MOA Flashcards
Chloropheniramine
Inhibit H1 and cholinergic receptors
Diphenhydramine
Inhibit H1 and cholinergic receptors
Dimenhydrinate
Inhibit H1 and cholinergic receptors
Loratadine
Selective H1 inhibition
Cetirizine
Selective H1 inhibition
Fexofenadine
Selective H1 inhibition
Cromolyn Sodium
directly inhibits mast cell degranulation (ion channel blockers)
Aldosterone
Binds to mineralocorticoid receptor
↑Na Channels and Na uptake into the cell
Glucocorticoids
↑Annexan A1 (which inhibits PLA2)
↓cytokine synthesis (TNF α )
↓Production of prostaglandin/leukotriene products (Cox 2)
11β-HSD2
inactivates cortisol by converting it to cortisone
Omalizumab
Binds to FC portion of IgE to block its ability to bind to mast cell
Montelukast
leukotriene receptor antagonist inhibits bronchoconstriction
Theophylline
Inhibits cAMP phosphodiesterase in smooth muscle
Ipratropropium Bromide
Block affects of Ach release from vagus on M3
↓smooth muscle contraction and mucus secretion
Tiotropium
Block affects of Ach release from vagus on M3
↓smooth muscle contraction and mucus secretion
Albuterol (SABA)
Bind to β2 and prevents Ca from coming in cell to relax smooth muscle causing airways to open
Inhibit release of mast cell mediators
Salmeterol (LABA)
Bind to β2 and prevents Ca from coming in cell to relax smooth muscle causing airways to open
Inhibit release of mast cell mediators
Fluticasone
Blocks gene transcription (cytokines, chemokines)
↓Inflammatory cells (cytokines)
↑β2 receptors
Prazosin
reversible α1 receptor blocker only
Phenoxybenzamine
irreversible α1 receptor blocker
somewhat selective over α2
Phentolamine
non-selectively blocks α1 and α2
Pindolol
↓CO, ↓plasma renin release and ↓ central sympathetic tone
Acebutolol
↓CO, ↓plasma renin release and ↓ central sympathetic tone
Propanolol
↓CO, ↓plasma renin release and ↓ central sympathetic tone
Timolol
β receptors produce aqueous humor so you block and ↓ aqueous humor and ↓IOP
Atenolol
↓CO, ↓plasma renin release and ↓ central sympathetic tone
Esmolol
↓CO, ↓plasma renin release and ↓ central sympathetic tone
Labetalol
Blocks β2α1 in 4:1 rtio
Carvedilol
Blocks β2α1 in 10:1 ratio
Clonidine
works directly at α2 receptors to
1. Tells enough NE and stops release by acting at presymaptic receptors on postganglionic neurons
- ↓Sympathetic outflow in the brain
α-methyldopa
must be metabolized to α-methyl-NE to
1. Tells enough NE and stops release by acting at presymaptic receptors on postganglionic neurons
- ↓Sympathetic outflow in the brain
Dexmedetomide
α2 receptors n locus coeruleus to
1. Tells enough NE and stops release by acting at presymaptic receptors on postganglionic neurons
- ↓Sympathetic outflow in the brain
Guanethidine
enters via NET and concentrates in vesicle to ↓ NE over time
NE that escapes is metabolized by MAO
Reserpine
enters terminal, membrane blocks VMAT causin ↓NE
NE that escapes is metabolized by MAO
Fiber
Releases FA that inhibit hepatic FA synthesis
Omega-3 Fatty Acids
↑ clearance of TGs
Atrovastatin
Direct inhibition of HMG CoA reductase which leads to
↓ cholesterol→
↑ synthesis of hepatic LDL receptors→
↑ LDL clearance
Pravastatin
Direct inhibition of HMG CoA reductase which leads to
↓ cholesterol→
↑ synthesis of hepatic LDL receptors→
↑ LDL clearance
Cholestyramine
