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113 Cards in this Set

  • Front
  • Back
What is Groud level ozone
it refers to ozone in the troposhere and is harmful
How is ground level ozone formed
it is formed by a chemical reaction b/w oxides of nitrogen and volatile organic compounds in the presence of sunlight and hot wheather
Ground level ozone is the primary constituet of ....
smog
whats the pathophys of ground level ozone
it damages Epi cells lining the Res. tract. and also damages type 1 alveolar cells
what are the chemical manifestations of groundlevel ozone
1. Coughing, and pain when taking a deep breath
2. Wheezing and breathing difficulties
3. Aggravation of asthma and increased susceptibilty to respiratory ilness
4. Permanant Lung Damage
How is CO formed
it is formed by incomplete combustion of carbon
56% of all CO emissons worldwide come from
Motor vehicle ehaust... other causes include
Cigarrette smoking
Residental wood burning
forest fires
the highest levels of CO in outdoor air occur during....
it occurs during the colder months. when inversions conditions are more frequent. aslo the air pollution becomes trapped near the gound becomes of the warm air.
CO binds to..
Hb.200 greater affinty
Cytochrome oxidase
CO leads to
hypoxia at 20-30%
at 60-70% lead to unconsis and death.
What happens during Chonic CO poisning
due to low level but peritent amount of CO

it is caused by widespread ischemic changes in CNS in the BG and LENTICUALR NUCLIE
What happens duirng Acute CO
due to accidental exposure on suicide attempts

CHERRY RE COLOR IN SKIN AND MUCOUS MEMBRANDE

BRAIN EDEMA AND PUNCTATE HEMORRHAGE, NERUONAL DEATH
CO LEVEL
.1-.9%
NORMAL
Carboxyhb levels correlate with acute Co poisinng
10-30 %
INCREASING HAche and dyspnea
Carbosyhb levels correlate with acute Co poisning
40-50
SEVER HA AND TACHYCARDIA
carboxyhemoglobin levels correlate with acute CO poisning
60-70%
COMA SEIZURES.. OFTEN FATAL
CarboxHb levels correlate to CO toxciity
80%
RAPILY FATAL
Sulfur oxides are formed when..
they are formed when fuel contaiing sulfur is burned, or when gasoline is extracted from oil... or metals extracted from ore.
when SO2 dissloves in vapor what does it form
it forms sulfurinc acid.. it then interacts other gasses to from sulfate
greater thatn 65% of SO2 released to air comes from what
electirc utilites..especially those that burn coal.
What problems does SO2 cause
respiratory problems...
WHat are nitrogen oxides
a group of highly reactive gases... usually colorless and odorless..but NO2 seen as a reddish brown layer over many urban areas
how are nitrogen oxides formed
when fuel is burned at high temperatures as in a combustion process
what are the primary manmade sources of NOx
are motor vehicles, electric utilities
N oxides can help produce...
ground level ozone
N oxides can react with ammonina and form
nitric acid,... and it can damage lung tissue and casu or worsen res. dis such as ephymesema and brochititis
Nitrogen can react with other substances in the air and form
acid rain.
major source of lead emmissoins
motor vehicles but now are near lead smelters... waste incenerators.... lead-acid battery manufectors
dont forget flanking lead paint...old building
most human exposure to lead occur by
Ingestion (children) and Inhalation.
Why are children are at a greater risk for leadt toxciity....
b/c children absorb >50% fo lead from contamnated foods while adults absorb 15%

2. they also have a more permable BBB.. more suceptable to brain damage.
when the lead is absorbed where does it go...
Bone 85%...1/2 life :20-30 yrs aslo in developing teeth

2. 5-10% remain in blood 1/2life 28-36 days
Why do women with prior lead exposrue and significant bone ead levels have a greater chance of exposing the fetus and infant to lead
b/c lead may be releasd from bones duirng times of Ca stress... suc as pregancny and lactation.
Pregnant women with elevated blood lead levels main hae an increased chance of ..
1. Preterm labor
2. Spot. abortion or still birth
3. LBW infant
4. impaired brain development in the fetus...
Lead competes with what and binds to what in the bone
Ca... PO4
lead binds to what type of enzymes
those containtng sulfhydrl groups... such as those that invovled in heme synthe
when lead inhibits Na and K dependent cell adenosin triPO4s what type of anmeia does it cause
hemolytic anemia... remembr lead aslo inhibts enzymes containg sulfhydryl groups such as those involved in heme syntheis and that can cause mychocytic anemia
what type of anemia develops when it inhibths sulfhydr. using enzymes
microcytic hypochromic anema... see this in lead poisining
with increasing dose what are the clinical manfestations of lead toxiciity
1. decreased learning and
memory and hyperactivity

2. fatigue, irritbable.. palor

3. Ab. pain vomiting.. constipation

4. paralysis, encephalopthy, death
what is the most usfull screnning and diagnositc test for recent or ongoing lead exposure
venous blood lead concentration (BLC)
BLC <10
no action req.
BLC 10-19
It a venous blood lead concetration. its a usefull screening nd diagnostic test for ongoing lead exposure.

