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
Parasympatholytics: Antinicotinics
*Drug classes with Drugs
NMJ Blockers: Depolarizing, Non-Depolarizing
Main cause of Nicotine Toxicity? Tx?
Eating cigs;
MAP formula
DBP + 1/3 [SBP-DBP]
How does an ACE Blocker Work
Blocks Angiotensin 1 from becoming 2, and blocks bradykinin from becoming inactive
Antidote for Nipride
Sodium Thiosulfate
How does an ARB work
Blockes receptor sites for Angiotensin 2; causes vasodilation and decreased Na+ absorption and decreased Blood Volume [blocks aldosterone secretion]
Contraindications for Atropine
Closed-Angle Glaucoma and BPH
Cholinomimetics in MG and Post-Op Ileus
MG - AChesterase inhibitors to help with more ACh reaching the nACh-R
Ileus - Increased motility, so increased chance to resolve
Nitrates: Nitro
*Amyl Nitrites
*Mononitro [Isosorbide]
NO release, 1-3 min onset, 20-30 min duration
En Passant Synapse
Where the Axon swells and releases NTM out
Sympathetic Activity
*Heart
*Blood Vessels
*Bronchioles
*Liver
*GI
*Kidney
- Increases/Accelerates Heart - B1,B2
*Relax skeletal muscle/constrict smooth muscle - A
*Relax Bronchioles - Relax B2
*Liver - Glycogenolysis B2
*GI - Relax/Contract A2,B2
*Contract Kidney
Sympathomimetics: Indirect Agonist
*2 examples
*Amphetamine - Displacement of NE, Reverse NET
*Cocaine - Block NET, DAT
In which Glaucoma do you avoid Atropine? Why?
Angle Closure/ Narrow Angle; atropine relaxes the ciliary muscle, which will increase ocular pressure by blocking the drainage of aqueous humor [blind]
Alpha Agonist Effect
IncreasedBP, Decreased HR [vagal], increased vascular tone
Cholinomimetics (Parasympathomimetics): Esters of Choline [Direct]
*With main use/effect
ACh - Miosis
Methacholine - Diagnosis for Asthma
Carbachol - IOP
Bethanechol - Bladder Dysfunction, GERD
Class 2 - Sympatholytic [bb]
Propanolol, esmolol
Indirect Acting Cholinomimetics: 3 classes w/examples
Simple Alcohols - Fast
*Edrophonium - Dx of MG
Carbamates - Moderate
*AChesterase Inhibitors
Organophosphates - Days
*Echothiophate - Glaucoma
Sympathomimetics: Direct Agonists
*Dobutamine, Phenylephrine, Midodrine, Clonidine, Precedex, Ephedrine
*Dobutamine - B1
*Neo - A
*Midodrine - A1
*Clonidine - A2
*Precedex - A2
*Ephedrine - Both direct and indirect
SNS: A1 with subtype and 2nd messenger
Gq [Excite]; Phospholipase C -> IP3, DAG
Class 4 - Block Cardiac Ca++ channel
Verapimil
3 Drug classes for Angina
Nitrates, CCB, BB
AntiHTN: Sympathoplegics 2 classes
*with drugs
Centrally Acting - A2>A1
*Methyldopa
*Clonidine
Andrenoreceptor Antagonist - A and B Blockers
*Prazosin
*Propanolol
Combination Vasodilators
CCB
Hydralazine toxicity resembles what AI disease
SLE
Triphasic Dopamine
D1 - Vasodilation and activates B1 in heart
Low dose - decrease peripheral resistance
High dose - mimics act of epi
Loveheim Cube of Emotion
NE, Serotonin, Dopamine
Cholinomimetics (Parasympathomimetics): Direct Groups
Esters of Choline
Plant Alkaloids
Sympatholytics: Alpha-Blockers
*2 Classes w/ meds
Reversible -
*Phentalomine - A1,A2
*Prazosin - A1 [BPH]
*Labetolol - A,B blocker
Irreversible -
*Phenoxybenzamine [pheochromocytoma] - Covalent bond At A1
Cholinomimetics (Parasympathomimetics): 3 Classes of Indirect
*Their main use, drugs included
Simple Alcohols - Fast
*Edrophonium - Dx of MG
Carbamates - Moderate
*AChesterase Inhibitors
Organophosphates - Days
*Echothiophate - Glaucoma
What drug blocks Renin production
Aliskiren
3 Types of Synapses per lecture
En passant, chemical, electrical
Main use of Methyldopa
Pregnancy induced HTN
Nicotinic vs Cholinergic Receptor Difference
N - takes places at NMJ
C - Takes place at Effector Cells
HTN Urgency
> 180/110 without organ damage
Direct Acting Cholinomimetics: 2 Classes w/ examples
Plant Alkaloids - Nictonine, Muscarine, Betel Nut, Pilocarpine
Esters - ACh, “chol or choline”
Sympatholytics: Beta Blockers
*4 Drugs
*Propanolol - B1,B2
*Metoprolol, Atenolol - B1 [safer in asthma]
*Labetolol - A1, B1, B2 [preeclampsia], pheochromocytoma
*Esmolol - B1
HTN Crisis
> 180/110 with organ damage
PNS: Nn location
Post Ganglia
Cholinomimetics (Parasympathomimetics): Plant Alkaloid [Direct]
*2 classes with meds
Muscarinic - Muscarine, Pilocarpine
Nicotine - Nicotine, Arecoline [Betel Nut]
Cholinoceptor Blockers (Parasympatholytics): 2 Types
Antimuscarinics, Antinicotinics
AntiHTN: Central Acting Sympathoplegics: Drugs w/purpose
1.) Methyldopa - not for 1st line, Pregnancy induced HTN
2.) Clonidine - Prolonged hypotension, Sedative, ADHA, tourettes, withdrawal
Class 1 - Na+ channel Blockade
Quinidine, Procainimide [prolong ADP]
CCB: Angina and HF
Most effective for variant angina; CCB make HF worse
Organophosphate Poisoning: S/S and Tx
Miosis, salivation, bronchiole constriction, n/v/d [SLUDGEM]; Atropine with Pralidoxime
B1 and B2 Receptors
B1 - Heart
B2 - Lungs
S/S Atropine OD; Tx
Blind, confused, hot, dry, flushed, tremors; Tx is AChesterase inhibitor or Pilocarpine
SNS: A2 w/subtype and 2nd Messenger
Gi [inhibitory]; blocks Ad. Cyclase - decreased cAMP
A1 and A2 Receptors
Smooth muscle, eyes, GI, presynaptic nerve terminal
SNS: B1,B2 w/ subtype and 2nd Messenger
Gs [excite]; Increase Ad. Cyclase - Increased cAMP
Class 3 - Prolonged AP duration
Amio
RAAS System
renin produced - renin stimulates angiotensinogen to angiotensin 1 - Angiotensin 1 - 2 via ACE in lungs - 2 constricts vessel and stimulates aldosterone being secreted [increased blood volume and renal absorption]
