Term
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Definition
Only NT in parasympathetic, first NT in sympathetic
Muscarninc and nictonic receptors
acetyl CoA + choline via choline acetyltransferase -> acetylcholine via acetylcholinesterase -> acetic acid + choline |
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Term
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Definition
Muscarinic cholinergic receptor agonist
Metabotropic receptor
M1/M3- increased IP3/DAG; increased internal [Ca2+]-> M1=nerve endings; M3=sm musc/glands/endothelium
M2- decreased cAMP; increased K+ channel opening-> heart, some nerve endings
Effects: miosis; vasodialation, slowing of HR (at higher levels of receptor activation); bronchial constriction, increased respiratory secretion; increased GI motility and secretion, sphincter relaxation
DUMBELSS |
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Term
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Definition
Nicotinic cholinergic receptor agonist
Ionotropic receptor- increased Na+ influx and depolarization
Nn receptor: PNS, SNS, ganglion cells
Nm receptor: neuromuscular junction
Activate both the sympathetic and parasympathetic nervous systems, but the net effect depends on
the organ and the predominant tone
Penetrates BBB
Toxicity: increased GI activity; increased BP |
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Term
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Definition
Muscarinic cholinergic receptor agonist
Effects: miosis; vasodialation, slowing of HR (at higher levels of receptor activation); bronchial constriction, increased respiratory secretion; increased GI motility and secretion, sphincter relaxation
DUMBELSS
Used for post-op urinary retention or paralytic ileus |
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Term
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Definition
Muscarinic cholinergic receptor agonist (partial agonist)
Effects: miosis; vasodialation, slowing of HR (at higher levels of receptor activation); bronchial constriction, increased respiratory secretion; increased GI motility and secretion, sphincter relaxation
DUMBELSS
Used for glaucoma, Sjogren Syndrome (impaired saliva/tear production) |
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Term
| Echothiophate; Malathione |
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Definition
AchE inhibitor; Organophosphate
MOA: Prevents breakdown of acetylcholine; phosphorylates the active site of AchE and forms a bond that is extremely stable; excess activation of muscarinic and nicotinic Ach receptors by excess Ach in synapse-> parasympathetic effects predominate
DUMBELSS
Hydrolyzes at an extremely slow rate (100s of hours)
Can undergo aging where there is strengthening of the AchE-phosphorus bond
Very well absorbed (except for echothiophate)
Uses: glaucoma |
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Term
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Definition
AchE inhibitor; 4° alcohol
MOA: Forms an electrostatic/H-bond with AchE that is reversible; excess activation of muscarinic and nicotinic Ach receptors by excess Ach in synapse-> parasympathetic affects predominate
DUMBELSS
Short-lived inhibition (~2-10 min)
Poorly absorbed in brain due to its permanent charge
Use: myasthenia gravis |
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Term
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Definition
AchE inhibitor; carbamate ester
MOA: forms covalent bond w/ AchE that is resistant to hydrolysis; excess activation of muscarinic and nicotinic Ach receptors by excess Ach in synapse-> parasympathetic affects predominate
DUMBELSS
Hydrolysis can occur but at a slow rate (30min-6hr)
Well absorbed but in general carbamates are not |
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Term
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Definition
Muscarinic receptor antagonist- competitive antagonist
Effects: eye dilation (mydriasis); tachydcardia; bronchodilation; dry mouth; reduced GI motility
Use: cholinergic poisoning; eye examination
Given IV, topical (drops) |
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Term
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Definition
Muscarinic receptor antagonist
Effects: eye dilation (mydriasis); tachydcardia; bronchodilation; dry mouth; reduced GI motility
Use: vertigo; nausea
Given IV |
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Term
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Definition
Nicotinic receptor antagonist- competitive inhibition
Effects: loss of accomodation; hypotension; reduced GI motility
Given orally |
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Term
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Definition
Acetylcholinesterase regenerator
Used for organophosphate intoxication
MOA: strong nucleophile-> breaks AchE phosphorous bond
Only works before aging occurs-> aging rate depends on the agent
