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Drugs acting on the heart Flashcards

1
Q

what is the definition of hypertension

A

160/95mmHg

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2
Q

what are the possible secondary causes of hypertension?

A

primary aldosteronism
cushing syndrome
phaechromocytoma
renal (Bright’s disease glomerulonephritis)

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3
Q

list the drug types used in the treatment of hypertension

A
  • thiazide diuretics
  • diuretics
  • Katp channel openers
  • calcium channel blockers
  • nitro-vasodilators
  • A1 adrenoreceptor antagonists
  • B adrenoreceptor antagonists
  • adrenergic blocking drugs
  • centrally acting anti-hypertensive drugs
  • ACE inhibitors
  • AT1 inhibitors
  • MR inhibitors
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4
Q

what is the mechanism of action of diuretics in reducing BP?

side effects?

A

example: bendrofluzaide

how they work:

  • they reduce blood volume, by increasing sodium and water excretion
  • this leads to reduced CO and blood volume
  • CO and blood volume return to normal
  • but BP remains low, due to direct smooth muscle relaxation
  • this SM relaxation is not the same for all anti-hypertensive diruetics

side effects:

  • hyperglycaemia
  • gout
  • hypokaleamia
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5
Q

what is the mechanism of action of Katp channel openers?

side effects?

A 
example:
diazoxide - given as IV in emergency 
minoxidil - only given when other drugs do not work 
causes hypertichosis 
very potent and long acting

hydralazine: acts on arteriolar SM, can cause SLE

those prevent the binding of ATP to the ATP sensitive channels

channel remains opened, causing K+ efflux, this causes membrane hyper polarisation. this prevents calcium L type voltage channels from opening thus causing SM relaxation

side effects:
- hyperglycaemia (Channels found in the beta cells of the pancreas)

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6
Q

what are diazoxide and minoxidil examples of?

A

Katp channel openers

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7
Q

how do calcium channel blockers work in lowering BP ?

A

examples

nifedipine: selective blocker for L type channels in vascular SM
verapamil: pronounced effect in heart

drugs work:

  • inhibit calcium influx into SM
  • prevents SM contraction

side effects:
flushing
headache
dizziness

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8
Q

what are nifedipine and verapamil examples of

A

calcium channel blockers

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9
Q

what are the side effects of calcium channel blockers

A

dizziness
facial flushing
headache

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10
Q

how do nitrovasodilators work in lowering BP?

A

drug breaks down to release NO
causes SM relaxation

example: sodium nitroprusside
used in severe hypertension
cannot be used on a day to day basis

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11
Q

how do alpha 1 adrenoreceptors antagonists work in lowering BP?

A

prazosin: can cause fainting due to massive BP drop
doxazosin: better tolerated and longer lasting

drugs used in conjunction with the other anti-hypertensive drugs

they inhibit the sympathetic tone of vascular smooth muscle

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12
Q

what are prazosin an example of?

A

A1 adrenoreceptor antagonist used in lowering BP

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13
Q

how do adrenergic blocking drugs work in reducing BP?

what are the side effects

A

example: guathendine

they prevent the release of noradrenaline

side effects:

  • postural hypotension
  • failure in ejaculation
  • nasal congestion
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14
Q

how does clonidine work in reducing BP?
where does it act?
what is the danger with using it?

A

it is a central acting anti-hypertensive
it is a selective A2 agonist, and thus reduces the central release of noradrenaline

acts on A2 receptors in the ventrolateral medulla at the nucleus of the solitary tract

when stopped rebound hypertension occurs due to sympathetic compensation

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15
Q

how does alpha methyl dopa work?
who can it work with?
what is it used for?

A

it is a centrally acting anti-hypertensive
it is a pro-drug converted into methyldopamine then methyl noradrenaline (a false neurotransmitter)

the false transmitter has a much higher affinity for A2 receptors than A1 receptors

safe to use in:

  • patients with asthma
  • patients with heart failure
  • pregnant women

it is used in pre-eclampsia
- women with high blood pressure and high protein content in their urine

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16
Q

how do beta adrenoreceptors work in lowering BP?
when are they contraindicated?
what are their side effects?
how can we slightly overcome the side effects?

