Potassium balance

Distribution of potassium

• The intracellular concentration of potassium

ranges from 140 to 150 mmol/L.
• The extracellular concentration of potassium
(3.5-5.0mmol/L) is considerable less.
Gains and losses

• Food is the main source of potassium intake.

• The kidneys are the main source of

potassium elimination.
Mechanisms of regulation

• Renal regulation through Aldosterone --- a

sodium-potassium exchange system.
Sodium is transported back into blood.
Potassium is secreted into tubular filtrate

• Transcellular shift between the intracellular

and extracellular compartments
Transcellular shifts
• Sodium-potassium ATPase
– Both insulin and epinephrine increase the activity of sodium-
potassium pump.
(An increase in potassium level stimulates insulin release. --- a
feedback mechanism)
• Potassium channels
– ECF osmolality↑→H2O leaves cell→ ICF K+↑→ K+ moves out
of cell through K+ channels →ECF K+
– Exercise
• Potassium-hydrogen exchange to maintain electrical
neutrality
– In acidosis
– In alkalosis
Functions of potassium
• Maintain the osmotic integrity of cells
– Osmotic pressure in ICF
• Maintain acid-base balance
– Through potassium-hydrogen exchange
• Contribute to the reactions that take place in cells
– Transform carbohydrates into energy
– Convert amino acid to protein
– Change glucose into glycogen
• Play a critical role in the excitability of skeletal,
cardiac, and smooth muscle.
 Hypokalemia

Hypokalemia refers to a decrease in

plasma potassium level below 3.5
mmol/L.
Causes of hypokalemia
• Inadequate intake
– inability to obtain or ingest food
– Diet deficient in potassium
• Excessive renal, gastrointestinal and skin losses
– Diuretic therapy (thiazide and loop diuretics)
– Increased aldosterone level (primary aldosteronism, stress-
cortisol)
– burn, sweating increase, vomiting and diarrhea
• Transcellular shift
– Administration of insulin (to treat diabetic ketoacidosis)
– β-adrenergic agonist----albuterol (bronchodilator)
– Alkalosis
Hypokalemia with alkalosis
• Vomitting (Loss of hydrogen ion increases plasma bicarbonate. Coexisting volume
depletion increases aldosterone secretion , sodium is retained and potassium excreted.)
• Diuretics (Bartter’s syndrome is usually diagnosed in childhood, sometimes associated with
growth and mental retardation. . Findings are similar to administration of a loop acting diuretic,
Gitelman’s syndrome mimic administration of a thiazide diuretic , Gitelman's syndrome, also known
as "hypocalciuric variant of Bartter's syndrome", is a cause of chronic hypokalemia and
hypomagnesemia in adults )

• Cushing syndrome
• Conn’s syndromr
Hypokalemia with acidosis
• Diarrhea
• Renal tubular acidosis
• Acetazolamide
• Partially treaTed DKA
Manifestations of hypokalemia
• Neuromuscular manifestations
– Muscle flabbiness, weakness and fatigue
– Muscle cramps and tenderness
– Paresthesia and paralysis (Hypokalemic periodic paralysis-
typically oriental men with thyrotoxicosis)
• Gastrointestinal manifestations
– Anorexia, nausea, vomitting,
– Constipation, abdominal distension, paralytic ileus
• Cardiovascular manifestations
– Arrhythmias, increased sensitivity to digitalis toxicity
• Metabolic alkalosis
ECG changes in hypokalemia
• Depression of the ST segment
• Flattening of the T wave
• Appearance of a prominent U wave
• Prolongation of PR interval
• Prolong QT

In hypokalemia U have no Pot and no T, but a

long PR and a long Qt
Treatment of hypokalemia

• Increasing the intake of foods high in

potassium content
• Oral potassium supplements
• Giving potassium intravenously when rapid
replacement is needed.
– Only if the renal function is adequate
 TREATMENT GOALS
prevent life-threatening and/or chronic consequences

replace the associated K+ deficit

correct the underlying cause and/or mitigate future

hypokalemia
Hyperkalemia

• Hyperkalemia refers to an increase in plasma

levels of potassium in excess of 5.0mmol/L.
Causes of hyperkalemia
• Decreased renal elimination
– Decreased renal function-renal failure
– Treatment with potassium-sparing diuretics
– Decreased aldosterone level
• Adrenal insufficiency (addison’s disease)
• Treatment with ACEI
• Angiotensin II receptor blocker
• Excessively rapid administration

• Movement of potassium from the intracellular to

extracellular compartment
– Tissue injury such as burns and crushing injuries
– Extreme exercise or seizures
– Acidosis
Manifestations of hyperkalemia

• Gastrointestinal manifestations
– Anorexia, nausea, vomitting, intestinal cramps,
diarrhea
• Cardiovascular manifestations
– Ventricular fibrillation and cardiac arrest
• Neuromuscular manifestations
– Paresthesias
– Weakness
– Muscle cramps
ECG changes in hyperkalemia

• Appearance a peaked T wave

• Widening of the QRS complex
• Prolongation of the PR interval
• Disappearance of the P wave
 Treatment of hyperkalemia

• Decreasing intake or absorption of potasssium.

