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Pharma > Pharma List A&B > Flashcards

Pharma List A&B Flashcards

1
Q

Papaverin and drotaverin

A

Drugs acting on gastrointestinal and urogenital smooth muscles. Drugs influencing uterine function

Smooth muscle relaxant

MOA:
- Ca2+-channel blocker
- Non-selective PDE inhibitor
Effect:
- SM relaxation

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2
Q

Butyl-scopolamine

A

Drugs acting on gastrointestinal and urogenital smooth muscles. Drugs influencing uterine function

Smooth muscle relaxation:

MOA:
- Non-selective muscarinic antagonist Effect:
- SM relaxation Indication:

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3
Q

Misoprostol

A

Drugs acting on gastrointestinal and urogenital smooth muscles. Drugs influencing uterine function

Agents contracting the pregnant uterus

MOA:
- PGE1 analog (Gq)
Effect:
- Uterus contraction, gastric mucus secretion

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4
Q

Oxytocin

A

Drugs acting on gastrointestinal and urogenital smooth muscles. Drugs influencing uterine function

Agents contracting the pregnant uterus

MOA:
- Induces uterine contraction (Gq-effect)àoxytocin receptor agonist
Effect:
- Secreted by posterior pituitary glandàuterus contraction + contraction of
myoepithelial cells of breast (milk ejection

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5
Q

Ergotamine

A

Drugs acting on gastrointestinal and urogenital smooth muscles. Drugs influencing uterine function

Agents contracting the pregnant uterus

MOA:
- α1 / 5HT-R agonist
Effect:
- Induce vasoconstriction and uterine contraction

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6
Q

Terbutaline

A

Drugs acting on gastrointestinal and urogenital smooth muscles. Drugs influencing uterine function

Tocolytic drugs - agents relaxing pregnant uterus:

MOA:
- Short-acting β2 agonists (SABA)
Effect:
- SM relaxationàuterus relaxation + bronchodilation

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7
Q

Atosiban

A

Drugs acting on gastrointestinal and urogenital smooth muscles. Drugs influencing uterine function

Tocolytic drugs - agents relaxing pregnant uterus:

MOA:
- Oxytocin receptor antagonist
Effect:
- Block the oxytocin pathway which leads to uterine contractionsàrelaxation

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8
Q

Mg++

A

Tocolytic drugs - agents relaxing pregnant uterus:

MOA:
- Ca2+-channel blocker
Indication:
- Tocolytic agent
- Torsades-de-Pointes, long QT syndrome, digitalis-induced arrhythmias

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9
Q

Ethanol

A

Tocolytic drugs - agents relaxing pregnant uterus:

MOA:
- Tocolytic agent

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10
Q

Solifenacin & oxybutinine

A

Smooth muscle relaxant
MOA:
- M3 antagonist(Gqàcontraction) Effect:
- Relax the muscle in the wall of the bladder (solifenacin)
- Decrease detrusor muscle spasms + short-acting (6h) (oxybutynin)

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11
Q

Tamsulosin

A

Agents acting on male reproductive system

MOA:
- α1-selective antagonist (primarily in the urinary tract)
Effect:
- Relax muscle of prostate + bladder neck allowing urine to flow more easily

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12
Q

Promethazine, diphenhydramine ,dimentinden

A

AntiHistamine

Is MOA:
- H1 receptor antagonists (1ST GENERATION)
- Also α1-AR, muscarinic, serotonergic antagonists
Effect:
- ↓vascular permeability, ↓nasal + bronchial mucus secretion,
↓bronchoconstriction

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13
Q

Levocetirizine, desloratadine, fexofenadine

A

AntiHistamine

MOA:
- H1 receptor antagonists (2ND GENERATION)

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14
Q

Chloropyramine

A

Antihistamine

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15
Q

Botulinum toxin

A

Direct-acting muscle relaxants

MOA:
- Inhibit SNARE fusion proteins Effect:
- Prevent synaptic exocytosis of ACh from terminals of motor axonsàflaccid paralysis

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16
Q

Levodopa carbidopa

A

Drugs used in Parkinson’s disease:

MOA:
- Levodopa is the metabolic precursor of dopamine
Effect:
- Levodopa can cross the BBB (dopamine cannot) and increase the synthesis of
dopamine in the brain
- Levodopa is converted by DOPA-decarboxylase à only 1-3% enters brain due to
extensive peripheral metabolism by the enzymeàgive carbidopa, which is a
peripheral inhibitor of the enzyme

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17
Q

Pilocarpine

A

Direct agonists: act directly on nicotinic or muscarinic receptors
Choline mimetic

MOA:
- Muscarinic agonist Effect:
- Increases salivation and sweat production (30 min – 2h)

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18
Q

Neostigmine

A

Indirect agonists: inhibit ACh-esteraseàprolonged ACh-mediated effects
Cholinomimetic
MOA:
- ACh-esterase inhibitor Effect:
- Peripheral actions (0,5 – 2h)

