Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
55 Cards in this Set
- Front
- Back
|
What happens if there is excess hormonal activity? Deficiency in hormone?
|
-Too much H: Dimunition of secretion of the hormone
-Not enough H: Inc in secretion |
|
|
How does Ca2+ regulate plasma Ca2+ lvls?
|
Through a ngative feedback loop
-Low plasma Ca2+ --> Stimulate parathyroid gland --> Inc syn and relese of parathyrid H --> Inc parathyroid H (PTH) secretion --> Acts on bone, kiney and gut --> inc plasma Ca2+ --> acts as a non-hormonal neg fdbk by acting on parathyroid glands |
|
|
What is the hormonal fdbk mechanism starting in the hypothalums?
|
-Stress acts on hypothalamus
-Inc CRH secretion -Inc Plasma CRH -Acts on anterior pituitary, Inc of ACTH secretion -Inc of plasma ACTH -Acts on adrenal cortex, Inc cortisol secretion -Inc plasma cortisol: this has neg fdbk on H in hypothalamus and anterior pituitary -Target cell of cortisol responds to inc cortisol levels |
|
|
What are the main endocrine glands?
|
-Anterior pituiatry
-Posterior pituitary -Thyroid Gland |
|
|
What are the two tissues of the pituitary gland? What kind of tissue are they?
|
-Anterior (adenohypophysis): Endocrine tissue
-Posterior (neurohypophysis): Neural tissue Posterior and anterior glands differ histologically |
|
|
How does signalling occur between the hypothalamus and the anterior pituitary and what organs are targeted?
|
1) GnRH--> (+) FSH and LH --> Gonads
2) GHRH --> (+) GH --> Liver and other cells, many organs and tissues 3) Somatostatin (SS) --> (-) GH --> Liver, cells, organs and tissues 4) SS --> (-) TSH --> Thyroid 5) TRH --> (+) TSH --> Thyroid 6) TRH--> (+) Prolactin --> Breasts 7) Prolactin releasing inhibiting H (PIH) --> (-) Prolactin --> Breasts 8) Prolacting Releasing H (PRH) --> (+) Prolactin --> Breasts 9) Corticotropin releasing H (CRH) --> (+) ACTH --> Adrenal cortex |
|
|
What is the relationship between Growth H releasing H (GHRH) and Somatostatin (SS)?
|
They have opposite affects on Growth hormone (GH)
|
|
|
What arethe functions of the target hormones?
|
Gonads: germ dev'l; hormones: estrogen, progesterone, testosterone
Liver: secretes IGF-1 (insulin-like growth factor) Organs and tissues: Growth and metabolism Thyroid: Secretes thyroxine and triiodothyronine Breasts: (prolactin) Breast dev'l, milk production, males: facilitates reproductive fct Adrenal cortex: Secretes cortisol |
|
|
What are the hormones of the hypothalamus?
|
-GnRH: gonadotroping releasing H)
-GHRH (hrowth hormone rekeasing H) -SS (Somatostatin) -TRH (Thyrotropin releasing H) -PIH (prolactin release inhibiting H) -PRH (prolactin releasing hormone) -CRH (corticotropin releasing hormone) |
|
|
What are the hormones of the anterior pituitary?
|
-FSH
-LH -ACTH (adrenocorticotropin H) -TSH (Thyroid stimulating H) -Prolactin -GH (Growth H) (FLAT PEG) |
|
|
What are the posterior pituitary hormones?
|
-Arginine vasopressin
-Oxytocin |
|
|
What us the genomic difference between vasopressin and oxytocin?
|
They differ by 2 aa
|
|
|
Which ormone is dopamine?
What is special about dopamine? |
-Dopamine= PIH (prolactin release inhibitin H)
-It is not a peptide hormone (all the other hypothalamus hormones are peptide hormones) |
|
|
What is the neurohypophysis?
|
Posterior pituitary gland
|
|
|
What does the posterior pituitary gland secrete?
|
Oxytocin
Vasopressin (ADH) |
|
|
Where are oxytocin and vasopressin made?
|
2 Hypothalamic nuclei (has axins that run down the pituitary stalk and end in the posterior pituitary near the capillary blood vessels)
|
|
|
Where and when are prohormones processed?
|
-In secretory granules
-During axinal transport |
|
|
What do the carrier molec of the posterior pituitary release?
|
The mature hormones (neurophysins) oxytocin and vasopressin
|
|
|
What is the function of oxytocin in males?
|
No known fct, but is probly secreted by the posterior pituitary
|
|
|
What is the fct of oxytocin in females?
