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Pharmacology > Drug mechanisms > Flashcards

Drug mechanisms Flashcards

1
Q

Mydriatics (eye)

A

Parasympatholytics/anticholinergic/muscarinic antagonist: antagonize M3 receptors on constrictor pupillae

Sympathomimetic: alpha 1 adrenergic agonist: agonize alpha 1 receptor on dilator pupillae

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2
Q

To decrease aqueous production (gluacoma) with no effect on pupil

A

Sympatholytics:

  • non-specific beta antagonist possibly via beta-2 receptors
  • B1 adrenoceptor antagonist: decrease aqueous production

Sympathomimetics:

epinephrine: non-specifc adrenoceptor agonist- decreases aqueous production via alpha 1 vasoconstriction of ciliary blood vessels
apraclonidine: alpha 2 adrenoceptor agonist (also weak alpha 1 agonist- capitalizing on this action)

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3
Q

Miosis (pupillary constriction) to open drainage angle (glaucoma)

A

Direct parasympathomimetic: non-specific muscarinic agonists (local application)

Indirect parasympathomimetic: acetylcholinesterase inhibitors–> increase [ACh] (targets NT rather than receptor)

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4
Q

To treat detrusor hypercontractility/spasticity (urinary incontinence)

A

Aim: decrease detrusor activity (M3 receptors)

Antimuscarinic: non-specific muscarinic antagonists

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5
Q

To treat detrusor atony (urinary retention)

A

Aim: increase activity–> cholinergic agonists

Bethanechol: Non-specific muscarinic agonist, but higher affinity for M3

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6
Q

Urethral sphincter incompetence (incontinence)

A

Aim: increase sphinctor tone

Alpha 1 agonists ideally

Oral phenylpropanolamine: non-specific alpha adrenergic agonists

Ephedrine: stimulates NA release, binds to alpha and beta receptors

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7
Q

Urethral spasticity (retention)

A

Aim: decrease urethral activity

Non-selective alpha antagonist: phenoxybenzamine- preferential binding to alpha 1

Prazosin and terazosin: selective alpha 1 antagonist

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8
Q

Aluminum salts and magnesium salts

A

alkaline chemicals that neutralize acid in stomach

neutralize gastric HCl, inhibit pepsin secretion

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9
Q

Histamine receptor antagonists (antacid)

A

i.e. cimetidine and ranitidine

competitive antagonism of H2 receptors in parietal cells; decreases production of HCl

[nb:Histamine receptor is couple to G-protein–> increase AC–>increase cAMP–>stimulate proton pump to secrete acid]

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10
Q

Sucralfate

A

sucrose sulfate-aluminum hydroxide complex

polymerizes to viscous gel at pH <4

forms long chains under acidic conditions–> exposted sulfate groups bind to protein in ulcerated area to create a bandage

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11
Q

Proton pump inhibitor

A

i.e. omeprazole

inhibits H+/K+ ATPase pump on luminal membrane of parietal cells

binding is irreversible; body has to synthesize new enzyme to create pump again

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12
Q

PGE2 analogues

A

e.g. misoprostol (methyl ester of prostaglandin)

PG analogue decreases acid secretion, increases blood flow and increases mucus production

Agonist at PG receptor

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13
Q

3% hydrogen peroxide

A

stimulates visceral afferents as a mild gastric irritant

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14
Q

Ipecac (huana)

A

local irriation (similar to hydrogen peroxide); direct central activation of receptors in CTZ

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15
Q

Xylazine

A

alpha 2 adrenoceptor agonist

direct central activation of receptors in CTZ (most species CTZ has alpha 2 adrenoceptors (cats have high amount))

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16
Q

Apomorphine

A

dopamine agonist; binds to receptors in CTZ

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17
Q

Phenothiazines (ACP)

A

block dopamine receptors in CTZ; weak anticholinergic and antihistamine also

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18
Q

Metoclopramide

A

dopamine antagonist; also some antimuscarinic effects

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19
Q

Diphenhydramine

A

antihistamine, antimuscarinic

effective for antiemesis (motion pathway)

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20
Q

Neurokinin antagonist

A

e.g. maropitant (cerenia)

NK-1 receptor antagonist

shuts down emetic pathway

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21
Q

Serotonin antagonist- Odansetron

A

blockade of serotonin receptors in CTZ

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22
Q

Adsorbents (diarrhea)

