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Stage 1 Blood > BLD.07 Haemostasis > Flashcards

BLD.07 Haemostasis Flashcards

1
Q

1) What does haemostasis mean?

2) What is its to function

A

1) blood stopping
2) Keep blood within damaged vessel
Still allowing blood flow

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2
Q

1) What is vasoconstriction?
2) Why is vasoconstriction necessary?
3) Which constrict the least effectively torn or cut vessels
4) what is the medical advice for a cut? why?

A

1) constriction of the blood
2) There is pressure in blood vessels due to heart pumping, so to allow a seal to occur pressure needs to be decreased this is done by arteries or arterioles smooth muscles contract and constrict these vessels, while capillaries and veins collapse
3) torn vessels constrict less effectively than cut vessels
4) apply pressure and raise above heart if possible, this reduces pressure within vessel helping formartion of platelet plug

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3
Q

What are the 3 main stages of haemostasis?

A
  1. Vasoconstriction
  2. Platelet aggregation (platelet ‘plug’)
  3. Coagulation
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4
Q

What is the fancy name for platelets?

A

thrombocytes

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5
Q

1) Where are platelets from?
2) How many platelets do we have per decilitre?
3) What is an important feature of platelets that make them an effective seal?
4) Where are platelets stored?
5) What stimulates production of platelets?
6) what negative feedback loop is occurring?
7) What is the lifespan of circulating platelets/

A

fragments that come of megakaryocytes, platelets do not contain nucleus
2)
150-400
3) smaller than RBC, most are circulating
4) Spleen
5) TPO
6) When platelets bind to TPO they inhibit further production
7) 8-12 days

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6
Q

What are the membrane receptor proteins that allows platelets to adhere to collagen? WHy is it important?

A

intergrin, the protein bound to plasma membrane

-important as target of drugs in anticoagulation

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7
Q

What is the initial stimulus in the formation of platelet plug?

A

exposure to collagen in sub endothelial tissue

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8
Q

What factor makes platelets “sticky”?

A

von Willebrands Factor (vWF) released - imagine it sticks to exposed collagen and is released

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9
Q

von Willebrands Factor (vWF) released by…

A

synthesised megakaryocytes and stored in alpha granules in platelets or synthesised and stored in endothelium cells
(makes them sticky)

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10
Q

What do active platelets do?

A

release contents of intracellular granules:

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11
Q
  1. What is the content released from granules in active platelets?
    b) what is the function of their contents?
    c) If possible state what else can release that substance? (other than platelets)
A

1) Serotonin (b) reinforce local vasoconstriction
2) ADP (b) platelet aggregation= platelet plug formation
3) Platelet activating factor (b) activate platelets and stimulates lots of other process including release of thromboxane A2
c) released by platelets and WBC
4) Thromboxane A2- (b)increase
aggregation and vasoconstriction

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12
Q

How is complete blockage of vessel prevented during formation of seal?

A

platelets cannot adhere to normal endothelium due to nitric oxide and prostacyclin

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13
Q

What are the 3 natural mechanisms that keep blood thin and prevent unwanted clotting?
THIS COULD BE VERY WRONG

A

1) secretion of nitric oxide and PGI2 from healthy endothelial cells =inactivation of platelets
2) thrombomodulin is a receptor on the epithelium wall, thrombin attaches to it activating it, thrombin activates protein C, activated protein C degrades factor 5 and 8
3) Heperin sulfate is attached to endothelial cells and activates antithrobin 2 which degrades clotting factor 2, 9 and 10

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14
Q

What initiates the:

1) Intrinsic pathway
2) Extrinisic pathway

A

1) exposed collagen which activates factor 12

2) damaged tissue exposing tissue thromboplastic (or Factor 3)

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15
Q

What occurs in the intrinisic pathway?

A

factor 12 is activated by exposed collagen, then tactivated 12 activates factor 11 with Ca++, activated 11 activates factor 9 with Ca++ .
von Willebrands Factor (vWF) activates 8.
Factor 8 and 9 activate factor 10- along with Ca++ and phospholipids (this is then the common pathway)

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16
Q

What occurs in the extrinsic pathway?

