Term
|
Definition
-non sulfonamide loop diuretic (high ceiling)
-used when patient w/sulfonamide allergy
-loop diuretic-high ceiling
-"semide" oral and IV
-secreted with PSOASS-->ascending loop of henle
-inhibition of NA/2CL/K cotransport
-increase urine volume,broncho/vaso dilation,smooth muscle relaxation,uric acid,glucose,TG,
-decrease renal 02 consumption,CSF production,CA,K,Mg,Ca,Cl,HDL,acid
-GFR and RPF unchanged-save on renal
-Ototoxicity-cochlear>vestibular
-IV use for glaucoma/IOP, ICP, pulmonary edema, ARF
-Oral use- decrease BP, Cardiac and Renal insufficiency |
|
|
Term
|
Definition
-"the" loop diuretic-high ceiling
-"semide" oral and IV
-secreted with PSOASS-->ascending loop of henle
-inhibition of NA/2CL/K cotransport
-increase urine volume,broncho/vaso dilation,smooth muscle relaxation,uric acid,glucose,TG,
-decrease renal 02 consumption,CSF production,CA,K,Mg,Ca,Cl,HDL,acid
-GFR and RPF unchanged-save on renal
-Ototoxicity-cochlear>vestibular
-IV use for glaucoma/IOP, ICP, pulmonary edema, ARF
-Oral use- decrease BP, Cardiac and Renal insufficiency |
|
|
Term
|
Definition
-Probenecide sensitive organic anion secretory system-PSOASS
-used to block receptor and keep penicillin in system
-transporter also competitive with uric acid |
|
|
Term
|
Definition
-coclhlear>vestibular
-caused by NSAIDS, Loops, Mycin (antibiotics), quinine, cisplatin (chemo)
-CAVE-combo chemo treatment-aminoglycoside (mycin) and cisplatin |
|
|
Term
|
Definition
-loop diuretic-high ceiling
-"semide" oral and IV
-secreted with PSOASS-->ascending loop of henle
-inhibition of NA/2CL/K cotransport
-increase urine volume,broncho/vaso dilation,smooth muscle relaxation,uric acid,glucose,TG,
-decrease renal 02 consumption,CSF production,CA,K,Mg,Ca,Cl,HDL,acid
-GFR and RPF unchanged-save on renal
-Ototoxicity-cochlear>vestibular
-IV use for glaucoma/IOP, ICP, pulmonary edema, ARF
-Oral use- decrease BP, Cardiac and Renal insufficiency |
|
|
Term
|
Definition
-loop diuretic-high ceiling
-"semide" oral and IV
-secreted with PSOASS-->ascending loop of henle
-inhibition of NA/2CL/K cotransport
-increase urine volume,broncho/vaso dilation,smooth muscle relaxation,uric acid,glucose,TG,
-decrease renal 02 consumption,CSF production,CA,K,Mg,Ca,Cl,HDL,acid
-GFR and RPF unchanged-save on renal
-Ototoxicity-cochlear>vestibular
-IV use for glaucoma/IOP, ICP, pulmonary edema, ARF
-Oral use- decrease BP, Cardiac and Renal insufficiency |
|
|
Term
|
Definition
| -loop, thiazide, potassium sparing, carboanhydrase inhibitors, xanthine derivitives |
|
|
Term
|
Definition
-thiazide-low ceiling-oral only
-secreted with PSOASS-->Early distal tubule-inhibition of NA/Cl cotransport
-increase urine volume moderately-->less than loops
-decrease urine volume in diabetes insipidus
-decrease CA, GFR and RPF, K,Mg, Cl, HDL, acids
-increase Ca,uric acid, glucose, TGs
-oral use: decrease BP, cardiac insufficiency(relaxes smooth muscle), diabetes insipidus, urinary calculi(keeps Ca+ out of kidney)
-combine with K sparing |
|
|
Term
|
Definition
| -chemically different from thiazides, but with exact same clinical use |
|
|
Term
|
Definition
| -chemically different from thiazides, but with exact same clinical use |
|
|
Term
|
Definition
-potassium sparing
-aldosterone antagonist-->steroid side effects
-spironolactone-->canrenone (both stop aldosterone binding to cyto receptor
-no aldosterone effects
-decrease Na and increase K
-oral only- 1/2 life 2 hours |
|
|
Term
|
Definition
-potassium sparing
-aldosterone antagonist-->steroid side effects
-spironolactone-->canrenone (both stop aldosterone binding to cyto receptor
-no aldosterone effects
-decrease Na and increase K
-IV only- 1/2 life 17 hours |
