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81 Cards in this Set
- Front
- Back
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When to use ion channel blockers vs. beta blockers in arrhythmias?
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ACUTE CONTROL:
Na or Ca channel blockers LONG TERM older beta blockers are best - ion channel blockers increase risk of recurring arrhythmias |
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Antiarrhtyhmics
- class I |
CLASS I: Na+ blockers
1. Quinidine 2. Procainamide (procan) 3. Disopyramide (Norpace) 4. Lidocaine (Xylocaine) 5. Mexiletine (mexitil) 6. Tocainide (tonocard) 7. Phenytoin (dilantin) 8. Flecaindie (tambocor) 9. Propafenone (rhythmol) - propafenone is also a weak beta blocker |
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ANTIARRHYTHMICS
CLASS II |
CLASS II: SNS (BETA) BLOCKER
1. Propranolol 2. Metoprolol 3. Sotalol (betapace) 4. Bretylium (generic) |
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ANTIARRHYTHMICS
CLASS III |
CLASS III: Blocks Na+ and others = PROLONG EFFECTIVE REFRACTORY PERIOD
1. Amiodarone (cordarone, pacerone) 2. Dofetilide (tikosyn) 3. Ibutilide (corvert) |
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ANTIARRHYTHMICS
CLASS IV |
CLASS IV: BLOCK CA2+
1. Verapamil (calan, isoptin, verelan, covera) 2. Diltiazem (cardizem, tiazac, dilacor) 3. Adenosine (adenocard, adenoscan) 4. Magnesium |
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general anti-arrhythmic drug mechanisms
- beta blockers - Na or Ca channel blockers - K channel blockers/class III |
DRUGS SLOW AUTOMATIC RHYTHMS BY ALTERING 1 OF 4 determinatns
1. DECREASE PHASE 4 SLOPE - beta blockers & Ca2+ channel blockers 2. Increase threshold potential/depolarization threshold, - Decreased upstroke velocity (phase 0) - membrane ion channels less responsive to depolarization stimulus = Na & Ca2+ channel blockers 3. Increase max diastolic potential (increase diastole?) - Na & Ca channel blockers (esp bepridil) 4. Increas ein AP duration - K+ channel blockers (class III) *decreased Kir (inward rectifier current) = decreased rate of depolarization & rate at which Na channels re-enter resting/nl state = ^ ERP |
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how do anti-arrhythmics block DAD/EADs and reentry arrhythmias?
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DAD/EADs
1. Inhibit development of ADs 2. Interfere w/ inward current - usu sodium or calcium = upstroke REENTRY: trickier 1. prolong AV nodal refractoriness 2. slow AVnodal conduction *Na & Ca channel blockers & beta blockers work here *Na channel blockers work best ot terminate FUNCTIONALLY determined reentry (2' myocardial ischemia) - prolong refractoriness/time for Na+ channels to recover |
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STATE-DEPENDENT ION CHANNEL BLOCK
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Ion channel blockers preferential bind ACTIVATED & INACTIVATED channel/receptor states
- esp studied in Na+ channels *Doesn't like the resting Na+ channel* Dissociation rate = key determinant of steady-state block of na channels - slower dissociation rate = ^ Na channel block GREAT: when HR ^, the time availble to unblocking decreases = INCREASED steady state Na+ channel block **Na+ channel blockers are great at normalizing rapid HRs (a/v-fib & flutter) |
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OCULAR PHARMACOLOGY
Prostaglandin analogues |
1. latanoprost (xalatan)
2. Travoprost (travatan) 3. Bimatoprost (lumigan) 4. Unoprostone (rescula) |
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OCULAR PHARM
BETA BLOCKERS |
1. betaxolol (beta-optic)
- beta1 selective 2. Carteolol (ocupress) 3. Levobunolol (betagan, akbeta) 4. Metipranolol (optipranolol) 5. Timolol (timoptic, timoptic xe, betimol) |
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OCULAR PHARM
