Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Ideal body weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

True or false:

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

A

False

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A
  • Pregnancy (category X)
  • Breastfeeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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?
A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are special side effects associated with bexarotene (an oral retinoid)? (2)

A
  • Agranulocytosis (neutropenia, eosinopenia)
  • Central hypothyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are notable interactions with systemic retinoids?

  • Food?
  • Acitretin in particular?
  • Isotretinoin in particular?
  • Bexarotene in particular?
A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are examples of TNF-alpha inhibitors?

  • Which is given as an infusion?
A
  • Etanercept (Enbrel)
  • Infliximab (Remicade), given as an infusion
  • Adalimumab (Humira)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are indications for TNF-alpha inhibitors?

  • What are they FDA approved for?
  • What are off label uses?
A
  • FDA approved for plaque psoriasis and psoriatic arthritis
  • Off label uses include bullous dermatoses, neutrophilic dermatoses, connective tissue diseases, granulomatous diseases, HS and PRP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

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?
A
  • Injection site reactions (etanercept > adalimumab), likely due to delayed-type hypersensitivity
  • Infusion reactions (infliximab)
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are important lab monitoring points with TNF-alpha inhibitors?

  • What should be checked at baseline? Annually?
A
  • PPD or quantiFERON gold (annually)
  • Viral hepatitis panel (at baseline)
  • CBC with diff
  • LFTs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

True or false:

TNF-alpha inhibitors can be used safely with active hepatitis C infection.

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the notable side effects of vismodegib, the sonic hedgehog pathway inhibitor used for BCC? (3)

A
  • Muscle spasms (#1)
  • Alopecia
  • Dysgeusia (distorted taste)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the mechanism of action of 5-fluorouracil?

  • What does it inhibit and prevent the conversion of?
A
  • A competitive inhibitor of thymidylate synthase, which normally converts doxyuridine to thymidine
  • Decreases DNA synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the FDA approved indications for 5-fluorouracil? (2)

A
  • AKs
  • sBCCs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the mechanism of action of imiquimod (Aldara)?

  • What does it activate? What is ultimately released?
A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the FDA approved indications for imiquimod (Aldara)? (3)

A
  • AKs
  • Superficial BCCs
  • Genital/perianal warts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

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?
A
  • Flu-like or GI symptoms if larger areas are treated
  • Psoriasis exacerbations
  • Pregnancy category C (i.e., risk cannot be ruled out)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the proposed mechanisms by which antimalarials work?

  • How do they affect DNA? Macrophages?
A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

If you develop retinopathy on antimalarials, can you continue taking it?

A

No! Retinopathy is an absolute contraindication.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the FDA approved indications for antimalarials? (3)

  • What are off label uses?
A
  • SLE
  • Malaria
  • Rheumatoid arthritis
  • Off label: DLE, dermatomyositis, PMLE, sarcoidosis, granuloma annulare, PCT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the notable side effects of antimalarials?

  • How might the eyes, blood, nails and skin be affected?
A
  • 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)​
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Which two antimalarials can you combine from the following:

hydroxychloroquine, chloroquine, quinacrine

A

Hydroxychloroquine and quinacrine

OR

Chloroquine and quinacrine

  • You cannot have two “chloroquines”!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Which antimalarial does not have risk of retinopathy?

A

Quinacrine

  • Can be combined with either hydrochloroquine or chloroquine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the eye monitoring recommendations when on antimalarials?

  • How often?
A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the mechanism of action of antihistamines?

  • How are they divided?
A
  • Competitive inhibitor (reversible) of histamine at tissue receptor sites
  • Either H1 or H2
  • H1 divided into sedating and non-sedating
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the 1st generation antihistamines?

A
  • Diphenhydramine (Benadryl)
  • Hydroxyzine (Atarax)
  • Promethazine
  • Cyproheptadine
  • Chlorpheniramine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Are antihistamines safe in pregnancy?

