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DT4- Exam 3 > IL- Environmental Path- Melissa > Flashcards

IL- Environmental Path- Melissa Flashcards

1
Q

Define “Disability-adjusted Life Years”. What is the equation used to determine this?

A

Sum of years of life lost to premature mortality, disability, or illness

Normal life expectancy for healthy individuals without disease…
Men = 80yrs
Women= 82.5yrs

Example: If 200 of 1000 healthy males suddenly die at 40, and the remaining live without liability until 80…

DAILY= 200men (80yrs-40yrs) = 8000man-year/1000men

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2
Q

What is the most common cause of global health loss?

A

Undernutrition

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3
Q

What is the most common cause of death in the developed vs. the developing world?

A

Developed: Heart/ Cerebrovascular disease
Developing: Infection

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4
Q

List the 5 most common causes of childhood death:

A
  • pneumonia
  • diarrhea
  • malaria
  • measles
  • prenatal/neonatal diseases
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5
Q

What are the three “emerging infectious diseases?

A
  • drug resistant organisms
  • pathogens introduced via other species (i.e HIV)
  • resurgence of infection
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6
Q

Define Xenobiotics:

A

Exogenous chemicals from environment (typically lipophilic for transmembrane movement)

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7
Q

What type or reactions are phase I reactions?
Do these reactions activate or inactivate drugs?
Which enzymes catalyze these reactions, and where do these reactions take place?

A

Phase I reactions:

  • hydrolysis, REDOX
  • CYP P450 system; mostly in liver
  • many genetic polymorphisms
  • can activate or inactivate

**Can make innocuous chemical toxic metabolite…

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8
Q

What type or reactions are phase II reactions? (4)

What is the point of phase II reactions?

A

These reactions metabolize materials to water soluble molecules for easy excretion; inactivation reactions

  • glucuronidation
  • sulfonation
  • methylation
  • conjugation
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9
Q

What is ground level ozone?

How does it act as a pollutant?

A
  • leads to free radical production

- injures respiratory tract epi

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10
Q

What is sulfur dioxide?
Where does it come from?
How does it act as a pollutant?

A
  • from fossil fuels and plants
  • becomes sulfuric acid + sulfuric trioxide
  • irritates respiratory tract
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11
Q

How do particulates (soot) act as pollutants? Where do they come from?

A
  • from coal + fossil fuel
  • UNDER 10 um irritate respiratory tract + eyes
  • engulfed by MQs; trigger release if inflammatory mediators that damage the RT
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12
Q

What kind of pollutant it CO?
How does it cause disease?
What are the acute and chronic manifestations of toxicity?

A

Colorless, oderless, tasteless, nonirritating gas; kills by asphyxiation

Binds Hb (STABLE)–> CarboxyHb CAN NOT CARRY O2–> Asphyxiation @ 20% CarboxyHb

Acute toxicity: CNS depression, cherry red skin/mucosa

Chronic Toxicity: Hypoxia w CNS impairment

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13
Q

What are 7 means of lead poisoning in modern day WV?

A
  • Mines
  • Foundries
  • Batteries
  • Paint from houses built BEFORE 1978
  • Leaded gasoline
  • Toys made before 2007 (REALLY, WTF?)
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14
Q

Where is lead absorbed in the body? With what element does it compete in mineralization? How long can it stay in the body?
How does it manifest clinically in the MSK system?

A
  • Absorbed by bone + teeth
  • Competes with Ca
  • t 1/2 = 20-30yrs
  • Interferes w cartilage remodeling, primary bone trabecular, and fracture healing
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15
Q

What are lead lines?

A

Result from increased Ca deposition; dense thick bone in the metaphysis seen with lead poisoning

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16
Q

What is Plumbism?
How does it manifest?
What do you see on peripheral smear?

A

Chronic lead poisoning–> Compromised heme synthesis–> ^ free RBC zinc bound protoporphyrin

Smear: Microcytic, hypo chromic anemia, basophilic stippling RBCs, ringed sideroblasts

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17
Q

What is basophilic stippling? ringed sideroblasts?

