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424 final > MOA > Flashcards

MOA Flashcards

1
Q

low to moderate noncompetitive antagonist at NMDA receptors, persistent stimulation of NMDA receptors by glutamate is thought to possibly contribute to the symptomology of AD

A

NMDA Receptor Antagonist; Memantine (Namenda) MOA?

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2
Q

reversibly and non-competitively inhibits centrally active acetylcholinesterase, which results in increased levels of Ach available for synaptic transmission in the CNS

A

AD drugs Donepezil and Rivastigmine MOA?

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3
Q

may inhibit burst firing without affecting normal neuronal excitability

A

Levetiracetam MOA?

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4
Q

may block sodium channels or potentiate GABA

A

Topirimate MOA?

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5
Q

increases GABA availability, enhances action of GABA, mimics action at postsynaptic sites

A

Valproic acid MOA?

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6
Q

exact MOA is unk, but blocks voltage dependent sodium and chloride channels

A

Zonisamide MOA?

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7
Q

thought to affect voltage sensitive sodium channels and inhibit presynaptic release of glutamate and aspartate in the neuron

A

Lamotrigine MOA?

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8
Q

exact MOA is unclear, but thought to affect the NA+ channels, slowing influx of NA+ in the cortical neurons and slowing spread of abnormal activity

A

Carbamazepine (Tegretol) MOA?

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9
Q

inhibit and stabilize electrical discharges in the motor cortex of the brain by affecting the influx of sodium ions during generation of nerve impulses

A

Phenytoin (Dilantin) MOA?

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10
Q

binding the circulating TNF-alpha, rendering it inactive; reduces chemostatic affect of TNF alpha by reducing IL-6 and CRP, resulting in reduced infiltration of inflammatory cells into the joint; cell lysis also occurs

A

Biologic DMARDS (Non-TNF Biologics) Rituximab and Abatacept MOA?

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11
Q

folic acid antagonist, thought to affect leukocyte suppression, decreasing inflammation, decreasing inflammation that results from immunological byproducts

A

Disease modifying anti-rheumatic drugs (DMARDS) like Methotrexate?

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12
Q

inhibits conversion of arachidonic acid to prostaglandin, prostacyclin, and thromboxanes, all of which are mediators of pain and inflammation

A

NSAIDS MOA?

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13
Q

decreases inflammation by suppressing migration of polymorphonuclear leukocytes (neutrophils, eosinophils, and basophils) and reversing increased capillary permeability

A

Corticosteroids (Prednisone) MOA?

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14
Q

inhibits activation, degranulation and migration of neutrophils to area of gout attack, decreases inflammation and pain associated with gout attack; takes 18-24 to work and full effect is at 48 hours

A

Colchicine MOA?

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15
Q

increases excretion of serum uric acid by competitively inhibiting reabsorption of uric acid in kidney

A

Probenecid MOA?

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16
Q

decrease uric acid by selectively inhibiting xanthine oxidase, uric acid decreases, reducing risk of crystallization and gout attack

A

Antigouts (Allopurinol and Febuxostat) MOA?

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17
Q

inhibit bone reabsorption by reducing osteoclast number and fxn

A

Bisphosphonates MOA?

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18
Q

thickens cervical mucus to inhibit sperm mitigation, suppresses ovulation, lower mid-cycle peak of FSH and LH; slow egg movement through fallopian tube; thins endometrium

A

Progesterone MOA?

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19
Q

primary effects are maturation and function of female reproductive system; in addition to breast, ovaries, and uterus, estrogen receptors also present in bone, CNS, GI tract and CV tissue

A

Estrogens and Anti-Estrogens MOA?

20
Q

luteinizing hormone (LH)- releasing hormone antagonists; creates reversible chemical orchiectomy state in males; creates reversible chemical oophorectomy state in females

A

GnRH Analogues (Leuprolide, Lupron) MOA?

21
Q

inhibits enzyme that converts testosterone to DHT

A

Finasteride (Proscar, Propecia) MOA?

22
Q

principle endogenous androgen responsible for promoting the growth and development of male sex organs and maintaining secondary sex characteristics

A

Testosterone MOA?

23
Q

after diffusing into the organism, it is thought that tinidazole causes cytotoxicity by damaging DNA and preventing additional DNA synthesis

A

Tinidazole MOA?

24
Q

diffuses into the organism and interacts with DNA to cause a loss of helical DNA structure and strand breakage, results in inhibition of protein synthesis and cell death

A

Metronidazole MOA?

25
Q

synthetic allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis in fungi, resulting in fungal cell death

A

Terbinafine MOA?

26
Q

interferes with fungal cytochrome p450 activity, decreasing ergosterol synthesis (principle sterol in fungal cell membrane), and inhibiting cell membrane formation

A

Fluconazole and itraconazole MOA?

27
Q

dependent endonuclease inhibitor that interferes with viral RNA transcription, resulting in inhibition of flu virus replication

A

Baloxavir marboxil MOA?

