Physiology of Ca2+ Flashcards
distinguish between free and total serum ca2+
- Plasma ( 2.5mmol/l)
- Free ca2+ = biologically important= can enter the cells ( 50% of plasma ca2+ is in this form )
- Non diffusible ca2+ = bound to albumin and globulin
What is the role of Vitamin D in Ca2+ homeostasis
-calcitriol & 1,25 dihydroxycholecalciferol
-found In dairy, eggs, cheese , it’s a steroid hormone
BONE : Osteoclast activity increases
KIDNEY : ca2+ absorption
INTESTINE :enhanced ca2+ absorption via transport proteins = calbindin-D
INCREASES Ca2+ levels in blood
What is the role of PTH in Ca2+ regualtion
1) Released from the parathyroid gland (behind thyroid)= chief cells produce PTH when ca2+ are low
-Mg2+ is needed for the normal function of the parathyroid gland
BONE :
-Causes resorption via osteoclasts ( osteoblast is activated, rank-L is activated and osteoprotegerin is inhibited so rank-L-binds to a rank receptor on osteoclast = activated = bone breaks down, and ca2+ released into the blood.
-Bone pool to ECF
KIDNEY :
-Reabsorption of ca2+
-Activated Vitamin D VIA 1-alpha hydroxylase
INTESTINE :
-Ca2+ is reabsorbed
so ca2+ levels increase
What is the role of calcitonin in ca2+ regulation?
- C cells (parafollicular )produce Calcitonin
- INHIBITS RESORPTION so blood ca2+ goes down
- increases osteoblast activity
What happens when you have vitamin D deficiency ?
bone wise
Lack of Vitamin D = Rickets, Osteomalacia ( soft bones )
elderly, those who don’t get sun exposure, women, south Asian, African origin
Effects of hypercalcemia
-primary hyperparathyroidism =tumour in the parathyroid gland
-secondary parathyroids (kidney failure = poor activation and synthesis of Vit D )
-Tertiary Parathyroidims = chronic
signs :
1-bone pain
2-kidney stones
3-short QT Interval
Bones , groans, stones and moans
causes of hypocalecemia
clinical tests x2
->Serum ca2+ decreases
causes:
1)Hypoparathyroidism
2)Pseudohypoparathyroidism (G-protein receptor mutation)
3)Vit D deficiency
CHVOSTEK’S sign =tapping on face anterior to ear = just below zygomatic bone = twitching of facial muscles
TROUSSEAU’S SIGN for hypocalecemia
what variables effect the levels of the free ca2+?
1) Albumin conc = of this goes down = more free ca2+ = Hypercalacemia
2) pH = H+ displaces ca2+ on albumin = more free ca2+ to enter cells = hypercalacemina
Process of VIT D activation
drop in Ca2+ –>PTH released
VIT D:
7-dihydrocholesterol on skin+ UV rays =cholicalciferol D3 Ergocalciferol, also known as vitamin D2 LIVER : D3-->Calcidiol (storage, circulation ) KIDNEY CALCIDIOL --> CALCITRIOL =ACTIVE VIT D enzyme : 1 alpha hydroxylase
what happens when you have too little Vit D
1) Rickets in children
2)Osteomalacia
( lack of Vit d, Failure to form calcitriol, mutation in enzyme 1-alpha hydroxylase, mutation in vitamins D receptor )
= bowing legs, soft bones,
QT intervals of hypo and hypercalcemia
Hypocalacemia = long QT Hypercalacemia = Short QT
What are the symptoms of Hyperthyroidism, thyrotoxicosis?
treatments ?
1-Tremors, hyper-reflexia,Sweaty , Tachycardiac, Hyperthyroidism
Treatment:
- Block the thyroid hormone being released = thioureylenes (inhibit thyroid peroxidase)
- beta blocker (propranolol = non selective beta blocker)
- Block are replace using carbimazole + Levothyroxine ( synthetic thyroid hormone )
- Radioactive iodine = radiation damages the thyroid follicle cells so you will need life long administration of T4
- Surgery
Thioureylenes - Case study -How does it work -How is taken (10)
Pro-drug carbimazole–>methimazole
- Taken orally
- 18-24months
Block the thyroid hormone from being produced!
- Thyroid peroxidase is inhibited so T3,T4 is not made
Side effects :
- rash , nausea
- Rare= Agranulocytosis (marrow suppression, infections and sore throat)
- Pregnancy = can cause goitre, it crosses the placenta so it can cause hypothyroid in the fetus
