The document discusses lead poisoning, including its causes, clinical features, diagnosis, and treatment. Lead poisoning occurs when lead is absorbed into the body, such as from lead-based paint, contaminated dust, or water. Symptoms depend on the amount of lead absorbed but can include abdominal pain, constipation, fatigue, and in more severe cases, damage to the nervous system. Diagnosis involves testing blood and urine samples to check for elevated lead levels. Treatment focuses on removing lead from the body through chelation therapy or other means while also preventing further exposure.

1. PREPARED BY:-
Chirag Marwah
B. Pharma

2. • Poisoning occurs when any substance interferes with normal
body functions after it is swallowed, inhaled, injected, or
absorbed.
• Barbiturates are derivatives of barbituric acid and are Non –
Selective CNS depressants.
• Barbiturate overdose is poisoning due to excessive doses of
barbiturates.
• Barbiturate overdose may occur by accident or purposefully in
an attempt to cause death.

3. • SEDATIVE-HYPNOTIC
• PRE-OPERATIVE SEDATION
• FEBRILE CONVULSIONS
• EPILEPSY

4. • ULTRA-SHORT ACTING BARBITURATES : -Duration of
action: >0.5 hours -Examples include: THIOPENTAL ,
METHOHEXITAL
• SHORT-ACTING BARBITURATES: -Duration of action : >3-4
hours -Examples include: PENTOBARBITAL ,
SECOBARBITAL
• INTERMEDIATE-ACTING BARBITURATES: -Duration of
action : >4-6 hours -Examples include: AMOBARBITAL,
APROBARBITAL, BUTABARBITAL, BUTALBITAL
• LONG-ACTING BARBITURATES: -Duration of action: >6-12
hours -Examples include: MEPHOBARBITAL ,
PHENOBARBITAL .

5. • Direct CNS depressants.
• Bind to GABA receptors.
• Prolong the opening of chloride channel.
• Inhibiting excitable cells of the CNS.
• Potent inducer of hepatic drug- metabolizing enzymes
especially CYP450 system, so liable to cause drug
interactions.
• Precipitate attacks of acute porphyria.
• Tolerance & dependence occur.

7. • Leading cause of poisoning due to their ready availability.
• Most of the cases are suicidal but some are due to error or
ungraded exploration in children.
• Short acting barbiturates are more dangerous than long acting.
• Shock & anorexia occur quickly.
• Coma is more severe with short acting barbiturates.

8. • Coma
• Peripheral circulatory collapse
• Slow or rapid breathing
• Pupils constricted & reacting to light initially but subsequently
develops paralytic dilatation
• Atelectasis
• Pulmonary edema
• Bronchopneumonia
• Acute renal shut down

9. METHODS:-
• Hospitalization
• Support vital functions
• Prevent further absorption
• Increase elimination of drug
• Conservative management with good nursing care
• Appropriate detoxification or psychiatric after care

10. • HOSPITALIZATION:
=) Admitted to the hospital.
• SUPPORT VITAL FUNCTIONS:
=) Consciousness.
=) Airway , breathing , circulation.
=)Blood pressure.
• PREVENT FURTHER ABSORPTION:
=) Emesis.
=) Gastric lavage.
=) Activated charcoal & catharsis.
• INCREASE ELIMINATION OF DRUG:
=) Forced diuresis.
=) Alkalization of urine.
=) Prophylactic antibiotic.
=) Peritoneal dialysis.
=) Hemodialysis.
=)Hemoperfusion.
• OTHER MEASURES:
=) Psychiatric after care.

11. • FOR PHENOBARBITONE : 6-10 GRAMS
• FOR AM0BARBITAL, SECOBARBITAL,
PENTOBARBITAL: 2-3 GRAMS

12. • Morphine poisoning is preventable and potentially lethal
condition that results from prescribing practices, inadequate
understanding on the patient's part of the risks of medication
misuse, errors in drug administration, and pharmaceutical
abuse.
• 50 mg morphine produce serious toxicity.
• Therapeutic dose : 10-50 mg oral, 2-6 mg i.v ., 10-15 mg i.m .
• Lethal dose : 250 mg.

