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Cardio Path > Cardio Pharma > Flashcards

Cardio Pharma Flashcards

0
Q

What are the uses of beta-blockers ?

A

Supraventricular tachycardia slows ventricular rate During atrial fibrillation and flutter

In glow coma it decreases aqueous humour secretion

At hypertension it decreases cardiac outputs and renin by blocking beta-1 receptors at JGA

@congestive heart failure it slows chronic failure progression

@angina pectoris by decreasing heartrate and contractility and therefore decreasing oxygen consumption For myocardial infarction in decreases mortality

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1
Q

What is the mechanism for beta-blockers ?

A

Decreases cyclic AMP which leads to decreased calcium currents which leads to Decreased phase 4 of pacemaker slope which leads to suppressing of abnormal pacemaker leading to AV sensitivity increasing PR interval therefore a D crease in AV conduction velocity

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2
Q

What are the toxicities from XS beta-blockers

A

COPD hypoglycaemia masking asthma impotence AV block bradycardia sedation and sleep alteration and congestive heart failure Chai A BSC

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3
Q

Specifically for Metoprolol what toxicity can it cause

A

Dyslipidaemia

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4
Q

Specifically for propanolol what toxicity can cause

A

Increased vasospasm at Prinzmetal angina

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5
Q

Who do you not give beta-blockers to i.e. contraindication and why? ?

A

Don’t give to cocaine users

Due to increased risk of unopposed Alpha-adrenergic receptor agonist activation

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6
Q

How do you treat an overdose of beta-blockers?

A

Glucagon

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7
Q

Give the names of beta-1’s electives And how do we remember which ones Are beta-1 selective?

A

Between a and M Acebutolol Atenolol betaxolol esmolol metoprolol

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8
Q

What are the non-selective beta antagonists and how do we remember them ?

A

From end to Z Nadolol pindolol propanolol and Timolol

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9
Q

Which ones are the alpha and beta non-selective antagonists and wondering about the suffixes ?

A

Modified suffix i.e. not – OLOL carbetalol and labetalol

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10
Q

What does Nerbivolol do?

A

Combines beta-1 blockade action with Beta three stimulation. beta three stimulation causes activation of nitric oxide synthase in the vasculature

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11
Q

What are the for antiarrhythmic drug classes.?

A

Class one sodium channel blockers, class 2 beta-blockers, class three potassium channel blockers, class for calcium channel blockers

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12
Q

What drugs block angiotensin I to angiotensin II?

A

ACE inhibitors and Angiotensin 2 receptor blockers i.e. Sara tans

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13
Q

What effects do a C inhibitors and sartans have?

A

Stuff first

Stop NA/H + activity
Prevent construction of different arterial at glomerulus therefore decreasing GFP NGF are which has negative feedback on rennin
Stops aldosterone therefore stops sodium absorption and therefore stops water retention
Prevent increase in total peripheral resistance as less angiotensin to acting on receptors at the smooth-muscle in the media
Prevent ADH therefore water absorption

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14
Q

What two things does ACE inhibitors effect?

A

Stops ace and stops bradykinin in activation causing increased bradykinin which is a dilator causes pain and vascular permeability.
Causes cough and angioedema

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15
Q

What effect does Sauternes have on bradykinin ?

A

No effect on bradykinin Therefore decreases the risk of cough and angioedema

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16
Q

What are ACE inhibitors used for ?

A

Congestive heart failure, hypertension therefore preventing unfavourable heart remodelling, Diabetic nephropathy, protein urea
CHDP MNEmonic

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17
Q

Give the names of three a’s inhibitors?What are the toxicities of ACE inhibitors?

A

Captopril, Enalapril and lisinopril

(Captopril to catchh)
Cough angio-oedema ( contra indicated at C1 esterase inhibitor deficiency )

Teratorn at fetus renal malformation
Increased create wind you to decreased GF are
Hypotension and hyperkalaemia

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18
Q

What are the contra indication is for ACE inhibitors?

A

Don’t give to bilateral renal artery stenosis due to already D creased GFR.
ACE inhibitor Will massively decreased GFR

Don’t give to see one esterase inhibitor deficiency due to worsening cough and angio-oedema

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19
Q

What is the mechanism for calcium channel blockers?

A

Blocks L-type calcium channels of myocyte and smooth muscle leading to D creased contractility
D creases smooth muscle tone therefore dilate

D creases conduction velocity therefore increases effective refractory period therefore increases PR interval

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20
Q

Which calcium channel blockers are best for the vascular smooth muscle ?

A

Dihydropyridine’s = Amlodipine and nifedipine

Better than

Non-dihydropyridine = dilitiazem and vermapril

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21
Q

Which Carson channel blockers are better for the heart?

A

Non-dihydropyridine = VermaPrill and dilitiazem

Better than

Hydropyridine = amlodipine and nifedipine

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22
Q

What is nimodipone used for?

A

Prevent subarachnoid haemorrhage by preventing Cerebral vasospasm

23
Q

What are dihydropyridined used for?

What are non-dihydropyridines used for?

A

For dihydropyridine = Raynaud angina and hypertension

For NON dihydropyridine = HTN, angina and atrial fibrillation

24
Q

What are the toxicities of calcium channel blockers ?

A

CCH A PFD

Cardiac depression and constipation, HYPERprolactinaemia, AV block, peripheral oedema, flushing and dizziness

25
Q

What’s nifedipine similar to ?

A

Nitrates

26
Q

What is the vermapril similar to ?

A

Beta-blockers

27
Q

What is the mechanism for thiazide diuretics?

A

Inhibits sodium chloride reabsorption at early distal tubule Therefore high concentration of sodium inside the nephron

Therefore decreasing the nephrons dilutes incapacity

Therefore increased sodium excretion

28
Q

What are the uses for thiazide diuretics?

