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Path SJSM > Radon/CO/Lead poisoning > Flashcards

Radon/CO/Lead poisoning Flashcards

1
Q

Radon is a byproduct of uranium that usually accumulates in which 2 areas of high exposure?

A

Soil & Basements

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2
Q

Describe how radon leads to DNA damage in lung cancer

A

The byproducts of radon decay are alpha-emitters which cause irritation to the respiratory epithelial cells and DNA damage.

Note if a patient presents with lung cancer before 40yrs of age & they’ve never smoked suspect RADON poisoning!!!

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3
Q

If a patient under 40yrs old presents with lung cancer & they’ve never smoked &/or had little/no secondhand smoke exposure what causal agent should you expect?

A

Radon Poisoning

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4
Q

Poisoning:

  • Burton’s lines (lead-lines on gingivae & metaphysis of long bones)
  • Encephalopathy
  • Erythrocyte basophilic stippling
  • Abdominal colic
  • Sideroblastic anemia
  • Wrist/foot drop

What’s the poisoning?

A

Lead poisoning

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5
Q

Poisoning:

Describe some of the signs of lead poisoning

A
  • Burton’s lines (lead-lines on gingivae & metaphysis of long bones)
  • Encephalopathy
  • Erythrocyte basophilic stippling
  • Abdominal colic
  • Sideroblastic anemia
  • Wrist/foot drop
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6
Q

Describe how exposure to high levels of lead leads to lead poisoning

A

Lead has a high affinity for sulfhydryl groups, disrupts heme synthesis in the bone marrow erythroblasts by inhibiting gamma

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7
Q

Poisoning:

Labs:
Normal PaO2
Left shift on the O2-Hb curve

A

CO poisoning, a non-irritating, colorless, & odorless gas that can come from motor exhaust, gas furnaces, & fires

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8
Q

Describe the pathophysiology about how CO causes extreme tissue hypoxia

A

Carbon monoxide (CO) is able to bind to hemoglobin (Hb) 200 times more strongly than oxygen, which means that it “steals” Hb and combines with it to form carboxyhemoglobin.

This disrupts aerobic metabolism & lipid peroxidation by inhibiting complex IV in the ETC (aka cytochrome C)

Because of the way carboxyhemoglobin affects the way cells use oxygen, it makes it harder for supplemental oxygen to help.

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9
Q

Which 2 tissues within the hypothalamus are most sensitive to the effects of CO poisoning?

A

Basal ganglia & Lenticular nuclei

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10
Q

Poisoning:

Headaches
Cherry red skin
Vomiting
Confusion
Coma (within 5 mins)
Visual disturbances
Short term memory loss

What’s the condition?

A

CO poisoning

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11
Q

Describe the neurological sequelae of CO poisoning (aka long term neuro effects)

A

Motor disturbances
Peripheral neuropathy
Hearing loss
Vestibular abnormalities
Dementia
Psychosis

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12
Q

What is considered criteria for a poor prognosis for a person suffering from CO poisoning?

A

They’re older than 35yrs
They had CO exposure for over 24hrs
They have acidosis or are unconscious
Cardiorespiratory arrest

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13
Q

Cherry red skin & mucus membranes are associated with what condition

A

Acute exposure to CO poisoning because CO is accumulated in the superficial capillaries

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14
Q

For long term survivors of CO poisoning tend to have neurophysiological sequelae

A

Motor disturbances
Peripheral neuropathy
hearing loss
Vestibular abnormalities
Dementia
Psychosis

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15
Q

Sources of lead poisoning

A

Lead paint chips
Corrosion of lead poisoning
Folk medicines (azarcon & greta)

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16
Q

Are children or adults more at risk of lead poisoning

A

Children absorb 45-50% lead

17
Q

What is a major risk of lead poisoning in pregnant women

A

Lead can be distributed in the blood through RBCs which can cross the placenta to affect the fetus

18
Q

What is the order or lead excretion

A

urine > poop >hair, nails, sweat

19
Q

Describe why patients chronic lead exposure may still experience side effects years-month later on

A

Distribution of lead from bones (up to 30YRS) into soft tissue can increase blood levels o lead for months to years after the source of contamination is removed

20
Q

Describe the pathophysiology of lead exposure on the body in heme synthesis

A

It inhibits Delta-aminolaevulinic acid dehydratase & ferrochetalase to ignore heme synthesis

21
Q

Describe the pathophysiology of lead exposure on the body in bones

A

It competes with Ca to deposit in bones and mess with metaphyseal & primary bone trabeculae in the epiphysis (aka lead stores on growth plates & increase bone densities.

