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HistoPathology > [P] Week 5: Environmental and Nutritional Disease - Part 2 > Flashcards

[P] Week 5: Environmental and Nutritional Disease - Part 2 Flashcards

1
Q

METALS AS ENVIRONMENTAL POLLUTANTS, enumerate

A
  1. Lead
  2. Mercury
  3. Arsenic
  4. Cadmium
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2
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Readily absorbed metal that binds to sulfhydryl groups in proteins

A

Lead

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3
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Lead interferes with ____ metabolism, effects that lead to ematologic, skeletal, neurologic, gastrointestinal, and renal toxicities

A

Calcium metabolism

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4
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Lead exposure may occur through?

A

contaminated air, food, and
water

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5
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Lead can be obtained from?

A

flaking old paint

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6
Q

METALS AS ENVIRONMENTAL POLLUTANTS

The effects of lead poisoningdepends on the blood lead level. At 150 ug/dL, it can even cause

A

Death

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7
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Lead poisoning of ____, there is:
- kidneys damage
- blood anemia
- nervous system damage
- brain (behavior problems, lower IQ, hearing loss, learning disabilities)
- body (decreased bone and muscle
growth)

A

Children

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8
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Lead poisoning In ____, this can be manifested by peripheral neuropathies

A

Adult

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9
Q

METALS AS ENVIRONMENTAL POLLUTANTS

used by swabbing an area and if it turns red, it indicates presence of lead.

A

Lead check swab

There is a different tool used in measuring
lead in the soil

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10
Q

METALS AS ENVIRONMENTAL POLLUTANTS

used to determine the concentration of lead in the blood of the time you extracted the patient.

A

Leadcare II Analyzer Kit

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11
Q

METALS AS ENVIRONMENTAL POLLUTANTS

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

A

Mercury

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12
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Mercury has had many uses throughout history, as a?

A
  • pigment in cave paintings
  • cosmetic
  • remedy for syphilis
  • component of diuretics
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13
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Ingested mercury can injure the gut and cause

A

ulcerations and bloody diarrhea

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14
Q

METALS AS ENVIRONMENTAL POLLUTANTS

In the kidneys, mercury can cause

A

acute tubular necrosis and renal failure

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15
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Chronic exposure of mercury can cause?

A

nephrotic syndrome

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16
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Today, the main sources of exposure to mercury are?

A

contaminated fish (methyl mercury) and mercury vapors released from metallic mercury in dental amalgams, a possible occupational hazard for dental workers.

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17
Q

METALS AS ENVIRONMENTAL POLLUTANTS

In some areas of the world, mercury used in ____ ____ has contaminated rivers and streams

A

Gold mining

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18
Q

METALS AS ENVIRONMENTAL POLLUTANTS

this variation of mercury enters the food chain, and in carnivorous fish such as swordfish, shark, and bluefish, mercury levels may be 1 million times higher than in the surrounding water

A

Methyl mercury

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19
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Almost 90% of ingested methyl mercury is absorbed in the

A

gastrointestinal tract

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20
Q

MERCURY CYCLE

1) Mercury is emitted to the ____.

A

Athmosphere

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21
Q

MERCURY CYCLE

2) Mercury is deposited in rain and snow and as ____ and ____
3) Mercury accumulates in ____, ____, and ____.

A

2) gasses and particles
3) Lakes, reservoirs, and forests

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22
Q

MERCURY CYCLE

4) Mercury is transported through watersheds and converted to ____.
5) Methylmercury bioaccumulates in ____

A

4) Methylmercury
5) Food webs

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23
Q

METALS AS ENVIRONMENTAL POLLUTANTS

interfere with several aspects of cellular metabolism, leading to toxicities that are most prominent in the gastrointestinal tract, nervous system, skin, and heart.

A

Arsenic salts

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24
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Because of its favored use as an instrument of assassination among royal families, arsenic has been called

A

the poison of kings and the king of poisons

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25
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Arsenic is found naturally in soils and water and is used in products such as

A

wood preservers and herbicides and other agricultural products

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26
Q

METALS AS ENVIRONMENTAL POLLUTANTS

TOF

Arsenic may be released into the environment from mines and smelting industries

A

True

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27
Q

METALS AS ENVIRONMENTAL POLLUTANTS

The most toxic forms of arsenic are the trivalent compounds

A
  • arsenic trioxide
  • sodium arsenite
  • arsenic trichloride
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28
Q

METALS AS ENVIRONMENTAL POLLUTANTS

If ingested in large quantities, arsenic causes?

