Environmental Flashcards

1
Q
  1. ‘Environmental diseases’ refers to injuries or disorders that are caused by
A

chemical or physical agents.

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2
Q
  1. A related field, occupational medicine, focuses on injuries that occur in the workplace from
A

environmental factors.

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3
Q

It has been estimated that in the US work-related injuries occur

A

2x more frequently than home injuries at an annual cost that exceeds $25 billion.

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4
Q
  1. US agencies involved in regulating environmental hazards include:
A

a. Environmental Protection Agency
b. Food and Drug Administration
c. Occupational and Safety Health Administration
d. Consumer Products Safety Commission

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5
Q
  1. Categories of Environmental Diseases:
A

a. Air Pollution – outdoor/indoor pollution
b. Industrial Exposures – coal, asbestos, other metals
c. Tobacco Smoke – major public health problem
d. Chemical agents – therapeutic & nontherapeutic drugs
e. Physical agents – mechanical trauma, thermal injury
f. Electrical injury
g. Radiation injury
h. Nutritional diseases

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6
Q

A. General – injuries can occur by

A

inhalation, ingestion, injection or absorption thru the skin.

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7
Q

Estimated 2 million potentially hazardous exposures each

A

year in the U.S. most (90%) are unintentional.

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8
Q
  1. Oral intake accounts for about
A

73% of exposures

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9
Q
  1. Children less than
A

6 yrs account for about 61% of exposures

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10
Q
  1. Adverse drug events account for about
A

2%

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11
Q

The most frequent environmental agents are common household items:

A

cleaning agents, analgesics, cosmetics, plants or cold preparations.

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12
Q

Factors that affect chemical injuries: “CLADME” which stands for:

A
  1. Concentration
  2. Liberation
  3. Absorption
  4. Distribution
  5. Metabolism
  6. Excretion
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13
Q

A. Injury by Therapeutic Agents – Adverse drug reactions (ADR’s) are common affecting an estimated

A

7-8% of hospitalized persons and about 10% of these are fatal.

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14
Q

Anaphylaxis can occur with any medication, but is most often associated with

A

antibiotics (penicillin is the classic).

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15
Q

The more potent the drug – the more likely it is to cause an

A

adverse reaction – anti-cancer drugs are the best examples.

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16
Q

Some other notable ADR’s:1. Acetaminophen (Tylenol®) – overdose occurs after

A

large ingestion (15-20 g).

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17
Q

Some other notable ADR’s: Aspirin (Acetylsalicylic acid or ASA) – overdose may be

A

accidental (young kids) or intentional (adolescents/adults). Ingestion of as little as 2-4 gms (kids) or 10-30 gms (adults) may be fatal.

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18
Q

Tylenol Toxicity is by damage to the

A

liver which occurs over several hours to days. Early symptoms are non-specific – nausea, vomiting, diarrhea, but will be followed by jaundice and shock as the liver failure progresses. There may also be heart and kidney damage as well.

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19
Q

Aspirin The major acute injury is a

A

metabolic one – first there is respiratory alkalosis followed by metabolic acidosis.

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20
Q

Aspirin: Chronic ingestion (3 gm or more per day) is associated with

A

headaches, dizziness, ringing in the ears (tinnitus), drowsiness, mental status changes, gastritis, GI bleeding, nausea and vomiting. It may progress to seizures and coma.

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21
Q

Some other notable ADR’s: 1. Exogenous Estrogens & Oral Contraceptives – until 2002, estrogens were widely used for

A

postmenopausal syndrome (hormone replacement therapy or HRT) and to prevent or slow progression of osteoporosis.

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22
Q

Estrogens: More recent studies indicate that patients receiving long term HRT are at increased risk for

A

breast cancer, strokes and blood clots.

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23
Q

Estrogens/oral contraceptives: The benefits of SHORT term therapy

A

(alleviation of severe peri-menopausal symptoms or prevention of osteoporosis if no other modality is effective) may outweigh these risks.

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24
Q

OCP’s have been in use for

A

> 30 yrs. Like all medications there are known risks (blood clots, hypertension, hepatic adenoma, cholecystitis, slightly increased risk in breast cancer) and benefits (contraception, protective effect for endometrial and ovarian cancers) to their use.

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25
Q

OCPS: have protective effect for

A

endometrial and ovarian cancers

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26
Q

A. Injury by Nontherapeutic Agents – the spectrum of agents is quite large ranging from

A

environmental exposures - lead, carbon monoxide, cleaning agents, cyanide, ethylene glycol, organophosphates (pesticides), mercury, plants (mushrooms), petroleum products and PCB’s to agents that may be ingested for mind/mood altering experiences.