22
Q

Describe the pathophysiology of lead exposure on the body in renal function

A

Lead can cause proximal tubule damage associated with intranuclear lead inclusions & protein aggregates which can lead to chronic renal damage (Interstitial & Renal failure)

23
Q

Labs:

Accumulation of urine coproporphyrin indicates what type of poisoning?

A

It indicates lead poisoning because it interferes with Delta-aminolaevulinic acid dehydratase

24
Q
  • Wrist drop (radial neuropathy due to elevated coproporphyrin)
  • Nausea/clumsy
  • Abdominal pain
  • Ringed sideroblasts (inhibited ferrochetalase)
  • Stippled RBCs
  • Microcytic & hypochromic anemia
  • Gingival lead lines (burtons)
  • Dense metaphyseal bands on long bones (burtons)
A

Lead poisoning

25
Q

What are sources of arsenic poisoning

A

Soil
Water
Wood preservatives
Herbicides
Mines
Smelting ind

26
Q

What are the 3 most toxic forms of arsenic?

A

Arsenic trioxide
Sodium arsenite
Aresenic trichloride

27
Q

Describe the pathophysiology of arsenic poisoning

A

It interferes with mitochondrial oxidative phosphorylation because it replaces 3 phosphate groups in ATP to inhibit enzyme activity and inhibits pyruvate dehydrogenase both causing apoptosis

28
Q

Describe neurological symptoms of arsenic poisoning

A

happens 2-8 weeks after exposure:
- Paresthesia
- Numbness
- Pain

29
Q

Describe the effects of chronic arsenic exposure

A
  • Hyperpigmentation (arsenic binds keratin & increases cell prolif)
  • Hyperkeratosis (Hands)
  • Patchy hair loss
  • Increase cancer risk
30
Q

Describe the high cancers seen in arsenic poisoning

A

Defective nucleotide excision repair:
- Squamous cell carcinoma
- Basal cell carcinoma
- Bowens disease

31
Q

Describe Bowens disease

A

Painless ulcers on the palms
Precancerous squamous cell carcinoma
Meese lines (nails)

Suspect HPV (if sexually promiscuous) or arsenic

32
Q

Describe the features of Cadmium toxicity

A

It’s toxic to the kidney & lung epithelium causing alveolar necrosis (Obstructive lung disease) & proximal tubular necrosis (Chronic renal disease)

Presents with flu symptoms (fever, weakness, chills) osteomalacia, & osteoporosis

33
Q

List some sources of Cadmium

A

Mining
Electroplating
Nickel-Cadmium battery factories
Soil
Plants/fertilizers
Ceramic food containers

34
Q

Which 2 conditions does cadmium toxicity lead to?

A

Obstructive lung disease & Chronic renal disease

35
Q

Acute exposure to Cadmium causes

A

flu-like symptoms (weakness, fever, headache, chills, sweating, & muscular pain)

36
Q

Long term exposure to cadmium can lead to

A
  • Lung cancer or obstruction
  • Kidney damage or chronic kidney disease
  • Pulmonary emphysema
  • Bone disease (osteomalacia & osteoporosis)
37
Q

93) A 52-year-old man visited ER complaining of coughing, shortness of breath and brown
expectorant for past 3 months. He works as a security guard and lives in the basement of
house, downtown, Chicago for the past 15 years. He smokes occasionally and social drinker. CT
scan showed mass in the right bronchus. Biopsy from the mass confirmed Squamous Cell
Carcinoma. Most likely risk factor for developing the cancer in this patient is due to.
A) Legionella pneumophila
B) Air pollution
C) Cigarette smoking
D) Arsenic toxicity
E) Radon

A

E) Radon

38
Q
A

Path SJSM (26 decks)

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