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BASIC Exam Study Guide > Adverse effects, monitoring and proper use of medications > Flashcards

Adverse effects, monitoring and proper use of medications Flashcards

1
Q

Name the mechanism of action for cyclosporine.

  • What does it form a complex with and what does it inhibit?
  • What is its ultimate effect on cytokines and immune cells?
A
  • Forms complex with cyclophilin, inhibiting calcineurin (an intracellular enzyme) and decreasing activity of NFAT-1 (nuclear factor of activated T-cells)
  • Leads to decreased IL-2 production and activity of T-cells
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2
Q

What weight should be used for calculating the cyclosporine starting dose?

A

Ideal body weight

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3
Q

What is the maximum daily dermatologic dose for cyclosporine?

  • What is the maximum duration of therapy?
A

5 mg/kg/day for up to 1 year

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4
Q

What are indications for cyclosporine?

  • What is it FDA approved and the treatment of choice for?
  • What are other off label uses?
A
  • FDA approved for psoriasis
  • Treatment of choice for erythrodermic psoriasis (along with infliximab)
  • Off-label uses are many and include atopic dermatitis, neutrophilic dermatoses (e.g., pyoderma gangrenosum), lichen planus, bullous dermatoses, connective tissue diseases and pityriasis rubra pilaris
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5
Q

What are the notable side effects associated with cyclosporine?

  • How does it affect the kidneys, gums, blood and skin?
  • What does it increase the risk of in psoriasis patients?
A
  • Nephrotoxicity
  • Known increased risk of NMSC in psoriasis patients
  • Gingival hyperplasia
  • Electrolyte derangements (uric acid, Mg, K)
  • Hypertension
  • Hyperlipidemia
  • Hypertrichosis
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6
Q

What are ways to reduce the risk of cyclosporine’s side effects?

  • Dosage?
  • When do you dose adjust?
  • Duration?
A
  • Use dermatologic doses (i.e., 2.5 to 5 mg/kg/day)
  • Dose adjust when Cr increases by 30%
  • Do not use for longer than 1 year
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7
Q

What is the preferred treatment for cyclosporine-associated hypertension?

  • Why are they the preferred treatment?
A

Calcium channel blockers (e.g., nifedipine or isradipine)

  • Because CCBs do not alter cyclosporine serum levels!
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8
Q

What should be monitored while on cyclosporine?

  • What physical exam finding and labs?
  • What baseline lab work should be obtained?
A
  • Blood pressure
  • Cr
  • Obtain baseline CBC, BMP, Mg, uric acid, LFTs and fasting lipid profile
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9
Q

What is the mechanism of action for methotrexate?

  • What does it inhibit and prevent the conversion of?
A
  • Competitively inhibits dihydrofolate (DHF) reductase, blocking folic acid
  • Prevents conversion of DHF to THF, which is needed to make purines
  • Inhibits cell division
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10
Q

What (2) medications is used for rescue of high-dose methotrexate adverse effects or overdose?

  • These medications bypases what enzyme?
A
  • Leucovorin (folinic acid), a naturally occurring version of folate (vitamin B9), or thymidine
  • These medications bypasses DHF reductase (which is inhibited by methotrexate).
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11
Q

True or false:

According to a recent Cochrane review, co-administration of folates and methotrexate REDUCES the efficacy of methotrexate.

A

False

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12
Q

What cumulative dose of methotrexate triggers concern for hepatic fibrosis?

  • What special populations should you be extra careful with?
A
  • Greater than 1.5 to 4 grams, especially for those with liver disease, hepatitis, alcohol abuse or psoriasis
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13
Q

What is the gold standard to assess for methotrexate-induced hepatic fibrosis?

  • What may be considered in special populations prior to starting methotrexate?
A

Liver biopsy

  • A pretreatment liver biopsy may be considered in those with baseline transaminitis, liver disease, heritable liver disease, diabetes, obesity, alcohol use or concurrent use of other hepatotoxic drugs.
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14
Q

What are indications for the use of methotrexate?

