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ACEM Part 1 > Pharmacology - CVS > Flashcards

Pharmacology - CVS Flashcards

1
Q

What is the mechanism, clinical effect and pharmacokinetics of GTN

A

-mechanism:
converted to nitric oxide, taken up by smooth muscle (all types, including vascular), causes increased cGMP
prevents interaction between myosin and actin, leading to SMC relaxation

-clinical effect: reduces myocardial oxygen demand
vascular = veins dilated at low concentration, causing reduced ventricular pre-load and stroke volume
arteries dilated at high concentration, causing reduced BP and dilation of epicardial artery

overall effect: reduce CO and myocardial oxygen demand and improved delivery of oxygen to heart

other = relax bronchi, GI tract, GU tract, decrease platelet aggregation

-pharmacokinetics: excretion via kidneys
GTN rapidly absorbed but high first pass metabolism, bioavailability <10-20% (ISMN oral bioavailability of 100%)
SL route avoids hepatic metabolism, onset 1-3 minutes, doa 10-30 minutes

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2
Q

What are the indications, side effects and contraindications of GTN

A

-indications:
angina, acs, hypertensive emergencies, APO, aortic dissection

-adverse effects:
orthostatic hypotension, tachycardia, headache, methaemoglobinaemia

-contraindications:
hypotension, inferior and posterior MI or right ventricular infarct

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3
Q

What is tachyphylaxis as it relates to GTN

A

-continuous exposure to GTN causes SMC to develop tolerance, seen with continuous infusions

-require a drug free interval of at least 8 hours between doses

-theory: diminished release of nitric oxide and systemic compensation

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4
Q

When should GTN be used with caution

A

hypotension
inferior/posterior MI
raised ICP
significant tachycardia

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5
Q

What are the effects of nitric oxide

A

smooth muscle relaxant
platelet inhibition
immune regulator
neurotransmitter

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6
Q

What are the therapeutic applications of nitric oxide

A

-vascular effects: angina
-hypertension associated with pregnancy
-respiratory disorders: newborns with pulmonary hypertension
-atherosclerosis: may act as an antioxidant and preventing foam cell formation in the vascular wall
-platelets: inhibitor of platelet aggregation
-CNS: may have a role in epileptic seizures

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7
Q

What drugs are used in hypertensive emergencies

A

GTN
nifedipine
diazoxide
hydralazine
nitroprusside
esmolol
labetalol

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8
Q

What is the mechanism of action, pharmackinetics and side effects of sodium nitroprusside

A

-mechanism:
release of NO leading to increased cGMP, causing smc relaxation
affects arteries and veins equally

-pharmacokinetics:
rapidly metabolised by uptake into RBC, release NO and cyanide
onset 1 minute, t1/2 2 minutes, duration of action 1-10 minutes, only parental form available, sensitive to light

-side effects:
accumulation of cyanide, hypotension, metabolic acidosis, arrhythmia

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9
Q

What is the mechanism of action, pharmacokinetics, indications and adverse effects of Adenosine

A

-mechanism:
act on the Adenosine receptor
activate inward rectifier K+ current and inhibit Ca+2 current causing hyperpolarisation/suppression of Ca+2 AP
directly inhibits AV nodal conduction and increases AV nodal refractory period, less effect on SA node

-pharmacokinetics:
very rapid metabolism by adenosine deaminase in RBC and endothelial cells
t1/2 <10 seconds, doa 30 seconds, must be given by rapid IV bolus

-indications: SVT

-adverse effects: flushing, SOB, chest pain, AF

-contraindications: AV block, SSS, acute asthma

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10
Q

How do you classify anti-arrhythmic drugs and give an example of each

A

-class 1 = Na+ channel blockers
a - procainamide, quinidine (prolongs AP)
b - lidocaine (shortens AP)
c - flecainide (minimal effect on AP)

-class 2 = beta blockers - propranolol

-class 3 = K+ channel blockers - amiodarone, sotalol

-class 4 = Ca+2 channel blockers - verapamil, diltiazem

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11
Q

What antiarrhythmic drugs can be used in the management of AF

A

class 1c (flecainide)
class 2 (metoprolol)
class 3 (amiodarone)
class 4 (verapamil)
unclassified (digoxin)