  • What are the best choices in pregnancy? (2)
A
  • 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the notable side effects of antihistamines?

A
  • Drowsiness
  • Anticholinergic symptoms (blurry vision, urinary retention, dry mouth, constipation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Which antihistamine is the treatment of choice for cold urticaria?

A

Cyproheptadine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Which 1st generation antihistamines are the safest in pregnancy?

A

Chlorpheniramine (Chlor-Tabs) or diphenhydramine (Benadryl)

  • Both are pregnancy category B.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What potential side effects does hydroxyzine (Atarax) specifically have that the other antihistamines do not? (2)

A

EKG changes and arrythmias

53
Q

What are the 2nd generation antihistamines?

A
  • Fexofenadine (Allegra)
  • Loratidine (Claritin)
  • Cetirizine (Zyrtec)
  • Levocetirizine
54
Q

What is the mechanism of action and potential side effects of doxepin?

  • 2 mechanisms of action
  • 2 notable side effects
A
  • Mechanism of action: TCA, H1/H2 antihistamine
  • Side effects: cardiotoxic (may prolong QT interval), decrease seizure threshold
55
Q

What is the mechanism of action of most -azole antifungals?

  • What is inhibited? Synthesis of what is blocked?
  • How does this affect the cell?
A
  • Inhibits 14 alpha-demethylase, blocking ergosterol synthesis
  • Less ergosterol means decreased cell membrane synthesis, increased membrane rigidity/permeability, growth inhibition and cell death
56
Q

What is the mechanism of action of griseofulvin?

  • What does it disrupt?
  • What protein does it induce?
A
  • Disrupts microtubule function (causing metaphase arrest)
  • Note: induces cytochrome p450 (may decrease warfarin level)
57
Q

What are the FDA approved uses of griseofulvin?

  • This is less preferred for a certain infection than what (2) other antifungal medications?
A
  • Dermatophyte onychomycosis
  • Tinea corporis/cruris/pedis/capitis
  • Less preferred for tinea pedis compared with oral terbinafine or oral fluconazole
58
Q

What is the shared mechanism of action of acyclovir/penciclovir/valacyclovir/famciclovir?

  • How is the medicine changed by the virus?
  • What is blocked?
A

Phosphorylated by herpes-specific viral thymidine kinase to acyclovir monophosphate, which blocks viral DNA polymerase –> stops DNA synthesis

59
Q

What are the indications for the following:

  • Acyclovir
  • Valacyclovir
  • Penciclovir
  • Famciclovir
  • Which covers all three viruses?
A
  • Acyclovir: HSV, VZV
  • Valacyclovir: HSV, VZV and CMV
  • Penciclovir: HSV, VZV
  • Famciclovir: HSV, VZV
60
Q

Which antivirals treat CMV? (4)

A
  • Valacyclovir
  • Gancyclovir
  • Cidofovir
  • Foscarnet
61
Q

What are the indications for foscarnet? (3)

A
  • CMV (retinitis)
  • Resistant HSV
  • Resistant VZV
62
Q

What are the indications for amantadine and rimantadine? (2)

A
  • Rubella
  • Influenza A & C
63
Q

What is the rare but unique side effect of IV acyclovir?

A
  • Crystalline obstructive nephropathy (seen with IV infusion)
64
Q

What is a rare but important side effect of valacyclovir?

  • What special patient populations does this occur?
A

TTP/HUS in advanced HIV patients and transplant patients on high doses

65
Q

What oral antifungals are FDA approved to treat dermatophyte onychomycosis? (2)

A

Itraconazole and terbinafine

66
Q

What are the shared side effects of all -azole antifungals?

  • On lab work?
  • Symptoms? (3)
A
  • Increased LFTs
  • GI upset (nausea, vomiting, abdominal pain)
  • Rash
  • Headache
67
Q

What are the FDA approved indications for oral itraconazole?

