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IPAP JUNIOR SEM. > Pharm IV Drug And MOA > Flashcards

Pharm IV Drug And MOA Flashcards

1
Q

What is the MOA and Clin use of Anithistamines

A

Mechanism of Action:
Competitive H1 antagonist, or an inverse agonist, of the early response

Nonselective 
(1st generation or sedating) 
Peripherally selective 
(2nd generation or
 non-sedating)

Exhibits anticholinergic and some α1 antagonist properties (1st generation) and may have some anti-inflammatory action

Clinical Use: temporarily relieves symptoms due to hay fever or other upper respiratory allergies and common cold, sneezing, runny nose, itchy, watery eyes, itchy throat and nose

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2
Q

Brompheniramine

A

Antihistamine

Preferred by ACOG in pregnancy

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3
Q

Chlophenirmamine

A

Antihistamine

Perferred by ACOG in pregnancy

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4
Q

Diphenhydramine

A

Antihistamine

Very sedative with high anticholinergic effect

CAt B preg

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5
Q

Promethazine

A

Antihistamine

Very sedative high Anticholinergic effect

Used primarily for N/V

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6
Q

Hydroxyzine

A

Antihistamine

Used primarily for urticaria and itching

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7
Q

Meclizine

A

Antihistamine

Used primarily for vertigo

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8
Q

Cyproheptadine

A

Antihistamine

Used for anti-serotonin effects to combat serotonin syndrome

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9
Q

Fexofenadine

A

2nd gen antihistamine

Non sedating

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10
Q

Loratadine

A

2nd gen antihistamine

Non sedating
Claritin

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11
Q

Desloratadine

A

2nd gen antihistamine

Non sedating loratadine metabolite

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12
Q

Cetirizine

A

2nd gen antihistamine

Low sedation, but can still cause slight

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13
Q

Levocetirizine

A

2nd gen antihistamine

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14
Q

Azelastine

A

Instranasal antihistamine

Can Crosses the BBB

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15
Q

Olopatadine

A

Intranasal antihistamine

Selective H1 with low ADE

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16
Q

What is the MOA of Decongestants

A

Sympathomometics

Direct and indirect α1 agonists producing vasoconstriction of respiratory mucosa

Relieves congestion (no effect on itching, sneezing, or rhinorrhea)

Relaxation of the bronchioles

Increased heart rate and contractility

Pseudoephedrine enters the CNS readily

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17
Q

MOA and C/U for phenylephrine

A

Mechanism of Action:
Direct-acting, synthetic α1-agonist

Increases BP (SBP & DBP), dilates the pupil, constricts engorged ocular, nasal, and rectal vasculature to decrease redness and congestion, and shrinks hemorrhoids

Clinical Use:
Treatment of hypotension/vascular failure 2º shock

Mydriatic for eye procedures
Relief of eye redness, hemorrhoids, and nasal congestion

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18
Q

MOA and C/u for Oxymetazoline

A

Mechanism of Action:
Direct-acting α1 and α2 agonist

Eye drops or nasal spray produces vasoconstriction that decreases blood flow resulting in decreases ocular redness and nasal congestion

Clinical Use: ocular and nasal vasoconstrictor (relief of redness and congestion)

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19
Q

MOA and C/U fro pseudoephedrine

A

Mechanism of action: direct-acting α and β agonist (α>β), while also displacing norepinephrine from storage sites

Clinical Use: relief of nasal congestion (i.e., decongestant)

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20
Q

C/U for Coricidin

A

Marketed for people who are unable to take decongestants (high blood pressure)

Multiple combination products that exclude decongestants
—Chlorpheniramine is the typical ingredient found in these products

Coricidin HBP Cough & Cold (Dextromethorphan and Chlorpheniramine) Tablets

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21
Q

MOA and C/u for montelukast

A

Mechanism of Action: inhibits cysteinyl leukotriene, an inflammatory mediator released by the mast cell (i.e., anti-inflammatory properties), on target cells (LTC4, LTD4, LTE4)
(Leukotrine antagonist)

Clinical Use: comparable efficacy to the antihistamines, but less than intranasal steroids

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22
Q

MOA and C/U for intranasal saline

A

Mechanism of Action: irrigates and cleanses the nasal passages of mucous and allergens reducing inflammation

Clinical Use: may be recommended in all patients including infants and pregnant women unless directed otherwise

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23
Q

MOA and C/U instranasal steroids

A

Mechanism of Action: anti-inflammatory agents that inhibits the mediators released in both the early and late phase reaction

Clinical Use: most effective drugs for allergic rhinitis relieving all four symptoms

NOTE: short course of ‘oral burst’ therapy (i.e., prednisone 40 mg daily for adults and 1-2 mg/kg/day for children QAM x 5-7 days) may be used for severe, debilitating allergic rhinitis

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24
Q

Beclomethasone

A

I/N steroid

May exert significant systemic effects and decrease growth velocity

Low incidence of local side effects

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25
Q

Budesonide

A

I/N steroid

Preferred INS if pregnant (Cat B)

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26
Q

Fluticasone propionate

A

I/N steroid

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27
Q

Flunidolide

A

I/N steroid

May exert significant systemic effects and decrease growth velocity

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28
Q

Mometasone

A

I/N steroid

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29
Q

Triamcinolone

A

I/N steroid

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30
Q

MOA and C/U of Azelatine HCL plus Fluticasone

A

Azelastine: antihistamine

Clinical Use:
Approved to treat symptoms of seasonal allergic rhinitis in people 6 years of age and older who need treatment with both azelastine HCL and fluticasone propionate

