Environmental Pathology Flashcards by Carson Spornhauer

Q

Environmental diseases

A

injuries or disorders that are caused by chemical or physical agents

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Q

Frequent adverse chemical agents

A

cleaning agents, analgesics, cosmetics, plants (ponsettia) and cold meds (i.e asprin)

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Q

Adverse drug events account for ___% of chemical agent exposures

A

2

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Q

children under the age of 6 account for ___% of chemical exposures

A

61

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Q

oral intake accounts for ___% of chemical exposures

A

73

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Q

how many hazardous exposures/yr are in the U.S?

A

2 million (90% are unintentional)

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Q

occupational medicine

A

injuries that occur in the workplace related to chimcal and physical agents
-U.S work injuries are 2x more frequent than at home injuries and are at an annual cost that exceeds 25 billion dollars

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Q

factors that affect chemical injuries

A

CLADME
c- concentration
l- liberation
a- absorption
d - distribution
m - metabolism
e - excretion

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Q

US agencies involved in regulating environmental hazards include

A

EPA, FDA, OSHA and consumer products safety administration

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Q

categories of environmental diseases

A

air pollution
industrial exposures
tobacco smoke
*physical agents
*chemical agents (therapeutic and non)
*radiation
*nutritional (caloric and vitamin forms)

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Q

how common are adverse drug reactions by therapeutic agents (things that are supposed to make us feel better)? of hospitalized people?

A

2% of adverse drug reactions are by therapeutic drugs

7-8% of people hospitalized are from therapeutic agents (10% of those in the hospital have fatal rxns)

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Q

what can major injury by therapeutic agents lead to?

A

most injury by therapeutic agents are minor, but major rxns can lead to anaphylaxis, blood clots, arrhythmias or hematologic conditions. potency dependent
ex. penicillin and anaphylactic shock or anti-cancer meds

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Q

ADR to aspirin

A

ingestion of 2-4 gm (7 tablets) for kids or 10-30 gm for adults may be fatal. respiratory alkalosis followed by metabolic acidosis. Chronic ingestion may result in tinnitus, dizziness, drowsiness etc.. and progress to seizures and comas
** think: when you are exercising you breathe quickly (resp alk) but you are not metabolizing the acid production from your mm. enough and you create lactic acid (metabolic acidosis)

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Q

ADR to acetaminophen (tylenol)

A

overdose has to be pretty significant (15-20 g) and damage to the liver occurs over hours or days which can lead to jaundice and shock or heart and liver damage

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Q

exogenous estrogens and BC injury

A

used in the past for perimenopausal symptoms and osteoporosis but assoc. with breast cancer and clots leading to strokes LONGTERM. Short term may have a better ratio of risk:reward

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Q

lead toxicity can affect (7 things) ….

A

blood - Pb competes with Fe for RBC synthesis so microhypochromic anemia results
Gingiva - hyperpigmentation from Pb deposits
Brain (CNS) - in adults leads to memory loss and kids it leads to neurological disorder, learning disabilities and sensory deficits
Peripherial nn. - in adults leads to demyleination (wristdrop and footdrop)
GI tract - stomach ache
kidney - interstitial fibrosis and possibly renal failure
bones - competes with Ca during bone formation and causes hyperdense lead lines to form on x-rays

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Q

Maximum allowable lead blood levels

A

5 ug/dl (reduced from 10)

** begin chelation treatment at 45, but chelation tx is not always effective, so AVOID Pb

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Q

Side effect of MDMA (ecstasy) is..

A

bruxism (hold a pacifier in their mouth to protect and store another hit)

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Q

physical agents

A

mechanical or temperature changes

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Q

mechanical injuries

A

abrasion (superficial layer i.e scrap)
contusion (does not break the skin, i.e bruise)
laceration (irregular violent tear)
puncture wounds and incisions

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Q

thermal burns cause how many deaths per year in the U.S?

A

5000 +

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Q

factors that affect the clinical significance of burns includes

A

1) percentage of the total body surface affected (rule of 9’s)
2) depth of the burn (deep vs. superficial)
3) internal inhalation of fumes
4) age (very young and old)
5) how fast/well is the tx (Ab or occluded quickly)

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Q

BSA in percentage (rule of 9’s)

A

head and neck - 9
trunk back - 18
trunk front - 18
each arm - 9
perineum - 1
each leg - 18

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Q

clinical consequences of burns (prognosis)

A

> 50% bsa then regardless of tx the prognosis is grave
20% then shock is common due to fluid drop (can lead to DIC), secondary infection and electrolyte and nutritional imblances
internal thermal injuries in any region of the resp. tract can result from fumes and may cause an acute resp. distress syndrome

