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MEH > Parathyroid glad and calcium regulation > Flashcards

Parathyroid glad and calcium regulation Flashcards

1
Q

how much calcium do we have? daily requirement? what is the net absorption of calcium?

A
  • adults contain 1000g
  • 800-1200mg
  • 175mg/day3/
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2
Q

in what form is calcium stored

A

hydroxyapatite crystals with phosphate so when broken down you also liberate some phosphate

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3
Q

what form is calcium in and which is biologically active

A
  • free ionised specie (biologically active) -complexed with organic anions ( can enter cells) - proteins ( storage b cant enter cell)
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4
Q

why is when they bound to organic anions than proteins better?

A
  • because can Enter cell
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5
Q

hormones involved in the regulation of ca.

A
  • parathyroid hormone : - Calcitriol (aka VD3) - Calcitonin (made in the C cells of the thyroid gland)(decreases calcium levels but doesnt do a lot in humans b if thyroid gain removed from patients they don’t suffer from hypocalciemia )
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6
Q

Functions of calcium

A
    • heart rhythm - low levels linked to insomnia - contrition of muscle - nerve function - clotting - activating enzymes - exocytosis
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7
Q

why put blood in EDTa tube

A
  • EDTA gathers ca2+ prevents it from acting so prevents it actions and so no b clotting
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8
Q

which factor in the clothing cascade effected by calcium

A
  • cofactor 4
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9
Q

why blood bags in citrate? and why is it important to monitor?

A
  • prevents ca2+ from clotting the blood - citrate colates calcium and so injected things that will c colating of calcium in the body c hypocalciuem a
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10
Q

PTH synthesis

A
  • raise serum ca2+ levels - doesnt need serum protein - synthesised, marginated in the membrane and only released where it goes to liver and is cleaved to activate form - don’t store a lot , you make it - calcium binds to receptor c synthesis of PTH ad released
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11
Q

calcitonin

A

-works to decreased b ca2+ levels - maintains lateral skeletal when she’s pregnant

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12
Q

anatomy of parathyroid gland

A

-

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13
Q

histokgy of parathyroid

A
  • chief cells make parathyroid hormones - oxyphil cells have unknown function
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14
Q

high serum ca. effect on 4th synthsis

A

decreases it

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15
Q

low serum

A

increases

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16
Q

half life of PTH and what does this mean

A

-short therefore rapid acting

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17
Q

when released what does PTH do?

A
  • low calcium - increases ca resorption in bone -increase activation of VIT D in GI wc means can absorb more ca2+ from gut - decreased ca2+ loss in urine (^ reabsorption)
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18
Q

ca2+ and phosphoruss

A
  • since we liberate calcium from bone as they form hypoxyapaptite crystal , by increases resorption of ca2+, so we can form inorganic phosphate wcneeds to be released b if it remains in the blood it will cause crystals to form - so we must increase phosphate release in the urine
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19
Q

complications of calcium balance and bon

A
  • roving a lot of calcium v ECM hence the v strength of bones
20
Q

what happens in lobng term hypo

A

-VITD is made with interactions of cholesterol and sunlight wc forms VITD 3 (cholecalciferol- get it from sunlight, margarine) wc is a precursor molecule - then goes to liver wc forms VItD (aka calcitriol) , which then goes to kidney and elsewhere

21
Q

what does VITD3 do

A
  • increases rate of calcium resorption
  • bone= c calcium removal
  • kidney ; calcium to be reabsorbed from urine and inorganic phosphate to be excreted
22
Q

whats the function of calcitonin

A
  • acts to lower calcium levels
23
Q

whats the function of calcitonin

A
  • acts to lower calcium levels
24
Q

hypercalcaemia

A
  • serum calcium >3.0mmol/L
  • polyuria wc exacerbates this v symptoms
  • renal calculi (renal stones)
  • increased kidney damage
  • constipated
  • tiredness
  • dehydration
  • muscle pain (stones, moans, groans bones)
  • won’t die from it
25
Q

hypocalaemia

A
  • more dangerous
  • <2.10mmol/L
  • hyper excitability at the neurones, b easier to fire action potential , muscle tetany , get convulsions
26
Q

