Potassium

Metabolism And
Disorders
BY
DR.B.E.KASIA
 OUTLINE
Introduction
Composition and compartments of
body fluid and Electrolytes
Physiology of water and electrolytes
with regulatory factors.
Potassium metabolism/homeostasis
Disorders- Hypo and Hyperkalaemia
Laboratory investigations
Conclusion
 Introduction
The Bible records that life began as a
spoken Word of God in Gen1. Life
specifically started from water.
Therefore, humans have to adapt to
terrestrial life. This adaptation
involves the development of complex
physiological systems to maintain
the composition of their internal
milieu.
Disorders of fluid and electrolytes may
arise from many factors both
external(Trauma)or internal(Disease)
Compensatory mechanisms may not
be adequate enough and so the
Chemical Pathologist is called upon
to provide valuable information to
guide therapy.
 Total Body Water
At birth 75% of the total body mass
is water and for roughly 1 year of
age through middle age this value is
60% for the average male and 55%
for females. After middle age this
falls to 50%. Approximately 2/3rd of
TBW is distributed into the ICF
compartment and 1/3rd exist in the
ECF compartment.
The ICF and ECF compartments are
physically separated by the cellular
membrane. ECF is subdivided into the
intestitial (3/4 of ECF) and intravascular
(approx. ¼ of ECF) fluid compartments, which
are separated by capillary endothelium. Within
the intravascular (whole blood) compartment,
plasma, the liquid fraction, constitutes 3.5L for
the average adult having a haematocrit of 40%
and a 5L blood volume.
It is therefore worthy of note that the
Analysis of hydration status, electrolytes
and acid-base status are performed on
samples from the intravascular (plasma,
serum, or whole blood) compartments.
 Total Body Water
Intestitial fluid

ICF
¾ ECF 28L

10.5L

Capillary endothel Cell membrane

Intravascular fluid
¼ ECF

Plasma 3.5L
 FLUID REQUIREMENTS OF THE BODY:-

Water intake ml/day Water output

ml/day
Drinking water 1200 Urine 1400
Water from food 1000 Insensible water
Water of oxidation 300 * Skin 400
Total 2,500 * Lungs 400
Sweat 100
Stool 200
Total 2,500
 ELECTROLYTES
The major ions of the body fluids are
collectively called electrolytes and
constitute the majority of osmotically active
particles. The primary cationic (positively
charged) electrolytes are sodium (Na+),
potassium (K +), calcium (Ca22+) and
magnesium (mg2+) whereas the anionic
(negatively charged) electrolytes include
chloride (Cl–), bicarbonate (HCo3–)
Phosphate (HPo42–, H2P04), sulfate
(S042–), organic ions such as lactate are
negatively charged compounds.
 ELECTROLYTE COMPOSITION AND VOLUME OF
VARIOUS GASTROINTESTINAL SECRETIONS IN A
NORMAL ADULT

Fluid Volume secreted Na+ K+ Cl– HCo3–

(ml/day)

Gastric juice 2500 8-120 1-30 8-100 0-20

Bile
700-1000 134-156 4-6 83-110 38
Pancreatic juice >1000
113-153 2-7 54-95 110
Small bowel 3000
72-120 3.5-7 69-127 30
Ileostomy 100-4000
112-142 4.5-14 43-122 30
Cecostomy 100-300
480-116 11-28 35-70 15
Faeces 100
<10 <10 <15 <15
 ELECTROLYTE COMPOSITION OF BODY
WATER COMPARTMENTS
Composition of body water compartment
Plasma Plasma water ISF Intracellular
(mmol/L) (mmol/L) water
 
