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Pharmacology 1 > drugs acting on the heart > Flashcards

drugs acting on the heart Flashcards

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1
Q

what is angina?

A

heart temporarily deprived of oxygen

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2
Q

what is dysrhythmia?

A

heart rhythm disturbed - arhythmia

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3
Q

what is heart failure?

A

heart doesn’t pump properly

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4
Q

what is a heart attack?

A

heart deprived of oxygen

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5
Q

what is a risk factors for angina, heart attack, dysrhythmia and heart failure?

A

hypertension

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6
Q

what is the function of the coronary arteries?

A

to supply heart with nutrients and oxygen to contract

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7
Q

what causes coronary artery disease?

A

excess cholesterol

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8
Q

in what way does excess cholesterol cause coronary heart disease?

A
  1. restricts blood flow
  2. blood clots can form round plaques
  3. clots can break off - causing stroke or MI
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9
Q

how can coronary artery disease be prevented?

A
  1. lifestyle choices - diet/ exercise/ stop smoking
  2. reduce blood pressure
  3. statins to reduce cholesterol
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10
Q

what are the symptoms of angina pectoris?

A

crushing pain radiating to arm, neck, jaw - usually on left hand side.

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11
Q

what is the pain associated with angina caused by?

A

cardiac ischaemia

K+, H+, bradykinin and adenosine stimulate pain signals

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12
Q

what is the problem with angina pectoris and what are the solutions?

A

problem: too little O2 in cardiac muscle

solutions: -reduce O2 demand

-increase O2 supply

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13
Q

how could O2 demand be reduced to treat angina?

A
  • rest
  • GTN - dilates periphral blood vessels
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14
Q

how could O2 supply be increased to treat angina?

A

increase airway size

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15
Q

how does glyceryl trinitrate (GTN) (or nitroglycerin) work?

A
  1. reduces cardiac workload - heart doesn’t push do hard so less blood returns to heart = reduced force of contraction
  2. improved blood supply - dilates collateral vessel to increase blood supply to heart
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16
Q

is GTN broken down by 1st pass metabolism? if so how is this avioded?

A

yes it is broken down by 1st pass metabolism

avoided by: spraying under tongue to avoid GI tract

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17
Q

what is atenolol used to treat?

A

angina

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18
Q

how does atenolol work?

A

ß blocker - acts on ß1 adrenoceptors in heart

ß1 adrenoceptors make heart work faster → atenolol blocks receptors reducing HR

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19
Q

how does atenolol reduce cardiac workload and improve blood supply?

A
  1. slows heart rate
  2. atria beat less forcibly
  3. venticles beat less forcibly

cardiac work rate and O2 demand reduced

  1. prolongs diastole to increase window for coronary blood flow

improves blood supply to heart

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20
Q

what is the differents between angina and a heart attack?

A

angina is a temporary blockage of the coronary artery - a heart attack (MI) is a prolonged blockage which leads to death of the heart muscle

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21
Q

name three treatments for heart attack

A
  1. GTN and propanolol
  2. tissue plasminogen activator
  3. angioplasty

must be treated as quickly as poss.

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22
Q

how does GTN and propanolol treat a heart attack?

A
  1. reduces workload and oxygen demand
  2. improves blood flow through coronary arteries
  3. reduces pain
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23
Q

what is a tissue plasminogen activator?

A

‘clot busting drug’ - enzyme breaksdown clot

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24
Q

what is an angioplasty?

