Calcium, Phosphate , Magnesium Flashcards
Disorders of calcium metabolism are (common or rare?) in clinical practice and they are closely associated with disorders of _______ and ______ metabolism
Common
phosphate and magnesium
Distribution of Body Calcium
The total body calcium depend on the amount _________ and the amount _________
absorbed from the diet
lost from the body
Distribution of Body Calcium
About ______% of Calcium in the body is part of bone.
The remaining __% is mostly in the _______ and ______
99
1; blood and ECF
Distribution of Body Calcium
The extra-osseous fraction is very important because of its effect in ____________ and ___________
neuromuscular excitability and cardiac muscle contraction.
Distribution of Body Calcium
The reference interval for plasma total calcium concentration is _______-_______ mmol/L
2.15-2.55
Calcium in blood is distributed among several forms.
T/F
T
Distribution of Body Calcium
About 45% circulates as _________
40% is ________________, mostly ______
15% is ______________ such as _________
free Calcium ions
bound to protein, mostly albumin
bound to anions, such as HCO3 , citrate, PO4 , and lactate.
Distribution of Body Calcium
About ____% circulates as free Calcium ions
_____% is bound to protein, mostly albumin
____% is bound to anions, such as HCO3 , citrate, PO4 , and lactate.
45
40
15
free Calcium ions
referred to as ______ Ca2
ionized
Distribution of Body Calcium
The free ionized calcium is the physiologically (active or inactive?) fraction.
Active
Distribution of Body Calcium
The albumin bound fraction is known as the physiologically (active or inactive?) fraction.
Inactive
Distribution of Body Calcium
The ____________ calcium functions in neuromuscular excitability and cardiac muscle contraction
M
free ionized
Distribution of Body Calcium
The reference interval for plasma free ionised calcium concentration is ______-____ mmol/L
1.1-1.4
Control of Plasma Calcium
Factors involved in the control of calcium include:
_______ supply of calcium
________
Normal functioning _______
________ glands
Normal functioning ________.
Dietary
Vitamin D.
intestines
Parathyroid
kidneys
Control of Plasma Calcium
Parathyroid Hormone
Secreted from the ________ gland
PTH is a _____ chain polypeptide containing _____ residues, the ____ N terminal amino acid largely determines its biological activity.
parathyroid
single; 84; 34
Control of Plasma Calcium
Actions of PTH
1. It increases the plasma concentration of ____________ by stimulating _______ bone __________
- On the kidneys, it causes decreased tubular re- absorption of ______ causing ____ and decreased ______ levels while it increases plasma ______ by increasing tubular reabsorption of ________.
calcium and phosphate; osteoclastic; resorption
phosphate; phosphaturia; phosphate
calcium; calcium
Control of Plasma Calcium
The control of PTH depends on:
- Plasma _________ concentration
- _____cellular ______ concentration
free ionized calcium
Extra; magnesium
plasma PTH conc. is _____eased by severe chronic hypomagnesaemia
decr
Control of Plasma Calcium
•Parathyroid Hormone Related Protein
This is a peptide hormone that has a similar ________ with PTH at the biologically ________
It is actively increased in certain ______ causing humoral __________ of malignancy
amino acid sequence
active end.
tumours
hypercalcaemia
Control of Plasma Calcium
Calcitonin
Calcitonin, which originates in the ______ cells of the ______ gland, is secreted when the concentration of Calcium in blood ____eases.
medullary; thyroid; incr
Control of Plasma Calcium
Calcitonin exerts its calcium lowering effect by _________________________
inhibiting the actions of both PTH and vitamin D.
Calcitonin is however secreted during normal regulation of the ionized Ca2 concentration in blood
T/F
.
F
not
Calcitonin is secreted in response to a _____calcemic stimulus
hyper
Control of Plasma Calcium
vitamin D –
Sources of vitamin D
Vitamin D3, aka ________, is obtained from the _________ or _______
cholecalciferol
diet or exposure of skin to sunlight
Control of Plasma Calcium
Vitamin D
____calciferol (vitamin D2) obtained from _____ in the _____
_____calciferol (vitamin D3) formed in the _____ by the action of ___________ on _____________
Ergo; plants; diet
Chole; skin
ultra violet light on 7 dehydrocholesterol
Control of Plasma Calcium
Metabolism of Vitamin D
Vitamin D is transported in blood bound to specific carrier protein – __________________
In the ____, cholecalciferol is hydroxylated to ——————————- by the enzyme __________.
