Datura - The Wonder Cure

Jimsonweed or Datura Stramonium

Chemicals

3ALPHA,6BETA-DITIGLOYLOXYTROPANE Plant:

4-HYDROXYLUBIMIN Plant:

ACETIC-ACID Plant:

ACETONE Leaf:

ACONITIC-ACID Plant:

ALKALOIDS Fruit 4,600 ppm; Leaf 2,500 - 5,100 ppm Plant 1,000 - 5,000 ppm Root 2,100 ppm; Seed 5,000 - 1,000 ppm Stem 2,500 - 2,600 ppm

ALPHA-KETO-GLUTARIC-ACID Plant:

APOATROPINE Plant:

ASCORBIC-ACID Plant:

ATROPAMINE Plant:

ATROPINE Plant 800 - 1,000 ppm

ATROPINESTERASE Plant:

BUTANOL Leaf:

CAFFEIC-ACID Plant:

CAPSIDOL Plant:

CHLOROGENIC-ACID Plant:

CITRIC-ACID Plant 750 ppm;

CUSCOHYGRINE Leaf:

DATUGEN Plant:

DATUGENIN Plant:

DITIGLOYL-D-DEHYDROXYTROPANE Plant:

EO Leaf 450 ppm;

ESCULETIN Plant:

ETHANOL Plant:

FAT Seed 150,000 - 300,000 ppm

FERULIC-ACID Plant:

FLURODATURATINE Plant:

FORMALDEHYDE Plant:

FORMIC-ACID Plant:

FUMARIC-ACID Plant:

GALACTOSE Leaf:

GLUCOSE Leaf:

GLYCOLIC-ACID Plant:

HOMOFLURODATURATINE Plant:

HYOSCINE Leaf 550 - 2,500 ppm Seed 1,200 - 5,000 ppm

HYOSCYAMINE Seed 80 - 490 ppm

ISOBUTYRALDEHYDE Plant:

LACTIC-ACID Plant:

LIGNOCERIC-ACID Plant:

LINOLEIC-ACID Seed 22,500 - 45,000 ppm

MALIC-ACID Plant 2,120 ppm;

METELOIDINE Leaf:

METHANOL Leaf:

NEO-CHLOROGENIC-ACID Plant:

NICOTINE Plant:

OLEIC-ACID Seed 93,000 - 186,000 ppm

PALMITIC-ACID Seed 15,000 - 30,000 ppm

POTASSIUM-NITRATE Plant:

PROPIONALDEHYDE Plant:

PROTEIN Seed 140,000 - 194,000 ppm

PUTRESCINE Plant:

RUTIN Plant:

SCOPIN Plant:

SCOPOLAMINE Seed 53 - 3,050 ppm

SCOPOLETIN Plant:

SCOPOLIN Plant:

SITOSTEROL Seed:

SOPHOROSE Leaf:

STEARIC-ACID Plant:

SUCCINIC-ACID Plant:

TANNIN Plant 70,000 ppm;

TIGLOYLMETELOIDIN Plant 5 - 25 ppm

UMBELLIFERONE Plant:

VITASTRAMONOLIDE Plant:

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Digoxin Sigma Pharmaceuticals Pty Ltd
MIMS Abbreviated Prescribing Information

Section: 2(g) Cardiac inotropic agents
Consumer Medicine Information: Available

Pregnancy Category: A

Sport Category: Permitted in sport

Uses/Indications: CHF, atrial fibrillation

Contraindications: Intermittent complete heart block; 2nd degree A-V block; ventricular tachycardia, fibrillation; arrhythmias induced by cardiac glycosides; supraventricular arrhythmias assoc. with accessory pathway; hypertrophic obstructive cardiomyopathy; hypersensitivity to other digitalis glycosides

Precautions: Carotid sinus hypersensitivity; acute glomerulonephritis with cardiac failure; Ca, K disturbance, hypoMg; thyroid disease; idiopathic hypertrophic subaortic stenosis; ischaemic heart disease, acute MI, myocarditis, myxoedema, severe pulmonary disease; hypoxia; sick sinus syndrome; rapid IV admin; malabsorption states; renal impairment; cardioversion; elderly, children, pregnancy

Adverse Reactions: GI upset; ECG effects: prolonged PR interval, depression of ST segment, false postive ST-T changes during exercise; arrhythmias incl sinus bradycardia (esp in intoxication in children); rash; gynaecomastia; visual disturbances; depression; others, see full PI

Drug Interactions: Complex, see full PI


Cardiac glycoside.

Pharmacology. Digoxin has a positive inotropic action on the heart, increasing the systolic force of contraction and so achieving more complete ventricular emptying. These effects are not easily seen in the normal heart because of homoeostatic adjustments in the circulatory system. In the failing heart, however, the increased contractile force results in an increase in cardiac output, a reduction in the end diastolic pressure of the ventricle, decrease in cardiac enlargement, reduction in venous pressure and improvement in renal function. Not only is the force of systole increased but its length is shortened, giving the heart more time to rest between contractions and more time for the ventricle to fill with venous blood. Owing to the increased cardiac output there is improvement in the peripheral circulation, with mobilisation of oedematous fluid, improved renal blood flow and resultant diuresis. The increased cardiac work is accomplished without a commensurate increase in oxygen consumption.

