Path Envr/Nutr Diseases (21)

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  1. ‘Personal Environment’
    • influenced by the use of tobacco, alcohol ingestion, therapeutic & non-therapeutic/recreational drug consumption, diet, & the like
    • factors in the personal environment generally have a larger effect on one’s health than those in the ambient environment → we can control a great deal of our own health
  2. Xenobiotic
    • a foreign chemical substance found within an organism that is not normally naturally produced by or expected to be present within that organism
    • once in the body can be metabolized to nontoxic or reactive/toxic metabolites
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  3. What is the 2 step process through which most chemicals go through in the body?
    • Phase I: chemicals undergo hydrolysis, oxidation, or reduction to produce a ‘Primary Metabolite’
    • Phase II: the ‘Primary Metabolite’ is converted into water-soluble compounds by glucuronidation, sulfation, methylation, & conjugation with glutathione (GSH)
    • [water-soluble compounds are readily excreted]
  4. Cytochrome P450 system (CYS)
    • most important drug-metabolizing enzyme involved in the biotransformation of xenobiotics & drugs
    • catalyzes reactions that either detoxify or activate xenobiotics into active compounds that cause cellular injury
    • ROS's generated in the process cause cell injury
    • variations in CYS activity in individuals can be due to inducers or genetic polymorphisms (eg. grapefruit juice inactivates CYP3A4 in the intestine, thus affecting the metabolism of certain orally administrated drugs → increasing their bioavailability)
  5. What are the most common air pollutants?
    • ozone
    • in combination w/ oxides & particulate matter forms smog, sulfur dioxide, acid aerosols, & particles of less than 10 μm in diameter
  6. Effects of Ozone
    • decreased lung function
    • increased airway reactivity
    • lung inflammation
    • free radical production → cell/tissue injury
  7. Effects of Nitrogen Oxide
    • increased airway reactivity
    • decreased lung function
    • increased respiratory infections
  8. Effects of Sulfur Dioxide
    • increased respiratory symptoms
    • increased mortality
    • decreased lung function
  9. Effects of Acid Aerosols
    • altered mucociliary clearance
    • increased respiratory infections
    • decreased lung function
    • increased hospitalization
  10. Effects of Particulates
    • increased respiratory infections
    • decreased lung function
    • increased asthmatic attacks
  11. What is Hemoglobin's affinity for Carbon Monoxide (CO) compared to its affinity for Oxygen?
    it has a 200-fold greater affinity for CO than for O
  12. Lead Exposure
    • occurs through contaminated air & food
    • flaking lead paint (tastes a little bit sweet) is a major hazard to young children
    • a single chip of lead paint, the size of a thumbnail, may contain 170 μg of lead; this amount, if consumes each day over time, will rapidly produce toxic lead levels
    • ingestion of 200mg/day can occur in heavily contaminated environment
  13. Effect of Lead Poisoning in Children Related to Blood Levels
    • the maximum allowable level is 10 μg/dL: decreased IQ, hearing, growth, impaired peripheral nerve function, & fetal affects by transplacental transfer
    • 20 μg/dL: increased nerve conduction vel. & erythrocyte protoporphyrin, decreased vitamin D metabolism & calcium homeostasis
  14. Excess Lead
    • causes neurologic effects in both adults & children
    • adults: peripheral neuropathies that are generally reversible w/ elimination of lead
    • exposure
    • children: low IQ, behavioral problems (hyperactivity, poor organizational skills etc.)
    • both peripheral and CNS abnormalities in children are generally IRreversible
  15. Effects of Lead on Skeletal System
    • excess lead interferes w/ the normal remolding of calcified cartilage & primary bone trabeculae in the epiphyses in children, causing increased bone density = ‘lead lines’
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    • cartilage mineralization is delayed
    • fractures heal poorly
  16. Effects of Lead on Hematopoietic system
    • lead interferes w/ normal heme biosynthesis
    • there's impaired incorporation of iron into heme
    • hypochromic anemia
    • basophilic stippling of RBC
    • hemolytic anemia due to the increase fragility of cell membranes
    • zinc-protoporphyrin is formed instead of heme (high levels in blood are indicative of lead poisoning)