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19
Q

Pyridostigmine

A

Indirect agonists: inhibit ACh-esteraseàprolonged ACh-mediated effects
Cholinomimetic
MOA:
- ACh-esterase inhibitor Effect:
- 3-6h

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20
Q

Rivastigmine

A

Indirect agonists: inhibit ACh-esteraseàprolonged ACh-mediated effects
Cholinomimetic antiholinesterase agents
MOA:
- ACh-esterase inhibitor
Effect:
- Long half-life

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21
Q

Atropine

A

Muscarinic receptor blocking

Atropine: (0.3 – 1.0mg) MOA:
- Non-selective muscarinic antagonist Effect:
- Duration of action (2-4h)

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22
Q

Butylscopolamine

A

Muscarinic receptor blocking
Smooth muscle relaxant

MOA:
- Non-selective muscarinic antagonist Effect:
- SM relaxation

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23
Q

Ipratropium

A

Muscarinic receptor blocking drugs

MOA:
- Non-selective muscarinic antagonist Effect:
- Bronchodilation

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24
Q

Procyclidine

A

Muscarinic receptor blocking drugs

MOA:
- Non-selective muscarinic antagonist
Effect:
- Improves tremor and rigidity

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25
Q

Solifenacin

A

Muscarinic receptor blocking drugs

MOA:
- M3 antagonist(Gqàcontraction)
Effect:
- Relax the muscle in the wall of the bladder

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26
Q

Cyclopentolate

A

Muscarinic receptor blocking drugs

MOA:
- Non-selective muscarinic antagonist
Effect:
- Mydriatic and cycloplegic agent (loss of accommodation)

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27
Q

Tiotropium

A

Muscarinic receptor blocking drugs

MOA:
- M3 antagonist(Gqàcontraction) Effect:
- Bronchodilation

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28
Q

Oxybutinin

A

Muscarinic receptor blocking drugs
MOA:
- M3 antagonist(Gqàcontraction)
Effect:
- Short-acting (6h)
- Decrease detrusor muscle spasms

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29
Q

Epinephrine

A

Catecholamines
MOA: (all adrenergic receptors)
- Small dose: β-stimulation predominates (HR, SV, CO, PP↑, TPR, BP↓,
bronchodilation)
- Large dose: α1-stimulation predominates (TPR, BP↑, reflex bradycardia)

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30
Q

Norepinephrine

A

Catecholamines

MOA:
- α1, α2 and β1 agonist
Effect:
- Vasoconstriction

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31
Q

Dopamine

A

Catheholimines
MOA:
- Small dose: D1 à vasodilation, RBF + GFR↑, Na+ excretion↑
- Medium dose: D1, β1 à heart = positive inotropic effect
- Large dose: α1 effects à vasoconstriction (TPR, BP↑)

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32
Q

Dobutamine

A

Catecholamines
MOA:
- β1 agonist
Effect:
- CO, SV↑

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33
Q

Isoprenalin

A

Catheholimines
MOA:
- Non-selective β-agonist
Effect:
- Positive inotropic and chronotropic effect via β1
- Bronchodilation via β2

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34
Q

Ephedrine

A

Indirect symoathomimetic
MOA:
- Indirect sympathomimetic + weak β2 agonist
Effect:
- Enhance monoamine release

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35
Q

Phenylephidrin

A

Indirect symphatomimetic alpha 1 agonist
MOA:
- α1-agonist
Effect:
- Vasoconstriction (increased BP, duration of action: 15-60 min)

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36
Q

Clonidine

A

Indirect sympathomimetics. Selective and α-2-agonists

MOA:
- α2-agonist (act as sympatholytic) + I2-agonist (imidazole)
Effect:
- Presynaptic α2 leads to decrease in release of NEàdecrease in BP

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37
Q

Rilmenidine

A

Indirect sympathomimetics. Selective and α-2-agonists

MOA:
- α2-agonist (+ I2-agonist)
Effect:
- Vasodilation

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38
Q

Methyldopa

A

Indirect sympathomimetics. Selective and α-2-agonists
MOA:
- α2-agonist
Effect:
- Inhibit NE release via presynaptic α2-receptor (cannot activate adrenergic receptors
àsafe in pregnancy)p Indirect sympathomimetics.

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39
Q

Oxymetazoline

A

Indirect sympathomimetics. Selective α-1 and α-2-agonists

MOA:
- Local α1-agonist
- Systemic α2-agonist (exception in effect from the sympatholytic effect of α2-agonists)
Effect:
- Vasoconstriction (local use)

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40
Q

Methylphenidat

A

Indirect sympathomimetics. Selective α-1 and α-2-agonists

MOA:
- α2-agonist
Effect:
- Inhibit NE release via presynaptic α2-receptor (cannot activate adrenergic receptors
àsafe in pregnancy)

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41
Q

Prazosin doxazosin tamsulozin

A

α-receptor antagonists
MOA:
- α1-selective antagonist
Effect:
- Relax muscle of prostate + bladder neck allowing urine to flow more easily

