General Toxicology
5
Corrosives
20
Pesticides
30
noxious gases and volatiles
40
Plant poisons
56
psychotropic drugs
74
Sedative Hypnotics
80
Contents
Substance dependance & abuse 88 Analgesics & antipyretics
96
Botulism
104
Animal Poisons
108
metallic irritant poisons
116
Miscellaneous & house hold
130
3
20
CASE
A 24 years old man complained of sore throat, dysphagia, epigastric pain & Vomiting that stopped later. He had delirium & convulsion then passed into coma. Catheterization showed dark urine that rapidly changed into green.
1- What is your provisional diagnosis? 2- Give the emergency & supportive measures for this case? 3- What are the possible mechanisms of death in this case?
Corrosives A
ny substance that if comes in contact with living tissues, will cause destruction by chemical action.
Acid Inorganic Sulfuric, Hydrochloric, Nitric acids. e.g.: toilet bowel cleaners & Drain cleaners.
Alkali Na-hydroxide (caustic soda): drain cleaners. Na. Carbonate: washing soda. Na-tri-polyphosphate: e.g. liquid automatic dishwasher detergents.
Organic “ACOT� Acetic Acid, Carbolic, Oxalic acid, Tartaric acids
KOH: caustic potash. Ca. carbonate: in cement. Ammonia: in industry, laboratories & refrigerators. Cosmetics: as hair relaxants.
Accidental Being widely used in industry and by children.
Circumstances of Poisoning Homicidal when thrown on face to cause disfigurement commonly by strong acids.
Suicidal rare but common in phenol.
21
Oxalic Acid Mechanism of Action Systemic It changes Ca 9 insoluble Ca–Oxalate that can’t be utilized by the body 9 fatal hypocalcemia Weak corrosion on stomach & skin. (blood decalcification) Dont forget ACIDS 9Co.agulative necrosis Local
Local Action (weak corrosion on the stomach and skin) - Acid sour taste in mouth with burning pain from mouth to stomach. - Severe V.: brown in colour with white crystals of the poison. - White patches on mouth Lip. - D. & tenesmus if the poison reaches the intestine. - Skin cracking, slow-healing ulcer. - Collapse: weak rapid pulse & hypotension. Remote Action: (fatal hypocalcemia and formation of calcium oxalate crystals) System Action Weakness, carpopedal spasm, twitchs & generalized convulsion. Lastly respiratory muscles are affected
Bradycardia, arrthymia & arrest.
Oligurea, haematuria, anuria & R.f.
Treatment (ABCDE+Antidote):
Enhancement of elimination:
Symptomatic TTT:
- Wash out Ca. oxalate crystals from renal tubules by alkaline I.V.fluids. - Haemodialysis in case of impairment of renal function.
1. Oxygen inhalation & artificial resp. in case of cyanosis (caused by spasm of respiratory muscles.) 2. Correct convulsion (relived by calcium replacement). Decontamination:
Physiological antidote: Calcium by every possible route (initial treatment): Calcium gluconate: - 10 ml slowly I.V. - with electrolyte and ECG monitoring.
- Gastro-intestinal: G.L. by Ca(OH)2 or milk. Milk is oral antidote because it is rich in calcium Calcium hydroxide: and demulcent & buffer. Orally or via gastric tube “precipitate oxalic - Skin & eye: as in general toxicology, ophthalmologist & dermatologist consultation is acid in stomach as calcium-oxalate” advisable. 26
SYSTEMIC ACTION CNS & Muscles (weakness, carrpopedal spasm, twitchs, genaralized convulsions & lastly respiratory muscles are affected)
Heart (bradycardiad, arrhythmia & cardiac arrest)
Kidney (oligurea, haematuria,anuria & Renal failure)
C/P Of oxalic acid LOCAL ACTION
White patches on mouth lip Acid sour taste
Burning sensation
Collapse (weak rapid pulse & Hypotension)
Severe Vomiting (brown with white crystals)
Diarrhea, Tenesmus
27
Postmortem Picture I- Sulphoric acid Causes of death: 1- Death Within 12 hours,Will result From Shock due to Local burning Pain Of acid. 2- Death From1-2 days , may result from : - Dehydration from Vomiting. - Peritonities due to perforation of the stomach. 3- Death Within 2-3 weeks may be due to exhaustion and general weakness. 4- Death after few years may result from stricture of the esophagus or stomach.
