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Derm Pharm 2020 > 2 - Vasoactive and Antiplatelet Agents > Flashcards

2 - Vasoactive and Antiplatelet Agents Flashcards

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Dermatology Board Prep flashcards
1
Q

Patients with Raynaud’s phenomenon have a deficiency of perivascular calcitonin gene related peptide-containing neurons

A

True

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2
Q

Pentoxifylline is known to reduce blood viscosity in the microcirculation

A

True

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3
Q

The endothelium produces prostacyclin which inhibit platelet activation and acts as a vasodilator

A

True

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4
Q

Endothelin-1 (ET-1) is a potent vasoconstrictor

A

True

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5
Q

Diffusion of nitric oxide (NO) from endothelial cells results in vascular smooth muscle relaxation and vasodilatation

A

True

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6
Q

Calcium channel blockers are well absorbed orally

A

True

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7
Q

Bioavailability varies between the calcium channel blocker drugs

A

True

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8
Q

Bioavailability for nifedipine (50-70%) and amlodipine (50-88%) are similar

A

True

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9
Q

Bioavailability for diltiazem is 20-40%

A

True

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10
Q

Calcium channel blockers are largely protein bound

A

True

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11
Q

Amlodipine reaches peak plasma level at 7-8 hours

A

True

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12
Q

Diltiazem reaches peak plasma level at 30 mins

A

True

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13
Q

Nifedipine reaches peak plasma levels at 1-2 hours

A

True

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14
Q

The dihydropyridine calcium channel blockers nifedipine, isradipine and amlodipine are principally excreted via the kidney

A

True

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15
Q

The non-dihydropyridine calcium channel blocker diltiazem is excreted via the faeces after extensive deacetylation

A

True

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16
Q

The plasma half life for nifedipine and diltiazem is 4 hours

A

True

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17
Q

The plasma half life for amlodipine is 35 hours

A

True

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18
Q

Amlodipine reaches peak plasma levels later than diltiazem and nifedipine

A

True

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19
Q

Amlodipine has a longer plasma half life than diltiazem and nifedipine

A

True

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20
Q

Calcium channel blockers prevent the transport of calcium across the plasma cell membrane of smooth muscle cells

A

True

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21
Q

Calcium channel blockers inhibit excitation contraction coupling and muscle constriction

A

True

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22
Q

Some calcium channel blockers I.e. Verapamil have varying effects on atrioventricular conduction and heart rate

A

True

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23
Q

Verapamil is predominantly used for dysrhythmias and not for cutaneous vascular diseases

A

True (verapamil is a strong depressor of AV conduction)

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24
Q

Beta1 adrenergic effect is vasodilatation

A

True

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25
Q

Alpha1 adrenergic effect is vasoconstriction

A

True

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26
Q

Alpha2 adrenergic effect is vasoconstriction

A

True

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27
Q

Thromboxane A2 induces vasoconstriction

A

True

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28
Q

Capsaicin induces vasodilatation

A

True (mediated by nitric oxide)

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29
Q

Calcitonin gene related peptide induces vasodilatation

A

True (mediated by nitric oxide)

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30
Q

Substance P induces vasodilatation

A

True (mediated by nitric oxide)

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31
Q

The calcium channel blocker agent of choice for Raynaud’s phenomenon is nifedipine

A

True

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32
Q

Nifedipine is superior to diltiazem in the treatment of recalcitrant chilblains

A

True

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33
Q

Nifedipine has in vivo anti platelet effects

A

True (in patients with systemic sclerosis)

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34
Q

The non-dihydropyridine calcium channel blocker verapamil is ineffective in treating Raynaud’s phenomenon

A

True

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35
Q

The non-dihydropyridine calcium channel blocker diltiazem may be useful in the treatment of calcinosis cutis

A

True (especially in patients with CREST syndrome)

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36
Q

Intralesional verapamil (non-dihydropyridine calcium channel blocker) has been used with some success in keloids and hypertrophic scars

A

True (and Peyronie’s disease)

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37
Q

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

A

True (CsA is a substrate of CYP3A4)

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38
Q

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

A

True (CsA is a substrate of CYP3A4)

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39
Q

Dihydropyridine Calcium channel blockers i.e. Amlodipine and nicardipine and the non-dihydropyridine calcium channel blocker diltiazem may reduce the necessary dose of cyclosporine

A

True (these calcium channel blockers have been shown to increase levels of cyclosporine via CYP 3A4 inhibition)

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40
Q

Calcium channel blockers rarely need to be ceased due to the adverse effects

A

True (although adverse effects are frequent, these rarely lead to cessation of therapy as dose reduction is typically sufficient to reduce the adverse effect)