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42
Q

Phentolamine

A

α-receptor antagonists
MOA:
- Non-selective α-antagonist (reversible competitive) Effect:
- Vasodilation, lower BP

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43
Q

Carvedilol

A

Alpha receptor antagonist
MOA:
- α1-selective antagonist, β-antagonist
Indication:
- Hypertension, CHF, chronic stable angina

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44
Q

Urapidil

A

Alpha receptor antagonist
MOA:
- α1-selective antagonist, α2-agonist
- Serotonergic agonist, β-antagonist

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45
Q

Propranolol

A

Non-selective β-antagonist
MOA:
- Non-selective β-antagonist
Effect:
- HR↓àdiastolic perfusion↑àO2 demand↓

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46
Q

Carvedilol

A

β1-selective antagonists:

MOA:
- α1-antagonist, β-antagonist

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47
Q

Timolol

A

Non-selective β-antagonist

MOA:
- Non-selective β-antagonist
Effect:
- Decreased aqueous humor secretion

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48
Q

Sotalol

A

Non-selective β-antagonist

MOA:
- Non-selective β-antagonist + (K+-channel blocker)
Effect:
- Decreases HR + AV conduction

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49
Q

Metoprolol

A

β1-selective antagonists:
Metoprolol: (2x 25-100mg) MOA:
- β1-selective antagonist Effect:
- Local anesthetic effect (inhibit Na+-channels)

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50
Q

Bisoprolol

A

β1-selective antagonists:
MOA:
- β1-selective antagonist
Indication:
- Hypertension, chronic stable angina, CHF

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51
Q

Nebivolol

A

β1-selective antagonist

MOA:
- β1-selective antagonist
Effect:
- NO-dependent vasodilation – better for young males

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52
Q

Esmolol

A

β1-selective antagonists
MOA:
- β1-selective antagonist Effect:
- Ultrashort effect (ca. 9 min)

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53
Q

Baclofen

A

Spasmolytic agents
MOA:
- GABAB receptor agonist
Effect:
- GiàK+-effluxàhyperpolarizationàlong-lasting muscle relaxant effect

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54
Q

Tolperison

A

Spasmolytic agents:

MOA:
- Unknown mechanism (may involve inhibition of Na+ and Ca2+-channels)
Effect:
- Reduction of muscle reflex

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55
Q

Diazepam

A

BDZ
Spasmolytic agents:

Diazepam: (benzodiazepine) MOA:
- GABAA receptor agonist Effect:
- Cl- influxàhyperpolarizationàmuscle relaxant effect

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56
Q

Tizanidine

A

Spasmolytic agents:
MOA:
- α2 agonist
Effect:

Pre-synaptic stimulationàinhibition of glutamate releaseàmuscle relaxation

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57
Q

Danntrolene

A

Direct-acting muscle relaxants:

MOA:
- Ryanodine receptor (RyR) antagonist
Effect:
- Inhibits Ca2+ release in ER in the skeletal muscleàreduce actin-myosin interaction

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58
Q

Cisatracurium

A

Choliergic antagonist
Non-depolarizing agents

MOA:
- Competitive antagonist of NM ACh-R
Effect:
- Bind to receptor instead of AChàno opening of ion channelàmuscle paralysis

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59
Q

Mivacurium

A

Non-depolarizing agents
MOA:
- Competitive antagonist of NM ACh-R
Effect: muscle paralysis

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60
Q

Pipecuronium

A

Neuromuscular junctiona blocker
Non-depolarizing agents
MOA:
- Competitive antagonist of NM ACh-R
Effect:
- Bind to receptor instead of AChàno opening of ion channelàmuscle paralysisk

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61
Q

Rocuronium

A

neuromuscular junction blocker
nondepolorazing agents
MOA:
- Competitive antagonist of NM ACh-R
Effect:
- Bind to receptor instead of AChàno opening of ion channelàmuscle paralysis

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62
Q

Succinylcholine (suxamethonium)

A

MOA:
- Selective agonist of NM receptor (depolarizing)
Effect:
- Skeletal muscle relaxant
- Provides depolarizing blockade that cannot be antagonized by ACh-esterase
inhibitors (phase 1 blockade)

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63
Q

Cocaine

A

Local anaesthetic
Esters:
MOA:
- Na+-channel blocker
Effect:
- Blocks NE re-uptake into nerve terminals (àvasoconstriction + psychostimulant)
• Intrinsic sympathomimetic effect

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64
Q

Lidocaine & articaine & bupivacaine

A

Local anaesthetics
Amides

MOA:
- Na+-channel blocker
Effect:
- Decreased Na+-influxàraise depolarization thresholdàno membrane
depolarizationàblock formation of APàblock generation + conduction of nerve
impulses

Bupivacaine - local surgical procedure

65
Q

Benzocaine

A

Local anaesthetics
Esters
MOA:
- Na+-channel blocker
Effect:
- Reversibly stabilizes the neuronal membraneàdecreases its permeability to Na+-
ionsàdepolarization of neuronal membrane inhibitedàblocking the initiation +
conduction of nerve impulses

