What is the oral bioavailability of Nimodipine?
Up to 28%.
What is the half-life of Nifedipine?
5 hours.
1/291
p.7
Digoxin Pharmacology

What is the oral bioavailability of Nimodipine?

Up to 28%.

p.8
Antihypertensive Agents Overview

What is the half-life of Nifedipine?

5 hours.

p.17
Beta-Blockers and Their Effects

What are the common uses of Phenoxybenzamine?

Hypertensive emergencies, especially caused by Phaeochromocytoma, cocaine, Reynaud’s phenomenon, and complex regional pain syndrome.

p.21
Diuretics and Their Mechanisms

How are diuretics used in renal failure?

Diuretics do not reverse renal failure but can control its symptoms.

p.17
Beta-Blockers and Their Effects

What is the typical dosage range for oral Phenoxybenzamine?

10–60 mg per day in divided doses.

p.13
Antihypertensive Agents Overview

How quickly does Clonidine become effective?

Effective within 10 minutes.

p.16
Antihypertensive Agents Overview

What is the typical starting dose of Prazosin?

0.5 mg t.d.s., increasing to a maximum of 20 mg/day.

p.8
Mechanism of Action of Digoxin

What is the mechanism of action of Nifedipine?

It is a competitive antagonist at slow calcium channels, causing decreased influx of Ca2+ into cells.

p.13
Antihypertensive Agents Overview

What are the available forms of Clonidine?

Tablets (100/250/300 μg) and solution (150 μg/mL).

p.30
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What dysfunction is related to reduced thromboxane production due to NSAIDs?

Platelet dysfunction.

p.17
Beta-Blockers and Their Effects

What central nervous system effects can occur with Phenoxybenzamine?

Sedation, meiosis, dizziness, and convulsions with rapid infusion.

p.11
Digoxin Pharmacology

What is the half-life of Nicorandil?

1 hour.

p.1
Digoxin Toxicity and Treatment

What are the serious effects of digoxin toxicity at plasma levels?

Toxic at levels > 2.5 μg/L; fatal at levels > 30 μg/L.

p.26
Diuretics and Their Mechanisms

What is the primary mechanism of action of Acetazolamide?

It acts as a non-competitive inhibitor of carbonic anhydrase at the proximal convoluted tubule.

p.4
Mechanism of Action of Digoxin

What effect does adenosine have on conduction velocity?

It selectively decreases conduction velocity in the nodes (negative dromotropic effect).

p.32
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is the maximum dose of Aspirin in 24 hours?

4 g.

p.4
Adenosine in Antiarrhythmic Therapy

What is the half-life of adenosine?

Less than 10 seconds.

p.15
Antihypertensive Agents Overview

What is the typical dosage range for Methyldopa?

0.5–3 g/day in 2–3 doses.

p.4
Adenosine in Antiarrhythmic Therapy

What is a primary use of adenosine in arrhythmias?

To differentiate between SVT and VT.

p.13
Antihypertensive Agents Overview

What is the oral bioavailability of Clonidine?

100%.

p.21
Diuretics and Their Mechanisms

What condition can loop diuretics help reduce?

Hypertension, congestive cardiac failure, and edema.

p.30
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What do NSAIDs reduce that is essential for maintaining gastric mucosal integrity?

Circulating prostaglandins.

p.4
Adenosine in Antiarrhythmic Therapy

What is adenosine?

A naturally occurring purine nucleoside.

p.30
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is the mechanism by which NSAIDs can induce acute kidney injury?

Reduced levels of prostacyclin, which are required to maintain renal perfusion.

p.7
Verapamil as a Calcium Channel Antagonist

What is the oral dosage of Nimodipine for subarachnoid hemorrhage (SAH)?

60 mg 6 times a day.

p.9
Digoxin Pharmacology

What is the typical starting dose of Captopril?

6.25 mg, titrating up to 12–50 mg/day.

p.28
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

How do NSAIDs exert their effects?

By inhibiting the action of the enzyme cyclo-oxygenase (COX), reducing the production of inflammatory prostanoids.

p.4
Mechanism of Action of Digoxin

Where are A1 receptors found?

In the sinoatrial and atrioventricular nodes.

p.17
Beta-Blockers and Their Effects

What are some side effects of Phenoxybenzamine?

Dry mouth, impotence, and contact dermatitis.

p.25
Diuretics and Their Mechanisms

What percentage of total water reabsorption is accounted for by Na+ reabsorption stimulated by aldosterone?

2%.

p.31
Paracetamol

What are some cardiovascular effects of Paracetamol when administered rapidly?

Hypotension and bradycardia.

p.15
Antihypertensive Agents Overview

What are the available forms and dosages of Methyldopa?

Tablets: 125/250/500 mg; Solution: 50 mg/mL.

p.8
Antihypertensive Agents Overview

What cardiovascular effects does Nifedipine have?

Decreases systemic vascular resistance (SVR) and blood pressure (BP), increases heart rate (HR) and contractility, and increases cardiac output (CO).

p.26
Diuretics and Their Mechanisms

What effect does Acetazolamide have on gastric and pancreatic secretions?

It decreases gastric and pancreatic secretions.

p.8
Antihypertensive Agents Overview

What are some central nervous system effects of Nifedipine?

Increased cerebral blood flow, headache, and vertigo.

p.33
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What percentage of asthmatics are sensitive to NSAIDs like Diclofenac?

20%.

p.12
Antihypertensive Agents Overview

What are the primary uses of Glyceryl Trinitrate (GTN)?

Prophylaxis/treatment of angina, congestive heart failure (CCF), pulmonary edema, myocardial infarction (MI), acute coronary syndrome (ACS), and hypertension.

p.28
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is the significance of inhibiting COX-2?

