Environmental Diseases Flashcards

1
Q

how does smoking cause emphasema

A

ROS inactivate anti-proteases (functional AT def) –> inc activity of neutrophil elastase –> tissue damage –> inc MMP and macrophage proteases –> more damage

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2
Q

gene that controls the response to injury after smoking

A

TGFB gene (TGF-beta reduced = inadequate repair)

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3
Q

effect of toxins in cigarette smoke on lungs

A
  1. Injure the mucociliary apparatus
    for escalating bacteria out of the lungs
  2. Cause inflammation recruiting phagocytes
    that leak their proteases
  3. Inhibit anti-proteases needed to protect
    against protease tissue injury
  4. Cause mucus production and secretion,
    yielding a place for bacteria to grow
  5. Inhibit phagocytosis and bacterial killing
    by phagocytes
  6. Cause squamous metaplasia, removing
    mucociliary clearance of bacteria
  7. Kill respiratory epithelial cells, removing
    a barrier to bacterial invasion
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4
Q

what is basophillic stippliang and what is it assc with

A

clumped ribosomes** assc w/ lead poisoning and disorders of RBC maturation (B12 and folate def)

**ribosomes clump bc pyrimidine 5- nucleotidase is inhibited thus causing the degradation of ribosomes

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5
Q

manifestations of lead tox in KIDS at low doses vs high doses

manifestations of lead tox in ADULTS at low doses vs high doses

A

KIDS

low: cognitive impairment, hyperactivity, dec verbal activity
high: abd pain, arthralgia, renal probs, tremor

ADULTS

low: short term meory loss, diff concentrating
high: periph demyelinating neuropathy, arthralgia, abd pain, renal

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6
Q

pathophys of lead toxicity (heme and neuro effects)

A

HEME
electropositivity = has high affinity for sulfhydryl groups and when it binds it inhibs enzymes such as ALA DH and ferrochelatase –> accumution of protoporphyins –> toxic

NEURO
Pb competes with Ca2+ for mitochondrial respiration–> disrupts processes/activates PKC –> problems

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7
Q

MC substance that is abused during pregnancy

A

cigarettes > alcohol > illicit drugs

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8
Q

how does alcohol cause hepatic steatosis

A

ethanol required NAD for its metabolism by alcohol and acetylaldehyde DH –> depletes NAD pool which is needed for lipid oxidation –> lipid cannot be broken down so it accumulates in the liver

alcohol also decreases assembly and secretion of lipoproteins

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9
Q

What are mallory-denk bodies

A

tangles of cytoskeleton (cytokeratin intermediate filaments)

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10
Q

how does alcohol cause hepatitis

A
  1. acetaldehyde induces lipid peroxidation + adducts proteins –> damage to membrane and cytoskeleton
  2. alcohol directly damages cytoskeleton
  3. generates ROS
  4. activates inflammation TNF
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