  17. Effects of Lead on Nervous system
    • brain damage, especially in children
    • peripheral neuropathy in adults
  18. Effects of Lead on Kidneys
    tubular damages, specifically the proximal tubules
  19. Treatment for Lead Poisoning
    • remove from source
    • chelation therapy for severe symptoms or markedly elevated blood levels
  20. People who smoke have a high chance of getting what type of cancer?
    • Bladder Cancer
    • toxic metabolites made soluble sit in the bladder waiting for excretion
    • smoking may reduce life expectancy by 7 to 8
    • years
    • other diseases strongly linked to cigarette smoking: atherosclerosis, myocardial infarction, peripheral vascular disease, cerebrovascular disease, cancers of the oral cavity, esophagus, & pancreas
  21. Smoke & smokeless tobacco interact with alcohol in the development of which type of cancer?
    laryngeal cancer
  22. Arsenic Metals as Environmental Pollutants
    • sources: naturally occurring, wood preservatives, herbicides, manufacturing processes for semiconductors, LED bulbs
    • Acute Toxicity: severe gastrointestinal, cardiovascular, & CNS disturbances that often progress to death
    • Chronic Toxicity: skin changes w/ hyperpigmentation & hyperkeratosis, basal & squamous cell carcinomas, & an increased risk of developing lung cancers
  23. Effects of Chronic Alcohol Abuse
    • fatty liver, alcoholic hepatitis, cirrhosis, portal hypertension, increased risk of hepatocellular carcinoma
    • gastritis, gastric ulcers, peripheral neuropathies, cardiomyopathy, acute/chronic pancreatitis
    • major risk factor for cancers of the oral cavity, pharynx, larynx, & esophagus
    • risk is GREATLY increased by concurrent smoking or use of smokeless tobacco
  24. Hormone Replacement Therapy (HRT)
    • estrogen therapy (w/ or w/o added progestins) is used primarily for distressing menopausal symptoms & in postmenopausal women to slow the progression of osteoporosis & reduce the likelihood of MI
    • it increases risk of endometrial carcinoma (E only formulary but less in E+P) & breast cancer (E+P)
    • there's little evidence to support the possible role of protection against MI
    • HRT also INCREASES the risk of thromboembolism (increases coagulability)
  25. Complications of Oral Contraceptives
    • Thromboembolism
    • Cardiovascular Diseases
    • Hepatic Adenoma
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  26. Acetaminophen Metabolism
    • normally done by detoxification/conversion (conjugation) to the non-toxic metabolite glucuronide sulfate
    • a side metabolic pathway is mediated by CYP450 enzymes (CYP2E1) yielding the toxic intermediate NAPQI (N-acetyl-p-benzoquinone imine)
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  27. NAPQI (N-acetyl-p-benzoquinone imine)
    • toxic metabolite of Acetaminophen produced by CYP450 enzymes
    • may cause hepatic cell death, but since it is normally produced in small quantities it is usually conjugated to glutathione and excreted before harm can be done
    • *when large amounts of NAPQI are formed, the capacity for glutathione conjugation can be exceeded
  28. What's one way to treat patients who have overdosed on Acetaminophen?
    • N-acetylcysteine, NAC (Mucomyst, Acetadote)
    • it's a precursor of glutathione
    • giving the drug within 16-24 hours of overdose can significantly reduce liver damage
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  29. Side Effects of Anabolic Steroids
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  30. What is the leading cause of death related to thermal injury?