|
|
Term
|
Definition
-potassium sparing-cycloamidine derivitive
-Na channel blocker and Na/H exchange blocker (alkoline urine)
-organic base- organice base cation exchange decretory system
-short half life (4-6 hours) because increased metabolism
-folic acid antagonism
-collecting duct |
|
|
Term
|
Definition
-do no combine any K+ increasing agents
-ACE, Potassium sparing, or K+ supplements |
|
|
Term
|
Definition
-potassium sparing-cycloamidine derivitive
-Na channel blocker and Na/H exchange blocker (alkoline urine)
-organic base- organice base cation exchange decretory system
-long half life (18-20 hours)
-collecting duct
-increase Ca+ |
|
|
Term
|
Definition
-carbo-anhydrase inhibitor
-sulfonamide group-->CA inhibitor
-PSOASS-->early proximal tubule
-prevention of mountain sickness-->induces acidosis in blood to keep breathing reflux
-secondary increase in urine volume/pH and K
-decrease glaucoma and IOP and nephron blockade |
|
|
Term
|
Definition
-xanthine derivitive
-Adenosine-1-receptor blocker-->vasodilation
--caffeine derivatives
-adenosine-1 receptor blocker
-high doses lead to unselective PDE inhibition
-decrease PDE, increase cAMP-->smooth muscle relaxtion
-seizure risk with high doses because of release of catacholomines
-1A2 metablism-induced by smoke and protien
-high doses-->switch to zero order-->tachycardia, N&V, tremor, rhabdomyolysis |
|
|
Term
|
Definition
-ace inhibitor
-only active drug (with lisinopril)
-short half life (2 hours)
-persistent dry cough, angioedema, hypotension, hyperkalemia, taste disturbance, fever, rash
-only sulfur containing -pril-->rashes and taste disturbance |
|
|
Term
|
Definition
-ace inhibitor
-only active drug (with captopril)
-half life 12 hours
-persistent dry cough, angioedema, hypotension, hyperkalemia, taste disturbance, fever, rash |
|
|
Term
|
Definition
-only ace inhibitor given IV-->ER
-captopril without sulfur group
-persistent dry cough, angioedema, hypotension, hyperkalemia, taste disturbance, fever, rash |
|
|
Term
|
Definition
-Ace inhibitor
-only one to be eliminated through liver (both kidney and liver)-->because of phosphate group
-persistent dry cough, angioedema, hypotension, hyperkalemia, taste disturbance, fever, rash |
|
|
Term
|
Definition
-ARB-block AT1 receptor
-only prodrug (with olmesartan)
-all distributed orally
-persistent dry cough, angioedema, hypotension, hyperkalemia, taste disturbance, fever, rash
-only one predominantly eliminated through kidney (rest through liver) |
|
|
Term
|
Definition
-ARB-block AT1 receptor
-only prodrug (except candesartan)
-all oral
-persistent dry cough, angioedema, hypotension, hyperkalemia, taste disturbance, fever, rash |
|
|
Term
|
Definition
--Ace inhibitor
-protects heart and against neuropath in diabetes patients and also reduces new cases of diabetes
-persistent dry cough, angioedema, hypotension, hyperkalemia, taste disturbance, fever, rash |
|
|
Term
|
Definition
-direct renin inhibitor
-hypertension medication
-high water solubility
-prevents conversion of angiotensin to angiotensin 1 |
|
|
Term
|
Definition
-broken down by ACE
-increased by ACE I
-increases NO and vasodilation |
|
|
Term
|
Definition
-caffeine derivatives
-adenosine-1 receptor blocker
-high doses lead to unselective PDE inhibition |
|
|
Term
|
Definition
-xanthine derivitive
-Adenosine-1-receptor blocker-->vasodilation
--caffeine derivatives
-adenosine-1 receptor blocker
-high doses lead to unselective PDE inhibition
-decrease PDE, increase cAMP-->smooth muscle relaxtion
-seizure risk with high doses because of release of catacholomines
-1A2 metablism-induced by smoke and protien
-high doses-->switch to zero order-->tachycardia, N&V, tremor, rhabdomyolysis |
