PLANTS POISONINGx
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Transcript PLANTS POISONINGx
PLANT POISONING
Dr. Hisham Zein Alabdin
POISONOUS PLANTS
The active principles in most of these plants
are alkaloids but glycosides (digitales) and
resinous materials, as cannabis also exist.
The plant poisons have mainly remote action
after their absorption. The route of poisoning
is usually the oral one, so gastric lavage is
indicated . each plant poison has its specific
physiological antidote.
Atropine poisoning
Atropa belladonnas. Datura fastiosa, Datura
strammonium ( thorn apple),
Plant contains ; atropine, hyoscine and
hyoscayamine. All parts of the plant contain the
active substance.
Atropine has 2 actions:
1. central action causes stimulation of the CNS . In
large toxic doses it causes depression.
2. peripheral action anticholenergic: atropine
blocks nicotinic and muscarinic effects of
acetycholine.
Uses
A- Therapeutic:
o Pre- anesthetic.
o Antispasmodics.
o In the treatment of peptic ulcer.
o Ophthalmic use.
o Nocturnal enuresis
o Toxicological use: as antidote in phosphate esters,
digitalis, aconite poison.
B- Non therapeutic: by addicts.
Toxicokinetics
Absorption : slowly absorbed from the gut.
Metabolism: is in the liver and muscle to
tropine tropic acid.
Excretion: is via the kidney in the urine, partly
unchanged and partly metabolized.
Pathophysiology
A- Central action:
stimulation followed by depression of CNS.
Except hyoscine has depressant action only.
B- Peripheral action:
By blocking the muscarinic action of
acetylcholine at the post ganglionic nerves
whether parasympathetic or sympathetic
(sweat glands)
Clinical picture
1- Central effects:
A- Stimulation phase:
1-Delirium ,disorientation, confusion, loss of short
term memory, talkativeness(acute toxic
psychosis).
2-Ataxia, in-coordination, hallucination(Lilliputian
type)
3-Occupational purposeless movements (picking
or grasping)
4- Tremors and convulsions.
B- Depressant phase: it follows pre-existing
stimulation phase . Patient is calm and falls
into sleep then into stupor and coma. The
respiration becomes slow and irregular. The
end result will be central asphyxia and death.
II- Peripheral effects:
1- Vital signs:
o Increased respiration.
o Increased blood pressure.
o Increased temperature up to atropine fever
resulting from anhydrosis.
o Rapid pulse and may be cardiac arrhythmia.
2- Diminished secretion:
o saliva
dryness of the mouth with
dysarthria and dysphagia.
o Sweat
dry skin
o GIT
constipation (decreased secretion and
motility)
o Urinary
oliguria and retention of urine
3- Blood vessels: Peripheral vasodilatation to
increase heat loss , leading to atropine flush
which may be misdiagnosed as scarlet fever.
4-Eye changes:
o Dilation and fixed pupils
blurred vision.
o Loss of accommodation due to cycloplegia
(ciliary muscle paralysis)
o Diplopia and photophobia
o Loss of light reflex.
• The eye symptoms may be the earliest ones,
thus the anticholinergic syndrome of
parasympathetic paralysis can be remembered
Blind as a Bat.
Red as a Beet.
Dry as a Bone.
Hot as a Hare.
Mad as a Hen.
Treatment
Support respiration.
Control convulsion if present by diazepam.
Stop further absorption by inducing emesis or
by gastric lavage.
The physiological antidotes ( physostigmine,
pilocarpine.).
Treat hyperthermia by ice packs
IV fluids to maintain urine output
DIGITALIS (FOX GLOVE)
Uses:
As cardiac tonic for cases of congestive heart
failure.
As diuretic.
As an anti-arrhythmic especially in atrial
flutter and. fibrillation as well as in paroxysmal
tachycardia
Toxicokinetics
• Digitalis preparations are rapidly absorbed
from the GIT and injection sites . Metabolism
takes place in the liver . Excretion is via the
renal route mainly, a small part in the bile (
enterohepatic circulation).
