ALL cards Flashcards

Question

Answer 1

Alpha 1 agonist

Answer 2

Alpha 2 agonist

Answer 3

Alpha 2 Agonist

Answer 4

Alpha 2 agonist

Answer 5

Alpha 2 agonist

Answer 6

Alpha 2 agonist

Answer 7

Alpha 2 agonist

Answer 8

Methyldopa alpha 2 agonist prodrug Metabolized into Methylnorepinephrine

Answer 9

Beta 1 agonist dopamine short acting easily metabolized by COMT and MAO

Answer 10

Dobutamine Methyl group can change selectivity and function

Answer 11

Beta 2 Agonist Albuterol

Answer 12

Beta 2 agonist

Answer 13

Beta 2 agonist

Answer 14

Beta 2 agonist

Answer 15

Beta 2 agonist

Answer 16

Salmeterol Beta 2 agonist super long chain

Answer 17

Beta 2 agonist

Answer 18

Beta 2 agonist

Answer 19

beta 2 agonist

Answer 20

Causes release of NE

Answer 21

Causes release of NE

Answer 22

Causes release of NE

Answer 23

Amphetamine causes release of NE

Answer 24

meth Releas NE

Answer 25

Release NE

Answer 26

Release NE

Answer 27

Release NE

Answer 28

Some what selective for alpha Covalent bond causes it to be an irreversible antagonist

Answer 29

Non selective antagonist

Answer 30

Alpha 1 antagonist

Answer 31

Alpha 1 antagonist

Answer 32

Alpha 1 Antagonist

Answer 33

Alpha 1 antagonist

Answer 34

Alpha 1 antagonist

Answer 35

Nonselective B antagonist

Answer 36

Nonselective B antagonist

Answer 37

Proptanolol Nonselective B antagonist

Answer 38

B1 antagonist

Answer 39

B1 antagonist

Answer 40

B1 antagonist

Answer 41

Carbidopa Inhibitor of AAD

Answer 42

Talcapone COMT I Nitro group with catechol system

Answer 43

Propargel group MAO I irreversible

Answer 44

Dopamine agonist Emetic Dopamine in locked conformation Previagra Apomorphine

Answer 45

D1-Excitatory decreased D2- Inhibitory increased

Answer 46

Compounds indicated in neuronal cell death

Answer 47

L-dopa (BBB+) MAO Dopamine (BBB-)

Answer 48

It is actively transported and the presence of both the Amino and Carboxylic acid group forms a zwitter ion and cause less unionizable things

Answer 49

Nigrostriatal cell death

Answer 50

Locked into trans alpha rotamer which is favorable to the receptor

Answer 51

Carbidopa Aromatic AA Decarboxylase Inhibitor and COMPT

Answer 52

Dose related dyskinesia (Impairement of voluntary movement) Pathological gambling CNS effects simialr to Schizo

Answer 53

Short T1/2 and should be taken with every dose of L-dopa

Answer 54

DA releaser ClogP = 2.0

Answer 55

Ctriple bond CH Irreversible inhibitor of MAO-B

Answer 56

Fewer adverse effects compared to L-deprenyl (Selegiline)

Answer 57

Reersible and selective MAO-B I

Answer 58

Can lower required dose of l-dopa Locked confomer of DA S-enatiomer has post synaptic D2 antagonism

Answer 59

Help reduce drooling and tremors

Answer 60

Longer acting tropone ring

Answer 61

* Irreversible MAO- Inhibitor * Triangle banana bond give it the irreversible nature * More likely to have toxic effects due to the covalent bond that is formed

Answer 62

* TCA * inhibits reuptake of S \> NE * more orthostatic hypotension than amitriptyline * Dealkylation will give active metabolites * Tertiary \> Anticholinergic SEs, But less than amitriptyline

Answer 63

* SSRI * 2D6 * Dont use with TCAs or MAOIs

Answer 64

* NMDA antagonist * Known to be faster acting compared to SSRIs and SNRIs this can be benficial because they take so long to take effect

Answer 65

* SNRI * Can be used to treat: * Diabetic Nueropathy * pain control in fibromyalgia * Chronic musculoskeletal pain

Answer 66

* Irreversible non-selective MAO I * Hydrazine group present

Answer 67

* Irreversible MAO I

Answer 68

* Irreversible non selective MAO I

Answer 69

* Reversible MAO-A Inhibitor * Less toxic effects compared to irreversible

Answer 70

* Reversible MAO-A Inhibitor * Less toxic effects compared to irreversible

Answer 71

* TCA * Activity more at NE

Answer 72

* Inhibits reuptake of both NE and S * Alkylation on the 3 carbon provides less anticholinergic SEs

Answer 73

* Mainly inhibits 5HT reuptake

Answer 74

* S\>NE * TCA * Does not contain a Nitrogen in ring instead has a C=C these have the same geometry though so they can be interchanged but steriochemistry becomes important

Answer 75

* TCA * S and NE equally

Answer 76

* TCA * NE more * C=C possible epoxidation

Answer 77

* TCA * NE and S * Used topically as H1 antagonist

Answer 78

* EPS * TCA * 51C - 2 and 3 * Similar to desipramine * Metabolite of Loxapine

Answer 79

* EPS * TCA * 51C - 2 and 3 * Similar to desipramine * Metabolite of Loxapine

Answer 80

* phenylpiperazine * 5HT uptake inhibitor * 5HT2A antagonist * Sedation * Piperazine with phenyl CL gives serotonin activity

Answer 81

* Phenylpiperazine * 5HT uptake inhibition * Some NE uptake inhibition * 5HT2 antagonist * Less sedation compared to TCAs and Trazodone

Answer 82

* Phenylethylamines * Weak dopamine uptake inhibitor * Very weak NE and S uptake inhibitor * Looks like amphetamine so the dopamine part makes sense * Less Sexual AEs

Answer 83

* SNRI * Contains chiral center

Answer 84

* NE/S reuptake inhibitor * a1 and H1 antagonist * 5HT2 and 3 not 1

Answer 85

* NE/S reuptake inhibitor * Low anticholinergic, sedation, and orthostatic hypo

Answer 86

* NE/S reuptake inhibitor * Low anticholinergic, sedation, and orthostatic hypo

Answer 87

* SSRI * less 2D6 so less interactions

Answer 88

* SSRI * methylenedioxy ring---\> more toxic * Michael acceptor * Quinone formation from methylene