III- Alkali Corrosive: 1- Lips, mouth and throat are corroded, stained with greyish colour and are soapy in appearance and touch. 2- The caustic effects are observed about the corners of the mouth & running down to the chin. 3- The gastric mucosa is swollen, hyperaemic and shows areas of corrosion Its colour is greyish and the contents of the stomach are coffee coloured (alkaline haematin ). 4- Perforation of the stomach isnot common . 5- The small intestine may show congestion. 6- In case of ammonia poisoning,in addition to the P.M.P of the alkaline corrosives. The followings may be present : -Characteristic odour of ammonia is smelled in the tissuses. -Perforation of the stomach may occur . -Inhalation of the ammonia fumes may lead to an inflamed swollen glottis. -Inflamamtion of themucous membranes of the respiratory passage with evidence of bronochopneumonia and pulmonary oedema.
IV- Carbolic acid 1- External and internal signs of asphyxia. Postmortem Picture: 2- Smell of phenol may be detected at the 1- The lips, the adjacent cheeks, chin and neck all are corroded with streaks of dark eschars as a mouth. 3- Greyish –white stains may be present at the result of dribbling of the acid and saliva. 2- The clothes may show stains of dark brownish angles of the mouth and on the chin. 4- Oesophageal and gastric mucosa are greyishcolour or they may be destroyed in spots . 3- The corrosions may extend through the mouth white or brown. It appears swollen and its and throat to the oesohagus and its mucosa may mucous folds are prominent with superficial erosions. be stripped off. 5- The kidneys are slightly swollen and show 4- The stomach is usually severely affected the whole mucous membrane may be corroded and haemorrhagic spots. The urinary bladder contains little amount of urine, which become stained black ,with streaks of altered blood. dark in colour after exposure to air. 5- The stomach may be perforated with escape of the gastric contents into the peritoneal cavity. V- Oxalic Acid 6- Evidence of chemical peritonitis may be 1- The mucous membrane of the mouth, throat, present. oesopahgus and stomach is whitish and covered with brown mucous. Erosions are superficial. II- Nitric Acid: 2- The stomach shows cloudy areas of Ca oxalate 1- The same as in sulphuric acid except of the crystals. deeply stained yellow orange colour of the 3- Kidneys are congested with whitish zones in affected tissues. the renal cortex(Ca oxalate Precipitation). 2- Perforation of the stomach isnot common. 4- Dilated heart. 3- Inflammation of the larynx, bronchitis and 5- Cyanosis in as phyxial deaths. pulmonary oedema may be present. 28
CASE
A 35-year-old man with a past psychiatric history was brought to the emergency department after claiming to have ingested an unidentified pesticide.Â? His vital signs were: blood pressure 120/70 mm Hg; pulse 45 beats/min; respiratory rate 28 breaths/min; and temperature 36.6ËšC). The patient was lethargic, sweating, incontinent of urine and stool, and had no evidence of trauma. The patient
had prominent fasciculations of his face and extremities, 3-mm pupils, and profuse oropharyngeal secretions requiring frequent suctioning. His pulmonary examination revealed scattered rhonchi, and his abdomen had hyperactive bowel sounds. His neurologic examination was significant for symmetric decrease in muscle strength, but he was fully oriented.
Pesticides Insecticides
- Insecticides: Compounds kill insects e.g. organophosphates, organochlorine, carbamates. - Rodenticides: Compounds kill rats, mice, rodents e.g. anticoagulants, thallium. - Herbicides: Compounds kill weeds e.g. paraquat, diquat. - Fungicides: Compounds kill fungi and molds e.g. dithiocarbamates, Captan. - Fumigants: Gases sterilize products e.g. ethylene dibromides, methyl bromide.
Rodenticides
Herbicides
Classification of insecticides Synthetic
Natural
Fungicides
Botanic Insecticides e.g Pyrethrins
Fumigants Synthetic Organic e.g Organophosphates, Carbamates & DDT
Synthetic Inorganic e.g Arsenic,Mercury
31
A
1- CO diplaces O2 from its receptors because the affinity of the receptors to bind with CO is 250 times more than O2.
After binding with CO at any site on Hb; Co prevents Hb from releasing the O2 carried at other sites.