Effective reduces stuffy nose, runny nose, itching, and sneezing

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31
Q

MOA of Anticholinergics

A

muscarinic antagonist, results in decreased nasal mucous secretion

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32
Q

Ipatropium

A

Atrovent

Anticholinergic
Preg Cat B

Mechanism of Action:
Short Acting Muscarinic Antagonist (SAMA)

Anticholinergic agent that appears to inhibit vagally-mediated reflexes by antagonizing the action of acetylcholine

Anticholinergics prevent the increases in intracellular concentration of Ca2+ which is caused by interaction of acetylcholine with the M3 receptor on bronchial smooth muscle

Clinical Use:
Use for the maintenance treatment of bronchospasm assisted with COPD

Not indicated for the initial treatment of acute episodes of bronchospasms where rescue therapy is required for rapid response

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33
Q

Cromolyn Sodium

A

Mechanism of Action: inhibits mast cell degranulation, which prevents the release of histamine and leukotrienes after contact with an antigen

Best used as preventative measure of symptoms

Preferred initial DOC during pregnancy for rhinorrhea and sneezing

Clinical Use: are extremely safe, but generally considered less efficacious than other therapies

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34
Q

Azelastine

A

H1 receptor antagonists decreases itching and vasodilation (tearing & swelling)

Non selective ocular antihistamine

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35
Q

Levocabastine

A

H1 receptor antagonists decreases itching and vasodilation (tearing & swelling)

Non selective ocular antihistamine

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36
Q

Ketotifen

A

Selective ocular antihistamine
OTC
Mechanism of Action: 2nd generation competitive H1 antagonist

Clinical Use:
Popular and likely the most effective agent

Combines fast-acting antihistamine relief with prophylactic actions

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37
Q

Olopatadine

A

Selective ocular antihistamine

RX! No OTC

Mechanism of Action: 2nd generation competitive H1 antagonist

Clinical Use:
Popular and likely the most effective agents
Combines fast-acting antihistamine relief with prophylactic actions

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38
Q

MOA of Ocular decongestants

A

Mechanism of Action: α-agonist that constricts conjunctival vessels thereby reducing redness & swelling

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39
Q

Naphazoline

A

Ocular decongestant

Most potent

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40
Q

Oxymetazoline

A

Ocular decongestant

Can cause rebound hyperemia

LONG acting

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41
Q

Tetrahydrozoline

A

Ocular decongestant

Intermediate acting

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42
Q

Lodoxamide

A

Ocular mast cell stabilizer

Mechanism of Action: stabilizes mast cells preventing degranulation and release of histamine and inflammatory mediators (e.g., leukotrienes, etc.)

Clinical Use:
The onset of action of ocular mast cell stabilizers is slower than other agents (i.e., prophylactic)

Therefore, it is most often used in combination with an ocular antihistamine

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43
Q

Nedocromil

A

Ocular mast cell stabilizer

Mechanism of Action: stabilizes mast cells preventing degranulation and release of histamine and inflammatory mediators (e.g., leukotrienes, etc.)

Clinical Use:
The onset of action of ocular mast cell stabilizers is slower than other agents (i.e., prophylactic)
Therefore, it is most often used in combination with an ocular antihistamine

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44
Q

Ketorolac

A

NSAID can be used in the eyes

Mechanism of action: decrease prostaglandin production resulting in relief of pain, inflammation, and ocular itching

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45
Q

Loteprednol

A

Ocular steroid

Can increase the risk of cataract formation

It is the only ocular steroid approved for use in seasonal allergic conjunctivitis

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46
Q

Albuterol

A

SABA

Mechanism of Action:
Act locally on β2 receptors in the bronchial to cause bronchodilation
Beta-adrenergic stimulation increase cycle AMP levels
Resulting in relaxation of bronchial smooth muscles and inhibition of the release of mediators from mast cells

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47
Q

L:evalbuterol

A

SABA

Mechanism of Action:
Act locally on β2 receptors in the bronchial to cause bronchodilation
Beta-adrenergic stimulation increase cycle AMP levels
Resulting in relaxation of bronchial smooth muscles and inhibition of the release of mediators from mast cells

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48
Q

Pirbuterol

A

SABA

Mechanism of Action:
Act locally on β2 receptors in the bronchial to cause bronchodilation
Beta-adrenergic stimulation increase cycle AMP levels
Resulting in relaxation of bronchial smooth muscles and inhibition of the release of mediators from mast cells

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49
Q

Formoterol

A

LABA

Mechanism of Action:
Act locally on β2 receptors in the bronchial to cause bronchodilation
Beta-adrenergic stimulation increase cycle AMP levels
Resulting in relaxation of bronchial smooth muscles and inhibition of the release of mediators from mast cells

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50
Q

Arformoterol

A

LABA

Mechanism of Action:
Act locally on β2 receptors in the bronchial to cause bronchodilation
Beta-adrenergic stimulation increase cycle AMP levels
Resulting in relaxation of bronchial smooth muscles and inhibition of the release of mediators from mast cells

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51
Q

Salmeterol

A

LABA

Mechanism of Action:
Act locally on β2 receptors in the bronchial to cause bronchodilation
Beta-adrenergic stimulation increase cycle AMP levels
Resulting in relaxation of bronchial smooth muscles and inhibition of the release of mediators from mast cells