CARBONIC ANHYDRASE INHIBITORS - TOPICAL ONES TOO |
1. Acetazolamide (diamox)
2. Methazolamide (glauctabs) 3. Dichlorophenamide (daramide) 4. Brinzolamide (azopt) 5.Dorzolamide (trusopt) *4 & 5 = topical CAIs |
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OCULAR PHARM
MUSCARINIC AGONISTS |
1. cARBACHOL (MIOSTAT, ISOPTO CARBACHOL)
2. PILOCARPINE (AKARPINE, PILOCAR, PILOSTAT) 3. ACH (MIOCHOL-E) |
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OCULAR PHARM
Acetylcholinesterase Inhibitors |
1. DEMECARIUM
2. ECHOTHIOPHATE (PHOSPHOLINE IODIDE) 3. PHYSOSTIGMINE (ERERINE) |
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OCULAR PHARM
- ALPHA AGONISTS |
1. APRACLONIDINE
(LOPIDINE) 2. BRIMONIDINE (ALPHAGAN) 3. DIPIVEFRIN (PROPINE) 4. ePINEPHRINE (MICRONEFRIN) |
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prostaglandin analogues (PGA)
LATANOPROST (XALATAN) - indications - mech - side effects: ^^ # of melanosomes** - similar drugs |
FIRST LINE DRUG FOR GLAUCOMA (esp open-angle)
MECH: decreases IOP 6-8 mmHg on average - Prodrug - Activated in cornea - binds Prostanoid FP receptor & lets aqueous leave via accessory uveoscleral outflow path SE'S: - Increased pigmentation (iris, eyelids) - Darkened & grew eyelashes =) - can cause PREMATURE LABOR =( Similar drugs: - travoprost & bimatoprost: active 24 hrs - Unoprostone: less IOP lowering efffects; 10 hrs active |
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glaucoma meds and babies
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ALL GALUCOMA MEDS CROSS THE PLACENTA AND SECRETED IN MILK
--> FETUS ALT TX: - LASER SURGER **XALATAN (PGA) can cause premature labor |
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TIMOLOL
(timoptic, betimol) - PHARM INDICATION - MECH - SE's - contraindication **beta receptors on ciliary epithelium help w/ secretion of aqueous humor** |
NONSELECTIVE beta blocker
- binds b1 & b2-R - PURE antagonist - no local anesthesia MECH:: - b2-R of ciliary body epithelium & blood vessels (80% receptors) - Decreased secretion - Decreases ocular blood flow = decreased ultrafiltration causing aqueous production (double effect) SEs: systemic effects - Bronchoconstrict (b2 in lungs) - Brady (b1 in heart) - can eff up verapamil & increase heart block risk + hallucinations, sex dysfxn, hair loss, depression, etc. CONTRAINDICATION - COPD - CHF |
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BETAXOLOL
pros & cons |
ONLY B1-SELECTIVE BLOCKER
used in ocular pharm - not as good as nonselective (eye = mostly b2-R) - Lowers IOP only by 3-4 mmHg PROS: 1. Less exacerbation of reactive airway dz / breathing difficulty 2. Ca2+ channel blocker; cna be used at high doses (neuroprotective?) 3. Preserves visual fields BETTER than timolol |
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CARTEOLOL - ocupress
- unique? - other drugs in this class |
MOST POTENT BETA BLOCKER
- decreased secretion & ocular BF - nonselective beta blocker (betaxolol = only b1 selective) other nonselective beta blockers: - levobunolol, metipranolol, timolol |
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SYSTEMIC CAIs
acetazolamide methazolamide dichlorophenamide - indication -mech - SEs |
INDICATION:
Sulfonamide derivative 2 tx open angle glaucoma - also treats macular edema & other macular degen. diseases MECH: CA (II, IV, XII) Inhibitor - CAs in ciliary processes of eye = Reduced bicarb & aqueous humor secretion - reduces 25-40% IOP many SE's: affects systemic CAs - numbness, tingling, sleepy, depression, fatigue, malaise, wt loss - decreased libido, GI irritation, Met. acidosis, kidney stones - transient myopia *contraindication: PTS W/ SULFA ALLERGY |
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TOPICAL CAIs
Dorzolamide (trusopt) Brinzolamide (azopt) - mech - SEs |
Indication: open angle glaucoma