  • What is it FDA approved for? (2)
  • What are other off label uses?
A
  • FDA approved for severe or recalcitrant psoriasis and Sezary syndrome
  • Off label use includes pityriasis lichenoides et varioliformis acuta (PLEVA), LyP, mycosis fungoides, bullous dermatoses, connective tissue diseases, sarcoidosis and cutaneous vasculitis
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15
Q

What are absolute contraindications for the use of methotrexate? (2)

A
  • Pregnancy (category X)
  • Breastfeeding
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16
Q

What are the notable side effects of methotrexate use?

  • How does it affect the lungs? Blood?
  • Kidneys? Skin? Bone marrow?
  • What other notable “reactions” may occur?
A
  • Acute pneumonitis and pulmonary fibrosis
  • Pancytopenia within first 4-6 weeks
  • GI upset
  • Nephrotoxicity
  • Phototoxicity
  • Myelosuppression (especially when used with other agents that inhibit folic acid metabolism, including sulfonamides, or increase methotrexate plasma levels, including tetracyclines, anticonvulsants and NSAIDs)
  • UV and radiation recall reactions
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17
Q

What are important lab monitoring points for methotrexate?

  • What should be obtained initially?
A
  • CBC with diff
  • BMP
  • LFTs
  • Viral hepatitis panel (initially)
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18
Q

Methotrexate can rarely cause what classic cutaneous reaction?

A

UV and radiation recall reactions

  • Radiation recall ranges from sunburn-like erythema to necrosis, ulceration and bleeding
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19
Q

What is the mechanism of action of retinoids?

  • What does it bind to?
  • What does it inhibit?
A
  • Binds cytosolic retinoid binding protein, which is transported to the nucleus, where it binds nuclear receptors, especially RAR-gamma of keratinocytes
  • Inhibits AP1, NF-IL-6 and TLR2 (all important in inflammation)
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20
Q

How do topical retinoids affect the layers of the skin?

  • How do they affect the epidermis?
  • What do they increase in the dermis?
A
  • Increase thickness of stratum corneum
  • Epidermal hyperplasia
  • Correction of atypia
  • Disperse melanin granules (increasing pigment uniformity)
  • Increase dermal collagen I
  • Increase papillary dermal elastic fibers
  • Increase hyaluronic acid
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21
Q

What nuclear factors and cytokines are affected by retinoids?

  • What do they inhibit?
  • What do they increase/decrease?
A
  • Inflammation is decreased by inhibiting AP1, NF-IL-6 and TLR-2
  • Increases Th1 cytokines and decreases Th2 cytokines (helpful in CTCL)
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22
Q

What are the notable mucocutaneous side effects associated with systemic retinoids?

  • How might they affect the nose and lips?
  • What special lesions may occur?
A
  • S. aureus colonization of nasal mucosa in isotretinoin patients
  • Pyogenic granuloma-like lesions
  • Cheilitis (dry lips)
  • Photosensitivity
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23
Q

What are the notable systemic side effects of systemic retinoids?

  • How might they affect the CNS? Blood? Bones?
A
  • Pseudotumor cerebri (especially when co-administered with tetracyclines)
  • Pancreatitis secondary to hypertriglyceridemia
  • Diffuse idiopathic skeletal hyperostosis (DISH)
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24
Q

What is the most common lab abnormality associated with systemic retinoids?

