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Medicine 1- mainly CVS > Drugs used in the treatment of the cardiovascular system > Flashcards

Drugs used in the treatment of the cardiovascular system Flashcards

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1
Q

What is meant by an antiplatelet agent?

A

a drug that reduces the activity of platelets and reduces their ability to cross link and form thrombus

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2
Q

What are the antiplatelet agents and why?

A

Aspirin (main one)- cyclooxygenase inhibitor and reduces production of Thromboxane A2 (active chemical that signals to platelets to reveal receptors that are involved in cross linking)

Clopidogrel/ Ticagrelor (other main ones) - irreversibly affect receptor on surface of platelets that is involved in platelet activation

Dipyridimole- Phosphodiesterase inhibitors )

(GPIIB/IIIA fibrinogen receptor antagonists)

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3
Q

What are the antiplatelet agent’s life span?

A

life span within circulation is about 7-10 days

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4
Q

What does the enzyme , cyclooxygenase, do?

A

converts fatty acid (Arachidonic acid) into various vasoactive mediators and inflammatory mediators called prostaglandins and thrombooxane A2

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5
Q

What are prostaglandins involved in?

A

involved in maintaining vascular tone in various vascular beds - in particular kidneys.
Where prostacyclin is important in maintaining perfusion within the kidneys involved in secretion of mucus within GI tract

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6
Q

What clinical problem does blocking cyclooxygenase within GI tract cause?

A

reduce the amount of mucus that’s produced in the GI tract and can lead to problems with indigestion.
Aspirin also makes you bleed and can irritate GI tract.
Bleeding from GI tract

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7
Q

What are the two isoforms of cyclooxygenase?

A

COX 1 - runs in background and produces prostaglandins to help with vascular tone and mucus production.
COX 2 - induced by pro-inflammatory signals and can produce a whole host of inflammatory mediators. These mediators are involved in pain reception.

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8
Q

When are antiplatelets used?

A

in secondary prevention

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9
Q

When is aspirin used?

A

used in patient who have got stable angina or have had a heart attack.
They will be left on aspirin and a small dose of aspirin for the rest of their lives.
High doses during first couple week after stroke and then switched to clopidogrel.

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10
Q

When is Clopidogrel used?

A

mainstay secondary prevention antiplatelet in patients with stroke disease

In combination with Aspirin- following Percutaneous Intervention in Stable patient and some Stroke patients

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11
Q

When is Ticagrelor used?

A

used In combination with Aspirin in all patient with ACS for upto 1 year in NHSG

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12
Q

Side effects of antiplatelet agents?

A

Bleeding
Roughly 0.25 to 1% annual risk of a significant bleed with a single agent,
synergistic effect (risk of bleeding goes up) when multiple agents used
Effect will last for up to 1 week as they irreversible

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13
Q

Interactions antiplatelet agents?

A

when used with anticoagulating can increase bleeding

NSAID and SSRIs - increased tendency to bleed

Clopidogrel and omeprazole - as omeprazole has risk of reducing patient to clopidogrel and therefore increasing risk of thrombosis.

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14
Q

What are the main receptors in the sympathetic nervous system?

A

alpha and beta adrenergic receptors

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15
Q

What does activation of alpha 1 receptors on smooth muscle mean?

A

smooth muscle contraction

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16
Q

What does activation of beta 1 receptors on heart mean?

A

activation of these receptors leads to tachycardia (increasing heart rate) and a more forceful contraction

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17
Q

What does activation of beta two receptors on vascular tree mean?

A

dilation of the arteries due to smooth muscle relaxation

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18
Q

What is the main neurotransmitter in sympathetic NS?

A

Noradrenaline

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19
Q

What is the stress hormone produced by the adrenal medulla?

A

adrenaline

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20
Q

What do alpha and beta receptors have a greater interaction with?

A

alpha receptors- noradrenaline
beta receptors-adrenaline

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21
Q

positive effects of beta blockers?

A

reduce mortality in ischaemic heart disease and heart failure

also reduce symptoms in angina (beta blockers slow heart down) , Atrial fibrillation and super ventricular tachycardia

Antihypertensive (2nd line now)- (multiple mechanisms of action both central and peripheral)

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22
Q

Where are beta I receptors found?

