• Pupil Dialation (Mydriasis)
• Blood Vessels (Vasoconstriction)
• Bladder (Contraction of Sphincter - Can't Pee)

• Inhibits the release of NT from presynaptic membrane

Heart - Activation increases heart rate, contraction force, velocity of impulse conduction through AV node

Kidney – causes release of rennin, which triggers release of angiotensin (a powerful vasoconstricter) resulting in increased BP due to vasoconstriction

Lungs - Bronchodialation

   (also dilates arterioles of heart & muscle)

Uterus - Relaxes uterine muscle

Liver - Promote glygogenolysis

Skeletal muscle - enhance contraction

Cholinesterase Inhibitor

Neostigmine (Reversible)

(Receptors it activats and what it does)

ü  Muscarinic Responses – similar to muscarinic agonist “Rest & Digest”

o   Increased glandular secretion, tone and motility of GI, urinary uregency, bradycardia, bronchiol constriction, miosis

ü  Neuromuscular effects – MUSCLE CONTRACTION (High/reduced)

o   increase force contraction, too high – reduce force in contraction d/t constant depolarization

Myasthenia Gravis

 Autoimmune process where antibodies block cholinergic receptors, Acetycholinesterase inhibitor increases Ach levels to complete with blocking antibody (respiration paralysis d/t diaphram tetany in overdose)

o   Same action as reversible cholinesterase inhibitors- just longer acting

o   Used primarily in treatment of glaucoma

o   Commonly founding insecticides and Nerve Gas

prevents the breakdown acethylcholine (more in blood) by inhibiting acetylcholinesterase

Cholinergic vs. myasthenic crisis;

use of drugs in diagnosis and treatment

ü  Myasthenic Crisis – patients inadequately medicated, low Ach causes muscle weakness and may result in respiratory paralysis. Treated with cholinesterase inhibitor

ü  Cholinergic Crisis – is d/t oversoe with cholinesterase inhibitor, like myasthenia crisis, cholinergic crisis is charterized by muscle weakness and frank paralysis. It is also accompanied by excessive muscarinic stimulation (rest or digest). Treated with respiratory support and atropine (Muscarinic anatagonis)

Adrenergic Agonist

Epinephrine - Theraputic Effects

ü  Therapuetic Effects

o   Alpha 1 activation vasconstriction: Delay absorption of local anethetics. Control superficial bleeding. Elevate blood pressure, Mydriasis for eye procedures,

o   Beta 1 activation: overcome heart block, restore cardiac function

o   Beta 2 activation:  in lung promotes bronchiodialation – asthma

ü

Adrenergic Agonist

Epinephrine - Adverse Effects

o   Hypertensive crisis

o   Dsyrhythmias

o   Angia pectoris

o   Necrosis following extravasation

o   Hyperglycemia

Mechanisms of adrenergic receptor activation

ü  Direct receptor binding (drug acts like agonist)

ü  Promotion of NE release (ie Amphetamines)

ü  Inhibition of NE reuptake (kinda like SSRI)

ü  Inhibition of NE inactivation (MAOI)

Catecholamines vs non-catecholamines; diff in oral usability, duration of action & action in the CNS

Concept of relative versus absolute receptor specificity

ü  Adrenergic therapy is more specific than muscarinic and we can say…

ü  We want to target Beta 1, but the more drug we give to go after Beta 1, the less specific we get – meaning it will begin to affect Beta 1 & 2

Anaphylactic shock; signs and symptoms & pharmacological treatment 

Propanolol (NON-selective beta blocker)

Uses & Side Effects:

Use: HTN, cardiac dysrhythmia, tachycardia, angina pectoris, MI

Adverse effects: Bradycardia, hypoglycemia in diabetics, AV block, heart failure, bronchoconstriction, CNS effects,

Metoprolol (selective beta-blocker)

Uses & Side Effects:

Uses: HTN, angina pectoris, heart failure and MI 

Adverse Effects: Bradycardia, AV block, low cardiac output, heart failure

Third generation beta blockers: proposed M of A

(know why these agents may be useful in some cardiac patients)  

Mechanism: cardioselective, act on blood vessels to cause dilation, thus decrease HTN

but may produce nonselevive or cardioselective beta blockade

Alpha 1 Agonist

Therapeutic Uses

Eyes: Dilation (Mydriasis) ---opposite is miosis

Blood Vessels:

- Hemostais

- Elevation of BP

- Nasal decongestion

- Adjunct to local anesthesia (delays anesthetic absorption, reduce blood flow to anesthetic SOA. Prolongs anesthesia to stay local and to lower dosage)

Hypertension 

Necrosis

Bradycardia 

Adrenergic Antagonist (Blockers) - Minipress

Therapeutic Uses

Eyes: Contraction (Miosis)

Blood Vessels:

-Treat essential hypertension

-Reduce alpha-agonist toxicity

-Treat pheochromacytoma (adrenal gland releases too much epi/NE)

-Treat Reynaud’s disease

Bladder: Relieve symptoms of BPH, can pee 

Adrenergic Antagonist (Blockers) - Minipress

Adverse Effects

Orthostatic hypotension

Reflex Tachycardia

Nasal congestion

Inhibition of ejaculation

Beta 1 Agonist

Therapeutic Uses

Cardiac arrest – initiate contraction in stopped heart

Heart failure – strengthen contractions of weak heart

Shock ­HR/heart contraction – maintain CO blood flow to organs

AV Heartblock – temporarily enhance impulse conducgtion thru AV node & overcomes AV block 

Altered HR

-tachycardia

- disrhythmia

Angina Pectoris

-d/t low O2 to the blood

Beta 1 Antagonist (Blocker) - Metroprolol & Propanalol

Therapeutic Uses

Blood Vessels:

Angina pectoris – slows heart so O2 demand is brought into balance

Hypertension - HR & contraction - ¯ cardiac output - ¯ b.p.

Cardiac dysrhthmias

Myocardial Infarction

Heart Failure

Hyperthyroidism

Migraine

Stage fright

Glaucoma 

Kidney:

Decrease Renin, Decrease BP

Bradycardia, reduced CO, heart fail, atreoventricular block, 

Beta 2 Agonist 

Therapeutic Effects

Lungs: Relieve Asthma

Uterus: Relaxes Uterine Contractions/Delay Labor

Liver: Promotes glycogenolysis

Skeletal Muscle: Enhance contraction

Tremor - activation of B₂ in smooth muscle

Beta 2 Antagonist - Propanalol

Adverse Effects

bronchoconstriction can cause onset of asthma symptoms in asthmatics

hypoglycemia in diabetics, due to decreased breakdown of glycogen