|
|
Term
|
Definition
-PDE III-inodilation
-increase stroke volume and CO-no increase in O2 consumption or BP
-smooth muscle relaxant |
|
|
Term
|
Definition
-PDE III-inodilation
-increase stroke volume and CO-no increase in O2 consumption or BP |
|
|
Term
|
Definition
-PDE IV inhibitor
-used for COPD-->increases cAMP and reduces inflammatory cells |
|
|
Term
|
Definition
-PDE V
-vasodilation-->ED
-can cause visual impairment
-3A4
-heartburn, headache, nasal congestion, flushing
-contraindicated with heart problems-->too much vasodliation-->decrease BP-->can't get blood to brain-->pass out
-don't use with nitrates
-also marketed under different trade name for pulmonary hypertension |
|
|
Term
|
Definition
-PDE V
-vasodilation-->ED
-can cause visual impairment
-3A4
-heartburn, headache, nasal congestion, flushing
-contraindicated with heart problems-->too much vasodliation-->decrease BP-->can't get blood to brain-->pass out
-don't use with nitrates |
|
|
Term
|
Definition
-PDE V
-vasodilation-->ED
-no visual impairment, PDE 11-no problems
-3A4
-prodrug with long half life
-heartburn, headache, nasal congestion, flushing
-contraindicated with heart problems-->too much vasodliation-->decrease BP-->can't get blood to brain-->pass out
-don't use with nitrates |
|
|
Term
|
Definition
-natural statins
-lovasatin, simvastatin, pravastatin |
|
|
Term
|
Definition
-synthetic
-atorvastatin, fluvastatin, rosuvastatin |
|
|
Term
|
Definition
-OAT-Rosuvastatin,pravastatin
-Diffusion-Lovastatin, Simvastatin, fluvastatin, atorvastatin |
|
|
Term
|
Definition
-decrease intracellular cholesterol-->activates genes for LDL receptor-->reduces extracellular chol.
-greatly reduces LDL-C, moderately reduces TGs (fibrates), slightly increases HDL-C (niacin)
-Atorvastatin and rosuvastatin-most potent
-plietropic effects-decrease protient prenylation-->decrease cancer, cardiovascular disorders, osteoporosis, multiple sclerosis, alzheimers
-decrease melvalonic acid-->which inhibits NO production less
-decreases arterial thickening and re-stenosis
-decrease CRP-->less aggregation and decreased risk of MI
-increase plaque stability-increased collagen production and decreased matrix protease and monocyte endothelial adherence
-decrease plasminogen activator inhibitor 1-->allows plasminogen-->plasmin-->fibrin degradation
-decreases osteoclast formation (~bisphosphonates)
-absorbed in GIT with high FPE
-most fecal elimination
-can lead to myotoxicity (increase with lipophilic and with fibrates) and hepatotoxicity
-category X
-all are single isomers with low bioavailability |
|
|
Term
|
Definition
-lipophilic-simvastatin, lovastatin,fluvastatin, atorvastatin
-hydrophilic-provastatin, -->more hepatic selective |
|
|
Term
|
Definition
-prodrug-lovastatin, simvastatin
-active-fluvostatin, pravastatin, atorvastatin, rosuvastatin |
|
|
Term
|
Definition
-only one with no cyp450 metabolism
-only 50% protien binding (the rest ~100)
- |
|
|
Term
|
Definition
-atorvastatin-14 hours
-rosuvastatin-20 hours
-all others around 1-3-->give in evening when most cholesterol is synthesized |
|
|
Term
|
Definition
-converts to NO with cysteine-->vasodilation
-trinitrate-shortest half-life
-no FPE
-nitrate tolerance-->depletion of sulfhydryl group needed for nitrates to vasodilate
-do not mix with PDE V inhibitors or alpha-1 blockers |
|
|
Term
|
Definition
-dinitrate-medium half-life
-used for angina and cyanide poisening-->sequesters cyanide as cyanomethemoglobin
-also used as "popper"
-do not mix with PDE V inhibitors or alpha-1 blockers |
|
|
Term
|
Definition
-mononitrate-longest half life (5 hours)
-dinitrate- medium (1 hour)
--do not mix with PDE V inhibitors or alpha-1 blockers |