2- Decrease O2 release from Hb leading to Tissue Anoxia “shift of O2 dissociation curve to the left
“Hb inside RBC inside Blood Vessels”
B- Block enzyme & interfere with cell respiration
“Mitochondrion inside cells”
C- Binding with Mb leads to muscle fatigue & impair Myocardial Contractility “Mb inside Muscles”
D- Direct toxic effect on Myocardium
“Heart” 42
CASE
A 72-year-old woman was brought to the hospital by her grandson. The grandson stated that she had lost her appetite for several days, refused her medications for 2 days, and had begun to vomit on the day of admission. The woman complained of being weak and having no appetite because of her constant nausea. Her past medical history was significant
for congestive heart failure and hypertension, for which she was chronically treated. the patient was not in acute distress, and was alert and oriented. Her vital signs were: blood pressure, 140/95 mm Hg; pulse, 50 beats/min respiratory rate, 16 breaths/min; and rectal temperature 37.1°C. Examination of the patient’s lower extremities revealed pitting edema.
PlantPoisons opium poppy
Marijuana
P
oisons from Plant source either addicted or drugs .
All plant poison early clinical picture are the same (GIT manifestations Then chracteristic C/P)
Erythroxylon Coca
PLANT POISONs
Opiates Cannabis Cocaine
Atropa belladonna
Atropine Digitalis Ergot
Digitalis purpurea
57
i- Opiates Toxicokinitics: Absorbtion: All routes Metabolism: Rapidly Hepatic Excretion: Mainly in urine & re-excreted also in stomach & bile
Action
Action
Dynamics Opioids share the ability to +++ specific opiate Rec. (Ο-K- Δ) present mainly in CNS +++ 3rd. Carnial N. Neuclus
P.P.P.
+++ Vagal Centres
,,, H.R.
+++ Vomting Centre
vomiting
--V.M.C
--Resp.Centres
,,, Bl.P.
1-Arrest 2-Chyne stocke Breath 3- Hypoxia 4-Non Cardiogenic pulmonary edema (D.t. Hypoxia)
--Seneory cortex
Coma Lethargy, somnolence
Clinical Picture System
Effect Coma Convulsion: with Mepridine - Propoxphene nBl.P.: (--VMC) nH.R.: (++ V.C.)
Serial ECG
PPP Dilatation: if there is (Hypoxia 9 Acidosis) nR.C.9Arrest Non.cardio.pulmonary edema Chyne stock breathing Constipation + ilieus ( nHCL-nMotility-nBile;Tone)
Chest X-Ray (Pul.Edema)
Urine Retention
Qualitative screening of the urine
Convulsion 9Rhabdomyolysis 9Renal failure)
C.P.K.
Traid of clinical diagnosis: 1- Pin Point Pupil (PPP) 2- CNS Depression 3- Respiratory Center Depression 58
Investigations Exclude other causes of Coma By 1-C.T. 2-CSF Culture
Convulsion 9 Rhabdomyolysis 9R.F.) nBl.P.: (--VMC) nH.R.: (++ V.C.)
P.P.P
Central --- or Respiration
Constipition + ilieus ( nHCL-nMotility-nBile;Tone)
Urine Retintion
59
Opiates
Mechanism
- ; 3rd Carnial N. Neuclus - ;Vagal Centres - ;Vomting Centre - nV.M.C. - nResp.Centres - nSensory cortex
Coma Convulsion: with Mepridine - Propoxphene
Urine Retention
nBl.P.: (--VMC) nH.R.: (++ V.C.)
PPP Dilatation: if there is (Hypoxia 9 Acidosis) nR.C.9Arrest Non.cardio.pulmonary edema, Cyanosis Chyne stock breathing Constipation + ilieus ( nHCL-nMotility-nBile;Tone)
CCC
66
Cannabis
Cocaine - ; CNS blocks the pre-synaptic reuptake of N.A. & dopamine 9overstimulation of sympathomimetic - Bind with anadamide R. of (B.G.-C.C.) 9;Cerebral system. Bl.flow - Sodium channels blocker - ;Symp. at: nPara symp9;H.R. - CVS: nconduction & contractility. - Nerve membrane 9local anesthetic effect. Euphoria - Hyperactivity Euphoria Restlessness then Tremors, Dream like state Hyperreflexia, Pleasant relaxation Convulsions then Coma Alteration of time and characterized by: space perception Hyporeflexia, Respiratory &/or CVS inhibition Shock - Renal A. spasm No Effect Rhabdomyolysis with myoglobinuria 9R.F. May occur rapidly after smoking or I.V. injection & mediated by sympathetic Bl.P.: unpredictable but overactivity. They include: orthostatic hypotension is 1- Fatal ventricular tachycommon cardia or fibrillation. ;H.R 2- SevereHTN: 3- Myocardial infarction 4- Shock Redness of eye
Mydriasis
pharyngitis Rhinitis Bronchitis
pulmonary infarction
Distress
N. – V. – D.- Abd.cramps
Convulsion 9Rhabdomyolysis 9R.F.)
