Chapter 3 Sanitary Permit Requirements
Chapter 3 Sanitary Permit Requirements
Chapter 3 Sanitary Permit Requirements
Example:
Therapeutic uses
•Treatment of anxiety disorders
•Muscular relaxation
•Treatment of seizure disorders
•Treatment of sleep disorders
•Pre-anesthetic agent
C. Enzyme bjective of metabolism: Convert drugs into: Inactive, Polar/Water Soluble (Ionized form), Non toxic and
Induction/ easily excreted metabolites.
Inhibition Main Site of Metabolism: LIVER
ENZYME INDUCTION: Occurs when a drug binds to the metabolizing enzyme and promotes enzyme activity.
(Stimulation of the enzyme activity→increased metabolism)
Drug-Drug Interaction involving enzyme induction
Ripampficin + Disopyramide (Reduced disopyramide level)
ENZYME INHIBITION-Occurs when a drug binds to the metabolizing enzyme and inhibits its activity. This leads
to decreased metabolism of the enzyme substrate
•POTENTIATION - a drug which has no therapeutic effect enhances the effect of a drug, i.e. 1 +0 = 2;
•example: potentiation of the CNS depressant effects of benzodiazepine by alcohol.
•SYNERGISM - the response elicited by the combined drugs is greater than the combined response of the
individual drugs i.e., 1 + 1 = 3
A. Neuronal Activation
•The neuron as a cell is responsive to changes in ion concentration in the cellular
environment.
•The membrane potential is maintained by the balance between cations and anions.
•regulated either by voltage control (voltage-gated channels) or by neurotransmitter
activation (ligand-gated channel)
•The resting state is maintained by the regulated efflux of POTASSIUM.
•The ACTION POTENTIAL is produced when the cell membrane charge becomes more
positive (DEPOLARIZATION) due to Na+ entry.
•After depolarization, when the Na channels close, potassium channels open and K+
goes out of the cell.
•This now leads to membrane REPOLARIZATION and the resting membrane potential is
restored.
2. GLYCINE
•Inhibitory
•Restricted to the spinal cord and brainstem
•Glycine receptors are pentameric which are selectively permeable to Cl-
•Blocked by strychnine
3. GAMMA AMINOBUTYRIC ACID (GABA)
•major inhibitory neurotransmitter in the brain
•derived from glutamate
•The receptor (e.g. GABAA) for glutamate is ionotropic and is coupled to a CHLORIDE CHANNEL. Activation of
this receptor leads to REPOLARIZATION/HYPERPOLARIZATION OF THE (post synaptic) NEURON à INHIBITION
4. ACETYLCHOLINE (Ach)
•Derived from choline and acetyl coA
Receptors:
•MUSCARINIC RECEPTORS (m1-m5)
•Metabotropic (G-protein coupled)
•NICOTINIC RECEPTORS (Ng or Nn)
•Ionotropic (sodium channel coupled)
5. CATECHOLAMINES
•NOREPINEPHRINE (NE)
•Derived from TYROSINE
•Receptors:
•α1, α2, β1, β2 adrenergic receptors
•sympathetic neurotransmitter
•DOPAMINE (DA)
•Synthesized from DOPA degraded by monoamine oxidase A (MAO A) in the brain and MAO B outside .
the CNS and catechol-Omethyl transferase (COMT)
•D1 and D2 receptors in the brain blocked by antipsychotic drugs
•Generally exerts a slow inhibitory action in the CNS neurons
•SEROTONIN (5HT)
•Synthesized by hydroxylation and decarboxylation of tryptophan
•Released by inhibitory neurons 5-HT1, 5HT2
•increases intestinal motility, bronchodilates and modulates vasodilation - LSD is an agonist
>CNS DEPRESSANTS
** Prototype is Alcohol
I. Primary Chemical Classes
i. Benzodiazepines
ii. Barbiturates
II. According to Use
i. Sedative (Anxiolytic): Relax, calm or tranquilize, and relieve anxiety.
ii. Hypnotics- induce sleep
iii. Anesthetics- loss of sensation
iv. Opiods Analgesic- relief from pain (Morphine and Codeine)
v. Antipsychotic or Neuroleptics-modify mood; used to treat psychoses, were called major tranquilizers
(1) Phenothiazine (Chlorpromazine and Thioridazine) (2) Butyrophenone (Haloperidol) (3) Clozapine,
Olanzapine and Risperidone.
vi. Antidepressants- Examples: MAOI’s (Phenelzine), TCA’s-SNRI(Amitryptyline, Imipramine, Clomipramine), SSRI’s
.. (Fluoxetine, Citlopram, Paroxetine) and 2nd and 3rd Gen Atidepressants (Amoxapine, Mirtazapine and
Trazodone)
vii. Antiparkinsons- Bromocriptine, Pergolide, Selegiline and Entacapone.
viii. Antiepileptics (AED’s) Carbamazepine, Phenytoin, Gabapentin and Topiramate
III. General Anesthetics
i. Inhalational (Volatile) eg. Isofluranr, Sevoflurane, diethyl ether and Nitrous oxide.
ii. Intravenous (non-volatile) eg. Propofol, Ketamine
MOA: (1) Activation of the GABA-a Receptor chloride channel
(2) Antagonism on the NMDA receptor
(3) Activation of potassium channel
(4) Decrease the duration of opening of nicotinic receptor.
(5) Action on glycine receptor.
STAGES of ANESTHESIA.
(Stage 1) ANALGESIA Conscious but drowsy|No response to painful stimuli | later part, amnesia is
produced.
