Pharmacology Cardio Flashcards
Class 1a Antiarrhythmic
(Class 1 = Na+ channel blockers
Quinidine
Procainamide
Disopyramide
Class 1b Antiarrhythmic
(Class 1 = Na+ channel blockers
Lidocaine
Hydrochloride
Class 1c Antiarrhythmic
(Class 1 = Na+ channel blockers)
Felcainide
Class 1c Antiarrhythmic
(Class 1 = Na+ channel blockers)
Felcainide
Class 2 Antiarrhythmic
(class 2 = β blocker)
(olol)
Bisoprolol
Atenolol
Propanalol
Timolol
Class 3 Antiarrhythmic
(class 3 = K+ channel blocker
Amiodarone
Class 3 Antiarrhythmic
(class 3 = K+ channel blocker)
Sotalol
Class 4 antiarrhythmic
Non-dihydropyridines
(class 4 = Ca2+ channel blocker)
Verapamil
Diltiazem
peripheral hypertensive calcium channel blockers
Amlodipine
Nifedipine
‘other antiarrhythmic’ need to know
Adenosine
‘other’ anti-arrhythmic
Digoxin
what is Quinidine
Procainamide
Disopyramide used for
Treats tachyarrhythmia caused by reentry circuit
Ventricular Fibrillation
what are Lidocaine , Hydrochloride used for
Treats tachyarrhythmia caused by reentry circuit
Local anesthetic
Ventricular Arrhythmias
Felcainide what is it used for
Treats tachyarrhythmia caused by reentry circuit. *tachyarrhytmia = tachycardia
Bisoprolol
Atenolol what is it used for
Tachyarrhythmias caused by increased sympathetic activity
Atrial Flutter
Atrial Fibrillation
AV nodal re-entrant tachycardia
In atrial fibrillation, the atria beat irregularly. In atrial flutter, the atria beat regularly, but faster than usual and more often than the ventricles
what is binding site for Quinidine
Procainamide
Disopyramide
Na+ channels
what is binding sites for Lidocaine
Hydrochloride
Na+ channels
what is binding site for felcainide
Na+ channels
what is bisoprolol and atenolol binding site
B1 receptor, Gs
what is propanolol and timolol binding site
β1 receptor
(non-selective)
what is amiodarone binding site
K+ channels
what is sotalol binding site
K+ channels and Beta receptors
what is verampil and diliazem binding site
Ca2+ channels (L type)
what is amlodipine and nifedipine binding site
Ca2+ channels
what is adenosine binding site- other arrhythmitic
alpha 1 purinergic receptors
what is digoxin binding site-other antiarrhythmic
Na+/K+, ATPase
what is digoxin used for
Used to control ventricular response rate in:
1. Atrial Fibrillation
2. Atrial Flutter
only given really if they’re bed bound otherwise use bisoprolol.
what is adenosine used for
Paroxysmal SVT
supraventicular tachyardia
what is verapamil and dilitazem used for
Stable angina
Supraventricular arrhythmias (supraventricular tachycardia, atrial flutter, atrial fibrillation)
Hypertension (Diltiazem)
what is sotalol used for
Inhibit reentrant tachycardias
Maintenance of sinus rythms in patients with:
1. Atrial Fibrillation
2. Atrial Flutter
3. Refractory paroxysmal SVT
4. Ventricular arrhythmias
what is amiodarone used for
Inhibit reentrant tachycardias
Tachycardias:
1. Atrial fibrillation,
2. Atrial flutter
3. Refractory ventricular fibrillation
what is the mechanism of action of Quinidine
Procainamide
Disopyramide
Moderate Na+ channel blocker
Decrease slope of phase 0
- They bind to the Na+ channels in the inactivate state (refractory period)
- This prevents more Na+ influx , thus slowing down the rapid upstroke during phase 0 - this causes a delay in the depolarisation
what is the mechanism of action of felcainide
Strong Na+ channel blocker
Decrease slope of phase 0
Flecainide suppresses phase 0 upstroke in Purkinje and myocardial fibers. This causes marked slowing of conduction in all cardiac tissue, with a minor effect on the duration of the action potential and refractoriness. Automaticity is reduced by an increase in the threshold potential, rather than a decrease in slope of phase 4 depolarization.
