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PBL SEM 2 > PBL 5 - PHARMACOLOGY - stable angina > Flashcards

PBL 5 - PHARMACOLOGY - stable angina Flashcards

1
Q

angina vs. acute coronary syndromes

A
  • both involve chest pain caused by cardiac ischaemia
  • stable angina resolves with rest, a few mins
  • ACS doesn’t resolve quickly or with rest
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2
Q

what are the 3 types of ACS?

A

get worse down list:

  • unstable angina
  • NSTEMI
  • STEMI
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3
Q

what is angina pectoris?

A

crushing pain in chest that may radiate to arm, neck or jaw “strangling the chest”
- pain that results from cardiac ischaemia

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4
Q

what pain mediators do muscles release when it doesn’t receive enough oxygen that send signals to the CNS?

A
  • protons
  • potassium
  • adenosine
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5
Q

where is referred pain?

A

in neck, arm or jaw instead of in centre of chest

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6
Q

what are 4 types of angina and what do they result from?

A

result from atherosclerotic plaque in a coronary vessel:

  1. stable angina
  2. unstable angina

result from vessel contracting/spasming

  1. Prinzmetal’s angina (variant angina)
  2. micro vascular angina (syndrome X)
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7
Q

describe and explain stable angina

A
  • angina of effort
  • the most common form of angina
  • atherosclerotic plaque is stable (fibrous cap protects it from rupture) — partially blocks artery and when the heart’s oxygen demand goes up, the oxygen demands of the heart muscle can’t be met as not enough blood can flow through this vessel
  • pain sets in
  • triggers = exercise, emotion, stress, cold weather
  • relieved by rest
  • caused by hyperlipidaemia
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8
Q

describe and explain unstable angina

A
  • brittle, crescendo angina
  • rarer but more serious
  • atherosclerotic plaque — plaque is weakened and ruptures — get a blood clot superimposed on top of plaque — blocks flow even more
  • can progress into a full-scale MI
  • triggers: unpredictable
  • not relieved by rest
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9
Q

what is the main problem in angina?

A

too little oxygen getting to cardiac muscle

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10
Q

what are the 2 solutions for treating angina?

A
  1. reduce heart’s oxygen demand (reduce workload)

2. increase oxygen supply (improve blood flow to ischaemic part of heart)

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11
Q

describe the NICE care pathway for stable angina

A
  1. initial drug - organic nitrates (short-acting) - relieve attacks
  2. beta-blockers or calcium channel blockers - prevent further attacks
  3. consider surgical approaches if can’t get control
  4. secondary prevention = prevent progression of atherosclerosis and also perhaps adding in drugs to prevent a blood clot forming
  5. surgical approaches which aim to revascularise
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12
Q

what 4 things can be used to treat the symptoms of angina itself?

A
  • organic nitrates
  • beta blockers
  • Ca++ channel blockers
  • K+ channel activator
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13
Q

when a drug enters the GI tract from the oral cavity, where is it absorbed into the circulation?

A

via the hepatic portal vein — liver detoxifies substances

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14
Q

what is the bioavailability of a drug?

A

the fraction of the drug that reaches systemic circulation (escapes metabolism in the liver)

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15
Q

name 4 organic nitrates

A
  1. glyceryl trinitrate (GTN/nitroglycerine)
  2. amylnitrite
  3. isosorbide dinitrate
  4. nicorandil
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16
Q

what is GTN subject to?

A

subject to extensive first pass metabolism — has a very very low bioavailability via oral route

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17
Q

side effect of GTN?

A

headaches — vasodilation of cranial blood vessels

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18
Q

how is GTN given?

A

sublingually or spray — to avoid first pass metabolism — goes into circulation 1st before liver

ineffective if swallowed

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19
Q

what are pro-drugs?

A

have to be metabolised before they become effective

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20
Q

where do organic nitrates have to be metabolised?

A

at site of action rather than in liver

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21
Q

what is the active principle of GTN?

A

nitric oxide

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22
Q

describe how vasodilation is induced by organic nitrates

A
  • NO is released at site of action
  • it is produced by breakdown of organic nitrates at their site of action
  • it is an endogenous natural signaling molecule that acts by cinerting soluble guanylyl cyclase in its inactive form to its active form
  • guanylyl cyclase turns GTP —> cGMP
  • cGMP works by activating protein kinase G — phosphorylate proteins — series of events which results in reduced Ca conc and vasodilation
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23
Q

how do nitrates relieve an attack of angina?

A
  • by dilating peripheral blood vessels — reduce preload (principle effect) and afterload
24
Q

what is preload?

A

amount of blood being returned to the heart

25
Q

what is afterload?

A

the resistance the heart has to push against when it is moving blood into the systemic circulation

26
Q

how do you reduce cardiac workload?

A

dilate peripheral blood vessels (capacitance veins)

  • heart doesn’t have to push so hard
  • less blood is returned to the heart — lower force of contraction
27
Q

how does dilation of capacitance veins result in reduced angina?

A
  1. dilation of capacitance veins
  2. reduced central venous pressure
  3. reduced venous return
  4. reduced EDV (preload) and EDP
  5. reduced myocardial stretch
  6. reduced contractile force and SV
  7. reduced cardiac work
  8. reduced angina
28
Q

large doses of nitrates cause arteriolar dilation. how does this reduced cardiac work?

