Term
Helminthic diseases
Nematodes:
Cestodes:
Trematodes: |
|
Definition
Nematodes: Pyrantel pamoate, Piperazine, Mebendazole
Cestodes: Praziquantel, Niclosamide
Trematodes: Praziquantel |
|
|
Term
Protozoan Infections
Trypanosomiasis
African:
American:
Leismaniasis:
Ambiasis:
Giardiasis:
Thrichomoniasis:
Balantidiasis: |
|
Definition
Trypanosomiasis
African: Suramin, Melarsoprol, Eflornithine
American: Nifurtimox
Leismaniasis: Sodium stibogluconate
Ambiasis: Metronidazole, Iodoquinol, Paramonycin
Giardiasis: Metronidazole, Nitazoxanide
Thrichomoniasis: Metronidazole
Balantidiasis: Tetracycline |
|
|
Term
|
Definition
Nematodes
USE: DOC-hydatid disease; combo w/ CSs for neurocysticercosis; also ascariasis, pinworm, hookworm infections
PK: admin PO to fasting pts with intraluminal parasites or with fatty meal when treating tissue infections
SE: generally well tolerated (1-3 days drug regime), long-term use -> enzymatic liver alterations and blood disorders
-careful use in pregnancy |
|
|
Term
|
Definition
Cestodes
salicylamide derivative
MOA: inhibition of oxidative phosphorylation
USE: treatment of most cestode infections
PK: oral admin
SE: mild or transient common GI rxns
-avoid alcohol |
|
|
Term
|
Definition
Cestodes and Trematodes
synthetic isoquinoline-pyrazine derivative
MOA: increases parasite cell membrane permeability to Ca2+ -> produce paralysis, dislodgement, death
USE: cestode and trematode infections, effective tx of schistosome infections of all specifies
PK: well absorbed from GI
SE: well tolerated and safe, nausea, dizziness, abdominal discomfort -> incidence and severity of SEs increases with dose
CI: pregnancy |
|
|
Term
|
Definition
Nematodes
MOA: inhibit microtubule synthesis
USE: ascariasis, pinworm, hookworm infections
PK: oral absorption increased if injested with fatty meal
SE: short term well tolerated
CI: pregnancy |
|
|
Term
|
Definition
Nematodes
MOA: inhibit ACh at myoneural junction -> produce nematode flaccid paralysis -> expulsion
USE: alternative to mebendazole for treatment of ascariasis
PK: rapidly absorbed
SE: may cause dizziness, urticaria
CI: known hypersensitivity, epilepsy, renal or hepatic disorders |
|
|
Term
|
Definition
Nematodes
ganglionic nicotinic ACh agonist
MOA: produce muscular contraction of nematode
USE: luminal ascariasis, pinworm, hookworm infections
PK: poorly absorbed
SE: well tolerated, generally only need single dose -> parasite paralysis and expulsion |
|
|
Term
|
Definition
|
|
Term
|
Definition
Giardiasis
MOA: blocks pyruvate:ferredoxin oxidoreductase pathway
USE: effective against G lamblia and metronizadole resistant protozoa strains and several tapeworm helminths |
|
|
Term
|
Definition
Amebiasis
USE: luminal amebecide
-little GI absorption, may accumulate in renal insufficiency and cause renal toxicity
SE: generally well tolerate, GI issues |
|
|
Term
|
Definition
Amebiasis
-derivative of Emetine
USE: effective against E histolytica trophozoites in bowel lumen but not in intestinal wall or extraintestinal tissues, combo w/ metronidazole
SE: generally well tolerated
-caution in pts with optic neuropathy, renal, thyroid disease, or iodine intolerance |
|
|
Term
|
Definition
Amebiasis, Giardaisis, Thrichomoniasis
Abebiasis: DOC, effectively eliminates intestinal and extraintestinal E histolytica infections
MOA: penetrates protozoan and bacterial cells, does not enter mammalian cells; affects the ferredoxin-like or flavodoxin-like low redox-potential electron transport proteins -> FUNCTIONS AS ELECTRON SINK -> toxic intermediates
PK: well absorbed after oral admin, widely distributed with intracellular conc. approaching extracelular levels, metabolized in liver
SE: nausea, vomiting, cramps, turns urine dark or red brown
CI: pregnancy or nursing, DO NOT DRINK ALCOHOL |
|
|
Term
|
Definition
Leismaniasis
antimonial
USE: choice drug for all forms, cutaneous and visceral, efficacy depends on many factors
PK: daily doses given IM or IV for 3-4 weeks (cure)
SE: intially relatively well tolerated but can produce dose related toxicity -> fever, GI changes, ECG changes (T-wave inversions/prolonged QT intervals) |
|
|
Term
|
Definition
American Trypanosomiasis
USE: tx of acute, but not chronic form of disease
-in many cases does not eradicate parasite and get chronic form
SE: severe GI, CNS, neurological toxicity |
|
|
Term
|
Definition
African Trypanosomiasis
MOA: inhibits enzyme ornithine decarboxylase -> blocks conversion of ornithin to putrescine which is required for cell proliferation
USE: tx of CNS advanced disease
TOX: better tolerated than arsenicals but still see significant blood and GI toxicity-reversible |
|
|
Term
|
Definition
African Trypanosomiasis
arsenical
USE: 1st line therapy for advanced CNS infections
PK: IV, penetrates CNS
TOX: use only when absolutely necessary-serious GI, CV, renal, hepatic SEs, encephalopathy (fatal), hemolysis in GP6D deficient pts |
|
|
Term
|
Definition
African Trypanosomiasis
USE: chemoprophylaxis and tx of early hemolymphatic infections, combo w/ pentamidine may increase efficacy
PK: IV, does not cross BBB -> not effective against advanced forms of disease
SE: serious GI, CV, neurological, blood |
|
|
Term
|
Definition
antimalarial agent
MOA: a rxn catalyzed by heme iron -> carbon-centered radical -> alkylates and damages parasite's macromolecules
USE: treat severe P falciparum infections, key role in combination therapy for drug-resistant infections
-CURRENTLY NOT FDA APPROVED
-not used alone because of incomplete efficacy and avoid drug resistance
-not used prophylactically |
|
|
Term
| Sulfonamides (Sulfoxadine) |
|
Definition
antimalarial agent
MOA: inhibit dihydropteroate synthase -> inhibit folate synthesis
USE: use in combo with chloroquine in tx and prevention of malaria |
|
|
Term
|
Definition
antimalarial agent
MOA: inhibits plasmodial dihydrofolate reductase -> inhibit folate synthesis
USE: used in combo with chloroquine for tx and prevention of malaria |
|
|
Term
|
Definition
antimalarial agent
MOA: unknown
USE: DOC-eradication of dormant P vivax and ovale liver forms-RADICAL CURE FOR THESE MALARIAL SPECIES, gametocidal against the 4 malaria species; active against hepatic stages but very weak against erythrocytic stage
PK: well absorbed from GI, long half life -> weekly dosing prophylaxis
-never give parenterally -> induce hypotension
SE: generally well tolerated, may produce GI symptoms