what is the mechanism of action of Bisoprolol and atenolol- CLASS 2
Decrease HR & conduction velocity
Indirectly alter conduction velocity
- Beta blocker will bind to the B1 receptor competitively
- The amount of cAMP is reduced
- This decreases the amount of L-type channels that open
- Less Ca2+ will enter the cell, therefore less Na+ will be pumped into of the cell
Less Ca2+ in the cell = less Ca2+ efflux = less Na+ influx = slower depolarisation = slows down the heart rate + contractility
what is the mechanism of action for propanolol and timolol- CLASS 2
Decrease HR & conduction velocity
Indirectly alter conduction velocity
- Beta blocker will bind to the B1 receptor competitively
- The amount of cAMP is reduced
- This decreases the amount of L-type channels that open
- Less Ca2+ will enter the cell, therefore less Na+ will be pumped into of the cell
Less Ca2+ in the cell = less Ca2+ efflux = less Na+ influx = slower depolarisation = slows down the heart rate + contractility
what is the mechanism of action of amiodarone- CLASS 3
Increase ERP
Class III agents block K+channels and, thus, diminish the outward K+current during repolarization (phase 4) of cardiac cells. These agents prolong the duration of the action potential and increased the refractory period
what is the mechanism of action of sotalol- CLASS 3
Increase ERP
Sotalolblocks a rapid outward K+current, known as the delayed rectifier current. This blockade prolongs both repolarization and duration of the action potential, thus lengthening the effective refractory period.
what is the mechanism of action of verapamil and diltiazem- CLASS 4
Decreases slope of phase 2
Slow down conduction velocity
Decrease contractility
Adjusts refactory period.
- The L-type Ca2+ channels on the T-Tubule are now blocked
- There is now little outflux of Ca2+ from the sarcoplasmic reticululm - no “Ca2+ induced Ca2+ release”
- Ca2+ cannot bind to troponin and therefore they’ll be less contraction - reducing the force and speed of contraction
- Little Ca2+ will leave the cell meaning little Na+ will enter the cell
- This means less K+ enters the cell
*They slow down the conduction of the AV nodes and the automaticty
* They supress the cardiac conduction down the Bundle of His - this slows down the ventricular rate and reduces cardiac contractility
how do amlodopine and nifedipine work -
act on blood vessels as calcium channel blockers to prevent dilation, reduces TBR by causing vasodilation. NOT CLASS 4 ANTIARRHYTHMICS . DECREASE BP BY DECREASE TPR.
