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pharmacology BM322 > arthlerosclerosis > Flashcards

arthlerosclerosis Flashcards

1
Q

what can vasoconstriction cause?

A

impaired blood flow, causing remodelling of the artery which then can cause hypertension and atherosclerosis

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2
Q

what is arthlerosclerosis?

A

its the thickening/ hardening of arteries caused by the build up of plaques in the inner lining of the vessel

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3
Q

what do atherosclerosis and hypertension increase the risk of?

A
  • Myocardial infarction
  • Heart failure
  • Anureism
  • Transient ischemia
  • Angina
  • Artery disease
  • Stroke
  • Renal failure
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4
Q

what is the development of atherosclerosis characterised by?

A

its characterised by a progressive narrowing of the blood vessel lumen, this reduces the flow of blood (and oxygen) to vital organs

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5
Q

what are the risk factors of arthlerosclerosis?

A
  • obesity
  • smoking
  • hypertension
  • activating endothelial cells
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6
Q

what are the stages of arthleroscelrosis?

A
  1. normal artery - 0% occlusion
  2. endothelial dysfucntion - 0% occlusion
  3. fatty streak - <30% occlusion
  4. increasing plaque- 65% occlusion
  5. obstructive plaque- 95% occlusion
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7
Q

what are the steps of plaque formation?

A
  1. endothelial cell injury (physical, reactive oxygen species, elevated blood glucose, infection
  2. increased endothelial permeability to lipids (low-density-lipoproteins (LDL))
  3. oxidation of trapped LDL by endothelial cells
  4. expression of endothelial adhesion molecules (ICAM & VCAM) and chemokines
  5. adhesion/ migration of monocytes, t-cells, platelets and smooth muscle cells
  6. fatty streak forms (macrophages and smooth muscle cells engulf oxidised lipids)
  7. plaque growth - continued uptake of lipids, lipid oxidation and inflammatory response, forming a necrotic core
  8. formation of fibrous cap over the foam cell layer
  9. growth, stiffening and calcification of artheroma, the plaques become brittle and may rupture, leading to thrombosis
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8
Q

what is the foam cell layer?

A

its the extracellular matrix proteins secreted by smooth muscle

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9
Q

what happens in the formation of fibrous cap?

A

the fibrous cap forms over the foam cell layer as platelets are release platelet derived growth factors, activating smooth muscle cells and then the muscle cells migrate into the plaque and form the fibrous cap (together with matrix proteins secreted by smooth muscle cells

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10
Q

what are some targets of the stabilisation and regression of arthleroscelrotic plaques?

A

plasma cholesterol concentration
endothelial cell function
platelet aggregation
smooth muscle cell migration
monocyte function

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11
Q

what happens if youre able to reduce the level of LDL?

A

you can reduce plaques and stop them growing

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12
Q

what is plasma cholesterol associated with?

A

its associated with an increased risk of arthleroscelrosis and cardiovascular disease

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13
Q

what does BAD HEART stand for?

A

BMI
Age
Diabetes
Hypertension
Excess fat (obesity)
Alcohol
Relatives with cardiovascular disease
Tobacco

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14
Q

what are the effects of having some of the risk factors of arthlerosclerosis?

A

reduced blood vessel lumen diameter, leads to lower blood flow at rest and a reduced oxygen supply
- vascular cell dysfunction leads to impaired vasodilation and faulty blood flow control
- increased risk of blood clots

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15
Q

what does ‘ischemia’ mean?

A

its where the blood flow is restricted to part of the body, it can be caused by blood clots in the blood vessels

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16
Q

what are the consequences of arthrosclerosis in cerebral arteries?

A
  • stroke
  • vascualr dementia
  • transient ischemic attacks
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17
Q

what are the consequences of atherosclerosis in coronary arteries?

A
  • angina
  • myocardial infarction
  • slient ischemia
  • arrhythmias
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18
Q

what is the name given to artherosclerosis of coronary arteries?

A

coronary heart disease

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19
Q

what are the consequences of atherosclerosis in the body apart from the brain and heart?

A

-decline in renal function
- renal artery occlusion
- abdominal angina
- aortic rupture/ dissection
- peripheral arterial occlusion

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20
Q

what is the origins of ‘angina pectorus’?

A

its from latin, angere (to strangle) and pectus (chest), a strangling feeling in the chest

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21
Q

what does angina pectorus occur due to?

A

its due to ischemial, a reduction in blood flow

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22
Q

what is angina characterised by?

A
  • episodes of pain/ pressure in the chest
  • breathlessness
  • impaired ventricular systolic performance
  • reduced coronary blood flow
  • irregular heartbeat (arrhythmia)
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23
Q

what is stable angina?

A

its brought on by effort and is short lived, only 2-3mins

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24
Q

what is unstable angina?

A

it can happen at rest and is an unpredictable increase in pain

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25
Q

what is variant angina?

A

its uncommon and caused by artery spasm

26
Q

what causes increasing severity of coronary heart disease and ischemia?