66
Q

Morphin

A

Natural opioids

MOA:
- Na+-channel blocker
Effect:
- Reversibly stabilizes the neuronal membraneàdecreases its permeability to Na+-
ionsàdepolarization of neuronal membrane inhibitedàblocking the initiation +
conduction of nerve impulses

67
Q

Codeine

A

Natural opioids

MOA:
- Weak agonist (MOR) + natural
- Centrally acting antitussiveàdecreases sensibility of cough centers
Effect:
- Antitussive (suppress cough reflex)
- Weak analgesic effect in combination with NSAIDs or acetaminophen

68
Q

Hydromorphone

A

Opioids
semi- synthetic Strong agonists:
- Semi-synthetic strong agonist
- 8x more potent than morphine – pharmacological effects similar to morphine
- Oral administration (fast absorbing tablets)

69
Q

Dihydrocodeine

A

opioids
Semisynthetic weak agonist
- Codeine derivative à more potent than codeine
- Antitussive effect, stronger analgesic effect than codeine

70
Q

Oxycodone

A

Opioid
Semi-synthetic strong agonist (potential drug of abuse!)
- Codeine derivative
- Similar to morphine – used in cancer associated pain + chronic musculoskeletal pain

71
Q

Buprenorphine

A

Opioids
Mixed agonist-antagonists:
- Partial μ agonist + κ antagonist (semisynthetic)
- 20x more potent than morphine (àresistant against naloxone)
- Indication: analgesia, respiratory depression

72
Q

Nalbuphine

A

Opioids

Mixed agonist- antagonist

  • μ antagonist + κ agonist (semisynthetic)
  • Indication: spinal anesthesia (given after cesarean section as it does not relax uterus)
  • Effect:
    • ‘’Ceiling effect’’: respiratory depression will reach a limit, where increasing the dose will not increase the depression
    • Fewer cardiovascular effects
    • Naloxone antagonism is weaker
73
Q

Meperidin

A

Opioids
Strong agonist
Meperidine: (pethidine)
- Synthetic strong agonist
- Shorter duration of action (2-4h) than morphine
- Indication: analgesic use (emergency ca

74
Q

Fentanyl

A

Opioids
- Synthetic strong agonist
- Similar to morphine à 100x more potent
- Short acting

75
Q

Methadone ‘

A

Opioids
Synthetic strong agonist
- Indication:
• Management of opioid withdrawal syndrome
• Maintenance programs for addicts (heroin, morphine)
- Longer duration than morphine + good oral bioavailability

76
Q

Tramadol

A

Opioid
Synthetic weak agonist
- Inhibitor of NE + 5-HT re-uptake
- Used in case of neuropathic pain

77
Q

Diphenoxylate& loperamid

A

opioid agonist
Synthetic weak agonists
- Anti-diarrheal agents à ↓GI motility + secretions
- Loperamide penetrates BBB with difficulty à no CNS effects

78
Q

Naloxone

A

Opioids
Pure antagonist
- Semisynthetic strong antagonist
- Antagonist on all opioid receptors (highest affinity to μ receptors)
- Short-acting, given IV/IM – oral naloxone together with oxycodone
- Indication: management of acute opioid overdose (IV only)

79
Q

Methyl naltrexone

A

zperipheral μ-opioid antagonist

Pure antagonist

  • Peripherally acting antagonist (cannot penetrate BBB)
  • For the treatment of opioid induced constipation – if other laxatives are ineffective
80
Q

Acetylaalicylic acid (aspirin)

A

NSAIDS

Cox inhibitor
MOA:
- Inhibition of platelet aggregation
Effect:
- Irreversible inhibition of COX enzyme in plateletsà↓thromboxane A2à↓effect
of platelet aggregation

81
Q

Colchicine

A

Management of acute gout attacks:

MOA:
- Microtubule assembly inhibitor
Effect:
- Binds to tubulin à prevents polymerization, inhibits migration of leukocytes +
phagocytosis, inhibits release of lysosomal enzymes
- Tubulin is necessary for normal cell division, motility etc. à mitosis inhibitor

82
Q

Allopurinol

A

-Managment of chronic gout
MOA:
- Uric acid synthesis inhibitor
Effect:
- Inhibits the enzyme (xanthine oxidase) responsible for the production of uric acidà
↓ serum uric acid

83
Q

Rasburicase

A

Managment of chronic gout
MOA:
- Recombinant urate oxidase Effect:
- Urate oxidase enzyme catalyzes the metabolism of uric acid to allantoinà↓serum uric acid, ↓uric acid preparation

84
Q

Metamizole

A

NSAIDs
-Excellent analgesic effect, weak anti-inflammatory drug
- Its use has decreased in many countries because of BM toxicityàagranulocytosis

85
Q

Naproxen

A

NSAIDs

Analgesic use + moderate anti-inflammatory action
- Management of dysmenorrhea à menstrual cramps (uterine relaxation)
- Acts for more than 12 hours