A
  • acute gastrointestinal
  • cardiovascular
  • CNS toxicities that are often fatal.
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29
Q

METALS AS ENVIRONMENTAL POLLUTANTS

What are the effects of arsenic poisoning?

A

Effects include:

  • Neurologic effects- paresthesias, numbness, & pain
  • Cardiovascular effects- hypertension
  • Skin changes- hyperpigmentation
  • Increased risk for the development of cancers is the most serious consequence of chronic exposure, particularly of the lung, bladder, and skin
  • Arsenic-induced skin tumors are often multiple; usually on the palms and soles
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30
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Preferentially toxic to the kidneys and the lungs through uncertain mechanisms that may involve increased production of ROS

A

Cadmium

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31
Q

METALS AS ENVIRONMENTAL POLLUTANTS

  • It is an occupational and environmental pollutant generated by mining, electroplating, and production of nickelcadmium batteries, which are usually disposed of as household waste
  • Can contaminate the soil and plants directly or through fertilizers and irrigation water.
A

Cadmium

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32
Q

METALS AS ENVIRONMENTAL POLLUTANTS

what is the most important source of cadmium exposure

A

Food

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33
Q

METALS AS ENVIRONMENTAL POLLUTANTS

The principal toxic effects of excess cadmium are a form of ____ that may progress to end-stage renal disease

A

obstructive lung disease

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34
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Cadmium exposure can also cause?

A

skeletal abnormalities associated with calcium loss.

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35
Q

METALS AS ENVIRONMENTAL POLLUTANTS

Cadmium exposure is also associated with?

A

elevated risk of lung cancer, which has been demonstrated in workers exposed occupationally and in populations living near zinc

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36
Q

OCCUPATIONAL HEALTH RISKS: INDUSTRIAL AND AGRICULTURAL EXPOSURES

the most readily preventable cause of death in humans

A

Smoking

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37
Q

OCCUPATIONAL HEALTH RISKS: INDUSTRIAL AND AGRICULTURAL EXPOSURES

TOF

The main culprit is sigarette smoking, but smokeless tobacco (e.g., snuff, chewing tobacco) is also harmful to health and an important cause of oral cancer.

A

False

Cigarette

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38
Q

OCCUPATIONAL HEALTH RISKS: INDUSTRIAL AND AGRICULTURAL EXPOSURES

The use of tobacco products not only creates personal risks, but passive tobacco inhalation from the environment (secondhand smoke) can cause lung cancer in nonsmokers.

A

PASSIVE SMOKING

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39
Q

EFFECTS OF SELECTED TOBACCO SMOKE CONSTITUENTS

Give the effect of the following substance:

  • Tar
  • Polycyclic aromatic hydrocarbons
  • Benzo[a]pyrene
  • Nitrosamine

TPBN

A

Carcinogenesis

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40
Q

EFFECTS OF SELECTED TOBACCO SMOKE CONSTITUENTS

Give the effect of the following substance:

  • Nicotine
A

Ganglionic stimulation and depression;
tumor promotion

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41
Q

EFFECTS OF SELECTED TOBACCO SMOKE CONSTITUENTS

Give the effect of the following substance:

  • Phenol
A

Tumor promotion; mucosal irritation

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42
Q

EFFECTS OF SELECTED TOBACCO SMOKE CONSTITUENTS

Give the effect of the following substance:

  • Carbon monoxide
A

Impaired oxygen transport and
utilization

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43
Q

EFFECTS OF SELECTED TOBACCO SMOKE CONSTITUENTS

Give the effect of the following substance:

  • Formaldehyde
  • Nitrogen oxides
A

Toxicity to cilia; mucosal= irritation

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44
Q

SUSPECTED ORGAN-SPECIFIC CARCINOGENS IN TOBACCO SMOKE

give the Organ of the specific carcinogen:
- Polycyclic aromatic hydrocarbons 4-(Methylnitrosoamino)-1-(3 pyridyl)-1- butanone (NNK)
- Polonium 210

