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MSK, Rheum, Derm > Monday Sweatman > Flashcards

Monday Sweatman Flashcards

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Dermatology Board Prep flashcards
1
Q

What are the most likely causative bugs in immunocompetent soft tissue infections? Complicated infections?

A
  • Immunocompetent: S. aureus, Strep pyogenes, or other beta-hemolytic strep
  • Complicated infections, e.g., w/burns, diabetes, infected pressure ulcers, or trauma/sx wound infections -> more commonly polymicrobial, and often include anaerones and G- bacilli like E. coli and Pseudomonas
  • NOTE: GAS, S. aureus, Clostridium spp (w/or w/o other anaerobes) can cause fulminant soft tissue infections and necrosis, esp in pts w/diabetes
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2
Q

What are the possible txs for uncomplicated, non-MRSA infections?

A
  • Usually susceptible to beta-lactamase-resistant penicillins (Dicloxacillin, Nafcillin, Oxacillin) or 1st-gen cephalosporins (Cefazolin)
  • If beta-lactam allergy, Clinda, a ribosomal INH, and Vanc, a cell wall INH
  • Oral drug tx most convenient, and pt doesn’t necessarily require hospitalization
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3
Q

Beta-lactam side chains and cross-reactivity

A
  • Some pt exhibit IgE-mediated allergy to penicillins: urticaria, angioedema, bronchospasm, anaphylaxis
  • POSSIBLE cross-reactivity w/1st, 2nd-gen Cephs
    1. Related to similarities in molecular structure of R1 SIDE CHAINS, rather than beta-lactam
  • VERY LOW risk in pt w/PMH of less severe rxn to Penicillin, when using 1st, 2nd-gen Ceph w/dissimilar side chain, or any 3rd, 4th-gen Ceph
  • Hypersensitivity still an issue w/all beta-lactam ABs
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4
Q

What are the resistance mechs for the beta-lactams, Vanc, and Clinda?

A
  • BETA-LACTAMS: orgs that lack cell wall, acquisition of resistance plasmid (beta-lactamase activity, reduced permeability, efflux pump, altered PBPs)
  • LINCOSAMIDES (Clinda): ribosomal target (50s) mut or methylation, drug efflux or inactivation
  • VANCOMYCIN: most G- bac intrinsically resistant bieng impermeable, expression of D-alanyl-D-lactate variation
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5
Q

What are the common toxicities of Dicloxacillin? Admin? Elim?

A
  • TOXICITY: hypersensitivity, GI pain, diarrhea, nausea, rarely interstitial nephritis
  • ELIM: renal; no adjustment in RF
  • ADMIN: oral
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6
Q

Which 3 penicillins do not require dose adjustment in renal failure?

A
  • Nafcillin
  • Oxacillin
  • Dicloxacillin (renal elim, but no dose adjustment necessary in RF)
  • These rely on biliary elim, so renal dysfunction is not an issue
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7
Q

Do Clinda and Vanc require dose adjustment in renal failure?

A
  • Clinda: NO
  • IV Vanc: YES -> eliminated unchanged (no metab)
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8
Q

What are the common toxicities of Cephalexin? Admin? Elim?

A
  • TOXICITY: hypersensitivity (don’t use if pt allergic to Ampicillin), diarrhea, rarely SJS
  • ELIM: renal, adjust in RF
  • ADMIN: oral
  • 1st-gen Cephalosporin
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9
Q

What are the common toxicities of Cefazolin? Admin? Elim?

A
  • TOXICITY: hypersensitivity, pruritis, diarrhea, eosinophilia, rarely SJS
  • ELIM: renal, adjust in RF
  • ADMIN: IV, IM
  • 1st-gen Cephalosporin
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10
Q

What are the common toxicities of Nafcillin? Admin? Elim?

A
  • TOXICITY: hypersensitivity, neutropenia, rarely interstitial nephritis, possible hypokalemia, INC ALT/AST
  • ELIM: primarily hepatic; dose adjust in hepatic + renal dysfunction
  • ADMIN: IV
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11
Q

What are the common toxicities of Oxacillin? Admin? Elim?