A

blood vessel is reopened with a stent

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25
what are the solutions if heart failure is present?
1. reduce blood pressure 2. make heart pump harder
26
what drug is commonly used to treat heart failure or atrial fibrillation?
digoxin
27
what is digoxin and who is it used for?
positive inotropic agent used for sympotomatic patients in sinus rhythm(despite ACE inhibitors and diuretics)
28
what is the action of digoxin?
increases cardiac output
29
why is digoxin used for sympotomatic patients in sinus rhythm?
* improves symptoms * improves exercise tolerance * reduces hospitalisation * however doesn't affect mortality
30
what is the molecular mechanism of action of digoxin on the heart?
* inhibition of Na+ /K+ ATPase that maintain resting potential * increase Ca+2 stores
31
what is the physiological effect of digoxin?
* increased force of contarction *without* increasing O2 consumption
32
what are the side effects of digoxin?
narrow therapeutic window - difficult to regulate dose (needs monitoring)
33
describe the electrical pathway of the conducting system in th heart
* SA node initiates cycle * AV node relays to ventricles * Purkinje fibres and bundle of His spread impulses through ventricles
34
name two possible problems with the conducting system in the heart and what effect this will have
_malfunctioning electrical system_ * poor pumping - inadequate blood supply _lack of coordination in pumping or very fast rate_ * turbulence - risk factor for blood clots→ strokes/ MI
35
what is the difference between arrhythmias and dysrhythmias?
arrhythmias - lack of rhythm dysrhythmias - disturbance both disruption of normal electrical conduction system of heart
36
how can dysrhythmias be classified?
site of origin - atrial / junctional (supraventricular) / ventricular true arrhythmias - very disorganised rhythm tachycardias - HR too fast bradycardia - HR too slow
37
how can arrhythmias/ dysrhythmias be treated?
drugs electrical surgical
38
name 5 dysrhythmic mechcanisms and explain what each is
_ectopic pacemaker_ - cardiac tissue other than SA node initates heart beat _delayed after-depolarisation_ - build up of calcium leads to train of APs _re-entry circuits_ - tissue damage/abnormality causes APs to travel in circles _congential abnormalities_ - additional conducting pathways between atria and ventricles _heart block_ - damage to conducting pathways disrupts atrial/ventricular signaling
39
who is more at risk of dysrhythmias?
* coronary heart disease - heart cells easily depolarise * heart valve disorders * blood chemistry disorders * dysrhythmias caused by drugs
40
name some drugs which can cause dysrhythmias
* beta blockers * psychotropics * sympathomimetics * caffeine * amphetamines * cocaine * some anti-dysrhythmic drugs
41
what is the cause of ventricular fibrillation?
ectopic foci / re-entry circuits - ventricles stop beating in a coordinated way
42
why is is important to act quick if a patient presents with ventricular fibrillation?
rapidly fatal DC electrical shock may be needed
43
describe the Vaughan-Williams classification of antidysrhythmic drugs
Class Target Examples I (a,b,c) sodium channels lidocaine II beta 1 adrenoceptors atenolol III potassium channels amiodarone unclassified various adenosine
44
describe the classification of dysrhythmic drugs by clinical utility
dysrhythmias of supraventicular origin - adenosine, verapamil dysrhythmias of supraventicular or venticular origin - amiodarone, flecainide, propranolol, quinidine dysrhythmias of venticular origin - lidocaine
45
what is hypertension defined as?
a sustained systolic BP \>140 mmHg or a sustained diastolic BP \>90 mmHg
46
what are the causes of hypertension?
1. genetic factors 2. low birth weight 3. environmental factors 4. diabetes 5. drugs 6. kidney/cardiovascular disease
47
what can high BP lead to?
damaged blood blood vessels - leading to stroke, ischaemic heart disease, peripheral vascular disease
48
what is the the formula for determining blood pressure?
BP = cardiac output x total peripheral resistance (TPR)
49
what is the intial treatment strategy for high BP?
reduce weight reduce alcohol reduce salt stop smoking more exercise less caffeine more fruit and veg
50
what controls BP?
baroreceptors in carotid sinus and aortic arch stimulate: 1. SA node to decrease cardiac rate and output 2. vasodilation in arterioles
51
what are the targets for antihypertensive drugs?
A - ACE inhibitors (+angiotensin receptor blockers) B - beta blockers C - calcium channel blockers D - diuretics
52
explain the renin - angiotensin system
