1/120
Asthma drugs, antihistamines, antianginals, nutraceuticals (only red text), diuretics, antihypertensives
Name | Mastery | Learn | Test | Matching | Spaced |
---|
No study sessions yet.
Acetazolamide
Diuretics
Carbonic Anyhydrase Inhibitor - block reabsorption of HCO3-
*PROTOTYPE OF THIS CLASS
Brinzolamide
Diuretics
Carbonic Anyhydrase Inhibitor - block reabsorption of HCO3-
Dorzolamide
Diuretics
Carbonic Anyhydrase Inhibitor - block reabsorption of HCO3-
Dichlorphenamide
Diuretics
Carbonic Anyhydrase Inhibitor - block reabsorption of HCO3-
Furosemide
Diuretics
Loop Diuretic - inhibit NaCl resabsorption in TAL
Butametanide
Diuretics
Loop Diuretic - inhibit NaCl resabsorption in TAL
Torsemide
Diuretics
Loop Diuretic - inhibit NaCl resabsorption in TAL
Vasopressin
Desmopressin
Diuretics
ADH Agonists
Lithium
Diuretics
ADH Antagonist - Inhibit effect of ADH by blocking the making of porins
Demeclocycline
Diuretics
ADH Antagonist - Inhibit effect of ADH by blocking the making of porins
Conivaptan
Diuretics
ADH Antagonist - Inhibit effect of ADH by blocking the making of porins
Tolvaptan
Diuretics
ADH Antagonist - Inhibit effect of ADH by blocking the making of porins
Bendroflumethiazide
Diuretics
Thiazides - Inhibit NaCL transport in DCT
Chlorothiazide
Diuretics
Thiazides - Inhibit NaCL transport in DCT
Hydrochlorothiazide
Diuretics
Thiazides - Inhibit NaCL transport in DCT
Hydroflumethiazide
Diuretics
Thiazides - Inhibit NaCL transport in DCT
Methyclothiazide
Diuretics
Thiazides - Inhibit NaCL transport in DCT
Polythiazide
Diuretics
Thiazides - Inhibit NaCL transport in DCT
Trichlormethiazide
Diuretics
Thiazides - Inhibit NaCL transport in DCT
Chlorthialidone
Indapamide
Metolazone
Quinethazone
Diuretics
Sulfonamides similar to Thiazides
Spironolactone
Diuretics
K+ Sparing Diuretic - Aldosterone antagonist (STEROID)- will cause inhibition of Na/K ATPase activity
Eplerenone
Diuretics
K+ Sparing Diuretic - Aldosterone antagonist (STEROID)- will cause inhibition of Na/K ATPase activity
Finerenone
Diuretics
K+ Sparing Diuretic - Aldosterone antagonist (STEROID) - will cause inhibition of Na/K ATPase activity
Amiloride
Diuretics
K+ Sparing Diuretic - Na+ channel blocker (NON-STEROID) - will directly inhibit Na+ channels (coupled to K+ secretion)
Triamterene
Diuretics
K+ Sparing Diuretic - Na+ channel blocker (NON-STEROID) - will directly inhibit Na+ channels (coupled to K+ secretion)
Mannitol
Diuretics
Osmotic Diuretics - enhance water excretion in water-permeable segements (PCT and descending limb)
Canagliflozin
Diuretics
SGLT2 Inhibitors - inhibit SGLT2 transporter, interrupting reabsorption of glucose in PCT
Dapagliflozin
Diuretics
SGLT2 Inhibitors - inhibit SGLT2 transporter, interrupting reabsorption of glucose in PCT
Empagliflozin
Diuretics
SGLT2 Inhibitors - inhibit SGLT2 transporter, interrupting reabsorption of glucose in PCT
Caffeine
Diuretics
A1 Antagonist - will interefere with activation of NHE3 in PCT, blocking adenosine-mediated enhancement of K+ secretion in collecting tubule
Asthma Drugs - Bronchodilators
Methylxantine - PDE inhibitor (increased cAMP and cGMP) and adenosine receptor antagonist (SM relaxation)
Theophylline
Diuretics
A1 Antagonist - will interefere with activation of NHE3 in PCT, blocking adenosine-mediated enhancement of K+ secretion in collecting tubule
Asthma Drugs - Bronchodilators
Methylxantine - nonselective PDE 3,4,5 inhibitor, will increase cAMP levels in all cells
Epinephrine
Ephedrine
Asthma Drugs - Bronchodilators
Sympathomimetics - increase release of NE
Albuterol
Asthma Drugs - Bronchodilators
