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PA20321 > The Drugs > Flashcards

The Drugs Flashcards

Include anti-anginal, anti-arrythmics, anti-hypertensives, anti-coagulants and diuretics

1
Q

Alpha1 antagonists (-azosin)

A

Eg. Doxazosin
Blocks action of noradrenaline/adrenaline
Causes vasodilation therefore decrease in blood pressure
Selective antagonists cause less tachycardia than non selective

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2
Q

Alpha2 antagonists (Yohimbine)

A

Clinically fucking useless
Causes vasodilation/stimulation
Can treat male impotence
Can enhance fat burn with excercise

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3
Q

Beta blockers (-olol)

A

Eg Bisoprolol, propanolol

Decreases blood pressure by decreasing cardiac output and renin release

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4
Q

Unwanted effects of Beta blockers

A

Also increases bronchoconstriction

Cardiac failure can occur as there is less sympathetic tone to maintain cardiac output. Also lower heart rate

Hypoglycaemia due to less glucagon release due to beta blockade

Can also cause erectile dysfunction and lucid dreams

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5
Q

Vascular selective CCB’s (-dipines)

1,4-Dihydropyrindines

A

Amlodipine, nifedipine

Antihypertensive via stopping influx of Ca2+ into smooth muscle stopping the contraction of the muscle

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6
Q

Cardiac selective CCB’s (-apamil)

Phenylalkylamines

A

Verapamil

Anti-arrythmic

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7
Q

Intermediate selective CCB’s (-iazem)

Benzothiazepines

A

Diltiazem

Anti-anginal/anti-arrythmic

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8
Q

NO donors (GTN)

A

Donates NO which activates GC
GC converts GTP to cGMP
cGMP increases activity of PKG
PKG inhibits contraction via enhancing the effect of MLCP which dephosphorylates MLC causing relaxation

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9
Q

PDE5 inhibitor (Sildenafil)

A

Treats erectile dysfunction and pulmonary arterial hypertension
Prevents the breakdown of cGMP allowing it to continue increasing the effect of MLCP

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10
Q

Prostacyclin analogues (Iloprost, selexipag)

A

Used in pulmonary arterial hypertension

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11
Q

Potassium channel activators (Cromakalim, Minoxidil)

A

Induces hyperpolarisation and causes relaxation
Can be used in hypertension and angina
Minoxidil used in severe resistant hypertension and causes excess hair growth

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12
Q

Carbonic anhydrase inhibitors (Acetazolamide)

A

Weak diuretic

Decreases Na+ reabsorption into interstitial fluid by inhibiting carbonic anhydrase (turns H20 and CO2 into carbonic acid which dissociates to give H+ and bicarb)

This means less H+ for exchange with Na+

Increased conc of Na+ in urine causes increased osmosis into urine

Can cause mild plasma acidosis and urine alkalosis
Used in glaucoma and altitude sickness

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13
Q

Osmotic diuretics (Mannitol)

A

Increases osmolarity of filterate

This increases volume retention and decreasing Na+ reabsorption as the conc of Na+ in filterate is lower due to increased volume of filterate

Used in glaucoma, cerebral oedema and acute renal failure

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14
Q

Loop diuretics (-emide)

A

Eg. Furosemide, bumetanide

Inhibits Na+/Cl-/K+ co transporter

Increases conc of these in fliterate
Increases uptake of Ca2+ and Mg2+

Secreted into fliterate by OAT
Very potent

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15
Q

Thiazide and thiazide-like diuretics (-thiazide)

A

Eg. Bendroflumethiazide,
Thiazide like diuretics include: Chlortalidone, indapamide, metolazone
Inhibits Na+/Cl- co transporter

Decreases reabsorption of Na+/Cl-
Decreases excretion moderately of K+ as K+ cannot be cotransported with Cl- into interstitial fluid
Increases Ca2+ reabsorption

Better tolerated than loop diuretics and have prolonged action. Has vasodilating properties

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16
Q

Uses of thiazide/thiazide like diuretics

A 
Hypertension 
Mild heart failure 
Severe resistant oedema (thiazide-like+loop)
Prophalaxis of kidney stones 
Nephrogenic diabetes insipidus

Can cause gout as less uric acid excreted and erectile dysfunction as well as hypokalaemia due to less K+ being excreted

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17
Q

Aldosterone antagonists (-one)

A

Eg. Spironolactone, eplenerone

Reduces production of Na+/K+ ATPase
therefore increasing Na+ in filterate but also increases K+ in plasma avoiding hypokalaemia