Given IV; regenerates AchE within 48 hours |
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Term
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Definition
Indirect acting sympathomimetic
Local anesthetic
MOA: mimicking sympathetic nervous system activation by inhibiting reuptake of catecholamines at noradranergic and dopaminergic synapses
Simultaneous vasoconstrictor not needed due to inherent vasoconstriction ability
Uses: local anesthetic (now primarily topical in upper respiratory tract)-> anesthesia is entirely superficial; vasoconstriction during surgery to reduce bleeding by shrinking mucous membranes
With abuse, increased sensitivity with decreased duration of effects
Toxicity: due to decreased uptake in CNS and PNS; euphoria |
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Term
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Definition
Local anesthetic given topically or injected near peripheral nerve or nerve trunks, parenterally, or orally; given with vasconstrictor to prevent diffusion and increase duration of action-> intermediate
Absorbed rapidly (decreased by epinephrine); excreted by urine
Toxicity: drowsiness; tinnitus; dizziness; dysphoria/euphoria; muscle twitching; loss of consciousness preceded by sedation; seizures; respiratory arrest |
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Term
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Definition
Local anesthetic given topically or injected near peripheral nerve or nerve trunks, parenterally, or orally; given with vasconstrictor to prevent diffusion and increase duration of action-> long-acting
Uses: pregnancy; post-op
Toxicity: arrythmia (blocks cardiac Na+ channels) |
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Term
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Definition
Spasmolytic-> benzodiazepine
MOA: inhibition by binding GABA-A receptors and increasing Cl- permeability, leading to hyperpolarization of alpha motor neurons; only works in the presence of GABA
Short term use for patients w/ muscle spasm of almost any origin, including trauma
Also used for IV anesthesia; anticonvulsant
SIde effects: sedation; dizziness; blurred vision; muscle weakness; ataxia |
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Term
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Definition
Spasmolytic
MOA: centrally acting alpha2 agonist that increases presynaptic inhibition of lower motor neurons neurons-> prevents glutamate release
Short duration of action for decreasing muscle tone and frequency of spasms; works better on polysynaptic pathways (but works for both)
Main use is for MS
Side effects: less muscle weakness and withdrawal compared to Baclofen; dry mouth; sedation; asthenia; dizziness; hypotension; bradycardia; hallucinations/delusions |
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Term
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Definition
Spasmolytic
MOA: GABA-B receptor agonist which inhibits presynaptic release of excitatory NTs (glutamate) by lower motor neurons and directly inhibits alpha motor neurons; inhibition is a result of increasing K+ channel conductance which causes hyperpolarization and reduces Ca2+ influx-> no vesicle exocytosis
Preferred for long term spasticity use-> ALS, spinal cord trauma, MS, cerebral palsy
Oral; intrathecal
Side effects: increased seizure activity; sedation dizziness; blurred vision; muscle weakness; ataxia-> effects are less severe compared to Diazepam |
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Term
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Definition
Autonomic nervous system neurotransmitter (given as L-Dopa clinically)
Defective release in Parkinson's Disease
Receptor = metatropic
D1 family receptors (D1 and D5) -> increase cAMP
D2 family receptors (D2, D3, D4) -> decrease cAMP
Synthesis: tyrosine-> L-dopa -> dopamine
Dopamine is small, charged does not cross BBB-> only L-DOPA form does (large, uncharged and travels via large a.a. carrier) |
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Term
| Epinephrine (aka Adrenaline) |
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Definition
Binds to alpha1, alpha2, beta1, beta2 receptors
alpha1 receptor-> increase IP3/DAG; increased [Ca2+]-> sm musc/glands
alpha2 receptor -> decreased cAMP-> nerve endings/sm musc
beta1/beta2 -> increased cAMP-> cardiac muscle/sm musc respectively
In vivo, released from adrenal medulla
Vasoconstrictor (alpha), cardiac stimulant (beta1), fall in diastolic BP (beta2)
If given in the presence of an alpha receptor antagonist there will be a decrease in peripheral resistance due to beta2 activation |
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Term
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Definition
Binds to alpha1/alpha2 and beta1 receptors; little activity at beta2 receptors
