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IV agents, :pharmacodynamics, Pharmacodynamics, Pharmacodynamics,…
IV agents
Propofol
Pharmacokinetics
Bioavailability
NA
Protein binding
95–99%
Metabolism
Liver glucuronidation
Onset of action
15–30 seconds[5]
Elimination half-life
1.5–31 hours[5]
Duration of action
~5–10 minutes
Liver
↓
Ring hydroxylation by Cytp450
↓
4 hydroxy propofol
↓
↓ cinjugation glucuronidation and sulfation
↓
Excreated via kidney
↓
Inactive metabolite
Etomidate
Pharmacokinetics
Absorption: absorbed after oral trans mucosal administration
Onset of action: 30–60 seconds.
Peak effect: 1 minute.
Duration: 3–5 minutes; terminated by redistribution.
Distribution: Vd: 2–4.5 L/kg.
Protein binding: 76%
Metabolism: Hepatic and plasma esterases
Half-life distribution: 2.7 minutes.
Half-life redistribution: 29 minutes
Liver and plasma esterase
↓
Hydrolysis of ethyl ester side chain
↓
Carboxylic acid ester
↓
Excreated in kidney
↓
Inactive metabolite
Ketamine
Pharmakinectics
Bioavailability
Intravenous: 100%
Intramuscular: 93%
Epidural: 77%
Intranasal: 45–50%
Sublingual: 24–30%
Rectal: 25–30%
By mouth: 16–20%
Protein binding
23 to 47%
Metabolism
Liver, intestine
Major: CYP3A4, CYP2B6
Elimination half-life
Ketamine: 2.5–3 hours
Norketamine: 12 hours
Liver
↓
Demethylation of ketamine by p-450
↓
Nor ketamine
Active metabolite
↓
Hydroxylated and conjugated
↓
Water soluble glyccuronide metabolite
↓
Excreated in urine
Bioavailability
Intravenous: 100%
Intramuscular: 93%
Epidural: 77%
Intranasal: 45–50%
Sublingual: 24–30%
Rectal: 25–30%
By mouth: 16–20%
Protein binding
23 to 47%
Metabolism
Liver, intestine
Major: CYP3A4, CYP2B6
Elimination half-life
Ketamine: 2.5–3 hours
Norketamine: 12 hours
Liver
↓
Demethylation of ketamine by p-450
↓
Nor ketamine
Active metabolite
↓
Hydroxylated and conjugated
↓
Water soluble glyccuronide metabolite
↓
Excreated in urine
:pharmacodynamics
CNS
CNS depressant
decreases cerebral metabolic rate
ICP
cause tremor , twitching
CVS
decreases CO,BP
tachycardia
caution in patient poor left ventricular function
Respiratory
depress the rate and depth of breathing
laryngospasm bronchospasm
coughing
GI
nausea and vomiting
Pharmacodynamics
RESPIRATORY
hypoventilation
hyperventilation
laryngospam
upper airway obstruction
CIRCULATORY SYSTEM
hypotension
hypertension
bradycardia
tachycardia
arrhythmias
GIT
nausea and vomiting and hiccups
ENDOCRINE SYSTEm
cause adrenocortical depression
CNS
Increases,CMR,ICP
Pharmacodynamics
CNS
increases cerebral mortality rate,ICP,cerebral blood flow
CVS
stimulates sympathetic nervous system
releasing catecholamines causing hypertension and tachycardia
RESPIRATORY SYSTEM
good bronchodilator causes respiratory depression
GIT
increased secretion, salivary bronchial
MUSCLOSKELETAL SYSTEM
increases skeletal muscle tone
Pharmacodynamics
CARDIOVASCULAR
hypotension
RESPIRATORY
Incidence of APNEA
bronchodilation in COPD patient
CEREBRAL
it posses anti convulsant property
GIT
it act as an anti emetic agent(even more effective than ondansetron)
IMMUNOLOGIC
it act s an antipuritic agent
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