A

a progressive narrowing or blockage of blood vessels by plaques or thrombus formation

27
Q

what does arthlerosclerosis of a stable plaque cause?

A

it causes stable angina

28
Q

what does arthleroscelrosis with an unstable plaque cause?

A

it either causes transient ischemia and unstable angina OR sustained ischemia and myocardial infarction leading to necrosis of tissue

29
Q

what does a prolonged reduction or cessation of blood flow cause?

A
  1. Subendocardial infarct (NSTEMI). Innermost layer is injured first (most distal).
  2. Transmural infarct (STEMI).
    Cell death extends throughout the whole thickness of the heart muscle
30
Q

what can necrosis cause?

A

irreversible cell death

31
Q

what can cell death result in?

A

arrhythmias
heart failure
cardiogenic shock

32
Q

what medication is used for the treatment of stable angina attacks?

A

nitrates

33
Q

what is the effect of nitrates on stable angina attacks?

A

they increase blood flow by increaseing the diameter of blood vessels (promoting vasodilation)

34
Q

what are some of the of the preparations of nitrates?

A

sublingual, translingual spray, ointment, sustained release tablets, intravenous infusion, etc.

35
Q

where do you find smooth muscle cells in terms of the arteries?

A

theyre wrapped around them

36
Q

what happens if the smooth muscle cells around the blood vessel are contracted?

A

they reduce the blood vessel diameter and restrict blood flow

37
Q

what happens if the smooth muscle cells around the blood vessel are relaxed?

A

they increase blood vessel diameter and facilitate blood flow

38
Q

what are the different types of nitrates used?

A

Nitroglycerin (NTG)
Isosorbide mononitrate (ISMN)
Isosorbide dinitrate (ISDN)

39
Q

what do nitrates donate?

A

NO- nitrogen oxide

40
Q

what pathway does NO take to cause relaxation in smooth muscle cells?

A

NO-cGMP-cGK-1 signalling pathway

41
Q

what is the NO-cGMP-cGK-1 signalling pathway?

A

NO activates solube gunanosine monophosphate and associated protein kinases which inhibit inositol-1,4,5-triphosphate-dependant calcium release

42
Q

what happens when calcium levels are decreased in smooth muscle cells?

A

they inhibit myosin light chain kinase and the unphosphorylated myosin light chain kinase, causing the myosin head to detach from the actin, resulting in smooth muscle contraction

43
Q

when are interventions for arthlerosclerosis needed?

A

when lifestyle changes are implimented too late to help prevent/treat it and its concequences

44
Q

what medications help stabilise and allow the regression of artheroscerosis?

A

lipid lowering drugs

45
Q

how do lipid lowering drugs work?

A

they lower plasma cholesterol and transport

46
Q

what medications are taken every day to prevent angina attacks?

A
  • antihypertensives
  • anticlotting drugs
47
Q

how do antihypertensives work?

A

they decrease heart rate/ force and relax arteries to increase blood flow

48
Q

how do anticlotting drugs work?

A

they work by preventing thrombosis

49
Q

what other intervention works apart from medication?

A

surgical intervention such as coronary angioplasty and stenting or coronary artery bypass graft

50
Q

what types of lipid-lowering drugs are there?

A

statins
fibrates
ezetimbe

51
Q

how do statins work in the treatment of atheroscelrosis?

A

they reduce circulaing LDL

52
Q

how do fibrates work in the treatment of artheroscelrosis?

A

they reduce circulating LDL

53
Q

how does ezetimibe work in the treatment of atherosclerosis?

A

it reduces cholesterol absorption in the intestine

54
Q

how do ACE inhibitors work to reduce hypertension?

A

they reduce Ang II levels and promote vasodilation

55
Q

how do beta-blockers work to reduce hypertension?

A

the decrease CO, reduce renin production (by the reduction of Ang II) and can indirectly cause vasidilation of peripheral arteries

56
Q

how do calcium channel blockers work to reduce blood pressure?

A

they block Ca2+ entry into the vascular smooth muscle cells and/or cardiac muscle cells, promoting the relaxation of the the muscle and vasodilation

57
Q

what types of lipid lowering drugs are there?

A

COX-1 inhibitors
ADP receptor inhibitors

58
Q

how do COX-1 inhibitors work in the treatment of artherosclerosis?

A

theyre anticlotting drugs
they irreversibly inhibit the enzyme responsible for the synthesis of thromboxane precursors and they reduce thromboxane, which is needed for platelet aggregation and activation

59
Q

how do ADP receptor inhibitors work in the treatment of artheroscelrosis?

A

the metabolites interfere with platelet function

60
Q

what are the three different types of anti-clotting drugs used in the treatment of artherosclerosis?

A
  • anti-platelet drugs which reduce platelet aggregation
    -anti-coagulants which work to target fibrin clot formation
  • thrombolytics which act as clot busters
61
Q

what do NSAIDs do in regards to heart attacks and strokes?

A

they increase the risk of strokes and heart attacks and are associated with increased blood pressure and adverse cardiovascular events

62
Q
A

pharmacology BM322 (7 decks)

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