what is adenosine mechanism of action
Decrease SAN firing and conductivity
Increase ERP
- Has potent effects on the SA node - resulting in sinus bradycardia
- Slows cardiac action thru the AV node
- Inhances the flow of K+ out of the cell - hyperpolarising the resting
acts on receptors in the cardiac AV node, significantly slowing conduction time. [3] This effect occurs by activation of specific potassium channels, driving potassium outside of cells, and inhibition of calcium influx, disrupting the resting potential of the slow nodal cardiac myocyte
how does digoxin work
Cardiac glycosides inhibit Na+/K+ pump, increase Ca2+ exchange, increase vagus effects
Increase contractile force
Decrease HR, AV conduction
- Digoxin binds to the Na⁺/K⁺ ATPase on the myocyte membrane and partially inhibits it. This increases the intracellular Na⁺ concentration and decreases the Na⁺ concentration gradient, the effect is downregulation of the Na⁺/Ca²⁺ transporter so excess Ca²⁺ remains in the cell to be stored in
- This enhances contractility
what is phenylephrine
a1 agonist
what is clonidine
a2 antagonist
what is dobutamine in
B1, B2, A1 agonist
what is salbutamol in
B2agonist
what is norepinephe
a1. a2 agonist
what is epinephrine in
a1, a2, b1, b2 agonist
what is doxazosin and prazosin in
a1 antagonists
what is atenolol, bisoprolol and metopralol
B1 antagonist
what is phenoxybenzamine in
a1 + a2 antagonists
what is propanolol and timolol in
B1 + B2 antagonist
what does phenylephrine used for
reduced nasal conjestion
what is clonidine used for
resistant hypertention
what is dobutamine used for
cardiogenic shock
what is salbutamol used for
bronchodilation
what is epinephrine used for
anaphylaxis and MI
what is dozasin used for
resistant hypertension
what is prazosin used for
resistant hypertension and benign prostatic hyperplasia
what is phenoxybenzamine used for
phaeochromocytoma
what is atenolol, bisoprolol and metoprolol used for
primarily hypertension, heart failure after MI (cardio selective B1 ONLY)
what is propanolol used for
hypertension, angina (non-selective, B1 and B2)
when can b blockers be used for angina and why
at rest they cause little change in HR, BP, and CO but decrease effects of excercise
what do non selective B blockers antagonise (meaning it binds to and competitibely antagonises both B1 and B2 receptors, likely causing bronchoconstriction, excaserbating patient’s asthma
B1 and B2
work calcium channels work best in the heart
diltiazem and verampamil
where are doxazosin and prazosin found
vascular smooth muscle
what is MOA of doxason + prozasoin ( alpha adrenoreceptor antagonists)
Prevents agonists such as epinephrine, norepinephrine and phenylepinephrine from binding to the α1 receptor and so prevents their MOA from occuring. This in turn causes vasodilation
what does clonidine do (a2 agonist)
cause vasodilation
what does phenoxybenzamine do a1 + a2 antagonist
Non-selective α antagonist that causes an irreversible blockade of all α adrenoreceptors
what does epinephrine do, a +B agonist
Causes increased HR, increased force of contraction & central shunting of blood
what does dopobutamine do , b1 receptor agonist
ionotropic effect increases contractility, leading to decreased end-systolic volume and, therefore, increased stroke volume.
what is aliskerin
renin inhibitor competitive antagonist
what is aliskirin used for
hypertension
what is normal MOA of renin, and what does aliskerin do
renin= Renin catalyses the conversion of angiotensin to ANG1
aliskerin= Aliskerin compeitively antagonises renin and prevents the formaiton of ANG1, which is needed for the prouction of ANG2
what is ramipril (any prils)
ACE inhibitor- competitively antagonise
what is ramipril used for
hypertension and heart failure
what is ACE normal MOA and what does ramipril do
ACE- ACE normally converts Angiotensin 1 into Angiotensin 2
In hypertension we can ventricular hypertrophy, which contributes to the diastolic component of heart failure via imparied diastolic filling
Ramipril- competitively antagonise the ACE enzyme to prevent the conversion of ANG1 to ANG2.
BP=COxTPR
↓ANG2 leads to vasodilation and ↓TPR
↓ANG2 reduces further hypertrophy
Results in CO from heart becoming sufficient for perfusion
what is losartan and valsaratan
Angiotensin 2 Receptor Blockers - ARBs
(sartans)- bind at AT2R competitive antagonist
what is losartan and valsartan used for
Hypertension
how does ANG2 and AG1 MOA usually work, and how does ARB stop this
-ANG2 normally binds to AT1 receptors, causing increased aldosterone levels
-ARBs competitively antagonise AT1 receptors in vascular, adrenal and neuronal tissue.