|
|
Term
|
Definition
-NO donor and K channel opener
-hyperpolarize-->smooth muscle relaxant
-mouth ulceration
-palpitation, weakness, N&V, headache, flushing
--do not mix with PDE V inhibitors or alpha-1 blockers |
|
|
Term
|
Definition
-first drug approved for alzheimers
-non-specific cholinesterase inhibitor
(AChE and BChe)
-SE-N&V and liver damage (increases LFTs) |
|
|
Term
|
Definition
-ChEI with greater specificity for AChE in the CNS (not BChE in perphery)
-NO liver damage
-1/2 life-70 hours-->once a day |
|
|
Term
|
Definition
-AChE and BChE inhibitor
-patch |
|
|
Term
|
Definition
-natural
-synthesized to intocostrin |
|
|
Term
|
Definition
| -blocks ACh receptor sites at nueromuscular junctions |
|
|
Term
|
Definition
non-depolarizing muscle relaxants
-used by surgeons to keep muscles loose
-block muscarinic receptors-->nerves don't interact with muscles
-no CNS involvment |
|
|
Term
|
Definition
-muscarinic blocking effect
-NDMR |
|
|
Term
|
Definition
-reversibly binds AChE-->increasing ACh-->out competes muscle relaxant after surgery
-no CNS penetration
-terminates action in 10 minutes
-fewer muscarinic effects than neostigmine
-low potency |
|
|
Term
|
Definition
-reversibly binds AChE-->increasing ACh-->out competes muscle relaxant after surgery
-no CNS penetration
-terminates action in 10 minutes
-more muscarinic effects than edrophonium
-higher potency
-lasts 20-30 minutes
-excreted in the urine |
|
|
Term
|
Definition
-AChE I used for Myaethania Gravis
-No CNS penetration, more potent, long acting
-pre-treatment for nerve gas (organo phosphate) exposure-->weaker AChE I |
|
|
Term
|
Definition
-anti-cancer drug
-blocks conversion of folic acid-->THF
by blocking dihydrofolic reductase
-given in low dose with folate will inhibit T-cell activation and be used as an immunosupressent w/ myaesthenia
-excretion can be competitive with beta-lactam (penicillin like antibiotics)-->cause toxicity
- |
|
|
Term
|
Definition
-calcineurin inhibitor (which is reponsible for IL-2)
-immunosupressent that can be used for myaesthenia |
|
|
Term
|
Definition
A-atropine
FL-fluid
O-oxygen
P- pyrodoxine-reactivates cholinesterase
or
pyrodostigmine-pre-exposure-weaker AChE I |
|
|
Term
|
Definition
-only AChE I that penetrates the brain
-used for treatment of anticholinergic syndrome
-"Niagerian trial" |
|
|
Term
|
Definition
-short acting cholinergic antagonist
-short acting mydriatic |
|
|
Term
|
Definition
alpha-andrenergic agonist
-short acting mydriatic |
|
|
Term
|
Definition
-muscarinic blocker (PS)
-mydriatic
-resuscitation (jump start heart~epi)
-decrease secretions and bronchoconstriction
-antidote for OP
-central anticholinergic syndrome |
|
|
Term
|
Definition
-weak atropine that can't enter brain
-no CAS |
|
|
Term
|
Definition
"tropium"
-only long acting inhalitive antimuscarinic
-used for asthma/COPD |
|
|
Term
|
Definition
-stops urinary incontinence (leakage)
-M3 receptor blocker-->stops smooth muscle bladder contraction |
|
|
Term
|
Definition
-M1 and M3 blocker
-less selective darifenicin
-may cause dry mouth |
|
|
Term
|
Definition
| -non-selective muscarinic blocker used for urinary incontinence |
|
|
Term
|
Definition
-atropine derivitive
-muscarinic blocker-->decreases ACh and restores ACh/dopamine imbalance in Parkinson's disease |
|
|
Term
|
Definition
| -antihistamine with strong anticholinergic effect |
|
|
Term
|
Definition
-anticholinergic, NMDA receptor antagonist, and antihistamine
-diphenhydramine derivitive
-2/3 atropine |
|
|
Term
|
Definition
-tertiary amine
-anticholinergic-->restors AcH/Dopamine balance and stops parkinson-like symptoms |
|
|
Term
|
Definition
-tertiary amine