TOX: blood dyscrasias, cardiac arrythmias; hemolysis or methomyoglobinemia (cyanosis) in persons with G6PD deficiency
CI: pts receiving myelosuppressive drugs or history of granulocytopenia
-avoid in pregnancy because of effects on fetus
STANDARD THERAPY: chloroquine to eradicate erythrocytic forms, if G6PD levels normal, then 14 day primaquine course to eradicate liver parasites and prevent relapse |
|
|
Term
|
Definition
antimalarial agent
MOA: strong blood schizonticidal activity against P falciparum and P vivax, not active against hepatic stages or gametocytes
USE: prophylactic agent in most malarial regions with chloroquine-resistant strains (weekly dosing)
PK: oral, well absorbed, widely distributed, elimated slowly allowing single-dose treatment regime
MOR: sporadic resistance-associated with quinine but not chloroquine
SE: CNS, blood dyscrasias, heart, GI
-FDA approved only for malaria prophylaxis |
|
|
Term
|
Definition
antimalarial agent
MOA: tx of choice/standard therapy in US for severe F malaria; gametocidal against P vivax and P ovale but not P falciparum
USE: 1st line therapy for F malaria; quinine-highly effective blood schizonticide against 4 forms of human malaria parasites; not used prophylactically
PK: oral quinine rapidly absorbed, or IV or IM, widely distributed
TOX: cardiac toxicity and unpredictable PKs (cardiac monitoring); discontinue if severe cinchonism, hypersensitivtiy, hemolysis occur
SE: cinchonism (tinnitus, headache, nausea, dizziness, flushing, visual disturbances); prolonged use -> GI disturbances, hypersensitivity (blackwater fever-hemolysis, hemoglobinuria), hematological abnormalities, hypoglycemia, uterine contractions
DI: do not give with mefloquine
-given with doxycycline to limit duration of use (3 days) due to toxicity
-not active against liver parasites |
|
|
Term
|
Definition
antimalarial agent
-few areas infested only by this drug-sensitive malaria parasites (Caribbean, Central America, Middle East)
MOA: interfere with heme handling -> failure to inactivate heme results in oxid. damage and causes parasite death
USE: DOC-treatment of nonfalciparum and sensitive falciparum malaria-rapidly terminates fever and clears parasitemia; preferred chemoprophylactic in regions without resistant F malaria
PK: well absorbed from GI, IM or IV not good, rapidly distributed, complex PKs
MOR: mutations in gene encoding chloraquine resistance transporter (crt); resistance common among P falciparum but not so common for P vivax
TOX: usually well tolerated, even with prolonged use; pruitis, anorexia, vision blurring; rare rxns-hemolysis in G6PD deficiency, confusion, ECG changes
CI: pts with psoriasis or porphyria
-highly effective blood schizonticide, principle antimalarial drug in world
-not active against liver parasites
-does not eliminate dormant liver forms of P vivax or P ovale
-safe in pregnancy and for small children |
|
|
Term
|
Definition
MOA: cyclic lipopeptide that interferes with bacterial membrane functions and pore formation
SOA: gram positives, esp. drug resistant bacteria
MOR: unclear
PK: IV
SE: elevated liver function tests and creatine phosphokinase-if pts have muscle weakness and pain -> discontinue drug |
|
|
Term
|
Definition
MOA: disrupts bacterial membranes by charge alteration
SOA: gram negatives
MOR: unclear
PK: topical (with neomycin and bacitracin), IV or IM as well
SE: few if used topically |
|
|
Term
|
Definition
MOA: not clear-attacks several pts of bacterial metabolism, mimics radiation damage
SOA: uncomplicated UTIs
MOR: altered levels of reduction enzymes
PK: PO, drug concentrated in urine
SE: turns urine brown, lung problems (pts on prolonged/prophylaxis treatment) |
|
|
Term
|
Definition
MOA: produces compounds toxic to DNA; reduced by pyruvate:ferridoxin oxidoreductase system -> promotes formation of intermediate compounds and free radicals that are toxic to the cell
MOR: not clear
SOA: obligate anaerobes and some protozoa (Giardia, Trichomonas)
PK: IV or PO, good tissue penetration (including CNS)
TOX: promote renal retention of lithium and decreased elimination of ergot derivatives, PTS SHOULD NOT DRINK ALCOHOL |
|
|
Term
|
Definition
allylamines (topical mucocutaneous infection)
MOA: block ergosterol biosynthesis by inhibiting squalene-2,3-epoxidase enzyme
USE: creams for tinia cruris and corporis
-broad spectrum antifungals |
|
|
Term
|
Definition
azole (topical mucocutaneous infection)
MOA: inhibit 14-alpha-sterol demethylase (microsomal CYP enzyme essential for ergosterol biosynthesis)
USE: cutaneous application-dermatophytic infections (tinea pedis, corporis, and cruris); shampoo form-seborrheic dermatitis and pityriasis versicolor; vaginal application-vaginal candidiasis
MOR: mutations in gene encoding 14-alpha-sterol demethylase |
|
|
Term
|
Definition
polyene antibiotic (topical mucocutaneous infection)
-same MOA and cross-resistance with amphotericin B
-not absorbed from GI, skin, vagina
USE: mucocutaneous candidal infections; stomatitis, vaginitis |
|
|
Term
|
Definition
azole (systemic mucocutaneous infection)
MOA: inhibit 14-alpha-sterol demethylase (microsomal CYP enzyme essential for ergosterol biosynthesis)
USE: similar spectrum of activity as itraconazole
MOR: mutations in gene encoding 14-alpha-sterol demethylase
TOX: visual disturbances (blurring and changes in color brightness or vision)-symptoms appear soon after admin and disappear after ~30 min |
|
|
Term
|
Definition
azole (systemic mucocutaneous infection)
MOA: inhibit 14-alpha-sterol demethylase (microsomal CYP enzyme essential for ergosterol biosynthesis)
USE: DOC treatment and secondary prophylaxis of C meningitis, IV treatment equiv to amphotericin B in candidemia in ICU pts with normal WBCs
MOR: mutations in gene encoding 14-alpha-sterol demethylase
PK: oral or IV, well absorbed from GI, good CSF penetration
-prophylactic use reduce fungal disease in bone marrow transplant and AIDS pts
TOX: relatively non-toxic |
|
|
Term
|
Definition
systemic mucocutaneous infection
MOA: similar to griseofulvin, but fungicidal agent; similar to azoles-inhibits ergosterol biosynthesis (inhibits fungal enzyme squalene epoxidase)
USE: dermatophytoses, particularly onychomycosis (cured in pts-1 tablet/d/12 weeks)
TOX: rare-GI, headaches |
|
|
Term
|
Definition
systemic mucocutaneous infection
-fungistatic