MECH: inhibits CA II in ciliary body epithelium - redcues formation of bicar ions, fluid transport, and IOP - Reduces IOP 18-22% ( less than systemic) SE's: - fewer than systemic agents - brinzolamide is better - burning/sitingin, eyelid edema |
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CHOLINERGIC AGONISTS (MITOTICS)
PILOCARPINE, CARBACHOL, ACH - INDICATION - MECH - SEs |
INDICATION:
Pilocarpine & carbachol: glaucoma Carbachol & ACh: Miosis in sx - Reduces IOP by 20-30% MECH: Musc Agonist contracts ciliary mm = tension on trabecular meshwork = open pores = easier outflow of aqueous humro 2 canal of schlemm = dec. IOP rapidly (4-8 hrs) SEs: - ciliary muscle spams = brow ache & myopia - headaches (contractions - pupilary constriction & blurry - cataracts -^ parasym effects |
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ACHEIs
demecarium echothiophate physostigmine - indication - SEs **no longer used in clinical practice normally** |
USE:
- Glaucoma - Accommodative esotropia * physostigmine: louse & mite infestation of lashes MECH: ache-inhibitor ^ ACh = ^ ciliary mm. contraction = increased reabs though canal of schlemm SEs: - vitreous hemorrhage - contact derm, allergic conjunctivitis - systemic: GI issues, ^ parasym **echothiophate = WORST SEs; photphobia, myopia |
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SYMPATHOMIMETICS
CLONIDINE vs. apraclonidine - indication - mech - SEs |
USE:
- Glaucoma - pre/post laser prphylaxis of IOP spikes = APRACLONIDINE MECH: a2-R agonist = + Gi = DECreased cAMP = reduced humor formation SEs: - pros: avoid miosis & browache of musc agonists - cons: major systemic hypoTN (--> CNS) *Apraclonidine: polar/hydrophilic analog; less cns EFFECTS |
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alpha agonists & the eye
- APRACLONIDINE - BRIMONIDINE - DIPIVEFRIN** - EPINEPHRINE** |
USE:
- Glaucoma - pre/post laser prphylaxis of IOP spikes = APRACLONIDINE MECH: - decrease production & increased outflow of aqueous humor *Dipivefrin: EPI prodrug; better corneal penetration & lipid solubility - less effective; fewer systemic SEs |
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APRACLONIDINE
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alpha agonist used to tx glaucoma & pre/postlaser sx prophylaxis against IOP spikes
*Apraclonidine: polar/hydrophilic analog 37% IOP reduction - bad SE's = A1-R effects - low potential for systemic SEs DECREASED HUMOR PRODUCTION (a2 agonist) |
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BRIMONIDINE
(Alphagan) - indication - mech - SEs |
USE: ~ CLONIDINE
- better penetration of cornea than apraclonidine - more systemic effects - glaucoma MECH: A2-R AGONIST & BETA ANTAGONIST - reduced humor flow/production - also increases uveoscleral outflow*** - lacks A1-R agnoism, quite lipophlic SE's: - dry mouth, red eye, eye pain, photphobia, - corneal staining - allergy rate = 30% |
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agents used in ocular dx
- phenylephrine (direct sympathomimetic) - indirect sympathomimetic |
PHENYLEPHRINE: mydriasis (dilation)
- also decongestant - sympathomimetic - also good in localizing lesions in horner's synd Cocaine, hydroxyamphetamine - require normal stores of catecholamines - differentiates b/w pre & post-ganglionic lesion in horner's **Pre-gang: WILL dilate **Post-gang: WON'T dilate (no NTs cause axon died), but WILL dilate w/ phenylephrine. |
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MISCELLANEOUS TREATMENT OF EYE
- CAFFEINE - MARIJUANA - ACUPUNCTURE |
CAFFEINE IS BAD FOR GLAUCOMA
Increases IOP by 3 mmHg 1 cup coffee MJ = LOWERED IOP - SE's increased HR & dec BP ACUPUNCTURE: - subjective improvement of central visual acuity - no change in IOP or visual field |
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Dacryoadenitis vs Dacryocystitis
- infected tissue? - most likely organism - tx? |
TX: SYSTEMIC ABX
Adenitis: lacrimal gland - younger pts - bact: S. auerus or Strep - Viral: mupms, influenza, zoster, Mono Cystitis: Lacrimal SAC - adults: S. aureus, diptheroids, candida, actinomyces israelii |
