pathophysiology of calcium-phosphorus metabolism

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Pathophysiology of calcium-phosphorus metabolism Ph.D. Ph.D. , , MD MD , , Assistant Professor Assistant Professor Ha Ha nna Saturska nna Saturska

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Pathophysiology of calcium-phosphorus metabolism. Ph.D. , MD , Assistant Professor Ha nna Saturska. Calcium 98 %. Phosphorus 86 %. Norm 1,22 – 2,2 mmol/l. Norm 2,35 – 2,75 mmol/l. - PowerPoint PPT Presentation

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Page 1: Pathophysiology  of calcium-phosphorus metabolism

Pathophysiology of calcium-phosphorus

metabolism

Ph.D.Ph.D., , MDMD,, Assistant ProfessorAssistant Professor HaHanna Saturskanna Saturska

Page 3: Pathophysiology  of calcium-phosphorus metabolism

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

Page 4: Pathophysiology  of calcium-phosphorus metabolism

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

Page 5: Pathophysiology  of calcium-phosphorus metabolism

Hypocalciemia

Violation of calcium-phosphorus metabolism

HypercalciemiaHypophosphatemia

Hyperphosphatemia

Page 6: Pathophysiology  of calcium-phosphorus metabolism

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

Page 7: Pathophysiology  of calcium-phosphorus metabolism

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

Page 8: Pathophysiology  of calcium-phosphorus metabolism

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

Page 9: Pathophysiology  of calcium-phosphorus metabolism

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

Page 10: Pathophysiology  of calcium-phosphorus metabolism

How does look osteoporosis?

Page 11: Pathophysiology  of calcium-phosphorus metabolism

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)

Page 12: Pathophysiology  of calcium-phosphorus metabolism

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

Page 13: Pathophysiology  of calcium-phosphorus metabolism

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

Page 14: Pathophysiology  of calcium-phosphorus metabolism

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.

Page 15: Pathophysiology  of calcium-phosphorus metabolism

Metastasic calcinosis

Calcinosis of aortic valve

Page 16: Pathophysiology  of calcium-phosphorus metabolism

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

Page 17: Pathophysiology  of calcium-phosphorus metabolism

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.

Page 18: Pathophysiology  of calcium-phosphorus metabolism

Pathogenesis unknown

Metabolic calcinosis (інтерстиціальне звапнення)

Limestone deposits in skin, tendons, fascias, muscles, along nerves and vessels

Page 19: Pathophysiology  of calcium-phosphorus metabolism

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

Page 20: Pathophysiology  of calcium-phosphorus metabolism

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

Page 21: Pathophysiology  of calcium-phosphorus metabolism

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

Page 22: Pathophysiology  of calcium-phosphorus metabolism

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 )

Page 23: Pathophysiology  of calcium-phosphorus metabolism

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

Page 24: Pathophysiology  of calcium-phosphorus metabolism