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.

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.

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.

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.

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).

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:

• 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

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.

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 is partially eliminated unchanged through the kidney and

expired air

• Addition of thiamine and pyridoxine enhance formation of nontoxic

metabolites.

Ethylene Glycol

Alcohol

dehydrogenase

Glycoaldehyde

Glycolic acid

Glyoxalic acid

Formic acid

Oxali Calcium oxalate

• 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.

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.

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.

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.

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

• 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

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.

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.