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Drug mechanisms Flashcards

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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
Aminosalicylates
cleaved by bacteria in bowel to sulfapyridine and 5-amniosalicylic acid (related to aspirin) have anti-inflammatory effect--\> inhibit PG synthesis?
26
Lubricant (laxative/ cathartic)
lubricate tract and soften feces mineral oil, liquid paraffin
27
Bulk (cathartic)
add dietary fiber to absorb H2O hydrophilic colloids absorb water, increase bulk--\> stimulate persistalsis
28
Osmotic cathartic
magenesium sulphate, lactulose non-absorbale salts/polymers retain water in intestinal lumen, decrease consistency, soften stools
29
Stimulant cathartics
bisacodyl, phenophthalein stimulate intestinal motility via irritant effect--\> promote organized peristaltic action
30
Beta-adrenergic agonists (respiratory)
adrenaline used for life threatning bronchoconstriction
31
Beta-2 specific agonists (respiratory)
bind to b2 receptors--\> increase cAMP --\> relaxation of bronchial smooth muscle also inhibit histamine release from mast cells--\> benefit in allergic reaction
32
Anticholinergics
antimuscarinics M3--\>increase IP3--\>increase cytosolic concentration of calcium--\> constriction of bronchial SM
33
Methylxanthines
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
34
Antihistamine (respiratory)
H1-receptor antagonists histamine--\> bronchoconstriction, local edema, vagal nerve stimulation
35
Sodium cromoglycate
inhibit release of inflammatory mediators (histamine, leukotrienes) from mast cells NO bronchodilator action, just prevents bronchoconstriction
36
Corticosteroids
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
NSAIDs (respiratory)
useful with inflammatory process i.e. PG mediated respiratory disease
38
Leukotriene inhibitors
1) lipoxygenase inhibitors 2) luekotriene receptor blocks
39
Opiates (antitussives)
directly depress cough center via mu and kappa receptors
40
Mucolytics
acetylcysteine: anti-oxidant compound that chemically interfereswith mucus
41
Saline expectorants
make a greater volume of mucus and stimulates coughing
42
decongestants
alpha agonists: vasoconstriction of BVs in upper respiratory tract--\> decreased producton of mucus antihistamines: decrease inflammation
43
Local anaesthetics
block Na+ channels to prevent initation/conduction of action potentials
44
Opioid analgesics
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
NSAIDs
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
Phenothiazines (tranquilizer)
non-selective dopamine antagonist (in basal ganglia, limbic system); also antagonist action at alpha 1, serotonin, histamine, muscarinic receptors
47
Butyrophenones
chemically unrelated to phenothiazines dopamine antagonist (some alpha 1 antagonism)
48
Alpha 2 agonists (sedative)
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
Benzodiazepines
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
Propfol (induction, TIVA)
enhanced GABA transmission (increased flux of Cl-), similar to BZP but at a different site
51
Alfaxalone (induction, TIVA)
enhances inhibitory action of GABA; it also possibly inhibits nicotinic ACh receptors and noradrenaline uptake
52
Barbiturates
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
Etomidate
imidazole derivative non-barbiturate, but similar to thiopentone enhance inhibitory action of GABA
54
Ketamine
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
Nitrous oxide
provides specific analgesia: NMDA receptor antagonist
56
Non-depolarizing NMBs
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
Depolarizing NMBs
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
Guaifenesin
blocks impulse transmission at internucial neurones within spinal cord and brain stem relaxes limbs more than respiratory muscles
59
AEDs
target: GABA, glutamate, voltage-gated channels (sodium, calcium, choloride) Act to hyperpolarize INSIDE of cell
60
Phenobarbital
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
Potassium bromide
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
Imepitoin
partial agonist at BZP recognition site of GABA receptor potentiates GABA receptor-mediated inhibitory effects on neurons weak calcium channel blocking effect
63
Beta 1 adrenergic agonists (positive inotropes for HF)
Dobutamine in cardiac muscle: beta-1 agonists stimulate AC via GCPR to form cAMP--\> increases Ca2+--\> contraction
64
PDE III inhibitor (positive innotrope/vasodilator)
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
Pimobendan (calcium sensitizer)
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
Calcium channel blockers (pure vasodilators)
Amplodipine: works vascularly blocks voltage operated Ca2+ channels that allow Ca2+ during depolarization--\> triggers Ca2+ release from SR to cause contraction
67
Hydralazine (vasodilator)
potent, but not sure how it works--\> suggestion that it has direct relaxant action on VSM
68
Prazosin (vasodilator)
alpha 1 adrenoceptor antagonist relaxation of VSM
69
Nitrates (vasodilators)
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
PDE V inhibitor (vasodilator)
selectively prevents pulmonary hypertension
71
ACE inhibitors (neuroendocrine modulating vasodilators)
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
Angiontensin II receptor antagonists
directed action against ATII receptors; blocks ATII formed by other routes; doesn't prevent breakdown of bradykinin
73
aldosterone antagonists
spirolactone (diurectic) used to block aldosterone escape
74
negative inotropes
Beta blockers (class 2); calcium channel blockers (class 4)
75
Class 1 AARDs
block sodium channels reduce rate of depolarization by blocking fast inward Na+ current
76
Class 2 AARDs
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
Class 3 AARDs
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
Class 4 AARDs
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
Cardiac glycosides
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
Treatment of bradyarrhythmias
muscarinic antagonists; methylxanthines, beta agonists
81
Muscarinic antagonists (bradyarrhythmia tx)
antagonism of muscarinic ACh receptors--\> positive chronotropes
82
Methylxanthines
mild pde inhibition- not specifc to III or V enhanced sympathetic drive--\> mild positive inotropic and chronotropic effects
83
beta agonists
stimulation of beta adrenergic receptors

Pharmacology (12 decks)

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