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Hordeolum
- tissue infected - organism - tx |
Infected meibomian, zeis, or Moll glands at LID MARGINS
- usu S. aureus tx: warm compress and TOPICAL abx |
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Blepharitis
- tissue infected - org - tx |
BL infalmm of EYELIDS
- irritated and burning - usu staph Topic abx: - Bacitracin zinc - gentaminc sulfate - polymyxin B - tobramycin sulfate SO DUMB |
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CONJUNCTIVITIS VS KERATITIS
- tissue infected - tx? |
CONJUNCTIVITS: infalmm of conjunctiva
- can range a lot - sulfacetamide sodium & levofloxacin + other abx KERATITIS: inflamm of corena - tx w/ chloramphenicol, ciprofloxacin, etc. |
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Endophthalmitis
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SERIOUS
- involves intraocular tissues - need to do vitreous taps for cx - inject w/ intravitreal abx |
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ANTIVIRAL AGENTS FOR THE EYE
- primary indication - MEDS/admin for viral retinitis, herpes ophthalmicus, viral keratitis, viral conjunctivitis |
Indications
- viral keratitis, herpes zoster opthalmicus, retinitis **not needed for viral conjunctivitis caused by adenovirus (self-ltd) HSV 1 & Varicella zoster cause viral keratitis - tx: trifluridine, vidarabine, etc. (oral) - AVOID topical glucocorticoids (active viral replication) *Use topical steroids in herpetic disciform keratitis (cell-mediated rxn) Herpes zoster opthalmicus (cn v) - systemic tx: valacyclovir, famciclovir, acyclovir **systemic b/c latent reactivation Viral retinitis: - tx w/ parenteral antivirals or intravitreal |
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ANTIFUNGAL AGENTS IN THE EYE
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NATAMYCIN = ONLY TOPICAL FOR EYE
- polyene: bind sterols in fungal membranes = punch holes |
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ANTIPROTOZOAL AGENTS IN THE EYE
- POPULATIONS? |
Acanthamoeba & Toxoplasma gondii & P. aeuruginosa in contact lengs & pools
--> keratitis tx w/ topical neosporin or imidazole TOXOPLASMOSIS: SYSTEMIC STEROIDS + ABX (?) |
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GLUCOCORTICOIDS IN THE EYE
TOPICAL: dexamethasone, prednisolone, fluorometholone |
used 2 manage ocular allergy & external eye inflamm disease
SEs: - cataract dev - 2' infxn - 2' glaucoma |
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QUINIDINE
- INDICATION - MECH/AXNS - CONTRAINDICATIONS **anticholinergic effects??** --> use w/ digitalis to tx a fib = increase vagal activity & offset anticholinergic effects of quinidine |
Oral antiarrhythmic agent
BROAD SPECTRUM Mech: Activated (steady-state) Na+ channel blocker Axns: 1. Hyperpolarizes resting Vm 2. Depresses phase 4 slope of pacemakers 3. Slows Vmax / phase 0 / upstroke 4. Prolongs QRS, repolarization (ERP) & AP duration in regular myocytes ****PARTIALLY BLOCKS K+ CHANNELS*** CONTRAINDICATIONS: 1. Anitcholinergic effects: can INCREASE AV nodal conduction - don't use in a. flutter/fib 2. CHF (neg. contractile) SE's - Cinchonism: headache, tinnitus, dizzy - OD = Severe <3 depression --> tachy & fibrillation asystole |
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PROCAINAMIDE & DISOPYRAMIDE
- mech/AXNS - use - differences - SEs |
broad spectrum class i antiarrhythmic
use: mainly Supraventricular (atrial) & ventricular arrhythmias AXNS: - Depress automaticity in pacemakers - similar effects as quinidine DIFFs: - Procainamide: LESS ANTI-ACH - Disopyramide; POTENT ANTICHOLINTERGIC; use w/ digitalis SEs: - don't use in CHF or hyperkalemic - PROCAINAMIDE = 1/3 pts get SLE (lupus) (skin rash, fever, & big liver) - Disopyramide: greater cardiac depression |
