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Medicine yr1 > CVS-atherosclerosis, circulation and clotting > Flashcards

CVS-atherosclerosis, circulation and clotting Flashcards

1
Q

what is an embolus?

A

material that causes blockage

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2
Q

what is an embolism?

A

when the embolus gets lodged in a blood vessel (e.g. pulmonary embolism)

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3
Q

name some types of embolism

A
  • blood clot (thrombus)
  • fat embolism (fat globule)
  • gas embolism (bubble of air)
  • amniotic fluid embolism (amniotic fluid)
  • foreign material
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4
Q

what is atherosclerosis?

A

development of an atherosclerotic plaque in tunica intima of large/ medium sized arteries (e.g. coronary arteries)

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5
Q

where do atherosclerotic plaques build up?

A

tunica intima of medium/ large arteries

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6
Q

what is plaque made up of?

A
  • fat
  • cholesterol
  • calcium
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7
Q

what happens to plaque over time and what does this cause?

A

plaque hardens and narrow arteries-decreasing blood flow to tissues

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8
Q

when does the formation of a lesion start (beginning of plaque build-up)?

A

in young children

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9
Q

what risk factor increasing the formation of lesions?

A

high fat diet

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10
Q

what is the earliest significant lesion called?

A

fatty streak

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11
Q

what do fatty streaks consist of?

A

lipid-containing foam cells in the artery just deep to the endothelium

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12
Q

what do fatty streaks evolve into?

A

evolve into atherosclerotic plaques; which remain stable or regress

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13
Q

outline the steps of fatty streaks formation and development into atherosclerotic plaques

A
  • injury to endothelium of artery caused monocyte adhesion and loosening of endothelial cell junctions
  • monocytes migrate deep to endothelium and differentiate into macrophages
  • macrophages phagocytose LDLs (enter initima via permeable endothelium) –>now foam cells
  • progressive accumulation of lipid/ smooth muscle in intima forms (via cytokines released by T cells)
  • growing lesion begins to raise endothelium and encroach on lumen of artery–>atherosclerotic plaque
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14
Q

what are the two types of atherosclerotic plaques?

A
  • stable

- unstable

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15
Q

how are stable atherosclerotic plaques formed?

A
  • they are slow growing plaques which expand gradually due to the accumulation of lipid in foam cells and migration and proliferation of smooth muscle cells
  • fibrin cap on lesion matures
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16
Q

what does atherosclerotic narrowing of coronary artery lead to?

A

stable angina

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17
Q

what is stable angina characterised with?

A

chest pain that comes on during exertion

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18
Q

how do unstable plaques form?

A
  • grow more rapidly as a result of more rapid lipid deposition
  • have a thin fibrin cap-prone to rupture-can trigger acute thrombosis (by activating platelets and clotting cascade)
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19
Q

what happens when an unstable plaque ruptures?

A

-mural thrombosis forms on top of ruptured plaque

–>causes variable obstruction of coronary artery–>unstable angina

(can also cause death of cardiac muscle just under endocardium->subendocardial infarction)

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20
Q

how is an acute transmural myocardial infarction caused?

A

-a thrombus forms on top of a ruptured plaque and occludes the lumen of the coronary artery -> leads to death of the full thickness of cardiac muscle supplied by that artery (myocardial infarction)

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21
Q

what is peripheral arterial disease (PAD)?

A

disease presentation that results when atherosclerosis of arteries of lower leg causes symptoms of ischaemia and/or infarction to occur

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22
Q

what is the most common presenting symptom of peripheral arterial disease?

A

intermittent claudication (pain/ cramping in legs relieved by rest)

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23
Q

what does fluid balance involve?

A

maintaining the amount of water as as a result the concentrations of ions in solution within healthy ranges

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24
Q

on average how many L of water is in the human body?

A

42L (in 70kg male)

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25
Q

what is hydrostatic pressure?

A

pressure of blood against the wall–>pushes substances out

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26
Q

what is oncotic pressure?

A

a form of osmotic pressure exerted by proteins in a blood vessel’s plasma -> holds substances in

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27
Q

which protein does oncotic pressure notably involve?

A

albumin

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28
Q

what is osmotic pressure?

A

related to total number of particles of solute

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29
Q

which force is the opposing force to HP?

