Drugs Flashcards

1
Q

Loop Diuretics

A

Inhibit NaCl reabsorption in the loop of Henle.
Strong and fast acting but short lasting.
eg: frusemide

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2
Q

What is the basic idea behind diuretics?

A

Decrease blood volume
> decrease preload and afterload
>decrease cardiac output
= less strain/O2 demand on heart.

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3
Q

Thiazide diuretics

A

Inhibit NaCl reabsorption in the distal tubule. This leads to decreased water absorption into the blood stream via osmosis.
Safe but weak.
eg: bendrofluazide

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4
Q

Potassium sparing diuretics

A

Weak, usually used in combination with others.
Can ^K
eg: Spirolactone

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5
Q

Diuretics - side effects

A

electrolyte imbalances (Us, Es, hypokalaemia)
Hypotension
^Uric acid

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6
Q

B-blockers work by?

A

inhibiting B1 receptors (sympathetic)
>reduce HR and CO
>reduce work performed by heart
>reduce O2 demands

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7
Q

Side effects/worries with beta blockers?

A
Can mask signs of hypoglycaemia
Cold hands and feet (vasoconstriction in peripheries)
Sleep - nightmares etc
Tiredness
Impotence

DO NOT GIVE TO ASTHMATICS!!!

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8
Q

How does dopamine work?

A

In the opposite way to beta blockers - it increases heart rate and blood pressure.

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9
Q

Basic m.o.a of nitrates?

A

Peripheral vessel dilators -> decrease preload.

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10
Q

M.o.a. of Ca channel blockers?

A

Dilates arteries (including coronary), leading to a reduced afterload and therefore workload and O2 demands of the heart.

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11
Q

Amlodipine is a…?

A

Ca channel blocker

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12
Q

ACE-inhibitors do what? How?

A

Reduce blood pressure.
Prevents vasoconstriction of both arteries and veins.

Blocks angiotensin II (a vasoconstrictor) which leads to reduction in aldosterone.

It can lead to renal failure.

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13
Q

What is amiodarone used for and how does it work?

A

Arrythmias - to reduce and stabilise HR
- in VT/VF arrest

Work by increasing repolarisation time to prolong the action potential.
Acts on: AVnode, purkinje fibres, cardiomyocytes.

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14
Q

What is quinidine used for and how does it work?

A

To reduce and stabilise HR in arrythmias.

Increases action potential threshold and refractory period.
Acts on cardiomyocytes, AVN, purkinje fibres.

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15
Q

Atropine: use and basic m.o.a?

A

Bradycardia

Antagonises (reduces) parasympathetic stimulation
> increases heart rate.

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16
Q

Use B-blockers in arrythmias caused by…?

A

MI
thyrotoxicosis
emotions

17
Q

Uses and basic m.o.a of digoxin?

A
Heart failure - increases force of contraction
Supraventricular tachycardia (SVT)

blocks Ca+ channels in the AVN and bundle of His

- increases refractory period
- slows conduction
18
Q

Adenosine - when would you use it and what does it cause?

A

SVT

transient heart block in the AV node.

19
Q

Lignocaine - how does it work and what do you use it in?

A

0blocks Na+ channels

use in ventricular arrythmias (except VF/VT arrest)

20
Q

What do aspirin and clopidogrel do?

A

Permanently block platelet activation sites.

Have to wait for new ones ~ long lasting!