what class is mannitol
osmotic diuretic
what is usage of mannitol
cerebral oedema, reduce ischameia, cerabral damage, acute traumatic brain injury
what is mannitol MOA vc normal MOA
normal MOA: 1. Na+ is actively pumped across basolateral membrane via Na+/K+ ATPase
2. Decreased Na+ conc, activates Na+ pumps on apical membrane
3. Na+/H+ transporter & Na+/glucose transporter move Na+ from the nephron lumen into the ICF.
mannitol MOA: Osmotic diuretics increase the concentration of solute in the nephron lumen, pulling water back into the lumen to dilute the concentration of the solute and so more water remains In the nephron lumen to be excreted
what is furosemide class
loop diueretic
what is furosemide usage
Oedema
Pulmonary oedema due to LVHF & Chronic HF
Resistant Hypertension
what is furosemide binding site
Na+/K+/2CL- receptor anatgonist
where are furosemide receptors found
ascending loop of henle
furosemide MOA vs normal MOA
NORMAL:
1. Na+ is actively pumped across basolateral membrane via Na+/K+ ATPase
2. Decreased Na+ conc, activates Na+ pumps on apical membrane
3. Na+/K+/2Cl- pumps ions across the apical membrane from the nephron lumen into the ICF
DRUG MOA:
Thiazide diuretics are antagonists of the Na+/Cl- receptor, so more sodium remains in the nephron lumen and is excreted. The water remains with the sodium and is excreted.
Bendroflumethiazide class
thiazide diuretic
bendroflumethiazide usage
Hypertension - lower doses
Oedema due to chronic HF - higher doses
bendroflumethiazide binding site and where
na/cl receptor antagonist distal convuluted tube
bendroflumethiazide MOA and normal MOA
normal MOA: 1. Na+ is actively pumped across basolateral membrane via Na+/K+ ATPase
2. Decreased Na+ conc, activates Na+ pumps on apical membrane
3. Na+/Cl- receptor pumps ions across the apical membrane from the nephron lumen into the ICF
drug MOA:
Block Na+/Cl- cotransporter so more Na+/Cl- excretion
Water loss
indapamide class
thiazide like diuretics
indepamide binding site and where
na/cl antagonist in distal convuluted tubule
indempamide MOA and normal MOA
normal MOA- 1. Na+ is actively pumped across basolateral membrane via Na+/K+ ATPase
2. Decreased Na+ conc, activates Na+ pumps on apical membrane
3. Na+/Cl- receptor pumps ions across the apical membrane from the nephron lumen into the ICF
indampemide MOA- Block Na+/Cl- cotransporter so more Na+/Cl- excretion
Water loss
amiloride class
potassium sparring diuretic
amiloride binding side and where found
ENaC-Na+ cotransporter antagonist in cortical collecting tubule
amiloride MOA and normal MOA
normal MOA - 1. Na+ is actively pumped across basolateral membrane via Na+/K+ ATPase
2. Decreased Na+ conc, activates Na+ pumps on apical membrane
3. Na+ channels are activated
amiloride MOA- Block Na+ cotransporter so more Na+ excretion
Water loss
Amiloride is an antagonist of the Na+ channel, so more sodium remains in the nephron lumen and is excreted. The water remains with the sodium and is excreted.
