1. E-learning topics in Clinical Toxicology
Gastric Lavage technique
Materials for gastric lavage
Wide bore (36-42F) orogastric lavage tube, funnel, jugs, bucket, oropharyngeal
airway, stethoscope, BP set.
Materials for immediate intubation (Functioning laryngoscope, endotracheal
tubes of different sizes, suction machine, suction catheters, Ambu bag with
proper fittings, oxygen supply, syringes).
Cardiac monitor (preferably supported with a defibrillator). In certain
poisoning, lavage should not be attempted unless well monitored e.g. Digoxin,
Organophosphates insecticides.
Materials for sample collection.
Gastric lavage technique
1. Technique must be explained to the patient if conscious.
2. An assistant (trained nurse to assist the physician).
3. Remove dentures, mucous, vomitus from the patient's mouth.
4. Choose the gastric tube's proper size for age.
5. Give the patient, if conscious, a glass of water.
6. Place the patient on his left side and elevate his waist by a pillow and make
his face out of the edge of the bed. This allows better washing of the fundus
and greater curvature and decreases the risk of aspiration.
7. Take the measure of length between the mouth and epigastrium; make a
mark with adhesive plaster on the tube so as not to introduce the tube beyond
this mark.
8. Lubricate the end of the tube with paraffin oil, if the patient is conscious and
cooperative, put the tube end on the back of his tongue and instructs him to
swallow while you gently push it till it reaches the mark previously
determined.
9. If you find resistance, or the patient coughs, it means that the tube entered the
trachea. Withdraw the tube and reintroduce.
10. Check for proper tube position by compressing the epigastrium to see the
regurgitated fluid contents of stomach or inject 50-100ml air in the tube to
auscultate the bubbling air in the stomach
11. Apply suction of the gastric contents by a syringe, for toxicological analysis.
12. Introduce about 200-400 ml of a room-temperature saline lavage solution by
a funnel then allow it to be removed by siphonage, and make sure that all the
fluid introduced should come out so as to avoid gastric distension and reflex
evacuation in the duodenum. This process should continue until fluid is clear
from any particle.
13. Give activated charcoal or oral antidotes at the end of lavage whenever
indicated.

2. 14. Gastric lavage tube is removed after clamping (to avoid dribbling of water in
upper airways during removal). The patient is ordered to cough while the
tube is pulled out.
Button Batteries
These are small disk-shaped batteries used in watches, calculators and
cameras. They contain caustic metal salts such as mercuric chloride and corrosive
alkalis such as sodium and potassium hydroxide. When swallowed or inhaled, they
can cause injury by corrosive effects resulting from leakage of the corrosive metal
salts or the alkali they contain.
Clinical presentation
- The case is always asymptomatic after ingestion. They cause serious injury
only if they become impacted in the esophagus, leading to burns and
subsequent strictures or perforation into the aorta or mediastinum. The clinical
presentation may be in the form of abdominal pain, vomiting, fever or signs of
bleeding due to perforation of the gut. If they reach the stomach without
impaction in the esophagus, they nearly always pass via the stools within
several days.
- The case is usually symptomatic after inhalation. Symptoms are in the form of
cough, dyspnea and stridor.
Diagnosis
1- History of ingestion or inhalation.
2- X-rays of the chest and abdomen will reveal impacted button batteries
(as shown in the x-ray. fig. 3).
3- Urine mercury levels have been reported to be elevated after button
battery ingestion.
Treatment
1- Airway assessment and initial stabilization.
2- If the battery is located in the respiratory tract it requires emergency
removal by endoscopy.
3- If the battery is located in the esophagus it is removed by esophagoscopy.
4- If the battery is located in the stomach or intestine and the patient is
asymptomatic, serial stool examination is done at home to check for battery
passage and another x-ray will be done in 5-7 days. But if the patient is
symptomatic, endoscopic or surgical removal should be done.
5- At any stage if the battery stops moving, it should be removed by
endoscopy or surgery.

