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101 Cards in this Set
- Front
- Back
2 types of biological work
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external work
internal work |
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external work
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movement of object by muscle contraction
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internal work
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work that is not used to move external objects
ex: hear contraction, ion pmp |
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what must energy for work be converted into?
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ATP which is then used for work
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What maintains body temp?
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heat generated by biochem rxns and work is used to maintain body temp
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metabolic rate
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rate that body expends energy doing external and internal work
in kcals/hr |
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what does metabolic rate depend on?
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activity
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one kilocalorie
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amt of heat needed to raise the temp of one gram water 1C at 15C
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How is metabolic rate measured?
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indirectly using oxygen consumption
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factors that influence metabolic rate
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age
gender height/weight menstration growth pregnancy |
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metabolic cost of living
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basal metabolic rate
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when is basal metabolic rate measured?
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during mental and physical rest and at comfortable temp
after fasted for 12 hrs |
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most important hormone influencing BMR
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Thyroid hormone
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Actions of thyroid hormone
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increase BMR
metabolism stimulate synthesis of beta adrenergic receptors required for maturation of fetus/infant pulmonary system GI needed for normal alertness and reflexes |
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how does thyroid increase BMR
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thyroid hormone stimulates Na/K ATPase.
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only tissue that does not have an increase in BMR
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brain
testes spleen |
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what happens to body when thyroid stimulates synthesis of beta adrenergic receptors?
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increases heart contractility
increasing beta adrenergic receptors also increases sensitivity to symp. activity and circulating catecholamines |
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what does absencse of thyroid hormone cause in fetus/infant?
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thyroid hormone is needed for brain dev. and maturation of skeleton of fetus. absence of thyroid hormone causes cretinism and dwarfism
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3 parts of thyroid gland
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follicular epithelial cells around the follicle
the folice colloid which is in the follicle where the thyroid hormone is |
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describe the synthesis and secretion of thyroid hormone
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iodide is in the BS and is taken up by Na/I cotransporter by follicular cell in thyroid. Iodide gets into follicle.
Thyroglobulin (which has lots of tyrosine on it) and thyroid peroxidase are synthesized by folliclar cell and put in follicle Iodide gets converted to Iodine in follicle by thyroid peroxidase. iodine binds to tyrosin on thyroglobulin to make MIT and DIT. MIT and DIT come together wi thyroglobulin to make T3 and 2 DITs come together to make T4. T3 and T4 bind to protin in plasma and go in BS. Free T3 and T4 enter tissue and T4 is converted to T3 by deiodinase. T3 then diffuses into nucleus, binds to receptor and alters gene expression |
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enzymre in cell that converts T4 to T3
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deiodinase
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actions of TSH
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increases uptake of thyroglobulin in ep cells and release of T3/T4
increases uptake of I and iodination of thyroglobulin increases size and vascularization of thyroid gland |
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goiter
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enlarged thyroid gland due to excess stimulation of TSH receptor causing hyperplasia of follicular ep cells
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what inhibits TSH and TRH by neg feedback?
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thyroxin
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How does thyroxine do neg feedback?
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thyroxiine inhibits TRH at hypothalmic neurons and inhibits TSH by down regulating TRH receptors on AP
this occurs with hi T3/T4 |
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hyperthyroidism
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hyperplasia of thyroid gland, iodide levels are normal but TSH is lo bc of neg feedback
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sympotoms of hyperthyroidism
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enlarged thyroid gland
increase BMR weight loss intolerance to heat excessive sweating increase adrenergic activity emotional lability dificulty swallowing/breathin |
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graves disease
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type of hyperthyroidism
autoimmune disease where Ab bind to TSH receptor on thyroid gland and cause constant stimulation of receptor so lots of T3/T4 released but due to neg feedback have decrease in TSH and TRH |
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Benign neoplasms
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make T3/T4 which goes and inhibits TRH and TSH
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How to treat hyperthryoid (graves/benign neoplasms)
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remove thyroid by radiation or surgery followed by thyroid replacement
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symptoms of hypothyroidism
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lo BMR
weight gain lo body temp/intol. to cold decrease sweating dry skin decrease adrenergic activty lethargy slow moves childhood retardation of grow in neonates get mental retard |
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hasimotos disease
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type of hypothyroidism
autoimmune disease where Ab attack the thyroid gland and kill it so you have a decrease in T3/T4 but due to pos feedback causes increase in TSH and TRH |
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iodine deficiency
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type of hypothyroidism
there is no I so you cannot make T3/T4 so due to lo neg feedback you get hi TRH and TSH which makes thyroid larger and makes more thyroglobulin but wo I you cant make any T3/4 so gland gets huge |
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therapy for hypothyroidism (hashimotos/Iodine def)
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replace with T4 synthroid
large doses of I if there is a I defiency |
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how does epi affect metabolic rate?