|
2 motor fcts
1)Parturition (giving birth): dilation of uterine cervix causes release of oxytocin which causes uterus to contract and helps expel fetus and placenta 2) Milk ejection: oxytocin causes milk filled ducts to contract and squeeze out milk |
|
|
What is the major component of the thyroid gland? Describe.
|
Thyroglobulin
-700 kDa ptn (large) -Contains H: Thyroxine (T4) & Triiodothyronine (T3) -Synthesis of thyroglobulin controlled by TSH of pituitary -Provides storage fr T3 and T4 before they are released |
|
|
Describe the thyroid gland.
|
-15- 20 g
-size varies with age, sex, diet, reproductive state, etc -Larger in females then males -only need 2g of healthy thyroid to maintain euthyroid state |
|
|
What do thyroid H contain?
|
Iodine
|
|
|
What do thyroid folllicular cell do?
|
Trap iodide and transport it across the cell against a chemical gradient (active transport)
|
|
|
How have terrestrial vertebrates evolved to deal with the availability of iodine?
|
Dev'l cellular mechanisms for concentration, utilization and conservatio of iodine in the thyroid gland
|
|
|
What are the thyroid H?
|
T4 & T3 (biologically active)
reverse T3 (biologically INactive :.: not bound by the H receptor) |
|
|
How are thyroid H synthesized?
|
-Iodine (I2) used to iodinate tyrosine residues of Thyroglobulin (TGB) to make mono- and di-iodotyrosine (MIT and DIT)
->oxidative coupling of 2 DITs-->T4 ->oxidative coupling of 1 MIT with 1 DIT --> T3 |
|
|
What controls thyroid activity?
|
TSH (Thyroid stimulating hormone)
|
|
|
What controls the synthesis and release of TSH?
|
The hypothalamic H thyrotropin releasing H (TRH)
|
|
|
What happens when lvls of T3 and T4 increase?
|
Exert neg fdbk at hypothalamic and pituitary lvls to decrease the release of TRH and TSH
|
|
|
Where does TSH bind? What does it do?
|
-TSH interacts with specific receptors on folllicular cells
-Induces activation of adenylyl cyclase (2nd messenger) and production on cAMP -> inc synthesis and release of T3 an T4 |
|
|
What happens during iodine deficiency?
|
-Synthesis of thyroid H dec
T4 and T3 circulating lvls dec -Inc release of TSH and the thyroid follicular cells are constantly stimulated (no neg fdbk loop) -Thyroid enlarges and might form a goiter (but non-toxic since can't make biologically active thyroid H) |
|
|
What are the effects of thyroid hormones?
|
1) Stimulation of calorigenesis in most cells
2)Effects on carbohydrate metabolism 3) Effects on lipid turnover 4)Effects on protein metabolism 5)Promote normal growth |
|
|
How do TH sitmulate calorigenesis in most cells?
|
-Increase cardiac output
-Increase rate and strength of cardiac contractions -Increase oxygenation of blood -Increase rate of breathing (inc number of RBC in circulation) |
|
|
How do TH effect carbohydrate mtabolism?
|
Promote glycogen formation in the liver
Increase glucose uptake into adipose and muscle (increase fuel sources) |
|
|
What effects do TH have on lipid turnover?
|
Increase lipid synthesis
Inncrease lipid mobilization Increase lipid oxidation ->probly as fuel source |
|
|
What effects do H have on protein metabolism?
|
Stimulate protein synthesis (indirect effect)
->can lead to ptn degradation |
|
|
How do TH promote normal growth?
|
-Stimulate GH secretion .: promote bone growth, IGF-I (insulin-like growth factor-1)production by the liver
-Promote dev'l and maturation of the nervous system -Promote neural branching and myelinization of nerves -->Neural dev'l |
|
|
What is the basic metabolic rate (BMR)?
|
Rate at which the organism burns up its stores of fuel to produce E in the form of heat or calories
|
|
|
How do T3 and T4 affect themetabolic rate?
|
-Inc BMR
->Inc the breakdown of carbs, lipids, ptns ->inc metabolic activity= increased need for oxygen |
|
|
What is the effect of TH on growth?
|
GH requires T4 and T3 to properly stimulate growth
.: T3 and T4 have permimssive effect on growth |
|
|
What is the effect of TH on the CNS?
