ATNAA

ATNAA Uses, Dosage, Side Effects, Food Interaction and all others data.

Atropine binds to and inhibit muscarinic acetylcholine receptors, producing a wide range of anticholinergic effects. Atropine is an anticholinergic agent which competitively blocks the muscarinic receptors in peripheral tissues such as the heart, intestines, bronchial muscles, iris and secretory glands. Some central stimulation may occur. Atropine abolishes bradycardia and reduces heart block due to vagal activity. Smooth muscles in the bronchi and gut are relaxed while glandular secretions are reduced. It also has mydriatic and cycloplegic effect.

Atropine, a naturally occurring belladonna alkaloid, is a racemic mixture of equal parts of d- and l-hyoscyamine, whose activity is due almost entirely to the levo isomer of the drug. Atropine is commonly classified as an anticholinergic or antiparasympathetic (parasympatholytic) drug. More precisely, however, it is termed an antimuscarinic agent since it antagonizes the muscarine-like actions of acetylcholine and other choline esters. Adequate doses of atropine abolish various types of reflex vagal cardiac slowing or asystole. The drug also prevents or abolishes bradycardia or asystole produced by injection of choline esters, anticholinesterase agents or other parasympathomimetic drugs, and cardiac arrest produced by stimulation of the vagus. Atropine may also lessen the degree of partial heart block when vagal activity is an etiologic factor. Atropine in clinical doses counteracts the peripheral dilatation and abrupt decrease in blood pressure produced by choline esters. However, when given by itself, atropine does not exert a striking or uniform effect on blood vessels or blood pressure.

Pralidoxime reactivates cholinesterase outside the CNS that had been inactivated by phosphorylation due to exposure to certain organophosphates by displacing the enzyme from its receptor sites. It removes the phosphoryl group from the active site of the inactivated enzyme by nucleophilic attack, regenerating active cholinesterase and forming an oxime complex. It also detoxifies certain organophosphates by direct chemical reaction.

Pralidoxime is to reactivate cholinesterase (mainly outside of the central nervous system) which has been inactivated by phosphorylation due to an organophosphate pesticide or related compound. The destruction of accumulated acetylcholine can then proceed, and neuromuscular junctions will again function normally. Pralidoxime also slows the process of "aging" of phosphorylated cholinesterase to a nonreactivatable form, and detoxifies certain organophosphates by direct chemical reaction. The drug has its most critical effect in relieving paralysis of the muscles of respiration. Because pralidoxime is less effective in relieving depression of the respiratory center, atropine is always required concomitantly to block the effect of accumulated acetylcholine at this site. Pralidoxime relieves muscarinic signs and symptoms, salivation, bronchospasm, etc., but this action is relatively unimportant since atropine is adequate for this purpose.

ATNAA
Uses
Dosage
Side Effect
Precautions
Interactions
Uses during Pregnancy
Uses during Breastfeeding
Accute Overdose
Food Interaction
Half Life
Volume of Distribution
Clearance
Interaction With other Medicine
Contradiction
Storage

Trade Name	ATNAA
Generic	Atropine + pralidoxime
Weight	2.1mg/0.7ml + 600mg/2ml,
Type	Intramuscular solution
Therapeutic Class
Manufacturer
Available Country	United States,
Last Updated:	September 19, 2023 at 7:00 am

Uses

Atropine is used for Non ulcer dyspepsia, Irritable bowel syndrome, Diverticular disease, Bradycardia, Organophosphorus poisoning, Premedication in anesthesia, Poisoning or overdosage with compound having muscarinic actions, Ophthalmic Inflammatory eye disorders, Eye refraction.

Pralidoxime chloride is used for an antidote:

In the treatment of poisoning due to those pesticides and chemicals (e.g., nerve agents) of the organophosphate class which have anticholinesterase activity and
In the control of overdosage by anticholinesterase drugs used in the treatment of myasthenia gravis.

The principal indications for the use of Pralidoxime chloride are muscle weakness and respiratory depression. In severe poisoning, respiratory depression may be due to muscle weakness.