A
  • Blastomycosis
  • Histoplasmosis
  • Onychomycosis
  • Oropharyngeal/esophageal candidiasis
  • Aspergillosis refractory to amphotericin B
68
Q

What are the important contraindications to itraconazole?

  • Disease?
  • Drugs?
A
  • CHF
  • Concurrent use of CYP3A4 drugs (pimozide, quinidine, cisapride)
  • Concurrent use of levomethadyl, dofetilide, statins, midazolam, triazolam, nisoldipine, ergot alkaloids
69
Q

What the FDA approved indications of fluconazole? (2)

A
  • Vaginal/oropharyngeal/esophageal candidiasis
  • Cryptococcal meningitis
70
Q

Why is oral ketoconazole not commonly used?

A

It has a high risk of hepatotoxicity!

71
Q

Which of the topical -azole agents are good for dermatophytes, Malassezia and Candida? (4)

A
  • Clotrimazole (Lotrimin)
  • Miconazole
  • Econazole
  • Ketoconazole
72
Q

What can voriconazole be used for?

A

Used in serious, invasive fungal infections in immunosuppressed patients (e.g., invasive aspergillosis, Candida, Fusarium)

73
Q

What are the side effects unique to voriconazole?

  • What can occur on the skin?
  • What is there an increased risk for?
A
  • Severe phototoxicity (pseudoporphyria, xeroderma pigmentosum-like changes)
  • Increased risk of SCC
74
Q

What is the most important serious side effect of oral ketoconazole?

A

Can cause increased QT if administered with cisapride, terfenadine or astemizole

75
Q

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?
A
  • Terbinafine, naftifine, butenafine
  • MoA: inhibits squalene epoxidase (catalyzes conversion of squalene to lanosterol) –> decreases cell membrane synthesis
76
Q

What are the FDA approved indications for terbinafine? (2)

A
  • Dermatophyte onychomycosis
  • Tinea capitis
77
Q

What is the most effective topical treatment for tinea pedis?

A

Terbinafine (Lamisil)

78
Q

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)
A
  • Taste/smell disturbance (dysgeusia/anosmia)
  • Exacerbation of SLE
  • Drug induced SCLE
  • Hepatitis/acute liver failure
  • SJS/TEN
  • Depression
79
Q

What is the “boards favorite” side effect of foscarnet?

A

Penile erosions

80
Q

What are the indications for topical selenium sulfide? (3)

A
  • Tinea versicolor
  • Seborrheic dermatitis
  • CARP
81
Q

What is the MoA and uses of nystatin?

  • What does it bind to?
  • What can it be used for?
A
  • MoA: binds Candidal cell membrane sterols, increasing permeability and causing cell death
  • Used for cutaneous/mucosal Candida infections
82
Q

What is the MoA and uses of the echinocandins (caspofungins, micafungin, anidulafungin)?

  • What does it inhibit?
  • What can it be used for?
A
  • MoA: inhibits beta-(1,3)-D-glucan synthase –> decreases glucan production –> disrupts cell wall synthesis
  • Used in invasive Candida and invasive aspergillosis
83
Q

Do corticosteroids achieve their desired dermatologic effects via glucocorticoid or mineralocorticoid activity?

  • Which effect is never desired?
A

Glucocorticoid

  • Mineralocorticoid effects (sodium and water retention, HTN) are never desired
84
Q

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?
A
  • 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
Q

What enzyme in the liver converts steroids to their active form?

A

11-beta-hydroxysteroid dehydrogenase

86
Q

Which is the active form: prednisone or prednisolone?

  • Which is better to give in patients with liver disease?
A

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
Q

How long does it take to see adrenal insufficiency (HPA axis suppression) in patients taking systemic corticosteroids?

A

3-4 weeks

88
Q

What are some noteworthy potential side effects of systemic corticosteroids?

  • How does it affect the skin?
  • Blood?
  • Bones?
  • Stomach?
  • Immune system?
A
  • Decreased wound healing, striae, atrophy, telangiectasias
  • Hypertriglyceridemia
  • Osteoporosis
  • Cushingoid changes
  • Peptic ulcers/GERD
  • Opportunistic infections
89
Q

What pregnancy category do systemic corticosteroids belong to?