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27
Q
  1. Lead – lead is found in many places in the environment –
A

urban air, soil, water, food, house dust, gasoline (historical), batteries, and older paints (lead-based). Exposure to lead also occurs in certain occupations – foundry workers and mining.

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28
Q

Lead has a high affinity for enzymes involved in the synthesis of

A

hemoglobin which blocks or hinders the incorporation of iron into the molecule.

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29
Q

Lead poisoned patients develop a

A

microcytic hypochromic anemia.

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30
Q

A majority (80-85%) of absorbed lead is taken up by the

A

bones and teeth.

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31
Q

Lead competes with

A

calcium and interferes with the normal remodeling process.

Bone becomes hyperdense with changes (lead lines) visible on x-rays.

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32
Q

Lead deposits in the gums causes

A

hyperpigmentation.

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33
Q

Lead toxicity in the CNS is most likely to occur in

A

kids.

A number of neurologic disorders may be seen – ranging from mild deficits to sensory, motor, cognitive and psychologic. Reduced IQ’s and learning disabilities may result.

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34
Q

In adults lead toxicity may lead to

A

peripheral neuropathies (wristdrop and footdrop).

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35
Q

Lead toxicity in the GU tract is characterized by

A

severe, poorly localized, “colicky” pain.

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36
Q

Lead is also toxic to the

A

renal tubules, which may lead to interstitial fibrosis and renal failure.

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37
Q

Monitoring lead exposure is a public health responsibility. The maximum allowable blood lead level was reduced from

A

10 to 5 ug/dL in 2012.

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38
Q

Lead Treatment is generally by

A

chelation therapy (starting at 45 ug/dL) and supportive measures.

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39
Q

a. Sedative-hypnotics –

A

alcohol, barbiturates, benzodiazepines

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40
Q

b. CNS stimulants –

A

cocaine, amphetamines, weight loss products

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41
Q

c. Opioids –

A

heroin, morphine, methadone, codeine

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42
Q

d. Cannabinoids –

A

marijuana

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43
Q

e. Hallucinogens –

A

LSD, mescaline, phencyclidine (PCP), ketamine

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44
Q

f. Inhalants –

A

glues, toluene, paint thinner, gasoline, amyl nitrate, nitrous oxide

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45
Q

g. Nonprescription drugs –

A

atropine, scopolamine, antihistamines, weak analgesics

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46
Q

Club Drugs – a collective term for substances that have become popular in dance clubs, bars, raves or trances. There are a variety of drugs including

A

methamphetamines (such as MDMA, ecstasy), hallucinogens (LSD, ketamine and, CNS depressants (GHB) and benzodiazepines (Rohypnol).

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47
Q

One of the side effects of MDMA is

A

bruxism – clenching of teeth. One way of dealing with this is by using a pacifier, reportedly used to store another “hit”.

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48
Q
  1. Abrasion - a wound produced by
A

scraping or rubbing leading to removal of a superficial layer of skin

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49
Q
  1. Contusion –
A

(bruise) a wound caused by a blunt object, doesn’t break the skin but may lead to damage to blood vessels and extravasation of blood in tissues.

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50
Q
  1. Laceration –
A

a tear in tissue – usually with irregular, jagged edges.

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51
Q
  1. Thermal burns – cause
A

> 5000 deaths per yr in the US.

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52
Q

Body operates in temperature range of

A

31o to 41oC (89-106oF)

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53
Q

Hyperthermia (burns) – cause

A

> 5000 deaths/yr in the US

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54
Q

a. Factors affecting clinical significance of burns

A

1) percentage of total body surface involved (Rule of 9’s)
- Head & neck 9%, Trunk front 18%, trunk back 18%, Arms 9% each, hands: 1% each, Legs 18% each, Perineum 1 %)
2) depth of the burn (full or partial thickness)
3) possible internal injuries from inhalation of hot gases and fumes
4) the age of the patient
5) how fast & how well is it treated?