MOA: deposited in newly forming skin -> binds to keratin protecting skin from new infection
USE: dermaphytosis (given 2-6 weeks), nail infections (given for months)
PK: poor solubility, GI absorption enhanced when given in microcrystalline form and fatty foods |
|
|
Term
|
Definition
echinocandin (systemic infection)
MOA: inhibit synthesis of beta(1,3)D-glucan -> disrupt cell wall structure
USE: esophageal candidiasis, candidema, and salvage therapy of aspergilliosis; azole resistant fungi susceptible to caspofungin
MOR: mutation in one of genes encoding beta(1,3)D-glucan
PK: only IV admin
TOX: generally well tolerated, SEs-GI disturbances, flushing |
|
|
Term
|
Definition
azole (systemic and mucocutaneous infection)
MOA: inhibit 14-alpha-sterol demethylase (microsomal CYP enzyme essential for ergosterol biosynthesis)
USE: replaced ketaconazole, broad spectrum; DOC for dimorphic fungi histoplasma, blastomyces, sporothrix
PK: oral or IV admin, absorption inc by food and low gastric pH, poor CSF penetration; interacts with hepatic microsomal enzymes, bioavail lowered when taken with rifamycins
MOR: mutations in gene encoding 14-alpha-sterol demethylase
TOX: relatively non-toxic
DI: interact with number of drugs -> fatal cardiac arrythmias |
|
|
Term
|
Definition
azole (systemic and mucocutaneous infection)
MOA: inhibit 14-alpha-sterol demethylase (microsomal CYP enzyme essential for ergosterol biosynthesis)
USE: only used when cost is primary determinant, broad spectrum
MOR: mutations in gene encoding 14-alpha-sterol demethylase
TOX: relatively non-toxic |
|
|
Term
|
Definition
cytosine analog (systemic infection)
MOA: toxic to fungal cells only when transported by cytosine permease into fungal cell; 5-FU -> 5-FUMP -> 5-FUTP (inhibit RNA synthesis) or 5-F-dUMP (inhibit DNA synthesis)
USE: narrow spectrum of action-cryptococcus neoformans, some candida, some molds; combo w/ amphotericin B for cryptoccal meningitis or w/ intraconazole for chromoblastomycosis
MOR: loss of cytosine permease enzyme, dec. activity of UPRTase or cytosine deaminase
PK: well absorbed from GI, widely distributed inc. CSF, renal excretion
TOX: renal insufficiency and AIDs-removed by dialysis, GI disturbances, leukopenia, thrombocytopenia, toxic enterocolitis, azotemia in AIDS pts
DI: synergy with amphotericin B and azoles |
|
|
Term
|
Definition
polyene antibiotic (systemic infection)
MOA: binds to ergosterol altering cell permeability by forming pores
USE: broad spectrum antifungal agent, yeasts, molds, fungi-causing endemic mycoses, initial induction regime for serious fungal infections -> replaced by azole drug for chronic therapy or relapse prevention; VERY IMPORTANT for immunosupp. pts, sever fungal pneumonia, crytococcal meningitis (intrathecal admin); corneal ulcer, keratitis, fungal arthritis, candiduria
PK: admin slow IV infusion, poorly absorbed from GI
MOR: alterations in ergosterol binding
TOX: immediate rxn-fever, chills, muscle spams, hypotension; culm. rxn-renal impairment, anemia, renal toxicity; hypersens. rxn and phlebitis @ site of injection; CNS SEs, hypokalemia, hypomagnesia, fever, pain, abnormal liver function test; intrathecal admin-seizures, chemical arachnoiditis |
|
|
Term
|
Definition
| non-nucleoside reverse transcriptase inhibitor MOA: alters conformation of RT USE: in combo with AZT and Lamivudine TOX: dizziness, headache, insomnia, rash DI: decreases conc. of Phenobarbital, Phenytoin, Carbamazepine, Methadone, Rifabutin -coadmin of Rifampin -> reduce levels of Efavirenz |
|
|
Term
|
Definition
nucleotide reverse transcriptase inhibitor
MOA: inhibits RT and terminates DNA chain elongation
USE: HIV pts and chronic hep B infections
TOX: flatulence, some renal toxicity
DI: do not give with didanisone, lamuvidine, abacavir combo |
|
|
Term
|
Definition
psoriasis treatment
MOA: protein that binds to TNF-a and b
USE: moderate-severe chronic plaque psoriasis
-not used with other immunosuppressive agents
SE: serious infections |
|
|
Term
|
Definition
acne treatment
-synthetic retinoid administered orally
USE: reserved only for sever cystic acne not responding to standard therapy, reduces size and function of sebaceous glands
SE: hypervitaminosis A, dryness and itching of skin and mucous membranes, headache, corneal opacities, alopecia, muscle/joint pains, TERATOGENIC
TOX: suspend drug at least 1 month before discontinuing contraceptives, start contraceptives at least 1 month before beginning this drug and for at least 1 menstrual cycle following drug cessation |
|
|
Term
|
Definition
acne treatment
MOA: naphtoic acid derivative resembling retinoic acid in structure and effects
-unlike RA, photochemically stable and shows little decrease in efficacy in combo with benzoyl peroxide
-applied topically
-less irritant than tretoin
USE: pts with mild to moderate acne vulgaris |
|
|
Term
| Retinoic acid (Tretinoin) |
|
Definition
acne treatment
-acid form of Vit A
MOA: decreases cohesion between epidermal cells and increases their turnover -> transformation of closed comedones into open ones -> expulsion; stabilizes lysosomes, increases RNA polymerase activity, PGE2, cAMP levels, incorporation of thymidine into DNA
USE: topically for acne vulgaris (remains mostly in epidermis)
PK: during 1st 4-6 weeks make seem to make acne worse, but after 8-12 weeks condition will improve
TOX: slight erythema with mild peeling, skin irritation; must avoid sun because drug may increase UV light potential to produce skin tumors
-apply to dry skin only |
|
|
Term
|
Definition
sunshade
MOA: contains opaque compounds known to reflect UV light, little used
USE: infants-6 months to 2 yrs |
|
|
Term
|
Definition
sunscreen
MOA: contain chemical compounds to absorb UV light responsible for most erythema and tannning sun exposure
-for children greater than two years old, adults
-half-life of about 2 yrs |
|
|
Term
| Psoralens (Trioxsalen, Methoxsalen) |
|
Definition
repigmentation
MOA: photoactivated by long-wavelength UV light -> intercalate with DNA
USE: repigment depigmented macules of vitiligo
TOX: long-term use -> cataracts and skin cancer |
|
|
Term
| Hydroquinone (reversible), Monobenzone (irreversible) |
|
Definition
depigmentation
H-MOA: inhibt tyrosinase -> block synthesis of melanin
M-MOA: toxic to melanocytes
USE: reduce skin hyperpigmentation |
|
|
Term
|
Definition
antiectoparasiticide
USE: pediculosis capitis, corporis, pubis, scabies
