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Cardiovascular > Drugs > Flashcards

Drugs Flashcards

1
Q

What is a dysrhythmia and what are some symptoms?

A

Any variation from the normal rhythm of the heart beat

Symptoms can include shortness of breath, fainting, fatigue, chest pain

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2
Q

What are some of the mechanisms that underlie dysrhythmias?

A
  • altered impulse formation (generation of AP at sites other than the SA node)
  • altered impulse conduction (conduction block or re-entry)
  • triggered activity (early or late after-depolarisations)
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3
Q

What are the 4 classes of antidysrhythmics?

A
  • Na+ channel blockers
  • Beta-adrenoceptor antagonists
  • K+ channel blockers
  • Ca2+ channel blockers
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4
Q

How do Na+ channel blockers work?

A

Reduce phase 0 slope and peak of ventricular AP

  • class 1 moderate block
  • class 2 mild block
  • class 3 marked block
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5
Q

How do beta-adrenoceptor antagonists work in dysrhythmias?

A

Inhibit the sympathetic influence –> decrease sinus rate, conduction velocity and aberrant pacemaker activity
- also have a membrane stabilising effect in Purkinje fibres

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6
Q

How do K+ channel inhibitors work?

A

Prolong the cardiac action potential by slowing the phase 3 repolarisation

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7
Q

How do Ca2+ channel blockers work in dysrhythmias?

A

Act preferentially on the SA and AV nodes to reduce rate, slow conduction velocity and increase refractoriness

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8
Q

What is the arbitrary cut off for hypertension?

A

> 140/90mmHg

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9
Q

What are the classes of drugs used to treat hypertension?

A
  • Angiotensin system inhibitors
  • Beta-adrenoceptor antagonists
  • Calcium channel blockers
  • Diuretics
  • Other (eg alpha-1 adrenoceptor antagonists, vasodilators)
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10
Q

How do ACE inhibitors work? What is an example?

A 
Block the conversion of Ang I to Ang II 
- reduce vascular tone
- reduce aldosterone production 
- reduce cardiac hypertrophy 
Eg. Captopril, enalapril
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11
Q

What are the adverse effects of ACE inhibitors?

A
  • first dose hypotension
  • dry cough (bradykinin)
  • hyperkalaemia
  • loss of taste
  • acute renal failure
  • itching, rash, angioedema
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12
Q

How do angiotensin receptor antagonists work? What is an example?

A 
Block AT1 receptors 
- reduce vasoconstriction
- reduce aldosterone
- reduce cardiac hypertrophy 
- reduce sympathetic activity 
Eg. Losartan
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13
Q

What are the adverse effects of angiotensin receptor antagonists?

A
  • hyperkalaemia

- headache, dizziness

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14
Q

How do beta-adrenoceptor antagonists work in hypertension? What is an example?

A 
Reduce CO
- rate, contractility 
Reduce renin release 
- blood volume, TPR 
Eg. propranolol, atenolol
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15
Q

What are the adverse effects of beta-adrenoceptor antagonists?

A
  • cold extremities (reflex alpha-1 constriction)
  • fatigue
  • dreams, insomnia (CNS effects)
  • bronchoconstriction (CONTRAINDICATED IN ASTHMA)
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16
Q

How do calcium channel blockers work in hypertension? What is an example?

A

Inhibit voltage gated L-type calcium channels in myocardium and vasculature
- reduce cardiac/vascular contractility
Eg. verapamil (cardiac and vascular)
nifedipine (vascular)

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17
Q

What are the adverse effects of calcium channel blockers?

A
  • oedema, flushing
  • headache
  • bradycardia (verapamil, diltiazem)
  • reflex tachycardia (dihydropyridines)
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18
Q

How do diuretics work?

A

Inhibit Na+/Cl- cotransporter in distal convoluted tubule

  • decrease Na+ and Cl- reabsorption in renal tubules
  • lower blood volume and reduce blood pressure
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19
Q

What are the adverse effects of diuretics?