3. Fig. (3): Impacted button battery
Naphthalene
ILOs
By the end of this chapter the student should be able to:
K1: Describe the mechanism of action of naphthalene.
K2: Describe the clinical picture of naphthalene toxicity.
K3: Discuss the management of naphthalene toxicity.
K4: Solve problems revolving around virtual cases presenting with
naphthalene toxicity.
A1: Realize the importance of urgent appropriate treatment in cases of
acute intoxication.
A2: Realize the importance of working in groups.
Introduction
• It is obtained from coal tar. Now, it contains paradichlorobenzene (tar
camphor) which is less toxic. It is used as a moth repellent and used as toilet
bowel deodorizer.
• Poisoning occurs through accidental ingestion (in children), or inhalation of
naphthalene vapor present in clothes and blankets.
Mechanism of action
• Its metabolite (alpha naphthoquinone) red cell hemolysis acts as an oxidative
agent in cells with G6PD deficiency.
Clinical picture
1. GIT: Nausea, vomiting and abdominal pain, diarrhea.
2. Neurologic: headache, restlessness, optic neuritis, lethargy, convulsions,
and coma may occur.
3. Hematologic: hemolysis in G6PD deficiency individuals which occurs
rapidly and with smaller dose, with hemolytic anemia hematuria….
4. Hepatic: hepatocellular injury, 3-5 days post ingestion.

4. 5. Renal: hemoglobinuria, oliguria, anuria.
6. Metabolic: fever, flushing, headache.
7. Pregnancy; hemolytic anemia of the newborn.
Investigations
1. CBC
2. Liver functions
Treatment
1. Emergency measures (ABCD)
2. Elimination
a. Remove to fresh air (in case of inhalation) and irrigate the eye with
copious amounts of water in case of eye affected.
b. Emesis by syrup ipecac.
c. Gastric lavage.
d. Activated charcoal 1 gm/kg.
3. Supportive treatment
Treatment of hemolysis by:
• Urine alkalinization:
• Blood transfusion
• Corticosteroids
Summary
Naphthalene is one of the household toxins. The clinical presentation
and management were discussed in this chapter.
Questions
1. Discuss the clinical picture and management of naphthalene toxicity.
2. Alkalinization of urine is used in the treatment of naphthalene toxicity for the
following reason:
a) To inhibit the precipitation of acid hematin in renal tubules.
b) To inhibit reabsorption of naphthalene.
c) To improve prognosis of rhabdomyolysis.
d) To control arrhythmias.

5. Anticoagulants
Coumarins (Warfarin)
Pathophysiology
• Coumarins depress the hepatic vitamin K dependent synthesis of substances
essential to blood clotting: prothrombin (factor II) and factors VII, IX, and
X. the antiprothormbin effect is the basis for detection and assessment of
clinical poisoning.
• Concurrently, the agents increase permeability of capillaries throughout the
body, predisposing the animal to widespread internal hemorrhage.
• Toxicity in humans follow regular consumption of coumarin contaminated
food over several days, or ingestion of very large amounts of the
rodenticide bait.
Clinical picture
Usually no apparent toxicity arise from a single modest dose of coumarins.
If any, it will usually appear after a delay of 48 hours consequent to increased
prothrombin time in the form of:
1. Ecchymosis, nasal bleeding.
2. Spontaneous hemorrhage: gingival bleeding, hematemesis, hematuria and
melena.
Investigations
1. Prothrombin time: detectable reduction in prothormbin occurs within 24-48
hours of ingestion. It usually reaches a maximum in 36-72 hours and
persists for 1-3 weeks..
2. Complete blood count daily. Repeat hemoglobin and hematocrit 6 hours if
prothrombin time is significantly prolonged to detect hidden bleeding.
3. Urine for hematuria, stool for occult blood.
Treatment
A- Emergency treatment: ABC
B- Elimination
Emesis using syrup Ipecac or gastric lavage followed by activated charcoal.
C- Antidote
Vitamin K1 (phytonadione)
a) If there is uncertainty about the amount of rodenticide ingested, phytonadione
(vitamin K1) given orally protects against the anticoagulant effect of this
rodenticide, with essentially no risk to the patient. Dosage is 15-25 mg for
adults; and 5-10 mg for children under 12 years.
b) Vitamin K 1 is given IM in a dose of 5-10 mg for adults or 1-5 mg for children
under 12 years if large amounts are consumed or if prothormbin time is > 2
times normal (INR > 2).

