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Y3R2 - Toxicology ☠️ > L14: Lead > Flashcards

L14: Lead Flashcards

1
Q

Sources of Lead

A
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2
Q

toxic compounds of Lead

A
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2
Q

Mode of poisoninig by Lead

A
  • Mostly accidental
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2
Q

Absorbtion of Lead

A
  • Lead is absorbed through GIT, respiratory tract and skin.
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3
Q

what increases/decreases Lead absorbtion?

A

Increased by
- Iron deficiency
- Low dietary calcium

Decreased by
- co-ingestion with food

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3
Q

Distribution of Lead

A
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4
Q

Metabolism of Lead

A

Lead metabolism is typically as Ca metabolism

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4
Q

what increases Deposition of lead in bone?

A
  • Alkalis as K citrate, Na citrate
  • Ca rich diet and Vitamin D
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5
Q

Execretion of Lead

A
  • It is mainly excreted through urine (70%).
  • Smaller amounts are eliminated via feces and scant amounts via the hair, nails and sweat.
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6
Q

what increases Mobilization of lead from bone?

A
  • Acids as NH3 chloride
  • lodides
  • Chelators
  • Parathormone.
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7
Q

Mechanism of Toxicity by Lead

A
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7
Q

Types of Lead toxicity

A
  • Acute Poisoning
  • Chronic Poisoning
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8
Q

Incidence of Acute Lead Poisoning

A

relatively uncommon

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9
Q

CP of Acute Lead Poisoning

A
  • Local (GIT)
  • Remote (CNS, Blood & Renal)
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9
Q

Remote effects of Acute Lead Poisoning

A

CNS
- Headache, lethargy, insomnia, paresthesia.

  • Lead encephalopathy: It is commonly preceded by several weeks of prodromal complaints, Including irritability, headache and sleep disturbance, Encephalopathy characterized by Ataxia, seizures, delirium, stupor and coma.

Toxic hepatitis

Haemolytic angemia.

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10
Q

Local effects of Acute Lead Poisoning

A
  • Metallic taste
  • Dry throat, thirst
  • Nausea, vomiting, cramping abdominal pain
  • Constipation.
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11
Q

Effects of Chronic Lead Exposure

A
  • Low levels may be associated with subslinical effects as Impairment of visualmotor dexterity, reaction time Slowing of motor nerve conduction velocity.
  • But Higher levels Cause chronic poisoning
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12
Q

Facial pallor in Chronic Lead Poisoning

A
  • Earliest sign around the mouth,
  • Due to vasospasm and produced by contraction of capillaries at arterial side.
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12
Q

CP of Chronic Lead Poisoning

A
  • Facial pallor
  • Hematological effect
  • GIT
  • Neurological effect
  • Reproductive system effects
  • Effects on the eye
  • CVS effects
  • Renal effects
  • Bones
  • Carcinogenic effect
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13
Q

Hematological effects in Chronic Lead Poisoning

A
  • Hypochromic anemia with normocytic or microcytic indices.
  • Reticulocytosis due to anemia
  • Punctuate basophilia (basophilic stippling of erythrocytes): early sign as consequences of lead-induced inhibition of pyrimidine-5 nucleotidase or cellular ribonucleases.
14
Q

GIT effects in Chronic Lead Poisoning

A
  • Burton’s/Burtonian (lead line)
  • Colic
  • constipation
15
Q

Burton’s/burtonian (lead line)

  • Incidence
A

50-70% cases

16
Q

Burton’s/burtonian (lead line)

  • Description
A
  • A stippled blue line on gingival surface due to subepithelial deposit of granules at junction of teeth, especially near dirty or carious teeth.
17
Q

Burton’s/burtonian (lead line)

  • Causes
A
  • Due to formation of lead sulphide (reaction of circulating leadt sulfur ions released by oral microbial activity) especially near dirty or carious teeth.
  • Seen in poisoning with copper, iron.
18
Q

Burton’s/burtonian (lead line)

  • Specifity
A

Not specific, Seen in poisoning with copper, iron.