It decreases pain and inflammation by reducing the formation of inflammatory mediators.

p.17
Beta-Blockers and Their Effects

What is the oral bioavailability of Phenoxybenzamine?

25%.

p.16
Beta-Blockers and Their Effects

What is the primary mechanism of action of Prazosin?

Highly selective α1 competitive antagonist.

p.20
Diuretics and Their Mechanisms

Where do diuretic drugs exert their effects in the nephron?

Proximal convoluted tubule, Distal convoluted tubule, Loop of Henle, and Collecting duct.

p.24
Diuretics and Their Mechanisms

What mechanism does Amiloride use to reduce potassium loss?

Blocks Na+/K+ exchange.

p.31
Paracetamol

How is Paracetamol primarily metabolized?

Mainly to glucuronide and sulfate metabolites (30%) in the liver.

p.24
Diuretics and Their Mechanisms

How is Amiloride metabolized?

Not significantly metabolized.

p.33
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is the chemical classification of Diclofenac?

Phenylacetic acid derivative NSAID.

p.24
Diuretics and Their Mechanisms

What is the absorption characteristic of Amiloride?

Poorly absorbed orally.

p.27
Diuretics and Their Mechanisms

What is the typical concentration of Mannitol solution?

10–20% clear colourless sugar alcohol solution.

p.14
Antihypertensive Agents Overview

What is the recommended dose range for Sodium Nitroprusside?

0.5–6 μg/kg/min, titrated to effect.

p.20
Diuretics and Their Mechanisms

Can mannitol be used repeatedly?

No, it cannot be used indefinitely due to the risk of rising serum osmolality and circulatory overload.

p.32
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is the typical dosage of Aspirin for angina and stroke prophylaxis?

75 mg once daily.

p.5
Antihypertensive Agents Overview

What is the effect of cardioselective β-Blockers like Atenolol?

They primarily act on β1 adrenoceptors, reducing heart rate and contractility.

p.12
Antihypertensive Agents Overview

What is the mechanism of action (MOA) of Glyceryl Trinitrate (GTN)?

GTN is broken down to liberate nitric oxide (NO), which increases cGMP, reducing Ca2+ uptake into smooth muscle, leading to vasodilation.

p.22
Diuretics and Their Mechanisms

How is furosemide primarily excreted?

Mostly unchanged in urine.

p.6
Antihypertensive Agents Overview

How do centrally acting drugs like clonidine work?

They stimulate central inhibitory presynaptic α2-adrenoceptors, reducing noradrenaline release and sympathetic outflow.

p.27
Diuretics and Their Mechanisms

What are the primary uses of Mannitol?

To reduce raised intracranial pressure and to force diuresis in major vascular surgery.

p.16
Beta-Blockers and Their Effects

What effect does Prazosin have on the urinary system?

Relaxes bladder sphincters.

p.9
Digoxin Toxicity and Treatment

What side effect of Captopril is caused by increased serum bradykinin?

Dry cough.

p.33
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What effect does Diclofenac have on renal function?

Inhibition of prostaglandins and prostacyclins causes local hypoxia and decreased renal perfusion.

p.25
Diuretics and Their Mechanisms

What is the oral bioavailability of Spironolactone?

70%.

p.3
Beta-Blockers and Their Effects

How does lipid solubility affect beta-blocker metabolism?

Low lipid solubility leads to minimal hepatic metabolism and excretion unchanged in urine; high lipid solubility leads to hepatic metabolism.

p.14
Digoxin Toxicity and Treatment

What are the signs of cyanide toxicity from Sodium Nitroprusside?

Tachycardia, arrhythmias, hyperventilation, sweating, rising SVO2, and metabolic acidosis.

p.24
Diuretics and Their Mechanisms

What is the common dosage for Amiloride tablets?

1–2 tablets per day.

p.24
Diuretics and Their Mechanisms

Where does Amiloride act in the kidney?

At the distal convoluted tubule.

p.11
Digoxin Pharmacology

What is the typical dosage range for Nicorandil?

10–30 mg, taken 12 hourly.

p.16
Antihypertensive Agents Overview

What is the oral bioavailability of Prazosin?

50–80%.

p.20
Diuretics and Their Mechanisms

How does mannitol reduce intracerebral pressure?

By decreasing the formation of cerebrospinal fluid (CSF) and plasma volume, encouraging water to move out of the brain.

p.25
Renin-Angiotensin-Aldosterone System (RAAS)

What does aldosterone stimulate in the kidneys?

Reabsorption of Na+ in exchange for K+.

p.27
Diuretics and Their Mechanisms

What is the recommended dose of Mannitol?

0.5–1 g/kg bolus over 20 minutes.

p.28
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is the role of COX in the inflammatory process?

COX catalyzes the formation of prostanoids, which are involved in inflammation.

p.20
Diuretics and Their Mechanisms

What happens if mannitol crosses the intact blood-brain barrier?

It can worsen edema by drawing water with it.

p.6
Antihypertensive Agents Overview

What are angiotensin-converting enzyme inhibitors (ACEIs) used for?

They affect the renin-angiotensin-aldosterone system to lower blood pressure.

p.14
Antihypertensive Agents Overview

What happens to Sodium Nitroprusside when exposed to sunlight?

It biodegrades, so use opaque giving sets or wrap in tin foil.

p.20
Diuretics and Their Mechanisms

What additional property does mannitol have?

It acts as a free radical scavenger, providing some neuroprotection.

p.5
Antihypertensive Agents Overview

What distinguishes non-cardioselective β-Blockers like Propranolol?

They act on both β1 and β2 adrenoceptors.

p.23
Diuretics and Their Mechanisms

What are the cardiovascular effects of Bendroflumethiazide?