A

factor 3 activates factor 7. factor 7 activates factor 10( along with Ca++ and phospholipids) and 9.

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17
Q

What occurs in the common pathway?

A

activated factor 10 and activated factor 5 as well as Ca++ and phospholipids activates prothrombin (factor 2) to form thrombin (activated factor 2), activated factor 2 causes fribinogen (soluble) to polymerise = fibrin (activated factor 1) (insoluble).
Activated factor 2 also activates factor 13, activated factor 13 and Ca++ causes cross-linking of fibrin= mesh that allows completion of thrombus (clot)

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18
Q

What are 3 positive feedback loops occurring in the coagulation pathway to allow for rapid blood clotting?

A

1) thrombin (activated factor 2) activates factor 11 along with Ca++
2) thrombin (activated factor 2) activates factor 8
3) activated factor 10 activates factor 7

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19
Q 
A) What produces 
1) Heparin
2) Anti-thrombin and thrombomodulin
3) Protein C
B) What are these?
A

1)Basophils
2) Anti-thrombin made in liver and circulates in blood
3) Protien C is made in liver and circulates in blood
B) Anticoagualants

20
Q

1) What does Heparin block?

2) WHat blocks the same things

A

1)Block thrombin and factors
IX, X, XI and XII
2) anti-thrombin and thrombomodulin

21
Q

1) What does anti-thrombin and thrombomodulin block?

2) WHat blocks the same things

A

1)Block thrombin and factors
IX, X, XI and XII
2) Heparin

22
Q

1) What does protein C block?
2) What activates it?
3) What does it work with?

A

1) Block factors
V and VIII
2) Vitamin K
3) Protein S that is also vitamin K-dependent plasma proteins

23
Q

What is fibrinolysis?

A

Fibrin broken down into fragments by plasmin (an enzeyme)

24
Q

What produces plasmin?

2) What is used as medication then for those who have had a myocardial infarction?

A

Plasminogen (found in the clot) is converted by Thrombin (factor 2) and Tissue plasminogen activator (tPA) (molecule on cell surface membrane of endothelial cells) to plasmin.
2) Synthetic tPA

25
Q

1) What occurs after fibrin is broken down by plasmin?

2) Where are fibrinolytic agents present in high concentrations?

A

1) fibrin degradation products are produced which act as anticoagulants.
Fibrinogen is also produced which si degraded by fibrinolytic agents to prevent conversion of fibrinogen back into fibrin.
2) saliva

26
Q

WHat can go wrong with haemostasis?

A

1) Inappropriate clotting leading to an thromboembolic episodes e.g. pulmonary embolus and Disseminated intravascular coagulopathy (DIC)

27
Q

Why do inappropriate clots form in vessels?

A

1) Scarring (atherosclerosis)
2) Foreign surfaces (prosthetic heart valves)
3) Slow blood flow (varicose veins in the legs, restricted circulation- pocket valves are damadged to blood doesn’t flow at a high pressure)
4) Altered blood factors

28
Q

What is Disseminated intravascular coagulopathy (DIC)?

A
  • this is when microclots form (clots forming all over body-they form due to release of factor 3 from lots of damadged tissues in the body
    –use up all factors, fibrin and platelets
    -increases in FDPs cause reduced fibrin production
    could bleed to death
29
Q

How are embolisms formed?

A

clots brake of and travel through blood vessels

30
Q

How can deep vein thrombosis (DVT ) lead to pulmonary embolus?

A

a clot dislodges forms in a deep vein (usually in the lower limb) , the clot brakes off and drains into the inferior vena cava and the heart pumps the embolus into the pulmonary vein, the embolus becomes lodged in pulmonary vein and if it is large enough causes pulmonary infarct.

31
Q

What are the 3 main reasons deep vein thrombosis occur?

A

1) slowed blood
2) damdge to blood vessel
3) blood has a higher tendency to clot than usually

32
Q

1) What does aspirin do?

A

prevents platelet plug formation by preventing synthesis of thromboxane 2 through inhibiting an enzyme

33
Q

1) What does warfarin do?