Answer 89

* SSRI * QT prolongation * Escitalopram is the S-enantiomer less prolongation

Answer 90

* Agonist at 5 HT 1A partial * SSRI

Answer 91

* SSRI * active at many receptors * antagonist at: HT1D, HT3, HT7 * Steric hinderance of ring decreases rate of metabolism

Answer 92

* NE and dopamine reuptake inhibitor

Answer 93

* NE and dopamine reuptake inhibitor

Answer 94

* SSRI * active at many receptors * antagonist at: HT1D, HT3, HT7 * Steric hinderance of ring decreases rate of metabolism

Answer 95

* Agonist at 5 HT 1A partial * SSRI

Answer 96

* SSRI * QT prolongation * Escitalopram is the S-enantiomer less prolongation

Answer 97

* SSRI * methylenedioxy ring---\> more toxic * Michael acceptor * Quinone formation from methylene

Answer 98

* SSRI * less 2D6 so less interactions

Answer 99

* NE/S reuptake inhibitor * a1 and H1 antagonist * 5HT2 and 3 not 1

Answer 100

* SNRI * Contains chiral center

Answer 101

* Phenylethylamines * Weak dopamine uptake inhibitor * Very weak NE and S uptake inhibitor * Looks like amphetamine so the dopamine part makes sense * Less Sexual AEs

Answer 102

* Phenylpiperazine * 5HT uptake inhibition * Some NE uptake inhibition * 5HT2 antagonist * Less sedation compared to TCAs and Trazodone

Answer 103

* phenylpiperazine * 5HT uptake inhibitor * 5HT2A antagonist * Sedation * Piperazine with phenyl CL gives serotonin activity

Answer 104

* TCA * NE and S * Used topically as H1 antagonist

Answer 105

* TCA * NE more * C=C possible epoxidation

Answer 106

* TCA * S and NE equally

Answer 107

* S\>NE * TCA * Does not contain a Nitrogen in ring instead has a C=C these have the same geometry though so they can be interchanged but steriochemistry becomes important

Answer 108

* Mainly inhibits 5HT reuptake

Answer 109

* Inhibits reuptake of both NE and S * Alkylation on the 3 carbon provides less anticholinergic SEs

Answer 110

* TCA * Activity more at NE

Answer 111

* Irreversible non selective MAO I

Answer 112

* Irreversible MAO I

Answer 113

* Irreversible non-selective MAO I * Hydrazine group present

Answer 114

* SNRI * Can be used to treat: * Diabetic Nueropathy * pain control in fibromyalgia * Chronic musculoskeletal pain

Answer 115

* NMDA antagonist * Known to be faster acting compared to SSRIs and SNRIs this can be benficial because they take so long to take effect

Answer 116

* SSRI * 2D6 * Dont use with TCAs or MAOIs

Answer 117

* TCA * inhibits reuptake of S \> NE * more orthostatic hypotension than amitriptyline * Dealkylation will give active metabolites * Tertiary \> Anticholinergic SEs, But less than amitriptyline

Answer 118

* Irreversible MAO- Inhibitor * Triangle banana bond give it the irreversible nature * More likely to have toxic effects due to the covalent bond that is formed

Answer 119

* Tertiary S \> NE * Secondary NE \> S

Answer 120

* Tertiary S \> NE * Secondary NE \> S

Answer 121

* Tertiary * S reuptake \> NE reuptake * More orthostatic hypotension than secondary * Generally more anticholinergic SEs * Secondary * NE reuptake \> S * less sedation compared to tertiaty * 3 carbons between tricyclic ring system and amine * **Halogen** on tricyclic system increases affinity for 5-HT transporter

Answer 122

* Tertiary * S reuptake \> NE reuptake * More orthostatic hypotension than secondary * Generally more anticholinergic SEs * Secondary * NE reuptake \> S * less sedation compared to tertiaty * 3 carbons between tricyclic ring system and amine * **Halogen** on tricyclic system increases affinity for 5-HT transporter

Answer 123

* Less cardiavascular toxicity than TCAs * Less sedation * Lower toxicity in OD compared to MAOIs and TCAs * AEs: Anxiety, sexaul dysfunction, nausea

Answer 124

* Less cardiavascular toxicity than TCAs * Less sedation * Lower toxicity in OD compared to MAOIs and TCAs * AEs: Anxiety, sexaul dysfunction, nausea

Answer 125

* Na+/KATPase Phase 4 * Contain a carbohydrate and a steriodal group

Answer 126

PDE- block cAMP --\> AMP B-adrenergic increase cAMP

Answer 127

Inamrinone is longer acting - inhibition of PDE Milrinon- Greater selectivity Dose adjustment in renal impairment

Answer 128

Dopamine analog, B1 agonist Active only with IV Short half life

Answer 129

Organic nitrates CCBs B BLOCKERs

Answer 130

* From L-arginine * NOS * Guanidine H bonding and Ionic * Stimulates cGMP

Answer 131

decreases myocardial workload this is very reactive Causes reduced O demand

Answer 132

Ester, Inhalation Fastest acting in class Short duration

Answer 133

Sublingual - most useful Prophylactic and acute pain Rapid onset not as fast at Amyl

Answer 134

Sub, chew, SR Slowest onset but longest DOA Metabolite 5-isosorbide mononitrate is active

Answer 135

INteraction with other vasodilators, alcohol Avoid Viagra fall Bp

Answer 136

Dihydropyridine Benxothiapine Aralkylamine CCBS inhibit Ca influx negative inotropic effects, vasodilation, Smooth muscle

Answer 137

Dihydropyridine Peripheral vasodilation Protein bound Inactive metabolites in urine

Answer 138

Dihydropyridine Selective for vascualr SM vs Myocardial Long DOA Inactive metabolites, Urine

Answer 139

Dihydromoeity essential Aromatic ring with ortho or meta required Ester functional group Can increase potency (amlodipine) Free NH at one position is REQUIRED

Answer 140

Dihydropyridine IV Fast short acting shortest of ester inactive

Answer 141

Chronic liver disease Grapefruit Azole fungal and CYp3A4 Displacement of protein binding with other drugs that protein bind

Answer 142

Benzothiazepine Somea activity with the weird one O and N inactive

Answer 143

* Phenylalkylamine * Ca2+ antagonist * Intry into Myocardial * CYP3A4 interaction * increase verapamil * Brady, Hypo, Edema

Answer 144

* 1 Membrane depressant, act on fast Na+ channels prevent conductance * B blockers * Repolarization prolongers blocking K+ * CCBS inward slow Ca2+