Effects: potent vasoconstriction (alpha), cardiac Stimulant (beta1), increases BP (systolic and diastolic)
Neurogenic orthostatic hypotension-> failure to release NE appropriately upon standing because activation of D2 receptors on sympathetic terminals prevents NE release |
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Term
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Definition
alpha2-adrenergic receptor agonist
MOA: inhibits adenylyl cyclase
Effects: decrease in peripheral vascular resistance and blood pressure, decrease in heart rate; mydriasis (pupillary dilation)
In the past used to treat spasticity (tizanidine used now-> fewer side effects)
Oral or transdermal |
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Term
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Definition
alpha1-adrenergic receptor agonist
Effects: increase in peripheral vascular resistance and blood pressure and decrease in heart rate; mydriasis (pupillary dilation)
Increased oral bioavailability b/c COMT in GI tract does not degrade it |
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Term
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Definition
Beta1/Beta2 adrenergic receptor agonist
Effects: increased cardiac output, vasodilation |
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Term
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Definition
Beta1/Beta2-adrenergic receptor agonist
Higher bioavailability and duration of effects than catecholamines
Excreted in urine |
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Term
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Definition
Beta1/Beta2-adrenergic receptor agonist
Effects: increased cardiac output, vasodilation
Used as a decongestant |
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Term
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Definition
Beta2-receptor agonist
beta2>>beta1>>>>alpha
Vasodilation, bronchodilation, decreased BP, increased heart rate
Uses: therapy of bronchial asthma, suppress premature labor |
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Term
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Definition
Indirect-acting sympathomimetics
MOA: mimic sympathetic nervous system-> increases release of catecholamines; blocks
transporter so more catecholamine in synapse
Readily enters CNS; D-isomer is most potent |
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Term
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Definition
Indirect acting sympathomimetic
Byproduct of tyrosine metabolism; found in fermented foods
MOA: increase synaptic levels of catecholamines by mimicking excitation of SNS; increases release
Use with caution in patients on MAO-A inhibitors-> normally degraded by MAO in liver
Low oral bioavailability b/c of first pass effect (concentration is reduced in liver); parenteral injection
Side effects: elevated BP |
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Term
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Definition
Indirect-Acting Sympathomimetics
MOA: inhibits both NE and dopamine transporters; increases interstitial concentrations not only of NE and dopamine, but also serotonin and glutamate while decreasing GABA levels
Used primarily to improve wakefulness in narcolepsy and some other conditions-> psychostimulant
Effects: increased BP and heart rate, though these are usually mild |
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Term
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Definition
Alpha adrenergic receptor antagonist
alpha1>>>>alpha2 (1000-fold difference)
MOA: reversible inhibition; relaxes arterial, venous, and prostate smooth muscle
Uses: management of HTN; lacks side effect of tachycardia; raises HDL; urinary obstruction
Oral; 50% bioavailability b/c of liver metabolism
Toxicity: orthostatic hypotension, dizziness |
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Term
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Definition
Alpha-adrenergic receptor antagonist
alpha1 > alpha2
MOA: forms a reactive ethyleneimonium intermediate that irreversibly binds the alpha receptor as well as receptors for histamine, acetylcholine, and serotonin; also inhibits NE reuptake
Uses: treatment of pheochromocytoma
Effects: lowers peripheral vascular resistance and BP; indirect baroreflex activation (rise in HR)
Oral, though low bioavailability
Toxicity: orthostatic hypotension, tachycardia, myocardial ischemia, nasal stuffiness, inhibition of ejaculation, fatigue, sedation, nausea |
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Term
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Definition
Alpha-adrenergic receptor antagonist-> competitive antagonist
alpha1 = alpha2
MOA: reversible inhibition of alpha receptors on vascular smooth muscle; minor inhibitory effect on serotonin and agonist of muscarinic and histamine receptors
Uses: antihypertensive, pheochromocytoma, erectile dysfunction
Oral or IV
