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PHYS 335
Exam 2
| Term | Definition |
|---|---|
| paracrine | local cell sends signals to surrounding cells |
| autocrine | cell sends signals to itself |
| endocrine | cell signaling into the blood stream |
| endocrine system | monitors the ECF and maintains homeostasis throughout many organ systems |
| exocrine galnds | raw materials from the blood, sent out of the body |
| endocrine galnds | raw materials from the blood, builds hormones to go back inot the blood |
| target cells | express hormone-specific receptors (high affinity and specifity for specific hormones) |
| peptide/protein hormones | prepro-->pro-->hormone+pro frgaments HYDROPHILLIC, synthesis in ER/golgi vesicle transport exists in plasma as a frely dissolved hormone receptor on plasma membrane of target cells FAST mobilization FAST metabolization |
| steroid hormone | synthesized from cholesterol HYDROPHOBIC, enzymatic modification of cholesterol simple diffusion requires plasma protein carriers for transport in blood receptor in nucleus of target cells SLOW mobilization SLOW metabolization |
| amine hormone | catecholamines: peptide/protein thyroid hormone: steroid hormone |
| down regulation of hormone receptors | continued activity of target hormone wil reducce the number of hormone receptors on target tissue |
| up regulation of hormone receptors | continued low-levels fo target hormone will increase the number of hormone receptors on target tissue |
| permissive effect | high levels of a non-target hormone will increase the presence of another hormone receptor on the target tissue. (TH permissive of epineprine) |
| tropic hormone | a hormone that effects the secretion of another hormone |
| trophic hormone | a hormone that promotes the growth of the target tissue |
| hypersecretion | ignoring of negative feedback (primary) excess secretion of hormone from a gland (secondary) |
| hyposecreteion | gland destruction (primary) loss of tropic hormone (secondary) |
| hyperresponsiveness | receptor upregulation or second messenger pathway over-activation |
| hyporesponsiveness | receptor downregulation or secondmessenger pathway under-activation |
| anterior pituitary | vascularized - turns hypophysiotropic hormones into anterior pituitary hormones hypthalamo-hypophyseal portal vessels |
| posterior pituitary | recieves signals from supraoptic nuclei - releases neurohormones median eminence oxytocin, ADH (vasopressin) - peptide neurohormones |
| funtional unit of the thyroid | follicles - colloidal fluid "pink lake" - follicular cells "rocky shoreline" |
| thyroglobulin | the T3 and T4 protein carrier in the colloidal fluid (steriod-like amine hormones) |
| T4 | 4 iodines 90% of storage converted to T3 inside of target cells |
| T3 | 3 iodines most active form |
| steps of thyroid hormone synthesis, storage and secretion | TSH binding and Iodine transport into colloid TG synthesis and exocytosis inot colloid T3+T4 synthesis TG+T3+T4 endocytosis and lysosomal liberation |
| actions of thyroid hormone | controls basal metabolic rate (increases amount of fuel burined to maintain organ system functions) ie body temp thyroid hormone is permissive of: beta-adrenergic receptors growth and development |
| Hypothyroidism (Hashimoto's) | causes: iodine deficiency, thyroid damge or autoimmune destruction symptoms: low metabolism, weight gain, cold intolerance, low blood pressure, low heart rate, fatigue, decreased alertness and cognitive function, stunted growth, goiter |
| Hyperthyroidism (Graves') | causes: tumors, autoimmune disease symptoms: high metabolism, weight loss, increased appetite, heat intolerance, increased heart rate, insomnia, nervousness/irritability, anxiety, constant fight-or-flight, goiter, exophthalmos |
| adrenal gland anatomy | CORTEX (steroids) zona glomerulosa: salt (aldosterone) zona fasciculata: sugar (cortisol) zona reticularis: sex (androgens) MEDULLA (catecholamines) :steroids |
| what determines the hormone produced in the adrenal galnd cortexes? | the enzymes present in that zone |
| physiological functions of cortisol (nonstress) | liver glucose production between meals permissive of adrenergic receptors in the cardiovascular system anti-inflammatory/anti-immune fetal/neonatal development |
| physiological functions of cortisol (stress) | activates catabolism bone resorption supports vasoconstriction stimulates erythropoietin anti-inflammatory/immunosuppression inhibition of nonessential function (growth,reproduction) |
| primary adrenal insufficiency (Addison's disesase) | caused by:destructive tumors, infection, autoimmune destruction results in: hypotension, low blood pressure, HIGH plasma ACTH and high CRH |
| secondary adrenal insufficiency | caused by: anterior pituitary dysfunction = loss of ACTH results in: hypotension, low blood pressure, LOWplasma ACTH and high CRH |
| Cushing's Syndrome (primary) | caused by: hyper-secreting tumor of the adrenal gland results in: osteoporosis, thin skin, muscle weakness, immunosuppresion, high blood glucose, hypertension, dcreased fertility, stunted growth, redistribution of fat |