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55
Q

b. Clinical consequences of burns:

A

1) > 50% total body surface involvement is grave 2) shock is frequent with > 30-40% total body surface involvement
a) massive fluid shifts causing hypovolemic shock
c) sepsis/infections – Pseudomonas spp., candida
d) other problems - electrolyte, and nutritional imbalances

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56
Q

3) Internal thermal injury

A

a) noxious fumes (CO, cyanide)
b) any part of respiratory tract may be damaged
c) delayed - acute respiratory distress syndrome (ARDS)

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57
Q
  1. Hyperthermia: Heat cramps –
A

vigorous exercise with loss of fluid & electrolytes (sweat)

58
Q
  1. Hyperthermia: b. Heat exhaustion –
A

most common, failure of the CV system to adjust to hypovolemia. Sudden onset, collapse, usually recover

59
Q
  1. Hyperthermia: c. Heat stroke -
A

abnormal elevation of the body temperature above 40oC, regulatory mechanisms fail and the body core temperature rises.

60
Q

In heat stroke, Peripheral vasodilatation causes

A

“pooling” and decreased circulating blood volume. Tissues become ischemic, necrosis of the muscles and heart may lead to disseminated intravascular coagulation (DIC). High mortality rate especially in elderly and persons under severe physical stresses (athletes).

61
Q
  1. Hypothermia
A

-Abnormally low core temperature
Promoted by high humidity, wet clothes, vasodilatation (EtOH)
Mild (core temp =) 32-35oC (89-95oF) ,Moderate 28-32oC (82-89oF), Severe < 28oC (< 82oF)
Bradycardia, atrial fibrillation, loss of consciousness

62
Q

a. Local chilling or freezing of cells and tissues:

A

rate dependent

63
Q

Hypothermia: direct effects due to

A

crystallization of water

64
Q

Hypothermia: 2) indirect effects -due to

A

circulatory changes, trench foot gangrene

65
Q

Hypothermia: b. Systemic reactions –

A

disorientation, including paradoxical undressing

66
Q
  1. Sources of radiation -
A

Cosmic rays, Ultraviolet light, Elements in earth’s crust, e.g. radon, medical (diagnostic and therapeutic), industrial products, nuclear power plants, nuclear weapons

67
Q

Radiation forms: Forms

A

a. Electromagnetic waves – x-rays and gamma rays

b. High-energy neutrons and charged particles (alpha and beta particles, protons)

68
Q

Gray (Gy) is a unit that expresses the

A

amount of energy absorbed by target tissue

69
Q

Sievert (Sv) roughly equal to Gy, but

A

dose also factors in relative biologic effect (RBE)
Single chest x-ray: 0.01 mSv
CT imaging: 2 mSv (head), 8 mSv (abdomen)
Single dental intraoral image: 0.002 mSv
Cone beam CT (CBCT): 0.02 - 0.08 mSv

70
Q

2.Occupational exposures should be

A

< 50 mSv/yr

71
Q

a. Radiation interacts with atoms and molecules by

A

excitation and ionization

72
Q

Radiation Interacts with biological systems in the following ways:

A

1) target effect - direct hit on DNA, causing mutations
2) indirect effect - production of free radicals that interact with
membranes, nucleic acids and enzymes

73
Q

1) target effect -

A

direct hit on DNA, causing mutations

74
Q

2) indirect effect -

A

production of free radicals that interact with

membranes, nucleic acids and enzymes

75
Q

Radiation a. Skin - changes occur

A

over time – erythema (redness) at 2-3 days, edema (2-3 wks), blistering and desquamation (4-6 wks), atrophy & cancers (months to yrs)

76
Q

Radiation: . Hematopoietic and lymphoid,

A

extremely susceptible: lymphocytes decrease in hours and rebound (hopefully) in weeks to months. Lymph nodes and spleen shrink in size. Granulocytes decrease over 1-2 wks and rebound in 2-3 months, pts are susceptible to infections at this time! Platelets and erythrocytes fall still later and have even more delayed recovery periods (erythrocytes resistant, but precursors are vulnerable)

77
Q

Radiation: c. Gonads

A

both sexes sensitive (possible sterility), uterus and cervix are resistant.

78
Q

Radiation: Lungs (sensitive because of the

A

rich vascularity), endothelial changes, pulmonary congestion and edema, ARDS, alveolar-capillary block

79
Q

Radiation: e. Gastrointestinal tract, very

A

sensitive; ulcers, strictures and later possible carcinomas

80
Q

Radiation:

f. Other: e.g. blood vessels exposed to radiation first have

A

endothelial

injury then later may become fibrotic and narrow

81
Q
  1. Total body radiation effects – even small amount of radiation to the whole body can be
A

devastating. The lethal range for humans begins about 2 Sv; at 7 Sv death is certain without medical care (even then mortality is quite high).