  • When should you discontinue them?
A

Hyperlipidemia/hypertriglyceridemia

  • Discontinue if fasting TGs > 800 mg/dL because of pancreatitis risk
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25
What is important to know about LFTs and **systemic retinoids**? * When does this usually occur? * When should **systemic retinoids** be discontinued? * Which **systemic retinoid** is most likely to cause this?
* Usually transient and early (i.e., **within 2 to 8 weeks of starting treatment**) * **If levels are greater than 3x upper limit of normal, then discontinue** * **More frequent with acitretin** than isotretinoin or bexarotene
26
What are special side effects associated with **bexarotene** (an oral retinoid)? (2)
* **Agranulocytosis** (neutropenia, eosinopenia) * **Central hypothyroidism**
27
What are notable interactions with **systemic retinoids**? * Food? * Acitretin in particular? * Isotretinoin in particular? * Bexarotene in particular?
* **Fatty meals increase bioavailability** because oral retinoids are lipophilic * **EtOH + acitretin = hepatotoxicity** * **Isotretinoin + tetracyclines = pseudotumor cerebri** * **Bexarotene + gemfibrozil = severe hypertriglyceridemia** due to increased bexarotene plasma levels
28
What are examples of **TNF-alpha inhibitors**? * Which is given as an infusion?
* **Etanercept** (Enbrel) * **Infliximab** (Remicade), given as an infusion * **Adalimumab** (Humira)
29
What are indications for **TNF-alpha inhibitors**? * What are they FDA approved for? * What are off label uses?
* FDA approved for **plaque psoriasis** and **psoriatic arthritis** * Off label uses include bullous dermatoses, neutrophilic dermatoses, connective tissue diseases, granulomatous diseases, HS and PRP
30
What are the notable side effects associated with **TNF-alpha inhibitors**? * What can occur at injection site? * What is special about infliximab? * What diseases may occur? Infections?
* Injection site reactions (etanercept \> adalimumab), likely due to delayed-type hypersensitivity * **_Inf_**usion reactions (**_inf_**liximab) * Infliximab-associated-antidrug antibodies * Unmasking of a demyelinating disease * Psoriasis, palmoplantar pustulosis, cutaneous vasculitis * Increased risk of lymphoma and skin cancer * Infections, including TB and opportunistic infections * Congestive heart failure (particularly infliximab, which is infused)
31
What are important lab monitoring points with **TNF-alpha inhibitors**? * What should be checked at baseline? Annually?
* PPD or quantiFERON gold (annually) * Viral hepatitis panel (at baseline) * CBC with diff * LFTs
32
True or false: TNF-alpha inhibitors **can be used safely** with _active_ hepatitis C infection.
**True**
33
What are the notable side effects of **vismodegib**, the sonic hedgehog pathway inhibitor used for BCC? (3)
* **Muscle spasms (#1)** * Alopecia * Dysgeusia (distorted taste)
34
What is the mechanism of action of **5-fluorouracil**? * What does it inhibit and prevent the conversion of?
* A **competitive inhibitor of thymidylate synthase**, which normally converts doxyuridine to thymidine * **Decreases DNA synthesis**
35
What are the FDA approved indications for **5-fluorouracil**? (2)
* AKs * sBCCs
36
What is the mechanism of action of **imiquimod** (Aldara)? * What does it activate? What is ultimately released?
* Activates TLR-7 and TLR-8, activating NF-κB transcription factor * Leads to TNF-alpha and IFN-gamma release, activating immune system * Also has antiangiogenic and proapoptotic properties * Ultimately, this leads to tumor destruction
37
What are the FDA approved indications for **imiquimod** (Aldara)? (3)
* AKs * Superficial BCCs * Genital/perianal warts
38
What are the notable adverse effects associated with **imiquimod** (Aldara)? * What can occur especially if large areas are treated? * What can be exacerbated? * What pregnancy category is it?
* Flu-like or GI symptoms if larger areas are treated * Psoriasis exacerbations * Pregnancy category C (i.e., risk cannot be ruled out)
39
What are the proposed mechanisms by which **antimalarials** work? * How do they affect DNA? Macrophages?
