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90 Cards in this Set
- Front
- Back
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Define conductivity*
(know differences between excitability, automaticity, dromotropism, and refractoriness) |
Ability of cell(s) to RECEIVE/TRANSMIT an AP
-excite: respond to stim (AP) -auto: initiate -dromo: rate conduction -refract: inability to receve/transmit! |
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Important disorder of impulse form?
of impulse conduction? |
-DAD (ca leak inside and spon depol)
-AV nodal re-entry (2nd/alt path of conduct A-->V that pre-excites ventric) -AV nodal block 1, 2, 3: 1: increased PR, slow 2: not all p waves pass AV 3: NO pwaves pass! no p/qrs rel -Ventric Re entry: one way blcok and re-entry of circuit, depol before next depol |
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Class 1 anti-dysrhythmics?
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Block Na+ channels, decrease excite of non-nodal/conductive tissue
-LOWERS AUTO, DELAYS COND, PROLONG ERP/ADP -Treats MI INDUCED DYSR (v dysr or digitalis) a: quinidine, procainamide, disopyramide b: lidocaine, phenytoin c: flecainide |
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Which drug classes affect NON NODAL tissue? (phase zero due to Na in)
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Class 1 (Na) and 3 (K) because affects ventricles
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Which drug classes affect NODAL tissue? (phase zero due to Ca in)
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Class 2 (bb) and 4 (Ca) affects nodal
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Class 1a agents?
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quinidine, procainamide, disopyramide
(quin is 1a pro(t) w/ dis) -moderate Na+ chann binding (delay 0) -K+ chann block (prolong qrs/QT, delayed 3) -Ca+ chann block high dose (low 2) |
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Class 1 b agents?
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lidocane
(liar-b 2faced, does 2 diff things) -weak bind Na+ -accel 3 repol *use digitalis/MI dysR (increase cond normal (lowers ERP/increase excite), decrease damaged tissue) |
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Class 1c agents?
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fleCainamide
(fle(e) C, depol) -Stongest binding to Na+ (slow on/off delayed depol 0) longer qrs/apd/PR (not qt) -depressed AV conduction (severe unstable MI) |
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Class 2 agents?
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propanoLOL, acebutaLOL, esmoLOL, metoproLOL (lol see 2 numeral w/o)
-block B rec that are G prot coupled to Ca+ chann: NODAL 0 low -low SA auto, AV cond*, V contract (by prolong PR) -Tx supraventric , digitalis dysR (also lower v ectopic depol) |
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Class 3 agents?
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amiodarone, dofetilide, ibutilide
(3 good amies/friends do-fetch boots w/soda @ hessen) -K+, Ca+, Na+, and B rec (in)direct) -prolong 3 repol, increase QT/erp (similar to class 1a!) Tx V re-entry/fibrillatory dysR |
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Class 4 agents?
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verapamil, diltiazem, bepridil
(4 seats in car, driver veers, beeps, and dilates eyes to drive) -Block Ca+, depress SA auto, AV cond*, decreased ventric contract (sim to class 2, aff 0) |
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Quinidine?
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1a, cinchona bark
SupraV/V dysR (low auto nodal, longer QT non-nodal) i.e. PAT/PSVT 1/3 discontinue/side effects! -cichonism (tinnitus, hear/blur) -hypoT-a block -Torsades de Pointes, increase QT (class 1 & 3, tx w/MgSO4 :)) Dose adjust if renal prob! (plasma prot binding/active metab = longer t1/2) |
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Procainamide?
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1a (no ester, little CNS)
metab depends on Hep N-actyltransferase/renal fxn -70% drug unchanged in urine -RAPID (t1/2 3 hrs) & SLOW**1/3 (5+hrs) acetylators be concerned! -slow can dev SLE like syndrome (arthralgia, pericard, fever, wk, skin, lymph, anemia, hepatomeg) -also see N/V, low renal/prodysR, torsades des pointes |
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Lidocaine?
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1b, unusual, b is 2 faced liar
-inhib re-entry in V tissue, suppress spont V depol -PREF axn on ISCH tissue, so use post MI/digoxin induced TACHY!! (post v fib tachy*) -shortens ERP/ADP in normal paths (excites) IV only/acute |
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flecainide?
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1c
greatly depress cardiac conduct -not 1st line bc prodysR (CAST1) -tx refractory life threat ectopic v dysR (prolong 0, widen qrs) |
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Propanolol?
