Term
|
Definition
| sustained adrenergic traffic ledasd to icnrased renin adn increased nagiotensin II. It raisesadlsoterone raising sodium retension. This leads to edema and pulmonary congestion in Heart fialure. |
|
|
Term
| downwrad spiral of herat faiulre |
|
Definition
decreased CO activated norep and angiotensin II and endothelin, which causes vasocinstriaction and incrased afterload . Further redjuction of ejection fraciton adn CO. This spiral.
look at downward spiral graph on right: ionotropes shfit the curve back up. and vasoidilators shift it to the left. |
|
|
Term
|
Definition
to decrease ecf volume/preload and curtial remodeling/foibrosis (ppironolactone).
control congestive symtpoms. dont decreasem ortality |
|
|
Term
| vasodilators over al lfunction |
|
Definition
| to dcrease preload/afterload |
|
|
Term
|
Definition
| reduce arrythmogenesis, curtail remodeling. reduce undsird ysmpathetic effects |
|
|
Term
|
Definition
| reduce arrythmogenesis, curtail remodeling. reduce undsird ysmpathetic effects |
|
|
Term
|
Definition
|
|
Term
|
Definition
| fluid enters glomerulus passign through prox tubule, thorugh thin dsecending limb through ascending limb through distal convulated utuble otu to collecting duct. |
|
|
Term
|
Definition
blocks na/k/2cl- mines nkcc2, in thick ascending limb .
loop agents also hae dirrect effects on blood flow through several vascular beds, leading to relif of pulmonary congestion before diuresis occurs. |
|
|
Term
|
Definition
|
|
Term
|
Definition
| loop diuretic, used only for sulfonamie allergies due to otoxicity |
|
|
Term
| loop diuretic side effects |
|
Definition
| enhace delivery of sodium and water to colelcting duct, leading to enhance k,h, mg2plus secretion, resulting in hypokalemic metabolic alkalosis an d hypomagnesemia. |
|
|
Term
|
Definition
| block symporter- NCC - nacl- . Less effective than loo pdiuretics, hwoever synergistic effect. |
|
|
Term
|
Definition
| enhance h and k secretion nthrough increased sodium deliver to moredistal sites. Causing hypokalemic metabolic alkalosis |
|
|
Term
| potassium sparing diuretics moa |
|
Definition
| act on collecting duct, priamrily of prinficple cel, antagonising aldosterone. |
|
|
Term
| potassium sparing diuretics moa |
|
Definition
| act on collecting duct, priamrily of prinficple cel, antagonising aldosterone. |
|
|
Term
| triamterone amiloride type and moa |
|
Definition
| potassium sparing diuretic. - block EnaC Na plus chanel. |
|
|
Term
| spironolactone type and moa |
|
Definition
| direct aldosterone antagonist (work at receptor). Thought to be effective more due to their ability to inhibit cardiac remodelling as opposted to diuretic ability |
|
|
Term
|
Definition
| direct aldosterone antagonist (work at receptor). better tolerated than spironoclatone because mroe specific. |
|
|
Term
|
Definition
| primary site of potassium secretion. |
|
|
Term
|
Definition
| higher in patients with heart failrue due to lwoer adlosterne degradationi nliver, k plus stimulated secretion, or angiotensin II levels icnreased |
|
|
Term
| k plus sparing diuretic side effects |
|
Definition
| increased potassium! leading to possible rhythmic changes |
|
|
Term
|
Definition
decrease afterload by lwoering peripheral resistance (increasign C.O and ejection fraction), reduce preload byreducing aldosterone secretion.
1. decrease conversion of angiotensin I to II.
2. Decreased aldosterone synthesis.
3. Decrease sympathetic activity by reducing NE.
4. Decreased logn term remodelling of heart and vessels due to decreases SNS and Aldosterone
venodilation in CHF. |
|
|
Term
| Ace inhibitors adverse effects |
|
Definition
increased risk of hyperkalemia due to decreased aldosterone syntehsis.
increased renin and angiotensin I levels due to negative feedback Decreased bradykinin degradation , which stimualted prostaglandin and NO leads to cough and angioneurotic ademea (swelling of nose, throat , glottic, tongue).
risk of hypotesion (as well as other drugs) |
|
|
Term
|
Definition
|
|
Term
|
Definition
| for grades II-IV CHF, support actions of diuretics. Are able to decrease mortality due toheart failure. |
|
|
Term
| angiotensin II receptor blockers |
|
Definition
block at1 and at2 recetpros. at1 receptors are g protein linked and use plc pathway to eleate free calcium. at2 recpetors: icnrease cGMP formation. |
|
|
Term
|
Definition
|
|
Term
|
Definition
| almost as e fefctie as AcCE inhibitors, but not quite. Decreasem ortality. have less side effects ecause do nott effect bradykininw in anyway |
|
|
Term
|
Definition
| used for acute setting. dilates both arterial and venous vessels, but must be given contiously via iV. |
|
|
Term
| hydralazine plus isorbide dintrate |
|
Definition
| helpful butless effective htan ace inhibitors. usually used as adjunct. esp useful in blacks. |
|
|
Term
|
Definition
| for use for chf in acute basis |
|
|
Term
|
Definition
| renin blocker, use like ace inhibitor ,but no bradykinin effects |
|
|
Term
|
Definition
reduce mortality.