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12
Q

What is the mechanism of action and cardiac effects of Amiodarone

A

-mechanism:
class 3 antiarrhythmic medication (potassium channel blocker)
blocks rapidly activating potassium current, causing markedly prolonged AP duration and QT interval
also: blocks Na+ channel, weak beta blocker, noncompetitive alpha blocker, weak Ca+ blocker

-effects:
prolongs AP duration, decrease HR and AV nodal automaticity, slows AV nodal conduction

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13
Q

Indications, side effects and drug interactions of Amiodarone

A

-indications: ventricular (vt) and supraventricular (af) arrhythmias

-adverse effects: heart block, pulmonary toxicity, hepatitis, hypo/hyperthyroidism, photodermatitis, torsades (rare)

-drug interactions:
amiodarone is a substrate for CYP3A4
inhibitors (cimetidine) - increase level of amiodarone
inducers (rifampicin) - decrease level of amiodarone
amiodarone inhibits several P450 enzymes, causing increased levels of - digoxin, warfarin, statin

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14
Q

What is the mechanism of action and pharmacokinetics of digoxin

A

-mechanism:
increases cardiac contractile force and decreases HR

mechanical =
inhibit Na+/K+ ATPase, causing increased intracellular Na+ and decreased intracellular K+
this causes decreased Ca+2 expulsion via Na+/Ca+2 exchange
increased concentration of Ca+2 causing increased contraction of cardiac sarcomere

electrical = indirectly modifies autonomic activity and increases efferent vagal activity
this causes decreased firing rate at SA node and increased refractory period at AV node

-pharmacokinetics:
well absorbed orally, moderate VOD, t1/2 36-40 hours, 2/3 excreted unchanged by kidneys

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15
Q

Are the parasympathetic effects of digoxin uniform throughout the heart

A

No
The atria and SA/AV node are more affected than purkinje or ventricular function

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16
Q

What are the features of toxicity of digoxin, antidote and why are patients in heart failure more prone

A

-features: hyperkalaemia, distorted vision (yellow-green vision), GIT effects, arrhythmia (bigeminy, 2nd degree HB)

-predisposition:
electrolyte disturbance = low K+, low Mg+2, high Ca+2
organ dysfunction = renal impairment
drugs that increase digoxin levels = amiodarone, nsaid, verapamil, quinine, antibiotics

-digoxin is renally cleared and requires dose adjustment in renal failure
-patients in heart failure have poor renal perfusion from lower CO
-K+ competes with binding of digoxin, so toxicity increased in setting of low K+ (may be on diuretics)

-antidote: digoxin immune fab, comes from sheep, binds to circulating digoxin and removes it
1 vial covers 500mcg digoxin, used in cardiac arrhythmias and hyperkalaemia

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17
Q

What is the mechanism of action, pharmacokinetics and contraindications of flecainide

A

-mechanism: class 1c antiarrhythmic (sodium channel blocker)
blocks Na+ and K+ channels with slow unblocking kinetics, prolongs QRS but no effect on AP duration

-pharmacokinetics: well absorbed orally, t1/2 20 hours, eliminated via liver and kidneys, dose 100-200mg OD

-indications: supraventricular arrhythmias in normal hearts

-contraindications: pre-existing ventricular tachyarrhythmia or IHD

18
Q

What distinguishes lidocaine from other class 1 antiarrhythmics

A

-lidocaine shortens the duration of the action potential
-lidocaine dissociates with rapid kinetics and has little effect on the ECG in NSR

19
Q

What is the mechanism of action of lidocaine on the heart

A

-mechanism: class 1b antiarrhythmic (sodium channel blocker), greater effect on ischaemic tissue
blocks activated and inactivated Na+ channels with rapid kinetics, binds refractory channels, shortens AP

-indications: arrhythmia associated with MI, local anaesthetic, post herpatic neuralgia

-adverse effects: hypotension, bradycardia, parasthesia, tremor, nausea, tinnitus, visual disturbance