* **Both immunosuppressive and anti-inflammatory** * Most likely intercalates into DNA, preventing further translation/transcription, therefore **inhibiting UV-induced cutaneous reactions** * Decrease ability of macrophages to express MHC complexes on cell surface * Reduces lysosomal size and impairs chemotaxis
40
If you develop _retinopathy_ on **antimalarials**, can you continue taking it?
**No! Retinopathy is an _absolute_ contraindication.**
41
What are the FDA approved indications for **antimalarials**? (3) * What are off label uses?
* **SLE** * **Malaria** * **Rheumatoid arthritis** * Off label: DLE, dermatomyositis, PMLE, sarcoidosis, granuloma annulare, PCT
42
What are the notable side effects of **antimalarials**? * How might the eyes, blood, nails and skin be affected?
* Ocular toxicity (most notable **retinopathy**) * **Hemolysis (if G6PD deficient)** * **Bluish-gray to black skin hyperpigmentation** (typically affecting **shins**) * **Nail hyperpigmentation** * Yellow pigmentation of skin (specifically quinacrine)​
43
Which _two_ **antimalarials** can you combine from the following: hydroxychloroquine, chloroquine, quinacrine
**Hydroxychloroquine and quinacrine** OR **Chloroquine and quinacrine** * _You cannot have two "chloroquines"!_
44
Which antimalarial **does not** have risk of retinopathy?
**Quinacrine** * Can be combined with either hydrochloroquine or chloroquine
45
What are the eye monitoring recommendations when on **antimalarials**? * How often?
* Baseline examination, then * Dilated exam and visual acuity testing **within first year** of starting therapy. * Dilated examination and visual acuity testing **yearly after 5 years** of treatment
46
What is the mechanism of action of **antihistamines**? * How are they divided?
* Competitive inhibitor (reversible) of histamine at tissue receptor sites * **Either H1 or H2** * **H1 divided into sedating and non-sedating**
47
What are the 1st generation antihistamines?
* **Diphenhydramine** (Benadryl) * **Hydroxyzine** (Atarax) * Promethazine * Cyproheptadine * Chlorpheniramine
48
Are antihistamines safe in pregnancy? * What are the best choices in pregnancy? (2)
* Likely safe in pregnancy, but none are FDA category A * Bests choices if needed are **diphenhydramine** (Benadryl) or **chlorpheniramine** (Chlor-Tabs; both are category B)
49
What are the notable side effects of **antihistamines**?
* Drowsiness * Anticholinergic symptoms (blurry vision, urinary retention, dry mouth, constipation)
50
Which antihistamine is the treatment of choice for **cold urticaria**?
**Cyproheptadine**
51
Which **1st generation antihistamines** are the safest in _pregnancy_?
**Chlorpheniramine** (Chlor-Tabs) **or diphenhydramine** (Benadryl) * Both are pregnancy category B.
52
What potential side effects does **hydroxyzine** (Atarax) specifically have that the other antihistamines do not? (2)
EKG changes and arrythmias
53
What are the **2nd generation antihistamines**?
* **Fexofenadine (Allegra)** * **Loratidine (Claritin)** * **Cetirizine (Zyrtec)** * Levocetirizine
54
What is the mechanism of action and potential side effects of **doxepin**? * 2 mechanisms of action * 2 notable side effects
* Mechanism of action: **TCA, H1/H2 antihistamine** * Side effects: cardiotoxic (**may prolong** **QT interval**), **decrease seizure threshold**
55
What is the mechanism of action of most **-azole antifungals**? * What is inhibited? Synthesis of what is blocked? * How does this affect the cell?
* **Inhibits** **14 alpha-demethylase, blocking ergosterol synthesis** * Less ergosterol means decreased cell membrane synthesis, increased membrane rigidity/permeability, growth inhibition and cell death
56
What is the mechanism of action of **griseofulvin**? * What does it disrupt? * What protein does it induce?
* Disrupts **microtubule function** (causing metaphase arrest) * Note: induces cytochrome p450 (may decrease warfarin level)
57
What are the FDA approved uses of **griseofulvin?** * This is less preferred for a certain infection than what (2) other antifungal medications?
* Dermatophyte onychomycosis * Tinea corporis/cruris/pedis/capitis * Less preferred for tinea pedis compared with oral terbinafine or oral fluconazole
58
What is the shared mechanism of action of **acyclovir/penciclovir/valacyclovir/famciclovir?** * How is the medicine changed by the virus? * What is blocked?