Answer 145

Quinidine, Procainamide, Disopyramide Quinide Phase 0 depol

Answer 146

Tubular excretion of DIgoxin leading to toxic Substrate for CYP3A4 unchanges urine

Answer 147

Dihydroquinidine more potent but toxic

Answer 148

analog of procain Ventricular arrythmias N-acetyl procainamide is active Unchanges in urine 50% Leukopenia and agranulocytosis

Answer 149

Cardiac activity like procainamide weak Anticholinergic AE- Anticholinergic SEs

Answer 150

Quinidine, Procainamide, Disopyramide Phase 0 depol

Answer 151

Tubular excretion of DIgoxin leading to toxic Substrate for CYP3A4 unchanges urine

Answer 152

analog of procain Ventricular arrythmias N-acetyl procainamide is active Unchanges in urine 50% Leukopenia and agranulocytosis

Answer 153

* Rapid rate of dissociation from Na+-ion channels. Shortens ‘Phase 3’ repolarization and action potential duration. Drug examples include: Lidocaine, and Phenytoin etc.

Answer 154

* Synthetic drug. An amide analog of the local anesthetic Procaine (example of bioisosteric drug design principle!) * Orally bioavailable. Parenteral (IV and IM) formulation also available. * Indicated for the treatment of ventricular arrythmias * Hepatic metabolism. Metabolites include N-acetyl procainamide (active) and p-aminobenzoic acid. Renal excretion of unchanged drug (~50%) and the metabolites. * Might require dose adjustment in hepatic and renal impaired patients * SEs- Drug induced lupus syndrome. Can also cause (0.5%) serious hematological disorders, particularly leukopenia and agranulocytosis.

Answer 155

* Synthetic drug. Cardiac activity similar to Procainamide, Also exhibit weak anticholinergic activity. * Good oral availability. T1/2= 5-7 hr. * Partially metabolized in liver (CYP3A4), mostly to a mono-N-dealkylated product. Renal excretion of unchanged drug (~50%) and metabolites. * Dose adjustment might be required in patients with liver/renal impairment * SEs- are primarily related to anticholinergic activities of the drug, and can include dry mouth, blurry vision, constipation, and urinary retention.

Answer 156

* Original use as a local anesthetic (Procaine-like). * Drug of choice for emergency treatment of ventricular arrythmia (IV). Also used parenterally for suppression of arrythmias associated with acute myo cardial infraction and cardiac surgery. * Rapid onset (1-2 min) and short duration of action (T1/2 = \< 30 min). * Liver metabolized (N-Deethylation and amidase hydrolysis). Renal excretion. * SEs- Dizziness, paresthesis and seizure in severe cases.

Answer 157

* Structurally analogous to barbiturates, but does not possess sedative properties. * Long history of use for the treatment of epileptic seizures. * Useful antiarrythmic agent for the treatment of digitalis induced arrythmias. * Orally active. Also available for parenteral (IV) use. * High plasma protein binding (~ 90%). T1/2 = 15 -30 hrs. * Slow hepatic (CYP450) metabolism to mono-p-hydroxyphenyl derivative, followed by glucuronide conjugation and excretion in urine. * Prevention of metabolism, or the presence of other plasma protein bound drugs can cause toxicity.

Answer 158

* Potent antiarrythmic drug with local anesthetic activity. * Orally administered for the treatment of ventricular arrythmias. * Plasma half-life ~14 hrs. * Part of the drug (~50%) is metabolized in liver (CYP2D6). Metabolism involves m-O-dealkylation. Urinary excretion of unchanged drug and the metabolites. * New or worsened arrythmias have been reported with the use of this drug. * Other adverse effects: Dizziness, blurred vision, nausea, and headache etc.

Answer 159

* Structural resemblance to class 1C antiarryhmics, as well as β-blockers * Used primarily for ventricular and supraventricular arrythmias * Oral drug. Metabolized in liver (CYP2D6; CYP3A4; CYP1A2). Dose adjustment might be required with simultaneous use of other drugs interacting with the above metabolic enzymes. * New or worsened arrythmias have been reported with the use of this drug. * Other adverse effects: Agranulocytosis, taste disturbance, dizziness, nausea, and constipation etc.

Answer 160

β-Adneregic blockers. Suppresses sympathomimetic activity. Slows ‘Phase 4’ depolarization. Propranolol

Answer 161

* K+-ion channel blockers. Prolongs ‘Phase 3’ repolarization and duration of action potential. * A quaternary ammonium salt. Originally developed as an antihypertensive. * Use limited for the treatment of emergency life threatening ventricular arrythmias resistant to other therapy. * Usually administered iv or im. * Adverse Effects : Hypotension (most common), nausea, and dizziness etc.

Answer 162

* Antiarrythmic effects similar to Bretylium. Approved for the treatment of life-threatening ventricular arrythmias refractory to other drugs. * Oral and parenteral formulations. Long half-life (several weeks) * Hepatic metabolism involving N-deethylation (active metabolite). * Severe toxicity limits the use of this drug (used in hospital setting only)

Answer 163

* Used orally for tachyarrythmias (esp. AF). T1/2 ~ 10 hr. * Due to the pro-arrhythmic potential of dofetilide, to be prescribe by physicians who have undergone specific training in the risks of treatment with dofetilide. * Hepatic metabolism (20%). Metabolites and unchanged drug excreted in urine. Dose adjustment in renal impairment. * Adverse effects: Induced arrythmia, headache, dizziness, nausea, rash, flu-like syndrome etc.

Answer 164

* Slows rate of dissociation from Na+-ion channels. Markedly slow ‘Phase 0’ depolarization * Flecainide, Propafenone

Answer 165

* Ca2+-ion channel blockers. Slows ‘Phase 4’ depolarization and duration. * Prototypical drug examples are Verapamil, and Diltiazem etc.

Answer 166

1. Agents which increase the rate of urine formation. 2. Diuretic usage leads to increased excretion of electrolytes (especially Na+ and Cl- ions) and water. 3. Useful in the treatment of edematous conditions caused by congestive heart failure, nephritic syndrome, chronic liver disease etc., and in the management of hypertension. 4. Diuretics are also used as the sole agent or as adjunctive therapy in the treatment of glaucoma, hypercalcemia, mountain sickness etc. 5. The primary site of action for the diuretics is the kidney, where these drugs interfere with the reabsorption of sodium and other ions.

