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PHA 222 > Angina 2&3 > Flashcards

Angina 2&3 Flashcards

1
Q

nitrates are prodrugs, what are prodrugs?

A

-drugs that need to be converted in vivo to the biologically active principle/metabolites
- nitrates + nitrites –> NO (in vivo)

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2
Q

what are the main treatments of stable coronary artery disease ( angina and INOC- variant/ microvascular)

A

nitrates and nitrites
B- adrenoreceptor antagonists
CALCIUM CHANNEL BLOCKERS
Misc Agents - Nicorandil, Ranolazine, Ivabradine

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3
Q

how do nitrates and nitrites work?

A

action on blood vessels -> vasorelaxation-> systemic vasodilatation -> therapeutic effect

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4
Q

what is the mechanism of vasodilation in nitrates and nitrites?

A
  • converted to NO (reduced)
  • This would activate guanylate cyclase, which would convert GTP to cyclic GMP
  • This would activate protein kinase G – cause blood vessels to relax.
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5
Q

how do nitrates and nitrites produce their anti-anginal effect?

A
  • peripheral venodilatation –> decrease preload MVO2
    -peripheral arterial and arteriolar dilatation –> decrease afterload and MVO2
  • coronary vasodilatation –> reverse/prevent spasm and inc collateral BF
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6
Q

what are the 3 ways that nitrates and nitrites are used clinically?

A

1-relief of acute angina attacks –GTN, amyl nitrate
2-prophylaxis of chronic angina –GTN, ISDN, ISMN
3-choice & mode of therapy (influenced by pharmacokinetic profile - sublingual, buccal, transdermal, inhaler, IV)

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7
Q

what are 4 side effects of nitrates and nitrites?

A

1) flushing & throbbing headaches (dilation of arterioes in the temples)
2) postural hypotension & syncope (low bp- take sitting down)
3) reflex tachycardia & inc myocardial contractility
4) tolerance
-depletion of thiol (-SH) groups
-physiological adaptation

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8
Q

name 1 problems associated with nitrates

A
  • must pass first pass metabolism

-

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9
Q

how long is a nitrate free period and why does it matter?

A

8-10 hours, body cant be saturated with nitrates 24/7 or else tolerance will build since thiols don’t replenish

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10
Q

what is the pharmacological action of b-adrenoceptor antagonists?

A

antagonise the effects of sympathetic nervous activation (i.e. noradrenaline & adrenaline) at β-adrenoceptors

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11
Q

how many subtypes of beta-adrenoceptors are there and effects of inhibiting?

A

3 but focus on 1 and 2
1-ARs –heart & kidney –> dec cardian output
2-ARs –heart, smooth muscle (e.g. vascular & bronchial) –> peripheral vasoconstriction, bronchoconstriction
3-ARs –adipocytes

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12
Q

what are the two subclasses of b-Blockers?

A

1) ‘non-selective’ –e.g. propranolol
2) ‘B1-receptor selective’ or ‘cardioselective’ -eg. atenolol, acebutolol, metoprolol

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13
Q

how do b-b produce their anti-anginal effect?

A

1) haemodynamic effects –> dec myocardial O2 demand
-dec myocardial contractility
-dec heart rate
-dec system blood pressure
2) Ancillary Effects
-inc diasoltic filling time –> inc myocardial perfusion
-antiarryhthmic activity –> inc electrical stability
-antiatherogenic and antithrombotic

Heart spends longer in diastole, promoting coronary flow and reduce isch

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14
Q

what is the first line treatment for prophylaxis of chronic stable angina (effeort induced)

A

beta-adrenoceptor antagonists

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15
Q

what are the two classes of drugs used to treat chronic stable angina classified based on?

A

where they are eliminated:
1 eliminated via hepatic metabolism
2 eliminated unchanged via the kidney

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16
Q

what are the features of drugs eliminated via hepatic metabolism?

A 
more lipid soluble
almost completely absorbed from the gut
largely metabolised in the liver
very variable bioavailability
short plasma half-life
17
Q

what are the features of drugs eliminated via the kidney?

A 
more water soluble
incompletely absorbed from the gut
largely eliminated unchanged
less variable bioavailability
longer plasma half-life
18
Q

what happens if you withdraw a Beta-blocker from treatment abruptly?

A

rebound phenomenon- increase force of contraction because more B receptors available for NA/AD to cause sympathetic effect- don’t stop taking unless doctor says/dose tapered down slowly- risk of angina agitation

19
Q

what are some adverse side effects of beta-blockers?

A
  • bronchoconstriction -exacerbation of asthma
    -peripheral vasoconstriction -cold extremities
    -myocardial depression -risk of heart failure
    -masking of signs of impending hypoglycaemia
    -sexual dysfunction –>poor patient compliance
  • CNS disturbances –nightmares, depression, confusion
    inc LV size =inc myocardial O2 consumption
20
Q

BB are contraindicated for patients with…

A

-Variant Angina (use CCB)
-Asthma with non-selctive BB

21
Q

what is the pharmacological action of Calcium channel blockers?

A

-inhibit entry of Ca into cells via L-type voltage-gated calcium channels i.e. if heart(node cells) blocks entry of calcium cells it reduces force of contraction

22
Q

What are the 3 types of CCBs

A

1 - Phenylalkylamines (verapamil)
2 - Dihydropyridines (nifedipine)
3 - Benzothisazepines (diltiazem)

Most CCBs are dihydropyridines
Diltiazem + verapamil are rate limiting

23
Q

What are the cardiac effects of rate limiting CCBs

A
  • block Ca influx into cadiac muscle cells, dec cardiac contractility
  • block Ca influx into nodal and conducting cells, dec HR
24
Q

what are the vascular effects that CCB have?

A

**Block of Ca influx into arterioles –> arteriolar dilatation
**-peripheral vasodilatation, dec SVR, dec arterial BP
-coronary dilatation, inc coronary BF, reversal of spasm, prevention of spasm

25
Q

what are the two mechanisms of anti-anginal effects of CCB?

A

1) Reduced myocardial O2 demand
-dec arterial BP
-dec myocardial contractility and HR (for RLCCB)
2) Inc myocarial blood flow
-coronary vasodilatation, inc CBF, spasm reversal and prevention

26
Q

What is CCB a first line treatment for?

A

chronic stable angina

also for management of variant angina

27
Q

The Adverse Effects of Dihydropridines

Amplodipine, Nifedipine

A

-Hypertension
-Light headedness
-Flushing
-Headache
-Peripheral Oedema

28
Q

The Adverse Effects of Non-dihydropyridines

Verapamil, Diltiazem

A

-AV block
-Bradycardia
-Cardiodepression
-Constipation
-Headache
-Hypotension
- Peripheral Oedema

29
Q

what does sublingual mean?

A

under tongue

30
Q

what does buccal mean?

A

between cheek and gum

31
Q

what are the 3 miscellaneous treatments of SCAD?

A

1-Potassium channel openers (Nicorandil)
-venodilatation, dec preload, dec MVO2
-arterial dilatation, dec afterload, dec MVO2
2-Sinus node (If current) inhibitors (Ivabradine)
-Inhibit If, dec HR, dec MVO2
3-Late Sodium Current Blockers (Ranolazine)
-Inhibit late sodium channel, anti-ischaemic effect

32
Q

what are the two revascularisation procedures?

A

Percutaneous Coronary intervention (PCI)-balloon

Coronary artery by-pass graft (CABG) -sew

33
Q

when do you consider a 3rd anti-anginal drug?

A

when 2 don’t satisify

PHA 222 (41 decks)

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