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QUINIDINE SIDE EFFECTS
(LOTS!) |
SE's
1. Quinidine induced thrombocytopenia - purpura 2.Torsades de pointes arrhythmias 3. Cinchonism: headache, tinnitus, dizzy - OD = Severe <3 depression --> tachy & fibrillation asystole *also anti-malarial* |
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LIDOCAINE = acute IV tx
- Oral Derivatives: mexiletin & tocainide = chronic tx - use - mech/axn - doc FOR??? |
DOC FOR DIGITALIS-INDUCED ARRHYTHMIAS
2' lidocaine's selectivity for depolarized myocardial cells - use for ventricular arrhythmias MECH: Blocks BOTH activated & inactivated Na+ channels - only depresses damaged or depolarized cells (not really normal) - depressed membrane responsiveness in ectopic VENT pacemakers & Purkinje fibers - DECREASE AP DURATION** |
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PHENYTOIN as an anti-arrhythmic
- use - mech - SE's |
USE:
2ND LINE DRUG FOR VENTRICULAR ARRHYTHMIAS - suppresses ectopic pacemakers MECH: - blocks both activated & inactivated Na+ channels - blocks Ca2+ channels too! = depressed membrane responsiveness ESP IN VENTRICLES & HIS-PURKINJE cells SEs: - tox: CNS - vertigo, nystag, slurrs, sedated - very variable from pt to pt - good = little antiAch effecs |
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FLECAINIDE
- mech/axn - use - contraindications / SEs |
USE: last resort -
- Resistant premature ventricular arrhtyhmias, - Resistant a-fib - Life threatening, resistant arrhythmias!! MECH: Blocks both activated & inactivated Na+ channels - slows conduction velocity in ventricles & purkinje cells = Depressed Phase 0 depolarization & Vmax MORE SO THAN ANY OTHER CLASS I AGENT!!! SO POTENT!! CONTRAINDICATIONS - CHF - Already on a negative inotropic agent (beta blocker or calcium channel blocker) SEs: - Dizzy, blurry, abd pain - tox = severe dec in CO & fibrillation asystole |
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ocular pharm
- effects on aqueous humor production or outflow? |
STOP MAKING/RELEASING IT!!
1. beta blockers 2. Systemic CAIs (25-40% reduction in IOP) 3. Alpha(2) agonists (clonidine too!) GET OUT OF HERE!! 1. PGAs 2. Cholinergic/musc agonists 3. ACHEI 4. alPHA AGONISTS = brimonidine |
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PROPAFENONE
- MECH/AXN - SE'S - |
mech:
- blocks activated & inactivated na+ channels - very strong depression of resting Vm like flecainide - can PRECIPITATE life threatening arrhythmias like flecainide (long diastole) **also weak beta blocker** |
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beta blockers in arrhythmias
- all beta1-blockers except propranolol - propranolol (nonsel) - sotalol ** - metoprolol - esmolol 1. mech/axn 2. uses 3. SE's /tox |
CARDIAC B1-R BLOCKERS
1. Depress phase 4 depolarization 2. Increase ERP of pacemakers 3. Slow SA nodal & AV conduction 4. Slow ectopic pacemaker automaticity (5. Sotalol: uniquely increases AP duration like class III drugs) USE: Prevent life-threatening ventricular arrhythmias w/ fewest SEs & lowest failure rate ********** BEST FOR PROPHYLACTIC USE =) =) =) =) =) - not great for suppressing acute arrhythmiaS |
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BRETYLIUM
- mech - axns - use -SEs |
MECH: SYMPATHOLYTIC
- antagonizes NE release from neurons to heart - maybe by affecting K+ channel or NKAtpase USE: EMERGENCY - tx v-fib or resistant recurrent tachy SEs hypertension followed by hypotension and ventricular ectopy --> SHOCK! |
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beta blockers & arrhythmias
3. SE's /tox **esmolol is NOT used for chronic prophylaxis - can't be oral** |
SE'S
1. Reduce <3 contractility - postural hypoTN 2. propranolol = bronchoconstrict **Persistent postural hypotension indicates toxicity contraindications: CHF |
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AMIODARONE
- MECH/AXNS - USE - TOXICITY |
MECH: blocks...
