Pharm IV Drug And MOA Flashcards
What is the MOA and Clin use of Anithistamines
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
Brompheniramine
Antihistamine
Preferred by ACOG in pregnancy
Chlophenirmamine
Antihistamine
Perferred by ACOG in pregnancy
Diphenhydramine
Antihistamine
Very sedative with high anticholinergic effect
CAt B preg
Promethazine
Antihistamine
Very sedative high Anticholinergic effect
Used primarily for N/V
Hydroxyzine
Antihistamine
Used primarily for urticaria and itching
Meclizine
Antihistamine
Used primarily for vertigo
Cyproheptadine
Antihistamine
Used for anti-serotonin effects to combat serotonin syndrome
Fexofenadine
2nd gen antihistamine
Non sedating
Loratadine
2nd gen antihistamine
Non sedating
Claritin
Desloratadine
2nd gen antihistamine
Non sedating loratadine metabolite
Cetirizine
2nd gen antihistamine
Low sedation, but can still cause slight
Levocetirizine
2nd gen antihistamine
Azelastine
Instranasal antihistamine
Can Crosses the BBB
Olopatadine
Intranasal antihistamine
Selective H1 with low ADE
What is the MOA of Decongestants
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
MOA and C/U for phenylephrine
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
MOA and C/u for Oxymetazoline
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)
MOA and C/U fro pseudoephedrine
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)
C/U for Coricidin
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
MOA and C/u for montelukast
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
MOA and C/U for intranasal saline
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
MOA and C/U instranasal steroids
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
Beclomethasone
I/N steroid
May exert significant systemic effects and decrease growth velocity
Low incidence of local side effects
Budesonide
I/N steroid
Preferred INS if pregnant (Cat B)
Fluticasone propionate
I/N steroid
Flunidolide
I/N steroid
May exert significant systemic effects and decrease growth velocity
Mometasone
I/N steroid
Triamcinolone
I/N steroid
MOA and C/U of Azelatine HCL plus Fluticasone
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
MOA of Anticholinergics
muscarinic antagonist, results in decreased nasal mucous secretion
Ipatropium
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
Cromolyn Sodium
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
Azelastine
H1 receptor antagonists decreases itching and vasodilation (tearing & swelling)
Non selective ocular antihistamine
Levocabastine
H1 receptor antagonists decreases itching and vasodilation (tearing & swelling)
Non selective ocular antihistamine
Ketotifen
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
Olopatadine
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
MOA of Ocular decongestants
Mechanism of Action: α-agonist that constricts conjunctival vessels thereby reducing redness & swelling
Naphazoline
Ocular decongestant
Most potent
Oxymetazoline
Ocular decongestant
Can cause rebound hyperemia
LONG acting
Tetrahydrozoline
Ocular decongestant
Intermediate acting
Lodoxamide
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
Nedocromil
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
Ketorolac
NSAID can be used in the eyes
Mechanism of action: decrease prostaglandin production resulting in relief of pain, inflammation, and ocular itching
Loteprednol
Ocular steroid
Can increase the risk of cataract formation
It is the only ocular steroid approved for use in seasonal allergic conjunctivitis
Albuterol
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
L:evalbuterol
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
Pirbuterol
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
Formoterol
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
Arformoterol
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
Salmeterol
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
Olodaterol
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
Indacaterol
Ultra long acting BA
Indacaterol and glycopyrrolate capsule
Ultra long acting BA
Tiotropium Bromide
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
Aclidinium
LAMA
Umeclidinium
LAMA
Theophylline/ Aminophyline
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
Roflumilast
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
Omalizumab
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
Montelukast / Zafirlukast
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
Zileuton
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
Bupropion
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
Varenicline
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
Glucocorticoids
Effects on intermediary metabolism and immune function
Major glucocorticoid is cortisol (also called hydrocortisone)
Has some mineralocorticoid effects
Mineralocorticoids
Primarily, sodium-retaining activity
Mineralocorticoids also act in the feedback regulation of pituitary
Cortiocotropin
Major mineralocorticoid is aldosterone
Clobetasol propionate
Very High Potency Steroid
Augmented betamethasone 0.05% Ointment and Gel
Very High potency Steroid
Fluocinonide 0.1%
Very High Potency Steroid
Augmented betamethasone 0.05 lotion and cream
High potency steroid
BEtamethasone o.o5 ointment
High Potency Steroid
Triamcinolone acetonide 0.05%
High Potency Steroid
Fluocinonide 0.05%
High potency steroid
Betamethasone dipropionate 0.05% lotion and cream
Medium potency steroid
Betamethasone valerate 0.1% and 0.12%(Luxiq)
Medium potency steroid
Triamcinolone acetonide 0.025%- 0.1% (Kenalog)
Medium potency steroid
Hydrocortisone valerate 0.2% (Westcort)
Medium potency steroid
Fluocinolone acetonide 0.025%
Medium potency steroid
Desonide 0.05% (Desonate)
Low potency steroid
Hydrocortisone (OTC) 0.5%
Low potency steroid
Hydrocortisone 1% (Cortizone-10) 2% and 2.5%
Low potency steroid
Hydrocortisone acetate 1%
Low potency steroid
Ointments
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)
Creams
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
Lotions and Gels
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
Foams, mousses, shampoos
Effective for applying to the scalp and hairy areas
Typically more expensive
Cortisone
Short acting oral steroid
primary and secondary adrenal cortical insufficiency (i.e., Addison’s)
Hydrocortisone
Short acting oral steroid
primary and secondary adrenal cortical insufficiency, joint injections, acute asthma (injection only), and ulcerative colitis
Prednisone
Formulations: tablets and syrup, no injection
Most prescribed oral medication for short term therapy in inflammatory disorders
Dexamethasone
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
Ketoconazole
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
Aldosterone
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
Fludrocortisone
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
