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Human Phiology Y4 > Platelets & Homeostasis (2) > Flashcards

Platelets & Homeostasis (2) Flashcards

1
Q

Where do platelets come from?

A

Platelets are cell fragments shed from megakaryotcytes

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2
Q

Do platelets have any organelles or nucleus?

A

No nucleus but a few organelles = mitochondria and ER fragments

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3
Q

What are megakaryocytes, and where are they found?

A

Extraordinarily large bone marrow-bound cells

Up to 60mm in diameter

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4
Q

What is haemostasis and its function?

A

Haemostasis stops blood loss from damaged small vessels

Stops haemorrhage

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5
Q

What are the steps to the formation of a platelet plug?

A
  1. Circulating platelets adhere to and are activated by exposed collagen at the site of vessel injury
  2. Activated platelets release ADP and Thromboxane A2

3.These chemical messengers work together to activate other platelets passing by

  1. Newly activated platelets aggregate onto the growing platelet plug and release even more platelet-attracting chemicals
  2. The uninjured endothelium releases prostacyclin and nitric oxide, which inhibits platelet aggregation = so platelet plug is confined to the site of injury
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6
Q

How do platelets adhere to collagen?

A
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7
Q

What do activated platelets release?

A
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8
Q

What molecules inhibit platelet aggregation?

A

Prostacyclin
Nitric oxide

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9
Q

What is aspirin used for?

A

Blood thinner = inhibits COX1 pathway
This is important in the release of inhibitors of platelet aggregation

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10
Q

What is the immediate response of an injured blood vessel?

A

Vascular spasm = vasoconstriction to physically reduce the flow of blood leaving the vessel

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11
Q

Overview of clot conversion

A

Prothrombin is converted into thrombin when blood clotting is needed

Thrombin then converts fibrinogen into fibrin

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12
Q

What is the role of fibrin?

A

Stabilizing the platelet plug

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13
Q

How is the fibrin mesh formed?

A

Fibrin monomers crosslink to each order facilitated by factor XIII (13) aka fibrin stabilizing factor

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14
Q

What activates factor 13?

A

Thrombin

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15
Q

What is the difference between the intrinsic and extrinsic clotting pathways?

A

Intrinsic pathway precipitates clotting within damaged vessels AND clotting of blood samples in test tubes

Extrinsic pathway initiates clotting of blood that as escaped into the tissues

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16
Q

What is the role of clot retraction?

A

Platelets trapped within the clot contract and shrink the fibrin mesh = pulling the edges of the damaged vessel closer together

Necessary for haemostasis and wound healing and to restore flow past obstructive thrombi

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17
Q

Describe the extrinsic clotting pathway

A
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18
Q

Describe the intrinsic clotting pathway

A
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19
Q

What initiates the extrinsic clotting pathway?

A

Tissue thromboplastin (factor 3) released from damaged tissue

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20
Q

Where are the clotting factors made and which need Vit K?

A

Liver

2, 7, 9 + 10

21
Q

What dissolves clots?

A

Fibrinolytic plasmin becomes trapped in the clot and later dissolves it by slowly breaking down the fibrin meshwork

22
Q

Why is plasmin important?

A

To prevent inappropriate clot formation

23
Q

What happens when a vessel is being repaired?

A

Fibroblasts form a scar at the vessel defect

24
Q

What is the precursor of plasmin and what converts it to plasmin?

A

Plasminogen converts to plasmin by plasminogen activators

Tissue plasminogen activator (tPA)
Urokinase, streptokinase, staphylokinase
Vampire bat plasminogen activator

25
Q

What is the role of PAI-1?

A

Inhibits tissue plasminogen activator (tPA)
leading to no conversion of plasminogen to active plasmin

26
Q

Where and in what concentrations is PAI-1 found?

A

Present in the blood in small concentrations

27
Q

What does α2-antiplasmin do?

A

Physiological inhibitor of plasmin = prevents fibrin being converted into fibrin degradation products

No degradation of fibrin clots (core of thrombus = prolongs clots

28
Q

What concentraiton is α2-antiplasmin found?

A

Present in blood in concentrations 6-8X exceeding therapeutic dose of plasmin

29
Q

What can inappropriate clotting produce?

A

Thromboembolism

30
Q

What is a thromboembolism?

A

Obstruction of a blood vessel by a blood clot that has become dislodged from another site in the circulation.

31
Q

What is a thrombus/

A

Thrombus = abnormal intravascular clot attached to a vessel wall

32
Q

What is an emboli?

A

Emboli = freely floating clots

33
Q

What causes haemophilia?

A

Deficiency of one of the clotting cascade factors

34
Q

What effect can liver disease have on blood clotting?

A

Inability to synthesize procoagulants
Inability to produce bile and to absorb fat and VitK

35
Q

What is our source of Vit K?

A

Half Vit K comes from gut bacteria other flat from diet

36
Q

What can cause Vit K defieciency?

A

Long-term antibiotic use results in Vit K deficiency and bleeding disorders

37
Q

What is thrombocytopenia?

A

Condition in which number of circulating platelets is too low (less than 50million/m)

Normal range = 200-500million/mL

38
Q

What does thrombocytopenia cause?

A

Spontaneous, widespread haemorrhage
Visible by small purple spots on the skin

39
Q

What causes thrombocytopenia?

A

Damage or destruction of bone marrow either due to cancer or chemotherapy

40
Q

What is the treatment for thrombocytopenia?

A

Fresh whole blood transfusions or platelet transfusion

41
Q

What causes thrombosis?

A

Inappropriate clotting due to roughened surface of a vessel, endothelial cell injury or disturbed blood flow (stasis)

42
Q

Define thrombus

A

Clot that develops and persists in an unbroken blood vessel

Thrombi can block circulation, resulting in tissue death

43
Q

How does blood pressure induce clots?

A

Affects endothelial cells and induces damage, which causes platelet activation

44
Q

What is atherosclerosis, and how does it induce clots?

A

Build up of oxidized LDL, fatty plaques in vessels

Narrows the blood vessels, causing less elasticity and higher blood pressure

45
Q

How is blood type determined?

A

Antigens are present on our RBCs

If RBC has antigen A then the antibody found in plasma will be B because otherwise our antigens would attack the RBCs

46
Q

What is Rh?

A

Resus factor found on RBCs

47
Q

What happens when Type B donates blood to Type A recipient?

A

The recipient has Type B antibodies which will bind to the Type B antigens on RBCs causing agglutination of the blood.

Clumping blocks blood flow in capillaries = oxygen and nutrient flow to cells and tissues is reduced

RBCs usually rupture because *** Hb precipitates in kidney = interfering with kidney function and sensinng

48
Q

What causes the haemolytic disease of the newborn?

A

This disease occurs during second or later pregnancies of an Rh- mother and Rh+ baby. During pregnancy, you don’t share blood with the fetus you’re carrying. However, a small amount of blood from the fetus can mix with your blood during labour and delivery.

The Rh- mother becomes sensitized when Rh+ blood caused her body to synthesize anti-Rh antibodies.

This means the mother has anti-Rh antibodies which cross the placenta and cause agglutination and haemolysis of fetal RBCs

49
Q

How is haemolytic disease of the newborn prevented?

A

Injected anti-RH antibodies eliminate Rh+ cells before they can stimulate the mother to produce her own anti-Rh antibodies

The injected anti-Rh antibodies get ‘washed out’ within weeks

Human Phiology Y4 (7 decks)

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