Beta-2 Selective Agonists - increased intracellular cAMP and subsequent smooth muscle relaxation
L-Albuterol
Asthma Drugs - Bronchodilators
Beta-2 Selective Agonists - increased intracellular cAMP and subsequent smooth muscle relaxation
Metaproterenol
Asthma Drugs - Bronchodilators
Beta-2 Selective Agonists - increased intracellular cAMP and subsequent smooth muscle relaxation
Terbutaline
Asthma Drugs - Bronchodilators
Beta-2 Selective Agonists - increased intracellular cAMP and subsequent smooth muscle relaxation
Pirbuterol
Asthma Drugs - Bronchodilators
Beta-2 Selective Agonists - increased intracellular cAMP and subsequent smooth muscle relaxation
Salmeterol
Asthma Drugs - Bronchodilators
Beta-2 Selective Agonists - increased intracellular cAMP and subsequent smooth muscle relaxation
Formoterol
Asthma Drugs - Bronchodilators
Beta-2 Selective Agonists - increased intracellular cAMP and subsequent smooth muscle relaxation
Theobromine
Asthma Drug - Bronchodilators
Methylxantine - PDE inhibitor (increased cAMP and cGMP) and adenosine receptor antagonist (SM relaxation)
Ipratropium
Asthma Drugs - Bronchodilators
Muscarinic Antagonist - blocks P-ANS bronchoconstriction and mucus release
Tiotropium
Asthma Drugs - Bronchodilators
Muscarinic Antagonist - blocks P-ANS bronchoconstriction and mucus release
Beclomethasone
Asthma Drugs - Anti-inflammatories
Glucocorticoids - Activate steroid receptor, repress gene expression of pro-inflammatory proteins, and promote expression of anti-inflammatory proteins
Triamcinolone
Asthma Drugs - Anti-inflammatories
Glucocorticoids - Activate steroid receptor, repress gene expression of pro-inflammatory proteins, and promote expression of anti-inflammatory proteins
Flunisolide
Asthma Drugs - Anti-inflammatories
Glucocorticoids - Activate steroid receptor, repress gene expression of pro-inflammatory proteins, and promote expression of anti-inflammatory proteins
Budesonide
Asthma Drugs - Anti-inflammatories
Glucocorticoids - Activate steroid receptor, repress gene expression of pro-inflammatory proteins, and promote expression of anti-inflammatory proteins
Flunisolide
Asthma Drugs - Anti-inflammatories
Glucocorticoids - Activate steroid receptor, repress gene expression of pro-inflammatory proteins, and promote expression of anti-inflammatory proteins
Zileuton
Asthma Drugs - Anti-inflammatories
Leukotriene Inhibitors - 5-lipoxygenase inhibitor, will decrease leukotriene production
Zafirlukast
Asthma Drugs - Anti-inflammatories
Leukotriene Inhibitors - LTD4 receptor antagonist (prevents leukotriene-induced bronchoconstriction)
Montelukast
Asthma Drugs - Anti-inflammatories
Leukotriene Inhibitors - LTD4 receptor antagonist (prevents leukotriene-induced bronchoconstriction)
Nedocromil
Asthma Drugs - Anti-inflammatories
Chromones - Alter Cl- function, reducing mast cell degranulation and nerve conduction in lungs mediating cough
Cromolyn
Asthma Drugs - Anti-inflammatories
Chromones - Alter Cl- function, reducing mast cell degranulation and nerve conduction in lungs mediating cough
Omalizumab
Asthma Drugs - Anti-inflammatories
Anti-IgE - Lower IgE levels
Diphenhydramine
Antihistamines
H1 Antagonist - 1st Gen; anti-motion sickness
Doxylamine
Antihistamines
H1 Antagonist - 1st Gen; Sleep aid
Hydroxyzine
Antihistamines
H1 Antagonist - 1st Gen
Chlorpheniramine
Antihistamines
H1 Antagonist - 1st Gen; OTC “cold” medicine
Astemizole
Antihistamines
H1 Antagonist - 2nd Gen; less CNS penetration, longer lasting due to active metabolites
Fexofenadine
Antihistamines
H1 Antagonist - 2nd Gen; less CNS penetration, longer lasting due to active metabolites