A

oncotic pressure

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30
Q

describe the structure pf capillaries in the circulatory system-what does this enable?

A

semi-permeable

  • ->enables fluids to pass across
  • ->larger proteins cannot
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31
Q

when HP and OP are in balance is there a net gain or loss of fluid from the cirulatory system?

A

no neither

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32
Q

what does movement of fluid across capillaries depend on?

A

the balance between:

  • capillary HP and interstitial fluid HP
  • plasma oncotic pressure and interstitial fluid oncotic pressure
33
Q

what is oedema?

A

an increased volume of interstitial fluid in a tissue or organ

34
Q

what are the 4 potential causes of oedema?

A
  • Raised hydrostatic pressure (e.g. cardiac failure after myocardial infarction)
  • Low oncotic pressure (e.g. liver disease → not enough albumin produced)
  • Impaired lymphatic drainage (e.g. tumours, lymph node removal → no lymphatic drainage of excess interstitial fluid); lymphoedema
  • Endothelial damage (e.g. inflammation → increased capillary permeability so more fluid leaks out)
35
Q

how can cardiac failure following a heart attack result in oedema?

A
  • infarction causes damage impairing cardiac function
  • blood not pumped effectively->blood backlogs in veins
  • pressure in veins increases->pressure at capillary bed increases
  • higher capillary HP at venous end->more fluid forced out–>oedema
36
Q

what is haemostasis?

A

the cessation of bleeding

opposite to haemorrhage-blood loss

37
Q

what does haemostatis do?

A
  • prevents loss of blood through walls of damaged vessels

- establishes a framework for tissue repair

38
Q

what are the 3 phases of haemostasis?

A
  • vascular
  • platelet
  • coagulation
39
Q

what triggers the vascular phase of haemostasis?

A

when a blood vessel is cut it triggers smooth muscle fibres of vessel wall–>vascular spasms

40
Q

what do vascular spasms cause?

A

a decrease in blood vessle diameter at the injury site and prevent flow of blood through vessel wall

41
Q

how long do vascular spasms last?

A

30 minuutes

42
Q

what do endothelial cells in the vascular phase release to stimulate smooth muscle contractions?

A

endothelins–>cause vasoconstriction of vessel

43
Q

what happens to endothelial cells at the end of the vascular phase ready for the platelet phase?

A

cells become sticky-ready for platelets to adhere to it in platelet phase

44
Q

what is Von Willebrand’s factor?

A

-A blood glycoprotein involved in haemostasis (specifically platelet adhesion)

45
Q

what is VWF produced by?

A

endothelial cells

46
Q

where does inactive VWF circulate?

A

in the plasma complexed with Factor VIII

47
Q

outline the steps in the platelet phase of haemostasis

A
  • Platelets adhere to sticky endothelial surfaces, basement membranes & exposed collagen fibres beneath the endothelium (via the collagen receptor called glycoprotein la/lla)
  • Adhesion occurs via bridging with von Willebrand’s factor (VWF)
  • When the collagen and VWF interact, a complex is formed that binds fibrinogen from plasma → platelet is activated
48
Q

which chemicals do activated platelets release in the platelet phase of haemostasis?

A
  • ADP
  • Thromboxane A2 & serotonin (vasoconstrictors)
  • Clotting factors, PDGF (platelet-derived growth factor) and calcium ions
  • > promote vasoconstriction and further platelet activation
49
Q

what does the release of ADP from activated platelets cause?

A
  • makes other platelets sticky → helps them aggregate and stick to the originally activated platelets → forms a platelet plug, which closes small breaks in the vessel
50
Q

what does the surface of activated platelets serve as a site for?

A

coagulation-formation of thrombus–>in coagulation phase

51
Q

how soon after injury does the coagulation phase begin?

A

30+ seconds after injury

52
Q

which 3 pathways does the coagulation phase involve?

A
  • intrinsic
  • extrinsic
  • —>both lead to common pathway
53
Q

where are most clotting factors synthesised?

A

in the liver

54
Q

which pathway in the coagulation phase is faster intrinsic or extrinsic?

A

extrinsic

55
Q

where does the extrinsic pathway of the coagulation phase begin?

A

in vessel wall outside bloodstream

56
Q

in the extrinsic pathway what does the damaged endothelium release and what does it cause?