A
  • K+ loss
  • gout
  • hyperglycaemia
  • allergic reactions
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20
Q

What is digoxin and how does it work?

A

Cardiac glycoside, inhibits the Na+/K+ ATPase

  • increased [Na] decreases Ca2+ extrusion
  • increased Ca2+ in sarcoplasmic reticulum
  • increased Ca2+ release with each AP
    • used in heart failure, but VERY narrow margin of safety –> low therapeutic index
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21
Q

How do beta adrenoceptor agonists and PDE inhibitors work in heart failure?

A

SHORT TERM support for acute heart failure/cardiogenic shock

  • increase the cardiac work, make it pump harder
  • this increases the O2 demand and increases the risk of arrhythmias
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22
Q

What drugs reduce preload?

A

Venodilators

  • nitrates
  • diuretics
  • aldosterone receptor antagonists
  • aquaretics
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23
Q

What drugs reduce afterload?

A
  • arterial vasodilators
  • ACE inhibitors (first line therapy)
  • AT1 receptor antagonist
  • B adrenoceptor antagonist
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24
Q

What is the confusion with beta-blockers in heart failure?

A

Despite beta-1 blockade, stroke volume increases as the heart has more time for filling

25
Q

What is the aim of treatment for heart failure?

A

Decrease cardiac work and improve cardiac function, reduce signs and symptoms and increase survival

26
Q

How does heparin work?

A

Enhances the activity of antithrombin III (inactivates Xa and thrombin) to act as an anti-coagulant
- needs to be given intravenously

27
Q

What is the difference between LMW heparin and heparin?

A

LMW heparin can be used by patients for self administration at home and have less of an effect on Xa

28
Q

How does warfarin work?

A

Inhibits the reduction of vitamin K thereby inhibiting the formation of clotting factors II, VII, IX and X
- ONLY ACTIVE IN VIVO, as it is affecting the formation of the clotting factors so there is a delayed onset of action and it does not affect the already active factors

29
Q

What are the adverse effects of warfarin?

A

Haemorrhage - need to titrate dose

  • reversal by vitamin K (oral)
  • need to monitor regularly (PT time, INR)
30
Q

What is low dose aspirin therapy?

A 
COX inhibitor (platelets produce thromboxane) 
Reduces thromboxane synthesis from platelets in the portal vein 
- decreased platelet aggregation and vasoconstriction 
- retains prostaglandin I2 from endothelium so inhibits platelet aggregation and promotes vasodilation
31
Q

When are fibrinolytic drugs used and how do they work?

A

Used in an acute setting, activate plasminogen and promote fibrinolysis

32
Q

How does streptokinase work?

A

Activates plasminogen, used IV

- microbial in origin, antigenic so only single use

33
Q

How does alteplase work?

A

Not antigenic so can be given in patients that have received streptokinase but EXPENSIVE

34
Q

What is the mechanism of action of statins?

A

Decrease mevalonic acid and therefore cholesterol synthesis by inhibiting HMG-CoA reductase

  • decrease LDL, increase LDL receptor, increase HDL and decrease TG
  • indications in hypercholesterolaemia and mixed hyperlipidaemia
35
Q

What is the mechanism of action of bile acid sequestrants/resins?

A

Bind bile acids preventing gut absorption
- increased demand for cholesterol for bile acid synthesis causes upregulation of hepatic LDL receptors, removal of LDL from plasma and more cholesterol metabolism

36
Q

What do you need to be aware of when prescribing resins?

A

Interactions with other drugs - decreases absorption of other drugs such as glycosides, thiazides, statins, aspirin
- need to give other drugs hours before resins

37
Q

What is the mechanism of action of Ezetimibe?

A

Specifically inhibits cholesterol absorption in the intestine by binding to a sterol transporter

  • does not allow the absorption of bile acids, fat soluble vitamins
  • lowers LDL
38
Q

What are possible side effects of Ezetimibe?