86
Q

(Dex)Ibuprofen & (dex)ketoprofen

A

NSAIDs

Non-selective COX inhibitor
- Analgesic use in children (safer than aspirin)
- Used to induce ductus arteriosus closure

87
Q

Phenylbutazone

A

NSAIDs

Strong anti-inflammatory drug, but significant toxicity
- BM toxic effect
- Gout, arthritis

88
Q

Indomethacin

A

NSAIDs

Short acting, strong anti-inflammatory drug
- Indication: acute gout attacks, ductus arteriosus closure, BM suppression

89
Q

Diclofenac

A

NSAIDs

Strong anti-inflammatory drug
- Indication: chronic rheumatic pain (accumulates in synovial fluid) à joints

90
Q

Paracetamol

A

Nsaids
Non-opioid analgesic

MOA:
- Popular analgesic + antipyretic drug
- No anti-inflammatory or antiplatelet effect
Effect:
- Inhibition of COX in the CNS
Indication:
- Analgesic and antipyretic agent
- Aspirin substitute à in children with viral infection or those with aspirin
hypersensitivity (can also be used in pregnant women)

91
Q

Meloxicam

A

NSAIDs

COX-2 > COX-1
- Anti-inflammatory

92
Q

Celocoxib

A

NSAIDs

MOA:
- COX-2 selective (reversible) inhibitor
- Not more effective than the non-selective COX inhibitor)
Effect:
- Analgesic, antipyretic, anti-inflammatory

93
Q

Sumatriptan

A

Drugs for headache symptoms

MOA:
- Selective 5-HT1D/1B agonist
Effect:
- Vasoconstriction of meningeal vessels, prevent release of vasoactive peptides,
inhibit pain pathway

94
Q

Galcanezumab

A

Migraine prophylactic therapy

MOA:
- CGRP antagonist (calcitonin gene-related peptide receptor)
Effect:
- Decrease inflammation in meninges caused by CGRP

95
Q

Cinnarizine

A

Migraine prophylaxis therapy

MOA:
- Ca2+-channel blocker, anti-histamine
Effect:
- Reduce neurogenic inflammation, promote cerebral perfusion

96
Q

Propranolol

A

Migraine prophylactic therapy

MOA:
- Non-selective β-antagonist
Effect:
- HR↓àdiastolic perfusion↑àO2 demand↓

97
Q

Verapamil

A

Migraine prophylactic therapy

MOA:
- Cardioselective Ca2+-channel blocker
Effect:
- Slower conduction by SA and AV nodes (Ca2+-dependent cells)à↓HR

98
Q

Valproate

A

Migraine prophylactic therapy

Effect:
- Facilitate inhibitory actions of GABA
Indication:
- Antiepileptic

99
Q

Amitriptyline

A

Tricyclic antidepressants (TCAs)
inhibit the NE and 5-HT reuptake transporters (NET + SERT)
- Action:
• Elevate mood, improve mental alertness, increase physical activity

100
Q

Nitrous oxide

A

Gas

Weak general anesthetic on its own (weakest among all inhaled anesthetics)à
cannot produce surgical anesthesia, but has analgesic effect

101
Q

Isoflurane

A

inhaled anaesthetic Volatile liquid

Isomer of Enflurane
- Irritates respiratory system (pungent) à only suitable for maintenancec

102
Q

Desflurane

A

Inhalerional anasthetic
Volatile liquids
Rapid onset + recovery
- Irritates respiratory system (pungent) à only suitable for maintenance

103
Q

Sevoflurane

A

Inhalationall anasthetics
Volatile liquid
Most commonly used inhaled anesthetic (potent)
- Rapid onset + recovery (à rapidly eliminated)
- Less irritation to respiratory system than the othersàused as anesthesia in childre

104
Q

Thiopental

A

Barbiturate (IV anaesthetic)

Mechanisms:
- Facilitate GABA-mediated inhibition at GABAA receptorsàCl- influx Indication:
- Induction of anesthesia
- Anesthesia for short surgical procedures

105
Q

Propofol

A

IV anaesthetic

Mechanisms:
- Facilitate GABA-mediated inhibition at GABAA receptorsàCl- influx
- Causes decreased level of consciousness and amnesia
Indication:
- Induction and maintenance of anesthesia
- Outpatient anesthesia
- Antiemetic effect (treat postoperative vomiting and nausea)

106
Q

Etomidate

A

IV anaesthetic

Mechanisms:
- Facilitate GABA-mediated inhibition at GABAA receptorsàCl- influx
Indication:
- Only for induction of anesthesia in patients with limited cardiac or respiratory
reserve (e.g. hypovolemic patients)

107
Q

Ketamine

A

IV anaesthetic

Mechanisms:
- NMDA receptor (glutamate) antagonist
- Produces ‘’dissociative anesthesia’’ à patient remains conscious but has marked
analgesia, amnesia and catatonia (lack of movement + communication) Indication:
- Induction of anesthesia only for short interventions (e.g. pediatrics, gynecology, burn patients that have to change bandages several times a day)

