2-4-16-Regulation Of Ca And PO4 Metabolism (Lopez) Flashcards
___ is twitching of the facial muscles elicited by tapping on facial n.
Chvostek sign
___ is carpopedal spasm upon inflation of a BP cuff
Trousseau sign
__ is characterized by a decreased QT interval, constipation, lack of appetite, polyuria, polydipsia, muscle weakness, hyporeflexia, lethargy, and coma
Hypercalcemia
___ reduces the activation threshold for Na channels –> easier to evoke an AP (less or no stimulus required to trigger an AP). THis results in increased membrane excitability and can produce numbness and tingling and muscle twitches
Hypocalcemia –> generation of spontaneous AP is the physical basis for hypocalcemic tetany
___ is characterized by decreased membrane excitability and the NS becomes depressed and reflex responses are slowed
Hypercalcemia
During ___, free ionized [Ca] increases because less Ca is bound to albumin
Acidemia –> leads to increased free ionized [Ca]; H+ kicks off the Ca2+ from albumin
During ___, free ionized [Ca] decreases, often accompanied by hypocalcemia
Alkalemia –> decreased ionized [Ca]; Ca stays on albumin since H+ does not displace it
Ca homeostasis is tightly regulated by these 3 organs ___ and these 3 hormones ___
Bones, kidneys, and intestine
PTH, calcitonin, Vit D
___ is an intracellular anion involved in the activation and deactivation of enzymes, as well as a buffer in bone, serum, and urine
PO4–> bone (85%), Plasma (
EC [Pi] is __ related to that of [Ca]
Inversely
The __ cells of the parathyroid glands synthesize and secrete PTH
Chief
What is the main stimulus for secretion of PTH?
Decreased plasma [Ca]
___ is characterized by long-term increased levels of plasma [Ca] and causes decreased synthesis and storage of PTH, increased breakdown of stored PTH and release of inactive PTH fragments into circulation
Chronic hypercalcemia
___ is characterized by long-term decreased plasma [Ca] and causes increased synthesis and storage of PTH, and hyperplasia of parathyroid glands (secondary hyperparathyroidism)
Chronic hypocalcemia
Severe hypomagnesemia can cause what?
Inhibition of PTH synthesis, storage, and secretion –> result of chronic Mg2+ depletion, as in alcoholism
PTH acts via this secondary messenger system___
Adenylate cyclase/cAMP
List the physiological affects of PTH on:
A-bone
B-Kidney
C-Intestine
A-Increased bone resorption
B-Decreased Pi reabsorption (phosphaturia), increased Ca reabsorption, increased urinary cAMP
C-Increased Ca reabsorption (via Vit D)
All will increase plasma [Ca] toward normal
__ promotes mineralization of new bone through its coordinated actions in the regulation of both Ca and Pi plasma concentrations
Vitamin D –> “steroid” hormone
In vitamin D synthesis, 7-dehydrocholesterol is converted to cholecalciferol via UV light. Cholecalciferol is then converted to 25-OH-cholecalciferol in the liver by this enzyme ___
25-hydroxylase
25-OH-cholecalciferol is converted to 1,25-(OH)2-cholecalciferol in the renal PCT by this enzyme ___
1-alpha-hydroxylase (CYP1alpha)
PTH receptors are located on these cells ___
Osteoblasts (not osteoclasts)
What are the short-term actions of PTH on bone?
What are the long-term actions of PTH on bone?
Short-term: Bone formation (via direct action on osteoblast) –> basis for use of intermittent synthetic PTH administration in osteoporosis treatment
Long-term: Increase bone resorption (indirect action on osteoclasts mediated by cytokines released from osteoblast)
___ acts synergistically with PTH to stimulate osteoclast activity and bone resorption
Vitamin D
In the formation and resorption in bone, ___ induces stem cells to differentiate into osteoclast precursors, mononuclear osteoclasts, and finally as mature multinucleated osteoclasts
M-CSF