A
  • BS: RNA aggregates in RBC

- RS: RBC precursors with stainable Fe

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18
Q

Describe the manifestations of plumbism in children:

A
  • lower IQ
  • poor organizational skills
  • Bx issues (^hyperactivity)
  • hearing loss
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19
Q

Describe the manifestations of plumbism in adults:

A
  • HA
  • Memory loss
  • Peripheral neuropathy (foot + wrist drop)
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20
Q

That are two miscellaneous findings associated with plumbism at any age?

A
  • Lead colic (nonspecific abdominal pain)

- Chronic TUBULOINTERSTITIAL DISEASE (renal toxicity)

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21
Q

What is the most common means of mercury toxicity

A

Exposure in via fish and shellfish –preggos beware

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22
Q

What are the symptoms of mercury toxicity win the fetus/child vs. the adult?

A
  • fetus/kiddos: major CNS damage

- adults: peripheral neuropathy/ CNS depression (mad as a hatter)

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23
Q

How do people become exposed to arsenic?

Describe the timeline of clinical manifestations (acute–> weeks–>long term effects)

A

Soil/ Water/ Agricultural preservatives especially in Bangladesh

Acute:
Stops OXPHOS–> CNS/ CV disturbance

2-8Wks:
Neuropathy/ msk cramping

Long term:
Lung + skin cancer on palms and soles; hyperpigmented/hyperkeratosis of palms and soles; anemia

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24
Q

How do patients become exposed to cadmium? (4)

A 
• Mining
• Electroplating
• Nickel-cadmium batteries
• Food
(elevated in 5% US adults)
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25
Q

Describe how cadmium poisoning manifests in the lung, kidney, and bone:

A

Lung
-COPD (alveolar MQs) + Cancer

Kidney
-TUBULAR damage + renal failure

Osteoporosis/osteomalacia

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26
Q

List the organic solvents (3)

A
  • Chloroform
  • CCl4
  • Benzene
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27
Q

What are the effects of acute exposure to chloroform or CCl4?
To which 2 organs are these compounds toxic? Which type of cancer is asstd with exposure to these toxins?

A
  • CNS depression, dizziness, confusion, coma
  • toxic to liver and kidney
  • ^ risk hepatocellular ca.
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28
Q

How is benzene toxic to the body? Which cancer is asstd with benzene exposure?

A
  • Causes dose dependent marrow aplasia–> pancytopenia

- ^ risk AML

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29
Q

How are humans exposed to polycyclic hydrocarbons?

With which three types of cancer are these toxins asstd?

A

Fossel fuels

  • scrotal cancer
  • lung + bladder cancer
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30
Q

What are organochlorines? List the three chemicals included in this group.

A
  • Lipophilic, halogenated compounds resistant to degradation
  • CYP inducers

DDT, PCBs, Dioxins

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31
Q

How would DDT, PCB, Dioxin toxicity manifest?

A
  • Endocrine dysfxn. (Anti E, Androgen activity)

- Chloracne: facial cysts, hyper pigmentation, hyperkeratosis (dermatitis, PCP or dioxin only)

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32
Q

What is chloracne?

A

PCB or Dioxin tox–> Dermatitis: facial cysts, hyper pigmentation, hyperkeratosis

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33
Q

Vinyl chloride increases the risk of what type of cancer?

A

Liver angiosarcoma

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34
Q

Phthalates toxicity has what two effects?

A
  • endocrine dysfunction

- testicular dysfunciton

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35
Q

What percent of lung cancers are caused by smoking?
What is the discrepancy in life expectancy between smokers and nonsmokers?
How long does it take one AFTER SMOKING CESSATION to decrease risk to level comparable with nonsmoker?

A
  • 90% lung cancers due to smoking
  • 50% smokers survive to 70 (vs. 80% for nonsmokers)
  • takes 30 years after smoking cessation to decrease risk to level of nonsmoker
36
Q

Passive smoking increases ones risk for lung cancer by how much compared to those not exposed?

A

1.3x

37
Q

What is the formula for pack years?

A

Pack Years = # packs per day x # years smoked

1.5 ppd for 20yrs = 1.5 x20 = 30 pack years

38
Q

List the 4 carcinogens in cigarettes:

Is nicotine a carcinogen?