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52
Q

Olodaterol

A

LABA

Mechanism of Action:
Act locally on β2 receptors in the bronchial to cause bronchodilation
Beta-adrenergic stimulation increase cycle AMP levels
Resulting in relaxation of bronchial smooth muscles and inhibition of the release of mediators from mast cells

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53
Q

Indacaterol

A

Ultra long acting BA

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54
Q

Indacaterol and glycopyrrolate capsule

A

Ultra long acting BA

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55
Q

Tiotropium Bromide

A

Long-Acting Muscarinic Antagonist (LAMA)

Anticholinergic agent that appears to inhibit vagally-mediated reflexes by antagonizing the action of acetylcholine

Anticholinergics prevent the increases in intracellular concentration of Ca2+ which is caused by interaction of acetylcholine with the M3 receptors on bronchial smooth muscle

Clinical Use:
Long-term, once daily maintenance treatment of bronchospasm associated with COPD, including chronic bronchitis and emphysema

Not indicated for the treatment of acute episodes of bronchospasms

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56
Q

Aclidinium

A

LAMA

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57
Q

Umeclidinium

A

LAMA

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58
Q

Theophylline/ Aminophyline

A

Mechanism of Action:
Methylxanthine (~caffeine)

Causes bronchodilation, diuresis, CNS and cardiac stimulation, and gastric acid secretion

Blocks phosphodiesterase (PDE) which increases tissue concentrations of cyclic adenine monophosphate (cAMP) which in turn promotes catecholamine stimulation of lipolysis, glycogenolysis, and gluconeogenesis and induces release of epinephrine from adrenal medulla cells

Clinical Use:
Adjunct to inhaled β2 selective agonists and systemically administered corticosteroids for the acute exacerbations of asthma and chronic lung diseases

Less effective and less well tolerated than inhaled LABA

Not recommended if long-acting bronchodilators are available and affordable

Some symptomatic benefit compared with placebo in stable COPD

Theophylline plus salmeterol produces greater increase in FEV1 and improve breathlessness post-bronchodilator lung function

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59
Q

Roflumilast

A

Mechanism of Action:

PDE4 inhibitor that reduces inflammation through inhibition of the breakdown of intracellular cyclic adenosine monophosphate (cAMP)

No direct bronchodilator activity

Clinical Use:
Daily treatment to reduce the risk of COPD exacerbations in patients with severe COPD (FEV1<50% of predicted) associated with chronic bronchitis and a history of frequent exacerbations

—COPD GOLD 3 and 4 patients
—History of exacerbations
—Chronic Bronchitis
—Reduces exacerbations treated with oral glucocorticosteroids

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60
Q

Omalizumab

A

Mechanism of Action:
Anti-IgE Monoclonal Anti-body:
Binds to circulating IgE, preventing it from binding to the high-affinity (FcRI) receptors on basophils and mast cells

Decreases mast cell mediator release from allergen exposure

Clinical Use:
Long-term control and prevention of symptoms in adults (12 yrs old) who have moderate or severe persistent allergic asthma inadequately controlled with ICS

Administered every 2 to 4 weeks; dependent on body weight and IgE level

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61
Q

Montelukast / Zafirlukast

A

Mechanism of Action: inhibits cysteinyl leukotriene, an inflammatory mediator released by the mast cell (i.e., anti-inflammatory properties), on target cells (LTC4, LTD4, LTE4)

Clinical Use:
Long-term control and prevention of symptoms in mild persistent asthma for patients

May be used with ICS as combination therapy in moderate persistent asthma

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62
Q

Zileuton

A

Mechanism of Action:
5-Lipoxygenase Inhibitor
Inhibits the production of leukotrienes from arachidonic acid

Clinical Use
Long-term control and prevention of symptoms in mild persistent asthma

Considered 2nd line agents (less effective anti-inflammatory agents than ICS)

May be used with ICS as combination therapy

May allow reduction in corticosteroid doses in some patients

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63
Q

Bupropion

A

Mechanism of Action: dopamine and norepinephrine reuptake (at high doses) inhibitor with minimal activity on serotonin

Clinical Use:
Smoking cessation
Brand Name Wellbutrin indicated for Depression

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64
Q

Varenicline

A

Mechanism of Action:
Partial neuronal α4 β2 nicotinic receptor agonist; prevents nicotine stimulation of mesolimbic dopamine system associated with nicotine addiction

Varenicline stimulates dopamine activity but to a much smaller degree than nicotine does, resulting in decreased craving and withdrawal symptoms

Clinical Use: smoking cessation

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65
Q

Glucocorticoids

A

Effects on intermediary metabolism and immune function

Major glucocorticoid is cortisol (also called hydrocortisone)

Has some mineralocorticoid effects

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66
Q

Mineralocorticoids

A

Primarily, sodium-retaining activity

Mineralocorticoids also act in the feedback regulation of pituitary
Cortiocotropin

Major mineralocorticoid is aldosterone

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67
Q

Clobetasol propionate

A

Very High Potency Steroid

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68
Q

Augmented betamethasone 0.05% Ointment and Gel

A

Very High potency Steroid

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69
Q

Fluocinonide 0.1%

A

Very High Potency Steroid

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70
Q

Augmented betamethasone 0.05 lotion and cream

A

High potency steroid

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71
Q

BEtamethasone o.o5 ointment

A

High Potency Steroid

72
Q

Triamcinolone acetonide 0.05%

A

High Potency Steroid

73
Q

Fluocinonide 0.05%

A

High potency steroid

74
Q

Betamethasone dipropionate 0.05% lotion and cream

A

Medium potency steroid

75
Q

Betamethasone valerate 0.1% and 0.12%(Luxiq)

