2 - Vasoactive and Antiplatelet Agents Flashcards
Patients with Raynaud’s phenomenon have a deficiency of perivascular calcitonin gene related peptide-containing neurons
True
Pentoxifylline is known to reduce blood viscosity in the microcirculation
True
The endothelium produces prostacyclin which inhibit platelet activation and acts as a vasodilator
True
Endothelin-1 (ET-1) is a potent vasoconstrictor
True
Diffusion of nitric oxide (NO) from endothelial cells results in vascular smooth muscle relaxation and vasodilatation
True
Calcium channel blockers are well absorbed orally
True
Bioavailability varies between the calcium channel blocker drugs
True
Bioavailability for nifedipine (50-70%) and amlodipine (50-88%) are similar
True
Bioavailability for diltiazem is 20-40%
True
Calcium channel blockers are largely protein bound
True
Amlodipine reaches peak plasma level at 7-8 hours
True
Diltiazem reaches peak plasma level at 30 mins
True
Nifedipine reaches peak plasma levels at 1-2 hours
True
The dihydropyridine calcium channel blockers nifedipine, isradipine and amlodipine are principally excreted via the kidney
True
The non-dihydropyridine calcium channel blocker diltiazem is excreted via the faeces after extensive deacetylation
True
The plasma half life for nifedipine and diltiazem is 4 hours
True
The plasma half life for amlodipine is 35 hours
True
Amlodipine reaches peak plasma levels later than diltiazem and nifedipine
True
Amlodipine has a longer plasma half life than diltiazem and nifedipine
True
Calcium channel blockers prevent the transport of calcium across the plasma cell membrane of smooth muscle cells
True
Calcium channel blockers inhibit excitation contraction coupling and muscle constriction
True
Some calcium channel blockers I.e. Verapamil have varying effects on atrioventricular conduction and heart rate
True
Verapamil is predominantly used for dysrhythmias and not for cutaneous vascular diseases
True (verapamil is a strong depressor of AV conduction)
Beta1 adrenergic effect is vasodilatation
True
Alpha1 adrenergic effect is vasoconstriction
True
Alpha2 adrenergic effect is vasoconstriction
True
Thromboxane A2 induces vasoconstriction
True
Capsaicin induces vasodilatation
True (mediated by nitric oxide)
Calcitonin gene related peptide induces vasodilatation
True (mediated by nitric oxide)
Substance P induces vasodilatation
True (mediated by nitric oxide)
The calcium channel blocker agent of choice for Raynaud’s phenomenon is nifedipine
True
Nifedipine is superior to diltiazem in the treatment of recalcitrant chilblains
True
Nifedipine has in vivo anti platelet effects
True (in patients with systemic sclerosis)
The non-dihydropyridine calcium channel blocker verapamil is ineffective in treating Raynaud’s phenomenon
True
The non-dihydropyridine calcium channel blocker diltiazem may be useful in the treatment of calcinosis cutis
True (especially in patients with CREST syndrome)
Intralesional verapamil (non-dihydropyridine calcium channel blocker) has been used with some success in keloids and hypertrophic scars
True (and Peyronie’s disease)
Dihydropyridine Calcium channel blockers i.e. Nifedipine and isradipine are the first line for managing cyclosporine-induced hypertension due to renal blood flow preservation and no CYP 3A4 inhibition
True (CsA is a substrate of CYP3A4)
Dihydropyridine Calcium channel blockers i.e. Amlodipine and nicardipine and the non-dihydropyridine calcium channel blockers diltiazem and verapamil have been shown to increase levels of cyclosporine via CYP 3A4 inhibition
True (CsA is a substrate of CYP3A4)
Dihydropyridine Calcium channel blockers i.e. Amlodipine and nicardipine and the non-dihydropyridine calcium channel blocker diltiazem may reduce the necessary dose of cyclosporine
True (these calcium channel blockers have been shown to increase levels of cyclosporine via CYP 3A4 inhibition)
Calcium channel blockers rarely need to be ceased due to the adverse effects