the vitamin D binding protein.
liver
25 hydroxycholecalciferol (25OHD3)
25- hydroxylase
Control of Plasma Calcium
_______________ is the main circulatory form and store of the vitamin.
25 hydroxycholecalciferol (25OHD3)
Control of Plasma Calcium
Vitamin D metabolism
In the _____ renal tubular cells of the kidney, _______ undergoes a second hydroxylation to form the active metabolite - __________________
proximal
25OHD3
1,25 dihydroxycholecalciferol
Control of Plasma Calcium
Vitamin D metabolism
The production of 1,25(OH)2D3 by ________________ may be stimulated by (low or high?) plasma phosphate concentration and ____eased PTH concentration
1-alpha - hydroxylase
Low
incr
Control of Plasma Calcium
Vitamin D metabolism
The 1-alpha -hydroxylase activity is inhibited by ____phosphataemia and (low or high?) levels of free ionized calcium
hyper
High
Control of Plasma Calcium
Vitamin D metabolism
The synthesis of the hormone 1,25 (OH)2 Vit D3 decreases in ____ disease and can lead to ____calcaemia.
renal
hypo
Control of Plasma Calcium
Actions of 1,25(OH)2 Vitamin D3
It Increases ____________ absorption by ___________ cells
calcium and phosphate
intestinal mucosal
Control of Plasma Calcium
Actions of 1,25(OH)2 Vitamin D3
It acts synergistically with _____ to stimulate ________ activity and release ______ from _____
PTH; osteoclastic
calcium from bone.
The action of PTH on bone is impaired in the absence of 1,25(OH)2 Vitamin D3.
T/F
T
PTH enhances _________ activity and therefore stimulation 1,25- (OH)2 Vit. D3 synthesis.
1- hydroxylase
Disorders of Calcium Metabolism: Hypercalcaemia
Hypercalcaemia has clinical consequences
Renal effects – renal damage, _____uria, renal calculi due to precipitation of ________
______kalemia
Neuromuscular effects – it (depresses or enhances?) neuromuscular excitability leading to ____tonia.
poly; calcium phosphate stones.
Hypo; depresses
hypo
calcium directly inhibits potassium reabsorption from the tubular lumen.
T/F
T
Disorders of Calcium Metabolism
Hypercalcemia
CNS effects –______, anorexia, nausea and vomiting.
GIT effect – _________, constipation and abdominal pain.
depression
peptic ulceration
Disorders of Calcium Metabolism
Hypercalcemia
Cardiac effect – ECG changes with _________ of the Q-T interval and ________ of the T waves.
At Ca >3.5mmoles/L, there is increased risk of sudden ________ or _________
shortening
broadening
cardiac arrest or ventricular arrhythmias.
Severe hypercalamia should be treated as a medical emergency.
T/F
T
Causes of Hypercalcaemia
_______ diuretics
____ metastasis
___________ abnormalities
(Low or High?) bone turnover
(Low or High?) levels of vitamin D
Thiazide
Bony
Parathyroid hormone
High
High
Causes of Hypercalcaemia
Thiazide diuretics (________________)
Bony metastasis- from breast, lung, prostate, kidney and thyroid carcinomas.
Parathyroid hormone abnormalities- ————- and ______
High bone turnover-__________, prolonged _________
reduced calcium excretion
primary and tertiary hyperparathyroidism
thyrotoxicosis; immobilization
Causes of Hypercalcaemia
Primary Hyperparathyroidism
This is caused by ________________________ causing hypercalcaemia.
inappropriate secretion of PTH by the PTH glands
Causes of Hypercalcaemia
It may be due to an ________, ________ or __________ of the parathyroid glands.
adenoma
hyperplasia or carcinoma
Causes of Hypercalcaemia
Tertiary Hyperparathyroidism
This may occur if the parathyroid glands have been subjected to ________________ by ______________ which has been subsequently corrected.
long standing and sustained positive feedback
hypocalcaemia of secondary hyperparathyroidism
Causes of Hypercalcaemia
Tertiary Hyperparathyroidism
The parathyroid glands ________, PTH secretion becomes _________ and not suppressed by ________ of ________
hypertrophy
partly autonomous
negative feedback of hypercalcaemia.
Causes of Hypercalcaemia
Hypercalcaemia of Malignancy
a)_________ of the _________
b)________________ of Malignancy
Malignant Disease of the Bone
Humoral Hypercalcaemia
Causes of Hypercalcaemia
Hypercalcaemia of Malignancy
a)Malignant Disease of the Bone
———- from tumours of the breast, lungs, prostate, kidney and thyroid cause hypercalcaemia.
Plasma ______ is also high from bone break down due to local action of malignant deposits
The malignant deposits stimulate a local _______ reaction and hence plasma _________ activity is raised.
Bony metastasis
phosphate
osteoblastic
alkaline phosphatase
Causes of Hypercalcaemia
Hypercalcaemia of Malignancy
B) Humoral Hypercalcaemia of Malignancy
Some malignant tumors secret ________.
This secretion is not subject to _________ by high plasma free ionized calcium concentration.
PTHRP
normal feedback control
Drugs/Medication
Various medication can cause hypercalcaemia such as _______ which decreases renal calcium excretion.
Others include _______ and ________
Vitamin ___ Excess
___________ treatment of hypocalcaemia.
thiazides
Lithium and Vitamin A.
D
Over enthusiastic
Causes of Hypercalcaemia
Sarcoidosis
The granulomatous tissue in sarcoidosis may _________________ , causing increased calcium absorption from the GIT.
_____________ and _________ may also produce the same effect.
synthesize 1,25(OH)2 cholecalciferol
Histoplasmosis and leprosy
Treatment of Severe Hypercalcaemia
Re-________
Bisphosphonates e.g. ________ (Ca binders)
________ especially in Vit. D intoxication and sarcoidosis
Calcitonin
hydration
pamidronate
Steroids
Hypocalcaemia Clinical Effects
_______,_______ spasm, generalized ________
__________ Sign
__________ sign
Tetany, carpo-pedal
seizure
Trousseau’s
Chvosteks’s
Hypocalcaemia Clinical Effects
Tetany, carpo-pedal spasm, generalized seizure, Laryngospasm, ______-reflexia, paraesthesiae _____tension, cataract, cardiac arrhythmias with prolonged _________ on ECG.
hyper; hypo
Q-T interval
Hypocalcaemia Clinical Effects
Trousseau’s Sign:______ and _______ evoked by _______________ to 10-20mmHg above systolic blood pressure for _________
Carpopedal spasm and tetany
inflating a blood pressure cuff
3-5minutes.
Hypocalcaemia Clinical Effects
Chvosteks’s sign can be elicited by tapping the ________ (anterior or o
posterior?) to the ear, when (ipsilateral or contralateral ?) facial muscle contraction may occur.
facial nerve
Anterior
ipsilateral
Hypocalcaemia can be classified into:
- Hypocalcaemia with ________
- Hypocalcaemia with ___________
hypophosphataemia
hyperphosphataemia
Hypocalcaemia with hypophosphataemia
Causes
In ______ hyperparathyroidism there is _____ and ________ deficiency causing hypocalcaemia
or _______ of calcium, vitamin D and
secondary
vitamin D and phosphate
inadequate intake
Hypocalcaemia with hypophosphataemia
Other Causes include
Impaired __________ of _______ in ________
Impaired _______ of vitamin D 1,25(OH)2 D3 due to _____ disease.
Increased _______ of vitamin D due to ________ therapy.
In renal tubular disorders of _______ reabsorption.
absorption of vitamin D in steathorhoea
metabolism; renal
inactivation
phosphate
Causes of Hypocalcaemia with Hyperphosphataemia
1)Renal dysfunction: ________ renal failure cause hyperphosphataemia because the __________ is affected and its synergestic effect on ____ is lost.
____________ develops within a few days of the onset of renal damage followed by _________.
.
acute and chronic
1- - hydroxylation; PTH
Hypocalcaemia
hyperphosphataemia
Causes of Hypocalcaemia with Hyperphosphataemia
_______ ______parathyroidism usually caused by _____ to the _______ during ___________.
Primary; hypo; surgical damage
parathyroids; partial thyroidectomy
Causes of Hypocalcaemia with Hyperphosphataemia
Pseudohypoparathyroidism
This is a rare in born error of metabolism with an impaired response of ______________________ to ________
There is ________________ to circulating parathyroid hormone
The PTH concentration is _____ but with
hypocalcaemia and hyperphosphataemia
both kidney and bone to PTH
end organ resistance
raised
Treatment of Hypocalcaemia
Mild hypocalcaemia - ________ and _______
oral calcium and vitamin D supplementation.
Treatment of Hypocalcaemia
Hypocalcaemia with life threatening symptoms such as cardiac arrhythmias, seizure, severe tetany or laryngospasm -
Give _______ as 10mls of 10% _______ for over _______ then continue with ______________
IV calcium; calcium gluconate
5 minutes
oral supplementation.
Phosphate Metabolism
Phosphate is a (mono or di?) valent (anion or cation?) .
80% is found in the _______
20% is distributed in __________________
Di; anion
bony skeleton.
soft tissues and muscle.
Phosphate Metabolism
______% is found in the bony skeleton.
______ % is distributed in soft tissues and muscle.
Phosphate is the major _____cellular anion.
80
20
intra
__________ is the major intracellular anion.
Phosphate
Phosphate Metabolism
(Acidosis or Alkalosis ?) can result in the shift of phosphate out of the cell in to the plasma.
Acidosis
Phosphate Metabolism
Protein rich foods, cereals and nuts are rich source of dietary phosphate.
Phosphate is ____% excreted via the renal route.
90
Functions of phosphate
Intracellular ______
_______ buffers – buffering ______ ions in _______.
It has structural role as a component of _____,_________, and ________.
buffer
Urine; hydrogen; urine
phospholipids, nucleo-proteins and nucleic acids
Functions of phosphate
Intracellular buffer
Plays a central role in cellular metabolic pathways, including ________ and ________
_________ regulates hemoglobin oxygen dissociation.
Component of nucleotides such as _______.
glycolysis and oxidative phosphoxylation.
2, 3 DPG
ATP
Treatment of Hyperphosphataemia
1. Use of ______________ agents e.g. ______ or ________
- ____dialysis or ________ dialysis may be indicated
oral phosphate binding
magnesium hydroxide or calcium carbonate
Hemo; peritoneal
Hypophosphataemia
Causes
Cellular redistribution
– Intravenous _______
– Alkalemia
–______ administration
glucose
Insulin
Hypophosphataemia
Causes
Poor _______
_________ states
Chronic _____-
Renal tubular (acidosis or alkalosis?)
_______parathyroidisms
intake
Malabsorbtion
alcoholism; acidosis
Hyper
Magnesium Metabolism
Predominantly an _____cellular ___valent ____ion.
It is an essential _______ to many enzymes as well as being important for _______ function.
intra; di; cation
co factor
Membrane
Magnesium Metabolism
It can act as an antagonist to _______ in cellular responses.
Magnesium is largely absorbed in the _____________ and its absorption (is or is not ?) vitamin D dependent.
calcium
upper small intestine ; Is not
Magnesium Metabolism
Cereals, nuts and vegetables are rich dietary sources of magnesium.
It is eliminated in _____ and via the ______ as well.
faeces; kidney
Magnesium Metabolism
__________,______, and ________ are thought to be important in its homeostatic control.
PTH, insulin and calcitonin
Hypermagnesaemia Causes
Increased _____
Impaired __________
__________ Causes
intake
renal excretion
Miscellaneous
Hypermagnesaemia Causes
Increased intake
_______
_________
____________
Impaired renal excretion
_______ and ___________
Miscellaneous Causes
_________
__________
Antacids
Purgatives
Parenteral nutrition
Acute and chronic renal failure
Hypothyroidism
Adrenal insufficiency
Clinical consequences of hypermagnesemia
Clinical consequences usually manifest at Mg. concentration >___ mmoles/L
Cardiac _______ ,Cardiac _____
Seizures, _____ reflexia
Paralytic ileus, Nausea
Respiratory _______
_____tension
2
arrhythmias; arrest
Hypo
depression
Hypo
Management of severe Hypermagnesemia
10ml of 10% _________ giving slowly
_____/______ infusion
________, if above fail.
calcium gluconate
Insulin/glucose
Dialysis
The symptoms of hypomagnesaemia are very different from those of hypocalcaemia.
T/F
F
similar
Hypomagnesaemia
Hypomagnesaemia can result in cardiac ________ , _______ sensitivity, ________ discomfort, anorexia and neuromuscular sequelae such as ____,______,______,______ etc.
arrhythmias; digoxin
Abdominal
parasthesia, vertigo, tetany, seizures, irritability
Hypomagnesaemia
Severe hypomagnesaemia can lead to ______calcaemia due to decreased _____ release and activity.
hypo
PTH
Long term magnesium deficiency may be a risk factor for coronary artery disease.
T/F
T
Some data suggest that reduced magnesium intake is associated with hypertension and insulin resistance.
T/F
T
