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Drugs Flashcards

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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?

Study These Flashcards
A

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

25
What is the aim of treatment for heart failure?
Decrease cardiac work and improve cardiac function, reduce signs and symptoms and increase survival
26
How does heparin work?
Enhances the activity of antithrombin III (inactivates Xa and thrombin) to act as an anti-coagulant - needs to be given intravenously
27
What is the difference between LMW heparin and heparin?
LMW heparin can be used by patients for self administration at home and have less of an effect on Xa
28
How does warfarin work?
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
What are the adverse effects of warfarin?
Haemorrhage - need to titrate dose - reversal by vitamin K (oral) - need to monitor regularly (PT time, INR)
30
What is low dose aspirin therapy?
``` 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
When are fibrinolytic drugs used and how do they work?
Used in an acute setting, activate plasminogen and promote fibrinolysis
32
How does streptokinase work?
Activates plasminogen, used IV | - microbial in origin, antigenic so only single use
33
How does alteplase work?
Not antigenic so can be given in patients that have received streptokinase but EXPENSIVE
34
What is the mechanism of action of statins?
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
What is the mechanism of action of bile acid sequestrants/resins?
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
What do you need to be aware of when prescribing resins?
Interactions with other drugs - decreases absorption of other drugs such as glycosides, thiazides, statins, aspirin - need to give other drugs hours before resins
37
What is the mechanism of action of Ezetimibe?
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
What are possible side effects of Ezetimibe?
Diarrhoea, headache, tiredness
39
What is the mechanism of action of Nicotinic acid/niacin?
Lowers atherogenic lipoprotein (a) (mechanism unclear) | - decreases secretion of VLDL particles from liver, reduces plasma LDL and TGs, increases HDL
40
What is the mechanism of action of fibrates?
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
What are the aims of drug treatment of angina?
Use drugs to - increase O2 supply --> dilate coronary arteries, reduce HR - reduce O2 demand --> decrease CO, reduce preload, reduce afterload
42
What is the mechanism of action of nitrates?
Drug undergoes biotransformation --> releases NO --> stimulates guanylate cyclase in VSM --> GTP converted to cGMP --> dephosphorylates myosin LC --> vascular relaxation
43
What is the major site of action of nitrates?
Veins --> reduce preload
44
How does GTN work and when is it given?
Given sublingually for acute attacks/anticipation of effort, transdermal for prophylaxis, IV for emergency
45
How does tolerance occur with GTN and how can it be managed?
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
How do calcium channel blockers work in treatment of angina?
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
How are beta blockers used in the treatment of angina?
Block the effects of sympathetic nervous system on cardiac beta-1 adrenoceptors - decrease HR, decrease contractility and SV * * first line therapy for prophylaxis
48
What is the mechanism of action of ivabradine?
Pure HR reduction by selective inhibition of the iFunny current --> reduces the steepness
49
What is the treatment for variant angina?
Relieve coronary spasm with short acting nitrate - prophylaxis with dihydropyridine Ca2+ channel blocker * ** BETA-ADRENOCEPTOR ANTAGONISTS CONTRAINDICATED
50
What is the treatment for unstable angina?
As for classic angina, but include aspirin to prevent thrombosis
51
What are diuretics?
Drugs that increase Na+ and water excretion
52
What are the 4 classes of diuretics?
Loop diuretics Thiazide diuretics Potassium-sparing diuretics Osmotic diuretics
53
What is the mechanism of action of loop diuretics?
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
What is the mechanism of action of thiazide diuretics?
Moderately powerful, act on the distal convoluted tubule to inhibit the Na+/Cl- cotransporter
55
What is the mechanism of action of potassium sparing diuretics?
Used in combination with potassium losing diuretics to prevent K+ loss - act on collecting tubule and ducts
56
What is the mechanism of action of spironolactone?
Aldosterone receptor antagonist to reduce activation of Na+ channels and simulation of Na+ pump synthesis ** can lead to hyperkalaemia if used alone
57
What is the mechanism of action of amiloride?
Block luminal sodium channels in collecting tubules and ducts to inhibit Na+ reabsorption and K+ secretion
58
What is the mechanism of action of osmotic diuretics?
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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