Term
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Definition
Organic Nitrate
Use: chronic or acute (post-MI IV, acute angina subling) |
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Term
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Definition
Isordil
Organic Nitrate
Dosed tid |
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Term
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Definition
Imdur
Organic Nitrate
Dosed qd |
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Term
Nitrates
Indications, MOA, SOA, ADRs, Tolerance |
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Definition
Use: angina
MOA: rel. NO from structure -> activates soluble GC -> cGMP -> PKG -> de-P's MLCK -> vasodil/sm musc relax
SOA: veins & coronary arteries
ADRs: dizziness, hypoTN, flushing, methemoglobinemia-> NO oxidizes Fe2 to Fe3+ -> oxygen cannot leave Hb -> bluish skin
Tolerance: There must be a nitrate-free period every day during the time pt is least symptomatic |
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Term
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Definition
Use: angina
MOA: causes inhibition of Na channel so decrease ca2+ buildup and therefore decrease preload and increase flow to coronary artery |
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Term
Direct Vasodilators
Indications, MOA |
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Definition
Use: HTN, CHF
MOA: act directly on smooth muscle cell to cause vasodil |
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Term
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Definition
MOA: bind K+ channel on sm musc cell -> (-) hyper polarized as K+ rushes out -> cell cannot contract -> vasodil
SOA: only arterial
ADR: hypertrichosis
Also branded as Rogaine |
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Term
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Definition
MOA: bind K+ channel on sm musc cell -> (-) hyper polarized as K+ rushes out -> cell cannot contract -> vasodil
SOA: only arterial
ADR: ^glucose; hyperpolarizes pancreatic Beta cells so they cannot release insulin
Also branded as Proglycim |
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Term
Hydralazine
MOA, SOA, Metabolism, ADR |
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Definition
MOA: unknown
SOA: only arterial
Metabolism: N-acetyl transferase
ADR: reversible lupus-like syndrome |
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Term
|
Definition
hydralazine + isosorbide dinitrate
SOA: balanced vasodilator
only approved for blacks |
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Term
Nitroprusside
MOA, SOA, Metabolism, Indication |
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Definition
IV only
MOA: releases NO from structure
SOA: balanced vasodilator
Metabolism: thiosulfate in liver converts CN- to thiocyanate & excreted renally; we coadmin thiosulfate to make sure
Use: HTN crisis |
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Term
|
Definition
Endothelin: Sm Musc Receptors EtA (bad:vasocon&sm musc prolif) & EtB (good: vasodil & antiprolif)
NItric Oxide: Sm Musc activation of GC -> cGMP -> PKG -> vasodil & antiprolif
Prostacyclin: Sm Musc Gs/prostacyclin receptor -> cAMP -> PKA -> vasodil & antiprolif |
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Term
|
Definition
Flolan
Prostacyclin Analog
Admin continously via central line; pump always on ice |
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Term
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Definition
Remodulin
Prostacyclin Analog
Admin continuously SC |
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Term
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Definition
Ventavis
Prostacyclin Analog
Admin via inhaler q3h |
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Term
Prostacyclin Analogs
MOA, ADRs |
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Definition
MOA: mimic Prostacyclin to -> decreased proliferation of sm musc & vasodil
ADRs: some reflex tachycardia, flushing, dizziness, orthostatic hypoTN, pain in mouth/jaw related to prostaglandin |
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Term
Endothelin Receptor Antagonists
ADRs |
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Definition
teratogenic: cannot take when pregnant
reversible hepatox |
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Term
|
Definition
nonselective endothelin receptor antagonist
oral
Use: PAH |
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Term
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Definition
A-selective endothelin receptor antagonist
oral
Use: PAH |
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Term
|
Definition
Revatio (PAH), Viagra (ED)
PDE-5 Inhibitor
Use: PAH & ED |
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Term
PDE-5 Inhibitors
MOA & ADRs & DDI |
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Definition
MOA: decreases cGMP breakdown -> more vasodilation
ADRs: dyspepsia via smooth muscle GIT relax; dizziness, flushing, hypoTN, bluish tinted vision
DDI: Nitrates -> you get incrased formation of cGMP from nitrate & decreased breakdown of cGMP from PDE-5i -> massive PKG activation -> massive vasodilation |
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
| Nonselective PDE Inhibitor |
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Term
|
Definition
Caverject-> penis injection
Muse-> transurethral suppository
PGE Analog
Use: erection |
