Drug revision general

Question 1

What is amiodarone

Answer 1

Amiodarone is used for VT, as an antiarhythmic, and in some cardiac arrests. It is a Class III anti arrhythmic, a K+ channel blocker, (think also Dronedarone)

Question 2

What is dronedarone

Answer 2

Dronedarone it is a Class III anti arrhythmic, a K+ channel blocker, (think also amiodarone)

Question 3

Name 5 anti hypertensive drug classes

Answer 3

ACE inhibitors
Angiotension-II-receptor blockers
α-blockers
β-blockers
CCB (calcium channel blockers)

Question 4

Name 3 ACE inhibitors

Answer 4

Ramipril, Lisinopril, Enalapril

Question 5

What are Ramipril, Lisinopril, Enalapril

Answer 5

ACE inhibitors

Question 6

Name 2 Angiotension-II-receptor blockers

Answer 6

Candesartan*, Losartan

Question 7

what are Candesartan*, Losartan

Answer 7

Angiotension-II-receptor blockers

Question 8

What is the MOA of Ace inhibitors

Answer 8

Block angiotensin converting enzyme and lowers BP by reducing angiotensin to anng-II, therefore also decreasing aldosterone production by adrenal cortex, reducing sodium and water retention.
These drugs also inhibit bradykinin breakdown by ACE (dry cough in 20%)
Reno-protective! Always consider for T2DM and early kidney failure.

Question 9

What is the MOA of Angiotension-II-receptor blockers?

Answer 9

Selectively inhibit angiotensin II at the AT1 receptor site
Therefore blocking causes VASODILATION and blockage of aldosterone release
Often used second to ACE inhibitors when dry cough side-effect (bradykinin) not tolerated (20% pts)

Question 10

Name an α-blocker

Answer 10

Doxazosin

Question 11

What is Doxazosin

Answer 11

α-blockers

Question 12

What is the MOA of doxazosin?

Answer 12

ALPHA BLOCKER: Doxazosin is a quinazoline derivative that acts as a competitive alpha1-antagonist at the post-synaptic receptor.
Doxazosin competitively inhibits post-synaptic alpha1-adrenergic receptors causing vasodilation of arterioles and veins, which results in decreased total peripheral resistance and blood pressure

Question 13

What is a CCB, name two

Answer 13

Calcium channel blocker - Amlodipine, Diltiazem, Verapamil. CCB reduces ca entry to cells which reduces their ability/strength of contraction- reduce heart contraction strength and dilate smooth muscle of arteries

Question 14

What are Amlodipine, Diltiazem, Verapamil

Answer 14

CCBs - calcium channel blockers

Question 15

CCB MOA?

Answer 15

Calcium channel blockers disrupt the flow of calcium through calcium channels.
-Cardioselective (aka ‘second generation’) amlodipine, verapamil and felodipine,
-Non-cardioselective, diltiazem and nifedipine.

CCB block slow calcium channels, and slow the rate of conduction through the SA and AV nodes -prolongs the PR interval, and reduces the sinus rate

Question 16

Which CCBs are unsafe in HF?

Answer 16

Short acting calcium channel blockers (diltiazem and verapamil) are particularly selective for cardiac muscle, and are strongly negatively inotropic. They reduce cardiac output and slow the heart rate and should be avoided in heart failure.

Question 17

How can CCBs activate the sympathetic nervous system

Answer 17

cause peripheral vasodilation, which can then in turn cause activation of the sympathetic nervous system

Question 18

Which CCbs are considered safe in HF

Answer 18

Dihydropyridine calcium channel blockers (e.g. amlodipine, felodipine, nifedipine) tend to affect vascular smooth muscle more than cardiac muscle, and are generally considered safe in heart failure.

Question 19

How can withdrawal of CCBs cause angina

Answer 19

Abrupt withdrawal of calcium-channel blockers has been known to result in angina due to rebound vasoconstriction

Question 20

What class of anti-arrythmics can CCBs be considered

Answer 20

They are sometimes classified as class IV anti-arrythmics because of their mechanism of action

Question 21

Why do CCBs only slow heart rate (negatively inotropic) but don’t prevent contraction?

Answer 21

Interfere with calcium uptake into cells through the ‘slow calcium channels’ found in the SA and AV nodes. These tissues depend on slow acting calcium currents to develop their action potentials.
Fast response myocardial tissues (in the atria, ventricles and accessory pathways) instead depend on sodium channels

Question 22

What are the first generation/typical antipsychotics

Answer 22

Not usually first line
Act mainly as D2 antagonists
Less cardiometabolic side effects compared to second generation
More extra pyramidal side effects compared to second generation

Haloperidol – Clopixol – Chlorpromazine - Depixol
(prochlorperazine)

Question 23

what are the second generation “atypical” antipsychotics?

Answer 23

Usually first line choice
Act on 5HT2, DA2/DA4 receptors
More cardiometabolic side effects compared to first generation
Less extra pyramidal side effects compared to first generation

Olanzapine – Quetiapine – Risperidone – Clozapine - Aripiprazole
(Lurasidone, Olanzapine, Paliperidone*)

Question 24

Which anti-psychotics are used as first line treatment and why

Answer 24

second generation “atypical” antipsychotics
Usually first line choice
Act on 5HT2, DA2/DA4 receptors
More cardiometabolic side effects compared to first generation
Less extra pyramidal side effects compared to first generation

Olanzapine – Quetiapine – Risperidone – Clozapine - Aripiprazole
(Lurasidone, Olanzapine, Paliperidone*)

Question 25

What are the side-effects of anti-psychotics?

Answer 25

Sedation
Cardiometabolic (Insulin resistance, weight gain, DMt2)
Extra pyramidal side effects EPSE
Raised prolactin (Galactorrhoea, Subfertility, Sexual dysfunction)
QTc prolongation
Constipation and dry mouth
!! Reduced seizure threshold!!
!!Neuroleptic malignant syndrome!!

Question 26

how do you monitor or assess side effects of antipsychotics?

Answer 26

Glasgow Antipsychotic Side effect Scale (GASS)