A

Lung, larynx

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45
Q

SUSPECTED ORGAN-SPECIFIC CARCINOGENS IN TOBACCO SMOKE

give the Organ of the specific carcinogen:

N′-Nitrosonornicotine (NNN)

A

Esophagus

46
Q

SUSPECTED ORGAN-SPECIFIC CARCINOGENS IN TOBACCO SMOKE

give the Organ of the specific carcinogen:

Polycyclic aromatic hydrocarbons 4-(Methylnitrosoamino)-1-(3 pyridyl)-1- butanone (NNK)

A

Pancreas

47
Q

SUSPECTED ORGAN-SPECIFIC CARCINOGENS IN TOBACCO SMOKE

give the Organ of the specific carcinogen:

4-Aminobiphenyl, 2-naphthylamine

A

Bladder

48
Q

SUSPECTED ORGAN-SPECIFIC CARCINOGENS IN TOBACCO SMOKE

give the Organ of the specific carcinogen:

  • Polycyclic aromatic hydrocarbons,
  • Polycyclic aromatic hydrocarbons 4-(Methylnitrosoamino)-1-(3
    pyridyl)-1- butanone (NNK)
  • N′-Nitrosonornicotine (NNN)
A

Oral cavity (smoking)

49
Q

SUSPECTED ORGAN-SPECIFIC CARCINOGENS IN TOBACCO SMOKE

give the Organ of the specific carcinogen:

  • Polycyclic aromatic hydrocarbons 4-(Methylnitrosoamino)-1-(3
    pyridyl)-1- butanone (NNK)
  • N′-Nitrosonornicotine (NNN)
  • Polonium 210
A

Oral cavity (snuff)

50
Q

EFFECTS OF ALCOHOL

After consumption, ethanol is absorbed unaltered in the stomach and small intestine and then distributes throughout the body in what proportion?

A

direct proportion to the blood level

51
Q

EFFECTS OF ALCOHOL

Less than what % is excreted unchanged in the urine, sweat, and breath.

A

Less than 10%

52
Q

EFFECTS OF ALCOHOL

The amount exhaled is proportional to the blood level and forms the basis for what test used by the law enforcement

A

Breath Test

53
Q

EFFECTS OF ALCOHOL

what concentration in the blood constitutes the legal definition of drunk driving in most states

A

80 mg/dL

53
Q

EFFECTS OF ALCOHOL

Not all is gloom and doom, however. Moderate amounts of alcohol (about 20 to 30 g/day, corresponding to approximately 250 mL of wine) appear to be protective against?

A

Coronary Heart Disease

53
Q

EFFECTS OF ALCOHOL

What are the possible mechanism of alchol be protective against coronary heart disease

A

Possible mechanisms include increase in:
- HDL levels
- inhibition of platelet aggregation
- lowering of fibrinogen levels.

53
Q

ACUTE ALCOHOLISM

Even with moderate intake of alcohol, multiple fat droplets accumulate in the?

A

cytoplasm of hepatocytes (fatty change
or hepatic steatosis)

54
Q

exerts its effects mainly on the CNS, but it may induce hepatic and gastric changes that are reversible if alcohol consumption is discontinued

A

Acute alcoholism

55
Q

ACUTE ALCOHOLISM

The gastric changes are?

A

acute gastritis and ulceration

56
Q

ACUTE ALCOHOLISM

In the CNS, alcohol is a?

A

depressant

57
Q

ACUTE ALCOHOLISM

TOF

Consequently, there is stimulation and disordered cortical, car, and intellectual behavior

A

False

MOTOR not car

58
Q

ACUTE ALCOHOLISM

At progressively higher blood levels, cortical neurons and then lower medullary centers are depressed, including those that regulate respiration. what arrest may follow?

A

Respiratory Arrest

59
Q

this alcoholism affects not only the liver and stomach, but virtually all other organs and tissues as well

A

Chronic Alcoholism

60
Q

this kind of alcoholism suffer significant morbidity and have a shortened lifespan, related principally to damage to the liver, gastrointestinal tract, CNS, cardiovascular system, and pancreas

A

Chronic Alcoholism

61
Q

CHRONIC ALCOHOLISM

What are the changes of liver in chronic alcoholism?

A
  • Fatty change
  • alcoholic hepatitis and cirrhosis;

Cirrhosis is associated with portal hypertension and an increased risk for the development of hepatocellular
carcinoma

62
Q

CHRONIC ALCOHOLISM

What are the changes of GIT in chronic alcoholism?