-lack of systemic side effects makes it a safe alternative scabicide in infants and pregnancy
SE: skin staining, unpleasant odor |
|
|
Term
|
Definition
antiectoparasiticide
USE: pediculosis capitis, corporis, pubis, scabies
PK: shampoo or lotion prep
TOX: neurotoxicity and nephrotoxicity (some systemic absorption may occur after cutaneous use), concentrated in fatty tissue and brain
-not used during pregnancy, infants, seizure-prone individuals |
|
|
Term
|
Definition
antiviral
USE: recurrent orolabial HSV infections in immunocompromised pts
-cream applied at first signs of infection, reapplied every 2h for 4d reduces time of viral shedding and decreases healing time by one day |
|
|
Term
|
Definition
antiviral
USE: primary cutaneous HS and limited mucocutaneous HS in immunocompromised pts, decreases duration of viral shedding |
|
|
Term
|
Definition
antifungal
USE: fingernail and toenail onychomycosis (6 or 12 weeks-daily dose)
SE: pt monitored for hepatic dysfunction |
|
|
Term
|
Definition
antifungal
USE: common dermatophyte infections-tinea infections of scalp and nonhairy skin, fingernails and toenails-relapse is common
SE: diarrhea, photosensitivity, headaches
CI: porphyria, hepatic failure, long-term use requires periodic evaluation of liver, hematopoietic and liver function |
|
|
Term
|
Definition
antifungal
SE: may interfere with ventricular function -> thorough cardiac examination and monitoring
CI: with midazolam or triazolam b/c prolong the sedative and hypnotic effects; use with HMG-CoA reductase inhibitors increases risk of rhabdomyolysis |
|
|
Term
|
Definition
antifungal
USE: cutaneous infections cause by epidermophyton, microsporium, trichophyton fungi
TOX: gynecomastia, hepatitis, increased liver function enzymes, long-term use-periodic evaluation
CI: with midazolam or triazolam b/c prolong the sedative and hypnotic effects; use with HMG-CoA reductase inhibitors increases risk of rhabdomyolysis |
|
|
Term
| Bacitracin, Clindamycin, Metronidazole, Mupriocin, Neomycin, Polymixin |
|
Definition
|
|
Term
|
Definition
immunomodulator
MOA: stimulate IFN-a release from peripheral mononuclear cells and macrophages
USE: perianal and external genital warts
-applied topically
SE: inflammatory rxn at site of application |
|
|
Term
|
Definition
immunomodulator
MOA: block release by mast cells of various inflammatory mediators
USE: atopic dermatitis
SE: burning sensation at application site |
|
|
Term
|
Definition
trichogenic
-5-alpha reductase inhibitor
MOA: blocks conversion of testosterone to dihydrotestosterone
USE: promotes hair growth, prevents further hair loss
-treat for at least 3-6 months, continued treatment to sustain benefit
SE: decrease libido, ejaculation disorder, erectile dysfunction |
|
|
Term
|
Definition
trichogenic
-reverse progressive miniaturization of terminal scalp hairs
-effect is not permanent and cessation of txt leads to hair loss in 4-6 months
-percutaneous absorption in normal scalp is minimal, but possible effects on blood pressure (monitor pts with cardiac disease) |
|
|
Term
|
Definition
antipruitic
USE: relief in pruitis associated with atopic dermatitis or lichen simplex chronicus
MOA: unknown
SE: drowsiness, anticholinergic effects, allergic dermatitis
CI: pts with untreated narrow-angle glaucoma or tendency to urinary retention |
|
|
Term
|
Definition
keratolytic
topical-absorbed percutaneously -> excreted in urine
MOA: solubilize cell surface proteins that keep stratum corneum intact -> desquamation of keratotic debris
TOX: salicylism, if toxic use hemodialysis
-children at high risk, careful use in pts with diabetes or peripheral vascular disease
SE: urticarial, anaphylactic, erythema multiforme rxs in pts allergic to salicylates |
|
|
Term
|
Definition
anti-inflammatories, anti-pruitic
USE: psoriasis, dermatitis, lichen simplex, chronicus
SE: folliculitis, phototoxicity, allergic contact dermatitis
-in pts with erythrodermal or generalized pustular psoriasis -> risk of total body exfoliation |
|
|
Term
| Betamethasone, Hydrocortisone |
|
Definition
anti-inflammatories, corticosteroids
very responsive: atopic dermatitis, seborrheic dermatitis
less responsive: psoriasis of palms and soles, vitiligo
least responsive: intralesional therapy (keloids, cysts)
-topical prep-variable absorption from healthy skin, increased absorption in damaged skin
SE: depressed, cigarette-like skin, steroid rosacea |
|
|
Term
|
Definition
psoriasis treatment
MOA: immunosuppressive protein-blocks lymphocyte activation
USE: moderate-severe chronic plaque psoriasis
-administered IM
-not to be used in pts with clinically significant infection or history of cancer |
|
|
Term
|
Definition
psoriasis treatment
MOA: synthetic vit D3 derivative
USE: plaque-type psoriasis vulgaris of moderate severity
-improvement noted after 2 weeks of treatment, continued improvement up to 8 weeks
SE: burning, itching, dryness of treatment area, avoid facial contact, may produce ocular irritation |
|
|
Term
|
Definition
psoriasis treatment
MOA: acetylenic retinoid prodrug hydrolyzed to active form tazarotenic acid -> binds retinoic acid receptors resulting in modified gene expression
-MOA in psoriasis is unknown
-teratogenic effects
-cautin if used in women of childbearing potential
SE: burning, stinging skin sensation, erythema, localized edema-minimize skin exposure |
|
|
Term
|
Definition
psoriasis treatment
MOA: etretinate metabolite
-effective orally in psoriasis (esp. pustular form)
TOX: similar to those seen for isotretinoin-hypervitaminosis, teratogenic
-not used by pregnant females or those who may become pregnant during treatment or for at least 3 years after treatment is discontinued
-ETHANOL strictly prohibited during treatment and 2 months after discontinuing therapy
-3 yr restriction in blood donation |
|
|
Term
|
Definition
treat leprosy
-alternative to dapsone
PK: has erratic absorption rate, stored in skin and reticuloendothelial tissues -> slowly released
USE: sulfone-reistant leprosy, sulfone intolerant pts
SE: skin discoloration from red brown to nearly black |
|
|
Term
|
Definition
treat leprosy
MOA: closely related to sulfonamides and comp. inhibit folate synthesis
PK: well absorbed from GI, widely distributed, eliminated in urine
USE: initial therapy combined with rifampin and clofazimine
TOX: generally well tolerated, hemolysis (pts with G-6-PD deficiency |
|
|
Term