Phosphorylated by **herpes-specific viral thymidine kinase** to acyclovir monophosphate, which blocks **viral DNA** **polymerase --\>** stops DNA synthesis
59
What are the indications for the following: * **Acyclovir** * **Valacyclovir** * **Penciclovir** * **Famciclovir** * Which covers all three viruses?
* Acyclovir: HSV, VZV * Valacyclovir: HSV, VZV _and CMV_ * Penciclovir: HSV, VZV * Famciclovir: HSV, VZV
60
Which antivirals treat **CMV**? (4)
* Valacyclovir * Gancyclovir * Cidofovir * Foscarnet
61
What are the indications for **foscarnet**? (3)
* CMV (retinitis) * Resistant HSV * Resistant VZV
62
What are the indications for **amantadine** and **rimantadine**? (2)
* **Rubella** * Influenza A & C
63
What is the rare but unique side effect of **IV acyclovir**?
* **Crystalline obstructive nephropathy** (seen with IV infusion)
64
What is a _rare but important_ side effect of **valacyclovir**? * What special patient populations does this occur?
**TTP/HUS in advanced HIV patients and transplant patients** on high doses
65
What **oral antifungals** are FDA approved to treat **dermatophyte onychomycosis**? (2)
**Itraconazole and terbinafine**
66
What are the shared side effects of all **-azole antifungals**? * On lab work? * Symptoms? (3)
* Increased LFTs * GI upset (nausea, vomiting, abdominal pain) * Rash * Headache
67
What are the FDA approved indications for **oral itraconazole**?
* **Blastomycosis** * **Histoplasmosis** * Onychomycosis * Oropharyngeal/esophageal candidiasis * Aspergillosis refractory to amphotericin B
68
What are the important contraindications to **itraconazole**? * Disease? * Drugs?
* **CHF** * Concurrent use of **CYP3A4 drugs (pimozide, quinidine, cisapride)** * Concurrent use of **levomethadyl, dofetilide, statins, midazolam, triazolam, nisoldipine, ergot alkaloids**
69
What the FDA approved indications of **fluconazole**? (2)
* **Vaginal/oropharyngeal/esophageal candidiasis** * **Cryptococcal meningitis**
70
Why is oral **ketoconazole** not commonly used?
It has a high risk of **hepatotoxicity!**
71
Which of the **topical -azole agents** are good for dermatophytes, Malassezia and Candida? (4)
* Clotrimazole (Lotrimin) * Miconazole * Econazole * Ketoconazole
72
What can **voriconazole** be used for?
Used in serious, invasive fungal infections in immunosuppressed patients (e.g., **invasive aspergillosis**, Candida, Fusarium)
73
What are the side effects unique to **voriconazole?** * What can occur on the skin? * What is there an increased risk for?
* Severe phototoxicity (pseudoporphyria, xeroderma pigmentosum-like changes) * Increased risk of SCC
74
What is the most important serious side effect of **oral ketoconazole**?
Can cause **increased QT** if administered with **cisapride, terfenadine or astemizole**
75
What medications are included in the **allylamines/benzylamines** family, and what is their MoA? * What is inhibited? * What does this prevent the conversion of? * How does this affect the cell?
* **Terbinafine, naftifine, butenafine** * MoA: **inhibits squalene epoxidase** (catalyzes conversion of squalene to lanosterol) --\> decreases cell membrane synthesis
76
What are the FDA approved indications for **terbinafine**? (2)
* Dermatophyte onychomycosis * Tinea capitis
77
What is the most effective topical treatment for **tinea pedis?**
**Terbinafine (Lamisil)**
78
What are the important (but rare) side effects of **oral terbinafine**? * What sensory functions are affected? * What rheumatologic conditions? * What internal organ is affected? * What other side effects? (2)
* **Taste/smell disturbance (dysgeusia/anosmia)** * **Exacerbation of SLE** * **Drug induced SCLE** * **Hepatitis/acute liver failure** * SJS/TEN * Depression
79
What is the "boards favorite" side effect of **foscarnet?**
**Penile erosions**
80
What are the indications for topical **selenium sulfide**? (3)
* Tinea versicolor * Seborrheic dermatitis * CARP
81
What is the MoA and uses of **nystatin**? * What does it bind to? * What can it be used for?
* MoA: **binds Candidal cell membrane sterols,** increasing permeability and causing cell death * Used for cutaneous/mucosal Candida infections
82
What is the MoA and uses of the **echinocandins (caspofungins, micafungin, anidulafungin)**? * What does it inhibit? * What can it be used for?