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Term
|
Definition
MOA: acts on PG receptor on blood vessels
Use: erection in those with CNS damage
ADR: priapism |
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Term
| 3 pathways to activate renin secretion from JG cells |
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Definition
1.) decreased BP in preglomerular cells
2.) decreased NaCl reabsorption in macula densa of kidney
3.) activation of B1 in JG Cells |
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Term
| 2 negative feedback mechanisms to stop renin secretion |
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Definition
1.) Long Loop: increased BP in preglomerular cells -> Cox2 decrease -> PG decrease -> less cAMP -> less renin
2.) Short Loop: adequate AngII -> binds AT1 on JGC -> Gq -> PLC -> Increased Ca++ -> decreased renin |
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Term
| 5 effects of AngII on AT1 |
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Definition
1.) kidney: vasocon of renal arteries -> decreased GFR
& increased Na & Cl reabsorp via aldosterone/ADH
2.) adrenal gland:
cortex: rel. aldosterone -> Na rebsorp
medulla: rel. catecholamines -> increased renin & contractil
3.) vascular sm musc: vasocon
& growth promoting factors
4.) CNS: increased ADH -> increased H2O reabsorp
5.) myocardium: increased contractility
& remodeling eventually |
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Term
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Definition
MOA:
1.) Block ACE -> decreased AngII -> decreased AT1 activity -> decreased vasocon, decreased Na/H20 rtn, decreased remodeling
2.) inhibit bradykinin bdown -> more bradykinin -> binds B2 Gq -> PLC -> Increased Ca++ -> eNOS -> NO -> cGMP -> vasodil
ADRs:
hypoTN (new dose), dry cough & angioedema (due to bradykinin), hyperkalemia (due to block of aldosterone which sec. K), increased SCr (due to decreased GFR), also beware Triple Whammy of ARF (ACEi, diuretic, NSAID)
Use: HTN, CHF, CKD
Oral prodrugs |
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Term
| 3 drugs to slow progress of CKD |
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Definition
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Term
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Definition
MOA: block AT1 receptor (Gq) -> decreased IC Ca++ -> decreased sm musc contraction -> vasodil
ADR: hypoTN, increased SCr, hyperkalemia
oral qd |
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Term
| ARB Affinity: Two best & two worst |
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Definition
Best: Azilsartan > Candesartan
Worst: Losartan < Valsartan |
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Term
Direct Renin Inhibitors
MOA & ADR & Use |
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Definition
| MOA: inhibits active form of renin by binding where angiotensinogen would bind; however since prorenin can still convert some angiotensinogen to AngI via PRR, not all AngII is stopped |
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Term
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Definition
Direct Renin Inhibitor
oral
Use: HTN (investig. CHF & CKD |
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Term
| 3 drug classes for treating CHF |
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Definition
Beta Blockers - bisoprolol, metaprolol, carvedilol
ACEi
Diuretics - Loop (don't decrease mortality) |
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Term
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Definition
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Term
proximal convoluted tubule
fxn & drug |
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Definition
reabsorb most Na & HCO3-
CAi |
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Term
proximal straight tubule
fxn & drug |
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Definition
a/b reabsorb
osmotic diuretics |
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Term
thin descending loop of henle
fxn & drug |
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Definition
H2O reabsorb
osmotic diuretics |
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Term
thick ascending limb of henle
fxn & drug |
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Definition
reabsorb 2nd most Na & Cl
Loop diuretics |
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Term
distal convoluted tubule
fxn & drug |
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Definition
reabsorb Na/Cl
TZ diuretics |
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Term
distal straight tubule & collecting duct
fxn & drug |
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Definition
fine tune Na reabsorb; couple with K & H secretion
Na channel inhibitors & aldosterone antagonists |
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Term
CAi
MOA, SOA, e-lyte effects, uses |
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Definition
MOA: disables Na/H antiport
via inhibition of CA which converts H2CO3 to CO2 + H2O in lumen then back to H2CO3 in cell where it donates a H+ to be secreted while Na is reabsorbed
SOA: PCT
e-lyte effects: acidosis; hypokalemia
uses: alkalosis, urine alkylization, epilepsy, altitude sickness, glaucoma |
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
Osmotic diuretics
MOA, SOA, uses |
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Definition
MOA: filtered but not reabsorbed; increases osmolarity
