Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Drugs > Final Review List > Flashcards

Final Review List Flashcards

1
Q

Aspirin Drug Class

A

NSAID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Aspirin mechanisms of action

A

NSAIDs inhibit COX -> reduced levels of prostaglandin E2 which plays important roles in both peripheral and central sensitization.

COX-1 inhibitor -> reduced synthesis prostaglandins and thromboxanes (TXA2) - platelets can’t create new COX so aspiring can irreversibly effect platlet aggregation - can modify COX-2 to produce asprin-triggered lipotoxin with lipoxygenase which has gastric mucosal protective actions so increased use -> decreased damage overtime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

altipamezol drug class

A

alpha2-adrenergic antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

atipamezol mechanism of action

A

-alpha2-adrenergic antagonist - competitively inhibits alpha2-adrenergic receptors (normally alpha-2 adrenergic receptors inhibit release norepinephrine by up regulating negative feedback loop decreasing release norepinephrine -> sedation an alpha2-adrenergic antagonist inhibits the alpha2-adrenergic receptor inhibiting the inhibition of norepinephrine release -> reversal of sedation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Carprofen drug class

A

NSAID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

carprofen mechanism of action

A

NSAIDs inhibit COX -> reduced levels of prostaglandin E2 which plays important roles in both peripheral and central sensitization.

inhibition of cyclooxyrgenase, phospholipase A2, and inhibition of prostaglandin synthesis - somewhat COX-1 sparing in dogs -> fewer COX-1 effects - COX-2 specificity depends on species, dose, tissue - not as COX-2 specific in horses and cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

deracoxib drug class

A

NSAID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

deracoxib mechanism of action

A

NSAIDs inhibit COX -> reduced levels of prostaglandin E2 which plays important roles in both peripheral and central sensitization.

  • COXIB class NSAID - predominantly inhibits COX-2 and spare COX-1 (theoretically inhibiting prostaglandins that -> plain and inflammation and sparing those maintaining normal GI and renal fx but not necessarily the case)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diazepam drug class

A

benzodiazepine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diazepam mechanism of action

A
  • enhance inhibitory actions of GABA - interact with specific site on GABAa receptor chloride channel complex that is associated with receptors that contain gama2subunit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Lidocaine drug class

A

Local Anestetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Lidocaine mechanism of action

A

From notes: - Na+ channel blockage sensory afferents and vasculature - have to be inside axon membrane to work; must be uncharged when crossing membrane then have nitrogen in amine protonated once inside axonal membrane and bond to Na+ channel and block it - major effect on axonal conduction of action potential - use dependent blockage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mepivacane drug class

A

Local aneshetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Mepivacane mechanism of action

A
  • Na+ channel blockage sensory afferents and vasculature - have to be inside axon membrane to work; must be uncharged when crossing membrane then have nitrogen in amine protonated once inside axonal membrane and bond to Na+ channel and block it - major effect on axonal conduction of action potential - use dependent blockage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

procaine drug class

A

local anesthetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

procaine mechanism of action

A
  • Na+ channel blockage sensory afferents and vasculature - have to be inside axon membrane to work; must be uncharged when crossing membrane then have nitrogen in amine protonated once inside axonal membrane and bond to Na+ channel and block it - major effect on axonal conduction of action potential - use dependent blockage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

tetracaine drug class

A

local anestetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

tetracaine mechanism of action

A
  • Na+ channel blockage sensory afferents and vasculature - have to be inside axon membrane to work; must be uncharged when crossing membrane then have nitrogen in amine protonated once inside axonal membrane and bond to Na+ channel and block it - major effect on axonal conduction of action potential - use dependent blockage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

edrophonium drug class

A

cholinesterase inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

edrophonium mechanism of action

A

anticholinesterase agent (aka indirectly acting agonist of acetylcholine) - combines with cholinesterases primarily at catalytic binding site forming rapidly reversible enzyme-inhibitor complex - inhibit AChE -> have more ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Meloxicam drug class

A

NSAID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Meloxicam mechanism of action

A

NSAIDs inhibit COX -> reduced levels of prostaglandin E2 which plays important roles in both peripheral and central sensitization.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

robenacoxib drug class

A

NSAID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

robenacoxib mechanism of action

A

NSAIDs inhibit COX -> reduced levels of prostaglandin E2 which plays important roles in both peripheral and central sensitization.