* MoA: **inhibits beta-(1,3)-D-glucan synthase** --\> decreases glucan production --\> disrupts cell wall synthesis * Used in invasive Candida and invasive aspergillosis
83
Do corticosteroids achieve their desired dermatologic effects via **glucocorticoid** or **mineralocorticoid** activity? * Which effect is *never* desired?
**Glucocorticoid** * Mineralocorticoid effects (sodium and water retention, HTN) are never desired
84
Name the **short-acting, intermediate-acting,** and **long-acting systemic** **corticosteroid** options. * How is the duration of activity (short, intermediate, long) relate to how much mineralocorticoid and glucocorticoid activity it has?
* **Short-acting:** cortisone, cortisol (hydrocortisone) * **Intermediate-acting:** prednisone, prednisolone, methylprednisolone, triamcinolone * **Long-acting:** dexamethasone, betamethasone * NOTE: The longer acting the steroid, the LESS mineralocorticoid activity and MORE glucocorticoid activity it has.
85
What enzyme in the liver converts steroids to their active form?
**11-beta-hydroxysteroid dehydrogenase**
86
Which is the active form: **prednisone** or **prednisolone**? * Which is better to give in patients with liver disease?
**Prednisone (inactive form)** is converted to **prednisolone (active form)** by 11-beta-hydroxysteroid dehydrogenase * Note: it is better to give the active form (i.e., prednisolone) in patients with liver disease
87
How long does it take to see adrenal insufficiency (HPA axis suppression) in patients taking **systemic corticosteroids**?
**3-4 weeks**
88
What are some noteworthy potential side effects of **systemic corticosteroids**? * How does it affect the skin? * Blood? * Bones? * Stomach? * Immune system?
* **Decreased wound healing, striae, atrophy, telangiectasias** * **Hypertriglyceridemia** * **Osteoporosis** * Cushingoid changes * Peptic ulcers/GERD * Opportunistic infections
89
What pregnancy category do **systemic corticosteroids** belong to?
**Pregnancy category C** (risk cannot be ruled out)
90
What are some risk factors for developing adrenal insufficiency while taking **systemic corticosteroids**? (4)
* **Abrupt cessation** (always taper if course is \> 4 weeks) * **Major stressor** (i.e., surgery, trauma, illness) * **Divided dosing** (i.e., BID or TID) * **Taking the pill any other time than in the morning**
91
What are the notable unique adverse effects of **intramuscular corticosteroids**? * Infection? * Adrenal gland? * Tissue? * What about in younger women?
* **Cold abscesses** (lack inflammation) * **Increased HPA axis suppression** (compared to oral due to steady state levels) * Subcutaneous fat atrophy * Purpura * Menstrual irregularities
92
What should you consider monitoring in a patient on **chronic oral steroids**? * Blood? * Bones? * Infection? * Other?
* Fasting glucose * Blood pressure * Triglycerides * Weight * DEXA (osteoporosis) * MRI if pain in large joint (osteonecrosis) * QuantiFERON gold * CXR
93
What makes **cidofovir** different than all the other **-virs?**
**Cidofovir does not require viral thymidine kinase** to activate it
94
Which (2) of the following are the most effective at **decreasing VZV pain:** * Acyclovir * Valacyclovir * Famciclovir * Penciclovir
**Valacyclovir and famciclovir**
95
**Bleomycin** is a chemotherapy agent that can be injected for warts. What are the side effects? (4) * What can happen right after injection? (1) * What can happen to the digit/nail? (2) * What skin change can occur? (1)
* Injection pain * Raynaud's phenomenon * Nail dystrophy * Flagellate hyperpigmentation (see photo)
96
What are the indications for **podophyllin** and **cantharidin**? * **Podophyllin** is FDA approved for what? * **Cantharidin** can be used for what two conditions?
* **Podophyllin**: FDA approved for genital warts * **Cantharidin**: warts, molluscum
97
What pregnancy category are **topical steroids**?
**Pregnancy category C** (risk cannot be ruled out)
98
What are the side effects of **topical steroids**? (5)
* Atrophy * Striae * Acneiform eruption * Hypertrichosis * Hypopigmentation
99
How do **topical steroids** work? * How do they affect keratinocytes? * Collagen? * Blood vessels?
