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Sodium (natrium) is the most important extra cellular ion and is an important determinant of
osmolality and permeability.
There is a calculation for calculating the osmolarity if the plasma is almost equal to osmolarity of
extra cellular fluid
This osmolarity of the plasma can be calculated by the concentration of sodium in the plasma
using this formula:
Calculated osmolarity = 2 Na + glycaemia /20 + Urea/3(all in mmol/L)
BUT if the urea/glycaemia is normal then osmolarity can be calculated only by using the
natremia.
The 3 factors (urea, glucose, Na) are important for the osmolarity but for tonicity Na and glucose
are important!
Urea doesnt modify tonicity of space because it diffuses through the space, different amount of
urea can modify the osmolarity but not tonicity.
Sodium and glucose modify both the tonicity and osmolarity
Glucose is the compound which modifies the tonicity and osmolarity of the plasma.
In diabetes mellitus when glycaemia is very increased glycaemia will produce dilution
phenomena.
Meaning in a sample from the patient you will measure glucose, natremia & acid base balance.
If this patient has high glucose it will attract the water from the cell so the natremia here is false
natremia because of the reduced water in the cell and here u have to make measurement for real
natremia.
The ultimate goal in this case should be to buffer the solution to level the acid base, the most
common buffer is sodium bicarbonate but it should be given according to the following:
Over 100 milligrams per deciliter (mg/dL) of glucose Glycaemia
Natremia decreases by dilution with 2.5 meq/L
So that means that this natremia is false decrease (pseudohyponatremia)
For instance:
If the patient has 400 glycaemia that is 300 above the normal so this means that this natremia is
decreased by 2.5 multiplied by 3 that means the natremia must be 140 + 3*2.5
So the natremia will be147.5 meq /L
So in an attempt to re-equilibrate this patient by acid base & electrolyte point of view you
must give him buffer to decrease acidosis but you have to take in account that he already have
enough Na so dont make enough imbalance over his imbalance.
So this was all about dilution effect in hyperglycemia.
NATRIUM
Sodium has many important body functions
- Most abundant extracellular cation along with constituent anion Cl
- regulates osmotic forces therefore regulates water
- very important determinant of osmolarity
- working with potassium and Ca, sodium is important for neuromuscular excitability
- regulates acid base balance
- near sodium chloride is the major anion in extracellular fluid transport following
sodium ,provides electroneutality
The kidney regulates the sodium balance under the influence of some hormone such as
aldosterone delivered by the osmoreceptor signaling done by decreased natrium and increased
potassium which leads to K secretion.
Aldosterone can be also stimulated by the renin-angiotensin aldosterone system by sympathetic
stimulation and decreasing renal perfusion. Renin is secreted by juxtaglomerular cell which
converts angiotensin 1 to angiotensin 2 which have well known effect
ANP and brain Natriuretic peptide and kidney natriuretic peptide
ANP: When the hemodynamic pressure in the atrium is increased this hormone is stimulated and
this fact will decrease the atrial blood pressure
Alteration in sodium chloride and water balance associates changes in tonicity and we have
already discussed dehydration
If we have lots of water, it is never lost alone it is lost with less or more sodium it will be
hypertonic if natremia is increased but hypotonic if its decreased so we can calculate the
deficiency of water in hypertonic and hypotonic dehydration to know how to recover the
imbalance.
The hyper hydration could be hypotonic cud be done by free water in cells, inadequate Na intake
or another important cause inappropriate secretion of ADH secreted by neurophypophysis.
Inappropriate secretion of ADH inhibit urine elimination and water retention cud be done by
brain trauma, surgery pain fear and a form of bronchogenic cancer in this form the cell that
secretes ADH
ADH will inhibit urine excretion and water retention and the extracellular space becomes
hypotonic so we have increased water SO the water have tendency to reestablish the balance of
tonicity establishing cellular hyper hydration and it has effect on tissues such as cerebral tissues
and can have cerebral edema coma
K potassium
Most important intracellular cation
-
Aldosterone levels it stimulates secretion of K in distal tubules, sweat glands , and in colon
Insulin stimulates the ATPAse pump promoting the K intake in hepatic cell, n promote glu
intake in these cells
Catecholamines increase the K secretion
Beta 2 adrenergic stimulates the movement of potassium into the cells
Alfa adrenergic pathway stimulates the shift of potassium out of the cells
have loss of K through urine cuz the diabetic patient urinates too much, so the total capital of K in
the body is decreased
4. we can have hyperkalemia assoc.. to acidosis
5. we can have hypokalemia by amydylosis
3. in diabetic patient total K is decreased
4. renal losses
5. we can have hypokalemia by mal distrubition of K in extra n intra cellular
compartments for example in the resp and metabolic alkalosis we know abt the shift of K n H ion in
the cell H ion tend to get out of the cell in exchange of K,so alkalosis usually associates hypokalemia
6. alkalosis it will aggravate hypokalemia
7. hyper insulinism this is another possiblty for redistrubition of K in intra cellular and
extra cellular fluid , insulin stimulates the entrance of K into the cells so if insulin is high we ll have
hypokalemia
8. hypokalemia has also some contributing factors to the maintanece of states for instance we can
have loss of K through vegetative fluids like diarrhea , vomiting laxative abuse and so on
9. we dont replace K loss in a balanced manner for example we have reducd intake of K , or if a
patient with K loss associates alkalosis the alkalosis will aggravate the hypokalemia
10 if at the kidney level if wwe have lots o K through some biological process such as Vomiiting n
diarrhea we have also hypovolemia which stimulates the RAAS system ultimately secreting
aldosterone which can lead to some more K loss through kidney
11 use of diuretics
12. if hypokalemia associates low magnesium ,low plasma Mg stimulates renin release which leads
to RAAs system activation and further K loss
These effect of hypokalemia cud be potentiated by hypercalcemia ,if Ca in the plasma is increased
in its concentrations the ca ion will increase the threshold potential it will be more postitive it will
increase the difference between resting membrane and threshold potential so the same the same
effect like hypokalemia but on opposite side so that means if both these modifications occurs at the
same time that means they will have accumulating bad effects prodcung decreased exictabilty og
neural and cardiac cells
2. also effect the renal fun it decreases the ability to concentrate urine if chronic for long term will
produce damage to renal tissue and producing interstitial fibrosis and tubular atrophy
3. cardiac effect
Cause of hyperkalemia
-
HYPERKALEMIA
Will increase the RESting membrane potential so will short the interval bw resting and
threshold potential leading to higher excitability but with no repolarization leading to higher
neuromusclular excitability
Because of the lack of recovery the cell becomes weaker and ends up in paralysis so the
clinical signs includes tingling of finger n lips, restlessness, diarhoea , intestinal cramps ,
ileus , On ECG we have rrapid repolarization with narrow and taller T waves Short QT
interval Depressed ST segment prolonge PR altered cardiac conduction with V Fibrillation
and finally cardiac arrest
These effects of hyperkalemia cud be accumulated by effects of hypocalcemia,
hypocalcemia will decrease threshold potential leading to increase in the difernce between
Resting membrane and threshold membrane potential but on the other side
DIABETES MELLITUS
Def: is metabolic disease with chronic evolution characterized by disturbances in glucid
metabolism with hyperglycemia or decreased glucose tolerance
Secondary distrurbance lipid and protein metabolisim
All thse phenomema is done by the relative or absolute deficiency of insulin
Classification :
Type 1 : insulin dependent appears in childhood , is characterized by absolute deficiency of
insulin for survival of pat insulin is needed
Genes and automimmunity involved
PATHOGENISIS:
Exoexaustion of the pancreas so the insulin production will decrease but not absolute,
relative deficiency of insulin usually continues with insulin resistance ,this ressistenace cud
be quantitative low number of receptors on peripheral cells but also cud be qualitative defect
secondary messenger and defected receptors
Defeiciency of incretins they are intestinal hormones delivered as an response to nutrition
and then effect is increase in insulin response in a glucose dependent manner
1. Glucose dependent insulinotropic polypeptide
Is prod in ileum n colon
Effects
2. Glucation like polypeptide
Produced in jejenum n duodenum
After injection of food these hormone will stimulate the secretion of insulin in beta cell so
food will increase the glucose thse hormone will stimulate the insulin secretion fromthese
cells and
Normal function of thses hormone increase the survival of beta cells cuz they decrease
apoptosis of beta cells and also they favourises the replication of the beta cells
They are used for theraphy and it was noticed their levels was decreaserd in type 2 DM
Sometimes with high success
impaired glucose tolerance after the lunch the level of glucose rises above normal but
normally there is no hyperglycemia
Gestational D.M glucose intolerance appears during pregnancy and disappears after
delivery
Clinical manifestation
Hyperglycemia with its consequences
Hyperglycemia may be seen in some condition like stress, during infection , physical trauma
These people have potential for developing the disease