A

example: atenolol - cardio selective B1 antagonist
reduces BP by reducing HR

mechanism fully understood? perhaps central switching off or resetting of baroreceptor reflex?

contraindicated?

  • asthamatics
  • diabetics
  • patients with peripherial vascular disease

side effects:

  • bronchoconstriction
  • fatigue
  • bradycardia
  • cold peripheries

partial agonist oxepranlol can be used which causes less bradycardia - so good for patients with heart failure of peripheral vascular disease

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17
Q

how do MR antagonists work in increasing plasma potassium

A

examples: spirolactone and eperolone

they block minerlocorticod receptors, which increase ENAC channels

ENAC channels increase sodium and water retention - so they cause slight dirusesis

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18
Q

what are the side effects of ACE inhibitors used to reduce BP?

A

severe hypotension with first dose, particularly with hypertensive patients with high plasma renin levels

renal impairment, hyperkalemia and angiodema

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19
Q

how are ACE inhibitors used to drop BP?

A

vasodilator effect:
- less production of angiotensin II

reduction in BV:
- due to excretion of sodium and water

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20
Q

what is the drug administeration for patients with hypertension

A
  1. thiazide diruetics
  2. beta blockers
  3. calcium channel blockers
  4. ACE inhibitors
  5. alpha blockers

they’re started one by one

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21
Q

what is angina?

when does it occur?

A

angina is a symptom and not a disease
it is severe pain in the chest radiating to the left arm -
it is not associated with irreversibly myocardial damage, but patients with angina have higher risks of MI attacks

angina occurs when there is an imbalance between oxygen supply and metabolic demand

the pain associated with angina occurs due to accumulation of metabolites

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22
Q

what are the three types of angina? and what are they caused by?

A

stable angina:

  • caused by narrowing of coronary vessels
  • occurs on exertion relieved by rest

unstable angina:

  • caused by rupture of atheromatic plaque, causing partial occlusion of coronary vessels
  • angina attacks are more frequent and more severe, they occur during rest or low level of exertion

spastic/variant angina:

  • occurs at rest
  • due to smooth muscle spasm
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23
Q

explain the mechanism of action of the organic nitrates in angina

A

glyceryl trinitrate and isosorbide mononitrate

the nitrates are denitrated inside the smooth muscle to make NO
nitrates first converted into NO2 by tissue sulphydryl (SH) groups, it can then be converted into NO

NO activates cellular guanylate cyclase, which increases cytosolic cGMP - this activates protein kinase G - this phosphorylates myosin light chains - and causes sequestration of intracellular calcium THUS leading to smooth muscle relaxation

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24
Q

what are glyceral trinitrates and isosorbide mononitrates used for?

A

organic nitrates in angina

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25
Q

what are they physiological consequences of organic nitrates?

what do they not act on?

A

they reduce after - load:
- this occurs through vasodilation

they reduce pre - load:

  • this occurs through venodilation
  • lower central venous pressure

they cause collateral coronary blood vessel dilation:
- this redistributes blood flow from well perfused areas into ischaemia myocardial areas WITHOUT increasing blood flow

the organic nitrates do not act directly on myocardium

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26
Q

what are the side effects of using organic nitrates?

A 
headaches 
increased intra-ocular pressure 
increased CSF pressure 
flushing of face 
warm skin 
hypotension 
methaglobinemia
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27
Q

how is GTN administered? what is its duration of action?

A

administered via:

  • buccal route (oral)
  • sublingual route

active for 20-30 minutes
readily absorbed by mucosa
metabolised in liver

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28
Q

how is isosorbid mononitrate administered? what is its duration of action?
what is the problem with this drug compared to GTN?

A

oral - 4-6 hours
sub-lingual: 1.5 hours
chewable: 2-3 hours
transdural: 24 hours

it is good because has longer duration of action. but easily tolerated
drug is given orally twice a day, with no administration at night to reduce tolerance

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29
Q

what is the mechanism of action of beta adrenoreceptor antagonists in angina?

when are they used as prophalyxis?