treatment for hypercalaemia and the bgl

A
  • >3 mmol/L - rehydration
27
Q

c of hypercalcemia

A
  • malignant osteolytic bone metastasis (osteolytic wc breaks down bones)
  • tumours of bones, lung., thyroid,renal and prostate cancer are common causes of bone metastasis and c hyperkalemia
28
Q

hyperparathyroidism

A
  • primary ; adenoma of one of the parathyroid glands so excess PTH so serum c to ^ and serum phosphate v - secondary : all 4 parathyroid glads become hyper-plastic and this is seen in vit d deficiency ( vit d deficiency = ca2+ absorption low so low ca2+ so ^ PTH is made - can reverse it with VITD
29
Q

letheary? confusion ? slow

A

hyperglycaemia

30
Q

tetany, convulsions paraesthisa

A

hypoglycaemia

31
Q

c of hypo and at what level does it begin b.ca.l

A
  • total thyroidectomy
  • <2.10 mmol/L or 6 hours within thyroidectomy
32
Q

what are sensory sings of

A
  • tinging of mouth and fingers
33
Q

motor sigs

A
  • tentany of muscles
  • carpopedal spasm
34
Q

image

A

carpopedal spasm

35
Q

imaeg

A
  • osteoporosis
  • incomplete filling of the osteoclast reasorption bays when remodelling
  • resulting in pore and large channels
  • 2 presentations : primary and secondary
  • PRIMARY; type 1 ;
    • menopausal women d lack of oestorgen , this lack of oestorgen c ^ in oestoclast number
  • PRIMARY; type 2 ; senile osteoporosis
    • ​more in older men and women ; d loss of osteoblast activity as a result of decrease in both androgen and oestrogen
  • SECONDARY ;
    • ​d drug therapy (corticosteroids)
    • process that affect bone remodelling like going to space, malnutrion, immobilisation
    • metabolic bone diseases (hyperthyroidism , metastatic cancers)
36
Q

imaeg

A
  • osteomalacia (rickets but in adults)
  • cant mineralise the bones because of vit d deficiency, so often seen with patients w kindey failure od disease since VD needs to be converted into calcitriol at the kidneys before it can function adn assit abosprtionof calcium
  • bowing of bones, kinda looks like rickets
37
Q

PThR

A
  • parathyroid related hormone, wc is produced by tumours especaillay tumours of the lungs, prostate, lungs, breasts.
  • it causes hypercalaemia
  • and leads to humeoral hypercalaemia of malignancy
  • no effect on pth so pateints present with hypercalaemia and normal PTH levels
  • small lung cancer cells produce PTH or ADH
38
Q

HHG

A

humeral hypercalaemia of maligancy

  • ca2+ release from tumours , so if pateint has normal PTH but still hypercalcaemia its probably this
39
Q

describe the parathyroid gland

A
  • 4 parathyroid glands on the posterior wall of the thyroid gland 2 on ach side,
  • 2 types of cells present ; cheif cells wc make PTH adn oxyphil cells wc hae unknown function
40
Q

how do you recognise parathyroid H&E stain

A
  • rich network of capilaries of varied diamter
  • oxyphil cells are closesly associated with adipocytes and more in the cytoplasm
41
Q
A
42
Q

action of PTH

A
  • c osteoblastic cells to secrete cytokines
  • they’re secreted onto the surface and c stimulation of differentiation of activity and protects osteoclasts so they do not undergo apoptosis so more breakdown of bone
43
Q

VITD pathwya

A
  • VD3 activated by sunlight and convertedinot VD in the liver
  • then in the kidny it is converted to calcitriol
  • c absorption of CA2+ in the gut
44
Q

do osteobalstic metastasis c hyperkalaemia

A

no b they c bone formation not osteolysis

45
Q

whats the effect of calicium on the neurones and hw does this relate ot hypo and hyper

A
  • calicum c increased threshold for depolarisation in nerve cells
  • so in hypo ; v ca2+ =vthreshold so more likely to fire and so thats why you get hypoerativity adn they symtpoms
  • hypercal = ^threshod so less likely to get AP firing hence the lethary, confusiion and coma
46
Q

treatment for osteoporosis

A
  • 700 mg /day of calcium for postmenopausal women
  • excerise since immobilisy can c bone atropy
  • cigarette smoking is directly linked to osteoporosis developmetn

MEH (24 decks)

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