It decreases blood pressure by reducing circulating volume.

p.16
Beta-Blockers and Their Effects

What cardiovascular effect does Prazosin have?

α1 blockade leading to vasodilation and decreased blood pressure.

p.22
Diuretics and Their Mechanisms

What is the bioavailability of furosemide compared to bumetanide?

Furosemide is 65% and bumetanide is 95%.

p.5
Antihypertensive Agents Overview

What is the mechanism of action for directly acting vasodilators?

They produce nitric oxide, activating guanylate cyclase and increasing cGMP levels to cause vasodilation.

p.28
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

Where is COX-2 primarily found?

In macrophages and other cells of inflammation; it is undetectable in most normal tissue.

p.22
Diuretics and Their Mechanisms

What are common uses of furosemide?

Congestive heart failure (CCF), peripheral and pulmonary edema, and to force diuresis in acute and chronic renal failure.

p.3
Beta-Blockers and Their Effects

Name a few examples of cardioselective beta-blockers.

Atenolol, Esmolol, Metoprolol, Bisoprolol, Carvedilol.

p.9
Digoxin Toxicity and Treatment

What serious adverse effect is more common in Afro-Caribbean patients taking Captopril?

Angioedema.

p.33
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

How does Diclofenac affect platelet function?

It causes reversible inhibition of platelet function with little effect on bleeding time.

p.17
Beta-Blockers and Their Effects

What is the primary mechanism of action of Phenoxybenzamine?

Non-selective irreversible α-blocker.

p.16
Antihypertensive Agents Overview

What are the main uses of Prazosin?

Hypertension, benign prostatic hypertrophy, Raynaud’s phenomenon, and treatment of nightmares associated with PTSD.

p.27
Diuretics and Their Mechanisms

What type of diuretic is Mannitol?

Osmotic diuretic.

p.11
Digoxin Pharmacology

How does Nicorandil affect preload?

It causes venous relaxation and reduces preload by donating nitric oxide to cells.

p.7
Mechanism of Action of Digoxin

What is the mechanism of action (MOA) of Nimodipine?

It is a competitive antagonist at slow calcium channels, decreasing Ca2+ influx into cells.

p.30
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

Which type of COX inhibitors are associated with platelet dysfunction?

Non-specific COX inhibitors.

p.6
Antihypertensive Agents Overview

What is the primary action of diuretics in antihypertensive therapy?

They reduce plasma volume, which decreases preload and cardiac output.

p.16
Antihypertensive Agents Overview

What is the volume of distribution (Vd) of Prazosin?

0.5–0.89 L/kg.

p.9
Digoxin Pharmacology

What are the common uses of Captopril?

Hypertension, reduction of progression of diabetic nephropathy, and post-MI to improve ventricular remodeling.

p.1
Digoxin Pharmacology

How is digoxin primarily excreted?

Unchanged in urine.

p.28
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What are the two types of cyclo-oxygenase (COX) relevant to NSAIDs?

COX-1 (constitutive) and COX-2 (inducible).

p.9
Digoxin Pharmacology

What effect does Captopril have on systemic vascular resistance (SVR) and blood pressure (BP)?

It decreases both SVR and BP.

p.1
Digoxin Toxicity and Treatment

What are common side effects of digoxin?

Anorexia, nausea, vomiting, diarrhea, headache, lethargy, visual disturbances, rashes.

p.14
Mechanism of Action of Digoxin

What is the mechanism of action of Sodium Nitroprusside?

It liberates nitric oxide (NO), increasing cGMP, which reduces Ca2+ uptake into smooth muscle, leading to vasodilation.

p.32
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

How is Aspirin metabolized in the body?

Hepatic and intestinal metabolism by ester hydrolysis to salicylic acid, further conjugated to salicyluric acid.

p.31
Paracetamol

What is the oral bioavailability of Paracetamol?

80%.

p.26
Diuretics and Their Mechanisms

What is the renal effect of Acetazolamide?

It causes mild diuresis and decreases the excretion of uric acid.

p.8
Antihypertensive Agents Overview

What should be noted about the use of Nifedipine with volatile anesthetics?

The negatively inotropic effects of Nifedipine are additive with those of volatiles, especially isoflurane, and should be used together with caution.

p.27
Diuretics and Their Mechanisms

What cardiovascular effect does Mannitol have?

Initial increase in circulating volume, which requires caution in patients with congestive heart failure (CCF).

p.27
Diuretics and Their Mechanisms

What central nervous system effect does Mannitol have?

Decreases intracranial pressure (ICP), but may worsen ICP if it crosses the blood-brain barrier (BBB) after head injury.

p.9
Digoxin Toxicity and Treatment

What should be avoided when using Captopril due to the risk of increased renal failure?

Potassium-sparing diuretics and NSAIDs.

p.3
Beta-Blockers and Their Effects

What are some common uses of beta-blockers?

Hypertension, Angina, MI, Tachycardias, Anxiety, Glaucoma, Migraine prophylaxis.

p.21
Diuretics and Their Mechanisms

What may be necessary to achieve optimum results with diuretics in renal failure?

Continuous infusion and combining various diuretics.

p.17
Beta-Blockers and Their Effects

What is the half-life of Phenoxybenzamine?

24 hours.

p.20
Diuretics and Their Mechanisms

What is the major indication for using mannitol?

Treatment of raised intracerebral pressure (ICP).

p.14
Antihypertensive Agents Overview

What is the appearance of Sodium Nitroprusside?

Red/brown powder.

p.13
Antihypertensive Agents Overview

What is the oral dosage range for Clonidine?

50–600 μg every 8 hours.

p.19
Beta-Blockers and Their Effects

What is the primary action of β-blockers?

