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137 Cards in this Set

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Incidence of Occupational Injury in US
7,400/100,000 (4.8/100,000 fatal)

{130 million US workers at risk)
Highest Risk occupations
Mining > Transportation > Agriculture > construction > public utilities#
# of Chemical agents used in US
# pesticides
# food additives
# tested (% carcinogenic)
80,000 chems in use
1500 pesticides
5500 food additives
600 tested (10% carcinogenic)
Types of chemical exposure
who gets ppm?
who gets ppb or ppt?
workers- ppm
general population- ppb or ppt
phases of toxin metabolism
Phase I reactions- generate primary metabolites and toxic byproducts (eg benzopyrene metabolism)

Phase II reactions- involve conjucation of primary metabolite with endogenous substrate for excretion (eg methylation of mercury and bioaccumulation)
variation in effects of a toxin, depends on
-Genetic variation in enzyme activity (eg glutathione in various cancers)
-Predominant metabolic pathway
-Nutritional/hormonal status
-Presence of other exogenous substances
-Adequancy of repair pathways
Dose Response Curve shows:
Response v. Dose

Threshold dose:
-measureable response
-permissible exposure

Ceiling effect
Nicotine's Mechanism
-crosses BBB
-stimulates Nicotine receptors, leading to release of Catecholamines
Nicotine
-crosses BBB
-stimulates Nicotine receptors, leading to release of catecholamines

What are the consequences?
Increase:
HR
BP
CBF
CO
FFA mobilization
ADDICTION
Tobacco related diseases
lung cancer
ischemic heart disease
acute respiratory tract infections
cold
fetal abnormalities
PUD
Tobacco can have synergistic effects on what other types of hazards?
workplace hazards:
-lung cancer
-bronchitis
-asthma
-pneumoconiosis
passive exposure to tobacco is associated with:
lung cancer
ischemic heart disease
AMI
SIDS
respiratory tract infections
asthma
most widely used/abused drug
ETHANOL
15-20 million alcoholics in US
100,000 deaths/ year in US
Acute, Chronic effects of Alcohol
Acute = CNS depressent
Chronic = systemic, vitamin deficiencies
elimination of alcohol, by fraction?
90% metabolized to acetaldehyde
rest unchanged in urine, breath, sweat
basis of alcohol tolerance
induction of cytochrom p450 CYP2E1 enzyme
basis for asian flush
reduced ALDEHYDE DH in Asian population
basis for lower alcohol tolerance in women
reduced levels of alcohol DH in women
Chronic Effects of Alcohol
FATTY LIVER (assymptomatic acute reversible)
ACUTE ALC HEPATITIS (symptomatic reversible)
LIVER CIRRHOSIS (10-15% of alcoholics)
WERNICKE-KORSAKOFF SYNDROME (thyamine deficiency)
DILATED CARDIOMYOPATHY
ELEVATED HDL (protective)
FETAL ALCOHOL SYNDROME (most common preventable cause of MR)
primary sites of alcohol absorption
stomach and small intestine
Main enzymes of ethanol metabolism
ADH
ALDH
CYP2E1
CATALASE
Fatty (alcoholic) liver
characteristics
mechanism
Asymptomatic, acute, reversible

Increased catabolism of peripheral fat
Increased NADH for lipid synthesis
Decreased FA oxidation in mito
Decreased transport of lipoproteins from liver (microtubule dysfunction)
Acute (alcoholic) Hepatitis
characteristics
pathology
mechanism
Symptomatic, reversible (fever, tender, jaundice)
Pathology: Necrosis, PMNs, Mallory's hyaline
Mechanism = direct toxicity
-Glutathione depletion
-Mito injury
-Altered methionine metabolism
-cytokine release from Kupffer cells--> activation of more inflammatory cells
-Hypoxia
Liver cirrhosis
-prevalence
-characteristics
-symptoms
-mechanism
10-15% of alcoholics
hard, shrunken, micronodules of hepatocytes surrounded by collagen bands (laid down by ITO cells)

weak, wasted, ascities, GI bleed, coma

mech = DIRECT TOXIC EFFECT or CYTOKINE mediated
Effects of ethanol on nervous system
Acute CNS depression

Addiciton

Wernicke's snydrome (via thiamine deficiency) = ataxia, cognitive problems, opthalmoplegia, nystagmus

