ibnkhaldonmed-toxicology.pdf

Ibnkhaldon Med | Toxicology Essay Questions with Answers 1

Toxicology Essay & Cases Questions

(General – Corrosives – Hydrocarbons – Insecticides)


General

1- Mention 2 differences between sympathomimetic & anticholinergic toxidromes. (October 2013)

Anticholinergic Sympathomimetic

Clinical pictures

Skin

Bowel sound

Urine retention

pupil

- dry - inhibited - present - dilated irreactive

- diaphoresis - hyperactive - absent - dilated irreactive

Causes Atropine , TCA , botulism Cocaine , amphetamines

2- Give reasons Salt and water should not be used as emetic. (May 2010)

As it may lead to fatal hypernatriemia that lead to severe cellular dehydration leading to convulsions leading to irreversible coma then death

3- Give full account on:

a- Complications of gastric lavage. (Sept 2004)

- Mech. injury to the gut. - Laryngospasm, cyanosis. - Aspiration pneumonia. - Bradycardia during introduction of the tube esp. with OP insecticides and digoxin

poisoning - Stress reaction, HTN, tachycardia because of CA secretion - Dilutional hyponatremia if performed with Tap water Especially children in whom

normal saline is preferable - Faulty passage of the gastric lavage tube in the trachea

b- Doses, contraindications and complications of activated charcoal. (May 2002-2005-2007)

Dose: 1 gm/kg ( if the amount of poison is not known )

5-10 times the weight of the ingested poison. ( if the amount is known) Contraindication:

1. Corrosives: - low absorptive power - Interfere with endoscopy. - Mask bleeding, melena. - Worse mediastinitis, peritonitis in case of perforation

2. Hydrocarbons:


- may cause vomiting →high risk of aspiration. 3. Intestinal obstruction, ileus or perforation.

4. Can't adsorb some poisons as:

Most metals: Fe.

Methanol, ethanol: usually mixed toxicity.

Cyanide: Death within 10 minutes. Complication:

1. Constipation, GIT obstruction in repeated doses. 2. It may adsorb oral medication making it not effective as : Syrup of Ipecac Oral antidotes as N-acetyl cysteine ( antidote of paracetamol poisoning )

4- Differentiate between Complications of peritoneal dialysis and hemodialysis in clinical toxicology.

(June 2012)

Hemodialysis Peritoneal dialysis

Complications

1- Hypotension 2- Elimination of therapeutically

administered drugs 3- Bleeding tendency due to

heparin 4- Air embolism 5- Electrolyte imbalance 6- Infection : HIV , hepatitis B or C

1- Infection leading to peritonitis 2- Injury to internal organs leading to

internal hemorrhage 3- Fluid overload or dehydration 4- Less effective

5- Explain a certain cocktail is used in cases of undiagnosed coma. (Sept 2014)

a- Naloxone 2 mg: pure opiate antagonist without any agonist activity “no CNS dep”. b- IV glucose ( dextrose 25 % 2-4 ml/kg ) for hypoglycemia to protect the brain c- Vit B1”Thiamine” 100 mg IM to prevent Wernick’s encephalopathy

6- Give reason: Flumazenil should not be administered routinely in comatose patients. (Sept 2012-2013)

- Reversal of benzodiazepine effect may result in seizures or arrhythmias with fatal outcomes if the patient ingested mixed drugs involving cyclic antidepressants.

7- Comatose patient requires change of position. (May 2010)

- To avoid bed sores on bony prominences and recumbent pneumonia 2ry to non drained lung lobes.

8- Explain: Mechanical ventilation can be used in some cases of respiratory failure


(June 2014)

- if PaO2 cannot be maintained above 60 mmHg or if there is progressive hypercapnea ( PCO2 is rising )

- If altered conscious level, interfere with normal resp. - Resp. ms paralysis or exhaustion.

9- Compare by giving three differences between Cardiogenic and non-cardiogenic pulmonary edema.

(May 2010)

Cardiogenic pulmonary edema Non-cardiogenic pulmonary edema

Result from left ventricular dysfunction Result from disruption of alveolar capillary membrane

Triggering Causes :

acute ischemia , myocarditis , rhythm or conduction abnormalities , high blood pressure

destruction of pneumocytes II lining alveoli that are responsible for surfactant synthesis

Toxic causes : Ca channel blockers , beta blockers ,

TCA , Scorpion myocarditis

Corrosive fumes , heroin , barbiturates , OPC ,

Salicylates

10- Give reasons: Hydration and alkalanization are recommended in treatment of rhabdomyolysis.

