Exam 2 Flashcards
Parasympathetic Activity on Body
*Heart
*Blood Vessels
*Bronchioles
*GI
*Urinary
*Decelerates Heart [M2]
*Relax smooth vessels [M3]
*Contract Bronchioles [M3]
*Contract Gi/Increase secretions [M3]
*Contract Bladder [M3]
PNS: PNS Plexi
Long Pre Fibers; Short Post Fibers
PNS: Nm location
skeletal muscle end plate
AntiHTN 4 Classes w/ main action
Diuretics - Deplete Na+
Sympathoplegics - Decrease PVR,CO
Direct Vasodilators - relax vascular smooth muscle
Anti-Angiotensins - Block activity or production
3 main sources to PVR
BV diameter, viscosity, BV length
CHF:
*Diuretics
*ACE/ARBS
*Vasodilators
*BB
Sympathomimetics: Direct Agonists
*Epi, Norepi, Isoproterenol, Dopamine
*Epi - A, B1, B2
*Norepi - A, B1
*Isoproterenol - B1, B2
*Dopamine - D, B1 [dose dependent]
CHF:
*Ca++
*Cardiac Glycosides
*PDE Inhibitor
*Catecholamines
*Cardiac Glycosides [digoxin] - + inotrope, inhibits NaK ATPase, Decrease AP and Na+ gradient
*PDE [Milrinone] - prolong cAMP and cGMP; + inotrope, Decrease PVR
*Catehcolamines - Dopamine, Dobutamine [+ inotrope]
Substitutions in Catecholamines
reduce potency; inactivated by COMT in the gut
Beta Agonist Functions
Decreased BP, Decreased vascular tones, increased heart functions
Parasympatholytics: Antimuscarinics
*4 Drugs with use
Atropine - Organophosphate poisoning [with pralidoxime], bradycardia
Scopalamine - motion sickness
Tropicamide - mydriasis and Dx of Cycloplegia
Ipratromine - asthma
AntiHTN: Angiotensin Inhibitors and Endothelin Receptor Antagonists
ACE, ARBS, Bosentan
AntiHTN: Sympathoplegic Adrenoreceptor Antagonist
*drugs w/ purpose
1.) Prazosin - more effective w BB
2.) Propanolol - not selective, prevents reflex brady
PNS: M1, M3, M5
Excite; CNS neurons, smooth muscle
4 Major Groups of Anti HTN meds
Diuretics, Sympathoplegics, Direct vasodilators, Anti-angiotensins
PNS: M2, M4
Inhibit: CNS Neurons, Myocardium, smooth muscle
How does Phentalomine turn Epi into a depressor
Alpha antagonist; blocks epi; used in pheochromocytoma
What is Minoxidil and how does it work
Rogain - Open K+ Channels; can cause tachycardia and hypertrichosis
How does Nipride work
Arterial and venous dilation by releasing more cAMP; be aware of CN poisoning [protect from light]
Where do Verapamil, Diltiazem, and Dyhydropyridines work
Verapamil - Heart
Diltiazem - Heart and Peripheral
Dyhydropyridines - Peripheral
Oral Vasodilators and MOA
Hydralazine [NO in endothelial cells], Minoxidil [Open K Channels to hyperpolarize]
Basic Structures of Catecholamines
Benzene ring w hydroxyl groups and amine group chain on the side
Innervation to Skeletal Muscle Blood Vessels
A1 Vasoconstriction - 20% @ Rest; 80% w/ activity
Cholinomimetics (Parasympathomimetics): Indirect
Simple Alcohols
Carbamates
Organophosphates
Substitutions in Alpha Carbons
MAO blocks oxidation = prolongs action
AntiHTN: Vasodilators 6 Types
Hydralazine - Stimulates NO release
Minoxidil - K+ channels
Nipride - NO/CN toxicity, dilate artery/vessels
Fenoldopam - D1 agonist
CCB - Verapamil [Heart], Cardizem, Dihydropyridines
Nitrates
6 Main NTM Classes with Examples
- Esters - ACh
*Monoamines[Catecholamines] - NE, Serotonin, Dopamine
*AA - GABA, Glutamate
*Purines - Adenosine, ATP
*Peptides - Substance P, Endorphins
*Inorganic Gases - NO
Parenteral Vasodilators and MOA
Nipiride [release NO from drug or endothelium]
Fenoldopam [activates Dopamine receptors]
SNS: Chain Ganglia
Short Pre Fibers; Long Post Fibers