108
Q

Midazolam

A

IV anaesthetic.Benzodiazepines

Mechanisms:
- Facilitate GABA-mediated inhibition at GABAA receptorsàCl- influx
Indication:
- Not real anesthetic à effect is not narcosis, but deep sleep
- Preoperative sedation
- Induction of anesthesia

109
Q

Dexmedetomidin

A

IV anaesthetic

Mechanisms:
- α2 agonist
Indication:
- Short-term sedation in ICU settings
- Hypertension, as it decreases BP

110
Q

Fentanyl

A

Opioid IV. Anaesthetic

Mechanisms:
- Opioid μ-receptor agonist
- Analgesic agent
Indication:
- Induction and maintenance of anesthesia

111
Q

Metoclopramide

A

Preoperative medication
Antiemetic

112
Q

Atropine

A

Parasympatolitic

Mechanism:
- Non-selective muscarinic antagonistàdecreases PARA tone
Indication:
- Reduce salivation and bronchial secretions before surgery
- Decrease of increased vagal tone due to administration of inhaled nar

113
Q

Antacid drug

A

IV anaesthetic

114
Q

Antihistamines

A

IV anaesthetic

115
Q

Analgesics

A

IV anaesthetic

116
Q

Diazepam

A

Benzodiazepines

MOA:
- GABAA receptor agonist
Effect:
- Cl- influxàhyperpolarizationàmuscle relaxant effect

117
Q

Nitrazepam

A

Benzodiazepines

MOA:
- GABA receptor agonist
Indication:
- Sleep disorders, insomnia
Extra:
- Short-acting
- Hepatic metabolism

118
Q

Midazolam

A

Benzodiazepines

MOA:
- GABA receptor agonist
Indication:
- Anesthesia (IV), preoperative sedation
Extra:
- Ultra-short-acting
- Hepatic metabolism

119
Q

Alprazolam (Xanax)

A

Benzodiazepines
MOA:
- GABA receptor agonist Effect:
- Cl- influxàhyperpolarizationàmuscle relaxant effect Indication:
- Anxiety, panic attacks and phobic disorders

120
Q

Clonazepam

A

Benzodiazepines

MOA:
- GABA receptor agonist
Effect:
- Cl- influxàhyperpolarizationàmuscle relaxant effect

121
Q

Flumazenil

A

Benzodiazepines

GABA antagonist (at BDZ binding site on GABAA receptor)
- Rapid onset, short duration
- Reverses effect of BDZs in sedation/anesthesia + overdose of benzodiazepines

122
Q

Zolpidem & zaleplon

A

Non benzodiazepine anxiolytics and non-benzodiazepine hypnotics
MOA:
- GABAA agonistàhigh affinity to BDZ receptors with α1 subunits
Indication:
- Sleep disorders (especially sleep-onset insomnia)

123
Q

Melatonin & ramelteon

A

Non benzodiazepine anxiolytics and non-benzodiazepine hypnotics

MOA:
- Non-GABAergic hypnotic
- Ramelteon = MT1 + MT2 agonists
Effect:
- Melatonin receptors have important roles in the regulation of the sleep-wake cycle
(suprachiasmatic nucleus)
- Decrease time of sleep onset during chronic insomnia à no rebound insomnia

124
Q

Buspirone

A

Non benzodiazepine anxiolytics and non-benzodiazepine hypnotics
MOA:
- Non-GABAergic anxiolytic
- 5-TH1A partial agonist (agonist on its own, antagonist together with full agonist) Indication:
- Generalized anxiety disorderso

125
Q

Haloperidol

A

Butyrophenons (1st generation (“typical”) antipsychotic agents )
Mechanism:
- Most widely used typical antipsychotic agentàhigh potency (D2&raquo_space; M, α1)
- Makes the patient calm and detached from the environment
Indication:
- Management of acute psychotic disordersàacute delirium

126
Q

Droperidol

A

Butyrophenons (1st generation (“typical”) antipsychotic agents)

D2 > α1, H1
- Has sedative effectàused in neuroleptanalgesia (together with fentanyl)

127
Q

Clozapine

A

Antipsychotic 2nd generation
Mechanism:
- High affinity for 5-HT2A, muscarinic and adrenergic receptors (antagonists!)
- Weak D2 antagonist
- No tardive dyskinesia
Indication:
- Schizophrenic patients resistant to 1st generation antipsychotics

128
Q

Olanzapine

A

Antipsychotic 2nd generation

Mechanism:
- 5-HT2AC > D2, M, H1, α1 à improves negative symptoms
Indication:
- First drug of choice in schizophrenia (most sedative drug)
- Also proven to be anti-maniac and have mood stabilizing effect

129
Q

Quetiapine

A

2nd generation antipsychotic

Mechanism:
- D2 > 5-HT2A receptor antagonist (but has good affinity for both)
Indication:
- Schizophrenia (most sedative drug together with olanzapine)
- Bipolar disorders