(June 2012)

- Hydration to treat hypovolemia that caused by sequestering of water within injured myocytes as also to avoid the enhancing effect of dehydration on rhabdomyolysis

- Alkalanization of urine to prevent renal insult and direct nephrotoxicity due to precipitation of myoglobin in renal tubules.

11- Give an account on Toxic rhabdomyolysis and its management. (Sept 2007)

- Def : it is the result of skeletal muscle injury which occurs due to excess energy and inadequate O2 SUPPLY to skeletal muscle resulting in myocytes break down and release of cellular toxic contents into plasma e.g. myoglobin , LDH , CPK , AST , uric acid , K+ , phosphates

- Factors enhancing rhabdomyolysis :

Seizures

Malignant hyperthermia

Extensive muscle VC ( cocaine )

Soft tissue compression with prolonged muscle ischemia as in coma

Dehydration - Clinical sequelae :

hypovolemia

hyperkalemia


hyperuricemia

metabolic acidosis

acute renal failure in 25% due to deposition of myoglobin in renal tubules leading to its obstruction

- toxic causes :

drugs ↑ muscular activity e.g. Salicylates , neuroleptics , caffeine , theophyline , TCA

abuse : alcohol , heroin , LSD , cocaine

drugs causing hypoxia : CO , toluene

direct toxic effect on muscle : black widow spider , massive bee envenomation - management :

good hydration

urinary alkalanization to prevent renal insult and direct nephrotoxicity due to precipitation of myoglobin in renal tubules

control of hyperkalemia by NaHCO3 , insulin/glucose , Ca+2 )

diuretics after good hydration


Corrosives

1- Give reasons: Endoscopy is recommended for all patients of corrosive intake. (Sept 2012-2014)

- It reveals different grades of severity :

Grade l : erythema

Grade ll :destruction of mucosa

Grade lll : destruction of all layers of the gut beyond the mucosa.

2- Give reasons: Giving steroids in corrosives ingestion. (May 2010)

- To prevent fibrosis.

3- Give an account on Clinical picture of concentrated potassium hydroxide ingestion. (June 2009)

KOH is alkali so lesions are usually located in the esophagus Clinical picture: severe irritation with: 1) Pain: is the main presenting s/o

- Severe burning pain : oropharyngeal , epigastric , retrosternal 2) Dysphagia 3) Oropharyngeal burns : light grayish to black ulcers in addition to edema of the tongue , lips ,gums, pharynx & epiglottis 4) Vomiting:

- Severe, repeated - May contain bl, shreds of mucosa

5) Sialorrhea d.t ↑Salivary sec due ti inflammation 6) Diarrhea 7) Hoarseness of voice if edema and burn extend to larynx 8) Stridor if edema if edema of vocal cords 9) Melena and hematemesis

4- Give a full account on

a- Complications of corrosive ingestion. (May 2002)

1. Acute :

Upper respiratory tract obstruction d.t laryngeal edema and severe stridor

Shock: hemorrhagic , neurogenic or hypovolemic "2ry to impaired feeding and vomiting"

Septicemia

DIC

Pre renal failure 2ry to dehydration and decrease blood supply to kidney

ARD$ due to aspiration

GIT hemorrhage : hematemesis or even regurgitation of fresh blood

Esophageal perforation


2. Delayed complication :

Pre – esophageal : - Time : by the end of first week - Cause : sloughing of the devitalized esophageal wall - They are :

1. Mediastinitis 2. Pleurisy

3. Tracheoesophageal fistula 4. Pericarditis

Chronic : - Time : occurs after weeks - Cause : scaring and stricture formation - They are :

1. Esophageal obstruction : malnutrition $ & cachexia 2. Pyloric stenosis & pyloric obstruction 3. Vocal cord : suffocation 4. GIT : Malabsorbtion and dehydration

b- Investigations and follow up of corrosive intake. (May 2004)

1. To diagnose the GIT lesions : a- Upper GI endoscopy :

- is recommended for all patients of corrosive intake - should be undertaken within the first 12 hours - It reveals different grades of severity :