A

-Damaged endothelium releases tissue factor (TF)/Factor III

-TF + other compounds form an enzyme complex
→ activates Factor X

57
Q

where does the intrinsic pathway of the coagulation phase begin?

A

Begins with circulating proenzymes WITHIN bloodstream

58
Q

what happens in the intrinsic pathway of coagulation phase?

A

-Activation of Factor XII exposed to collagen

-Platelets release factors (e.g. PF-3)
→ series of reactions activates Factor X

59
Q

outline the steps of the common pathway

A
  • Activated Factor X combines with Factor V in presence of Ca2+ to form active prothrombinase
  • Prothrombinase converts prothrombin to thrombin
  • Thrombin converts fibrinogen to fibrin
60
Q

what is fibrin?

A

insoluble protein that covers the platelet plug

61
Q

what causes the conversion of prothrombin—->thrombin?

A

prothrombinase

62
Q

what causes the conversion of fibrinogen—>fibrin?

A

thrombin

63
Q

give an example of positive feedback in clotting

A

Positive feedback -

generation of thrombin amplifies clotting cascade

Stimulates further formation of tissue factor & further release of PF-3 → accelerates clotting

64
Q

give examples of negative feedback in clotting

A

Negative feedback; factors that restrict blood clotting:

  • Anticoagulants (plasma proteins) e.g. antithrombin-III
  • Heparin; released by basophils and mast cells
  • Aspirin, protein C; activated by thrombomodulin
  • Prostacyclin (inhibits platelet aggregation)
65
Q

what is fibrinolysis?

A

-the dissolving of the fibrin strands

  • Plasminogen is activated to produce plasmin (which digests fibrin strands)
  • > restores normal blood flow through repaired vessel
66
Q

which ion and vitamin are essential to the clotting process?

A

Ca2+

vitamin K

67
Q

what type of vitamin is Vitamin K?

A

fat soluble

68
Q

where can vitamin K be obtained?

A

via green vegetables and bacteria in the gut

69
Q

what is vitamin K essential for?

A
  • Required for liver to synthesise prothrombin, Factor VII, Factor IX, and Factor X
  • Deficiency in Vit K affects coagulation
  • Antagonist of Vit K = warfarin
70
Q

what is Virchow’s triad?

A

three broad categories of factors that influence the occurrence of thrombosis (formation of a blood clot):

71
Q

what are the 3 categories of Virchow’s triad?

A

hypercoagulability, vascular damage & circulatory stasis

72
Q

In an average 70kg male, how much water is present in the blood plasma?

A-10.5 litres
B-28 litres
C-14 litres
D-7 litres
E-3.5 litres
A

E

73
Q

What stimulates the migration of smooth muscle from the tunica media into the tunica intima during atherosclerosis?

A-Foam cells
B-LDLs
C-Cytokines
D-Monocytes
E-Calcium ions
A

C

74
Q

Which of the following is a circulating plasma protease inhibitor that inhibits thrombin?

A-Intrinsic factor
B-Tissue factor
C-Factor X
D-Factor XII
E-Factor V
F-Heparin
G-Warfarin
H-Thrombin
I-Antithrombin
A

I-Antithrombin

75
Q

Which clotting factor is involved in the intrinsic pathway?

A-Intrinsic factor
B-Tissue factor
C-Factor X
D-Factor XII
E-Factor V
F-Heparin
G-Warfarin
H-Thrombin
I-Antithrombin
A

D-Factor XII

76
Q

Which of the following cleaves fibrinogen to form insoluble fibrin?

A-Intrinsic factor
B-Tissue factor
C-Factor X
D-Factor XII
E-Factor V
F-Heparin
G-Warfarin
H-Thrombin
I-Antithrombin
A

H-thrombin

77
Q

Which of the following is a mixture of mucopolysaccharides derived from mast cells & activates antithrombin?

A-Intrinsic factor
B-Tissue factor
C-Factor X
D-Factor XII
E-Factor V
F-Heparin
G-Warfarin
H-Thrombin
I-Antithrombin
A

F-Heparin

78
Q

Which of the following is a vitamin K antagonist ?

A-Intrinsic factor
B-Tissue factor
C-Factor X
D-Factor XII
E-Factor V
F-Heparin
G-Warfarin
H-Thrombin
I-Antithrombin
A

G-Warfarin

Medicine yr1 (55 decks)

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