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41
Q

Adverse effects are frequent in calcium channel blockers

A

True

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42
Q

Calcium channel blockers adverse effects are typically due to vasodilatation

A

True

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43
Q

Calcium channel blockers may cause dizziness

A

True (due to vasodilatation)

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44
Q

Calcium channel blockers may cause headaches

A

True (due to vasodilatation)

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45
Q

Calcium channel blockers may cause peripheral oedema

A

True (due to vasodilatation)

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46
Q

Calcium channel blockers may cause nausea

A

True (due to vasodilatation)

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47
Q

Calcium channel blockers may cause flushing

A

True (due to vasodilatation)

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48
Q

Symptomatic hypotension is uncommon in patients on calcium channel blockers

A

True

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49
Q

Nifedipine has more severe side effects than amlodipine

A

True

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50
Q

Nifedipine has more severe side effects than diltiazem

A

True

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51
Q

Calcium channel blockers may cause gingival hyperplasia

A

True (diltiazem > verapamil > nifedipine)

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52
Q

Calcium channel blockers may cause facial and truncal telegiectasia

A

True (vasodilatation)

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53
Q

Calcium channel blockers may cause new onset or exacerbation of psoriasis

A

True

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54
Q

Diltiazem may cause photodistributed hyperpigmentation particularly in African American women

A

True

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55
Q

Long term use of calcium channel blockers is associated with the development of chronic eczematous reactions in the elderly

A

True

56
Q

Calcium channel blockers may cause gynaecomastia

A

True

57
Q

Calcium channel blockers may cause oral ulcers

A

True

58
Q

Propanolol is a lipophilic beta blocker with a short half life and readily cross the blood brain barrier

A

True

59
Q

Carvedilol is a lipophilic beta blocker with a short half life and readily cross the blood brain barrier

A

True

60
Q

Metoprolol is a lipophilic beta blocker with a short half life and readily cross the blood brain barrier

A

True

61
Q

Propranolol is metabolised by the liver (lipophilic)

A

True

62
Q

Carvedilol is metabolised by the liver (lipophilic)

A

True

63
Q

Atenolol is a hydrophilic beta blocker with a longer half life and do not cross the blood brain barrier

A

True

64
Q

Sotalol is a hydrophilic beta blocker with a longer half life and do not cross the blood brain barrier

A

True

65
Q

Atenolol is excreted by the kidneys (hydrophilic)

A

True

66
Q

Sotalol is excreted by the kidneys (hydrophilic)

A

True

67
Q

Blockage of beta1-adrenergic receptor is cardio selective

A

True

68
Q

Metoprolol is a cardio selective beta blocker

A

True

69
Q

Atenolol is a cardio selective beta blocker

A

True

70
Q

Blockage of beta2-adrenergic receptor by non-selective agents I.e. Propranolol interferes with dilation of bronchioles and blood vessels

A

True

71
Q

Blockage of beta2-adrenergic receptor by non-selective agents I.e. Propranolol causes lipolysis

A

True

72
Q

Blockage of beta2-adrenergic receptor by non-selective agents I.e. Propranolol causes glycogenolysis

A

True

73
Q

Non-selective beta blocker I.e. Sotalol also possesses class III antiarhythmic features and increased risk of cardiac arythmias

A

True (not suitable for use in dermatology)

74
Q

Non-selective beta blocker I.e. Labetalol and Carvedilol also have alpha-adrenergic activity result in vasodilatation and further reducing blood pressure

A

True

75
Q

The non-selective beta blocker Propanolol (beta2-adrenergic reception blockade) has been successfully used to treat infantile haemangiomas

A

True (interferes with dilation of bronchioles and blood vessels)

76
Q

Non-selective beta blockers I.e. Propanolol and Carvedilol have been used in flushing with mixed success

A

True

77
Q

Bradycardia is a common side effect of beta blockers

A

True

78
Q

Hypotension is a common side effect of beta blockers

A

True

79
Q

Bronchospasm is a common side effect of beta blockers

A

True

80
Q

Fatigue is a common side effect of beta blockers

A

True

81
Q

Hypoglycaemia is a side effect of beta blockers reported in some paediatric patients undergoing treatment for infantile haemangioma

A

True

82
Q

Beta blockers have been associated with lichenoid drug, eczematous and psoriasiform eruptions

A

True

83
Q

Beta blockers may induce or worsen psoriasis

A

True (same as calcium channel blockers) - though more guttate psoriasis

84
Q

Salicylates I.e. Aspirin is rapidly absorbed and widely distributed

A

True

85
Q

Salicylates I.e. Aspirin reach peak plasma levels after 2 hours and slowly decline

A

True

86
Q

Salicylates I.e. Aspirin are mainly protein bound (50-80%) to plasma albumin and only the free drug is active

A

True

87
Q

Salicylates I.e. Aspirin is metabolised by the liver

A

True

88
Q

The amount of salicylates I.e. Aspirin metabolised by the liver is dependant on the rate of urinary excretion