Grade l : erythema

Grade ll :destruction of mucosa

Grade lll : destruction of all layers of the gut beyond the mucosa - Contraindicated in :

Airway obstruction

The presence of signs of perforation 2. To diagnose the complications :

a- Radiography :

Chest X-ray : - Detect air in the mediastinum in case of esophageal perforation

Abdominal X-ray - In upright position - Demonstrate free abdominal air in case of gastric perforation

Barium swallow : - Done 21 days post ingestion - Demonstrate the site of stricture

b- CT scan : Accurate detection for the site of perforation

c- Laboratory studies :

CBC

ABG

Electrolytes

glucose


5- Differentiate between:

a- Clinical picture of oxalic acid and carbolic acid poisoning. (June 2012)

Oxalic acid Carbolic acid

Local symptoms 1. Ingestion

Irritation

Swelling of Oropharynx and esophagus

Abdominal pain

Smell of phenol

Nausea , vomiting

Bloody diarrhea

Abdominal pain

White patches in the oral cavity

2. Inhalation

Sore throat , cough , wheezing

Chemical pneumonitis , pulmonary edema

Irritation and Chemical pneumonitis

3. Skin Irritation and burning Painless skin lesions " white

patches turns to red then to brown"

4. Eye Irritation and corneal

damage Irritation and corneal damage

Systemic effect 1. Renal

symptoms 2. CNS symptoms 3. Cardiac

symptoms 4. Others

Dysuria and hematuria

Oliguria and anuria Weakness

Titanic convulsions

Dysrhythmias and cardiac arrest

Acute glomerulonephritis with Oliguria and anuria

Seizures

Lethargy

Coma

Tachycardia followed by bradycardia

Hypotension Hypothermia

Metabolic acidosis

Methemoglobinemia

Anemia and jaundice due to Hemolysis


b- Mechanisms of toxic actions of carbolic acid and oxalic acid intoxications. (Sept 2012)

Carbolic acid Oxalic acid

General protoplasmic poison , causing cell wall disruption , protein coagulation , coagulative necrosis and Hemolysis to RBCs

Highly irritating and corrosive causing acute hypocalcaemia resulting from precipitation of insoluble calcium oxalate salt in brain , kidney , heart and other sites causing serious systemic damage

6- Mention 2 differences between: Renal effects of oxalic & carbolic acids. (October 2013)

Oxalic acid Carbolic acid

Renal effects

Dysuria and hematuria

Oliguria and anuria

Precipitation of calcium oxalate salts

Acute glomerulonephritis

Oliguria and anuria

Metabolic acidosis

Increased Hemolysis of RBCs and Precipitation of acid hematin in renal tubules which is toxic and leading to its obstruction and failure

Dark urine that turns dark green if left in air due to oxidation of the excretory products of phenol "Hydroquinone"

7- Explain: Urine examination helps in diagnosis of phenol toxicity (June 2014)

- urine turns dark green if left in air due to oxidation of the excretory products of phenol "Hydroquinone"

8- Cases: A 3-year-old child was transferred to the E.R of the poisoning control center after ingestion of a disinfectant fluid 3 hours ago. He was drowsy, pale and thirsty. On examination: pulse 60/min.,BP85/50 mmHg, R.R29/min. laboratory results revealed Hb 4.8gm%, k 6.9 mEq/L with dark urine

(Sept 2008)

a- What is your diagnosis? - Phenol ( carbolic acid ) poisoning

b- What are the additional investigations to confirm diagnosis?

- Kidney function tests : urea and creatinine - Urine analysis :

Turn dark green if left in air due to oxidation of the excretory products of phenol "Hydroquinone"


Albuminuria and renal casts may be present in renal affection - If corrosive injury to GIT is suspected : endoscopy should be done - Blood for methemoglobinemia

c- What are the therapeutic measures to be adopted in such a case?