    • organ system failure resulting from burn sepsis
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  31. Hyperthermia
    • prolonged exposure to elevated ambient temperatures
    • can have detrimental effects on the body
  32. Heat Cramps
    • loss of electrolytes via sweating
    • cramping of voluntary muscles, usually in association w/ vigorous exercises
  33. Heat Exhaustion
    • sudden onset, prostration, & collapse
    • failure of Cardiovascular system to compensate for hypovolemia (state of decreased blood volume) secondary to water depletion
    • equilibrium is usually spontaneously re-established
    • can progress to heat stroke
  34. Heat Stroke
    • associated w/ high ambient temperature & high humidity
    • thermoregulatory mechanisms fail, sweating ceases, core temperature rises
    • 50% mortality in those w/ rectal temperature of 106°F/41°C
    • marked generalized peripheral vasodilation
    • peripheral pooling of blood
    • decreased effective circulating blood volume
    • change in mental stasis
    • arrhythmias
    • disseminated intravascular coagulation can occur
    • at risk population: elderly people, persons w/ cardiovascular disease, & otherwise healthy people undergoing physical stress
  35. Major Morphologic Consequences of Radiation Injury
    • Ionizing radiation may injure the cells directly or, MORE importantly, indirectly by generating free radicals from water or molecular oxygen
    • Ionizing radiation damage DNA
    • Rapidly dividing cells such as germ cells, bone marrow, & GI are VERY sensitive to radiation injury
    • DNA damage that is not adequately repaired may result in mutations that predispose the cells to neoplastic transformation
  36. Acute Radiation Syndromes (Radiation Poisoning)
    • a constellation of health effects that present within 24 hours of exposure to high amounts of ionizing radiation
    • it causes cellular degradation by damaging DNA & other key molecular structures within cells in various tissues
    • the destruction, particularly as it affects ability of cells to divide normally, in turn causes the symptoms
    • types of death can be Hemopoietic, Intestinal, or Cerebral
  37. Hemopoietic Death from Radiation Poisoning
    • dose: 300
    • latency: 2 weeks
    • death: 3 weeks
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  38. Intestinal Death from Radiation Poisoning
    • dose: 1000
    • latency: 3 days
    • death: 2 weeks
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  39. Cerebral Death from Radiation Poisoning
    • dose: 2000
    • latency: 1 hour
    • death: 1 day
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  40. What is the late manifestation of radiation injury in tissues?
    ionizing radiation may cause vascular damage & sclerosis, resulting in ischemic necrosis of parenchymal cells & their replacement by fibrous tissue
  41. Nonneoplastic Complications of Radiation
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  42. What are the 2 protein compartments in the body?
    • 1. Somatic: proteins in the skeletal muscles
    • 2. Visceral: proteins stores in the viscera, primarily the liver
    • the 2 compartments are regulated separately
  43. Marasmus
    • a type of PEM that manifests as a primary deficiency of energy
    • there is a loss of body mass but hepatic/visceral proteins (eg. albumin) are maintained
    • is a chronic condition that progresses over weeks to months; body fat is lost to a greater extent than lean tissue (until fat stores are depleted)
    • advanced Marasmus is characterized by severe loss of fat + skeletal muscle & children below average height for their age (60%)
  44. What is the most obvious symptom of Marasmus?
    • loss of subcutaneous fat
    • extremities are emaciated, head appears disproportionally large
    • anemia, multivitamin deficiencies, immune deficiency, concurrent infections
  45. Kwashiorkor
    • dietary protein deficiency with varying degrees of energy deficiency; can occur as a result of not enough protein or essential AA intake
    • What is the translation of Kwashiorkor?
    • "the sickness the [first] baby gets when the new baby comes"
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  46. What are characteristic symptoms of Kwashiorkor?
    1. reduced circulating concentrations of proteins such as albumin (hypoalbuminemia)

    2. edema from a DECREASE in oncotic pressure

    3. characteristic skin lesions: alternating zones of hyperpigmentation, areas of desquamation, & hypopigmentation (‘flaky paint’)

    4. Hair changes: overall loss of color or alternating bands of pale & dark hair (‘flag sign’), straightening, fine texture, & loss of firm attachment to the skull

    5. fatty liver, apathy, listlessness, loss of appetite

    6. multivitamin deficiency, immune deficiency, secondary infections
  47. Which progresses more quickly, Marasmus or Kwashiorkor?
    • Kwashiorkor's progression of is highly variable but is usually more rapid than Marasmus
    • if kwashiorkor persists, muscle wasting will become evident
  48. How can Marasmus be distinguished from Kwashiorkor?
    • kwashiorkor (pregnant babies) is protein deficiency w/ adequate energy intake whereas Marasmus (skeletons) is INadequate energy intake in all forms, including protein
    • Marasmus: depletion of skeletal muscle protein (after a while), but maintenance of visceral protein (until late stage of the disease)
    • Kwashiorkor: depletion of visceral protein (primarily), but maintenance of skeletal muscle protein (b/c of insulin)
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  49. Vitamin A
    • family = retinoids, which refers to retinol, metabolites in the body, & synthetic analogs
    • it plays a role in reproduction & bone growth
  50. What role does vitamin A play in vision?
    • the retina requires retinal to adapt to dim light because 11-cis-retinal is a critical part of the rhodopsin molecule of the rods
    • also retinoic acid is required for normal corneal differentiation
  51. How does a vitamin A deficiency affect eyesight?
    • it can cause night blindness
    • dryness (xeropthalmia)
    • Bitot’s spots (accumulation of keratinized tissue on the cornea) which if left untreated will lead to blindness
    • Keratomalacia (cornea erosion)
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  52. What role does vitamin A play in cell division & differentiation?