Answer 167

* 120 * 1-2% * 98%

Answer 168

* Chemical Class (eg. thiazides); * Mechanism of Action (eg. Carbonic Anhydrase Inhibitors); * Site of Action within the nephron (eg. Loop Diuretics); * Effects on Urine contents (Potassium- Sparing Diuretics) etc.

Answer 169

* Low molecular weight compounds * Passively filtered through Bowman’s capsule into renal tubule. * Limited reabsorption. * Undergoes negligible metabolism * Forms hypertonic solution, causing water to secrete into renal tubule, producing a diuretic effect

Answer 170

Proximal Tubule; Loop of Henle; Collecting Tubule

Answer 171

1. Agents which increase the rate of urine formation. 2. Diuretic usage leads to increased excretion of electrolytes (especially Na+ and Cl- ions) and water. 3. Useful in the treatment of edematous conditions caused by congestive heart failure, nephritic syndrome, chronic liver disease etc., and in the management of hypertension. 4. Diuretics are also used as the sole agent or as adjunctive therapy in the treatment of glaucoma, hypercalcemia, mountain sickness etc. 5. The primary site of action for the diuretics is the kidney, where these drugs interfere with the reabsorption of sodium and other ions.

Answer 172

* 120 * 1-2% * 98%

Answer 173

* Chemical Class (eg. thiazides); * Mechanism of Action (eg. Carbonic Anhydrase Inhibitors); * Site of Action within the nephron (eg. Loop Diuretics); * Effects on Urine contents (Potassium- Sparing Diuretics) etc.

Answer 174

* Low molecular weight compounds * Passively filtered through Bowman’s capsule into renal tubule. * Limited reabsorption. * Undergoes negligible metabolism * Forms hypertonic solution, causing water to secrete into renal tubule, producing a diuretic effect

Answer 175

Proximal Tubule; Loop of Henle; Collecting Tubule

Answer 176

* Isosorbide greater absorption longer t half * Mannitol greater DOA * Not a frequently used class of diuretics in current practice, except in the prophylaxis of acute renal failure to inhibit water reabsorption and maintain urine flow. * Mannitol is the agent most commonly used as an osmotic diuretic. * Administered as an intravenous solution. * Isosorbide (a bicyclic form of sorbitol!) is primarily used for the treatment of glaucoma.

Answer 177

* Carbonic anhydrase (CA), a metalloenzyme (Zn2+-ion at active site), catalyzes the formation of carbonic acid (H2CO3) from carbon dioxide and water. * At least seven CA isozymes in human, present mainly in blood cells, gastric mucosa, pancreatic cells, and renal tubules. * In the proximal tubule, promotes reabsorption of Na+ and HCO3 – ions from the glomerular filtrate, and excretion of H+ ions. (Acidic nature of urine and alkalinity of blood) * Inhibition of carbonic anhydrase induces diuresis via excretion of sodium and bicarbonate ions, and associated water molecules. * Accidental initial discovery of carbonic anhydrase inhibitory activity (in dog urine!) of Sulfanilamide, a sulfonamide antibacterial.

Answer 178

* Presence of an acidic sulfonamide group (pKa= 7–9). Free N–H required for activity. * Site of Action: Proximal Convoluted Tubule * Not very efficacious (increases renal excretion of sodium only by 2%–5%) * Limited use, mostly for the treatment of glaucoma (oral and topical formulations) * First orally effective CA inhibitor diuretic in clinical use § Diuretic effect lasts for 8 – 12 hrs § Limited use because of systemic acidosis * AEs- * Development of metabolic acidosis on prolonged use * Can cause electrolyte disturbance (hypokalemia) and renal effects (kidney stone) * Hypersensitivity reactions possible (attributable to sulfonamide group)

Answer 179

* Isosorbide greater absorption longer t half * Mannitol greater DOA * Not a frequently used class of diuretics in current practice, except in the prophylaxis of acute renal failure to inhibit water reabsorption and maintain urine flow. * Mannitol is the agent most commonly used as an osmotic diuretic. * Administered as an intravenous solution. * Isosorbide (a bicyclic form of sorbitol!) is primarily used for the treatment of glaucoma.

Answer 180

* Used in the treatment of edema caused by congestive heart failure as well as in hepatic or renal disease. Also useful in the treatment of hypertension (reduction in blood volume) * Compared to Chlorothiazide, the double bond reduced analog Hydrochlorothiazide (HCT) is more potent and has a longer half-life. * Adverse Effects: Gastric irritation, hypersensitivity, nausea, and electrolyte disturbance. Long-term use may also result in decreased glucose tolerance and increased blood lipid content (TC, LDL, TG).

Answer 181

* C7-position: Sulfonamide group is required for activity * C6-position (R1): Electron-withdrawing group (e.g. Cl, CF3 etc) required for activity * 3–4-position: Saturation of the double bond results in more potent (~ 10-fold) analogs * C3-position (R2): Lipophilic group improves diuretic potency * 2-position (R3): N-alkyl substitution increases the duration of diuretic action

Answer 182

* Contains a quinazolin-4-one structural core (ring-SO2 of thiazides replaced with a CO group) * Diuretic effects similar to the thiazide class of compounds * Orally active. Long duration of action (upto 24 hrs) * Adverse effects similar to the thiazide diuretic class

Answer 183

* Carbonic anhydrase (CA), a metalloenzyme (Zn2+-ion at active site), catalyzes the formation of carbonic acid (H2CO3) from carbon dioxide and water. * At least seven CA isozymes in human, present mainly in blood cells, gastric mucosa, pancreatic cells, and renal tubules. * In the proximal tubule, promotes reabsorption of Na+ and HCO3 – ions from the glomerular filtrate, and excretion of H+ ions. (Acidic nature of urine and alkalinity of blood) * Inhibition of carbonic anhydrase induces diuresis via excretion of sodium and bicarbonate ions, and associated water molecules. * Accidental initial discovery of carbonic anhydrase inhibitory activity (in dog urine!) of Sulfanilamide, a sulfonamide antibacterial.

Answer 184

* Contains a carboxylic acid functional group (pKa ~4) * 8 – 10 Times stronger saluretic action than the thiazides. * Causes excretion of Na+, K+, Ca2+, Mg2+, Cl- and HCO3 - ions * Orally active. Parenteral form for faster onset of action. * Extensive plasma protein binding (\> 90%). Mostly excreted unchanged (kidney). * **Uses**-Most important use in the treatment of pulmonary edema. Additional uses include, treatment of edemas associated with cardiac, hepatic and renal malfunctions. Also useful in the treatment of hypertension. * **Side-Effects**: Electrolyte Imbalance; Hyperuricemia; Gastrointestinal side-effects, and hypersensitivity etc. Can also cause ototoxicity (temporary hearing loss). This effect can be additive with concurrent usage of aminoglycoside antibiotics.