6. c) Vitamin K1 is given IV as infusion (10 mg for adults; 5 mg for children) if
patient is bleeding. Repeat in 24 hours if bleeding continue.
D) Symptomatic treatment
Blood transfusion, fresh frozen plasma for severe bleeding.
Nitrites and Nitrates
− They may be inorganic or organic
− They are used as fertilizers, food processing and in medicine. High levels of
nitrates have now contaminated soil and water supplies especially shallow
wells in ruler areas..
Mechanism of toxicity:
Nitrites and nitrates are potent smooth muscle relaxants that produce
cardiovascular effects through coronary and peripheral vasodilatation.
• They also oxidize hemoglobin to methemoglobin by oxidizing iron from
ferrous (fe2+) to (fe3+) state.
• Iron in the ferric state is incapable of binding oxygen.
• Methemoglobin also causes shift of oxygen dissociation curve to the left
and consequently impairs unloading of oxygen to tissues.
• Methemoglobin is normally present as less than 1% of total hemoglobin
under physiologic conditions.
• Reduction of hemoglobin occurs through two enzymatic pathways in
erythrocytes. The most active is the NADH-dependent methemoglobin
reductase system. This accounts for 95% of methemoglobin reduction.
• The second pathway is catalyzed by NADPH-dependent methemoglobin
reductase. In this pathway NADPH combines with methemoglobin
(MetHb) in the presence of the cofactor methylene blue.
• NADPH pathway depends on functioning hexose monophosphate shunt,
which requires in its first step G6PD. This account for less than 5% of
MetHb reduction.
Clinical Picture
• The clinical effects are determined by the cardiopulmonary status and the
total methemoglobin rather than just the methemoglobin percentage.
• Vasodilatation may lead to a throbbing headache and flushed face up to
rapid fall in blood pressure and cardiogenic shock.
• The heart would compensate by increasing heart rate and force of
contraction to elevate blood pressure.
• In severe toxicity the heart may be unable to respond leading to
hypotension, shock and cardiovascular collapse.
• In addition to cardiovascular effects, the major toxic effect of nitrates and
nitrites is methemoglobinemia:

7. • The initial manifestation of methemoglobinemia is cyanosis.The patient
may appear deeply cyanosed and application of oxygen does not improve
this cyanosis
• At 50% to70%, arrhythmias, coma, seizures, respiratory distress, and lactic
acidosis develop.
• Levels more than 70% cause cardiovascular collapse and have a high
degree of mortality
Investigations
1. ABGs
2. Serum electrolytes.
3. ECG
4. Serum methemoglobin levels
Treatment
I- Emergency measures (ABCD)
II- Elimination
• Gastric lavage followed by activated charcoal
III- Toxin-specific measures
1- Methylene blue
• Is the first-line antidotal therapy. It accelerates the enzymatic reduction
of methemoglobin by NADPH-methemoglobin reductase
• The initial dose is 1-2 mg/kg IV over 5 min. Its effects should be seen
in approximately 20 min to 1h.
• Patients may require repeated dosing, but the total dose should not
exceed 7 mg/kg.
• The methemoglobin level should be significantly improved within one
hour of methylene blue infusion.
• Methylene blue should be avoided in patients with G6PD deficiency, if
possible, because this antidote may induce hemolysis in this patient
population
2- Exchange transfusion
Should be used for:
1. Infants.
2. Patients who do not respond to methylene blue within 30 to 60 minutes.
3. Patients with G6PD deficiency.
4. Patients with metHb levels of more than 70%.
Lithium
Uses

