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67 Cards in this Set

  • Front
  • Back
Donezipil
Achase (-)

Tx: Alzheimers

(also Galantamine and Rivastigmine)
Galantimine

Rivastigmine
also Donezapil

carbamate Achase (-)

Tx: Alzheimers
Pseudocholinesterase and Ach analogs
CAn't BE Metabolized

-Carbachol
-Bethanechol
-Methacholine

-longer activity, slow metabolize in body
Methocholine
-Dx asthma
-Ach analog

-cannot be metabolized w/ pseudocholinesterase
-only muscarinic effects
Muscarinic specific Choline esters
-Methacholine- Dx asthma
-Bethanechol- Tx urinary retention
How to block hypoTN w/ i.v. choline ester admin:
Atropine

-activate K+ channels to hyperpolarize cells
-prevent Ach-like increase in cGMP/ NO
Pilocarpine
Ach agonist

-miosis
-fixate pupils at far distance
-lower IOP

-contraction of meridional fibers of ciliary muscle
-align trabecular plates through canal of Schlem
Nicotine
-tertiary amine
-not hydrolyzed by pseudocholinesterase
-metabolized by liver

-increase HR and BP--> vasodilation
-increased GI Motility and respirations
Carbamates
ACHase (-)--> phyostigmine, neostigmine, edrophonium
Edrophonium
4' amine ACHase (-)

-Dx myasthenia gravis
-differentiate between MG and choinergic crisis

Tx MG w/ neostigmine
Neostigmine
3' amine ACHase (-)

Tx Myasthenia Gravis
Organophosphates
-Malathion
-Parathion
-Isoflophosphate (DFP)

-toxins in home, agriculture and biochemistry labs
-Sx: lacrimation, salivation, miosis, blurred vision, urination, sk. muscle fasciculations, pulm. edema, dyspnea

Tx: atropine + pralidoxime
Phyostigmine
indirect Ach agonist

Tx: anticholinergic toxicity (atropine OD)
Tx urge incontinence
-Solifenacin
-Tolterodine

Ach antagonist
Ach antagonists Tx Parkinsons
-Diphenhydramine
-Trihexphenidyl
-Benztropine
Tx Menier's Disease
Meclazine

-Ach antagonist anti-emetic
DOC Fundoscopic exam
Tropicamide

Ach antagonist
DOC determination refractive error
Cyclopentolate
Tx anterior uveitis pain, keratitis, choroiditid
long-acting muscarinic antagonists

-Scopolamine
-Atropine
Ganglionic blocking drugs
-Trimethaphan
-Hexamethonium

-antagonist N1 receptors in autonomic ganglia
-(-) Epi release w/ hypoglycemia
Atropine w/ NE
blocks baroreflex bradycardia

i.v.
Haloperidol + DA
-DA nl. increase BF to kidneys and GI
-haloperidol blocks increase in BF

-DA will still increase contractility (beta-1)
-high dose DA will increase DBP
DA effects on body
-increase contractility (beta-1)
-HIGH dose increase DBP

-increase RBF and BF to GI (block w/ haloperidol)
EPI + halothane
cardiac arrythmias
EPI effects
-vasodilation on skeletal muscle
-vasoconstriction to GI, kidneys, skin

-increased HR, contractility, CO, SBP, PP
-decrease PP
increase PP
Epinephrine

-increase BF muscles
-decrease BF to GI, kidneys, skin

-increase SBP w/ no change in DBP
alpha blockers
-prazosin
-phentolamine
-phenoxybenzamine

Epi + alpha block = lower BP, TPR, ERP, increase HR and RBF
Epi + alpha blocker
-Prazosin
-Phenoxybenzamine
-Phentolamine

-lower TPR, BP, ERP
-increase HR and RBF
Ritodrine
beta2 agonist

-prevents premature labor
selective beta-2 agonists
Albuterol
Tertbutaline
-less incidence of tachycardia

Isoproterenol= non-spec. beta agonist w/ increase HR
Isoproterenol
non-specific beta-agonist

Tx: asthma

-tachycardia prominent
Clonidine
pre- and post-synaptic alpha agonist
Methylphenidate
Amphetamines
-dump catecholamines and DA (amphetamines)
-prevent reuptake
Ergotamine
partial alpha agonist

Tx: migraines
S/E: angina via vasospasm
Tx Pheo. to reverse effects of Epi
Phentolamine

-alpha blocker
-lowers the BP a/ EPI secretion
Beta-blockers specificity
Propanolol, Isoproterenol, Timolol = nonspecific