| Erythromycin, Azythromycin, Ciprofloxacin |
|
Definition
| drugs to treat atypical mycobacterial infections |
|
|
Term
|
Definition
2nd line drug-treat TB
-folate synthesis antagonist
SE: GI irritation and hypersensitivity rxn |
|
|
Term
|
Definition
1st line drug-treat TB
MOA: unclear
USE: M TB, M avium complex, M kansaii (always given in multidrug regime and treatment continued for several months)
PK: poor penetration into cells-effective mostly against extracellular TB; used when injectable (IM or IV) therapy recommended (TB meningitis, disseminated infection, when TB resistant to other drugs)
MOR: point mutation in rpsL gene (S12 ribosomal protein gene) or rrs gene (16S ribosomal protein gene) -> alter ribosomal binding site
TOX: dose-related ototoxicity and nephrotoxicity, vertigo, hearing loss; risk increased in elderly and pts with impaired renal function |
|
|
Term
|
Definition
1st line drug-treat TB
-bacteriostatic agent
MOA: inhibit mycobacterial arabinosyl tranferase enzymes, encoded by the embCAB operon -> polymerization of arabinoglycan (component of mycobacterial cell)
USE: given as daily dose with INH and rifampin, effective against most M TB strains
MOR: mutations resulting in overexpression of emb gene products or within emb structural gene
PK: well absorbed from GI, excreted in feces and urine, accumulates in renal failure and reaches CSF only during inflammation
SE: dose-related retrobulbar neuritis -> loss of visual acuity and red-green color blindness (disappears after discontinuation of drug), hypersensitivity to drug is rare
-contraindicated in children |
|
|
Term
|
Definition
1st line drug-treat TB
MOA: synthetic analog of nicotinamide, converted to pyranzinoic acid (active form) by mycobacterial pyrazinamidase (encoded by pncA)
MOR: mutations in pncA, decreased drug uptake
USE: combo with INH and rifampin in short course regmine (6 months) as sterilizing agent to prevent relapse
PK: well absorbed from GI, widely distributed
-no cross-resistance between this drug and other anti-TB agents
SE: hepatotoxicity, GI disturbances, hyperuricemia (not reason to stop txt unless develops gout) |
|
|
Term
|
Definition
1st line drug-treat TB
MOA: analog of antibiotic rifamycin, binds to beta-subunit of bacterial DNA-dependent RNA polymerase -> inhibit RNA synthesis
USE: various bacteria, in combo with other drugs is effective in some atypical M infections and leprosy; as single drug-alternative to INH prophylactic tx for TB
MOR: point mutation in rpoB -> reduced rifampin binding to RNA polymerase
PK: well absorbed (oral admin), excreted into bile, penetrates most tissues and fluids and CSF
SE: SECRETIONS ARE RED ORANGE COLOR, proteinuria, rash, nephritis, jaundice, hepatitis; intermittent admin -> flu-like syndrome; strongly induces P450 enzymes |
|
|
Term
|
Definition
1st line drug-treat TB
MOA: acts only upon M, prodrug-activation by mycobacterial catalase peroxidase KatG -> forms complex with AcpM and KasA -> blocks mycolic acid synthesis and kills cell
MOR: over-expression of inhA gene, mutation/deletion of katG gene, promoter mutation resulting in overexpression of ahpC, mutations in kasA
PK: well absorbed (oral admin), widespread distrib. including brain and CSF
USE: chemoprophylaxis in individuals with greatest risk factors, young children, immunocompromised individuals; pyroxidine recommended for slow acetylators (neuropathy)
TOX: hepatitis, risk increases with age, greater risk in alcoholics, pregnancy and post-partum period |
|
|
Term
|
Definition
MOA: bind to cellular receptors -> JAK/STAT pathway; induce many proteins -> inhibit protein synthesis
USE: genital warts, chronic hep B and C, kaposi's sarcoma in HIV pts, multiple myelomas, MS
-Peg-interferon 2A + Ribavirin -> chronic hep C
TOX: IM or SC injection give flu-like symptoms, high dose/chronic therapy -> bone marrow suppression, fatigue, inc suscep. to bacterial infections, anorexia, diarrhea, psychiatric syndrome (depression and anxiety) |
|
|
Term
|
Definition
fusion inhibitors
E-MOA: binds to HIV viral envelope glycoprotein and prevents conformational change
E-USE: injected twice daily in HIV pts, used with other drugs
E-TOX: pain, redness, nodule and cyst formation at site of injection
M-MOA: maraviroc is a chemokine receptor 5 inhibitor
M-USE: HIV pts
M-TOX: most common are cough, fever, dizziness, headache, lowered blood pressure, nausea, bladder irritation, may cause liver problems and cardiac events, an increased risk for some infections, slight increase in cholesterol levels |
|
|
Term
|
Definition
protease inhibitor combo
PK: lopinavir is metabolized by CYP3A, ritonavir is inhibitor of CYP3A -> raise levels of lopinavir
USE: treat HIV strains that are resistant to multiple protease inhibitors
TOX: well tolerated, diarrhea, nausea, fatigue, headache, hyperlipidemia, hyperglycemia, altered body fat
DI: inhibit activity of CYP4A4 and CYP2D6 |
|
|
Term
| Atazanavir, Indinavir, Ritonavir, Lopinavir, Nelfinavir, Amprenavir, Saquinavir |
|
Definition
protease inhibitors
MOA: interfere with proteoylsis of gag-pol precursor -> nonfunctional virions
USE: HIV pts must take drugs continuously in combo with AZT and Lamivudine or other NRTI
MOR: cross resistance often occurs among protease inhibitors, but HIV strains may still be susceptible to Amprenavir
TOX: well tolerated, sometimes get nausea, vomiting, diarrhea, lipodystrophy, hyperglycemia |
|
|
Term
|
Definition
non-nucleoside reverse transcriptase inhibitor
MOA: binds and inhibits RT
USE: in combo with Zidovudine and Didanosine, least potent NNRTI
DI: inhibits CYP3A4,drugs that induce CYP3A4 reduce levels of delaviridine, also inhibits CYP2C9 |
|
|
Term
|
Definition
non-nucleoside reverse transcriptase inhibitor
MOA: alters conformation of RT
USE: in combo with Didanosine or Stavudine
TOX: rash, fever, nausea, severe dermatological effects and fatal hepatotoxicity
DI: st. john's wort -> lowers conc. of nevirapine, nevirapine induces CYP3A4, nevirapine lowers plasma conc. of ethinyl estradiol so pts should be given alternative birth control |
|
|
Term
|
Definition
| nucleoside reverse transcriptase inhibitor MOA: inhibits RT and terminates DNA chain elongation USE: given with AZT or alone for those who cannot tolerate AZT-treatment, Hep B and HIV MOR: RT becomes mutated TOX: peripheral neuropathy, rash and stomatitis on initial treatments |
|
|
Term
|