-anticholinergic-->restors AcH/Dopamine balance and stops parkinson-like symptoms |
|
|
Term
|
Definition
|
|
Term
|
Definition
-nonselective muscarinic agonist
-decreases IOP and gluacoma |
|
|
Term
|
Definition
-M3 agonist
-increases saliva production (~clozapine)
-used for dry mouth |
|
|
Term
|
Definition
-nonselective alpha receptor blocker
-vasodilation-->decrease BP in hypertensive emergencies
-used for emergency phaeochromocytoma or cocaine induces hypertension |
|
|
Term
|
Definition
-"osin"- alpha 1 A blockers (specific for prostate)
-uroselective blocker
-"flomax"-increases flow
-1:40 beta:alpha |
|
|
Term
|
Definition
"osin"-alpha 1 blocker
-non uroselective (prostate and peripheral)
-side effect->hypotension |
|
|
Term
|
Definition
"osin"-alpha 1 blocker
-non uroselective (prostate and peripheral)
-side effect->hypotension |
|
|
Term
|
Definition
"osin"-alpha 1 blocker
-functionally uroselective |
|
|
Term
|
Definition
| "osin" alpha 1 blocker -ueoselective -->alpha 1 a -no orthostatic hypotension -inhibit ejeculation, not orgasm |
|
|
Term
|
Definition
-central alpha 2 and imidazoline agonist--> negative feedback on presynaptic terminal-->decrease NT release
-turn off sympathetic activity
-imidazoline-decrease BP and reduce anxiety
SE:bradykardia, constipation, water retention
- alpha 1-analgesia, sedation
SE: dry mouth, parotid pain
-"nidine" |
|
|
Term
|
Definition
-alpha 2 agonist (not imidazol)
-pregnancy category B-> safe way to lower BP during pregnancy |
|
|
Term
|
Definition
-sedative anciolytic without respiratory depression
-clonidine like drug (only alpha 2) |
|
|
Term
|
Definition
| -clonidine like-selective for imidazol->specific for decreasing BP |
|
|
Term
|
Definition
-alpha 1 agonist->nasal vasocontriction for decongestion
-use too much, go to system-> increase BP
"zoline"
-can lead to nasal necrosis |
|
|
Term
|
Definition
-alpha 1 agonist->nasal vasocontriction for decongestion
-use too much, go to system-> increase BP
"zoline"
-can lead to nasal necrosis |
|
|
Term
|
Definition
-alpha 1 agonist->nasal vasocontriction for decongestion
-use too much, go to system-> increase BP
"zoline"
-can lead to nasal necrosis |
|
|
Term
|
Definition
-beta 2/beta 1 agonist-4/1
"terol"-beta 2 agonist
-also called salbutamol
-secreted in urin
-racemic with eutomer and distomer
-ROSA reliever asthma inhalent |
|
|
Term
|
Definition
-beta 2/beta 1 agonist-4/1
"terol"-beta 2 agonist
-also called albuterol
-secreted in urin
-racemic with eutomer and distomer
-ROSA reliever asthma inhalent |
|
|
Term
|
Definition
-beta 2/beta 1 agonist-4/1
"terol"-beta 2 agonist
-ROSA reliever asthma inhalent
-concentrated eutomer of albuterol |
|
|
Term
|
Definition
-beta 2 agonist
-true SOLA controller for asthma |
|
|
Term
|
Definition
-beta 2 agonist
-only ROLA-->can be a controller or reliever in asthma |
|
|
Term
|
Definition
-beta 2 agonist
-true SOLA controller for asthma |
|
|
Term
|
Definition
-beta 2 agonist
-only ROLA-->can be a controller or reliever in asthma |
|
|
Term
|
Definition
-psuedo beta 1 agonist
-beta 1>>beta 2 agonism
-racemic mixture- cancels out alpha effects
-increase HR and + ionotropic
-support failing heart |
|
|
Term
|
Definition
small dose- D1 agonist-in periphery acts on kidney and GI to increase profusion
"renal dose"-->protects kidneys
-medium dose-beta 1 agonist-increase HR and + ionotropic
-high dose- alpha 1 agonist-vasoconstriction and increase BP |
|
|
Term
|
Definition
-synthetic catecholamine
-increase cAMP through beta 1 and beta 2
-increase HR and contraction while vasodilating
-same as PDE III inhibitor-->inodilator |
|
|
Term
|
Definition
-non selective, no ISA beta blocker
-fat soluble-dreams and hepatic metab.