Loratadine
Antihistamines
H1 Antagonist - 2nd Gen; less CNS penetration, longer lasting due to active metabolites
Cetirizine
Antihistamines
H1 Antagonist - 2nd Gen; less CNS penetration, longer lasting due to active metabolites
Methyldopa
Antihypertensives - Sympathoplegics
CNS-Acting: Alpha 2 Agonists - can be converted to active products in nerves
Clonidine
Antihypertensives - Sympathoplegics
CNS-Acting: Alpha 2 Agonists
Prazosin
Antihypertensives - Sympathoplegics
Alpha 1 Blockers - will inhibit ligand binding, causing vascular SM relaxation
Terazosin
Antihypertensives - Sympathoplegics
Alpha 1 Blockers - will inhibit ligand binding, causing vascular SM relaxation
Doxazosin
Antihypertensives - Sympathoplegics
Alpha 1 Blockers - will inhibit ligand binding, causing vascular SM relaxation
Propranolol
Antihypertensives - Sympathoplegics
Beta Blockers - nonspecific beta antagonist, will cause decrease CO and renin release
Antianginals
Beta Blockers - Nonselective beta antagonist
Metaprolol
Atenolol
Nadolol
Antihypertensives - Sympathoplegics
Beta Blockers - Beta 1 selective antagonist
Antianginals
Beta Blockers - Beta 1 selective antagonist
Hydralazine
Antihypertensives - Direct Acting Vasodilators
Dilate arteries (not veins)
Minoxidil
Antihypertensives - Direct Acting Vasodilators
Dilate arteries (not veins), opens SM membrane K+ channels causing depolarization of SM
Diazoxide
Antihypertensives - Direct Acting Vasodilators
Increase K+ conductance, preventing SM contraction
Nitroprusside
Antihypertensives - Direct Acting Vasodilators
NO release and activation of guanylyl cyclase
Fenoldopam
Antihypertensives - Direct Acting Vasodilators
D1 Agonist
Amlodipine
Antihypertensives - Direct Acting Vasodilators
Calcium Channel Blockers (Dihydropyridines) - blockade of open Ca2+ channels located on SM, reduce myocardial oxygen requirement
Antianginals
CCB: Dihydropyridines
Felodipine
Antihypertensives - Direct Acting Vasodilators
Calcium Channel Blockers (Dihydropyridines) - blockade of open Ca2+ channels located on SM, reduce myocardial oxygen requirement
Antianginals
CCB: Dihydropyridines
Nimodipine
Antihypertensives - Direct Acting Vasodilators
Calcium Channel Blockers (Dihydropyridines) - blockade of open Ca2+ channels located on SM, reduce myocardial oxygen requirement
Antianginals
CCB: Dihydropyridines
Verapamil
Antihypertensives - Direct Acting Vasodilators
Calcium Channel Blockers (Non-dihydropyridines) - blockade of open Ca2+ channels located on SM, reduce myocardial oxygen requirement + decrease contraction, conduction velocity and rate
Antianginals
CCB: Non-dihydropyridines
Diltiazem
Antihypertensives - Direct Acting Vasodilators
Calcium Channel Blockers (Non-dihydropyridines) - blockade of open Ca2+ channels located on SM, reduce myocardial oxygen requirement + decrease contraction, conduction velocity and rate
Antianginals
CCB: Non-dihydropyridines
Captopril
Antihypertensives - Angiotensin Production or Receptor Blockers
ACE Inhibitors - prevent binding of angiotensin I and cleavage to angiotensin II; also prevent degradation of bradykinin
Lisinopril
Antihypertensives - Angiotensin Production or Receptor Blockers
ACE Inhibitors - prevent binding of angiotensin I and cleavage to angiotensin II; also prevent degradation of bradykinin
Benazepril
Antihypertensives - Angiotensin Production or Receptor Blockers
ACE Inhibitors - prevent binding of angiotensin I and cleavage to angiotensin II; also prevent degradation of bradykinin
Fosinopril
Antihypertensives - Angiotensin Production or Receptor Blockers