A

Pregnancy category C (risk cannot be ruled out)

90
Q

What are some risk factors for developing adrenal insufficiency while taking systemic corticosteroids? (4)

A
  • 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
Q

What are the notable unique adverse effects of intramuscular corticosteroids?

  • Infection?
  • Adrenal gland?
  • Tissue?
  • What about in younger women?
A
  • Cold abscesses (lack inflammation)
  • Increased HPA axis suppression (compared to oral due to steady state levels)
  • Subcutaneous fat atrophy
  • Purpura
  • Menstrual irregularities
92
Q

What should you consider monitoring in a patient on chronic oral steroids?

  • Blood?
  • Bones?
  • Infection?
  • Other?
A
  • Fasting glucose
  • Blood pressure
  • Triglycerides
  • Weight
  • DEXA (osteoporosis)
  • MRI if pain in large joint (osteonecrosis)
  • QuantiFERON gold
  • CXR
93
Q

What makes cidofovir different than all the other -virs?

A

Cidofovir does not require viral thymidine kinase to activate it

94
Q

Which (2) of the following are the most effective at decreasing VZV pain:

  • Acyclovir
  • Valacyclovir
  • Famciclovir
  • Penciclovir
A

Valacyclovir and famciclovir

95
Q

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)
A
  • Injection pain
  • Raynaud’s phenomenon
  • Nail dystrophy
  • Flagellate hyperpigmentation (see photo)
96
Q

What are the indications for podophyllin and cantharidin?

  • Podophyllin is FDA approved for what?
  • Cantharidin can be used for what two conditions?
A
  • Podophyllin: FDA approved for genital warts
  • Cantharidin: warts, molluscum
97
Q

What pregnancy category are topical steroids?

A

Pregnancy category C (risk cannot be ruled out)

98
Q

What are the side effects of topical steroids? (5)

A
  • Atrophy
  • Striae
  • Acneiform eruption
  • Hypertrichosis
  • Hypopigmentation
99
Q

How do topical steroids work?

  • How do they affect keratinocytes?
  • Collagen?
  • Blood vessels?
A
  • Inhibits epidermal mitosis and DNA synthesis
  • Decreases collagen crosslinking
  • Vasoconstriction (which is directly proportional to anti-inflammatory potency of the particular agent)
100
Q

What is tachyphylaxis?

  • What might be required if this should develop?
A
  • Efficacy lost over time
  • Seen in topical steroids
  • Therefore, structurally different steroid required
101
Q

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)
A
  • MOA: binds to C55-prenol pyrophosphatase to disrupt bacterial cell wall synthesis
  • Active against Neisseria and gram positives but NOT MRSA
102
Q

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)
A
  • MOA: increases cell membrane permeabiliy via detergent-like phospholipid interaction
  • Active against gram negatives (e.g., Pseudomonas)
103
Q

What is neosporin comprised of? (3)

A
  1. Neomycin
  2. Bacitracin
  3. Polymyxin B
104
Q

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?
A
  • 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
Q

What is the mechanism of action of gentamicin, and what does it treat?

  • What does it bind to?
  • What is it active against? (2)
A
  • MOA: binds to bacterial 30s ribosomal subunit to decrease protein synthesis
  • Active against gram positives and gram negatives (including Pseudomonas)
106
Q

What is a good topical option for burn wounds?

  • What is it active against? (2)
  • What are rare side effects? (2)
A

Silver sulfadiazene

  • Active against GPs and GNs
  • Rare SEs include: hemolysis in G6PD; methemoglobinemia
107
Q

What antibacterial coverage does benzoyl peroxide have?

A

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
Q

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?
A
  • 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
Q

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?
A
  • 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
Q

What (2) classes of antibiotics have a beta-lactam ring? How do these antibiotics work?