| Cushing's disease (secondary) | caused by: hyper-secreting tumor of the anterior pituitary results in: osteoporosis, thin skin, muscle weakness, immunosuppresion, high blood glucose, hypertension, dcreased fertility, stunted growth, redistribution of fat |
| stress effects on hormone production | increases: aldosterone, vasopressin, growth hormone, glucagon, beta-endorphin, epinephrine + norepinephrine decreses: insulin |
| steps of bone growth (in epiphysis) | newest chondrocytes undergo hyperplasia to form cartilage older chondrocytes undergo hypertrophy to increase in size osteoblasts convert oldest chondrocytes (cartilage) to bone |
| factors influencing bone growth | adequate nutrition freedom from chronic illness/disease freedom from psychosocial stress sleep |
| hormonal factors of growth | growth hormone insulin-like growth factors (IGFs) Insulin Thyroid hormone - permissive testosterone - closes epiphyseal plates + stimulates protin production estrogen/DHEA - closes epiphyseal plates cortisol - ANTi-growth effects |
| gigantism | too much GH BEFORE epiphyseal plates close |
| acromegaly | too much GH AFTER epiphyseal plates close |
| gonads | primary reproductive organs |
| gametogensis | production of the reproductive cells/gametes |
| sex hormones | steroid hormones secreted by the gonads |
| genotype | PRIMARY sex determination (genetics) |
| phenotype | SECONDARY sex differentiation (hormones) |
| polar bodies | only in ovary production, designed to donate cytoplasm to developing zygote (oocytes much more energetically expensive than sperm) |
| aromatase | enzyme that converts testosterone into estrogens |
| 5-alpha-reductase | converts testosterone into DHT |
| gonadotropins | FSH - follicle stimulating hormone LH - lutenizing hormone |
| kisspeptin | begins puberrty in both male and females by stimulating the production og GnRH (gonadotropin-Releasing Hormone) |
| oogonium | divides mitotically to give rise to 2-4 million oogonia |
| oogonia | before birth, these undergo their first meiotic divison but do not complete it PRIMARY OOCYTES in state of meiotic arrest |
| follicular phase | produces a mature follicle |
| luteal phase | prepares for pregnancy if fertilization occurs |
| primordial follicles | primary oocytes surrounded by granulosa cells |
| early antral follicles | a portion of the resting primordial follicles progress to this during childhood and the menstrual cycle |
| dominant follicle | at beginning of the menstrual cycle, 10-25 of the early antral follicles will begin to enlarge, only one survives |
| secondary oocyte | completed just prior to ovulation, the primary oocyte completes its first meiotic division |
| corpus luteum | leftover granulosa and theca cells after ovulation, becomes active steroidogenic tissue (progesterone mostly), stores cholesterol, vascularization |
| corpus albicans | the dying tissue of the corpus luteum if fertilization does not occur |
| estrogen | dominates the first 14 days of the ovarial cycle |
| progesterone | dominates the last 14 days of the ovarian cycle |
| LH surge | the cause of ovulation, a positive feedback loop. terminating event = ovulation |
| proliferative phase | estrogen increases the thickness of the endometrium |
| secretory phase | progesterone increases the vascularization and fueling of the endometrium to prepare for implantation of an embryo |
| menstrual phase | decreased estrogen and progesterone cause the release of prostaglandins causing hemmorhage of the endometrium |
| Human Chorionic Gonadotropin (hCG) | secreted by the developing embryo, saves the corpus luteum (LH-like), turns on testosterone production in male fetus, present until placenta takes over this role ~3 months |
| life of a sperm | 1. testes/seminiferous tubules (sperm production) 2. epididymus (sperm storage) 3. vas deferens (duct work) 4. seminal vesicles (fructose, prostaglandins) 5. prostate (alkaline mucus, clotting factors) 6. bulbourethal gland (lubrication) 7. penis |
| seminiferous tubules | 250 meters long |
| sertoli cells "nurse cells" | walls of the seminiferous tubules, form blood-testes barrier, sprem differentiation/proliferation, nourish developing sperm |
| leydig cells "interstitial" | surrounding seminiferous tubules, make and release testosteron |
| skeletal muscle | - uses ATP - striated - somatic/voluntary - requires calcium |
| cardiac muscle | - uses ATP - striated - autonomic/involuntary - requires calcium |
| smooth muscle | - uses ATP - autonomic/involuntary - requires calcium |
| sarcomere | functional unit of skeletal muscle (z-line to z-line) |
| heavy chain segment | long, rod like portions of the myosin that form the core of the filament |
| globular cross-bridge heads | the parts of myosin that interacts with actin contains 2 binding sites: one for actin, one for ATP |
| G-actin | globular actin that acts as the binding site for myosin cross-bridge heads |
| F-actin | the filamentous form of actin that is seen in muscle tissue |
| tropomyosin | spans 7 G-actins and blocks the binding sites |