Definition
nucleoside reverse transcriptase inhibitor
MOA: inhibits RT and terminates DNA chain elongation
USE: HIV infected adults and children in combo with AZT and Lamivudine or protease inhibitor
TOX: hypersensitivity resulting in fever, GI distress, malaise, rash |
|
|
Term
|
Definition
nucleoside reverse transcriptase inhibitor
MOA: inhibits RT and terminates DNA chain elongation
USE: pts with HIV in combo with AZT (resistance to AZT develops more slowly when used in combo), hep B
TOX: pancreatitis in pediatric pts
-triziir: zidovudien, lamivudine, abacavir; also lamivudine and abacavir |
|
|
Term
|
Definition
nucleoside reverse transcriptase inhibitor
MOA: inhibits RT and terminates DNA chain elongation
USE: HIV infections
TOX: peripheral neuropathy, potentially fatal lactic acidosis, peripheral lipoatrophy, central fat accumulation, hyperlipidemia |
|
|
Term
|
Definition
nucleoside reverse transcriptase inhibitor
MOA: inhibits RT and terminates DNA chain elongation
USE: pts with AZT-resistant HIV infections
MOR: RT becoes mutated
TOX: pancreatitis (fatal), GI disturbances, dose-limiting peripheral neuropathy, non-cirrhotic portal HTN (fatal)
DI: toxicity increases when combo with stavudine |
|
|
Term
|
Definition
nucleoside reverse transcriptase inhibitor
MOA: thymidine kinase converts drug to AZT-TP which is incorporated into viral DNA and terminates chain elongation
USE: HIV pts (protects fetus from become infected by HIV mother)
MOR: mutated RT that has lower affinity for AZT-TP
TOX: bone marrow (anemia and leukopenia), headaches; potentially fatal lactic acidosis, peripheral lipoatrophy, central fat accumulation, hyperlipidemia
DI: Probenecid, Acetaminophen, Lorazepam, Indomethacin, Cimetidine -> increase toxicity of AZT
-Trizivir: Zidovudine, Lamivudine, Abacavir |
|
|
Term
|
Definition
synthetic guanosine analog
MOA: inhibits viral mRNA synthesis
USE: ribavirin w/ IFN -> hep C; infants and young children with respiratory syncytial virus infection -> bronchiolitis and pneumonia, influenza A and B, parainfluenza, paramyoxvirus, arenavirus, HIV
TOX: aerosol well tolerated, systemic doses -> anemia, teratogenic -> no pregnant women |
|
|
Term
|
Definition
neuraminidase inhibitors
MOA: inhibit neuraminidases -> decreased release of virus from infected cells, increased formation of viral aggregates, decreased viral spread
Z-USE: shortens duration and may be used to prevent flu (within 30 hrs of onset)
Z-TOX: nasal and throat discomfort, headaches, bronchospasm in asthma pts
O-USE: shortens the duration and may be used to prevent flu (within 36 hrs of onset)
O-TOX: nausea (reduced if taken with food), vomiting, headaches
-both treat influenza A and B, H1N1 |
|
|
Term
|
Definition
iodinated thymidine analog
MOA: inhibits viral DNA synthesis, incorporated into viral and cellular DNA -> more susceptible to breaks -> error-prone transcription
USE: topical txt of HSV keratitis
TOX: pain, inflammation, edema of eyes or lips |
|
|
Term
|
Definition
pyrimidine analog
MOA: inhibits viral DNA synthesis
USE: HSV keratoconjunctivitis and keratitis
TOX: inflammation of cornea
-replaced the drug Idoxuridine |
|
|
Term
|
Definition
inorganic pyrophosphate analog
MOA: reversibly inhibit viral DNA and RNA polymerases
USE: IV treatment for CMV retinitis in HIV-infected pts who are resistant to ganciclovir, herpes pts resistant to acyclovir
TOX: nephrotoxicity, anemia, nausea, fever, hypocalcemia, hypomagnesemia |
|
|
Term
|
Definition
guanine nucleoside analog
MOA: comp inhibit viral DNA polymerase, block elongation
USES: CMV retinitis in immunocomp pts, prevention of CMV in transplant pts
TOX: dose-dependent neutropenia, CNS effects (heachache, behavioral changes, convulsions, coma), carcinogenic
-half life: > 24 hrs
-ganciclovir conc. 10X that of acyclovir |
|
|
Term
|
Definition
guanine nucleoside analog
MOA: viral thymidine kinase gene phosphorylates drug -> acyclovir triphosphate which competes with dGTP and incorporated into DNA -> premature chain termination
USES: HSV and VZV
MOR: due to altered/deficient thymidine kinase or polymerase
TOX: nausea, headache, diarrhea, vomiting, transient renal dysfunction @ high doses or when given IV to dehydrated pt
-oral or IV admin (systemic)
-half life: 2.5hrs |
|
|
Term
| Ciprofloxacin, Levofloxacin |
|
Definition
fluoroquinolones
-DNA replication inhibitors
MOA: inhibit type II topoisomerases (DNA gyrase, topo IV), bactericidal
SOA: broad spectrum
-ciproflaxin: gram negs, esp. pseudomonas
-levoflaxacin: gram negs and gram pos (strep and staphy), atypical respiratory pathogens (mycoplasma, legionella), also active against myco-not 1st line agent
-used in ear or eye drops-staph, strep, pseduomonas
MOR: target modification in DNA gyrase, topo IV genes; altered uptake or efflux; plasmid-mediated drug modification by quinolone transacetylase
PK: well absorbed from upper GI tract, given orally or IV, tissue distrib good
-not recommended in pregnant pts or those under 18 bc of athropathy
AR: levofloxacin-elongation of QT interval -> arrythmias (not given to pts with heart condition); arthropathy in elderly pts, discontinued in pts who develop joint pain or tendonitis (achilles tendon) |
|
|
Term
|
Definition
protein synthesis inhibitor
MOA: inhibit isoleucine tRNA synthetase
SOA: gram positives, esp. drug resistant S. aureus
MOR: target site mutation
PK: topical on skin or mucosal surface, used to treat nasal carriage of S. aureus
AR: unclear |
|
|
Term
|
Definition
protein synthesis inhibitor
MOA: binds 50S subunit
SOA: broad, seldom used nowadays
MOR: acetylation, efflux pumping
PK: IV or PO
AR: aplastic anemia, bone marrow suppression, Gray syndrome (circulatory collapse, coma, death), dose adjustment for pt with liver problems |
|
|
Term
| Tetracycline, Doxycycline, Tigecycline |
|
Definition
tetracyclines
-protein synthesis inhibitors
MOA: bind 30S ribosomal subunit
SOA: broad, many unusual bacteria and some protozoa
MOR: frequently occuring, often found on plasmids and transposons, efflux pumping, some bact produce protein that binds to ribosome and blocks tetracycline action
-tigecycline not affected by these MOR
PK: IV or PO, good absorption from GI tract and reasonable tissue distribution (including CNS)
-antagonistic to beta-lactams
AR: nausea and photosensitivity common, sun exposure -> rash, not given to children under 8 and pregnant women b/c of teeth discoloration |
