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Multisystems > Path- Environmental Pathology > Flashcards

Path- Environmental Pathology Flashcards

1
Q

What are the 6 air pollutants that have set National Ambient Air Quality Standards?
Which 2 are the most widespread health threats?

A
  1. particles
  2. ground-level ozone
  3. carbon monoxide
  4. lead
  5. sulfur dioxide
  6. nitrogen oxides

Particles and ground-level ozone are the most widespread health risks

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2
Q

What is particle pollution?

What size particles have the highest potential for causing health problems?

A

Particle pollution is a mixture of small particles [ injury.

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3
Q

Describe:

  1. inhalable coarse particles
  2. fine particles

in terms of where they are found and what size they are

A

Inhalable coarse particles:

  • found near roadways and dusty industries
  • less than 10 but greater than 2.5 micrometers

Fine particles

  • smoke from forest fires, power plants, industries, cars
  • less than or equal to 2.5 micrometers
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4
Q

What is ground-level ozone?

A

Ozone in the trophosphere that is harmful [as opposed to ozone in the stratosphere which protects life on earth from the suns rays]

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5
Q

How does ground-level ozone form?

What is the seasonal preference?

A

Forms by a chemical reaction between nitrogen oxides and volatile organic compound in the presence of HEAT and SUNLIGHT
-motor vehicle exhaust, industrial emission, gasoline vapor, chemical solvents

  • Summertime air pollutant
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6
Q

What is the primary constituent of ground-level ozone?

How does this effect our health?

A

Smog is the major constituent.

03 produces free radicals that injure epithelial cell lining of the respiratory tract and type 1 alveolar cells causing:

  1. airway irritation, coughing, pain with deep breath
  2. wheezing during exercise or outdoor activity
  3. aggravation of asthma,
  4. increased risk for bronchitis, pneumonia
  5. permanent damage of lung after repeat exposure
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7
Q

What are the major sources of CO?

A
  1. car exhaust
  2. construction equipment/ boats
  3. industrial processing [metals and chemicals]
  4. wood burning [residential]
  5. natural wood burning [forest fires]
  6. wood stoves, gas stoves, smoking cigs, unvented space heaters
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8
Q

What is the seasonal preference for high levels of CO in outdoor air? Why?

A

Colder months because there are “inversion conditions” where air pollution gets trapped near the ground beneath a layer of warm air

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9
Q

How much greater is the Hb affinity for CO over O2?
What levels cause systemic hypoxia?
What levels can cause unconsciousness and death?

A

200x affinity for CO

20-30% CO –> systemic hypoxia
60-70% CO –> unconsciousness and death

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10
Q

What is the major effect of chronic CO poisoning [low levels but persistent exposure]?

A

Widespread hypoxic damage to the CNS

  • basal ganglia
  • lenticular nuclei
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11
Q

What are the major effects of acute CO poisioning [suicide, accidental exposure]?

A
  1. cherry-red color of skin and mucous membranes
  2. brain edema
  3. punctate hemorrhages
  4. neuronal death
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12
Q

Sulfur is present in which materials?
When are sulfur oxides formed?
Once sulfur oxide is released into the air, what 2 things can it form?

A

It is in crude oil, coal and ore.
SO2 is formed when fuel containing sulfur is burned [gas extraction from oil, metal extraction from ore]
-electric utilities, petroleum refinery, cement factory, metal processing plants, large ships

S02 can dissolve with:

  1. water –> sulfuric acid [acid rain]
  2. other gases –> sulfate particles

Both sulfuric acid and sulfate particles can cause respiratory problems esp in people with asthma

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13
Q

What is the normal appearance of Nitrogen oxides?

How does the appearance differ when it is NO2?

A

Nitrogen oxides are highly reactive gases that are ODORLESS and COLORLESS.

However, nitrogen dioxide along with particulates are reddish-brown layer over urban areas

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14
Q

When do nitrogen oxides form?

What are the man made sources?

A

When fuel is burned at high temperatures [as in combustion process].
-cars, electric utilities, industrial, commercial, residential sources of burn fuels

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15
Q

What are the 4 negative effects of nitrogen oxides?

A
  1. react with volatile organic compounds in the heat to make ground-level ozone
  2. react with other substances to form acids [acid rain]
  3. react with ammonia and moisture to form nitric acid that damages lungs and worsens emphysema and bronchitis
  4. react with organic chemicals and ozone to form nitrate radicals, nitroarenes and nitrosamines that can lead to cancer
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16
Q

What were the main sources of lead emissions historically?

What has changed?

A

Historically:

  1. cars and trucks
  2. industrial sources [metal processing]

Now metal processing is the major source over cars because the phasing out of leaded gasoline

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17
Q

What is the most widespread source of lead today for US children?

A

flaking lead paint from old buildings and soil contamination

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18
Q

Why are children at greater risk of lead toxicity?

A
  1. Children absorb over 50% of lead from contaminated food, and adults absorb only 15%
  2. the BBB is more permeable in children
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19
Q

When lead is absorbed from food, where does it distribute?

A
  1. 80-85% is taken up by bones and teeth [20-30yr T1/2]
  2. 5-10% stay in blood [1 month T1/2]
  3. remainder goes to soft tissue
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20
Q

What is the effect of lead on pregnancy?

A

Lead competes with calcium and binds phosphate in the bones.
When a woman is pregnant or lactating, this is a calcium stress and Lead is released into the blood where it can expose the fetus/infant.

  1. preterm labor
  2. spontaneous abortion
  3. low birth weight
  4. impaired brain development
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21
Q

What enzymes are inhibited by lead?

What is the clinical result of inhibiting these enzymes?

A
  1. enzymes with sulfhydryl groups in heme synthesis like aminolevulinic acid, ALA dehydratase, or ferrochelatase
    - results in MICROCYTIC, HYPOCHROMIC ANEMIA
  2. Na/K ATPase
    - results in HEMOLYTIC ANEMIA
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22
Q

What are the indicators of lead toxicity in the blood?

A

When ferrochelatase is inhibited there will be elevated blood:

  1. zinc protoporphyrin
  2. free RBC protoporphyrin
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23
Q

Lead affects every organ system, but what are the most notable?

A
  1. RBCs
  2. brain/peripheral nerves
  3. GI
  4. kidney
  5. skeleton
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24
Q

What is the most useful screening and diagnostic test for recent or ongoing lead exposure?

A

venous blood lead concentration {BLC}

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25
Q

What chelating agents are used for lead toxicity?

A
  1. Calcium disodium edetate
  2. dimercaprol
  3. D-penicillamine
  4. succimer
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26
Q 
What should be done at BLC levels:
1. below 10
2. 10-20
3, 20-44
4. 45-69
5 > 70 OR encephalopathy
A
  1. nothing
  2. retest every 3 months and if elevated:
    - follow guidelines or 20 to 44
    - lead education
    - if a lot of children have it, community poison prevention
  3. retest monthly, clinical eval and chelator of necessary, education, environment intervention
  4. clinical eval and chelators within 48hrs, retest monthly, education, environment intervention
  5. medical emergency, hospitalize and chelate immediately, education, intervention
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27
Q

Where does organic mercury [methylmercury] accumulate?

What does it cause in fetuses, infants and children?

A

It accumulates in fish, shellfish and animals that eat fish.

It can impair neurological development by accumulating in the brain and blocking ion channels

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28
Q

How does elemental mercury [metallic] get into the body?

What does it cause?

A

It is absorbed through the lungs and causes

A lot of neuro problems like:

  1. tremors
  2. emotional changes
  3. insomnia
  4. neuromuscular changes [weakness, atrophy]

At higher levels it can also involve renal failure, respiratory failure and death

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29
Q

How does inorganic mercury get into the body?

What does it cause?

A

It is absorbed in the GI tract and damages:

  1. GI tract
  2. nervous system
  3. kidneys

Skin rash, emotional changes, memory loss, cognitive disturbances, muscle weakness

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30
Q

Where is arsenic found?
What is the pathology?
What would you see with acute toxicity? Chronic?

A

It is in drinking water in Chile, Bangladesh and China
It interferes with mitochondrial oxidative phosphorylation

Acute:
GI, cardio, CNS–> death

Chronic:

  1. skin hyperpigmentation, hyperkeratosis
  2. SCC, BCC
  3. lung carcinoma
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31
Q

What are the 4 adverse effects of cadmium?

A
  1. obstructive lung disease
  2. renal tubular damage
  3. osteoporosis
  4. osteomalacia
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32
Q

What are the negative effects of benzene?

A
  1. aplastic anemia

2. AML

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33
Q

What are the negative effects of polycyclic hydrocarbons?

A
  • most potent carcinogens– found in cigarette smoke
    1. lung cancer
    2. bladder cancer
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34
Q

What are the negative effects of organochlorines?

A
  1. anti-estrogen

2. anti-androgen

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35
Q

What are the negative effects of dioxins, polychlorinated biphenyls?

A
  1. folliculitis

2. chloaracne - acne, cysts, hyperpigmentation, hyperkeratosis

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36
Q

What are the negative effects of vinyl chloride?

A

hepatic angiosarcoma

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37
Q

What are the negative effects of mineral dusts?

A
  1. pneumoconiosis

2. cancer [asbestos]

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38
Q

What is the mechanism of action of nicotine?

A

It is an alkaloid that binds receptors in the brain that lead to catecholamine release:

  1. increase d HR
  2. increased BP
  3. increased cardiac contractility

It is also responsible for addiction

39
Q

Cigarette smoke is responsible for 90% of lung cancers and multiplies the carcinogenic effects of what 2 things?

A
  1. ethanol - laryngeal cancer

2. asbestos/uranium - lung cancer

40
Q

What are the 6 chemical carginogens in cigarettes?

A
  1. polycyclic hydrocarbons - LUNG, oral cavity, larynx cancer
  2. Naphthylamine - bladder carcinoma
  3. Nitroso [NNN, NNK] -esophagus, pancreas, mouth
  4. polonium -210 = lead= mouth larynx, LUNG
  5. arsenic - skin, LUNG
  6. nickel, chromium- LUNG, nasal sinus
41
Q

What are the 3 ways constituents of cigarette smoke affect respiratory health?

A
  1. ciliatoxin - decreases tracheobronchial clearance
  2. Respiratory irritants [NO2, formaldehyde] induce submucousal gland hypertrophy, increase goblet cells
  3. ROS deplete antioxidants
42
Q

What are the 5 ways smoking negatively affects cardio health?

A
  1. increased platelet adhesion/aggregation
  2. decreased myocardial O2 supply b/c of lung problems
  3. increased cardio demand because of nicotine
  4. triggers arrhythmias
  5. Atherosclerosis, MI, stroke
43
Q

What does maternal smoking increase the risk of?

A
  1. spontaneous abortion
  2. placental abruption
  3. rupture of membranes
  4. placenta previa
  5. prematurity
  6. low birth weight
44
Q

What are people exposed to second hand smoke at an increased risk for?
Who is most at risk?
How can second hand smoke be estimated?

A

Increased risk for LUNG CANCER, and ISCHEMIC HEART DISEASE.

Infants and children are most at risk:

  1. SIDS
  2. respiratory/ear infections
  3. exacerbation of asthma

The second hand smoke can be estimated by:
measuring cotine [metabolite of nicotine]

45
Q

What are the 2 forms of excessive ethanol use?

A
  1. Heavy drinking
    - more than 2 drinks a day on average for men
    - more than 1 drink per day on average for women
  2. Binge drinking
    - more than 4 drinks on one occasion for men
    - more than 3 drinks on one occasion for women
46
Q

What is the legal limit to be considered drunk?
What is the limit for coma/death?
What can the BAC be up to in chronic alcholics?

A

Drunk is 0.08

Coma/death is above 0.3g/dL
Chronic alcoholic coma/death is up to 0.7g/dL

47
Q

What 3 things oxidize alcohol to acetaldehyde?

A

It is oxidized to acetaldehyde by:

  1. alcohol dehydrogenase [major]
  2. microsomal p450 [important at high BAC]
  3. peroxismal catalase
48
Q

What enzyme converts acetaldehyde to acetic acid in the metabolism of alcohol?
What happens if this enzyme is mutated [like in 50% of asians]?

A

Acetaldehyde dehydrogenase

If it is low activity, there will be flushing, tachycardia, hyperventilation

49
Q

What ratio promotes fatty acid synthesis and leads to hepatic steatosis in alcohol drinkers?

A

Alcohol dehydrogenase enzyme requires the conversion of NAD to NADH.
If the ratio of NADH to NAD is too high, this will inhibit FA oxidation and promote FA synthesis

50
Q

What is the negative effect of oxidation of ethanol by microsomal p450s?

A

ROS which cause membrane injury by lipid peroxidation

51
Q

What are the 3 major signs of acute ethanol toxicity?

A
  1. hepatic steatosis
  2. gastritis/gastric ulcers
  3. CNS depression –> respiratory arrest [occurs rapidly]
52
Q

What are the 6 major signs of chronic ethanol toxicity?

A
  1. AFLD- cirrhosis, hepatocellular carcinoma
  2. GI bleeds from gastric ulcers, esophageal varices [due to portal HTN]
  3. Thiamine deficiency
    - wet/dry beriberi, Wernickes, Korsokoff, etc
  4. Congestive cardiomyopathy
    - decreased HDL, increased atherosclerosis
  5. acute/chronic pancreatitis
  6. increased risk of cancer
    - oral, esophageal, hepatic, breast
53
Q

A baby is born with growth retardation, microcephaly, short palpebral fissures, maxillary hypoplasia, holoprosencephaly, atrial septal defect and genitourinary defects. What is the likely cause?

A

FAS

54
Q

What is a safe amount of alcohol to drink in pregnancy?

What trimester?

A

NONE EVER [but first trimester is particularly harmful]

55
Q

What signaling pathway is impaired in fetal alcohol syndrome?

A

hedgehog signaling involved in organogenesis and body patterning

56
Q

A patient presents with blurred vision, vomiting and seizures. Labs show a large anion gap metabolic acidosis and osmolar gap.
What is it likely that this man consumed?

A

Methanol - antifreeze/bad shine

57
Q

A man presents with anuria, vomiting seizures and is slipping into a coma. Labs show a metabolic acidosis with large anion gap and an osmolar gap. There are oxalate crystals in his urine. What did he consume?

A

ethylene glycol [antifreeze]

58
Q

A man presents with vomiting, hematemesis, melena. Despite all this, he has fruity breath. He has doesn’t have a metabolic acidosis with anion gap but he DOES have an osmolar gap. What is it likely he comsumed?

A

Isopropyl alcohol

59
Q

What 3 things are patients on hormone replacement therapy WITHOUT progestin at risk for?

A
  1. breast and ovarian cancer
  2. endometrial cancer [reduced/eliminated with progestin]
  3. DVT and thromboembolisms
60
Q

What 2 cancers do OCPs put patients at increased risk for?
What 2 cancers have DECREASED risk?
What cancer is not effected?

A

Increased risk for:

  1. hepatic adenoma
  2. cervical cancer

No risk for: breast cancer

Decreased risk for:

  1. endometrial
  2. ovarian
61
Q

How is acetaminophen metabolized?

What happens at toxic levels of Tylenol?

A

95% by glurcuronide or sulfate in the liver
5% by p450 –> NAPQ1

NAPQ1 is metabolized by glutathione in the liver, but if there are toxic doses, this gets overwhelmed. NAPQ1 build up and causes centrilobular necrosis

62
Q

What is the reversal/treatment for acetaminophen toxicity?

A

NAC - N acetyl cysteine which repletes glutathione to metabolize NAPQ1

63
Q

A patient presents with a respiratory alkalosis followed by a metabolic acidosis. What is it likely she had an acute overdose of?

A

Aspirin

64
Q

A patient presents with headache, dizziness, tinnitus, confusion, drowsiness, nausea, vomiting, diarrhea, and convulsions. She has GI bleeds from ulcers and gastritis. She has mucosal and skin petechiae. What is it likely that she has chronic toxicity from?
What does she have the petechiae?
What will her kidneys look like?

A

Chronic saliylism
Petechiae- due to inhibition of platelet cyclooxygenase blocking formation of thromboxane A2.

Kidneys- tubulointerstitial nephritis with papillary necrosis

65
Q

What are the cardio effects of cocaine?

A

Coke is sympathomimetic [blocks reuptake of dopamine in CNS and NE, epi in the periphery]

  1. tachycardia
  2. HTN
  3. peripheral/coronary vasoconstriction –>stroke, MI, arrhythmia

NOT DOSE DEPENDENT

66
Q

What are the CNS effects of cocaine?

A
  1. hyperpyrexia

2. seizures

67
Q

A mother comes into the ER. She has a spontaneous abortion due to placental abruption [as evidenced by hematoma in the placenta]. What drug can cause this?

A

Cocaine

68
Q

What are the effects of cocaine on the fetus during pregnancy?

A
  1. spontaneous abortion/placental abruption

2. fetal hypoxia with subsequent brain damage

69
Q

What are the 3 chronic effects of cocaine abuse?

[one specific for snorters, one for crack smokers]

A
  1. septal perforation [snorter]
  2. COPD [inhalers]
  3. dilated cardiomyopathy
70
Q

A teen comes in with tachycardia and HTN. They seem like they are going to have a heart attack but deny drug use.
What drug are you suspicious they are on and what would you find in the urine?

A

Cocaine- benzoylecognine in the urine

71
Q

What are the overdose symptoms from heroin?

When does an overdose usually occur?

A

Symptoms:

  1. respiratory depression
  2. arrhythmia, cardiac arrest
  3. pulmonary edema

Overdoses occur:

  1. unknown purity so they take too much
  2. loss of tolerance [stint in rehab then tried to do same amount]
72
Q

What are the renal complications of heroin?

A
  1. amyloidosis

2. focal segmental glomerulosclerosis

73
Q

What terms describes mechanical trauma that is superficial damage, limited to the epidermis produced by rubbing or scraping?

A

abrasion

74
Q

What term describes mechanical trauma that is extravasation of blood produced by blunt trauma?

A

Contusion- bruise

Color change from red–> black/blue–> yellow is due to breakdown of Hb

75
Q

What term describes an irregular tear [jagged] with intact bridging veins due to blunt trauma?

A

laceration

76
Q

What term describes a linear cut produced by a sharp object?

A

incision

77
Q

What is the difference between a peforating and penetrating wound?

A 
penetrating = in 
perforating = in and out [entry/exit wound]
78
Q

What is a partial thickness burn?

Which two “degrees” apply to this?

A

Basal layer is still intact and the skin an regenerate.
Appendages are spared.

  1. first degree = sunburn that involves epidermis. red, swollen, tender
  2. second degree is epidermis and superficial/deep dermis with deep red wet, painful blisters
79
Q

What is a full thickness burn?

What is destroyed?

A

It is destruction of skin, dermis, and extends deeper destroying:

  1. nerve endings
  2. skin appendages

No basal layer so no regeneration

80
Q

What do burns affecting over 20% of the body lead to?

Over 40% of the body?

A

Over 20 = hypovolemia and shock because fluid shifts to interstitium

Over 40 = doubling of resting metabolic rate

81
Q

When will inhalation injuries from inhalation of heated gases manifest?
What are the manifestations?

A

24-48hrs

  1. upper airway obstruction [gases forming acids/alkali incite inflammation and edema]
  2. chemical pneumonitis
82
Q

Sepsis resulting in shock and multisystem failure is the leading cause of death in burn patients. What three organisms are responsible?

A

Staph aureus
Pseudomona areuginosa
candida

83
Q

A young child presents with skin irritation due to excessive sweating on a hot, humid day. what is this?

A

heat rash

84
Q

A teen experiences cramping of voluntary muscles during vigorous exercise. What is this called? What is their core body temp? What is the cramping due to?

A

Heat cramps due to electrolyte loss via sweating.

Core body temp is NORMAL

85
Q

A man is outside on a July day in Houston and suddenly collapses. His core temperature is normal. He is given a glass of water and he feels better. What is this called and what is the cause?

A

Heat exhaustion - the body becomes hypovolemic due to water depletion from sweat and the CV system cannot compensate

86
Q

Who is most likely to have a heat stroke?
What happens to the core body temp?
What are the sequelae?

A

Elderly with physical stress and pre-existing cardio disease.
Core temp rises with the failure of thermoregulatory mechanisms.
-sweating stops
-peripheral vasodilation
-decreased volume

Sequelae: muscle necrosis, arrhythmia, encephalopathy, etc

87
Q

A homeless alcoholic is brought into the hospital on a snowy January evening. He seems to have no physiological function. What must you do before you declare him dead?

A

Warm him up! He might have hypothermia and once warmth is restored, physio function can be restored

88
Q

Compare low voltage and high voltage electical currents.

A

Low - home electricity [120-220V].
Patient will have ventricular fibrillation and muscle tetany so they will remain holding the device that is eletricuting them until they are pulled off

High - power lines, lightening
Patient will be blown away from the source and will have stunned respiratory centers

89
Q

What tissue are high sensitivity for radiation?

A 
Gonads
Endothelial cells
Lymphoid tissue 
bone marrow
intestinal mucosa
skin appendages
90
Q

What are the acute effects of ionizing radiation?

A
  1. direct injury of DNA via formation of free radicals

2. activation of TFs for cell cycle arrest, DNA repair apoptosis

91
Q

Where is the damage likely to occur for ionizing radiation that is :

  1. 1-5Gy
  2. 5-50 Gy
  3. over 50 GY
A
  1. hematopoietic
  2. GI
  3. cerebral
92
Q

How does ionizing radiation cause cerebral defect?

A

Damages vasculature–> edema, improper delivery of nutrients, O2 etc

NOT damage to neurons

93
Q

What can develop years later after exposure to ionizing radiation ?

A

Leukemia

Multisystems (29 decks)

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