* Inhibits epidermal mitosis and DNA synthesis * Decreases collagen crosslinking * Vasoconstriction (which is directly proportional to anti-inflammatory potency of the particular agent)
100
What is **tachyphylaxis?** * What might be required if this should develop?
* Efficacy lost over time * Seen in **topical steroids** * Therefore, structurally different steroid required
101
What is the mechanism of action of **bacitracin**, and what type of bacteria does it treat? * What does it bind to and disrupt? * What is it active against? (2)
* MOA: binds to **C55-prenol pyrophosphatase** to disrupt **bacterial cell wall synthesis** * Active against **Neisseria and gram positives but NOT MRSA**
102
What is the mechanism of action of **polymyxin B**, and what type of bacteria does it treat? * How does it affect the cell membrane? * What is it active against? (1)
* MOA: **increases cell membrane permeabiliy via detergent-like phospholipid interaction** * Active against gram negatives (e.g., **Pseudomonas**)
103
What is **neosporin** comprised of? (3)
1. **Neomycin** 2. **Bacitracin** 3. **Polymyxin B**
104
What is the mechanism of action of **mupirocin**, and what type of bacteria does it treat? * What does it bind to? * What is it active against? (2) * What pregnancy category is it?
* MOA: binds to bacterial **isoleucyl tRNA synthetase** to decrease RNA and protein synthesis * Active against **MRSA** and **Strep pyogenes** (GAS) * Note: pregnancy category B (no evidence of risk)
105
What is the mechanism of action of **gentamicin**, and what does it treat? * What does it bind to? * What is it active against? (2)
* MOA: **binds to bacterial 30s ribosomal subunit** to decrease protein synthesis * Active against **gram positives and gram negatives (including Pseudomonas)**
106
What is a good topical option for **burn wounds**? * What is it active against? (2) * What are rare side effects? (2)
**Silver sulfadiazene** * Active against GPs and GNs * Rare SEs include: **hemolysis in G6PD; methemoglobinemia**
107
What antibacterial coverage does **benzoyl peroxide** have?
**It is _broad spectrum_!** * **No bacterial resistance reported to date** * Works through its strong oxidizing properties * Most common side effect is local irritation, bleaching of hair/fabric
108
What kind of organisms does **topical metronidazole** treat? * What is it active against? (2) * What is it NOT active against? * What pregnancy category is it? * What is it primarily used for?
* Active against **protozoa** and **anaerobes** * **​NOT** active against P. acnes, staph, strep, fungi or Demodex * Pregnancy category B (no evidence of risk) * Primarily used for **rosacea** due to _anti-inflammatory_ properties
109
How does **topical sodium sulfacetamide** work and what skin diseases can it be used in? * What does it inhibit and prevent the conversion of? * What is it active against? * What can it be used for?
* MOA: **inhibits bacterial dihydropteroate synthetase, preventing conversion of PABA to folic acid** * Active against P. acnes * Used in **acne and rosacea** with or without sulfur
110
What (2) classes of antibiotics have a **beta-lactam ring**? How do these antibiotics work? * What does it inhibit?
* Penicillins and cephalosporins * MOA: inhibit formation of **peptidoglycan cross-links** in the bacterial cell wall, leading to **cell wall breakdown**
111
What is the bacterial coverage of **clindamycin?** (2)
* **Gram positive** **cocci (including MRSA)** * **Anaerobes** (*Bacteriodes, Clostridium*)
112
What is the antibiotic of choice for **animal or human bites**? * What is this notably NOT effective against? * What does it cover?
**Amoxicillin-clavulanate (Augmentin)** * **NOT effective against MRSA or Pseudomonas** * Covers Strep, MSSA, anaerobes, most GNs (except Pseudomonas)
113
What is the mechanism of action and bacterial coverage of **vancomycin**? * What does it inhibit? * What does it cover? (1)
* MOA: tricyclic glycopeptide that **inhibits bacterial cell wall synthesis** * Covers **gram positives (including MRSA)**
114
What _medication_ is the most common cause of **linear IgA bullous dermatosis**? * What antibodies are involved? * What is the antigen target? (2)
**Vancomycin** * Due to IgA antibodies to LAD285 and IgA/IgG to BP180
115
Name the side effects of **vancomycin**. (4)