8. The salt of lithium carbonate is used as mood stabilizer in acute mania and
manic depressive psychosis.
Pharmacokinetics
• Rapid absorption from GIT
• Delayed tissue distribution so serum levels after single acute overdose do not
reflect the biologically active intracellular lithium.
• Distribution in tissue follows water distribution, mainly excreted by the
kidney..
• It has a narrow therapeutic index and toxicity is enhanced by dehydration,
thiazide diuretic and renal failure.
Clinical picture of acute toxicity
I- CNS
• Mild toxicity: mental confusion, ataxia, tremors and exaggerated reflexes
• Severe toxicity: convulsions and coma
II- Renal
• Polyuria, polydepsia, nephrogenic diabetes insipidus and renal failure
III- CVS
• Arrhythmias
IV- GIT
• Nausea, vomiting and diarrhea
Investigations
1. Serum lithium level (therapeutic level 0.4-1.3 meq/L)
2. Renal functions.
3. ECG
Treatment
I- Stabilization of the patient (ABCD)
II- Elimination
• Induction of emesis or G. lavage
• Charcoal is not effective
• Whole-bowel irrigation is effective especially in sustained-release
preparations.
III- In mild to moderate cases with serum level < 4 meq/L
1. Good hydration with IV infusion of normal saline.

9. 2. Maintenance of electrolyte and fluid balance
3. ECG monitoring
4. Serial estimation of lithium level
IV- Hemodialysis
1. Severe toxicity (coma, convulsions or arrhythmias)
2. Serum lithium level > 4 meq/L
N.B. slow distribution of lithium may account for delayed improvement of
patients treated from lithium toxicity
Ethylene Glycol
Ethylene glycol is widely used as an engine coolant.
Mode of Toxicity
Accidental oral ingestion. Ethylene glycol has low volatility and does not cause
poisoning by inhalation.
Pathophysiology and kinetics
Once absorbed ethylene glycol is rapidly distributed to total-body water.
Ethylene
Glycol
Alcohol
dehydrogenase
Glycoaldehyd
e
Glycolic
acid
Glyoxalic
acid
Formic
acid
Oxali Calcium
oxalate
• Ethylene glycol is partially eliminated unchanged through the kidney and
expired air
• Addition of thiamine and pyridoxine enhance formation of nontoxic
metabolites.

10. • Glycolic , glyoxalic and oxalic acid metabolites are the cause of metabolic
acidosis
• Oxalic acid metabolite binds with calcium:
1- Forming Calcium oxalate crystals which precipitate in the renal tubules,
leading to acute renal failure which may be caused also by direct toxic
effect of ethylene glycol.
2- Causing hypocalcaemia and QTC prolongation with dysrhythmias and
cranial nerve abnormalities.
Clinical Pictures
• Tingling and numbness
• Twitches
• Convulsions
• Tetany
• Arrhythmia
• Acute renal failure
• Other features are similar to ethyl alcohol toxicity
Investigations
• Routine investigations: CBC, ABG, electrolytes (Ca, K).
• ECG changes.
• Urine analysis: calcium oxalate.
• Renal profile: urea, creatinine.
Treatment
I- Emergency Measures
II- Antidotes
• Ca gluconate IV slowly
• Ethanol and 4 Methyl pyrazol (fomepizole) are used to prevent
glycolate accumulation.
• Thiamine and Pyridoxine enhance metabolism to less toxic products
III- Symptomatic treatment.
• Correct acidosis.
• IV fluids: prevent calcium oxalate precipitation in the kidney.
• Dialysis in case of renal failure
Mercury
Forms and Sources
1. Elemental mercury vapor, dental amalgam, mercury of medical instruments
as glass thermometer and sphygmomanometers. It causes toxicity after
inhalation and has no toxic effects when swallowed as it is poorly absorbed.
2. Inorganic salts of mercury used as laxatives, teething powder, mercuric
fulminate which is an explosive, mercuric Cl used as disinfectant.