1. inactivated Na+ channels: depressed conduction in depolarized cells 2. delayed rectifier K+ block = PROLONGED AP duration 3. Slow SA nodal automaticity & ventricular ectopic pacemakers - beta- blocker 4. Blocks inward Ca2+ current CLINICAL: - Arrhythmias 2' rapid SA nodal firing - resistant - extracardiac tox = limiting factors TOXICITY: - Deposition in skin & cornea = vision aff'd - Hypo & hyperthyroidism ( 5%) - hepatocelular necrosis |
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DOFETILIDE
- MECH/AXN - USE - TOX |
Selective Kir (inward rectifier) blockers
- slow phase 4 repolarization = LONGER AP USE: A-fib --> restore sinus rhythm TOX: - pRLONGED qt INTERVAL - Pro-arrhythmic (esp if hypoK+) - can induce torsades de pointes **MORE blockage w/ hypokalemia - Kir is dept on extracell K+ |
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IBUTILIDE
- MECH / axn - use - tox |
SIMILAR TO DOFETLIDE
- BLOCKS Kir - also blocks Kslow rectifying = SLOWED PHASE 4 repolarization & lONGER AP use: IV a-fib/flutter --> normal sinus rhythm TOXICITY: - PROLONGED QT INTERVAL --> ARRHTYHMIAS --> TORSADE DE POINTES (LIKE DOFETILIDE) |
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VERAPAMIL & DILTIAZEM
- USE (ESP IN ARRHYTHMIAS) - MECH - SE'STOX |
multi-use
- Superventricular tachy - angina - hypertension MECH: CALCIUM CHANNEL BLOCKER in <3 & smooth muscle cells VERAPAMIL: DOC for superventricular tachy (2' a. tachy & flutter) - depressed AV node conduction DILTIAZEM: also inhibits AV conduction - less potent than verapamil - less dec in contractility - use in CHF pts w/ supervent tachy 2' atrial tachy/flutter se's & tox: - hypotension / syncope - OD: severe hypoTN & AV blok & CHF --> tx w/ isoproterenol (+ inotropic) & clacium gluconate |
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ADENOSINE IN ARRHYTHMIAS
- mech - use - SE's & tox |
MECH:
Rapid activation of Kir channels 1. Major hyperpolarization 2. Suppress voltage-gated Ca2+ channels DOC: Paroxysmal supraventricular tachy (resotre sinus rhythm) - stops heart (short asystole) - IV admin SE'S TOX: - Flushing & SOB (bronchospasm) - Induced AV block (short-lived) |
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MAGNESIUM & ANTIARRHYTHMIAS
- USE? - COMBO W/ DOFETILIDE? |
alters Na, K, & Ca fxn
USE: - IV in pts w/ TORSADES DE POINTES - Prevent a-fib post-cardiac sx COMBO W/ DOFETILIDE - Increases cardioversion rate of dofetilide during a-fib |
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MAGNESIUM & ANTIARRHYTHMIAS
- USE? - COMBO W/ DOFETILIDE? |
alters Na, K, & Ca fxn
USE: - IV in pts w/ TORSADES DE POINTES - Prevent a-fib post-cardiac sx COMBO W/ DOFETILIDE - Increases cardioversion rate of dofetilide during a-fib |
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AGENTS USED TO TREAT ACNE
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A.) RETINOIDS: TAIP
1. Tretinoin (all trans RA) 2. Adapalene (differin) 3. Photodynamic therapy (5-ALA + light) 4. Isotretinoin (accutane) B.) Antibacterial: BACMES 1. Benzoyl Peroxide 2. Azelaic acid (azelex) 3. Clindamycin 4. Erythromycin 5. Metronidazole 6. Sodium Sulfacetamide |
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ACNE
- organism - process - pimples vs black/white heads |
MC skin disorder in USA
7% population Disease of pilosebaceous unit - plugged follicle - accum of sebum - growth of Propinoibacterium acnes & inflamm Pimple = papule, pustule, nodule, cyst Blackhead = OPEN comedone - open & see the dirt White head = closed comedone |
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RETINOIDS
*Photodynamic therapy: painful, acute inflamm, & transient skin tanning - accumulation of porphyrins |
used to tx Acne
- normalize maturation of follicular epithelium - reduce inflamm - enhance pentration of other topicals a.) tretinoin: all-trans - helps with wrinkles too - use with topical antimicrobials - avoid SUN b.) adapalene: deriv of naphthoic acid - less iritating than tretinoin; mild-moderate acne c.) isotretinoin - synthetic - only for severe cystic acne - may inhibit sebaceous gland size/fxn - SEs: hypervitaminosis; headaches, teratogen, lipid abnls |