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Class 2, b block (indirect Ca+ block)
-decrease HR/CO/conduction A/V/AV -Tx: atrial flutter/fib, PAT side effects: hypoT, asystole, BRONCHOSPASM, rebound w/drawl (rec up reg-don't miss doses!) |
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Amiodarone?
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class 3, alters K+ in 3
-lengthen ERP/APD! (low excite V) -purported less prodysR potential (cheaper, safer) side eff: 75% if chronic PO-lung toxic, photosens (micro deposit eye), thyroid* disorder/tumors |
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Verapamil?
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Class 4, CCB
Tx: supraV tachy (also diltiazem) -slow Ca+ in affected, nodal ***more useful than digox in Afib since CCB PERSISTS during SYMP STIM! -decrease HR, SA auto, AV conduct "Cardiac Depression" v contract/hr/co/sv -increase PR, qt, torsades de point -IV: rapid convert SVT -PO: maintain recurr SVT (high lipophillic, hemodial ineff to rid) side eff: *GI constip (give stool soft to avoid VALSALVA), hypoT, worsen CHF, AV heart block w/lol's |
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ADENOSINE?
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OTHER CLASS 5
-purine nucleoside, converts re-entry SVT to NSR!! ******ADENOSINE SUBTYPE 1 (A1) RECEPTOR FOR SVT ON AV NODE************************ -less toxec than verapamil (shorter 1/2) -AV node hyperpol, b/c adenosine stim open K+ out hyperpol! (prod complete AV block) -must give IV BOLUS (6-12mg) CLOSE TO HEART (rapid degrade in plasma) t 1/2 = 10-15 sec -stops heart, then picks up normal |
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Digoxin?
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Directly stim VAGUS/PS
Tx chronic A fib, but CCB are preferred cadiac glycoside w/2 MECHANISMS! -CHF: Na/K/ATPase inhib** -Afib: vag stim, neg dromo @ AV, causes PROLONG ERP! (slow v rate by decreasing p waves reaching V) ***SYMP CAN OVERIDE! (bc not CCB) Side eff: prodysR due to hypoKalemia (class IB/2 can tx digoxin induced dysR)* |
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Treatment for other dysR?
-bradycardia -sinus tachycardia |
-brady: atropine (vagal block to increase HR), isoproterenol (B1 stim to increase HR), pacemaker
-sinus tachy: vagal stim through carotid sinus/valsalva to decrease HR to normal (bear down/cold H2O) |
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Characterize heart failure?
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Reduction SV/CO at any given EDV
-due to MI, chronic hyperT (untx) |
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Describe the Frank Starling Relationship?
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V contract varies DIRECTLY w/ musc fiber length (EDV/preload)
-as EDV (fiber length) increases SV (tension) increases |
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What do pos/neg iontropic influence directly alter for any given EDV?
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CONTRACTILE FORCE
@ same EDV, pos or neg iontrope will increase or decrease SV (contractile force) |
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Low output congestive heart failure results from ______? graph
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Decreased contractile capacity, lowest curve (on EDV vs SV)
added digoxin tx shifts whole curve up, but NEVER as high as normal |
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3 major clinical sxs of CHF?
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1) Ventric hypertrophy (cardiomeg)
2) edema (pulm/periph) 3) weak, rapid**, pulse (baroreflex: if decrease MAP (CO x TPR), symp increases HR, but still wk pulse) -goal of tx = reverse these sxs |
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Primary (and other) treatments for CHF?
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-DIURETICS/ACEI/VASODIL
-diet/Na+ restrict -exercise -pos iontropic (rarely) |
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What should you know about DIGITALIS?
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Cardiac Glycosides use for Afib
*inhib Na/K/ATPase* HOCKEY STICK* (ST) forced exchange (Na out/Ca in) more Ca+ for musc fiber contract! LD higher than ED! -rest memb pot (4 v contract) more pos -phase 2 shortened (altered Ca+) -phase 3 altered, rapid repol, APD shorter changes in plasma K/Ca augments prodysR effects (prob if combine w/diuretics that deplete K+) not diuretic but 2nd fluid loss (pt low SV/kid perf takes digoxin to increase CO/renal/UO-->cath/meas) |
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How would you correct adverse elevations of plasma digoxin?
