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101 Cards in this Set

  • Front
  • Back
2 types of biological work
external work
internal work
external work
movement of object by muscle contraction
internal work
work that is not used to move external objects

ex: hear contraction, ion pmp
what must energy for work be converted into?
ATP which is then used for work
What maintains body temp?
heat generated by biochem rxns and work is used to maintain body temp
metabolic rate
rate that body expends energy doing external and internal work

in kcals/hr
what does metabolic rate depend on?
one kilocalorie
amt of heat needed to raise the temp of one gram water 1C at 15C
How is metabolic rate measured?
indirectly using oxygen consumption
factors that influence metabolic rate
metabolic cost of living
basal metabolic rate
when is basal metabolic rate measured?
during mental and physical rest and at comfortable temp

after fasted for 12 hrs
most important hormone influencing BMR
Thyroid hormone
Actions of thyroid hormone
increase BMR


stimulate synthesis of beta adrenergic receptors

required for maturation of fetus/infant

pulmonary system


needed for normal alertness and reflexes
how does thyroid increase BMR
thyroid hormone stimulates Na/K ATPase.
only tissue that does not have an increase in BMR
what happens to body when thyroid stimulates synthesis of beta adrenergic receptors?
increases heart contractility

increasing beta adrenergic receptors also increases sensitivity to symp. activity and circulating catecholamines
what does absencse of thyroid hormone cause in fetus/infant?
thyroid hormone is needed for brain dev. and maturation of skeleton of fetus. absence of thyroid hormone causes cretinism and dwarfism
3 parts of thyroid gland
follicular epithelial cells around the follicle

the folice

colloid which is in the follicle where the thyroid hormone is
describe the synthesis and secretion of thyroid hormone
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
enzymre in cell that converts T4 to T3
actions of TSH
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
enlarged thyroid gland due to excess stimulation of TSH receptor causing hyperplasia of follicular ep cells
what inhibits TSH and TRH by neg feedback?
How does thyroxine do neg feedback?
thyroxiine inhibits TRH at hypothalmic neurons and inhibits TSH by down regulating TRH receptors on AP

this occurs with hi T3/T4
hyperplasia of thyroid gland, iodide levels are normal but TSH is lo bc of neg feedback
sympotoms of hyperthyroidism
enlarged thyroid gland
increase BMR
weight loss
intolerance to heat
excessive sweating
increase adrenergic activity
emotional lability
dificulty swallowing/breathin
graves disease
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
Benign neoplasms
make T3/T4 which goes and inhibits TRH and TSH
How to treat hyperthryoid (graves/benign neoplasms)
remove thyroid by radiation or surgery followed by thyroid replacement
symptoms of hypothyroidism
lo BMR
weight gain
lo body temp/intol. to cold
decrease sweating
dry skin
decrease adrenergic activty
slow moves
childhood retardation of grow
in neonates get mental retard
hasimotos disease
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
iodine deficiency
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
therapy for hypothyroidism (hashimotos/Iodine def)
replace with T4 synthroid

large doses of I if there is a I defiency
how does epi affect metabolic rate?
it increase BMR by increasing lipolysis and glycogenolysis
satiety center
paraventricular nucleus
hunger center
lateral hypothalmic area and perifomical area
where are satiety and hunger center both located
in hypothalmus
what does nucleus tractus solitarius in Bs do?
tells you to stop eating when you are full
short term regulation of food intake
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
long term regulation of food intake
uses leptin from adipose to stimulate neurons in hypothalmus. the hypothalamic neurons go to the NTS to enhance satiation. leptin also increases metabolic rate
make in tummy during fasting it increases hunger and decreases metabolism and increase gastric mobility and increases gastric acid secretion
normal body temp
37 C

limit is 43 C
what does body temp vary with?
part of body (perph vs core)
circadian variation
menstral cycle-hi at last 1/2
what must be equal to maintain constant temp
heat gain equals heat loss
2 thermoreceptors
peripheral on skin

central in hypothalmus,SC, and abs
what happens in decrease in temp
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"
emission of heat by electromagnetic waves
transfer of heat by collision molecules
how does evaporation remove heat?
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
what happens when increase temp
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"
heat acclimation
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
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
hyperthermia (with fever)
with fever elevation above set pt body reacts to new set point by retaining heat.

