UCF Human Physiology Test3 SummerB Endocrine

- inactive.

-active.

Seven-transmembrane domain receptors

-tyrosine kinase

-tyrosine kinase

-autophosphorylation

JAK2

tyrosine kinase

-Guanylyl cyclase receptor

increased NO and vasodilation/relaxation

steroids and thyroid hormones

-freely

-with a carrier

-anterior = blood vessels

-posterior = nerves

CRH

Thyroid hormones and prolactin

dopamine

somatostatin

under control of CRH* -> function is to stimulate the 3 adrenal cortex hormones

concentration increases in first two weeks of menstrual cycle b/c it is required for the development of folicle

development of folicle = development of ovum (located in folice)

level increases in mid cycle (day 13-15) bc LH helps in the last steps of folicular development -> required for the rupture of the folicle, elimination of the ovum from the folicle, and movement of ovum from ovary to the fallopian tube -> in general LH is important for elimination

has receptor in testis -> controls spermatogenesis (development of mature sperm from germ cells)
Deficient FSH = infertility

has receptor on cell membranes (leydig cell) located in testis  stimulates testosterone secretion from leydig cells

level increases during pregnancy because it prepares the mammary glands for production of milk during breast feeding; increase also suppresses secretion of FSH and LH -> prevents 2nd pregnancy during pregnancy

increase in non-pregnant females = infertility

behavior hormone; important for contacts.

suppresses FSH = abnormal sperm

suppresses LH = low testosterone

has receptor on myometrium of uterus that causes the contraction of myometrium during delivery. Also has receptor on myoepithelial cell of mamary gland and causes ejection of milk during breast feeding

important for ejaculation and causes vasoconstriction of smooth muscle blood vessels of penis

Glumeruloasa = outter cortext
fasciculata

mineralocorticoids (aldosterone)

mostly glucocorticoids (cortisol)

sex hormones (mostly androgens, dehydroepiandro-sterone and androstenedione)

Is under tonic control by ACTH, but is separately regulated by the
renin-angiotensin system and the potassium.

tumor of zone glumerlosa of adrenal cortex = oversecretion of aldosterone = HTN, hypernatremia, hypokalemia

increase renal H+ secretion (action on the intercalated cells of the late distal tubule and collecting duct).

-Stimulation of gluconeogenesis

adrenocortical insufficiency

hypotensive, hyponatremia, and hyperkalemia; hypoglycemia (cortisol); impared immune function; hair loss due to androgen deficiency; hyperpigmentation of face/lips/palms/nails

primary = adrenal gland

secondary = ACTH or CRH

Adrenocortical excess

oversecretion of aldosterone, cortisone, androgen
HTN, hypernatremia, hypokalemia, hyperglycemia, cortisol stimulates the appetite and the pt has accumulation of fat in abd cavity and shoulder area and posterior region of neck. Cortisol alterates the collagen – skin has lines in it; Cortisol = breaking down of proteins = thinner upper and lower limbs = atrophy Female has hair on face

moon face

Cushings is all 3 cortical hormones. Conn's is aldosterone

T3 is more active

T4 can cross placental membrane during pregnancy but it is converted to T3

Folicular cell

peroxidase

T4

T3

secreted by the hypothalamus and stimulates the secretion of TSH by the anterior pituitary.

increases both synthesis and secretion of thyroid hormones by the follicular cells via an adenylate cyclase- cAMP mechanism.

hypertrophy of the thyroid gland

T3

B1 receptors

A1 receptors

a. Increases glucose absorption from the gastrointestinal tract
b. Increase glycogenolysis, gluconeogenesis, and glucose oxidation
c. Increases lipolysis
d. Increases protein synthesis and degradation. The overall effect is catabolic.

memory disorder and learning disorder, cold/temperature regulation, weight gain, hypotension, speech disorder, sleep disorder

nervousness/anxiety, htn(adrenergic), increased CO, palpitations, sleep disorder, high metabolism (weight loss), feel extremely hot

hypothyroidism

Hashimoto's thyroiditis – autoimmune -> hypothyroidism

parathyroid - blood calcium

pancreas - BGL

binding of PTH to receptor causes increase in calcium reabsorption by small intestine capilary

binding causes reabsorption of calcium by peritubular capilary of DT

binding causes the removal of ca from bone and releases it into blood stream

converts the precursor of vitamin D into active form of vitamin D

-25 hydroxy colicalciferol

-1.25 dehydroxy colicalciferol

prevents -> phosphate is excreted

Decreased calcium

mild decrease in magnesium

- inhibits PTH secretion and produce
symptoms of hypoparathyroidism

cAMP

results in hypocalcemia

Alterates action potential – especially SA node
Alterates neuromuscular junction
Alterates the synapse and release of NT and activation of next neuron
Alterates bone development
Tetany – not exactly the same as tetanus  or tetany seizure is a medical sign consisting of the involuntary contraction of muscles; spasms and then weakness

Role of vitamin D = reabsorption of calcium by the bone -> deficiency = weak bones

Hypercalcemia
Overstimulation/excitation of SA node = extrasystole
Htn

alpha cells

glucagon

beta cells

insulin

-delta cells

-somatostatin

-gastrin

gap junctions

cAMP

glycogenolysis
gluconeogensis
fatty/keto acid concentration
urea production

insulin increases glucose uptake

activates GLUT2 -> GLUT2 inserts into membrane and glucose continue to enter -> K+ channels close and K+ remains inside cell -> calcium channels are activated and calcium enters beta cell -> high concentration of calcium causes stimulation of secretory vesicles full of insulin -> exocytosis + release of insulin

insertion of GLUT4 into target cell membrane -> GLUT4 then allows glucose to pass through channels

Autoimmune disease -> destruction of Beta cells in the pancreas -> leads to deficiency of insulin production -> low blood insulin = glucose cant enter target cell and remains in blood = hyperglycemia

insulin decreases blood K+ concentration, increases K+ uptake into cells, which decreases blood K+ concentration.

insulin

Possibly due to genetic disorder -> alteration/mutation to insulin receptor -> the receptor becomes resistant to insulin

exercise, diet, metformin

somatostatin

serotonin

-pineal gland

-melatonin

HCG – non-pregnant females do not have this hormone; hormone is important for positive sign of pregnancy (urinalysis);
Hormone controls the corpus luteum which produces progesterone. Progesterone maintains the endometrium for the pregnancy

Relaxin – during delivery relaxin relaxes the cervix and joints of pelvic cavity for delivery

after the first trimester of pregnancy

maintains endometrium, important for proliferation of cell proliferation after menstruation; responsible for secondary sex characteristics

arachidonic acid

cyclooxygenase

lipoxygenase into leukotrienes

decreased cortical hormones causes feedback to increase ACTH, CRH, and POMC -> POMC is precursor to alpha-melanocyte = hyperpigmentation

alpha-melanocyte
enkephalin
ACTH
MSH

K+ channels close - can't leave

Ca++ channels open - rushes in

Interleukin 1 and 2

cyclooxygenase

arachidonic acid to PGE2

PGE2 irritates temperature center of the hypothalamus = fever