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it increase BMR by increasing lipolysis and glycogenolysis
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satiety center
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paraventricular nucleus
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hunger center
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lateral hypothalmic area and perifomical area
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where are satiety and hunger center both located
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in hypothalmus
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what does nucleus tractus solitarius in Bs do?
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tells you to stop eating when you are full
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short term regulation of food intake
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determines the size of individual meals
neural signals from mechanical and chem stimulation of tummy during food intake. also neural input from liver and hormone in GI like CCK go to NTS to say your full |
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long term regulation of food intake
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uses leptin from adipose to stimulate neurons in hypothalmus. the hypothalamic neurons go to the NTS to enhance satiation. leptin also increases metabolic rate
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ghrelin
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make in tummy during fasting it increases hunger and decreases metabolism and increase gastric mobility and increases gastric acid secretion
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normal body temp
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37 C
limit is 43 C |
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what does body temp vary with?
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part of body (perph vs core)
activity circadian variation menstral cycle-hi at last 1/2 |
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what must be equal to maintain constant temp
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heat gain equals heat loss
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2 thermoreceptors
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peripheral on skin
central in hypothalmus,SC, and abs |
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what happens in decrease in temp
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the peripherial and core thermoreceptors send signals to the hypothalmus. the hypothalmus sends sigals to:
skeletal m. to shiver constrict arteries at skin increase epi at adrenal med. CC to say "I am cold" |
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radiation
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emission of heat by electromagnetic waves
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transfer of heat by collision molecules
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conduction
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how does evaporation remove heat?
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w/sweat glands stimulated by symp (ACTH to activate M)
when env is above core temp, max vasodialation does not remove enough heat so use evaporation |
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what happens when increase temp
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periperhal and core thermoreceptors send signal to hypothalmus. hypothalmus sends signal to:
dialate arteries of skin increase sweat glands CC to say "I am hot" |
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heat acclimation
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person moves from NY to CA
pt reacts to heat sooner and increases the amt of sweat. Na conc in sweat decreases to minimize the amt of Na lost |
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fever
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elevated temp due to resetting of thermostat in hypothalmus due to infection which is caused endogenous pyrogens (IL)
get chill with rapid onset of fever |
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hyperthermia (with fever)
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with fever elevation above set pt body reacts to new set point by retaining heat.
shiver and vasoconstriction |
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what happens when fever breaks
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set point returns to normal and sweating and vasodialation occurs to eliminate excess heat
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heat exhaustion
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state of collapse, faintness bc decrease in sweating and increased vasodialation
with extreme heat exhaustion also have decrease in CO and peripheral resistance |
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2 limbs of stress response
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glucocorticoid response (cortisol)
symp nervous system |
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how is glucocorticoid release w/ stress
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hi stress-CRH secreted from hypothalmus-ACTH secreted from AP-cortisol secreted from adrenal cortex
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neg feedback with cortisol
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cortisol release causes inhibited release of CRH in hypothalmus and ACTH in AP
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when is cortisol released
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released in circadian rhythm
released in early morning and late afternoon |
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besides stress, CRH, and ACTH pathway what elso causes release of glucocorticoids?
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vasopressin
epi cytokines (IL-1) |
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effects of cortisol under non stress conditions
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permissive effects on norepi and epi actions on blood vessels and symp nervous control of BP
maintains enzymes for gluconeogenisis in liver important in fetal dev. |
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effects of increased cortisol levels during stress
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opposite of insulin
leads to mobilization of fuels(aa,glucose,fa,glycerol) protein catabolism in muscle so aa can go to liver to undergo gluconeogenisis. inhibits glucose uptake except in brain lipolysis enhance vascular rxn to norepi inhibit phospholipase A (prostaglandins and leukotriens) |
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pts with v. hi cortisol levels have symptoms similiar to what?
