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Step 1 - Elise > UWorld Pharmacology - Derm drugs > Flashcards

UWorld Pharmacology - Derm drugs Flashcards

1
Q

Tx of dermatophytosis. MOA

A

Terbinafine.

MOA: inhibits squalene epoxidase, which inhibits fungal cell membrane formation by inhibiting ergosterol synthesis

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2
Q

Antifungal that has MOA of binding to ergosterol, creating pores in the fungal membrane.

A

amphotericin B and nystatin

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3
Q

Drug class that blocks Beta-1,3-D-glucan, blocking fungal cell wall synthesis. Especially in aspergillus and candida.

A

the echinocandins - caspofungin, anidulafungin, micafungin

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4
Q

Drug that binds to polymerized microtubules and disrupts fungal mitotic spindle, preventing fungal mitosis.

A

Griseofulvin

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5
Q

Antimetabolite antifungal that is transformed into 5-Fluorouracil in fungal cell. Inhibits fungal protein sythesis by replacing uracil with 5-Fluorouracil in fungal mRNA. Used for systemic fungal infections (crypto).

A

Flucytosine.

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6
Q

Tx for androgenetic alopecia (polygenic inheritance).

A

5-alpha-reductase inhibitors (finasteride) to inhibit testosterone conversion to dihydrotestosterone

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7
Q

Name viral dependent nucleosides.

MOA

A

Acyclovir, valacyclovir, famcyclovir - all HSV, VZV
Gancyclovir (CMV)

MOA - complete inhibition of viral DNA polymerase

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8
Q

Name nucleoside monophosphate. how are they different from viral dependent nucleosides?

A

They are nucelotides, so they only require cellular kinases for activation. Cidofovir and Tenofovir.

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9
Q

An eczematous dermatitis patient presents with atrophy of dermis and loss of dermal collagen, drying, cracking, and or tightening of skin. Telangiectasia,also possible.

What is the person being treated with?

A

This is dermal atrophy due to topical corticosteroid use.

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10
Q

What drug inhibits NFAT (nuclear factor of activated T cells) from entering nucleus and modulating transcription activity?

A

cyclosporin

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11
Q

What antiviral is a recombinant form of human TNF that binds to TNF-alpha.

A

Etanercept

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12
Q

Antifolate metabolite that reversibly binds to DHFR, resulting in inhibition of purine and thymidylic acid syntehsis.

A

MTX

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13
Q

Antiviral class that inhibits influenza neuraminidase, decreasing progeny release from virus.

A

Neuraminidase inhibitors - oseltamivir, zanamivir

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14
Q

Antiviral drug class that inhibits uncoating of virus.

A

Amantadine - used for Parkinson

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15
Q

Abacavir, tenofovir, zidovudine - MOA and use

A

HIV antiviral therapy - NRTI. Impairs viral RNA replication.

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16
Q

Antifungal class/drugs that bind to ergosterol molecules in fugnal cell mamrbeans creating pores and causing cell lysis.

A

polyenes -amphotericin B, nystatin

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17
Q

Antifungal class/drugs that inhibits syntehsis of ergosterol

A

triazoles - ketoconazole, fluconazole, itraconazole, voriconazole

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18
Q

Antifungal class/drugs that inhibit synthesis of glucan, a component of the fungal cell wall.

A

Echinocandis - caspofungin, micafungin

19
Q

Antifungal class/drugs that conver 5-fluorouracil within fungal cell and interfer with fungal RNA and protein syntehsis

A

pyrimadines- flucytosine

20
Q

name the three beta-lactamase inhibitors

A

clavulanic acid, sulbactam, tazobactam (CAST)

21
Q

What class has MOA that interferes with DNA gyrase (topoisomerase 2)?

A

Fluoroquinolones

22
Q

What drug combination is effectinve against most gram negative anaerobic rods (psudomonas and bacteroides)? Why?

A

Pipercillin-tazobactam

Add tazobactam because it protect the antibiotic form dstruction by beta-lactamase (penicillinase).