Rhabdomyolysis Diffuse myalgias.
Convulsion 9Rhabdomyolysis 9R.F.)
PPP Constipition Vomiting
Pharyngitis Hoarseness Fever Euphoria Dream like state
- Nasal septal perforation - sympathetic overactivity - Hyperthermia (cocaine fever) It is one of the major causes of death.
CASE
A 63 year old hypertensive and diabetic man, with suicidal tendencies, in a mood of depression he swallowed tablets of a prescription medication. There was no history of convulsions, vomiting, urinary incontinence or tongue bite. At the time of admission, the patient (On examination) was in an unconscious state with no response to deep painful stimu-
li, a-reflexic and cyanotic, temperature 36ºC; Blood pressure 80/60; pulse 90; respiratory rate 16; Pupils were constricted and minimally reactive to light, corneal reflex absent. Neither naloxone nor flumazenil were effective in relieving the coma. Breath sounds, cardiac exam, and abdominal exam (except diminished peristalsis) were all within normal limits.
Sedative-Hypnotics Classification
Benzodiazepines
Carbamazepine
Barabiturates
Carbatrol® Epitol® Equetrol® Tegretol® Slow
(e.g. Oxazepam)
Intermediate-acting (e.g. Lorazepam)
Rapid
Short acting
Long-acting
(e.g. Diazepam)
(e.g. sentobarbitone)
(e.g. phenobarbitone)
Ultra-slow
Intermediate-acting
Ultrashort-acting
(e.g. Diazepam)
(e.g. amobarbitone)
(e.g. thiopentone).
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82
CASE
15 year old male presented in a suicide attempt with agitation, dystonia, constricted pupils, tachycardia, hypotension and a GCS fluctuating between 6 to 11. ECG showed sinus tachycardia, ST depression and prolonged QTc interval.
1- What is your provisional diagnosis? 2- DD of pupillary constriction? 3- How to treat this case?
Psychotropic Drugs T
hey are group of drugs that exerts their effect on the higher function of CNS. They change the mood, thinking, behavior and emotions.
Classification
Psychodysleptics
Psychotherapeutics
(Hallucinogens) Cannabis
ttt of Psychosis: neuroleptics, antipsychotics
Psychostimulants Increase level of motivation
ttt of anxiety: anxiolytics, Benzodiazepins
ttt of Mood disorders: Antidepressants, Mood stabilizers
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i-Antipsychotics USES Antipsychotics have been used to treat : 1-schizophrenia: and other types of psychosis. 2-sedatives, preanesthetics 3-treatment of drug induce hallucinations, vomiting and tension headache. Classification Pharmacokinetics and Toxicokinetics: Typical - e.g: Chloropmazine - Block D2 receptors mainly - Treat +ve symptoms of schizophrenia: Hallucination, dellusions, paranoia, disorganization of thought - More extrapyramidal syndrome(EPS) Atypical - e.g:Benzipines, Benzamides - Block 5HT2A receptors mainly -Treat -ve symptoms of schizophrenia: Social withdrawal, flattening of affect - Less extrapyramidal syndrome Absorption: - lipophylic & generally well absorbed - Anticholinergic effects may delay absorption 9Delayed gastric lavage can be done up to 6 hours. Distribution: Highly bound to plasma protein with large volume of distribution 9Enhancement of elimination has no role. Metabolism: Hepatic cytochrome p450 Elimination: Metabolites are excreted in urine and stool after conjugation and enterohepatic circulation respectively 9Multible doses of activated charcoal can be given(GIT dialysis). Mechanism of action: - Block receptors - Block Na channels: Quinidine like action on heart - Interfere with reuptake of neurotransmitter Receptor block: 1- Dopamine (D2) receptor block at the following sites: 84
