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36 Cards in this Set
- Front
- Back
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causes of hypoxia
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1) high altitude
2) poor ventilation 3) CO poisoning 4) impaired mitochondrial function 5) severe anemia 6) local restriction of blood flow |
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what is the effect of hypoxia?
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decrease of ATP -> anaerobic glycolysis -> lactic acid -> \/ pH -> Na/K pump malfunction
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What three indications are there that ischemic/hypoxic injury is irreversible?
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1) profound membrane damage
2) permanent loss of ability to generate ATP 3) cytoskeletal abnormalities 4) glycine is lost -> membrane injury all lead to cell death - necrosis |
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reperfusion injury
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after irreversible injury, ROS are produced to remove damaged cells and surrounding healthy cells can be damaged.
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what is the final and subsequently lethal effect of ischemic/hypoxic events that will ultimately cause cell death?
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profound membrane damage
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threshold dose
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lowest dose at which a response occurs
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subthreshold dose
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no measurable response, "safe dose"
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ceiling effect
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plateau is reached at higher doses
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xenobiotic
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chemical which is found in an organism but which is not normally produced or expected to be present in it. most xenobiotics are lipophilic and are metabolized to hydrophilic substances.
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phase I reactions
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in liver, polar group is added to xenobiotic to create a more soluble metabolite. if not hydrophilic enough, then goes to phase II reactions. CYP P450 are heavily used here.
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phase II reactions
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metabolites conjugated with endogenous hydrophilic substances to increase hydrophilicity for clearance.
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what type of tissue do xenobiotics love to sit in?
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fatty tissue. they are naturally lipophillic, which is why the liver must go through phase I and phase II processes to increase hydrophilicity to allow elimination.
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biotransformation
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the overall term to describe the phase I and phase II conversion of lipophilic to hydrophilic compounds.
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what is the significance of CYP1A1 gene?
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people express this gene has an increased risk of lung cancer.
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What activities work synergistically with smoking to compromise health?
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1) asbestos worker
2) chronic drinker |
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What percent of lung cancers are due to smoking?
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90% !
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Is increased risk of cancer isolated to lungs for smokers?
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No! larynx, oral, esophageal, pancreas, bladder
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what is the legal limit for DUI blood levels?
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< 80 mg/dL
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how is ethanol metabolized?
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1) alcohol dehydrogenase in gastric mucosa & liver
2) CYP2E1 in liver and catalase in liver assists 3) acetaldehyde (toxic) is converted to acetic acid (water soluble) by aldehyde dehydrogenase |
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what does alcohol do to the CNS?
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acute CNS depressant
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wernicke encephalopathy
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thiamine (vit B1) deficiency - ataxia, conitive impairment, ophthalmoplegia, nystagmus
commonly grouped with korsakoff as "Wernicke-Korsakoff syndrome" |
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korsakoff psychosis
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thiamine (vit B1) deficiency - severe memory loss, confabulation, hallucination
commonly grouped with wernicke as "Wernicke-Korsakoff syndrome" |
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effects of alcohol on liver
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fatty liver (triglycerides in hepatocytes), acute hepatitis, cirrhosis
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how does ethanol hurt the liver?
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ethanol is directly toxic to hepatocytes caused by glutathione depletion, hepatocyte necrosis and fibrosis occurs around central veins, and cirrhosis
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What is cirrhosis?
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irreversible formation of micronodules of regenerating hepatocytes surrounded by collagen bands. this leads to portal hypertension, varices, GI bleeding
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what are the cardiovascular effects of alcohol?
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directly toxic to cardiac cells, dilated cardiomyopathy, hypertension caused by increased catecholamines
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what are the cardiovascular benefits of alcohol?
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moderate use (1-2 drinks/day) increases HDL, decreases platelet aggregation
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fetal alcohol syndrome
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microcephaly, dysmorphic facies, organ malformation, growth retardation, mental retardation
most common form of preventable mental retardation |
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common cancers associated with alcohol use
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oral cavity, pharynx, esophagus, liver
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methanol metabolism
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metabolized by alcohol dehydrogenase to formaldehyde and formic acid.
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methanol poisoning clinical characteristics
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metabolic acidosis, dizziness, vomiting, blindness, respiratory depression
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methanol poisoning tx
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ethanol - competitive inhibitor
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ethylene glycol metabolism
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component of antifreeze, metabolized by alcohol dehydrogenase to aldehydes, glycolate, oxalate, lactate
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ethylene glycol poisoning clinical characteristics
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metabolic acidosis, mental status, nausea, vomiting, acute renal failure due to oxalate crystal obstruction of renal tubules
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ethylene glycol poisoning tx
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ethanol - competitive inhibitor
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