heamostasis

Question 1

define heamostasis

Answer 1

blood stoping process by combination of fibrin clot and platelets aggregate

Question 2

define thrombosis

Answer 2

formation/precense of a clot within a vessel

Question 3

define embolism

Answer 3

obstruction of vessel from blood clot that got stuck travelling through blood stream

Question 4

platelets normal functioning

Answer 4

stick to damaged blood vessels and begin heamostasis process. needed for cuts or constant cuts in mouth, uterus, skin etc…

Question 5

too much platelet sticking

Answer 5

attaching to blood vessels and block blood pathway
= arterial thrombosis

Question 6

too little platelet sticking

Answer 6

from low/dysfunctional platelets
= bleeding from mucosal surfaces, GI, bruising

Question 7

Coagulation - what is it, too little, too much

Answer 7

jelly component, made of fibrin.
too much causes clot forming in veins eg:; DVT
too little causes bleeding disorders from lacking coagulative factors eg: patients on anticoagulant meds

Question 8

thrombin role

Answer 8

converts fibrinogen to fibrin

Question 9

platelets in injury repair (4)

Answer 9

normally epithelium secretes anticlotting agents.
1. blood vessel lining is activated or damaged
2. platelets stick to damaged endothelium and underlaying matrix
3. platelets secrete ADP and thromboxane to recruit more platelets
4. platelets use fibrinogen and von Willebrand factor to stick together. they activate the coagulation system to reinforce fibrin plug

Question 10

platelets: adhesion and activation

Answer 10

endothelial cells at injure site release von willebrand which binds to receptors on platelets and sub-endothelial collagen

Question 11

Von Willebrand factor - description and disease

Answer 11

big protein critical for platelets plug
most common bleeding disorder, autosomal dominant genetic.
deficiency = loss of platelet function = mucosal bleeding (menorrhagia, gingival, bruising, GI bleeding)

Question 12

thrombocyptopenia - def, causes, symptoms

Answer 12

low platelet count
causes: autoimmune, chemotherapy, drug reaction
symptoms: bruising, petechia, mucosal bleeding

Question 13

coagulation - clotting cascade overview

Answer 13

different clotting factors are activated
they all activate factor Xa
causes conversion of prothrombin to thrombin
thrombin converts fibrinogen to fibrin.
there are naturally occurring anticoagulants aswell.

Question 14

hemophilia A

Answer 14

factor 8 deficiency
on X chromosome, male disease

Question 15

bleeding disorders - coagulation factor deficiency

Answer 15

heamophilia
acquired factor 8 deficiency:
- liver disease - fails to synthesise the clotting factors
- warfrin - anticoagulant that blocks complete synthesis of clotting factors

Question 16

venous thromboembolism

Answer 16

excessive coagulation causes thrombosis, esp in deep veins of leg.

Question 17

DVT - causes, what can it lead to

Answer 17

from post surgery, immobilisation: obesity, cast, bed..
worse when in pro-thrombic states (older, cancer, genetic, woman).
can lead to pulmonary embolism where clot travels to lungs and causes ischemia.

Question 18

Venous thrombus - cause, consequences,

Answer 18

coagulation forms a clot - fibrin gel is the most key factor not platelets.
consequences: loacl pain, swelling, discoloration, ppl 50% asymptomatic from blood flowing into collateral vessels = ppl dont realise until it embolises and tey get SOB, chest pain or drop dead.

Question 19

venous thrombosis c- omplications

Answer 19

pulmonary embolism
- SOB, chest pain, bloody sputum
post thrombotic syndrome
- pain, oedema, heaviness, itching, skin hardening + discolouration
- vessel doesnt recanalise = blocked (so need to treat asasp)
venous ulceraion
- severe post thrombotic syndrome

Question 20

Pulmonary embolism - predisposition

Answer 20

cancer patients
immoblised
hypercoagulable state

Question 21

pulmonary embolism - factors of presentation + outcome

Answer 21

dependent on extent of pulmonary arterial BF obstruction, size of occluded vessel, number of alveoli, over all CV health

Question 22

PE consequences

Answer 22

death
resp compromise
hemodynamic compromise
risk of recurrence

Question 23

extrinsic pathway of coagulation

Answer 23

damage of endothelial calls makes them produce tissue factor
tissue factor converst 7 -> 7a
7a converts 10 ->10a
10 a converts prothrombin -> thrombin

Question 24

intrinsic pathway of coagulation

Answer 24

convert 12 ->converts 11 -> converts 9 -> converst 10 -> prothrombin -> thrombin

Question 25

effects of inadequate CV function or larger PE

Answer 25

tisseu downstream fom occlusion is infarcted
haemorrhagic infarct:
- ischemic necorsis, leaky vessles, heamorrhagic, fibrous scarring, RBC lysing in first 48h = pale infarct

Question 26

effects of multiple PE over time

Answer 26

pulmonary hypertension (clot blocks in blood in the right side so tension develops)
right ventricular failure = cor pulmonare

Question 27

D dimers - definition, significance

Answer 27

protein frgaments prpoduced by fibrinolysis (fibrin break down).
elevated in DVT and PE, cancer, infection, age, pregnancy
D dimer presence = indication of PE of DVT

Question 28

thrombophilia

Answer 28

abnormality of coagulation which predispose patients to thrmobosis
acquired or inherited

Question 29

anticoagulants for venous thrombosis

Answer 29

rivaroxaban
dabigatran
wafrin

Question 30

DVT/PE prophylaxis

Answer 30

from anticoag meds
post op mobilisation + physio
compression stocking

Question 31

Arterial thrombosis

Answer 31

platelets bind to damaged endothelium. this forms arterial clots

Question 32

arterial thrombosis - normal endothelial vs injured endithelium

Answer 32

produces anticlotting and antiplatelets to prevent things sticking to it.
on damaged endothelium, platelets stick and recruit coagulation. tissue factor also recruits coagulation process

Question 33

consequences of platelet thrombi

Answer 33

heart attack: coronary artery atherosclerosis = thrombosis = MI
storke: carotid artery emboli and cerebral artery thrombosis
leg ischemia: peripheral vascular disease
intestinal infarction: mesenteric artery atherosclerosis

Question 34

platelets activation + antiplatelet drugs

Answer 34

they have receptors for activators: thrombin, ADP, fibrinogen, thromboxane.
antiplatelets: aspirin (blocks thromboxane production), clopidogrel (blocks ADP receptor)

Question 35

atrial fibrilation

Answer 35

inefficient pumping which can cause clot formation in left atrial appendage and embolise to brain = stroke