Cations 153 164.6 153 195
Na+ 142 152.7 145 10
K+ 4 4.3 4 156
Ca2++ 5 5.4 2.3 3.2
Mg2+ 2 2.2 1.2 26
Anions 153 164.6 153 195
Cl– 103 110.8 116 2
HCo3– 28 30.1 31 8
Proteins 17 18.3 - 55
Others 5 5.4 6 130
PHYSIOLOGY OF FLUID AND ELECTROLYTES
AND THE REGULATORY FACTORS
Physiological functions:
Water (ECW) constitutes the medium
through which all metabolic exchange
occurs. Water within the cell (ICW)
constitutes the medium in which chemical
reactions of cell metabolism occur. Water
generally is the medium in which body
solutes, both organic and inorganic, are
dissolved, and transported around the
body.
Electrolytes especially the four major ones
(Na+, K+, Cl– and HC03–) are responsible
for maintenance of osmotic pressure and
water distribution in the various body fluid
compartment. They in addition play
important role in the maintenance of pH,
proper heart and muscle function,
oxidation-reduction reactions, and as co-
factors for enzymes.
Physiology and pathophysiology of body
water and electrolytes
Water is the most abundant constituent of
the human body, accounting for
approximately 60% of the body mass in a
normal adult. Water is important not only
because of its abundance but also because
it is the medium in which body solutes, both
organic and inorganic, are dissolved and
metabolic reactions takes place.
Compartment Volumes

% of % of Volume in 70kg
Body weight TBW man
 
TBW 60 - 42L
ECW 20 33 14L
Plasma 5 8 3.5L
ISF 15 25 10.5L
Intracellular 40 67 2.8L
Water
POTASSIUM METABOLISM