A
  • massive bleeding from gastritis
  • gastric ulcer
  • esophageal varices
63
Q

CHRONIC ALCOHOLISM

What are the changes of Neurologic Effects in chronic alcoholism?

A

Thiamine (vitamin B1) deficiency

64
Q

CHRONIC ALCOHOLISM

What are the changes of Cardiovascular effects in chronic alcoholism?

A

increased incidence of
hypertension, & coronary heart disease

65
Q

CHRONIC ALCOHOLISM

What are the changes of Pancreatitis effects in chronic alcoholism?

A

excessive alcohol intake increases the risk of acute and chronic pancreatitis

66
Q

CHRONIC ALCOHOLISM

What are the changes of Pancreatitis effects in chronic alcoholism?

A

The use of ethanol during pregnancy can cause fetal alcohol syndrome, which is marked by microcephaly, growth retardation, and facial abnormalities in the newborn and reduction in mental functions as the child grows older.

Consumption during the first trimester of pregnancy is particularly harmful.

67
Q

CHRONIC ALCOHOLISM

What are the changes of Malnutrition in chronic alcoholism?

A

ethanol is a substantial source of energy (empty calories). Chronic alcoholism leads to malnutrition
and nutritional deficiencies, particularly of the B vitamin

68
Q

CHRONIC ALCOHOLISM

What are the changes of Carcinogenesis in chronic alcoholism?

A

increased incidence of cancer of the oral cavity, esophagus, and liver.
- In women, low to moderate intake (12 oz beer or 5 oz of wine) incurs a slightly higher risk of breast cancer.

69
Q

CHRONIC ALCOHOLISM

considered to be the main agent
associated with alcohol-induced laryngeal and esophageal cancer

A

Acetaldehyde

70
Q

CHRONIC ALCOHOLISM

synergize in the causation
of various cancers.

A

Alcohol and cigarette smoke

71
Q

Enumerate the affected organs in chronic alcoholism

A
  • Liver
  • GIT
  • Neurologic Effects
  • Cardiovascular effects
  • Pancreatitis
  • Fetus
  • Malnutrition
  • Carcinogenesis
72
Q
  • refer to untoward effects of drugs that are given in conventional therapeutic settings.
  • An exotic, but easily seen example is discoloration of the skin caused by accumulation of an oxidized metabolite of the antibiotic minocyclin
A

Adverse drug reactions

73
Q

what aret the adverse drug reacion

A
  1. Anticoagulants
  2. Menopausal Hormone Theraphy
  3. Aspirin (ACETYLSALICYLIC ACID)
74
Q

INJURY BY THERAPEUTIC DRUGS (ADVERSE DRUG REACTIONS

The two drugs that most frequently cause adverse reactions reported to the US Food and Drug Administration are the oral anticoagulants warfarin and dabigatran.

A

Anticoagulants

75
Q

INJURY BY THERAPEUTIC DRUGS (ADVERSE DRUG REACTION

increases the risk of breast cancer after a median time of 5 to 6 years.

A

Combination estrogen-progestin

76
Q

INJURY BY THERAPEUTIC DRUGS (ADVERSE DRUG REACTION

increases the risk of stroke and venous thromboembolism including deep vein thrombosis and pulmonary embolism

A

Menopausal Hormone Therapy

77
Q

INJURY BY THERAPEUTIC DRUGS (ADVERSE DRUG REACTION

overdose may result from accidental ingestion of a large number of tablets by young children; in adults, overdose is frequently suicidal. Much less commonly, poisoning is caused by the excessive use of ointments containing oil of wintergreen (methyl salicylate).

A

ASPIRIN (ACETYLSALICYLIC ACID)

78
Q

INJURY BY THERAPEUTIC DRUGS (ADVERSE DRUG REACTION

causes alkalosis as a consequence of the stimulation of the respiratory center in the medulla eventually leading to coma

A

Acute salicylate overdose

79
Q

INJURY BY THERAPEUTIC DRUGS (ADVERSE DRUG REACTION

may develop in persons who take 3 g or more daily for long periods of time for treatment of chronic pain or inflammatory conditions.