11. 3. Organic Mercury compounds: which have been incorporated and
concentrated in the aquatic food as eating contaminated fish due to
discharge of contaminated waste.
Mercury absorption
• After inhalation: 60-80% of mercury vapours are absorbed.
• After dermal exposure 3-15% is absorbed.
• After ingestion only <0.2 % of metallic mercury and about 15% of
inorganic mercury are absorbed. However, more than 90% of organic
mercury are absorbed via the GIT.
Pathophysiology
1- Mercury has a high affinity for SH groups, which attributes to its effect on
enzyme dysfunction. Choline acetyl transferase is one of the inhibited
enzymes, which is involved in acetyl choline production. This inhibition
may lead to acetyl choline deficiency, contributing to the signs and
symptoms of motor dysfunction.
2- Glomerulonephritis is attributed to an immune mechanism.
3- Elemental mercury is pulmonary irritant and toxic to the CNS.
4- Inorganic mercury salts are corrosive to the skin and the GIT. Deposition of
mercuric ions in the renal tubules causes acute tubular necrosis.
5- Organic mercury is especially toxic to the CNS and has teratogenic effects.
Acute Mercury Toxicity
A- Acute ingestion of liquid metallic mercury:
• Since it is poorly absorbed in the GI, it causes no harm and needs no
treatment.
B- Acute inhalation of mercury vapors
• Severe chemical pneumonitis, cough and dyspnea.
• Acute respiratory distress syndrome.
• Pulmonary fibrosis.
• Mouth ulcers, metallic taste, nausea, vomiting, and diarrhea.
• Metal fume fever: pyrexia, cough, malaise, flu-like symptoms
• Kidney is final target organ where mercury accumulates as body tries to
clear toxin
• Erethism
It is constellation of neurologic abnormalities collectively referred to as
erethism and including mood alteration (emotional lability), shyness,
anxiety, sleep disturbances, memory impairment, parasthesia, ataxia,
muscle rigidity, visual and hearing impairment.
C- Acute ingestion of inorganic mercurous salts
Ingestion of single large dose of mercurous chloride does not usually cause
symptoms, since it is poorly absorbed.

12. D- Acute ingestion of inorganic mercuric salts
Accidental or suicidal ingestion of mercuric Chloride
Clinical picture
1. GIT manifestations: irritation leading to nausea, vomiting, severe abdominal
cramps, hematemesis, dehydration and collapse, burning sensation with
metallic taste, dysentery (mercury is re-excreted in the caecum), also due to its
re-excretion in the saliva leads to stomatitis, increased salivation and gingivitis
(gingivostomatitis).
2. Acute toxic renal tubular necrosis with hematuria and casts.
3. Shock and death may occur.
Causes of death
• Within 24 hours: dehydration.
• Later, in 1-2 weeks: uremia.
Treatments
I- Emergency measures (ABCD)
II- Elimination
• Induction of emesis or gastric lavage if ingested
III- Antidote (chelators)
• Immediate chelation therapy is the standard of care for a patient showing
symptoms of severe mercury poisoning or the laboratory evidence of a
large total mercury load (blood/urine mercury persistently > 100 – 150
mg/l).
• Chelators of mercury include: Dimercaprol "BAL", D-penicillamine,
Dimercapto succinic acid "DMSA" or 2, 3-Dimercapto-1-
propanesulphonate "DMPS".
• DMPS is the chelation therapy of choice for mercury for both acute and
chronic mercury poisoning and for all forms of Hg (inorganic, metallic and
organic).
IV- Symptomatic treatment
• IV fluids for dehydration, mouth hygiene, hemodialysis in renal failure.
Chronic Mercury toxicity "Mercurialism"
Mode of exposure
Industrial: chronic inhalation of mercury fumes.
Clinical picture
1. GIT irritation: recurrent stomatitis, ptyalism, gingivitis, grey line, recurrent
vomiting and diarrhea and weight loss.
2. Nervous affection: kinetic intention tremors, first appearing in the tongue
leading to hesitant speech, then in the hands. There is also affection of the
visual cortex leading to contraction of the visual field.