Approximately 98% of the total body potassium

is found in the ICW space, reaching a
concentration there of about 150 – 160 mmol/L.
In the ECW space, the concentration of
potassium is only 3.5 – 5 mmol/L. Total body K+
in an adult male is about 50 mmol/kg of body
weight and is influenced by age, sex and very
importantly, muscle mass, because most of the
body’s K+ is contained in the muscle.
 Homeostasis
In normal subjects potassium is
taken orally in diet and balance is
achieved in feces, sweat and urine
Kidney is the major excretory organ,
others are relatively insignificant
Redistribution between the ICF and
ECF is also impt. Due to effect of
memb polarization and rapid
increase in ECF K+ which may be
buffered by cellular K+ intake.
Intake orally depends on diet- 50-
100mmol/day.Virtually all are
absorbed in the gut with <10mmol/
day appearing in feces. There is No
physiological control over intake.
Distribution: Disturbances in the ECF
K+ is more than changes in the ICF
content.
 Distribution contd.
Potassium distribution b/w the ICF and ECF
is via Na/K-ATPase pump where both ions
diffuse across the cell walls and maintains
their ionic conc on both sides of the cell
membrane by pumping K into the cell and
Na out of it.
The factors affecting distribution are-
K load- 50% of ECF(oral or IV) crosses to
ICF:mechanism unclear but perceived local
ATPase pump.
40% of excess is excreted renally in 3hrs.
Insulin-directly induces cellular uptake of
K+ while insulin deficiency cause K leaking
from cells, hence insulin is useful in
treatment of hyperkalemia.
Cathecholamine- Adrenalin and β-
adrenegic receptor agonist like salbutamol
increase cellular K uptake causing
hypokalemia.Biphasic in action via initial
hepatic release before uptake.
Aldosterone- Acts at the distal renal
tubules by secretion into the urine in
exchange for H+. Acts on other cells
like the large gut cells, sweat gland
and mammary gland cells. Plays
minor role in uptake by other cells
PH –High pH(alkalaemia)- K goes
inwards (ICF) to maintain electro-
chemical neutrality.
This can lead to hypokalaemia in
addition, there is increased renal K
excretion.
The reverse is seen in low pH
(acidemia)-leads to hyperkalaemia.
 Output
Under normal circumstances potassium balance is
maintained by renal excretion; only a small
amount (5-10mmol/day) is excreted in the sweat
and faeces.
Renal potassium excretion
About 700 mmol/day of potassium is filtered by
the glomerulus. Most of this ( ˃95%) is
reabsorbed in the proximal nephron and the major
part of the urinary potassium results from
secretion by the distal nephron.
Proximal tubule. About 70% of the filtered
potassium is actively reabsorbed by a process that
is independent of sodium reabsorption.
Loop of Henle. In the thick ascending limp
(diluting segment) of the loop of Henle 20 to 25%
of the filtered potassium is reabsorbed along with
sodium consequent to active chloride reabsorption.
Output
Distal tubule and collecting duct. Secretion of
K+ occurs in the distal tubule along the
electrochemical gradient caused by the active
reabsorption of Na+. This is not a 1:1 coupling
with sodium ions (Na+ reabsorption can be more
than the sum of K+ and H+ secretion and occurs
mainly in the distal portion).
Control of potassium excretion
The renal secretion (and excretion) of potassium
is governed mainly by two factors: the
potassium concentration in the distal renal
tubular cells, and the rate of urine flow past these
cells.
The intracellular potassium ions rapidly
equilibrate with the luminal fluid across the
luminal side of the cell membrane. The following
relationships apply: an increased cellular (K+)
associated with a normal flow rate will result in
increased secretion wheras (a low (K+) with
normal flow gives a low excretion); a normal
cellular (K+) and an increased flow rate produces
an increased secretion and (a normal (K+) and a
 Cell potassium content. Factor increasing the cellular
(K+ ) (and renal excretion) are:
Increased aldosterone
Alkalaemia (low ECF (H+) due to H+-K+ exchange across
the cell wall. Thus primary metabolic alkalosis is nearly
always associated with hypokalaemia due to increased
renal potassium excretion
Increased potassium load
The reverse situations, hypoaldosteronism, acidaemia, and
decreased potassium load result in a low cell (K+ ) and
decreased excretion.
Urine flow rate. Factors which increase the urine flow
rate and renal potassium excretion are:
Increased sodium load (sodium diuresis)
Osmotic diuresis
Diuretics acting proximal to the distal tubule (sodium
diuresis)
A decreased flow rate and potassium retention occur if
there is a decreased GFR (dehydration, shock, etc) and in
acute renal failure
Disorders of potassium metabolism
An acute load of potassium is ‘buffered’ in the first
instance by the cells: 50% is taken up by cells and
40% is excreted by the kidney over the next 2 to 3
hours (hence only 10% is retained in the extracellular
fluid).
This occurs even in potassium-depleted states, i.e.;
50% of replacement potassium is excreted in the
urine.
Potassium deficiency is generally due to increased
loss in the face of normal or decreased intake
(negative potassium balance), and potassium excess
usually represents decreased renal potassium
excretion in the face of a normal or increased intake
(positive potassium balance).
As stated above the plasma (K) does not
necessarily reflect the total body potassium
content. For example, hypokalaemia can be
associated with a normal body potassium
content, as in the hypokalaemia associated with
salbutamol therapy; and hyperkalaemia, with a
low body potassium content, as occurs in diabetic
ketoacidosis.
The importance of hyper-and hypokalaemia lies
in the fact that such conditions represent an
abnormal intracellular- extracellular gradient that
may require vigorous therapy.
From a therapeutic view hypokalaemia is usually
associated with potassium deficiency, whilst
hyperkalaemia generally implies that potassium
has to be removed from the extracellular
compartment
 HYPERKALAEMIA
Hyperkalaemia is defined as a plasma potassium
value in excess of 5.0 mmol/L (our reference
range: 3.5-5-0 mmol/L). It is a common problem
presenting in up to 5% of hospital patients