Treats hypokalaemia, heart failure, resistant hypertension (due to low renin)

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18
Q

Na+ channel blockers (Amiloride, Triamterene)

A

Stops reabsorption of Na+ into plasma but maintains levels of K+ in plasma

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19
Q

Adverse effects of K+ sparing drugs

A

Hyperkalaemia

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20
Q

Renin inhibitors (Aliskiren)

A

Inhibits renin which is the precusor molecule for the RAAS system

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21
Q

ACE (angiotensin converting enzyme) inhibiters (-pril)

A

Eg. Ramipril, enalapril
Acts as antagonist for ACE

Causes cough as it is no longer breaking down bradykinin

Therefore build up of bradykinin occurs
Increased bradykinin causes vasodilatation and cough
Conntra indicated in afro-carribean patients

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22
Q

ARB’s (Angiotensin receptor blockers) (-sartan)

A

Eg. Candasartan, Losartan

Blocks angiotensin receptors (AT1)

23
Q

The weird direct acting vasodilator (Hydralazine)

A

Causes vasodilation

Use in severe hypertension in pregnancy

Use in heart failure in afro-carribean patients

Can cause lupus, tachycardia, hypotensions and oedema

24
Q

Central acting alpha2 agonists (Monoxidine, alpha-methyldopa)

A

Monoxidine used only in resistant hypertension when 1st line doesn’t work

Methyldopa in pregnant hypertension

They work by reducing the release of NA into the system

25
Q

Adrenergic nerve blockers (Reserpine, Guanethidine)

A

Guanithidine is taken up by NET and then by VMAT

It slowly displaces the NA in the vesicles meaning the NA cannot be released

Respirine inhibits the action of VMAT meaning NA cannot be taken up into the vesicles

26
Q

The classes of anitarrythmics

A

Class 1: Na channel blockers
Class 2: Beta blockers
Class 3: AP prolonging drugs
Class 4: Ca channel blockers

27
Q

Na channel blockers (Disopyramide, lidocaine, Flecainide)

A

Blocks fast Na channels preventing depolarisation

Lidocaine is short acting can cause CNS effects

Disopyramide is intermediate acting, can cause myocardial infraction

Flecainide is long acting can cause sudden cardiac death in patients that have had MI

28
Q

Beta blockers (-olol)

A

Blocks b1 receptor, slows conduction at AVN
Propanolol is long acting non-selective
Atenolol is b1 selective and water soluble
Esmolol is short acting b1 selective

Can cause bradycardia, cardiac depression, bronchoconstriction, sleep disturbance,

29
Q

AP prolonging drugs (Amiodarone, Sotalol)

A

Blocks the hyperpolarisation caused by K channels in phase 3 of AP

Amiodarone blocks Na and Ca channels and decreases expression of beta receptors and is a alpha receptor antagonist

Can cause thyroid abnormalities

Sotalol is a non selective b blocker

30
Q

CCB’s for arrythmias (Verapamil, Diltiazem)

A

Blocks Ca channels affecting phase 0 in pacemaker AP

Verapamil is more selective than diltiazem

Can bradycardia, reduced cardiac contractility, constipation and hypotension

31
Q

Anticoagulant: Heparin (-parin)

A 
Eg Enoxaparin, dalteparin, tinzaparin
Unfractionated heparin (UFH) is naturally occurring heparin

LMWH are heparins with MW <8000

They bind to antithrombin III (ATIII) and enhance its binding to FXa

UFH also inhibits thrombin (LMWH not long enough to bind both)

Can cause thrombocytopenia as UFH, LMWH and PF4 bind

32
Q

The heparin antidote

A

Protamine sulfate

Very +ve and binds to UFH and LMWH forming stable inactive ion pairs

33
Q

Fondaparinux

A

Based on unique pentasaccharide sequence responsible for ATIII binding to heparin

Does not cause thrombocytopenia

34
Q

Novel oral anticoagulants (NOAC’s) (-xaban)

A

Eg Rivaroxaban, apixaban

Directly inhibits FXa

Long lasting but no available antidotes

35
Q

Direct thrombin inhibitors (-irudin)

A

Eg Lepirudin, Bivalirudin

36
Q

Dagitran

A

Directly inhibits thrombin

Given as dagitran etexilate a pro-drug substrate of p-glycoprotein in GI tract

Hydrolysed to active dagitran

Inhibits both free and fibrin bound thrombin
Antidote is Idarucizumab

37
Q

Warfarin

A

Inactivates Vit K reductase (VKORC1)