A
  • fall in peripheral resistance
  • reduction in cardiac afterload
  • reduces cardiac work
29
Q

how does GTN improve perfusion of tissues?

A

dilates the collateral vessels

30
Q

what are the 2 mechanisms for organic nitrates?

A
  1. reduce cardiac workload by dilating peripheral vessels to reduce cardiac workload through reduction of preload and afterload
  2. dilate collateral vessels to improve blood supply within the heart itself
31
Q

what are 2 long acting organic nitrates?

A
  • isosorbide mononitrate

- isosorbide dinitrate

32
Q

describe the long acting organic nitrates

A
  • effective when swallowed
  • dinitrate is metabolised in initially to mononitrate by 1st pass metabolism
  • mononitrate form travels to tissues
  • NO released at site of action
  • duration of action of sustained release tablets can be up to 12 hours
  • development of tolerance likely (can be minimised if doses spaced)
33
Q

which has a better bioavailability and duration of action: mononitrate or dinitrate?

A

mononitrate

34
Q

how is isosorbide dinitrate given?

A

tablets, sustained release tablets, sublingual tablets and sprays, transdermal patches, i.v. injection

35
Q

how is isosorbide mononitrate given?

A

tablets and sustained released tablets

36
Q

when are long acting organic nitrates used?

A

only when other drugs haven’t worked properly

37
Q

what are unaffected effects of nitrates?

A

often due to vasodilation properties

  • flushing of skin
  • throbbing headache (dilation of cranial vessels)
  • postural hypotension (fainting)
  • reflex tachycardia (due to drop in BP) (baroreceptors detect change and increase HR)
38
Q

describe nicorandil

A
  • activator of K+ ATP channels and NO donor
  • dilate arteries and veins
  • effects vs angina similar to nitrates
  • unwanted effects: headache, flushing, hypotension, nausea, vomiting
39
Q

what are the main effects of beta blockers in relieving angina?

A

reduction in cardiac work and hence reduction in oxygen demand

by slowing the HR down, the atria and ventricles beat less forcibly and the cardiac work rate will decrease — reduction in O2 demand

40
Q

when beta 1 adrenoceptors are activated, what is the effect on cardiac O2 demand?

A

increases cardiac oxygen demand — HR increases and heart beating harder so uses more O2

41
Q

name a beta blocker that works principally by slowing down the HR and reducing the force of contraction

A

atenolol

42
Q

name 2 calcium channel blockers/antagonist

A
  • verapamil

- amlodipine

43
Q

describe verapamil in stable angina

A
  • acts principally on the heart
  • blockade of Ca++ channels is use-dependent
  • more potent on heart than vascular smooth muscle — cardiac selective
  • Ca++ channel blockade in cardiac tissue reduced HR and CO
  • dilation of arterioles reduced cardiac afterload
  • CARDIAC WORK AND O2 DEMAND ARE REDUCED
  • unwanted effects: same as hypertension
44
Q

describe amlodipine in stable angina

A
  • blockage of Ca++ channels is NOT use-dependent
  • more potent on vascular smooth muscle than heart (it is a vasculature selective calcium channel blocker)
  • dilation of arterioles — reduced cardiac afterload (heart won’t have to push as hard to pump blood out)
  • dilation of capacitance veins reduce cardiac preload (wont get as much blood going back to the heart, not as much stress, heart won’t pump as hard)
  • CARDIAC WORK AND O2 DEMAND ARE REDUCED
  • unwanted effects same as hypertension
45
Q

what is nifedipine?

A

a calcium channel blocker used to treat angina but is not use-dependent

46
Q

what is nicorandil?

A

used to treat angina but is a nitrovasodilator and activator if KATP channels. both contribute to anti angina actions

47
Q

what is flecainide?

A

a sodium channel blocker used as an antidysrhythmic agent

48
Q

what is verapamil?

A

a use-dependent blocker of L-type calcium channels useful for treating stable angina

49
Q

what is dilitazem?

A

a calcium channel blocker

50
Q

when are surgical approaches used to treat angina?

A

only when drug options have not brought the angina under control

51
Q

what are the 2 surgical options?

A
  1. coronary artery angioplasty (aka percuatneous coroanry intervention or PCI)
  2. coronary artery bypass (CABG)
52
Q

describe PCI

A
  • stent inserted to keep artery open
  • also used as an emergency treatment for HA
  • performed under local anaesthetic with sedation
53
Q

what are some adverse effects of PCI?

A
  • stroke and MI due to angioplasty either triggering the formation of a blood clot of dislodging one
  • some studies suggest cognitive decline due to blockage of very small blood vessels in the brain
  • restenosis (re-closing) of the artery
54
Q

describe CABG

A
  • open heart surgery
  • much more invasive
  • involves removing a non-essential blood vessel from antlers part of the body and using it to restore blood flow to part of the heart in which the blood supply is compromised
  • normally use internal mammary artery and the great saphenous vein (leg)
  • used to treat angina that is resistant to drug treatment run and where the location of the blockage means that stents cannot be used
  • need to be replaced after 15 years
55
Q

what are some adverse effects of CABG?

A
  • poor wound healing
  • blood loss
  • dysrhythmias induced by use of general anaesthetic
  • MI and stroke due to embolisms and debris from surgery
  • cognitive decline?

PBL SEM 2 (44 decks)

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