-Na CB |
|
|
Term
|
Definition
not selective, no ISA beta blocker
-water soluble |
|
|
Term
|
Definition
-not selectrive with ISA beta blocker
-water soluble-kindeys
-Na CB
-partial 5-HT-1a agonist |
|
|
Term
|
Definition
selective, no ISA beta blocker
-fat soluble-dreams and hepatic metab |
|
|
Term
|
Definition
selective, no ISA beta blocker
-water soluble-kidney |
|
|
Term
|
Definition
selective with ISA
-fat soluble-dreams
-renal elimination
-Na CB |
|
|
Term
|
Definition
-beta blocker used by anaesthetists because of ultra-short half life
-ester compound=ultra short half life |
|
|
Term
|
Definition
| mixed-non cardio specific alpha and beta blocker (1:3) |
|
|
Term
|
Definition
| mixed-non cardio specific alpha and beta blocker (1:3) |
|
|
Term
|
Definition
| -cardioselective Beta 1 blocker with vasodilation by NO |
|
|
Term
|
Definition
-beta blocker overdose
-increases cAMP without beta receptor |
|
|
Term
|
Definition
| -first inhaled anesthetic for surgery |
|
|
Term
|
Definition
-inhaled anesthetic with lowest MAC,highest potency and lipid solubility
-first introduces, rarely used in western world
-can trigger malignant hyperthermia (release of Ca)
-20% metabolized (most)-->hepatitis
-slow onset/offset |
|
|
Term
|
Definition
-inhaled anesthetic
-2% metabolized
-increased risk of seizures |
|
|
Term
|
Definition
-inhaled anesthetic
-.2% metabolized |
|
|
Term
|
Definition
-inhaled anesthetic
-4 % metabolized
-kidney damage |
|
|
Term
|
Definition
-highest MAC of inhaled anesthetics, lowest fat solubility and potency
-.004% metabolized
-rapid onset/offset |
|
|
Term
|
Definition
-laughing gas-NMDA antagonist(not GABA agonist) inhaled anesthetic
-highest MAC, lease fat soluble and potent
-cannot use alone for proper anesthesia
-sympatho-mimetic (like ketamine)
-inhibits B12 dependent enzymes-myelin production (paralysis) and RBC production (megoblastic anemia) |
|
|
Term
|
Definition
-"cronium"-aminosteroid NDMR
-less vasolytic->increases HR
-longest length (90-120 min)
-renal/hepatic elimination |
|
|
Term
|
Definition
"curonium"aminosteroid NDMR
-very vagolytic-->increase HR-->don't give to patients with CAD
-second longest lasting (60-90) |
|
|
Term
|
Definition
"curonium" aminosteroid NDMR
-hepatic/renal/bile elimination
-intermediate acting (30-40min) |
|
|
Term
|
Definition
-"curonium"-aminosteroid NDMR
-not metabolized-->renal/bile elimination
-intermediate acting (30-40min) |
|
|
Term
|
Definition
-"curium" isoquinoline NDMR
-histamine release->bronchoconstriction and tachycardia
-ester-shortest acting (5-15 min) |
|
|
Term
|
Definition
-"curium" isoquinoline NDMR
-histamine release->bronchoconstriction and tachycardia
-mixture of 10 isomers
-partially degraded by Hofmann
-rest by plasma esterases-->laudanosine (increases CNS and causes seizures)
-intermediate duration (20 min) |
|
|
Term
|
Definition
| -"curium" isoquinoline NDMR -histamine release->bronchoconstriction and tachycardia -cleaner atracurium-->only active isomers -Hoffman with laudanosine (increased CNS and seizures) -intermediate (30min) |
|
|
Term
|
Definition
-"curium" isoquinoline NDMR
-histamine release->bronchoconstriction and tachycardia
-not metabolized-renal
-long duration (120 min) |
|
|
Term
|
Definition
-di-acetyl-choline
-depolarizing muscle relaxant
-only 1-10% reaches target (unless atypical)
-ultra-short 1/2 life (3 minutes)
-very rapid onset (60 seconds)
-train four response-fade
-fasiculations, myalgia (young women), increased pressure (ICP, IOP, intragastric)-->don't give with head trauma, glaucoma, eye injury
-bradycardia, bronchospasm
-hyperkalemia (higher ith muscle disease or burns)
-masseter muscle spasm and malignant hypertherm |
|
|
Term
|
Definition
-test to determine the amount of ChE in plasma
-should get broken down 80%, if less-->less ChE present |
|
|
Term
|
Definition
-large polysaccharide, water soluble, not protein bound-->short 1/2 life (fast acting)
-safe for pregnancy
-parenterally-->in plasma
-catalyzes antithrombin III to inactivate 2,9,10,11,12 (intrinsic), also inhibits FII (thrombin)
-measured with partial thromboplastin time (PTT)
-can cause HIT(heparin induced thrombocytopenia)-long term-->autoimmune against platelets-->bleed more and clot
-osteoporosis
-antagonist-protamine (a vasodilator or anticoag)
-LMW-clean-only AT III activator-increased 1/2 life, expensive with no reliable antagonist |
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Term
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Definition
-small, lipid soluble-->goes to liver, protein bound-->long half life (displaced by fibrates)
-oral
-binds to vit. K epoxide reductase-->stops production of vit. K dependent factors-2,7, 9, 10, s, c (extrinsic)
-don't take if pregnant
-measured with Prothrombin time (PT), or INR- INR increases with efficacy (decrease in Vit. K)
-VKORC1 and CYP2C9 polymorphism
-antagonize with Vit. K (long term) or Frozen Fresh Plasma
-can lead to skin necrosis (avoid if heparin bridge)
-ADR-osteoporosis, purple toe (necrosis) |
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Term
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Definition
-direct thrombin inhibitor (from leech)