COX-2 specific inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

grapiprant drug class

A

NSAID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

grapiprant mechanism of action

A

non-cox inhibiting blocks EP4 receptor that is primary mediator OA pain and inflamation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Acetylcholine drug class

A

cholinergic neurotransmitter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Acetylcholine mechanism of action

A

cholinergic neurotransmitter, rarely used as a drug because effects too generalized - prototypic cholinergic agonist - in periphery cholinergic transmission occurs both with autonomic and somatic NS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

atracurium drug class

A

muscle nicotinic antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

atracurium mechanism of action

A

Acetylcholine receptor non depolarizing blockers (competitive antagonist that binds to acetylcholine receptor but does not create response)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

bethanechol drug class

A

muscarinic agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

bethanechol mechanism of action

A

-direct acting muscarinic agonist (produce only muscarinic effects so parasympathomimetic) - mostly effects GI and bladder - Choline ester

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

dantrolene drug class

A

ryanodine recetpor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

dantrolene mechanism of action

A

decreases amount of calcium released into cytoplasm from sarcoplasmic reticulum by interacting with ryanodine receptor in muscle (ryanodine is involved in Ca2+ release -> muscle contraction) this blocks ryanodine receptor and therefore Ca2+ release and ultimately decreases muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

dexmedetomidine drug class

A

sedative, alpha-2 adrenergic agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

dexmedetomidine mechanism of action

A

inhibits neuronal firing in brain and spinal cord by diminishing release of norepinephrine from presynaptic neuro terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

gabapentin drug class

A

analgesic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

gabapentin mechanism of action

A
  • structural analogue of GABA - binds axillary subunit (a2S-1) of voltage-gated Ca2+ channels inhibiting Ca2+ channels -> decreased NT release

(inhibiting nerve injury-induced trafficking of Ca2+ channels at pre-syn terminals DRG neurons (inhibit Ca2+ channels -> decrease NT release)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

ketamine drug class

A

glutamate receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

ketamine mechanism of action

A

NMDA receptor antagonist (activate glutamate synapses more likely to be inhibited by dissociate anesthetics bc NMDA-type glutamate receptors in pain pathways that are stimulated more likely to be blocked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

morphine drug class

A

opiod

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

morphine mechanism of action

A
  • activate opioid receptor -> -inhibition voltage-sensitive Ca2+ channels in presynaptic neuron -> less NT released - activation inwardly rectifying K+ channels (GIRKs) in post synaptic neuron -> membrane hyperpolarization - modulation cAMP-gated K+ channels These activities attenuate neuronal excitability and reduce neurotransmitter release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

pancuronium drug class

A

muscle nicotinic antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

pancuronium mechanism of action

A

-non depolarizing acetylcholine receptor blocker - binds to acetylcholine receptor, does not produce a response - ammonio steroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

phenobarbital drug class

A

barbiturate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

phenobarbital mechanism of action

A

allosteric agonist that binds GABAa receptor, works at allosteric site called barbiturate site and increases Cl- influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

pyridostigmine drug class

A

cholinesterase inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

pyridostigmine mechanism of action

A

-indirectly acting agonist (cholinesterase inhibitor ie anticholinesterase) - carbamylating ester, reversibly inhibits AchE for a few hours via covalent modification (carbamylation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

succinylcholine drug class

A

depolarizing nicotinic blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

succinylcholine mechanism of action

A

acetylcholine receptor depolarizing blocker; binds to acetylcholine receptor and produces response (depolarizaiton) but rapidly desensitizes the receptor this temporarily blocks further activation of receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

