Final Review List Flashcards
Aspirin Drug Class
NSAID
Aspirin mechanisms of action
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
altipamezol drug class
alpha2-adrenergic antagonist
atipamezol mechanism of action
-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
Carprofen drug class
NSAID
carprofen mechanism of action
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
deracoxib drug class
NSAID
deracoxib mechanism of action
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)
Diazepam drug class
benzodiazepine
Diazepam mechanism of action
- enhance inhibitory actions of GABA - interact with specific site on GABAa receptor chloride channel complex that is associated with receptors that contain gama2subunit
Lidocaine drug class
Local Anestetic
Lidocaine mechanism of action
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
Mepivacane drug class
Local aneshetic
Mepivacane mechanism of action
- 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
procaine drug class
local anesthetic
procaine mechanism of action
- 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
tetracaine drug class
local anestetics
tetracaine mechanism of action
- 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
edrophonium drug class
cholinesterase inhibitor
edrophonium mechanism of action
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
Meloxicam drug class
NSAID
Meloxicam mechanism of action
NSAIDs inhibit COX -> reduced levels of prostaglandin E2 which plays important roles in both peripheral and central sensitization.
robenacoxib drug class
NSAID
robenacoxib mechanism of action
NSAIDs inhibit COX -> reduced levels of prostaglandin E2 which plays important roles in both peripheral and central sensitization.
COX-2 specific inhibitor
grapiprant drug class
NSAID
grapiprant mechanism of action
non-cox inhibiting blocks EP4 receptor that is primary mediator OA pain and inflamation
Acetylcholine drug class
cholinergic neurotransmitter
Acetylcholine mechanism of action
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
atracurium drug class
muscle nicotinic antagonist
atracurium mechanism of action
Acetylcholine receptor non depolarizing blockers (competitive antagonist that binds to acetylcholine receptor but does not create response)
bethanechol drug class
muscarinic agonist
bethanechol mechanism of action
-direct acting muscarinic agonist (produce only muscarinic effects so parasympathomimetic) - mostly effects GI and bladder - Choline ester
dantrolene drug class
ryanodine recetpor antagonist
dantrolene mechanism of action
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
dexmedetomidine drug class
sedative, alpha-2 adrenergic agonist
dexmedetomidine mechanism of action
inhibits neuronal firing in brain and spinal cord by diminishing release of norepinephrine from presynaptic neuro terminal
gabapentin drug class
analgesic
gabapentin mechanism of action
- 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)
ketamine drug class
glutamate receptor antagonist
ketamine mechanism of action
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
morphine drug class
opiod
morphine mechanism of action
- 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
pancuronium drug class
muscle nicotinic antagonist
pancuronium mechanism of action
-non depolarizing acetylcholine receptor blocker - binds to acetylcholine receptor, does not produce a response - ammonio steroid
phenobarbital drug class
barbiturate
phenobarbital mechanism of action
allosteric agonist that binds GABAa receptor, works at allosteric site called barbiturate site and increases Cl- influx
pyridostigmine drug class
cholinesterase inhibitor
pyridostigmine mechanism of action
-indirectly acting agonist (cholinesterase inhibitor ie anticholinesterase) - carbamylating ester, reversibly inhibits AchE for a few hours via covalent modification (carbamylation)
succinylcholine drug class
depolarizing nicotinic blocker
succinylcholine mechanism of action
acetylcholine receptor depolarizing blocker; binds to acetylcholine receptor and produces response (depolarizaiton) but rapidly desensitizes the receptor this temporarily blocks further activation of receptor
thiobarbital drug class
barbituate
thiobarbital mechanism of action
allosteric modulator of GABAa receptor - acts at allosteric barbiturate site and directly at neurotransmitter receptor site as direct agonist - decreases responsiveness of membrane
tramadol drug class
opiod
tramadol mechanism of action
- synthetic analgesic - functions as agonist for MOP (and probably KOP) - inhibits serotonin and norepinephrine reuptake - mainly works on CNS
atropine drug class
muscarinic antagonist
atropine mechanism of action
-inhibits acetylcholine and other cholinergic stimulants at postganglionic parasympathetic neuroeffector sites - high dose can block nicotinic receptors at autonomic ganglia and NMJ
Pralidoxime (2-PAM) drug class
OP reversal agent
Pralidoxime (2-PAM) mechanism of action
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)
Flunixin meglumine Drug class
NSAID
flunixin meglumine mechanism of action
NSAIDs inhibit COX -> reduced levels of prostaglandin E2 which plays important roles in both peripheral and central sensitization.