1. low BP in kidney - renin secreted 2. renin stimulates angiotensinogen to convert to angiotensin I 3. angiotensin converting enzyme (ACE) then converts angiotensin I to angiotensin II 4. this stimulates aldosterone to be produced and vasoconstriction to occur
53
what is the action of ACE inhibitors?
blocks ACE→ vasodilation occurs thus reducing periphral resistance
54
name five ACE inhibitors
* captopril * enalapril * trandolapril * ramipril * lisinopril
55
what are the side effects of ACE inhibitors?
* persistant dry cough * rash * renal problems (DO NOT use in patient with renal disease) * hypotension * DO NOT use in pregnancy
56
what can be used instead of ACE inhibitors?
angiotensin receptor antagonists (ARBs)
57
what is the action of ARBs?
selectively block AT2 receptors→ vasodilation occurs
58
give four examples of ARBs
* losartan * candesartan * valsartan * eprosartan
59
what are the pros and cons of using ARBs?
_pros_ * well tolerated * don't produce cough _cons_ * dizziness * hyperkalaemia
60
what is the antihypertensive action of ß blockers?
1. reduce cardiac output 2. reduced renin release 3. reduced sympathetically mediated vasoconstriction
61
where do ß blockers act?
sympathetic nervous system
62
can ß blockers be used in pregnancy?
yes - eg. labetalol (mixed alpha/beta blockers)
63
give five examples of ß blockers
atenolol bisoprolol sotalol\* metoprolol propranolol\* \* none selective - act on ß1 and ß2 receptors
64
what are the side effects of ß blockers?
* lathargy * impaired concentration/memory * aching limbs during exercise * erectice dysfunction * exacerbation of Raynauds disease * aggrevation of asthma
65
what is the action of alpha receptor antagonist ?
blocks action od NAdr and adrenaline on blood vessels→ vasodilation occurs
66
name 3 alpha receptor antagonists
prazosin doxazosin terazosin
67
describe the action of prazosin
short acting alpha1 anatagonist → arteriolar/ venous dilation \*may cause postural hypotension
68
what are the effects of calcium?
* increase AV node conduction * incraese arterial tone * incraese myocardial contractility * increase HR
69
what do calcium channel blockers do?
_block calcium therefore:_ * dilates arteries * reduces heart contractility * and or reduces heart rate
70
give examples of calcium channel blockers (CCBs) which are more potent on blood vessels than heart
1. nifedipine 2. amlodipine 3. nicardipine
71
what are the side effects of nifedipine, amlodipine, nicardipine?
* headache * flushing * dizziness * peripheral oedema
72
give two examples of CCbs which are more potent on the heart than the blood vessels
1. verapamil 2. diltiazem
73
what are the side effect of verapamil and diltiazem?
* constipation * heart block - could precipitate cardiac failure
74
what is the action of thiazide like (and thiazide) diuretics?
increase urine output → which decreases blood volume and reduces blood pressure
75
give five examples of thiazide like and thiazide diuretics
1. chlorothiazide 2. hydrochlorothiazide 3. metolazone 4. Chlortalidone 5. Bendrothiazide
76
what are the side effects of thiazide like (and thiazide) diuretics?
* Hypokalaemia (reduced potassium) * reduced insulin release * increased plasma lipids and urates → gout * erectile dysfunction
77
can potassium-sparing diuretics be prescribed alongside thiazide diuretics?
yes
78
what are possible difficulities occuring with the use of potassium-sparing diuretics?
don't reduce potassium as with thiazide diuretics but can increase potassium and reduce sodium in blood → hyperkalaemia / hyponatraemia
79
give two examples of potassium-sparing diuretics
1. amiloride 2. spironolactone
80
when would loop diuretics be most useful?
in severe hypertension - short duration of action
81
what are the side effects of loop diuretics?
* can affect hearing * may cause gout * may cause hypokalaemia
82
give an example of a loop diuretic
furosemide
83
give 3 examples of other vasodilators and when they may be used
1. hydrazaline - short acting, non-selective K+ channel opener 2. minoxidil - powerful vasodilator used in extreme hypertension 3. sodium nitroprusside (intravenous nitrates) - used in hospital emergencies
84
outline the use of multiple drug therapy to control hypertension
85
summerise antihypertensive drugs
A - ACE inhibitors → block angiotensin II production (or ARBs) B - ß blockers → reduce HR, dilate arteries, reduce renin release C - calcium channel blockers → reduce HR, dilate arteries D - Diuretic → increases urine output which lows blood volume

Pharmacology 1 (11 decks)

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