A

examples: propanalol, atenolol and metoprolol

they reduces sympathetic effects on the heart
they reduce effect of circulating adrenaline in the peripheries

overall, they reduce cardiac work and therefore cardiac oxygen demand

the drugs reduce frequency of angina attacks, but also reduce frequency of MI attacks

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30
Q

what is the mechanism of action of calcium antagonists in angina?

clue: cardiac and vascular effects

A

verapamil - acts on heart
nifedipine - acts on vasculature
diltiazem - has intermediate effects

the drugs have cardiac effects:

  • reduce cardiac contractility, by reducing calcium influx during plateau phase
  • prevents transient inwards current, T1 (prevents ecotopic beats)
  • depression of conduction, because blocking calcium dependant calcium release
  • causes increased resistance to cardiac damage

the drugs have vascular effects:

  • vasodilation in small arterioles and arteries
  • causes coronary artery dilation in those with variant angina
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31
Q

what are the effects of nifedipine? what is the drug used for?

A 
antihypertensive 
angina 
reduces BP and peripheral resistance dramatically 
has no affect on AV conduction 
massive increase in coronary flow 
massive increased IN CO
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32
Q

what is diltiazem used for? what are its effect?

A

dysrthymias and angina

increased coronary blood flow
reduce heart rate
reduce AV conduction

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33
Q

what is verapamil used for? what are its effects?

e.g. on blood flow

A

dysrthymias

does not cause massive increase in coronary blood flow
but causes a massive decrease in AV conductance

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34
Q

what are the side effects of calcium channel blockers?

A

headaches: due to massive vasodilation
constipation: particularly when using verapamil, GI motility dependant on calcium influx

verapamil and diltiazem:

  • slow HR
  • they can cause bradycardia and high degree AV block
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35
Q

what should verapamil and diltiazem not be given with? and why?

A

beta adrenoreceptor antagonists

those two drugs are calcium channel blockers, and cause high degree AV block

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36
Q

what is the difference in blood flow distribution in coronary circulation when dipyridamole and organic nitrates are given?

A

dipyridamole dilates coronary vessels, but not collaterals
this means blood flow is redirected towards already well perfused areas, and taken away from ischaemic areas

organic nitrates: they dilate collaterals meaning blood flow is redirected from well perfused areas to ischaemic cardiac areas without an increase in blood flow

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37
Q

how does dipyridamole work?

key drug action to know

A

inhibits the uptake of adenosine, adenosine is thought to increase vasodilation in hypoxic myocardium

inhibits platelet aggregation, useful in preventing thrombosis

maybe used in invariant angina

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38
Q

why is aspirin used in cardiovascular medicine?

how does it work?

A

used as prophalyxis for thrombus formation (in low doses)
inhibits thromboxane A2 formation, while allows PG12 formation which inhibits platelet aggregation

the drug works by inhibiting cylco-oxgenase, which synthesiezes A2

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39
Q

why are statins used?

A

they’re thought to lower cholestrol, by inhibiting the rate limiting step in cholestrol formation
HMG-coA enzyme
aims at treating underlying arthematous disease

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40
Q

why is heparin used?

how can it be give?

A

IV or subcutaneous injections

inhibits coagulation by activating ANTI - thrombin iii, THIS PREVENTS THROMBUS FORMATION

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41
Q

what are the drugs administered for angina?

A

the drugs:

  • organic nitrates as the first line drugs
  • beta blockers as the gold standard, with organic nitrates in conjunction

if the used of beta blockers is contraindicated, then calcium blockers used with short acting organic nitrates

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42
Q

what is congestive heart failure? and what is the most common cause of congestive heart failure?

A

congestive heart failure is when the cardiac output of the heart is siginificantly reduced so that it is not enough to meet the body’s metabolic demands

it is most commonly caused by ischaemic heart disease

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43
Q

what are some of the symptoms of congestive heart failure?

A 
SOB 
fatigue and fluid retention 
reduced patient survival 
tachycardia 
cardiomegaly
44
Q

what is the definitive physiological indication of congestive heart failure?

A

adenosine depletion

45
Q

how are diruetics used in congestive heart failure?
how are they administered? dosage?
what are their side effects?
what are their effects on mortality and symptoms?

A

they’re used to decreased pre-load, by reducing blood volume

administered:

  • orally
  • IV
  • I.M

symptomatic dosages: the more odema a patient has the higher the dosage

side effects include:

  • hyponatremia
  • hypotension
  • gout
  • impotence

no studies to show that they reduce mortality
but they’re used to improve symptoms

46
Q

What is spirolactone? why is it used in congestive heart failure?

what are the side effects of the drug?