13. 3. Psychiatric disturbances "erethism" in the form of shyness, fear, irritability,
loss of self confidence, insomnia, mental deterioration.
4. Renal affection: toxic tubular necrosis.
5. Cutaneous affection in the form of dermatitis.
Investigations
• CBC, renal function tests, electrolytes.
Treatment
A. Prophylactic
• Prophylactic measures to decrease exposure as masks, gloves,
...etc
• Periodic medical examination of workers.
B. Curative
I- Stop further exposure
II- Chelation therapy
Chelation therapy using penicillamine, or DMSA
III- Symptomatic e.g. renal affection: hemodialysis.
Cocaine
• It is extracted from the leaves of erythroxylon coca, known for more than two
centuries for the stimulant and anti fatigue properties.
• Purified cocaine is now used by sniffing the powder, usually adulterated by
other less expensive substances as salicylates, boric acid, quinine, talc powder,
mannitol, sucrose, lactose or caffeine.
• It is rarely smoked as freebase (crack) or taken intravenously (usually with
heroin).
Mechanism of action
1- Sympathomimetic action due to inhibition of reuptake of catecholamines.
2- Local anesthetic action of sensory nerves.
3- Vasoconstriction of blood vessels.
Clinical picture of acute toxicity
A. CNS stimulation followed by depression:
• Euphoria, delayed fatigue and insomnia.
• Irritability, talkativeness and hyperthermia.
• Tremors up to convulsions.
• Hallucinations.
• Drowsiness, confusion up to coma.
• Cyanosis and death from central respiratory depression.
B. Peripheral sympathomimetic action:
• Tachycardia, arrhythmia, tachypnea, dilated reactive pupil, hypertension which
may be so severe to cause subarachnoid or intracranial hemorrhage and
produces neurologic sequelae.

14. C. Vasoconstriction of the blood vessels:
• Pallor, renal vasospasm (infarction and acute renal failure), cerebral VC
(infarction), acute myocardial infarction and necrosis (occurs shortly after
snuffing and is due to coronary vasospasm), and cardiac arrest which is a
common incident in cocaine abusers.
D. Irritation followed by paralysis of nerve endings leading to:
• Numbness in the nose and throat on snuffing, then in the limbs.
• Local anesthesia.
Investigations
1. Urine screening to identify cocaine metabolites.
2. ECG.
Treatment
I- Emergency measures (ABCD).
II- Elimination: Gastric lavage and activated charcoal (if leaves are chewed).
III- Symptomatic treatment:
1. Treatment of arrhythmia.
2. Treatment of hypertension using labetalol or IV Na nitropruside
(vasodilator).
Cocaine Dependence
(Cocainism)
Cocaine is euphoriant. It decreases physical and mental fatigue and
increases sexual activity. Tolerance and physical dependence to cocaine develop
rapidly.
Picture of dependence
1- Mental change:
• Decrease power of concentration with dementia (amnesia, decrease
intelligence, decrease mental faculties).
2-Physical changes:
• Anorexia and progressive weight loss (wasting).
• Pallor of face due to vasoconstriction.
• Dilated reactive pupils, irritability, tremors, insomnia and hypertension .
• Loss of the sense of smell.
• Perforated nasal septum due to:
1. Continuous vasoconstriction of nasal blood vessels by snuffed
cocaine → devitalisation and sloughing.
2. Irritation by adultrants (Boric acid, quinine, salicylates).
3. Cocaine anesthesia: patient can not feel pain of necrosis →more
snuffing →more necrosis.
3-Moral changes
• Patient becomes aggressive and dangerous.
4-Psychological changes

