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SD IV: Block 3 Week 2 > Environmental Disorders 02 - Metals and Air pollutants > Flashcards

Environmental Disorders 02 - Metals and Air pollutants Flashcards

1
Q

What is the treatment for CO poisoning?

A

O2 via tight fitting mask or endotracheal tube (100% O2), hyperbaric oxygen chamber

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2
Q

How would you diagnose someone of chronic CO poisoning?

A

measure carboxyhemoglobin levels in the blood

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3
Q

Radon exposure can lead to what cancer?

A

lung cancer in uranium miners

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4
Q

How can one expose themselves to radon?

A

indoor air: produced when naturally occurring uranium in soil and water decays, is odorless, tasteless and invisible. It is present indoors and#out, in all types of buildings, and radon levels vary geographically from location to location

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5
Q

What is formaldehyde used for?

A

manufacture of building materials (cabinetry, furniture, adhesives)

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6
Q

Is formaldehyde a carcinogen for only humans?

A

classified as a carcinogen for humans and animals

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7
Q

What is sick building syndrome?

A

Exposure to one or more indoor pollutants, possibly poor ventilation

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8
Q

CDC measures lead poisoning to what amount?

A

> 5ug/dL

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9
Q

When is treatment for lead poisoning in children mandated?

A

≥ 45 ug/dL

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10
Q

What are some clinical findings evidenced upon examination of children with led poisoning?

A

encephalopathy

growth retardation: lead is deposited in the ephiphysis of growing bone

Lead “colic in GI

Kidneys: Chronic renal damage leads to interstitial fibrosis/renal failure, decrease in uric acid excretion leads to gout (“saturnine gout”)

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11
Q

How is a child prone to developing encephalopathy when they have lead poisoning?

A

There is higher intestinal absorption and the more permeable blood-brain barrier of children creates a high susceptibility to brain damage

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12
Q

What are the clinical findings evidenced in adults who have lead poisoning?

A

Peripheral neuropathy : foot drop (peroneal nerve palsy), wrist drop (radial nerve palsy), and claw hand (ulnar nerve palsy)

lead line in gums - usu. in adults with preexisting gingivitis

Lead “colic in GI

Kidneys: Chronic renal damage leads to interstitial fibrosis/renal failure, decrease in uric acid excretion leads to gout (“saturnine gout”)

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13
Q

What may you find in a blood smear of those with lead poisoning?

A

Sideroblastic anemia - microcytic, hypochromic RBCs with punctate basophilia on peripheral smear, ring sideroblasts on bone marrow

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14
Q

What is the pathogenesis of sideroblastic anemia?

A
  • inhibition of Ferrochelatase (Iron cannot bind with protoporphyrin to form heme, FEP proximal to the enzyme block is increased) - iron accumulates in the erythroblasts (sideroblasts)
  • inhibition of Ribonuclease: Ribosomes cannot be degraded and persist in the RBC, results in coarse basophilic stippling
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15
Q

What are tests that can be performed to determine if one has lead poisoning?

A
  • Increased whole blood and urine lead levels
  • Increase in free or zinc-bound red cell protoporphyrin
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16
Q

Treatment for lead poisoning?

A

Chelation therapy
* Succimer
* Dimercaprol
* Ethylene Diamine Tetra Acetic acid (EDTA)

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17
Q

Minamata disease?

A

Disease caused by mercury poisoining through consumed fish containing methyl mercury

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18
Q

How does Mercury poisoning occur in general?

A

mercury binds to sulfhydryl groups in certain proteins with high affinity, leading to damage in the CNS and kidney

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19
Q

Where is arsenic typically found?

A

– Naturally found in soil and water
– Used in wood preservers, herbicides

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20
Q

What is the best treatment for acute promyelocytic leukemia?

A

A-ll Trans Retinoic Acid + Arsenic Trioxide is used in treatment for acute promyelocytic leukemia

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21
Q

What is this condition and what can it be seen in?

A

Mees lines can be seen in thallium and arsenic poisoning

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22
Q

Chronic exposure to arsenic can present as what? (What are the clinical features?)

A

– Skin changes: hyperpigmentation, hyperkeratosis
– Mees lines: transverse bands in nails
– ↑ risk for cancers of lungs, bladder and skin
– Arsenic induced skin tumors - multiple, usually on palms and soles (differ from the sunlight
induced skin cancers)
– Non-malignant respiratory disease

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23
Q

What is the best treatment for arsenic toxicity?

A

chelating agents: Succimer or dimercaprol

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24
Q

What is cadmium toxic to in the body the most?

A

kidneys and lungs mostly

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25
Q

What are some clinical features of Cadmium toxicity?

A
  • Obstructive lung disease , ↑risk of lung cancer
  • Renal tubular damage progressing to end-stage renal disease
  • Skeletal abnormalities associated with calcium loss
  • Itai-Itai (ouch-ouch): Cadmium-containing water used to irrigate rice fields in Japan lead to osteoporosis and osteomalacia in post-menopausal women, associated with renal disease
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26
Q

Where is benzene found and what can this toxicity in the body lead to? (Explain pathogenesis as well.)

A

occupational exposure of rubber worker, oxidized by hepatic CYP2E1 to toxic metabolites, leading to dose-dependent marrow aplasia and inc. risk of AML

27
Q

Where can one get polycyclic hydrocarbon toxicity and what complications can result from it?

A

combustion of fossil fuels (in steel foundries), present in tar and soot.

Lung and Bladder cancer

28
Q

Where can one get vinyl chloride toxicity and what complications can result from it?

