Parathyroid glad and calcium regulation Flashcards
(46 cards)
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/
2
Q
in what form is calcium stored
A
hydroxyapatite crystals with phosphate so when broken down you also liberate some phosphate
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)
4
Q
why is when they bound to organic anions than proteins better?
A
- because can Enter cell
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 )
6
Q
Functions of calcium
A
- heart rhythm - low levels linked to insomnia - contrition of muscle - nerve function - clotting - activating enzymes - exocytosis
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
8
Q
which factor in the clothing cascade effected by calcium
A
- cofactor 4
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
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
11
Q
calcitonin
A
-works to decreased b ca2+ levels - maintains lateral skeletal when she’s pregnant
12
Q
anatomy of parathyroid gland
A
-
13
Q
histokgy of parathyroid
A
- chief cells make parathyroid hormones - oxyphil cells have unknown function
14
Q
high serum ca. effect on 4th synthsis
A
decreases it
15
Q
low serum
A
increases
16
Q
half life of PTH and what does this mean
A
-short therefore rapid acting
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)
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
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
hypocalaemia
- more dangerous
- \<2.10mmol/L
- hyper excitability at the neurones, b easier to fire action potential , muscle tetany , get convulsions
26
treatment for hypercalaemia and the bgl
- \>3 mmol/L - rehydration
27
c of hypercalcemia
- 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
hyperparathyroidism
- 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
letheary? confusion ? slow
hyperglycaemia
30
tetany, convulsions paraesthisa
hypoglycaemia
31
c of hypo and at what level does it begin b.ca.l
- total thyroidectomy
- \<2.10 mmol/L or 6 hours within thyroidectomy
32
what are sensory sings of
- tinging of mouth and fingers
33
motor sigs
- tentany of muscles
- carpopedal spasm
34
image
carpopedal spasm
35
imaeg
- 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
imaeg
- 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
PThR
- 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
HHG
humeral hypercalaemia of maligancy
- ca2+ release from tumours , so if pateint has normal PTH but still hypercalcaemia its probably this
39
describe the parathyroid gland
- 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
how do you recognise parathyroid H&E stain
- rich network of capilaries of varied diamter
- oxyphil cells are closesly associated with adipocytes and more in the cytoplasm
41
42
action of PTH
- 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
VITD pathwya
- 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
do osteobalstic metastasis c hyperkalaemia
no b they c bone formation not osteolysis
45
whats the effect of calicium on the neurones and hw does this relate ot hypo and hyper
- 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
treatment for osteoporosis
- 700 mg /day of calcium for postmenopausal women
- excerise since immobilisy can c bone atropy
- cigarette smoking is directly linked to osteoporosis developmetn