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Cholestyramine
digoxin immune Fab: bind free/bound cardiac glycosides (out kid) IV: immediate axn but therapeutic/ clinical affects reversed |
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Isoproterenol?
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B1 agonist, increase cAMP/Ca+ for membrane excite/contract
acute use only to increase contractility (CO) and HR |
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Dopamine?
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low dose: DA1/2 periph vasc, vasoD to increase GFR/UO
**MOD DOSE: additional stim B1 to increase Contraction and slight HR. TX: LOW CO but already HIGH HR high dose: additional stim a1, periph vasoC |
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Dobutamine?
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less B1 tachy (and less a1)
PREF INCREASE CONTRACT (CO) short term manage of heart fail after MI |
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Phosphodiesterase Inhib?
-Inamrinone -Milrinone |
INHIB ENZ FOR DEGRADE cAMP
INCREASED CAMP/Ca+ by IV (acute) to improve contractility, vasoD |
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Remember the Baroreceptor Reflex and why it becomes a problem in Rx treatment for hyperT?
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HyperT pts MAINTAIN a higher homeostatic set point for BP, so the body will fight the decrease in BP due to drugs
mech include: carotid sinuses, CN 9, NTS, AP, RVLM, CVLM, CN 10, cardiac accelerans/medullary efferents ***IF Rx VASOD, BP DROPS: Reflex increase by body: kidney decrease RBF, sodium/H2O retention, increase BP, HR, CO** (increase symp) major cause hyperT = primary/essential 90% -idiopathic, genetic, middle aged (non-essential/secondary: I.D cause-renal, tumor, stenosis so tx surgery) dx 2+ times, 4 wks apart AHA: >140/90 WHO: >160/95! |
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First Step in tx hyperT?
Then? (next steps if inadequate response) |
1) NON-PHARM LIFESTYLE, lose wt, lower alc/Na+/sugar/fat/CE, exerc, maintain K+, Ca+, Mg+, stop smoke
2) modif + PHARM 3) increase dose, substitute Rx, 2nd drug 4) add 2nd/3rd, etc (one must be diuretic!!) -consider life-long, cost, side eff/interactions, non-Cx, step care |
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Most drugs have initial drop in ____ (but comes back)
BUT LONG TERM ______ stays low! |
CO
TPR MAP = CO x TPR******** CO = HR x SV******** So MAP/BP = HR x SV x TPR (can choose any 1 factor to lower BP) |
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Importance of Diuretics to lower BP?
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1st lower CO but returns
2nd LOWERS TPR** =thiazides (HCTZ), loop, K+ sparing moderate monotherapy 20/10 AUGMENTS antihyperT of OTHER Rx's! -works better in AA/OLD ****activ RAS so MALPRACTICE to NOT GIVE DIURETIC!!!!!!!!!!!!!!!!! AND don't give to hyperlipidemia** pts! will increase LDL/TG onset axn 2-4 wks, max 3-4 mo no benefit if increase dose (just side effects) |
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B Blockers to lower BP?
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PROPANOLOL class 2 antidysR
decrease HR/contractility(CO) = to lower BP decrease Renin/ang2 to VASOD moderate mono, better combined *+ Diuretic (SMOKERS DON'T RESPOND WELL) -->7-9% will stop (asthma-B2, hyperlipid, male sex dysfxn, masks sxs hypoglycemia!, worsen CHF) labetalol/carvedilol: block B1/2, a1 -lower BP AND vasoD vasc sm musc (B1 blocked so no reflex tachy!!!!) -long term manage (CHF/high BP) short ER BP lower |
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Centrally Acting Sympatholytic?? to lower BP (1 of 2)
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CLONIDINE (activ a2) decrease HR/TPR
-affects/blocks all symp activ decreases NE release from post-gang Nerve Term (35/20 combine w/diuretic) |
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Centrally Acting Sympatholytic?? to lower BP (2 of 2)
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a-methyldopa: CHILD-BEAR AGE WOMEN (also stim a2)
ADVERSE EFF: + COOMBS (presence auto-Ab to RBC) prod frank hemolytic anemia |
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Peripherally-Acting Sympatholytics??
3 big ones ____end in? |
AZOSIN (prazosin, terazosin, doxazosin) BLOCK a1 vasc sm musc*
15/10 mono, 25/15 w/diuretic -helps to lower LDL/TG/total CE :) -but mild reflex tachycardia* -b/c direct vasoD, TAKE @ NIGHT! (to avoid orthostatic when baroreflex slow at vasoC for blood to head) |
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CCB to lower BP?