A

Predominant receptor in the Heart- SA, AV Nodes and myocardial cells.

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23
Q

Effect of beta blockers on the beta I receptors in kidneys?

A

Kidneys- reduce secretion of Renin (see ACE inhibitors)

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24
Q

Positive effects of beta blockers?

A

Slows heart rate and conduction (Negatively Chronotropic (and Dromotropic)), Increases Diastolic Time,
Reduces BP,
Antiiaryhthmic Protects heart from effects of Catecholamines

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25
Negative effects of beta blockers?
reduces contractility (negatively Inotropic), high doses can lead to bradycardia and heart block
26
Where are the beta two receptors?
Smooth muscle eg Airways, Peripheral vasculature (to lesser extent present on myocardial cells) skeletal
27
Positive effects of beta blockers on beta 2 receptors?
Reduces tremor
28
Negative effects of beta blockers on beta II receptors?
bronchospasm in asthmatics, vasoconstriction in PVD
29
Examples of beta blockers ?
For beta 1 receptors Bisoprolol Atenolol Metoprolol for beta one and beta two carvediol propanolol
30
Side effects of beta blockers?
Lethargy/sexual dysfunction- in males especially Breathlessness Wheeze Cold extremities- some effect still on beta II receptors peripherally- causing vasoconstriction
31
Interactions of beta blockers?
hypotensive effect with other agents, extreme bradycardia with certain Ca channel blockers and other antiarrhythmics
32
How are calcium ions crucial to function of smooth muscle and myocardium?
Calcium needed for contractile mechanisms of both muscle types Calcium ingress into cardiac nodal tissue (sinoatrial and atrioventricular node) responsible for action potential
33
How does calcium get into muscle cells?
via L -type calcium channels
34
Why do calcium channels respond differently to different classes of drugs?
Different isoforms in the Heart and Smooth Muscle means they respond differently to different classes of drug
35
Who are the calcium channels the first line antihypertensive agent for?
for older patients
36
What do calcium channel blockers reduced symptoms of?
Angina - dihydropyridine (peripherally) and non dihydropyridine(work on heart rate) Atrial fibrillation and SVT (supraventricular tachycardia)- non dihydropyridine
37
What are the two big classes of calcium channel blockers?
dihydropiridine non-dydropyridine
38
Characteristics of dihydropyridine?
Block calcium entry into smooth muscle Cause vasodilation Less effect on myocardial pacemaking tissue Eg. Amlodipine, felodipine, nifedipine Side effects- postural hypotension, peripheral oedema (capillary leakage of fluids from vasodilation), reflex tachycardia (particularly Short acting ones), rarely bradycardia (unless in overdose)
39
Characteristics of non-dydropyridine?
Block calcium entry to smooth muscle Blocks calcium entry in the myocardial pacemaking tissue Slow SA node function Slow AV conduction Eg. Verapamil and Diltiazem Side effects- Bradycardia, heart block (particularly if prescribed with beta blocker), postural hypotension, peripheral oedema
40
What is the renin-angiotensin-aldosterone axis for?
Preserves circulating volume to maintain perfusion of the vital orgains Central hormonal axis to the development of Heart failure Liver failure Kidney failure
41
What are the first choice of drugs for hypertension in the young?
Angiotensin converting enzyme inhibitors and angiotensin receptor antagonists (ARBS)
42
What are the positives of use of Angiotensin converting enzyme inhibitors and angiotensin receptor antagonists (ARBS)?
Reduction in mortality and progression of disease in IHD, CVD and renal disease with proteinuria (particularly diabetic nephropathy) Prevent aberrant remodelling following MI Reduction in symptoms in heart failure
43
Describe the renin-angiotensin-aldosterone axis?
angiotensinogen produced by the liver converted to angiotensin I by renin angiotensin I converted into angiotensin II by ACE Angiotensin II , potent vasoconstrictor (Peripheral vasculature Efferent Arteriole of the glomerulus ) and acts on the adrenals -releasing aldosterone (Retention of Na (and therefore H20) at the expense of K in the DCT of the kidneys (sweat glands, Gut) )