A

Kaolin (Al3+ salt) suspension

absorbs toxins; provides prtective coating on inflamed mucosa (changes consistency of feces)

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23
Q

Opioids (antidiarrheal)

A

diphenoxylate and loperamide won’t cross BBB- no typical CNS effects of opioid

inhibits ACh release in myenteric plexus–> slows gut, allows for reabsorption of water

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24
Q

Anticholinergics (antidiarrheals)

A

muscarinic antagonism (buscopan, atropine)

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25
Q

Aminosalicylates

A

cleaved by bacteria in bowel to sulfapyridine and 5-amniosalicylic acid (related to aspirin)

have anti-inflammatory effect–> inhibit PG synthesis?

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26
Q

Lubricant (laxative/ cathartic)

A

lubricate tract and soften feces

mineral oil, liquid paraffin

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27
Q

Bulk (cathartic)

A

add dietary fiber to absorb H2O

hydrophilic colloids absorb water, increase bulk–> stimulate persistalsis

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28
Q

Osmotic cathartic

A

magenesium sulphate, lactulose

non-absorbale salts/polymers

retain water in intestinal lumen, decrease consistency, soften stools

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29
Q

Stimulant cathartics

A

bisacodyl, phenophthalein

stimulate intestinal motility via irritant effect–> promote organized peristaltic action

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30
Q

Beta-adrenergic agonists (respiratory)

A

adrenaline

used for life threatning bronchoconstriction

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31
Q

Beta-2 specific agonists (respiratory)

A

bind to b2 receptors–> increase cAMP –> relaxation of bronchial smooth muscle

also inhibit histamine release from mast cells–> benefit in allergic reaction

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32
Q

Anticholinergics

A

antimuscarinics

M3–>increase IP3–>increase cytosolic concentration of calcium–> constriction of bronchial SM

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33
Q

Methylxanthines

A

PDE inhibitors

PDE breaks down cAMP to 5’AMP

PDE inhibitiors increase cAMP–> bronchial smooth muscle relaxation

also decreases inflammatory mediators

inhibit adenosine: circulating substance that causes bronchoconstriction

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34
Q

Antihistamine (respiratory)

A

H1-receptor antagonists

histamine–> bronchoconstriction, local edema, vagal nerve stimulation

35
Q

Sodium cromoglycate

A

inhibit release of inflammatory mediators (histamine, leukotrienes) from mast cells

NO bronchodilator action, just prevents bronchoconstriction

36
Q

Corticosteroids

A

decrease inflammation associated with inflammatory pulmonary diseases by inhibiting transcription of certain genes involved in producing inflammatory mediators

also enhance action of beta-2 agonists: slow down down-regulation process–> enhance length of efficacy

37
Q

NSAIDs (respiratory)

A

useful with inflammatory process i.e. PG mediated respiratory disease

38
Q

Leukotriene inhibitors

A

1) lipoxygenase inhibitors
2) luekotriene receptor blocks

39
Q

Opiates (antitussives)

A

directly depress cough center via mu and kappa receptors

40
Q

Mucolytics

A

acetylcysteine: anti-oxidant compound that chemically interfereswith mucus

41
Q

Saline expectorants

A

make a greater volume of mucus and stimulates coughing

42
Q

decongestants

A

alpha agonists: vasoconstriction of BVs in upper respiratory tract–> decreased producton of mucus

antihistamines: decrease inflammation

43
Q

Local anaesthetics

A

block Na+ channels to prevent initation/conduction of action potentials

44
Q

Opioid analgesics

A

bind to opioid receptors in brain, spinal cord, periphery

GCPR: inhibit adenylate cyclase and decrease cAMP

promote opening of K+ channels (hyperpolarization, decreased neuronal excitability)

inhibit opening of voltage-gated calcium channels (decrease NT release)

45
Q

NSAIDs

A

inhibit cyclooxygenase to decrease production of PGs and thromboxanes

act peripherally: decrease PG production at site of inflammation and reduce sensitization of nociceptive nerve endings to inflammatory mediators

act centrally: block PG release and neuronal excitation; decreased central sensitization

46
Q

Phenothiazines (tranquilizer)

A

non-selective dopamine antagonist (in basal ganglia, limbic system); also antagonist action at alpha 1, serotonin, histamine, muscarinic receptors

47
Q

Butyrophenones

A

chemically unrelated to phenothiazines

dopamine antagonist (some alpha 1 antagonism)

48
Q

Alpha 2 agonists (sedative)

A

Alpha 2 agonism–> inhibit adenylate cyclase, decrease cAMP–> inhibit voltage gated Ca2+ channels and activate Ca2+ dependent K+ channels.