13. • First, opioid analgesic overdose can have life-threatening toxic
effects in multiple organ systems.
• Second, normal pharmacokinetic properties are often disrupted
during an overdose and can prolong intoxication dramatically.
• Third, the duration of action varies among opioid formulations,
and failure to recognize such variations can lead to
inappropriate treatment decisions, sometimes with lethal results

14. • Although the classic toxidrome of apnea, stupor, and meiosis
suggests the diagnosis of opioid toxicity, all of these findings are not
consistently present.
• The sine qua non of opioid intoxication is respiratory depression.
Administration of therapeutic doses of opioids in persons without
tolerance to opioids causes a discernible decline in all phases of
respiratory activity, with the extent of the decline dependent on the
administered dose.
• At the bedside, however, the most easily recognized abnormality in
cases of opioid overdose is a decline in respiratory rate culminating in
apnea. A respiratory rate of 12 breaths per minute or less in a patient
who is not in physiologic sleep strongly suggests acute opioid
intoxication, particularly when accompanied by meiosis or stupor.
• Miosis alone is insufficient to infer the diagnosis of opioid intoxication.
Polysubstance ingestions may produce normally reactive or mydriatic
pupils, as can poisoning from meperidine, propoxyphene, or
tramadol. Conversely, overdose from antipsychotic drugs,
anticonvulsant agents, ethanol, and other sedative hypnotic agents
can cause miosis and coma, but the respiratory depression that
defines opioid toxicity is usually absent

15. Stupor or coma
Flaccidity
Shallow
breathing
Cyanosis
Pinpoint pupil
Fall in b.p . And
shock
Convulsions
Pulmonary edema
Death due to
respiratory failure.

17. Urine sample
10 ml
Negative
Positive Urine hydrolysis
Urine extraction for
solid or liquid
phase
Opiate confirmation
TLC/GC/HPLC
CONFIRMED
CONFIRMED
Morphine

18. Naloxone therapy MOA: Modulate the release of catecholamines.
Plasma E, NE, DA concentrations are increased.
Dose : 0.4-0.8 mg i.v. every 2-3 minutes (maximum 10 mg)
antagonizes all actions of morphine. Respiration is stimulated.
Pediatric dose: 0.1-2 mg iv/im depending on the weight. Interaction :
decrease analgesic activity of narcotics.
Use : To reverse respiratory depression. Diagnosis of opioid
dependence-ppt withdrawal sym. Reverse alcohol intoxication. Elevates
bp in endotoxic/hypovolemic shock, stroke, spinal injury.

19. Nalmefene MOA :
Competitive antagonist of
opioid receptor sites
resp. depression, sedation,
hypotension.
Dose : 0.5 mg/70 kg iv/ im
and repeat with 1 mg/70 kg
in 2-5 min.
Pediatric : 0.25 mcg/kg/ iv
or im .

20. Determine is airway
and circulation is intact.
volume should be 10-15
ml/kg.
01
GUT DECONTAMINATION :
Activated charcoal (not
in tramadol overdose)
lavage with endotracheal
intubation is safer than
induced emesis. Iv infusion
naloxone is administered.
02
ANTEDOTE : Naloxone 0.4-
mg i.v. (1-5 ampules)
repeated every few
Max: 10 mg. Child 0.01-
mg/kg 4-8 mg is added to
dextrose in water infused
100ml/hr(0.4-0.8 mg
naloxone)
03

21. • Airway maintenance for ADEQUATE RESPIRATORY
VENTILATION , O2 source.
• Supportive care to maintain FLUID AND ELECTROLYTE
BALANCE.
• Patients with atropinism or CNS depression-admitted in
hospital For urinary retention, catheterization required.
• IC MONITORISING THE: Vital Signs Fluid Balance Level Of
Consciousness Pupil Size Arterial Blood Gases , must be
recorded continuously to guide and status and response to
naloxone administration. Should not be discharged until
respiratory rate and depth, state of consciousness CV and
pulmonary examination should indicate normal function.