Atenolol, Metopropolol = beta-1 (cardiac effects)

Albuterol, Tertbutaline = beta=2 (respiratory effects)
beta-blockers and angina
-lower O2 demand by lowering HR
-lower venous return
Reserpine
-depletes NE stores
-poisons NE vesicles
S/E beta-blockers
-hypoglycemia
-bronchospasm
-AV block
-CHF
Propanolol
-non-specific beta blocker

-prevents peripheral conversion T4--> T3
-lowers HR and BP
MAO-A
MAO-B
MAO-A= metab. NE and 5-HT

MAO-B= metab. 5-HT
-Selegine MAO-B specific

-Phenelezine, Tranylcypromide hits both MAO
Drugs that decrease plasma NE
-Clonidine
-Reserpine
-alpha-methyldopa
-Guanethidine
-ganglionic blockers
Drugs that increase plasma NE
-alpha-blockers
-hydralazine, minodoxil, diazoxide
-Nifedipine
-nitroprusside
-HCTZ
-Cocaine
Arterial vasodilators
-Hydralazine- SLE-like, edema
-Minodoxil- hirsituism, additive w/ finisteride
-Diazoxide- inhibit insulin release

-increase cGMP---> increase NO
DOC HTN emergency
-Labetolol
-Diazoxide- activate K+ ATPase channel
-Nitroprusside
-Fenoldopam- agonist vascular D1-rec
Nitroprusside
-balanced vasodilation- increase cGMP and NO

Tx: CHF, HTM emergency

-not for G6PD def.
-beware CN toxicity and thiocyanate toxicity
drugs which decrease contractility
-beta-blockers

-calcium channel blockers
RAAS and the heart
-aldosterone = increase fibrillar deposition in cardiac ECM

-AngII- increase BP via vasoconstriction
ACE(-) and Bradykinin
ACE normally breaksdown Bradykinin

ACE(-) ---> increase Bradykinin
-cough
-facial edema
-potentiate vasodilatory effects of Bradykinin

-will see no change of Bradykinin w/ ARBs
Cough with ACE(-)
Tx w/ aspirin

-due to increased Bradykinin and PGs
-ARBs will not have cough associated
ACE (-) renal fxn
-always give to diabetics

-preserves renal fxn
-prevents proteinuria
Aliskiren
renin inhibitor

Tx: HTN
Acetazolimide
MOA (-) carbonic anhydrase in PT/ eye/ CSF

Tx: glaucoma, mild diuretic, clearance of acidic drugs, mild decrease gastric acid
-altitude sickness

S/E: hyperchloremic metabolic acidosis
-loss of bicarb, K+, and Na+
To make urine acidic
ammonium chloride
hyperchloremic metabolic acidosis and diuretics?
acetazolimide
hypochloremic metabolik alkalosis
Loop diuretics (furosemide + ethacrynic acid)
Diuretics and digoxin
loss of K+ will potentiate digoxin
-loop diuretics
-THiazides
bilateral hearing loss exacerbated w/ aminoglycosides (gentamycin)
loop diuretics

-furosemide
ethacrynic acids
diuretic with low GFR
use a loop diuretic (furosemide/ ethacrynic acid)

thiazides will not work
S/E Loop diuretics
-hypokalemic, hypochloremic metabolik alkalosis
-increase Hct due to loss plasma volume

-ototoxicity worse w/ aminoglycosides
-hyperuricemia
-lithium toxicity

-enhance digoxin (hypokalemia)
limitations of Thiazides
-will not work w/ GFR <25 (use loop diuretic)
-will lower GFR in all pts.

(does not apply to metolazone)
Metolazone
thiazide diuretic works at low GFR

will not lower GFR like other thiazides
K+ sparing diuretics
tASK

Triamterene
Amilioride
Spirinolactone

-ALL contraindicated in renal insufficiency due to HYPERKALEMIA
Amilioride
Triamterene
-block Na+ channels in principle cells of DCT

-increase Na+ excretion
-decrease K+ excretion

-make urine alkaline via (-) H+ secretion from intercalcated cells

-K+ sparing--> contraindicated w/ renal insufficient pts.
Spirinolactone
-antagonist aldosterone
-partial androgen/ estrogen agonist

-increase excretion Na+
-reverse cardiac remodeling
Tx Conns syndrome
Spirinolactone
REMINDER
GO OVER ELECTROLYTE AND FLOW ALGORYTHIM