Toxicity: tachycardia (baroreflex activation), arrhythmias, myocardial ischemia |
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Term
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Definition
Alpha adrengergic receptor antagonist
alpha2>>alpha1
Indole alkaolid
MOA: promotes NE release
Uses: orthostatic hypotension; erectile dysfunction; can reverse antihypertensive effects of alpha2 adrenergic agonists
Toxicity: anxiety |
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Term
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Definition
Mixed-adrenergic receptor antagonist-> competitive antagonist
beta1 = beta2 ≥ alpha1 > alpha2
MOA: reversible antagonist
Partial agonist activity and local anesthetic action
Use: lowers BP w/ limited heart rate increase during hypertensive emergencies
Oral or parenteral |
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Term
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Definition
Beta1/Beta2 adrenergic receptor antagonist-> inverse agonist
beta1 >>> beta2
Local anesthetic action; highly metabolized in liver by cytP450s w/ little unchanged drug presence in urine
Effects: lower HR and BP; reduce renin
Uses: bronchoconstriction; ischemic heart disease; chronic heart failure; migraine headaches
Safer for use in patients who experience bronchoconstriction w/ propranolol; high beta1 selectivity so must use w/ caution in asthmatic patients; benefits outweigh risks in patients w/ diabetes or peripheral vascular disease (b/c beta2 antagonists are important in liver and BVs)
Toxicity: bradycardia, fatigue, vivid dreams, cold hands |
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Term
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Definition
Beta adrenergic receptor antagonist
beta1 = beta2
Oral or parenteral; when given orally, low bioavailability-> first-pass metabolism by cytP450s in liver
Local anesthetic action; very lipophilic-> crosses BBB
Uses: management of essential tremor; inhibits sympathetic NS stimulation of lipolysis; ischemic heart disease; hyperthyroidism; migraine headaches; alcohol withdrawal
Toxicity: bradycardia; lowered BP; reduced renin; cold hands/feet; bronchoconstriction (use caution with asthmatic patients); sedation; vivid dreams; depression |
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Term
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Definition
Beta adrenergic receptor antagonist
beta1 = beta2
Topical drops (good for eyes b/c lack anesthetic properties); oral
Uses: "Beta-Blocker" for acute angle glaucoma-> decreased aqueous secretion to reduce pressure; ischemic heart disease; migraine headaches
Toxicity: may be absorbed and cause lowered HR and BP and reduced renin; worsened asthma; fatigue; vivid dreams; colds hands |
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Term
| Metyrosine (aka alpha-methyl tyrosine) |
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Definition
Tyrosine hydroxylase inhibitor-> competitive inhibitor
Sympatholytic-> inhibits postganglionic functioning of sympathetic NS
MOA: blocks tyrosine hydroxylase and reduces catecholamine synthesis
Effect: lowers BP, may elicit extrapyramidal effects in CNS b/c of low [dopamine] (parkinsonian symptoms)
Used for pheochromocytoma (adrenal gland tumor)
Toxicity: extrapyramidal symptoms, orthostatic hypotension (fainting on standing), crystalluria |
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Term
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Definition
Adrenergic-neuron blocking agent
Sympatholytic; effects CNS and PNS
MOA: inhibits vesicular monoamine transporter (VMAT) irreversibly, resulting in depletion of catecholamine stores by inability to fill vesicles
Oral w/ long duration
Uses: Huntington's Chorea (depletes neuronal stores of dopamine); HTN (lowers BP by decreased cardiac output and peripheral vascular resistance)
Toxicity: Parkinsonian syndromes; sedation, lassitude (mental exhaustion); nightmares; depression; diarrhea; GI cramps and increases gastric acid secretion |
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Term
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Definition
Immunomodulator
MOA: suppresses movement of Tcells into CNS by binding VLA-4 on Tcells and inhibitng Tcell expression of MMP; inhibits Tcell proliferation by blocking binding of costimulatory molecules (B7 and CD40); shifts cytokine profile from pro (Th1) to anti (Th2) inflammatory
Use: for relapsing/remitting attacks in MS
Parenteral
Side effects: flu-like symptoms; headache; nausea; leukopenia/lymphpenia; injection site reaction; hypersensitivity
Contraindicated in pregnancy |
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Term
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Definition
Immunomodulator
Random-sequence polypeptide made up of Ala, Lys, Glu, Tyr
MOA: binds MHC II-DR to induce CD4+ Tcells to secrete Th2 cytokines
Used for relapsing/remitting attacks of MS