although factitious values (haemolysis, etc) are
the commonest cause
Causes/pathophysiology
A useful practical classification is to divide the
causes of hyperkalaemia into three groups:
– Pseudohyperkalaemia,
– increased potassium input into the ECF
– decreased renal excretion.
Pseudohyperkalaemia
– Haemolysis
– Leucocytosis
– Thrombocytosis
Increased intake/load to ECF
Exogenous: Oral/IV therapy
Endogenous: Tissue necrosis: crush injury, burns,
malignancy
Disturbed intracellular/extracellular
distribution
Acidaemia
Insulin deficiency: diabetes mellitus
Drugs: digoxin toxicity, succinylcholine
Hypertonicity: glucose, sodium
Familiar Hyperkalaemic periodic paralysis
 Decreased renal excretion
Renal failure: Acute, Chronic
Drugs;
– Potassium-sparing diuretics: amiloride,
triamterene, spironolactone
– Prostaglandin inhibitors: indomethacin, ibuprofen
– Captopril
– Heparin
Mineralocorticoid deficiency syndromes
– Low cortisol and aldosterone: Addison’s disease,
– Adrenal hyperplasia, C21-hydroxylase defect
– Selective aldosterone deficiency:
– Hyporeninaemic hypoaldosteronism
– Prostaglandin inhibition (indomethacin)
Mineralocorticoid resistant syndromes
– Interstitial nephritis
– Sickle cell disease
– Obstructive uropathy
– Systemic lupus erythromatosus
– Amyloidosis
– Pseudohypoaldosteronism
Thrombocytosis often has a factitiously high
potassium concentration due to release of
potassium from these elements during clotting.
This can be overcome by taking a fresh sample
into heparin and quickly separating the plasma.
In vitro haemolysis and seepage of potassium
from red cells due to delayed separation of the
serum (˃4 hours) is a common problem.
Pseudohyperkalaemia is the commonest cause of
a high serum (K) encountered in the laboratory.
Tissue destruction.Acute tissue necrosis (crush
injuries, burns, chemotherapy of malignancy) will
release large amounts of potassium into the ECF.
These patients often have compromised renal
function which worsens the hyperkalaemia.
Extracelllular hypertonicity. Hypertonicity due to
high ECF concentrations of sodium or glucose is
associated with efflux of potassium from cells which
may produce a mild hyperkalaemia.
Hyperkalaemic periodic paralysis. This is a rare
inherited condition associated with bouts of
muscular paralysis and hyperkalaemia (potassium
release from cells). It can be precipitated by
exercise, cold exposure, or potassium therapy. The
cause is unclear.
Drugs and hyperkalaemia. The drugs that may
be associated with hyperkalaemia are the
potassium-sparing diuretic, prostaglandin inhibitors,
digoxin, succinylcholine, captopril, and heparin.
Potassium-sparing diuretics. Amiloride,
spironolactone, and triamterene act on the distal
tubule inhibiting sodium reabsorption. This is
associated with inhibition of potassium and
hydrogen ion excretion and may cause hyper-
kalaemic hyperchloraemic metabolic acidosis.
 Prostaglandin inhibitors. Normal
prostaglandin metabolism is necessary for the
normal secretion of rennin and aldosterone and
the prostaglandin inhibitor drugs, such as
indomethacin and ibuprofen, can produce a
syndrome similar to the syndrome of
hyporeninaemic hypoaldosteronism (see below).
Digoxin. Hyperkalaemia may be associated with
digoxin toxicity (potassium release from cells).
Succinylcholine. This muscle relaxant (used as
an anaesthetic) depolarizes the muscle cells and
allows potassium to escape into the ECF.
Captopril. This agent and other ACE inhibitors
have the potential to produce hypoaldosteronism
and hence hyperkalaemia. However,
hyperkalaemia is not a common complication of
these drugs but it will occur if there is an
associated increased potassium uptake.
Heparin. Large doses of heparin can suppress
the synthesis of aldosterone and result in
hyperkalaemia.
Renal failure. Chronic renal failure may have an
associate hyperkalaemia whereas acute renal
shutdown is usually accompanied by
hyperkalaemia.
In uncomplicated chronic renal insufficiency the
remaining nephrons are able to maintain
potassium excretion by increasing their workload
(increased fractional excretion) by up to 30 –
fold, but there comes a stage when this is
insufficient due to decreased number of nephrons
and potassium is retained causing hyperkalaemia.
This occurs when 70-80% of the nephrons are
destroyed (serum creatinine ˃0.35 mmol/L or
thereabout).
In acute renal shutdown renal function is severely
compromised and hyperkalaemia is usual.
Mineralocorticoid deficiency syndromes
Aldosterone increases potassium excretion by
increasing the distal tubular cell uptake.
Aldosterone deficiency has the reverse effect.
Syndrome of hyporeninaemic
hypoaldosteronism (SHH)
This syndrome is commonly seen in elderly
patients where it presents as hyperkalaemia
which may be associated with a mild
hyperchloraemic metabolic acidosis.
There may be mild renal insufficiency (serum
creatinine ˂0.20 mmol/L) and around 50% of the
subjects will have diabetes mellitus, most of the
others will have interstitial nephritis.
The hyperkalaemia is due to decreased renal
potassium excretion as a consequence of
hypoaldosteronism.
Evaluation of the renin-aldosterone axis reveals
depressed secretion of both hormones – the exact
cause is unknown. A similar biochemical and
clinical presentation can be seen in patients on
long term prostaglandin inhibitor (e.g.,
indomethacin) therapy.
Mineralocorticoid resistance syndromes. In
these disorders, the synthesis and secretion of
aldosterone is normal but there is end organ
resistance. The disorder may be primary
(pseudohypoaldosteronism) or secondary to a
variety of diseases which affect the kidney.
Consequences of hyperkalaemia
The patient’s response to hyperkalaemia depends on the
rate of rise of the ECF potassium concentration and the level
reached. Mild degrees of hyperkalaemia ( <6.0 mmol/L) are
usually asymptomatic, but if there is a rise beyond this
figure (particularly if rapid) some or all of the following may
occur.
The problems of most concern are cardiac arrhythmia and
possible arrest.
Listlessness, mental confusion
muscle weakness
nausea and vomiting
paralytic ileus
parasthesia
cardiac arrhythmia and arrest
ECG changes: tall T-waves, wide QRS- complex,
wide PR-interval.
 Laboratory evaluation

