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Physiology with pharmacology - L1 > Pathophysiology of clotting > Flashcards

Pathophysiology of clotting Flashcards

1
Q

What components are within the ECF (plasma)?

A
  • erythrocytes
  • leukocytes
  • platelets
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2
Q

What is plasma?

A

pale white watery solution of electrolytes, plasma proteins, carbohydrates & lipids

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3
Q

What does pink blood indicate?

A

haemoglobin has been released by haemolysis (rupture of erythrocytes)

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4
Q

What does brown/green blood indicate?

A

high bilirubin (erythrocyte breakdown), liver or gallbladder issue

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5
Q

What does cloudy blood indicate?

A

high levels of cryoglobulins (immunoglobulin) - abnormal increase in viscosity (with cooling), which leads to vessel obstruction + local thrombosis

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6
Q

What is the hematocrit made of?

A

red blood cells (erythrocytes)

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7
Q

How do you establish the hematocrit %?

A

height of erythrocytes/total height

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8
Q

What are the 3 principal proteins found in plasma?

A
  • albumin
  • fibrinogen
  • immunoglobulins
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9
Q

What is the role of albumin?

A

oncotic pressure, binds steroids, Y3 bilirubin, bile salts, FA)

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10
Q

What is the role of fibrinogen?

A

clotting protein, precursor fibrin

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11
Q

What is the role of immunoglobulins?

A

humoral immunity from plasma/B cells

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12
Q

what is factor 1 in the blood coagulation cascade?

A

fibrinogen

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13
Q

what is factor 2 in the blood coagulation cascade?

A

prothrombin

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14
Q

what is factor 3 in the blood coagulation cascade?

A

tissue factor

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15
Q

How many plasma proteins are involved in the blood coagulation cascades?

A

14 (factor 1-13 & vWF)

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16
Q

What is vWF?

A

Von Willebrand factor

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17
Q

What is the most prevalent factor in plasma?

A

albumin

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18
Q

What is fibrinogen important for?

A

important in blood clotting

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19
Q

What is the role of vWF (Von Wilebrand Factor)?

A

Mediates platelet adhesion to damaged vascular subendothelium & subsequently platelet aggregation

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20
Q

What cells in blood play a big role in determining blood viscosity?

A

erythrocytes

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21
Q

Why do erythrocytes have a non-nucleated biconcave disc shape?

A

maximising SA:Vol

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22
Q

What is the main component in erythrocytes?

A

haemoglobin

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23
Q

What maintains the shape of erythrocytes?

A

cytoskeleton

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24
Q

What are erythrocytes anchored to?

A

plasma membrane

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25
Q

What are the 3 main functions of erythrocytes?

A
  1. O2 carriage from lungs to systemic system.
  2. CO2 carriage from tissues to lungs.
    3.Buffering of acids/bases
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26
Q

What are 2 types of white blood cells (leukocytes) are there?

A

granulocytes & non-granular

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27
Q

What are the 3 types of granulocytes?

A
  1. neutrophils
  2. eosinophils
  3. basophils
28
Q

What is the role of neutrophils?

A

phagocytose bacteria

29
Q

What is the role of eosinophils?

A

combat parasites & viruses

30
Q

What is the role of basophils?

A

release IL-4, histamine, heparin & peroxidase

31
Q

What are the 2 types of non-granular leukocytes?

A
  1. lymphocytes
  2. monocytes
32
Q

What is the function of lymphocytes?

A

mature into T cells & B cells (plasma cells)

33
Q

What is the function of monocytes?

A

macrophages & dendritic cells

34
Q

Where are platelets made?

A

bud off from megakaryocytes in bone marrow (TPO - thrombopoietin & IL-3 dependent)

35
Q

Describe the feedback mechanism by which platelets are made?

A
  1. Platelet receptor TPO
  2. Abundant platelets bind TPO
  3. Megakaryocytes not generated
  4. Platelets not made
  5. Receptors don’t bind TPO
  6. TPO stimulates megakaryocytes production
  7. Platelets generated
36
Q

What nucleus-free fragments are found in a platelet?

A
  • mitochondria
  • lysosomes
  • peroxisomes
  • alpha granules (VWF, fibrinogen, clotting factor)
  • dense-core granules (ATP, ADP, Ca2+)
37
Q

Why is it beneficial for platelets to have a circumferential band tubulin microtubules in its inner skeleton?

A

allows for the ability for the platelets to change shape?

38
Q

What is haemostasis?

A

the prevention of haemorrhage

39
Q

What is used in haemostasis?