A

Medium potency steroid

76
Q

Triamcinolone acetonide 0.025%- 0.1% (Kenalog)

A

Medium potency steroid

77
Q

Hydrocortisone valerate 0.2% (Westcort)

A

Medium potency steroid

78
Q

Fluocinolone acetonide 0.025%

A

Medium potency steroid

79
Q

Desonide 0.05% (Desonate)

A

Low potency steroid

80
Q

Hydrocortisone (OTC) 0.5%

A

Low potency steroid

81
Q

Hydrocortisone 1% (Cortizone-10) 2% and 2.5%

A

Low potency steroid

82
Q

Hydrocortisone acetate 1%

A

Low potency steroid

83
Q

Ointments

A

More lubrication and occlusion than other preparations

Occlusive property improves steroid absorption

More useful for treating dry or thick hyperkeratotic lesions

Should NOT be used on hairy areas (may cause maceration and folliculitis if used on intertriginous areas)

84
Q

Creams

A

Good lubricating properties; ability to vanish into the skin (patient preference)

Generally less potent than ointments of same medications; often contain preservatives

Acute exudative inflammation responds well to creams because of their drying effect

85
Q

Lotions and Gels

A

Least greasy and occlusive of all topical steroid vehicles

Lotions contain alcohol (drying effect on an oozing lesion)

Lotions are useful for hairy areas

Gels dry quickly and can be applied to the scalp or hairy areas

Beneficial for exudative inflammation, such as poison ivy

86
Q

Foams, mousses, shampoos

A

Effective for applying to the scalp and hairy areas

Typically more expensive

87
Q

Cortisone

A

Short acting oral steroid

primary and secondary adrenal cortical insufficiency (i.e., Addison’s)

88
Q

Hydrocortisone

A

Short acting oral steroid

primary and secondary adrenal cortical insufficiency, joint injections, acute asthma (injection only), and ulcerative colitis

89
Q

Prednisone

A

Formulations: tablets and syrup, no injection

Most prescribed oral medication for short term therapy in inflammatory disorders

90
Q

Dexamethasone

A

Long Acting Oral Steroid

Clinical Use:
Respiratory Diseases
Allergic states
Dermatologic Diseases

Endocrine disorders: 1st or 2nd adrenocortical insufficiency (hydrocortisone or cortisone is still the DOC)

Gastrointestinal Disease
Hematologic Disorders
Ophthalmic Diseases
In oncology for N/V

91
Q

Ketoconazole

A

Corticosteroid antagonist

Mechanism of Action:
Potent and nonselective inhibitor of adrenal gonadal steroid synthesis
Decreases the body’s production of corticosteroids

Clinical Use:
FDA approved as an antifungal but used for the treatment of hyper-adrenocorticalism (unapproved use)

Possible application in Cushing’s Disease when surgical resection is not possible

92
Q

Aldosterone

A

Mechanism of Action:
Target distal tubule and collecting ducts in the kidney

Results in sodium, bicarbonate, and water reabsorption

Clinical Use:
Addison Disease: adrenal glands do not produced enough cortisol and aldosterone

Target cells for aldosterone contain mineralocorticoid receptors that interact with the hormone in a manner similar to that of glucocorticoid receptors

Treatment:
Supplement cortisol and aldosterone deficiency with hydrocortisone and fludrocortisone

Hydrocortisone is identical to natural cortisol, is given to correct the deficiency; failure to do so results in death

93
Q

Fludrocortisone

A

Mechanism of Action:
Exogenous mineralocorticoid

Not used as a Glucocorticoid but has 15 times more glucocorticoid activity than hydrocortisone

Clinical Use:
Used to replace aldosterone activity in primary and secondary adrenocortical insufficiency, i.e. Addison’s Disease

94
Q

Pimecrolimus

A

Topical immuno modulator

Inhibit T cell activation in inflamed skin by blocking transcription of pro-inflammatory cytokines (i.e., interleukins and interferon gamma)

Bind to the FKBP-12 surface protein inhibiting calcineurin which blocks cytokine transcription

Calcineurin is a protein phosphate involved in activating T-cells of the immune system

95
Q

Tacrolimus

A

MOA: Inhibit T cell activation in inflamed skin by blocking transcription of pro-inflammatory cytokines (i.e., interleukins and interferon gamma)

Bind to the FKBP-12 surface protein inhibiting calcineurin which blocks cytokine transcription

Calcineurin is a protein phosphate involved in activating T-cells of the immune system

96
Q

Mupirocin

A

Topical antibiotic of choice for impetigo

Mechanism of Action: inhibits bacterial protein synthesis

Comes in a 2% cream and ointment

97
Q

benzoyl peroxide, retinoids, azelaic acid

A

Normalize follicular keratinization in acne treatment

98
Q

retinoids, hormone manipulation

A

Decrease sebum production in acne treatment

99
Q

antibiotics, benzoyl peroxide, retinoids, azelaic acid

A

Suppresses bacteria in acne treatment

100
Q

antibiotics, retinoids

A

Prevent inflammatory response in acne treatment

101
Q

Tropical metronidazole

A

DOC for papulopustular rosacea

102
Q

Azelaic acid

A

Mild to mod rosacea tx

Mechanism of Action: unknown, efficacy appears secondary to a combination of antimicrobial activity against acne-related microorganisms and anti-keratinizing effects on the follicular epidermis