A 
Congestive heart failure
Hypertension
Diabetes insipidus nephrogenic
Idiopathic hypercalciuria 
Osteoporosis
29
Q

What are the toxicity is caused by thiazide diuretics?

A

Hyper GLUC
Hyperglycaemia, lipidaemia, uricaemia, calcemia

Hypo NK
Hyponatraemia, kalemic metabolic ALKalosis

Inhibits Insulin release

30
Q

What other contraindications for thiazide diuretics ?

A

Thiazide is a sulphur allergic do not take

31
Q

What is the mechanism for hydralazine ?

A

Increases cyclist GMP
Causes smooth-muscle relaxation
Arterioles dilate more than veins
Therefore D creased afterload

32
Q

What are the uses of hydralazine?

A

Congestive heart failure, hypertension, hypertension in pregnancy
For hypertension in pregnancy use meet L-dopa with hydralazine

33
Q

For hypertension and pregnancy what is hydralazine also administered with ?

A

Methyldopa and hydralazine

34
Q

Hydralazine is given with a beta-blocker to prevent what ?

A

Reflex tachycardia

35
Q

What are the toxicities of Hydralazine?

A 
Lupus like syndrome
Compensatory tachycardia
Headache
Angina
Nausea
Fluid retention
36
Q

In a hypertensive emergency what to drugs are used ?

A

Nitroprusside and fenoldopam

37
Q

What does nitroprusside do?

What does fenoldopam do?

A

Nitroprusside releases nitric oxide Which causes an increase in cyclically GMP which causes dilation of the arterioles more than the veins therefore decreased afterload

Fenoldopam is it dopamine one agonist
It causes vasodilation of coronary peripheral renal and Splanchnic arterioles therefore decreasing blood pressure

D creasing of the renal vascular smooth muscle also increases natriuresis

38
Q

Give the names of two nitrates? What are their mechanisms ?

A

Nitroglycerin and isosorbide dinitrate increases nitric oxide and vascular smooth muscle
Increasing cycling GMP
Causing smooth-muscle relaxation
Causing dilation of the veins more than arterioles
Therefore decreasing preload

39
Q

What are nitrate used in?

A

Pulmonary oedema, acute coronary syndrome, angina

PAAn

40
Q

What causes Monday disease? What happens in Monday disease?

A

Nitro glycerin and isosorbide dinitrate
Monday to Friday use the spray due to stress at work therefore developed tolerance for vasodilating action

During the weekend you lose tolerance due to no stress therefore you do not use it therefore lose tolerance

On Monday start work again therefore start stress therefore re-exposure causes tachycardia dizziness and headache

41
Q

What’s are the three classes of sodium channel blockers and what do they each do ?

A

1a lengthens AP duration
1B decreases at AP duration
1C has no effect on capital a P and promotes sodium current depression more so than group 1a and 1B

42
Q

What is the mechanism for antiarrhythmics sodium channel blockers class 1a?

A

Increases action potential duration
Causing increase in effective refractory period
Causing an increase in the Q-T interval
This QT interval increase can cause torsade de pointes’s at Dizopyramide

43
Q

What are class 1A sodium channel blockers used for?

A

For atrial and ventricular arrhythmias especially re-entrant and ectopic SVT and VT

44
Q 
What's are the class 1A sodium channel blockers names?
 What's toxicities do these drugs cause?
A

Quinidine causes Cinchonism =headache and tinnitus
Procainamide causes SLE like syndrome
Diso pyramid causes heart failure thrombocytopenia and torsades de points increased QT interval

45
Q

What is the mechanism for class 1B drugs? and what are their class 1B drugs called?

A

Decrease action potential duration and preferentially affect ischaemic/depolarised Purkinje and ventricular tissue

46
Q

What are classed Ib lidocaine and mexiletine used for?

A

Ventricular arrhythmia after MI

Digitalis introduced arrhythmia after MI

47
Q

What are the toxicities of Lidocaine and mexiletine?

A

CNS stimulation

Cardiovascular depression

48
Q 
What is the mechanism for class 1C sodium channel blockers?
Give the name of two sodium channel blockers ?
A

Flecainide and propafenone

49
Q

What is the mechanism for class 1C sodium channel blockers?

A

Prolongs the refractory period

50
Q

What our class 1C drugs flecsinimide and propafenone used for?

A

SVT – Atrial fibrillation

51
Q 
Toxicities of sodium channel blockers class W1C flicainimide and propafenone?
Contraindications of class 1c sodium channel blockers?
A

Proarrhythmic

Don’t use if have structural/ischaemic Capital HD

52
Q

Give the names of four potassium channel blockers?

What is the mechanism of potassium channel blockers?

A

Cutting channel blockers increased the action potential duration therefore increasing the effective refractory period therefore increasing Q-T interval

53
Q

What are potassium channel blocker is used for?

A

Atrial fibrillation and flutter

Ventricular tachycardia

54
Q

What are the toxicities caused by potassium channel blockers?

A

Sotalol can cause XS beta-blockade Therefore cause torsades the pointes

Ibutilide causes torsade de pointes’s

Amiodarone causes corneal deposits skin deposits hepatotoxicity hypertension bradycardia congestive heart failure and heartblock and hypo/hyperthyroidism Amiodarone alters lipid membrane

55
Q

Give the names of other antiarrhythmics?

Their mechanisms?

A

Adenosine increases potassium out of cells causing hyper polarised cell And decreased intracellular calcium

Used for supraventricular tachycardia
Toxicity causes chest pain hypotension and flushing

Magnesium Is for torsades de points and digitoxin toxicity

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