22. • Arsenic poisoning, or arsenicosisis a medical condition that
occurs due to elevated levels of arsenic in the body.
• Arsenic is a type of carcinogen that’s gray, silver, or white in
color.
• it doesn’t have any taste or odor.
• arsenic is naturally occurring
• it also comes in inorganic (or “man-made”) formulas.
• used in agriculture, mining, and manufacturing

23. Symptoms of arsenic poisoning are:
• red or swollen skin
• skin changes, such as new warts or lesions
• abdominal pain
• nausea and vomiting
• diarrhea
• abnormal heart rhythm
• muscle cramps
• tingling of fingers and toes

24. Contaminated groundwater is the most common cause of
arsenic poisoning. Arsenic is already present in the earth
and can seep into groundwater. Also, groundwater can
contain runoff from industrial plants. Drinking arsenic-laden
water over a long period of time can lead to poisoning.
Other possible causes of arsenic poisoning can include:
• breathing air that contains arsenic
• smoking tobacco products
• breathing contaminated air from plants or mines that use
arsenic
• living near industrialized areas
• eating arsenic-contaminated food —some seafood and
animal products may contain small levels of arsenic

25. Long-term exposure to arsenic can cause cancer.
The most common types of arsenic-related cancers are
associated with the:
• bladder
• blood
• digestive system
• liver
• lungs
• lymphatic system
• kidneys
• prostate
• skin

26. MECHANISM DEPENDS ON THE TARGET:
• Arsenic-induced cardiovascular dysfunction
• Arsenic-induced diabetes mellitus
• Arsenite-induced neurotoxicity
• Arsenic-induced nephrotoxicity and hepatotoxicity
• Arsenic-induced carcinogenicity

27. • ROS generated during arsenite exposure increases the
expression of atherosclerosis related genes such as heme
oxygenase-1 (HO-1), monocyte chemo-attractant protein (MCP-1),
and interleukin-6 (IL-6) and thus its exposure promotes the
attachment, penetration, and migration of monocytes in VSMC.
• Chronic exposure to arsenic induces oxidative stress and alters
the release of vasoactive mediators in blood vessel leading to
elevation of blood pressure.
• Taken together, it may be suggested that arsenic induces
cardiovascular dysfunction by inducing high oxidative stress,
reducing the activation of eNOS and enhancing the
phosphorylation of MLCK, which may be targeted for preventing
arsenic exposure-associated cardiovascular complications

29. • Brain is a soft target for arsenic toxicity as it freely crosses
blood-brain barrier.
• The deficiency of thiamine (vitamin B1) is well known to
induce neuronal complications. It is worthwhile to note that
arsenic causes thiamine deficiency and inhibits pyruvate
decarboxylase, which elevates blood pyruvate and hence
causes encephalopathy.
• The chronic arsenic exposure is associated with
morphological changes in axons and nerve fibers of the
striatum which disturbs central structural organization.
Hence, oxidative stress, induction of thiamine deficiency,
and inhibitions of pyruvate decarboxylase, acetyl
cholinesterase, reduction in biogenic monoamines seem to
play a pivotal role in arsenic-induced neurotoxicity

31. • Chelation:-
Dimercaprol and dimercaptosuccinic acid are chelating
agents that sequester the arsenic away from blood
proteins and are used in treating acute arsenic poisoning.
The most important side effect is hypertension.
Dimercaprol is considerably more toxic than
succimer. DMSA monoesters, e.g. MiADMSA, are
promising antidotes for arsenic poisoning.