-Mesolimibic and mesocortical 9ttt of psychosis. - Basal ganglia 9EPS. - Heat regulating center in hypothalamus 9hyperthermia. - Pitutary gland - Chemoreceptor trigger zone (CTZ) 9Decreased vomiting. 2- serotonin: 5-HT2A receptor 3- Muscarinic receptors block 9anticholinergic syndrome 4- H1 histamine receptors block 9atropine like action 5- Alpha adrenergic receptors block 9Vasodilatation & hypotension(take the upper hand) 6- GABA receptors (inhibitory) 9Convulsions & seizures Clinical picture 4 possible toxic scenarios I- Dopamine blocking effect, extra pyramidal syndrome 1)Dystonia: sustained involuntary muscle contraction including -Eye lid: Blepharospasm -Oculogyric crisis: Upward gaze -Torticolis & tortipelvis 2)Dyskinesia: parkinsonism, rigidity, tremors, shuffling gate, mask face. 3)Akathesia: sensation of restlessness(unable to sit still). II- Anticholinergic effects III- Cardiac toxicity -Hypotension more than hypertension -Tachycardia more than bradycardia. -Ventricular tachy arrhythmia. -Wide QRS complex, prolonged PR interval. IV- CNS toxicity, sedation, seizures Others -Mydriasis or myosis. -Hyperthermia or hypothermia. -Impaired air way reflexes. Cause of hypotension:
-Direct myocardial depression -Alpha blocking effect lead to vasodilatation 9Give I.V fluids
Investigation:
Treatment: ABCDE + no specific antidote
- ECG includes widening of the QRS complex, prolongation of the QT interval. - Abdominal radiography may reveal densities in the GIT. - ECG is the most probably accurate predictor of toxicity for neuroleptics poisoning.
Treatment from clinical picture as follow: 1-Seizures 9Diazepam 2-Arrhythmia 9Na bicarbonate, Mg infusion 3-Hypotension 9I.V fluids, vasoconstrictors e.g: Alpha agonists(Norepinephrine & phenyl ephrine). - Drugs with Beta 2 activity e.g (epinephrine, isoprotenerol) may worsen hypotension. 4-Dystonic reactions 9Anticholinergic(diphenh ydramine or benztropine) , Benzodiazepines. 5-Parkinsonism 9anticholinergics, dopamine agonists as bromocriptine or amantadine.
Q- Differentiate between neuroleptic malignant syndrome & serotonin syndrome Neuroleptic malignant syndrome Serstonin syndrome Causes 1- Abrupt withdrawal of dopamine agonist (Bro;Synaptic serotonin in the brain & spinal cord mocryptine). by different mechanisms e.g: 2- Increase dosing of neuroleptics. SSRI, TCA, MAOI 3- Cessation of anticholinergic medication. Charachterized by: Triad ofANA: 1- Altered mental state. HAFTER: 2- Neuromuscular abnormalities: tremors, rigidiHyperpyrexia, Autonomic instsbility, Fluctuation ty, myoclonus. of level of consciousness, Tremors & Rigidity. 3- Autonomic effects: nausea, vomiting, tachycardia, fever. Treatment - Stop the drug. Give dopamine agonist, Benzodiazepines &/or -Symptomatic ttt. Dantrolene (muscle relaxant). -Seretonin receptor antagonist: Methysergid.
Pitfalls
- Atypical antipsychotic are extremely safe. - Most common symptom of overdose includes mental state changes, coma, tachycardia and hypotension. - Supportive care is enough.