potent COX inhibitor (NSAID)
aminocaproic acid drug class
inhibits fibrinolysis
aminocaproic acid mechanism of action
inhibits fibrionolysis via inhibitory effects on plasminogen activator substances via some antiplasmin action
xylazine drug class
alpha-2 adrenergic agonist
xylazine mechanism of action
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
warfarin drug class
vit k antagonist
warfarin mechanism of action
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
heparin drug class
anticoagulant
heparin mechanism of action
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
EDTA drug class
lead chealator
EDTA mechanism of action
chelator of Ca2+ which arrests coagulation because Ca2+ is what allows factors to bind phosphatydyl serine on platelets
amantadine drug class
antiviral drug/ dopamine receptor agonist
amantadie mechanism of action
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
clopidogrel drug class
ADP receptor antagonist
clopidogrel mechanism of action
antiplatlet drug that blocks platlet ADP receptor which prevents ADP from activating platelets
aluminum hydroxide drug class
phosphate binder
aluminum hydroxide mechanism of action
-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
epoetin alpha drug class
erythropoietin receptor agonist
epoetin alpha mechanism of action
-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
Telmisartan drug class
angiotensin II receptor blocker
Telmisartan mechanism of action
Selectively blocks angiotensin-II AT1-receptor -> reduction in synthesis and secretion of aldosterone -> vasodilation and decreased K+ and increased Na+ excretion
Tumil-k drug class
K+ supplement
Tumil-k mechanism of action
- 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
Maropitant drug class
NK1 receptor antagonist
Maropitant mechanism of action
-NK1 receptor antagonist that acts in CNS by inhibiting substance P = key neurotransmitter involved in V+
famotidine drug class
H2-histamine receptor antagonist
famotidine mechanism of action
- 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
Furosemide drug class
Diuretic
Furosemide mechanism of action
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
enalapril drug class
ACE inhibitior
enalapril mechanism of action
- 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
Diltiazem Drug class
Ca2+ channel blocker
Diltiazem Mechanism of Action
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
Pimobendan drug class
inodilator
pimobendan mechanism of action
- 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)
spironolactone drug class
Mineralocorticoid antagonist
spironolactone mechanism of action
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**
albuterol drug class
beta 2 adrenergic agonist
albuterol mechanism of action
stimulates production of cAMP by activation of adenyl cyclase via Gs -> relaxation bronchial, uterine, and vascular smooth muscle; beta 2 adrenergic agonist
epinephrine drug class
hormone and adrenergic agonist
epinephrine mechanism of action
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
isoproterenol drug class
beta adrenergic agonist
isoproterenol mechanism of aciton
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
norepinephrine drug class
neurotransmitter and adrenergic agonist
norepinephrine mechanism of action
- 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
phenylephrine drug class
alpha adrenergic agonist
phenylephrine mechanism of action
- 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
prazosin drug class
alpha adrenergic antagonist
prazosin mechanism of action
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
propranolol drug class
beta adrenergic antagonist
propranolol mechanism of action
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.)
metoprolol drug class
beta 1 adrenergic antagonist
metoprolol mechanism of action
B1 adrenergic antagonist can block B2 at high dose - negative inotropic and chronotropic actions
atropine drug class
muscarinic antagonist
atropine mechanism of action
-inhibits acetylcholine and other cholinergic stimulants at postganglionic parasympathetic neuroeffector sites - high dose can block nicotinic receptors at autonomic ganglia and NMJ
Theophyline drug class
methylxanthine
theophylline mechanism of action
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
dexamethasone drug class
corticosteroid
dexamethasone mechanism of action
- 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)
albuterol drug class
beta 2 adrenergic agonist
albuterol mechanism of action
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
epinephrine drug class
hormone and adrenergic agonist
epinephrine mechanism of action
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
atropine drug class
muscarinic antagonist
atropine mechanism of action
-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
Apomorphine drug class
D-2 Dopamine receptor agonist
Apomorphine mechanism of action
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
bismuth subsalicylate drug class
(aka pepto bismol) Drug class: None Given
bismuth subsalicylate mechanism of action
bismuth: adsorbs bacterial enterotoxins and endotoxins and has GI protective effect salicylate: has anti prostaglandin and anti secretory activity in intestine
butorphanol drug class
(Aka torbugesic) Drug Class: Synthetic Opiod agonist-antagonist analgesic
cimetidine drug class
H2-histamine receptor antagonist
cimetidine mechanism of action
-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
lactulose drug class
synthetic sugar
lactulose mechanism of action
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
loperamide drug class
(aka as immodium) opiod
loperamide mechanism of action
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
metaclopramide drug class
D-2 dopamine receptor antagonist
metaclopramide mechanism of action
inhibits D2 dopamine receptors in CTZ which normally-> relays info of stimulation to emetic center ->stimulation V+ so inhibit them inhibit V+
butorphanol mechanism of action
competitive mu receptor antagonist, exerts analgesic effects by acting as agonist at kappa receptor
midazolam drug class
short acting hypnotic-sedative benzodiazepine drug with anxiolytic and amnestic properties
midazolam mechanism of action
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
omeprazole drug class
proton pump inhibitor
omeprazole mechanism of action
-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
PEG 3350 drug class
(aka miralax) Drug Class: Osmotic laxative
PEG 3350 mechanism of action
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
Propofol drug class
ultra-short acting parenteral anesthetic in the US
Propofol mechanism of action
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
sucralfate drug class
mucosal protectant
sucralfate mechanism of action
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