82
Q

Fatal acute radiation syndromes (FARS)

A

a) Hematopoietic
b) Gastrointestinal
c) Cerebral

83
Q

Hematopoietic FARS:

A

2-10 Sv, GI symptoms, decreased white blood cells, platelets, and anemia; resultant sepsis and bleeding problems, death in 2 to 6 weeks

84
Q

Gastrointestinal FARS –

A

10- 20 Sv, severe GI symptoms, bloody diarrhea, producing dehydration, shock, sepsis and death in 5-14 days

85
Q

c) Cerebral (FARS)-

A

> 50 Sv – listlessness, drowsiness, followed by seizures, coma and death in 1-4 hrs.

86
Q

A. An adequate diet is one that should provide:

A
  1. sufficient CHO’s, protein & fats for the daily metabolic needs
  2. essential amino acids and fatty acids for synthesis of structural and functional proteins and lipids
  3. vitamins & minerals – coenzymes or hormones
87
Q

A. Primary malnutrition – diet is deficient in

A

1 or more components

88
Q

Secondary malnutrition – supply is

A

adequate, but there may be a problem with absorption, storage, utilization, excessive losses, or drug effects

89
Q

E. Protein-Energy Malnutrition (Protein-Calorie Malnutrition)

A

IDK, know that this is a thing?

90
Q

Ways to assess nutritional status –

A

body weight (compared to age, sex & height norms), rate of growth (charts)

91
Q

There are 2 protein compartments in the body:

A

somatic, visceral

92
Q
  1. Somatic protein compartment –
A

skeletal muscles – can assess loss of this compartment by measuring skinfold thickness

93
Q
  1. Visceral protein compartment – mainly the
A

liver - can assess this compartment by measuring serum proteins (albumin, transferrin)

94
Q

The 2 major disorders in which the intake of protein and/or calories is inadequate:

A

marasmus and kwashiorkor.

95
Q

In marasmus there is deficiency of

A

caloric intake which results in growth retardation and loss of muscle mass as the body catabolizes protein (amino acids) as a source of energy.

96
Q

Marasmus: As a result the somatic protein compartment is

Subcuatneous fat is also

A

depleted. Subcutaneous fat is also broken down.

97
Q

When weight falls to < 60% of normal – child has

A

marasmus. The extremities are emaciated.

98
Q

Other marasmus manifestations include

A

anemia and immune deficiency, especially the T-cell-mediated immune system.

99
Q

Thrush is a common finding and an indicator of

A

immune system deficits.

100
Q

Body temperature and pulse rate may be decreased with

A

marasmus

101
Q

In kwashiorkor there is a greater deficiency of

A

protein than total calories.

102
Q

Kwashiorkor is the most common form of PEM found in

A

Africa, it is also found in SE Asia. Kwashiorkor is more severe than marasmus.

103
Q

Kwashiorkor: There is severe loss of the

A

visceral protein compartment.

104
Q

Kwashiorkor: The decreased albumin causes a loss of

A

vascular oncotic pressure and generalized fluid retention and edema may result (which can mask the true extent of the weight loss).

105
Q

Kids with kwashiorkor will classically have skin changes

A

– hyperpigmentation, desquamation and hypopigmentation – a “flaky paint” appearance, hair changes, fatty liver, vitamin and immune deficiencies also occur.

106
Q

PEM is common in third world countries; it contributes to high mortality rates in kids less than

A

5 years old. Comparison of individual body weight with normal weight for age, sex and height of the child is used to assess nutritional status. Comparison with past rate of growth is helpful

107
Q

When the weight falls to less than 80% of normal the child is felt to be

A

malnourished.

108
Q

Secondary forms of PEM can be seen in

A

chronically ill/hospitalized patients (even in the US).

109
Q

A form of wasting that is encountered in cancer patients – cachexia – probably results from decreased

A

intake (loss of appetite) as well as an increase in catabolism (cytokine-mediated).

110
Q

A. Vitamin Deficiencies – are common in people living in lower socioeconomic groups and are usually a part of general malnutrition. Deficiencies may be primary: ——– or secondary: ———-

A

(insufficient diet) or secondary (problem with absorption, transport, storage, utilization, metabolism, etc).

111
Q

Vitamins are classically divided into

A

fat-soluble (A, D, E, K) and water-soluble.

112
Q

Fat-soluble vitamins need

A

healthy intestinal mucosa, bile and pancreatic secretions for absorption.