85
Mechanism of action & clinical picture of acute salicylate toxicity “CHARG” CVS CNS - Stimulation followed by depression of the - Hypotension due to nof VMC cerebral cortex. C - C/P: Hypotension & tachycardia. - C/P: Excitation, convulsions, hyperreflexia then coma & death. Hyperthermia Hematologic effects due to increased basal metabolic rate and - Salicylate decreases plasma prothrombine un-coupling of oxidative phosphorylation. by: C/P: sweating & dehydration 1- Interfering with vitamine K utilization in the liver. H 2- Asprin is transformed into dichomarol that competes with vitamine K. 3- Interference with platelet function. - C/P: Hypoprothrombinemia 9bleeding: - Petechial&subconjunctival hemorrhage - Ecchymosis of the eye lids Acidosis Allergic reaction - Skin rashes - Metabolic acidosis occurs due to: - Hypersensitivity reactions 1- Depletion of energy storage leads to in- Bronchospasm creased lactic & pyruvic acids. - Angioneurotic edema & anaphylactic 2- Stimulation of lipid metabolism leads to shock. increased ketone bodies. A 3- Inhibition of kreb’s cycle enzymes leads to increased organic acids. 4- Inhibition of amino acids’ metabolism leads to increased amino acids. - C/P: Hyperacidity: Peptic ulcer & hematemesis RBCs Respiration Destroyed in G6PD deficiency (favism). - Respiratory stimulation by: 1- Direct action on respiratory center and/or 2- Indirect action by: increasing basal metabolic rate with co2 accumulation and hyperventilation. R - C/P: 1- Hyperventilation(hyperpnea) 9Acidosis 2- Pulmonary edema (cyanosis, tachycardia & hypoxia which lead to vasodilatation & edema). 3- Respiratory failure may occur Glucose GIT - Local: Irritation & may be painless ulcer. - Small dose: Hypoglycemia - Central: Chemoreceptor trigger zone G leads to vomiting. - Large dose: Hyperglycemia - C/P: Nausea, vomiting, & burning pain in mouth, throat & abdomen. 98
CASE
2 sisters came to emergency hospital giving a history of sharing canned food at dinner (fool). They complained of dry mouth, nausea, vomiting, dysphagia, dysarthria, blurred vision & ptosis. The pupils wrere dilated & fixed. Within 2 hours in the ED descending muscle weakness was noticed with difficulty in breathing. They were put on ventilator.
1- What is the mechanism of toxicity in this case? 2- Do you think that the 2 sisters wouldn’t develop this toxicity if they boil the food before eating? 3- Mention differential diagnosis of the case & how to treat?
Botulism There are 4 clinical pictures of botulism: - Food borne botulism 925% - Infant botulism 970% - Wound botulism 91-2% - Adult intestinal 9 1-2% I- Food borne botulism: - A paralytic disease caused by a neurotoxin produced from the germination of clostridium botulinum spores. - The toxin is a heat-labile neurotoxin and can be destroyed by heating to 100 C for 10 min. - Rare outbreaks are usually associated with improper canning, processing, or storage of food, allowing spores to remain, germinate and form toxin. - Spores germinate in an anaerobic environment with a pH greater than 4.6.
Mechanism of toxicity: Neuorotoxin binds irreversibly to cholinergic nerve terminals. n Prevent acetyle choline release into synapse lead to muscle paralysis. n Affection of respiratory muscles may end in death from respiratory failure. - The neurotoxin does not cross blood brain barrier. - Botulinum toxin is extremely potent,as little as one taste of toxin-contaminated food may be fatal.
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108
CASE
A 43-year-old professional snake trainer was demonstrating how to handle a snake at a show, suddenly he suffered a bite to his right thumb, he immediately stop the show & drove himself to the nearest hospital within 15 minutes. At this time he complained of severe pain, nausea, he was pale , sweating & his thumb was noted to be swollen. Vital signs on admission revealed: elevated pulse rate, respiration, blood pressure. His CBC was
within normal limits except for prothrombin time after 2 hours was 15.1 sec. & INR 1.56 after 90 minutes. He complained of bilateral ptosis, dysphagia, generalized flaccidity & confusion, 2 hours after the bite, the patient was endotracheally intubated & placed on mechanical ventilation. 1- What is the probable identity of the snake bite him? 2- What are the lines of treatment in this case?
Animal Poisons According to its poisonus effect,animals are classified into two main categories: 1- Reptiles “e.g:snakes” 2- Arthrpodes “e.g: scorpions,spiders & bees”
1- SNAKES Charachterized by: 1- Ability to swallow its prey fast as there is no mandibular joint. 2- Ability to pull food into throat without chewing as their teeth are curved backwards 3- Periodic sheeding and replacemant of their (teeth,fangs and skin) 4- They have fixed or movable short front fangs connected to the venom gland which lies superficially behind the eye 5- Difficulty in seeing due to their poor eye sight, but they have great sense to moving objects as their hearing is responsive to ground viberation
Morphology of a Venomous Snake
N.B: Not all snakes are venomous, so what are the differences between venomous and non venomous snakes ?
non-Venomous snakes Eyes: Rounded No front fangs Bite: 2 rows of tiny shallow wounds (1-2mm deep).