In most patients presenting with true hyperkalaemia the

cause is clinically obvious, e.g. diabetes mellitus, severe renal
failure and the like.
Again it is worth noting that the commonest cause of a high
serum potassium is pseudohyperkalaemia and this should be
excluded, by analyzing a fresh sample if necessary, before
pressing on to further tests.
Factors to note are haemolysed specimens, time between
venesection and cell separation, and the possibility of
haematological disorders.
The general approach is to exclude obvious causes such as
pseudohyperkalaemia, diabetes mellitus, severe renal failure,
and drug-induced hyperkalaemia. Then continue the
evaluation on the basis of the plasma bicarbonate and anion
gap. The ACTH (Synacthen) stimulation test may necessary to
exclude or confirm the mineralocorticoid deficiency syndromes
and the evaluation of rennin and aldosterone status may be
required.
 Therapy
Decreasing potassium intake (dietary, IV fluid).
Increasing excretion from the body (use of oral
Resonium A, an ion exchange resin which
binds potassium, or dialysis)
In the emergency situation, pushing the
potassium into cells with insulin. In
the very acute situation calcium, which
antagonizes the effects of potassium at the
tissue level, can be given as IV calcium
chloride.
HYPOKALAEMIA
Hypokalaemia, a plasma (k+) less than ~3.5
mmol/L, is the commonest disorder of potassium
homeostasis occurring in around 3 to 6% of all
hospitalised patients. The commonest causes of
hypokalaemia are diuretic therapy, vomiting, and
diarrhoea
Causes/pathophysiology
Although the commonest mechanism of
hypokalaemia is loss from the body, decreased
intake plays a significant role because the kidney is
not efficient at conserving potassium (50% of intake
appears in the urine within 3 to 4 hours). A useful
approach is to consider the causes in terms of ;
– Decreased intake
– Transcellular shifts
– Renal loss
– Extrarenal loss
 Causes of Hypokalaemia
Decreased intake
• Inappropriate iv therapy
• Anorexia nervosa
• Chronic alcoholism
Transcellular shifts
• Insulin,
• Vitamin B12
• Salbutamol, Barium toxicity
• Periodic paralysis
Extrarenal loss
Renal loss
• Metabolic alkalosis
• Diuretic therapy
• Mineralocorticoid excess
syndromes
• Renal tubular acidosis
• Bartter’s syndrome
• Magnesium depletion
• Gentamycin therapy
• Leukaemia

