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Dermatology Board Prep > DERM (12) Medical Therapy > Other Systemic Medications > Flashcards

Other Systemic Medications Flashcards

1
Q

What are the primary histamine receptors involved in cutaneous itch?

A

H1, not H2

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2
Q

What is a disease for which histamine levels are clearly elevated?

A

Urticaria and angioedema (some forms). This is in contrast to atopic dermatitis where histamine levels likely are not a large contributor

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3
Q

Though H1 receptor antagonists are primarily used in dermatology for what disease can H2 blockers be added?

A

In chronic urticaria a H2 receptor blocker can be considered, but there is poor evidence for this

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4
Q

Which antihistamines are most often used during pregnancy?

A

Usually diphenhydramine or chlorpheniramine due to long safety record

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5
Q

What is the primary difference seen between the first and second-generation antihistamines and why is this seen?

A

Second-generation antihistamines are less sedating because they are less lipophilic and have decreased ability to cross the blood-brain barrier.

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6
Q

Main adverse effects of first-generation H1 antihistamines?

A

Sedation, impaired cognitive function and anticholinergic effects (dry mouth, constipation, dysuria, blurred vision) [use caution with these medications in men with enlarged prostate and dysuria. Likewise, avoid in elderly patients]

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7
Q

What are some important side effects of cyproheptadine?

A

Interferes with hypothalamic function and increases appetite, can also slow/inhibit growth in children

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8
Q

What are the first-generation H1 antihistamines metabolized by?

A

P450 system

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9
Q

Side effects of second-generation H1 antihistamines?

A

Less sedating, anticholinergic effects much less common (but caution must still be used in high-risk patients).

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10
Q

What is the most sedating of the second-generation antihistamines?

A

Cetirizine, 10% get drowsiness

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11
Q

What should be done in patients with hepatic or renal diseases taking second-generation antihistamines?

A

Loratidine, Cetirizine and derivatives should be dose reduced

fexofenadine is not metabolized by the liver and is largely excreted as is

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12
Q

What is the strongest of the oral antihistamines that we typically use in dermatology?

A

Doxepin. This tricyclic antidepressant has both H1 and H2 properties and is a much stronger antagonist of these than typical antihistamines

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13
Q

What is a potential side effect of topical doxepin?

A

Can cause allergic contact dermatitis and drowsiness

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14
Q

Some important side effects and contraindications for doxepin?

A

Do not give with other antidepressants, don’t give in those with severe heart disease, can decrease the seizure threshold, may induce manic episodes in patients with manic-depressive disorder

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15
Q

What is the mechanism of hydroxyurea?

A

Impairs DNA synthesis through inhibition of ribonucleotide diphosphate reductase; hypomethylates DNA resulting in altered gene expression

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16
Q

What are the dermatologic uses for hydroxyurea?

A

off label treatment of recalcitrant psoriasis, Sweet’s syndrome, erythromelalgia, and hypereosinophilic syndrome

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17
Q

What is the most common side effect of hydroxyurea?

A

Megaloblastic anemia (myelosuppressive)

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18
Q

What skin eruptions can hydroxyurea cause?

A

Dermatomyositis-like eruption, lichenoid drug eruption resembling graft-versus-host disease, leg ulcers, alopecia, photosensitivity, radiation recall, and hyperpigmentation of the skin and nails.

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19
Q

What is the mechanism of cyclophosphamide?

A

An alkylating agent (directly damages DNA via cross-linking).

  • Nitrogen mustard derivative
  • Aldophophamide is one of the metabolites and is cleaved intracellularly into acrolein and enhances cellular damage by depleting glutathione stores.
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20
Q

Uses of cyclophosphamide in dermatology?

A

Mycosis fungoides (advanced, FDA approved)

  • Off label: ocular cicatricial pemphigoid, severe systemic vasculitides, neutrophilic dermatoses, and autoimmune connective tissue diseases.
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21
Q

How frequent is hemorrhagic cystitis and what causes it in cyclophosphamide administration?

A

This occurs in 5-41% as a result of acrolein.

