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Oral Biology > Mineral Homeostasis > Flashcards

Mineral Homeostasis Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

activation of amino acid based hormones

A

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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2
Q

activation of steroid hormones

A

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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3
Q

phosphodiesterase

A

breaks down cAMP and cGMP

5 - types

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4
Q

type 5 phosphodiesterase

A

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

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5
Q

what can inhibit phosphodiesterase

A

caffeine

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6
Q

what is the only thing PTH responds to

A

decrease in calcium

so released in response to low plasma Ca++

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7
Q

expanded epiphyseal growth plate

A

seen in rickets

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8
Q

rickets symptoms

A

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

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9
Q

primary action of vitamin D

A

increases Ca++ absorption by intestine

PERMISSIVE FACTOR WITH PTH

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10
Q

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

A

TRUE

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11
Q

PTH works as a control factor for what

A

enzyme in the kidney

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

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12
Q

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

A

NO

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

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13
Q

sudden drop in Ca++ results in

A

tetany of skeletal muscles

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14
Q

normal Ca++ level in the plasma

A

10mg/100ml normal plasma Ca++

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15
Q

possible sources of Calcium

A

diet supplement or from skeletal source

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16
Q

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

A

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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17
Q

what happens in calcitonin gene knockout in mice?

A

increased bone mineral content in these mice

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18
Q

pro-calcitonin implications if present

A

marker for sepsis

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19
Q

describe calcitonin

A

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

20
Q

when given intramembranous invusion of calcitonin

A

hypocalcemic

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

21
Q

calcitonin actions

A

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

22
Q

high calcitonin or no calcitonin?

A

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

23
Q

what does calcitonin inhibit?

A

release of sphingosine-1-phosphate from osteoclasts

24
Q

cholecalficerol is also called…

A

Vit D3 - this is the type that is in supplements

25
Q

sources of vitamin D

A

sunlight exposure - through skin

or ingesting it as a supplement

26
Q

vitamin D from sun reaction

A

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

27
Q

does cholecalciderol have biological activity?

A

no

28
Q

toxicity of Vit D?

A

starting to lean away from this and say not really

29
Q

deficient in 1-alpha hydroxylase?

A

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

30
Q

systemic growth factors

A

growth hormone and thyroid hormone

31
Q

thyroid hormone deficiency?

A

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

32
Q

IGF-1 stimulation

A

stimulated by growth hormone

so growth hormone stimulates IGF-1 from the liver

33
Q

laron dwarfism

A

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
34
Q

excess GH in adults and children

A

adults - acromegaly and adults DO NOT INCREASE IN HEIGHT

children - gigantism

35
Q

control of GH

A

both stimulatory and inhibitory at level of the hypothalamus

36
Q

what type is PTH in terms of treatment for osteoperosis?

A

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

37
Q

Osteoantiresorptive agents

A

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

BISPHOSPHONATES
CALCITONIN
ESTROGENS

38
Q

osteoclast activating factor is…

A

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

39
Q

effects of increased IL-1 and IL-6

why do they increase

A

increased bone resoprtion

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

40
Q

role of estrogen

A

inhibits inflammatory mediator syntehsis

without estrogen inhibiting - IL-1 and IL-6 will increase and causes increased bone resorption

41
Q

what are osteoblasts role in osteoporosis?

A

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

42
Q

do osteoclasts have PTH receptors?

A

NO

43
Q

what controls the differentiation of osteoclasts?

A

osteoblasts mediate this

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

44
Q

where is RANK-L and RANK

A

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

45
Q

what does binding of RANKl and RANK do?

A

this binding stimulates differentiation of osteoclasts

46
Q

Osteoprotegrin

A

OPG

Oral Biology (12 decks)

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