Re test in 3 months x2, if persienty elevated follow the 20-44
lead exposure
BLC 20-44
retest monthly
perform clinical evaul
provide lead education
BLC 45-69
perform clinical evaul and manage with chelators witin 48 hurs
retest montholy
BLC >70
its a medical emergence
hospitlzie and begin immediate chelation therapy
pr
what are some of the chealing agents for lead
Ca disodium edetate
dimercaprol
d-penicillamine
succimer
mercury exists in what 3forms
(metallic quick silver
inorganic mercury (salts)
organic ...methylmerucury
methymercury comes from what type of food
fish... shellfish, and animals that eat fish
all forms of merucury cause what type of symptoms
1. neuromuscualr signs
2. renal failure
Elemen. Mercury...it specifcally cause
inhalation.. respiratory failure
inorganic mercury causes...
Skin rashes
Emotinal changes
Mem. Loss and Congnitve Distu
Muscle Weakness
why is methymercury so toxic
b/c it is very lipophilic
Arsenic interferes with what
mito. oxidative phosporlation
acute Arsenic toxcitity signs and symptoms
GI,
Cardio
CNS
Chronic Arsenic toxciity
skin hyperpig. hyperkeratosis
sq. cell and basal cell carin
lung carn.
cadmium casues
Obsturctive lung dx
Renal tubular damage
osteoporiss
osteomalcia
benzene causes
aplastic anema
AML
polycyclic hydrocarbons
very potent carcinogen... in cig.
oral cavity larnx and lung

p53?
organochlorines
antiestrogenic
antiandrogenic
vinyl choloride.. and industrial or agriculture exposure
hepatic angiosarcoma
what is the most common eogenous cause of huma cancer and most preventable cause of death
tobacco
what is responsible for 90 % of lung cancers
cigarette smoke... it also multiples the carcinogenic potential of ethanol and / uranium cancer
what are the componets of cigar. smoke
polycylci hydrocargons (beznene)
Naphthylamine
nitroso
polonium-210
arsenic
nicel, chromium
Napthylamine
urinary bladder cancer

one of the carcinogens found in cigarettes
nitroso
Cancer of esophagus, pancreus, oral cavity

one of the carcinogens in ciggarettes
polonium 210
Cancer in the oral cavity laryns LUNG

it is one of the carcinogen in ciagrettes
ARSENIC..chronic exposure to this toxin can cause
cancer of skin and lung
nickel chromium
cancer of nasas sinuses

one of the carcinogens in cigarette smoke.
smokeless tobacco is an important cause of
oral carcinoma
smoking can
1. increase platlet adhesion
2.decrease myocardial oxygen supply.. as result of res. dx
3. increase oxygen demand
4. trigger arrythima
is smoking is a riskfactor for development of atheroscleroiss and acute mocardial infaction
yes
maternal smoking increases the risk of
1. Spot. abortion
2. placental abrubtion
3. premature rupture of membranes
4. placenta previa
5. LBW
6. Prematurity.
the only way to prevent second hand smoke
is the eliminate active smoking competly.
what is the most common drug of abuse
ethanol
whats heavy drinking
drinking more than 2 drinks per day on average for men or more that noe drink per day on average for women
what is binge drnking
drinking more that 4 drinks during a single occasion for men or more that 3 drinks dring a single occaseion for women
breath ethanol is proportionoal to what
blood ethanol lvel
what is the definition of drunk.
80 mg/dl of ethanol in the blood is the legal definition of drunk
what 3 enzymes metabolize ethanol... which is oxidized to acetaldehyde.
1. alchol deydrogenase (major)
2 microsmoal cytochrome P-450.. this is important at high blood ethanol levels
3. peroxisomal catalase (minor)
Whats the mech. for mito. actealdyde dehydrogenase
acetaldehyde is oxidized to acetic acid...
why do they say they have empty calories when driking beer.
when ethanol is oxidized by alcohol dehydrogenase requres the conversion NAD to NADH. and it is the increased ratio to NADH to NAD inibits fatty acid oxidation and promotes fatty acid synthesiss... leading to hepatic steatosis or fatty liver... also this inhibits oxidation of lactate to pyruvate ( producing metabolic aciosis)
oxidation by cytochrome p450 produces
ROS that cause membrane injury by lipid peroxidation
Ciliatoxins (hydrogen cyanide
one of the constituents of cig SMOKE THAT affects res. heath.... it impairs tracheobronchial clearacne
One of the things you see in CIG SMOKE
respiratory irritants
(NO2 and formaldeyhede)
one of the constituents affect res. health... it induce sumbucosal gland hypertrophy., increase in goblet cells

and chronic bronchitis
Smokers are prone to (in terms of the respiratory system)
1. Acute res tract infectoin
2. acute and chronic sinusitis
3. chronic obstructive airway dx

