Pharmacology Flashcards
Class IA Antiarrhythmics. Mechanism. Drugs.
Na channel blockers.
-Class IA is moderately strong, decreases slope of phase 0
-Prolongs the refractory period
-Prolong AP duel to K+ blockage in phase 3 (at higher doses)
Procainamide
Quinidine
Disopyramide
Procainamide. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class IA
Decrease vascular resistance causing hypotension
Hepatic metabolism (NAPA is active metabolite that has Class III activity and a longer half life than Procainamide)
Use for Atrial or Ventricular Arrythmias
-2nd or 3rd choice for sustained ventricular arrhythmia with MI
Adverse: Long QT leading to Torsades, Lupus* like disease in chronic use
Quinidine. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class IA
Hepatic metabolism
Rarely used
Adverse: Long QT leading to Torsades, NV&D
Disopyramide. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class IA and also Antimuscarinic
Atropine like effects (urine retention, dry mouth, blurred vision, constapation)
In US only approved for ventricular arrythmias, but also could be used for supra ventricular arrhythmias. DO NOT use in heart failure
Adverse: Long QT leading to Torsades
Class IB Antiarrhythmics. Mechanism? Drugs?
Na channel blockers. -Shortens ERP -WEAK phase 0 changes -Depression of conduction in depolarized cells, NO effect if patient is in NSR Lidocaine Mexiletine Tocainide
Tocainide. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class IB
Glucuronidation reaction in liver
NOT used in US
Minimal adverse effects
Lidocaine. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class IB
Extensive first pass metabolism (GIVE PARENTERALLY)
Use: Sustained Vtach, Vfib, Post cardioversion in acute ischemia. DO NOT USE prophylactically
Adverse: Very minimal
Mexiletine. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class IB (ORAL lidocaine) Also used for chronic pain or neuropathy Hepatic metabolism Use for Ventricular arrhythmias Adverse: Minimal (tremor, blurred vision, lethargy, N&V)
Class IC Antiarrhythmics. Mechanism? Drugs?
Na channel blockers -Strongest Class I drugs -Significant decrease in phase 0 slope -NO change in ERP Flecainide Propafenone Moricizine
Flecainide. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class IC
-Also Class III effects
Hepatic and renal metabolism
Use for PVC SUPPRESSION and supra ventricular arrhythmias
Adverse: Exacerbation of arrythmias in a patient with a history of arrhythmia or past MI
Propafenone. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class IC -Also a weak B-blocker Hepatic metabolism Use for Supraventricular Arrhythmias Adverse: Arrhythmia exacerbation, metallic taste
Moricizine. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class IC
Extensive first pass metabolism (Give PARENTALLY)
NOT used in US, used in ventricular arrhythmia elsewhere
Class II Antiarrhythmics. Mechanism? Drugs?
Beta Blockers -Inhibit SNS activity in the SA node -Decrease HR -Decrease BP -Decrease Contractilty -Increase coronary perfusion Propranolol Acebutolol Esmolol Solatol Metoprolol Adverse: May cause HYPOglycemia in Diabetics*
Metoprolol. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Cardioselective B1 blocker, MUCH less B2 blocking than propranolol
CYP2D6 Substrate, extensive first pass metabolism
Use: Hypertension in asthma patients, DM, PVD (peripheral vascular disease), CHF, MI
Adverse: Bradycardia
Sotalol. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class II antiarrhythmic
-Some Class III activity
Use in AFIB*, Vfib, Vtach, HTN
Adverse: Long QT leading to Torsades
Acebutolol. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class II Antiarrhythmic
-Cardioselective (B1)
-Partial AGONIST of B2 receptor
Very good to control HTN in asthma patients
Also used for HTN in PVD or patients with bradyarrythmias
Has intrinsic sympathomimetic activity so DO NOT use with ANGINA (may exacerbate it)
Propranolol. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class II Antiarrhythmic
-B1 blocking
-Non specific B blocker
Use for HTN, Prophylaxis of ANGINA, CHF, MI, Reflex tachycardia from vasodilation
DO NOT USE IN ASTHMA PT, PVD, or DM
Adverse: bradycardia, bronchospasm, fatigue
Esmolol. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class II Antiarrhythmic
-B1 selective (cardioselective)
Rapidly metabolized by RBC esterases, must be on a drip (9-10 minute half life)
Used for intra/post operative HTN or in Acute arrhythmia
Class III Antiarrhythmics. Mechanism? Drugs?