23
Q

tx of N. gono/Chlamydia

A

Azithromycin (inhibit protein synthesis by binding to 23S rRNA of 50s ribsosome) + Ceftriaxone (beta-lactam drug that inhibits cell wall synthesis).

24
Q

The two methods of gene INH resistance

A
  1. decreased bacterial expression of catalase-peroxidase enzymes that are required for INH activation once drug enters bacterial cell.
  2. Modification of protein target binding site for INH
25
Q

When can you use INH monotherapy?

A

positive PPD with negative chase XR - no evidence of clinical disease.

26
Q

Anaerobic above v. below diaphragm

A

Above - clindamycin (clean gym)

Below - metronidazole

27
Q

A 19 year old male presents with an ulcer on his penis. It is indurated, painless, and no surrounding erythema or inguinal LAD. College student. What is this and what drug?

A

Treponema pallidum

Tx with Penicillin - bc they are gram negative with peptidoglycan cell wall.

28
Q

MOA of penicillins

A

They are structurally similar to D-ala-D-ala, inhibiting transpeptidase by binding COVALENTLY to the acitve site. Results in failed synthesis of bacterial peptidoglycan cell wall.

29
Q

How is penicillin and vancomycin MOA differen?

A

Vanc binds DIRECTLY to D-ala-D-ala.

Penicillins bind covalently.

30
Q

What class of antibiotics compete with Para-aminobenzoic acid for incirportaitn into folic acid.

Whatcalss blocks another step in folic acid synthesis by inhibiting dihydrofolate reductase?

A

sulfonamides

trimethoprim

31
Q

What is the most potent diuretic, used especially in acute decompensated HF. Where is its MOA?

A

Loops (furosemide) act on Thick ascending loop. Na/K/2Cl.

32
Q

What diuretic acts on the Dct?

A

thiazides - Cl/Na reabs

33
Q

What diuretics act on CT?

A

K-sparing - spironolactine and Na-CB (amelioride)

34
Q

A person with high plasma renin levels and volume depletion or HF is started on ACEinhibitor (lisinopril). What is a likely side effect.

A

First dose Hypotension.

35
Q

CYP inducers do what to a paerson on warfarin?

CYP inhibitors do what to a person on warfarin?

A
  • inducers will decrease effect of warfarin, increasing its metabolism. (CHRONIC ALCOHOLICS, ST. johns wart, PHENytoin, PHENobarbitol, NEvirapine, Rifampin, GRiseofulvin, CARBamazepine).
  • inhibitors will potentiate warfarin by blocking its metabolism, increasing bleeding risk. (Acute Alcohol Abuse, Ritonavir, Amiodarone, Cimetidine, Ketoconazole (azoles), Sulfonamides, INh, Grapefruit Juices, Quinidine, MAcrolides (except azithromycin).
36
Q

SE of antipsychotic - akisthisia

A

inability to sit still

37
Q

SE of antipsychotic - NMS

A

fever, rigidity, mental status changes, autonomic instabiltiy

38
Q

SE of antipsychotic - tardive dyskinesia

A

lip smacking, choreathetoid movements - involuntary mvmts after chronic use

39
Q

What is indicated for treatment of bradycardia bc it decreases vagal influence on SA and AV nodes. When is this contraindicated?

A

ATropine. CI if the person has glaucoma bc the increased intraocular pressure may precipitate close angle galucoma (severe unilateral eye pain and visual disturbances).

40
Q

When would a SERM (i.e. tamoxifen) be appropriate to use in a male?

A

If he is getting tx with androgen-deprivation therapy (ADT) for prostate cancer.

41
Q

Role of desmopressin in tx Hemophilia A or vWF disease

A

Incrases factor 8 and endothelial secretion of vWF.

42
Q 
What do opioids do to:
histamine release
gut motility
pariteal cell acid secretion
hepatocytes
skeletal muscle
pancreas
A 
increase
decrease
decerase
no effect
no effect
no effect
43
Q

Digoxin, B-blockers, and CCB can all cause what change on ECG?

A

prolonged PR interval (First degree block - PR >200 msec).

44
Q

Diuretic that can cause gout.

A

thiazide

Step 1 - Elise (30 decks)

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