4. Chronic bronchiits (centriacinar emphysema)
Smoking can
1. increse platelet adhesion and aggregation
2. decrease myocardial oxyen supply as a result of respiratory dx
3. increase cardiac oxygen demand
4. trigger cardiac arrhythmia
smoking is a rskf factor for develoment of
atherosclerosism, and acute MI and stroke
maternal smoking increases the risk of
Spontaneous abortions
• Acute placental abruption
• Premature rupture of
membranes
• Placenta previa
• Prematurity
• Low birth weight infants
Ethanolo may release what from intestinal bacteria
endotoxin.. the latter produces from cell injury by stimulating RES cells to release cytokines such as tumor necrosis factor.
Methano toxciity is caused by
Inebriation, vomiting, blurring of vision (“as if looking
through a snowstorm”), metabolic acidosis, anion and
osmolar gaps
ethelyene glycol
Inebriation, acute renal failure, oxalate and glycolate in
urine, metabolic acidosis, anion and osmolar gaps
Isopropyl alcohol
Inebriation, fruity odor in breath, osmolar gap
Acute ethanol toxciity causes
hepatic statosis
gastritis and gastric ulceration.
cns depression that may lead to respiratry arrest
Chronic ethanol toxcity can casue
o Alcoholic fatty liver disease
o Gastrointestinal bleeding (gastritis, ulcers, varices)
o Malnutrition and vitamin deficiencies (thiamine
deficiency)
o Congestive cardiomyopathy
o Acute and chronic pancreatitis
o Increased risk of oral, esophageal, hepatic, and breast
cancers
Fetal alcohol syndrome
• Growth retardation and developmental defects
o Craniofacial dysmorphism:
 microcephaly, short palpebral fissures, smooth philtrum
o Brain malformations: holoprosencephaly
o Cardiovascular defects: atrial septal defect
o Genitourinary malformations
o 0.2 to 1.5 per 1,000 live births
the most common tpe of preventable mentla retardatin in the us is
FAS
in regards to alchol and preg.
There is no known safe amount of alcohol to
drink while pregnant and there also does not
appear to be a safe time to drink during
pregnancy (CDC
what are te risks nof HRT
it increase the risk of
ovarian ca/breatcancer
endometrial cancer.. although this is reduced if given progestins,

it increased the risk of venous thromboembolism (DVT, PE, and stroke)
Oral Contracetpties
increase the risk of Venous thromboembolism
increase risk of atherosclerotic cardio dx in women smoker older than 35 yrs

increased rsik of heaptic ademoms with prolonges use
increased risk of cerveral cnaer..

no increase in risk of breast cancer
decreased risk of endo and ovarian cancers...
95 % of Acetamnophen is ..
conjugated in liver with glucuronide or sulfate
5 % of Aceaminophen is ...
converted to NAPQI.. via cytochorme p450 enxyme...
at toxic does of ACPN
thats 12- 15 grams... NAPQI accumulates i the liver and prouces CENTRILOBAR (ZONE 3 NECROSIS).. BY COVALENT BINDING TO HEPATIC PROTEINS AND DEPLETION OF REDUCED GLUTAHIONE
glutahione can be repleted by
inve N-acetylcysteine
Acute overdose of Aspirin cna lead to
res. alkalosis folowied by metabolic acidosis that may be fatal
in chronic toxicity of asprin the clinica manfestations that you see are
HA
Tinnitus
Hearing diffculty
Confusion
drowsy
N/v
GI bleedin
blood diathesis
analgesic nephropathy
Reyes syndrome you see
acute encephl. microvesical
hepatic failure
high mortality
after adminstraion of asprin ton child
mito. dysfxn.
What are the acute affects of Coocaine
Cardioeffects
>>>sympathometic. blocks the reuptake of DA in the CNS and epi and NE reuptake in the peripheral nerve

>>> disrupts ion transport in myocardium

>>>> taky HTN Perpheral an coronary VC

CNS effects
>>> hyperpyrexia seziures
what are the chronic effects of coccaine abuse
nasal septal performatoin in snorters

decreaed pulmanory diffusing capacity insmoke inhaliers

dilated cardio.
Maternal cocaine abuse affects the fetus...
spontaneous abortions, placental abruptoion

fetal hypoxia and brain damange
what are the features of nonionzing radiation.
o Long wavelengths, low frequencies
o Electric power, radio waves, microwaves, infrared
light, visible light, ultraviolet light
o Produce vibration and rotation of atoms
Ionzing radiation
o Short wavelengths, high frequencies
o Electromagnetic - X-rays, gamma rays, cosmic rays
o Particulate - alpha and beta particles
acute effects of Ionizing radiatoin
Acute Effects..
1. Direct injury or via fomration of free radicals

2. DNA-protein and DNA-DNA cross links, degradation of bases, cleavage of suar-phosphate bonds, DNA breaks

3. Activation of TF and corresponding genes invovled in cell cycle arrest, DNA repair, apoptosis
What are the chronic effects of ionzing radiation
1. Vascualr injury-ischemia-fibrosis
2. chronic ulcers and strictures
3. Poor wound healing
4. Cataracts
5. infertility
Carcinogenesis of ionizing radiation
o Persistent DNA lesions
o Epigenetic mechanisms
(CpG methylation,
telomere shortening)
o All leukemias except for
chronic lymphocytic
leukemia
o Carcinomas and sarcomas
n