Answer 185

* Ring substitution pattern different than furosemide * Greater bioavailability than furosemide * Marked increase in diuretic potency (~ 40 times of furosemide) * Uses and side effect profile similar to furosemide

Answer 186

* Sulfonylurea side-chain instead of sulfonamide * Same site / mechanism of action as furosemide and bumetanide * Available in oral and parenteral (IV) forms * Partially metabolized by hepatic cytochrome P450 enzymes. A major metabolic route involves oxidn of the Ar-Me group to carboxylic acid. * Uses: Treatment of hypertension; Congestive heart failure and cirrhosis associated edema. * Adverse Effects : Fatigue, dizziness, muscle cramps, nausea and orthostatic hypotension.

Answer 187

* A phenoxyacetic acid derivative. Lacks a sulfonamide group. * Same site / mechanism of action as the above loop diuretics * Rapid onset (~ 30 min) and long duration of action (6 – 8 hr) * Oral and parenteral. Highly plasma protein bound (\> 95%) * Relatively less potent than the other drugs in this category. However, useful in patients who are allergic to the sulfonamides. * Adverse effects: Greater incidences of ototoxicity and more serious gastrointestinal effects

Answer 188

* Aldosterone, a steroid hormone, is secreted by the adrenal cortex, and is a potent mineral corticoid. * Acting on the distal tubule and collecting ducts of the nephron, it causes increased reabsorption of Na+ and Cl– ions and water, while increasing K+-ion ion excretion * Aldosterone action leads to increase in water retention, and increased blood pressure / volume. * The biologic effect of Aldosterone is caused by its binding to the mineralcorticoid receptor (MR), a nuclear transcription factor * Inhibition (antagonism) of aldosterone function can lead to diuresis (excretion of Na+, and Cl– ions and water) * Such inhibitors are also classified as Potassium-Sparing Diuretics

Answer 189

* A semi-synthetic drug. Prevents aldosterone binding (antagonist) to the MR in the distal convoluted tubule and the collecting system. * Causes increased amount of Na+ / water excretion, and retention of K+-ion. * Oral drug (90% availability). Undergoes significant first-pass metabolism to form Canrenone (loses Me–CO–SH), an active metabolite. Excretetion mainly in urine. * Adverse effects: Can cause hyperkalemia. Use of other K+-sparing diuretics, potassium supplements and food rich in potassium should be avoided. Anti-androgenic effects, hypersensitivity reactions, GI disturbances, and peptic ulcer have also been reported.

Answer 190

* An aldosterone antagonist. Compared to Spironolactone, lower affinity for MR, however a more selective inhibitor (does not inhibit AR, PR, and GR) * Oral drug (~70% availability). T1/2≃ 5 hr. Hepatic metabolism (CYP3A4). Metabolites inactive and excreted in urine and feces. * Adverse effects: Can cause hyperkalemia. However, unlike spironolactone, limited/fewer sexual side effects.

Answer 191

* Contains a pteridine sturctural core. * Renal epithelial Na+ channel blocker. Blocks the reabsorption of Na+ ion and prevents excretion of K+ ion in the distal tubule (but no effect on aldosterone action). * Oral drug (~70% absorption). Metabolized extensively (4’-OH analog and its sulfate conjugate). Excreted in the urine * Adverse Effects: Can cause hyperkalemia, nausea, vomiting and headache. Potassium supplements are contraindicated, and serum potassium levels should be monitored.

Answer 192

* An aminopyrazine derivative. * Renal epithelial Na+ channel blocker. Blocks the reabsorption of Na+- ion and secretion of K+-ion in DCT. No effect on aldosterone action. * Oral drug (~50% absorption). Excreted (mostly unchanged) in urine and feces. Renal impairment can increase half-life. * Adverse Effects: Similar to triamterene.

Answer 193

* Presence of an acidic sulfonamide group (pKa= 7–9). Free N–H required for activity. * Site of Action: Proximal Convoluted Tubule * Not very efficacious (increases renal excretion of sodium only by 2%–5%) * Limited use, mostly for the treatment of glaucoma (oral and topical formulations) * First orally effective CA inhibitor diuretic in clinical use § Diuretic effect lasts for 8 – 12 hrs § Limited use because of systemic acidosis * AEs- * Development of metabolic acidosis on prolonged use * Can cause electrolyte disturbance (hypokalemia) and renal effects (kidney stone) * Hypersensitivity reactions possible (attributable to sulfonamide group)

Answer 194

* Further modified sulfonamides, characterized by the presence of a benzothiadiazine 1,1-dioxide core * Weakly acidic compounds (pKa ~ 7). Actively secreted into the proximal tubule and are carried to the site of action. * **Site of Action**: Thick ascending loop of Henle and distal convoluted tubule * **Mechanism of Diuretic Action**: Binds to the Na+/Cl– symporter and inhibits the reabsorption of sodium and chloride ions (saluretic agents) * Used alone, or as add-on therapy. Rapid oral absorption. Excreted mainly unchanged (urine)

Answer 195

* Used in the treatment of edema caused by congestive heart failure as well as in hepatic or renal disease. Also useful in the treatment of hypertension (reduction in blood volume) * Compared to Chlorothiazide, the double bond reduced analog Hydrochlorothiazide (HCT) is more potent and has a longer half-life. * Adverse Effects: Gastric irritation, hypersensitivity, nausea, and electrolyte disturbance. Long-term use may also result in decreased glucose tolerance and increased blood lipid content (TC, LDL, TG).