A

Chronic aspirin toxicity (salicylism)

80
Q

INJURY BY THERAPEUTIC DRUGS (ADVERSE DRUG REACTION

this salicylism is manifested by headaches, dizziness, ringing in the ears (tinnitus), hearing impairment, mental confusion, drowsiness, nausea, vomiting, and diarrhea. The CNS changes may progress to convulsions and coma.

A

Chronic salicylism or Chronic aspirin toxicity

81
Q

Injury induced by physical agents is divided into the following categories:

A
  • mechanical trauma
  • thermal injury
  • electrical injury
  • injury produced by ionizing radiation
82
Q

INJURY BY PHYSICAL AGENTS

  • Due to wounds produced by shooting, stabbing, blunt force, traffic accidents, etc.
  • Type of injury depends on:
    o Shape of colliding object
    o Amount of energy discharged at impact
    o Tissues or organs that bear the impact
  • Patterns of Injury:
    o Abrasion (Gasgas)
    o Contusion (Pasa)
    o Laceration (Hiwa)
    o Incised wound
    o Puncture wound
A

MECHANICAL TRAUMA

83
Q

INJURY BY PHYSICAL AGENTS

  • 80% of burns are caused by fire or by scalding, the latter being a major cause of injury in children
  • The clinical significance of a burn injury depends on the
  • following factors:
    o Depth of the burns (Is it just the epidermis or dermis)
    o Percentage of body surface involved (Is it just the finger or entire body)
    o Internal injuries caused by the inhalation of hot and toxic
  • Promptness and efficacy of therapy, especially fluid and electrolyte management and prevention or control of wound infections
A

THERMAL BURNS

84
Q

INJURY BY PHYSICAL AGENTS

What are the consequences of Thermal Burns

A
  • Pulmonary edema
  • Infected burn site with Pseudomonas aeruginosa (or methicillin-resistant S. aureus, and Candida)
  • Pneumonia or septic shock with renal failure
  • In burn survivors the development of hypertrophic scars, both at the site of the original burn and at donor graft sites.
85
Q

HYPERTHERMIA VS. HYPOTHERMIA

  • Happens when there is prolonged exposure to elevated ambient temperatures which can result in heat cramps, heat exhaustion, and heat stroke
A

Hyperthermia

86
Q

HYPERTHERMIA VS. HYPOTHERMIA

A genetic condition resulting from mutations in genes such as RYR1 that control calcium levels in skeletal muscle cells

A

Malignant Hyperthermia

87
Q

HYPERTHERMIA VS. HYPOTHERMIA

In affected individuals of malignant hypethermia, exposure to certain ____ during surgery triggers a rapid rise in calcium levels in skeletal muscle, leading to muscle rigidity and increased heat production

A

Anesthetics

88
Q

HYPERTHERMIA VS. HYPOTHERMIA

Patients with malignant hyperthermia have problems in controlling their?

A

**calcium levels ** secondary to mutation

89
Q

HYPERTHERMIA VS. HYPOTHERMIA

Heat cramps, Heat exhaustion, or Heat stroke

✓ It is probably the most common hyperthermic syndrome.
✓ Onset is sudden, with prostration and collapse
✓ Results from a failure of the cardiovascular system to compensate for hypovolemia
caused by dehydration

A

Heat exhaustion

90
Q

HYPERTHERMIA VS. HYPOTHERMIA

Heat cramps, Heat exhaustion, or Heat stroke

✓ result from loss of electrolytes via sweating.
✓ Cramping of voluntary muscles, usually in association with vigorous exercise, is the hallmark.
✓ Heatdissipating mechanisms
are able to maintain normal core
body temperature

A

Heat cramps

91
Q

HYPERTHERMIA VS. HYPOTHERMIA

Heat cramps, Heat exhaustion, or Heat stroke

✓ associated with high ambient temperatures, high humidity, and exertion.
✓ Thermoregulatory mechanisms fail, sweating ceases, and the core body temperature rises to more than 40°C, leading to multiorgan dysfunction that can be rapidly fatal.

A

Heat stroke

92
Q

HYPERTHERMIA VS. HYPOTHERMIA

Prolonged exposure to low ambient temperature leads to hypothermia, a condition seen all too frequently in homeless persons.