• Using calcium to antagonize the potassium.
• Using insulin and glucose
• Increasing potassium excretion
– hemodialysis
– peritoneal dialysis
CALCIUM
 Biological functions of Calcium
• Bone and teeth mineralization
• Regulate neuromuscular excitability
• Blood coagulation
• Secretory processes
• Membrane integrity
• Plasma membrane transport
• Enzyme reactions
• Release of hormones and neurotransmitters
• Intracellular second messenger
Distribution
 Different Forms of Calcium
 Calcium in the plasma:
45% in ionized form (the physiologically active form)

45% bound to proteins (predominantly albumin)

10% complexed with anions (citrate, sulfate,

phosphate)

 Both total calcium and ionized calcium measurements are available

in many laboratories
 Body requirements
Age (in years) Calcium Requirement
1–3 500mg
4-8 800mg
9 - 18 1300mg
19 - 50 1000mg
51+ 1500mg

*Pregnant and lactating women are

recommended a daily calcium intake of 1000mg.
 source
• Calcium is found in milk and dairy products,
• Green leafy vegetables,
• seafood,
• almonds,
• blackstrap molasses,
• broccoli,
• enriched soy and rice milk products, figs,
• soybeans and tofu.
 Absorption of Ca
• Absorption is taking place from the first and second
part of duodenum
• Increased absorption-
- calcitriol , active form of Vit-D
- PTH
- acidic pH
- Lys and Arg
• Inhibiting absorption -
- phytic acid
- oxalates
- phosphate
- Mg
- caffeine
 Hormone regulation of
calciummetabolism
• Parathyroid hormone (PTH)
• Vitamin D
• Calcitonin
 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 synthesis
4. increase of ca absorption indirectly in the
intestine
 Vitamin D3
• in the liver, cholecalciferol undergoes 25-hydroxylation to yield
25(OH) Vit-D ( calcidiol) .In the kidney , calcidiol undergoes further
1α-hydroxylation to produce 1,25 –dihydroxy Vit-D (Calcitriol). Its
production in the kidney is catalyzed by 1α -hydroxylase .

 Action of 1,25-dihydroxycholecalcififerol(Calcitriol)
• Increases intestinal Ca2+ absorption (the main action)
• Increases intestinal phosphate absorption
• Increase renal reabsorption of Ca2+ and phosphate
• It acts on osteoblasts which produce a signal that activates
osteoclasts to resorb Ca++ from the bone matrix. (Osteoblasts, but
not osteoclasts have vitamin D3 receptors)

•
Vitamin D3 and Calcium Control
 Calcitonin
• This is produced from the C-cells of the thyroid.
Organ-target :bones osteoclast
Function - decrease of Ca concentration in
plasma
• The major stimulus of calcitonin secretion is a
rise in plasma Ca++ levels
• Calcitonin is a physiological antagonist to PTH
with regard to Ca++ homeostasis
 Calcium metabolism disorders:
Calcium metabolism disorder include:

• Hypercalcemia

• Hypocalcemia

• hyperparathyrodism
 hypercalcemia
• Is condition in which the calcium level in
the body is above the normal.
• The need of the calcium for the bone
formation and muscle contraction,
releasing hormone .
• The main cause is over activity of the
parathyroid gland.
• cancer and some medication may cause
over activity of the calcium level.
 Etiology of hypercalcemia
Increased GI Absorption:
Vitamin D excess
Elevated PTH
Decreased Urinary Excretion:
Thiazide diuretics ,antiacids
Increased Loss From Bone:
Elevated PTH
Hyperparathyroidism
Malignancy
Osteolytic metastases
Other
Sarcodosis
 symptoms and signs
• Bones,stones ,groans and psychic moans
• Abdominal pain and constipation
• Polyuria and polydipsia
 Complication:
• Metastatic calcification
• Renal stones
 Management
• Rehydration with normal saline
• Calcitonin
• bisphosphonate
 hypocalcaemia

• Is a condition in which the calcium level below

The normal level

• Is caused by low level of PTH , low level of

magnesium, deficiency of vitamin D

• The kidney dysfunction play role in

hypocalcuimia
 Etiology of the hypocalcemia

• Poor dietary intake of calcium,impaired GI

absorption
• Increased Urinary Excretion
• Decreased Bone Resorption/Increased
Mineralization
• Low PTH
• PTH resistance (low Mg)
• Vitamin D deficiency,
 Complication

Tetany: condition of mineral imbalance .

in the body that results in severe muscle
spasms. usually occurs when the
concentration of calcium ions (Ca++) in
extracellular fluids below normal
Trousseau Sign
Chvostek Sign
 Management
• Acute:
• IV calcium gluconate
• ECG monitoring
• Treatment of the underlying cause
• Correction of low magnesium
 Hyperparathyroidism.
• Hyperparathyroidism occur in two major
forms:
• Primary: most common cause of
hypercalceimia.it represents autonomous
production of PTH.
• Secondary:is caused by any chroinc
condition assocaited with chroinc
depression in the calcuim level.
• Tertiary hyperparathyroidism: rarely
occur
 Deficiency:
Deficiency of calcium levels in the body
may induce several diseases:

• Rickets disease

• Adult osteomalacia

• osteoporosis
Rickets :
is a softening of bones in children potentially leading to
fractures and deformity. The predominant cause is a
vitamin D deficiency, lack calcium in the diet may also
leads to rickets

 Osteomalacia :
is the softening of the bones due to
defective bone mineralization It may
show signs as diffuse body pains, fragility
of the bones. A common cause of the disease is
deficiency in vitamin D, which is normally obtained
from the diet and/or sunlight exposure
Osteoporosis
a disease characterized by low bone mass and
structural deterioration of bone tissue, leading
to bone fragility and an increased risk of
fractures of the hip spine, and wrist, leading to
bone fragility. Men as well as women are
affected by osteoporosis. women had high rate
to be affected by osteoporosis