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Cardiovascular Drugs Flashcards

(61 cards)

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1
Q

What does Ivabradine do?

A

Decrease If current hence decreases heart rate

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2
Q

What do beta blockers do to the heart?

A

Decrease cAMP hence decreases If and Ica hence decreased HR

Also decrease contractility

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3
Q

What do CCBs do to HR

A

Decrease it, blocks Ica current

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4
Q

What are the two classes of calcium antagonists?

A
  • rate slowing (cardiac and smooth muscle)

- non rate slowing (smooth muscle action)

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5
Q

Types of rate slowing calcium antagonists

A
  • Phenylalkylamines (verapamil)

- Benzothiazepines (diltiazem)

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6
Q

Types of non rate slowing calcium antagonists

A
  • Dihydropyridines (amlodipine)
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7
Q

How do non rate slowing calcium antagonists cause tachycardia

A

Vasodilation can lead to reflex tachycardia

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8
Q

What drugs influence myocardial oxygen supply/demand

A
  • organic nitrates
  • potassium channel openers (nicorandil)

Induces hyperpolarisation hence decreased cardiac contractions as decreased afterload and preload (demand) and increased coronary blood flow

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9
Q

Side effects of beta blockers

A
  • worsening of heart failure as reduced Q and less b2 mediated vasodilation hence increased vascular resistance
  • bradycardia
  • cold extremities
  • impotence
  • CNS effects
  • fatigue
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10
Q

How can the heart side effects of beta blockers be minimised?

A
  • use pindolol (intrinsic sympathetic activity)

- cardevilol (alpha blockade decreases TPR)

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11
Q

Why should diabetic avoid beta blockers?

A

When you have a hypo, the SNS warns you. This is lowest if taking beta blockers

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12
Q

Side effects of verapamil?

A
  • AV block and bradycardia

- constipation (blocks gut Ca channels)

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13
Q

Side effects of the dihydropyridines

A
  • ankle oedema (vasodilation and gravity)
  • headache (vasodilation)
  • palpitations (reflex tachycardia)
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14
Q

Aims for treatments for cardiac rhythm abnormalities

A
  • reduce risk of sudden death
  • prevent stroke (blood clots in heart to ICA)
  • alleviate symptoms
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15
Q

Types of arrhythmias or dysrhythmias

A
  • Supraventricular
  • ventricular
  • complex

These can be tachyarrythmias or bradyarrythmias

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16
Q

How does adenosine work as a drug for supraventricular arrhythmias?

A
  • binds to the A1 receptor on SAN and AVN stimulates Gi hence decreased cAMP hence decreased chronotropy and dromotropy
  • binds to A2 receptors on VSMC, triggers Gs hence increased cAMP meaning vasodilation (via eNOS)
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17
Q

How does verapamil work as a supraventricular arrhythmia drug?

A

Stops atrial arrhythmias by decreasing automaticity of SAN by decreasing upstroke of Ca

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18
Q

What is amiodarone used for?

A

Supraventricular and ventricular arrhythmias

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19
Q

How does amiodarone work?

A

Blocks reentry signals by prolonging repolarisation. This means less jerky contractions.

Does this by complex block of many ion channels

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20
Q

Sid effects of amiodarone

A
  • pulmonary fibrosis
  • photosensitive skin rashes
  • thyroid disorders
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21
Q

What is digoxin used for?

A

Cardiac glycoside used for AF and flutter

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22
Q

How does Digoxin/digitalis work?

A
  • inhibition of NaK ATPase
  • means sodium builds up in the cell
  • Na/Ca exchanger means more Ca binds to troponin
  • inotropy is increased
  • central vagal stimulation means decreased rate of AV conduction

This means cardiac output isn’t really affected

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23
Q

Side effects of digoxin

A
  • AV block leads to dysthymias
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24
Q

How does hypokalaemia caused by diuretics increase side effects of digoxin

A

Digoxin competes with potassium for potassium binding site. Hence low potassium means digoxin has more of an effect.