|
|
Term
| Streptomycin, Gentamicin, Tobramycin |
|
Definition
aminoglycosides
-protein synthesis inhibitors
MOA: bind to 30S subunit, usually bactericidal, initially penetrate by disrupting magnesium bridges b/w LPS moieties -> transported across cytoplasmic membrane in energy-dependent manner (inhibit by divalent cations, inc. osmolarity, acidic pH, anaerobic environ)
SOA: broad, most effect against gram negs, often given along with other antibiot (esp. beta-lactams), inactive vs anaerobes
MOR: common problem-resist genes found on plasmids/transposons; efflux pumping, dec uptake by outer membrane changes, enzymatic inactivation by acetylation, phosphorylation, adenylation
PK: post antibiotic effect (PAE) and conc. dependent killing, synergistic effect with other antibiotics, esp cell wall agents (beta-lactams)
AR: nephrotoxicity-serum levels of drugs and kidney function monitored, ototoxicity; not given to pts with dec. renal function
-admin IV or IM |
|
|
Term
|
Definition
Lincosamide
-protein synthesis inhibitor
MOA: binds the 50S ribosomal subunit
SOA: gram positives and some protozoa, but not gram negs (do not get across outer memb)
MOR: ribosome RNA methylation, altered ribosomal proteins, adenylation; both chromosomal and plasmid resistance genes
PK: well absorbed after oral uptake and good tissue penetration-but no CNS, given IV, PO, or topically
AR: some allergic rxns |
|
|
Term
| Erythromycin, Clarithromycin, Azithromycin |
|
Definition
macrolides
-protein synthesis inhibitors
MOA: bind 50S ribosomal subunit
SOA: broad, many unusual bacteria and respiratory pathogens, used as alternative for pts with PCN allergy
MOR: methylation of ribosomes, efflux pumping
PK: reasonable oral bioavail, given IV or PO, good tissue distrib
-azithromycin has longer half-life, taken less often; given to children and pregnant women
-extended release version of clarithromycin available
AR: erythromycin -> more nausea than others and greater risk of QT elongation (seldom used) |
|
|
Term
|
Definition
oxazolidinones
-protein synthesis inhibitor
MOA: bind to 50S subunit
SOA: gram positives, but not gram negs, usually used with multiply resistant staph and and enterococci
MOR: mutation of 23s rRNA
PK: IV or PO, good absorption
AR: thrombocytopenia-pts on long term therapy monitor platelets, CBC, creatinine, LFT; not give to pts on SSRIs |
|
|
Term
| Quinupristin/dalfopristin combo (synercid) |
|
Definition
streptogramins
-protein synthesis inhibitors
MOA: bind to 50S ribosomal subunit
SOA: gram positives, esp. drug resistant enterococci
MOR: target alteration by ribosome methylation, efflux pumping but resistance readily occurs if only one of two given
PK: IV
AR: athralgias and myalgias, dose needs adjustment of pt has liver problems |
|
|
Term
| Sulfamethoxazole, Sulfadiazine, Dapsone, Trimethoprim (structure and MOA) |
|
Definition
-all sulfa drugs are derivatives of para-aminobenzene sulfonamide
Trimethoprim: analog of dihydrofolic acid-binds bacterial dihydrofolic acid reductase blocking formation of folic acid, used in conjunction with sulfa drug (TMP-SMX, Bactrim)
Dapsone: analog of PABA, useful against mycobacteria (esp. leprosy), pnemocystis jirovecii/carinii (fungus) |
|
|
Term
| Sulfamethoxazole, Sulfadiazine, Dapsone, Trimethoprim (SOA, MOR, PK, AR) |
|
Definition
folate metabolism inhibitor
-cell wall synthesis inhibitor
-broad spectrum drugs active against gram positives and negatives, pneumocystis jirovecii/carinii (fungus), toxoplasma (protozoa)
MOR: major problem-mutated genes for target enzymes, high levels of expression of enzymes, newly transferred genes w/ resistant enzymes, altered uptake and efflux, resistance found on both chromosome and plasmids
PK: good bioavail, IV or PO, sulfa given with silver ions -> topical cream
AR: HIV pts -> neutropenia and exfoliative dermatitis; allergic rxns that can be severe (anaphylaxis), not given to those who have glucose 6-phosphate deficiency or are pregnant
-sulfa and trimethoprim -> synergistic |
|
|
Term
|
Definition
cell wall synthesis inhibitor (polypeptide)
MOA: inhibits dephosphorylation of the lipid carrier (blocks transfer of cell wall components)
SOA: gram positives mostly
MOR: unclear
PK: topical, often used with neomycin or polymixin B
AR: very few, rarely allergic rx -> anaphylaxis |
|
|
Term
|
Definition
-cell wall synthesis inhibitor (glycopeptide)
-binds to D-alanine and prevents cross-linking by steric hindrance
SOA: gram positives mostly, often used against gram positive infections in which organisms are resistant to other antibiotics (beta-lactams)
MOR: set of genes on transposon that encode enzymes that make cell wall with D-serine or D lactate
PK: usually IV, can be given orally, good tissue avail, not CNS w/o inflamm, conc of vanco monitored to determine time above MIC
AR: rapid IV admin -> red man syndrome (histamine mediated rxn-flushing and redness of upper body), nephrotoxicity (esp. w/aminoglycosides), linear IgA bullous dermatosis |
|
|
Term
|
Definition
monobactam
-cell wall synthesis inhibitor
-admin IV
-same target as penicillin |
|
|
Term
|
Definition
carbapenem
-cell wall synthesis inhibitor
-administered IV
-same target as penicillin
-cilistatin has no antibacterial action but prolongs half-life of Imipenem, prevents nephrotoxic effects |
|
|
Term
| Cephalexin, Ceftazidime, Cefotaxime, Ceftriaxone |
|
Definition
cephalosporins
Cephalexin: 1st gen (PO)
Ceftazidime, Cefotaxime, Ceftriaxone: 3rd gen (IV)
-same target as penicillin
-cell wall synthesis inhibitor
-each generation has broader SOA and more resistant to beta-lactamases
-PCN allergic pts have 5-10% incidence of cross-hypersensitivity rxns to cephalosporins |
|
|
Term
| Amoxycillin/Clavulanate, Ampicillin/Sulbactam, Piperacillin/Tazobactum |
|
Definition
penicillin/beta-lactamase inhibitor combos
-amoxicillin/clavulanate given PO and often used when IV admin not cared for
-piperacilllin/tazobactum only given IV |
|
|
Term
| Penicillin, Nafcillin, Dicloxacillin, Ampicillin, Amoxicillin |
|
Definition
cell wall synthesis inhibitor
MOA: bind transpeptidases and prevent crosslinking
SOA: very broad, drug of choice when organism is sensitive, increasing resistance -> combos given now
MOR: mutations in genes encoding transpeptidases, penicillin binding proteins; beta-lactamases that hydrolyze beta-lactam ring; altered uptake