thiobarbital drug class

A

barbituate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

thiobarbital mechanism of action

A

allosteric modulator of GABAa receptor - acts at allosteric barbiturate site and directly at neurotransmitter receptor site as direct agonist - decreases responsiveness of membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

tramadol drug class

A

opiod

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

tramadol mechanism of action

A
  • synthetic analgesic - functions as agonist for MOP (and probably KOP) - inhibits serotonin and norepinephrine reuptake - mainly works on CNS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

atropine drug class

A

muscarinic antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

atropine mechanism of action

A

-inhibits acetylcholine and other cholinergic stimulants at postganglionic parasympathetic neuroeffector sites - high dose can block nicotinic receptors at autonomic ganglia and NMJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Pralidoxime (2-PAM) drug class

A

OP reversal agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Pralidoxime (2-PAM) mechanism of action

A

Removes phosphate from serine to reactivate cholinesterase (In OP poisoning phosphate binds to serine -> permanent inactivation of enzyme unless 2-PAM reverses this because next step is loss of alkyl group and then v hard to reverse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Flunixin meglumine Drug class

A

NSAID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

flunixin meglumine mechanism of action

A

NSAIDs inhibit COX -> reduced levels of prostaglandin E2 which plays important roles in both peripheral and central sensitization.

potent COX inhibitor (NSAID)

61
Q

aminocaproic acid drug class

A

inhibits fibrinolysis

62
Q

aminocaproic acid mechanism of action

A

inhibits fibrionolysis via inhibitory effects on plasminogen activator substances via some antiplasmin action

63
Q

xylazine drug class

A

alpha-2 adrenergic agonist

64
Q

xylazine mechanism of action

A

alpha-2 adrenergic agonist; binds alpha-2 receptor leads to decreased release norephinephrine (b/c receptor -> negative feedback -> inhibition of norepinephrine relrease)

Also binds alpha2 adrenergic receptor in CTZ stimulateing them -> relays info to emetic center ->stimulation V+

  • causes sedation and CNS depression - can also have alpha-1 agonist activity, less selective for alpha-2 receptors than dexmidetomidine
65
Q

warfarin drug class

A

vit k antagonist

66
Q

warfarin mechanism of action

A

inhibits vit k epoxide reductase which = necessary for recycling fit k to active form in vit k epoxide cycle - vit k = essential cofactor in carboxylation of y-glutamic acid (GLA-) residues of amino terminal domains of factors II, VII, IX, X - carboxylation GLA- residues= what lets coagulation factors bind Ca2+ which = required to bind phosphatydil serine on platlet surface

67
Q

heparin drug class

A

anticoagulant

68
Q

heparin mechanism of action

A

inhibits secondary hemostasis by promoting action of antithrombin which is an inhibitor of many coagulation factors especially FXa and thrombin

Ignore rest of this card

inhibits clotting by potentiating action of antithrombin - binds to antithrombin and activates it -> inactivation of thrombin, factor II, factor X, factor IX, factor XI, factor XII - at low concentrations heparin combined with anthrombin III inactivate factor Xa and prevent conversion prothrombin to thrombin - in higher doses it inactivates thrombin and blocks conversion of fibrinogen ot fibrin and when combined with antithrombin III inactivates IX, X, XI, XII - by inhibiting activation of factor XIII it prevents formation of stable fibrin clots - does not lyse clots but can prevent growth of existing clots

69
Q

EDTA drug class

A

lead chealator

70
Q

EDTA mechanism of action

A

chelator of Ca2+ which arrests coagulation because Ca2+ is what allows factors to bind phosphatydyl serine on platelets

71
Q

amantadine drug class

A

antiviral drug/ dopamine receptor agonist

72
Q

amantadie mechanism of action

A

inhibits post-synaptically localized NMDA receptors that play central roles in pain sensitization

antiviral activity = bc interferes with replication by interfering with influenza A virus M2 protein

73
Q

clopidogrel drug class

A

ADP receptor antagonist

74
Q

clopidogrel mechanism of action

A

antiplatlet drug that blocks platlet ADP receptor which prevents ADP from activating platelets