20
Q

Describe the pharmacodynamics, pharmacokinetics and side effects of propranolol

A

-mechanism:
non-selective beta block, Na+ channel block, inhibit conversion of T4 to T3, antagonise renin release

-effects: reduce BP and HR

-pharmacokinetics:
high first pass metabolism, high lipid solubility, readily crosses the BBB

-side effects:
bradycardia, hypotension, bronchoconstriction, sedation, VF arrest in OD

21
Q

How does carvedilol differ from propranolol

A

carvedilol has no local anaesthetic action but has alpha 1 block

22
Q

Describe the mechanism of action, pharmacokinetics and effects of metoprolol

A

-mechanism:
beta 1 selective beta blocker

-pharmacokinetics:
PO or IV, well absorbed, bioavailability 50% (first pass effect), large VOD, metabolised by liver

-effects:
negative chronotropic and inotropic, slows AV node conduction

23
Q

Why do beta blockers lower BP

A

-BP is determined by cardiac output (HR x SV) and TPR
-beta blockers lower HR and reduce force of contraction

24
Q

How does metoprolol differ from propranolol

A

equipotent at B1
metoprolol is 50-100 times less potent at B2

25
Q

Describe the pharmacodynamics/kinetics and side effects of sotalol

A

-mechanism:
class 2 and 3 antiarrhythmic
blocks K+ channels causing a prolonged AP duration
non-selective beta blocker causing decreased HR

-pharmacokinetics:
well absorbed, bioavailability of 100%, not metabolised, excreted unchanged by kidneys

-side effects:
prolongs QT and torsades, CCF, asthma, AV blockade

26
Q

What drug interactions occur with sotalol to prolong the QT

A

phenothiazines
macrolides
antidepressants
drugs that cause hypokalaemia

27
Q

What are the pharmacokinetic principles, effects and side effects of beta blockers

A

-well absorbed, low bioavailability, large VOD, most metabolised in liver

-effects: negative chronotropic and inotropic, AV block, increased survival after MI, bronchospasm

-side effects: hypotension, bradycardia, cardiogenic shock, bronchospasm, seizure

28
Q

What are the effects of calcium channel blockers on smooth muscle

A

smc relaxation
arterioles are more sensitive than veins but both are dilated

29
Q

How do calcium channel blockers control angina and what are the toxic effects

A

-voltage-gated L-type calcium channels is dominant in cardiac and smooth muscle

blocking these channels cause decrease opening and decreased calcium current, leading to:
-reduced myocardial contractility - causing reduced oxygen demand
-decreased SA node rate and AV node conduction velocity
-relaxation of vascular smooth muscle - causing decreased afterload

-toxicity: cardiac depression, bradycardia, AV block, cardiac arrest, heart failure, peripheral edema

30
Q

Differentiate verapamil from other calcium channel blockers

A

-verapamil and diltiazem are mainly antiarrhythmic (more marked in tissues that fire frequently)
side effects: bradycardia

-nifedipine and nimodipine (dihydropyridines) are predominantly vasodilating
side effects: flushing, headache, tachycardia

31
Q

What is the mechanism of action and uses of verapamil

A

-mechanism:
class 4 antiarrhythmic, blocks activated and inactivated slow L-type Ca+2 channels
works on vascular smc, cardiac myocytes and cardiac nodal tissue
AV node conduction time and effective refractory period are prolonged
directly dilates coronary arteries

-indications:
angina, hypertension, atrial arrhythmia, migraine

-side effects:
hypotension, bradycardia, AV block, constipation, edema

-antidotes in toxicity:
calcium, insulin

32
Q

What are the sites of action of antihypertensive drugs

A

-diuretics: lower BP by depleting Na+
example. frusemide, thiazide, spironolactone

-centrally active: lower BP by reducing sympathetic outflow from vasomotor centers in the brain
example. methyldopa, clonidine, moxonidine

-beta-blockers: lower blood pressure by beta antagonism causing negative inotropic and chronotropic effects
example. metoprolol

-alpha-blockers: lower BP by alpha antagonism dilating capacitance and resistance vessels
example. prazosin

-vasodilators: lower BP but sympathetic reflexes remain intact, no orthostatic hypotension
example. hydralazine (dilate arteries only), GTN (dilate veins>arteries), nifedipine (dilate arteries>veins)