-"rudin"
-reversal of HIT |
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Term
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Definition
-"rudin"-direct thrombin inhibitor
-IV-->reversal of HIT from heparin |
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Term
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Definition
-direct thrombin inhibitor and anticoagulant
-IV-->reversal of HIT from heparin
-can be used in replace of heparin as an anticoagulant |
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Term
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Definition
-"gatran"- oral
-direct thrombin inhibitor |
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Term
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Definition
(+) 5-HT, adrenalin, ADP, TXA2, PAF, Thrombin
(-) adenosine, NO/EDRF, PGI2, cAMP, cGMP |
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Term
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Definition
-low dose-inhibits platelet aggregation
-inhibits COX on platelets->inhibits TXA2 (which causes platelet aggregation) |
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Term
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Definition
-decreases platelet aggregation
-ADP-inhibitor- stops the activation of P2Y12->which then cannot activate IIbIIIa
-used when ASA cannot be used, but is not being used in place of
-ester, only 15% makes it to liver |
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Term
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Definition
-decreases platelet aggregation "grel"
-ADP-inhibitor- stops the activation of P2Y12->which then cannot activate IIbIIIa
-used when ASA cannot be used, but is not being used in place of
-pro-drug
-ester, only 15% makes it to liver |
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Term
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Definition
-decreases platelet aggregation "grel"
-ADP-inhibitor- stops the activation of P2Y12->which then cannot activate IIbIIIa
-used when ASA cannot be used, but is not being used in place of
-pro-drug
-ester, only 15% makes it to liver |
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Term
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Definition
| -direct GP-IIb/IIIA inhibitor |
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Term
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Definition
| -direct GP-IIb/IIIA inhibitor |
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Term
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Definition
| -direct GP-IIb/IIIA inhibitor |
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Term
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Definition
-adenosine-re-uptake inhibitor
-increase adenosine-->decreases platelet aggregation
-also reduces heart rate
-PDE I do the same thing (cAMP and cGMP decrease aggregation) |
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Term
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Definition
-thrombolytic->catalyze formation of plasmin
-tissue plasminogen activator (tPA)
-use post surgery, MI, Stroke, etc.
-binds to clot itself, more specific
-cost more
-also increases platelet aggregation by increasing thrombin levels (must counter with ASA) |
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Term
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Definition
-thrombolytic
-catalyzes formation of plasmin
-binds to plasminogen (not clot)-less specific, can cause increased bleeding
-can form antibodies against
-use post surgery, MI, Stroke, etc.
-also increases platelet aggregation by increasing thrombin levels (must counter with ASA) |
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Term
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Definition
-TB
-stops bacteria RNA polymerase
-potent inducer of metabolism
-red child syndrome-orange skin and secretions and contact lenses |
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Term
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Definition
-TB
-stops bacteria RNA polymerase
-potent inducer of metabolism
-red child syndrome-orange skin and secretions and contact lenses
-less drug interaction-used in HAART for HIV treatment |
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Term
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Definition
-TB
-stops bacteria RNA polymerase
-potent inducer of metabolism
-red child syndrome-orange skin and secretions and contact lenses
-longer half life |
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Term
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Definition
-TB
-inhibits arabinosyl-->bacterial cell wall synthesis
-OPTIC NEURITIS, red/green discrimination, decrease uric acid-->goute
-neuropathy, nystagmus |
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Term
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Definition
-TB
-prodrug-->INA-->gets incorporated into NAD-->decreases mycolic acid synthesis-->cell death
-uses acetyl transferase-->sight for polymorphism in people
-NAT-2 gene-further north, better acetylators-->less toxicity
-can be measured with xanthine metab.