75
Q

aluminum hydroxide drug class

A

phosphate binder

76
Q

aluminum hydroxide mechanism of action

A

-aluminum salts reduce amount of phosphate absorbed from intestine by physically binding to dietary phosphate extra: as antacid hydroxyl ions interact with hydrogen ions in gut

77
Q

epoetin alpha drug class

A

erythropoietin receptor agonist

78
Q

epoetin alpha mechanism of action

A

-Erythropoietin = naturally occurring substance produced in kindey = hormone that regulates erythropoiesis - stimulates erythrocyte production by stimulating differentiation and proliferation of committed red cell precursors -EPO also stimulates release of reticulocytes - recombinant Human EPO alpha serves as substitute or endogenous EPO

79
Q

Telmisartan drug class

A

angiotensin II receptor blocker

80
Q

Telmisartan mechanism of action

A

Selectively blocks angiotensin-II AT1-receptor -> reduction in synthesis and secretion of aldosterone -> vasodilation and decreased K+ and increased Na+ excretion

81
Q

Tumil-k drug class

A

K+ supplement

82
Q

Tumil-k mechanism of action

A
  • K+ = principle intracellular cation in body - essenital for maintaining cellular tonicity, nerve impulse transmission; smooth, skeletal, and cardiac muscle contraction, and maintenance of normal renal fx - giving supplementation just helps provide adequate K+ in cases of or cases where worried about K+ deficits
83
Q

Maropitant drug class

A

NK1 receptor antagonist

84
Q

Maropitant mechanism of action

A

-NK1 receptor antagonist that acts in CNS by inhibiting substance P = key neurotransmitter involved in V+

85
Q

famotidine drug class

A

H2-histamine receptor antagonist

86
Q

famotidine mechanism of action

A
  • Competitive antagonist of H2 receptors that inhibit gastric acid secretion so inhibits basal and food stimulated acid secretion and promote healing of gastric and duodenal ulcers
  • Normally histamine released by ECL cells b/c gastrin or acetylcholine and histamine directly stimulates acid secretion by binding H2 receptors on parietal cells
  • by decreasing amount of gastric juice produced H2-blockers reduce amount of pepsin secreted
87
Q

Furosemide drug class

A

Diuretic

88
Q

Furosemide mechanism of action

A

Loop diuretic - main location of action is thick ascending limb of loop of Henle - Block Na+-K+-2Cl transporter in luminal membrane of loop of Henle preventing reabsorption of Na+ from tubular lumen -> decrease Na+ in medullary interstitial -> decreased osmolary gradient -> decreased urine concentration -> decreased H2O retention -> decreased blood volume -> decreased blood pressure

89
Q

enalapril drug class

A

ACE inhibitior

90
Q

enalapril mechanism of action

A
  • converted by liver to active compound enalprilat which competes with angiotensin I for ACE (angiotensin converting enzyme) (ACE has higher affinity for Enalaprilat than angiotensin I) -> prevents formation angiotensin-II which is a vasoconstrictor - decreased angiotensin-II [] -> decreased aldosterone secretion and plasma renin activity increased - decreases total peripheral resistance, pulmonary vascular resistance, mean arterial and R atrial pressures, and pulmonary capillary wedge pressure - increase renal blood flow and decrease glomerular efferent arteriole resistance
91
Q

Diltiazem Drug class

A

Ca2+ channel blocker

92
Q

Diltiazem Mechanism of Action

A

binds to L-type Ca2+ channels preventing Ca2+ entry into cell -> inhibit cardiac and vascular smooth muscle contractility dilating main systemic and coronary artieries; TPR, BP, cardiac afterload all = reduced - Slows AV node conduction and prolongs refractory time

