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OTC analgesics & antipyretics
OTC analgesics & antipyretics
OTC drugs available:
salicylates (aspirin, choline salicylate, Mg salicylate and Na salicylate)
Paracetamol (acetaminophen)
ibuprofen
Naproxen Na
Ketprofen
All are similar but Naproxen has slightly a longer duration of action
The strength of these products available OTC is less than same products available on prescription
Onset of all of these drugs is ½-1 hr, maximum effect between 2-3 hrs and duration of action is 4-6 hrs.
All will reduce temp by (1.1°- 1.7°C),
Salicylates
Active moiety: salicylic acid (irritating)
Choline salicylate: stable in oral solution
Mg salicylate + Na salicylate: can be used for patients allergic to aspirin
Inhibit COX in periphery and CNS
Aspirin
Indication: (1) mild to moderate pain of musculoskeletal NOT visceral origin. (2) Fever
DOC in RA
Aspirin
Pharmacokinetics:
- ASA is absorbed by passive diffusion of the nonionised from from the stomach/small intestine
- Factors affecting absorption (=5, what are they?)
- Rectal absorption is slow and unreliable (60-75%)
Enteric-coated ~:
1. Eliminates local gastric irritation
2. Delayed absorption by food (why?)
3. Not suitable for acute pain relief. Preferred for RA (why?)
Buffered ~:
1. no difference in gastric damage from plain ASA
2. Absorbed more rapidly than non buffered ASA
Effervescent ~: rapidly absorbed, but no evidence if rapid analgesia. Avoid in patients with restricted Na+ intake (CHF, RF, HTN)
Therapeutic Considerations:
1. Impaired platelet aggregation
acetyl group (good and bad?!!)
ASA should be D/C 48 hrs before surgery and shouldn’t be used as analgesic in dental extraction, or surgery etc
C/I: haemophilia, hypoprthrombinemia, vit K deficiency, Hx of bleeding or PUD
The prostaglandin thromboxane A2 (TxA2) causes platelets to aggregate
Aspirin inhibits synthesis of TxA2 by irreversible acetylation of COX enzyme.
Other salicylates & NSAIDs also inhibit COX but have a shorter duration of inhibitory action because they cannot acetylate COX; that is, their action is reversible.
. Effect on uric acid elimination (dose-dependent)
Avoid all salicylates in all patients with Hx of gout or hyperuricemia (why?)
1-2 g/day plasma level of uric acid
2-3 g/day little/ no effect
> 5 g/day plasma level of uric acid
(Toxicity)
3. GI irritation & bleeding
two mechanisms of gastric damage (what are they?)
Avoid in: elderly, PUD or bleeding, alcoholic liver disease
Ingesting alcohol + ASA= incidence of GI bleeding
4. Aspirin Allergy
- If you experience gastritis or heart burn after aspirin use
Aspirin allergy is uncommon, < 1% of patients
within 3 hours of ASA ingestion: urticaria, oedema, difficulty in breathing, rhinitis, bronchospasm or shock
Most common in patients with asthma, urticaria or nasal polyps
15% cross-reaction with Tartrazine (colour)
Cross reaction with other NSAIDS (rate for acetaminophen 6% and for ibuprofen 97%)
patients allergic to ASA > avoid all NSAIDs > use acetaminophen or nonacetylated salicylates (eg, Na salicylate) instead
5. Pregnancy/ Lactation
- Avoid ASA in both
Avoid ASA especially during the 3rd trimester/pregnancy
Why? > Effect on mother (=3), effect on fetus (haemorrhage, growth retardation, congenital intoxication, premature closure of ductus arteriosus > still birth)
Paracetamol is the analgesic of choice in these periods
Unlabelled/Investigational Use:
Low doses have been used in the prevention of pre-eclampsia, recurrent spontaneous abortions, pematurity, fetal growth retardation (including complications associated with autoimmune disorders such as lupus)
60-80 mg/day during gestational weeks 13-26 (patient selection criteria not established)
6. Reye’s Syndrome
Acute potentially fatal illness (50%) occurs almost exclusively in children < 15 years of age
Produces fatty liver + encephalopathy
Occurs usually within 1-7 days of viral infections with influenza or chickenpox.
Ch.Ch: persistent vomiting, CNS damage, signs of hepatic injury & stupor > convulsions > coma
Nonacetylated NSAIDs > not associated with Reye’s
Aspirin toxicity
Overdose:
with chronic therapy (100 mg/kg per day for at least 2 days)> mild intoxication- HA, dizziness, N & V, hyperventilation, mental confusion, lassitude….
Acute intoxication- dose-dependent:
<150 mg/kg mild
150-300 mg/kg moderate
>300 mg/kg severe
Symptoms: lethargy, tinnitus, tachypnea, pulmonary edema, convulsions, coma, haemorrhage and dehydration.
First respiratory alkalosis followed by metabolic acidosis (why?)
Hypoglycemia (why?) and fever may be severe in children.
Bleeding from GIT or mucosal surface > petechiae at autopsy
OD Management: ipecac syrup, gastric lavage, activated charcoal
Administration of ipecac syrup or any oral solution to a pt who’s convulsing is absolutely C/I aspiration
in children < 1yr old > vomiting should be induced only under medical supervision
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