| troponin | the molecule that controls the blocking and unblocking of actin binding sites via tropomyosin |
| actin:myosin ratio | 2:1 |
| sarcolemma (plasma membrane) | T-tubules (ECF) |
| sarcoplasmic reticulum (smooth ER) | terminal cisternae (stores Ca2+) |
| alpha motor neuron | sends signals from the somatic motor system to the target motor unit |
| nueromuscular junction | the place on the skeletal muscle fiber where a synapse is transferred from the motor neuron |
| motor end plate | highly folded region of the sarcolemma that lies directly beneath the alpha motor neuron nerve terminal (high in nACh receptors) |
| end plate potential (EPP) | a huge excitatory graded potential (30-50 mV) that generates one muscle fiber action potential |
| acetylcholinesterase | breaks down acetylcholine in muscle fibers to control the length of the action potential |
| botulinium toxin | breaks down SNARE proteins in the alpha motor neuron (no contraction) |
| organophosphates | inhibits acetylcholinesterase activity in the muscle fiber (all contract) |
| curare | antagonist of nACh (paralysis) |
| succinylcholine | agonist of nACh (paralysis) |
| Dihydropyridine Receptor (DHPR) | voltage sensor within the T-tubule membrane |
| Ryanodine Receptor (RyR) | Calcium channel within the terminal cisternae of the sarcoplasmic reticulum |
| Sarcoplasmic-Endoplasmic Reticulum Ca2+-ATPAse pump (SERCA pump) | primary active transporter within longitudal membrane of the sarcoplasmic reticulum |
| load | force exerted by an object on a muscle |
| tension | force exerted by muscle on an object |
| isometric contraction | - tension development - XBs cycle - same length - tension = load |
| isotonic contraction | - tension development - XBs cycle - change in length concentric (shortening) tension > load eccentric (lengthening) tension < load |
| twitch | the mechanical response of a single fiber or whole muscle to a single AP |
| fast-twitch fibers | contraction times quick faster calcium release out of SR via RyRs faster calcium reuptake via SERCA |
| slow-twitch fibers | contraction times slow slower calcium release out of SR via RyRs slower calcium reuptake via SERCA |
| what determines the tension developed? | number of XB heads bound to actin |
| latent period | time for the contraction to occur isometric always shorter that an isotonic |
| shortening velocity | (slope) slower with increasing loads |
| shortening determination | (x-axis) gets shorter with increasing loads |
| distance shortened | (y-axis) gets smaller with increasing loads |
| tetanus | the sustained contraction in response to repetitive stimulation unfused vs fused |
| summation of single-fiber contraction | involves number of crossbridges not APs |
| active tension | determined by # of XBs bound to actin |
| passive tension | determined by stretch of titin |
| Slow-Oxidative fibers (SO) | low myosin-ATPase activity high oxidative capacity fatigue resistant small fibers and neurons recruited first |
| Fast-Oxidative-Glycolytic fibers (FOG) | high myosin-ATPase activity high oxidative capacity intermediate glycolytic capacity intermediate fatigue resistance medium fibers and neurons recruited second |
| Fast-Glycolytic fibers (FG) | high myosin-ATPase activity high glycolytic activity low fatigue resistance large fibers and neurons recruited last |
| causes of muscle fiber fatigue (high intensity, short duration activity) | decrease in ATP concentration buildup of metabolites ADP and Pi buildup inhibits power stroke motion |
| causes of muscle fiber fatigue (low intensity, long duration activity) | high activity reasons AND persistent calcium from leaky RyRs decrease in muscle glycogen, low blood glucose, dehydration central command fatigue not usually significant loss of ATP supply |
| isometric equation | wt x d = wt x d |
| lever ratio | pivot point to object/pivot point to insert |
| hand velocity | Vh = Vm x lever ratio |
| activation of smooth muscle cells | neurotransmitters hormones local factors stretch (mechnoreceptors) spontaneous electrical activity |
| tone | the contiuous and partial contraction of the smooth muscle |
| sources of cytosolic calcium (smooth muscle) | leak channels (ECF) stretch-sensitive channels (ECF) voltage-gated channels (ECF) ligand-gated channels (ECF) sarcoplasmic reticulum (ICF) |
| IP3 receptor | IP3 presence in the cell activates pumping od calcium out of the sarcoplasmic reticulum via a second messenger cascade |
| thick filament regulation of smooth muscle contraction | myosin light-chin kinase activated by calcium bound calmodulin MLCK phosphorylates myosin XB cross bridge cycle occurs myosin head dephosphorylated by myosin light-chain phosphatase (MLCP) |
| phasic contraction | tone and phasically active contractions |
| tonic contraction | normally relaxed and normally contracted |
| single-unit smooth muscle | gap junctions sheet contracts together self-excitatory (pacemaker activity) |
| multi unit smooth muscle | independent, uncoupled cells cells is activated (or inhibiited) bt autonomic nerves, hormones, or local factors |
Created by:
educhateau1