93
Q

Pimobendan drug class

A

inodilator

94
Q

pimobendan mechanism of action

A
  • inhibition of phosphodiesterase III (PDE III) -> increased inotropy and arteriodilation - increases intracellular Ca2+ sensitivity on troponin C making -> enhancement cardiac contractility w/o inc in myocardial O2 consumption bc does not increase intracellular Ca2+ levels (Ca2+ sensitization -> increased ionotrophy)
95
Q

spironolactone drug class

A

Mineralocorticoid antagonist

96
Q

spironolactone mechanism of action

A

Overall effect is decrease aldosterone induced production of Na+/K+ channels that get put into the DCT which in turn dec Na+ reabosprotion and K+ excretion

competitively binds mineralocorticoid receptor -> release heat shock protein 90 -> inhibits production of aldosterone-induced proteins and blocks effects of aldosterone ie -> dec Na+ uptake b/c aldosterone normally increases synthesis of lumina Na+ channels and increases K+ channels increasing K+ secretion driving force secondary to Na+ secretion so if inhibit aldosterone inhibit the luminal Na+ channels and in turn inhibit that secondary K+ secretion ** At low doses does not have diuretic effects**

97
Q

albuterol drug class

A

beta 2 adrenergic agonist

98
Q

albuterol mechanism of action

A

stimulates production of cAMP by activation of adenyl cyclase via Gs -> relaxation bronchial, uterine, and vascular smooth muscle; beta 2 adrenergic agonist

99
Q

epinephrine drug class

A

hormone and adrenergic agonist

100
Q

epinephrine mechanism of action

A

endogenous adrenergic agent w/ alpha and beta activity -> - relaxation smooth muscle in bonchi and iris - antagonizes effects histamine - inc glycogenolysis - raise blood sugar - give rapidly IV -> inc systolic BP - give slow IV -> modest rise systolic pressure and dec diastolic pressure - dec TPR bc beta effects

101
Q

isoproterenol drug class

A

beta adrenergic agonist

102
Q

isoproterenol mechanism of aciton

A

B1 and B2 adrenergic agonist; isoproterenol stimulates B-adrenergic receptors of intracellular adenyl cyclase which catalyzes conversion of adenosine triphosphate to cAMP -> inc cAMP levels-> -inc inotropism and chronotropism, - relax bronchial smooth muscle - peripheral vasodilation - +/- inc perfusion to skeletal muscle

103
Q

norepinephrine drug class

A

neurotransmitter and adrenergic agonist

104
Q

norepinephrine mechanism of action

A
  • directly stimulates adrenergic receptors strong affinity for alpha than beta receptors (GPCRs) - also some B1 activity - acts as peripheral vasoconstrictor (a) and inotropic cardiostimulant and coronary artery dilator (b) -> TPR inc -> inc BP - high doses can -> decreased perfusion to vital organs, skin, and skeletal muscle
105
Q

phenylephrine drug class

A

alpha adrenergic agonist

106
Q

phenylephrine mechanism of action

A
  • a1 seletive - predominantly post-synaptic alpha-adrenergic effects at therapeutic doses Act through Gq which activates PLC -> formation IP3 and DAG -> increased cytosolic Ca2+ -> contraction -> - vasoconstriction -> inc in diastolic and systolic BP - small dec in cardiac output - increase in circulation time
107
Q

prazosin drug class

A

alpha adrenergic antagonist

108
Q

prazosin mechanism of action

A

competitive inhibition of a1-adrenergic receptors -> no stim PLC via Gq so no formation IP3 and DAG so no increase in cytosolic Ca2+ so no contraction -> decrease BP and peripheral vascular resistance; has dilatory effects on arterial and venous side also decreases RA pressure; CO increased in patients with CHF

109
Q

propranolol drug class

A

beta adrenergic antagonist

110
Q

propranolol mechanism of action

A

blocks B1 and B2 receptors in myocardium, bronchi, and vascular smooth m muscle - B1 block -> dec HR dec force contraction and dec AV nodal conduction velocity and dec renin secretion - B2 block -> constriction smooth muscle (vascular, bronchial ect.)