Vit K is usually used to activate FII and FX which are involved in the extrinsic pathway

S isomer 5x potent than R

Metabolised by p450
NSAIDS and alcoholism contraindicated

38
Q

Factors affecting Warfarin action

A

Alcoholism- p450 elevated therefore higher metab of warfarin

Drugs reducing GI absorption eg colestyramine

Diet- green things have lots of Vit k

39
Q

Fibrinolytic agents (-ase)

A

Eg Alteplase, reteplase

Used in actue MI, thrombotic stroke and life threatening thromboembolisms

Increase conversion of plasminogen to plasmin which breaks down the fibrin network

40
Q

Antifibrinolytic (Tranexamic acid)

A

Derived from lysine

Competitively blocks lysine binding sites on plasminogen reducing conversion to plasmin thereby maintaining clotting

Used in haemorrhages due to fibrinolytic therapy, prophylaxis of haemorrhage in post/pre surgery patients at high risk of haemorrhage as well as heavy menstrual bleeding

Can cause nausea, vomiting and diarrhoea

41
Q

Positive inotropes: Phosphodiesterase inhibitors (PDE3) (-one)

A

Eg. Milrinone, enoximone

Blocks action of PDE3 conversion of cAMP to AMP

This means more PKA produced meaning it can continue inhibiting MLCK which means more contraction (in cardiac muscle)

42
Q

Calcium sensitisers

A

Eg. Levosemendan

Binds to troponin c (TnC) and prolongs its action thereby increasing contraction

Good as does not cause extra ATP production or Ca increase

Also inhibits PDE3 and causes vasodilation via activation of K+ channels on blood vessels

43
Q

Digoxin

A

Inhibits Na+/K+ATPase by binding competitively to extracellular K+ site

This causes a build up of Na in the cell

This build causes NCX to reverse and pump 3Na out for every Ca

This means there is extra Ca available in SR meaning stronger contraction

44
Q

The mechanism by which Digoxin toxicity occurs and adverse effects

A

Ca2+ build up causes NCX to reverse again and start pumping Na+ back into the cell

The Na+ is not beng pumped out by Na+/K+ATPase

This causes a build up of +ve charge within the cell and can lead to a depolariastion which can lead to arrythmias (DAD)

Can also cause GI disturbance, yellow/blurred vision, dizziness and headaches

45
Q

Factors which can effect Digoxin action

A

Hypo/hyperkalaemia- hypo means more binding to CV while hypermeans more GI effects

Hyperthyroidism- Untreated requires higher doses

Renal impairment- less excretion mean higher plasma levels

Drugs that affect or damage to GI lining- Digoxin is dependant on uptake from GI. Drugs such as amiodarone are contraindicated

46
Q

Nitrate vasodilators

A

Eg. GTN and Isosorbide Mono/dinitrate

Short acting is glyceryl trinitrate

Longer acting is isosorbide mono/dinitrate
Activates GC which produces cGMP involved in vasodilation

They cause dilation of blood vessels which decreases cardiac pre/afterload which reduces cardiac work and increases CBF

47
Q

Nicorandil

A

NO donor

Activates ATP sensitive K channels

Causes vasodilation

48
Q

Ivabridine

A

Inhibits pacemaker If current in SA node
Causes a decrease in HR
Do not use with cardiac selective CCB (Diltiazem/Verapamil)

49
Q

Ranolazine

A

Inhibits the late Na current caused by ischaemia

This late current can cause a Na overload which reverses the NCX function which causes a Ca overload which causes reduced relaxation

Can be used 1st line in stable angina to prevent ischaemic damage

Can however cause arrythmias

50
Q

COX inhibitor

A

Aspirin, irreversibly binds to COX 1

COX1 is necessary for the production of TXA2 which is involved in platelet aggregation

51
Q

P2Y12 inhibitors (-grel and -grelor)

A

Eg, Clopidogrel, prasugrel, ticagrelor and cangrelor
-grelor’s are reversible while -grel’s are irreversible prodrugs
P2Y12 allows for aggregation of platelets and its shape change.

Therefore inhibition will reduce thrombus formation

52
Q

Glycoprotein IIA/B inhibitors (GPIIA/B)

A

eg. Abciximab, eptifibatide, tirofiban

GPIIA/B is necessary for platelets to adhere to fibrinogen. With this process inhibited the fibrin network cannot form

53
Q

Antiplatelet PDE inhibitors

A

Dipyridamole
Blocks PDE which increases cAMP and cGMP
This inhibits TXA2 synthesis and causes vasodilation

PA20321 (6 decks)

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