1. Emergency treatment : Care of respiration , convulsion , … etc

If corrosive injury to GIT is suspected : endoscopy should be done 2. Decontamination :

Do not induce emesis for fear of CNS depression

GL is possibly formed 3. Symptomatic treatment :

If methemoglobinemia occurs : give methylene blue

Alkalanization of urine to decrease PPT. acid hematin

Dialysis in case of renal failure

d- Explain the causes of the mentioned laboratory abnormalities in this case. - Due to the systemic effects of phenol causing :

Hemolysis of the RBCs leading to anemia ( Hb 4.8gm% )

Acid hematin in urine making it dark

Hyperkalemia ( k 6.9 mEq/L ) : due to impaired kidney functions caused by : Direct toxic effect of phenol on kidney causing toxic glomerulonephritis Increased Hemolysis of RBCs and Precipitation of acid hematin in renal tubules

which is toxic and leading to its obstruction

e- Explain the absence of GIT manifestations in this case. - Phenol ( carbolic acid ) has local anesthetic effect and paralysis to the local sensory

nerves

f- What are the possible risks and complications? - Early within 48 h CNS depression leading to coma - Late more 48 h toxic glomerulonephritis leading to acute renal failure


Hydrocarbons 1- Give full account on: Mechanism of respiratory tract and lung injury in kerosene

toxicity.(May 2005)\ and CNS. (Sept 2007)

a- On lung : - Kerosene has low viscosity , low surface tension and low volatility , these lead to high

risk of aspiration with increasing rate of penetration into terminal bronchioles and alveoli - Kerosene also destroy the surfactant lining the alveoli - As a result , Acute chemical pneumonitis will develop , hemorrhagic pulmonary edema ,

interstitial inflammation and alveolar collapse may occur b- On CNS :

- Direct effect :

When large amount is ingested leading to direct CNS depression - Indirect effect :

Secondary to pulmonary involvement with resulting hypoxia that leads to irritation of CNS followed by depression

2- Give reasons: Kerosene inhalation may end in sudden death. (June 2012)

- Kerosene make the heart more sensitive to the circulating catecholamine that may result in severe dysrhythmias either by itself or by the induced effect of hypoxia from pulmonary injury resulting in sudden death

3- Cases: A clear fluid with a characteristic smell (used as fuel by poor people) was accidentally drunk by a child. When transmitted to the hospital he was drowsy with dyspnea and fever, crepitation were heard over the chest. X-ray was done.

a- What is the suggested toxic agent in this case? - Kerosene toxicity

b- What is its effect on the lungs? - Kerosene has low viscosity , low surface tension and low volatility , these lead to

high risk of aspiration with increasing rate of penetration into terminal bronchioles and alveoli

- Kerosene also destroy the surfactant lining the alveoli - As a result ,

Acute chemical pneumonitis will develop

hemorrhagic pulmonary edema , interstitial inflammation, bronchopneumonia and alveolar collapse may occur

c- What is the treatment of this case? (May 2003)

- Emergency measure : ABCD - Elimination :

Contaminated clothes should be removed and skin should be washed by soap and water

GL is done after introduction of cuffed ETT to prevent aspiration


- Symptomatic treatment :

Treatment of pulmonary edema - Drug therapy :

No specific antidote

Corticosteroid help in chemical pneumonitis

Prophylactic antibiotics

4- Four-year-old child presented with abdominal pain after ingestion of colorless fluid, on examination his vital data were normal, pupils were normal and reactive to light & there was characteristic smell in his breath. The doctor performs gastric lavage, gave the child activated charcoal & discharged him. Few hours later the child returns with marked respiratory distress & examination revealed marked tachycardia, tachypnea, intercostal retraction, wheezes & basal crepitation on lung auscultation.

a- What is the most probable diagnosis & enumerate 4 other toxins with characteristic

smell? - Kerosene poisoning - other toxins with characteristic smell :

1. Phenol ( carbolic acid ) 2. Ammonia 3. Morphine 4. Ethanol 5. OPC

b- Explain finding mentioned in this case & what are the other possible finding?

- Gastric Lavage induce aspiration of kerosene that has low viscosity , low surface tension and low volatility with increasing rate of penetration into terminal bronchioles and alveoli

- Kerosene also destroy the surfactant lining the alveoli - As a result, Acute chemical pneumonitis will develop with :

Intercostal retraction Dyspnea , tachypnea crepitation and wheezes and decreased breath sounds

- kerosene increase sensitivity of the heart to the circulating CA result in tachycardia

c- Comment on the doctor’s behavior? - He had to do gastric Lavage after introduction of cuffed endotracheal tube

d- What are the investigation & treatment of this case? (June 2013)

- Investigations :

ABG

ECG monitoring

Chest X-ray every 2-3 days

Serum electrolytes - Treatment: Discussed before


Insecticides

1- Give an account on: Clinical picture of cholinergic crises of organo-phosphorus toxicity. (June 2009)