Subcutaneous administration |
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Term
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Definition
MOA: alkylating agent-> inhibits B/Tcell proliferation
Treatment for relapsing/remitting MS attacks and secondary progressive MS
SE: acrolein made as a breakdown product, toxic to bladder-> neutralize w/ MESNA |
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Term
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Definition
MOA: intercalates DNA and suppresses cellular and humoral response-> inhibits B/Tcell proliferation
Treatment for relapsing/remitting MS attacks and secondary progressive MS
Tolerated only up to an accumulated dose of 100-140 mg/m^2
Contraindicated in cardiac disease |
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Term
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Definition
Glucocorticoid
Treatment of acute attacks of MS to improve function and quality of life
Given IV in pulsatile fashion
Targets inflammation without targeting autoimmunity |
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Term
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Definition
Treatment of Parkinson's Disease
Synthesis: tyrosine-> L-dopa -> dopamine
Crosses BBB-> large, uncharged and travels via large amino acid carrier
Given orally-> absorbed in small bowel on empty GI tract; not taken with a protein heavy meal as it competes for absorption; given w/ peripheral decarboxylase inhibitor (Carbidopa) to prevent conversion to dopamine so it can cross BBB
Carbidopa + L-Dopa = Sinemet
Adverse effects: nausea, vomiting, mydriasis, may precipitate acute glaucoma, tachyarrhythmias, postural hypotension, hypertension, dyskinesias (impairment of voluntary movement-> including choreoathetosis), wearing off (decreased durations of response w/ each dose), on-off fluctuations (better and worse condition), hallucinations/confusion/psychosis
Contraindications: psychosis, closed-angle glaucoma, melanoma
Drug interactions: vitamin B6, non-selective MAO inhibitors |
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Term
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Definition
Peripheral decarboxylase inhibitor
Given w/ L-DOPA to prevent conversion of L-DOPA to Dopamine before it reaches the brain
Carbidopa itself is unable to cross BBB
Fewer GI and cardiovascular side effects of L-DOPA when given in conjunction; more behavioral effects when given in conjunction compared to L-DOPA alone |
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Term
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Definition
Sinemet = L-DOPA + Carbidopa
Treatment of Parkinson's Disease
Patients often given a low dose of Sinemet, then Dopamine is added slowly to prevent patients from becoming resistant and to prevent on/off fluctuations and wearing off |
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Term
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Definition
Dopamine receptor agonist
(Derived from ergot)
Treatment of Parkinson's Disease
MOA: preferentially binds D2 receptor, with partial D1 receptor binding
Does not require conversion to active form; lower response fluctuations and dyskinesias than treatment w/ L-DOPA; useful in treating on/off fluctuations
Fewer side effects than L-DOPA because more selective for receptors -> use of Dopamine agonists before L-DOPA in treatment
Side effects: painless digital vasospasms
Rarely used anymore; highly variable absorption via GI tract |
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Term
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Definition
Dopamine receptor agonist
(Ergot derivative)
Treatment of Parkinson's Disease
MOA: stimulates both D1 and D2 receptors-> more effective than Bromocriptine in reducing symptoms with an increased on time
Does not require conversion to active form; lower response fluctuations and dyskinesias than treatment w/ L-DOPA; useful in treating on/off fluctuations
Fewer side effects than L-DOPA because more selective for receptors -> use of Dopamine agonists before L-DOPA in treatment
Side effects: no longer used because of association w/ development of valvular heart disease; painless digital vasospasms |
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Term
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Definition
2nd generation dopamine agonist
Affinity: D3>>D2
MOA: neuroprotective by scavenging H2O2 and enhancing neutrophil activity
Most commonly used Dopamine agonist for treatment of Parkinson's Disease-> more effective in relieving resting tremor, movement problems, and minimizing off times; decreased risk of dyskinesias and wearing off b/c used as a monotherapy
Readily absorbed orally; excreted in urine
Side effects: narcolepsy |
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Term
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Definition
2nd generation dopamine agonist-> D2 agonist