A

Diarrhoea, headache, tiredness

39
Q

What is the mechanism of action of Nicotinic acid/niacin?

A

Lowers atherogenic lipoprotein (a) (mechanism unclear)

- decreases secretion of VLDL particles from liver, reduces plasma LDL and TGs, increases HDL

40
Q

What is the mechanism of action of fibrates?

A

Agonists at PPAR-alpha, increases synthesis of LPL which leads to increased breakdown of TGs
** major effect is on TGs, but also decreases LDL and increases HDL

41
Q

What are the aims of drug treatment of angina?

A

Use drugs to

  • increase O2 supply –> dilate coronary arteries, reduce HR
  • reduce O2 demand –> decrease CO, reduce preload, reduce afterload
42
Q

What is the mechanism of action of nitrates?

A

Drug undergoes biotransformation –> releases NO –> stimulates guanylate cyclase in VSM –> GTP converted to cGMP –> dephosphorylates myosin LC –> vascular relaxation

43
Q

What is the major site of action of nitrates?

A

Veins –> reduce preload

44
Q

How does GTN work and when is it given?

A

Given sublingually for acute attacks/anticipation of effort, transdermal for prophylaxis, IV for emergency

45
Q

How does tolerance occur with GTN and how can it be managed?

A

Depletion of tissue thiols required for NO production/increased release of and/or sensitivity to constrictors etc
- drug free period required to minimise tolerance, eg remove patch overnight

46
Q

How do calcium channel blockers work in treatment of angina?

A

Block Ca2+ entry into the heart through L-type channels leading to decreased HR and decreased SV and CO
- mostly verapamil and diltiazem
Block Ca2+ entry into vessels through voltage operated (L-type) and receptor operated channels –> arterial dilation, reduced afterload and demand
- nifedipine, felodipine

47
Q

How are beta blockers used in the treatment of angina?

A

Block the effects of sympathetic nervous system on cardiac beta-1 adrenoceptors

  • decrease HR, decrease contractility and SV
    • first line therapy for prophylaxis
48
Q

What is the mechanism of action of ivabradine?

A

Pure HR reduction by selective inhibition of the iFunny current –> reduces the steepness

49
Q

What is the treatment for variant angina?

A

Relieve coronary spasm with short acting nitrate

  • prophylaxis with dihydropyridine Ca2+ channel blocker
  • ** BETA-ADRENOCEPTOR ANTAGONISTS CONTRAINDICATED
50
Q

What is the treatment for unstable angina?

A

As for classic angina, but include aspirin to prevent thrombosis

51
Q

What are diuretics?

A

Drugs that increase Na+ and water excretion

52
Q

What are the 4 classes of diuretics?

A

Loop diuretics
Thiazide diuretics
Potassium-sparing diuretics
Osmotic diuretics

53
Q

What is the mechanism of action of loop diuretics?

A

Most powerful diuretic, causes “torrential” urine flow

  • Frusemide
  • acts on the thick ascending limb of LoH, inhibiting the Na+/K+/2Cl- carrier
    • normally given with a K+ supplement or used with K+ sparing diuretic
54
Q

What is the mechanism of action of thiazide diuretics?

A

Moderately powerful, act on the distal convoluted tubule to inhibit the Na+/Cl- cotransporter

55
Q

What is the mechanism of action of potassium sparing diuretics?

A

Used in combination with potassium losing diuretics to prevent K+ loss
- act on collecting tubule and ducts

56
Q

What is the mechanism of action of spironolactone?

A

Aldosterone receptor antagonist to reduce activation of Na+ channels and simulation of Na+ pump synthesis
** can lead to hyperkalaemia if used alone

57
Q

What is the mechanism of action of amiloride?

A

Block luminal sodium channels in collecting tubules and ducts to inhibit Na+ reabsorption and K+ secretion

58
Q

What is the mechanism of action of osmotic diuretics?

A

They are pharmacologically inert and have their main effects on water permeable parts of the nephron
- not really used for Na+ retention

Cardiovascular (8 decks)

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