    retinoic acid is required for gene expression of enzymes & structural proteins
  53. What effect does Vitamin A deficiency have on the immune system?
    • vitamin A DEFICIENCY results principally in squamous metaplasia, especially in glandular epithelium
    • it causes immune deficiency → increases the risk of viral ailments such as measles or respiratory infections
    • can also lead to hyperkeratinization
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  54. Vitamin D Metabolism
    • to achieve biological potency, vitamin D must be hydroxylated to active metabolites in the liver & kidney
    • the active form, 1,25(OH)2D promotes calcium & phosphate absorption from the small intestine & may directly influence mineralization of bone (with PTH)
  55. Vitamin D Form Order
    • Vitamin D2, Vitamin D3, or 7-dehydrocholesterol
    • 25(OH)D 25-hydroxyvitamin D (form in the liver)
    • 1,25(OH)2D *ACTIVE FORM
    • 1,25-dihydroxyvitamin D
    • (formed in the kidney)
  56. What stimulates the hydroxylation of 25-hydroxyvitamin D to the active form of vitamin D, 1,25(OH)2D?
    • Parathyroid Hormone
    • which itself is secreted from the parathyroid when blood calcium levels are LOW
  57. parathyroid hormone (PTH)
    • hormone made by parathyroid gland chief cells that INCREASES blood calcium (opposes the action of calcitonin)
    • increases osteoclast activity - bone breakdown & liberation of calcium
    • stimulates vitamin D activation in kidney, which stimulates calcium resorption in GI tract & kidney)
    • *is a vital hormone
  58. What is the basic derangement in both rickets and osteomalacia?
    an excess of unmineralized matrix
  59. Rickets
    • softening of bones in immature mammals due to deficiency or impaired metabolism of vitamin D, phosphorus or calcium
    • can lead to fractures & deformity
    • is characterized by growth retardation + bowing of lower extremities
  60. Osteomalacia
    • softening of the bones caused by defective bone mineralization secondary to low levels of phosphorus & calcium
    • is characterized by diffuse bone & muscle pain, muscle weakness, & frailty
    • long term osteomalacia increases the risk of osteoporosis
    • is caused by vitamin D deficiency which can lead to overactive resorption of calcium from the bone as a result of hyperparathyroidism
  61. Vitamin C (Ascorbic acid)
    • functions in a number of biosynthetic pathways by accelerating hydroxylation & amidation reactions; also functions as an antioxidant
    • activation of prolyl & lysyl hydroxylases from inactive precursors, providing for hydroxylation of procollagen
    • inadequately hydroxylated procollagen lacks tensile strength; is more soluble & more vulnerable to enzymatic degradation
    • collagen is affected: results in a predisposition to hemorrhages in scurvy
  62. What does a deficiency of vitamin C lead to?
    • scurvy
    • weakness and lassitude
    • skin and soft tissue (impaired wound healing, petechial hemorrhage, perifollicular hyperkeratosis, ecchymosis)
    • oral issues: swollen gums that bleed easily & are friable, tooth loss
    • coiled hair
    • joint issues: bleeding into joints, arthralgias
    • cardiopulmonary issues: shortness of breath, pericardial bleeding
    • bone: impaired growth & bowing, subperiosteal hemorrhage, impaired healing
    • CNS issues (depression, confusion, hysteria, hypochondriasis)
    • infection
    • internal bleeding
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  63. What are the major consequences of vitamin C deficiency caused by?
    • impaired formation of collagen
    • they include bleeding tendency because of poor vascular support, inadequate formation of osteoid matrix, & impaired wound healing
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  64. Cadmium
    • obstructive lung disease & kidney damage
    • skeletal abnormalities associated w/ calcium loss
  65. Obesity
    • a disorder of energy regulation
    • increases the risk for insulin resistance, type 2 diabetes, hypertension, hypertriglyceridemia, atherosclerosis, non-alcoholic fatty liver disease (which may progress to fibrosis & cirrhosis), formation of cholesterol gallstones, & endometrial and breast cancer
Card Set:
Path Envr/Nutr Diseases (21)
2014-03-11 02:31:45
MBS Pathology
Exam 3
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