Venomous snakes Eyes: Slit like It has one or 2 front fangs Bite: one or two fang punctures connected by a row of very small punctures. 109
N.B: the common venomous snakes in Egypt are - Cobra (Family Elapidae) - Cerastes Cerastes (Family Viperidae)
Cerastes Cerastes (Family Viperidae)
Cobra (Family Elapidae)
Factors affecting severity of snake bite: Snake
1- Amount of venom,which depends on the length of time that the snake last Eaten..longer period allows high amount of venom to be injected & vice versa 2- The way the snake bites its victim will affect its ability to inject venom Eg.coral snakes must grasp its victim before penetrating the skin so large amount of venom will be injected. 3- Number of fangs
Victim 1- General health, weight &age..so the extremes of age are more likely to develop toxicity. 2- Site of bite determines: - The effect of tissue swelling - Time needed to reach vital organs, bites around head and neck > swelling > constriction of air passages and dangerous suffocation. 3- Type of tissue bitten , injection in fatty tissue will reduce the toxic effect of venom d.t decreased bl supply. 4- Physical activity following bite increase blood supplyTo the wound and so increase circulation of venom. 5- Time passed between bite and ttt 9;toxicity
How does snake venom components suit its action ? venom is a mixture of ptns Phospholipase Victim Proteolytic Enzymes Nerve Toxin Protease & Transaminase 1-Intravascular haemolysis of RBCs due to direct action 1- Digestion of tissue ptns on its membrane 2- Alteration of neuromuscular conduction 2- Hyaluronidase enzymes of snake venom: hydrolyzes the gel between cell spaces & fibers 3- Facilitates the penetration of other neuro-pharmacologically active venom components thus reducing the viscosity of tissues into nerve tissue 110
Mechanism Part affected
Effect
Investigation Finding
Mechanism
2- Remote Action I- Hematologic effect Bind to SH group contaning enzymes & proteins B.M RBCs - nGlutathion nHeme synthesis - nRBCs survival Microcytic hypochromic anaemia ;Heme Precursors BM compensation CBC, Urine analysis Free Erythrocyte Pro- Corporphorin III Reteculocytosis toPorphyrin - Urinary ALA II- Soft Tissue Lead’s toxicity is largely due to its capacity to mimic Calcium and substitute it in many of the fundamental cellular processes that depend on calcium.
Organ affected
Effect Brain Disruption of BBB 9Brain edema Mild Severe Encephalopathy - Headache (delirium ,ataxia, - Irritability Convulsions, - Lethargy Coma) more common in children Treatment: Hypertonic solutions as mannitol to reduce cerebral edema
Prepheral nerves wrist & foot drop (lead palsy)
Treatment: Splint
Chronic nephritis (Oligurea, Hematurea, Albuminurea) Reproductive Smooth muscle Contraction Visual
CVS
- Female: fetal abortion & menstrual - Face pallor (circum oral pallor) also disorder due to - Male: impotence disorder - Anemia - Male & female: sterility - Vasospasm of arterioles & capillaries Lead deposition around optic disk 9optic neuritis 9Optic atrophy & diminution of vision
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Mercury (Hg) Poisoning Types
Elemental Mercury
Inorganic Mercury
Sources
In glass thermometers, sphygmomanometers, dental amalgam.
- Mercuric chloride: in disinfectants, diuretics. - Mercurous chloride: in teething powder & laxative (calomel).
Mechanism of toxicity & action:
- By ingestion: It is non toxic (poor absorption). - By inhalation: it passes through alveoli to blood stream 9accumulate in brain. It is oxidized in RBCs & brain to inorganic mercury 9binds with SH group of enzymes & proteins 9degenerative changes.
- Toxicity mainly via GIT (or skin) 9irritation. - It affects the kidney 9 acute renal failure & nephrotic syndrome.
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Organic Mercury - Methyl & ethyl mercury incorporated in the aquatic food chain as in Minamata disease. - Mercurous fulminate is an explosive compound.
- It crosses blood brain barrier & placental barrier 9 degenerative changes in CNS & teratogenic disorders.
C/P of elemental Mercury
Acute
Chronic
Inhalation
CNS
- Bronchitis & pneumonitis “Fever, Dyspnea� , non cardiogenic pulmonary edema - Pulmonary fibrosis may occur 9respiratory failur
Intention tremors - In muscles That perform fine motor functions 9Hand writing suffers Severely - Used as gualtative measure of ttt - Then progress to generalized tremors
Erethism - Irritability, Anxiety - Emotional liability - Depression - Shyness - Memory loss
Mouth: - Gingivitis& salivation - Gray line in gum
Eye: - Mercurialentis: brownish discoloration of the lens due to mercury deposition
Kidney: Renal impairment
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