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systemic pharm > ED > Flashcards

ED Flashcards

1
Q

Phosphodiesterase Inhibitors
Alpha-2 Antagonists
Prostaglandin-E1 Analogs

A

ED Drug classes

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2
Q

what does phosphodiesterase do?

A

it forms phosphate bonds

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3
Q

ED has many physical and psychological causes, including what?

A

vascular disease, diabetes, medications, depression, and sequelae to prostatic surgery

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4
Q

Erectile dysfunction (ED) is the inability to maintain what?

A

maintain penile erection for the successful performance of sexual activity

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5
Q

first line therapy for men with ED?

A

Because of the efficacy, ease of use, and safety of oral phosphodiesterase (PDE) inhibitors, these drugs are now considered to be first-line therapy for men with ED

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6
Q

-afil suffix

A

ED therapy

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7
Q 
INDICATION
Erectile Dysfunction (Viagra®)
Pulmonary Arterial Hypertension (Revatio®)
DOSING [25, 50, 100 mg]
1 tab qd prn
A

SILDENAFIL CITRATE

INDICATION

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8
Q

CLINICAL PHARMACOLOGY
Vasodilator
Mechanism of Action
PDE-5 Inhibitor; sustains the vasodilatory effects of nitric oxide-dependent synthesis of cGMP

A

sildenafil citrate moa

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9
Q

nitric oxide is what?

A

free radical –> binds to anything –> causes damage

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10
Q

key mechanism of attack used by white blood cells

A

free radicals –> will kill invading organism

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11
Q

what does NO do?

A 
stimulates vasodilation
inhibits platelet aggergation
inhibits monocyte adhesion
inhibits ldl oxidation
inhibits superoxide radical elaboration (in low doses antiinflammatory)
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12
Q

what are 6 things NO do?

A

stimulates vasodilation
inhibits platelet aggergation
inhibits LDL oxidation
inhibits superoxide radical elaboration (in low doses antiinflammatory)
inhibits smooth muscle cell proliferation (seen in artherosclerosis)
inhibits monocyte adhesion (adhesion of monocytes to vessel wall –> first step of it leaving blood stream and entering tissue=antiinflammatory)

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13
Q

what cell makes no?

A

endothelial cell

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14
Q

larginine + no –> NO (lipid soluble) –> enters muscle cell –> GC is stimulated (has heme moiety) –> converts GTP into cyclicGMP –> energy of cleavage produces GMP

A

no induced vasodilation mechanism

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15
Q

cyclic GMP –> activates kinases that activate ion channels that lead to closure of ion channels and muscle relaxation

A

how does cyclic gmp work?

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16
Q

pde5 does what?

A

breaks cgmp and turns it into GMP

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17
Q

IF WE inhibit cgmp, what happens?

A

continues to stimulate kinase causing relaxation

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18
Q

where else is pde5 found?

A

lungs; therefore is also used in pulmonary hypotension

19
Q

if pde5 is not selected, and pde3 is what will happen?

A

inhibit contraction of heart muscle

20
Q

why is pde6 special?

A

its selectivity is only 10 percent less than pde5; and its responsible for color vision and retinal phototransduction

21
Q

why is pde6 special?

A

its selectivity is only 10 percent less than pde5; and its responsible for color vision and retinal phototransduction

22
Q

disc of rod is important because?

A

contains rhodopsin, which in the presence of light takes trans configuration; in absence of light takes cis

23
Q

light –> rhodopsin –> isomerization –> activates transducin –> pde6 activation –> degrade cGMP –> ion channels will close –> (in light, less sodium is entering the cell) –> hyperpolarization

A

rod phototrandsuction and pde mechanism

24
Q

viagra depends on what molecule to initiate vasodilation?

A

NO

25
Q

lack of selectivity of viagra, will inhibit activity in what?

A

possibly phototransduction –> impacting vision

26
Q

ADVERSE EFFECTS
Common: headache, abnormal vision, dizziness, nasal congestion
SERIOUS ADVERSE EFFECTS
CV: MI, stroke, ventricular tachycardia, hypotension/shock
Hematology: anemia, leukopenia
OCULAR ADVERSE EFFECTS
Ocular: Retinal heme, NAION, vision loss, elevated IOP, cyanopsia

A

sildenafil citrate (adverse effects)

27
Q

ADVERSE EFFECTS
Common: headache, abnormal vision, dizziness, nasal congestion
SERIOUS ADVERSE EFFECTS
CV: MI, stroke, ventricular tachycardia, hypotension/shock
Hematology: anemia, leukopenia
OCULAR ADVERSE EFFECTS
Ocular: Retinal heme, NAION, vision loss, elevated IOP, cyanopsia

A

sildenafil citrate (adverse effects)

28
Q

SILDENAFIL CITRATE
DRUG INTERACTIONS
Azole Antifungals, Erythromycins, Cyclosporine (Reduced metabolism)
Alpha-Blockers, Beta-Blockers (Additive)

A

SILDENAFIL CITRATE

DRUG INTERACTIONS

29
Q

SILDENAFIL CITRATE
DRUG INTERACTIONS
Azole Antifungals, Erythromycins, Cyclosporine (Reduced metabolism)
Alpha-Blockers, Beta-Blockers (Additive)

A

SILDENAFIL CITRATE

DRUG INTERACTIONS

30
Q

pde5 and seratonin do what to blood?

A

pde5 is found in platelets; seratonin helps form platelets

31
Q

pde5 and seratonin do what to blood?

A

pde5 is found in platelets; seratonin helps form platelets

32
Q

pde5 and seratonin do what to blood?

A

pde5 is found in platelets; seratonin helps form platelets

33
Q

how is viagra eliminated?

A

hepatic metabolism involving p450-3a4 enzyme

34
Q

retinitis pigmentosa is partly a genetic disorder of what?

A

retinal phosphodiesterases

35
Q

what is released during sexual arousal?

A

NO

36
Q

what do PDE’s promote?

A

cyclic GMP (cGMP) degradation

37
Q

PDE5 is found where?

A

arterial wall smooth muscle of the penis and lung vasculature

38
Q

PDE3’s selectivity is what?

A

> 700 (cardiac contractility)

39
Q

PDE6’s selectivity is what?

A

10 less (retinal phototransduction; color vision)

40
Q

PDE6’s selectivity is what?

A

10 less (retinal phototransduction; color vision)

41
Q

what is PDE5?

A

in platelets, thus, its inhibition poses a potential risk of hemorrhage

42
Q

PDE5 is found where?

A

skeletal muscle

43
Q

what does pde5 do?

A

arterial venous dilation

systemic pharm (16 decks)

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