Calcium Flashcards
Anatomy of parathyroid gland.
it is suseptible to being damaged during thyroid surgery
Cells of the parathyroid gland?
Cheif and Oxyphil cells
Chief (its the boss!)>> produce PTH
Oxyphil> no one cares?
what is Calcium?
what is normal serum calcium?
what is biologicall active free Ca levels?
-most abundant metal in our body
Normal serum calcium levels are 2.2-2.6 M
– biologically active free ionized [Ca2+] closely regulated to 1.0-1.3 mM
– Remained bound to plasma proteins or complexed with citrate
functions of Calcium?
unlike calcium, the plasma phosphate concentration is not very strictly regulated, and its levels fluctuate throughout the day, particularly after meals
what forms the hydroxyapatite crystals?
importance of the crystal?
Calcium and phosphate!
it is a major portion of the mineral phase of the bone!
Ca+ and phosphate r regulated by 3 hormones.
Name them and what organs do they act on to control these ions? (in order) (3)
- PTH
- Cacitrol
- Calcitonin
- GI tract
- Bone
- Kidenys
actions of these hormones on calcium and phosphate are opposed …how?actions of these hormones on
a particular hormone may elevate the level of one ion while lowering that of the other.
where is most Calcium located?
In the bone!
the calcium in our bones is constantly being recycled round
cuz bone is a dynamic tissue
ok
typical daily dietry intake of Ca+?
major source of it?
800-1200mg
Dairy products
Describe the distribution of Ca+ in our body!
In plasma, Calcium exists in 3 physiochemical forms:
which form is the physiologically active form?
1) 45% free
2) 45% Bound to serum proteins (especially albumin)
3) 10% Bound to small organic anions (e.g., citrate and oxalate).
* Freeeeee*
Alkaline phosphatase
ALP is an enzyme made mostly in the liver and in bone with some made in the intestines and kidneys . It also is made by the placenta of a pregnant woman.
what effect does hypercalcemia have on the CNS?
what symptoms can result?
Normally in the neuron, the resting state of Na channels is stabilized by Ca+>> this prevents spontaneous depolarisation!
but in hypooo….
sometimes total Ca levels in the blood can vary a bit, depenidng on the blood’s PH & protein levels!
explain
during acidosis (LOW PH) , means theres alot of H+ ions floating around , albumin’s “Coo-“ groups pick up the protons and become COOH,
this makes it more positively charges and therefore repels Ca+!
*Free ioniz**ed calcium increases in blood!*
What hormones r involved in regulation of serum Ca2+?
Short term>> PTH
Long term>> active form of V.D (calcitrol)
lol. .
* they both raise serum Ca+!*
active form of Vitamin D? half life?
(calcitrol)
0.25days
what is VD?
how is it activated?
a collective term for a group of prohormones:
the two major forms of which are:
vitamin D2 (ergocalciferol) & vitamin D3 (cholecalciferol)
must undergo 2 hydroxylation reactions to be activated in the body>>>>Calcitriol (1,25- dihydroxycholecalciferol)
activated by PTH
where do we get our Vitamen D from?
Vitamin D obtained from sun exposure, food, and supplements, is biologically inert.
So it MUST undergo 2 hydroxylation reactions to be activated in the body.
functions of VD
– Increases intestinal absorption of dietary Calcium and renal
reabsorption of Calcium
– Increases bone resorption (breakdown of bone tissue to release calcium)
what 3 target organs does PTH act upon?
what is PTH
roles?
fucntions of PTH and calcitonin on maintaining calcium levels
what happens if Ca levels r low in the body?…
(what mechanism does body do to proper this?
how is PTH different from insulin?
insulin is made and stored
PTH is NOT stored
how is PTH synthesis produced and released?
when Ca+ binds to recepter (Gq) > slows down realease of PTH and its production
which region in the kidney does PTH have an effect on to release Ca+ levels?
Distal Tubule!
what happens when our hydroxyapeptite is broken down?
they’re freeing calcium and phosphate, these 2 in high concentrations can form crystals>> and that is a problem in the kidenys!
soooo..
The kidney needs to reguale this..
when we increase the amount of calcium reabsorption in the kidenys( via PTH)
We also Increase the amount of Phosphate the kidney looses!
How is calcium reabsorbed in the thick ascending loop of henle?
what is PTHrP
PTH action on the gut?
absorption is increased in the presence of VD!
Remember……..PTH stimulates conversion of vitamin D to its active form which ↑uptake of Ca2+ from gut.
how does PTH act on bone?
- increases bone turnover by increasing the activity of Osteoclasts! (via cytokines)
- it decreases osteoblast activity
Calcitonin?
released and produced by C cells (parafollicular cells) of the thyroid gland.
-
if we remove the thyroid gland from a patient.(thyroidectomy) do they loose the ability to regulate serum Ca2+ levels?
Explain?
NO, cuz Calcitonin doesnt play a major role in Ca + homeostasis
what is EDTA?
its a calcium chelator
it binds all the calcium in the blood
when u take a full blood count, u’ll put it in this bottle which contains EDTA, to let the blood clot
ROle of calcium in the clotting cascade and VK
Vk adds a carboxyl group on the Gla domain of the promthrombin, this makes the gla super negative charged>> attracts Ca+ and on the other end calcium adheres to the platelet membrane at site of wound!
(so Ca+ acts like a bridge btw prothrombin and the platelet memebrane))
when we want to give blood transfusion we obviously dont want the blood to clott in the transfusion bag.
what is contained in the bag to prevent this clotting from occuring?
it contains Citrate, which chelates Ca+,
& Ca+ is whipped out of this bag by the citrate> bag doesnt clot yay!
calcium is clotting factor number____
4
after giving a blood transfusion of about 5ooml of blood to a patient, why should we give the IV Ca+
cuz remember the bag had citrate which removed the calcium, and so the patient will not have any calcium after tranfused
Hyper & Hypo calcemia effects
Symptoms of hyper and hypo Calcemia
Hypocalcaemia
hyper- excitability in the nervous system,
paraesthesia>> tetany>> paralysis and even convulsions.
hypercalcaemia
kidney stones (renal calculi),
constipation>> dehydration
kidney damage>>tiredness and depression.
when looking at Ca+ levels in the body, what value should u make sure you’re looking at?
Adjusted Ca+
(its adjusted for the ALBUMIN level)
what are the 2 most common cause of HYPERCALCEMIA in a hospital setting?
- Malignant metastases that have gone to bone & r osteolytic
- Multiple myeloma
what is multiple myeloma?
Multiple myeloma affects the plasma cells inside the BM.
what r common causes of cancers that metastasise to bone causing lytic lesions and hypercalcemia?
- Breast
- lung
- Renal
- thyroid
what is the commonest cancer in men? does it cause hypercalcemia?
Prostate cancer
no, it causes osteoblastic metastases that do not cause hypercalcemia
what r the common sites for metasteses?
- vertebrae
- pelvis
- proximal femur
- ribs
- proximal humerus
- skull
- (these r the sites that r particulary active in formation of RBC’s, so if uve got metastases, they would want to lodge at thea reas that have got good blood supply)*
what is this xray showing?
osteoblastic activity
Metastatic prostate cancer
what causes primary hyperparathyroidsim?
what can this lead to?
the parathyroid gland develops an Adenoma and secretes excessive PTH> which will increase osteoclastic activity> serum calcium levels rise (hypercalcemia)
what causes secondary hyperparathyroidism
All 4 parathyroid glands become hyperplastic.
due to Vitamin D deficiency > this means that their Ca+ absorption is low resulting in low serum Ca+ levels,
parathyroid gland go hang on? we need to make more Ca+! > PTH levels to rise.> activates osteoclasts> in an attempt to maintain normal serum calcium
osteomalacia vs osteoporosis
what is the stimulus for the release of VD?
osteomalacia?
defective bone mineralization due to lack of VD (which is needed to absorb Ca from the gut)
The osteoid is produced, BUT, Ca+ salts r not adequetly deposited>> bones r soft and weak
osteoid is the ground matrix which consists of ground substance
rickets?
is osteomalacia but in children.
bc the epipheseal plate cannot caldify, long bone become abnormally long and widen
risk factors for Osteoporosis?
consequences of Osteoporosis
The control of plasma Ca2+ differs from the regulation of Na+ and K+ in 2 important ways
alkaline phosphatase?
if raised, what is it an indication of?
what r the 2 main mechanisms by which malignancy can cause hypercalcaemia:
structure of bone
Name these findings
what r they sign of?
HYPOCALCEMIA
1) Chvostek’s sign
tap on facial nerve at angle of Jaw> mouth will twitch
is a clinical sign of existing nerve hyperexcitability (tetany) seen in hypocalcemia. When the facial nerve is tapped at the angle of the jaw (i.e. masseter muscle), the facial muscles on the same side of the face will contract momentarily (typically a twitch of the nose or lips) because of hypocalcemia
2) Carpopedal spasm
Causes of Hypocalcemia
Symtoms of HYpocalcemia
symptoms of severe hypercalcemia occur whe clacium serum levels r higher than______
how do u treat it?
3.0mmol/L
High calcium levels the kidney tries to dump then in the urine> the polyurea can lead to dehydration> must REHYDRATE THEM
Sensory symptoms of Hypocalcemia
why can hypocalcemia kill?
Hypocalcemia can kill due to laryngeal muscle tetany, so needs treating quickly
