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Integ > Drugs > Flashcards

Drugs Flashcards

1
Q

Erythromycin and Clindamycin:

MOA, Clinical, Adverse Effects,

A

MOA: It is a 50S subunit inhibitor, and is a bacteriostatic and inhibits protein synthesis.

Bacteriostatic.

Clindamycin causes pseudomembranous colitis

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2
Q

Benzoyl Peroxide

A

MOA: absorbed by skin –> benzoic acid –> metabolized by purine–> oxidize of bacterial proteins. Is

Clinical: acne rosacea.

Used in combo with antibiotics. Greater efficacy and decreased resistance.

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3
Q

Dapsone

MOA
Adverse Effects:

A

MOA: antibacterial and antibacterial

Adverse Effects: Methemoglobinemia and orange staining of skin benzoyl peroxide.

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4
Q

Azelaic Acid

MOA, Clinical Uses

A

MOA: anti comedome, anti-hyperproliferation, competitive inhibitor of mitochondrial oxidoreducatases and 5 alpha reductase, which lowers hyperpigmentation.

Clinical: Lightens post inflammatory hyperpigmentation, mild inflammatory acne, and comedonal acne.

Adverse Effects: Hypo-pigmentaton of the skin

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5
Q

Doxyxlycline, Minocycline, Tetracycline

MOA, Clinical Uses

A

MOA: 16rRNA of the 30s subunit, preventing binding of aminoacyl tRNA to the acceptor site

Clinical Uses: for inflammatory acne vulgaris

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6
Q

Clotrimazole and Miconazole.
MOA:
Adverse Effects:

A

MOA: Inhibit CYP450 14 alpha- demethylase (essential enzyme in ergosterol synthesis)

Clinical: Tinea Corporis, Tinea Cruris, tinea pedis, tine versicolor, Tina nigra.

Miconazole: is used for diaper dermatitis complicated by Candida albicans infection.

Adverse Effects: irritation, burning/ stinging,

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7
Q

Ketaconazole:

MOA:

Clinical Uses: (Topical)

Adverse Effects (oral)

Contraindications:

Do not use:

A

MOA: same as all azoles

Shampoo/ foam: seborrheic dermatitis, white and black piedra.

Clinical Uses:

Shampoo: Seborrheic Dermatitis

Topical: Tinea pedis, Tinea Cruris, Tinea Corporis

Clinical oral: chromomycosis, paracoccidioidimycosis, mucocutaneous candidiadis.

Do not use: if patient has achrohydria, is on bicarb, antacids, H2-blockers or PPIs

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8
Q

Itraconazole and Fluconazole
MOA
Clinical Aspects

A

MOA: CYP-450 14 alpha Demethylase needed for ergosterol synthesis.

Clinical Aspects: Used for onychomycosis.

Itraconzole: white pierdra, lobo mycosis, chromoblastomycosis

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9
Q

Terbinafine:

MOA
Clinical Use:
Oral Use:
Topical:

Side Effects:

A

MOA: It affects squalene epoxidase–> stops ergosterol synthesis

Clinical: first line for the dermatophytosis

Topical: tinea corporis, curries, versicolor and nigra

Oral: First choice for onychomycosis

Side Effects: Are change or loss of taste and smell. Not recommended in patients with renal or hepatic failure or in pregnant women.

Not recommended for renal or hepatic failure in women.

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10
Q

Naftinine:
MOA:
Clinical:
Adverse Effects:

A

MOA: same as any oral allylamine.
Clinical: tinea, corporis, pedis, curries.
Anti-inflammatory activity.
Adverse Effects:

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11
Q

Butenafine:

MOA:
Clinical
Adverse Effects

A

works as general allylamine

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12
Q

Griseolfulvin:
MOA:
Clinical:
Contraindications:

A

MOA: inhibition of mitotic spindle and inhibition of fungal mitosis

Clinical: Tinea Capitis , fungistatic and requires long time to be useful

Contraindications: pregnancy, patients with poryphria and hepatic failure

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13
Q

Ciclopirox Olamine

A

MOA: chelation of polyvalent cations resulting in stopping of metal dependent enzymes that are responsible for degradation of peroxides within fungal cell.