A
  • nitrosamines
  • polycyclic aromatic hydrocarbons
  • tar
  • formaldehyde

NICOTINE IS NOT CARCINOGENIC (but is addictive)

39
Q

What causes lung cancer in cigarette smokers? Which compounds are synergistic with cigarette smoke for this purpose?

A
  • secondary local inflammation leads to lung cancer

- asbestos + uranium are synergistic w cigarettes

40
Q

What is synergistic with cigarettes to cause oral cancer?

A

ETOH; note that oral cancer also associated with chewing tobacco

41
Q

List the 6 cancers associated with cigarette smoke:

A
  • lung
  • oral
  • esophageal (squamous cell)
  • pancreatic
  • bladder
  • renal
42
Q

Which metabolite of nicotine can be found in the blood?

A

Cotinine

43
Q

Which chronic diseases are associated with smoking (2)

A
  • atherosclerosis

- COPD ( emphysema + chronic bronchitis )

44
Q

How is smoking dangerous to preggos (4)?

A
  • spontaneous abortion
  • preterm birth + LBW
  • intrauterine growth restriction
  • SIDS
45
Q

How is ETOH absorbed?
What is the legal definition of drunk?
Which BACs will make you drowsy, stuporous, dead?

A

Absorbed unchanged in the stomach and sm bowel

  • Drunk = 0.08% (80mg/dL)
  • Drowsy = 0.2%
  • Stuporous = 0.3%
  • Dead = 0.4%
46
Q

How is ETOH excreted?

Describe the metabolic process and name the location of each enzyme involved…

A

10% excreted unchanged in urine and breath

Metabolism occurs in the LIVER:
ETOH + cytosolic ALD + microsomal CYPS–>
Acetaldehyde + mitochondrial ALDH–>
Acetic acid/Acetate–> Enters mitochondrial resp chain

  • ALD= alcohol dehydrogenase
  • ALDH= acetaldehyde dehydrogenase
47
Q

What are the ALDH variants; which is wild type and which will render patient unable to metabolize ETOH?

A

ALDH2*1 = normal allele

ALDH2*2 = unable to metabolize acetaldehyde–> acetate

  • Hetero= reduced ability
  • Homo = complete disability
48
Q

How does acute alcoholic affect the liver, stomach, CNS?

Which are also issues associated with chronic disease?

A

Liver–> hepatic steatosis
Stomach–> gastritis + ulcers
CNS–> cognitive + motor impairment; ^^ resp depression

**all of the above can become chronic issues with chronic etoh abuse as well…

49
Q

How does CHRONIC alcoholism affect the liver?

Which livercancer is asstd with chronic ETOH abuse?

A
  • hepatic steatosis
  • alcoholic hepatitis
  • cirrhosis (portal HTN–> esophageal varacies)
  • ^ risk hepatocellular carcinoma
50
Q

How are the pancreas and CV system, affected by chronic ETOH abuse?

A
  • pancreas: acute and chronic pancreatitis

- CV system: dilated cardiomyopathy, HTN

51
Q

Which nutrient is commonly deficient in alcoholic patients?

What are the affects of this deficiency?

A

Patients generally malnourished with exceptional deficiency in THIAMINE (B1)–> peripheral neuropathy + wernicke-korsakoff syndrome (psychosis–>memory impairment)

52
Q

When does delirium tremors onset? how does it manifest?

A

3-10 days after last drink; global confusion + sympathetic overdrive

53
Q

Which three cancers are associated with ETOH abuse?

A
  • hepatocellular ca
  • esophageal squamous cell ca
  • oral cancer
54
Q

During what point in pregnancy is ETOH most dangerous to fetus?
Describe the findings associated with fetal alcohol syndrome (4).

A

ETOH most dangerous within first trimester (very littler ETOH causes massive effects)

Characteristics of disease:

  • growth retardation
  • microcephaly
  • flat philtrum, small upper lip, short palpebral fissures
  • cognitive impairment
55
Q

What is are 2 benefits to HRT? What are 3 risks?