Pathophysiology
Digitalis toxicity is an exacerbation of the drug
Pharmacological actions:
Positive inotropic action: it increases the
force and velocity of myocardial contraction
by increasing intracellular Ca++ . This increase
in the excitability and contractility of the atria
and ventricles may result in extrasystoles and
tachyarrhythmias.
Negative chronotropic action: (rate) It
increases the vagal tone in the early stage
leading to decreased heart rate.
Negative dromotropic action: (conduction
velocity) It slows AV node conduction velocity
that can be depressed resulting in Saor AV
block.
It increases the refractory periods of AV
node and depresses that of the atria and
ventricles, resulting in prolonged PR interval ,
AV block and shortened QT interval.
Alteration of impulse formation with
suppressant and excitatory effects.
Mechanism of action:
Digitalis inhibit active transport of Na+ ,K+
across cell membranes by binding to the Na+ K+ ATP ase , and inhibiting Na+ - K+ pumps .
The net result
Increase extracellular potassium
Increase intracellular sodium.
Increase intracellular calcium
Predisposing factors
Patient factor: (old age, myocardial infarction,
core pulmonale, renal failure.)
Electrolyte abnormalities: ( hypo and
hyperkalemia, hypomagnesemia, hyper and
hypocalcemia.)
Drug interaction: (diuretics, antibiotics,
quinidine , reserpine.)
Clinical picture
Asymptomatic period of several minutes to
several hours follows a single oral toxic dose. The
toxic effects include non cardiac and cardiac
effects
A- Non cardiac :
o GIT: may be the first complaints. (nausea,
vomiting, abduminal pain and diarrhea)
o CNS: headache, trigeminal neuralgia, confusion,
delirium, disorientation, drowsiness and
hallucination.
o Visual transient amblyopia, diplopia, blurring,
scotoma and abnormal colour vision including
yellow halos (xanthopsia).
o Endocrine : Gynecomastia.
o Allergic : Urticaria.
B- Cardiac:
Early slow full pulse (vagus) , with hypotension,
followed by any type of dysrhythmia (altration
in cardiac rate and rhythm):
o AV block.
o Atrial tachycardia with AV block.
o Sino-atrial block.
o Atrial flutter, fibrillation.
o Ventricular premature extrasystoles , flutter.
Digoxin toxicity
Acute
1- following acute
overdose
2- Usually young
3-normal heart
4-high digoxin level
5- K+ normal to high
6-AV conduction blocks
more common
7-Lessnon cardiac
manifestations
Chronic
Following long term
therapy
Usually elderly
Heart disease.
High digoxin or therapeutic
K+ normal to low
Various dysrhthmias
Non cardiac symptoms
prominent
MANAGEMENT
Investigations:
1-ECG:
o Prolonged PR interval
o Shortened QT interval
o ST segment depression, inverted T wave.
2- Laboratory :
o Electrolytes (K+ )
o Serum digoxin: toxic level is above 2ng/ml and
is above 25ng/ml for digitoxin.
Treatment
Stop drug administration.
monitor the patient in an ICU.
Establishment of respiration.
Dicontamination.
Atropine sulphate 1-2mg IM for bradycardia.
Phenytoin or diphenyl hydantoin is the drug of
choice for tachyarrhythmia.
Cholestyramine help excretion of digitalis
Determine electrolytes hourly and correct
electrolytes and acid base disturbances.
o For hypokalaemia: potassium chloride5g in
fruit juice every hour until ECG show
improvement or peaking of T wave.
o For hyperkalaemia : give 20 units of insulin
with 5% Dextrose.
o For hypocalcemia: avoid replacement
because intracellular calcium is very high.
Antidotal therapy: Digoxin specific antibody
(Digibind ).They bind to the free digoxin and
increase the renal excretion of digoxin bound
to FAB fragment.
Indications for (DIGIBIND )
Hyperkalaemia (k + > 5 mEq/L).
Bradyarrhythmias unresponsive to atropine.
High degree AV block.
Life threatenting ventricular tachycardia and
ventricular fibrillation.
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