A
  • TOXICITY: hypersensitivity, diarrhea, nausea, fever, rash, rarely interstitial nephritis
  • ELIM: hepatic; NO dose adjust in RF
  • ADMIN: oral
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12
Q

What are the common toxicities of Clindamycin? Admin? Elim?

A
  • TOXICITY: rash, diarrhea, GI pain, N/V, jaundice, rarely C-difficile infection, SJS
  • ELIM: hepatic; NO adjust in LF or RF
  • ADMIN: oral
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13
Q

What are the common toxicities of Vancomycin? Admin? Elim?

A
  • TOXICITY: Red Man and hypotension (rapid IV), fever, nausea, rash, tinnitus, INC BUN/Cr
  • ELIM: hepatic/renal; dose adjust in RF
  • ADMIN: IV; used oral to tx enterocolitis
  • Think NEPHROTOXICITY, OTOTOXICITY, THROMBOPHLEBITIS
    1. Hypotension: histamine-related thrombophlebitis
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14
Q

Why is Vanc administered IV for systemic infection? What is the exception?

A
  • Poor bioavailability
  • Remember: oral dosing is sometimes used for enterocolitis, where retention of drug in the GI tract is a therapeutic advantage and has little discernible systemic toxicity
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15
Q

Which ABs have risk of hypersensitivity?

A
  • Beta-lactams
  • Dicloxacillin
  • Cephalexin (don’t use if pt allergic to Ampicillin)
  • Cefazolin
  • Nafcillin
  • Oxacillin
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16
Q

Which ABs have potential for interstitial nephritis?

A
  • Penicillinase-resistant penicillins
  • Dicloxacillin
  • Nafcillin
  • Oxacillin
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17
Q

How can Vanc affect the ear?

A
  • IV admin may cause damage to auditory branch of 8th cranial nerve
  • Permanent hearing loss has been reported
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18
Q

How can Vanc affect the kidney?

A
  • Vanc-induced NEPHROTOXICITY usually shows transient INC in BUN or serum creatinine, and presence of hyaline and granular casts and albumin in the urine
  • Generally reversible after discontinuation of the drug, but deaths have occurred
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19
Q

What is CA-MRSA? What does it cause? How should it be treated?

A
  • Community-acquired MRSA: predominant cause of suppurative skin infections in many parts of US
  • Usually causes furunculosis (painful, pus-filled bump under the skin caused by infected, inflamed hair follicles), cellulitis, and abscesses, but necrotizing fasciitis and sepsis can occur
  • For simple abscesses and o/less serious CA-MRSA skin and soft tissue infections, I & D alone may be effective
  • If not, CA-MRSA strains are usually susceptible to oral: Trimethoprim-Sulfamethoxazole (BACTRIM), Minocycline, Doxycycline, Clinda, Linezolid
  • Fluoroquinolones should NOT be used empirically to treat MRSA infections bc RESISTANCE is common and INC in both community and nosocomial settings
    1. Floxacins
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20
Q

What is the MOA of Bactrim?

A
  • PO/IV
  • Folic acid antagonists: sequential antagonists of folate synthesis
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21
Q

What is the MOA of Minocycline and Doxycycline?

A
  • PO/IV tetracyclines
  • Bind 30s ribosomal subunit, INH binding of aminoacyl-tRNA molecules
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22
Q

What is the MOA of Clinda?

A
  • IV/IM
  • Lincosamide: 50s ribosomal INH of translocation
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23
Q

What is the MOA of Linezolid?

A
  • PO/IV
  • Oxazolidinone: binds 23s ribosomal RNA of 50s subunit, preventing initiation complex formation with 70s ribosomal subunit
24
Q

What are the resistance mechs to the folic acid antagonists, tetracyclines, and oxalidinones?

A
  • FOLIC ACID ANTAGONISTS: permeability barrier and/or efflux pumps, natural target insensitivity, change in target enzyme expression or mutational, recombinational changes, and acquired resistance by drug-resistant target enzymes
    1. May be different mechs for e/component
  • TETRACYCLINES: drug efflux or metabolism, ribosome protection
  • OXALIDINONES: mutation (plasmid carried Cfr rRNA methyltransferase) of 23s rRNA and ribosomal proteins L3 and L4, drug efflux, biofilm formation and DEC cell wall penetration
25
Q

What are the common toxicities of Trimethoprim/Sulfamethoxazole (Bactrim)? Admin? Elim?