Effective monotherapy for mild Parkinson's Disease; helps to smooth L-DOPA response in advanced stages; decreased incidence of dyskinesia
Side effects: narcolepsy |
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Term
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Definition
Dopamine agonist
Affinity: D4>>D2=D3>>D1
Rescue therapy for acute, intermittent treatment of Parkinson's Disease off episodes-> only used when other options have failed
Given subcutaneously
Side effects: similar to other Dopamine agonists and also vomiting; dyskinesias; drowsiness; chest pain; sweating; hypotension |
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Term
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Definition
MAO-B inhibitor-> irreversible
MOA: inhibits breakdown of dopamine by monoamine oxidase-B, allowing an increased release of dopamine at synapses
Provides symptomatic relief early on in Parkinson's Disease; may reduce on/off and wearing off
Used as initial therapy or as adjunct in later stages
Side effects: may inhibit MAO-A (in periphery) at higher doses; may exacerbate L-DOPA side effects when given in adjunct (dyskinesias, psychosis, hallucinations) b/c it increases amount of Dopamine
Contraindications: SSRIs, tricyclic antidepressants, Meperidine-> all may cause stupor, rigidity, hyperthermia; may block serotonin metabolism-> restlessness, sweating, twitches, hyperreflexes, shivering, tremor, seizures, coma, death |
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Term
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Definition
MAO-B inhibitor-> irreversible
More potent than Selegiline
MOA: inhibits breakdown of dopamine by monoamine oxidase-B, allowing an increased release of dopamine at synapses
Provides symptomatic relief early on in Parkinson's Disease; may reduce on/off and wearing off
Used as initial therapy or as adjunct in later stages
Side effects: may inhibit MAO-A (in periphery) at higher doses; may exacerbate L-DOPA side effects when given in adjunct (dyskinesias, psychosis, hallucinations) b/c it increases amount of Dopamine
Contraindications: SSRIs, tricyclic antidepressants, Meperidine-> all may cause stupor, rigidity, hyperthermia; may block serotonin metabolism-> restlessness, sweating, twitches, hyperreflexes, shivering, tremor, seizures, coma, death |
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Term
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Definition
COMT Inhibitor
MOA: prevents conversion of L-DOPA to 3-O-methyldopa by COMT; 3-O-methyldopa nomally competes w/ L-DOPA for transporters in brain and gut
Used as an adjucnt to L-DOPA+Carbidopa for Parkinson's Disease; COMT inhibitor activity is upregulated by Carbidopa decarboxylase inhibition-> increases on time and improves wearing off
Works in periphery and CNS
Side effects: liver failure (possibly fatal)-> requires signed patient consent for use |
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Term
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Definition
COMT Inhibitor
MOA: prevents conversion of L-DOPA to 3-O-methyldopa by COMT; 3-O-methyldopa nomally competes w/ L-DOPA for transporters in brain and gut
Used as an adjucnt to L-DOPA+Carbidopa for Parkinson's Disease; COMT inhibitor activity is upregulated by Carbidopa decarboxylase inhibition-> increases on time and improves wearing off
Works in periphery only-> not CNS |
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Term
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Definition
Antiviral medication with anti-Parkinson's activity
MOA: enhances production and promotes release of dopamine; inhibits metabolism of dopamine; has some anti-glutamate activity
May be used as initial therapy or an antidyskinetic in late stage Parkinson's; short-lived but effective benefits
Oral
Side effects: blocks glutamate receptor-> confusion, restlessness, hallucinations, depression, toxic psychosis; Livedo Reticularis (swelling of veins making them more visible under the skins); peripheral edema
Contraindications: history of seizures or cardiovascular disease |
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Term
| Benztropine, Trihexyphenidyl |
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Definition
Muscarinic receptor antagonist
MOA: reduces excessive acetylcholine release that arises due to dopamine loss
Used as monotherapy in early Parkinson's Disease or in conjunction w/ L-DOPA later, but benefits are short lived
Best used to treat prominent tremor or early morning dystonia
Side Effects: sedation/confusions; dry mouth; blurred vision; mydriasis; glaucoma; urinary retention
Contraindications: prostatic hyperplasia; obstructive GI disease; closed angle glaucoma; other anti-muscarinic drugs |
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Term
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Definition
Chelation of copper or lead; oral
Rapidly enters CNS to decrease copper levels in Wilson's disease