Potassium channel blocker -phase 3 prolongation -Increase in AP and ERP duration, longer QT Amiodarone Dofetilide Ibutilide
Amidorone. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class III Antiarrhythmic
-Also has Class I, II, and IV effects
Extra: peripheral vasodilation
CYP3A4 substrate (levels of statins, warfarin, and digoxin will GO UP in patients if you give Amiodorone and do not decrease dosing)
First line treatment for sustained VTACH, Vfib, Afib, Aflutter
DO NOT use in a patient with SA or AV nodal disease
Adverse: Pulmonary toxicity*, Hepatitis, corneal deposits, skin deposits, thyroid issues
Dofetilide. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class III anti arrhythmic
CYP3A4 substrate
Use for AFIB* as maintenance
DO NOT use if patient has long QT, bradycardia, or hypokalemia
Adverse: Life threatening ventricular arrhythmias
Ibutilide. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class III anti arrhythmic
-Also slow inward sodium channel ACTIVATOR
-Delays depolarization and inhibits sodium channel INactivation, Increases ERP
Use for Acute conversion of AFLUTTER*, Afib to NSR
Adverse: Long QT leading to Torsades
Class IV Antiarrhythmics. Mechanism? Drugs?
Calcium channel blockers
-Smooth muscle relaxation: Vasodilation
-Reduced contractility of myocytes: shortens phase 2
-Decreases HR, conduction, and CONTRACTILITY: Slows phase 0 in Nodal cells
-Increases coronary blood flow
-Decreases Aortic diastolic pressure (reduces preload)
Dihydropyridines
Non-Dihydropyridines (Verapamil, Diltiazem)
Dihydropyridines. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class IV antiarrhythmics -Smooth muscle SELECTIVE -drugs end in '-pine' Use to treat HTN DO NOT USE WITH A BETA BLOCKER Adverse: HA, flushing, hyptension, reflex tachycardia, edema
Verapamil. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class IV antiarrythmic
-NONdihydropyridine
-Myocardium selective, decreases HR and contractility
Use for SVT, Afib, Aflutter, Angina, coronary vasospasm
DO NOT USE with a B-BLOCKER or in WPW
Adverse: bradycardia, AV block
Diltiazem. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class IV antiarrhythmic
-NONdihydropyridine
-Smooth muscle and cardiac, slows HR, Contractility, and increases vasodilation
Use for hypertension or prophylaxis of angina (will NOT get reflex tachycardia like the dihydropurines may produce)
DO NOT USE with a B-Blocker
Adenosine. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Activation of inward K channels
Inhibition of Ca channels (hyperpolarization), slowing of APs in nodal cells
Slowed conduction velocity
Increased ERP
First line treatment for SVT conversion to NSR
DO NOT USE if pt has preexisting 2’ or 3’ block
Adverse: hypotension
Digitalis. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Inhibits Na/K ATPase pump -increase intracellular Na -decreases action of Na/Ca pump so more Ca IN CELL -increases CONTRACTILITY -Depolarizes RMP -Activates vagal efferents to heart -Decreases SA/AV conduction -Increases ERP -Decreases Ventricular rate Use in HEART FAILURE*, Afib, Aflutter DO NOT use if AV block, WPW, Hypokalemia Adverse: AV block, digitalis effect on EKG (increase PR, flat T waves, decreased QT)
Nitrates & Nitrites. Mechanism? Drugs?