⊕charged so binds to bile acids (cholesterol metabolites) → prevents reabsorption of bile acids → ↑conversion of cholesterol to bile acids→ ↑LDL receptors and ↑LDL clearance from plasma
Can also lead to up regulation of HMG-CoA reductase
Niacin (vit B3)
Inhibits lipase and ↓ TG transport to liver→ ↓TG synthesis in liver
Gemfibrozil
Agonist for PPAR α receptor (a transcription factor)
Evolocumab
blocks degredation of LDL receptor
Nitroglycerin
Converted to NO →↑Guanylate cyclase →↑cGMP→dephosphorylates MLC→↓conractile smooth muscles
Verapamil
Block influx of Ca→↓contractile state of smooth muscle
Diltazem
Block influx of Ca→↓contractile state of smooth muscle
Nifedipine
Block influx of Ca→↓contractile state of smooth muscle
more potent on vessel than heart
Nimodipine
Block influx of Ca→↓contractile state of smooth muscle
more potent on vessel than heart
high affinity for cerebral vessels
Propanolol
Block β1 R on heart→↓HR and ↓contraction due to ↓Calcium influx
Blocks β1 and β2
↓renin secretion→↓Ang II
Hydrochlorothiazide
block Na Cl pump
↑Na in lumen→depolarizing luminal membrane→↑loss of K
Captopril
Blocks ACE which blocks conversion of Ang I → Ang II (normally causes vasoconstriction)
Losartan
Block pathway at receptor level AT1
Hydralazine
Vasodilate arterial smooth muscle → baroreceptor reflex response
Minoxidil
Vasodilate arterial smooth muscle → baroreceptor reflex response
Sodium Nitroprusside
Vasodilate arterial smooth muscle → baroreceptor reflex response
Prazosin
Blocks binding of NE to to α1 receptors
Guanethidine
Transported into vesicles and replace NE and blocks exicatation secretion coupling at Post ganglionic peripheral nerurons
Reserpine
Binds to storage vesicles and inhibits transmitter uptake→dysfunctional vesicles bc depletion of NE at Central and peripheral vesicles
Methyldopa
↓sympathetic activity→vasoconstriction
Clonidine
↓sympathetic activity→vasoconstriction
Effect of nitroglycerin on the body
Vasodilates
Dilates large epicardial arteries →↓coronary steal→↓LV pressure
↓Preload
↓Wall tension
Effect of Calcium Channel Blockers on the body
↓contractility
Effect of Dihydropyridine Calcium Channel Blockers on the body
More coronary and peripheral vasodilation than non-dihydros
↓BP
↑HR
↑Contractility
Effect of Propanolol on the body
↓HR
↓contraction
↑Preload and tension (might want to use in combo w/ ↓preload)
Effect of Hydrochlorothiazide on the body
↓preload and blood volume
Effect of Captopril on the body
vasodilation
↓preload and blood volume
↓LV hypertrophy
Effect of Losartan on the body
↓preload and blood volume
Effect of α2 Agonists on the body
Vasoconstriction
↓Sympathetic Activity
↓BP
Lidocaine
Block Na channels→ ↑ERP
Inc K+ out→ ↓ AP
Selective for sick cells
Mexiletine
Block Na channels→ ↑ERP
Inc K+ out→ ↓ AP
Selective for sick cells
Flecainide
Selectively Na channel blocker→ ↑ERP
Inc K+ out→ ↓ AP
Quinidine
Blocks Na channels in normal cells → ↑ERP
Anticholinergic ↓vagal influences
Procainamide
Blocks Na channels in normal cells → ↑ERP
Anticholinergic ↓vagal influences
Disopyramide
Blocks Na channels in normal cells → ↑ERP
Anticholinergic ↓vagal influences
Amiodarone
Blocks K+ efflux → ↑APD and ↑QT
Blocks Na channels→ ↑ERP
Dronedarone
Blocks K+ efflux → ↑APD and ↑QT
Blocks Na channels→ ↑ERP
Sotalol
Blocks K+ efflux → ↑APD and ↑QT
Blocks Na channels→ ↑ERP
Ibutalide
Blocks K+ efflux → ↑APD and ↑QT