Answer 196

* C7-position: Sulfonamide group is required for activity * C6-position (R1): Electron-withdrawing group (e.g. Cl, CF3 etc) required for activity * 3–4-position: Saturation of the double bond results in more potent (~ 10-fold) analogs * C3-position (R2): Lipophilic group improves diuretic potency * 2-position (R3): N-alkyl substitution increases the duration of diuretic action

Answer 197

* Diverse structural classes * The most efficacious among the various diuretic classes * Peak diuresis produced \> other commonly used diuretics (High-Ceiling Diuretics) * Site of Action: Loop of Henle (thick ascending limb) * Inhibits the luminal Na+/ K+/ 2Cl- co-transporter * Characterized by quick onset (~ 30 min) and relatively short duration of action (~ 6 hrs)

Answer 198

* Contains a quinazolin-4-one structural core (ring-SO2 of thiazides replaced with a CO group) * Diuretic effects similar to the thiazide class of compounds * Orally active. Long duration of action (upto 24 hrs) * Adverse effects similar to the thiazide diuretic class

Answer 199

* Contains a carboxylic acid functional group (pKa ~4) * 8 – 10 Times stronger saluretic action than the thiazides. * Causes excretion of Na+, K+, Ca2+, Mg2+, Cl- and HCO3 - ions * Orally active. Parenteral form for faster onset of action. * Extensive plasma protein binding (\> 90%). Mostly excreted unchanged (kidney). * **Uses**-Most important use in the treatment of pulmonary edema. Additional uses include, treatment of edemas associated with cardiac, hepatic and renal malfunctions. Also useful in the treatment of hypertension. * **Side-Effects**: Electrolyte Imbalance; Hyperuricemia; Gastrointestinal side-effects, and hypersensitivity etc. Can also cause ototoxicity (temporary hearing loss). This effect can be additive with concurrent usage of aminoglycoside antibiotics.

Answer 200

* Ring substitution pattern different than furosemide * Greater bioavailability than furosemide * Marked increase in diuretic potency (~ 40 times of furosemide) * Uses and side effect profile similar to furosemide

Answer 201

* Sulfonylurea side-chain instead of sulfonamide * Same site / mechanism of action as furosemide and bumetanide * Available in oral and parenteral (IV) forms * Partially metabolized by hepatic cytochrome P450 enzymes. A major metabolic route involves oxidn of the Ar-Me group to carboxylic acid. * Uses: Treatment of hypertension; Congestive heart failure and cirrhosis associated edema. * Adverse Effects : Fatigue, dizziness, muscle cramps, nausea and orthostatic hypotension.

Answer 202

* A phenoxyacetic acid derivative. Lacks a sulfonamide group. * Same site / mechanism of action as the above loop diuretics * Rapid onset (~ 30 min) and long duration of action (6 – 8 hr) * Oral and parenteral. Highly plasma protein bound (\> 95%) * Relatively less potent than the other drugs in this category. However, useful in patients who are allergic to the sulfonamides. * Adverse effects: Greater incidences of ototoxicity and more serious gastrointestinal effects

Answer 203

* First ACE inhibitor drug (1981); Contains a sulfhydryl (SH) group * Oral drug; Rapid absorption; Bioavailability ~ 75%; T1/2 = 2 hrs * Partially eliminated unchanged in urine (~50%), remainder as disulfide dimer and captopril-cysteine disulfide * Used for the therapy of hypertension and heart failure * Food reduces oral bioavailability by 25-30% * Sulfhydryl group implicated in skin rashes and taste disturbance

Answer 204

* An ester prodrug. Hydrolyzed by hepatic esterase to the active carboxylic acid form. Dicarboxylate class of ACE inhibitor. * More potent than Captopril. * Oral drug; Readily absorbed; Oral bioavailability ~ 60%, not reduced by food. Eliminated unchanged in urine * Enalaprilat not absorbed orally. Available in IV formulation. * Used for the therapy of hypertension and heart failure; Only ACE inhibitor approved for pediatric use.

Answer 205

* A prodrug; Ester hydrolysis produces the active drug. * Belongs to the dicarboxylate class of ACE inhibitors * More potent than captopril or enalaprilat * Oral drug. Indicated for hypertension. * Readily but incompletely absorbed. Glucuronide conjugate excreted via urine and bile. * Also available in combination with Hydrochlorothoazide (Lotensin HCT®) or Amlodipine (Lotrel®)

Answer 206

* Phosphinate group containing ACE inhibitor. * A prodrug. Cleavage of the ester moiety by hepatic esterases generates the active drug Fosinoprilat * Slowly and incompletely (36%) absorbed after oral administration. * Fosinoprilat and glucuronide conjugate excreted in urine and bile; Clearance not significantly altered by renal impairment. * Indicated for the treatment of hypertension and heart failure.

Answer 207

* The N-ring carboxylic acid is essential (mimics the C-terminal carboxylate of ACE substrates) * Large hydrophobic functionalities in the N-ring increases potency * Zn-ion binding groups (sulfhydryl, carboxylate, phosphinic acid etc) required for potency * ‘X’ is usually methyl (mimics the side-chain of alanine), the exception being Lisinopril * For optimum activity, stereochemistry should be consistent with natural L-amino acid

Answer 208

* Aldosterone, a steroid hormone, is secreted by the adrenal cortex, and is a potent mineral corticoid. * Acting on the distal tubule and collecting ducts of the nephron, it causes increased reabsorption of Na+ and Cl– ions and water, while increasing K+-ion ion excretion * Aldosterone action leads to increase in water retention, and increased blood pressure / volume. * The biologic effect of Aldosterone is caused by its binding to the mineralcorticoid receptor (MR), a nuclear transcription factor * Inhibition (antagonism) of aldosterone function can lead to diuresis (excretion of Na+, and Cl– ions and water) * Such inhibitors are also classified as Potassium-Sparing Diuretics

Answer 209

* A semi-synthetic drug. Prevents aldosterone binding (antagonist) to the MR in the distal convoluted tubule and the collecting system. * Causes increased amount of Na+ / water excretion, and retention of K+-ion. * Oral drug (90% availability). Undergoes significant first-pass metabolism to form Canrenone (loses Me–CO–SH), an active metabolite. Excretetion mainly in urine. * Adverse effects: Can cause hyperkalemia. Use of other K+-sparing diuretics, potassium supplements and food rich in potassium should be avoided. Anti-androgenic effects, hypersensitivity reactions, GI disturbances, and peptic ulcer have also been reported.

Answer 210

* The first clinically approved ARB drug (1995) * Highly protein bound (~98%); Adequate oral bioavailability (33%) * Approximately 14% of an oral dose is oxidized by the isozymes CYP2C9 and CYP3A4 to a more potent (10-40 times) carboxylic acid metabolite * (-CH2OH ----\> -CO2H) * Primarily excreted by the fecal route.

Answer 211

* Inactive ester prodrug. Completely hydrolyzed during absorption from the GI tract to form the active drug Candestran; High plasma protein binding (99%); Oral bioavailability = 15%; T1/2 = 9 hrs.