Arteriole and Venodilation -VENODILATION > arteriol dilation -Decreases Preload (V filling pressure) -Decreased pulmonary resistance -Decreases LV end-diastolic pressure -Slight decrease in TPR -Minimal INCREASE in HR at high doses (reflex response) -MINIMAL change in coronary blood flow, but less pressure redistributes it to endocardium Nitroglycerine Isosorbide Dinitrate Isosorbide Mononitrate
Nitroglycerine. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Releases NO in smooth muscle, activates guanylyl cyclase and increases cGMP
-Smooth muscle relaxation (VEINS>arterioles)
-Decreased venous return and heart size
-May increase coronary blood flow
USE: Angina
sublingual for acute episodes, oral and transdermal for prophylaxis, IV for acute coronary syndrome
HIGH first pass metabolism (sublingual dose much smaller than oral)
Adverse: Orthostatic HPTN, REFLEX tachycardia, HA
Synergistic hypotension if patient is on other phosphodiesterase type V inhibitor (viagra, cialis, levitra)
Isosorbide Dinitrate
Mechanims similar to nitroglycerin but has a slightly longer duration of action
Isosorbide Mononitrate
Active metabolite of isosorbide denigrate used ORALLY for prophylaxis of Angina
Nifedipine. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class IV antiarrythmic -Dihydropyridine -Blocks vascular Ca L-type channels MORE than cardiac Ca channels Use in prophylaxis of ANGINA, HTN Adverse: HPTN, reflex tachycardia
Atenolol. Mechanism? Effects? Pharacokinetics? Use? Adverse?
Class II anti arrhythmic -B1 Selective Decrease HR, BP, Contractility Increase coronary blood flow Use: HTN or ANGINA Adverse: HPTN, bronchospasm (but less risk than propranolol)
Aspirin
Mech: Inhibitor of plately COX1&2 -inhibits thromboxane A2 -Irriversible -Platelets cannot aggregate -Decreases risk of thrombosis Use in MI
Hydralazine
Arteriole vasodilator
Enalapril
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Diabinase
L
Zaroxolyn
Loop dieuretic
-Use in CHF if allergy to furosemide
Warfarin
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Furosemide
s
Acetazolamide
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Dobutamine
Used in acute CHF in hospital
Apresoline
Arterial vasodilator
ACE inhibitors
CHF!!!
Catopril
Enalapril
ARBs (Angiotensin II Receptor Blockers)
Losartan
Spironolactone
Aldosterone antagonist
CHF
Carvedilol
Cardio selective B-Blocker
- Decreases catecholamines
- Improves survival in CHF
What drug do you never use in a patient with diastolic dysfunction CHF?
Diuretics and Vasodilators
Indirect-Acting Sympathomimetics
Induce release of NE but not dopamine B hydroxylase
-Reverse direction of axoplasmic catecholamine transporter
-Inactive in presence of axoplasmic pump inhibitors (imipramine, cocaine)
Tyramine
Amphetamine
Ephedrine
Alpha 1 Receptor
Epinepherine > Norepi»_space;> Isoproterenol
-Smooth muscle contraction
-Vasoconstriction
Activates phophsolipase C, Gqalpha dependent, increases intracellular Ca
Alpha 2 Receptor
Epinepherine > NE»_space;> Isoproterenol
- Inhibition of neural NE release
- Decreases cAMP
- Activates Na/H antiporter
- Gialpha dependent
Beta 1 Receptor
Isoproterneol > Epi = NE
- Adrenergic cardiac effects (SA node inc.)