(hint: 2 from class 4 antidysR) |
Verapamil(30/20) & dilitiazem(20/15)
direct vasoD (inhib Ca+entry vasc sm musc and release from SR) CONCERN: CARDIODEPRESS (may counteract reflex tachy-direct on AV node to no increase HR/CO) |
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Other CCB to lower BP?
(hint: dipine, so what do you need to use??????????????) |
NIFEDIPINE (dihyropyridine class ccb)
-direct vasoD (inhib ca+ vasc musc and SR -LESS CARDIODEPRESS (no direct AV node) so PROMINENT REFLEX TACHY!!!!****must use w/B BLOCKER! to block reflex (EXAM) |
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Direct vasoD to lower BP? #1
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HYDRALAZINE
guan cyclase stim, increase cGMP, Ca+ sequestered causes sm musc RELAX! (arterioles/afterload* & some venous/preload) 25/25 Need B blocker/diuretic again! to prev increase HR/CO/Na+/H2O retention TOLERANCE DEV (TACHYPHYLAXIS) due to this baroreflex! -adverse: SLE like syndrome (n-acetlyation metab) palp, tachy -only for tx R*, fulminant hyperT, ER |
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Direct vasoD to lower BP? #2
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MINOXIDIL
topical rogaine & oral for severe, non-responding hyperT -stim vasc sm musc K+ out (hyperpol) lowers BP -but tachyphylaxis baroreflex increase symp tone so use Bblock/diur! AGAIN |
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Direct vasoD to lower BP? #3
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Sodium NITROprusside (NO* & CN)
-parenterally infused, POTENT Dilator -decreases afterload AND preload (venoD) *EDRF = cGMP/Ca+ seq -extended cont infusion = >24hrs methemoglobinemia, CN poisin, inhib cell respire/death |
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ACE Inhibitors to lower BP?
___end in? -2 reasons to take off/avoid?* |
captoPRIL, enalaPRIL, linsinoPRIL
*most widely used antihyperT! 25/20 ****ang2 on AT1 receptor***exam 2 mech***** 1) DECREASE ANG 2 -3mo lower bp, but same ang 2 due to block ang (ang2 = vasoC) at micro/cell level 2) INCREASE bradykinin -blocks kinase 2 which breaks down bradykinin (more brady = vasoD) -max in 4-8wks, less for AA -ADVERSE: DRY COUGH 1/3 must take off ACEI -PREGNANCY CONTRAINDICATION (renin-ang fetal dev) |
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Angiotensin Rec Blockers to lower BP?
___end in? 1 reason to avoid** |
loSARTAN, candeSARTAN, irbeSARTAN, valSARTAN
-newest, +diuretic, low side effects -antag ang 2 at AT1 REC********* (on vasc sm musc*, adrenal cortex, brain, sp cord, heart) -NO COUGH (b/c no bradykinin increase) but DON'T USE IN PREGNACY!! |
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Angina is due to ____?
importance of vessel radius and flow? |
Angina (severe press/constrict pain) is due to Cardiac Ischemia (low flow/O2 delivery to heart)
-sm decrease in radius = LG DECREASE IN FLOW (exp 4th) |
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How can the pain of angina be counteracted?
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= improving myocardial perfusion/vasoD OR decrease metab demands
ischemia when increase work load more than oxygen supply -increase after/preloads create imbalance |
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What is the "Steal Phenomenon"**?
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= vasoD do not improve isch attack by producing coronary vess dilation
**in chronic isch, vessels incld downstream @ MAX DILATION (body-reactive hyperemia) **so vasoD therapy helps by dilating ven/art on BOTH sides of heart = LOWERS PRELOAD AND AFTERLOAD = lower O2 demand (so lower flow is now sufficient)*** |
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2 mech of vasoD?
2 types of 2nd mech? |
1) block endog vasoC
2) direct relax vasc sm musc a) endoth dep (ach, bk) b) NON-endoth dep vasoD**** -NO donators (nitrovasoD) provide their own EDRF****** causes immed drop in BP! |
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2nd use of NITROprusside? (other than antihyperT)
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ER (short-term or build up CN) parenteral to REDUCE PRELOAD & AFTERLOAD
***REDUCE MYOCARDIAL O2 DEMAND! |
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NitroGlycerine used for?
