Final Exam Greatest Hits Flashcards
hormones
moves thru blood, impact based on receiving end
hormone classes
protein/peptide (insulin, adh), catecholamines, thyroid (modified amino acids), steroid (inc sex hormones, aldosterone, cortisol)
how is blood hormone conc regulated
production changes, degradation stays stable
thyroid hormone production
made in colloids (spheres of cells where amino acids are modified) and made when attached to protein backbone. leaves colloid and diffuses out upon release from this peptide
adrenal gland medulla
makes catecholemines
adrenal gland cortex
makes steroids inc cortisol, aldosterone
pituitary and hypothalamus anatomy
middle of brain, pituitary dangles from hypothalamus. ant pituitary is endocrine, posterior is NS
posterior pituitary
neurosecretory cells release nonapeptides. inc ADH and oxytocin
oxytocin effects
birth, bonding, monogamy
anterior pituitary
makes peptide hormones (usually prohormones) responding to releasing or inhibiting hormones from hypothalamus. = thyroid-stimulating hormone, adrenocorticotropic hormone (ACTH), growth hormone (goes to liver, tissue, cell metabolism), LH and FSH, and prolactin which is actually a real hormone for milk secretion
portal system
capillaries btwn tissues ie. hypothalamus to pituitary
adrenocortical stress hormone response (+ pathway)
hypothalamus releases corticotropin-releasing hormone (CRH), ant pituitary ACTH, goes to adrenals which release cortisol which - feedbacks the CRH and ACTH prod. this results in increased blood glucose, suppressed immune system, stimulates aldosterone
cushings syndrome
overactive pituitary ACTH leads to too much cortisol
glucose obtained from sympathetic vs adrenocortical stress
sympathetic uses glycogen, cortisol takes it from proteins and fats
mineralocoracoids
stimulate salt/water retention (inc ase of blood loss)
why is cortisol long term stress response
steroid, so changes gene expression
stress and cognition
low stress improves performance, high stress impairs
cortisol other uses
inhibits inflammation (for injuries)
muscle cell structure
myofibrils wrapped in sarcoplasmic reticulum with t tubules, nuclei and mitochondria around
sarcomere contraction basic
thin filaments climb toward center of thick filament to contract. z lines are where actin is anchored
thin filament
actin with troponin (binds Ca2+ to move tropomyosin from active sites) and tropomyosin(regulates binding)
myosin
heads pull on actin during contraction, require atp. heads are out of phase so not all must be active at once or stop working all at once. binding actin releases prod from ATP dephos and releases energy for myosin to climb
stabilizing components in sarcomere
nebulin stabilizes actin, titin anchors actin, is elastic, helps muscle return to og state (largest protein, length = 1/2 sarcomere)
AP moves to sarcomeres..
AP from NMJ travels thru t-tubules, channels on SR become unblocked by the t-tubule and Ca is released to sarcomere