They are competitive antagonists at β adrenoreceptors.

p.31
Paracetamol

What treatments are recommended for Paracetamol overdose?

Oral methionine and/or IV N-acetylcysteine (Parvolex).

p.12
Antihypertensive Agents Overview

What are the available forms of Glyceryl Trinitrate (GTN)?

Tablets, buccal, spray, patch, and solution.

p.18
Antihypertensive Agents Overview

What is the typical dose range for Phentolamine?

1–5 mg, titrated to effect.

p.23
Diuretics and Their Mechanisms

What is the mechanism of action of Bendroflumethiazide?

It acts on the early distal convoluted tubule to inhibit reabsorption of Na+ and Cl-, increasing their excretion along with H2O.

p.19
Beta-Blockers and Their Effects

How does lipid solubility affect the metabolism of β-blockers?

Low lipid solubility results in minimal hepatic metabolism and excretion unchanged in urine, while high lipid solubility leads to hepatic metabolism.

p.18
Antihypertensive Agents Overview

What is the onset time for Phentolamine?

1–2 minutes.

p.12
Antihypertensive Agents Overview

How quickly does sublingual GTN take effect?

Effective in 3 minutes and lasts for 1 hour.

p.25
Diuretics and Their Mechanisms

What is the typical dosage range for Spironolactone?

100–400 mg/day.

p.11
Digoxin Toxicity and Treatment

What are common side effects of Nicorandil?

Flushing, vertigo, headache, nausea, vomiting, angio-oedema, and hepatic dysfunction.

p.3
Beta-Blockers and Their Effects

What are 'cardioselective' beta-blockers aimed to block?

β 1 receptors but not β 2 receptors.

p.5
Antihypertensive Agents Overview

How do calcium channel blockers like Amlodipine work?

They are antagonists at L-type calcium channels in vascular smooth muscle, causing vasodilation.

p.10
Antihypertensive Agents Overview

How is Losartan metabolized and excreted?

It undergoes hepatic metabolism and is excreted in urine and bile.

p.13
Antihypertensive Agents Overview

What are the primary uses of Clonidine?

Hypertension, agitation and anxiety in ICU, adjunct in neuroaxial anaesthesia, migraine, and analgesia.

p.22
Diuretics and Their Mechanisms

What cardiovascular effect does furosemide have?

Arteriolar vasodilation causes decreased systemic vascular resistance (SVR) and preload.

p.6
Antihypertensive Agents Overview

What are common side effects of β-blockers?

Bronchospasm and peripheral vasoconstriction, especially in patients with COPD and peripheral vascular disease.

p.32
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What gastrointestinal risks are associated with Aspirin?

Increased risk of GI bleeding and ulceration due to inhibition of prostaglandin synthesis.

p.1
Digoxin Toxicity and Treatment

What ECG changes are associated with digoxin toxicity?

Long PR interval, 'inverted tick', flat T wave at therapeutic level.

p.13
Antihypertensive Agents Overview

What central nervous system effects does Clonidine produce?

Sedation, anxiolysis, and decreased minimum alveolar concentration (MAC).

p.19
Beta-Blockers and Their Effects

How can non-selective β-blockers affect diabetic patients?

They can increase resting blood glucose and mask symptoms of hypoglycemia.

p.23
Diuretics and Their Mechanisms

What are some other side effects of Bendroflumethiazide?

Impotence, rash, photosensitivity, and pancreatitis.

p.21
Diuretics and Their Mechanisms

Why might large doses of diuretics be needed in renal failure?

Their efficacy is decreased due to low renal blood flow, reducing delivery to the target organ.

p.20
Diuretics and Their Mechanisms

How does mannitol function as an osmotic diuretic?

It increases the osmolality of the filtrate, causing water to follow the drug and be excreted.

p.1
Digoxin Pharmacology

What is the therapeutic range of digoxin?

1–2 μg/L.

p.9
Renin-Angiotensin-Aldosterone System (RAAS)

What is the primary mechanism of action of Captopril?

It is an ACE inhibitor that prevents the conversion of angiotensin I to angiotensin II.

p.25
Diuretics and Their Mechanisms

What is the mechanism of action of Spironolactone?

Acts as a competitive antagonist of aldosterone at the distal convoluted tubule and collecting ducts.

p.5
Antihypertensive Agents Overview

What are the major categories of antihypertensive drugs?

Antihypertensive agents can be categorized based on their site of action: heart and blood vessels.

p.8
Antihypertensive Agents Overview

What is the oral bioavailability of Nifedipine?

60%.

p.5
Antihypertensive Agents Overview

How do β-Blockers function as antihypertensive agents?

They are competitive antagonists at β-adrenoceptors, reducing cardiac output and renin release.

p.14
Antihypertensive Agents Overview

How should Sodium Nitroprusside be reconstituted?

With 5% dextrose.

p.11
Digoxin Pharmacology

What are the primary uses of Nicorandil?

Treatment and prophylaxis of angina.

p.31
Paracetamol

What are the common uses of Paracetamol?

Analgesia and antipyretic.

p.18
Mechanism of Action of Digoxin

What is the mechanism of action of Phentolamine?

Competitive α blocker with 3x higher affinity for α1 than α2.

p.23
Diuretics and Their Mechanisms

How does Bendroflumethiazide affect renal function?

It decreases renal blood flow and glomerular filtration rate (GFR).

p.12
Antihypertensive Agents Overview

What is the oral bioavailability of Glyceryl Trinitrate (GTN)?

5%.

p.11
Digoxin Pharmacology

How is Nicorandil metabolized and excreted?