113
Q

chronic malabsorption states

A

(inflammatory bowel diseases – for example Crohn’s disease or cystic fibrosis)

114
Q

in chronic malabsorption states and alcoholic liver disease the absorption of the

A

fat-soluble vitamins will be poor. On the other hand, because of lipid solubility, these vitamins can be easily stored and deficiency usually develops slowly.

115
Q

A. Vitamin A – first described in 1909, found to prevent night blindness in 1925, is made up of 3 biologically active forms:

A

retinol, retinal and retinoic acid.

116
Q

Vitamin A found in

A

yellow and leafy green vegetables and in some animal products (liver, fish, eggs, milk & butter).

117
Q

Over 90% of vitamin A is stored in the

A

liver, where there are reserves for 6-12 months. When needed retinol is released by the liver and is bound to a carrier protein (retinol-binding protein).

118
Q

Vitamin A functions:

A

Functions:

  1. maintain normal vision in reduced light
  2. augments differentiation of specialized epithelial cells (mucus-secreting)
  3. enhance immunity to infections, esp in children
119
Q

Vitamin A deficiency: Early sign is impaired

A

vision at night. If the deficiency persists, then there will be dryness of the conjunctiva (xerosis).

120
Q

vitamin A deficiency: The mucosa of the lacrimal glands will be replaced by

A

keratinized epithelium and keratin debris may accumulate. Further drying may lead to damage to the cornea and total blindness is possible.

121
Q

Vitamin A: In addition to the ocular changes – the epithelium of the respiratory and urinary tracts may be undergo

A

squamous metaplasia. This will predispose to infections.

122
Q

Finally the immune system is affected by vitamin A deficiency – common infections such as

A

measles, pneumonia and infectious diarrhea may result.

123
Q

Toxicity – excessive ingestion (25,000 IU or more daily) of vitamin A can result from

A

over use of vitamin supplements and rarely from using topical retinoids (for acne).

124
Q

Infants are especially susceptible to

A

vitamin A toxicity.

125
Q

Symptoms of acute Vitamin A toxicity =

A

nausea, vomiting, irritability, headache, blurred vision (papilledema).

126
Q

Symptoms of Vitamin A chronic toxicity =

A

anorexia, hair loss, dry skin, pruritis, dry mucus membranes, fissured lips, fatigue, weight loss, bone & joint pain.

127
Q

A. Vitamin C – a

A

water-soluble vitamin, ascorbic acid was isolated in 1932 as an antiscurvy agent.

128
Q

Vitamin C is an essential vitamin (we cannot synthesize it) that is found abundantly in

A

citrus fruits, vegetables (tomatoes, g. peppers, cabbage, leafy greens, potatoes). It is also found in milk and some animal products.

129
Q

Ascorbic acid is

A

heat labile so fresh and uncooked foods have highest content.

130
Q

Vitamin C Functions:

A
  1. formation and stabilization of collagen (hydroxylation of proline & lysine)
  2. conversion of tyrosine to catecholamines
  3. role as an antioxidant
131
Q

Scurvy is a disease of impaired

A

collagen synthesis.

132
Q

Weakened collagen doesn’t support the walls of

A

capillaries & venules – thus hemorrhages are a common finding in the skin and gingival mucosa. Other sites for bleeding include the joints (hemarthrosis), behind the eye, subarachnoid space and within the brain (can be fatal).

133
Q

Scurvy: Skeletal changes are found in infants and kids –

A

there is insufficient production of osteoid matrix resulting in cartilaginous overgrowth, bowing of the long bones (esp the legs), depression of the sternum.

134
Q

Scurvy: Wound healing

A

(needs collagen) is impaired, Ability to localize infections is impaired, anemia (due to bleeding and iron deficiency) is common.

135
Q

With scurvy the following are common:

A

Gingival bleeding, swelling and periodontal infections are common.

136
Q

The idea that high doses of vitamin C prevents colds has

A

not been conclusively established.

137
Q

Some protection from gastric and esophageal cancers has been reported

A

due to high doses of Vitamin C

138
Q

. Large daily ingestions of Vitamin C can enhance

A

iron absorption which could create iron overload in susceptible persons.

139
Q

Ingesting large doses of Vitamin C will

A

acidify the urine which may increase risk for stone formation (data is controversial).

140
Q

Finally if a person abruptly ceases taking megadoses of Vitamin C they may precipitate

A

“rebound scurvy” because of enhanced clearance mechanisms.