Pharmacology II Dentistry 1
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Transcript of Pharmacology II Dentistry 1
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PHARMACOLOGY II DENTISTRY
GENERAL & LOCAL ANESTHESIA
Dr Mohammed Shamssain
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Course Contents
General & local anesthetics
Sedative hypnotics & pharmacology of
alcoholism
Treatment of epilepsy & parkinsonism
Antipsychotics, anti depressant & anxiolytics
Pharmacology of pain Adrenal cortex hormones & steroidal anti-
inflammatory drugs
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Course Contents
Thyroid hormones & anti-thyroid drugs
Calcium metabolism
Gonadal hormones & their antagonists
Oral contraceptives
Pharmacology of diabetes mellitus
Antimicrobial agents
Antifungal & antiviral agents
Treatment of cancer & parasitic infestation
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Assessment
Quiz one: one hour; 20%; date: Monday 19th
March (1-2 pm)
Mid-term exam: one hour; 20%
Quiz two: one hour; 20%; date: Monday 14th
May (1-2 pm)
Final exam: two hours; 40%
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General
Noradrenaline: noradrenergic transmission is important in
control of mood (functional deficiency resulting
depression)
controlling wakefulness, and alertness Dopamine: is important in
motor control (parkinsonism is due to dopamine
deficiency)
has behavioural effects (excessive dopamine activity isimplicated in schizophrenia)
hormone release (prolactin, GH)
dopamine in chemoreceptor trigger zone causes nausea
& vomiting
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General
5-HT: physiological functions associated with 5-HTpathways include: feeding behaviour, behaviouralresponse, control of mood and emotion, control ofbody temperature and vomiting
Ach: has effects on arousal, on learning, and on shortterm memory. Dementia and parkinsonism areassociated with abnormalities in cholinergicpathways.
GABA (Gamma-AminoButyric Acid): is an inhibitoryNT in CNS
Glycine: an inhibitory NT , acts on GABA like receptorin spinal cord
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Anesthetics
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Ion Channels
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Synapse
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AnestheticSuppression ofPhysiologicalResponse to
Surgery
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Essential Components of Anesthesia
Analgesia- perception of pain eliminated
Hypnosis- unconsciousness Depression of spinal motor reflexes
Muscle relaxation
* These terms together emphasize the role ofimmobility and of insensibility!
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Stages of Anesthesia
In general anesthesia: the patient is
unconscious and has no awareness or othersensations.
The relationship between the amount ofgeneral anesthetic administered and the
depression of the brain's sensory usefullydivided into stages to describe the depth ofanesthesia.1,3,5
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Mechanism of Action
General Anesthetics CNS modifyingfunctions of ION CHANNELSmodifying theelectrical activity of neurons at a molecular level
This may occur by anesthetic molecules binding directly to ion channels or
by their disrupting the functions of molecules thatmaintain ion channels.
a general anesthetic is a drug that has the abilityto bring about a reversible loss of consciousness by act on CNS via shutting off the brain from external
stimuli
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Anesthetics divide into 2 classes:
InhalationAnesthetics
Gasses or Vapors
Usually Halogenated
IntravenousAnesthetics
Injections
Anesthetics or inductionagents
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What are General Anesthetics?
A drug that brings about a reversible loss of
consciousness. Administered by an anesthesiologist in order
to induce or maintain general anesthesia tofacilitate surgery.
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Pathway for General Anesthetics
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Pathway for General Anesthetics
Partial Pressure in brain quickly equilibrates
with partial pressure in arterial blood whichhas equilibrated with partial pressureperfused alveoli.
DEPTH of anesthesia induced by an inhaled
anesthetic depends primarily on thePARTIAL PRESSURE!!! Of the anestheticsin the brain
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Pathway of General Anesthetics
Rate of induction and recovery from
anesthesia depends on the rate of change ofpartial pressure in the brain.
These drugs are small lipid-solublemolecules that cross the alveolar membrane
easily. Move into and out of the blood basedon the partial pressure gradient.
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Variables that Control Partial Pressure
in Brain
Direct Physician's Control Solubility of agent
Concentration of agent in inspired by air
Magnitude of alveolar ventilation
Indirect Physicians Control Pulmonary blood flow-function of CO
Arteriovenous concentration gradient
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Rate of Entry into the Brain: Influence
of Blood and Lipid Solubility
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Rate of Entry into the Brain
LOW solubility in blood= fast induction and
recovery HIGH solubility in blood= slower induction
and recovery.
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General Anesthetics
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General Anesthetics
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General Actions of Inhaled Anesthetics
Respiration
Depressed respiration and response to CO2 Kidney
Depression of renal blood flow and urine output
Muscle
High enough concentrations will relax skeletalmuscle
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Cont
Cardiovascular System
Generalized reduction in arterial pressure andperipheral vascular resistance. Isofluranemaintains CO and coronary function better thanother agents
Central Nervous System Increased cerebral blood flow and decreased
cerebral metabolism
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Inhaled Anesthetics
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Inhaled Anesthetics
Halothane
Enflurane
Isoflurane
Desflurane
Halogenatedcompounds:
ContainFluorineand/orbromideSimple, small
molecules
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Injectable Anesthetics
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Intravenous Anesthetics
Used in combinationwith Inhaled
anesthetics to: Supplement general
anesthesia
Maintain generalanesthesia
Provide sedation
Control blood pressure
Protect the brain
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Adjunct Agents
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Anticholinergic Drugs
Block the effects of Ach and other cholinergic
drugs at cholinergic receptors of effector cells
Two major types
Antinicotinics include ganglion blockers and
neuromuscular blockers
Anti muscarinics include tertiary amines (e.g:
atropine , scopolamine, etc)
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Mechanism of Action of Anesthesia
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MAC:Minimum Alveolar Conc
MAC is a concept used to compare the
strengths, or potency, of anaesthetic vapours
Defined as the concentration of the vapour in
the lungs that is needed to prevent movement
(motor response) in 50% of subjects in response
to surgical (pain) stimulus.
A lower MAC value represents a more potent
volatile anesthetic.
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Overton Meyer Theory
O-M Theory: The MAC of a volatile substance isinversely proportional to its lipid solubility (oil:gascoefficient)
MAC is inversely related to potency i.e. high macequals low potency.
The hypothesis correlates lipid solubility of ananaesthetic agent with potency (1/MAC)
Onset of anaesthesia occurs when sufficientmolecules of the anaesthetic agent havedissolved in the cell's lipid membranes, resultingin anaesthesia
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Indications
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Side Effects
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Local Anesthetics
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Types of Local Anesthetics
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Parenteral Anesthetic Agents
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Drug Effects
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Indications
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Side Effects
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Neuromuscular Blocking Agents
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NMBAs
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NMBAs:Depolarizing Agents
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NMBAs:Non-Depolarizing Agents
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NMBAs
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NMBAs:Indications
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NMBAs: Side Effects
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NMBAs: Overdose
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Depression of respiratory drive
Decreased CO2 drive (medullary chemoreceptors),
Takes MORE CO2 to stimulate respiration
Depressed cardiovascular drive
Gaseous space enlargement by NO
Fluoride-ion toxicity from methoxyflurane
Metabolized in liver = release of Fluoride ions
Decreased renal function allows fluoride toaccumulate = nephrotoxicity
Toxicity and Side Effects
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Moderate Sedation
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Dentistry Implications
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Dentistry Implications
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Dentistry Implications
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Dentistry Implications