A

spirolactone is an aldosterone inhibitor, it is used in conjunction with ACE inhibitors because it is shown to improve mortality

also potentiates the effects of loop diuretics

side effects:

  • hyponaetremia
  • hyperkaelmia
  • gynaecomastia
47
Q

what is the problem with using hydralazine in the long term?

A

repeated dosage over a long amount of time can cause SLE

48
Q

what vasodilators are used in congestive heart failure?
what are their effects on mortality and symptoms?
when are they used?

A

nitrates and hyradalazine are used in conjunction
used when ACE is not tolerated or contra-indicated
when combined they reduce pre-load and afterload

improve symptoms and reduce mortality

side effects:

  • hypotension
  • headache
  • facial flushing
  • tachycardia
  • SLE with prolonged use of hydralazine
49
Q 
what beta adrenoreceptor antagonists are used in CHF? 
what are their mechanism of action?
what are their effects?
how are they administered? dosage?
what are their adverse effects?
A

carvedilol and bisoprolol

  • they prevent the activation of the sympathetic effects on the heart
  • they prevent exarcerbation of hear failure through RAS activation

they improve symptoms and MORTALITY

the dosage is started off as low then gradually increased

administered:
- topically
-orally
IV

side effects;

  • tirdness
  • hypotension
  • impotence
  • wheezing in asthamatics
50
Q

give examples of the ionotropes used in congestive heart failure

A

cardiac glycosides
- digoxin

beta adrenoreceptor agonists:
- dobutamine (given IV)

Type III phosphodiesterase inhibitors:
- milrionone (IV)

51
Q

what are cardiac glycosides mainly used for?

A

cardiac failure with atrial arrhythmia

52
Q

what are studies to shows the effectiveness of digioxin?

A

there is no evidence to show that digioxin improves mortality in congestive heart failure

53
Q

what are the side effects of cardiac glycosides? and why so?

A

most peripheral side effects are on the gut:
- nausea
- vomitting
- anorexia
- diarrhoea
thought to be due to vagal and chemoreceptor trigger zone activation

cardiovascular effects:

  • AV block (caused by vagal reflexes)
  • extrasystoles (caused by calcium overload)
  • can cause dysrthmyias
54
Q

why are cardiac glyosides dangerous? when are they most toxic?

how can their toxicity be treated?

A

because they have a very low therapeutic index
must be kept within the narrow range of 0.7-3ng/ml

cardiac glycosides compete with potassium ions to enter into the cell, therefore, they’re most toxic in cases of hypokalaemia

to treat:

  • administer KCl
  • withdraw the drug
  • administer anti-dysrthymic drugs (lidocaine and phenytoin)
  • use Fab fragments to remove drug
55
Q

what is the mechanism of action of cardiac glycosides?

A

they inhibit the Na/K+ Atpase channel by binding to the K+ binding site

this has the secondary effect of reducing the exchange of extracellular Na+ with intracellular calcium

this causes a build of calcium within the cells, leading to an increased contractility

but build up of calcium can lead to increased automocitity and excitability which can lead to tacchyarhythmias

56
Q

what are the side effects of digoxin on cardiac muscle?

A

the calcium overload can lead to automocity and excitability of the cells leading to arrythmias

digoxin also leads to vagal activation, which can cause AV block

57
Q

what are the therapeutic effects of cardiac glycosides?

A 
reduction in heart rate (Reduction in reflex tachycardia)
an increase in CO (then decreases) 
a reduction in odema 
an increase in urine flow 
a decrease in body weight 
a reduction in cardiac muscle area
58
Q

apart from cardiac glycosides what other drugs can be used in congestive heart failure?

A

beta adrenoreceptor antagonists (Carvedilol)
vasodilators (Esp. nifedipine, which affects vasculature more than the heart)
diruetics
ACE inhibitors

phosphodiesterase inhibitors (theophyline and milrinone)

59
Q

what is the consequence of inhibiting PDE 3?

when are milrinone and enoximone used?