(Stage 2) EXCITEMENT- Delirious and may vocalize but is definitely amnesic | Irregular respiration |
Retching and Vomiting may occur if stimulated | Dangerous Stage
(Stage 3) SURGICAL ANETHESIA –Respiration is regular but slow | No Movement
(Stage 4) MEDULLARY PARALYSIS – Vasomotor and respiratory support ceases | Death may occur
in few minutes
>CNS STIMULANT
Categories:
1.Category 1 Convulsants & Respiratory Stimulants
Doxapram, nikethamide, leptazol, strychnine
2.Category 2 Psychomotor Stimulants
Amphetamine, caffeine, cocaine
3.Category 3 Psychomimetic drugs
LSD (Lysergic Acid Diethylamide), phencyclidine, cannabinoids (THC)
I. STRYCHNINE-
–Alkaloid from Strychnos nux vomica which is a vermin poison
MOA: Blocks postjunctional glycine inhibition at the receptor in the CNS and Spinal Cord
Causes violent extensor spasm (voluntary muscle), Seizures and CNS excitation
Effects: Rhisus sardonicus
Treatment: DIAZEPAM to prevent Seizures
II. AMPHETAMINES AND METHYLPHENIDATE
-CNS Stimulant, anorectic, sympathomimetic actions
MOA: (1) Indirect acting dopaminergic and noradrenergic agonist
(2) Release biogenic amine (NE, DOPAMINE and SEROTONIN) from storage vesicles
(3) Can be attenuated by dopamine antagonist (Chlorpromazine and Haloperidol)
INDICATION (1) For treatment of ADHD and Narcolepsy (2) Adjunct therapy for obesity
ADVERSE EFFECTS: (1) Increase arousal and wakefulness, mood alteration
(2) Increased confidence, ability to concentrate, Euphoria, Increased Motor Activity, Anorexia and
Insomnia
(3) Prolonged exposure may cause “Amphetamine Psychosis”
TOLERANCE and DEPENDENCE (1) Very addictive and often abused
OVERDOSE TREATMENT: (1) Acidify the urine, (2) Give chlorpromazine to treat CNS Symptoms and (3) Alpha-receptor
blockers to lower the BP
DRUG INTERACTION:
(1) MAO Inhibitors: Effects: Hypersensitive crisis, CNS Overstimulation
(2) Barbiturates: Super additive mood elevation
(3) TCA: Potentiate CNS Stimulation, inhibit metabolism of amphetamine.
VI. COCAINE
Alkaloid from the leaves of Erythroxylon coca
MOA: Blocks reuptake or NE, Serotonin and Dopamine resulting to Increase arterial pressure, Tachycardia and
Ventricular Arrhythmias.
ADVERSE EFFECTS: (1) Loss of appetite, Insomnia and Hyperactivity. (2) Increased risk of intracranial hemorrhage, MI
and generalized/partial seizures (3) High addiction potential together with amphetamines (4) Overdose can
lead to hyperthermia, coma and death
DRUG INTERACTION: MAOI’s: Life threatening
GASTROINTESTINAL DRUGS
• Cholinergic antagonist
Atropine
• MOA: competes with Ach at the muscarinic receptors causing blockade of cholinergic effects
resulting to DECREASE GI MOTILITY
• Reversible (Surmountable)
• Indirectly acting cholinergic agonist (Acetylcholinesterase inhibitor)
Neostigmine • MOA: Carbamate esters by binding with acetylcholinesterase resulting to Increase Acetylcholine
at the synaptic cleft increasing the cholinergic effect resulting to INCREASE GI MOTILITY.
Dicyclomine, • Inhibit Muscarinic cholinergic receptors
Hyoscyamine • USES: Antispasmodics
(N-Hyoscine-
butyl bromide
• OPIOD AGONIST
• (Loperamide and Diphenoxylate)
• MOA: Inhibition of presynaptic cholinergic nerves
• USES: Treatment of Diarrhea
• Kaoiin and Pectin (Kopectate)
• Kaolin (Hydrated Magnesium Silicate or Attapulgite) + Pectin (Indigestible Carbohydrate
derived from apples.
ANTIDIARRHEAL • MOA: Adsorbent of bacteria, toxins and fluid decreasing the stool liquidity.
AGENTS • USES: Antidiarrheal
• BILE SALT BINDING RESINS
• Example: Cholestyramine and Colestipol)
• MOA: Adsorbs bile salt (which cause secretory diarrhea and C. difficile toxin
• USES: Treatment of diarrhea caused by C. difficile and bile salts
• SOMATOSTATIN, OCTREOTIDE
• MOA: Regulatory peptide slows the GI motility and intestinal fluid secretion
• USES: Effective for diarrhea due to vagotomy, short bowel syndrome
AGENTS THAT • Antacids
REDUCE • H2-Receptor Blocker
GASTRIC • Proton Pump Inhibitor
ACIDITY
MUCOSAL • Sucralfate
PROTECTIVE • Prostaglandin analog
AGENTS
LAXATIVES • Bulk
• Osmotic
• Stool Softener
• Cathartic
Clinical Techniques for Evaluating Cholinergic Blocking Agents
•Pathophysiologic Considerations
•Anticholinergic drugs inhibit the neuronic or vagal mechanism of gastric secretion.
•The more effective agents decrease both volume and acidity of gastric secretions.
•Anticholinergic drugs also block vagal stimulation of smooth muscle and depress GI motility.
•Pharmacologic Considerations
•Acetylcholine is the mediator of nerve impulses at the ganglionic synapses of both subdivisions of the ANS
and of impulses from the post ganglionic parasympathetic fibers to the effector organ.
•The classic parasympathetic depressant, atropine, lacks sensitive action, so that blockade of the peripheral
effects of Ach includes not only the GIT but also the sphincter muscle of the iris, ciliary muscle of the lens, and
salivary gland.