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Pharmacology > CVS > Flashcards

CVS Flashcards

1
Q

Digoxin: Mechanism of Action

A

It is negatively chronotropic as it slows conduction at the AV node by increasing vagal tone.
It is positively intotropic as it inhibits Na+/K+ pumps. This causes an increase in intracellular sodium, and therefore reduces Ca2+ excretion so Ca2+ accumulates in the myocytes and their contractility is increased.

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2
Q

Digoxin: Indications

A

AF and atrial flutter, though a B blocker or CCB is usually more effective
In severe heart failure, as 3rd line treatment after B blocker and ACEI and spironolactone/ARB

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3
Q

Digoxin: Adverse Effects

A

Bradycardia, GI upset, rash, dizziness, visual disturbance.

It is pro-arrhythmic

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4
Q

Digoxin: Warnings and Interactions

A

Low therapeutic index. OD can cause weird and wonderful arythmias.
It is contraindicated in those at risk of ventricular arrhythmia or heart block
It is really excreted so dose should be reduced in renal impairment
Hypokalaemia and hypercalcaemia increase the risk of digoxin toxicity

Interacts with loop/thiazide diuretics as they can cause hypokalaemia

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5
Q

Digoxin: Prescription

A

Oral or IV
Large volume of distribution so loading dose is required
Cardiac monitoring!

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6
Q

Diuretics, Loop (Furosemide): Mechanism of Action

A

Inhibit Na/K/2Cl transporter in ascending limb. Also causes dilation of capacitance veins.

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7
Q

Diuretics, Loop (Furosemide): Indication

A

Acute pulmonary oedema
Chronic heart failure
Other oedematous states

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8
Q

Diuretics, Loop (Furosemide): Adverse effects

A

Dehydration, hypovolemia, loss of electrolytes

Hearing loss at high doses

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9
Q

Diuretics, Loop (Furosemide): Warnings and Interactions

A

Contraindicated in dehydration or hypotension, and hypokalaemia
Can worsen gout as they inhibit uric acid excretion

Increase levels of renal excreted drugs
Increase ototoxicity of ahminoglycosides
Cause digoxin toxicity by hypokalaemia

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10
Q

Diuretics, Loop (Furosemide): Prescription

A

Oral and IV

Periodic monitoring of electrolytes for safety

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11
Q

CCBs (Amlodipine): Indications

A

Hypertension

Non-dihydropyridine drugs (verapamil) are anti-arrhythmic and can be used to treat SVT, AF and flutter

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12
Q

CCBs (Amlodipine): Mechanism of Action

A

Decrease Ca2+ entry, so decrease smooth muscle contractility. They also slow conduction, especially across the AV node.

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13
Q

CCBs (Amlodipine): Adverse Effects

A

Ankle swelling, flushing, headache and palpitations

Verapamil can cause bradycardia

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14
Q

CCBs (Amlodipine): Warnings and Interactions

A

Verapamil SHOULD NOT be prescribed alongside a B blocker as this can cause dangerous bradycardia or even ayststole
Should be avoided in unstable angina as they can increase myocardial oxygen demand

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15
Q

CCBs (Amlodipine): Prescription

A 
Taken orally (except verapamil can be given IV for acute arrhythmia)
Amlodipine has a long half life so can be given once daily
Monitering is based on symptoms and BP measurements
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16
Q

Lidocaine: Indications

A

Local anaesthetic

Uncommonly as anti arrhythmic for VT and VF that cannot be cardioverted

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17
Q

Lidocaine: Mechanism of Action

A

Na+ channel blocker, so prevents initiation and propagation of action potentials
In the heart it reduces the duration of the action potential, slows conduction and increases the refractory period

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18
Q

Lidocaine: Adverse Effects

A

Drowsiness, tremor, fits
Effects more pronounced when used systemically
OD can cause hypotension and arrhythmia

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19
Q

Lidocaine: Warnings and Interactions

A

Dose reduction in patients with reduced CO

Beneficial interaction with adrenaline (local vasoconstrictor)

