pharma fouda 3_p096-097.pdf

Preparations and doses  Morphine sulphate: 10 mg s.c. or i.m. In acute MI it is given 5 mg i.v.  Intrathecal (epidural) injection: produce long lasting analgesia which is useful for critically ill patients at risk of RC depression.  Sustained release preparatio...

Preparations and doses  Morphine sulphate: 10 mg s.c. or i.m. In acute MI it is given 5 mg i.v.  Intrathecal (epidural) injection: produce long lasting analgesia which is useful for critically ill patients at risk of RC depression.  Sustained release preparations &transdermal patches are available. Adverse effects: CNS  Tolerance & physical dependence (addiction) with prolonged use: – Physical dependence can occur within 24 h if given /4 h. – Tolerance may occur to analgesia and euphoria but not to respiratory depression.  ↑↑ intracranial tension.  RC depression: the most important effect and is dose-dependent. Resp  Bronchoconstriction. CVS  Postural hypotension GIT  Nausea, vomiting, and constipation.  Increased biliary tract pressure and biliary colic. Genito-  Urine retention especially in patients with enlarged prostate. Urinary  Prolongation of labor. Eye  Miosis is a consistent finding in morphine addiction. Contraindications & precautions  Head injury & increased intracranial pressure: Morphine causes respiratory depression & CO2 retention. The ↑ CO2 causes cerebral VD and ↑ intracranial tension.  Respiratory depression.  Bronchial asthma: Morphine causes bronchoconstriction due to (a) vagal stimulation; (b) histamine release. It also causes RC depression.  Biliary colic & gallstones: due to spasm of the sphincter of Oddi → ↑ biliary pressure.  Senile enlarged prostate: Morphine ↑ detrusor muscle tone with spasm of the internal urethral sphincter → feeling of urinary urgency with difficult micturition.  Hypotension and hypovolemia: because morphine causes postural hypotension.  Hepatic damage: Due to: (a) morphine is metabolized by the liver; (b) morphine increases the risk of hepatic encephalopathy due to marked CNS depression.  Hypothyroidism and adrenal insufficiency (Addison’s disease). Why? Because those patients have prolonged and exaggerated response to morphine. 332  Undiagnosed acute abdominal pain: Morphine masks the pain (which may be dangerous e.g. appendicitis) and interferes with the correct diagnosis.  Infants and old patients: are more susceptible to respiratory depression. ▌Chronic opioid toxicity (addiction)  There are behavioral changes, constipation, itching &miosis.  Sudden withdrawal (abstinence syndrome): – Consists of: irritability, nervousness, tremors, hypertension & ms cramps starts after 6-10 hrs from the last dose - peak effect at 48 hrs - gradually subsides over 5-10 days. – Mechanism: chronic administration of opioids ↓↓ endogenous production of endorphins and NA. Following sudden withdrawal, there is an immediate deficiency of endogenous opioids with rebound ↑ of NA release. Treatment of chronic morphine addiction: – Gradual withdrawal of morphine with substitution by methadone, then gradual withdrawal of methadone. – Clonidine: to stimulate central α2 receptors and ↓ NA release. – Sedatives: e.g. diazepam. ▌Acute opioid toxicity Manifestations:  Coma with depressed respiration, miosis, and shock.  Death occurs from respiratory depression. Treatment:  Gastric lavage. N.B.  Establish a patent airway Opioid blockers are and artificial respiration if indicated in acute morphine needed. toxicity but they are  Opioid antagonists: absolutely contraindicated – Naloxone: pure opioid in chronic morphine antagonist and can addiction because they reverse RC depression precipitate severe withdrawal within minutes (0.4 - 0.8 syndrome. mg i.v. for 2-3 doses). – Nalorphine: it is mixed agonist-antagonist (partial blocker). N.B.  The duration of opioid antagonists is shorter than morphine. The patient should be watched carefully because he may go back into coma.  Care should be taken to avoid withdrawal syndrome. 333