-angiotensin modulators: lower BP by inhibiting RAS
example. ACE inhibitor (enalapril), angiotensin II blocker (losartan)

33
Q

Describe the mechanism of action of ACE inhibitors (also asked as Catalopril and Ramipril)

A

-mechanism:
competitively block conversion of angiotensin I to angiotensin II
inhibits RAS: normally would cause arteriolar vasoconstriction, Na+/Cl- reabsorption, aldosterone/ADH secretion
stops inactivation of the kallikrein-kinin system

-effects: decreased vascular tone, decreased BP

34
Q

Describe the pharmacokinetics, uses and side effects of ACE inhibitors

A

-pharmacokinetics: eliminated mainly by the kidneys, need renal adjusted dosing

-uses: CHF, post MI, diabetic nephropathy to stabilise renal function, hypertension

-adverse effects: AKI, hyperkalaemia, dry cough, dizziness, hypotension, angioedema

-interaction: hypotension with diuretics, lithium toxicity with lithium, hyperkalaemia with potassium sparing diuretics

35
Q

Describe the pharmacodynamics of medications that modulate the effect of angiotensin

A

-ACE inhibitors:
reversibly block conversion of angiotensin I to angiotensin II

-angiotensin blockers:
competitive antagonists at AII receptors, does not increase level of bradykinin

36
Q

What are the advantages of angiotensin receptor blockers over ACE inhibitors

A

-no effect on bradykinin, so reduced incidence of cough and angioedema

-more complete inhibition of actions of angiotensin II

37
Q

What is the mechanism of action and side effects of prazosin

A

-mechanism: selective alpha 1 blocker affecting arterioles and venules
reduces arterial pressure by dilating both resistance and capacitance vessels

-side effects: dizziness, palpitations, headache, lassitude, first dose hypotension, postural hypotension

38
Q

What is the mechanism and effect of acetazolamide

A

-mechanism: inhibition of carbonic anhydrase enzyme
causes reduced H+ excretion and increased Na+/K+ excretion leading to diuresis

-toxic effect: hyperchloraemic normal anion gap metabolic acidosis, renal K+ wasting, low pH of CSF, renal stones

39
Q

What is the mechanism of action, indications and adverse effects of thiazide

A

-mechanism:
inhibits the Na+/Cl- cotransporter on the luminal side of the early distal convoluted tubule
prevents re-absortion of NaCl and promotes diuresis

-indications:
hypertension, heart failure, nephrogenic diabetes insipidus, edema, nephrotic syndrome, cirrhosis

-adverse effects:
hypokalaemic metabolic alkalosis, hyperlipidaemia, hyponatraemia, hyperuricaemia

40
Q

What are the pharmacokinetics and side effects of frusemide

A

-mechanism
loop diuretic, acting by inhibiting Na+/K+/2Cl- transporter on luminal side of ascending loop
prevents reabsorption of Na+ and Cl- and causes diuresis

-pharmacokinetics:
rapidly absorbed, onset post oral 1-3 hours/post IV 15-30 minutes, t1/2 1.5-2 hours
highly protein bound, 50% conjugated in kidney, 50% excreted in urine unchanged

-side effects:
electrolyte = hypokalaemic metabolic alkalosis, hyponatraemia, hypomagnesaemia, hyperuricaemia
others = orthostatic hypotension, dehydration, ototoxicity (reversible)

-drug interactions:
nsaid, aminoglycosides, digoxin, lithium, propranolol, thiazides

41
Q

Why is mannitol used in management of head injury and what are the toxic effects

A

-used to reduce intracranial pressure

-mechanism: osmotic diuretic, does not cross BBB, draws water out of cells and reduced intracellular volume

-freely filtered by glomeruli, not reabsorbed

-other clinical effect: reduces rate of CSF production, reduces intraocular pressure

-dose in raised intracranial pressure: 1-2g/kg as IV bolus over 15 minutes

-toxic effects: extracellular volume expansion, hypovolaemia, hyponatraemia, hypokalaemia

ACEM Part 1 (38 decks)

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