beneficial action; lower adverse effects ofh igh catecholamiens (icnludinga poptosis). upregulation of beta-1 receptors- for increased catech resposniveness.
reduced remodeling.
decreased heart rate adn arrythmogenesis |
|
|
Term
|
Definition
|
|
Term
|
Definition
| racemid mixture of nonselective beta blocekr and alpha 1 antagoninst |
|
|
Term
| carvedilol short term effects and logn term |
|
Definition
| short term: vasodilation without lwoering of C.O. long term: prevents detioration of myocardial function and reverse adrenergically mediated myocardial dysfunction. Unlike metaprolol has no effects on beta 1 receptor numbers. |
|
|
Term
| carvedilo ladverse efects |
|
Definition
| symptomatic hypotensioa nd bradycardia, alelviated by starting with very low doses |
|
|
Term
| nitortopic agents general moa |
|
Definition
| icnrease intracellular calcium levels , adrenergic agonists also do simliar things |
|
|
Term
| digatlis MOA/ cardiac glycosides |
|
Definition
inhibition of sodium potasisum atpase. leading to decreased calcium kicking out via na/ca2plsu channel. Binding of digtalis is inhibited by potassium.
increaased itnracelluar free clacium promotes cardiac contraciltity viat he cardiac torpnoin system.
Movest the cardiac output curve verticallly upwards.
doesnt decrease moratliy, and doenst work syngerstically wtih acei nhbiitors |
|
|
Term
|
Definition
early breif prolognation fo AP , folwoed by protracted pe riod of shortening, which elads to shortened artial/ventricualr refractoriness. this is due to cholineric innervation stiulation.
It also reduces resting membrane potenial (lessn egative due to blockign ofh te atpase. It also sensitizes myocardium to sypathetic trnsmitters. digitalis can cause v irutally an ydegree of arrythmia |
|
|
Term
| cardiac glycosides farm actions |
|
Definition
increases C.O. , decreases heart size, decreases venosu pressure, and decrease EDV,produce diuresis, adn decrease blood v olume.
consequences: decreases symapthetic output (direct and reflex and incresed vagal activity- decresed herat rate nad icn reased vasodialtion.
increased renal perfusion.
inhibiton of renal sodium/potassium atpase promoting sodium exretion and iuresis.
improving renlal perfusion nd reduced renin oputput. |
|
|
Term
| three variants of glycosides cardiac |
|
Definition
| ouabin, digoxin and digitoxin. Oubain not vyr lipid solube so used epremtianlly . digoxin only one really sued clinically |
|
|
Term
|
Definition
| ivnestigational steroid driate increased cardiac contratiliy via na/ka apte but also faciliates calcium sequesteration making it lessa rrythmogenic htan digoxin |
|
|
Term
| pharmacokinetics of digoxin are complciated |
|
Definition
| needst o be itnroduced with care |
|
|
Term
|
Definition
| calcium sensiizer- increase calcium binding to troponin. |
|
|
Term
|
Definition
| phosphodiesterase inhibitors. Icnreases Camp and photrphosylaciton/activaiton fo l tyep calcium channels. Incresing calcium fluxx in heart and contractility. Also inhibition of myosin light chain phsorphyrlation leading to vasodilation. |
|
|
Term
| phosphidesterase inhibitorsu se |
|
Definition
| long term usei s not warranted due to increased arrythmias, thrombocytopenias and liver toxicity. |
|
|
Term
| beta adrenergic agonists main effects |
|
Definition
| rsult in icnrease calciu m influx and alterin calcium kienticsi n SR, resulting in phosphorylation of troponin. |
|
|
Term
|
Definition
| depepdnant upon infusion rate. at low levels acivated d1 and d2, at higherl evels also acivated beta 1, at highest rates actives alpha1 whichi s udnesirable because of its vasoconstrictive effects. |
|
|
Term
| dobuatmine compositioand action |
|
Definition
| racmic mixture of beta1 more htan beta 2 agonists , with an alpha1 agonist. Overall see mostly b1 adrenergic repsonse. |
|
|
Term
| acute vs chronic heart failure |
|
Definition
acute- ie. after mi, or shock. maintain pbp and icnrease cardiac output.
Chronic- congestive hear faiulare. Control ECF expansion, icnrease CO an d decrease periph resitance. INcrease excercise tolerance nad preent cardiac hypertrophy and remodleigng |
|
|
Term
|
Definition
| ptoassium sparing diuretic |
|
|
Term
|
Definition
|
|
Term
| hydralazine and isodorbide dinatrate |
|
Definition
|
|