19
Q

Incidence of colic in patients with Chronic Lead Toxicity

A

85% cases

19
Q

Characters of colic in patients with Chronic Lead Toxicity

A
  • The pain is spasmodic, paroxysmal, occurs at night may be very severe.
  • Pain is slightly relieved by application of pressure over abdomen.
20
Q

Neurological effects of Chronic Lead Toxicity

A
  • Deficits in cognitive function
  • Irritability, fatigue, headache, sleep disturbance and depressed mood
  • Lead palsy (peripheral neuropathy, Mainly Motor)
  • Lead. encephalopathy
21
Q

Deficts in cognitive functions in Chronic Lead Toxicity

A

IQ decreased and attention impairment especially in Children

22
Q

Local encephalopathy in Chronic Lead Toxicity

A

Symptoms include

  • Changes in personality
  • Restlessness, hyperkinetic and aggressive behavior disorders
  • Mental dullness,
  • Learning disorders
  • Refusal to play
  • Headache and insomnia.
22
Q

Lead palsy in Chronic Lead Toxicity

A
  • a late and uncommon phenomenon
  • There may be tremors and cramps before the actual muscle weakness.
  • Later the extensor muscles of wrist (Wrist drop) and anterior tibial muscles (foot drop) are affected.
  • it may occur in male adults” workers exposed chronically to high lead levels.
22
Q

Reproductive system effects of Chronic Lead Toxicity

A
23
Q

Effects of Chronic Lead Toxicity on eyes

A
  • Optic atrophy in severely intoxicated patients.
  • Retinal stippling noticed by ophthalmoscope with grayish glistening lead particles, in early phase of chronic lead poisoning.
24
Q

CVS effects of Chronic Lead Toxicity

A

Hypertension (vasoconstriction)

24
Q

Renal effects of Chronic Lead Toxicity

A
  • Interstitial nephritis.
  • Renal insufficiency.
  • Decreased renal clearance of uric acid.
  • Fanconi-like syndrome (aminoaciduria, glucosuria, hypophosphatemia, hyperphosphaturia).
25
Q

Carcinogenic effects of Chronic Lead Toxicity

A
  • Lead is considered a probable human carcinogen.
  • Clinical presentation of lead toxicity (listed in approximate order of appearance).
25
Q

Bones affection in Chronic Lead Toxicity

A

Lead osteopathy in children and young adults,

  • It is deposited beyond the epiphysis of growing long bones leading to abnormal development.
26
Q

why are children more susceptible to Chronic Lead Toxicity?

A
27
Q

Dx of Chronic Lead Toxicity

A

Depends on
- History of exposure
- Blood lead level.

28
Q

Investigations for Chronic Lead Toxicity

A
29
Q

Emergency TTT of Lead Toxicity

A
  • Maintain airway, breathing and circulation.
  • Provide adequate fluids to maintain urine flow.
29
Q

Decontamination in Lead Toxicity

A
  • Remove the patient from the sourco of exposuro.
  • Gastric lavage and whole bowel irrigation.
  • For Lead-containing shots, shrapnel, or bullets in or adjacent to a synovial space or CSF, should be surgically removed if possible.
30
Q

Antidotes in Lead Toxicity

A
  • Edetate calcium disodium (CaNa2EDTA)
  • BAL (British Anti-Lewisite, dimercaprol)
  • Succimer (dimercaptosuccinic acid DMSA)
  • Antidoes for asymptomatic patients
31
Q

Edetate calcium disodium (CaNa2EDTA)

A
  • As 30 mg/kg/day in 4-6 divided doses or as a continuous infusion for 5 days.
  • Prolonged dosing has risk of nephrotoxicity.
32
Q

BAL (British Anti-Lewisite, dimercaprol)

A
  • An oily solution.
  • The most effective in preventing renal damage if administrated within 4 hours after acute ingestion of lead salts.
  • Dose 3-5 mg/kg IM every 4-6 hours for 3 days.
  • Side effects: HTN, nausea, vomiting, headache, pain at the injection sites, priapism and convulsions.
33
Q

Succimer (dimercaptosuccinic acid DMSA)
oral, IM, IV

A

In severe acute poisoning
- 3-5 mg/kg every 4 hours by IV infusion over 20 min in the first day then continue orally

In chronic poisoning
- 10 mg/kg orally every 8 h for 5 days, Every 12 h for 2 weeks.

34
Q

Antidotes (Chelation Therapy) For asymptomatic patients

A
  • Children with blood lead concentration ≥ 45 ug/dl or Adults > 80-100 ug /dl
  • Administer oral succimer.
  • There is no consensus regarding the value of chelation at lower levels.
34
Q

Enhanced Elimination in lead toxicity

A

There is no role for enhanced elimination of lead.

35
Q

Symptomatic TTT in Lead Toxicity

A

Y3R2 - Toxicology ☠️ (15 decks)

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