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Mini II > Environmental Pathology 1 > Flashcards

Environmental Pathology 1 Flashcards

1
Q

which 2 cell types does ozone affect?

A

free radicals cause injury to:

1) epithelial cells
2) type I pneumocytes

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2
Q

ozone is more dangerous for patients with which conditions?

A

asthma or emphysema (causes upper respiratory inflammation)

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3
Q

sources of sulfur dioxide?

A

power plants and paper mills

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4
Q

sulfur dioxide gives what symptoms clinically?

A

burning sensation in throat. rise to bronchitis over time

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5
Q

what size of particulate matter is most harmful?

A

ultra fine particles (less than 10 micrometers)

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6
Q

what do ultra-fine particles of particular matter result in clinically?

A

Myocardial Ischemia!

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7
Q

what is the mechanism of action of particulate matter inducing symptoms clinically (i.e. asthma, irritation, MI?)

A

phagocytozed by macrophages and neutrophils in ALVEOLI –> releases macrophage, inflammatory protein 1a and ENDOTHELIN

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8
Q

what are the 2 main sources of CO?

A

1) incomplete oxidation of carbon materials (car engines, heating appliances)
2) chronic poisoning in individuals working in confined environments with high exposure to fumes (i.e. tunnels, underground garages)

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9
Q

pathophysiological effects of CO?

A

CO binds to Hb with 240 greater affinity than O2 binds. –> Cb-hb does not carry oxygen.

systemic asphyxia (CO kills by inducing CNS depression)

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10
Q

Acute CO poisoning results in what clinically?

A

Cherry Red color of skin and mucous membranes

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11
Q

Chronic CO poisoning results in what clinically?

A

carboxy-hb levels rise to life-threatening levels and cause widespread CNS ischemia

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12
Q

6 indoor air pollutants

A

1) Tobacco
2) wood smoke
3) radon
4) bio-aerosols
5) formaldehyde
6) sick bldg syndrome

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13
Q

What can Radon pollutant cause clinically?

A

Lung cancer in uranium miners (indirectly)

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14
Q

Where is formaldehyde often found? and what population does it pose most danger to?

A

manufacture of building materials (cabinetry, furniture)

Refugees from environmental disasters living in poorly ventilated trailers (i.e. Katrina 2005)

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15
Q

what are the main environmental, occupational and recreational causes of lead poisoning?

A

environmental:
1) lead containing house paints & gasoline
2) flaking lead paint in older homes and soil contamination
3) Pica (childhood craving) for eating lead-based paint

occupational:

1) mining, foundries
2) pottery painter
3) automobile factory (incinerate batteries!)

recreational:
glazed pottery making, painting

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16
Q

clinical features of lead exposure in children and adults

A

children: low intellectual capacity and behavioral problems (at subclinical levels)
adults: BLUE LINE on gums “lead lines”, CNS symptoms, anemia

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17
Q

Effects of lead exposure in the CNS (children & adults)

A

children –> encephalopathy

adults –> peripheral neuropathies

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18
Q

effects of lead exposure in bone

A

impaired remodeling of calcified cartilage in epiphyses of children. “lead lines” – impairs healing of fractures

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19
Q

What type of anemia results from lead poisoning?

A

Microcytic, hypochromic anemia.

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20
Q

what is the mechanism of heme deficiency in lead poisoning? (i.e. inhibition of what two enzymes in heme synthesis?)

A

1) gamma-aminolevulinic acid (ALA) dehydratase

2) Ferrochelatase (inhibition causes rise in PROTO-PORPHYRIN LEVELS)

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21
Q

Diagnosis of lead poisoning in children (and definitive diagnosis)

A

1) neurological and behavioral changes
2) unexplained anemia with BASOPHILIC STIPPLING IN RED CELLS

Definitive diagnosis = elevated blood lead levels & free (or zinc-bound) red cell “protoporphyrin”

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22
Q

Microscopic changes in BM and peripheral blood from lead poisoning

A

BM: RINGED SIDEROBLASTS (red cell precurors with iron-laden mitochondria)

Peripheral blood: microcytic, hypochromic anemia with basophilic stippling of red cells

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23
Q

microscopic changes in brain from lead poisoning

A

in children: Brain Edema
gama-ALA damages neurons and increases vessel permeability

in adults: peripheral demyelinating neuropathy
(wrist drop & foot drop)

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24
Q

how are the kidneys and GIT affected from lead poisoning?

A

kidneys – PCT damage with intra-nuclear lead inclusions. interstitial fibrosis which can lead to renal failure and gout.

GIT- lead colic

25
Q

inorganic mercury

A

mercury chloride

26
Q

organic mercury

A

methyl mercury

27
Q

sources and mechanism of mercury poisoning?

A

contaminated fish & vapors from dental amalgams

inorganic (mercury chloride) converted to organic (methyl mercury) by bacteria (usually from industrial sources) and gets concentrated in carnivorous fish.

28
Q

minamata disease

A

from mercury poisoning.

cerebral palsy, deafness, blindness, mental retardation and major CNS defects in children exposed in utero

29
Q

acute mercury exposure

A

bread made from grain with “methyl mercury based fungicide” (iraq 1971)

30
Q

2 main effects of mercury toxicity?

A

1) Nephrotoicity - Kidney = main target.
Acute = PCT necrosis
chronic = nephrotic syndrome with proteinuria

2) Neurotoxicity
clinical findings: constriction of visual fields, paresthesia, ataxia, dysarthria, hearing loss.
cerebellum- atrophy of granular layer. spongy softening in visual cortex

31
Q

common sources of arsenic poisoning?

A

wood preservers, herbicides

ground water used for drinking (bangladesh, chile, china)

32
Q

acute arsenic poisoning

A

sensorimotor neuropathy (parasthesia, numbness and pain) 2-8 weeks post exposure

GIT, CVS, CNS disturbances (interference with mitochondrial ox phos since trivalent arsenic can replace phosphates in adenosine triphosphate. causes vomiting, abd pain, and diarrhea)

33
Q

chronic arsenic poisoning (4 things)

A

1) increased risk of cancers (lung, liver-angiosarcoma, skin, GI)
2) skin changes:
i- hyperpigmentation & hyperkeratinosis
ii- basal and squamous cell carcinoma
3) nail changes “mees’ lines”
4) non-malignant resp. disease

34
Q

sources of cadmium poisoning

A

production of nickel-cadmium batteries, food, cigarette smokers (through inhalation), soil and plants via fertilizers

35
Q

toxic effects of excess cadmium (4 things)

A

1) obstructive lung disease (necrosis of alveolar macrophages)
2) kidney damage
3) skeletal abnormalities related to calcium loss “Itai Itai”(post-menopausal women, japan, osteoporosis and osteomalacia)
4) *increased risk of lung cancer!

36
Q

which 3 toxicants can cause lung cancer?

A

1) radon
2) asbestos,
3) arsenic

37
Q

health risks and uses of chloroform and carbon tetrachloride

A

found in dry cleaning agents and paint removers

CNS depression/coma
liver and kidney toxicity

38
Q

health risks and uses of Benzene

A

widely used in industrial processes

marrow aplasia (aplastic anemia) and acute myeloid leukemia

(oxidized by hepatic CYP2E1 to toxic metabolites)

39
Q

Health risk and uses of Ethylene glycol

A

used as anti-freeze and substitute for ethanol by alcoholics (+ adulterate wines)

toxicity = toxic within minutes due to “oxalic acid” metabolite. Results in metabolic acidosis, CNS depression, nausea, vomiting, hypocalcemia-related cardiotoxicity, renal failure

40
Q

health risks and uses of polycyclic hydrocarbons

A

uses: potent carcinogen (released during combustion of fossil fuels, etc)

LUNG AND BLADDER CANCER

41
Q

health risks and uses of methanol

A

used as substitute for ethanol

poisoning due to metabolism of formaldehyde and formic acid

42
Q

health risks and uses of organo-chlorines

A

uses: pesticides

anti-estrogenic or anti-androgenic activity

43
Q

health risks of Dioxins and Polychlorinated biphenyls (PCBs)

A

1) skin disorders (folliculitis and chloracne-dermatosis). around face and behind ears
2) Liver and CNS abnormalities

44
Q

health risks of mineral dusts

A

pneumoconiosis (from inhalation)– chronic, non-neoplastic lung disease.

(mineral dusts = coal, silica, asbestos, beryllium)

45
Q

Occupational exposure to asbestos linked to (4)

A

1) localized fibrous plaques
2) parenchymal interstial fibrosis (asbestosis)
3) lung carcinoma
4) Mesothelioma

46
Q

What are the 2 forms of asbestos?

A

1) amphibole

2) serpentine

47
Q

what are the differences between amphibole and serpentine asbestos?

A

Amphibole is less prevlanet and more pathogenic. Contains straight, stiff fibers that are delivered deep into lung tissues

serpentine is more flexible and less likely to be impacted in upper airways. More prevalent in industry but less carcinogenic

48
Q

What is the oncogenic effect of asbestos?

A

tumor initiator and promoter.

Increases LUNG carcinoma 5 fold (more common in smokers)

Increases Mesothelioma 1000 fold

49
Q

Gross characteristics of asbestos (3)

A

1) diffuse pulmonary interstitial fibrosis
2) pleural plaques
3) mesothelioma

50
Q

Microscopic characteristics of asbestos (3)

A

1) spindle cells or plump rounded cells
2) asbestos bodies – golden brown fusiform or beaded rods
3) ferruginous bodies– inorganic particles coated with iron-protein complexes

51
Q

vinyl chloride

A

leads to angiosarcoma of liver

52
Q

what are the 3 major toxicants that lead to lung cancer?

A

1) radon
2) asbestos
3) arsenic

53
Q

what are the 2 major toxicants that lead to fibrosis in lung?

A

1) silica

2) asbestos

54
Q

what are the 2 major toxicants that lead to hypersensitivity and irritation of lung?

A

1) beryllium

2) formaldehyde

55
Q

what are the 2 major toxicants that lead to Bladder cancer?

A

1) napthylamines

2) rubber products

56
Q

what toxicant leads to leukemia?

A

benzene

57
Q

what toxican leads to liver angiosarcoma?

A

vinyl chloride

58
Q

what indoor air pollutant is responsible for legionella pneumonia?

A

Bio-aerosols

Mini II (17 decks)

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