It undergoes hepatic metabolism and is excreted in urine and bile.

p.6
Renin-Angiotensin-Aldosterone System (RAAS)

What effects does angiotensin II have in the body?

It causes peripheral vasoconstriction, aldosterone release, increased thirst, and increased ADH release.

p.19
Beta-Blockers and Their Effects

What potential side effects can β-blockers cause in the respiratory system?

Bronchospasm, particularly in susceptible patients, necessitating the use of cardioselective drugs in asthma or COPD.

p.32
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is a significant risk associated with NSAID use in asthmatics?

20% of asthmatics may be sensitive to NSAIDs, causing bronchoconstriction.

p.12
Antihypertensive Agents Overview

What cardiovascular effects does Glyceryl Trinitrate (GTN) have?

Decreases systemic vascular resistance (SVR) and blood pressure (BP), predominantly through venodilation, which reduces preload.

p.19
Beta-Blockers and Their Effects

What central nervous system side effects can β-blockers cause?

Hallucinations, nightmares, depression, and fatigue.

p.10
Antihypertensive Agents Overview

What is the half-life (t½) of Losartan?

2 hours.

p.26
Diuretics and Their Mechanisms

What are the common uses of Acetazolamide?

It is used as a weak diuretic, for mountain sickness prophylaxis and treatment, and for glaucoma.

p.5
Antihypertensive Agents Overview

What is the effect of magnesium in the context of antihypertensive therapy?

Magnesium acts as a natural antagonist to calcium, contributing to vasodilation.

p.21
Diuretics and Their Mechanisms

What are the side effects of thiazides and loop diuretics?

Refer to the appropriate spider diagram for detailed side effects.

p.24
Diuretics and Their Mechanisms

What type of diuretic is Amiloride?

A potassium-sparing diuretic.

p.11
Digoxin Pharmacology

What is the chemical name of Nicorandil?

Nicotinamidoethyl nitrate.

p.31
Paracetamol

What is the mechanism of action of Paracetamol?

Central action via COX-3 inhibition, associated with decreased brain PGE2 levels.

p.1
Digoxin Pharmacology

What is digoxin extracted from?

Foxglove leaves (Digitalis lanata).

p.30
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

In which patients can acute kidney injury be induced by NSAIDs?

In vulnerable patients such as those with pre-existing renal dysfunction, diabetics, the elderly, or dehydrated patients.

p.11
Mechanism of Action of Digoxin

What is the primary mechanism of action (MOA) of Nicorandil?

Activates K+ channels, causing hyperpolarization of the membrane and reducing Ca2+ concentration.

p.7
Verapamil as a Calcium Channel Antagonist

What type of drug is Nimodipine?

A dihydropyridine calcium channel antagonist.

p.8
Antihypertensive Agents Overview

What are the common dosage forms of Nifedipine?

Capsules (5–10 mg) and tablets (10–60 mg).

p.4
Adenosine in Antiarrhythmic Therapy

What is the typical dose of adenosine?

6 mg, followed by 12 mg and another 12 mg if needed, given as fast bolus into a large vein.

p.1
Mechanism of Action of Digoxin

What is the mechanism of action of digoxin?

It binds to and inhibits the Na+/K+ ATPase pump, increasing intracellular Na+ and Ca2+, which enhances contractility.

p.17
Beta-Blockers and Their Effects

What cardiovascular effects does Phenoxybenzamine have?

α1 blockade causes vasodilation and decreased blood pressure, while reflex tachycardia increases cardiac output.

p.10
Antihypertensive Agents Overview

What type of drug is Losartan?

A substituted imidazole AII receptor antagonist.

p.4
Mechanism of Action of Digoxin

What is the mechanism of action of adenosine?

It binds to adenosine (A1) receptors, opening K+ channels to hyperpolarize the membrane.

p.33
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What are the available forms of Diclofenac?

Tablets, suppositories, solution, and topical gel.

p.31
Paracetamol

What happens when glutathione is exhausted in Paracetamol overdose?

NAPQI accumulates, leading to liver failure.

p.10
Antihypertensive Agents Overview

What are the available tablet dosages for Losartan?

25 mg and 50 mg.

p.16
Digoxin Toxicity and Treatment

What are some common side effects of Prazosin?

Profound orthostatic hypotension, syncope, nasal congestion, fatigue, headache, vertigo, nausea, and vomiting.

p.24
Diuretics and Their Mechanisms

What is a common use for Amiloride?

In combination with loop diuretics to decrease hypokalaemia.

p.18
Antihypertensive Agents Overview

What is the chemical classification of Phentolamine?

Imidazoline.

p.9
Digoxin Pharmacology

What is the oral bioavailability of Captopril?

75%.

p.33
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is the adult dosage of Diclofenac?

50 mg every 8 hours.

p.7
Digoxin Pharmacology

How is Nimodipine metabolized and excreted?

It undergoes hepatic metabolism and is excreted in urine.

p.10
Antihypertensive Agents Overview

What is the typical dosage range for Losartan?

50–100 mg/day.

p.15
Antihypertensive Agents Overview

What is the chemical classification of Methyldopa?

Phenylalanine derivative.

p.19
Beta-Blockers and Their Effects

What are 'cardioselective' β-blockers?

Drugs that aim to block β1 but not β2 receptors, such as Atenolol, Esmolol, Metoprolol, Bisoprolol, and Carvedilol.

p.8
Antihypertensive Agents Overview

What are the primary uses of Nifedipine?

Angina, hypertension, reduction of vasospasm during coronary angiography, and Raynaud’s phenomenon.

p.22
Diuretics and Their Mechanisms

What is the primary mechanism of action of furosemide?

It acts mainly on the thick ascending limb of the loop of Henle to inhibit reabsorption of Na+ and Cl-.

p.27
Mechanism of Action of Digoxin

How does Mannitol work in the body?