A

those inhibitors prevent the breakdown of cAMP
inhibition leads to an increase and prolongation of calcium influx in the heart - this increases cardiac contractility

in vasculature inhibiting this enzyme leads to vasodilation

they’re given IV: post cardiac surgery of chronic heart failure. they’re superseding the use of glycosides or diruetics

60
Q

what is the consequence of inhibiting PDE 4 and PDE5?

A

inhibition of PDE 4 can be useful in the treatment of athsma
(rolipram)

inhibition of PDE5 leads to vasodilation in the corpus caverneosum, leading to erections

61
Q

give examples of non selective phosphodiesterase inhibitors

A

theophyilline and aminophyliine , caffeine

62
Q

what is the gold standard for the treatment of heart failure?

A

Carvedilol with ACE inhibitor and spirolactone

63
Q

how does dobutamine work?

A

it is a Beta 1 adrenoreceptor agonist
it increases cAMP formation, therefore calcium influx, thereby increasing cardiac contractility

it is a positive ionotrope

64
Q

what is the potency of a LA determined by?

what is the duration of an LA determined by?

A

its ability to cross the lipid bilayer

its ability to bind to the protein

65
Q

what is the pKA of an LA

A

the pH at which 50% of the LA is in ionised form, while the other 50% is in non - ionised form

pKa= pH + log (BH+/B)

66
Q

how do local anaesthetics work?

A

they reversibly bind to the sodium channels from inside the cell, preventing the conduction of an AP by preventing sodium influx

the LA do not change resting membrane potential, they reduce the amplitude of an impulse (can complete degrade an impulse)
they also reduce the rate of conduction through the axon

67
Q

what are most LA administered as? what are they?

A

they’re weak bases, administered as water soluble hydrochlorides

68
Q

what happens to the ionised and non ionised form of an LA?

A

the non-ionised form can cross straight into the axoplasm, where it becomes ionised by the relatively acidic pH - it then goes on to bind to the sodium channels from the inside

the ionised form, which is a weak base, liberated due to the alkaline pH of surrounding tissue, enters the axoplasm when sodium channels open and bind to them from the inside

69
Q

what is meant by the term ‘frequency dependant’

A

this refers to the fact LA have higher affinities for axons which are conducting AP at a higher rates, than those conducting AP at lower rates

two reasons for this:

  • LA have a higher affinity for inactivated sodium channels
  • a cell which is frequently depolarised, on average has a more positive charge, which drives the LA through the sodium channels
70
Q

what type of nerve fibres do LA work best on? what is the implication of this during anaesthesia?

A

they work best on small myleinated fibres
they do not work very well on large diameter nerve fibres

meaning in LA: pain sensation will be lost first, followed by temperature, pressure and deep touch sensation

LA does not work to anesthesise motorneurones

71
Q

in LA why dos the overall AP decrease in a nerve trunk?

A

compound AP in a trunk is reduced in amplitude - because not all nerve fibres are firing to contribute to an AP

slowing of conduction through anesthesised regions leads to the nerve impulse spreading out (temporal dispersion)

72
Q

how can surface anesthetics be applied (give examples)

A

mucous membrane: via spray, lozenges, solution
- lidocaine
benzocaine - can be given as a powder to anesthesize burnt or ulcerated skin regions

lidocaine and prilocaine can be given as a non-crystallised mixture forming complete anesthesia within one hour

73
Q

what is infiltration anesthesia?

what are the dangers?
why are vasoconstrictors used with them?

A

anesthesia given to anesthesise nerve endings
large amounts maybe required, predisposing to systemic toxicity

IV danger:
- local tissue irriation and necrosis

vasoconstrictors: adrenaline, noradrenaline, ADH, felypressin
1. to prolong the duration of action
2. to reduce systemic toxicity

examples: lidocaine

74
Q

what is nerve block anesthesia?

A

when you block an entire nerve trunk, so that all area supplied by that nerve is blocked

e.g. mandibular nerve block in denistry
brachial nerve block: in hand surgery

75
Q

what is spinal anesthesia?

side effects?

A

drug injected into subarachnoid space (L3-L5)
glucose can be given with drug, to alter density

examples: liocaine and procaine are used

side effects:

  • respiratory paralysis
  • headache and paralysis
  • vomitting and visceral pain
  • neurological complication
  • severe hypotension
  • post- operative pain
76
Q

what is epidural anaesthesia?

