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Pharmacology 1 > drugs acting on the heart > Flashcards

drugs acting on the heart Flashcards

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
Q

what are the solutions if heart failure is present?

A
  1. reduce blood pressure
  2. make heart pump harder
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26
Q

what drug is commonly used to treat heart failure or atrial fibrillation?

A

digoxin

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27
Q

what is digoxin and who is it used for?

A

positive inotropic agent

used for sympotomatic patients in sinus rhythm(despite ACE inhibitors and diuretics)

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28
Q

what is the action of digoxin?

A

increases cardiac output

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29
Q

why is digoxin used for sympotomatic patients in sinus rhythm?

A
  • improves symptoms
  • improves exercise tolerance
  • reduces hospitalisation
  • however doesn’t affect mortality
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30
Q

what is the molecular mechanism of action of digoxin on the heart?

A
  • inhibition of Na+ /K+ ATPase that maintain resting potential
  • increase Ca+2 stores
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31
Q

what is the physiological effect of digoxin?

A
  • increased force of contarction without increasing O2 consumption
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32
Q

what are the side effects of digoxin?

A

narrow therapeutic window - difficult to regulate dose (needs monitoring)

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33
Q

describe the electrical pathway of the conducting system in th heart

A
  • SA node initiates cycle
  • AV node relays to ventricles
  • Purkinje fibres and bundle of His spread impulses through ventricles
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34
Q

name two possible problems with the conducting system in the heart and what effect this will have

A

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
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35
Q

what is the difference between arrhythmias and dysrhythmias?

A

arrhythmias - lack of rhythm

dysrhythmias - disturbance

both disruption of normal electrical conduction system of heart

36
Q

how can dysrhythmias be classified?

A

site of origin - atrial / junctional (supraventricular) / ventricular

true arrhythmias - very disorganised rhythm

tachycardias - HR too fast

bradycardia - HR too slow

37
Q

how can arrhythmias/ dysrhythmias be treated?

A

drugs

electrical

surgical

38
Q

name 5 dysrhythmic mechcanisms and explain what each is

A

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
Q

who is more at risk of dysrhythmias?

A
  • coronary heart disease - heart cells easily depolarise
  • heart valve disorders
  • blood chemistry disorders
  • dysrhythmias caused by drugs
40
Q

name some drugs which can cause dysrhythmias

A
  • beta blockers
  • psychotropics
  • sympathomimetics
  • caffeine
  • amphetamines
  • cocaine
  • some anti-dysrhythmic drugs
41
Q

what is the cause of ventricular fibrillation?

A

ectopic foci / re-entry circuits - ventricles stop beating in a coordinated way

42
Q

why is is important to act quick if a patient presents with ventricular fibrillation?

A

rapidly fatal

DC electrical shock may be needed

43
Q

describe the Vaughan-Williams classification of antidysrhythmic drugs

A

Class Target Examples

I (a,b,c) sodium channels lidocaine

II beta 1 adrenoceptors atenolol

III potassium channels amiodarone

unclassified various adenosine

44
Q

describe the classification of dysrhythmic drugs by clinical utility

A

dysrhythmias of supraventicular origin - adenosine, verapamil

dysrhythmias of supraventicular or venticular origin - amiodarone, flecainide, propranolol, quinidine

dysrhythmias of venticular origin - lidocaine

45
Q

what is hypertension defined as?

A

a sustained systolic BP >140 mmHg or a sustained diastolic BP >90 mmHg

46
Q

what are the causes of hypertension?

A
  1. genetic factors
  2. low birth weight
  3. environmental factors
  4. diabetes
  5. drugs
  6. kidney/cardiovascular disease
47
Q

what can high BP lead to?

A

damaged blood blood vessels - leading to stroke, ischaemic heart disease, peripheral vascular disease

48
Q

what is the the formula for determining blood pressure?

A

BP = cardiac output x total peripheral resistance (TPR)

49
Q

what is the intial treatment strategy for high BP?

A

reduce weight

reduce alcohol

reduce salt

stop smoking

more exercise

less caffeine

more fruit and veg

50
Q

what controls BP?

A

baroreceptors in carotid sinus and aortic arch stimulate:

  1. SA node to decrease cardiac rate and output
  2. vasodilation in arterioles
51
Q

what are the targets for antihypertensive drugs?

A

A - ACE inhibitors (+angiotensin receptor blockers)

B - beta blockers

C - calcium channel blockers

D - diuretics

52
Q

explain the renin - angiotensin system

A
  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
Q

what is the action of ACE inhibitors?