- Renin Release (inc BP, volume)
- Increases cAMP via Gsalpha
Beta 2 Receptor
Isoproterenol > Epi»_space; NE
- Relaxation of smooth muscle Bronchiodilation in LUNG (use Epi in anaphylaxis)
- Vasodilation
- Increase cAMP via Gsalpha
Dopaminergic Receptor
Dopamine
-Dilation of renal and mesenteric vasculature
Muscarinic Receptor
NE
Nicotinic Receptor
Ach, Nicotine release from preganglionic neuron
- Nicotinic receptor on post ganglionic neuron
- Stimulates release of ACh from vagus nerve on muscarinic receptor (heart and vessels)
- Stimulates release of NE if adrenergic neuron (heart, vessels)
- Stimulates ACh if cholinergic neuron, muscarinic rec. (sweat glands, vessels)
- Stimulates release of dopamine if dopaminergic neuron (renal vessels)
- Stimulates release of NE, EPI into blood if acting in ADRENAL gland (heart and vessels)
COMT
Inactivates catecholamines in liver
MAO
Oxidizes catecholamines
-Pargyline
Dobutamine
Selective B1 AGONIST
-Positive inotrope (inc. HR, BP)
Use in CHF or acute MI
DO NOT USE in AFib
Dopamine
B1 Agonist, Dopaminergic agonist
-At high doses A1 Agonist
-Inc. HR, BP (positive inotrope)
Use in Shock (maintains renal blood flow), HPTN, Chronic refractory HF
Phenylephrine
A1 AGONIST
-Vasoconstriction (inc. BP)
Use in HPTN or for paroxysmal atrial tachycardia
Metaproterenol
B2 AGONIST -Bronchodilation in lungs Use for Asthma, difficulty breathing Adverse: Tachycardia (B1), tremor, HA (B2 vasodilation) -Decreases BP
Albuterol
B2 AGONIST -Bronchodilation in lungs Use for Asthma, difficulty breathing Adverse: Tachycardia (B1), tremor, HA (B2 vasodilation) -Decreases BP
Isoproterenol
B1 and B2 Agonist -Vasodilation* -Bronchodilation -Increase HR What about BP? -MAP = HR*SV*TPR -HR and SV increase -TPR decreases (but much more than HR and SV (radius^4)) -So BP WILL DROP* Use: Cardiac stimulant
Norepinepherine
A1 Agonist, B1 Agonist -Vasoconstriction -Positive Inotrope -HR, Contractility, SV, BP all increase -Then reflex reduction in HR Used to treat HPTN
Terazosin
A1 ANTAGONIST
- Vasodilation
- Decreased BP
Epinepherine
A1 Agonist, B2 Agonist, B1 Agonist -Vasoconstriction -Bronchodilation -Vasodilation -Positive Inotrope (Inc. HR) -Reflexive decrease in HR -If large dose it will RAISE BP Used in hypersensitivity Reactions or with local anesthetics
Loop Diuretics
Furosemide, Torsemide
-inhibit Na K Cl pump in acending loop lf Henle
Used in CHF or to reduce pulmonary hypertension
ALWAYS check electrolyte levels*
Furosemide
Loop Diuretic
Torsemide
Loop Diuretic
Thiazide Diuretics
Block NaCl transporter in distal convoluted tubule -Used to treat HTN Chlorthalidone Hydrochlorothiazide Metalzone Adverse: HYPERGLYCEMIA (thiazides are sufonylureas, bind to SUR (sufonyl urea receptor) on potassium channel and OPENS it, hyper polarizing the cell - thus suppressing insulin release) Hyperuricemia (GOUT) Hypokalemia Hyperlipidemia Hyponatremia
Chlorthalidone
Thiazide Diuretic
Hydrochlorothiazide
Thiazide Diuretic
Metalzone
Thiazide Diuretic
Why are using thiazide diuretics with ACE inhibitors Synergistic?