• Vomiting
• Diarrhoea
• Laxative abuse
• Villous adenoma of colon
• Urine diversion to gut
Causes of Hypokalaemia Contd.
Decreased intake. Hyperkalaemia due only to a decreased
potassium intake is unusual, there being usually an associated
increased loss, but it may occur in subjects on potassium-
deficient IV therapy, in chronic alcoholics and in anorexia nervosa
Transcellular shift. Severe
hypokalaemia associated with normal total body potassium may
occur with a variety of drugs, in barium toxicity (rare), and in
hypokalaemia periodic paralysis (uncommon).
Drugs. Hypokalaemia may complicate insulin therapy in diabetic
ketoacidosis if potassium supplements are not given because
these patients are potassium deficient.
The administration of salbutamol (B2- agonist), particularly when
given as infusions for the prevention of premature labour, can be
associated with quiet low plasma potassium levels (e.g., ˂2.5
mmol/L).
Newly diagnosed patients with pernicious anaemia, when given
vitamin B12, can develop a severe life-threatening hypokalaemia
(due to rapid uptake of potassium by newly developing red cells).
Causes of Hypokalaemia Contd
Hypokalaemic periodic paralysis. This condition presents
with bouts of muscle paralysis associated with hypokalaemia.
It is due to increased cellular potassium uptake (cause
unknown) which can be initiated by physical stress, large
carbohydrate meals, and cold exposure.
Barium toxicity. Several cases of have been recorded
where severe hypokalaemia has been due to increased
cellular potassium uptake.
Renal loss.
This is a very important cause for hypokalaemia and is most
commonly seen in patients undergoing diuretic therapy.
Diuretic therapy. Therapy with the following groups of
diuretics may be associated with hypokalaemia due to
excessive renal loss. Although diuretic therapy is a common
cause of hypokalaemia in clinical practice, it occurs in less
than 5% of patients on therapy.
Causes of Hypokalaemia Contd
Carbonic anhydrase inhibitors. These drugs (e.g.,
acetazolamide) inhibit proximal tubule bicarbonate reabsorption
and the increased sodium bicarbonate presented to the distal
nephron increases urine flow and hence encourages potassium
excretion. This hypokalaemia is associated with a low plasma
bicarbonate (metabolic acidosis) rather than the high plasma
bicarbonate seen with the other groups of diuretics. These drugs
are rarely used as diuretics now but find a use in the treatment of
glaucoma.
Loop diuretics. Furosemide and ethacrynic acid prevent chloride
reabsorption in the thick ascending limb of Henle which in turn
prevents the reabsorption of sodium ions. Direct causes of the
associated hypokalamia are similar to those for the thiazide
diuretics.