A

Hypothermia

93
Q

HYPOTHERMIA

sometimes exacerbated by dilation of superficial blood vessels due to ingestion of alcohol, hasten the lowering of body temperature

A

High humidity and wet clothing

94
Q

HYPOTHERMIA

loss of consciousness occurs, followed by bradycardia and atrial fibrillation at lower core temperatures

A

At a body temperature of about 90°F

95
Q

often fatal, can arise from contact with low-voltage currents (i.e., in the home and workplace) or high-voltage currents carried by high-power lines or produced by lightning.

A

Electrical injuries

96
Q

ELECTRICAL INJURY

what are the two types of electrical injuries

A
  1. Burns
  2. Ventricular fibrillation or cardiac and respiratory center failure, resulting from disruption of nerve impulse conduction. (For low voltage currents)
97
Q

ELECTRICAL INJURY

The type of injury and the severity and extent ofburns
depend on the

A
  • strength (amperage)
  • duration
  • path of the electric current within the body
98
Q

ELECTRICAL INJURY

Voltage in the household and workplace ____ is high enough that with low resistance at the site of contact (as when the skin is wet), sufficient current can pass through the body to cause serious injury, including ventricular fibrillation

A

120 or 220 V

99
Q
  • Radiation is energy that travels in the form of waves or high-speed particles.
  • Radiation has a wide range of energies that span the electromagnetic spectrum; it can be divided into nonionizing and ionizing radiation.
A

INJURY PRODUCED BY IONIZING RADIATION

100
Q

INJURY PRODUCED BY IONIZING RADIATION

The energy of nonionizing radiation such as

A

UV and infrared light, microwave, and sound waves
can move atoms in a molecule or cause them to vibrate but is not sufficient to displace bound electrons from atoms

101
Q

INJURY PRODUCED BY IONIZING RADIATION

double-edged sword. It is indispensable in medical practice, being used in the treatment of cancer, in diagnostic imaging, and in therapeutic or diagnostic radioisotopes

A

Ionizing radiation

102
Q

INJURY PRODUCED BY IONIZING RADIATION

Ionizing Radiation produces what effect?

A

short-term and long-term effects such as fibrosis, mutagenesis, carcinogenesis, and teratogenesis

103
Q

MAIN DETERMINANTS OF BIOLOGIC EFFECTS OF
IONIZING RADIATION

A
  1. Rate of delivery
  2. Field size
  3. Cell proliferation
  4. Oxygen effects and hypoxia
  5. Vascular Damage
104
Q

MAIN DETERMINANTS OF BIOLOGIC EFFECTS OF IONIZING RADIATION

Fractionated doses of radiant energy have a cumulative effect only to the extent that repair during the “recovery “intervals is incomplete

A

Rate of delivery

105
Q

MAIN DETERMINANTS OF BIOLOGIC EFFECTS OF IONIZING RADIATION

The body can sustain relatively high doses of radiation when delivered to small, carefully shielded fields, whereas smaller doses delivered to larger fields may be lethal.

A

Field Size

106
Q

MAIN DETERMINANTS OF BIOLOGIC EFFECTS OF IONIZING RADIATION

  • Because ionizing radiation damages DNA, rapidly dividing cells are more vulnerable to injury than quiescent cells
  • Tissues with a high rate of cell division, such as gonads, bone marrow, lymphoid tissue, and the mucosa of the gastrointestinal tract, are extremely vulnerable to radiation, and the injury is manifested early after exposure.
A

Cell proliferation

107
Q

MAIN DETERMINANTS OF BIOLOGIC EFFECTS OF IONIZING RADIATION

Poorly vascularized tissues with low oxygenation, such as the center of rapidly growing tumors, are generally less sensitive to radiation therapy than non-hypoxic tissues.

A

Oxygen effects and hypoxia

108
Q

MAIN DETERMINANTS OF BIOLOGIC EFFECTS OF IONIZING RADIATION

Damage to endothelial cells, which are moderately sensitive to radiation, may cause narrowing or occlusion of blood vessels leading to impaired healing, fibrosis, and chronic ischemic atrophy.
- These changes may appear months or years after exposure.

A

Vascular Damage

109
Q

MAIN DETERMINANTS OF BIOLOGIC EFFECTS OF IONIZING RADIATION

used to treat certain cancers however; it can also lead to development of secondary cancers elsewhere

A

Radiotherapy

HistoPathology (10 decks)

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