Answer 212

* All the ARBs are acidic drugs. The tetrazole ring has a pKa ≃ 6, and the carboxylic acid pKa = 3-4. * Azilsartan medomoxil and Olmesartan medomoxil are prodrugs that are completely hydrolyzed during absorption from the GI tract to generate the active carboxylic acid metabolites.

Answer 213

* An aldosterone antagonist. Compared to Spironolactone, lower affinity for MR, however a more selective inhibitor (does not inhibit AR, PR, and GR) * Oral drug (~70% availability). T1/2≃ 5 hr. Hepatic metabolism (CYP3A4). Metabolites inactive and excreted in urine and feces. * Adverse effects: Can cause hyperkalemia. However, unlike spironolactone, limited/fewer sexual side effects.

Answer 214

* Development of Aliskiren: The First (and only) Renin Inhibitor in Clinical Use

Answer 215

* Contains a pteridine sturctural core. * Renal epithelial Na+ channel blocker. Blocks the reabsorption of Na+ ion and prevents excretion of K+ ion in the distal tubule (but no effect on aldosterone action). * Oral drug (~70% absorption). Metabolized extensively (4’-OH analog and its sulfate conjugate). Excreted in the urine * Adverse Effects: Can cause hyperkalemia, nausea, vomiting and headache. Potassium supplements are contraindicated, and serum potassium levels should be monitored.

Answer 216

* An aminopyrazine derivative. * Renal epithelial Na+ channel blocker. Blocks the reabsorption of Na+- ion and secretion of K+-ion in DCT. No effect on aldosterone action. * Oral drug (~50% absorption). Excreted (mostly unchanged) in urine and feces. Renal impairment can increase half-life. * Adverse Effects: Similar to triamterene.

Answer 217

Stroke, MI, Renal Failure, CHF, Progressive Atherosclerosis and Dementia

Answer 218

Highly regulated pathway, integral in regulating arterial blood pressure, body fluid volume, and electrolyte balance

Answer 219

Renin and Angiotensin Converting Enzyme

Answer 220

* Potent vasodilator * Angiotensinogen * Production of Aldosterone which in turn contributes towards an increase in plasma volume and Bp.

Answer 221

Renin to release angiotensin I

Answer 222

Protease Angiotensinogen to form Angiotensin I

Answer 223

to Ang II by ACE

Answer 224

* Zn2+ * Tripeptide sequence but not cleave peptides with penultimate prolyl residue * Bradykinin and Substance P

Answer 225

Stimulate Aldosterone secretion which increases plasma volume and blood pressure

Answer 226

* Generation of a potent hypertensive agent Angiotensin II * Release of a hypertensive agent Aldosterone * Degradation of a potent antihypertensive agent Bradykinin (a vasodilator) * The outcome of all the above actions of ACE is hypertension, an increase in blood pressure.

Answer 227

* Sulfhydryl (SH) group containing inhibitors (e.g. Captopril) * Dicarboxylate-containing inhibitors (e.g. Enalapril) * Phosphonate-containing inhibitors (e.g. Fosinopril)

Answer 228

* In their potency * Whether the activity is due to the drug itself, or the conversion of a prodrug to an active metabolite * Pharmacokinetics (extent of absorption; effect of food; plasma half-life; tissue distribution; mechanism of elimination etc)

Answer 229

* Further modified sulfonamides, characterized by the presence of a benzothiadiazine 1,1-dioxide core * Weakly acidic compounds (pKa ~ 7). Actively secreted into the proximal tubule and are carried to the site of action. * **Site of Action**: Thick ascending loop of Henle and distal convoluted tubule * **Mechanism of Diuretic Action**: Binds to the Na+/Cl– symporter and inhibits the reabsorption of sodium and chloride ions (saluretic agents) * Used alone, or as add-on therapy. Rapid oral absorption. Excreted mainly unchanged (urine)

Answer 230

* Diverse structural classes * The most efficacious among the various diuretic classes * Peak diuresis produced \> other commonly used diuretics (High-Ceiling Diuretics) * Site of Action: Loop of Henle (thick ascending limb) * Inhibits the luminal Na+/ K+/ 2Cl- co-transporter * Characterized by quick onset (~ 30 min) and relatively short duration of action (~ 6 hrs)

Answer 231

* Generally well-tolerated drugs. Serious untoward reactions are rare. * Side effects may include, hypotension, hyperkalemia, dry cough (in 5-20% of patients), dizziness, renal insufficiency, skin rash, neutropenia (rare), and angioedema etc. * The use of ACE inhibitors during pregnancy (especially during 2nd / 3rd trimester) is contraindicated * Renal elimination is the primary route of elimination for majority of the ACE inhibitors (except Fosinopril). Therefore, dosage should be reduced in patients with renal impairment.

Answer 232

* Antacids may reduce bioavailability. NSAIDS (including aspirin) may reduce the anti-hypertensive response to ACE inhibitors.

Answer 233

* Also called receptor antagonists, displace/prevents binding of angiotensin II at the binding site * Located in brain, neuro, vascular, renal, hepatic, adrenal, myocardial mediate effects at these sites * 2 is growth, development

Answer 234

* All the ARBs are approved for the treatment of hypertension. Can be used as stand-alone drugs, or in combination with other anti-hypertensive agents (e.g. Diuretics; Calcium channel blockers). * Additionally, some of the ARBs also find use in the treatment of nephropathy in type 2 diabetes (Losartan / Irbesartan), heart failure (Candesartan / Valsartan), and cardiovascular risk-reduction of MI and stroke (Telmisartan) etc. AEs * ARBs are generally well tolerated. Unlike ACE inhibitors, does not effect the levels of bradykinin or prostaglandins. The most common side-effects include: * Headache; Dizziness; Fatigue; Hypotension; Upper respiratory tract infection etc. q ARBs are contraindicated during pregnancy. DIs * ARBs are relatively free of clinically important drug interactions. Telmisartan is the only agent among this class reported to increase the plasma concentration of Digoxin. * However, non-steroidal antiinflammatory drugs (NSAIDs) may alter the response to ARBs and other anhtihypertensive agents (including ACE inhibitors and Ca2+-channel blockers) due to the inhibition (COX) of vasodilatory prostaglandins. *

Answer 235

* First ACE inhibitor drug (1981); Contains a sulfhydryl (SH) group * Oral drug; Rapid absorption; Bioavailability ~ 75%; T1/2 = 2 hrs * Partially eliminated unchanged in urine (~50%), remainder as disulfide dimer and captopril-cysteine disulfide * Used for the therapy of hypertension and heart failure * Food reduces oral bioavailability by 25-30% * Sulfhydryl group implicated in skin rashes and taste disturbance

Answer 236

* An ester prodrug. Hydrolyzed by hepatic esterase to the active carboxylic acid form. Dicarboxylate class of ACE inhibitor. * More potent than Captopril. * Oral drug; Readily absorbed; Oral bioavailability ~ 60%, not reduced by food. Eliminated unchanged in urine * Enalaprilat not absorbed orally. Available in IV formulation. * Used for the therapy of hypertension and heart failure; Only ACE inhibitor approved for pediatric use.

