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Potassium and Sodium Metabolism
Dr Zahid AzeemAJK Medical College
Muzaffarabad
For. . MBBS- batch-2018
DEFINITION Sodium is the most abundant ion of the
extra cellular compartment.
Water is the most abundant constituent of the body 50% of body weight in women & 60% of the body wt in men is water, out of which 40% is intracellular and 20% is in extracellular compartment.
Total body water (60% of body wt
I.C.F. (40 of body wt)
E.C.F. (20% of body wt)
Interstitial fluid 15% Intravascular 5%
IONIC COMPOSITION OF DIFFERENT
BODY FLUID COMPARTMENTS
SODIUM • Sodium -> the a abundant cation of ECF
• Sodium salts -> important part of osmotically active solutes in plasma & interstitial fluid.
• Sodium and its corresponding anions represent almost all of the osmotically active solutes in the extracellular fluid under normal conditions…………. Tonicity
.
Small changes in osmolality are counteracted by thirst regulation,
antidiuretic hormone (ADH) secretion, and renal concentrating or diluting
mechanisms.
Preservation of normal serum osmolality (i.e., 285-295 mOsm/L) guarantees
cellular integrity by regulating net movement of water across cellular
membranes.
ADHIts mechanism of action
•ADH is also called arginine vasopressin or simply vasopressin.
•ADH is a small peptide hormone produced by the hypothalamus that binds
to the vasopressin 1 and 2 receptors(V1 and V2).
•Vasopressin release is regulated by osmoreceptors in the hypothalamus, which
are sensitive to changes in plasma osmolality of as little as 1 % to 2%.
•Under hyperosmolar conditions, osmoreceptor stimulation leads to stimulation
of thirst and vasopressin release.
These two mechanisms result in increased water intake and retention, respectively.
•Vasopressin release is also regulated by
baroreceptors in the carotid sinus and aortic arch; under conditions of hypovolemia, these receptors stimulate vasopressin release to
increase water retention by the kidney.
Regulatory systems Detects ECF volume changes Detects Sodium concentration
Modify rate of sodium
absorption/excretion SODIUM HOMEOSTASIS
DEFENSE OF ECF VOLUME AND DEFENSE OF ECF VOLUME AND IONIC COMPOSITION OF THE BODYIONIC COMPOSITION OF THE BODY
Angiotensin
Angiotensin -I
Angiotensin -II
Hypothalamus
ADH
Thirst
Hypovolemia
Hyperosmalarity
Vasoconstriction
Adrenal cortex
Aldosterone
Kidney
Na+, water retention
Renin
ACE
KIDNEY -- > homeostasis
At a GFR of 125 ml/ min & serum sodium -> 145 mmol/L , kidney filters > 26 mol/ day of sodium ( 1.5
kg of NaCl )
More than 99% of filtered sodium is reabsorbed along nephrons
In KIDNEY :
Sodium is reabsorbed along different
segments of nephrons :
1) 50-75 % of filtered sodium reabsorbed via secondary active co transporters
2) Thin ascending loop of Henle doesn’t reabsorb sodium
3) Thick ascending loop of Henle reabsorbs 20-25%
4) Distal convoluted tubule: i) early DCT : 5-10% reabsorption by NaCl
co transporter ii) late DCT : 2-5% enters here * fine regulation, under control of
Aldosterone * Although sodium reaching here is a small
fraction of filtered sodium, it is here where it is decided how much sodium will be excreted
Hyponatremia
Hyponatremia is defined as a serum sodium concentration lower than 136 mmol/L.
Hyperglycemia can also cause hyponatremia, via osmotically induced water movement from cells into the blood (translocational hyponatremia)
Hyponatremia in a patient with hypovolemia
Hypovolemic hyponatremia represents a decrease in total body sodium in excess of
a decrease in total body water. REASONS;
Simultaneous sodium and water loss can be due to renal
(such as diuretic use) or extrarenal causes.
Hypovolemia results in a decrease in renal perfusion, a decrement in the glomerular filtration
rate, and an increase in proximal tubule reabsorption of
sodium and water;
How does hypervolemic hyponatremia differ from
hypovolemic hyponatremia?
Increase in total body water exceeds increase in total body sodium. Patients are edematous.
RENAL CAUSES(urinary sodium > 20mEq/L): Acute or Chronic renal failure
NON RENAL CAUSES: CHF, Cirrhosis, nephrotic syndrome
Hypervolemic Hyponatremia
In general, hypervolemic hyponatremia due to an extrarenal cause is
characterized by a low urine sodium concentration (<10 - 20 mEq/L)
This distinguishes it from hypervolemic hyponatremia due to intrinsic renal
causes, where the urine sodium is > 20 mEq/L
{ In renal causes, kidney can not re-absorb Na } .
Patient has a normal store of sodium but an excess of total body water
The most common form seen in hospitalized patients. The most common cause is the inappropriate administration of hypotonic fluid
The syndrome of inappropriate antidiuresis is the most common cause of euvolemic hyponatremia
Euvolemic Hyponatremia
Clinical Signs of Hyponatrema
Nausea, vomiting, anorexia, muscle cramps, confusion, and lethargy, and culminate ultimately in seizures and coma.
Seizures are quite likely at [Na+] of 113 mEq/L or less.
Hypernatremia
Defined as a serum sodium concentration greater than 145
mEq/L, occurs when too little total body water exists relative to the
amount of total body sodium, thereby raising the sodium concentration.
An increase in serum sodium concentration is almost always a reflection of water loss rather than sodium gain.
Water loss results in the development of plasma hyperosmolality; via hypothalamic sensors, this acts as a stimulant to thirst and production of ADH.
•Given that even small rises in the serum osmolality trigger the thirst mechanism, •Hypernatremia is relatively uncommon
unless the thirst mechanism is impaired or access to free water is restricted.
As a result, hypovolemic hypernatremia tends to occur in the very young, the very
old.
It is typically due to extracellular fluid losses accompanied by inability to take in adequate amounts of free
water.
Febrile illnesses, vomiting, diarrhea, and renal losses are
common causes.
Hypervolemic hypernatremia
Although uncommon. Sodium bicarbonate injection during cardiac arrest,
administration of hypertonic saline solution and inappropriately prepared infant
formulas are several examples of induced hypernatremia.
Regulation of Na/K
How much sodium does the patient need?
Sodium deficit = Total body water x (desired Na – actual
Na)
Total body water is estimated as lean body weight x 0.5 for
women or 0.6 for men
Question:In elderly patients : Decreased GFR with age limits ability to
excrete sodium prone to over expansion of ECF
Why Hyponatremia?????????????
Impaired thirst mechanism with decreased ability to concentrate urine
Why Hypernatremia????????
Thanx
BODY POTASSIUM
-K+ is the major intracellular ion
-serum potassium is normally regulated within a narrow range of 3.5 to 5.0 mmol/L.
-75% of which is in skeletal muscles
-K+ is taken up by all cells via the Na-K ATPase pump
-K+ is one of the most permeable ion across cell membranes and exits the cells mostly via K channels (and in some cells via K-H exchange or via K-Cl cotransport)
Introduction The total body stores are approximately 50 to 55
meq/kg. The main intracellular cation. 98% located ICF,150 meq/L. 2% located ECF,4meq/L.90% readily exchangeable10% non exchangeableAmount ingested = up to 100meq/d = 2.5 gm/d92% urinary excretion8% GIT excretion
32
Redistribution of K
potassium homeostasis External potassium balance is determined by rate of potassium intake
(100 meq/day) and rate of urinary (90 meq/day) and fecal excretion (10 meq/day).
Internal potassium balance depends on distribution of potassium between
muscle, bone, liver, and red blood cells (RBC) and the extracellular fluid (ECF).
Physiological roles of potassium
1.Roles of intracellular K+: Cellular volume maintenance Intracellular pH regulation Cell enzyme function DNA/protein synthesis Cell growth2.Roles of transcellular K+ ratio: Resting cell membrane potential Neuromuscular excitability Cardiac pacemaker rhythmicity
35
Potassium homeostasis
1.Internal balance ( ICF and ECF K+ distribution)2. External balance ( Renal excretion of K+)1.Internal balancePhysiological and pathological conditions can influence this
process.o Hormones like insulin , catecholamines ,aldosterone o Acid base imbalanceo Changes in osmolarityo Exerciseo Cell lysis
Hormonal control of K+ homeostasis Insulin and beta 2agonsists shifts K+ to the cell, by increase the
activity of Na+,K+-ATPase, the 1Na+-1K+-2Cl- symporter, and the Na+-Cl- symporter.
Aldosterone acting on uptake of K+ into cells and altering urinary K+ excretion.
Stimulation of α-adrenoceptors releases K+ from cells, especially in the liver.
insulin and epinephrine act within a few minutes, aldosterone requires about an hour to stimulate uptake of K+ into cells.
02/12/15 37Potassium homeostasis and its renal handling
39
Hormonal control of K+ homeostasis
Miscellaneous factors …..1.Acid base imbalance Metabolic acidosis increases the plasma [K+].
Metabolic alkalosis decreases the plasma [K+] .2.Plasma osmolarity Hyperosmolarity associated with hyperkalemia . A fall in plasma osmolality has the opposite effect. 3.Cell lysiso Crush injury,burns,tumor lysis syndrome, rhabdomyolysis
associated with destruction of cells and release of K+ to ECF. 4. Exercise vigorous exercise, plasma [K+] may increase by 2.0 mEq/L.
…………Cont’d
Physiological: Keep Plasma [K+] Constant Epinephrine Insulin Aldosterone Pathophysiological: Displace Plasma [K+] from Normal Acid-base balance Plasma osmolality Cell lysis Exercise Drugs That Induce Hyperkalemia Dietary K+ supplements ACE inhibitors K+-sparing diuretics Heparin
Renal handling of potassium
The PCT reabsorbs about 67% of the filtered K+ under most conditions by K+-H+ exchanger and K+-Cl- symport.
20% of the filtered K+ is reabsorbed by the TALH.
The distal tubule and collecting duct are able to reabsorb or secrete K+.
02/12/15 Potassium homeostasis and its renal handling
42
……….cont’d
The rate of K+ reabsorption or secretion by the distal tubule and collecting duct depends on a variety of hormones and factors.
Most of the daily variations in potassium excretion is caused by changes in potassium secretion in the distal and cortical collecting tubules.
02/12/15 Potassium homeostasis and its renal handling
43
……………cont ’d
02/12/15 Potassium homeostasis and its renal handling
44
K+ SECRETION BY PRINCIPAL CELLS
Secretion from blood into the tubule lumen is a two-step process:
1.uptake of K+ from blood across the basolateral membrane by Na+,K+-ATPase and
2. diffusion of K+ from the cell into tubular fluid via K+ channels.
Three major factors that control the rate of K+ secretion by the distal tubule and the collecting duct
A. The activity of Na+,K+-ATPase .B. The driving force (electrochemical gradient) for movement of
K+ across the apical membrane. C. The permeability of the apical membrane to K+ .
Cellular K buffering When K is added to the ECF, most of the added K is
taken up by the cells, reducing the ECF K+ increase If K is lost from the ECF, some K+ leaves the cells,
reducing the ECF K decline Buffering of ECF K through cell K uptake is impaired in
the absence of aldosterone or of insulin or of catecholamines
Cell K exit to the ECF increases when osmolarity increases (as in diabetes mellitus) and in metabolic acidosis, when it is exchanged for ECF protons (H+)
When cells die, they release their very high K content to the ECF
Copyright ©1998 American Physiological Society
Renal regulation of Potassium
Sources of K
Banana, orange, apple, pineapple Almond, dates, beans, potatoes
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