MOA: chelation via -NH2 and -SH; forms ring complex with copper
Rapidly excreted in urine
SE: hypersensitivity, nephrotoxicity, pancytopenia, myasthenia, optic neuropathy |
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Term
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Definition
Antimicrobial
Treatment of meningitis due to Neisseria meningitidis; good for gram (-) organisms
MOA: prevents cell wall synthesis
MOR: penicillinase (infrequent w/ N. meningitidis)
High dose given IV; not good for carrier state |
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Term
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Definition
Antimicrobial-> 3rd generation cephalosporin
Treatment of meningitis due to Neisseria meningitidis; able to penetrate CNS
MOA: interferes w/ cell wall synthesis
MOR: beta-lactamase |
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Term
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Definition
Antimicrobial
Treatment of meningitis due to Neisseria meningitidis; used in patients w/ beta-lactam allergy
MOA: inhibits microbial protein synthesis by binding 50S peptidyltransferase
MOR: inactivation by acetyltransferases; many strains resistant to Penicillin G are also resistant to Chloramphenicol
Side Effects: inhibits synthesis of IMM proteins, anemia/leukopenia/thrombocytopenia, aplastic crisis/fatal pancytopenia (<1%) |
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Term
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Definition
Antimicrobial
Treatment of meningitis due to Listeria monocytogenes-> usually in immunocompromised
N. meningitides has high levels or resistance
MOA: inhibition of cell wall synthesis
MOR: beta-lactamase |
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Term
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Definition
Antimicrobial
Prophylactic therapy for bacterial meningitis or treatment for leprosy (Mycobacterium leprae)
Kills the carrier state-> bacteriocidal
MAO: inhibits microbial RNA synthesis by inhibiting DNA-dependent RNA polymerase
MOR: target mutations |
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Term
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Definition
Antiprotozoal
Treatment of trypanosomiasis due to T. brucei gambiense early and late stage
MOA: inhibits ornithine decarboxylase, resulting in decrease polyamine synthesis |
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Term
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Definition
Antiprotozoal
Treatment of trypanosomiasis due to T. brucei gambiense early stage |
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Term
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Definition
Antiprotozoal
Treatment of trypanosomiasis due to T. brucei gambiense and T. brucei rhodesiense early stages
Slow acting |
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Term
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Definition
Antiprotozoal
Treatment of trypanosomiasis due to T. brucei gambiense and T. brucei rhodesiense late stages
Usually given after Suramin
MOR: transport deficits |
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Term
| Pyrimethamine-Sulfadiazine |
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Definition
Antiprotozoal
Primary treatment of toxoplasmosis (T. gondii)
MOA: blocks dihydrofolate reductase; inhibition of dihydropteroate synthase-> prevents use of PABA
MOR: mutations in DHFR
Side effects: toxic in 40% of cases |
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Term
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Definition
Antiprotozoal
2nd line treatment of toxoplasmosis (T. gondii)
MOA: binds 50S peptidyltransferase to block translocation; also work on apicoplast ribosome
SE: diarrhea, pseudomembranous colitis (kills GI bacteria except C. dificile)-> can be fatal |
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Term
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Definition
Antiprotozoal
Treatment of toxoplasmosis (T. gondi) during pregnancy-> concentrates in placenta
MOA: inhibits protein synthesis via reversible blockade of 50S subunit-> bacteriostatic |
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Term
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Definition
Antiprotozoal
Treatment of Acantamoeba infections-> mainly in eye
Topical
MOA: cell membrane disruption |
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Term
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Definition
Treatment of leprosy (M. leprae)
MOA: inhibits RNA synthesis by inhibiting dihydropteroate synthase and decreasing PABA-> bacteriostatic
Resistance is increasing-> multi-drug regimen suggested |
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Term
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Definition
| Treatment of leprosy (M. leprae) |
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