Term
|
Definition
| venodilator decreases preload which decreases work on heart |
|
|
Term
|
Definition
angina SL for acute attack
not great preventitive |
|
|
Term
| drugs good vo vasospasm angina |
|
Definition
never BB
CCB vascular specific - amlodipine |
|
|
Term
| drugs good for stable angina prevention |
|
Definition
#1 is BB
any CCB will work (amlodipine, ditilzaim, verapmil) |
|
|
Term
|
Definition
| work on ascending loop of henle targeting Na/K/2Cl diuretic |
|
|
Term
|
Definition
loops loose Ca
ototoxic
K loss and thus H loss so metabolic acidosis |
|
|
Term
|
Definition
| DOC acute pulmonary edema |
|
|
Term
|
Definition
| works on DCT NaCl channels |
|
|
Term
| hydrochlorothiazide: SE 4 |
|
Definition
K loss and thus H loss so metabolic acidosis
thiazides save Ca
hyperglycemia |
|
|
Term
| hydrochlorothiazide: use 2 |
|
Definition
DOC daily fluid balance duiretic (long half life)
DI NOT caused by lithium |
|
|
Term
| what is used to tx DI caused by lithium, why |
|
Definition
| amularide: becaue lithium and Na are similar in size and charge. comes into CD through Na channels |
|
|
Term
|
Definition
works in CD as direct Na channel blocker
K sparing |
|
|
Term
| eplerone and spironolactone: MOA |
|
Definition
works in CD as ALD receptor blocker decreasing number of Na chennals, thus indirect CD blocker
K sparing |
|
|
Term
|
Definition
| if you save K you save H causing metabolic acidosis |
|
|
Term
|
Definition
lowers VLDL, TG
raises HDL |
|
|
Term
|
Definition
|
|
Term
|
Definition
bile acid sequesterant (ie cholesterol)
complexes with bile so you cannot recycle them and you loose them from the body and liver needs to make more bile acids and thus need to pull cholesterol from the blood to do it |
|
|
Term
| cholestyramine: contrindications, why |
|
Definition
| hyperTG patients: further increases TG because when liver starts making more bile acids it starts making other lipids too |
|
|
Term
|
Definition
HMG CoA reductase (rate limiting step in cholesterol synthesis) inhibitor
benifit all aspects of lipid profile |
|
|
Term
| which statin is most likley to raise HDL, which is least |
|
Definition
| atrivostatin > simvastatin |
|
|
Term
|
Definition
| muscle toxicity (myalgia, myositis, rhabdomyalgia) |
|
|
Term
|
Definition
| take with P450 inhibitor increases statin levels and risk of muscle toxicity (never drink grapefruit juice!) |
|
|
Term
|
Definition
| increases gene expression of PPARy which increases lipoprotein lipase which lowers TG |
|
|
Term
| what two NT and change in parkinsons disease |
|
Definition
decreased dopamine
increased ACh (Relative) |
|
|
Term
|
Definition
taken into CNS and turned into dopamine
use carbadopa to avoid DOPA decarboxylase break down in periphery |
|
|
Term
|
Definition
| dopamine agonist directly stimulates D2 receptors |
|
|
Term
|
Definition
| stops metabolism of dopamine by MAOB blocking it |
|
|
Term
|
Definition
in periphery and CNS levodopa is converted to 3-o-methyodopa by COMT
drug blocks COMT to increases levadopa conversion to dopamine |
|
|
Term
|
Definition
targets ACh, muscarinic blocker
lowers effect of ACh in parkinsons |
|
|
Term
|
Definition
|
|
Term
| drugs used for parkinsons |
|
Definition
levodopa/carbadopa
ropinerole
selegiline
entacapone
benzotropine |
|
|
Term
| explain the break down process of ethanol and the SE 3 |
|
Definition
| ethanol > alcohol DH > acetaaldehyde > aldehyde DH > acid aldehyde > acidosis, N/V, headache |
|
|
Term
| explain break down process of methanol and the SE 2 |
|
Definition
| methanol > alcohol DH > formeldahyde > aldehyde DH > formic acid > acidosis, eye damage |
|
|
Term
| explain break down process of ethylene glycol and the SE 2 |
|
Definition
| ethylene glycol > alcohol DH > aldehyde > aldehyde DH > acid aldehyde > acidosis, kidney damage |
|
|
Term
|
Definition
| blocks aldehyde DH causing aldehyde buildup which causes toxic effects deturing from alcohol use |
|
|
Term
|
Definition
methylphenidate
dextroamphetamine |
|
|
Term
|
Definition
| promote release of NE and dopamine |
|
|
Term
|
Definition
|
|
Term
|
Definition
tachycardia
sweating
increased BP |
|
|
Term
|
Definition
uses antithombin III to cleave IIa, IXa, XIa, XIIa
works on activated factors so works rapidly |
|
|
Term
|
Definition
protamine: directly complexes with heparin stopping its action
rapid onset |
|
|
Term
|
Definition
| heparin induced thrombocytopenia (stop all drugs working through antithrombin III if induced, not just heparin) |
|
|
Term
| how can heparin be monitered |
|
Definition
|
|
Term
|
Definition
| low molecular weight heparin |
|
|
Term
|
Definition
| takes time, decreased synthesis of II, IV, IX, X by stopping vitamin K |
|
|
Term
| warfarin antidote and MOA |
|
Definition
Vit K: never going to be fast
fresh frozen plasma: fast, replenishes clotting factors |
|
|
Term
| how is warfarin monitered |
|
Definition
|
|
Term
| rivaroxban: MOA, how monitored |
|
Definition
blocks factor Xa
no need to monitor |
|
|
Term
| dabigatran: MOA, how monitored |
|
Definition
direct thrombin inhibitor
no need to monitor |
|
|
Term
|
Definition
ADP receptor blocker
cannot activate platelets
good back up to aspirin |
|
|
Term
|
Definition
| glycoprotein IIb/IIIa inhibitor blocks fibrinogen receptors prevents cross linking in platelet aggregation |
|
|
Term
|
Definition
angioplasty
acute coronary syndromes
unstable angina |
|
|
Term
|
Definition
tPA
fibrinolytic
breaks down clots |
|
|
Term
|
Definition
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