130
Q

Risperidone

A

2nd generation antipsychotic

Mechanism:
- 5-HT2AC > D2, H1, α1 à improves negative symptoms
Indication:
- First drug of choice in schizophrenia
- Tics of Tourette disorder in children

131
Q

Tiapride

A

2nd generation antipsychotic

Atypical antipsychotic, D2/D3 antagonistàused in management of alcohol psychosis

132
Q

Aripiprazole

A

2nd generation antipsychotic

Mechanism:
- 5-HT2Aàimproves negative symptoms
- Partial D2 agonist
Indication:
- Schizophrenia
- Bipolar disorder (long-acting, T1/2 up to 3 day

133
Q

Cariprazine

A

2nd generation antipsychotic

Atypical antipsychotic, D2/D3 antagonistàschizophrenia, bipolar disorder (Hungarian development)

134
Q

Amitryptiline & clomipramine

A

Antidepressant

Tricyclic antidepressants (TCAs) inhibit the NE and 5-HT reuptake transporters (NET + SERT)
- Action:
• Elevate mood, improve mental alertness, increase physical activity
- Uses:
• Major depression, phobia/panic anxiety, neuropathic pain, migraine,

135
Q

Moclobemide

A

MAO INHIBITOR
Antidepressants
MOA:
- Selective and reversible MAO-A inhibitor
Effect:
- Increased NEàhypertensive crisis (TCAs)
- Symptoms: increased BP, arrhythmias, hyperthermia, excitation

136
Q

Fluoxetine & sertaline & citalopram

A

Antidepressants
Selective serotonin reuptake inhibitors

First line therapy against depression à GOLD STANDARD!
- Indication:
• Depression à 2 weeks to show improved mood (4-6w for max benefit)
• Other: generalized anxiety disorder, OCD, PTSD, bulimia
• Contraindication: pregnancy
- Effect:
• Selective inhibition of 5-HT reuptake
• Little blocking activity at M, H1, α1 receptorsàless side effects

136
Q

Fluoxetine & sertaline & citalopram

A

Selective serotonin reuptake inhibitors

First line therapy against depression à GOLD STANDARD!
- Indication:
• Depression à 2 weeks to show improved mood (4-6w for max benefit)
• Other: generalized anxiety disorder, OCD, PTSD, bulimia
• Contraindication: pregnancy
- Effect:
• Selective inhibition of 5-HT reuptake
• Little blocking activity at M, H1, α1 receptorsàless side effects

137
Q

Venflaxine & duloxetine

A

Selective serotonin and NE reuptake inhibitors

Selective inhibition of 5-HT + NE reuptake
- Used to treat patients that do not respond to SSRIs
- Little blocking activity at M, H1, α1 receptors à less side effects

138
Q

Reboxetine

A

Selective NE reuptake inhibitor

Selective NE reuptake inhibitor
- Increases mental alertness, motivations, activity
- Side effects: dry mouth, hypertension, constipation

139
Q

Mirtazapine

A

Norepinephrine and serotonin receptor antagonist antidepressants.

MOA:
- α2 selective antagonist (presynaptic)
- 5-HT2A/C, 5-HT3, H1 receptor inhibition
Effect:
- Increased NE synthesis + release à weight gain
- 5-HT2C inhibition: stimulation of DA + NE pathways à anxiolytic effect
- 5-HT3 inhibition: lack of nausea, vomiting and diarrhea à antiemetic
- H1 inhibition: sedative

140
Q

Agomelatine

A

Norepinephrine and serotonin receptor antagonist antidepressants.

MOA:
- Melatonin (MT1 + MT2) agonist
- 5-HT2C antagonist
Effect:
- Recovery of circadian rhythm
- Better sleep and sexual function

141
Q

Lithium

A

Norepinephrine and serotonin receptor antagonist antidepressants

Indication:
- Acute treatment of bipolar disorders (manic-depressive diseases)
- Maintenance therapy à decrease frequency and magnitude of mood swings (‘’mood
stabilizer’’)àusually an antidepressant/antipsychotic is also required MOA: (follow figure above)
- Prevent recycling of inositolàdecreased IP3 + DAG (diacylglycerol)àinterfere with actions of Gq/s-coupled receptorsà↓ second messengersà↓neuronal activity in pathologically overactive circuitsàmood stabilization

142
Q

Phenytoin

A

Antiepileptics used in partial seizures and generalized tonic-clonic seizures

MOA:
- Inhibition of VG Na+-channel
Effect:
- Prevent seizure propagation, but not initiation

143
Q

Carbamazepine

A

Antiepileptics used in partial seizures and
generalized tonic-clonic seizure

MOA:
- Inhibition of VG Na+-channel
Effect:
- Prevent seizure propagation, but not initiation

144
Q

Phenobarbital

A

Antiepileptics used in partial seizures and generalized tonic-clonic seizures

MOA:
- Inhibits GABA metabolism
- May also block Na+ / Ca2+ channels at higher concentrations Effect:
- Prevent tonic-clonic or partial seizures (2nd or 3rd in line due to SE)

145
Q

Ethosuximide

A

Antiepileptics used in absence seizures. “Broad spectrum” antiepileptic drugs.

