ملخص

HYPOKALEMIA

Decrease in K+ causes decreased excitability of cells, therefore cells are less responsive to normal stimuli

ICF conc. = 150- 160 mEq/ L

Hypokalemia can only occur for four reasons:

1-Decreased intake

2-Shift into cells
1. Alkalosis
2.Insulin
3. Beta adrenergic drugs or epinephrine
3-Extra-renal losses..GIT
A-Hypokalemia from loss of gastric fluid.
B-Diarrheal losses are usually accompanied by metabolic acidosis
4-Renal losses
A-Primary hyperaldosteronism ( Conns syndrome),
B-Cushing syndrome and increased steroids.
C-Diuretic therapy
D-diabetic ketoacidosis
E-Renal tubular acidosis (RTA)


Neuromuscular disorders
Muscle Weakness, flaccid paralysis, respiratory arrest
GIT
nuasia , constipation
Acquired Nephrogenic DI
Heart
Arrhythmias, Postural hypotension

Management

treat underlying cause
correction of alkalosis
Oral KCL
infusion of KCL

Hyperkalemia

Severe: above 6.5 mmol/l carry
Risk of cardiac stand still in diastole
c/p: progressive muscular weakness or no symptoms

Of Hyperkalemia Causes

1.(spurious) Pseudohyperkalemia
Hemolysis
Delay in processing of blood
Severe leukocytosis or thrombocytosis

2.Excessive intake (diet, iv therapy..)

3.Redistribution out of cells
1.Metabolic acidosis
2.Insulin deficiency
3.B-BLOCKERS

4.Endogenous increase K Load

Rhabdomyolysis
Hemolysis

5.Medications

ACEI,B-BLOCKER,K-sparingD
6.Renal retention of K
A. Sever Acute Renal Failure
B. Chronic Renal Failure


Conditions with Hyperkalemia due to Renal Tubular Secretary Failure with NORMAL GFR

1.Addison disease

2.Congenital adrenal enzyme defect
3. Drugs : ACEIs , B-blockers ,NSAIDs and K Sparing Diuretics
4.Tubulointerstial disease

Treatment of Hyperkalemia

1- Stabilize myocardial membrane
Calcium Gluconate
2- Drive extracellular potassium into the cells
1- 2 Agonists
2- Insulin
3- If Acidosis , IV Sodium Bicarbonate
3- Removal of Potassium from the body
1.Frusemide IV with Normal Saline if renal function is normal
2.Ion Exchange Resin
decreasing total body potassium
3.Dialysis if significant renal impairment

Investigations

1-Serum Electrolytes
2-Renal Function tests
3-bicarbonate level
4-ECG


Hypomagnesemia
Causes :
1- decrease Intake :
Starvation ,Malnutrition
2-Shift to Cells
Insulin, Pancreatitis
3-Excretion (Renal)
Diuretics loop
Post-obstructive
primary hypoaldosteronism
Post-renal transplant
4-GIT Loss
Prolonged vomiting and chronic Diarrhea

Cardiovascular

Arrhythmia
Vasocostriction &Hypertention

Metabolic

Hypocalcemia is frequently associated with Hypomag.
occasionally Hypokalemia & Hyponatremia


Neurological
Tetany
Seizures

Hypomagnesemia Treatment

1-Treat underlying cause
2-If Diuretics Contribute.. Then use K sparing diuretic
3-Oral Mg Salts
4-Mg sulfate
5-Mg Cl

Hypermagnesemia

1-nearly always Acute or Chronic renal failure (Mg retention) is the underlying cause
2- increase INTAKE
Mg-containing antacids/laxatives , Iatrogenic IV magnesium replacement
3-SHIFT
Diabetic ketoacidosis , Tissue injury

Clinical Consequences

Vasodilatation..Hypotention
Inhibition of cardiac conduction Bradycardia
Inhibition of neuromuscular transmission
Respiratary muscle depression
muscle paralysis


Treatment
Loop diuretic which promote excretion
calcium gluconate to reverse cardiac ill effects
Dialysis in renal failure

Phosphorous

has inverse relationship to Calcium

Hypophosphotemia

Causes
Shift into cells: starvation, Alkalosis
Decrease Intake or absorption from gut: Malabsorption, chronic diarrhea
Increase renal loss: Hyperparathyroidism , Diuresis

Clinical manifestations

Skeletal Muscles: weakness respiratory failure
Cardiac Muscle: congestive heart failure
CNS: Convulsion ,coma
Treatment Hypophosphatemia.
high protein/dairy Dietary supplements
Oral phosphate salt supplements
In sever cases IV Potassium phosphate


Hyperphosphatemia
Causes:
usaully Acute or chroniv renal failure
Hypoparathyroidism
Tumor lysis syndrome &Catabolic states
Inaproppriete Vit D therapy

Clinically features related to the usually associated Hypocalcemia &renal failure

Treatment by phosphate restriction & use of oral phosphate binders