Thiazide diuretics. These drugs prevent sodium reabsorption in

the thick ascending limb of the loop of Henle and the early part of
the distal tubule; there is also minimal carbonic anhydrase
inhibition.
The potassium depletion is due to increased renal
excretion as a consequence of:
– increased Na+-K+ exchange in the distal nephron
– (increased sodium delivery)
– Hyperaldosteronism secondary to minimal
hypovolaemia
– Increased distal tubule urine flow rate (sodium
diuresis)
The hypokalaemia is almost always associated with a
high plasma bicarbonate (metabolic alkalosis) which is
due to increased renal tubular H+ secretion resulting
from:
– direct stimulation by thiazide drugs
– hyperaldosteronism
– potassium depletion per se
Causes of Hypokalaemia Contd
Extrarenal losses.
Both vomiting and diarrhoea are important causes of potassium
being lost via extrarenal routes. They may at times be difficult
to diagnose as certain patients who induce vomiting or use
laxatives surreptitiously may not readily admit to these actions
during history-taking.
Vomiting. Prolonged vomiting is nearly always associated with
hypokalaemia and in addition the loss of HCI results in metabolic
alkalosis. The potassium is lost from two sources.
Vomitus. Small but significant amounts
Kidney. Mostly lost in the urine due to increased potassium
excretion as a consequence of alkalosis and hyperaldosteronism
secondary to hypovolaemia (dehydration due to water loss).
Diarrhoea. Diarrhoeal fluid is rich in bicarbonate (60-80
mmol/L) and potassium (6.0-9.0 mmol/L) and hence the
condition results in hypokalemic metabolic acidosis. Any
associated dehydration will result in extra potassium loss via the
kidney (secondary hyperaldosteronism).
Two similar conditions are laxative abuse and villous
adenoma of the colon or rectum.
Laxative abuse results in chronic diarrhoea which
may present as hypokalaemia of obscure origin
(patient reluctance to admit to self medication).
Some large bowel villous adenomas present with
hypokalaemia because of the loss of potassium-rich
secretions in the faeces (diarrhoea may not
necessarily be a feature).
Renal tubular acidosis (RTA). RTA type 1 always
presents with hypokalaemia: in RTA type 2,
hypokalaemia generally only occurs after
commencement of bicarbonate therapy.
Urine diversion to large gut. If urine is allowed to
collect in the colon, as in ureterosigmoidostomy or
vesico-colic fistulae, the urinary chloride is
reabsorbed by the gut in exchange for bicarbonate
and potassium is secreted into the gut in exchange
for ammonium (and sodium) ions, resulting in a
hypokalaemic metabolic acidosis. A similar metabolic
abnormality occurs with an ileal bladder.
Mineralocorticoid excess syndromes. A
characteristic feature of aldosterone excess is
hypokalaemia and metabolic alkalosis due to
renal loss of potassium and hydrogen ions.
Miscellaneous causes of hypokalaemia.
These include the following:
Gentamicin therapy. Patients on gentamicin
therapy may develop occasional hypokalaaemia
due to renal potassium loss (? inhibition of
tubular reabsorption).
Magnesium depletion. Severe deplection may
be associated with hypokalaemia which is
refractory to potassium therapy until the patient
is malgnesium replete.
Leukaemia. Occasional hypokalaemia due to
renal potassium loss (? toxic effect of lysosomes
associated with lysosomuria) is seen in acute
myeloid leukaemia.
 Laboratory evaluation
In clinical practice the commonest causes of
hypokalaemia are diuretic therapy, vomiting,
diarrhoea, and drug therapy.
If after considering these conditions the cause is
obscure, the urinary potassium concentration on
a spot (untimed) sample should be estimated and
the result considered in tandem with the patient’s
plasma bicarbonate level.
It is important that the urine sample be collected
before giving the subject any potassium therapy
as this will invalidate the result (oral or IV
potassium appears in the urine regardless of the
clinical condition).
Note: A number of seriously ill patients, e.g. with
myocardial infarction, will present with a transient
hypokalaemia (i.e., normalizes without therapy).
This most likely represents an intracellular shift due to
adrenaline stimulation of the cell β-receptors and is
seen in stress associated conditions (stimulation of
catecholamine secretion) such as trauma, myocardial
infraction etc.
Consequences of hypokalaemia
The clinical picture is non-specific and depends on the
severity of the deficiency: muscle weakness and
polyuria (nocturia) are the most characteristic
symptoms.
The range of signs and symptoms includes:
Muscle weakness: both skeletal and smooth muscle
(paralytic ileus). Paralysis of the limbs can occur.
Loss of tendon reflexes
Fatigue and apathy
Polyuria (hypokalaemia nephropathy)
Hypotension and postural hypotension
Tachycardia, cardiac arrhythmia ECG
changes: T-wave depression and occasional
inversion, ST depression. In severe cases
there may be U waves and widening of the
QRS and QT complexes.
Patients with hypokalaemia associated with
conditions known to cause potassium losses
from the body are generally potassium
deficient to the tune of 300-350 mmol per
1.0 mmol/L drop in the plasma potassium
below 4.0 mmol/L; and will usually require
potassium replacement therapy..
 Therapy
Potassium can be given orally or intravenously.
The oral preparations are either effervescent KCI
tablets with ~14 mmol of K+ per tablet or slow
release preparations with ~8 mmol of K+ per tablet.
Effervescent KCl tablet. Sando K: 12mmol K per
tablet as bicarbonate and chloride
Intravenous potassium can be given at the rate of 10
to 20 mmol/hour at a concentration less than 40
mmol/L (to prevent sudden rises in the blood level).
The amount of potassium given per day (oral or IV)
should be at least 90 mmol because of the ongoing
loss in the urine.
Close monitoring is essential to prevent the
development of hyperkalaemia, particularly with IV
therapy.
 Conclusion
Usefulness of potassium should not
be over-emphasized.
Note its homeostatic roles
(intake ,distribution and output)
Disorders
Laboratory evaluation
Management.
THANKS FOR

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