28
Q

neuraminidase is a viral enzyme responsible for cleaving viral attachment to the host cell surface, allowing for viral circulation, inhibiting this enzyme prevents release of virus and halts the spread of infection

A

Neuraminidase inhibitors (Oseltamivir, zanamivir, peramivir) MOA?

29
Q

inhibit HCV protein necessary for viral replication

A

Hep C Tx (Ledipasvir/Sofosbuvir) and (Sofosbuvir/Velpatasvir) MOA?

30
Q

interferes with DNA synthesis and inhibit viral replication

A

Nucleoside analogues (Acyclovir, Famiciclovir, and Valacyclovir) MOA?

31
Q

activated by bacteria to re-activate intermediates that inactivate or alter bacterial ribosomes, leading to inhibition of protein synthesis, aerobic energy metabolism, DNA, RNA, and cell wall synthesis

A

Nitrofurantoin MOA?

32
Q

competitively inhibit dihydrofolate synthetase, which is necessary for the conversion of para-aminobenzoic acid (PABA) to dihydrofolate acid, inhibiting this pathway prevents folic acid synthesis, which is important for some bacteria to survive

A

Sulfonamides and Trimethroprim (Bactrim) MOA?

33
Q

bactericidal through interference with enzymes required for the synthesis and repair of bacterial DNA and promote breakage of DNA strands

A

Fluoroquinolones (Cipro and Levo) MOA?

34
Q

inhibit protein synthesis by reversibly binding to the 30S subunit of the bacterial ribosome

A

What is the MOA of Tetracyclines?

35
Q

binds to the 50s subunit of the bacterial ribosome and suppresses protein synthesis

A

What is the MOA of both lincosamides (clindamycin) and macrolides (erythromycin, azithromycin, and clarithromycin)?

36
Q

inhibit bacterial cell wall synthesis by blocking glycopeptide polymerization through binding tightly to the D-A1a-D-A1a portion of cell wall precursor

A

What is the MOA of glycopeptides (vancomycin)?

37
Q

prevent bacterial cell wall synthesis during active multiplication, causing cell wall death; bactericidal against susceptible bacteria

A

What is the MOA of Penicillins and Cephalosporins

38
Q

competitively inhibits postsynaptic alpha 1 receptors which results in vasodilation of veins and arterioles and a decrease in total peripheral resistance and BP

A

Alpha 1 selective antagonists (doxazosin, tamsulosin, or terazosin) Hypertension MOA

39
Q

competitively inhibits postsynaptic alpha-1 receptors in prostatic stromal and bladder neck tissues, which reduces the sympathetic tone induced urethral stricture causing BPH sxs

A

Alpha 1 selective antagonists (doxazosin, tamsulosin, or terazosin) BPH MOA?

40
Q

stimulates alpha-2 receptors in the brain stem, activating an inhibitory neuron, resulting in reduced sympathetic outflow from the CNS, decreasing peripheral resistance, HR, BP, & renal vascular resistance; * this all occurs due to down regulation of alpha-2 receptors after chronic use

A

Alpha 2 agonists: central (Clonidine/Catapres)
HTN MOA?

41
Q

MOA unknown; thought that it regulates activity in the prefrontal cortex responsible for emotions, attention & behaviors

A

Alpha 2 receptors: central (Clonidine/Catapres)
MOA ADHD?

42
Q

stimulation of central alpha-2 receptors by methyldopa’s metabolite alpha-methylnorepinephrine, which produces a decrease in sympathetic outflow to the heart, kidneys, & blood vessels; can build tolerance over 2-3 months & may have to increase dose or add on diuretic

A

Alpha 2 agonists: central
Methyldopa MOA?

43
Q

block beta-1 receptors at the SA node to decrease HR, decrease contractility in the atria & ventricles and conduction velocity, and slow conduction at the AV node

A

Selective BBs: Metoprolol and Atenolol MOA

44
Q

competitively block response to beta-1 & beta-2 stimulation, which results in decreased HR, myocardial contractility, BP & myocardial oxygen demand

A

Nonselective BBs: Propanolol (Inderal) MOA

45
Q

nonselective beta receptor blockade & alpha-1 receptor blockade thereby decreasing BP & peripheral resistance; these combined effects decrease myocardial oxygen demand & lower cardiac workload

A

Combined Alpha and Beta-Adrenergic Agonists and Antagonists: Carvedilol MOA

46
Q

nonselective beta receptor blockade & alpha-1 receptor blockade thereby decreases BP & peripheral resistance; these combined effects decrease myocardial oxygen demand & lower cardiac workload

A

Combined Alpha and Beta-Adrenergic Agonists and Antagonists: Labetalol MOA

47
Q

decreases the vasodilation & vascular permeability that occur during anaphylaxis; relaxes smooth muscles, relieves bronchospasm, wheezing, dyspnea, pruritus, angioedema, & urticaria

A

Combined Alpha and Beta-Adrenergic Agonists and Antagonists: Epinephrine MOA

424 final (2 decks)

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