Korsakoff syndrome = toxicity and thyamine deficiency
-memory loss
effects of ethanol on the CV system
hypertension (via catecholamine release)
dilated cardiomyopathy
protective effects (increased HDL, decreased platelet aggregation)
most common preventable cause of mental retardation
1200/ year
FETAL ALCOHOL SYNDROME
due to maternal alcohol consumption
growth retardation, microcephaly, short palpebral fissures, maxillary hypoplasia, ASD

?via acetaldehyde toxicity to fetal brain?
Prevalence of Drug abuse in the US
7.5 % US residents aged 15-54
Risk factors for drug abuse
family Hx
male
pschiatric disorders
ethanol abuse
access
peer pressure
drug associated with highest number of drug deaths in NH
METHADONE
examples of sedative hypnotics
ETHANOL
BARBITURATES (associated with tolerance, enzyme induction)
BENZODIAZEPINES (safer)
Stimulants of Abuse
Amphetamines
Cocaine
Amphetamine
-Acute intoxication
long term problems
sweating, tremors, restlessness, confusion, delerium, convulsions, arrhythmias, coma, death

Fetal malformations and withdrawal

MDMA toxic to serotonin neurons (depression, anxiety, panic disorder)

Tolerance and withdrawal
Cocaine
alkaloid extracted from Erythroxylon coca
crack = freebase cocaine
Acute toxicity: rapid high of short duration
chronic abuse: insomnia, anxiety, paranoia, hallucinations
overdose: seizures, cardiac arrhythmias, respiratory arrest
mechanism: blocks reuptake of dopamine, serotonin, catecholamines in presynaptic terminals
mechanism of cocaine's actions
blocks reuptake of dopamine, serotonin, catecholamines in presynaptic terminal
CV effects of cocaine
increased BP
increased HR
coronoary spasm
accelearted atherosclerosis
-enhanced platelet activation/aggregations
-increased PAI
-increased endothelial permeability
Opioid Narcotics
heroin, codeine, morphine
acute effects of opiod narcotics
anxiolytic, sedation, mood changes, nausea, respiratory depression
overdose of opiod narcotics
convulsions, cardiorespiratory arrest, death
problems associated with opioid narcotic abuse
Infection (IVDA)
ski, subcutaneous,
R. sided heart valves (S. aureaus tricuspid)
Liver (viral hepatitis)
lungs
Natural hallucinogens
Mescaline (peyote)
Psilocybin (morning glory flower)
Teonanacatl mushrooms
Marijuana (hemp plant Cannabis sativa)
Chemical hallucinogens
PCP
LSD
active ingredient in Marijunana
THC
effects of marijuana use
induces relaxation, heightened sensation, impaired cognitive, motor functions

chronic use may induce lung damage (not carcinogenic)
what consitutes and ADVERSE DRUG REACTION
undesired response at "therapeutic" doses
frequency of Adverse Drug Reactions
2 million hospitalized patients and 106,000 deaths/ year in the US

unpredictable, related to invidual variations in drug metabolizing enzymes
OC use is associated with increased risk of:
STROKE
MI
THROMOSIS/PE
HPV?
Hormone replacement Tx is associated with increased risk of:
STROKE
MI
THROMOSIS/PE
BREAST CANCER
GALLBLADDER CANCER
Acetominophin therapeutic dose
0.5gm
toxic dose of acetominophen
-symptoms
15-25 gm (hepatic, centrilobular necrosis)
early symptoms: N/V/D/ ... shock
late: jaundice, liver failure, necrosis
ASPIRIN
acute toxicity
-dose
-Cx presentation
2-4 gm kids
10-30 gm adults

Cx: respiratory alkalosis, follwed by metabolic acidosis
ASPIRIN
chronic toxicity
-dose
-Cx presentation
-Pathology
dose: 3+ gm/day

Cx: HA, dizzy, tinnitus, N/V/D, confusion, drowsy, convulsions, coma

Path morphology: acute erosive gastritis due to ulcertaion, petechiae (COX inhibition), renal papillary necrosis
Six Major outdoor air pollutants
OZONE
Nitrogen oxides
sulfur dioxide
particulates
CO
lead
Who is at highest risk for outdoor air pollutants?
kids
asthmatics
chronic heart/lung Dx patients
effect of most outdoor air pollutants
Respiratory tract irritants
sources of lead poisoning
contaiminates air, soil, house dust, ceramics, food and drink
lead absorption is enhanced by:
CA/Fe/Zn deficiencies