Blocks Na channels→ ↑ERP
Verapamil
L type Ca channel blockade
↓SA and AV node conduction
↓ contractility
Diltiazem
L type Ca channel blockade
↓SA and AV node conduction
↓ contractility
Metoprolol
↓AV node conduction
↓excitability
↓SA node rate
↓contractility
Digoxin
Inhibits Na+/K+ ATPase→
↓resting mem potential
↓conduction velocity
↑vagal activity→ ↓recractory period and ↓conduction in AV node
Adenosine
↑K+ efflux and hyperpolarizes cell→ ↓ability for Ca to enter→ ↓AV node conduction and ↓automaticity
Alcohol
↑GABA binding at inhibitory GABAaR
↓Glutamate activation of excitatory NMDAR
Facilitate release of endogenous opioids in VTA
Barbiturates
↑GABA binding at inhibitory GABAaR
Can directly open GABAa at high concentrations
Benzodiazepines
↑GABA binding at inhibitory GABAaR
Abuse w/ faster acting BZ (alprazolam, diazepam)
Heroin/Opioids
Activity mu-opioid receptor
Nicotine
Nicotine stimulates nAchRs in reward pathway
Marijuana, hashish, oils
THC binds to cannabinoid receptors (GPCR) and activates the reward pthwy
Amphetamines
and
Methamphetamine
↑ DA and NE release and block MAO
Cocaine
Blocks reuptake of NA so ↓ NE and serotonin
Psychedelics related to serotonin
LSD, Psilocybin, DMT
Agonist at 5HTR, DA receptors and adrengeric receptors
Psychedelics related to dopamine and aphetamines
MDA, MDMA, mescaline
Induce 5HT and DA release
5HT reuptke inhibitor
Agonist at 5HT, DA & adrenergic receptor
Dissociatives
PCP, ketamine
Inhibit glutamatergic NMDA receptors
Acetazolamide
CAH inhibitor→↓HCO3⁻ in → ↓ Na⁺ resoprtion→ ↑ luminal Na⁺ concentration (which will retain water and Cl⁻)
↓ H⁺ in
Secondary: ↑tubular Na⁺→TGF activation → ↓GFR
Osmotic diuretics
↑ conc in tubule that cant be resorbed so holds onto more water
↑plasma osmolality, ↑ECFV→ ↑ RBF & ↓ osmotic gradient
Na⁺/K⁺/2Cl⁻ Blockers (Loop diuretics)
↓ Na⁺/K⁺/2Cl⁻ Symporter → ↓ osmotic gradient
Changes in macula densa sensing of Na is duiretic braking
Na⁺/Cl⁻ Blockers (Thiazide diuretics)
Inhibits Na⁺/Cl⁻ cotransporter
ENaC Inhibitors
Block ENaC → ↓ Na resoprtion and ↓ K backleak & excretion
Aldosterone Antagonists
Prevents aldosterone & blocks production of ENaC channel, Na/K ATPase and K channel→ ↑Na resportion→ ↑K+ excretion
Vasopressin (ADH) Antagonists
Block V2 receptor → block aquaporins→ ↓ water resorption
Captopril
Block conversion of ang I to ang II → ↓ preload by ↓ vasoconstriction
↓aldosterone stimulation → ↓ preload
Enalapril
Block conversion of ang I to ang II → ↓ preload by ↓ vasoconstriction
↓aldosterone stimulation → ↓ preload
ARBs
Blocks after ang II so no cough but still ↓afterload by ↓ vasoconstriction
Ivabradine
↓ HR
Blocks Na funny current in SA node which determines HR and ↓ leak
Isosorbide
Releases organic nitrates→release of NO→ ↑cGMP→ uphosphorylated Myosin LC→ vasodilation
Dinitrate/hydralazine
Dilates arterioles → ↓ afterload
Ivabradine
↓ HR
Blocks Na funny current in SA node which determines HR and ↓ leak
Isosorbide
Releases organic nitrates→release of NO→ ↑cGMP→ uphosphorylated Myosin LC→ vasodilation
Dinitrate/hydralazine
Dilates arterioles → ↓ afterload
Milirinone
Myocardium: Blocks cAMP destruction → ↑ Ca⁺⁺ levels → ↑ contraction
Also affects arterioles → MLCK inactivated → relaxation→ ↓ afterload
Digoxin
Blocks Na⁺/K⁺ ATPase → ↓ Na⁺ outside the cell → ↓ driving force → ↑ Ca⁺⁺ inside cell → ↑ contractility