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insulin deficiency
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why do you remember stressful situation?
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bc ACTH faciliates learning and memory
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medical implications with cortisol
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pts who are ill/surgery have increased protein catabolism
diabetic w/infection will need more insulin kids w/stress have retarded growth |
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what does symp nervous system do during stress
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increase glycogenolysis
increase lipolysis increase ventiliation increase CO shunt blood from viscera to muscle decrease fatigue in muscle increase coagulation of blood |
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cushings syndrome
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hypersecretion of cortisol
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is cushings more common in men or women?
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9x more likely in woman
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symptoms of cushings
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muscle weekness bc of protein catabolism
osteoporosis bc demineralization of bine glucose intolerant obese-fat goes from extremities to trunk hypertension due to aldosterone reabsorbing Na decrease immune function emotional crap retarded growth in youth |
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what 4 things can cause Cushing's disease?
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1.hypercortisolism due to excess ACTH due to tumor in AP
2. hypercortisolism due to increase release of ACTH by ectopic loci 3. hypercortisolism due to secretion of CRH by ectopic loci 4. excess secretion of cortisol by adrenal cortex neoplasm |
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addisons disease
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cortisol hyposecretion
must have lost over 90% of adrenocortical tissue to see symptoms |
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is addisons more likely in girl or boy
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girl
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symptoms of Addisons
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weak
hypotension weight loss decrease plasma Na increase plasma K hyperpigmentation |
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therapy for Addisons
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replacement of cortisol and mineralcorticoids
cortisol taken 2x/day in morning and in late afternoon |
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factors that influence growth
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genetics
endocrine environment |
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what does growth require?
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cell divison and protein synthesis
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what determine height?
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bone growth of vertebral column and legs
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ends of bone
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epiphysis
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chondrocytes
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in interior epiphyseal growth plate these cells form new cartilage
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osteoblasts
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bone forming cells at shaft of epiphyseal growth plate
coverts cartilagous tissue to bone |
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closure of ep plate
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occurs in late puberty
when ep plate is converted to bone. growth stops |
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environmental factors controlling growth
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nutrition (malnutrition bad!)
illness stress |
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when is growth retardation most severe?
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malnutrition early in life
maternal malnutrition causes low birth wieht and death and decrease growth and intelectual dev. |
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main hormone that controls growth post natally
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Growth hormone
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Growth hormone
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most important hormone for post natal growth
stimulates cell division promotes bone lengthening |
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actions of GH
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stimulates cell division
promotes bone lengthening stimulates release of IGF from liver simulates protein synth. by increasing uptake of aa in tissue and making RNA |
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what mediates most of GH activities?
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IGF
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anti insulin effects of GH
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stimulates lipolysis
stimulates gluconeogenesis by liver reduce glucose uptake |
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neg feedback of GH
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IGF-1 inhibits GH and GHRH and activates somatostatin
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% of GH bound to protein
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40%
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when is GH release?
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in pulses it is elevated during slow wave sleep
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actions of IGF-1
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stimulates defferentiation of prechondrocytes to chondrocytes in epiphyseal plates
stimulates secretion of IGF-1 from chondrocytes stimulates division of chondrocytes to bone |
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how is T3/T4 required for growth and fetal dev?
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they are required for secretion of GH
required for dev. of CNS in fetus |
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besides GH what other hormones aid in growth?
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thyroid hormone
insulin sex hormones corisol |
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why is insulin needed for growth?
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to supply cells with insulin
and stimulate aa uptake by cells for protien synthesis needed to make IGF-1 |
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insulin actions in fetus
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promotes cell differentiatin and division in fetus and is needed to produce IGF-1
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major effect of sex hormones
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increase GH and IGF-1 secretion
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what causes closure of epiphyseal plates to stop bone growth?
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hi sex hormones
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anabolic effect of testosterone
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increase muscle mass in males
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cortisol effects on growth
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antigrowth bc ...
inhibits DNA syn. protein catabolism inhibit bone growth bone reabsorbtion inhibit GH |