20
Q

Lidocaine: Prescription

A

Maximum dose is based on body weight

Foundation doctors should not prescribe it systemically

21
Q

Amiodarone: Indictions

A

A wide range of tachyarrhythmias e.g. AF, SVT, VT, VF…

Generally when other treatments have been ineffective

22
Q

Amiodarone: Mechanism of Action

A

It is a Class III drug so blocks K+ channels (It actually also blocks Ca2+, Na+ and antagonises adrenoreceptors)
This reduces spontaneous depolarisation, decreases conduction velocity and increases resistance to depolarisation

23
Q

Amiodarone: Adverse Effects

A

Hypotension

When taken chronically: pneumonitis, hepatitis, bradycardia

24
Q

Amiodarone: Warnings and Interactions

A

Actually quite a dangerous drug, so consider risks and benefits
Avoid in thyroid disease, hypotension or heart block
It interacts with lots and lots of drugs; especially digoxin and verapamil

25
Q

Amiodarone: Prescription

A

Requires senior input

Continous cardiac monitoring

26
Q

Beta Adrenoceptor Blockers: Indications

A 
Ischaemic Heart Disease
Chronic Heart Failure
Atrial Fibrillation
SVT
HTN, when ACEIs and CCBs have not worked
27
Q

Beta Adrenoceptor Blockers: Mechanism of Action

A

Then antagonise B1 receptors. They are negatively chronotropic and inotropic
They also increase the refractory period at the AV node
They reduce renin secretion

28
Q

Beta Adrenoceptor Blockers: Adverse Effects

A

Hypotension, cold peripheries, GI upset, fatigue, headache

29
Q

Beta Adrenoceptor Blockers: Warnings and Interactions

A

Should be avoided in asthmatics (bronchospasm)
In heart failure, start at a low dose and slowly increase as they can initially impair cardiac function
AVOID with VERAPAMIL as this is bad (bradycardia, asystole)

30
Q

Beta Adrenoceptor Blockers: Prescription

A

Monitoring is based on symptoms and heart rate

Timing doesn’t matter

31
Q

ACEI: indications

A

First line treatment of HTN
Heart failure
Ischaemic Heart Disease

32
Q

ACEI: Mechanism of Action

A

Inhibit ACE. Reduces AT2 levels, so reduces after load. Reduces aldosterone levels so less sodium retention

33
Q

ACEI: Adverse Effects

A

Coughing, hypotension,

Rare: idiosyncratic angiooedema

34
Q

ACEI: Warnings and Interactions

A

Can cause hyperkalaemia and worsen renal failure, so should be avoided in AKI
Should be avoided in combination with other potassium elevating drugs
Combination with NSAID increases the risk of renal failure

35
Q

ACEI: Prescription

A

Taken orally
Can be useful to take before bed to reduce hypotension
Tell patient to avoid NSAIDs
Monitoring is based on symptoms, BP and checking electrolytes for safety before treatment and after 1-2 weeks

36
Q

ARB: Indications

A

HTN , esp. when ACEI is not tolerated

37
Q

ARB: Mechanism of Action

A

Block AT1 receptor

Reduces vasoconstriction and aldosterone levels

38
Q

ARB: Adverse Effects

A

Hypotension, hyperkalaemia and renal failure

39
Q

ARB: Warnings and Interactions

A

Avoid in renal disease e.g. AKI
Avoid in combination with other potassium elevating drugs
Combination with NSAIDs increases risk of renal failure

40
Q

ARB: Prescription

A

Taken orally, dose before bed to reduce effects of hypotension
Advise to avoid NSAIDs
Monitoring is based on symptoms, BP and checking electrolytes for safety before treatment and after 1-2 weeks

41
Q

Statins: Indications

A

Primary and prevention of cardiovascular disease

Primary hyperlipidaemia

42
Q

Statins: Mechanism of Action

A

Inhibit HMG-CoA Reductase so decrease cholesterol production by the liver and reduce LDL/Cholesterol levels

43
Q

Statins: Adverse Effects

A

Generally well tolerated: headache, nausea, muscle aches
Rarely cause more serious muscle issues : rhabdomyolysis, myopathy
Rare but serious: hepatitis

44
Q

Statins: Warning and Interactions

A

Caution in hepatic impairment
Dose reduction in renal impairment
CYP450 interactions!

45
Q

Statins: Prescription

A

Taken orally once daily
Lipid level before starting treatment
ALT/AST for safety

Pharmacology (7 decks)

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