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Endocrine Revision
Revision of the endocrine system
| Question | Answer |
|---|---|
| A gland that secretes its products into another organ or onto body surface by way of a duct | Exocrine gland |
| A ductless gland that secretes hormones into the bloodstream | Endocrine gland |
| Name the hormones produced by the anterior pituitary | ACTH, TSH, Growth hormone, FSH, LH, Prolactin |
| Name the 9 endocrine glands in the body | Hypothalamus, pituitary, pineal gland, thyroid gland, parathyroid gland, thymus, adrenal, pancreas, kidneys & gonads |
| These hormones are carried in the blood dissolved in plasma | Protein hormones |
| Where are the hormone receptors for protein hormones? | Plasma membranes. |
| How does the message from protein hormones enter the cell | hormone interacts with fixed membrane receptor, this cause the release of a SECOND MESSENGER which activates a series of enzyme reactions that alter the cell function |
| What is the rate of excretion for protein hormones | are readily filtered in glomerulus & removed from the blood because of their solubility |
| If this hormone is taken orally it is destroyed | Protein. digestive enzymes break their peptide bonds |
| These hormones need a protein carrier to transport them in the blood | Lipid - steroid |
| What is the importance of a hormone-protein complex | the extent to which the hormone is bound to carrier determines the rate it leaves the blood & enters the cells. The free hormone is the active portion |
| Where are the receptors for steroid hormones | in cytoplasm because they can pass through the membrane |
| What effects the rate of excretion for steroid hormones | plasma proteins are too large to be filtered, therefore only the free hormone can be excreted, making excretion slow |
| Define target cell | cells which carry receptors for a particular hormone |
| define target tissues | are made up of target cells |
| This mechanism reduce the difference between a variable & it's "set" level | negative feedback |
| Define positive feedback | an increase in output leads to a further increase in the input. |
| What is the embryological development of the posterior pituitary | derived from the base of the brain, contains axon terminals from neurosecretory cells of the hypothalamus. |
| another name for posterior pituitary | neurohypophysis |
| Describe the embryological development of the anterior pituitary | derived from the roof of the mouth and composed of glandular tissue which produces & secretes hormones |
| what is another name for anterior pituitary | adenohypophysis |
| what are tropic hormones | they stimulate endocrine glands |
| what is the function of calcium | structural components of teeth, nerve impulse conduction, blood clotting, muscle contraction, exocytosis, acid-base balance, second messenger & cofactor |
| how does parathormone increase plasma calcium | facilitates the release of calcium from bone, enhance reabsorption of calcium by the kidney & in the small intestine |
| effects of hypercalcaemia | decreased neuromuscular excitability, cardiac arrhythmia and arrest, muscle weakness, confusion, kidney stones, emotional disturbances, nausea & vomiting, coma |
| effects of hypocalcaemia | increased neuromuscular excitability, tingling fingers, tremor, muscle cramps, tetany, convulsions, affects bone growth |
| what can cause hypocalcaemia | vitamin D deficiency, diarrhoea, thyroid tumors, under active parathyroid, pregnancy & lactation |
| how does calcitonin effect calcium levels | reduces calcium levels by osteoclast inhibition , which release less calcium from the bone & osetoblast stimulation, which deposit calcium into the bone |
| adult calcium levels are entirely under control by parathormone. Explain it's effects | rise calcium levels by osetocyte & osteoclast stimulation, reduces excretion of calcium & increases excretion of phosphate, vitamin D synthesis |
| describe calcitrol | most active form of vitamin D, via skin, liver, kidney & small intestine. promote intestinal absorption of calcium & phosphate, and reduces excretion of both |
| what diseases are caused by hyper & hyposecretion of growth hormone? | hyper: <20 years - gigantism >20 years - acromegaly Hypo: pituitary dwarfism |
| what are the symptoms of gigantism | an abnormal increase in the length of long bones. Person grows tall but body proportions are abnormal |
| what are the symptoms of acromegaly | cannot grow tall because epiphyseal plates are closed. hands, feet & facial features thicken |
| what are the symptoms of pituitary dwarfism | slow bone growth, epiphyseal plates close before normal height is reached. body is child like |
| what are the diseases from hyper and hypo secretion of ADH | hyepr: syndrome of inappropriate ADH (S.I.A.D.H) Hypo: diabetes insipidus |
| what does S.I.A.D.H cause | fluid retention & sodium dilution, hyponatraemia, hypo osmolarity of blood, weight gain, brain oedema, coma & death |
| what are the symptoms of diabetes insipidus | polyuria 3-30L a day polydipsia, sever dehydration |
| what does hyper and hypo secretion of T3 & T4 cause | Hyper: Graves disease Hypo: myxoedema, endemic goiter & cretinism |
| what are the symptoms of graves disease | enlarged thyroid, oedema behind the eyes,thinning hair, hand tremors & difficulty sleeping |
| what are they symptoms of cretinism | short stature, thick & protruding tongue, floppy infant, unproportional, prolonged jaundice |
| what are the symptoms of myxoedema | oedema that causes the face to swell |
| what diseases are caused by hyper and hyposecretion of aldosterone | Hyper: aldosteronism Hypo: addisons disease |
| What are the effects of aldosteronism | hypernatraemia hyperchlorhydia hypervolaemia hypokalaemia |
| what are the characteristics of addisons disease | weight loss, muscle weakness, fatigue, low blood pressure & darkening skin |
| what are the diseases caused by hyper & hypo secretion of cortisol | Hyper: cushings disease/syndrome Hypo: addisons |