greater in kids (80-85% in bone/teeth, 5-10% in blood, rest in soft tissue)
Lead toxicity
organ/system involved (effect)
1) BLOOD (hypochromic anemia via inhibition of iron incorporation into heme)
2) CNS (inverse correlation betwen IQ and blood lead level)
3) Bone, nervous system (competes w/ Ca)
4) GI tract (lead colic)
5) Kidneys (renal failure)
Agricultural hazards
INSECTICIDES (organochorines like DDT, organophosphates, carbamates)
HERBICIDES (dioxins, eg: agent orange)
NATURAL TOXINS (mycotoxins, eg aflatoxin B1, phytotoxins, animal toxins like saxitoxin)
Carbon Monoxide
colorless, odorless gas byproduct of gasoline, oil, coal, wood, natural gas and cigarette smoke

200x affinifity for Hb as O2 and impairs release of O2 from Hb

HA, dizzy, loss motor fxn, coma

900 deaths/ year in US
Radon:
-source?
-effect?
-incidence of toxicity?
radioactive gas decay product of uranium

decay products emit alpha radiation associated with lung cancer in miners

10,000 lung cancer cases per year in US
Industrial sources of lead
beatteries
alloys
exterior lead paint
ammunition
mining
smelting
spray painting
recycling
radiator repairs
Environmental sources of lead
air (leaded gasoline)
soil (exterior lead paint)
water (lead plumbing)
house dust (interior lead paint)
ceramics (lead glaze)
food/ soft drinks (lead solder)
moonshine
insecticides
ORGANOCHLORINES: ddt bioaccumultaes, chlordane and lymphomas?
ORGANOPHOSPHAGES (neurotoxins) irreversibly inhibit cholinesterases (40% of farm workers)
CARBAMATES (reversibly inhibit cholinesterase)
Agent Orange is a:
DIOXIN (an Herbicide)
-increased incidence of leukemia, lymphoma, sarcoma
-immunosuppresive, teratogenic and carcinogenic in lab animals
Natural Toxins
mycotoxins (aflatoxin B1 and liver cancer)
Phytotoxins (cycasin and ALS)
animal toxins (saxitoxin and paralytic shellfish poisoning)
ETOH is involved in what % of traffic deaths?
40%
Types of Physical hazards
Mechanical
Thermal
Electical
Pressure
Types of Thermal injuries
Burns
Hypothermia
Hyperthermia
Thermal injury- burns:
5000 deaths/yr in US
vary in severity (partial/ full thickness)
shock at 20% BSA
>50% BSA = FATAL

Shock, inhalation injury, secondary infection, hypermetabolic state
Rule of 9
used to guage % BSA involved in burn
Head = 9% (18% in infants)
neck = 1%
arm = 9% each
trunk = 18% each side
leg = 18% (13.5% infant) each
total = 100% BSA
Partial thickness burns
1st degree (epidermis only)
2nd degree
Full thickness burns
3rd and 4th degree
-dry, white or charred
-total destruction of epidermis, dermis
mechanism of Shock due to Thermal burn
@ 20% BSA burned

increased local interstitial osmotic pressure and increased vascular permeability
mechanims/ Cx features of inhalation injury due to thermal injury
direct head and gas toxins

