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38 Cards in this Set

  • Front
  • Back

Parasympathetic Nervous System

-Rest and Digest:


-Cervical and Sacral origin


-Long presynaptic ganglia, give of ACh which pass signal onward to short postsynaptic ganglia.


-Secrete ACh on M type receptors


-Effects: cardiac and smooth muscle, gland cells

Sympathetic Nervous System

-Fight or Flight!


-Thoracic and Lumbar origin


-Short presynaptic chain secrete ACh at nicotinic receptors


Long postsynaptic ganglia reach end organ to secrete ACh, NE, and eventually Epi at Alpha and Beta receptors

Somatic Nervous System

Voluntary Motor Nerves


-Long axon directly to end organ


-Skeletal Muscle

Alpha 1 Adrenergic Receptor

G Protein Q- Phospholipase C hydrolyzes IP3 and DAG, leads to mobilization of Ca+2 and Protein Kinase C===> Smooth Muscle Contraction



Increased: Smooth Muscle Contraction, mydriasis, GI sphincter contraction.

Alpha 2 Adrenergic Receptor

G Protein I- leads to inhibition of adenylyl cyclase, decreased cAMP, and increased K+ = Hyperpolarization



Decrease: Sympathetic outflow, insulin release, lipolysis,



Increase: Platelet Aggregation

Beta 1 Adrenergic Receptor

G Protein S- increased adenylyl cyclase activity, leads to increase cAMP, and Ca+2 Influx



Primary Excitatory impulse on heart rate, Contraction, renin release, lipolysis

Beta 2 Adrenergic Receptor

G Protein S- Increase Adenylyl Cyclase, increase cAMP, and Ca+2 influx



Vasodilation, bronchodilation, insulin release,

M1 Receptor

G-Protein Q- Phospholipase C produce IP3 and DAG---> Protein Kinase C and Ca Influx



CNS and Enteric Nervous System

M2 Receptor

G Protein I- Inhibits Adenylyl Cyclase, decreased cAMP, decreased Protein Kinase A and decreased Ca+2



Leads to decreased HR and Contractility

M3 Receptor

G protein Q- Increased- Phospholipase C--- DAG and IP3. Increased Influx of Ca+2



Increased: exocrine secretion, peristalsis, bronchoconstriciton, bladder contraction, miosis, accomodation

Atropine

Muscarinic Antagonist- treats bracdycardia



Hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter.

Epinephrine

secreted by adrenal glands in response to sympathetic activation



Beta > Alpha (low concentration)



Anaphylaxis, asthma, glaucoma, hypotension



Increase Systolic/Decrease Diastolic

Norepinephrine

Alpha 1> Alpha 2> Beta 1



Treats hypotension



Increase systolic/increase diastolic

Isoproterenol

Beta Adrenergic Receptors



evaluation of tachyarrythmias, worsens ischemia through increasd 02 need



Neutral Systolic/Decreased Diastolic

Dopamine

D1 and D2> Beta> Alpha (low dose)



Unstable bradyarrythmias, heart failure, shock,

Dobutamine

Beta 1> Beta 2> Alpha



heart failure, cardiac stress testing

Phenylephrine

Alpha 1> Alpha 2



Hypotension, ocular procedures, decongestant

Amphetamine

indirect agonist- via reuptake inhibition and catecholamine release



narcolepsy, ADD, obesity

Cocaine

reuptake inhibitor



causes vasoconstriction and local anesthesia

Ephedrine

releases catecholamine



nasal decongestion, urinary incontinence, hypotension

Phenoxybenzamine

irreversibbly blocks Alpha receptors



treats- pheochromocytoma

Phentolamine

reversible Alpha blocker



reduces BP, and TPR

Prazosin and -Osin

Alpha 1 selective blocker



decrease TPR, and BP.

Beta Blockers- (-lol)

A-M are Beta 1 selective


N-Z are Beta 2 Selective


Nonselective don't have -olol



Decrease HR and Contractility===> decreased 02


MI mortality, decreased AV conduction, and renin secretion

Class IA Antiarrythmic



The Queen Proclaims Diso's Pyramid

Quinidine, Procainamide, Disopyramide



Slowed Na channel depolarizion and slowed K channel repolarization



Atrial and Ventricular arrythmias, reentry and ectopics

Class IB Antiarrythmics



IB is best post-MI

Lidocaine, Mexilitene



slows Na channel depolarization

Class IC Antiarrythmics



Can I have Fries Please

Flecainide, Propafenone



slows Na channel depolarization



SVT and atrial fibrillation

Class II

Beta Blockers- olols



Decrease SA and AV activity by decrease cAMP and Ca+2 current. Phase 4 prolonged

Class III



AIDS

Amiodarone, Ibutilide, Dofetilide, Sotalol



K+ channel blocker


used when other drugs fail



AFib, Flutter and Vetnricular Tachy

Class IV

Verapamil and Diltiazem



Ca Channel Blockers, slows Phase 0 in pacemaker cells



Prevents nodal arrythmias

Adenosine

Increase K+ out of cell leads to hyperpolarization and decreasing Ca+.



Use for SVT

ACE Inhibitors

Angiotensin Converting Enzyme- Take Angiotensin I and form Angiotensin II



Useful in the treatment of CHF by reducing preload through natriuresis and venodilation



-pril

ARB's

Angiotensin II Receptor Blockers- stop production of aldosterone



-sartan



cause dizziness and hyperkalemia

Cardiac Glycosides

Digoxin



Treat CHF and certain arrythmias



Inhibit Na/K Pump, this in turn increase Na inside cell. This decreases the need for Na/Ca exchanger and thus leads to increased Ca in the cell. Ca= increased contractility and Decreased HR



Van Gogh Symtpoms- ear, halo's, yellow

Hydralazine

Increased cGMP--> smooth muscle relaxation and decrease in afterload



Used for HTN, CHF



Lupus Like Syndrome

Types of Angina

Classical Angina- occurs when O2 demands exceed O2 supply. (during exercise)



Prinzmetal Angina- spasmatic constriction of Coronary Arteries causes random angina

Anti-Anginal Therapy

reduce myocardial needs by decreasing end diastolic, blood pressure, contractility, HR.



Nitrates (affect preload)



Beta Blocker (affect afterload)



Calcium Channel Blockers

Hypertensive Emergency

Nitroprusside- direct release of NO



Fenoldapam- D1 agonist