2) What do patients recieve warfarin have to carry due to risks?

A

blocks action of vitamin K which is essential to lots of clotting factors e,g, thrombin,
2) patients who receive this carry an anticoagulation alert card/wear bracelet

34
Q

What treatment would someone who has had a myocardial infarction recieve?
2) Why?

A

1) synthetic tPA
and anti-platelet drugs
2) as the heart attack is caused by death of cardiac cells due to artery being blocked by clot and this medication will reduce the number of thrombi formed in the entire body

35
Q

WHat does synthetic tPA do?

2) WHat does anti-platelet drugs do?

A

1) is tissue plasminogen activator works with thrombin to form plasmin from plasminogen, = plasmin brakes down thrombus
2) inhibit integrin receptors on platelets binding to collagen= no platelet plug formed

36
Q

What the 3 main causes of haemostatic disorders?

A

1) vascular abnormality
2) platelet disorders
3) reduced fibrin production (coagulopathy)

37
Q

1) What are the causes of vascular abnormalities that lead to haemostatic disorders?

A

1) Collagen disorder –Marfan syndrome as means intrinsic pathwya isn’t initaited and vessels are weaker
Vit C deficiency (scurvy)- as platelets can’t bind properly to collagen

38
Q

What are the causes of platelet disorders that lead to haemostatic disorders:

1) quantitiative
2) qualitative

A

1) Thrombocytopenia at less than 60 x 10^9/dl ( lack of platelets)
Thrombocythaemia (too many platelets)

2)Thrombopathy
issue in quality of platelets,

39
Q

What are the causes of reduced fibrin production (coagulopathy)that lead to haemostatic disorders?

A
  1. haemophilias

2. von Willebrand disease

40
Q

What is the cause of thrombocytopenia?

A

1) idiopathic(unknown)
2) bone marrow suppression:
- chemotherapy,
- leukaemia

41
Q

1) what is petechiae?
2) What are purpura?
3) What is on cause of these 2 marks?

A

1) Less than 3mm red spot on skin that doesn’t disappear when pressure is applied
2) larger than 3mm red spot on skin that doesn’t disappear when pressure is applied
3) thrombocytopenia- as it causes little bleeds all over the body

42
Q

What is the cause of thrombopathy?

-issue to do with platelet quality

A

-drug induced: aspirin, clopidogrel

These drugs prevent platelets adhering to one another

43
Q

1) How is haemophilia A and B inherited?
2) WHich factor do each lead to a deficiency in?
3) Which is more common?
4) What is the treatment for haemophilias?
5) What are the effects of haemophilia on the patient? What treatment should be considered in more detail due to the patient having the condition?

A

1) X-linked recessive
2) A= factor 8
B= factor 9 (Memory builder: also known as christmas disease as was discovered in a man called christmas, haemophilia B factor nine deficiency around the christmas tree)
3) Haemophilia A is more common
4) Infusion of factors in blood, expensive so are also looking at gene therapy
5) Spontaneous bleeding in joints which lead to deformities and also cause spontaneous gingival bleeding which is something to consider when your going to do an extraction

44
Q

What is haemophilia?

WHat occurs as usual? what isn’t occuring? Why is this bad?

A
  • which is when a factor is defective or lacking, There is a normal vascular and platelet
    haemostatic response so platelet plug is formed but no clotting occurs so no thrombosis is formed. This is bad as platelet plug is weak
45
Q

What is von Willebrand disease?

2) what doesn’t happen then that normally would in certain types of von Willebrand disease?
3) What are the effects on the patient of this condition? what can it eventually cause?
4) Will the patient have all these symptoms?

A

the most commonly inherited bleeding disorder

2) - platelet adhesion to collagen and thus no platelet aggregation either= no platelet plug formed
- factor 8 activation and preservation doesn’t occur so common pathway cannot be activated by intrinsic pathway
3) nose bleeds, bruising, gingival bleeding, heavy menstruation, post surgery bleeding =leading to anaemia
4) no there are varying levels of the condition

Stage 1 Blood (7 decks)

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