Clinical Use:
Used for rosacea (15% foam/gel) or acne (20% cream)

Studies show efficacy comparable to tretinoin 0.05%, benzoyl peroxide 5% or erythromycin 2% (mild/moderate acne)

Advantage is minimal toxicity (cutaneous and systemic)

103
Q

Sodium Sulfacetamide 10% and Sulfur 5%

A

Sulfacet-R) combination therapy originally used to treat acne and seborrheic dermatitis, also effective in rosacea

104
Q

Brimonidine

A

Gel for the treatment of persistent (non-transient) erythema of rosacea in adults 18 years of age or older

Mechanism of Action:
Selective alpha-2 adrenergic agonist
May reduce erythema through direct vasoconstriction

Clinical Use: topical treatment of persistent (non-transient) erythema of rosacea in adults 18 years of age or older

105
Q

Benzoyl peroxide

A

Mechanism of Action:
Dual mode of action
Releases oxygen; lethal to the P. acnes (anaerobe)

An irritant; increases the turnover rate of epithelial cells

Increased sloughing

Promotes of resolution of comedones

Clinical Use:
Effective against both inflammatory and non-inflammatory acne vulgaris

The most effective topical acne vulgaris treatments

50-75% reduction in inflammatory lesions in 8-12 weeks

Efficacy enhanced when combined with other agents especially topical erythromycin

106
Q

What are the ABX that can Suppress P. acnes which minimizes the inflammatory response

A

Clindamycin 1% topical solution (Cleocin-T)

Erythromycin 2% topical solution (T-Stat)

Combination: Clindamycin and Benzoyl Peroxide (Benzaclin) and Erythromycin and Benzoyl Peroxide (Benzamycin)

Clinical Use:
Topical treatment of severe acne vulgaris (off-label for rosacea)

Most effective when combined with benzoyl peroxide or retinoids
Benzoyl peroxide reduces risk of resistance

107
Q

Retinoids

A

Mechanism of Action:
Vitamin A analogs

Reduces the production of sebum which is required by P. acnes

Reduces inflammation by inhibiting neutrophil and monocyte chemotaxis

Clinical Use:
Usually used for acne vulgaris after Benzoyl Peroxide trial and topical antibiotic failure

Can be used first line in inflammatory and non-inflammatory acne

Pregnancy (not recommended):
Tretinoin, adapalene are C; tazarotene and isotretinoin are X

Retinoids are degraded by UV light, should apply at evening/night

108
Q

Tretinoin

A

Topical retinoids

109
Q

Adapalene

A

Topical Retinoid

110
Q

Tazarotene

A

Topical retinoid

Shown to have best efficacy

Gel form appears to be more irritating than tretinoin

Indicated for psoriasis

111
Q

Isotretinoin

A

Clinical Use:
Only effective agent in severe cystic acne vulgaris

iPLEDGE registration: provider, patient, and pharmacy have to register to get the product

Pregnancy Category X
A negative pregnancy test must be obtained within 2 weeks before starting therapy

Initiated only on the second or third day of the next normal menstrual period

Two forms of contraception must be used during isotretinioin therapy and for one month after treatment has ended

112
Q

Azelaic Acid MOA and CU

A

Mechanism of Action: unknown, efficacy appears secondary to a combination of antimicrobial activity against acne-related microorganisms and anti-keratinizing effects on the follicular epidermis

Clinical Use:
Used for rosacea (15% foam/gel) or acne (20% cream)

Studies show efficacy comparable to tretinoin 0.05%, benzoyl peroxide 5% or erythromycin 2% (mild/moderate acne)

Advantage is minimal toxicity (cutaneous and systemic)

113
Q

MOA and Clin use of Topical Corticosteroids

A

Clinical Use:
1st line for mild to moderate Psoriasis

Can combine or alternate with vitamin D analogues, tazarotene or emollient to improve efficacy and reduce adverse effects

114
Q

Coal Tar MOA and C/U

A

Clinical Use:
Mild to moderate plaque psoriasis
Less effective than topical steroids
Consider for patients who can’t afford prescription options

Not used as much any more

115
Q

Vitamin D3 Analogs MOA and C/U

A

Mechanism of Action:
Calcitriol is an active form of vitamin D (D3)

Calcitriol is an endogenous hormone in the blood that regulates the concentration of calcium and phosphate in the bloodstream and promoting the healthy growth and remodeling of bone

Mechanism in psoriasis is unknown
Affect neuromuscular and immune function

Slows skin cell growth, flatten lesions, and remove scales

116
Q

Calcitriol Ointment 3mcg/g

A

Vitamin D3 Analog

117
Q

Calcipotriol aka calcipotriene 0.005%

A

Vitamin D3 Analog

118
Q

Calcipotriene 0.005% and Betamethasone dipropionate 0.064%.