ATNAA is also used to associated treatment for these conditions: Amblyopia, Atrioventricular Heart Block, Bradycardia, Bronchospasm, Crying, Detrusor Hyperreflexia, Excessive bronchial secretion, Hypertonic uterine contraction, Hypertonicity of the small intestine, Ocular Inflammation, Parkinsonism, Peptic Ulcer, Poisoning by parasympathomimetics (cholinergics), Poisoning caused by mushrooms, Poisoning caused by organophosphate anticholinesterase nerve agents, Poisoning caused by organophosphorus pesticides, Pylorospasm, Rhinorrhoea, Sinus Bradycardia, Spasms, Toxic effect of organophosphate and carbamate, Hypermobility of the colon, Laughing, Muscarinic side effectsToxic effect of organophosphate and carbamate, Anticholinesterase overdose

How ATNAA works

Atropine binds to and inhibit muscarinic acetylcholine receptors, producing a wide range of anticholinergic effects.

Pralidoxime is an antidote to organophosphate pesticides and chemicals. Organophosphates bind to the esteratic site of acetylcholinesterase, which results initially in reversible inactivation of the enzyme. Acetylcholinesterase inhibition causes acetylcholine to accumulate in synapses, producing continuous stimulation of cholinergic fibers throughout the nervous systems. If given within 24 hours after organophosphate exposure, pralidoxime reactivates the acetylcholinesterase by cleaving the phosphate-ester bond formed between the organophosphate and acetylcholinesterase.

Dosage

ATNAA dosage

Adult:

IV: Bradycardia: 500 mcg every 3-5 mins. Total: 3 mg.
IV/IM: Organophosphorus poisoning: 2 mg every 10-30 mins until muscarinic effects disappear or atropine toxicity appears.
IM/SC: Premedication in anesthesia: 300-600 mcg 30-60 mins before anesthesia.
IV/IM/SC: Poisoning or overdosage with compound having muscarinic actions: 0.6-1 mg, repeat 2 hrly.
Ophthalmic: Inflammatory eye disorders: As 0.5-1% solution: 1-2 drops 4 times/day.
Ophthalmic: refraction: 1% solution 1 drop twice daily for 1-2 days before procedure.
Oral: Non ulcer dyspepsia, Irritable bowel syndrome, Diverticular disease: 0.6-1.2 mg as a single dose at bedtime.

Usual Pediatric Dose for Anesthesia:

7 to 16 pounds: 0.1 mg, IV, IM, or subcutaneously
17 to 24 pounds: 0.15 mg, IV, IM, or subcutaneously
24 to 40 pounds: 0.2 mg, IV, IM, or subcutaneously
40 to 65 pounds: 0.3 mg, IV, IM, or subcutaneously
65 to 90 pounds: 0.4 mg, IV, IM, or subcutaneously
Over 90 pounds: 0.4 to 0.6 mg, IV, IM, or subcutaneously

Intramuscular-

Organophosphorus poisoning:

Adult: Mild: 600 mg, repeat 1-2 times at 15 min intervals as needed. Severe: 1.8 g given as 3 inj of 600 mg in rapid succession. Persistent: May repeat the entire series (1.8 g) beginning 1 hr after admin of the last inj.
Child:<40 kg: Mild: 15 mg/kg, repeat as needed every 15 min. Max: 45 mg/kg. Severe: 15 mg/kg, repeat twice in rapid succession to a total dose of 45 mg/kg. Persistent: May repeat the entire series (45 mg/kg) beginning 1 hr after admin of the last inj; ≥40 kg: Same as adult dose.

Intravenous-

Organophosphorus poisoning:

Adult: In combination with atropine: Loading dose: 1-2 g by infusion over 15-30 min or slow inj over at least 5 min, may repeat dose after 1 hr then 10-12 hrly, as needed. Administer as soon as the effects of atropine are observed. Maintain atropinisation for at least 48 hr.
Child: ≤16 yr Loading dose: 20-50 mg/kg (max: 2 g/dose) by inj over 15-30 min followed by 10-20 mg/kg/hr as continuous infusion. Alternatively, a repeat bolus of 20-50 mg/kg after 1 hr and repeated 10-12 hrly as needed; >16 yr Same as adult dose.