15. • Hallucinations; the chronic effect on the sensory nerve endings gives rise to
Magnan's symptom, which is the feelings of sand under the skin or to
Cocaine bugs, with sensation as if insects creep under the skin with severe
itching.
5-Withdrawal symptoms
• Physical dependence occurs to cocaine but withdrawal symptoms are not
serious as that with opiates. It includes irritability, neurologic pain in arms
and legs, tendency to violence, depression and fatigue.
Treatment
1. Abrupt withdrawal in an institute.
2. Good diet, vitamins and health care.
3. Psychological care, tranquilizers and analgesics.
4. Symptomatic treatment for hypertension and arrhythmia.
Performance Enhancing Drugs
Doping in Sports
Definition
Doping is defined as administration of or use by a competing athlete
of any substance foreign to the body with the sole intention of increasing
performance in competition.
• The use of the performance enhancing drugs is linked to an epidemic
number of deaths among competitors. Also, these drugs have shown
unhealthy side effects in athletes.
• The International Olympic Committee (IOC) and other sport organizations
agreed to ban certain substances which could be used in the attempt to
enhance performance, some commonly used and potentially harmful
performance enhancers are: anabolic steroids, creatine, sympathomimetics,
human growth hormones, amino acids, and erythropoietin. We shall focus
on a commonly used performance enhancer i.e. anabolic steroids.
Anabolic steroids
Anabolic steroids (ASs) are a class of synthetic molecules structurally
related to testosterone. They exert anabolic i.e. muscle building properties.
Unfortunately, these steroids are not purely anabolic. In fact, they possess
androgenic properties as well. These androgenic properties affect different organ
systems.
In 1991, the anabolic steroids were classified as controlled dangerous
substance and were put in schedule ΙΙΙ of the Controlled substance Act.
The similarities of anabolic steroid abuse to the classic substance abuse are
suggested through the facts that (ASs) are used over long periods than desired,
failure of the attempts to stop taking the drug, continuing use despite the
knowledge of health problems caused by ASs, and the occurrence of characteristic

16. withdrawal symptoms that lead to the use of the hormone to relieve these
symptoms.
Anabolic effects
ASs adds to the building up of body tissues and assimilation of proteins and hence,
promotes increasing muscle mass. When they are taken in combination with a
specific diet and a programme of intensive training, they accelerate muscle growth
and increase body mass thus enhancing performance or appearance of an
individual. ASs are available as tablets, capsules for oral use, also preparations for
intramuscular injections are available.
Adverse and toxic effects of ASs
1. Reproductive effects:
ASs suppress gonadotrophin secretion, Male athletes may suffer of
testicular atrophy; decreased sperm count and increase in morphologically
abnormal sperm, prostate enlargement, loss of libido and impotence.
Female athlete may suffer of irregular menses or amenorrhea, miscarriage
or stillbirth.
2. Feminization in male athletes
Male athletes, who administered parenteral ASs, can develop gynecomastia
and increased fat deposition.
3. Virilizing effect
ASs possess some androgen effects. Women and children using ASs suffer
from deepening of voice, hirsutism and decreased body fat. In addition,
female may suffer of acne, male balding pattern and change in breast size.
4. Cardiovascular effects
ASs cause numerous cardiovascular effects as: hypertension, decline in
high density lipoprotein (HDL) and increased low density lipoproteins
(LDL).also biventricular and interventricular septum hypertrophy are
reported. Vasospasm, thromboemboli and increased platelet aggregation
may also occur. Risk of congestive heart failure may be increased due to
fluid retention. Case reports described myocardial infarction and sudden
cardiac death in young bodybuilders taking ASs.
5. Hepatotoxicity:
ASs use may be associated with elevated liver enzymes, cholestatic
jaundice, and hepatic neoplasms (benign adenomas and malignant
carcinomas).
6. Erythropoiesis:
Ass stimulate erythropoiesis, can cause polycythemia, increased hematocrit
value and increased leukocyte and platelet count.
7. Muscular effects:
Rupture of tendons and ligaments of muscle size.
8. Infections:
Through contaminated shared needles which may result in abscess
formation, hepatitis, HIV and infected joints.

17. 9. Psychological effects:
Such as: aggression, irritability, memory effects, mood-swings, criminal
acts and manic behavior.
10. Withdrawal effects:
Include depression, insomnia, anorexia, fatigue, decreased libido and loss
of physical and muscular power. The dramatic change in body image and
performance often drive the athlete to resume use of ASs.