Neuropharmacology

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Neuropharmacology by Mind Map: Neuropharmacology

1. Sites of Action

1.1. Axon

1.1.1. Conduction of signals

1.1.2. Carry action potential

1.2. Synapse

1.2.1. Synaptic Transmission: Transmission of signals / Carries messages across neural gap

1.2.1.1. Make it

1.2.1.1.1. Increase in production

1.2.1.1.2. Decrease in production

1.2.1.1.3. Causing more effective product to be made

1.2.1.2. Store it

1.2.1.2.1. Vesicle contents decreased

1.2.1.3. Signal its use

1.2.1.4. Use it

1.2.1.4.1. Bond to receptor

1.2.1.4.2. Bond to receptor components

1.2.1.5. Get rid of it

1.2.1.5.1. Reuptake

1.2.1.5.2. Degradation

1.3. Receptor

1.3.1. Selectivity

1.3.1.1. Beta Blockers

1.3.1.1.1. Agonist

1.3.1.1.2. Antagonist

1.3.2. Receive signals

2. Neurotransmitters

2.1. Peripheral Nervous System

2.1.1. Somatic nervous system

2.1.1.1. Acetylcholine

2.1.1.1.1. Skeletal muscles

2.1.2. Autonomic nervous system

2.1.2.1. Sympathetic nervous system

2.1.2.1.1. Acetylcholine

2.1.2.1.2. Norepinephrine

2.1.2.1.3. Epinephrine

2.1.2.1.4. Dopamine

2.1.2.2. Parasympathetic nervous system

2.1.2.2.1. Acetylcholine

2.1.2.2.2. Nicotine

2.1.2.2.3. Muscarine

3. Pharmacokinetics

3.1. ACE Inhibitors

3.1.1. Most administered orally (except enalaprilat)

3.1.2. Excreted by kidneys

3.1.2.1. dosages must be reduced in patients with kidney disease

3.1.3. Most have prolonged half-lives (except captopril)

3.1.3.1. can be administered once or twice a day

3.1.4. Most are prodrugs- lisinopril is an exception

3.1.4.1. have to undergo conversion in small intestines and liver

3.1.5. Can be administered with food (except captopril and moexipril)

3.2. Aldosterone Antagonist

3.2.1. Eplerenone

3.2.1.1. absolute bio-availability unknown

3.2.1.2. undergoes metabolism by CYP3A4

3.2.1.3. excretion in urine and feces

3.3. Calcium Channel Blockers

3.3.1. Verapamil

3.3.1.1. Can be administered orally or IV

3.3.1.2. undergoes extensive first pass metabolism

3.3.1.3. elimination primarily through hepatic metabolism

3.3.1.3.1. dose must be reduced in patient's with hepatic impairment

3.3.2. Diltiazem

3.3.2.1. undergoes extensive first pass metabolism

3.3.2.1.1. bioavailability is only 50%

3.3.3. Nifedipine

3.3.3.1. undergoes extensive first pass metabolism

3.3.3.1.1. bioavailability only about 50%

3.4. Competitive neuromuscular blockers

3.4.1. Renal elimination

3.4.1.1. Pancuronium

3.4.2. Hepatic/biliary elimination

3.4.2.1. Rocuronium

3.4.2.2. Veruronium

3.4.3. Spontaneous degradation

3.4.3.1. Cisatracurium

3.4.4. Plasma cholinesterase elimination

3.4.4.1. Succinylcholine

3.4.4.2. Mivacurium

3.4.4.3. Atracurium

3.5. Adrenergic Agonists

3.5.1. Epinephrine

3.5.1.1. Cannot be given orally- only topically or by injection

3.5.1.1.1. Absorption more rapid following IM- Immediate with IV administration

3.5.1.2. has a short half-life due to enzymatic inactivation and uptake into adrenergic nerves

3.6. Adrenergic Antagonists

3.6.1. Prazosin

3.6.1.1. undergoes extensive hepatic metabolism

3.6.1.2. only 10% eliminated in urine

3.7. Beta-Adrenergic Antaganosts

3.7.1. Propranolol

3.7.1.1. Highly lipid soluble

3.7.1.1.1. can cross membranes including CNS

3.7.1.2. undergoes extensive first pass metabolism

3.7.1.3. excretion in urine

3.8. Indirect Acting Antiadrenergic Agents

3.8.1. Clonidine

3.8.1.1. Very lipid soluble

3.8.1.1.1. widely distributed including CNS

3.8.1.2. eliminated through hepatic metabolism and renal excretion

3.9. Muscarinic Agonists

3.9.1. Bethanechol

3.9.1.1. Quaternary ammonium compound

3.9.1.1.1. crosses membranes poorly and only a small fraction of each dose is absorbed

4. Nervous system Physiology

4.1. Peripheral nervous system

4.1.1. Somatic nervous system (Voluntary / 1 neuron pathway)

4.1.1.1. Sensory (afferent) nervous system

4.1.1.2. Motor (efferent) nervous system

4.1.2. Autonomic nervous system (involuntary / 2 neuron pathway)

4.1.2.1. Sympathetic division

4.1.2.1.1. Regulate cardiovascular system

4.1.2.1.2. Regulating body temperature

4.1.2.1.3. Implementing acute stress response

4.1.2.2. Parasympathetic division

4.1.2.2.1. Slow Heart rate

4.1.2.2.2. Increase gastric secretion

4.1.2.2.3. Constrict pupils

4.1.2.2.4. Empty bladder

4.1.2.2.5. Empty bowel

4.1.2.2.6. Focus for nearvision

4.1.2.2.7. Contract bronchial/smooth muscle

4.2. Central nervous system

4.2.1. Brain and spinal cord

5. Receptors

5.1. Parasympathetic Nervous systems

5.1.1. Cholinergic

5.1.1.1. Nicotinic

5.1.1.1.1. Non-neuronal (skeletal muscle)

5.1.1.1.2. Neuronal

5.1.1.2. Muscarinic

5.1.1.2.1. increased glandular secretions

5.1.1.2.2. contraction of smooth muscle in the bronchi and GI

5.1.1.2.3. Slowing of heart rate

5.1.1.2.4. contraction of iris resulting in miosis

5.1.1.2.5. contraction in eye for near vision

5.1.1.2.6. dilation of blood vessels

5.1.1.2.7. voiding of urinary bladder

5.2. Sympathetic Nervous system

5.2.1. Adrenergic

5.2.1.1. Alpha 1

5.2.1.1.1. Vasoconstriction

5.2.1.1.2. Ejaculation

5.2.1.1.3. Contraction of bladder neck and prostate

5.2.1.2. Alpha 2

5.2.1.2.1. regulate transmitter release

5.2.1.3. Beta 1

5.2.1.3.1. Heart

5.2.1.3.2. Kidney

5.2.1.4. Beta 2

5.2.1.4.1. Bronchial dilation

5.2.1.4.2. Relaxation of uterine muscle

5.2.1.4.3. Vasodilation

5.2.1.5. Dopamine

5.2.1.5.1. Dilates renal blood vessels