SOA: thin descending loop & straight proximal tubule
uses: emergency ICP&IOP |
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Term
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Definition
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Term
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Definition
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Term
Loop Diuretics
MOA, SOA, e-lyte effs, other ADRs, uses |
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Definition
MOA: inhibit NaK2Cl symporter -> Na & Cl don't reabsorb ->urine must be diluted -> pee :)
SOA: thick ascending limb
e-lyte effs: hypokalemia (Na exchanges with K in collecting duct), alkalosis (Na exchanges with H in collecting duct), hypocalcemia&hypomagnesemia (Ca & Mg rely on symporter to create membrane potential to absorb via tight jxn)
ADRs: resistance (usu combine w/TZ), hypersensitivity (if sulfa), ototoxicity
Uses: CHF, ARF (works when GFR<30), hypercalcemia due to breast/prostate cancer |
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
Thiazide Diuretics
MOA, SOA, e-lyte effs, uses |
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Definition
MOA: inhibit Na/Cl symporter -> Na & Cl don't absorb -> urine must be diluted -> pee :)
SOA: DCT
e-lyte effs: hypokalemia, hypercalcemia (Ca is reabsorbed at DCT; drug causes more o_o)
uses: HTN |
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Term
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Definition
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Term
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Definition
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Term
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Definition
TZ-Like Diuretic
thus effective w/GFR < 30 |
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Term
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Definition
TZ-Like Diuretic
thus effective w/GFR < 30 |
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Term
Na Channel Inhibitors
MOA, SOA, e-lyte effs, uses |
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Definition
MOA: bind & inhibit Na channel by bein' similar :)
SOA: straight distal tubule & collecting duct
e-lyte effs: hyperkalemia (due to Na/K exchange being blocked)
Uses: Combo w/TZ or Loop |
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Term
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Definition
Na Channel Inhibitor
used Liddle syndrome- mutation in epithelial of channels --> excessive Na+ reabsorption(hypernatremia) and potassium reabsorption(hypokalemia) that causes HTN |
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Term
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Definition
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Term
Aldosterone Antagonists
MOA, SOA, e-lyte effs |
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Definition
MOA: binds mineralocorticoid receptor in place of aldosterone -> decreased Na Channels, decreased Na/K ATPase -> decreased Na reasbsorp & K secretion
SOA: distal straight tubule & collecting duct
e-lyte effs: hyperkalemia due to block of secretion |
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Term
|
Definition
aldosterone antagonist
nonsel; also binds progesterone receptor -> hirsutism & manboob |
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Term
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Definition
aldosterone antagonist
selective; causes worse hyperkalemia thus caution in ACEi or ARF |
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Term
| Vasopressin V2 Effects & Use |
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Definition
Gs -> increased synthesis & transloc of aquaporins -> more H2O reabsorbed during high blood osmolarity
use: central diabetes insipidus (pt cannot synth ADH) |
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Term
| Vasopressin V1 Effects & Use |
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Definition
Pressor
Gq -> increased IC Ca -> sm musc contraxn
use: shock/gastric bleeding |
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Term
Desmopressin/DDAVP
Use, Admin |
|
Definition
V2 agonist
peptide
uses: central diabetes insipidus, nocturnal enuresis, clotting disorders (V2 exists on endothelial cells which sec VWF)
admin: po, iv, in |
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Term
conivaptan
use, effects, admin |
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Definition
nonsel vasopressin antagonist
use: SIADH
effects: aquaresis
admin: IV |
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Term
tolvaptan
use, effects, admin |
|
Definition
V2 selective
use: SIADH
effects: aquaresis
admin: IV, po |
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Term
|
Definition
ACEi (DOC)
ARB
BidiL
nitroprusside (acute)
nitroglycerine (acute)
nisiritide (acute) |
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Term
|
Definition
Diuretics
Vasodilators
(+)Inotropes
B1 Antagonists |
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Term
|
Definition
B1 agonist (dobutamine) (acute only)
dopamine (Gs) (acute only)
glucagon (Gs) (acute only)
PDE-3 inhibitors (acute only)
digoxin (acute or chronic) |
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Term
PDE-3 Inhibitors
MOA, SOA, Uses |
|
Definition
MOA: raise cAMP -> increased PKA -> increased phosphorylation of SR -> increased contractility
SOA: heart muscle
Use: CHF |
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Term