A

drug injected into epidural space, limits CNS involvement = because epidural space ends at the foreman magnum
much higher concentrations needed (careful with subarachnoid injection)

examples: lidocaine and bupivacaine

77
Q

what is IV regional anaesthesia?

A

injection of IV distal to cuff
anaesthesia diffuses retrogradely into tissue

danger of systemic toxicity if cuff is released too early

lidocaine or prilocaine used

78
Q

what are the CNS effects of LA?

A

STIMULATION with hyperactivity and manic behaviour

followed by coma and respiratory depression

79
Q

what are the side effects of LA?

A

tissue necrosis or local injury after infiltration or spinal anesthesia

vasodilator action, depression of myocardium and cardiac slowing

allergic reaction: very rare, but occur due to breakdown products of one of the ester types
para-amino benzoate

80
Q

what is prolonged after depolarisation? why can it cause dysrhtymia?

A

depolarisation, occurs after an AP is triggered
caused by high intracellular calcium concentration, leading to an exchange between sodium and calcium - this is known as transient inward current

may trigger an ectopic beat

81
Q

what is a disorder conduction pattern? what is its main features? why can it lead to dysrhtymias?

A

this occurs in areas of dead myocardium, where there is a unidirectional myocardial block
so that a slowly moving AP can re-excite areas of myocardium that is no longer refractory

this results in a re-enterant dysrythmia
- for this type of dysarrhythmia the refractory period must be shorter than the circulating time of the impluse

conduction through depolarised areas of the myocardium, is dependant on calcium influx rather than sodium - this causes a slow response AP

this type of arryhtmia is very sensitive to calcium modifying agents

82
Q

how can abnormal pacemaker activity lead to dysrhytmias

A

damaged myocardium can lead to ecotopic beats,

this initiates beats which are out of synchrony with the normal rhythm

83
Q

how can heart block lead to dysrhtymia?

why is this a special type of abnormal conductivity?

A

if cardiac impulse fails to be propogated through AV node, then the Purkinjie fibres propagate the nervous impulse - however they’re slow and unreliable

this type leads to bradycardia rather than a tachycardia dysrhtymia

84
Q

what is atrial flutter?
what is atrial fibrillation?
what are they both caused by

A

flutter atria contracts at 300bpm

fibrillation contraction at 350- 600bpm (caused by re-entrant arrhytmias)

85
Q

what is paraoxysmal atrial tachycardia?

A

atrial contraction: 120-240bpm

it is caused by ecotopic beats

86
Q

what is ventricular tachycardia?

how is this different from ventricular fibrillation?

A

ventricular tachycardia is caused by successive ecotopic beats

ventricular fibrillation is caused by re-entrant arrhythmia - which can lead to death

87
Q

what are the class Ia anti-dysryhtmic drugs?
give an example?
how do they alter the shape of an AP?
when are they used?

A

example: disopyramide, quinidine
work:
- the are medium effect on blocking sodium channels
- the increase the refractory period, thereby prolong the duration of an AP
- decrease the amplitude of an AP(not as much as IC)

supraventricular and ventricular dysrythmia

88
Q

what are class Ib anti-dysrhytmic drugs?
give an example
how do they alter the shape of an AP?
when are they used?

A

example: lidocaine
work:
- they’re weak sodium voltage gate blockers
- preferentially bind to depolarised areas, because have high affinity for inactivated sodium channels

shape of AP:

  • do not prolong an AP, infact decrease the refractory period
  • only minimally reduce the amplitude of an AP

used in:
- ventricular tachycardia, particularly following an MI

89
Q

what are class Ic anti-dysrhtmic drugs?
give an example?
how do they alter shape of an AP?
when are they dangerous?

when are they used?