A
  • REDUCES osteoporotic fractures
  • DECREASES CVD risk if STARTED BEOFRE 60yoa
  • ^ thromboembolic risk
  • ^ breast cancer risk
  • ^ hepatic adenoma risk
56
Q

What are 3 risks associated with OCP use?
How are the risks amplified for smokers?
What is one BENEFIT to OCP use

A
  • ^ thromboembolic risk
  • ^ risk CVD (ESPECIALLY W SMOKERS)
  • ^ risk hepatic adenoma
  • DECREASED risk endometrial + ovarian cancer
57
Q

8 effects of anabolic steroid (AS) use?

A
  • Inhib FSH, LH release (AS–> estrogens)
  • gynecomastia
  • testicular atrophy
  • stunt adolescent growth
  • acne
  • premature MI
  • cholestasis–> jaundice
  • psychosis (roid rage)
58
Q

Describe how acetaminophen is metabolized.
Describe how toxicity manifests.
How does toxicity present clinically early on? later?
How is it treated?

A

Metabolized in the LIVER; typically conjugated to sulfate/ glucuronate –> nontoxic metabolites

OVERDOSE overwhelms system–> CYP rxns–>
TOXIC METABOLITES–> Glutathione reductase overwhelmed (glutathione depleted)

Presents w n/v/d–> centrilobular necrosis–> liver failure
(50% acute liver failure cases in US!!!)

Treat with n-acetylcystine (restore glutathione)

59
Q

Describe the physiological course of ACUTE (overdose) Acetylsiacylic acid toxicity. How does this manifest clinically?

A

Respiratory center stimulation–> RESPIRATORY ALKALOSIS–> ^^ Lactate + pyruvate –> METABOLIC ALKALOSIS

Krebs + OXPHOS dysfunction–> Nausea–> Coma

60
Q

Describe the clinical manifestations of CHRONIC acetylciacylic acid toxicity in the CNS, GI, and heme systems?

A

CNS: HA/ dizziness, tinnitus, confusion/ drowsiness, coma
GI: acute gastritis; bleeding + ulceration
Heme: platelet inhibition–> bleeding

61
Q

What is analgesic nephropathy?

A

ASA + Acetaminophen–> tubulointerstitial nephritis + papillary necrosis

62
Q

What is the MOA for cocaine? How does toxicity present?

What might one indicator of chronic abuse be?

A

^NE release; prevents NE, Epi, DA reuptake

  • *causes generalized sympathomimetic effects in CV, CNS, etc.
  • *look for perforated nasal septum to indicate abuse
63
Q

What is the MOA for heroine? What are the effects?

A

Opioid agonist; causes euphoria, sedation, somnolence, etc; sympatholytic effects (dry mouth, miosis, etc.)

64
Q

What are some complications that can occur with heroine use? How about from just cutting the drug?

A

Remember that heroine abuse can cause arrhythmia + pulmonary edema (in addition to other more obvious stuff)

Cutting heroine can cause GRANULOMATOUS inflammation in the lungs, spleen, liver, and lymph nodes due to inhalation of particulate matter.

65
Q

What can you get if you inject heroine?

A

AN INFECTION, duh.

possible septic emboli/ endocarditis , HIV/HBV, access/ cellulitis

66
Q

How does heroine use affect the kidneys?

A

Causes nephrOTIC syndrome

67
Q

How do methamphetamines work? What kind of effects do they have? What can result with chronic use?

A

^^DA release in synapse; sympathomimetic effects

Chronic use can clean to violence, psychosis, paranoia, confusion/hallucinations

68
Q

How does MDMA work?

A

^^5HT release; induces euphoria, mydriasis, hyperpyrexia, hallucinations

69
Q

What is the active ingredient in marijuana? Describe the acute and chronic effects of abuse? How long will one’s urine test + after cessation?

A

Delta-9-THC
Sensory distortion + impaired coordination–> Inability to judge time, speed, distance + pulm disease

Urine will test positive up to 3 mos after cessation

70
Q 
Define the following: 
Abrasion 
Contusion 
Laceration 
Incised wound 
Puncture

What should one be aware of when assessing patient injuries?

A

Abrasion: scrape/ friction
Contusion: bruise (local RBC extravasation)
Laceration: tear; irregular boarders +/- tissue bridging
Incision: no tissue bridging, straight line borders
Puncture: penetration (enter only), perforation (enter + exit!)

