Mineral Homeostasis Flashcards by Abigail Cook

activation of amino acid based hormones

through acitvation of cyclic AMP and cGMP with G-protein receptors and activating PROTEIN KINASE A

through PIP second messenger - uses phospholipase c and more rapid on/off responses
Protein kinase C

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activation of steroid hormones

direct gene activation mechanism

may take longer for effects to be seen but can LAST LONGER
crosses membrane and gets into cell and to the nucleus for transcription of genes

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phosphodiesterase

breaks down cAMP and cGMP

5 - types

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type 5 phosphodiesterase

target for drugs for asthma, obstructive pulmonary disease, heart failure, and erectile dysfunction

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what can inhibit phosphodiesterase

caffeine

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what is the only thing PTH responds to

decrease in calcium

so released in response to low plasma Ca++

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expanded epiphyseal growth plate

seen in rickets

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rickets symptoms

deficient grwoth in long bones
chronic hypocalcemia
expanded epiphyseal growth plate
bowing of legs

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primary action of vitamin D

increases Ca++ absorption by intestine

PERMISSIVE FACTOR WITH PTH

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T/F if vitamin D deficient - you wont respond to PTH

TRUE

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PTH works as a control factor for what

enzyme in the kidney

enzyme produces the 1-25 dihydroxy vit D and PTH stimulates this enzyme

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will excessive vit D lead to higher levels of 1-25 dihydroxy metabolite?

- but will see an increase in the precursor that is produced at the liver (25 hydroxy)

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sudden drop in Ca++ results in

tetany of skeletal muscles

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normal Ca++ level in the plasma

10mg/100ml normal plasma Ca++

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possible sources of Calcium

diet supplement or from skeletal source

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hypercalcemia
describe
when is it a problem
short term vs. long term

Problem on chronic, not acute level. so becomes a problem when there is long term high calcium levels and can get soft tissue calcification in heart/cardiac valves and kidney tubules

can see lethargy, digestive tract abnormalities, possible cardiac arrhythmia’s

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what happens in calcitonin gene knockout in mice?

increased bone mineral content in these mice

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pro-calcitonin implications if present

marker for sepsis

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describe calcitonin

single chain polypeptide of 32 amino acids
secreted by the parafollicular cells of the thyroid and present in all vertebrate classes
normal function is UNKNOWN

when given intramembranous invusion of calcitonin

hypocalcemic

- calcium will be deposited into the bone - treatment method in osteoporosis?

calcitonin actions

hypocalcemic in mammals
no effect in other classes
secreted in response to high plasma Ca++, so causes Ca++ depositon in bone

high calcitonin or no calcitonin?

high - meduallry carcinoma of the thyroid or low due to thyroid removal - BONE AND CALCIUM METABOLSIM SEEM TO BE NORMAL

what does calcitonin inhibit?

release of sphingosine-1-phosphate from osteoclasts

cholecalficerol is also called…

Vit D3 - this is the type that is in supplements

sources of vitamin D

sunlight exposure - through skin or ingesting it as a supplement

vitamin D from sun reaction

7-dehydrocholesterol converted to cholecalciferol (vit d3) in skin

does cholecalciderol have biological activity?

toxicity of Vit D?

starting to lean away from this and say not really

deficient in 1-alpha hydroxylase?

genetic deficiency in this enzyme causes rickets unresponsiveness to vit D but responds to exogenous calcitriol (vit d 1,25 version) because cannot metabolize the vitamin d so these individuals can resume normal growth when given the medication of exogenous calcitriol

systemic growth factors

growth hormone and thyroid hormone

thyroid hormone deficiency?

can lead to a syndrome known as cretinism even if growth hormone is present - thyroid hormone is needed for it to elicit its effects and the child will have stunted growth and mental cognitive dysfunctions as well

IGF-1 stimulation

stimulated by growth hormone so growth hormone stimulates IGF-1 from the liver

laron dwarfism

lack of GH receptors or mutations in IGF-1 receptor so even if have GH - these individuals cannot respond to it -no treatments right now - in comparison to children who have a lack of GH - if treated can resume 'normal' growth

excess GH in adults and children

adults - acromegaly and adults DO NOT INCREASE IN HEIGHT children - gigantism

control of GH

both stimulatory and inhibitory at level of the hypothalamus

what type is PTH in terms of treatment for osteoperosis?

OSTEOANABOLIC - stimualtes bone growth - decreases the frequency / rate of fractures GIVEN IN PULSES

Osteoantiresorptive agents

treatment method for osteoporosis but these DO NOT decrease/change the fracture rate - they just INHIBIT THE RESORPTION PROCESS BISPHOSPHONATES CALCITONIN ESTROGENS

osteoclast activating factor is...

an inflammatory mediator (interleukin) and is a potent stimulator of bone resorption

effects of increased IL-1 and IL-6 | why do they increase

increased bone resoprtion due to the loss of inhibition by estrogen (post menopausale osteoporosis)

role of estrogen

inhibits inflammatory mediator syntehsis without estrogen inhibiting - IL-1 and IL-6 will increase and causes increased bone resorption

what are osteoblasts role in osteoporosis?

they can produce Il-1 and IL-6 and TNF -alpha

do osteoclasts have PTH receptors?

what controls the differentiation of osteoclasts?

osteoblasts mediate this high PTH results in increased osteoclasts but effect is mediated through the osteoblasts

where is RANK-L and RANK

RANK-L is produced by osteoblasts and RANK is on the membrane of osteoclast pre cursor cells

what does binding of RANKl and RANK do?

this binding stimulates differentiation of osteoclasts

Osteoprotegrin

OPG