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ASforP > Cardiovascular medication > Flashcards

Cardiovascular medication Flashcards

1
Q

When are antihypertensive drugs prescribed?

A

When diet and physical activity changes are not successful or practical

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2
Q

How do antihypertensive drugs generally work?

A

Relaxing and dilating blood vessels or acting on the kidneys to help increase urination

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3
Q

What is considered hypertensive?

A

140/90

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4
Q

How is blood pressure calculated?

A

Cardiac output x systematic vascular resistance

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5
Q

What factors do antihypertensive act on?

A

Blood volume
Contractility
Heart rate
Systemic vascular resistance

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6
Q

How do thiazide diuretics work?

A

Reducing sodium reabsorption at the distal convoluted tubule

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7
Q

What are the most commonly prescribed diuretics alongside an antihypertensive?

A

Bendeoflumethiazide
Indapamide

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8
Q

Why do patients on thiazide diuretics need to have potassium levels checked?

A

Thiazide diuretics aren’t potassium sparing and higher levels of potassium will be excreted

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9
Q

How do loop diuretics work?

A

They increase sodium excretion in the loop of Henle

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10
Q

What are the most powerful and fastest acting types of diuretics?

A

Loop diuretics

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11
Q

What are potassium sparing diuretics?

A

Diuretics which do not waste potassium

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12
Q

How do potassium sparing diuretics work?

A

By blocking the sodium potassium pumps in the last part of the distal tubule and the start of the collecting duct

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13
Q

What do ACE inhibitors do?

A

Stop angiotensin 1 turning into angiotensin 2

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14
Q

What patients are given ACE inhibitors?

A

Patients with:
Hypertension
Heart failure
ACS
Chronic kidney disease

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15
Q

What are ARBs?

A

Angiotensinogen II receptor blockers

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16
Q

How do calcium channels blockers work?

A

Inhibition of muscle contraction and nerve transmission

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17
Q

What tissues do Nifedipine and Amlodipine have their main effect on?

A

Vascular smooth muscle

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18
Q

What tissues does Verapamil have its main effect on?

A

Conductive tissue

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19
Q

What tissues does Diltiazem have its main effect on?

A

Coronary vasculature

20
Q

What do beta blockers inhibit?

A

Adrenaline and noradrenaline

21
Q

Are atenolol and bisoprolol selective or non selective beta blockers?

A

Selective

22
Q

Are propranolol and labetalol selective or non selective beta blockers?

A

Non-selective

23
Q

What are non-selective beta-blockers prescribed for?

A

Cardiac arrhythmias, anxiety and migraines

24
Q

What are HMG-CoA reductase inhibitors?

A

Statins - Drugs that lower cholesterol

25
Q

How do statins lower cholesterol?

A

Interrupting the cholesterol synthesis pathway in the liver, inhibiting HMG-CoA reductase, preventing mevalonic acid from forming and activating its pathway which leads to reduced cholesterol synthesis

26
Q

How do statins affect the levels of LDLs and HDLs in the body?

A

Reduces LDLs
Increases HDLs (promotes production)

27
Q

What is the difference between LDLs and HDLs?

A

LDL cholesterol (“bad” cholesterol) makes up most of your body’s cholesterol. LDLs form plaque and cause atherosclerosis. High levels of LDL cholesterol raise your risk for heart disease and stroke.

HDL cholesterol (“good” cholesterol) absorbs cholesterol in the blood and carries it back to the liver. The liver then flushes it from the body. High levels of HDL cholesterol can lower your risk for heart disease and stroke.

28
Q

What are the 4 classes of anti-arrhythmic medications?

A

Class I - Sodium channel blockers
Class II - Beta blockers
Class III - Potassium channel blockers
Class IV - Calcium channel blockers

29
Q

What are class I anti arrhythmic medications?

A

Sodium channel blockers (end in -dipine)

30
Q

What are class I anti-arrhythmic medications used to treat?

A

Atrial fibrillation and supra-ventricular tachycardias

31
Q

What are the two most common cardiac specific sodium channel blockers?

A

Flecainide
Propafenone

32
Q

What effect at low and high doses does Sotalol have?

A

At low doses it acts as a beta-blocker and at higher doses it acts as a sodium channel blocker

33
Q

What are class II anti arrhythmic medications?

A

Beta blockers (end in -olol)

34
Q

How do class II anti-arrhythmic medications work?

A

Blocking the beta receptors in the SA and the AV node -extending the action potential

35
Q

What are class II anti-arrhythmic medications used to treat?

A

AF, SVTs, VTs

36
Q

What are class III anti-arrhythmic medications?

A

Potassium channel blockers

37
Q

What do class III anti-arrhythmic medications do?

A

Prolong the QT

38
Q

Which patients should not be given class III anti-arrhythmic medications?

A

Patients with prolonged QTs such as patients with Brugada’s syndrome

39
Q

Why should you be mindful of potassium channel blocker overdoses?

A

Patients may take low doses of non-cardiac specific potassium channel blockers for other conditions, usually having no effect on the heart. During an overdose higher levels of these drugs may cause arrhythmias

40
Q

What are class IV anti-arrhythmic drugs and what are they used to treat?

A

Calcium channel blockers - primarily SVTs (can also treat VTs but potassium channel blockers shown to be much more effective)

41
Q

What are the two types of class IV anti-arrhythmic drugs and how do they differ?

A

Dihydropyridines (DHPs)
e.g. nifedipine and amlodipine

Non-dihydropyridines (Non-DHPs)
e.g. diltiazem and verapamil.

The two classes both help to relax and widen arteries but non-dihydropyridines have an additional effect on the heart’s conduction system and can help to control certain fast heart rhythms (such as atrial fibrillation). This is because non-dihydropyridines also block calcium going into the conducting cells in the heart, which has the effect of slowing down the heart rate.

42
Q

What are thrombocytes?

A

Platelets

43
Q

Where are platelets produced?

A

The bone marrow

44
Q

What is the lifespan of platelets?

A

7-10 days

45
Q

What do platelets do once activated?

A

Become ‘sticky’ and release clotting mediators

46
Q

What are the three parts of haemostasis?

A

Adhesion
Activation
Aggregation

47
Q

What stage of haemostasis do anti-platelets usually act on?

A

Activation

ASforP (22 decks)

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