  • Can be prevented by good hydration and administration of mesna (binds acrolein in blader and reduces irritation)
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22
Q

What are some common side effects of cyclophosphamide administration?

A

Nausea and vomiting are the most common side effects. Can give ondansetron and dexamethasone to decrease these

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23
Q

What are the long term effects of cyclophosphamide administration and hemorrhagic cystitis and how should they be monitored?

A

Associated with an increased risk of transitional cell carcinoma of the bladder, non-Hodgkin’s lymphoma, leukemia, and squamous cell carcinoma.

  • Monitor with periodic urine analysis with cytologic examination
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24
Q

What side effect is possible in women of childbearing age?

A

Infertility amenorrhea (27-60%); premature ovarian failure (up to 80%)

25
Q

Cutaneous side effects of cyclophosphamide?

A

permanent pigmented band on the teeth, anagen effluvium, and hyperpigmentation of the skin and nails

26
Q

What is the mechanism of action for Chlorambucil?

A

Alkylating agent which damages DNA via cross-linking

27
Q

What the uses for Chlorambucil for dermatology?

A

NXG, pyoderma gangrenosum, and several immunobullous and connective tissue diseases, such as Behcet’s’ and dermatomyositis

28
Q

Contraindication for chlorambucil?

A

Allergy to nitrogen mustard

29
Q

Side effects of chlorambucil?

A

nausea, vomiting, azoospermia, amenorrhea, pulmonary fibrosis, hepatotoxicity, bone marrow suppression, and oral ulcers

-Epileptogenic and mood-altering potential

30
Q

What ist he mechanism of spironolactone for dermatologic purposes?

A

Antiandrogen and blocks androgen receptor. This decreases androgen production

31
Q

Dermatologic uses for spironolactone?

A

Hirsutism, acne, and androgenetic alopecia

32
Q

What is the mechanism of action of finasteride and dutasteride?

A

Finasteride = Type II 5-alpha reductase inhibitor (5-alpha reductase converts testosterone to dihydrotestosterone

Dutasteride = Type I and type II 5-alpha reductase inhibitor

33
Q

Uses for finasteride/dutasteride in dermatology?

A

Hirsutism, hidradenitis suppurativa and androgenic alopecia (Dutasteride may be more effective based on recent trials)

34
Q

Side effects of finasteride/dutasteride?

A

Decreased libido, impotence, and abnormal ejaculation, gynecomastia, decreased risk of prostate cancer but a slight increase in high-grade prostate cancer and breast cancer. It is teratogenic

35
Q

What is the mechanism of Danazol and stanozolol?

A

Complex, involves an increase in production of proteins made by the liver including clotting factors, inhibitor of first component of complement (C1 INH), fibrinolytic proteins

36
Q

What are the dermatologic uses for Danazol and Stanozolol?

A

Hereditary angioedema, cryofibrinogenemia, lipodermatosclerosis, and livedoid vasculitis

37
Q

Side effects of Danazol and Stanozolol?

A

Hormone-related: hirsutism, deeper voice, alopecia, acne, and menstrual irregularities

  • Muscle cramps, myalgias, myopathy (in patients on statins especially), hematuria/hemorrhagic cystitis, insulin resistance, headaches, worsening HTN and CHF, hyperlipidemia, and hepatic effects like jaundice and liver tumors

DON’T GIVE IN PREGNANCY OR CHILDHOOD

38
Q

What is clofazimine used for in dermatology?

A

Riminophenazine dyne, it’s used as an antibiotic and anti-inflammatory

Antibiotic: antimycobacterial, especially multibacillary leprosy and erythema nodosum leprosum

Anti-inflammatory: SLE, pyoderma gangrenosum, erythema dyschromicum perstans, and discoid lupus

39
Q

Side effects of clofazimine?

A

Reversible orange-brown skin and body fluid discoloration, xerosis, and crystal deposition in organs which can lead to enteropathy/splenic infarction/eosinophilic enteritis/cardiac dysrhythmia

40
Q

Mechanism of action for colchicine?

