Exam 2 ANS Agonist & Antagonist Flashcards
Hormonal feedback loop
Kidneys sense low blood flow -> release Renin -> activates Renin angiotensin aldosterone system -> activates Angiotensin -> releases Aldosterone -> retain more water -> blood volume, SV, CO, SV -> increase MAP.
Autonomic Feedback Loop: sympathetic
Baroreceptors activates Vasomotor center -> activate Sympathetic autonomic NS -> release NE -> Increases HR, contractility & venous tone -> Increased CVP, CO, SV -> Increased MAP.
Sympathetitic organ responses
i. Heart:
1. Beta-1 increases HR & Contractility
ii. Blood vessels
1. Skeletal: Beta-2 relax
2. Smooth: Alpha-1 contract
iii. Bronchioles smooth muscle:
1. Beta-2 relax
iv. GI tract:
1. Alpha-2 & Beta-2 relax wall (no food moving)
2. Alpha-1 contract sphincters
3. Overstimulation can cause constipation.
v. Renal:
1. Beta-1 release Renin
2. Beta-2 relax bladder
3. Alpha-1 contract sphincter
vi. Liver:
1. Alpha & Beta-2= Glycogenolysis
Parasympathetic organ response
i. Heart:
1. M2 decreases HR & contractility
ii. Blood vessels
1. Smooth: M3 relax
iii. Bronchioles smooth muscle:
1. M3 contract (Dust can get trapped if no contraction, keeps things out)
iv. GI tract:
1. M3 contract walls, relax sphincters & increase secretions (food moving)
2. Overstimulation can cause diarrhea.
v. Renal:
1. M3 contract bladder & relax sphincter
Autonomic nervous system
Includes Sympathetic, Parasympathetic & Enteric
ii. Effectors are cardiac & smooth muscle & glands
iii. Not under consciousness control
iv. Neurons start in CNS will have 2nd cell body ganglia (PNS)
v. All ANS preganglionic fibers release ACh
vi. Postganglionic fibers release either ACh or Norepinephrine & effect is either stimulatory or inhibitory (depends on receptor).
Somatic nervous system
i. All neurons are myelinated
ii. Neurons start in brain go thru nuclei (CNS) to body
iii. Conscious control
List the most common toxicities associated with sympathomimetics.
HTN, cerebral hemorrhage, pulmonary edema, angina, cardiac tamponade, MI.
Delineate the decision in selecting a specific adrenergic agonist.
- Which receptor activation is required.
- Route of administration
- Dosing/ monitoring therapeutic response.
List the major clinical applications (7) of the adrenoceptor agonists & treatment.
- Hypotension / Hypotensive crisis: –> Direct Acting α agonists: NE, phenylephrine
- Cardiogenic Shock: Treat heart & avoid peripheral vasoconstriction
- Shock: Volume replacement, NE
- Reduced blood flow: Epi + Lidocaine for facial Sx.
- Cardiac arrest / Complete HB: Target vasodilation of coronaries. Epinephrine & Isoproterenol
- Respiratory: Bronchial asthma –> Beta-2 agonists Albuterol, terbutaline.
- Anaphylaxis: Nebulized epinephrine for asthma attack –> open airway.
List tissues that contain significant numbers of α1 or α2 receptors.
- α1: Peripheral vascular
- α2: CNS (hypothalamus) (Overall decreases BP)
Describe what happens in the cardiovascular system after the administration of an alpha-agonist, a beta-agonist, or a mixed agonist.
- Alpha: Increase PVR, decrease CO, Increase MAP
- Beta: Decrease PVR, increase CO, decrease MAP
- Mixed: Increase or decrease PVR, increase CO, increase MAP
Describe the MOA of direct and indirect acting catecholamines.
- Direct: Bind to receptor & elicit similar effect of endogenous ligand.
- Indirect: Does not bind to receptor & Increases amount of catecholamine in synapse
Non depolarizing muscle relaxants.
- half life?
- Origin?
- MOA?
- Reversal?
- Short, intermediate & long acting
- Curare derivatives
- MOA: Competitive antagonist with ACh
- Reversal: Sugammadax for Rocuronium & Vecuronium
Depolarizing muscle relaxants
- MOA?
- Example? Metabolism?
- Depolarizes the post-synaptic cell –> flaccid paralysis
- Succinylcholine: It is an agonist
a) Not metabolizes by AChE as it is not recognized by AChE.
b) Continuous end-plate depolarization causes muscle relaxation.
c) Phase 1 & Phase 2
What cholinomimetic is associated with myasthenia gravis?
- For what is it used & describe that?
- Edrophonium (lasts 5mins) used as diagnostic test.
- Baseline muscle strength test –> 2mg given to assess for negative reaction –> 8mg given if improvement then indicative of MG. Can also be used to see if long-acting AChE inhibitors will work.
List the signs, symptoms, and treatment of atropine overdose.
- S/S: Dilated pupils, hyperthermia, dry mouth, shaking, confusion, flushed skin, tachycardia, absent bowel sounds, vision loss, grabbing invisible objects, urinary retention.
- Treatment: Antimuscarinic
Define the different types of glaucoma and the use of cholinomimetics.
- Open angle:
a) Constricting the pupil/iris –> further opens canal of Schlemm. - Narrow angle:
a) Iris is bulged forward to narrow & partially obstruct the drainage angle
b) Atropine is contraindicated –> it relaxes the ciliary muscle –> completely obstructing Canal of Schlemm
c) Atropine causes Mydriasis= Enlargement of pupil.
Describe the pharmacodynamics of direct-acting cholinomimetic agents and give examples of each.
- Mimics ACh binding to receptor.
a) Esters of Choline: ACh, Succinylcholine.
- Permanently charged & insoluble in lipids. Cannot cross BBB
b) Alkaloids: Plant based (Muscarinic, Nicotine, Lobeline)
- Some can cross BBB.
- Excretion enhanced by urine acidification.