* **Red man syndrome** * **Linear IgA bullous dermatosis** * **Hearing loss** (in renal failure patients) * **Nephrotoxicity** (if given with aminoglycosides)
116
Name the **macrolides**. (3) * What drug reaction are they associated with?
* Azithromycin * Clarithromycin * Erythromycin * Associated with **acute generalized exanthematous pustulosis (AGEP)**
117
What kind of antimicrobial coverage do **macrolides** have? * What do they bind to? * What do they cover and NOT cover?
* MoA: bind to **50s subunit** of bacterial ribosome to **decrease protein synthesis** * Good for **atypicals and gram positives, except MRSA**
118
What is the treatment of choice for **cutaneous anthrax**? (1)
**Ciprofloxacin**
119
What is the mechanism of action and bacterial coverage of **fluoroquinolones**? * What do they inhibit? (2) * What do 1st and 2nd generation fluoroquinolones cover? (1) Why? * What do 3rd and 4th generation fluoroquinolones cover? (2) Why?
* MoA: **inhibits DNA gyrase** (a.k.a. topoisomerase II) +/- **topoisomerase IV** --\> DNA fragmentation * 1st and 2nd generations (**ciprofloxacin**, ofloxacin, nalidixic acid): **GNs** only because only targets DNA gyrase * 3rd and 4th generations (**levofloxacin**, moxifloxacin, sparfloxacin, gatifloacin): **both GN and GP** because they target both enzymes
120
What is the treatment of choice for **Lyme disease**? (1)
**Doxycycline**
121
What is the treatment of choice for **CARP** (confluent and reticulated papillomatosis)? (1) * What are second line therapies? (3)
**Oral minocycline** * Can also try topical selenium sulfide, ketoconazole and retinoids
122
What is the mechanism of action for **tetracyclines?** * What do they bind to? * What secondary actions do they have, conferring anti-inflammatory properties?
* **E.g., doxycycline, minocycline** * **Binds 30s subunit** of bacterial ribosome --\> decreases protein synthesis * Also **inhibits MMPs**, neutrophil migration and cytokines, conferring anti-inflammatory properties
123
What is the bacterial coverage of **tetracyclines**?
* **Good coverage for GPs, _including MRSA_** (doxycycline and minocycline), **and GNs** * **Chlamydia** (doxycycline) * **Rickettsial infections** (doxycycline) * **Syphilis**, if PCN allergic * **Lyme Disease** (doxycycline) * Mycoplasma * Atypical mycobacteria
124
What are notable side effects of **tetracyclines**? * CNS side effects? Especially when combined with what other medication? (1) * GI side effects? (1) * Skin side effects? (2)
* Pseudotumor cerebri (increased risk when combined with isotretinoin) * GI symptoms (e.g., pill esophagitis and GI upset) * Photosensitivity * Gram-negative acne/folliculitis
125
At what age should you NOT give patients **tetracyclines**? Why?
**_Under 8 years old_, due to risk of tooth discoloration**
126
What is the MoA, use and most notable side effects of **rifampin?** * ​What does it bind to? * What is it effective against? (1) * What side effect can it cause? (1) * What condition can it worsen? (1)
* MoA: binds bacterial **DNA-dependent RNA polymerase** * Effective against mycobacteria * SEs: **orange-red discoloration of body fluids; can lead to worsening of porphyria**
127
What is the mechanism of action of **trimethoprim-sulfamethoxazole**? * What does each component inhibit? * What does this ultimately decrease the production of?
* **Dihydrofolate reductase inhibitor** (trimethoprim) + **dihydropteroate synthetase inhibito**r (sulfamethoxazole) --\> **decreases tetrahydrofolic acid** --\> decrease bacterial nucleic acid/protein synthesis
128
What is the MoA, bacterial coverage and notable side effects of **linezolid?** * What does it bind to? * What does it cover? * What notable side effect can occur, especially when combined with psychoactive drugs?
* MoA: binds **23s portion of 50s** **ribosomal subunit** * Good for skin infections caused by staph and strep **_(including MRSA)_** * SEs: **serotonin syndrome (when combined with serotonergic drugs like SSRIs, MAOs and TCAs)**
129
What are good options for **MRSA**? (7)
* Doxycycline, minocycline * Vancomycin * Trimethoprim-sulfamethoxazole * 5th generation cephalosporin (IV ceftaroline) * Linezolid * Daptomycin

BASIC Exam Study Guide (11 decks)

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