Freely filtered by glomerulus and not reabsorbed; water follows mannitol as osmolality of filtrate is increased.

p.30
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

Are selective COX-2 inhibitors associated with platelet dysfunction?

No, they are not associated with platelet dysfunction.

p.31
Paracetamol

What is NAPQI and why is it significant?

N-acetyl-p-amino benzoquinoneimine (NAPQI) is a toxic metabolite produced from Paracetamol metabolism.

p.8
Antihypertensive Agents Overview

What is the typical onset time for Nifedipine?

15–20 minutes.

p.1
Digoxin Pharmacology

What are the loading and maintenance doses of digoxin?

Loading: 500 μg followed by 500 μg or 250 μg 6 hours later; Maintenance: 62.5–500 μg/day.

p.32
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is the mechanism of action of Aspirin?

Irreversible COX-1 inhibitor and modifies the action of COX-2.

p.13
Antihypertensive Agents Overview

What is the mechanism of action (MOA) of Clonidine?

Agonist at presynaptic α2 receptors, decreasing sympathetic tone.

p.24
Diuretics and Their Mechanisms

What metabolic effect can Amiloride cause?

Hyperkalaemia.

p.33
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is the mechanism of action (MOA) of Diclofenac?

Inhibits cyclo-oxygenase (COX) with equal effect on COX-1 and COX-2.

p.17
Beta-Blockers and Their Effects

How is Phenoxybenzamine metabolized and excreted?

Hepatic metabolism; excreted in urine and bile.

p.26
Diuretics and Their Mechanisms

How does Acetazolamide affect intra-ocular pressure?

It decreases intra-ocular pressure by reducing the rate of aqueous humour production.

p.28
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

Where is COX-1 found?

In most cells throughout the body.

p.9
Digoxin Toxicity and Treatment

Why is Captopril contraindicated in renal artery stenosis?

It reduces plasma angiotensin II, which can decrease renal perfusion and lead to renal failure.

p.18
Antihypertensive Agents Overview

What is the oral bioavailability of Phentolamine?

20%.

p.4
Adenosine in Antiarrhythmic Therapy

How does adenosine affect pulmonary vascular resistance?

It increases pulmonary vascular resistance.

p.13
Antihypertensive Agents Overview

What cardiovascular effects does Clonidine have?

Decreases systemic vascular resistance (SVR) and blood pressure (BP); can cause rebound hypertension if stopped suddenly.

p.15
Antihypertensive Agents Overview

What are the primary uses of Methyldopa?

Hypertension and pregnancy-induced hypertension/pre-eclampsia.

p.18
Antihypertensive Agents Overview

What cardiovascular effects does Phentolamine have?

α1 blockade causes vasodilation and decreased BP, while α2 blockade enhances noradrenaline release, increasing HR and CO.

p.6
Diuretics and Their Mechanisms

What electrolyte imbalances can loop and thiazide diuretics cause?

Hyponatraemia, hypokalaemia, hypomagnesaemia, and hypochloraemic alkalosis.

p.19
Beta-Blockers and Their Effects

What is a potential gastrointestinal side effect of β-blockers?

Dry mouth and gastrointestinal upset.

p.23
Diuretics and Their Mechanisms

What is the typical dosage of Bendroflumethiazide?

2.5–5 mg orally once daily.

p.23
Diuretics and Their Mechanisms

How is Bendroflumethiazide metabolized and excreted?

It undergoes hepatic metabolism to active compounds, with 30% excreted unchanged in urine.

p.10
Antihypertensive Agents Overview

What is the mechanism of action (MOA) of Losartan?

It acts as an antagonist at angiotensin II receptors.

p.11
Digoxin Pharmacology

What are some cardiovascular effects of Nicorandil?

Decreased preload, decreased LVEDP, and decreased cardiac work.

p.7
Digoxin Pharmacology

What are the primary uses of Nimodipine?

Reduction of vasospasm following subarachnoid hemorrhage (SAH) and treatment of migraines.

p.7
Beta-Blockers and Their Effects

What cardiovascular effects does Nimodipine have at doses greater than 2 mg/hr?

It decreases systemic vascular resistance (SVR) and blood pressure (BP).

p.10
Antihypertensive Agents Overview

Why might Losartan be used instead of ACE inhibitors?

When the dry cough caused by ACE inhibitors is unacceptable.

p.25
Diuretics and Their Mechanisms

How is Spironolactone metabolized and excreted?

Hepatic metabolism and excreted in urine.

p.4
Adenosine in Antiarrhythmic Therapy

What are some side effects of adenosine?

Shortness of breath, flushing, chest discomfort, and a sense of impending doom.

p.23
Diuretics and Their Mechanisms

What biochemical changes occur with Bendroflumethiazide use?

It decreases K+, Cl-, Na+, Mg2+, and H+, while increasing Ca2+ and uric acid.

p.26
Diuretics and Their Mechanisms

What type of metabolic change can Acetazolamide induce?

It can cause hyperchloraemic metabolic acidosis and alkaline urine.

p.31
Paracetamol

What is the protein binding percentage of Paracetamol?

10%.

p.15
Antihypertensive Agents Overview

What is the range of oral bioavailability for Methyldopa?

8–60%.

p.5
Antihypertensive Agents Overview

How do α-Blockers like Prazosin contribute to antihypertensive effects?

They antagonize α1-adrenoceptors, causing vasodilation of both arterial and venous vessels.

p.10
Antihypertensive Agents Overview

What cardiovascular effects does Losartan have?

It decreases systemic vascular resistance (SVR) and blood pressure (BP).

p.25
Diuretics and Their Mechanisms

What hormonal side effects can occur with Spironolactone?