ACE Inhibitors - prevent binding of angiotensin I and cleavage to angiotensin II; also prevent degradation of bradykinin
Moexipril
Antihypertensives - Angiotensin Production or Receptor Blockers
ACE Inhibitors - prevent binding of angiotensin I and cleavage to angiotensin II; also prevent degradation of bradykinin
Perindopril
Antihypertensives - Angiotensin Production or Receptor Blockers
ACE Inhibitors - prevent binding of angiotensin I and cleavage to angiotensin II; also prevent degradation of bradykinin
Quinapril
Antihypertensives - Angiotensin Production or Receptor Blockers
ACE Inhibitors - prevent binding of angiotensin I and cleavage to angiotensin II; also prevent degradation of bradykinin
Ramipril
Antihypertensives - Angiotensin Production or Receptor Blockers
ACE Inhibitors - prevent binding of angiotensin I and cleavage to angiotensin II; also prevent degradation of bradykinin
Trandopril
Antihypertensives - Angiotensin Production or Receptor Blockers
ACE Inhibitors - prevent binding of angiotensin I and cleavage to angiotensin II; also prevent degradation of bradykinin
Losartan
Antihypertensives - Angiotensin Production or Receptor Blockers
Angiotensin II Receptor Antagonists (ARBs) - block AT1 receptors, prevent angiotensin II from binding and activating (no bradykinin accumulation)
Valsartan
Antihypertensives - Angiotensin Production or Receptor Blockers
Angiotensin II Receptor Antagonists (ARBs) - block AT1 receptors, prevent angiotensin II from binding and activating (no bradykinin accumulation)
Candesartan
Antihypertensives - Angiotensin Production or Receptor Blockers
Angiotensin II Receptor Antagonists (ARBs) - block AT1 receptors, prevent angiotensin II from binding and activating (no bradykinin accumulation)
Eprosartan
Antihypertensives - Angiotensin Production or Receptor Blockers
Angiotensin II Receptor Antagonists (ARBs) - block AT1 receptors, prevent angiotensin II from binding and activating (no bradykinin accumulation)
Telmisartan
Antihypertensives - Angiotensin Production or Receptor Blockers
Angiotensin II Receptor Antagonists (ARBs) - block AT1 receptors, prevent angiotensin II from binding and activating (no bradykinin accumulation)
Olmisartan
Antihypertensives - Angiotensin Production or Receptor Blockers
Angiotensin II Receptor Antagonists (ARBs) - block AT1 receptors, prevent angiotensin II from binding and activating (no bradykinin accumulation)
Valsartan
Antihypertensives - Angiotensin Production or Receptor Blockers
Angiotensin II Receptor Antagonists (ARBs) - block AT1 receptors, prevent angiotensin II from binding and activating (no bradykinin accumulation)
Nifedipine
Antianginals
Calcium Channel Blockers (Dihydropyridines) - blockade of open Ca2+ channels located on SM, reduce myocardial oxygen requirement
Isradipine
Antianginals
Calcium Channel Blockers (Dihydropyridines) - blockade of open Ca2+ channels located on SM, reduce myocardial oxygen requirement
Nicardipine
Antianginals
Calcium Channel Blockers (Dihydropyridines) - blockade of open Ca2+ channels located on SM, reduce myocardial oxygen requirement
Nisoldipine
Antianginals
Calcium Channel Blockers (Dihydropyridines) - blockade of open Ca2+ channels located on SM, reduce myocardial oxygen requirement
Bepridil
Antianginals
Calcium Channel Blockers (Non-dihydropyridines) - blockade of open Ca2+ channels located on SM, reduce myocardial oxygen requirement + decrease contraction, conduction velocity and rate
Nitroglycerin
Antianginals
NO Donors - stimulate GC to cause cGMP-induced SM relaxation via dephosphorylation of MLC = vasodilation of veins and arteries, reducing myocardial oxygen requirement