32. • Nutrition
Supplemental potassium decreases the risk of
experiencing a life-threatening heart rhythm problem from
arsenic trioxide
• Vitamin E and selenium supplements have been used as
alternative remedies to limit the effects of arsenic
exposure.
• Gastric lavage
• Whole bowel irrigation with pollyethylene

33. • Insecticides - malathion, parathion, ethion,
diazinon
• Nerve gases - (sarin, woman, tabun - German
military used it for warfare), VX(invented by the
English for warfare)
• ophthalmic agents - echothiophate,
isoflurophate
• Herbicides - tributes [DEF], merphos
ORGANOPHOSPHATE POISONING
SOURCES

34. • Inhibition of carboxyl ester hydrolyses,
particularly acetylcholinesterase (AChE).
• AchE degrades Ach into choline and acetic acid
OP phosphorylates the serine hydroxyl group
• Once AChE has been inactivated, ACh
accumulates throughout the nervous system,
resulting in overstimulation of muscarinic and
nicotinic receptors
PATHOPHYSIOLOGY

35. Clinical effects are manifested via activation
of the autonomic and central nervous
systems and at nicotinic receptors on
skeletal muscle.
MECHANISM

36. • Organophosphates can be absorbed cutaneously,
ingested, inhaled, or injected.
• Although most patients rapidly become symptomatic, the
onset and severity of symptoms depend on the specific
compound, amount, route of exposure, and rate of
metabolic degradation
MODE OF TRANSMISSION

37. MUSCARINIC EFFECTS
NICOTINIC EFFECT
CNS EFFECTS
CLINICAL SYMPTOMS AND SIGNS

38. • SLUDGE (salivation, lacrimation, urination, diarrhea, GI
upset, emesis)
• DUMBELS (diaphoresis and diarrhea; urination;
miosis; bradycardia, bronchospasm, bronchorrhea;
emesis; excess lacrimation; and salivation)
MUSCARINIC EFFECTS

39. • muscle fasciculations, cramping, weakness, and
diaphragmatic failure.
• Autonomic nicotinic effects include hypertension,
tachycardia, mydriasis, and pallor
NICOTINIC EFFECTS

40. Anxiety, Emotional lability, Restlessness,
Confusion, Ataxia, Tremors, Seizures, Coma,
impaired memory, lethargy, psychosis
Respiratory paralysis
CNS EFFECTS

41. Remove clothing and cleanse patient with soap and
water - OPs hydrolyze easily in aqueous soon with
high pH
Discard clothing properly - hazardous waste!
Protect yourself- OPs penetrate latex and vinyl
gloves; use neoprene gloves and gowns!
Irrigate the eyes of patients with ocular exposure
using isotonic sodium chloride solution or lactated
Ringer’s solution
TREATMENT

42. LEAD POISONING

43. Pb + essential SH-groups of certain enzymes
Increase in permeability
Potassium leakage

44. INORGANIC Pb exposure:- Abd. Colic
obstinate constipation
loss of appetite
blue lines on gums
stippling of red cells
anaemia
wrist drop
foot drop

45. Organic Pb compounds:- (toxic effect mainly on CNS)
Insomnia
Headache
Mental confusion
Delirium etc..

46. History
Clinical features
Laboratory diagnosis
a)Coproporphyrin in urine(CPU)
Normal- <150µg/L
b)Amino levulinic acid in urine(ALAU)
>5mg/L

47. c)Pb in blood and urine
(In urine Nl is 0.2-0.8mg)
In urine- >0.8mg/L
In blood- >70µg/100ml
Indicates
Pb absorption
d)Basophilic stippling of RBC

48. a) To prevent further absorption
b) To remove lead from soft tissues
c) To prevent recurrence
• TREATMENT
 Saline purge (remove lead from the gut)
 d-penicillamine(promote Pb excretion in urine)
Aim

49. a)Substitution
Pb compounds should be substituted by less toxic
materials.
b)Isolation
Pb dust or fumes should be enclosed and segregated
c)Local exhaust ventillation
To remove dust & fumes