It consists of muscarinic, nicotinic and central effect: a- Muscarinic effects : DUMBBELS

Diarrhea

Urination

Miosis ( pin point pupil = constricted irreactive )

Bradycardia, prolonged QT interval, hypotension

Broncho constriction→ wheezes →↑pul. Sec (bronchorrhea)

Emesis

Lacrimation

Salivation , sweating b- Nicotinic action: MATCH

muscular fasciculation typically started around eyelids and peri-oral region followed by weakness & respiratory paralysis

adrenal medullary hyperactivity with transient hyperglycemia

tachycardia , dysrhythmias

cramps

hypertension c- CNS effects :

Vertigo

Confusion

Tremors

Convulsions

Coma due to inhibition of brain AChE coincides with true AChE in RBCS

2- Give an account on: Antidotes of Organophosphorus toxicity. What is the specific treatment of Organophosphorus insecticide poisoning?

(June 2008, June 2014)

- Atropine: "the life saving measure" Dose: 2-5 mg IV, repeated after 15 m till full atropinization mainly until relief of

bronchospasm and dryness of chest secretions " the greatest life threats " Action: antagonizes muscarinic effect only. Precautions:

presence of cyanosis may necessitate correction of hypoxia to avoid arrhythmia

avoid sudden withdrawal to prevent relapse and keep the patient atropinized for 1-2 days

3- Cases: A female child was brought to poison control center after local application of a pesticide solution to her scalp by her mother. Arrival following clinical findings: Pulse: 58/min and respiration 12/min, drowsiness and pin-point pupils.


a- What are the two possible groups of pesticides causing such presentation? - Organo-phosphorous compounds - Carbamates

b- By investigation how can you differentiate between the two types of pesticides? - By assessment of true ( in RBCs) and pseudo ( in plasma ) cholinesterase enzyme :

Normal level of true AChE and low level of pseudo AChE which rapidly replenished within few Hours in Carbamates poisoning

Low level of both true and pseudo AChE in OPC poisoning

c- What are cutaneous, neuron-muscular and respiratory manifestations in such cases? - Cutaneous : sweating ( muscarinic action on sweat glands ) and pallor - Respiratory: broncho constriction→ wheezes →↑pul. Sec (bronchorrhea) - Neuron-muscular :

muscular fasciculation typically started around eyelids and peri-oral region followed by weakness & respiratory paralysis

cramps of the skeletal muscles , tremors

d- How can you treat this case? 1. Prophylactic: by using masks, gloves and keeping away from children. 2. Curative:

a- Emergency:

ABC, care of coma. Convulsion, pul. Edema

Start:

Antidotes " atropine ' which is life saving :

Dose: 2-5 mg IV, repeated after 15 m till full atropinization mainly until relief of bronchospasm and dryness of chest secretions " the greatest life threats "

Action: antagonizes muscarinic effect only. Precautions:

presence of cyanosis may necessitate correction of hypoxia to avoid arrhythmia

avoid sudden withdrawal to prevent relapse and keep the patient atropinized for 1-2 days

Oximes:

Members: Obidoxime " more potent " , pralidoxime " PAM " Mechanism of action : choline esterase reactivators by forming oxime

phosphate complex Indication : Severe toxicity of OPC only

Predominance of nicotinic manifestations

b- Decontamination: - Remove contaminated cloth - Cut the hair for rapid control and prevention of relapse from continuous

exposure - Wash the skin for at least 15 min with water and soap


c- Symptomatic treatment : - Management of dysrhythmias - Diazepam to control seizures, ↓cardiomyopathy - AVOID:

Succinylcholine: (-) choline esterase enzyme.

Antihistamines: marked CNS (-)

Class 3 antiarrythmics: cause bradycardia, ht block

Phenothiazines

d- Treatment of complications : - Intermediate $ : Assisted ventilation, - Monitoring of vital data to detect relapsing of S/O and evaluation for

peripheral neuropathy and other long term effects

4- Case : A farmer was found unconscious in his farm. He had repeated vomiting, diarrhea and abdominal colic. On examination he was in grade III coma, with pin point pupils, muscle twitches and crepitating all over the chest.

a- What are the criteria of grade III coma?

- Comatose - No response to pain - Absent of deep reflexes - Normal circulation and respiration

b- What is the general treatment of a comatose patient?