A

Binds tubulin dimers in leukocytes which then causes mitotic arrest in metaphase and decreases chemotaxis

41
Q

Dermatologic uses for colchicine?

A

Familial Mediterranean fever (treatment of choice), neutrophilic dermatoses like Behcet’s, cutaneous small-vessel vasculitis autoimmune connective tissue disorders and gout

42
Q

What are the principle side effects of colchicine?

A

GI (cramping, diarrhea, and abdominal pain) more rarely there can be bone marrow suppression, neuropathy, and myopathy

43
Q

What is the mechanism of action for nicotinamide (B3)?

A

Inhibits PARP1 which leads to decreased NFkappaB transcription which then leads to decreased leukocyte chemotaxis lysosomal enzyme release, and it stabilizes leukocytes by inhibiting PDE which leads to immunomodulatory effects. There is also decreased lymphocytic transformation/antibody production and decreased mast cell degranulation

44
Q

Side effects for nicotinamide?

A

Rare, occasional GI complaints, flushing and headaches

45
Q

Dermatologic uses for nicotinamide?

A

Pellagra, autoimmune bullous disorders (combined with tetracyclines), NMSC chemoprevention (23% reduction according to NEJM study)

46
Q

What is the mechanism of action for potassium iodide?

A

Unknown, likely antiinflammatory (especially towards neutrophils)

47
Q

Dermatologic uses for potassium iodide?

A

sporotrichosis erythema nodosum, and erythema induratum

48
Q

Side effects are seen with potassium iodide?

A

Hypothyroidism (with chronic high-dose treatment mostly in people that had preexisting thyroid dz), acneiform, dermatitic, and vascular, GI (most common), iodism (metallic taste, sore/burning mouth, and headache), and exacerbation of dermatitis herpetiforms

49
Q

Contraindications and screening for potassium iodide?

A

Don’t give high doses in pregnancy, can lead to goiter and hypothyroidism in the fetus (pregnancy class D)

  • Check for pre-existing thyroid dz prior to starting
50
Q

Mechanism of action of thalidomide?

A

Anti-inflammatory effects are the main ones for dermatology

Anti-inflammatory: Inhibits TNF-alpha and IFN-gamma, decreased IL-12 production, decreased t-helper cells, decreased PML chemotaxis, and decreased histamine/acetylcholine/prostaglandins

Vascular: decreases angiogenesis –> effect on Kaposi’s sarcoma and AVM in the GI tract

51
Q

Dermatologic uses for thalidomide?

A

Neural effects: prurigo nodularis

vascular effects: Kaposi’s sarcoma

Erythema nodosum leprosum (FDA approved), HIV-related disorders, lupus erythematosus, GVHD, neutrophilic dermatoses (Behcet’s dz)

52
Q

Side effects of thalidomide?

A

Teratogenic (category X, most common defect is phocomelia), peripheral neuropathy (proximal muscle weakness + painful paresthesias/sensory loss), venous thrombosis, hypersensitivity reaction, (more common in HIV patients), sedation/drowsiness (most common), constipation and various drug interactions

53
Q

What is the program that monitors thalidomide in the US?

A

STEPS, it is like I-Pledge for thalidomide

54
Q

What is the mechanism of Pentoxifylline?

A

Phosphodiesterase inhibitor: increased erythrocyte/leukocyte deformability, decreased platelet aggregation, decreased TNF-alpha, decreased neutrophil adhesion

55
Q

What is pentoxifylline used for in dermatology?

A

Raynaud’s livedoid vasculopathy, necrobiosis lipoidica, venous ulcers, and lipodermatosclerosis

56
Q

What are the side effects of pentoxifylline?

A

GI mostly, decrease dose in renal dysfunction

57
Q

What are two anticholinergics for hyperhidrosis?

A

glycopyrrolate and oxybutynin

58
Q

What are the side effects of glycopyrrolate and oxybutynin?

A

glycopyrrolate: dry mouth and blurred vision, seizures (rare), hyperthermia (rare)
oxybutynin: urinary retention, constipation and the ones above

DERM (12) Medical Therapy (7 decks)

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