MOA

A

Vit. D3 Analog

119
Q

What is the Clin Use of Vit D3 Analogs

A

Clinical Use:
Use for mild psoriasis as monotherapy and moderate to severe in combination

Used in various plaque psoriasis conditions

Combination with corticosteroid is more effective than either agent alone

Consider for maintenance; slower onset than topical steroids, sustained remission

Acids inactivate; other topical agents may be acidic should not apply at the same time; reasonable to alternate steroid in AM and Calcitrol/Calcipotriene PM

Calcitrol = calcipotriene in efficacy but calcitrol has less skin irritation

120
Q

Tazarotene MOA and C/U

A

Mechanism of Action:
Topical Retinoid

Vitamin A derivative

Modulates differentiation and proliferation of epithelial tissue

Reduces inflammation by inhibiting neutrophil and monocyte chemotaxis

Clinical Use:
Mild plaque psoriasis

Used with topical corticosteroid to reduce side effects and improve efficacy

Efficacy maintained for 12 weeks after stopping treatment

Indicated for acne vulgaris

121
Q

Acitretin PO MOA and CU

A

Mechanism of Action:
Oral Retinoid

Reduces inflammation by inhibiting neutrophil and monocyte chemotaxis

Clinical Use:
Monotherapy or adjunct to UVB phototherapy, biologics, potent corticosteroids, or calcipotriene (calcipotriol) for disease that is too severe, refractory, or extensive for topical

Less risk of organ toxicity than methotrexate or cyclosporine

122
Q

Cyclosporine PO

A

Clinical Use:
Disease that is too severe, refractory, or extensive for topicals

Example: Severe disease of the palms, soles, or scalp; involvement of 10% or more of body surface

Alternative to biologics for patients who prefer cheaper, oral option

Can be used along with topical vitamin D3 analogs or topical corticosteroids

123
Q

Apremilast

A 
Mechanism of Action:
Phosphodiesterase 4 (PDE4) Inhibitor

Reduction of numerous inflammatory mediators (eg, decreased expression of nitric oxide synthase, TNF-α, and interleukin [IL]-23, as well as increased IL-10)

Clinical Use:
Moderate to severe psoriasis in patients who are candidates for phototherapy or systemic therapy
Consider for patients who prefer an oral treatment with no lab monitoring

Less efficacious than cyclosporine but also fewer ADE’s

124
Q

Methotrexate

A

Mechanism of Action:
Folic acid antagonist, inhibits PURINE SYNTHESIS by acting on dihydrofolate dehydrogenase!!

Folic acid required for synthesis of amino acids required for DNA, RNA, and protein

Inhibits cytokine production and purine nucleotide biosynthesis
Leads to immunosuppressive and anti-inflammatory effects

Clinical Use:
Disease that is too severe, refractory, or extensive for topicals

Ex: severe disease of the palms, soles, or scalp; involvement of 10% or more of body surface

Trials show that less efficacious than biologics, but is much cheaper

125
Q

Adalimumab MOA and CU

A

HUMIRA!

Human IgG antibody to TNF-α

Moderate to severe psoriasis

Can be combined with methotrexate or acitretin

Risk of infections such as TB, lupus, demyelinating disorders, lymphoma and other cancers

Less toxic to the liver, kidneys, and bone marrow compared to methotrexate, acitretin, and cyclosporine

126
Q

Infliximab MOA and C/U

A

Remicade

Chimeric antibody to TNF-α (most effective)

Moderate to severe psoriasis
Can be combined with methotrexate or acitretin

Risk of infections such as TB, lupus, demyelinating disorders, lymphoma and other cancers

Less toxic to the liver, kidneys, and bone marrow compared to methotrexate, acitretin, and cyclosporine

127
Q

Etanercept MOA and CU

A

TNF-alpha for psoriasis

Clinical Use:
Moderate to severe psoriasis
Can be combined with methotrexate or acitretin

Risk of infections such as TB, lupus, demyelinating disorders, lymphoma and other cancers

Less toxic to the liver, kidneys, and bone marrow compared to methotrexate, acitretin, and cyclosporine

128
Q

Ustekinumab

A

Human antibody to IL-12 and IL-23

Clinical Use:
Moderate to severe psoriasis
Can be combined with methotrexate or acitretin

Risk of infections such as TB, lupus, demyelinating disorders, lymphoma and other cancers

Less toxic to the liver, kidneys, and bone marrow compared to methotrexate, acitretin, and cyclosporine

129
Q

Cervarix/ Gardasil

A

Prevention of Warts (HPV)

130
Q

Salicylic Acids

A

Most common Wart treatment

expect improvement in 1-2 weeks and resolution in 4-6 weeks

17% Liquid (DuoFilm, Compound W)
40% Plaster (Mediplast) – 2”X3” patches

131
Q

Podofilox

A

Gel solution for HPV warts

Podofilox is the active ingredient of podophyllum plant resin

Mechanism of action is unknown, but causes mortality of effective cells
Only used for external warts

Applied twice daily for 3 days, stop for 4 days and repeat up to 4 times

132
Q

Podophyllum resin

A

Treatment for HPV warts

Podofilox is the active ingredient of podophyllum plant resin

Mechanism of action is unknown, but causes mortality of effective cells
Only used for external warts

Applied twice daily for 3 days, stop for 4 days and repeat up to 4 times

133
Q

Imiquimod

A

Treatment for HPV warts

Mechanism of Action: topical immunomodulator that induces local cytokine induction

Clinical Use:
Cutaneous, genital and perianal warts (external only)

In combination with salicylic acid may be more effective for plantar warts than cryotherapy

Actinic keratoses on the face and scalp
Superficial basal cell carcinomas

134
Q

Sinecatechins Ointment

A

Partially purified fraction of green tea leaves from Camellia sinensis and consists of a mixture of catechins and other green tea components

Upregulate apoptosis-associated genes and to modulate and downregulate genes involved in the proinflammatory response to human papillomavirus (HPV) infection

