Physio 2 - Endocrinology 5

drraythe's version from 2015-06-09 01:45

Ca-P homeostasis

Question Answer
in plasma, how much of Ca is doing what? (such as _________% is this, etc)41% protein bound, 9% complexed to anions, 50% IONIZED.
physiological fxns of Ca? (7 things) and how much disturbance of Ca+ can cause effects (in general terms)*small disturbances in Ca homeostasis can have major effects. **Stabilizes Na+ channels in membranes, electromechanical coupling, mm contraction, release of hormones and enzymes, reduces basement membrane permeability, co-factor in blood clotting, component of bone+teeth
physiological functions of phosphate? (4 things) and how much disturbance of phosphate can cause effects (in general terms)*even large fluctuations are well tolerated. It is a constituent of many compounds (nucleic acid ATP, cAMP, creatine phosphate, membranes), **phosphorylation processes, buffer, and component of teeth and bones
where and in what percentage does phosphate lie in the body?85% bone, 14% intracellular, 1% ECF (plasma forms are HPO4(2-) or H2PO4(-) )
what are the two components of adult bone, in what proportions?(1) organic matrix (30%) which is collagen fibers and ground substance. (2) salts (70%) which are crystalline hydroxyapatite [Ca10(PO4)6(OH)2]
how does bone calcification occur?osteoblasts secrete collagen molecules--> polymerization--> collagen fibers (osteoid). Then, Precipitation of amorphous (=noncrystaline) calcium salts (CaHPO4). Then conversion into hydroxyapetite crystals.
how does Ca/P precipitation (in terms of bone calcification) occur? what prevents it elsewhere?when Ca/P concentrations are close to their saturation point, they will precipitate. in other tissues precipitation is avoided via inhibitors (pyrophosphate)
explain remodeling of bone (how, why?)continual process of bone deposition (osteoblasts) and absorption (osteoclasts) --> bone can adjust to altered stress
explain the exchangeable Ca++ poolaka Ca++ buffer system, since some amorphous salts are usually present and can be mobilized rapidly, this pool exists
*Plasma calcium conc must be maintained within what %?+/- 5% of normal.
what are the three hormone systems that control Ca++ (and phosphate)?(1) to INC Ca++ use parathyroid hormone (2) to INC Ca++ use vitamin D/ D hormone (3) to DEC Ca++ use calcitonin (made in the thyroid)
what is the most powerful hormone controlling plasma Ca++ and phosphate levels?PTH (parathyroid hormone)
what are the 4 ways parathyroid hormone controls Ca++ and phosphate?(1) stim bone mobilization (resorption) which inc plasma Ca and P. (2) stim renal Ca++ absorption which inc plasma Ca. (3) inhibits renal phosphate absorption which dec plasma P (4) stim activation of vit D which inc plasma Ca via GI ABSORPTION
what is the overall effect of PTH (parathyroid hormone)?plasma Ca inc and plasma P decreases
what happens with hypocalcemia? chronic hypocalcemia?acute= small changes lead to immediate PTH response (chronic hypocalcemia--> compensatory hypertrophy of parathyroid glands)
what happens in hyperphosphatemia?indirect effect because of high phosphate levels--> binding of Ca ions to for CaPO4--> HYPOCALCEMIA
D hormone is aka? overall affect?aka calcitriol, inc plasma Ca via GI absorption.
What is vitamin D3 derived from? where is it activated into D hormone? it is derived from vit D from diet or by de novo synth in liver followed by UV(B) activation in skin. It is activated to D hormone in the liver and kidney
conversion to the active form (full name of the active form?) of D hormone in the kidney needs what?active=1.25-dihydroxycholecalciferol aka calcitriol. conversion in the kidney required PTH (parathyroid hormone) which is stimulated by low plasma Ca level
what are the two actions of calcitriol?(D-hormone) it (1) inc intestinal and renal Ca and phosphate absorption (2) inc mobilization of bone (in *high conc)
What is calcitonin stimulated by? what does it do?it is stimulated by hypercalcemia, and decreases calcium and phosphate levels.
Where does calcitonin come from, and what is interesting to note about this?From C-cells in the thyroid. Calcitonin seems more important in young animals than adults and the removal of the thyroid gland/ C-cells has little effect on Ca balance (im assuming esp. since PTH is the most important)
Explain how lack of dietary vit D or lock of UV exposure causes hypocalcemiawithout vit D/D hormone, there is a reduced absorption of Ca which leads to hypocalcemia (rickets in young or osteomalacia in adult, resp. MBD= metabolic bone disease in reptiles/birds)
explain how dietary IMBALANCES lead to hypocalcemia (state the norms also)normal 2Ca:1P but cereals and innards are 1Ca:20P--> hyperphosphatemia--> P binds to/inactivates Ca--> hypocalcemia
explan how a renal disease with insufficient P excretion can lead to hypocalcemia?build up in P (no longer 2Ca:1P ratio) binds all the necessary free Ca, leads to hypocalcemia.
What happens to the body with chronic hypocalcemia?chronic hypocalcemia-->body releases PTH (high conc)-->mobilizes bone tissue--> plasma Ca returns to low/normal-->in long term, leads to softening of bone (DEMINERALIZATION) and COMPENSATORY HYPERPARATHYROIDISM [saw pic of "rubber jaw" here]
what is a good example of acute hypocalcemia? (nameS for it, brief description)parturient paresis (milk fever.) acute hypocalcemia within 72 hrs post partum due to a rapid loss of Ca via milk.
Why does release of PTH not help during milk fever?the osteoclasts are reduced in numbers or inactive because insufficient stim during dry period (6wks before birth) (because low Ca demand and low PTH) OR inhibition by calcitonin (high dietary Ca)--> so the bone cant respond fast enough= acute hypocalcemia.
pathophysiology of acute hypocalcemia? in cows?inc. conductivity of Na channels--> excitability, tremors, seizures, tachycardia. (In cows mostly: uncoupling of neuromuscular transmission--> flaccid paresis. may be caused/exacerbated by concomitant Mg increase)
symptoms of acute hypocalcemia? (three stages) (stage 1) nervousness, excitability, tremor. Mild, short phase. (stage 2) sternal recumbency, flaccid paresis, GI stasis, low temp. (stage 3) lateral recumbancy, complete flaccid paresis, coma, death.
what happens with dogs and horses with hypocalcemia?Eclampsia / puerperal (after birth) tetany. Acute hypocalcemia during first weeks of lactation, symptoms relate to inc nerval/muscular excitability= spasms, tetany