|
Definition
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Term
|
Definition
PDE-3 inhibitor
ADR of thrombocytopenia |
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Term
digoxin
MOA, ADRs, Metabolism, Use |
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Definition
MOA: EC inhibits Na/K ATPase pump (3Na/2K) -> Na buildup -> Na leaves by Na/Ca exchange -> Ca buildup -> increased contractility
ADRs: nausea, yellow tinted vision, arrhythmias
Metabolism: unchanged by kidney
Use: CHF |
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Term
| Nesiritide MOA, Effects, Uses |
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Definition
Natrecor MOA: binds BNP receptor -> memb guanylate cyclase -> cGMP -> PKG -> sm musc relax/vasodil Effects: decreased preload/afterload & increased GFR & diuresis due to dilation of renal artery
Uses: acute HF (not given chronically can increase mortality and kidney failure)
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Term
| Name 5 causes for arrhythmias |
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Definition
ectopic beats due to ischemic tissue
e-lyte abnormality e.g. high K
adrenergic drugs increasing HR
digoxin increasing IC Ca++
re-entry circuit |
|
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Term
| 4 Classes of Slow Conduction Tissue Decreasing Agents |
|
Definition
Adenosine
B Blockers
CCB (nonDHP)
Digoxin |
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Term
|
Definition
1.) inhibit Na/K ATPase -> increase IC Ca++ -> (+)ino
2.) central vagal (parasymp) effect -> ACh onto Gi (M2/M4)
a.) -> decreases cAMP -> decreased Ca entry into fast conduction tissue -> decreased pacemaker current
b.) -> opens K channels -> fast conduction tissue hyperpolarizes -> longer refractory period |
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Term
Adenosine
MOA, admin, indications |
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Definition
MOA: activates A1 receptor on SA/AV Node -> similar to M2/M4 effects of digoxin
Admin: rapid IV bolus so cells don't absorb it all before it reaches the heart (stored for ATP creation)
Uses: SupraVentricular Tachycardia acutely -> actually stops heart for a sec |
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Term
| 4 Classes of Antiarrhythmics |
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Definition
I) Na Channel Blockers
II) Beta Blockers
III) K Channel Blockers
IV) NonDHP CCBs |
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Term
lidocaine
uses, monitoring |
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Definition
Class IB Na Channel Blocker
use: IV drip after MI
monitor blood levels -> too high = coma, seizure, slurred speech |
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Term
|
Definition
| Class IB Na Channel Blocker |
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Term
Class IB Na Channel Blockers
Tau Recovery |
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Definition
Rapid dissc from resting state
Preferentially block ischemic tissue bc more are inactive @ a given time due to more depolarized state (-75mV vs -90mV healthy) |
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Term
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Definition
| Class IC Na Channel Blocker |
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Term
|
Definition
| Class IC Na Channel Blocker |
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Term
|
Definition
Class IA Na Channel Blocker
antimuscarinic ADRs |
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|
Term
procainamide
class
metabolism
ADR |
|
Definition
Class IA Na Channel Blocker metabolized by PII N-acetyl transferase --> Lupus like syndrome
Agranulocytosis = decrease in WBC |
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Term
|
Definition
Class IA Na Channel Blocker
can cause cinchonism -> visual disturbances& ear ringing |
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Term
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Definition
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Term
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Definition
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Term
|
Definition
Tikosyn
K Channel Blocker
excr. unchanged in kidney so monitor levels |
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Term
amiodarone
benefits & ADRs |
|
Definition
K Channel Blocker
shown to decrease mortality*
really REALLY long t1/2; in your body a year after d/c
ADRs: pulmonary fibrosis, liver dysfxn, thyroid dysfxn, blindness |
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Term
|
Definition
K Channel Blocker
shorter t1/2 than amiodarone |
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Term
Class IC Na Channel Blockers
Tau Recovery |
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Definition
Very slow dissc from resting state
-> can slow a healthy heartbeat |
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Term
|
Definition
| Increases refractory period by taking some inactive receptors out of equilibrium for longer |
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Term
K Channel Blockers
MOA, ADRs |
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Definition
MOA: prolong plateau & delays delayed rectifier current -> Na channels stay inactive for longer bc they can't recover yet
ADRs: Torsades de Pointes arrhythmia due to increased IC Ca++ |
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