PK: good bioavail, cross BBB when inflamm, short half-lives, some IV, others PO, some both
AR: allergies, desensitization |
|
|
Term
|
Definition
atypical anti-psychotic
-increase QT interval -> arrythmias |
|
|
Term
|
Definition
atypical anti-psychotic
-potent D2 blocker
TX: schizo, schizoaffective DO, bipolar DO, mania, tourette's
TOX: low doses-dec. EPS, higher doses-inc. EPS w/ elevated prolactin
SEs: EPS, inc. prolactin, weight gain |
|
|
Term
|
Definition
atypical anti-psychotic
-blocks 5HT, D2, alpha-2 receptors
TX: schizo, schizoaffective DO, bipolar DO, mania, tourette's
TOX: weight gain, metabolic syndrome
-may help with negative signs |
|
|
Term
|
Definition
atypical anti-psychotic
-stronger D4 and 5HT, weaker D2 (many features like CPZ)
-may help with neg symptoms
TX: schizo, schizoaffective DO, bipolar DO, mania, tourette's
TOX: orthostatic hypotension, EPS, AGRANULOCYTOSIS, dec. seizure threshold, sialorrhea (M4) |
|
|
Term
|
Definition
atypical anti-psychotic
-partial D2 and 5HT1A agonist
TX: schizo, schizoaffective DO, bipolar DO, mania, tourette's
-less SEs
-minimal or no weight gain (as opposed to olanzopine) |
|
|
Term
|
Definition
typical anti-psychotic (low dose, high potency)
MOA: potent DA block
TX: schizo, schizoaffective DO, bipolar DO, mania, tourette's
TOX: severe EPS and TD, little CV or sedation, no anti-musc effects, NEUROLEPTIC MALIGNANT SYNDROME
-injectable prep available (IM) |
|
|
Term
|
Definition
typical anti-psychotic (high dose, low potency)
-blocks DA, alpha-1, muscarinic, histamine receptors
TX: schizo, schizoaffect DO, bipolar DO, mania, tourette's
TOX: DA-inc. EPS, prolactin, wt gain; mACH-anti-cholinergic effects; a1-orthostatic hypotension
-sedation, jaundice, photosensitivity, parkinsonism, TD, sexual dysfunction, arrythmias, anti-emetic effect (block CTZ)
-not drugs of abuse |
|
|
Term
|
Definition
halogenated hydrocarbons (inhaled)
-decrease in minute volume (++)
-skeletal muscle relaxation (++)
-clinical use (+++) |
|
|
Term
|
Definition
halogenated hydrocarbons (inhaled)
-high MAC -> slow induction
-sensitization of myocardium to catecholamines -> arrythmias
-myocardial function: depressed sympathetic stimulation (++)
-severe hepatitis
-cerebral flow increased (++) |
|
|
Term
|
Definition
halogenated hydrocarbons (inhaled)
-changes in renal concentration ability
-myocardial function: depressed sympathetic stimulation (++)
-decrease in minute volume (++)
-skeletal muscle relaxation (+++) |
|
|
Term
|
Definition
halogenated hydrocarbons (inhaled)
-nephrotoxic due to inorganic fluoride released during metabolism
-clinical use (+++) |
|
|
Term
|
Definition
halogenated hydrocarbons (inhaled)
-clinical use (+++) |
|
|
Term
|
Definition
inhaled
-low MAC -> fast induction
-low anesthetic potency
-marked analgesia, amnesia
-clinical use (+++) |
|
|
Term
|
Definition
short-acting barbituates (intravenous)
-bolus dose or IV drip
-rapid onset (~30sec), very short anesthesia (10min)
-rapid diffusion out of brain and redistribution; slow liver metabolism -> hangover
-myocardial and respiratory depressant
-decreased cerebral blood flow -> good for pts with head injuries, brain tumors
-may reduce hepatic blood flow, GFR
-not analgesic |
|
|
Term
|
Definition
benzodiazepine (intravenous)
-slower onset of central action
-sedative but central depression below true anesthesia
-prolong recovery
-anterograde amnesia -> given before induction (premedication)
-minimal respiratory or CV depression
-not analgesic |
|
|
Term
|
Definition
opioids (intravenous)
-analgesic, only large dose anesthetic
-little effect on circulation
-respiratory depression (severe with high dose)
-effects can be reversed by naloxone (opioid antagonist)
-sufentanil is 5-10x more potent than fentanyl |
|
|
Term
|
Definition
intravenous
-most popular IV anesthetic
-rapid onset, rapid recovery
-feels better
-hypotension
-respiratory depressant
-ANTIEMETIC
-pain at site of injection; ~expensive |
|
|
Term
|
Definition
intravenous
-rapid onset, loss of consciousness within seconds
-recovery occurs in 3-5 min
-minimal CV and respiratory depression
-no analgesic effects, requires premedication
-high incidence of nausea, vomiting, pain on injection |
|
|
Term
|
Definition
intravenous
-catatonia, amnesia, analgesia
-blocks glutamate (NMDA) receptors
-CV stimulation: increases HR, BP, CO
-increases cerebral blood flow, intracranial pressure
-little respiratory depression
-post-op disorientation, illusions, vivid dreams -> so little used in US |
|
|
Term
|
Definition
ester
-Novocaine
-readily hydrolyzed in plasma -> short duration
-often combined with epi for infiltration, nerve block, spinal anesthesia |
|
|
Term
|
Definition
ester
-short duration of action |
|
|
Term
|
Definition
ester
-Potocaine
-effective topical LA
-most commonly used drug for spinal anesthesia
-more lipophilic -> more potent, long lasting, and toxic than procaine and cocaine |
|
|
Term
|
Definition
ester
-surface use only
-ester of PABA (lacks the terminal amino group)
-poorly water soluble -> dusting powder or ointment for wounds and ulcerated surfaces w/o systemic toxicity issues |
|
|
Term
|
Definition
amide
-Xylocaine
-intermediate duration of action
-well tolerated, one of most commonly used
-more prompt, intense, longer lasting, more extensive anesthetic than procaine
-DOC for pts with ester sensitivity
-may produce drowsiness
-used as antiarrythmic agent |
|
|
Term
|
Definition
amide
-intermediate duration of action |
|
|
Term
|
Definition
amide
-intermediate duration of action
-more rapid, longer action than lidocaine
-used to be widely used in obstetrics -> less now because of transient neurobehavioral effects in neonate |
|
|
Term
|
Definition
amide
-long duration of action
-some nerve block lasts >24 hrs -> advantage for postoperative analgesia
-used for epidural an. in obstetrics -> low pain of labor but permits motor activity to aid expelling fetus
-no behavioral effects in neonate
-more lipophilic -> more potent, toxic (heart) |
|
|
Term
|
Definition
amide
-longer duration of action than bupivacaine |
|
|
Term
|
Definition
vasoconstrictor
-decreases rate of absorption of anesthetic to...
1) localize anesthetic at desired site and prolong drug action
2) allow body's ability to metabolize drug keep pace with rate at which drug is absorbed into circulation -> reduce systemic toxicity of local anesthetic |
|
|