Applied daily for 16 weeks
Medication was 55% vs. 35% clearance with placebo

135
Q

How do male condoms work

A

Thin sheath

collect sperm

Latex and polyurethane reduce risk of STDs

Lambskin do not prevent STDs

Disposable after single use

136
Q

How do female condoms work

A

Thin flexible plastic pouches

Prevents sperm from entering uterus

Reduces the risk of STDs

Disposable after a single use

137
Q

How do Diaphram contraceptives work

A

Shallow, flexible cup

Latex or soft rubber

Blocks sperm from entering uterus

Used with spermicidal cream or jelly
Remain in place for 6-8 hours

Remove within 24 hours

Fitted by a healthcare provider
Replace after 1 to 2 years

138
Q

How does a cervical cap contraceptive work

A

Small, rigid, thin silicone cup

Inserted into vagina before intercourse

Used with spermicidal cream or jelly

Remain in place for 6-8 hours

Remove within 48 hours

Fitted by healthcare provider
Can be used for 2 years

139
Q

How does a birth control sponge work

A

Soft, disposable, spermicide-filled foam sponges

Inserter before intercourse

Blocks sperm from entering uterus and kills sperm cells

Remain in place for 6 hours after intercourse

Remove within 30 hours

140
Q

How does spermicides work

A

Destroys sperm

Used alone or with diaphragm or cervical cap

Most common agent is nonoxynol-9
Available as foam, jelly, cream, suppository, and film

Insert close to uterus, < 30 mins prior to intercourse

Remain in place for 6 hours

141
Q

How do tubal implant contraceptives work

A

Nonsurgical blocking of fallopian tubes

Soft, flexible insert in Fallopian tube

Scar tissue forms and blocks tubes

142
Q

How does Tubal ligation work

A

Surgical procedure to cut, tie, and seal Fallopian tubes

Blocks path from ovaries to uterus

Egg cannot reach uterus

Sperm cannot reach egg

143
Q

How does a vasectomy work

A

Surgical cut and close off two vas
Deferns

Male still produces sperm

Sperm does not move out of testicles

May be reversible but is difficult

144
Q

How does and IUD work

A

Small, T-shaped device inserted in uterus
Fitted and removed by healthcare provider

Copper IUD 
—Remain in place for 12 years
Hormonal IUD
—Releases progestin in uterus
Remain in place for 3-5 years
145
Q

How does the vaginal ring contraceptive work

A

Thin, flexible, 2 inches in diameter

Delivers synthetic estrogen and a progestin analogs for 3 weeks

Remove for 4th week, insert new ring 7 days later

High estrogen content increases risk of blood clots, stroke, heart attack, or cancer

146
Q

How do BC implants work

A

Matchstick-sized rod placed under the skin of the upper arm

Releases a low dose of progestin

Protects for up to 3 years

Requires local anesthetic for insertion

Removed anytime before 3 years

147
Q

How do contraceptive patches work

A

Thin plastic patch

Releases hormones through skin into bloodstream

Place on lower abdomen, buttocks, outer arm, or upper body

Apply new patch once a week for 3 weeks

No patch on 4th week

High estrogen content increases risk of blood clots, stroke, heart attack, or cancer

Less effective in women weighing more than 198lbs (90kg), should NOT be used

148
Q

How does injectable BC work

A

Injection of a medroxyprogesterone

Given in arm or buttocks once every 3 months (IM vs SubQ)

Should eat diet rich in calcium and vitamin D

In adolescents can cause temporary loss of bone density

Most of the bone loss occurs during the first two years of therapy

149
Q

What is the role of estradiol, estrone, and estriol ?

A

Signals for growth of uterine lining during first part of menstrual cycle
Causes changes in breasts during adolescence and pregnancy
Regulates metabolic processes (i.e., bone growth and cholesterol levels)
Suppress LH and FSH release

Forms:

Ethinyl estradiol (EE)
Estradiol valerate (Natazia only)
Mestranol (not used often)
150
Q

What is the MOA of combined oral contraceptives

A

Suppress release of LH and FSH from pituitary gland via negative feedback by providing exogenous estrogen/ progesterone

Preventing ovulation

Thinning endometrium

Thickening cervical mucus

151
Q

What are the FDA approved uses of Oral contraceptives

A

Prevent pregnancy

Acne (Estrostep, OrthoTri-Cyclen, YAZ, Beyaz)

Premenstrual dysphoric disorder (YAZ, Beyaz)

Reduce heavy periods

152
Q

Natazia Clin use

A

First birth control pill clinically proven to help heavy monthly periods

153
Q

Levonorgestrel

A

Is an progestin component in OC

154
Q

Norethindrone

A

Progestin component in OC

155
Q

Desogestrel

A

Progestin component in OC

156
Q

Drospirenone

A

Progestin component in OC

Parent compound is spironolactone
No diuretic effect, has anti-mineralocorticoid effects, decreases bloating effect of ethinyl estradiol
Low androgenic: best for acne, hirsutism, or male pattern balding in women
Drug Interactions: drugs that increase potassium such as high doses of NSAIDs, heparin, ACE inhibitors, and potassium sparing diuretics

(YAZ)

157
Q

What is a low dose estrogen vs a high dose estrogen

A

20 -30 mcg is low dose

50 is high does

158
Q

Norgestimate

A

Progestin component in OC

159
Q

Dienogest

A

Progestin Component in OC

160
Q

Depo-Medroxyprogesterone Acetate (DMPA)