|
Req'd for normal dev'l of the brain
Absence of TH at early stages of dev'p lead to irrev mental retardation ->TH stimulate synthesis of Nerve Growth Factor (NGF), which induces dendritogenesis and regeneration of sympathetic neurons |
|
|
What are the molecular mechanisms of action of TH? (3)
|
1) Analagous to mech of action of steroid H: T3 and T4 enter target cell nucleus and bind to their cognate nuclear receptor, where it alters the transcription of specific genes and .: lvls of encoded ptns
-->Effects blocked by ptn synthesis inhibitors 2)TH may induce some effects by interaction with plasma mb and mitochondria: T3/4 interact w/ specific repceptor in the IMM and inc O2 consumption and produce heat in the mitochondria --> NOT blocked by ptn synthesis inhibitors 3) T3/4 act directly at plasma mb and inc uptake of aa: also independent of ptn synthesis inhibitors |
|
|
What are the abnormalities of thyroid fct?
|
1) Hypofct (NOT enough): Hypothyroidism, low lvls of TH (congenital: present at birth)
2) TOO MUCH: Hyperthyroidism, high lvls of TH |
|
|
What are he major physiological consequences of hyperthyroidism?
|
-Elevated T3/4 lvls
-Elevated BMR (hypermetabolism) -Inc, perspiration -Rapid pulse, inc cardiac output, hypertension -Inc body T -Heat intolerance -Sweaty palms -Nevousness, anxiety, excitabililty, restlessness, insomnia -Weight loss -Inc appetite -Muscle wasting -Menstrual irregularities -Exophtalmos (eyes bulge out) -Goiter (primary/secondary in origin) |
|
|
What are he major physiological consequences of hypothyroidism?
|
-Dec/absent T3/4
-Low BMR (hypometabolism) -Dec perspiration -Slow pulse, dec cardiac output, hypotension -lower body T -cold intolerance -coarse, dry skin, subdermal thickening -lethargy, dec mentation, depression, paranoia, sleepiness, tiredness -Weight gain -loss of hair, dry brittly texture -edema of face and eyelids -Menstrual irregularities -carotenemia (inc plasma lvls of carotenes) -goiter (may/not be present) |
|
|
What is primary hypothyroidism?
|
Myxedema
-at lvl of thyrod gland ->inabillity of tyroid gland to make active TH -more common in women then men (appears 40-60 years of age) Caused by: ->atrophy of thyroid ->autoimmune thyroiditis: destruction by AB vs cell components of thyroid (Hashimoto's disease) ->Goitrous hypothyroidism/Non-toxic goiter: block in T3/4 synthesis, causing inc of thyroid gland and goiter formation |
|
|
What is secondary hypothyroidism?
|
-at lvl of pituitary
-synthesis of little/no TSH |
|
|
What is tertiary hypothyroidism?
|
-at hypothalamic lvl
-synthesis of little/no TRH |
|
|
What is infantile hypothyroidism?
|
-Absence of thyroid gland or incomplete dev'p of thyroid gland at birth
->baby normal at birth cuz fetus uses it's mother's T3/4. But after a few months, baby shows dec physical growth and mental dev'p. Need early treatment or can get dwarfism or mental retardation ass't with cretinism |
|
|
How can all types of hypothyroidism be treated?
|
Giving them thyroid hormone
|
|
|
What is primary hyperthyroidism?
|
-level of thyroid gland
1)Toxic diffuse goiter (Graves Disease): autoimmune disease; presence of LATS (long acting thyroid stimulator) that mimics actions of TSH and stimulatng release of T3 and T4. Cst stimulation by LATS inc mass of thyroid -> goiter formation which makes T3/4 .: toxic goiter 2)Thyroid adenoma/thyroid cancer: synthesize TH independent of TSH stimulation |
|
|
What is secondary hyperthyroidism?
|
level of anterior pituitary gland
-no neg fdbk from inc lvls of T3/4 and autonomous synthesis of TSH -often due to presence of pituitary tumor |
|
|
What is tertiatry hyperthyroidism?
|
at level of hypothalamus
-no neg fdbk of high T3/4 to decrease the synthesis of TRH -often due to presence of hypothalamic tumour |
|
|
How can hyperthyroidism be treated?
|
Depends on severity of hyperthyroidism
1)Surgery + replacemet treatment (admin of TH) 2)Admin of radioactive Iodide (131-I) (~5 mCi). This concentrates in the cells of thyroid follicles and destroys them. Can use replacement therapy if needed 3) Admin of antithyroid drugs like Propylthiouracil (blocks addition of iodine to TGB). Must be carfeul not to stop the synthesis of TH too much, don't want to caue hypothyroidism. |