Poisoning or overdosage with compounds having muscarinic actions:

Adult: Initially, 1-2 g, followed by 0.5-1 g/hr as infusion. Alternatively, the initial dose may be repeated after 1 hr and then 3-8 hrly as needed.

Intramuscular: Dilute 1 g with 3.3 mL sterile water for inj to a final concentration of 300 mg/mL.

Intravenous: Dilute 1 g with 20 mL of sterile water for inj to make a concentration of 50 mg/mL to be administered in fluid-restricted patients or when rapid admin is required; for all other patients, further dilute with normal saline to a final concentration of 20 mg/mL.

Side Effects

Injection: Dry mouth, dysphagia, constipation, flushing and dryness of skin, tachycardia, palpitations, arrhythmias, mydriasis, photophobia, cycloplegia, raised intraocular pressure. Toxic doses cause tachycardia, hyperpyrexia, restlessness, confusion, excitement, hallucinations, delirium and may progress to circulatory failure and resp depression.

Eye drops or ointment: Systemic toxicity esp in children, on prolonged use may lead to irritation, hyperaemia, oedema and conjunctivitis. Increased intraocular pressure.

Drowsiness, dizziness, visual disturbances, nausea, HTN, tachycardia, headache, hyperventilation, muscle weakness, impaired renal function, elevated liver enzymes, transient increase in creatine phosphokinase, transient neuromuscular blockade; mild to moderate pain at inj site.

Toxicity

Oral, mouse: LD₅₀ = 75 mg/kg. Symptoms of overdose includes widespread paralysis of parasympathetically innervated organs. Dry mucous membranes, widely dilated and nonresponsive pupils, tachycardia, fever and cutaneous flush are especially prominent, as are mental and neurological symptoms. In instances of severe intoxication, respiratory depression, coma, circulatory collapse and death may occur.

Precaution

Reflux oesophagitis; elderly; infants and children; Pregnancy.

Patient with myasthenia gravis receiving anticholinesterase agents. Not indicated in the treatment of poisoning due to phosphorous, inorganic phosphates, or organophosphates without anticholinesterase activity and carbamate pesticides. Renal impairment. Pregnancy and lactation.

Interaction

Additive anticholinergic effects with quinidine, antidepressants and some antihistamines.

Elimination Route

Atropine is rapidly and well absorbed after intramuscular administration. Atropine disappears rapidly from the blood and is distributed throughout the various body tissues and fluids.

Half Life

3.0 ± 0.9 hours in adults. The half-life of atropine is slightly shorter (approximately 20 minutes) in females than males.

74-77 minutes

Elimination Route

Much of the drug is destroyed by enzymatic hydrolysis, particularly in the liver; from 13 to 50% is excreted unchanged in the urine.

The drug is rapidly excreted in the urine partly unchanged, and partly as a metabolite produced by the liver.

Pregnancy & Breastfeeding use

Pregnancy Category C. Animal reproduction studies have not been conducted with atropine. It also is not known whether atropine can cause fetal harm when given to a pregnant woman or can affect reproduction capacity. Atropine should be given to a pregnant woman only if clearly needed.

Pregnancy Category C. Either studies in animals have revealed adverse effects on the foetus (teratogenic or embryocidal or other) and there are no controlled studies in women or studies in women and animals are not available. Drugs should be given only if the potential benefit justifies the potential risk to the foetus.

Contraindication

Glaucoma, chronic respiratory disease, sick sinus syndrome, thyrotoxicosis, cardiac failure, pyloric stenosis, prostatic hypertrophy.

There are no known absolute contraindications for the use of Pralidoxime Chloride. Relative contraindications include known hypersensitivity to the drug and other situations in which the risk of its use clearly outweighs possible benefit.

Acute Overdose

May cause hyperthermia, hypertension, increased respiratory rate, nausea and vomiting. May also lead to CNS stimulation. Severe intoxication may lead to CNS depression, coma, respiratory failure and death.

Manifestations of Overdosage: Observed in normal subjects only: dizziness, blurred vision, diplopia, headache, impaired accommodation, nausea, slight tachycardia. In therapy it has been difficult to differentiate side effects due to the drug from those due to the effects of the poison.