-inactivates pyridoxal (B6)-peripheral neuropathy
-stops conversion of glutamate->GABA- CNS stimulant-BDZ resistant siezures
-stops conversion of lactic acid to pyruvate-->lactic aciduria
-decreases conversion from tryptophan->niacin (vit. B3)-pellegra (dermatitis, diarrhea, dementia, death)
-hepatotoxicity->lupas-like symptoms |
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Term
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Definition
-diamino diphenyl sulfone (DDS)
-rafampin and clofazamine
-used for leprocy |
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Term
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Definition
-blocks the conversion of PABA to folate
-dihydropteroate synthetase
-hemolysis w/ glucose6P dehydrase deficiency (also caused by fava beans)
- |
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Term
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Definition
-inhibits DNA replication
-anti-inflammatory-->given for leprosy
rxn erythema nodosum leprosum-->hypersensitivity rxn |
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Term
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Definition
-stops the conversion of dihydrofolate to tetrahydrofolate-->inhibits diyhydrofolate reductase
-slows DNA and RNA synthesis-->anti-cancer (trimethoprim and pyrimethaprim)
-immunosuppressent because it stops t-cell activation (used for AI-rheumatoid arthitis, crohns, psoriasis)
-supplement with folate
-renal comp. and toxicity with B-lactams
- |
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Term
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Definition
-cause toxicity of methyltraxate
-penicillin, cephalosporin, carbapenems, monolactam |
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Term
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Definition
-binds to cyclophilin and inhibit calcineurin-->decreases IL-2
-immunosuppresent-used for rhematoids
-can cause neprhotoxity, increased malignancy, 3A4 substrate (induced by BCGPRS)-inhibited by grapefruit |
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Term
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Definition
=rapamycin
-"limus"-immunosupressent |
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Term
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Definition
-tsukuba macolide immunosupressent
-similar to cyclopsporin (calcineurin-IL2) |
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Term
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Definition
-tsukuba macolide immunosupressent
-similar to cyclopsporin (calcineurin-IL2) |
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Term
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Definition
-inhibits purine synthesis->slows DNA synthesis (B and T cells)
-pro-drug-->6-merpcaptopurine
-bone marrow toxicity
-teratogenic
-metabolized by TPMT-polymorphisms
(also metabolizes 6-thioguanine)
TPMT deficient-->leads to hematotoxicity |
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Term
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Definition
-inhibits purine synthesis-->DNA synthesis-->T and B cells
-delayed onset of action (6-12 months)
-no side effects
-expensive |
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Term
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Definition
-inhibits microtubule polymerzation, decreases mitosis
-affects axonomal transport
-stops luekocytes from getting to inflamed area-->stops acute flare from gout arthritis (big toe) |
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Term
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Definition
-interferes with excretion and increases the elimination of uric acid
-used for gout |
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Term
| xanthine oxidase inhibitor |
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Definition
-stops the synthesis of uric acid
-used for gout |
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Term
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Definition
-used in the treatment of solid tumors
-polymorphism-->dihydro-pyrimidine-dehydrogenase (DPD)-rate limiting step in catabolism-->toxicity if absent
-toxicity-myolsupression, mouth ulcers, skin changes, neuro tox, diarrhea |
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Term
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Definition
-used in the treatment of solid tumors
-polymorphism-->dihydro-pyrimidine-dehydrogenase (DPD)-rate limiting step in catabolism
-toxicity-myolsupression, mouth ulcers, skin changes, neuro tox, diarrhea |
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Term
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Definition
-5 lipoxidase (LO)inhibitor-decreases leukotrienes
-broad spectrum antibiotic |
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Term
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Definition
-decreases macrophage activation
-gold |
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Term
tnf-alpha inhibitor/IL-1 antagonist
-cept, ximab, zumab, mumab, ra |
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Definition
-cept-receptor Ab fusion protein
-ximab-chimeric monoclonal Ab
-zumab-humanized monoclonal Ab
-mumab-human monoclonal Ab
-ra-receptor agonist |
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