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25
How do ACEis and ARBs decrease blood pressure
- less vasoconstriction - decreased salt and water retention (decreasing preload) - less aldosterone - less SNS/thirst
26
What are ACEis used for?
Eg Enalapril - hypertension - HF - diabetic nephropathy
27
Side effects of ARBs?
ARBs are better tolerated than ACEis - they cause cough as less bradykinin broken down by ACE - orthostatic hypotension - hyperkalaemia (as less sodium reabsorbed)
28
What are ACEis contraindicated for bilateral renal artery stenosis?
Angiotensin II increases GFR by constricting the efferent arteriole. This is very useful in renal artery stenosis as the pressure in the glomerulus is low due to reduced Renal blood flow. This is exacerbated by ACEis
29
What is dabigatran?
DOAC, inhibits thrombin
30
What is rivaroxaban?
Factor 10a inhibitor DOAC
31
When would you use dalteparin?
Antithrobin enhancer (and FXa inhibitor), low molecular weight heparin has fast onset of action
32
What factors do warfarin decrease.
2,7,9,10
33
Risk for DvT
Chest pain and SOB due to PE
34
List some anticoagulants
Dabigatran Rivaroxaban Warfarin Heparin
35
List antiplatelets
Clopidogrel Aspirin Abciximab
36
How does oral clopidogrel work?
P2Y-12 receptor antagonist
37
How does Aspirin work as an antiplatelet?
Irreversible COX inhibitor, inhibits TXA2 productions hence prevents platelet aggregation via GPiib/iiia
38
How does Abciximab work as an antiplatlet?
Monoclonal antibody against platelet integrin
39
What is Alteplase used for?
- clot buster (thrombolytic or fibrinolytic) | Used to break infarcts of the brain (stroke treatment)
40
Drugs for atherosclerosis
- bile acid sequestrants - nicotinic acid - statins - fibrates - ezetimibe
41
How do statins work?
- inhibition of HMGCoA reductase means less cholesterol produced - this leads to more LDLR expression on hepatocytes - means more LDL uptaken from the blood (hence lowered) Also they are anti thrombotic, anti inflammatory and have vasodilator properties
42
What is the rule of 6
If you double the statin dose, you lower LDL by 6%
43
How do fibrates like gemfibrozil work?
Activate PPAR alpha receptors Decreasing plasma fatty acids and triglycerides
44
How does nicotinic acid (niacin) work?
Lowers LDL, increases HDL, reduces inflammation
45
How does ezetimibe work?
- inhibits cholesterol absorption - prodrug which is activated by Glucuronidation in intestines - used in conjunction with statins to add more lipid lowering
46
How do PCSK9 inhibitors improve statin efficacy?
PCSK9 is also upregulated with LDLR when statins are given PCSK9 is a inhibitor of LDLR Hence antibodies against PCSK9 means less LDLR inactivation hence more LDL uptake by the liver
47
What is the most powerful diuretic?
Ascending Loop diuretic like furosemide (blocks Na/2Cl/K transporter which affects the countercurrent multiplier)
48
Effects of loop diuretics
- less water is reabsorbed as the tubular fluid osmolality increases - as more Na is delivered to the DCT, it causes an increase in potassium leakage as the DCT tries to transport more sodium - calcium and magnesium loss
49
How do thiazides work?
They block NaCl transporter in the early DCT, less potent as it does affect the counter current multiplier.
50
Effects of thiazides
- less diuresis than loops - increased delivery of Na causes potassium loss - mg loss - unknown cause of calcium reabsorption
51
Why do RAS inhibitors need to be given with thiazides and loops?
- Decreased sodium loading into the macula densa cells as the transporter has been blocked - this increases renin secretion hence causes hypertension
52
How does spironolactone work?
Aldosterone receptor antagonist hence decreased sodium reuptake and inhibits NaK pump (which maintains sodium gradient)
53
How does Amiloride work
Inhibits the aldosterone sensitive sodium channels
54
Why are amiloride and spironolactone potassium sparing diuretics?
Blocks NaK-ATPase hence less leakage into the urinary filtrate Sodium reabsorption drives potassium leakage so if this is stopped so will hypokalaemia
55
Effects of potassium sparing diuretics
- mild diuresis - decreased reabsorption of sodium - hence increased H+ retention (due to Na/H exchanger)
56
Side effects of loops and thiazides
- hypovolaemia - hyponatraemia - hypokalaemia - metabolic alkalosis (due to loss of Cl-) - hyperuricaemia
57
Side effects of potassium sparing diuretics
Hyperkalaemia
58
How do loops and thiazides cause hyperuricaemia?
Diuretics access the lumen by being actively secreted by an organic anion transporter. Uric acid uses this transporter too as they are not freely filtered hence diuretics compete with uric acid hence build up in the blood
59
Why are thiazides better antihypertensives than loops even though loops are better diuretics
Chronic thiazides use not only reduces plasma volume, it also decreases TPR by activating eNOS, antagonises Calcium channels, opens K channels in smooth muscle.
60
What would you use loop diuretics for?
To reduce congestion acutely in heart failure patients by diuresis
61
Why do chronic loop diuretic use cause worsening of HF?
- increases cardiac remodelling - increases RAS activity - hence must give potassium sparing diuretic too to negate this effects

Pharmacology (8 decks)

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