A
  • vasoconstriction (e.g. thromboxane A, serotonin, thrombin & endothelin-1)
  • increased tissue pressure (decreased transmural pressure - pressure difference between inside & outside of blood vessel)
  • platelet plug (transient) - small breaches in vascular endothelium
  • stabilisation of weak platelet plug with fibrin
40
Q

What are the 3 roles of the platelet plug?

A
  • adhesion
  • activation
  • aggression
41
Q

How is the platelet plug with fibrin?

A

with the addition of fibrin - coagulation/clot formation, a semisolid mass of platelet + fibrin mesh with trapped cells + serum

42
Q

What occurs during platelet adhesion?

A
  • platelet adhesion mediated by platelets receptors bound to ligands
  • breach of endothelium exposes:
  • plasma VWF, which binds to collagen exposed in damaged tissue & platelet receptors
  • endothelial cell VWF factor release also triggered - forming addition links
43
Q

What leads to platelet activation?

A

ligand binding leads to conformation change in receptors. This leads to an intracellular signalling cascade being initiated

44
Q

What is released following platelet activation?

A
  • dense storage granules (ATP, ADP, serotonin, Ca2+)
  • alpha granules (vWF, clotting factor V, fibrinogen)
45
Q

What cytoskeletal changes occur following platelet activation?

A
  • lamellipodium/filopodia
46
Q

What occurs during platelet aggression?

A
  • activation leads to conformation change in the receptors
  • this allows it to bind to fibrinogen - forming molecular bridges between platelets
47
Q

What is a blood clot composed of?

A

semisolid mass of:
- erythrocytes
- leukocytes
- serum
- mesh of fibrin (and platelets)

48
Q

What is the main process that occurs during platelet aggression?

A

activation triggers chain reaction converting precursors to activated factors
- controlled proteolysis amplifies clotting signals

49
Q

What is a thrombus?

A

intravascular clot (not wanted)

50
Q

Describe the intrinsic pathway of clotting

A

initiated by factors within blood in contact with the negatively charged membrane surface of the activated platelet.

  • this causes a cascade of protease reactions. Positive feedback acts at several upstream levels, ending in activated FACTOR XA (FACTOR 10)
51
Q

Describe the extrinsic pathway of clotting

A

Injury to endothelium allows ‘tissue factor’ (receptor) in subendothelial cells to become activated when blood factor VII in contact

  • this leads to activated FACTOR XA (FACTOR 10)
52
Q

What is the function of FACTOR XA (FACTOR 10)?

A

FACTOR XA (FACOTR10) from both intrinsic & extrinsic pathways enters a common pathway to generate THROMBIN (enzyme) and produce stable fibrin?

53
Q

What does generation of thrombin (enzyme) lead to?

A

production of stable fibrin

54
Q

Do velocities increase of decrease from wall to centre?

A

increase (thin layer next to wall cannot move)

55
Q

What is laminar flow?

A

parabolic profile, with maximal velocity (Vmax) at centre

56
Q

What is abnormal (turbulent) flow?

A

non-laminar blood flow leads to endothelial injury

57
Q

What can cause turbulent flow?

A
  • local stenosis (narrowing of blood vessel)
  • large radium (e.g. aorta)
  • high velocity (e.g. high CO - cardiac output)
58
Q

What is arterial thrombosis?

A

the formation of an atherothrombosis (clot in artery), following erosion or rupture of atherosclerotic plaque

59
Q

What is the Virchow triad?

A

the 3 primary factors which can lead to the development of thrombosis:

  1. Endothelial injury
  2. Abnormal blood flow
  3. Hyper-coagulability
60
Q

What is stenosis?

A

The narrow of a blood vessel

61
Q

What is an example of abnormal blood flow?

A

turbulent or stasis (plane/car/bedrest)

62
Q

What is an example of endothelial injury?

A

platelet activation (inflammation/cholesterol)

63
Q

Why might a person experience hyper-coagulability?

A

inherited or through infection or injury

64
Q

What do homeostatic mechanisms to prevent haemostasis aim to achieve?

A

Prevention of blood clot development:
- balance between pathological states of inadequacy & overactive clotting

65
Q

Describe how homeostatic mechanisms promote an anti-thrombotic state

A
  • normal endothelial cells maintain normal blood fluidity through paracrine factors & anticoagulant factors
  • paracrine factors - e.g. prostacyclin promotes vasodilation, nitric oxide (NO) inhibits platelet adhesion & aggregation
66
Q

Describe how homeostatic mechanisms promote a pro-thrombotic state

A
  • event of vascular damage
  • hypoxia (expression of procoagulants)

Physiology with pharmacology - L1 (17 decks)

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