A
  • TOXICITY: N/V, rash, photosensitivity, dizziness, dyspepsia, human fetal risk
  • ELIM: renal; dose adjust in RF
  • ADMIN: PO/IV
  • Maintain hydration -> a sulfamethoxazole metabolite has limited aqueous solubility
26
Q

What are the common toxicities of Minocycline/Doxycycline? Admin? Elim?

A
  • TOXICITY: N/V, rash, photosensitivity, hepatotoxicity (most evident in pre-existing dysfunc and with pregnancy), tinnitus, vertigo, ataxia, discolored teeth (dysplasia, discoloration of teeth enamel), human fetal risk
  • ELIM: hepatic/renal; dose adjust in RF
  • ADMIN: PO/IV
27
Q

What are the common toxicities of Clindamycin? Admin? Elim?

A
  • TOXICITY: rash, diarrhea, GI pain, N/V, jaundice, rarely C-difficile infection, SJS
  • ELIM: hepatic; NO adjust in RF/LF
  • ADMIN: IV/IM
28
Q

What are the common toxicities of Linezolid? Admin? Elim?

A
  • TOXICITY: diarrhea, N/V, headache, anemia, thrombocytopenia, myelosuppression, rash, HTN, rarely SJS, optic and peripheral neuropathy, vision loss, serotonin syndrome, seizures, lactic acidosis
    1. Usually well-tolerated, w/few described AEs
    2. Serious AEs in bold require withdrawal of the drug
  • ELIM: hepatic/renal; caution in RF
  • ADMIN: IV/PO
29
Q

Which CA-MRSA ABs are teratogenic?

A
  • Bactrim
  • Tetracyclines
30
Q

How can Linezolid cause optic neuropathy?

A
  • Damage is thought to be caused by mitochondrial dysfunction in the optic N bc mammalian mito DNA uses ribosomes that more closely approximate that of bacteria and are therefore susceptible to drug INH
  • Mito DNA dysfunction a common mechanism to several classes of drugs possessing specific organ toxicity
31
Q

Serotonin syndrome

A
  • Caused by excessive levels of circulating serotonin in CNS/periphery
  • Mental status changes, autonomic hyperactivity, and neuromuscular abnormalities ranging from imperceptible to almost lethal -> MOST cases appear w/in 6 hours
  • Lg # of diverse drugs assoc w/SS: SSRIs, TCAs, MAOIs, some opiate analgesics, Isoniazid, amphetamines, Procarbazine, St. John’s Wart, Ginseng (herbals)
  • Overall low incidence of SS when Linezolid and SSRIs simulataneously administered -> paucity of prospective data
  • Effective treatments for SS
32
Q

How should pts with serious MRSA be treated?

A
  • Pts w/complicated MRSA skin, soft tissue infections should be hx and tx w/IV Vanc (even if SUSPECTED, should be treated empirically)
  • While not bactericidal against staph, Linezolid appears to be as effective as Vanc for serious MRSA infection -> advantage (over Vanc) of INH bacterial toxin production (protein synthesis inhibition)
  • Daptomycin bactericidal for MRSA in vitro and appears to be as effective as Vanc for tx of MRSA skin and soft tissue infection
    1. Inactivated by surfactant
33
Q

How should complicated polymicrobial infections be treated?

A
  • Add an MRSA drug to broad spectrum parenteral AB
  • Piperacillin/Tazobactam or Imipenem-cilstatin, Meropenem
  • Ceftaroline fosamil is a new (5th-gen) IV Cephalosporin with activity against MRSA that may be effective as monotherapy if infection w/P. aeruginosa and anaerobic bacteria is unlikely
34
Q

Ceftaroline fosamil

A
  • IV Cephalosporin binding to PBPs
  • Bactericidal against S. aureus, Strep pneumo, Strep agalactiae (GBS), E. coli, Kleb pneumo, Kleb oxytoca
    1. Noninferior to Vanc + Aztreonam
  • Mainly renal elim; dose adjust in RF
  • Common AEs: diarrhea, nausea, rash, constipation, hypokalemia, phlebitis
    1. C. difficile, ALT/AST elevation, and hemolytic anemia are rare but reported in post-marketing studies
    2. MONITOR pts for devo of ANEMIA (CBC)
35
Q

MOA, admin, and resistance of Daptomycin?