Answer 237

* A prodrug; Ester hydrolysis produces the active drug. * Belongs to the dicarboxylate class of ACE inhibitors * More potent than captopril or enalaprilat * Oral drug. Indicated for hypertension. * Readily but incompletely absorbed. Glucuronide conjugate excreted via urine and bile. * Also available in combination with Hydrochlorothoazide (Lotensin HCT®) or Amlodipine (Lotrel®)

Answer 238

* Phosphinate group containing ACE inhibitor. * A prodrug. Cleavage of the ester moiety by hepatic esterases generates the active drug Fosinoprilat * Slowly and incompletely (36%) absorbed after oral administration. * Fosinoprilat and glucuronide conjugate excreted in urine and bile; Clearance not significantly altered by renal impairment. * Indicated for the treatment of hypertension and heart failure.

Answer 239

* The N-ring carboxylic acid is essential (mimics the C-terminal carboxylate of ACE substrates) * Large hydrophobic functionalities in the N-ring increases potency * Zn-ion binding groups (sulfhydryl, carboxylate, phosphinic acid etc) required for potency * ‘X’ is usually methyl (mimics the side-chain of alanine), the exception being Lisinopril * For optimum activity, stereochemistry should be consistent with natural L-amino acid

Answer 240

* The first clinically approved ARB drug (1995) * Highly protein bound (~98%); Adequate oral bioavailability (33%) * Approximately 14% of an oral dose is oxidized by the isozymes CYP2C9 and CYP3A4 to a more potent (10-40 times) carboxylic acid metabolite * (-CH2OH ----\> -CO2H) * Primarily excreted by the fecal route.

Answer 241

* Inactive ester prodrug. Completely hydrolyzed during absorption from the GI tract to form the active drug Candestran; High plasma protein binding (99%); Oral bioavailability = 15%; T1/2 = 9 hrs.

Answer 242

* All the ARBs are acidic drugs. The tetrazole ring has a pKa ≃ 6, and the carboxylic acid pKa = 3-4. * Azilsartan medomoxil and Olmesartan medomoxil are prodrugs that are completely hydrolyzed during absorption from the GI tract to generate the active carboxylic acid metabolites.

Answer 243

* Development of Aliskiren: The First (and only) Renin Inhibitor in Clinical Use

Answer 244

Stroke, MI, Renal Failure, CHF, Progressive Atherosclerosis and Dementia

Answer 245

Highly regulated pathway, integral in regulating arterial blood pressure, body fluid volume, and electrolyte balance

Answer 246

Renin and Angiotensin Converting Enzyme

Answer 247

* Potent vasodilator * Angiotensinogen * Production of Aldosterone which in turn contributes towards an increase in plasma volume and Bp.

Answer 248

Renin to release angiotensin I

Answer 249

Protease Angiotensinogen to form Angiotensin I

Answer 250

to Ang II by ACE

Answer 251

* Zn2+ * Tripeptide sequence but not cleave peptides with penultimate prolyl residue * Bradykinin and Substance P

Answer 252

Stimulate Aldosterone secretion which increases plasma volume and blood pressure

Answer 253

* Generation of a potent hypertensive agent Angiotensin II * Release of a hypertensive agent Aldosterone * Degradation of a potent antihypertensive agent Bradykinin (a vasodilator) * The outcome of all the above actions of ACE is hypertension, an increase in blood pressure.

Answer 254

* Sulfhydryl (SH) group containing inhibitors (e.g. Captopril) * Dicarboxylate-containing inhibitors (e.g. Enalapril) * Phosphonate-containing inhibitors (e.g. Fosinopril)

Answer 255

* In their potency * Whether the activity is due to the drug itself, or the conversion of a prodrug to an active metabolite * Pharmacokinetics (extent of absorption; effect of food; plasma half-life; tissue distribution; mechanism of elimination etc)

Answer 256

* Generally well-tolerated drugs. Serious untoward reactions are rare. * Side effects may include, hypotension, hyperkalemia, dry cough (in 5-20% of patients), dizziness, renal insufficiency, skin rash, neutropenia (rare), and angioedema etc. * The use of ACE inhibitors during pregnancy (especially during 2nd / 3rd trimester) is contraindicated * Renal elimination is the primary route of elimination for majority of the ACE inhibitors (except Fosinopril). Therefore, dosage should be reduced in patients with renal impairment.

Answer 257

* Antacids may reduce bioavailability. NSAIDS (including aspirin) may reduce the anti-hypertensive response to ACE inhibitors.

Answer 258

* Also called receptor antagonists, displace/prevents binding of angiotensin II at the binding site * Located in brain, neuro, vascular, renal, hepatic, adrenal, myocardial mediate effects at these sites * 2 is growth, development

Answer 259

* All the ARBs are approved for the treatment of hypertension. Can be used as stand-alone drugs, or in combination with other anti-hypertensive agents (e.g. Diuretics; Calcium channel blockers). * Additionally, some of the ARBs also find use in the treatment of nephropathy in type 2 diabetes (Losartan / Irbesartan), heart failure (Candesartan / Valsartan), and cardiovascular risk-reduction of MI and stroke (Telmisartan) etc. AEs * ARBs are generally well tolerated. Unlike ACE inhibitors, does not effect the levels of bradykinin or prostaglandins. The most common side-effects include: * Headache; Dizziness; Fatigue; Hypotension; Upper respiratory tract infection etc. q ARBs are contraindicated during pregnancy. DIs * ARBs are relatively free of clinically important drug interactions. Telmisartan is the only agent among this class reported to increase the plasma concentration of Digoxin. * However, non-steroidal antiinflammatory drugs (NSAIDs) may alter the response to ARBs and other anhtihypertensive agents (including ACE inhibitors and Ca2+-channel blockers) due to the inhibition (COX) of vasodilatory prostaglandins. *

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