may be delayed 24-48 hours
Complications of Thermal burns
Shock
inhalation injury
Secondary infection
hypermetabolic state (40% BSA doubles metabolic rate)
Manifestations of Hyperthermia
Head cramps
Heat exhaustion
Heat stroke
most common manifestation of hyperthermia
HEAT CRAMPS
voluntary muscle cramps d/t electrolyte imbalance d/t exertional sweating
normal core temp
characteristics of HEAT EXHAUSTION
prostration and collapse d/t hypovolumia, d/t water depletion, d/t sweating with inadequate fluid replacement
Normal core temp
heat stroke
characteristics of HEAT STROKE
failure of thermoregulation at high ambient temperature and humidity
-elderly, militar recruits, athletes at risk
-loss of sweating results in ELEVATED CORE TEMP, vasodilation and reduced circulating blood volume
-myonecrosis, arrythmia, DIC
-50% mortality if T > 106 F
Hypothermia
loss of thermoregulation aggravated by humity and ethanol (cutaneous vasodilation)
systemic effects of hypothermia
at T < 90F there is LOC, bradycardia, AFib
local effects of hypothermia
direct: crystallization of water with increased salt
indirect: vasoconstriction and permeability (edema, ischemia)
Electrical injuries
low vs high voltage
low voltage - cause vFib
high voltage- cause paralysis of medullary centers, asystole
Result of electrical injuries
no effect, sudden death, thermal burns
type of electrical current that causes tetany
AC (vs. DC)
Effects of high altitude (4000m +)
Pulmonary Edema (HAPE)
Cerebral EDEMA (HACE)
Examples of Barotrauma/decompression sickness
Rapid decompression
CAGE
bends, chokes, staggers
Caissons disease of bone
Primary causes of malnutrition
Ignorance
Poverty
Self-imposed
Secondary causes of malnutrition
Malabsorption
Impaired utilization/storage
Excess losses
Increased BMR
Protein Energy Malnutrition
inadequate intake of protein and calories
25% of kids in dvpg world
-SOMATIC (skeletal muscle) depleted in MARASMUS)
-VISCERAL (organs, eg liver) depleted in KWASHIORKOR
Dx of Protein energy malnutrition
body wt for height
fat stores (skin fold thickness)
muscle mass (midarm circum)
serum proteins (reflect visceral stores)
MARASMUS
severe reduction in cals
<60% normal body weight
growth retardation, muscle loss, fat loss (wasted extremities, large head)
-preserved albumin
-anemia, immune deficiencies (infection)
KWASHIORKOR
protein deprivation (CHO diet)
60-80% normal body weight
severe loss visceral stores (LOW ALBUMIN) leads to edema
relative sparing of fat and muscle stores
skin changes (flaky paint), hair changes, fatty liver, loss of appetite, apathy, listlessness, immune deficiency (infections)
Secondary cuases of Protein Energy malnutrition
cancer, AIDS, chronic GI disease, bedridden patients

signs: depletion of subcutaneous fat, muscle wasting, sacral/pedal edema
Anorexia nervosa
amenorrhea, reduced bone density, anemia, hypoalbuminemia at risk SCD
Bulimia
less amenorrhea, at risk for aspiration, esophageal/gastric rupture, SCD
obesity (BMI > 30)
related diseases:
diabetes, hypertension, CAD, osteoarthritis, hypoventilation, pancreatitis, NASH, ischemic stroke, venous thrombosis)
% of adults in US-
OVERWEIGHT:
OBESE:
35 % overweight
30% obese
Dx obesity:
BMI:
normal: 18.5-24.9 kg/m^2
overweight = 25-29.9 kg/m^2
obese: >30kg/m^2
skin fold measurements
body circumferences (waist to hip ratio)
SYNDROME X
abdominal obesity
insulin resistance
increased TAG
decreased HDL
hypertension
coronary artery disease
etiology of syndrome X
disorder of energy balance
genetic environmental and psychological factors
neurohumoral mechanism
-afferent system (humoral signals from fat, pancreas, stomach)
-CPU (hypothalamus)
-effector system (feeding behavior and energy expenditures)
Leptin
cytokine secreted by adipocytes
crosses BBB and binds leptin receptors
inhibits anabolic circuits and triggers catabolic circuits
reduces food intake and promotes energy expenditure
Leptin deficient mice are morbidly obese
elevated blood levels (low CSF levels) in most obses persons
6 known genetic causes of obesity
Leptin receptor, POMC and PC1 (4)
-autosomal recessive, rare
-hyperphagia, childhood onset massive obesity

Melanocortin receptor (1)
-common (5-8% obese persons)
-inability to stimulate energy consumption

SIM1 transcription factor (1)
-essential factor for formation of second order Leptin enurons
these reduce risk of fatal MI and sudden cardiac death
Omega-3 Fatty acids
restricting sodium has beneficial effect on what?
BP
dietary fiber prevents what disease?
diverticulosis
fruits and veggies with limited meat and processed foods lowers risk of?
MI
calorie restriction, increases what?
lifespan
fruits and vegetables lower risk of cancer via???
anticarcinogenic effect of carotenoids (vit A)?
High animal fat and low fiber diets are associated with what type of cancer?
-supposed mechanism?
COLON CANCER
-increased bile acids alter intestinal flora
-intestinal floral alter bile acids
-altered bile acids carcinogenic or promotor
why might a high fiber diet be protective against colon cancer?
decreased transit time
certain fibers bind carcinogens
Pneumoconioses
non-neoplastic LUNG RXN to inhalation of mineral dusts in workplace