MOA:
- Inhibits T-type Ca2+ channels in the thalamus
- Narrow spectrum
Indication:
- Absence seizures ONLY!

146
Q

Valproate

A

Antiepileptics used in absence seizures. “Broad spectrum” antiepileptic drugs

MOA + Effect:
- Inhibits VG Na+ channels, T-type Ca2+ channels
- Enhances GABA transmission, decreases glutamate Indication:
- All seizures (including absence seizures)àbroad spectrum
- Bipolar disorders, migraine

147
Q

Lamotrigine

A

Antiepileptics used in absence seizures. “The Broad spectrum” antiepileptic drugs

MOA:
- Inhibits Na+ channels + reduces glutamate release
Indication:
- Most seizuresàbroad spectrum
- Not teratogenic (unlike others)àcan be given to pregnant women

148
Q

Clonazepam

A

Antiepileptics used in absence seizures. “Broad spectrum” antiepileptic drugs.

MOA + Effect:
- Benzodiazepine
- Enhances effect of GABA
Indication:
- Absence seizure (first line), panic + anxiety disordersl

149
Q

Levetiracetam

A

Antiepileptics used in absence seizures. “Broad spectrum” antiepileptic drugs.

MOA + Effect:
- Prevents synaptic release of glutamate (SV2A receptor blockade)
Indication:
- Tonic-clonic, partial, myoclonic seizures in childrenàbroad spectrum
- Not teratogenicàcan be given to pregnant women

150
Q

Vigabatrine

A

Antiepileptics used in partial seizures and generalized tonic-clonic seizures except for the “broad spectrum

MOA:
- Inhibits GABA metabolism (GABA-transaminase inhibitor)
Effect:
- Decreased GABA metabolismàmore GABA released
Indication:
- Partial seizures + infantile (juvenile) spasm

151
Q

Levodopa + carbidopa

A

Drugs used in Parkinson’s disease

MOA:
- Levodopa is the metabolic precursor of dopamine
Effect:
- Levodopa can cross the BBB (dopamine cannot) and increase the synthesis of
dopamine in the brain
- Levodopa is converted by DOPA-decarboxylase à only 1-3% enters brain due to
extensive peripheral metabolism by the enzymeàgive carbidopa, which is a
peripheral inhibitor of the enzyme

152
Q

Ropinirole & pramipexole

A

Drugs acting in the extrapyramidal motoric system.

Drugs used in Parkinson’s disease

MOA:
- Dopamine D2 agonists (non-ergot derivatives)
Effect:
- Longer duration of action than levodopa and effective in patients with fluctuations
in response to levodopa
- Pramipexole is a potential anti-oxidant

153
Q

Selegiline: (Hungarian development, REMEMBER IT!)

A

Drugs acting on extrapiramidal system
Drugs against Parkinson’s Disease
MOA:
- Selective + reversible MAO-B inhibitor Effect:
- Decreases metabolism of dopamine à increased dopamine activity in the brain
- No ‘’cheese effect’’ as seen with non-selective MAO inhibitors
- Neuroprotective (enhancement of scavenger function)

154
Q

Amantadine

A

Drugs acting on extrapyramidal system
Drugs agains Parkinson’s disease

MOA:
- Antiviral drug (influenza prevention)
Effect:
- Uncertain mechanism à increased dopamine release / block dopamine reuptake,
block muscarinic receptors
- Weaker than levodopa and tolerance develops against it

155
Q

Procyclidine

A

Drugs acting on extrapyramidal system
Drugs against Parkinson disease

MOA:
- Muscarinic receptor antagonist Effect:
- Decreases resting tremor and rigidity, but little effect against bradykinesia

156
Q

Memantine

A

Drugs acting on extrapyramidal system
Drugs acting against Alzheimer’s Disease

MOA:
- Glutamate NMDA receptor blocker Effect + Indication:
- Stimulation of CNS glutamate receptors appears to be critical in formation of certain memories, but overstimulation may result in excitotoxicity
Side-effects:
- Confusion, agitation

157
Q

Rivastigmine

A

Drug acting on extrapyramidal system
Drugs used for Alzheimer’s disease

MOA:
- ACh-esterase inhibitor (centrally-acting)
Effect + Indication:
- 1st line agent for Alzheimer’s diseaseàprovide moderate reduction in rate of loss of
cognitive function

158
Q

Piracetam

A

Drug caring on extrapyramidal system
Drug used for Alzheimer’s disease

Interferes with NT release by binding to synaptic vesicle protein (SV2A)
- Used as cognition enhancers and in treatment of ADHD (attention deficit
hyperactivity disorder), Parkinson’s disease and schizophrenia

Pharma (2 decks)

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