Pimecrolimus
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
Tacrolimus
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
Mupirocin
Topical antibiotic of choice for impetigo
Mechanism of Action: inhibits bacterial protein synthesis
Comes in a 2% cream and ointment
benzoyl peroxide, retinoids, azelaic acid
Normalize follicular keratinization in acne treatment
retinoids, hormone manipulation
Decrease sebum production in acne treatment
antibiotics, benzoyl peroxide, retinoids, azelaic acid
Suppresses bacteria in acne treatment
antibiotics, retinoids
Prevent inflammatory response in acne treatment
Tropical metronidazole
DOC for papulopustular rosacea
Azelaic acid
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)
Sodium Sulfacetamide 10% and Sulfur 5%
Sulfacet-R) combination therapy originally used to treat acne and seborrheic dermatitis, also effective in rosacea
Brimonidine
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
Benzoyl peroxide
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
What are the ABX that can Suppress P. acnes which minimizes the inflammatory response
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
Retinoids
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
Tretinoin
Topical retinoids
Adapalene
Topical Retinoid
Tazarotene
Topical retinoid
Shown to have best efficacy
Gel form appears to be more irritating than tretinoin
Indicated for psoriasis
Isotretinoin
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
Azelaic Acid MOA and CU
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)
MOA and Clin use of Topical Corticosteroids
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
Coal Tar MOA and C/U
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
Vitamin D3 Analogs MOA and C/U
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
Calcitriol Ointment 3mcg/g
Vitamin D3 Analog
Calcipotriol aka calcipotriene 0.005%
Vitamin D3 Analog
Calcipotriene 0.005% and Betamethasone dipropionate 0.064%.
MOA
Vit. D3 Analog
What is the Clin Use of Vit D3 Analogs
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
Tazarotene MOA and C/U
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
Acitretin PO MOA and CU
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
Cyclosporine PO
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
Apremilast
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
Methotrexate
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
Adalimumab MOA and CU
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
Infliximab MOA and C/U
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
Etanercept MOA and CU
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
Ustekinumab
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
Cervarix/ Gardasil
Prevention of Warts (HPV)
Salicylic Acids
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
Podofilox
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
Podophyllum resin
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
Imiquimod
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
Sinecatechins Ointment
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
How do male condoms work
Thin sheath
collect sperm
Latex and polyurethane reduce risk of STDs
Lambskin do not prevent STDs
Disposable after single use
How do female condoms work
Thin flexible plastic pouches
Prevents sperm from entering uterus
Reduces the risk of STDs
Disposable after a single use
How do Diaphram contraceptives work
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
How does a cervical cap contraceptive work
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
How does a birth control sponge work
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
How does spermicides work
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
How do tubal implant contraceptives work
Nonsurgical blocking of fallopian tubes
Soft, flexible insert in Fallopian tube
Scar tissue forms and blocks tubes
How does Tubal ligation work
Surgical procedure to cut, tie, and seal Fallopian tubes
Blocks path from ovaries to uterus
Egg cannot reach uterus
Sperm cannot reach egg
How does a vasectomy work
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
How does and IUD work
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
How does the vaginal ring contraceptive work
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
How do BC implants work
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
How do contraceptive patches work
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
How does injectable BC work
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
What is the role of estradiol, estrone, and estriol ?
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)
What is the MOA of combined oral contraceptives
Suppress release of LH and FSH from pituitary gland via negative feedback by providing exogenous estrogen/ progesterone
Preventing ovulation
Thinning endometrium
Thickening cervical mucus
What are the FDA approved uses of Oral contraceptives
Prevent pregnancy
Acne (Estrostep, OrthoTri-Cyclen, YAZ, Beyaz)
Premenstrual dysphoric disorder (YAZ, Beyaz)
Reduce heavy periods
Natazia Clin use
First birth control pill clinically proven to help heavy monthly periods
Levonorgestrel
Is an progestin component in OC
Norethindrone
Progestin component in OC
Desogestrel
Progestin component in OC
Drospirenone
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)
What is a low dose estrogen vs a high dose estrogen
20 -30 mcg is low dose
50 is high does
Norgestimate
Progestin component in OC
Dienogest
Progestin Component in OC
Depo-Medroxyprogesterone Acetate (DMPA)
IM andSUBQ contraceptives
Q11-13 weeks
Copper IUD
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
Progestin IUD
Mechanism of Action:
Foreign object in uterus, prevents implantation
Thickens cervical mucus, thins endometrium, and inhibits sperm motility
Products
Mirena (5yrs) and Skyla (3yrs)
Implanon and Nexplanon
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
Levonorgestrel
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
Ulipristal Acetate Rx
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
Clin Use of Estrogen in Menopause
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
Alendronate
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
Risedronate
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
Ibandronate
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
Zoledronic Acid
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
What is the CU of Bisphosphonates
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
Denosumab
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
What is the CU of Calitonin in OSteo
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)
Teriparatide
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
Raloxifene
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