Gynaecomastia in men and irregular menstruation due to anti-androgenic effects.

p.12
Antihypertensive Agents Overview

What rare condition can occur with Glyceryl Trinitrate (GTN) use?

Methaemoglobinaemia.

p.10
Antihypertensive Agents Overview

What caution should be taken when using Losartan with NSAIDs?

There is an increased chance of renal failure.

p.3
Beta-Blockers and Their Effects

How can non-selective beta-blockers affect diabetics?

They can increase resting blood glucose and mask symptoms of hypoglycemia.

p.16
Antihypertensive Agents Overview

How is Prazosin metabolized and excreted?

Hepatic metabolism and excreted in bile.

p.27
Diuretics and Their Mechanisms

What is the half-life of Mannitol?

100 minutes.

p.13
Antihypertensive Agents Overview

How is Clonidine metabolized and excreted?

Hepatic metabolism; 50% excreted unchanged in urine.

p.19
Beta-Blockers and Their Effects

What are some common uses of β-blockers?

Hypertension, angina, myocardial infarction, tachycardias, anxiety, glaucoma, and migraine prophylaxis.

p.1
Digoxin Pharmacology

What is the half-life of digoxin?

35 hours, increased in renal failure.

p.15
Mechanism of Action of Digoxin

What is the mechanism of action of Methyldopa?

Metabolised to α-methyl noradrenaline, which is an α2 agonist that decreases sympathetic tone.

p.10
Antihypertensive Agents Overview

What is the oral bioavailability of Losartan?

30%.

p.25
Diuretics and Their Mechanisms

What are some clinical uses of Spironolactone?

Ascites, nephrotic syndrome, and Conn’s syndrome (primary hyperaldosteronism).

p.33
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is a significant risk associated with Diclofenac?

Risk of thrombosis.

p.3
Beta-Blockers and Their Effects

What cardiovascular effects do beta-blockers have?

They decrease heart rate, cardiac output, and blood pressure, and increase time in diastole and coronary artery perfusion.

p.15
Antihypertensive Agents Overview

What cardiovascular effects does Methyldopa have?

Decreases systemic vascular resistance (SVR) and blood pressure (BP); rare postural hypotension.

p.3
Beta-Blockers and Their Effects

What potential side effect can occur in patients with peripheral vascular disease when using beta-blockers?

Inhibition of β 2 receptors can cause constriction, compromising circulation in the peripheries.

p.22
Diuretics and Their Mechanisms

How does furosemide affect serum lithium levels?

It raises serum lithium levels.

p.25
Diuretics and Their Mechanisms

What are the available tablet dosages of Spironolactone?

25 mg, 50 mg, and 100 mg.

p.33
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is the oral bioavailability of Diclofenac?

60%.

p.3
Beta-Blockers and Their Effects

What is the primary action of beta-blockers?

They are competitive antagonists at β adrenoceptors.

p.10
Antihypertensive Agents Overview

What are the primary uses of Losartan?

Hypertension and to reduce progression of diabetic nephropathy.

p.19
Beta-Blockers and Their Effects

What cardiovascular effects do β-blockers have?

They act as negative inotropes and chronotropes, decreasing heart rate and cardiac output, and increasing time in diastole.

p.31
Paracetamol

What is the maximum dosage of Paracetamol for adults?

1 g every 6 hours.

p.1
Mechanism of Action of Digoxin

What is the effect of digoxin on heart rate?

It decreases conduction in the SA & AV node, slowing heart rate.

p.15
Antihypertensive Agents Overview

How is Methyldopa metabolized and excreted?

Hepatic metabolism; excreted in urine, 50% unchanged.

p.18
Antihypertensive Agents Overview

What are the primary uses of Phentolamine?

Hypertensive emergencies, especially from pheochromocytoma, cocaine, and MAOI reactions with tyramine.

p.23
Diuretics and Their Mechanisms

What hematological side effects are associated with Bendroflumethiazide?

Blood dyscrasias including anemia, leucopenia, agranulocytosis, and thrombocytopenia.

p.32
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What cardiovascular effects does Aspirin have?

Decreases platelet aggregation and vasoconstriction, providing cardioprotective effects.

p.26
Diuretics and Their Mechanisms

What is the typical dosage range for Acetazolamide when taken orally?

250 mg to 1 g per day in divided doses.

p.10
Antihypertensive Agents Overview

Why is Losartan contraindicated in renal artery stenosis?

It can cause decreased renal perfusion and renal failure.

p.3
Beta-Blockers and Their Effects

What central nervous system side effects can beta-blockers cause?

Hallucinations, nightmares, depression, fatigue.

p.22
Diuretics and Their Mechanisms

What condition can furosemide cause related to acid-base balance?

Hypochloraemic alkalosis.

p.6
Renin-Angiotensin-Aldosterone System (RAAS)

What is the role of renin in the renin-angiotensin-aldosterone system (RAAS)?

Renin converts angiotensinogen into angiotensin I in response to low renal perfusion.

p.14
Antihypertensive Agents Overview

How is Sodium Nitroprusside metabolized?

It reacts with sulphydryl groups on plasma proteins and undergoes hydrolysis in red blood cells to liberate NO and cyanide ions.

p.32
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What are the common uses of Aspirin?

Analgesia, anti-inflammatory, and anti-platelet in myocardial infarction and cerebrovascular accidents.

p.18
Antihypertensive Agents Overview

What percentage of Phentolamine is excreted unchanged in urine?

10%.

p.7
Digoxin Toxicity and Treatment

What central nervous system effects can Nimodipine cause?

Increased cerebral blood flow, headache, and vertigo.

p.14
Antihypertensive Agents Overview

What are the cardiovascular effects of Sodium Nitroprusside?

