By Dr Sameh AM Abdel-Ghany

Natural alkaloids

atropine

scopolamine

Synthetic atropine substitutes

hyoscinebutylbromide

emepronium

Chemistry:

natural plant alkaloid (tertiary amine)

from Atropa belladonna plant.

Absorption:

good after oral administration.

Distribution:

all tissues including CNS.

Metabolism:

40% metabolized by liver.

Excretion:

60% excreted unchanged in urine.

Non-selective muscarinic blocker.

CNS:

Brain: (Minimal CNS stimulant effect)

Stimulate RC and CIC

Large dose produce excitation – agitation-hallucination and coma → coma.

Basal ganglia:

anti-parkinsonian effect.

Vestibulocerebellar pathway:

anti-motion sickness and antiemetic effects

Eye:

Passive mydriasis

(due to paralysis of constrictor pupillae ms ).

Cycloplegia :

(paralysis of ciliary ms ) → loss of accomodation for near vision.

Decrease aqueous drainage

Sweat glands:

↓ sweating → atropine fever.

Children are more sensitive to this effect.

CVS:

Heart:

Initial bradycardia (due to transient stimulation of vagal nucleus in the medulla) followed by persistant tachycardia

BV:

Therapeutic doses → no effect.

Toxic doses → direct VD (atropine flush).

BP:

no effect in therapeutic doses but toxic doses produce hypotension.

Bronchi:

Bronchodilatation.

↓ bronchial secretions.

GIT:

↓ salivary secretion (dry mouth).

↓ HCl secretion.

↓ motility (antispasmodic action).

Urinary tract:

Relaxation (antispasmodic action)

Urine retention.

Neurological:a. Motion sickness. • Blocking (M1) in the vestibulocerebellar pathway → ↓

vertigo.• Blocking (M1) in the CTZ → ↓ vomiting (antiemetic).

b. Parkinsonism. To block (M1) in the basal ganglia → ↓ excitatory effect of

Ach.

Eye (eye drops):

to produce mydriasis in the following conditions:

a. Fundus examination.

b. To counteract the effect of miotics.

Cardiovascular:

a. Bradycardia and heart block.

Atropine ↑ HR and ↑ A-V conduction

b. Bradycardia due to excessive β-blockers.

Because β1 agonists are useless when β receptors are blocked. Atropine will ↑ HR via blocking the vagal inhibitory effect on the heart.

Respiratory:

Bronchial asthma: atropine is not preferred.

Non-selective → many systemic and CNS side effects.

Produces dryness of the bronchial secretions which become difficult to expell.

Gastrointestinal:

a. Abdominal colic and diarrhea.

Antispasmodic action.

↓ intestinal secretions.

b. Peptic ulcer.

Antispasmodic action.

↓ HCl secretion.

Urinary system:

a. Cystitis and renal colic.

Antispasmodic action → ↓ pain, urgency and frequency of micturition.

b. Nocturnal enuresis

Pre-anaesthetic medication:

Atropine is given ½ h before general anaesthesia.

a. To ↓ bronchial and salivary secretions and prevent bronchial obstruction.

b. To prevent bronchoconstriction due to excessive vagal tone.

c. To protect the heart from excessive vagal tone (bradycardia) occurred during general anesthesia.

d. To counteract the inhibitory effect of morphine on the RC.

1. May Precipitate acute attack in patients with glaucoma.

2. Dry mouth

3. Tachycardia

4. Constipation

5. urine retention (especially with senile enlarged prostate)

6. In children: atropine flush and fever.

(Toxicity dry as bone , blind as bat , red as beet and mad as a hatter)

1. Glaucoma

2. Constipation.

3. Old male patients with senile enlarged prostate.

4. Children for fear of atropine toxicity.