A

blocks ACE→ vasodilation occurs thus reducing periphral resistance

54
Q

name five ACE inhibitors

A
  • captopril
  • enalapril
  • trandolapril
  • ramipril
  • lisinopril
55
Q

what are the side effects of ACE inhibitors?

A
  • persistant dry cough
  • rash
  • renal problems (DO NOT use in patient with renal disease)
  • hypotension
  • DO NOT use in pregnancy
56
Q

what can be used instead of ACE inhibitors?

A

angiotensin receptor antagonists (ARBs)

57
Q

what is the action of ARBs?

A

selectively block AT2 receptors→ vasodilation occurs

58
Q

give four examples of ARBs

A
  • losartan
  • candesartan
  • valsartan
  • eprosartan
59
Q

what are the pros and cons of using ARBs?

A

pros

  • well tolerated
  • don’t produce cough

cons

  • dizziness
  • hyperkalaemia
60
Q

what is the antihypertensive action of ß blockers?

A
  1. reduce cardiac output
  2. reduced renin release
  3. reduced sympathetically mediated vasoconstriction
61
Q

where do ß blockers act?

A

sympathetic nervous system

62
Q

can ß blockers be used in pregnancy?

A

yes - eg. labetalol (mixed alpha/beta blockers)

63
Q

give five examples of ß blockers

A

atenolol

bisoprolol

sotalol*

metoprolol

propranolol*

* none selective - act on ß1 and ß2 receptors

64
Q

what are the side effects of ß blockers?

A
  • lathargy
  • impaired concentration/memory
  • aching limbs during exercise
  • erectice dysfunction
  • exacerbation of Raynauds disease
  • aggrevation of asthma
65
Q

what is the action of alpha receptor antagonist ?

A

blocks action od NAdr and adrenaline on blood vessels→ vasodilation occurs

66
Q

name 3 alpha receptor antagonists

A

prazosin

doxazosin

terazosin

67
Q

describe the action of prazosin

A

short acting alpha1 anatagonist → arteriolar/ venous dilation

*may cause postural hypotension

68
Q

what are the effects of calcium?

A
  • increase AV node conduction
  • incraese arterial tone
  • incraese myocardial contractility
  • increase HR
69
Q

what do calcium channel blockers do?

A

block calcium therefore:

  • dilates arteries
  • reduces heart contractility
  • and or reduces heart rate
70
Q

give examples of calcium channel blockers (CCBs) which are more potent on blood vessels than heart

A
  1. nifedipine
  2. amlodipine
  3. nicardipine
71
Q

what are the side effects of nifedipine, amlodipine, nicardipine?

A
  • headache
  • flushing
  • dizziness
  • peripheral oedema
72
Q

give two examples of CCbs which are more potent on the heart than the blood vessels

A
  1. verapamil
  2. diltiazem
73
Q

what are the side effect of verapamil and diltiazem?

A
  • constipation
  • heart block - could precipitate cardiac failure
74
Q

what is the action of thiazide like (and thiazide) diuretics?

A

increase urine output → which decreases blood volume and reduces blood pressure

75
Q

give five examples of thiazide like and thiazide diuretics

A
  1. chlorothiazide
  2. hydrochlorothiazide
  3. metolazone
  4. Chlortalidone
  5. Bendrothiazide
76
Q

what are the side effects of thiazide like (and thiazide) diuretics?

A
  • Hypokalaemia (reduced potassium)
  • reduced insulin release
  • increased plasma lipids and urates → gout
  • erectile dysfunction
77
Q

can potassium-sparing diuretics be prescribed alongside thiazide diuretics?

A

yes

78
Q

what are possible difficulities occuring with the use of potassium-sparing diuretics?

A

don’t reduce potassium as with thiazide diuretics but can increase potassium and reduce sodium in blood → hyperkalaemia / hyponatraemia

79
Q

give two examples of potassium-sparing diuretics

A
  1. amiloride
  2. spironolactone
80
Q

when would loop diuretics be most useful?

A

in severe hypertension - short duration of action

81
Q

what are the side effects of loop diuretics?

A
  • can affect hearing
  • may cause gout
  • may cause hypokalaemia
82
Q

give an example of a loop diuretic

A

furosemide

83
Q

give 3 examples of other vasodilators and when they may be used

A
  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
Q

outline the use of multiple drug therapy to control hypertension

A
85
Q

summerise antihypertensive drugs

A

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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