what is amiloride usually used in conjuction with
This drug is used for fine tuning and so is normally used in cojunction with another diuretic (usually thiazide)
what is spironalactone class
aldosterone antagonist
what is spironolactone binding site
mineralcoricoid receptor antagonist
what is spironalactone MOA vs normal MOA
normal MOA- 1. Aldosterone is a steroid hormone that binds to mineraloorticoid receptor and acts principally by modulating gene transcription
2. Aldoseterone increases the activity of several key proteins involved in Na+ transport it does this by:
* increasing the amount of Na+/K+ ATPase - this causes more Na+ reabsorption on the apical membrane
* Increases the expression of the apical Na+ channels and the Na+/K+/Cl- cotransporters - this increases the Na+ reabsorption and water follows (less is secreted in the urine)
drug MOA-
Aldosterone antagonist so blocks MR so decrease in AIP so fewer Na+/K+ pumps, Na+ channels and K+ channels so increased Na+ excretion
Water loss
Spironolactone blocks the following actions:
Aldosterone on the apical membrane causes:
More ENaC channel phosphorylation meaning they stay open for longer allowing more sodium entry to the cell from the lumen
Less ENaC channels to be endocytosed so more remain in the membrane
Aldosterone on the basolateral membrane causes:
More Na+/K+ pumps to be inserted into the membrane increasing the Na+ extrusion from the cell, increasing the driving flux for Na+
what is spironolactone usually used in conjunction with
usually used with a thiazide diuretic
what class is unfractionated heparin
heparin
what is usage of unfractionated heparin
Prevention of VTE - following an operation, in patients with angina and following acute MI
Treatment of VTE
what is MOA of unfractionated heparin
Increase affinity of ATIII to to clotting factors
Heparin increases the affinity og antithrombin III (ATIII) to clotting factors XIIa (12a), XIa (11a), IXa (9a), Xa (10a) and IIa (thrombin)
This interupts the coagulation cascade and no fibrinogen is converted to fibrin and no clotting can occur
what class is enoxaparin
low molecular weight heparin(LMWH)
what is enoxaparin usage
Prevention of VTE - following an operation, in patients with angina and following acute MI
Treatment of VTE
what is enoxabin moa
LMWH inhibit Xa (10a), via increasing afinity of ATIII
This will inhibit the conversion of II (prothrombin) to Iia (thrombin)
what is fondaparinux MOA
inhibits factor Xa
what class is warfarin
anticoagulant antagonists
what is warfarin usage
- Prevention of venous thrombosis or pulmonary embolus
- Prevention of arterial thromboemboli (in patients with AF or a cardiac disease)
what is warfarin binding site
vitamin K reductase
where are warfarin receptors found
blood
what is warfarin MOA and normal MOA
- Vitamin K is reduced to form its reduced form (hydroquinone)
- This activates the clottings factors (II, VI, IX, X)
normal MOA
1. Warfarin inhibits vitamin K epoxide reductase
2. This prevents the reactivation of Vitamin K to its reduced form
3. Inactives vitamin K dependent clotting factors (II, VII, IX and X) can’t bind stable to the blood vessel endothelium and so can’t activate clotting
what class is dibigratran
anticoagulant competetive antagonist
what is dibitgatran usage
- Prevention of stroke and embolism in patients with AF
- Prophylaxis of venous thromboembolism after hip or knee replacement surgery
what is dibigatran binding site
Factor IIa
where is dibigatran receptors found
blood
what is dibigatran MOA
Competitively binds (reversibly) to the free and fibrin bound factor Iia which inhibits the production of fibrin
what is rivaroxaban/apixaban class
anticoagulant competitive antagonist
what is rivaroxaban/apixaban usage
Prophylaxis of VTE after hip or knee replacement surgery
what is rivaroxaban/aprixaban binding site
factor Xa
what is rivoroxaban/apixaban where are the receptor found
blood
what is the MOA of rivaroxaban /apixaban
Competitively antagonsises factor Xa, which inhibits thrombin (Iia) production from prothromin (II)
what class is aspirin
antiplatelet
what is usage of aspirin
Used prophylactically to prevent arterial thrombosis leading to:
Transient ischaemic attack
Stroke
MI
what is binding site of aspirin
COX-1
(cyclooxygenase-1)
where a aspirin receptors found
platelets
what is aspirin MOA and normal MOA
aspriin- 1. Aspirin irreversibly inhibits COX-1 , therefore the synthesis of TXA2 is inhibited.