now includes rxns to organic and inorganic particulates, fumes and vapors
Pathogenesis of Pneumoconioses
-amt of dust retained (concentration, duration of exposure, clearance mechanisms)
-size/shape of particles (1-5micrometers most dangerous)
-particle solubility and reactivity (inflamm/immun response)
-other irritants (cig. smoke)
Coal Workers' Penumoconisosis
decreased incidence with dust reduction
<10% develop PMF (pulmonary hypertension and cor pulmonale)
NO increased TB susceptibility
NO predisposition to lung cancer (unless smokers)
INCREASED INCIDENCE chronic bronchitis, emphysema
morphology of CWP
asymptomatic anthracosis:
asymptomatic anthracosis:
inhaled carbon engulfed by M0s in CT and lymphoid tissue)
morphology of simple CWP
coal macules and nodules
upper lobes most, upper lower lopes at respiratory bronchioles
morphology of complicated CWP (PMF)
multiple massive (up to 10 cm blackened scars)
most prevalent chronic occupational disease in the world
SILICOSIS
SILICOSIS results from:
inhalation of crystalline silicon dioxide (silica)
most prevalent chronic occupational disease in the world (sandblasters, mine workers)
characteristics of Silicosis
slowly progressive, nodular, fibrosing (over decades)
less commonly, acute accumulation of lipoproteinaceous material in alveoli (mos to yrs)
Pathogenesis of Silicosis
crystalline (more fibrogenic) or amorphous silica
-engulfed by M0s
-release of mediators (eg TNF)
-amplification of inflammatory response
early stages of Silicosis
nodules in upper lung zones containing BIREFRINGENT silica
later stages of silicosis
-coalesced hard collagenous scars
-cavitation
-eggshell calcification
-PMF
clinical course of silicosis
-fine nodularity in upper lung zones on chest xray
-shortness of breath (PMF)
-increased TB susceptibility
-carcinogenic?
Asbestos related diseases
(involve chrystalline hydrated silicates that form fibers)
Occupation:
-fibrous pleural plaques
-pleural effusions
-interstitial fibrosis (asbestosis)
-lung cancer
-mesotheliomas
-extrapulmonary neoplasms
Increased incidence of asbestos related cancer in family members
Pathogenesis of Asbestos related diseases determined by:
concentration, side, shape and solubility of fibers
longer fibers more pathogenic
SERPENTINE (most common, less pathogenic, soluble)
AMPHIBOLE (more pathogenic, deeper penetration, only exposure correlated with meothelioma)
Oncogenicity of Aspestos
initiator and promoter activity
reactive free radicals
adsorbed toxic chemicals (synergy w/ tobacco smoke ~5x to 55x risk)
Morphology of asbestosis
-lower lobes, subpleural around bronchioles, ducts
-diffuse interstitial fibrosis with honeycombing (pulmonary hypertension, core pulmonale)
-asbestos bodies (golden brown beaded rods)
Morphology of Pleural plaques (most common asbestos disease)
well circumcribed collagen plaques with Ca
no asbestos bodies
Lung cancer (risk increase associated with smoking)
5x risk increased with smoking
Meothelioma (risk increase with smoking?
1000x risk
clinical course of Asbestosis
-delayed 10 or 20 yrs after exposure
(dyspnea on exertion to rest, cough with sputum production)
-CXR irregular linear densities lower lung lobes, plaques
-may progress to respiratory failure, cor pulmonale, death
hypersensitivity pneumonitis
hypersensitivity of alveoli to inhaled organic dusts (allergic alveolitis)
-thermophilic bacteria (actinomycetes, Farmer's lung)
-true fungi
-animal proteins (pigeon breeder's lung/bird fancier's disease)
-bacterial products
immune-mediated pathogenesis in hypersensitivity pneumonitis
-increased chemokines in BAL specimins
-increased T cells in BAL speciments
-specific Abs in serum
-complement and immunoglobulins in vessel walls
-noncaseating granulomas in most
morphology of HP (hypersensitivity pneumonitis)
interstitial pneumonitis (lymphocytes, plasma cells M0s)
-noncaseating granulomas
-interstitial fibrosis and obliterative bronchiolitis
-intra-alveolar infiltrate
Cx features of HP (hypersensitivity pneumonitis)
-acute attacks of fever, dyspnea, cough, leukocytosis, 4 to 6 hours after exposure
-diffuse and nodular infiltrates on chest radiograph
-acute restrictive disorder on PFTs
-progression with protracted exposure to respiratory failure, dyspnea, cyanosis, decreased TLC and compliance