| what are the symptoms of cushings syndrome | breakdown of muscle proteins & redistribution of body fat results is spindly arms & legs and a "moon" face, "buffalo" hump & hanging abdomen, flushed face |
| what cells of the pancreas produce insulin, and what effect does it have on BGL | beta cells. Target cells plasma membranes capacity to transport glucose & amino acids. Glycolysis. decreases BGL |
| what cells of the pancreas produce glucagon & what is its effect on BGL | alpha cells. primarily acts on liver to break down glycogen & release glucose. Increases BGL |
| This hormone is produced by delta cells of the pancreas & acts locally inhibiting the secretion of both insulin & glucagon | Somatostatin A.K.A growth inhibiting hormone |
| Name the nucleus that produces oxytocin | paraventricular nucleus |
| Name the nucleus that produces ADH | supraoptic nucleus |
| How do hormones get from the hypothalamus to the posterior pituitary, how long does it take | transported down the axons to nerve cells, and stored bound to proteins in axon terminals in the pituitary. Takes about 10hours |
| how are hormones from the posterior pituitary released | Are released from the terminals in response to nerve impulse, when released in neurohypophysis they diffuse into the blood |
| what is the relationship between they hypothalamus & the posterior pituitary | Pituitary gland hangs from hypothalamus & is connected by the infundibulum. |
| hypothalamic-hypophyseal tract | tract of unmyelinated nerves connecting the hypothalamus to posterior pituitary, route of stimulation for hormone release |
| what are the different controls for the posterior & anterior pituitary | Anterior- chemical control Posterior- electrical control |
| hypotalamo-hypophyseal portal system | releasing hormones from the hypothalamus are carried to anterior pituitary by this special circulatory network |
| where do the male hormones come from | hypothalamus- Gonadotropin.R.H anterior pituitary- F.S.H & L.H Testes- testosterone |
| what is the function of F.S.H in males | stimulates steroli cells lining seminiferous tubules & initiate spermatogenesis. stimulates production of androgen binding protei |
| what is the function of L.H (I.C.S.H) in males | stimulate Leydig cells of the testes to secrete testosterone |
| What is the function of testosterone | Growth & development of primary sex organs, secondary sex characteristics, anabolic activity, vigour in muscles & bones, enhancese RBC production & provides positive feedback to hypothalamus |
| what is the function of inhibin in males | produced by sustentacular cells when sperm count is too high, slows sperm production without inhibiting testosterone |
| function of L.H in females | Causes ovulation of the follicle producing the corpus luteum, secreting progesterone |
| function of F.S.H in females | stimulates the development of ovarian follicles leading to oestrogen production |
| role of oestrogen in the menstrual cycle | stimulates growth of endometrium in preparation for ovulation |
| Role of progesterone in the menstrual cycle | only during luteal phase of ovarian cycle. works with oestrogen to prepare the endometrium for implantation of the fertilized ovum with increase blood cells and glycogen stores |
| what causes the "L.H surge" and what does it result in | high oestrogen levels in follicular phase have a positive feedback effect on hypothalamus & anterior pituitary causing a rise in L.H production which causes ovulation |
| corpus luteum | what becomes of the ruptured graafian follicle after release of an ovum |
| corpus albicans | the degenerated corpus luteum if fertilization of the ovum doesn't occur |
| what are the phases of the menstrual cycle | menstrual phase, proliferative phase (building up endometrium) secretory phase (progesterone from corpus luteum) menstruation of fertilization doesn't occur |
| Hormones produced by thyroid | T3 & T4 calcitonin |
| Hormones produced by the adrenal cortex | aldosterone cortisol sex hormones |
| what causes menstruation | if fertilization doesn't occur the corpus luteum degenerates to the corpus albicans & is shed with the lining of the endometrium & dead blood cells in preperation for another follicle |
| what are the target organs, the action & stimulus for production for growth hormone | Target: most cells, bone, skeletal & muscle Action: Increase in cell size & cell division. promotes protein synthesis & favors use of lipids for ATP (anabolic effects) Stimulus: GHRH/GHRIH |
| what is the stimulus for production for ADH, the cells it targets and the effect | Stimulus: Increased osmotic pressure of blood Target: DCT, sweat glands & arterioles Action: conserve h2o & retain blood volume |
| what is the action of oxytocin, the stimulus for production & the target organs | Action: smooth muscle contraction & positive feedback Stimulus: stretch receptors in uterus & touch in nipple Target: smooth muscle in uterus & nipple |
| What is the target organ for T3 & T4, the stimulus for production & the action | Target: most cells Stimulus: TSH Action: increases metabolic rate & heat production. Helps control BP & regulate tissue G & D |
| What is the stimulus for calcitonin, the target organ & the action | Stimulus: Increased plasma calcium Target: Bone Action: decrease plasma calcium by stimulating osetoblast & inhibiting osteoclast |
| what is the target for aldosterone, the stimulus for production & the action | Target: DCT of kidney Stimulus: Low blood volume by low BP, hyponatraemia & hyperkalaemia Action: Stimulates Na reabsorption & K secretion |
| what is the stimulus for cortisol, the target organ and the action | Stimulus: ACTH Target: most cells Action: Energy metabolism & resistance to stress |
| what is the target of sex hormones & the stimulus for production | Target: Female libido, pubic & axillary hair, oestrogen post menopause Stimulus: ACTH |
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