Pharmacology Autonomics- FirstAID

Clearance decreases. Therefore, maintenance dose decreases. Loading dose will stay the same (not dependent on clearance)

A substance that produces the opposite physiologic effect of an agonist but does not act at the same receptor (epinephrine can act as a bronchodilator by stimulating beta2 receptors in asthma patients that have muscarinic overactivity).

Adrenal medulla
Sweat glands

Increase vascular smooth muscle contraction, INCREASE PUPILLARY DILATOR MUSCLE (MYDRIASIS), INCREASE intestinal and bladder sphincter muscle contraction

Decrease sympathetic outflow, decrease insulin release

Increase heart rate and contractility, increase renin release, increase lipolysis

Vasodilation, bronchodilation, increase heart rate (because of vasodilation), increase contractility, increase lipolysis, increase insulin release, DECREASE UTERINE TONE

CNS, enteric nervous system

Decrease heart rate and contractility of ATRIA

Increase exocrine gland secretions (sweat, gastric acid), increase gut peristalsis, increase bladder contraction, BRONCHOCONSTRICTION, INCREASE PUPILLARY SPHINCTER MUSCLE CONTRACTION (MIOSIS), CILIARY MUSCLE CONTRACTION (accomodation), Increase release of NO (EDRF)

Relaxes renal vascular smooth muscle

Modulate neurotransmitter release in the brain

Increase nasal and bronchial mucus production, CONTRACTION OF BRONCHIOLES, puritus, pain (allergies)

Increase gastric acid secretion

Increase vascular smooth muscle contraction

Increase H2O permeability and reabsorption in the medullary collecting tubules of the kidney

Autoreceptor- NE binds presynaptic a2 receptors that block further release
AII- Increases
M2- Decreases it

Hemicholinium- Blocks choline transport into the nerve terminal (RLS)
Vesamicol- blocks choline acetyltransferase
Botulinum toxin- Blocks release of ACh into the synapse

Metyrosine- Blocks Tyrosine hydroxylase (converts tyrosine to DOPA)
Reserpine- Blocks dopamine conversion to NE
Guanethidine, bretrylium- Blocks NE release into the synapse

Mechanism: Direct muscarinic agonist
Use- Postoperative and neurogenic ileus and urinary retention (contracts bowel and bladder smooth muscle)

Mechanism: Direct muscarinic agonist
Use- Glaucoma, pupillary contraction, and relief of intraocular pressure

Mechanism: Direct muscarinic agonist. Resistant to AChE
Use- Potent stimulator of sweat, tears, and saliva, glaucoma (contracts ciliary muscle of eye- open angle; contracts pupillary sphincter- closed angle)

Mechanism: Direct muscarinic agonist
Use- Challenge test for diagnosis of asthma (stimulates receptors when airway is inhaled- bronchoconstricts)

Mechanism- AChE inhibitor
Use- Postoperative and neurogenic ileus and urinary retention, MG, reversal of NMJ blockade. NO CNS PENETRATION

Mechanism- AChE inhibitor
Use- MG (long acting); does NOT penetrate CNS

Mechanism- AChE inhibitor
Use- Diagnosis of MG (very short acting- 30 minutes)

Mechanism- AChE inhibitor
Use- Glaucoma (crosses BBB) and ATROPINE OVERDOSE

Mechanism- AChE inhibitor
Use- Glaucoma

DUMBBELSS- Diarrhea, urination, miosis, bronchoconstriction, bradycardia, lacrimation, excitation of skeletal muscle and CNS, salivation, sweating

Mechanism- Muscarinic antagonist
Use- Eye exams (mydriasis)

Mechanism- Muscarinic antagonist
Use- Parkinson's

Mechanism- Muscarinic antagonist
Use- Motion sickness

Mechanism- Muscarinic antagonist
Use- Asthma, COPD

Mechanism- Muscarinic antagonist
Use- Reduce urgency in mild cystitis and reduce bladder spasms (urge incontinence)

