Brainscape's Knowledge GenomeTM

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


See full index

blood > haemostasis > Flashcards

haemostasis Flashcards

coagulation & anticoagulation

1
Q

what are primary and secondary haemostasis?

A

primary: formation of platelet plug
secondary: formation of blood clot

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

what is thrombopoiesis?

A

the process of forming thrombocytes/platelets in the bone marrow

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

what is the process of thrombopoiesis?

A

thrombopoietin (TPO) activates myeloid stem cells→ megakaryocytes→ thrombocytes→ negative feedback (↓TPO)

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

what is the process of formation of platelet plug (primary haemostasis)?

A

exposed collagen→ platelets adhere & activate→ platelets form appendages to increase attachment surface, and release granules containing platelet agonists for aggregation→ attract more platelets→ platelets aggregate to form plug→ positive feedback loop (release more platelets)

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

how do platelets adhere to exposed collagen

A
  • primary haemostasis
  • mediated by Von Willebrand’s Factor (vWF) (plasma proteins produced by platelets)
  • vWF binds platelets to exposed collagen via Gp1b
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what factors mediate platelet aggregation? (3)

A

platelets release granules containing agonists:
1. ADP: attracts & activates more platelets
2. Thromboxane A2: promotes aggregation & further vasoconstriction
3. fibrinogen: links platelets through glycoprotein receptors (link r WEAK! need secondary haemostasis)

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

what are the triggers of intrinsic pathway? (2)

A
  1. exposure to collagen fibres
  2. exposure to foreign surface eg glass
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the triggers of extrinsic pathway? (1)

A

damaged tissues releasing tissue factor or thromboplasin

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

what is the process of coagulation cascade?

A

extrinsic: 12a→ 11a→ 9a→(+8a)→ 10a
intrinsic: 7→ (+ tissue factor/thromboplastin/3)→7a→ 10a
common pathway: 10a→ (+5a)→ thrombin/2a→ fibrin/1a→ (+13)→ fibrin meshwork

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the actions of thrombin? (2)

A
  1. activates factor 13→ 13a (fibrin stabilising factors for fibrin→ meshwork)
  2. cleaves & activates fibrinogen (fibrin→ fibrin monomer)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the process of fibrin meshwork formation?

A

10→ 10a→ prothrombin→ thrombin→ fibrinogen→ fibrin monomer (→ fibrin strand)→ + factor 13 (crosslinks strands)→ fibrin meshwork

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

what are the measures of coaguation cascade? (2)

A
  1. PT (prothrombin time)
  2. aPTT (partial thromboplastin time)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what does PT evaluate?

A

extrinsic pathway
normal time: ~10s (less time)

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

what does aPTT evaluate?

A

intrinsic pathway
normal time: ~25-35s (more time)

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

what factors require Vit K for production? (4)

A

2, 7, 9, 10
(2+7=9)+1=10

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

what are (most) common factors made of?

A

plasma protein
(except factor 3/tissue factor/thromboplastin that is a mixture of glycoprotein & phospholipids)

17
Q

where are (most) common factors of coagulation cascade produced in?

A

liver
(except factor 3 that’s produced by damaged tissues)

18
Q

what is the pathology of non-palpable/blanchable rashes + frequent nose bleeding

A

problem with primary haemostasis (small damages in capillary are usually healed by platelet plugs)→ vWF disease?

19
Q

what are the 3 processes of anticoagulation?

A
  1. plug prevention (primary haemostasis): NO + prostacyclins
  2. clot prevention (secondary haemostasis): TFPI + APC/S + AT
  3. clot removal (fibrinolysis)
20
Q

how are aberrant plug & clot prevention carried out? (3)

A

intact & smooth endothelial cells release:
1. Nitric Oxide (NO) & prostacyclins that inhibit platelet activation/aggregation
2. TFPI (Tissue Factor Pathway Inhibitor) to inhibit extrinsic pathway
3. thrombomodulin & protein C receptor that sequesters/inactivates thrombin & activates protein C/S

21
Q

what is the process of protein C & S activation?

A

thrombomodulin binds to thrombin and EPCR binds Protein C→ bring Protein C to thrombin-thrombomodulin complex→ activate Protein C→ binds circulating Protein S→ forms APC-PS complex (active protease)→ cleaves & inactivates factor 5a & 8a (common pathway)

22
Q

what are anti-thrombins (AT) and its functions?

A
  • plasma protein produced by liver
  • binds & inhibits thrombins & 10a & 9a that leak from clots (ensure clotting is localised to damaged site)
23
Q

what is the process of clot removal (fibrinolysis) after wound healing?

A

intact endothelial cells release Tissue Plasminogen Activator (TPA)→ binds to plasminogen in presence of fibrin→ forms plasmin (protease)→ fibrin degradation products (FDP) released into circulation

24
Q

how is fibrinolysis regulated? (3)

A
  • no TPA from damaged vessels (only INTACT endothelial cells)
  • low TPA affinity to plasminogen in absence of fibrin
  • circulatory PAI (plasminogen activator inhibitor) & anti-plasmin inhibits TPA & plasmin that strays into circulation
25
Q

what are the clinical uses of FDP?

A

crosslinked fibrins release D-dimers (fibrin fragment containing 2 D domains & crosslink) upon fibrinolysis→ circulatory D dimers indicate thrombotic event

26
Q

what is thrombosis?

A

clot formation that results in occlusion of a blood vessel (clotting > anti-clotting)

27
Q

what factors increase the risk of thrombus formation?

A

VIRCHOW’S TRIAD
1. venous stasis
2. hypercoagulability
3. endothelial damage

28
Q

what is venous stasis + examples?

A

slow blood flow reduces propensity of anti-coagulants to interact w coagulation factors
e.g. surgery, prolonged immobilisaition

29
Q

what is hypercoagulability + examples?

A

thrombophilia: conditions that increase tendency for clot formation (love to clot!)
e.g. oral contraceptives, cancer/tumour, hereditary thrombophilia

30
Q

what is endothelial damage + examples?

A

intact & smooth endothelial walls inhbit plug/clot formation→ destroyed :(
e.g. high blood pressure, smoking, fatty foods, atherosclerosis

31
Q

examples of hereditary thrombophilia (4)

A

less anticoagulants:
1. Anti-thrombin 3 deficiency
2. protein C deficiency
3. protein S deficiency

stronger factors:
4. factor 5 Leiden (factor 5 resistant to cleavage activity by APC-PS complex)

32
Q

what is haemophilia?

A
  • love to bleed! (not enough clotting factors)
  • X-linked recessive disorder
33
Q

what are the causes of haemophilia? (4)

A

less platelets:
- von Willebrand’s disease

less factors:
- congenital haemophilia A (factor 8 deficient)
- congenital haemophilia B (factor 9 deficient)
- acquired haemophilia (due to autoantibodies)

congenital haemophilia lead to bleeding into joints

blood (2 decks)

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