Pre-synaptically: alpha 2s inhibit NT release via inhibiting cAMP production

Post-synaptically: alpha 2 agonism–> vasoconstriction

49
Q

Benzodiazepines

A

BZPs potentiate GABA (not actually agonists)

In the presence of GABA, BZPs facilitate opening of GABA activated Cl- channels

BZP binding site is distinct from GABAa site

BZP increases affinity of GABA for its receptor–> enhanced agonist effect.

50
Q

Propfol (induction, TIVA)

A

enhanced GABA transmission (increased flux of Cl-), similar to BZP but at a different site

51
Q

Alfaxalone (induction, TIVA)

A

enhances inhibitory action of GABA; it also possibly inhibits nicotinic ACh receptors and noradrenaline uptake

52
Q

Barbiturates

A

reversibly depress activity of all excitable tissue; reticular activating system is particularly susceptible

enhances inhibitory action of GABA at an allosteric site; promote binding of GABA to GABAa receptor; enlarge GABA-induced chloride currents

53
Q

Etomidate

A

imidazole derivative

non-barbiturate, but similar to thiopentone

enhance inhibitory action of GABA

54
Q

Ketamine

A

dissociative agents

interrupts association between limbic and cortical regions by acting on NMDA receptor (excitatory) ion changes which receptor is an intergral part of

Inhibits NMDA receptors

can also physically block the open ion channel, but it also decreases frequency of opening by binding modulatory sites

55
Q

Nitrous oxide

A

provides specific analgesia: NMDA receptor antagonist

56
Q

Non-depolarizing NMBs

A

competitive antagonist at the nicotinic ACh receptor. bind to receptor as antagonists, leaving fewer receptors for ACh to bind (need to block at least 80% of receptors)

reversed by anticholinesterases (i.e. increase ACh overcomes block)

57
Q

Depolarizing NMBs

A

agonist at nicotinic ACh receptor but metabolized slowly.

ACh is normally rapidly cleared from the synapse

depolarizing NMB has persistence of action, leading to a rapid loss of muscle control and eventual muscle relaxation

has effect of initial fasciculations

58
Q

Guaifenesin

A

blocks impulse transmission at internucial neurones within spinal cord and brain stem

relaxes limbs more than respiratory muscles

59
Q

AEDs

A

target: GABA, glutamate, voltage-gated channels (sodium, calcium, choloride)

Act to hyperpolarize INSIDE of cell

60
Q

Phenobarbital

A

enhances activity of GABA and thereby increases nueronal inhibition

reduces neuronal excitability through interaction with glutamate receptors

inhibits voltage-gated calcium channels

competitive binding of chloride channel picrotoxin site

61
Q

Potassium bromide

A

not fully understood but involves bromide interaction with chloride channels

Cl- channels modulated by GABA and function to hyperpolarize cell membrane, making it more stable

Bromide cross the chloride channels in preference of Cl- has it has a smaller hydrated diameter. Bromide facilitates the neurotransmitters acting on GABA channel by hyperpolarizing cell membrane.

62
Q

Imepitoin

A

partial agonist at BZP recognition site of GABA receptor

potentiates GABA receptor-mediated inhibitory effects on neurons

weak calcium channel blocking effect

63
Q

Beta 1 adrenergic agonists (positive inotropes for HF)

A

Dobutamine

in cardiac muscle: beta-1 agonists stimulate AC via GCPR to form cAMP–> increases Ca2+–> contraction

64
Q

PDE III inhibitor (positive innotrope/vasodilator)

A

Vasodilator: In VSM: cAMP causes relaxation due to inhibitory effect on myosin kinase. if you increase amount of cAMP using PDE III inhibitor–> relaxation

In cardiac muscle: cAMP causes contraction to do effect of activating Ca2+ channels. increase PDE III inhibitor–> increase cAMP

