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17 Cards in this Set
- Front
- Back
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What are the therapeutic effects of taking steriods to treat asthma?
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It lowers inflammatory cells reaching lungs and prevents mucus buildup in airways. It also prevents synthesis and induces apoptosis of inflammatory agents.
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What do steroids do on the molecular level to treat asthma?
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They bind to glucocorticoid receptors, which dimerize, travel to cell, recruits HATs, and activate transcription of anti-inflammatory and other anti-asthma genes. They also actively repress expression of pro-inflammatory genes.
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What could possibly go wrong on the molecular level in a patient who cannot respond to steroid treatment for her asthma?
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GR receptors can't dimerize
GR receptors can't be released from chaperone GR receptors cannot bind DNA, HATs, HDACs, or some other regulatory molecules. There may be a problem in post-translation modification of the receptor, that would result in a variety of different functions. |
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You want to figure out if a patient is not responding to steroid therapy because she/he may have Cushing's Syndrome. What signs would you look for in order to determine this?
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In Cushing's patients, presence of a fatty abdomen and neck, thin arms/legs, bruising, poor wound healing, red cheeks, and a "moon face." Cushing's syndrome is caused by a manifestation of increased glucocorticoid.
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Different isoforms of the glucocorticoid receptor, GR, have different functions in asthma patients. Describe this.
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GR-alpha:GR-beta Dimer: no transcription of anti-inflammatants
GR-alpha:GR-alpha: active transcription Patients with increased levels of the GR-beta isoform of the receptor have more steroid resistance when treating asthma. Kd is increased. |
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T/F: treatment of COPD patient and those with asthma is similar.
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False; COPD patients cannot be treated with steroids.
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How is gene regulation altered in smokers?
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Oxidative damage from smoking results in repression of HDAC, and thus, no transcription deactivation.
More specifically, inflammatory cytokines are released because there is no HDAC to repress transcription of certain mediators of these cytokines. |
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What are some clinical symptoms of fetal alcohol syndrome?
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CNS dysfunction
-cognitive problems like hyperactivity and learning disabilities craniofacial abnormalities -microcephaly (small head circumference) -smooth philtrum ("cleft lip" - restricted range of lip motions) -palpebral fissures (eye width decreases) -flat midface -epitcanthal folds stunted growth |
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T/F: incidence of fetal alcohol syndrome is higher in whites than in blacks/Native Americans.
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False; it is 2-3 times higher in the two minority populations; it is also higher among lower socioeconomic classes
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What part of development is affected most by teratogenic insult?
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Gastrulation
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What are some specific molecular reasons explaining some of the symptoms seen in FAS?
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-affected neural crest formation
-less purkinje cells in the cerebellum -midline of the brain is not formed correctly -neural crest derivatives do not migrate property |
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What is the relationship between ethanol and the GABA receptor?
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Normally, the GABA receptor opens Cl- channels, and allows Cl- inside the cell, resulting in hyperpolarization and reduced brain activity. Ethanol binds to GABA and allows it to release MORE Cl- into the cell.
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Does FAS have genetic roots?
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Possibly; homozygotes of ADH1B gene are more likely to have children with FAS.
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Describe the anti-oxidant properties of the fetus.
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The fetus has no superoxide dismutase, and overall less anti-oxidants. Ethanol, in high amounts, causes oxidative stress that the fetus cannot counteract.
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How is the Beta-Adrenergic Receptor activated? Desensitized?
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Epinephrine and Norepinephrine bind to receptor. ACase is (+). cAMP is (+). PKA is (+). Increase in calcium. High force and rate of contraction. It is desensitized when arrestin binds it.
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T/F: African Americans have more GRK (G protein coupled receptor kinase) polymorphisms than whites.
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True. AA have the L41 allele more in their GRKs. This is like having a built in beta blocker. Leu42 is not associated with disease, however.
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T/F: beta blockers do not increase survival of patients with L41 allele.
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True; they work for the more common, Q41, allele. The survival rate is the same as those who do not take beta blockers and have the L41 allele.
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