True (although adverse effects are frequent, these rarely lead to cessation of therapy as dose reduction is typically sufficient to reduce the adverse effect)
Adverse effects are frequent in calcium channel blockers
True
Calcium channel blockers adverse effects are typically due to vasodilatation
True
Calcium channel blockers may cause dizziness
True (due to vasodilatation)
Calcium channel blockers may cause headaches
True (due to vasodilatation)
Calcium channel blockers may cause peripheral oedema
True (due to vasodilatation)
Calcium channel blockers may cause nausea
True (due to vasodilatation)
Calcium channel blockers may cause flushing
True (due to vasodilatation)
Symptomatic hypotension is uncommon in patients on calcium channel blockers
True
Nifedipine has more severe side effects than amlodipine
True
Nifedipine has more severe side effects than diltiazem
True
Calcium channel blockers may cause gingival hyperplasia
True (diltiazem > verapamil > nifedipine)
Calcium channel blockers may cause facial and truncal telegiectasia
True (vasodilatation)
Calcium channel blockers may cause new onset or exacerbation of psoriasis
True
Diltiazem may cause photodistributed hyperpigmentation particularly in African American women
True
Long term use of calcium channel blockers is associated with the development of chronic eczematous reactions in the elderly
True
Calcium channel blockers may cause gynaecomastia
True
Calcium channel blockers may cause oral ulcers
True
Propanolol is a lipophilic beta blocker with a short half life and readily cross the blood brain barrier
True
Carvedilol is a lipophilic beta blocker with a short half life and readily cross the blood brain barrier
True
Metoprolol is a lipophilic beta blocker with a short half life and readily cross the blood brain barrier
True
Propranolol is metabolised by the liver (lipophilic)
True
Carvedilol is metabolised by the liver (lipophilic)
True
Atenolol is a hydrophilic beta blocker with a longer half life and do not cross the blood brain barrier
True
Sotalol is a hydrophilic beta blocker with a longer half life and do not cross the blood brain barrier
True
Atenolol is excreted by the kidneys (hydrophilic)
True
Sotalol is excreted by the kidneys (hydrophilic)
True
Blockage of beta1-adrenergic receptor is cardio selective
True
Metoprolol is a cardio selective beta blocker
True
Atenolol is a cardio selective beta blocker
True
Blockage of beta2-adrenergic receptor by non-selective agents I.e. Propranolol interferes with dilation of bronchioles and blood vessels
True
Blockage of beta2-adrenergic receptor by non-selective agents I.e. Propranolol causes lipolysis
True
Blockage of beta2-adrenergic receptor by non-selective agents I.e. Propranolol causes glycogenolysis
True
Non-selective beta blocker I.e. Sotalol also possesses class III antiarhythmic features and increased risk of cardiac arythmias
True (not suitable for use in dermatology)
Non-selective beta blocker I.e. Labetalol and Carvedilol also have alpha-adrenergic activity result in vasodilatation and further reducing blood pressure
True
The non-selective beta blocker Propanolol (beta2-adrenergic reception blockade) has been successfully used to treat infantile haemangiomas
True (interferes with dilation of bronchioles and blood vessels)
Non-selective beta blockers I.e. Propanolol and Carvedilol have been used in flushing with mixed success
True
Bradycardia is a common side effect of beta blockers
True
Hypotension is a common side effect of beta blockers
True
Bronchospasm is a common side effect of beta blockers
True
Fatigue is a common side effect of beta blockers
True
Hypoglycaemia is a side effect of beta blockers reported in some paediatric patients undergoing treatment for infantile haemangioma
True
Beta blockers have been associated with lichenoid drug, eczematous and psoriasiform eruptions
True
Beta blockers may induce or worsen psoriasis
True (same as calcium channel blockers) - though more guttate psoriasis
Salicylates I.e. Aspirin is rapidly absorbed and widely distributed
True
Salicylates I.e. Aspirin reach peak plasma levels after 2 hours and slowly decline