44
Examples of ACE inhibitors?
Eg Ramipril, Lisinopril, captopril, perindopril
45
What are positive effects of ACE inhibitors?
Reduce blood pressure, reduce afterload on heart, prevents aberrant remodelling after MI and reduces proteinuria
46
What are negative effects of ACE inhibitors?
reduces perfusion pressure in glomerulus leading to renal impairment; hyperkalaemia via effect on aldosterone levels,; cough; orthostatic hypotension
47
Examples of ARBS?
Eg, losartan, candersartan
48
Positive effects of ARBS?
Positive effects- Reduce blood pressure, reduce afterload on heart, prevents aberrant remodelling and reduces proteinuria
49
Negative effects of ARBS? (angiotensin receptor blockers)
reduces perfusion pressure in glomerulus leading to renal impairment; hyperkalaemia via effect on aldosterone levels, No cough; orthostatic hypotension
50
What are examples of aldosterone antagonists?
Spironolactone and eplenerone- used in heart failure (frequently coprescribed with ACE/ARB). Spiro sometimes used in hypertension
51
Positives of aldosterone antagonists?
Enhanced diuretic effect, vasodilation Reduces mortality in IHD and Heart failure
52
Side effects of aldosterone anatgonists?
Renal impairment, hyponatraemia, HYPER KALAEMIA Gynaecomastia (Spiro > Eplenerone) -avoid using aldosterone antagonists alongside ibuprofen and other NSAIDs (as NSAID will reduce the production of cyclin- which is important in maintaining blood flow withing the kidney and if turn off angiotensin II-marked renal failure.
53
What is entresto useful in?
useful drug in patients with symptomatic , chronic heart failure
54
When does entresto reduce mortality?
when used in combination with an angiotensin receptor blocker
55
Why don't you prescribe ace inhibitors with entresto?
risk of angiodema
56
When are statins important?
Primary prevention- reduce cardiovascular risk if patients 10 year risk is > 20% Secondary prevention after cardiovascular event
57
What are examples of statins?
Simvastatin, Rosuvastatin and Atorvastatin
58
Side effects of statins?
muscle aches and pain but low risk of myostitis (inflammation of muscle - which leads to leak of muscle proteins- leads to oxidative damage to kidneys and marked renal failure) myositis is rare and more likely if statin coprescribed with certain agents
59
What are the effects of using diuretics?
Antihypertensive effects- Thiazides eg. Indapamide and Bendroflumethizide Symptomatic treatment in heart failure- generally loop diuretics eg. Furosemide and Bumetanide Promote Sodium and Water loss in the kidney (also can lead to hypokalaemia)
60
What is the function of thiazide diuretics?
Act by blocking NaCl reabsorption in distal convoluted tubule of the kidney Mild diuretic effect Vasodilatory effect
61
Examples of thiazide diuretics?
Eg. Indapamide, Bendroflumethiazide
62
Common side effects of thiazide diuretics?
Electrolyte disturbance (Low Na and K in particular but also Hypercalcaemia) Hyperuricaemia (causing gout and increased Cardiovascular risk) Hyperglycaemia Dehydration, renal impairment Orthostatic Hypotension
63
How do loop diuretics work?
Act by blocking NaCl Reabsorption in the ascending limb of the loop of Henle Intense diuretic effect Pronounced vaso and venodilatory effect
64
What are examples of loop diuretics?
Eg. Furosemide and Bumetanide
65
Common side effects of loop diuretics?
Electrolyte disturbance (Low K, Na and Mg and Ca) Dehydration, renal impairment Orthostatic Hypotension
66
Other cardiovascular drugs?
Antianginals- Nitrates Short acting eg GTN Long acting eg Isosorbide Mononitrate Directly act to cause vasodilation via nitic oxide Headache and postural hypotension Nb. Need to have nitrate free period Nicorandil Nitrate effect K+ Channel blocker Vasodilation Headache, postural hypotension and ulceration in GI tract Antihypertensives- Alpha (adrenoreceptor) blockers Cause peripheral vasodilation eg doxasocin

Medicine 1- mainly CVS (58 decks)

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