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EDRF donor (manage angina since '79)
freq dosing = tachyphylaxis (tol dev) SUBLINGUAL (1-3min) + psych best, but many forms avail **Nit Ox stim increase cGMP/Ca+ seq, sm musc relax in art(after) and ven(pre), so reduces heart work by......DECREASE heart TENSION during diast/systole***** (vasoD's induce reflex high HR/contractility, but nitrogly decreases O2 demand to relieve pain) Adverse: HA b/c cerebral vasoD, flush, subling burn **effective :) -Isosorbide diNITRate-ISDN (similar) -nifedipine also reduce afterload -ACEI/Bblock also "" prophy & CHF |
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EDRF and ENDOTHELIN?
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EDRF = NO, sol gas prod by vasc endoth, cGMP vasoD, underprod lead to angina, vasospasm, hyperT?
ENDOTHELIN = PEPTIDE by vasc enoth, rec mediated (ETa)/ca+ vasoC, same Cx w/OVERproduction ENDOTHELIAL LAYER produces the most potent VASOD & VASOC |
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What are sarafotoxins?
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primary toxin made in SNAKE
(Atractaspis engaddensis kills 50ppl/yr by ***vasoC HEART ATTACK) we have 3 similar endothelin peptides made in our body |
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Acetazolamide?
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Carbonic Anhydrase Inhib (CAI)
85% decrease in HCO3- reabsorp! Increase urine pH/metab ACID!**** -decrease acid/NH4+ excr (+ decrease new HCO3-) CAI4: PCT* brush border inhib CAI2: cytoplasmic inhib -->H+ secr (for Na+ in), combines w/HCO3-, makes H2CO3**CA4 splits this into H2O & CO2 -->CO2 diffuses into cell, combines w/H2O, makes H2CO3- INSIDE** by CA2 -->H2CO3 splits into H+ (secr) & HCO3- (INTO BLOOD w/Na+), maintained by Na+out/K+ in cell ATPase |
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Clinical Indications for CAI's?
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-Glaucoma (CA in ciliary body)
-Acute mountain sickness -Urinary Alkalization (to excrete Rx) -Edema: combined w/NKCC or NCC inhib Adverse? metab acid (block HCO3 reab), renal stone/loss K+(high flow) Don't use in cirrhosis pts (hyperammonemia) |
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Mannitol?
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Osmotic Diuretic: increase tub osmotic P at THIN loop* mostly
Decrease tubular fluid reab/K+ secr Tx: acute renal fail, cerebral edema, dialys disequal, acute glauc Adverse: ECV expansion, pulm edema, low/high Na+ (don't use in renal dis UR, impaired liver, cranial bleed) |
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Furosemide?
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LOOP DIURETIC, NKCC inhib (Na+K+2Cl- Cotransporter)-inhibits reab of solute from THICK ASC
-VenoDIL to decrease RA press for ppl w/pulm edema/CHF |
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Mechanism of loop diuretics?
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increase Ca+ excretion by 30%
MOST EFFICACIOUS DIUR! -block reab Na/K/Cl (decrease lumen pos transepith pot that helps Ca reab) -increase Mg excretion by decreasing volt dep paracell transport |
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Uses and adverse for NKCC inhib?
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Tx: pulm edema, CHF, acute renal fail, hyperCa+
Adverse: low Na+/K+/Ca+/Mg+, hyperuricemia, ototoxicity |
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Chlorthiazides, Metolazone?
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NCC inhib (thiazides/sulfonamides)
Inhib DCT Na/Cl co transporter/reab DECREASE Ca+ EXCRETION (more Ca+ into cell b/c pos in lumen) = vasoRELAX (Ca+ activ K+) Tx: hyperT, edema/CHF, HyperCa+, nephrolith/DI |
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Amiloride?
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Inhib of Renal Epith Na+ chann late DCT/collect duct (Na OUT, K stays IN)
-K+ SPARING in hypoK alkalosis |
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Spironolactone?
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Aldosterone rec antag
decrease Na reab (Na stays out) K stays IN! |
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Aldosterone Rec Antag Mech?