A

example: flecainide

work:

  • they’re potent binders to sodium gates
  • do not have a preference to already depolarised areas
  • reduces general excitability

AP:

  • reduce amplitude the most
  • do not affect the RP, therefore have no affect on the duration of an AP

they increase mortality in patients with sudden death syndrome

used in:
atrial fibrillation
re-enterrant ventricular dysrythmia

90
Q 
what are class II anti-dysrythmic drugs?
when are they used?
A

beta blockers: propanaolol
- block sympathetic activity to B1 receptors

used in:
tacharythmias provoked by sympathetic activity

91
Q 
what are class III anti-dysrthmic drugs?
when are they used?
A

example: amiodarone
potassium channel blockers
increase the refractory period, prolonging AP

used in:
supraventricular arryhtmias
ventricular dysrhtmias

amiodarone: has a very long half life and many side effects

92
Q

what are class IV anti dysrthmic drugs?

A

example: veramapil
they’re calcium channel blockers
- inhibit slow inwards calcium current
- therefore, indirectly T1 currents

used for:
supra ventricular tachycardia

93
Q

what other drugs apart from anti-dysrthymic drugs can be used to treat dysrhtmias

(2 main classes)

A

cardiac glycosides:

  • although they can cause dysrthymia, by increasing calcium concentration
  • they have increased vagal activity
  • used to treat atrial fibrillation

adensoine:

  • treats paraoxysmal supraventricular tachycardia
  • activates A1 receptors in cardiac channels, whcih inhibits calcium channels and increase potassium permeability
  • potent AV blocker

used to terminate AV nodal re-entrant supraventricular tachycardia

94
Q

what is long QT syndrome?

what can it be caused by>

A

characterised by a prolonged QT interval on an ECG (meaning takes longer time to repolarise the ventricles)
the problem with delayed repolarisation, it predisposes to after depolarisation

predisposes to a specific type of ventricular dysrthymia known as Torsade de pointes (which can cause ventricular fibrillation leading to death)

can be inherited:
- genetic mutation in a potassium channel LQT1-7
can be caused by drugs that bind to the potassium
channels: potassium channels involved with phase 2 AND 3 of cardiac AP
- antibiotics
- anti pyscotics
- anti-histamines
- can be caused by anti-dysrthymics themselves

electrolyte disturbance:

  • hypokalemia
  • hypomangeisa
  • hypocalcemia
95
Q

what are they symptoms long QT syndrome ?

how can it be treated?

A

syncope
fatigue
seziures
Torsade de Pointes

treated using Class II anti - dysrthymics (beta blockers) - first line of choice, prevents cardiac events in 70% of patients
DC defibrillators
- used when the patients is already on drugs but unresponsive

96
Q

what are pacemaker cells dependant on for their AP spike?

what are myocardial cells dependant on for their AP spike?

A

calcium influx

sodium influx

97
Q

what are ergot alkaloids?

give the uses of ergotamine and ergometrine

give other uses of ergot alkaloids

A

ergot alkaloids are alpha adrenoreceptor antagonists, but they can also have affects on dopamine and 5HT receptors

ergotamine - used in migranes in acte atacks
ergometrine (this is a very important drug)
- used to prevent post-martum haemorrahage

hydergine: cerebral vasodilator

other effects:
LSD
dopamine receptors: agonists
- bromocriptine for PD and galacatorrhea (Fetility drug)

5HT receptors: agonist/ antagonist

  • methysergide
  • used for migranes
98
Q

how are glycoprotein IIa and IIb receptor antagonists used in cardiovascular medicine?

A

they’re used to prevent platelet aggregation, by inhibiting the receptors involved in their activation.
those drugs are given intravenously

99
Q

what is nicorandil?

A

potassium channel activator

100
Q

what is ivadradine?

A

it inhibits the funny current, thereby reducing pacemaker activity
slow heart rate allows more time for ventricular filling
can be used in CHF, or angina

101
Q

what is bupivacaine used for?

A

this has a long duration of action (although slow onset)

- used in epidural anaesthesia during childbirth

102
Q

what are the characteristics of lidocaine?

A
  • fastest onset

- most stable

103
Q

what are the characteristics of prilocaine?

A
  • less toxic in equipotent dosage
104
Q

what are the characteristics of benzocaine? and when is it used?

A
  • low potency
  • water insoluble
  • for non-inflammed tissue (for ulcers and burns) applied as powder
105
Q

what is a nor-adrenegric neurone blocking drug?

A

e.g. guathendine and this prevents the release of noradrenaline from a post-ganglioinic sympathetic neurone

Pharmacology (17 decks)

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