A

(synthesis of polyvinyl resins)

angiosarcoma of the liver

29
Q

Where can one get bisphenol A toxicity and what complications can it lead to?

A

(polycarbonate food and water containers, epoxy resins that line food bottles and cans)

potential endocrine disruptor in children

heart disease in adult populations

30
Q

Where can one get organochlorine toxicity?

A

pesticides: DDT, lindane, aldrin

Non-pesticides: PCBs and Dioxin

31
Q

What are some complications of organochlorine toxicity? (MOA needs to be explained as well)

A
  • Dioxins and PCBs : Skin disorders (folliculitis, chloracne), Liver and CNS toxicity
    – PCBs induce CYPs leading to abnormal drug metabolism
32
Q

What is the treatment for organophosphate poisoning?

A

atropine; pralidoxime

33
Q

What are some important lab findings to consider when you suspect organophosphate poisoining?

A

dec. serum and RBC cholinesterase levels

34
Q

What are some sources that can predispose one to pneumoconioses?

A

coal dust (mining of hard coal)
Silica (sandblasting, stonecutting)
Asbestos (mining, fabrication, insulation work)

35
Q

What are sources of cyanide poisoining?

A

house fires
odor of bitter almonds

36
Q

What are treatment modalities for cyanide poisoining?

A

amyl nitrite followed by thiosulfate

37
Q

What is the treatment of choice in concurrent cyanide and CO poisoining (as in house fire)

A

infusion of hydroxycobalamin

38
Q

What is the best way to check lab values of those with cyanide poisoining?

A

Quick bedside or laboratory confirmatory test, and it remains a clinical diagnosis.

Fire victims with soot in their mouth, altered mental status, and metabolic acidosis with extremely high lactate levels suggest cyanide poisoning

39
Q

Smoke inhalation is a unique challenge because of what substances that the victim is exposed to?

A

CO and cyanide

40
Q

What are the drugs that are not recommended for CO poisoining because of adverse effects associated with them? What are the complications?

A
  • Amyl and sodium nitrites can cause methemoglobinemia and hypotension and therefore are not recommended if carbon monoxide poisoning is also suspected
41
Q

What is an advantage of using hydroxycobalamin in cases of cyanide and CO poisoining?

A

faster onset of action

42
Q

What is the formula for pack years?

A

(avg cigarette packs per day x number of years of smoking)

43
Q

What are some acute effects of smoking linked to nicotine use?

A

(↑HR, BP, cardiac contractility and output)

44
Q

What is the most important metabolite of nicotine? What is the best screening for nicotine users to test it?

A

Cotinine

Cotinine screening test for blood or urine is used to detect if a person is a nonsmoker

45
Q

What is a major noxious chemical in cigarette smoking?

A

Tar contains most of the carcinogenic agents in cig smoke

46
Q

What is an effective treatment for UC?

A

nicotine patch

47
Q

What can Ecigs cause?

A

EVALI

e-cigaratte, or vaping, product use associated lung injury

48
Q

What are complications of using smokeless tobacco/chewing tobacco?

A
  • Can cause nicotine addiction
  • ↑ risk of oral cancer
49
Q

What are the complication of passive (second-hand) smoke inhalation in adults and children?

A
  • In children
    – ↑risk of respiratory/middle ear infections in children
    – Exacerbates asthma
  • In adults
    – ↑risk for lung cancer and coronary artery disease
50
Q

How can smoking cause bronchitis?

A

Direct irritant effect on tracheobronchial mucosa, produces inflammation and↑ mucus production

51
Q

How can smoking cause emphysema?

A

Recruitment of leukocytes to the lung, with ↑ local elastase production and subsequent injury to lung tissue, leads to emphysema

52
Q

T/F. Polycyclic hydrocarbons and nitrosamines are potent carcinogens in smoking?

A

True

53
Q

The risk of developing complications of smoking is related to what?

A

number of pack years

54
Q

What is the laryngeal cancer of greatest concern with smokers?

A

squamous cell ca

55
Q

What are the lung cancers that are associated with smoking?

A

squamous cell carcinoma, small cell carcinoma, some types of adenocarcinoma

56
Q

T/F. There is a decreased risk of carcinogenic influence from asbestos in smokers?

A

F

57
Q

What are some CVS effects related to smoking?

A

– Acute myocardial infarction (atherosclerosis of coronary arteries)

  • Sudden cardiac death
  • peripheral vascular disease (atherosclerosis of femoral and popliteal arteries)
58
Q

What are some complications found in the GIT of smokers?

A

– ↑ risk for oropharyngeal cancer: squamous cell carcinoma
– ↑ risk for upper and mid-esophageal cancer: squamous cell carcinoma
– ↑ risk for stomach cancer: adenocarcinoma
– ↑ incidence of GERD : ↓ tone of lower esophageal sphincter
– ↑ risk for peptic ulcers and delayed healing of peptic ulcers
– ↑ risk for pancreatic cancer: adenocarcinoma

59
Q

What are major genitourinary complications of smoking?

A

– ↑ risk for cervical cancer: squamous cell carcinoma
– ↑ risk for urinary bladder cancer: transitional cell carcinoma

60
Q

What are some effect on fetus linked to maternal smoking?

A

– Low birth weight in newborns
– Intrauterine growth retardation

61
Q

What condition that affects the CNS is smoke related to?

A

stroke

62
Q

What are some MSK findings in those who smoke?

A

Osteoporosis, ↓ estrogen in females and ↓ free testosterone in males

63
Q

What hematopoietic condition is smoking linked to?

A

inc. risk for AML

SD IV: Block 3 Week 2 (8 decks)

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