111
Q

metoprolol drug class

A

beta 1 adrenergic antagonist

112
Q

metoprolol mechanism of action

A

B1 adrenergic antagonist can block B2 at high dose - negative inotropic and chronotropic actions

113
Q

atropine drug class

A

muscarinic antagonist

114
Q

atropine mechanism of action

A

-inhibits acetylcholine and other cholinergic stimulants at postganglionic parasympathetic neuroeffector sites - high dose can block nicotinic receptors at autonomic ganglia and NMJ

115
Q

Theophyline drug class

A

methylxanthine

116
Q

theophylline mechanism of action

A

not fully understood; possiblities:

  • inhibit PDE which breaks down cAMP so when inhibit it
  • > incrased cAMP -> stimulation of PKA which phosphorylates targets -> relaxes smooth muscle; overall potentiates effect of B2 agonists -> enhanced bronchodilation
  • adenosine receptor antagonist (adenosine -> release histamine and leukotrienes from mast cells -> bronchoconstriction and therefore inhibits adenosine -> bronchodilation
  • antiinflamatory effects on cells in airway
117
Q

dexamethasone drug class

A

corticosteroid

118
Q

dexamethasone mechanism of action

A
  • prevents transricption of genes of various inflamatory proteins (by inhibition of phospholipase A2 which converts phospholipids to arachadonic acid) this prevents transrciption of cytokines
  • stimulates production of anti-inflamatory proteins which interact with inflamatory cells and structural cells in airways
  • b/c effect transrcption effects are not immeduate usually take a few days to develop fully (full effect on bronchial hyper-responsiveness can require weeks or months of therpay)
119
Q

albuterol drug class

A

beta 2 adrenergic agonist

120
Q

albuterol mechanism of action

A

stimulates production of cAMP by activation of adenyl cyclase via Gs -> relaxation bronchial, uterine, and vascular smooth muscle; beta 2 adrenergic agonist

Stim B2 receptor -> stim Gs -> Adenyl cyclase stimulated

  • > ATP converted to cAMP -> stim PKA -> phosphorylated target proteins ->
  • increase Ca2+-activated K+ channel activation
  • decrease PLC-IP3-Ca2+ pathway activity
  • increase Na+/Ca2+ exchange
  • incrase Na+/Ca2+ ATPase
  • decrease MLCK
  • > smooth muscle
121
Q

epinephrine drug class

A

hormone and adrenergic agonist

122
Q

epinephrine mechanism of action

A

endogenous adrenergic agent w/ alpha and beta activity -> - relaxation smooth muscle in bonchi and iris - antagonizes effects histamine - inc glycogenolysis - raise blood sugar - give rapidly IV -> inc systolic BP - give slow IV -> modest rise systolic pressure and dec diastolic pressure - dec TPR bc beta effects

123
Q

atropine drug class

A

muscarinic antagonist

124
Q

atropine mechanism of action

A

-inhibits acetylcholine and other cholinergic stimulants at postganglionic parasympathetic neuroeffector sites - high dose can block nicotinic receptors at autonomic ganglia and NMJ

Ach binds M3 -> stimulation Gq -> activate phospholipase C -> produce IP3 -> intracellular Ca2+ -> smooth muscle contraction

125
Q

Apomorphine drug class

A

D-2 Dopamine receptor agonist

126
Q

Apomorphine mechanism of action

A

stimulates D2 dopamine receptors in CTZ -> relays info to emetic center ->stimulation V+ - will have depressant effect on emetic center so don’t give multiple doses if first doesn’t work

127
Q

bismuth subsalicylate drug class

A

(aka pepto bismol) Drug class: None Given

128
Q

bismuth subsalicylate mechanism of action

A

bismuth: adsorbs bacterial enterotoxins and endotoxins and has GI protective effect salicylate: has anti prostaglandin and anti secretory activity in intestine

129
Q

butorphanol drug class

A

(Aka torbugesic) Drug Class: Synthetic Opiod agonist-antagonist analgesic

130
Q

cimetidine drug class

A

H2-histamine receptor antagonist

131
Q

cimetidine mechanism of action

A

-Competitive antagonist of H2 receptors that inhibit gastric acid secretion so inhibits basal and food stimulated acid secretion and promote healing of gastric and duodenal ulcers - Normally histamine released by ECL cells b/c gastrin or acetylcholine and histamine directly stimulates acid secretion by binding H2 receptors on parietal cells - by decreasing amount of gastric juice produced H2-blockers reduce amount of pepsin secreted