when you use a thiazide it shifts body to use renin-angiotensin system.. So blocking both is SYNTERGISTIC*
Potassium Sparing Diuretics
Inhibit aldosterone receptos in collecting duct (SPIRONOLACTONE)
-Inhibit Na exchange for K and H (E NAC channels) in the cortical collecting duct (AMILORIDE, TRIAMTERENE)
Used in hyperaldosteroneism or to PREVENT K WASTING caused by other diuretics
Use in HEART FAILURE or POST MI
Adverse: Hyperkalemia, hyperchloremic metabolic acidosis, kidney stones
Spironolactone
K Sparing Diuretic
-Inhibits aldosterone receptor in collecting duct
Adverse: hyperkalemia, acidosis, Gynecomastia
Amiloride
K Sparing Diuretic
-Inhibits E NAC channels, inhibits Na exchange for K and H in collecting duct
Triamterene
K Sparing Diuretic
-Inhibits E NAC channels, inhibits Na exchange for K and H in collecting duct
Adverse: RENAL Failure
Vasopressin (ADH)
Natural hormone that uses G-protein coupled receptors in the collecting duct of the nephron to recruit aquaporins and increase water reabsorption to CONCENTRATE urine
-Desmopressin is a synthetic congener of ADH
Used to treat diabetes insipid us and bed wetting in young children
Desmopressin
Vasopressin (ADH) congener
Reason to use a potassium sparing diuretic?
HTN in Heart Failure or Post MI patient
Demecocycline
Antibiotic that has some ADH antagonistic activity
Osmotic Diuretics
Mannitol is the primary osmotic diuretic
-It is NOT reabsorbed in the nephron, therefore it exerts and osmotic effect to RETAIN water IN the nephron, thus increasing urine output
-Reduces body water or intracranial/ocular pressure
Adverse: Extracellular volume expansion, dehydration, hyperakalemia
Mannitol
Osmotic Diuretic
Carbonic Anhydrase Inhibitors
Acetazolamide is major CA inhibitor
-Not useful as diuretic since it has so many large effects in body
Used to treat Glaucoma, to ALKALINIZE urine (anecdote for barbiturates), treating metabolic ALKALOSIS, Acute Mountain Sickness
Adverse: Hyperchloremic metabolic acidosis, Renal stones, Renal K wasting (hypokalemia)
Acetazolamide
Carbonic Anhydrase Inhibitor
Organic Anion Transporters
Transport small hydrophilic molecules into or out of nephron
-Dicarboxylate drives this process (an alpha keto glutamate)
Used in the treatment of GOUT (along with NSAIDS, DO NOT use ASA)
Probenicid
Sulfinpyrazone
-Inhibits renal organic acid transporters of irate to facilitate excretion
Allopurinol
Inhibits xanthine oxidase
-Used to treat GOUT
Probenicid
Inhibits Organic Anion Transporters (OATs)
-Used for Gout
Sulfinpyrazone
Inhibits Organic Anion Transporters (OATs)
-Used for Gout
How to thiazides cause Gout?
Thiazides are substrates
Eplerenone
Potassium sparing diuretic
-Aldosterone Receptor blocker similar to spironolactone
What do you use to acidify urine?
Ammonium Chloride
-Probably will never use
What is important to monitor when using Loop Diuretics?
Electrolyte levels, hypokalemia can be and adverse effect
What reasons (comorbidities) should thiazide diuretics be used?
HTN and high risk of STROKE
HTN in diabetics (even though hyperglycemia may be an AE)
HTN and Coronary Artery Disease
Pindolol. Mechanism? Use? Adverse?
Class II Antiarrhythmic
-Cardioselective (B1)
-Partial AGONIST of B2 receptor
Very good to control HTN in asthma patients
Also used for HTN in PVD or patients with bradyarrythmias
Has intrinsic sympathomimetic activity so DO NOT use with ANGINA (may exacerbate it)
Treatment for polycystic kidney disease along with HTN?
ACE Inhibitors
- Reduce HTN
- Increase renal blood flow
- Renal protective
Methamphetamine
Facilitates release of NE from post ganglionic neuron in the synaptic junction.
- NE stimulates alpha 1 adrenergic receptors causing smooth muscle contraction leading to hypertension
- NE stimulates beta 1 adrenergic receptors in the SA node causing an increased HR - it is a positive inotrope