A

True

89
Q

The rate and amount of salicylates I.e. Aspirin excreted in the urine depends on urinary pH

A

True (greater excretion in alkaline urine as salicylates are acidic)

90
Q

The urinary excretion of salicylates I.e. Aspirin is greater in alkaline urine

A

True

91
Q

Low dose aspirin acetylates platelet enzymes which are responsible for the synthesis of thromboxane A2

A

True

92
Q

Higher dose aspirin inhibits synthesis of prostacyclin (endogenous inhibitor of platelet aggregation)

A

True (this reverses the anti platelet effect of prostacyclin)

93
Q

Salicylates may cause exacerbation of asthma

A

True

94
Q

Hypersensitivity reactions I.e. Angioedema, urticaria, rhinitis may occur with salicylates

A

True

95
Q

Dyspepsia, peptic ulcer disease and upper GI bleeding are potential complications of aspirin therapy

A

True

96
Q

Dipyridamole is largely bound to plasma proteins

A

True

97
Q

Dipyridamole is metabolised in the liver

A

True

98
Q

Dipyridamole is excreted in the bile

A

True

99
Q

Dipyridamole inhibits platelet aggregation

A

True

100
Q

Dipyridamole is a vasodilator

A

True

101
Q

Dipyridamole has pro-fibrinolytic quality

A

True

102
Q

Dipyridamole may cause gastric upset

A

True

103
Q

Dipyridamole may cause worsening of coronary heart disease

A

True (causes tachycardia)

104
Q

Dipyridamole is contraindicated after recent myocardial infarction and in rapidly worsening angina

A

True (contraindicated as may cause worsening heart disease with tachycardia)

105
Q

Dipyridamole may cause dizziness

A

True (vasodilation)

106
Q

Dipyridamole may cause headache

A

True (vasodilation)

107
Q

Dipyridamole may cause hypotension

A

True (vasodilation)

108
Q

Dipyridamole may cause tachycardia

A

True (Contraindicated in recent myocardial infarction and rapidly worsening angina)

109
Q

Pentoxifylline is a non-specific phosphodiesterase inhibitor

A

True

110
Q

Pentoxifylline is a methyl-xanthine derivative

A

True

111
Q

Pentoxifylline is well absorbed

A

True

112
Q

Pentoxifylline undergoes extensive first pass metabolism in the liver

A

True

113
Q

Pentoxifylline is excreted in the urine

A

True

114
Q

Pentoxifylline reaches peak plasma levels within 2 hours

A

True

115
Q

Pentoxifylline has a half life of 4-6 hours

A

True

116
Q

Pentoxifylline reduces blood viscosity in the microcirculation

A

True

117
Q

Pentoxifylline has been used for the treatment of Raynaud’s phenomenon

A

True (reduces blood viscosity in the microcirculation)

118
Q

Pentoxifylline has been used for the treatment of venous insufficiency with ulcers

A

True (reduces blood viscosity in microcirculation)

119
Q

Pentoxifylline should be used with caution in patients with severe cardiac disease

A

True

120
Q

The dose of Pentoxifylline should be reduced in significant renal impairment

A

True (renal excretion)

121
Q

Sildenafil (Viagra) is a phosphodiesterase-5 inhibitor

A

True

122
Q

Sildenafil (Viagra) causes an increase in cyclic-GMP in the vasculature resulting in vasodilatation

A

True

123
Q

Sildenafil (Viagra) is metabolised in the liver primarily by CYP 3A4 and to a lesser extent by CYP 2C9

A

True

124
Q

Sildenafil (Viagra) has been used in systemic sclerosis associated Raynaud’s phenomenon

A

True

125
Q

Sildenafil (Viagra) is contraindicated with nitrates or nitric oxide donors

A

True

126
Q

Headache is a common adverse effect of sildenafil (Viagra)

A

True

127
Q

Flushing is a common adverse effect of sildenafil (Viagra)

A

True

128
Q

Nasal congestion is a common adverse effect of sildenafil (Viagra)

A

True

129
Q

Dyspepsia is a common adverse effect of sildenafil (Viagra)

A

True

130
Q

Sildenafil (Viagra) must be used cautiously in patients with history of risk factors for myocardial infarction and unstable angina

A

True

131
Q

Sildenafil (Viagra) must be used cautiously in patients with history of hypotension

A

True

132
Q

Sildenafil (Viagra) must be used cautiously in patients with history of hypertension

A

True

133
Q

Iloprost is a prostacyclin analog and a vasodilator

A

True

134
Q

Iloprost causes vasodilation and is used in Raynaud’s phenomenon

A

True

135
Q

Iloprost inhibits skin fibrosis

A

True

Derm Pharm 2020 (47 decks)

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