**Remember that superficial injuries may make damage look minor when patient has deeper serious injuries (i.e. internal bleed)

71
Q

What are the 4 major factors to consider when assessing burn wounds?

A
  • depth
  • surface area
  • internal injuries (inhalation, trauma)
  • promptness of treatment (prevent dehydration, infection)
72
Q

Define superficial, partial thickness, and full thickness burns

A

Superficial (1st degree): epi only, painful i.e. sunburn

Partial thickness (2nd degree): dermis; painful; blistering

Full thickness (3rd degree): SQ tissue; PAINLESS (damaged nerves); tissue charring

73
Q

When does hypovolemic shock take place in response to burn injury?

A
  • rapid onset after burn

- presents w generalized edema

74
Q

Why should nutrition be watched in burn patients?

A

hypermetabolic state causes heat loss and ^ in nutritional demand

75
Q

What are three infectious agents highly dangerous to burn patients?

A

1 pseudomonas

  • candidiasis
  • s. aureus

***sepsis is a real threat

76
Q

When will injury to airway in burn patients become apparent if not recognized on addition; is this dangerous?

A
  • 24-28 hours after injury
  • look for bronchial charring; consequences of missing this will be fatal
  • **THIS WAS WHY KEPNER WAS FIRED AFTER THE MERGER ON GRAY’S SHE DIDN’T LOOK IN THE MOM’S THROAT AND THEN SHE HAD TO LIVE WITH IT FOR AN ENTIRE 4-5 EPISODE STORY ARCH
  • **ALWAYS CHECK THE THROATS OF BURN PATIENTS
77
Q

Describe the progression in severity from heat cramps–> heat exhaustion–> heat stroke

A

Heat cramps: Loss of electrolytes w/ normal core temp–>

Heat Exhaustion: Hypovolemia (hypoTN) beyond capacity of CV system to compensate; patient may vomit or pass out

Heat STROKE: CORE TEMP OVER 40C; vasodilation, tacky/ arrhythmia; HYPERkalemia

**I had heat exhaustion at disney world waiting for Brittany Spears to come by in an Easter parade when I was in 5th grade. I vomited, then I passed out, and then I got to eat popsicles all day and cut lines. It was awesome, but it really sucked at first.

78
Q

What are three things that can facilitate HYPOthermia?

A
  • ambient temp
  • wetness (cold + wet = BAD)
  • drugs (ETOH dilates superficial aa’s –> release heat)
79
Q

Define hypothermia; how does it present?

A

Core temp UNDER 90F; patient has LOC, bradycardia, a-fib

80
Q

What is trench foot?

A

slow chilling of wet feet–> vasoconstriction–> edema + ischemia–> infarction–> amputation

81
Q

Describe the types of injury that can result from electrocution (3):

A
  • burn
  • v fib; muscle tetany; medullary central paralysis
  • involuntary msk contraction (police taser)
82
Q

What are some examples or non ionizing radiation?

A

UV, infrared, microwave

83
Q

What are some examples of ionizing radiation (4) ?

A
  • x/gamma rays
  • high energy neutrons
  • alpha particles (helium nuclei)
  • beta particles (electrons)
84
Q

What units do we use to measure radiation?

How about damage from an absorbed dose of radiation?

A
  • gray (Gy) = absorbed/unit mass

- sievert (Sv) = measures damage from absorbed dose

85
Q

How is damage due to radiation injury determined (5)

A
  • Rate of delivery (fractioned delivery = time to repair)
  • Feld size (smaller = less damage)
  • Proliferating cells (spermatogonia, hematopoietic cells, GI epi) MORE SUSCEPTIBLE to damage
  • Oxygenation (highly O2 areas worse bc ROS; tumor centers = hypoxic)
  • Endothelial damage due to radiation = atrophy + fibrosis
86
Q

What are the physical consequences of radiation (4)

A
  • ^ risk cancer
  • Bone marrow suppression
  • GIT injury (w higher doses than BM suppression) diarrhea/ dehydration/ infxn
  • Fibrosis (endothelial injury)

DT4- Exam 3 (14 decks)

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