Clinical: Mild to moderate onychomycosis of fingernails and toenails. Seborrheic dermatitis, white piedra.

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14
Q

Imiquimod:
MOA:
Clinical:
Adverse Effects:

A

MOA: TLR7 agonist for immune cells and induces production of interferons alpha and gamma

Clinical: genital and perianal warts, common warts and cutaneous warts

Molluscum contagium

HSV off label.

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15
Q

Cimetidine:

MOA
Clinical
Adverse Effects:

A

MOA: immunoomdulatory effects by histamine induced T suppressor cell activity.

Clinical: warts in children, and molluscum contagious in small children

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16
Q

Lindane:
MOA:
Clinical Use
Contraindications:

A

MOA: It is directly absorbed by the parasites and ova through exoskeleton.

It activates the nervous system–> causes seizures and death of parasitic arthropods.

Clinical: scabies and lice.

Contra: potential for neurotoxicity and hematoxivity.

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17
Q

Crotamiton:
MOA:

A

MOA: scabicidal activity, and antipruritic effects.

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18
Q

Permethrin:

MOA:
Clinical:

A

MOA: inhibits sodium ion channel through sodium ion cell membranes channels. Paralysis and death of the parasite.

Clinical: head lice and nits (lotion and cream), and scabies

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19
Q

Ivermectin:

MOA:
Clinical:

A
  1. Glutamate gated chloride channel binding–> increases cl ions, and hyperpolarization of nerve of muscle cell and death of parasite

Clinical: topical heals lice and rosacea in adults, and immature onchocerciasis.

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20
Q

Praziquantel

MOA:
Clinical:

A

MOA: increases cell permeability to schistosomes, and causes there to be strong contractions and paralysis of worm musculature.

Clinical: Schistosoma adult forms

`

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21
Q

Glucocorticoids

MOA:
Clinical Uses:

A

MOA: anti-inflammatory and immunosuppressive effects. Used for inflammatory and pruritic conditions.

MOA: bind to glucocorticoid response elements in DNA.

Adverse Effects: Tachyphylaxis

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22
Q

Hydrocortisone

Clinical:

A

Clinical: corticoid responsive dermatoses

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23
Q

Betamethasone

A

Clinical: corticoid responsive dermatoses, plaque psoriasis

24
Q

Halobetasol

A

Clinical: corticosteroid responsive dermatoses, plaque psoriasis

25
Clobetasol
Clinical: Corticosteroid responsive dermatoses, psoriasis. Adverse: growth retardations
26
Adapalene MOA: Clinical: Adverse Effects:
MOA: binds to RAR. Comedolytic, normalize desquamation. Clinical: bactericidal with activity abasing P. Acnes
27
Tretinoin:
MOA: comedlytic, normalize desquamation
28
Tazarotene:
MOA: prodrug hydrolyzed to tazoretinic acid. Binds to RAR. Anti-inflammatory, anti proliferative and immunological activity. Clinical: acne vulgaris, psoriasis, facial mottled hyper and hypopigmentation, and benign facial lentigenes. Pregnancy Category X
29
Isotretinoin
MOA: Decreased sebum, C.acnes concentration and inflammation. Strong comedolytic effects, Teratogen, patients f childbearing age must be on 2 forms of contraception and monthly pregnancy checks should be done.
30
How do antihistamines work?
Sedating and used for nighttime itch. Non-sedating H1 receptor and H2 receptor have almost limited effect in treatment of chronic itch. Elderly population: may be confusion and urinary retention.
31
Diphenhydramine MOA: Clinical/ Adverse:
MOA: blocks the H1 receptor Clinical: for chronic urticaria, nocturnal itch, and drug related itch Contra: not for neonates, premature infants, and nursing mothers. Note: topical products are not OTC for children under 2 yeas.
32
``` Doxepin MOA: Clinical: Adverse Effects: Contraindications: ```
MOA: blocks H1 and H2 receptors Clinical: nocturnal urticaria Contraindication: QT prolonging.
33
Hydroxyzine
MOA: it is basically a H1 receptor blocker. Clinical: Histamine mediated pruritis, and pruritis due to allergic conditions
34
Hydroquinone: MOA: Adverse Effects:
MOA: inhibits tyrosine kinase Clinical: temporarily reduces hypo pigmentation There is possible carcinogenicity
35
Monobenzone
MOA: irreversible depigmentation Clinical: for vitiligo patiens, some percutaneous absorption takes place.
36
Mequinol Contraindications:
MOA: Substrate for the enzyme tyrosinase, competitive inhibitor of formation of melanin precursor. Clinical: solar lentigenes Contraindications: mequinol and tretinoin can cause fetal harm
37
Minoxidil
MOA: Stimulates hair growth secondary to vasodilation. Androgenic Alopecia: reverses progressive miniaturization of terminal scalp hairs.
38
Finasteride
MOA: 5 alpha reductase inhibitors --> blocks testosterone to DHT conversion. Clinical: promotes hair growth and prevents further hair loss
39
Bimatoprost
MOA: synthetic analog of prostaglandin Clinical: hypertrophichosis of eyelashes.
40
Acitretin
check the slide
41
Calcipotriene
Synthetic Vitamin D3, binds to D3 receptors and inhibits keratinocyte proliferation Clinical: Plaque type psoriasis vulgaris.
42
Calcitriol
Better tolerated and used treat plaque psoriasis
43
Etanercept
TNF receptor dimer that binds to both TNF alpha and TNF beta. Decoy receptor not a monoclonal antibody.
44
Infliximab
Partially humanized mouse antibody against TNF alpha
45
Adalimumab
Fully human IgG1 antibody. that binds to TNF Clinical: moderate to severe plaque psoriasis, psoriatic arthritis
46
Certolizumab
binds selectively and neutralizes TNF alpha activity. Does not induce complement activation, ab dependent cell mediated cytotoxicity or apoptosis. Moderate to severe plaque psoriasis, psoriatic arthritis
47
Ustekinumab
MOA: human Ig1K monoclonal antibody. Binds with high affinity and specificity to p40 subunit of IL-12 and IL-23 --> inhibits chemokine and cytokine release used for moderate to severe plaque psoriasis
48
Guselkumba, Tildrazkizumbab, Rizankizumab
IgI1 monoclonal antibody. Binds to p-19 subunit of IL-23 same as ustekinumba.
49
Secukinumab, Ixekizumab
binds to IL-17A, inhibits release of pro inflammatory cytokines and chemokine. S--> IgG1 I--> IgG 4
50
Brodalumab
Humanized Ig2 monoclonal antibody that binds selectively to IL-17A receptor suicidal ideation and behavior.
51
Ipilimumab
Ig1- Anti-CTLA-4 antibody that binds to CTLA 4 that down regulates the T cell activation. Treats melanoma + metastatic to the brain
52
Nivolumab and Pembrolizumab
Ig4-Anti-PD antibody to L1/L2 Melanoma and lymph nodes cancer
53
Aldesleukin
IL-2--> increases WBC, lymphocyte toxicity, killer cell activity, IFN-gamma production. Adverse: capillary leak syndrome CI: only for patients with normal cardiac and pulmonary function
54
Encororafenib Cobimetinib
BRAF inhibitor and combined with +Binemetinib + Vermurafinib and reversible MAPK inhibitor
55
Dabrafenib
+Trametinib V600E +K inhibits mutated BRAF including 600E
56
Actinic Keratosis
Topical treatment for precancerous Actinic keratosis--> Diclofenac/ Doclifenyak

Integ (3 decks)

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