(Spironolactone) |
1) prevent LV remodel/fibrosis
2) prevent sudden Cardiac Death 3) hemodynamic effects (bp lower, diur/naturesis) 4) Vasc Effects: reduce ROS, NADPH oxidase, increase NO bioact Tx: edema, high BP, heart fail, hyperaldosteronism (2nd aldost- edema) Adverse: HYPERKALEMIA (metab acid in cirr pts) |
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Conivaptan?
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ADH REC ANTAG on basolat* epith of renal collect tubule
*decreases H20 reab Tx: inapp ADH secr/CHF Adverse: nephr DI, renal fail |
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With Diuretic Therapy, why does your BP stay decreased even though your body volume and CO are eventually restored?
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TOTAL BODY NA+/H2O excretion is maintained
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Describe Endocrine, Neurocrine, and Paracrine pathways of stomach acid secretion
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Endocrine: Gastrin stim par & ECL
Neurocine: Ach stim par & ECL Paracrine: Hist (from ECL) stim par, PGE2 to decrease secr par Other Inhib: -PG/Ach promote HCO3 from gastric epith -Gastric D: somatostatin inhib gastrin release from G cells (decrease acid x2, ecl/par) |
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Mechanism and ex's of Antacids?
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NEUTRALIZE gastric ACID (Cx-infect/bioavail) by add base, stim PG by gastric epith
-Sodium Carbonate: fast, Cx(metab alk, too much Na+, gas/CO2) -Calcium Carbonate: Cx(Ca+ signal H+ secr, gas) -Magnesium Hydroxide: slow, Cx(osmo D, high Mg) -Aluminum Hydroxide: slow, Cx(constip, high Al/Ca, low PO4, bone resorp) |
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Antacids used to Tx?
How efficacious? |
-GERD (1/2), peptic ulcers(80%), dyspepsia
= efficacious to H2 rec antag, just shorter |
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Mechanism and ex's of H2 rec antag?
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-COMP inhib hist at H2 rec (selective!)
-decrease gastrin/Ach influence on par -inhib 60-70% 24hr acid secr: (in)direct, works 6-10hrs ANY "TIDINE" (Cx: HA, D, contip, inf, IV-brady/hypo) -cimentidine Cx: CNS**, endocrine, inhib CYP metab(drug interaxns) |
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H2 rec ANTAG Tx?
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GERD (1/2), peptic ulcers(80%), dyspepsia, gastritis
**Absorbed by GI (absorb, blood, GI) = to antacids, but longer |
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Mechanism and ex's of PPI's?
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Block neuro/endo/para by blocking H+/K+ exchanger on APICAL
-coated b/c activ by low pH, absorp in blood and back to GI to conc at gastric pit-irrev bind proton pump (3-4D max effect, exhaust suppl/new -activ pump req NEW synth -PRAZOLE, safe, Cx (bioavail, nut absorp/B12!, resp inf-aspirate) |
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PPI Tx?
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GERD & peptic ulcers (90%)
-also dyspepsia, gastritis, hypergastrin secr, NSAID/H.pylori ulc **MOST EFFICACIOUS INHIB |
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Mech of Mucosal Protective Agents?
-2nd line agents to PPI's (6hrs) (3)* |
adhere to ulcer/makes barrier (stim pg)
-Sucalfate: prevent stress bleeds (w/o acid suppress) Cx(Constip, renal prob) -Misoprostol*: for NSAID ulcers, Cx(cramp, D, ABORT!) PG analog -Bismuth subsal: absorb toxins of H.pyl/Travel's D, dyspepsia, Cx(black tongue, high dose toxicity) *intest* low pg? |
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Serotonin (5HT) vs DOPAmine and Motilin?
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Serotonin: ENS NT that stim MOTILITY (Ach-GI sm musc)
**Inhib ACE to INCREASE Dopamine: decrease firing ENS/decrease GI motility **ANTAG to INCREASE motility Motilin: increase motility (motilin rec on GI sm musc) |
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Metoclopramide?
Bethanechol? Neostigmine? Erythromycin? |
PROKINETIC!!!!!!!!!!!!!!!!!!!!!!!!
-"metoc: block Dop" (inhib D2 inhib), cx(park sxs) -Beth: M3 agon for motility "has to go at bethel" -neostig: AchE inhib to tx UR/distention "new stomach" -eryth: motilin agonist (abx also) "red riding" along |
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Methylcellulose?