A
  • ADMIN: IV
  • MOA: lipopeptide -> binds to and depolarizes bacterial membrane, inhibiting DNA/RNA/protein synthesis
  • RESISTANCE: changes in cell wall thickness, drug binding site mutations, biofilm production
36
Q

MOA and admin of Piperacillin/Tazobactam?

A
  • IV
  • Beta-lactam + inhibitor: cell wall synthesis INH
  • Tazobactam: inhibits beta-lactamase activity, sustaining active drug levels
37
Q

MOA and admin of Imipenem/Cilastatin, Meropenem?

A
  • ADMIN: IV
  • MOA: carbapenem (beta-lactams) -> cell wall synthesis inhibitors
  • Cilastatin: inhibits renal dihydropeptidase I (brush border), preventing metabolism
    1. Dihydropeptidase produces inactive, but renotoxic metabolite
38
Q

Elim and common toxicities of Daptomycin? Monitoring?

A
  • ELIM: renal; dose adjust in RF
  • TOXICITY: diarrhea, vomiting, throat pain, rarely myopathy, rhabdomyolysis, renal failure
    1. MONITOR pt creatinine kinase levels
    2. Remember that rhabdomyolysis is most commonly associated with antilipidemic statin drugs
39
Q

Elim and common toxicities of Piperacillin/Tazobactam? Monitoring?

A
  • ELIM: renal; dose adjust in RF
  • TOXICITY: GI distress, headache, rash, hypersensitivity rxns, rarely SJS, agranulocytosis, leukopenia, neutropenia, C. difficile
    1. MONITOR for changes in BUN/serum Cr
40
Q

Elim and common toxicities of the Carbapenems? Monitoring?

A
  • Imipenem/Cilastatin, Meropenem
  • ELIM: renal; adjust dose in RF
  • TOXICITY: GI distress, skin rash, seizures at high serum drug levels
    1. MONITOR for changes in BUN/serum Cr
  • REMEMBER: Meropenem not susceptible to dihydropeptidase activity, and w/lower risk of seizures
41
Q

What is the tx for the two types of leprosy?

A
  • Tuberculoid: Dapsone + Rifampicin daily -> 12 mos, then therapy discontinued
  • Lepromatous: Dapsone + Rifampicin + Clofazimine daily -> 24 mos, then therapy discontinued
    1. Dead bacilli may remain in tissues for several years
    2. Clofazimine is no longer widely available
42
Q

Dapsone metabolism

A
  • Metabolized to a series of inactive, but potentially toxic products, esp. Hydroxylamine -> hemolysis + methemoglobinemia
    1. Methemoglobinemia: iron in Hb oxidized, and less capable of carrying O2 -> O2 sats can fall, w/blue nail beds/lips, esp. in pts w/already compromised pulmonary reserve
  • CONTRAINDICATED in pts with G6PD deficiency
  • Drug interxns w: Rifampicin -> INC toxicity
    1. Cimetidine/Omeprazole (for gastric hyperacidity) -> DEC toxicity
    2. Trimethoprim -> INC serum level of both drugs
  • Renal func important; DEC clearance will lead to potential drug accumulation (i.e., w/Probenecid)
43
Q

Dapsone mechanism(s)

A
  • Folate antagonist producing bacteriostatic effect
    1. Distinct from actions of Sulfamethoxazole and Trimethoprim
  • INH of 2nd messenger pathways involved in poly chemotaxis (incompletely understood)
44
Q

How do Sulfamethoxazole and Trimethoprim inhibit folate synthesis?

A
  • Sulfamethoxazole: structural analog of p-aminobenzoic acid (PABA) that competes with PABA for binding to bac dihydropteroate synthase
  • Trimethoprim: binds to and reversibly INH dihydrofolate reductase, preventing formation of tetrahydrofolic acid, the metabolically active form of folic acid
    1. W/o THF, bacteria cannot synthesize thymidine, leading to interference with bacterial nucleic acid and protein formation
  • Synergistic combo against some bacteria
45
Q

Dapsone (Sulfone) Syndrome

A
  • Long-term use of Dapsone is assoc w/a # of AEs (see attached table)
  • In combo, called Dapsone (Sulfone) Syndrome
    1. Sequence: dermatitis, LAD (esp. along posterior border of SCM mm), hepatitis
  • Liver enzyme abnormalities worsen over the period of the exposure, but are reversible once tx ends
    1. Hemolysis also resolves, albeit over a longer time scale
  • Maculopapular rash (upper limbs + forehead, or disseminated)
    1. SJS also reported
46
Q

What are the clinical utilities of Dapsone?