132
Q

lactulose drug class

A

synthetic sugar

133
Q

lactulose mechanism of action

A

synthetic disaccharide metabolized by bacteria in LI producing acetic, lactic, and formic acids which have osmotic effect drawing fluid into intestine by osmosis -> increase fluid content of feces -> intestinal distention and promotion of peristalsis

134
Q

loperamide drug class

A

(aka as immodium) opiod

135
Q

loperamide mechanism of action

A

synthetic opiate specifically targets GI tract w/o causing other effects act on mu and delta receptors decreasing propulsive intestinal contractions increasing segmentation and increase GI sphincter tone; stimulate absorption of fluids, electrolytes, and glucose

136
Q

metaclopramide drug class

A

D-2 dopamine receptor antagonist

137
Q

metaclopramide mechanism of action

A

inhibits D2 dopamine receptors in CTZ which normally-> relays info of stimulation to emetic center ->stimulation V+ so inhibit them inhibit V+

138
Q

butorphanol mechanism of action

A

competitive mu receptor antagonist, exerts analgesic effects by acting as agonist at kappa receptor

139
Q

midazolam drug class

A

short acting hypnotic-sedative benzodiazepine drug with anxiolytic and amnestic properties

140
Q

midazolam mechanism of action

A

bind and activate benzodiazepine receptor bidding site on game subunit of GABAa -> increase frequency of opening of Cl- ion channels -> decreased GABA required to open channels and hyperpolarization of postsynaptic neuron and decreased neuronal transmission -> CNS depression Also possible mechanisms: - antagonism of serotonin - diminished release or turnover of acetylcholine in CNS

141
Q

omeprazole drug class

A

proton pump inhibitor

142
Q

omeprazole mechanism of action

A

-prodrug activated in acid environment - gains access to parietal cell via systemic circulation -> accumulates in acidic canaliculi as weak base -> protein-catalyzed conversion to sulfenamide -> drug activation and prevents diffusion of drug across canalicular membrane -> activated drug binds H+-K+-ATPase irreversibly inactivating it (acid secretion will return to normal after new pump proteins are synthesized and inserted into luminal membrane) Role of parietal cell proton pump in molecular mechanism of acid secretion: - pump uses ATP hydrolysis to drive extrusion of H+ into lumen of gastric gland in exchange for K+; K+ recycled into lumen through symporter that caciltations secretion of Cl- into gastric lumen -> net increase HCl and increase of parietal cell pH -> passive uptake H2O and CO2 which = converted to HCO3- and H+ by carbonic anhydrase -> HCO3- leaves cell via CL- HCO3- exchanger in basalt membrane which replensihes intracell Cl- -> fuels net movement HCl (gastric acid) onto apical membrane

143
Q

PEG 3350 drug class

A

(aka miralax) Drug Class: Osmotic laxative

144
Q

PEG 3350 mechanism of action

A

Large molecular weight water-soluble polymer that forms hydrogen bonds with 100 molecules of H2O per molecule -> high osmotic pressures and preventing absorption of H2O out of lumen

145
Q

Propofol drug class

A

ultra-short acting parenteral anesthetic in the US

146
Q

Propofol mechanism of action

A

not well understood: - decreases rate of GABA dissociation from receptors -> increase opening of chloride channels -> hyperpolarization of postsynaptic cell membranes and inhibition of postsynatpci neurons -> hypnosis and amnesia

147
Q

sucralfate drug class

A

mucosal protectant

148
Q

sucralfate mechanism of action

A

Undergoes extensies cross-linking in acidic environment (pH <4) -> forms sticky polymer that adheres to epithelial cells and ulcer craters -> promotes ulcer healing and limits proton diffusion - also cytoprotective effects (local production prostaglandins and epidermal growth factor)

+ inhibits pepsin-mediated hydrolysis of mucosal proteins

Drugs (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions