Chapter 7 - Environmental Pathology Flashcards

0
Q

What is the most important preventable cause of death in the United States?

A

Smoking: most important preventable cause of death in United States

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1
Q

What is the leading cause of premature death in developed countries?

A

Tobacco use leading cause of premature death in developed countries

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2
Q

What is nicotine?

A

Nicotine: addictive component in tobacco

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3
Q

Besides addiction, nicotine patch can be used to treat what?

A

Nicotine patch used to Rx ulcerative colitis

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4
Q

What is cotinine?

A

Cotinine: nicotine metabolite; used for screening

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5
Q

What does tar in cigarette smoke contain?

A

Tar contains carcinogenic agents

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6
Q

What are the carcinogens in cigarette smoke?

A

Carcinogens: polycyclic hydrocarbons, phenol, nitrosamine

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7
Q

What can smokeless tobacco cause?

A

Smokeless tobacco: addictive; ↑risk for oral squamous cancer

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8
Q

What does passive smoke increase the risk of in children?

A

Passive smoke: ↑risk of respiratory/middle ear infections in children

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9
Q

What does secondhand smoke exacerbate in children?

A

Smoking exacerbates asthma

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10
Q

What does passive smoke increase the risk for in adults?

A

Passive smoke: risk for lung cancer; CAD

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11
Q

What are the beneficial effects of smoking cessation?

A

Live longer; ↓risk for heart disease, lung cancer, stroke

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12
Q

What is the most common recreational drug taken in the U.S.?

A

Alcohol MC recreational drug

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13
Q

Where is alcohol metabolized and reabsorbed?

A

Stomach/liver metabolize alcohol; stomach/small bowel reabsorb alcohol

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14
Q

Why are women at risk for acute/chronic alcohol complications?

A

Women at risk for acute/chronic alcohol complications; ↓alcohol dehydrogenase

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15
Q

What are the enzymes that metabolize alcohol?

A

Enzymes metabolizing alcohol: alcohol dehydrogenase, CYP2E1, catalase

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16
Q

What is the rate-limiting enzyme in alcohol metabolism?

A

ADH: rate-limiting enzyme in alcohol metabolism

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17
Q

What is key to lab abnormalities in alcohol metabolism?

A

↑NADH key to lab abnormalities

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18
Q

How does role of increased NADH in alcohol metabolism?

A

↑NADH: ↑synthesis lactic/β-OHB acids; ↑liver TG synthesis

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19
Q

Acetyl CoA is used to synthesize what?

A

Acetyl CoA used to synthesize fatty acids/ketoacids

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20
Q

Describe why there is increased risk for fasting hypoglycemia in alcohol metabolism.

A

NADH enhances pyruvate conversion to lactate → ↓pyruvate → fasting hypoglycemia

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21
Q

What anions are present in the increased anion gap metabolic acidosis of alcohol abuse?

A

↑Anion gap metabolic acidosis: lactic acid, β-OHB acid

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22
Q

Which ketone is not detected with standard urine/blood tests for ketone bodies?

A

β-OHB not detected with standard urine/blood tests for ketone bodies

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23
Q

Besides fasting hypoglycemia and acidosis, what are the other laboratory findings in alcohol abuse/alcoholic liver disease?

A

Lactic acid/β-OHB → hyperuricemia (potential for gout); hypertriglyceridemia
Alcohol liver disease: AST > ALT; ↑GGT

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24
Q

What is the most common systemic complication of IVDU?

A

Hepatitis C: MC systemic complication of IVDU

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25
Q

What are the effects of acetaminophen overdose?

A

Acetaminophen: chemical hepatitis; renal papillary necrosis

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26
Q

What are the general symptoms of aspirin overdose?

A

Aspirin: tinnitus, vertigo, tachypnea

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27
Q

What is the initial acid-base disorder in aspirin overdose?

A

Initial respiratory alkalosis

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28
Q

What is the mixed acid-base disorder in aspirin overdose in adults?

A

Mixed primary respiratory alkalosis and metabolic acidosis (adults)

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29
Q

What is there danger of in salicylate poisoning?

A

Salicylate poisoning: danger of hyperthermia

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30
Q

Both acetaminophen and aspirin toxicity may cause what?

A

Both acetaminophen and aspirin toxicity may cause fulminant hepatitis

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31
Q

Unopposed estrogen increases the risk for what?

A

Unopposed estrogen: adenocarcinoma endometrium/breast
Risk venous thromboembolism; intrahepatic cholestasis
Risk myocardial infarction/stroke

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32
Q

OCPs increase the risk for what?

A

OCP: risk breast adenocarcinoma, cervical SCC
Risk folic acid deficiency (macrocytic anemia)
OCP MCC hypertension in young women → ↑angiotensinogen → ↑ATII
Risk hepatic adenoma causing intraperitoneal hemorrhage
Risk of intrahepatic cholestasis/cholesterol gallstones

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33
Q

What is the most common cause of death due to a venomous bite?

A

Bee/wasp/hornet sting: MCC death due to a venomous bite

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34
Q

What is a contusion?

A

Contusion: blunt force injury to blood vessels with blood leaking into tissue

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35
Q

What is an abrasion?

A

Abrasion: superficial excoriation of epidermis

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36
Q

What is a laceration?

A

Laceration: jagged tear with intact bridging vessels/nerves/connective tissue

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37
Q

What is an incision?

A

Incision: wound with sharp margins; severed blood vessels

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38
Q

Describe contact gunshot wounds.

A

Contact wound: stellate-shaped; fouling (soot + gunpowder)

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39
Q

Describe an intermediate-range gunshot wound.

A

Intermediate-range wound: powder tattooing

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40
Q

Describe a long-range gunshot wound.

A

Long-range wound: no powder tattooing

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41
Q

Describe exit gunshot wounds.

A

Exit wounds: larger than entrance wound

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42
Q

What is the most common cause of death ages 1 to 44 years?

A

MVAs MCC death ages 1 to 44 years

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43
Q

What accounts for more than 50% of deaths from child abuse?

A

Shaken baby syndrome: >50% deaths from child abuse

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44
Q

What is the key finding in shaken baby syndrome?

A

Key finding: retinal hemorrhages

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45
Q

What is the most common cause of burns?

A

MCC burns is fire

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46
Q

What is the most common site for burns?

A

MC site for burn is upper extremities

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47
Q

What is the common denominator in all burns?

A

Common denominator in burns is protein denaturation

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48
Q

What does the center of a burn have?

A

Center of burn has irreversible coagulation necrosis

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49
Q

Describe the zone of ischemia of a burn.

A

Zone of ischemia has reduction in dermal microcirculation

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50
Q

Describe the zone of hyperemia in a burn.

A

Zone of hyperemia due to immediate and transient increase in perfusion

51
Q

What does the depth of a burn determine?

A

Depth of burn determines potential for skin regeneration

52
Q

What are the sources for skin regeneration?

A

Sources for skin regeneration: basal layer of cells at margins; dermal skin appendages

53
Q

What is a first degree burn?

A

1st degree burn: limited to epidermis

54
Q

What is a superficial second-degree burn?

A

2nd degree superficial: extends into papillary dermis; partial-thickness burn

55
Q

What is a deep second-degree burn?

A

2nd degree deep: extends into reticular dermis; partial-thickness burn

56
Q

What is a third-degree burn?

A

3rd degree burn: extends through epidermis/dermis; full-thickness

57
Q

What common occurs following a third-degree burn? What can potentially develop?

A

SCC risk in keloids

58
Q

What is a fourth-degree burn?

A

4th degree burn: extends thru skin, subcutaneous fat, muscle/bone

59
Q

What is a possible effect of losing plasma from the burn surface?

A

Hypovolemic shock from loss of plasma; pitting edema

60
Q

What is the most common cause of infection of a burn wound?

A

P. aeruginosa MCC infection of burn wound

61
Q

What may develop in the small intestine as a complication of a severe burn?

A

Curling ulcers of proximal duodenum

62
Q

What is hypermetabolic syndrome?

A

Hypermetabolic syndrome: heat loss from damaged skin surface → ↑BMR

63
Q

Smoke inhalation may result in what type of poisoning?

A

Smoke inhalation: CO/CN poisoning

64
Q

What is heat edema?

A

Heat edema: mild swelling feet, ankles, hands

65
Q

What is heat edema due to?

A

Cutaneous vasodilation with gravitational pooling

66
Q

Who is affected by heat edema?

A

Elderly in tropical/semitropical area; healthy traveler coming from cold to hot area

67
Q

What are heat cramps?

A

Heat cramps: painful, spasmodic muscle contractions postexercise

68
Q

Describe the electrolyte derangement in heat cramps.

A

Deficiency Na+, Cl−, and fluids in muscle

69
Q

What is heat exhaustion?

A

Heat exhaustion: volume depletion under conditions of heat stress

70
Q

What are the clinical findings in heat exhaustion?

A

Heat exhaustion: <104° F); profuse sweating/no mental status changes

71
Q

Describe the laboratory findings in heat exhaustion.

A

Hemoconcentration, variable serum Na+

72
Q

What are the predisposing factors for heatstroke?

A

CHS: high ambient temperature; poor, elderly without air-conditioning
CHS: chronic disorders (psychiatric, alcoholism) requiring medication

73
Q

What are the clinical findings in classic heatstroke?

A

Core body temp >40° C (104° F); skin hot/dry; mental status abnormal; CNS dysfunction

74
Q

What are the laboratory findings in classic heatstroke?

A

Mild respiratory alkalosis; mild ↑serum CK

75
Q

What are the predisposing factors for exertional heatstroke?

A

EHS: athletes/military recruits; endogenous heat production overrides cooling mechanisms

76
Q

What are the clinical findings in exertional heatstroke?

A

EHS: Core body temp >40° C (104° F); profuse sweating; severe CNS dysfunction

77
Q

What are the lab findings in exertional heatstroke?

A

Lactic acidosis, rhabdomyolysis, ARF, DIC, liver damage, hypocalcemia

78
Q

What is the most common freezing injury to tissue?

A

Frostbite MC freezing injury to tissue

79
Q

What is trench foot/immersion foot?

A

Trench foot/immersion foot: nonfreezing injury; exposure to wet cold

80
Q

What is chilblain?

A

Chilblain: nonfreezing injury; exposure to dry cold

81
Q

What is the pathogenesis of frostbite?

A

Frostbite: tissue exposed to temperature <0° C
Frostbite: ice crystallization; stasis of blood flow

82
Q

What occurs during the prefreeze phase of frostbite?

A

Prefreeze: endothelial plasma leakage; vasoconstriction; ↑plasma viscosity

83
Q

What occurs during the freeze-thaw phase of frostbite?

A

Freeze-thaw phase: extracellular ice crystallization; intracellular volume depletion → death

84
Q

What occurs during the postthaw phase of frostbite?

A

Postthaw: microvascular collapse → necrosis

85
Q

Describe the epidemiology of electrical injury.

A

Most injuries in children or work-related

86
Q

What is the main determinant of tissue injury in electrical injury?

A

Current main determinant of tissue injury

87
Q

What is Ohm’s law?

A

Ohm’s law: Current (I) = Voltage (V)/Resistance (R)

88
Q

What change in resistance or voltage results in a decrease in current?

A

↑Resistance (R) or ↓Voltage (V) = ↓Current (I)

89
Q

What change in resistance or voltage results in an increase in current?

A

↓Resistance (R) or ↑Voltage (V) = ↑Current (I)

90
Q

How does AC exposure compare to DC exposure at the same voltage?

A

AC 3× more dangerous that DC at same voltage

91
Q

How do muscle contractions differ during AC and DC exposure?

A

AC induces tetanic contractions (hold on); DC induces single muscle spasm (throws away)

92
Q

How does wet skin affect resistance and current?

A

Wet skin ↓R causing ↑I

93
Q

How does dry skin affect resistance and current?

A

Dry skin ↑R causing ↓I

94
Q

What is the most common cause of death in an electrical injury?

A

Cardiorespiratory arrest MCC death electrical injury

95
Q

What is the most common cause of death from lightening injury?

A

Cardiorespiratory arrest MCC death from lightening injury

96
Q

Who is most at risk for drowning?

A

Children 1 to 4 and 10 to 14 years old most at risk for drowning

97
Q

Define drowning.

A

Drowning: death by suffocation from immersion in a liquid

98
Q

What is wet drowning?

A

Wet drowning: aspiration of water; MC type of drowning

99
Q

What is immersion syndrome?

A

Immersion syndrome: sudden death from submersion in cold water; vagally mediated cardiac arrest

100
Q

What is dry drowning?

A

Dry drowning: asphyxia from laryngospasm without aspiration

101
Q

Describe two features of the diving reflex.

A

Diving reflex protective; shunts blood to vital areas

102
Q

Describe the cause of death in drowning.

A

Death in drowning: laryngospasm/closed glottis; hypoxemia with respiratory/metabolic acidosis

103
Q

How are O2 concentration and atmospheric pressure affected at high altitude?

A

High altitude: O2 concentration 21%, ↓atmospheric pressure

104
Q

Describe the effect of hypoxemia at high altitude.

A

Hypoxemia stimulates peripheral chemoreceptors → respiratory alkalosis

105
Q

Describe the effect of respiratory alkalosis on OBC.

A

Respiratory alkalosis → activates PFK → ↑2,3-BPG → right-shifted OBC

106
Q

Acute mountain sickness occurs at what elevation?

A

AMS occurs at elevations >8000 feet (2440 m)

107
Q

What are the clinical findings in acute mountain sickness?

A

Headache, fatigue, dizziness, anorexia, nauseous, insomnia

108
Q

Describe the pulmonary edema in high altitude pulmonary edema.

A

HAPE: noncardiogenic pulmonary edema

109
Q

What are the clinical findings in high altitude cerebral edema?

A

HACE: ataxia, stupor, coma

110
Q

Give two examples of ionizing radiation.

A

Ionizing radiation: x-rays, γ-rays

111
Q

Describe the pathophysiology of ionizing radiation.

A

Damage to DNA by hydroxyl free radicals

112
Q

Which tissue is most sensitive to ionizing radiation?

A

Lymphoid tissue most sensitive to ionizing radiation

113
Q

Which tissue is least sensitive to ionizing radiation?

A

Bone least sensitive to ionizing radiation

114
Q

What is the first hematologic sign of total body radiation?

A

Total body radiation: lymphopenia first hematologic sign

115
Q

What are the vascular effects of radiation?

A

Vascular system: thrombosis/fibrosis; ischemia

116
Q

What are the acute integumentary effects of radiation?

A

Acute—erythema, edema, blisters

117
Q

What are the chronic integumentary effects of radiation?

A

Chronic—radiodermatitis; danger of SCC

118
Q

What are the acute and chronic GI effects of radiation?

A

Acute—diarrhea; chronic—bowel adhesions

119
Q

What is the most common cancer caused by radiation?

A

Acute leukemia MC cancer caused by radiation

120
Q

What other cancers are caused by radiation besides acute leukemia?

A

Other radiation cancers: papillary carcinoma of thyroid, osteogenic sarcoma

121
Q

Describe the pathogenesis of injury with UVB light.

A

UVB: ↑pyrimidine dimers distort DNA helix
UVB: inactivates p53 suppressor gene; activates RAS proto-oncogene

122
Q

What are the general effects of UVB light injury?

A

Sunburn, actinic (solar) keratosis (danger SCC), corneal burns from skiing

123
Q

What are the cancers associated with UVB light injury?

A

UVB cancers: BCC (MC), SCC, melanoma

124
Q

What type of radiation may cause third-degree burns?

A

Laser radiation: third-degree burns