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hyperthermia

an increase in the ambient (surrounding) temperature or exercise an increase in temp that increases the internal body temperature without causing burns)

forms of hyperthermia

heat cramp (vigrous exercise and fluid loss), heat exhaustain (CV system fails to adjust to the hypovolemia and pt. collapses) and heat stroke (high mortality rate )

heat stroke

abnormal elevation of body temp above 40 degrees celsius, peripheral vasodilation causes "pooling" and the amount of circulating blood decreases leading to ischemic tissues and mm. necrosis. Can lead to DIC

hyopthermia

abnormally low core temperature that is exacerbated by high humidity, wet clothes and alcohol (vasodilation)

hypothermia leads to (locally)

chilling and crystallization of water that can cause cells to burst and die (frost bite) if the cells don't die then circulatory changes occur (to keep the vital organs alive) and vasoconstriction edema to the peripheries may result (trench foot), long term this can lead to atrophy ad fibrosis

hypothermia (systemically)

disorientation - paradoxical undressing (exactly what it sounds like)

forms of radiation

waves (gamma and x) and particles (high energy neutrons)

mechanisms of radiation injury

directly damages DNA (mutations arise) or indirectly through free radicals interacting with enzymes, nucleic acids and membranes **cytoplasm is also affected in cells

organ systems that are affected by radiation

** cells that turn over quickly are the most susceptible to radiation skin, hematopoeitc, gonads (sterility?), lungs, GI and any blood vessel exposure

what is the occupational exposure limit

less than 20 mSv/yr

what are the units that measure radiation

Gray (Gy) and Sievert (Sv) | -Sv factors in the relative biologic effect

explain the changes in the skin after radiation therapy

erythema (2-3 days) -->edema (2-3 weeks) --> blistering (4-6 wks) --> atrophy, fibrosis and neoplasia months or years later

changes in the hematopoietic/lymphoid system after radiation therpay

**** extremely sensitive lymphocyte number decreases in hours, but rebounds in wks/mo (lymph and spleen may shrink) PMN (granulocytes) decrease in 1-2 weeks and rebound in 2 to 3 mo. (pt susceptible to infection!!!) and platelets and RBC decrease and take longer to rebound, but precursors are more vulnerable

lung changes after radiation therapy

sensitive because of vascularity | -pulm congestion and edema (sets up infection), ARDS, endothelial changes, alv-capillary block

lethal full body radiaiton

begins at 2 Sv, but 7 Sv is certain death without tx | ** after like an atomic bomb

fatal acute radiation syndromes (3)

1) hematopoietic - (2-10 sv) - decreased WBC, platelets and anemia with bleeding problems (die in 2-6 weeks) 2) GI - (10-20 sv) - bloody poop, dehydration, shock and sepsis (die in 5-14 days) 3) cerebral (>50 sv) - listless, drowsy, coma, death in min-hrs. (i.e star trek reference)

primary malutrition vs. secondary malnutrition

primary - diet is deficient in 1 or more components secondary - supply adequate, but problem with absorption, storage, utilization, excessive losses or drug effects (ex. Chrohns)

an adequate diet has 3 components

1. carbs, protein and fats (macros) 2. essential amino acids and fatty acids for structural and functional proteins and lipids 3. vitamins and minerals

what are the 2 important protein compartments

somatic (skeletal mm. ) - marasmus -measure skinfold thickness visceral (liver mainly) - serum proteins

marasmus

- PEM deficiency in caloric intake (when weight falls below 60%) - body is wasting (cachexia looking) - somatic compartment is taken away, but keep the visceral - anemia, immune deficiency (T mediated) so THRUSH may result - the smaller the pt. gets, the more everything slows down

kwashiorkor

greater deficiency in protein than total calories - africa and SE asia - more of a problem than marasmus - visceral protein lost (albumin lost so edema results) - PUFFY look, so weight appears to be normal (60-80%) - fatty liver, skin changes (hyperpigmentation), vitamin and immune deficiency

how many kids under the age of 5 are affected by PEM?

25%

if a childs weight falls below 80% what are they considered?

malnurished

secondary forms of PEM

chronically ill patients (i.e cancer and aids) cachexia results because of decreased intake (loss of apetite) and an increase in catabolism from cytokines (IL-1 and 6 and TNF)

fat soluble vitamins

-healthy intestinal mucosa, bile and pancreatic secretions are required -stored easily because of lipid solubility (6 - 12 mo last) BUT need to keep replenishing because we don't make them or deficiency will result slowly -decreased absorption in alcoholic liver disease and chronic malabsorption states like crohns

3 biologically active forms of vitamin A

retinol, retinal and retinoic

vitamin A found in

leafy green and yellow plants and eggs and fish

where is vitamin a stored?

in the liver (90% of vit a) and is released with retinol binding protein so if you have liver disease

functions of vitamin A

maintain vision in reduced light, augments differentiaiton of specialized epi cells (mucous secreting) and enhances immunity to infections

vitamin A deficiency

in 3rd world countires - early sign is impaired night vision - persistent deficiency is dry eyes that can lead to cornea damage and complete blindness - squamous metaplasia of the respiratory and urinary tracts (increased rick of infection and stones) - impaired immunity

vitamin A toxicity

excessive use of supplement or rarely acne medication (topical retinoids) - infants are susceptible -acute toxicity is blurred vision and nasuea chronic toxicity is anorexia, hair loss, dry skin and cracked lips etc..

Vitamin C

- water soluble - found in citrus fruits and veggies and some milk and animal products - heat liable so fresh food is the best

Vit C deficiencies are from

being old AF, alcoholics, erratic eating habits (fads), dialysis pts, and infants that are not fed vit c fortified milk

vit c functions

stabilize and form collagen, convert tyrosine to catecholamines and is an antioxidant

vit C deficiences result in

-hemorrhaging in the skin and gingival mucosa (weak collagen) and a lot of other places, insufficient production of osteoid matrix so skeletal changes to more cartilage (causes bowing), impaired wound healing PERIO infection COMMON

Such a thing as vit c toxicity?

high doses of vit c prevents colds? acidic urine causes stones? some cancer risk goes down with high doses, enhanced iron absorption, iron overload??, megadoses that are stopped can cause rebound scurvy. excessive ingestion possible