1. Emergency measures :

Airway , breathing and circulation

Arterial blood gases

Administration of coma cocktail if undiagnosed patient : - Naloxone 2 mg: pure opiate antagonist without any agonist activity “no CNS dep.” - IV glucose ( dextrose 25 % 2-4 ml/kg ) for hypoglycemia to protect the brain - Vit B1”Thiamine” 100 mg IM to prevent Wernick’s encephalopathy

2. Care of comatose patient :

Urinary catheterization and daily monitor input and output of fluids

Mouth , eye , skin care

Protect against : - Stress gastric ulcer : H2 blockers or proton pump inhibitors - Infection : prophylactic antibiotics - Deep venous thrombosis : heparin

Frequent change of position To avoid bed sores on bony prominences and recumbent pneumonia 2ry to non drained lung lobes

Nutrition and proper hydration : Ryle tube or total parental nutrition

Physiotherapy for chest , limb muscle and joints

Daily clinical examination : electrolytes , glucose , urea , hematocrit


c- What is your proper diagnosis? Why? - Organo Phosphorus Compounds poisoning - Causes :

1. Occupational exposure : Usually occurs during agricultural applications and he is a farmer

2. Cholinergic $ c/p : Muscarinic effects:

repeated vomiting, diarrhea and abdominal colic

Pin point pupils

crepitating all over the chest due to bronchorrhea Nicotinic effects :

muscle twitches 3. CNS effects : coma

d- What is the specific treatment in this case? (May 2001)

Discussed before + prevent reexposure to OPC

5- Case: After suicidal attempt, a female student was transmitted to the hospital with constricted pupil, sweaty face, vomiting, diarrhea, salivation, generalized weakness and muscle fasciculation. Crepitation were heard all over the chest

(Sept 2003)

a- What is your most probable diagnosis? - Organo Phosphorus Compounds poisoning

b- How do you correlate the signs and symptoms to the mechanism of action of the suspected poison? - Mechanism of action : inhibition of AChE enzyme that hydrolyze Ach which in turn

accumulate profusely stimulating : 1. Muscarinic receptors result in : constricted pupil, sweaty face, vomiting, diarrhea,

salivation , Crepitation all over the chest due to bronchorrhea 2. Nicotinic receptors result in : generalized weakness and muscle fasciculation

c- Discuss treatment of the case. - Discussed before + patient should go psychiatric evaluations

6- Case: A 28-year-old farmer was found comatose in his farm after ingestion of a clear fluid. He had been brought to the emergency department. On examination, he was found in grade II coma. The pupils were constricted, the pulse was 50 beats/min, blood pressure was 90/60 mmHg, and there were also crepitation all over the chest.

a- What is the possible diagnosis for this case and why? - Organo Phosphorus Compounds poisoning - Reasons :

1. Occupational exposure :

Usually occurs during agricultural applications and he is a farmer


2. Cholinergic $ c/p :

- Muscarinic effects :

constricted pupils

crepitating all over the chest due to bronchorrhea

bradycardia , hypotension - CNS effects : coma

b- What are the criteria of grade II coma? - Comatose - No response to pain - Intact deep reflexes - Normal circulation and respiration

c- How can you investigate this case? - ABG , Electrolytes , glucose , urea or creatinine - ECG and cardiac monitoring - Assessment of true ( in RBCs) and pseudo ( in plasma ) cholinesterase enzyme

50 % of normal : subclinical or mild poisoning

30-40% of normal : mild to moderate toxicity

Less than 20-25% of normal : severe poisoning

Chest X-ray :evidence of aspiration pneumonia and bronchospasm

d- How can you treat this case? (May 2006) - Discussed before

7- What is the specific treatment of Warfarin intoxication? (Sept 2014)

- Emergency treatment : ABC - Elimination :

Emesis using syrup ipecac or GL followed by Activated charcoal - Antidote : vit.K1 " phytonadione "

Uncertain amount ingested : oral route

Large amount are consumed or if PT or INH is doubled : IM route

Bleeding patient : infusion route - Symptomatic TTT :

Blood transfusion and/ or fresh frozen plasma for severe bleeding

ibnkhaldonmed-toxicology.pdf

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clinical toxicology

hepatitis b

trachea b doses

gastric lavage tube

mixed drugs

administered drugs

ingested poison

cases of undiagnosed