Arteriolar dilation, decreased systemic vascular resistance (SVR) and blood pressure (BP), venodilatation, and decreased left ventricular end-diastolic pressure (LVEDP).

p.26
Diuretics and Their Mechanisms

What is the oral bioavailability of Acetazolamide?

100%.

p.27
Diuretics and Their Mechanisms

What is a potential adverse effect of Mannitol?

Allergy, though rare.

p.6
Antihypertensive Agents Overview

What side effects can vasodilators cause?

Postural hypotension and headaches due to vasodilatation of capacitance and cerebral vessels.

p.28
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

Why is it challenging to develop COX-2 inhibitors without side effects?

Because COX-2 inhibitors still show the side-effect profile of non-specific agents.

p.25
Diuretics and Their Mechanisms

What are some common side effects of Spironolactone?

Nausea, vomiting, decreased response to vasopressors, and increased response to cardiovascular depressants.

p.15
Antihypertensive Agents Overview

What gastrointestinal side effects are associated with Methyldopa?

Constipation and impaired liver function with long-term use.

p.5
Antihypertensive Agents Overview

What is the role of potassium channel activators like Nicorandil?

They activate ATP-sensitive K+ channels, leading to hyperpolarization and arteriolar vasodilation.

p.1
Digoxin Toxicity and Treatment

What can be used to treat bradycardia caused by digoxin?

Atropine or pacing.

p.28
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is COX-3?

An isoenzyme discovered in 2002, likely a CNS variant of COX-1, and the site of action of paracetamol.

p.12
Antihypertensive Agents Overview

What is a notable side effect of Glyceryl Trinitrate (GTN) related to the central nervous system?

Increased intracranial pressure (ICP) causing headache.

p.14
Digoxin Toxicity and Treatment

What conditions increase the risk of toxicity from Sodium Nitroprusside?

Liver/renal failure and vitamin B12 deficiency.

p.25
Diuretics and Their Mechanisms

What biochemical effects does Spironolactone have?

Increases K+ and Na+ levels.

p.22
Diuretics and Their Mechanisms

What metabolic side effect is associated with furosemide?

Hyperglycemia (less common than with thiazides).

p.14
Antihypertensive Agents Overview

What is the half-life of Sodium Nitroprusside?

10 minutes.

p.32
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What is a potential drug interaction concern with Aspirin?

Care with warfarin, as NSAIDs may displace warfarin due to high protein binding.

p.26
Diuretics and Their Mechanisms

How is Acetazolamide metabolized and excreted?

It undergoes hepatic metabolism and is excreted in urine.

p.18
Antihypertensive Agents Overview

What potential side effect related to insulin secretion can occur with Phentolamine?

Hypoglycemia.

p.15
Antihypertensive Agents Overview

What hematological effects can Methyldopa cause?

Direct Coombs test positive in 10–20%, hemolytic anemia, thrombocytopenia, and leucopenia (rare).

p.15
Antihypertensive Agents Overview

What effect does Methyldopa have on MAC?

Decreases MAC.

p.23
Diuretics and Their Mechanisms

What metabolic effects does Bendroflumethiazide have?

It decreases glycogenesis and insulin secretion, while increasing glycogenolysis, cholesterol, and triglycerides.

p.18
Antihypertensive Agents Overview

What effect does Phentolamine have on respiratory function?

Increases VC and FEV1, and prevents bronchospasm caused by histamine release.

p.13
Antihypertensive Agents Overview

Does Clonidine affect platelet aggregation?

No increase in platelet aggregation despite surface α2 receptors.

p.22
Diuretics and Their Mechanisms

What biochemical changes can furosemide cause?

Decreases in K+, Cl-, H+, Na+, and Mg2+, and an increase in Ca2+.

p.27
Diuretics and Their Mechanisms

Why should the dose of Mannitol not be repeated indefinitely?

It causes rise in serum osmolality, circulatory overload, and may ultimately cross the BBB, causing increased ICP.

p.12
Antihypertensive Agents Overview

What should be done to prevent tolerance when using GTN patches?

Have a 'patch-free period' each day.

p.13
Antihypertensive Agents Overview

What is the half-life of Clonidine?

9–18 hours.

p.6
Antihypertensive Agents Overview

Why are ACEIs contraindicated in renal artery stenosis?

They can reduce renal perfusion pressure, leading to renal failure in patients with impaired renal circulation.

p.6
Antihypertensive Agents Overview

What persistent side effect may some patients experience with ACEIs?

A persistent cough due to increased bradykinin levels.

p.28
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What are the adverse effects of NSAIDs attributed to?

The lack of prostaglandin due to COX inhibition.

p.15
Antihypertensive Agents Overview

What central nervous system effects can Methyldopa cause?

Sedation, vertigo, and uncommon depression or nightmares.

p.18
Antihypertensive Agents Overview

How does Phentolamine affect gastrointestinal function?

Increases GI motility, salivation, and gastric acid secretions.

p.14
Antihypertensive Agents Overview

What are common side effects of Sodium Nitroprusside?

Nausea, vomiting, muscle twitching, and tachyphylaxis.

p.32
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What syndrome is associated with Aspirin use in children?

Reye's syndrome.

p.23
Diuretics and Their Mechanisms

What are the primary uses of Bendroflumethiazide?

Hypertension and heart failure.

p.15
Antihypertensive Agents Overview

What is a rare hypersensitivity reaction associated with Methyldopa?

Myocarditis.

p.22
Diuretics and Their Mechanisms

What is a potential risk of rapid IV injection of furosemide?

Ototoxicity, which can cause deafness.

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Study Smarter, Not Harder