Toxicology Essay & Cases Questions

(General Corrosives Hydrocarbons Insecticides)

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

Anticholinergic
Clinical pictures
Skin
Bowel sound
Urine retention
pupil
Causes

- dry
- inhibited
- present
- dilated irreactive
Atropine , TCA , botulism

Sympathomimetic
- diaphoresis
- hyperactive
- absent
- dilated irreactive
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:

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- 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
1- Hypotension
2- Elimination of therapeutically
administered drugs
3- Bleeding tendency due to
Complications
heparin
4- Air embolism
5- Electrolyte imbalance
6- Infection : HIV , hepatitis B or C

Peritoneal dialysis
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 B1Thiamine 100 mg IM to prevent Wernicks 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

Ibnkhaldon Med | Toxicology Essay Questions with Answers

(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

Result from left ventricular dysfunction
Triggering Causes :
acute ischemia , myocarditis , rhythm
or conduction abnormalities , high
blood pressure
Toxic causes :
Ca channel blockers , beta blockers ,
TCA , Scorpion myocarditis

Non-cardiogenic pulmonary edema

Result from disruption of alveolar capillary
membrane
destruction of pneumocytes II lining alveoli that
are responsible for surfactant synthesis
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

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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

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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

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2. Delayed complication :
Pre esophageal :
- Time : by the end of first week
- Cause : sloughing of the devitalized esophageal wall
- They are :
1. Mediastinitis
3. Tracheoesophageal fistula
2. Pleurisy
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
Electrolytes
ABG
glucose

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5- Differentiate between:
a- Clinical picture of oxalic acid and carbolic acid poisoning.

Oxalic acid
Local symptoms
1. Ingestion

2. Inhalation

3. Skin
4. Eye

Systemic effect
1. Renal
symptoms

Irritation
Swelling of Oropharynx
and esophagus
Abdominal pain
Sore throat , cough ,
wheezing
Chemical pneumonitis ,
pulmonary edema
Irritation and burning
Irritation and corneal
damage
Dysuria and hematuria
Oliguria and anuria

Carbolic acid

Smell of phenol
Nausea , vomiting
Bloody diarrhea
Abdominal pain
White patches in the oral cavity
Irritation and Chemical pneumonitis

Painless skin lesions " white

patches turns to red then to brown"
Irritation and corneal damage
Acute glomerulonephritis with
Oliguria and anuria

Seizures
Lethargy
Coma
Tachycardia followed by
bradycardia
Hypotension

2. CNS symptoms
3. Cardiac
symptoms

4. Others

(June 2012)

Weakness
Titanic convulsions
Dysrhythmias and
cardiac arrest

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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

Renal
effects

Dysuria and
hematuria
Oliguria and
anuria
Precipitation
of calcium
oxalate salts

Carbolic acid

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"

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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

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10

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

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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 doctors 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

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12

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.

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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

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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 B1Thiamine 100 mg IM to prevent Wernicks 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

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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

5Case: 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

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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

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