Digoxin increases the excitability of cardiac muscle, which results in the production of ectopic beats when excessive doses are administered. Conduction in the atrioventricular bundle is depressed, with increase in atrioventricular conduction time and lengthening of the PR interval on the ECG. Digoxin increases vagal tone in the heart resulting in slowing of the sinoatrial nodal rate and further depression of conduction in the atrioventricular bundle. This action may be abolished by atropine.

Pharmacokinetics. Absorption. Approximately 60 to 85% of an oral dose of digoxin from either tablet or elixir is usually absorbed. Absorption of digoxin is mainly from the small intestine, presumably by a passive, nonsaturable process. Delayed gastric emptying or the presence of food may slow the absorption rate but not the extent of absorption of orally administered digoxin. Gastric pH does not affect the degree of digoxin absorption. Intestinal absorption of the drug may be impaired in patients with certain malabsorption states, but absorption is not substantially changed by partial gastrectomy or jejunoileal bypass.

After oral administration in undigitalised patients onset of peak effect occurs in 0.5 to 2 hours and peak effect occurs in six to eight hours. After intravenous administration of a single dose of digoxin in previously undigitalised patients, the onset of action occurs in 5 to 30 minutes and peak effects occur in one to five hours. Pharmacological effect may persist three to four days after withdrawal of digoxin in digitalised patients.

If plasma concentrations of digoxin are to be determined, blood samples should be obtained at least six to eight hours after the daily dose and preferably just prior to the next scheduled daily dose. Therapeutic plasma concentrations of digoxin in adults are generally 0.5 to 2 nanogram/mL. In some patients with atrial fibrillation, slowing of ventricular rate may require steady-state plasma concentrations of 2 to 4 nanogram/mL. In adults toxicity is usually but not always associated with plasma concentrations greater than 2 nanogram/mL. Although neonates and infants appear to tolerate higher plasma concentrations of digoxin than do adults, evidence suggests that plasma concentrations greater than 2 nanogram/mL are associated with little, if any, additional therapeutic benefit in these patients.

Distribution. With therapeutic plasma concentrations, about 20 to 30% of digoxin in blood is bound to plasma proteins. Digoxin protein binding is not appreciably changed in uraemic patients. Patients with severe renal impairment have smaller apparent volumes of distribution of digoxin than do normal subjects.

Metabolism. In most patients, only small amounts of digoxin are metabolised, but the extent of metabolism is variable and may be substantial in some patients. Some metabolism presumably occurs in the liver, but digoxin is also apparently metabolised by bacteria within the lumen of the large intestine following oral administration and possibly after biliary elimination following parenteral administration.

Excretion. Digoxin has an elimination half-life of 34 to 44 hours. In patients with renal failure the elimination half-life is increased, for example in anephric patients the half-life is about 4.5 days or longer. Elimination half-life is prolonged in hypothyroid patients and decreased in hyperthyroid patients. In undigitalised patients, institution of a fixed daily dose of digoxin maintenance therapy without an initial loading dose results in steady-state plasma concentrations after four to five elimination half-lives (about seven days in patients with normal renal function).

Digoxin is excreted mainly in the urine, principally as unchanged drug, by glomerular filtration and active tubular secretion; tubular resorption may also occur. In most patients, small amounts of reduced metabolites are also excreted in urine. However, in some patients, about 40% or more of orally administered digoxin excreted in urine will consist of reduced metabolites. In healthy individuals, about 50 to 70% of an intravenous dose is excreted unchanged in urine. Small amounts of cardioactive metabolites and unchanged digoxin are also excreted in the bile and faeces.

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Digoxin immune Fab GlaxoSmithKline Australia Pty Ltd
MIMS Abbreviated Prescribing Information

Section: 20(a) Detoxifying agents, antidotes
Consumer Medicine Information: Available

Pregnancy Category: B2

Sport Category: Permitted in sport

Uses/Indications: Potentially life threatening digoxin intoxication

Precautions: Multiple drug overdose; monitor potassium; impaired cardiac, renal function; sheep protein allergy, prior treatment (perform skin test, see full PI); pregnancy, lactation, infants

Adverse Reactions: Sensitivity reactions; hyper/ hypokalaemia; exacerbation of CHF, AF (withdrawal of digitalis)

DIGIBIND INJECTION (Infusion) Prescription required. S4
Digoxin specific immune antigen binding fragments; sorbitol 75 mg, NaCl 28 mg; powder for reconstitution; vial;

Dose: Calculate dose according to serum digoxin conc or amount ingested; if unavailable admin 760 mg as 9.5 mg/mL IVI over 30 mins; see full PI
Pack: 38 mg (solv. needed) [1]

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DIGOXIN

Digoxin is obtained from leaves of the plant Digitalis lanata and is one of a family of cardiac glycosides all of whom share a steroid nucleus and an unsaturated lactone ring attached to the C-17 position (wherein the pharmacological activity resides), combined with one to four molecules of sugar attached to the C-3 position (Figure 1). The sugar modifies the lipid and water solubilities, and thus absorption, duration, and excretion properties of the drug.

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Patients presenting to the Colombo CCU with sinus bradycardia <40 bpm

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