shiver and vasoconstriction
what happens when fever breaks
set point returns to normal and sweating and vasodialation occurs to eliminate excess heat
heat exhaustion
state of collapse, faintness bc decrease in sweating and increased vasodialation

with extreme heat exhaustion also have decrease in CO and peripheral resistance
2 limbs of stress response
glucocorticoid response (cortisol)

symp nervous system
how is glucocorticoid release w/ stress
hi stress-CRH secreted from hypothalmus-ACTH secreted from AP-cortisol secreted from adrenal cortex
neg feedback with cortisol
cortisol release causes inhibited release of CRH in hypothalmus and ACTH in AP
when is cortisol released
released in circadian rhythm

released in early morning and late afternoon
besides stress, CRH, and ACTH pathway what elso causes release of glucocorticoids?
cytokines (IL-1)
effects of cortisol under non stress conditions
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.
effects of increased cortisol levels during stress
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


enhance vascular rxn to norepi

inhibit phospholipase A (prostaglandins and leukotriens)
pts with v. hi cortisol levels have symptoms similiar to what?
insulin deficiency
why do you remember stressful situation?
bc ACTH faciliates learning and memory
medical implications with cortisol
pts who are ill/surgery have increased protein catabolism

diabetic w/infection will need more insulin

kids w/stress have retarded growth
what does symp nervous system do during stress
increase glycogenolysis

increase lipolysis

increase ventiliation

increase CO

shunt blood from viscera to muscle

decrease fatigue in muscle

increase coagulation of blood
cushings syndrome
hypersecretion of cortisol
is cushings more common in men or women?
9x more likely in woman
symptoms of cushings
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
what 4 things can cause Cushing's disease?
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
addisons disease
cortisol hyposecretion

must have lost over 90% of adrenocortical tissue to see symptoms
is addisons more likely in girl or boy
symptoms of Addisons
weight loss
decrease plasma Na
increase plasma K
therapy for Addisons
replacement of cortisol and mineralcorticoids

cortisol taken 2x/day
in morning and in late afternoon
factors that influence growth
what does growth require?
cell divison and protein synthesis
what determine height?
bone growth of vertebral column and legs
ends of bone
in interior epiphyseal growth plate these cells form new cartilage
bone forming cells at shaft of epiphyseal growth plate

coverts cartilagous tissue to bone
closure of ep plate
occurs in late puberty

when ep plate is converted to bone. growth stops
environmental factors controlling growth
nutrition (malnutrition bad!)
when is growth retardation most severe?
malnutrition early in life

maternal malnutrition causes low birth wieht and death and decrease growth and intelectual dev.
main hormone that controls growth post natally
Growth hormone
Growth hormone
most important hormone for post natal growth

stimulates cell division

promotes bone lengthening
actions of GH
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
what mediates most of GH activities?
anti insulin effects of GH
stimulates lipolysis

stimulates gluconeogenesis by liver

reduce glucose uptake
neg feedback of GH
IGF-1 inhibits GH and GHRH and activates somatostatin
% of GH bound to protein
when is GH release?
in pulses it is elevated during slow wave sleep
actions of IGF-1
stimulates defferentiation of prechondrocytes to chondrocytes in epiphyseal plates

stimulates secretion of IGF-1 from chondrocytes

stimulates division of chondrocytes to bone
how is T3/T4 required for growth and fetal dev?
they are required for secretion of GH

required for dev. of CNS in fetus
besides GH what other hormones aid in growth?
thyroid hormone
sex hormones
why is insulin needed for growth?
to supply cells with insulin
and stimulate aa uptake by cells for protien synthesis

needed to make IGF-1
insulin actions in fetus
promotes cell differentiatin and division in fetus and is needed to produce IGF-1
major effect of sex hormones
increase GH and IGF-1 secretion
what causes closure of epiphyseal plates to stop bone growth?
hi sex hormones
anabolic effect of testosterone
increase muscle mass in males
cortisol effects on growth
antigrowth bc ...

inhibits DNA syn.
protein catabolism
inhibit bone growth
bone reabsorbtion
inhibit GH