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module 103 - theme 3 > drug treatments for cardiovascular disease (lectures 1-4) > Flashcards

drug treatments for cardiovascular disease (lectures 1-4) Flashcards

1
Q

what is hypertension?

A

persistently higher than normal blood pressure

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2
Q

when do you treat hypertension?

A

when mean BP is >150/95 mmHg

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3
Q

how do you treat hypertension?

A

appropriate pharmacological treatment required a knowledge of the physiological regulation of BP and knowledge of how drugs work

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4
Q

what is the equation of blood pressure?

A

BP = CO x TPR

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5
Q

what is the equation of cardiac output?

A

cardiac output = stroke volume x heart rate

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6
Q

what regulates stroke volume?

A

the ventricles

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7
Q

what regulates heart rate?

A

SA node

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8
Q

what is the total peripheral resistance a measure of?

A

the degree of constriction of the arterioles

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9
Q

how does extrinsic regulation work?

A
  • autonomic nervous system
  • sympathetic system increased frequency and force of contraction via beta 1 receptors —> increased cAMP
  • –> increased calcium —> increased rate and force of contraction
  • parasympathetic system decreases frequency by decreasing cAMP via M2 receptors
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10
Q

how does the sympathetic nervous system regulate TPR?

A
  • SNS –> NA –> alpha 1 receptor –> IP3 –> Ca2+ –> constriction
  • SNA –> A –> beta 2 receptor –> cAMP –> relaxation
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11
Q

how do you generally regulate TPR?

A
  • increase in Ang II —> increase IP3 —> increase intracellular [Ca2+]
  • causes constriction of arterioles and an increase in total peripheral resistance and increases in BP
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12
Q

how do you regulate preload by RAAS?

A
  • constriction of venules via AT1-R
  • RAAS also facilitates Na+ and H2O retention
  • aldosterone activates cytoplasmic receptors which bind to the nucleus to increase expression of Na+ channels and so aid Na+ and water retention
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13
Q

what factors affect the choice of drug treatment?

A
  • age: <55 years old ACE inhibitor/angiotensin receptor blocker (ARB); >55 year old or all-black African/American calcium channel blocker
  • race: ACE inhibitors/beta blockers may be less efficacious in black African/Americans
  • co-existing diseases
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14
Q

what are the different classes of anti-hypertensives?

A
  • ACE inhibitors and angiotensin receptor blockers
  • calcium channel antagonists
  • diuretics
  • beta-blockers
  • vasodilators
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15
Q

what are the side effects and contraindications of ACE inhibitors?

A
  • dry cough
  • 1st dose hypotension
  • renal impairment
  • contraindicated in bilateral renal artery stenosis
  • may cause hyperkalaemia
  • no adverse effect on serum glucose or lipids
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16
Q

what is hyperkalaemia?

A

high potassium levels

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17
Q

what do angiotensin receptor antagonists do?

A

block the actions of Ang II on AT1-R

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18
Q

what is an example of an aldosterone antagonist?

A

spironolactone

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19
Q

when do you use spironolactone?

A

used as an add on for resistant hypertension but FRONTLINE for hypertension in patients with primary aldosteronism

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20
Q

what are the different types of calcium channel antagonists and how do they work?

A
  • main type = dihydropyridines
  • target L-type calcium channels on smooth muscle of arterioles
  • phenylalkylamines and benzothiazepines target L-type channels in the heart and decrease the frequency and force of contraction
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21
Q

what are the side effects of calcium channel antagonists?

A
  • peripheral oedema

- flushing and headaches

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22
Q

how does peripheral oedema occur?

A

preferential dilation of pre-capillary arteriole and impairment of the function of the pre-capillary sphincter increases hydrostatic pressure across the capillary and reducing fluid reabsorption

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23
Q

what enhances the action of calcium antagonists?

A

grapefruit juice

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24
Q

how do thiazide and thiazide-like diuretics work?

A

some diuretic action but also acts via activation of Katp in smooth muscle of blood vessel to dilate arteriole and decrease blood pressure

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25
Q

how does indapamide work?

A

it hyperpolarises smooth muscle cells causing relaxation/dilation of the arteriole and decrease in total peripheral resistance

26
Q

what are the side effects and contraindication of hiazide and thiazide-like diuretics?

A
  • hypokalaemia
  • increase in urate
  • increase in glucose
  • increase in blood lipids
27
Q

what are the side effects and contraindications of beta blockers?

A

fatigue

28
Q

how do beta blockers cause vaso/bronchoconstriction?

A

smooth muscle cell in the airways of peripheral arterioles perfusing skeletal muscle

29
Q

what does low blood glucose activate?

A

the release of adrenaline, mobilises glucose release from liver leading to tremor, palpitations and sweats

30
Q

what blocks the action of low blood glucose?

A

beta blockers

31
Q

what combination of 2 drugs is contraindicated in diabetics?

A

beta blockers and thiazides

32
Q

what are the different types of beta blockers?

A
  • non selective (beta 1 and beta 2)

- selective beta 1 anatgonists

33
Q

what type of drug are vasodilators?

A

alpha 1 antagonists

34
Q

how do vasodilators work?

A

NA –> alpha 1 –> IP3 –> calcium ion –> constriciton

35
Q

when are vasodilators used to treat hypertension?