A
  • Labeled: acne vulgaris, dermatitis herpetiformis, leprosy (Henson’s disease)
  • Off-label, recommended: granuloma annulare, ITP, malaria prophylaxis, pneumocystis pneumo
47
Q

Rifampin

A
  • INH bacterial and mycobac RNA synthesis via beta-subunit of DNA-dependent RNA polymerase
    1. Eukaryotic cells unaffected
  • Effective against rapidly growing + slowly dividing orgs -> no antiviral activity (shouldn’t be used)
  • Widely distributed in body: crosses inflamed meninges, placenta; elim in BREAST MILK
  • Hepatic metabolism and elim: enterohepatic recirc
  • CYP inducer: 1A2, 2B6, 2C19, 2C9, 3A -> multiple drug-drug interaxns
48
Q

Why is Rifampin activity variable?

A
  • Genotype (from pt to pt)
  • Pts can express differences in CYP activity or polymorphisms in genomic targets (PXR, RXR) upon which inducers act
  • Differences in P-gp activity and capacity
  • Drug-drug interactions are possible, but NOT absolute
49
Q

Rifampin AEs

A
  • Transient INC in hepatic enzymes and severe, sometimes fatal, liver toxicity
  • Makes mgmt of diabetes more difficult
  • Therapy interval -> not less than twice weekly
    1. Hemolysis, hemoglobinuria, hematuria, renal insufficiency/failure
    2. Flu-like syndrome of fever, chills, myalgias
  • Can discolor bodily fluids -> warn patient (urine, saliva, tears, sputum, contact lenses)
50
Q

Clofazimine

A
  • Preferential binding (not intercalator) to mycobac guanine in DNA -> freq of mycobac guanine and cytosine >>>>> human DNA
  • Progressive, dose-dependent anti-inflam and immunosuppressive effects -> can tx reversal rxns and erythema nodosum leprosum
  • Highly lipophilic w/long (mos) persistence in fatty tissues and reticuloendothelial system
  • Hepatic elim, unchanged -> hepatitis, jaundice reported
  • Staining of body, bodily fluids, suckling infant
    1. Skin discoloration may trigger depression -> suicides reported
  • Feces may appear black or tarry (misinterpreted as GI hemorrhage)
51
Q

What routine monitoring is required for patients being treated for leprosy (table)?

A
  • Basically, CBC and LFTs + screening for renal/hepatic disease and G6PD before starting tx
52
Q

What 3 drugs are used in leprosy tx when Clofazamine is contraindicated?

A
  • Drug resistance remains rare; no need for baseline resistance testing
53
Q

What types of adverse rxns are possible with leprosy tx? How are they treated?

A
  • Type 1 rxns: red patchy skin lesions, erythema, swollen hands and feet, joint pain -> GCS anti-inflam therapy
  • Type 2 rxns (erythema nodosum leprosum): sudden eruption of numerous, painful, nodules and neuritis -> GCS, Clofazamine, Thalidomide
  • Primarily tx w/GCS and NSAIDs; Clofazamine and Thalidomide also used for this purpose
54
Q

Thalidomide

A
  • INH NFkB-mediated transcriptional upregulation and TNF-alpha production (among o/intermediates)
    1. Blocks leukocyte migration: inflammation intimately involved in disease process
    2. Also anti-angiogenic (used in tx of myeloma)
  • TERATOGEN
  • INC in plasma HIV viral load (MONITOR)
  • AEs: somnolence (sleepiness) > rash > headache
  • Rarely peripheral neuropathy
55
Q

What are the clinical uses for the antivirals (table)?

A
  • Famciclovir is metabolized to active product, Penciclovir
  • Valacyclovir and Valganciclovir are pro-drugs for acyclovir and ganciclovir

MSK, Rheum, Derm (21 decks)

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