AAA

• SALICYLATES DESCRIPTION

  PAST → only as analgesic and anti-inflammatory drugs

  PRESENT → as prophylaxis of thromboembolic disorders, myocardial infarction, and stroke
• Salicylates

  MECHANISM OF TOXICITY CENTRAL STIMULATION OF RESPIRATORY CENTER → HYPERVENTILATION ➔ Respiratory Alkalosis

  ➔ Compensatory Metabolic Acidosis

  ➔ Dehydration
• Salicylates

  Mechanism of Toxicity

  ALTERATION OF PLATELET FUNCTION → ➔ Affect bleeding time ➔ Prolong prothrombin time
• aspirin molecular structure


  ???

  
• Aspirin PRINCIPAL MANIFESTATIONS

  1. Hyperpnea (abnormal rapid or deep breathing)
  2. Disturbed Acid-Base Balance
• ASPIRIN ACUTE INTOXICATION

  1. Vomiting (shortly after ingestion) 2. Hyperpnea, Tinnitus, & Lethargy 3. Respiratory Alkalemia & Metabolic Acidosis (in arterial blood gases) 4. Coma, Seizures, Hyperglycemia, Hyperemia, Hyperthermia & Pulmonary Edema (severe) 5. Central Nervous System Failure & Cardiovascular Collapse (DEATH)
• ASPIRIN CHRONIC INTOXICATION (usually in young children or confused elderly)

  1. Confusion, Dehydration, & Metabolic Acidosis (attributed to the next symptoms) 2. Sepsis, Pneumonia, or Gastroenteritis 3. Cerebral & Pulmonary Edema (more common than in acute intoxication) 4. Central Nervous System Failure & Cardiovascular Collapse (DEATH)
• ASPIRIN EMERGENCY AND SUPPORTIVE MEASURES

  1. Maintain the airway & assist ventilation if necessary 2. Treat coma, seizures, pulmonary 4 edema, & hyperthermia if they occur 3. Treat metabolic acidosis with intravenous sodium bicarbonate
• Aspirin antidote?

  None
• Aspirin: NO SPECIFIC ANTIDOTES (However, sodium bicarbonate is frequently given both to prevent acidemia and to promote salicylate elimination by the kidneys)
• ASPIRIN: DECONTAMINATION 1. Induce emesis or perform gastric lavage 2. Administer activated charcoal and a cathartic NOTE: not necessary for patients with chronic intoxication
• Acetaminophen/ paracetamol: Found in many analgesics and cold remedies (whether OTC or prescription)
• Paracetamol + Codeine or Propoxyphene = more dramatic acute symptoms of early
• acetaminophen toxicity → delayed recognition and antidotal treatment.
• MECHANISM OF TOXICITY

  1. Formation of hepatotoxic NAPQI from cytochrome P450 metabolism
  2. ➔ NAPQI directly reacts with hepatic macromolecules ➔ LIVER INJURY
• NAPQI = N-acetyl-p-benzoquinoneimine
• Renal damage may also occur by the same mechanism owing to renal metabolism
• STructure of acetaminophen


  C8H9NO2

  
• Acetaminophen/ paracetamol

  PRINCIPAL MANIFESTATION: Hepatic failure
• Acetaminophen/ paracetamol:

  ACUTE INTOXICATION

  ➔ Nausea & Vomiting ➔ Drowsiness ➔ Confusion ➔ Liver Tenderness ➔ Low Blood Pressure ➔ Cardiac Arrhythmias ➔ Jaundice ➔ Acute Hepatic & Renal Failure (Liver Necrosis results to DEATH)
• Acetaminophen/ Paracetamol

  CHRONIC INTOXICATION

  HEPATIC DAMAGE is reported after daily ingestion of acetaminophen for a year or more

  Chronic intoxication is generally RARE

  (Liver Necrosis results to DEATH)
• Acetaminophen/ Paracetamol

  EMERGENCY MEASURES

  1. Induce emesis with Syrup of Ipecac, unless respiration is depressed
  2. Give Saline Cathartic
• Paracetamol: ANTIDOTE

  1. N-acetylcysteine (NAC) (best if given within 10 hours from ingestion)
  2. MOA: NAC is a mucolytic agent that also increases glutathione synthesis by providing cysteine.
• Paracetamol:

  GENERAL MEASURES

  1. Keep the patient warm and quiet
  2. Give Phytonadione (if the prothrombin time ratio exceeds 3.0)
  3. MOA: Phytonadione (Vitamin K1) stops bleeding as a cofactor for the synthesis of liver coagulation factors (II, VII, IX, and X).
• ANESTHETICS DESCRIPTION: A local anesthetic on mucous membranes and one of the most popular drugs of abuse
• Anesthetics:

  Administered through: → Sniffing into the nose (snorting) → Injected intravenously, occasionally combined with heroine (aka. speedball) → Smoking
• Anesthetics:

  When purchased from the streets, it is usually of high purity (however, it may occasionally contain substitute stimulants: caffeine, phenylpropanolamine, ephedrine, or phencyclidine)
• Anesthetics

  MECHANISM OF TOXICITY (Three Primary Action) ● Local Anesthetic Effects ● CNS Stimulation ● Inhibition of Neuronal Uptake of Catecholamines
• Cocaine PRINCIPAL MANIFESTATIONS ● Convulsions ● Circulatory Failure
• Cocaine ACUTE INTOXICATION

  Restlessness, excitability, hallucinations, tachycardia, dilated pupils, chill or fever, sensory aberration, abdominal pain, vomiting, numbness and muscular spasms

  • Irregular respiration, convulsions, coma, and circulatory failure
• Cocaine CHRONIC INTOXICATION

  Hallucinations, mental deterioration, weight loss, and change of character.

  PERFORATION OF THE NASAL SEPTUM (when sniffed)
• Cocaine: Step 1

  • Maintain airway and respiration
  • Delay absorption of ingested drug by giving charcoal
  • Remove ingested drug from the stomach by gastric lavage or emesis
• Cocaine: Step 2

  • Control convulsions by giving diazepam -
  • Control tachycardia and other cardiac arrhythmias by giving propranolol
• Cocaine Treatment 3

  Control hypertensive reactions by giving phentolamine (non-selective a-adrenergic antagonist)