pathophysiology of calcium-phosphorus metabolism
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Pathophysiology of calcium-phosphorus
metabolism
Ph.D.Ph.D., , MDMD,, Assistant ProfessorAssistant Professor HaHanna Saturskanna Saturska
Calcium98 %
Phosphorus86 %
Са10 (РО4)6 (ОН2)
Norm2,35 – 2,75 mmol/l
Norm1,22 – 2,2 mmol/l
Role - Bones- Tooth- Blood coagulation- Membranes permeability- Nervous impulses pass- Muscle contraction- Enzymes activation (succinatdegydrogenasa, lecetinasa)
Role - Bones- Tooth- ATP, КPh)- Phosphorillation of carbohydrates- DNA and RNA synthesis- Phospholipids of membranes- Phosphate buffer
Са10 (РО4)6 (ОН2)
Daily need – 1,0-1,2 g
Depends on:- entrance (main source – milk food)- absorption (max. – duodenum, main quantity – intestine), only 30 % of Ca absorbs from food - excretion (intestine, kidney)
Daily need – 1,5 g Source – all food(there is no exogene deficit) Absorption - 70 % from used foodPhosphorus of fish absorbs in 100 %
Calcium 98 %
Phosphorus86 %
Norm2,35 – 2,75 mmol/l
Norm1,22 – 2,2 mmol/l
Parathyroid hormone (PTH)
Organ-target: bones, kidneys
Function of PTH - increase of Ca concentration in plasma
Mechanisms: 1. Releasing of Са by bones
(activation of osteoclasts – resumption of bones)
2. Increase of Са reabsorbing in kidneys
3. Activation of vit. Dз synthesisand increase of absorption in the intestine
Vitamin D
Hormone regulation of calcium-phosphorus metabolism
Thyreocalcitonin
Organ-target - bones
Function - decrease of Ca concentration in plasma
Hypocalciemia
Violation of calcium-phosphorus metabolism
HypercalciemiaHypophosphatemia
Hyperphosphatemia
ETIOLOGY Hypoparathyreosis (primary, secondary, tertiary) Pseudohypoparathyreosis (increasing of sensitivity of receptors to PTH) Hyperphosphatemia (insoluble salts of Ca phosphate form – in
children who were fed on cow's milk) D3 hypovitaminos (deteriorating of absorption of Са in GIT, which
are at the controlling of vit. Dз) Illness of GIT (diarrhea, steatorrhea) Hyperproduction of thyreocalcitonin (medullary thyroid cancer) Chronic renal failure (leads to loss of Ca and decrease of
sensitivity to PTH)
HypocalcaemiaPathological state, at the quantity of Са in blood
less than 2,35 mmoll/l
Cramps
Clinical manifestations of hypocalcaemia
Tetanus
The process of tetanus potentiation at the motor neurons and interneuron of spinal cord violate
Conduction of impulses at reflex arch become easier
Activate a reflex muscles contraction on mechanical and other stimuli
Spasm of larynx, bronchus
asphyxia
death
Coronarospasm (cardiotetanus)
angina
Stop of heart
Ricket
Гіпокальциемія
Acquired forms- Lack of vit. Dз in food - Lack of insolation – insufficient of synthesis
Congenital forms (calcipenia form )
– Dependence on vit. Dз type 1 (reason – hereditary defect of synthesis vit.
Dз in kidneys)There is easy to treat by synthetic vit. Dз
- Dependence on vit. Dз type 2 (reason – insensitivity of target organs to
1,25(ОН)2 Dз Very difficult clinical manifestation
Clinical manifestations of hypocalcaemia
Osteomalacia The bones become soft
(as a result of metabolic violations of Са and Р in organic part of bones)
ГіпокальциеміяOsteodythtrophy
OsteoporosisAthrophia of bones
Increasing of quantity Ca in blood
Decreasing of quantity PTH
Activate of resorption of bone
Activate of osteoclastes which: - produce a lot of organic acids especially
citric for solution hydroxilapatit- produce lisosomal enzymes for solution
organic matrix
Implications: frequent fractures, disability
Clinical manifestations of hypocalcaemia
How does look osteoporosis?
HypercalciemiaPathological state, at the quantity of Са in blood
more than 2,75 mmoll/l
ETIOLOGY Primary hyperparathyrosis (appear at multiple adenomatosis of
endocrine glands, inheritance autossomal-dominant disease)
Hypervitanosis Dз (overdoses of drugs doses cause to excessive absorption Са in GIT)
Heavy and massive fractures – the balance between construction of bone (slowing) and resorption (without changes)
Osteodystrophy (Recklinhauzen disease)Clinical manifestations of hypercalciemia
Recklinhauzen disease – hyperparathyreoid osteodystrophy in 24 years old female. Damaging of lower jaw. The patient complains only on not pain deformation of face. Roentgenexam of whole skeleton revealed multiple changes.
Cystosis swelling in the distal ends of both fibula bones
MechanismHyperparatireosis – increasing of Са in blood – waste of Са from bones by resorbtion – osteoporosis – overgrowth of connective tissue (but Са isn’t deposited) - osteofibrosis
KINDS
Clinical manifestations of hypercalciemiaCALCINOSIS
(звапнення, calcification) – accumulation of insoluble salts of Са In soft tissues
The main case – alkalosis in tissue
CellularExtracellular
LocalGeneral
MetaplasticDystrophyMetabolic
Matrix for calcification
1. Mitochondria
2. Lisosomes
1. Collagen and elastic fibers
2. Glicozaminglican
The main reason - hypercalciemia
Clinical manifestations of hypercalciemiaMetastasic calcinosis
The main case – alkalosis condition
Appears1. Vessels (arteries )2. Myocardium3. Lungs4. Mucous of stomach5. Kidneys
Substances which are emitted or contacted these organs – acids. These tissues have a high alkalinity for saving a normal
state.
Metastasic calcinosis
Calcinosis of aortic valve
It arises in necrotic and dystrophic tissues - tuberculosis center , infarctions, dead fetus, chronic focus of inflamations (lungs and
heart like an armor ), focuses of atherosclerosis, scar tissue
Dystrophic static calcinosis (petrification)
Mechanism: alkalinity conditions – increased absorption Са from blood – The increased activity of phosphatases, which prodused from necrotic cells
– formation of insoluble salts of Са
The woman gave birth stone baby! A resident of Morocco Zara became pregnant in 1959 at the age of 26. Nine months of pregnancy
passed without complications. The contractions were long and very painful, and, fearing for her life, her husband took Zara to the hospital.
In the hospital room Zara saw as young woman in the throes died, doctors couldn’t save her child. Fearing that a similar fate awaits her as well, Zara escaped from the hospital. Over the next few days the contractions continued, but the long-awaited baby was never born. Many years later, when Zara
was 75 years old, the pain suddenly returned, and the woman went to doctors. Ultrasound examination revealed the presence of abdominal foreign body, the origin of which doctors could not
explain. There have been more thorough examination of the Zara, which resulted in doctors admitted that the
solid mass in the her body - nothing like petrified body of her child, who was not born. It was necessary to conduct operation because the subsequent delay would inevitably lead to the
death of the patient. The operation continued four hours. The doctors managed to pull out of a woman's body fetus weighing just over 3 kilograms and 42 centimetres in length. Thus, in 46 years,
"Stone Child" of Zara has finally emerged into the light. This phenomenon is very rare, to 1900 were described only 38 such cases, today they number no
more than 300. The oldest fossilized fetus was found during excavations of burial sites in the U.S., his age is more than 1000 years.
Pathogenesis unknown
Metabolic calcinosis (інтерстиціальне звапнення)
Limestone deposits in skin, tendons, fascias, muscles, along nerves and vessels
Implications of calcinosis
Negative Positive
Calcinosis atherosclerotic plaque – provokes thrombosis
Calcinosis of tendons – violation of muscles constriction
Lungs and heart like an armor – violation of function of these
organs
Petrification of tuberculosis center –
sign of healing
CALCIPHILAXIA The state of increased sensitivity of organism to
Increased quantity of Ca
Clinical manifestations of hypercalciemia
H.Selye (1960-1963) described the phenomenon andcreated an experimental model
1. Sensitizing factor – hypercalcaemia2. Decisive factor – degranulation of mass cells, mechanical
damage, salts of Аl, Fe
This phenomenon promotes the localization of process of organ calcification
That cam explain the systemic destruction of the cardiovascular system
ETIOLOGY1. Chronic kidneys insufficiency (loosing by kidneys)2. Diseases of GIT (vomiting, malabsorption syndrome )3. Hypovitaminosis D (increased absobtion in the GIT)4. Liver diseases5. Using of insulin at treatment of diabetes mellitus and
ketoacidosis (Increase of glucose phosphorylation – increase of extracellular Р using)
6. Restoring of nutrition after full starvation (mechanism is same like previous point)
Hypophosphatemia (norm of P in blood 1.22 – 2.2 mmoll/l)
Pathological state, at the quantity of Р in blood less than 1.22 mmoll/l
Rickets (in children)/osteomalacia (in adults)
Clinical manifestations of hypophosphatemia
(long-term decline of Р)
X-linked hypophosphatemia
Autossomal-dominant hypophosphatemial
damage of the bones
Autossomal-dominant hypophosphatemial ricket
Fanconi’s syndrome (group of diseases, which are manifested
general dysfunction of renal tubules + lossing of Р)
The main sign of all forms of rickets – heredity defect of enzyme’s
synthesis, which are responsible for transportation of Р in kidneys
Clinical manifestations:- Hypophosphatemia - Bones become soft- Delay of growth- In difficult case + violation of functions of
liver, heart, brain and development of coma (reason – violation of phosphorylation and deficit macroergs )
ETIOLOGY1. Intensive capture of Р by kidneys (CKI, hypoparathyreosis,
hyperthyroidism)2. Over use of Р from the bones (rapid bone growth, healing of fractures,
tumor of bones)3. Intensive absorption Р in GIT (Dз hypervitaminosis, acute intestinal
obstruction)4. Massive destruction of cells (hemolytic anemia, leucosis)
HyperphosphatemiaPathological state, at the quantity of Р in blood
more than 2.2 mmol/l
Don’t have independent value.Increasing of quantity of Р causes formation insoluble
phosphates Ca in blood. Concentration of ionizing Ca decreases and
hypocalcaemia is dominant in clinical manifestation
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