65
Q

Pimobendan (calcium sensitizer)

A

Calcium sensitizer: enhances Ca2+/troponin interaction by increasing the affinity of Ca2+ for binding site; increased force of contraction without an increase in Ca2+ concentration

Inodilator: PDE III inhibitor effects

Decrease pulmonary hypertension: PDE V inhibitor in pulmonary blood vessels

positive lusitropic effects: diastolic relaxation of ventricles for better filling and CO

66
Q

Calcium channel blockers (pure vasodilators)

A

Amplodipine: works vascularly

blocks voltage operated Ca2+ channels that allow Ca2+ during depolarization–> triggers Ca2+ release from SR to cause contraction

67
Q

Hydralazine (vasodilator)

A

potent, but not sure how it works–> suggestion that it has direct relaxant action on VSM

68
Q

Prazosin (vasodilator)

A

alpha 1 adrenoceptor antagonist

relaxation of VSM

69
Q

Nitrates (vasodilators)

A

Nitrates act like endogenous system of vasodilation.

Primary stimulus for production of NO is shearing force generated by blood flow–stimulates endothelium nitric oxide synthase to convert L-arg to NO

NO stimulates guanylate cyclase to convert to cGMP–> relaxation of smooth muscle

Nitrates spontaneously donate NO which diffuses and causes relaxation

70
Q

PDE V inhibitor (vasodilator)

A

selectively prevents pulmonary hypertension

71
Q

ACE inhibitors (neuroendocrine modulating vasodilators)

A

ACE inhibitor blocks formation of angiotensin II. Angiotensin II stimulates aldosterone secretion, increase BP, increase ADH, increase sympathetic activity

ACE breaks down bradykinin which is a vasodilator. ACE inhibitors result in increased amounts of bradykinin, thereby increasing vasodilation.

72
Q

Angiontensin II receptor antagonists

A

directed action against ATII receptors; blocks ATII formed by other routes; doesn’t prevent breakdown of bradykinin

73
Q

aldosterone antagonists

A

spirolactone (diurectic)

used to block aldosterone escape

74
Q

negative inotropes

A

Beta blockers (class 2); calcium channel blockers (class 4)

75
Q

Class 1 AARDs

A

block sodium channels

reduce rate of depolarization by blocking fast inward Na+ current

76
Q

Class 2 AARDs

A

Beta-blockers: reduce sympathetic drive; slow AV node conduction; negative inotrops (decrease force of contraction, decrease O2 consumption, offset any hypoxia that may be contributing)

B1 in heart; B2 in bronchial and VSM, also in nodal tissue

77
Q

Class 3 AARDs

A

Block outward K+ channels (responsible for repolarization)

markedly increases AP duration and refractory period

also have effects on other classes

Amiodarone is a sodium channel blocker, alpha and beta block and calcium channel blocker

Sotalol has beta blocking actions also

78
Q

Class 4 AARDs

A

block L-type calcium channels (voltage operated Ca2+ channels that allows Ca2+ during depolarization–> triggers Ca2+ release from SR to cause contraction)

reduce AP height, prolong AP at node

shorten AP at cardiacmyocytes

negative inotropes: decrease force of contraction

positive lusitropes: diastolic relaxation of ventricles

79
Q

Cardiac glycosides

A

inhibit Na+/K+ pump so that sodium can’t be extruded, intracellular sodium concentraions increase, and calcium levels also build up inside the cell.

Increased cytoplasmic concentrations of calcium cause increased calcium uptake into SR–> more powerful contraction

Refratory period of AV node is increased

Increased parasympathetic activity results in a decreased sinus rate, decreased speed of AV node conduction, prolonged refractory period; slow ventricular response to atrial flutter.

80
Q

Treatment of bradyarrhythmias

A

muscarinic antagonists; methylxanthines, beta agonists

81
Q

Muscarinic antagonists (bradyarrhythmia tx)

A

antagonism of muscarinic ACh receptors–> positive chronotropes

82
Q

Methylxanthines

A

mild pde inhibition- not specifc to III or V

enhanced sympathetic drive–> mild positive inotropic and chronotropic effects

83
Q

beta agonists

A

stimulation of beta adrenergic receptors

Pharmacology (12 decks)

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