A

when the patient have benign prostatic hypertrophy

36
Q

what do vasodilators such as minoxidil do?

A

open potassium channels

37
Q

what increases myocardial oxygen supply?

A
  • work rate (heart rate, force)

- work load (TPR)

38
Q

what decreases myocardial oxygen supply?

A
  • thrombus
  • atheroma
  • vasoconstriction
39
Q

what helps with the regulation of coronary blood flow?

A

endothelium derived relaxing factor (nitric oxide)

40
Q

how do you regulate cardiac workload?

A
  • end diastolic volume (preload) regulated by smypathetic system, RAAS
  • heart rate (sympathetic system/Ca2+)
  • contractility (sympathetic system/Ca2+)
  • total peripheral resistance (sympathetic system RAAS)
41
Q

what is the definition of stable angina?

A

a predictable pattern of pain during exercise that is relieved by rest

42
Q

what is the treatment for angina?

A

drug treatment designed to decrease work done by the heart and/or increase blood supply and treat risk factors

43
Q

what are the side effects of drug treatment for angina?

A
  • postural hypotension
  • headache
  • dizziness
  • reflex tachycardia
44
Q

why does reflex tachycardia occur and how do we stop it?

A
  • it is due to activation of the sympathetic nervous system

- we look to block effects of the sympathetic nervous system with beta blockers

45
Q

what do beta blockers do?

A

inhibit release from the kidney and inhibit RAAS

46
Q

what are the side effects of beta blockers?

A
  • bronchoconstriction
  • fatigue
  • contraindicated in patients with peripheral vascular disease
47
Q

what are calcium channel antagonists used for?

A

in asthmatics or other groups where beta blockers are contradicted the cardiac selective calcium channel blockers can be used

48
Q

what happens when you use a mixture of cardiac selective calcium eds and beta blockers?

A

can cause severe bradycardia and even heart block

49
Q

what do calcium channel blockers do?

A

can reduce heart beat by blocking L-type channels in the SA and AV nodes which slows the rate of depolarisation and therefore reduces the rate of action potential generation
- they also decrease the force of contraction of the ventricles by reducing calcium entry through L-type channels

50
Q

what does ivabradine do?

A
  • blocks the pacemaker current (Ih/f) in the nodal tissue of the heart
  • it reduces the Na+ entry through If channels and slows the rate of depolarisation of the SA node cells and reduce firing frequency and therefore heart rate
  • it will not directly alter the force of contraction of the heart
51
Q

what are the side effects of ivabradine?

A
  • luminous phenomena (ih) in retina
  • blurred vision
  • dizziness
52
Q

what are the alternatives to ivabradine?

A
  • long acting nitrates (isosorbide mononitrate)
  • decreased preload
  • nicorandil
  • ranolazine
53
Q

how do you treat to reduce hypercholesterolaemia 2 degrees prevention?

A
  • cholesterol from 2 main sources
  • drugs designed to either inhibit uptake from GI tract or reduce production in liver
  • frontline treatment are the statins
54
Q

how do statins prevent cholesterol synthesis?

A
  • statins decrease the production of cholesterol in the liver by inhibiting the HMG CoA enzyme
  • this stimulates the liver cells to express LDL receptors and allows the liver cells to scavenge LDL cholesterol from the plasma
  • this reduces plasma LDL cholesterol levels
55
Q

what are the secondary prevention methods cholesterol synthesis?

A
  • aspirin: antiplatelet agents

- ACE inhibitors: decrease the workload on the heart

56
Q

how do you treat acute coronary syndromes?

A
  • same as for stable angina and antiplatelet

- aspirin and clopidogrel

57
Q

what is the mechanism of action for some key antiplatelet agents?

A
  • platelet activation occurs when the endothelial cells become damaged
  • this releases ADP which on P2Y12 receptors to stimulate the platelet to express GPIIb/IIIa receptors
  • fibrinogen binds to these receptors to cross link different platelets
  • activation of COX also helps platelet activation through the production of Thromboxane A2
  • aspirin inhibits COX irreversibly
  • clopidogrel and prasugrel are ADP antagonists and block P2Y12 receptors
58
Q

how do you diagnose chronic coronary syndromes?

A
  • pain

- sweating, tachycardia, cold clammy skin

59
Q

how do you treat chronic coronary syndromes?

A
  • pain relief: diamorphine to decrease pain, anxiety, sympathetic drive and vasodilators
  • oxygen
  • aspirin/GTN
  • clot busting drugs: tenecteplase
  • beta blockers: decrease cardiac workload, prevents arrhythmias
  • ACE inhibitors: decrease cardiac workload, prevents remodelling development of heart failure
  • anticoagulants: in case of long term best rest, prevents thrombus formation
60
Q

how does digoxin work to treat heart failure?

A
  • digoxin binds to the Na+/K+ ATPase and inhibits its action
  • this will increase levels of Na+ ions inside the heart muscle cells
  • this increase will in turn inhibit the Na+/Ca2+ exchanger which will lead to a build up of Ca2+ inside the muscle cell and a stronger contraction
61
Q

how does amiodarone treat dysrhythmias?

A
  • K+ channel blockers that increase the refractory period of ventricular myocytes and can terminate arrhythmias

module 103 - theme 3 (17 decks)

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