

Heparin
- Liver disease
- Fibrinogen deficiency
- Hyperfibrinolysis

41
Q

low platelet count
normal PT
normal aPTT
normal TT

A

thrombocytopenia

42
Q

low platelet count
long PT
long aPTT
normal TT

A

Massive transfusion
- Liver disease (could affect thrombopoietin prod & CF prod)

43
Q

low platelet count
long PT
long aPTT
long TT

A

DIC
acute liver disease

44
Q

haemostatic investigations (further tests): factor assays

A

testing for deficiencies
If pt plasma diluted in normal plasma the prolonged clotting time should be corrected.
Diluting in various plasmas that are deficient in specific CFs can indicate which factor missing/reduced.

45
Q

haemostatic investigations (Further tests): inhibitor assays

A

If pt plasma is added to normal plasma & incubated for 2h, any inhibitors present in pt plasma will cause the normal plasma to have prolonged clotting times.

46
Q

haemostatic investigations (Further tests): PCR

A

Families w/ bleeding disorders may undergo risk assessment by analysis of
Pedigree
Phenotype
Genotype
Mutations commonly identified by PCR amplification of DNA.
Most commonly used for analysis of Haemophilia A/B & von Willebrands Disease.

47
Q

D-dimer assays:

A

Raised w/ fresh venous thrombosis.
Also elevated in cancer, inflammation after surgery or trauma, but -ve result helps exclude DVT.

48
Q

which CFs are involved in intrinsic?

A

12
11
9
8
(10)

49
Q

which CFs are involved in extrinsic?

A

3
7
(10)

50
Q

which CFs are involved in common?

A

1
2
5
10
13

Clinical Biomedicine (23 decks)

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