  • What does it inhibit?
A
  • Penicillins and cephalosporins
  • MOA: inhibit formation of peptidoglycan cross-links in the bacterial cell wall, leading to cell wall breakdown
111
Q

What is the bacterial coverage of clindamycin? (2)

A
  • Gram positive cocci (including MRSA)
  • Anaerobes (Bacteriodes, Clostridium)
112
Q

What is the antibiotic of choice for animal or human bites?

  • What is this notably NOT effective against?
  • What does it cover?
A

Amoxicillin-clavulanate (Augmentin)

  • NOT effective against MRSA or Pseudomonas
  • Covers Strep, MSSA, anaerobes, most GNs (except Pseudomonas)
113
Q

What is the mechanism of action and bacterial coverage of vancomycin?

  • What does it inhibit?
  • What does it cover? (1)
A
  • MOA: tricyclic glycopeptide that inhibits bacterial cell wall synthesis
  • Covers gram positives (including MRSA)
114
Q

What medication is the most common cause of linear IgA bullous dermatosis?

  • What antibodies are involved?
  • What is the antigen target? (2)
A

Vancomycin

  • Due to IgA antibodies to LAD285 and IgA/IgG to BP180
115
Q

Name the side effects of vancomycin. (4)

A
  • Red man syndrome
  • Linear IgA bullous dermatosis
  • Hearing loss (in renal failure patients)
  • Nephrotoxicity (if given with aminoglycosides)
116
Q

Name the macrolides. (3)

  • What drug reaction are they associated with?
A
  • Azithromycin
  • Clarithromycin
  • Erythromycin
  • Associated with acute generalized exanthematous pustulosis (AGEP)
117
Q

What kind of antimicrobial coverage do macrolides have?

  • What do they bind to?
  • What do they cover and NOT cover?
A
  • MoA: bind to 50s subunit of bacterial ribosome to decrease protein synthesis
  • Good for atypicals and gram positives, except MRSA
118
Q

What is the treatment of choice for cutaneous anthrax? (1)

A

Ciprofloxacin

119
Q

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?
A
  • 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
Q

What is the treatment of choice for Lyme disease? (1)

A

Doxycycline

121
Q

What is the treatment of choice for CARP (confluent and reticulated papillomatosis)? (1)

  • What are second line therapies? (3)
A

Oral minocycline

  • Can also try topical selenium sulfide, ketoconazole and retinoids
122
Q

What is the mechanism of action for tetracyclines?

  • What do they bind to?
  • What secondary actions do they have, conferring anti-inflammatory properties?
A
  • 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
Q

What is the bacterial coverage of tetracyclines?

A
  • 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
Q

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)
A
  • Pseudotumor cerebri (increased risk when combined with isotretinoin)
  • GI symptoms (e.g., pill esophagitis and GI upset)
  • Photosensitivity
  • Gram-negative acne/folliculitis
125
Q

At what age should you NOT give patients tetracyclines? Why?

A

Under 8 years old, due to risk of tooth discoloration

126
Q

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)
A
  • MoA: binds bacterial DNA-dependent RNA polymerase
  • Effective against mycobacteria
  • SEs: orange-red discoloration of body fluids; can lead to worsening of porphyria
127
Q

What is the mechanism of action of trimethoprim-sulfamethoxazole?

  • What does each component inhibit?
  • What does this ultimately decrease the production of?
A
  • Dihydrofolate reductase inhibitor (trimethoprim) + dihydropteroate synthetase inhibitor (sulfamethoxazole) –> decreases tetrahydrofolic acid –> decrease bacterial nucleic acid/protein synthesis
128
Q

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?
A
  • 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
Q

What are good options for MRSA? (7)

A
  • Doxycycline, minocycline
  • Vancomycin
  • Trimethoprim-sulfamethoxazole
  • 5th generation cephalosporin (IV ceftaroline)
  • Linezolid
  • Daptomycin

BASIC Exam Study Guide (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions