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Disorder of Potassium Metabolism

This document discusses disorders of potassium metabolism, including hypokalamia and hyperkalemia. It covers the distribution of potassium in the body, factors influencing intracellular and extracellular potassium levels, and the role of the kidney in potassium homeostasis. The key causes, clinical effects, and treatment approaches for hypokalemia and hyperkalemia are summarized.

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Saif Ali
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116 views28 pages

Disorder of Potassium Metabolism

This document discusses disorders of potassium metabolism, including hypokalamia and hyperkalemia. It covers the distribution of potassium in the body, factors influencing intracellular and extracellular potassium levels, and the role of the kidney in potassium homeostasis. The key causes, clinical effects, and treatment approaches for hypokalemia and hyperkalemia are summarized.

Uploaded by

Saif Ali
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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DISORDER OF POTASSIUM

METABOLISM
WHOLE BODY POTASSIUM DISTRIBUTION

 In contrast to sodium (Na+), most potassium


(K+) in the body is located within cells, as
shown in the table below:
INTRODUCTION
 Plasma K+ is a small fraction of, and hence not always an
accurate reflection of whole body K+ status.
 For example, in diabetic ketoacidosis, accumulated H+ ions
force K+ ions out of cells into the plasma, from where they are
filtered by the kidney and lost in the urine.
 In this situation, although plasma K+ is normal or high,
intracellular K+ (and hence total body K+) may be severely
depleted. Why is intracellular [K+] so much higher? As a result
of two forces, both acting to drive K+ into cells:
INTRODUCTION
 1. Intracellular anions, consisting of organic phosphate in
various forms (creatine phosphate, ATP, phosphorylated
glycolytic intermediates) as well as protein, provide binding sites
for cations (e.g. K+).
 2. The Na/K ATPase in the cell membrane pumps Na+ out and
K+ in against their respective concentration gradients, thus
ensuring that K+, rather than Na+, remains in the cell and
balances the intracellular anions.
K+ AND THE CELL MEMBRANE POTENTIAL:

 K+ leaks out down its concentration gradient through K+


channels in the cell membrane, leaving the ICF negative
relative to the ECF. This continues until equilibrium is reached,
where the outwardly-directed concentration gradient is matched
by an inwardly-directed electrical force. The voltage at
equilibrium is the resting membrane potential, and can be
predicted from the Nernst equation, i.e. Membrane potential = -
60 x log[K+in]/[K+out]
 = - 60 x log 30 = - 60 x 1.5 = - 90 mV (inside negative)
 Thus, membrane potential is directly related to the ratio of
[K+in] to [K+out], and hence is affected by the following
factors:

 Hypokalaemia enhances K+ efflux from the cell by increasing the


K+ concentration gradient from IN to OUT. K+ efflux
hyperpolarizes excitable cells, making it increasingly difficult to
initiate an action potential.
 Hyperkalaemia opposes K+ efflux, reducing membrane potential,
and facilitating depolarization. In the heart this hyperexcitable state
can lead to ectopic beats and ventricular fibrillation.
 • Certain drugs, the sulphonylureas, used to
treat diabetes, specifically block K+ channels
in pancreatic β-cells. By inhibiting K+ efflux
down its concentration gradient, these drugs
decrease cell membrane polarization and
facilitate depolarization, which triggers insulin
release.
K+ HOMEOSTASIS :

 The kidney plays a central role in maintaining K+ balance.


Filtered K+ is practically all reabsorbed in the proximal
convoluted tubule (PCT) and Loop of Henle.
 Hence, net K+ excretion depends on the SECRETION of K+
by the distal convoluted tubule (DCT), a passive process
depending on a transtubular electrical gradient (lumen negative)
created by Na+ absorption under the influence of aldosterone
(see diagram below).
The factors which are affected
on renal k+ excretion:
 Na+ delivery to the distal convoluted tubule (DCT). K+
cannot be excreted by the DCT unless there is Na+ present
with which it can exchange.

 Aldosterone. Reabsorption of Na+ in exchange for K+ and H+


in the DCT is under control of the steroid hormone,
aldosterone.
 Hydrogen ion availability. Since Na+ is reabsorbed in the
DCT in exchange for either K+ or H+, a reciprocal relationship
exists between K+ and H+ excretion.
Endocrine Regulation Of K+
Homeostasis :
 Aldosterone promotes K+ excretion mainly by
the renal mechanism described, but also
stimulates Na+/K+ exchange in the GIT and sweat
glands. Hyperkalaemia directly stimulates
aldosterone release.
 Insulin promotes K+ entry into cells as a
consequence of its stimulation of glucose uptake
and protein synthesis.
 Catecholamines enhance K+ uptake into cells by
stimulating glycogenolysis .
Hypokalaemia :
Clinical Features Of Hypokalaemia:
 Cardiac arrhythmias:
can be induced by hypokalaemia, and are often heralded by
tell-tale ECG features, including an increased PR-interval.
 Muscle weakness:

It usually involves peripheral muscles, sparing facial


muscles and muscles of respiration.
 GIT smooth muscle weakness :

manifests as constipation, progressing to paralytic ileus.


Hypokalaemia :
Clinical Features Of Hypokalaemia:
 Polyuria and dehydration.
K+ is required for salt and water reabsorption via the
Na+/K+/2Cl- co-transporter in the thick ascending limb
of the loop of Henle.

 Glucose intolerance.
Hypokalaemia impairs insulin release (fortunately, since
insulin would aggravate hypokalaemia). It can mimic
diabetes mellitus and resolves promptly once K+ is
replaced.
Causes Of Hypokalaemia:
1. DECREASED K+ INTAKE
A-Starvation – e.g. anorexia nervosa
B-Alcoholism.
C-Parenteral nutrition, without adequate K+ supplementation.

2. Renal K+ loss
A-Diuretic therapy
B- Mineralocorticoid excess
C- Renal tubular acidosis
D- The diuretic phase of acute renal failure
E- Magnesium deficiency
Causes Of Hypokalaemia:
3. GASTRO-INTESTINAL K+ LOSS :
A- Diarrhea.
B- Enteric fistulae that discharge small
intestinal contents, eg. ileostomy or colostomy.
C- Vomiting is a frequent cause of
hypokalaemia.
D- Villous adenoma of the rectum, a benign
tumour oozing K+ rich secretions, is a rare cause
of GIT K+ loss.
Causes Of Hypokalaemia:
4. MOVEMENT OF K+ FROM ECF TO ICF:

A-Acute alkalosis.
B-Diabetic acidosis treated with insulin.
C-β-adrenergic drugs.
Treatment Of Hypokalaemia:
 Intravenous infusion is required, K+
must be infused slowly (<20mmol/hr),
well-mixed, in dilute solution
(<40mmol/l).
HYPERKALAEMIA 
CAUSES OF HYPERKALAEMIA:
 These can be divided into excess intake, impaired
renal excretion, redistribution of K+ from ICF to
ECF, or spurious.
1. EXCESSIVE K+ INTAKE
 Excess oral intake rarely causes hyperkalaemia, as
the healthy kidney readily excretes a K+ load.
Only patients with renal impairment or those
treated with K+ sparing diuretics are at risk from
excess intake.
CAUSES OF HYPERKALAEMIA:
2. DECREASED RENAL K+ EXCRETION:
 Acute renal failure .
 Certain drugs interfere with the ability of the kidney
to excrete K+. For example: K+-sparing diuretics,
including spironolactone or amiloride, interfere with the
ability of the distal tubular to secrete K+; spironolactone
by inhibiting aldosterone action on the DCT, and
amiloride by blocking the luminal Na+ channels
through which Na+ enters the DCT cells.
CAUSES OF HYPERKALAEMIA:
 Adrenal insufficiency.

 Hyporeninaemic hypoaldosteronism is
a primary failure of renin secretion,
usually seen in association with diabetes
mellitus.
CAUSES OF HYPERKALAEMIA:
 3. MOVEMENT OF K+ FROM ICF TO ECF:
 Acute tissue injury may result in K+ efflux, eg. crush injury to
muscle or acute haemolysis. Liberation of myoglobin or
haemoglobin, respectively, into the plasma can cause secondary
renal damage, which in turn aggravates hyperkalaemia.
 Acidosis will displace K+ from intracellular sites into the
plasma.
 Depolarizing muscle relaxants, like succinyl choline (scoline),
can cause a transient hyperkalaemia by preventing K+ re-uptake
from acutely depolarized muscle cells.
CAUSES OF HYPERKALAEMIA:
4. Spurious hyperkalaemia:
 This refers to the reporting of hyperkalaemia in a patient in
whom circulating K+ is, in fact, normal. It has a variety of
causes:

 Release from red cells during or after venepuncture.


 Drip arm contamination.
 Release of K+ from white cells or platelets. In patients with a
particularly high white cell or platelet count (leukaemia or
thrombocytosis), white cells and/or platelets release their K+ into
the serum during the clotting process.
EFFECT OF HYPERKALAEMIA ON THE
HEART:
 Hyperkalaemia can kill without warning.
 It lowers the resting membrane potential.
 Increases the rate of repolarization.
 predisposes to ventricular arrythmias.
 Cardiac arrest in ventricular fibrillation may be
the first sign.
 Ecg changes are characteristic (peaked T-waves,
absent P-waves, widening of the QRS complex),
and provide early warning.
EFFECT OF HYPERKALAEMIA ON
THE HEART:
MANAGEMENT OF HYPERKALAEMIA:
 For mild hyperkalaemia, limit K+ intake (less
fruit) and give non-absorbable cation-exchange
resins (Kay-exalate) by mouth.
 Insulin and glucose infusion (100 gram glucose +
20 units insulin in 30 min), which causes K+ to be
taken up into cells.
 NaCl infusion with diuretics to promote urinary
K+ excretion.
MANAGEMENT OF HYPERKALAEMIA:
 NaHCO3 infusion to induce alkalosis, with movement of
K+ into cells.
 Dialysis (haemo- or peritoneal) is often required for
long-term control of hyperkalaemia; a plasma K+ > 7mM
in acute renal failure is an absolute indication for dialysis.
 In an acute situation, with imminent cardiac arrest, IV
infusion of calcium gluconate affords some protection
against hyperkalaemia by antagonizing its effect on
cardiac excitability.
Thank you

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