Mechanism- Muscarinic antagonist
Use- Peptic ulcer treatment (reduce acid secretion), decrease salivation, decrease motility

Increased body temperature (decreased sweating), dry mouth, dry skin, rapid pulse, constipation, DISORIENTATION (DELIRIUM), cycloplegia

Mechanism- Blocks nAchR (ganglionic). Only used in experiments to prevent vagal reflexes to changes in blood pressure (reflex bradycardia caused by NE)
Toxicity- Severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction

Mechanism- a1, a2, b1, b2 (low doses selective for b1)
use- Anaphylactic shock, open angle glaucoma, asthma, hypotension (2nd line)

Mechanism- a1, a2 > b1 (no b2)
Use- Hypotension (but decreases renal perfusion), septic shock

Mechanism- b1=b2
Use- AV block (rare)

Mechanism- D1=D2 > b > a; ionotropic and chronotropic
Use- Cardiogenic shock (increases renal perfusion via D1), heart failure

Mechanism- B1>B2, ionotropic but not chronotropic. Increases cardiac conduction velocity (can lead to arrhythmia)
Use- Heart failure, cardiac stress testing

Mechanism- a1 > a2
Use- Pupillary dilation, vasoconstriction, nasal decongestion (stops epistaxis)

Mechanism- B2 selective
Use- Acute asthma

Mechanism- B2
Use- Long term asthma

Mechanism- B2
Use- Reduce premature uterine contractions (tocolytic)

Mechanism- B2
Use- Reduce premature uterine contractions

Mechanism- Releases stored catecholamines
Use- Narcolepsy, obesity, ADD, MDD

Mechanism- Releases stored catecholamines
Use- Nasal decongestion, urinary incontinence, hypotension

Mechanism- Prevents reuptake of catecholamines
Use- Vasoconstriction and local anesthesia

Mechanism- a2 agonists, decrease central adrenergic outflow
Use- Hypertension, especially if patient has renal disease because no decrease of blood flow to kidney (a-methyldopa safe in pregnancy; clonidine will give rebound hypertension if a dose is missed).
Note- causes hemolytic anemia (Coombs positive)

Mechanism- Blocks a1 and a2 irreversibly
Use- Pheochromocytoma before removing tumor
Toxicity- Orthostatic hypotension, reflex tachycardia

Mechanism- Blocks a1 and a2 reversibly
Use- Pheochromocytoma
Toxicity- Orthostatic hypotension, reflex tachycardia

Mechanism- Selective a1 blocker
Use- Hypertension, urinary retention in BPH
Toxicity- 1st dose orthostatic hypotension (give at bed time), dizziness, headache

Mechanism- a2 selective blocker
Use- Depression
Toxicity- Sedation, increased serum cholesterol, increased appetite

Hypertension: Decrease cardiac output, decrease renin secretion (via b1 on JGA cells)
Angina: Decrease heart rate and contractility (decrease oxygen demand)
MI: Decrease mortality
SVT: Decrease AV conduction velocity
CHF: Slows progression to chronic failure
Glaucoma: Decreases secretion of aqueous humor

Impotence, exacerbation of asthma, cardiovascular (bradycardia, AV block, CHF), CNS adverse effects (sedation, sleep alterations), mask the signs of hypoglycemia in diabetics because they stop sweating and tachycardia

Propanolol, timolol, nadolol, and pindolol (N-Z)

Acebutolol (partial agonist), betaxolol, esmolol (short acting), atenolol, metoprolol (A-M)

Pindolol, aceputolol

Metoprolol, carvedilol

Propanolol, esmolol

Timolol

Propanolol

Because all the adrenergic receptors are activated, including b2 which is actually good because it is causing vasodilation to temper the increase in blood pressure caused by cocaine. If you block beta receptors then only the alpha effects will be seen which is bad