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ANTIMICROBIALS USED IN ACNE
(BACME) |
1. Benzoyl Peroxide
- peeling & comedolytic effects - used w/ clinda or erythro - Contact sensitizer - can bleach your skin 2.) Azelaic acid - dicarboxylic acid - mild SEs 3.) Clinda: - abx assc'd colitis & bloody diarrhea 4.) Erythro: - drug resistant bugs can develop 5.) Metronidazole - tx: acne rosacea - mech unknown 6.) Sodium Sulfacetamide - combined w/ sulfur - tx: acena veulgaris & acne rosacea - inhibits P. acnes by competitive inhibtion of p-ABA - don't use in pts w/ sulfa allergy |
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TRICHOGENIC & ANTITRICHOGENIC AGENTS
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1.) Minoxiddil (rogaine)
2.) Finasteride (propecia) 5a-reductase inhibitor - decreases dihydrotestosterone 3.) Eflornithine (vaniqa) - REDUCES facial hair growth |
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MINOXIDIL
- use - mech - seS |
AKA ROGAINE
mech: - Stimulates hair growth, enhances follicular size --> thicker shaft - first used as anti-HTN ( opens Katp channels in VSM) TX: Androgenic alopecia - male/female pattern baldness - use for 4 mos SEs: - allergic contact derm - hair growth in undesirable locations =/ |
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FINASTERIDE (PROPECIA)
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TX: androgenic alopecia
MECH: TYPE 2 5-alpha reductase inhibitor - prevent conversion of testosterone to dihydrotestosterone SEs: - decreased libidio - erectile dysfxn - ejaculation disorders **PREGNANT FEMALES SHOULDN'T TOUCH BROKEN TABS - it also decreases serum PSA levels |
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EFLORNITHIN
(VANIQA) |
TX: REDUCES FACIAL HAIR GROWTH
MECH: Irreversible inhibitor of ortnithine decarboxylase (rate limiting enzyme in polyamine biosyntheiss) SEs: - stinging, burning, folliculitis |
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Digoxin as an anti-arrhythmic
- mech - use **Quinidine, Verapamil, Amiodarone INCREASE digoxin levels/effects |
MECH: Na/K pump blocker
= enchanced contractility Anti-Arrhythmic: Parasym effects: Slows AV conduction USE: A-fib & A-flutter - slows ventricular response rate |
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Affects of CLASS 1 anti-arrhythmics on ERP
Ia/b/c/d |
1A. Queen Proclaims Diso's Pyramid
- INCREASE ERP Moderate na+ channel block 1b. Lidocaine Weak Na+ channel block DECREASE ERP 1b = Best post-MI 1c: Flecainide NO CHANGE IN ERP strong Na+ channel block 1c = Contraindicated post-MI |
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ADENOSINE
"class 5" MECH of axn |
MECH: ^ K+
A1, A2a Receptors in heart: Gi = dec cAMP? Activates ACh-sensitive K+ current in SA, AV nodes & atrial myocardiocytes 1. Hyperpolarizes cells 2. Prevents abnl automaticity - decreases Ca2+ current 3. Inhibits Ca2+ mediated DAD triggered activity 4. Increases refractory period in slow conducing AV pathways - prevent re-entry DOC: Supravent Tachycardia - prevents premature impulses & re-entry *can cause transient asystole (^ K+ and Dec Ca2+) Slows/blocks conduction in the AV node by hyperpolarizing AV node via ↑IK and ↓Ica so causes short asystole (stops heart) |
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ADENOSINE SEs
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sHORT LIVED SEs
- rapid deamination 1. Transient asystole & hypotension ^ k+ and Dec Ca2+ = hyperpolarizes & decreased conduction 2. Bronchospasm, Dyspnea - A2b-R: Gq --> DAG & IP3 3. Flushing *Effects & SEs potentiated by DIPYRIDAMOLE - adenosine reuptake inhibitor *Effects/SEs are REDUCED by CAFFEINE & THEOPHYLLINE - adenosine receptor blocker |
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AMIODARONE
- MECH - class |
Synthetic analogue of thyroid hormone
- binds to nuclear thyroid-R CLASS 3 anti-arrhythmic - has properties of all 4 classes 1a. Blocks inactivated Na+ fast channel********* 2. Beta-blocker 3. Blocks delayed rectifier K+ current 4. Blocks inward Ca2+ current |
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AMIODARONE
- SEs - USES |
SEs:
Acute: Hypotension Chronic: Pulmonary fibrosis, thyroid dysfunction, liver tox, visual problems (deposits in cornea & skin) INDICATIONS: DOC FOR.. 1. Symptomatic/Pulseless V.tach & V. fib - out of hospital OR in-hospital - after DC cardioversion is attempted/fails 2. Asymptomatic V. tach - in hospital - 2nd line: Lidocaine & Procainamide **also used in a.fib |
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MAGNESIUM
- MECH - INDICATIONS |
UNKNOWN MECH
"CLASS 5 ANTI-ARRHYTHMIC" - does NOT shorten QT interval - may decrease transient inward Ca2+ current DOC for.. 1. Torsades de pointes - terminate & prevent recurrence 2. Digoxin toxicity-induced arrhythmias |
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DOFETILIDE (tikosyn)
& Ibutilide (Corvert) - mech - DOC |
CLASS 3 AGENTS:
MECH: Block rapid component of delayed rectifier K+ current - slower repolarization = Longer ERP - Longer QT = Longer AP doc: - restore sinus rhythm in pts w/ a.flutter & A.FIB |
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OVERVIEW OF A.FIB
- Goals of drug tx - importance of sinus rhythm |
If it's UNLIKELY a.fib will RECUR --> restore sinus rhythm w/ electrical cardioversion or drug
--> Once sinus rhythm restord, give long term drug 2 prevent recurrence of a.fib LIKELY THAT A.FIB WILL RECUR? - Leave pt in a.fib - give long term drug to keep the ventricular rate bw 60-80 bpm (by decreasing AV conduction) |
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drugs for ATRIAL FIBRILLATION
PRESENT <48 HRS OR > 48 HRS? **acute resolution** |
PRESENT <48 hrs
- REestablish sinus rhythm w/ 1. electrical cardioversion 2. OR DRUG A. Dofetilide or ibutilide (class 3) B. Propafenone or flecainide (class 1c) C. Amiodarone (class3,1a,2,4) IF present >48 hrs 1. Anticoagulate w/ warfarin for 3 weeks - prevent systemic embolization 2. Cardioversion after 3 wks or drugs above |
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LONG TERM DRUGS FOR ATRIAL FIBRILLATION
- in presence of other diseases? - pt. likely to have recurrent Afib? |
DOC depends on underlying CV diesease
1. NO underlying dz: Class 1c & 3 - Propafenone - flecainide - sotalol: greatest AP prolonger 2. + CAD: Sotalol - careful for brady - blocks Na+ and K+ 3. CHF or HTN - Amiodarone - Dronedarone If AFIB LIKELY TO RECUR - Leave pt in AF - Control ventricular rate DOC: decrease AV conduction rate 1. EF > 40% - Diltiazem or Verapamil - Propranolol or metoprolol 2. EF <40% - Amiodarone |
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Drugs that increase digoxin?
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Quinidine
Amiodarone Verapamil (QuAV) |
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Drugs that decrease mortality following MI
(DECREASE RISK OF SUDDEN DEATH) |
Propranolol & Metoprolol
- decrease ventricular ectopy - decrease sudden death risk |
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WHAT DRUGS TO GIVE BEFORE QUINIDINE IN CASE OF A.FIB/FLUTTER
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ALWAYS GIVE
Digoxin, Verpamil, or beta blocker BEFORE quinidine - if using it to restore sinus rhythm in a.fib/flutter QUINIDINE ALON: - Increases AV node conduction & ventricular response rate Above drugs = decrease AV conduction & prevent increase in ventricular response rate |
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DRUG COMBOS THAT CAN PRECIPITATE CARDIAC ARREST FROM 3RD DEGREE AV BLOCK
- anti-arrhythmics |
1. verapamil + digoxin
2. verapamil + beta blockers |
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SIDE EFFECT PEARLS
- quinidine - procainamide - lidocaine - amiodarone |
QUINIDINE:
- LONG QT - CINCHONISM (headache, tinnitius, vertigo) PROCAINAMIDE: SLE (rarely affects kidneys) LIDOCAINE: SEIZURES AMIODARONE: Pulmonary fibrosis Thyroid dysfxn (low/high) |
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DRUGS PRECIPITATING CHF
(anti-arrhtyhmics) |
any drug that decreases CONTRACTILITY
1. dISOPYRAMIDE - greater <3 depressant effect than other class1a drugs 2. VERAPAMIL & DILTIAZEM (calcium channel blocker) 3. FLECAINIDE: (CLASS1C = contraindicated post-MI) 4. PROPAFENONE: also class1c *also beta-blockers? |
