Investigation of electrolite balance

Electrolytes are minerals in your body that have an electric charge. They are in your blood, urine and body fluids. Maintaining the right balance of electrolytes helps your body's blood chemistry, muscle action and other processes. Sodium, calcium, potassium, chlorine, phosphate and magnesium are all electrolytes. You get them from the foods you eat and the fluids you drink.

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

Hormones (al-Greek.. Ὁρμάω - exciting, urge) - the biologically active substances of organic nature, is produced in specialized cells of the endocrine glands, entering the blood and have a regulating effect on metabolism and physiological functions. Hormones are humoral (blood-borne) regulators of certain processes in the various organs and systems.

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

Hypertonic Fluids

Used to temporarily treat hypovolemia Used to expand vascular volume Fosters normal BP and good urinary output

(often used post operatively) Monitor for hypervolemia !

Not used for renal or cardiac disease. THINK – Why not?

D5% 0.45% NS D5% NS D5% LR

Osmolarity Concentration of particles in solution The greater the concentration (Osmolarity) of a solution,

the greater the pulling force (Osmotic pressure) Normal serum (blood) osmolarity = 280-295 mOSM/kg

A solution that has HIGH osmolarity is one that is > serum osmolarity = HYPERTONIC solution

A solution that has LOW osmolarity is one that is < serum osmolarity = HYPOTONIC solution

A solution that has equal osmolarity as serum = ISOTONIC solution

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

Hypertonic Fluids

Osmotic pressure is therefore the same inside & outside the cellsCells neither shrink nor swell in an isotonic solution, they stay the same

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?

Cell membranes are semipermeable allowing water to pass through

Osmosis- major way fluids transported Water shifts from low solute concentration to high solute concentration to reach homeostasis (balance).

Osteoporosis ("porous bones", from Greek: οστούν/ostoun meaning "bone" and πόρος/poros meaning "pore") is a progressive bone disease that is characterized by a decrease in bone mass and density which can lead to an increased risk of fracture. In osteoporosis, the bone mineral density (BMD) is reduced, bone microarchitecture deteriorates, and the amount and variety of proteins in bone are altered.

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)

Hypercalcaemia (British English) or hypercalcemia (American English) is an elevated calcium (Ca2+) level in the blood.[1] (Normal range: 9–10.5 mg/dL or 2.2–2.6 mmol/L). It can be an asymptomatic laboratory finding, but because an elevated calcium level is often indicative of other diseases, a workup should be undertaken if it persists. It can be due to excessive skeletal calcium release, increased intestinal calcium absorption, or decreased renal calcium excretion.

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

Petrification is the process in which organic substance exposed to minerals over an extended period is turned into a stony material. This process is known as silicification and the organic substance are converted into stone by impregnation using silica.

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

Hypophosphatemia is an electrolyte disturbance in which there is an abnormally low level of phosphate in the blood. The condition has many causes, but is most commonly seen when malnourished patients (especially chronic alcoholics) are given large amounts of carbohydrates, which creates a high phosphorus demand by cells, removing phosphate from the blood (refeeding syndrome).

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