Glycerin? Lactulose? Senna? Tegaserod? Lubiprostone? |
Methylcellulose: fiber/bulk, retain H2O
Glycerin: Surfact/soften "glisten coat" Lactulose:Osmo, non-absorp sugar/salt (mom, polyeth gly) Senna: Stim ENS*, leak muc, Na+ lumen accum Tegaserod? LAST RESORT STIM SEROTONIN REC, extreme constip, Cx: CV/GI Lubiprostone? lubricate Cl- Chan, secr into lumen/H2O follows, PG derive, later resort |
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Most important thing to consider w/anti D tx?
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TREAT UNDERLYING CAUSE FIRST
-infection, inflam, osmo D/lactose intol, tumors -THEN use opiods, bismuth*inhib PG intest**, kaolin/pect, bile salt res, octreotide |
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Loperamide?
Diphenoxylate? Bismuth sub? Kaolin/Pectin? Cholestyramine? Octreotide? |
Loperamide: Opiod+, increase absorb time H2O and sphincters, decrease motlity and distend percep, Cx: contip/safe
Diphenoxylate: "opiod", Cx CNS, atropine unpleasant dizzy Bismuth sub: intest inhib PG, absorb toxins, tx travel's D Kaolin/Pectin: bulk, absorp toxins Cholestyramine: tie up bile acids/salt (only tx low bild salt absorp), H2O out (bloat, low fat absorp) Octreotide: LAST RESORT, somatostatin agonist-stop G on par, shut down pancr/bile secr! Cx: glucose disrupt (low motility** promotes fluid REAB, rid lumen) IV bc peptide |
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Know antiemetic Receptors in body!
-GI?* -CTZ -Vomit center? -Vestibular? |
-GI: mechanorec, chemorec, serotonin
-CTZ: D2, NK1, serotonin -vomit center: H1, M1, NK1, serotonin Vestib: : H1, M1 |
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Ondansetron?
Scopolamine? Metocpramide? Dimenhydrate? Aprepitant? Prochlorperazine? |
DIRECT ANTAG for ANTIEMETIC
Ondansetron: serotonin antag, Cx (CV/GI) "tx so you can keep on dancing" Scopolamine: M1 antag for MOTION sickness**** "scoop My puke" Metocpramide: D2 antag (inhib inhib-park) "metoc block dop" Dimenhydrate: H1 antag, motion sickness "DRAMAMINE" "dizzy from diamonds" Aprepitant: NK1 antag for chemo, Cx(CYP3A4 drug interaxns/metab) "new kids new a prep course or will have drug prob" Prochlorperazine: M1, D2, H1 antag, MIXED LAST RESORT "proc is a mad hatter" |
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Lorazepam?
Nabilone? Dexamethasone? |
-INDIRECT AGONIST (antiemetic)
-lorazepam: GABA +, "lorax book/gaba gaba" Tx ANXIETY -Nabilone: Cannabinoid+, "want nabiscos w/pot" for CHEMO -Dexamethasone: glucocorticoid+ will INCREASE effectiveness of SEROTONIN ANTAG for chemo (not used mono) Cx(wt gain, UR) |
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IBS tx?
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idiopathic, relapsing
-abd discomfort + D/C/both -Loperamine, osmo lax, TCA, antispasmodics/antimusc for pain *Tegaserod: ser AGON for constip (cx cv/gi) *Alosetron: ser ANTAG for D/last resort, CX: ISCH COLITIS (not effective in MEN!) |
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IBD tx?
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ASA: inhib IL's, TNF, COX, free rads, works Topically*
Glucocorticoids: supp inflam (cytokines) Purine analog: inhib immune prolif Anti-TNF Ab: inhib TNF alpha imm |
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5-ASA's? for IBD
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Sulfasalazine: oral to colon, malaise and don't feel right
Mesalamine-Pentasa: oral to intest, time release "vegans w/chron's(IBD) eat SALADS to lower inflam" |
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Glucocorticoids? for IBD
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Prednisone: suppress inflam, risk infect
Hydrocortisone: same |
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Antimetab? for IBD
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6MP and azathioprine: inhib purine synth, decrease cell prolif
methotrextate: inhib DHFR, decrease cell prolif, MAINTAIN IMS for CHRON'S (but bone marr depress) "Get your AZ out of bed at 6aM, to eat MyTrix" |
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INFLIXIMAB?
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IBD, TNF alpha Ab binds TNF alpha to inhib imm response "IMS"
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