2. The TXA2 cannot recruit more platelets
Because platelets do not contain RNA or DNA they cannot synthesise new COX-1 - making this reaction irreversible
normal MOA - Activated platelets cover and adhere to exposed subendothelial surface of damaged endothelium
Activated platelets release chemical mediators inclusive of
ADP promotes platelet adhesion
PAF promotes platelet activation
Serotonin promotes platelet aggregation
TXA2 recruits more platelets to the plug and causes platelet aggregation
what class is clopidogrel
anti platelet
what is usage of clopidogrel
Patients who have coronary artery stents
Stroke Prevention
Post MI - STEMI & NSTEMI
Unstable angina
what is binding site for clipidogrel
P2Y12 (ADP) receptor
where are clopidogrel receotors found
platelet
what is clopidogrel MOA and normal MOA
normal MOA- Activated platelets cover and adhere to exposed subendothelial surface of damaged endothelium
Activated platelets release chemical mediators inclusive of
ADP promotes platelet adhesion
PAF promotes platelet activation
Serotonin promotes platelet aggregation
TXA2 recruits more platelets to the plug and causes platelet aggregation
clopidogral MOA- Prevents ADP-mediated P2Y12 depedent platelet activation and aggregation
Irreversible binding
what class is tricagrelor
Anti-platelet
what is tricargelor usage
Patients who have coronary artery stents
Stroke Prevention
Post MI - STEMI & NSTEMI
Unstable angina
what is tricagretor receptor found
P2Y12 (ADP) receptor
where are tricagrelor receptors found
platelets
what is tricagrelor MOA and normal MOA
tricagrelor MOa- Prevents ADP-mediated P2Y12 depedent platelet activation and aggregation
Irreversible binding
normal MOA-
Activated platelets cover and adhere to exposed subendothelial surface of damaged endothelium
Activated platelets release chemical mediators inclusive of
ADP promotes platelet adhesion
PAF promotes platelet activation
Serotonin promotes platelet aggregation
TXA2 recruits more platelets to the plug and causes platelet aggregation
what class is dypyridamol
antiplatelet
what class is alteplase
fibronlytic agonist
what is the usage of alteplase
Dissolve clots that result in MI and ischaemic stroke
Massive PE - high risk of bleeding so not first choice
Restoring catheter and shunt function - by lysing clots causing occlusions
what is the binding site of alteplase
Plasminogen
what is the receptor of alteplase found
blood
what is alteplase MOA and normal MOA
alteplase MOA- Catalyses the conversion of plasminogen to plasmin
normal MOA- There is always a balance between the breakdown (fibrinolysis) and the formation of thrombosis
Fibrinolysis happens by plasminogen being converted to plasmin which breaks down the fibrin fibres formed during the coagulation cascade
atropine what class
anti muscarinic receptor. M1, M2, M3, M4 and M5 antagonist
atropine what is usage
first line SVT
atropine MOA
Atropine binds to and inhibits muscarinic acetylcholine receptors, competitively blocking the effects of acetylcholine and other choline esters
what receptors do atropine bind to
binds to M1, M2, M3
what is the most importany plasma protein
albumin
what is the most importany plasma protein
albumin * a high plasma protein bound drug will show slower acting and prolonged therapeutic effects
why should tetracuclines not be used in children
they accumulate slowly in bones and teeth because HIGH AFFINITY FOR CALCIUM
what is asprin hydrolysed to
salicyclic acid
what do ACEi and thiazide diuretics together lead to
lead to fainting
aspirin MOA
decrease formation of thromboxaneA2. reversible cox 1 and cox 2 inhibitor
what receptors does adrenaline work on
a1, a2, b1, b2
warfarin contrainsndications
Warfarin is contraindicated in hemorrhagic stroke, in patients with significant bleeding, and in pregnancy
who shouyou not give beta blockersn
heart failuire and asthmatics
When do you use mannitol
Only in cranial hypertension
Where does mannitol work
Proximal convultaed tubule
What does ivabradine moa
Ivabradine aims to inhibit funny current HCN channels ONLY ON PACEMAKER CELLS ON SAN AND AVN. Slows down heart rate