True
Salicylates I.e. Aspirin are mainly protein bound (50-80%) to plasma albumin and only the free drug is active
True
Salicylates I.e. Aspirin is metabolised by the liver
True
The amount of salicylates I.e. Aspirin metabolised by the liver is dependant on the rate of urinary excretion
True
The rate and amount of salicylates I.e. Aspirin excreted in the urine depends on urinary pH
True (greater excretion in alkaline urine as salicylates are acidic)
The urinary excretion of salicylates I.e. Aspirin is greater in alkaline urine
True
Low dose aspirin acetylates platelet enzymes which are responsible for the synthesis of thromboxane A2
True
Higher dose aspirin inhibits synthesis of prostacyclin (endogenous inhibitor of platelet aggregation)
True (this reverses the anti platelet effect of prostacyclin)
Salicylates may cause exacerbation of asthma
True
Hypersensitivity reactions I.e. Angioedema, urticaria, rhinitis may occur with salicylates
True
Dyspepsia, peptic ulcer disease and upper GI bleeding are potential complications of aspirin therapy
True
Dipyridamole is largely bound to plasma proteins
True
Dipyridamole is metabolised in the liver
True
Dipyridamole is excreted in the bile
True
Dipyridamole inhibits platelet aggregation
True
Dipyridamole is a vasodilator
True
Dipyridamole has pro-fibrinolytic quality
True
Dipyridamole may cause gastric upset
True
Dipyridamole may cause worsening of coronary heart disease
True (causes tachycardia)
Dipyridamole is contraindicated after recent myocardial infarction and in rapidly worsening angina
True (contraindicated as may cause worsening heart disease with tachycardia)
Dipyridamole may cause dizziness
True (vasodilation)
Dipyridamole may cause headache
True (vasodilation)
Dipyridamole may cause hypotension
True (vasodilation)
Dipyridamole may cause tachycardia
True (Contraindicated in recent myocardial infarction and rapidly worsening angina)
Pentoxifylline is a non-specific phosphodiesterase inhibitor
True
Pentoxifylline is a methyl-xanthine derivative
True
Pentoxifylline is well absorbed
True
Pentoxifylline undergoes extensive first pass metabolism in the liver
True
Pentoxifylline is excreted in the urine
True
Pentoxifylline reaches peak plasma levels within 2 hours
True
Pentoxifylline has a half life of 4-6 hours
True
Pentoxifylline reduces blood viscosity in the microcirculation
True
Pentoxifylline has been used for the treatment of Raynaud’s phenomenon
True (reduces blood viscosity in the microcirculation)
Pentoxifylline has been used for the treatment of venous insufficiency with ulcers
True (reduces blood viscosity in microcirculation)
Pentoxifylline should be used with caution in patients with severe cardiac disease
True
The dose of Pentoxifylline should be reduced in significant renal impairment
True (renal excretion)
Sildenafil (Viagra) is a phosphodiesterase-5 inhibitor
True
Sildenafil (Viagra) causes an increase in cyclic-GMP in the vasculature resulting in vasodilatation
True
Sildenafil (Viagra) is metabolised in the liver primarily by CYP 3A4 and to a lesser extent by CYP 2C9
True
Sildenafil (Viagra) has been used in systemic sclerosis associated Raynaud’s phenomenon
True
Sildenafil (Viagra) is contraindicated with nitrates or nitric oxide donors
True
Headache is a common adverse effect of sildenafil (Viagra)
True
Flushing is a common adverse effect of sildenafil (Viagra)
True
Nasal congestion is a common adverse effect of sildenafil (Viagra)
True
Dyspepsia is a common adverse effect of sildenafil (Viagra)
True
Sildenafil (Viagra) must be used cautiously in patients with history of risk factors for myocardial infarction and unstable angina
True
Sildenafil (Viagra) must be used cautiously in patients with history of hypotension
True
Sildenafil (Viagra) must be used cautiously in patients with history of hypertension
True
Iloprost is a prostacyclin analog and a vasodilator
True
Iloprost causes vasodilation and is used in Raynaud’s phenomenon
True
Iloprost inhibits skin fibrosis
True