A

IM andSUBQ contraceptives

Q11-13 weeks

161
Q

Copper IUD

A

Mechanism of Action:
Copper ions inhibit sperm motility and acrosomal enzyme activation so that sperm seldom reach fallopian tube and are unable to fertilize the ovum

Does not interfere with ovulation and is not an abortifacient

Remain in body for up to 12 years

162
Q

Progestin IUD

A

Mechanism of Action:
Foreign object in uterus, prevents implantation

Thickens cervical mucus, thins endometrium, and inhibits sperm motility

Products
Mirena (5yrs) and Skyla (3yrs)

163
Q

Implanon and Nexplanon

A

Mechanism of Action:
Rod inserted in upper arm
Slowly releases progestin etonogestrel (3rd generation), which acts similarly to other progestin-only contraceptive

Active metabolite of desogestrel

Hormone: etonogestrel

60-70mcg/day during weeks 5-6 and then decreases to 35-45mcg/day by the end of the first year; 30-40 mcg/day after the second year; and 25-30mcg/day at the end of 3 years

Effective for up to 3 years

Clinical Use: long-term prevention of pregnancy

Not tested in women weighing more than 130% of their ideal body weight; may be less effective in overweight women

164
Q

Levonorgestrel

A

Mechanism of Action:
Inhibits ovulation
Prevents fertilization
Increases thickness of cervical mucus

Prevents implantation
By medical standards, not considered an abortifacient; does not disrupt an implanted and fertilized egg

Clinical Use:
Used after intercourse to prevent pregnancy

Should not be used as a routine method of contraception

Routine use of emergency contraceptives are less effective than other methods and may have greater incidence of adverse effects

165
Q

Ulipristal Acetate Rx

A

Emergency contraceptive

Prevents progestin from binding to the progesterone receptor
Indicated for emergency contraception within 120hrs of unprotected intercourse

Possibly 42% more effectiveness in preventing pregnancy than levonorgestrel at 72 hours

166
Q

Clin Use of Estrogen in Menopause

A

Clinical Use: symptomatic menopause and prevention of postmenopausal osteoporosis in women without a uterus (hysterectomy)

Hormone therapy in women who have not undergone hysterectomy should include a progestin in addition to estrogen

Without treatment, hot flushes typically subside within 1 to 2 years; in some pts continue for more than 20yrs

167
Q

Alendronate

A

Bisphosphonates

Selectively bind to the anti-resorptive surfaces of bone and may be incorporated into the bone

Works to decrease osteoclast activity
Decrease bone resorption, increase bone density, and prevent fractures
Inhibits normal and abnormal bone resorption

168
Q

Risedronate

A

Bisphosphonates

Selectively bind to the anti-resorptive surfaces of bone and may be incorporated into the bone

Works to decrease osteoclast activity
Decrease bone resorption, increase bone density, and prevent fractures
Inhibits normal and abnormal bone resorption

169
Q

Ibandronate

A

Bisphosphonates

Selectively bind to the anti-resorptive surfaces of bone and may be incorporated into the bone

Works to decrease osteoclast activity
Decrease bone resorption, increase bone density, and prevent fractures
Inhibits normal and abnormal bone resorption

170
Q

Zoledronic Acid

A

Bisphosphonates

Selectively bind to the anti-resorptive surfaces of bone and may be incorporated into the bone

Works to decrease osteoclast activity
Decrease bone resorption, increase bone density, and prevent fractures
Inhibits normal and abnormal bone resorption

171
Q

What is the CU of Bisphosphonates

A

1st line in most patients with osteoporosis

Treat osteoporosis and Paget’s Disease (excessive bone breakdown with disorganized remodeling)

Most reduce vertebral and non-vertebral fractures by 30-50%

Exception: Ibandronate reduces only vertebral fractures

172
Q

Denosumab

A

Member of the TNF receptor family
Monoclonal antibody that binds to RANK ligand (RANKL), inhibiting osteoclast formation and activity

Clinical Use (not enough long-term use data):
Due to lack of evidence, cost and ADE’s usually not first line agent for osteoporosis

Treatment of osteoporosis/bone loss in men and women due to:
Androgen depravation (men)
Estrogen depravation (women)
All other etiologies

Used as initial therapy in patients at high risk for fracture

173
Q

What is the CU of Calitonin in OSteo

A

Clinical Use:
No longer recommended for treatment of Osteoporosis (use bisphosphonates or denosumab)

Only benefit is to reduce pain from osteoporotic fracture (use short-term then switch)

FDA indications:
Treatment of osteoporosis in women more than 5 years post menopause

Hypercalcemia

Paget’s disease (bone cancer)

174
Q

Teriparatide

A

Mechanism of Action: chronic exposure to PTH or PTHrP results in bone resorption.

However, intermittent administration of recombinant human PTH (either full-length 1-84 or fragment 1-34) or PTHrP 1-34 has been shown to stimulate bone formation more than resorption and reduce fractures.

Clinical Use:
Patients with high risk of fractures (T-score of -3.5 or below )

Unable to tolerate bisphosphonates or have failed
Glucocorticoid-induced osteoporosis

175
Q

Raloxifene

A

SERM

Clinical Use:
Prevention and treatment of osteoporosis in:
—Postmenopausal women at high risk of breast cancer
—Postmenopausal women who cannot take bisphosphonate therapy

Women in their 50s or 60s concerns about long-term bisphosphonate safety

IPAP JUNIOR SEM. (43 decks)

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