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Symptoms and Signs – Differential Diagnosis of Hypoimmunoglobulinemia
• IgM: congenital deficiency, lymphocytic leukemia, nephrotic syndrome
• IgG: congenital or acquired deficiency, lymphocytic leukemia, phenytoin, methylprednisolone, nephrotic syndrome, proteinlosing enteropathy
• IgE: hypogammaglobulinemia, neoplasm (breast, bronchial, cervical), ataxia-telangiectasia
• IgA: nephrotic syndrome, protein-losing enteropathy, congenital deficiency, lymphocytic leukemia, ataxia-telangiectasia, chronic sinopulmonary disease
• IgM: congenital deficiency, lymphocytic leukemia, nephrotic syndrome
• IgG: congenital or acquired deficiency, lymphocytic leukemia, phenytoin, methylprednisolone, nephrotic syndrome, proteinlosing enteropathy
• IgE: hypogammaglobulinemia, neoplasm (breast, bronchial, cervical), ataxia-telangiectasia
• IgA: nephrotic syndrome, protein-losing enteropathy, congenital deficiency, lymphocytic leukemia, ataxia-telangiectasia, chronic sinopulmonary disease
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Symptoms and Signs – Differential Diagnosis of hypokalemia
• β-Adrenergic agonists (e.g., terbutaline), decongestants, bronchodilators, theophylline, caffeine
• Vitamin B12 therapy for megaloblastic anemias, acute leukemias
• Renal tubular acidosis (RTA): distal (type 1) or proximal (type 2)
• Postobstruction diuresis, diuretic phase of tyrosinase-negative oculocutaneous albinism (ATN)
• Osmotic diuresis (e.g., mannitol)
• Magnesium deficiency
• Insulin administration
• Increased renal excretion secondary to medications: diuretics, including carbonic anhydrase inhibitors (e.g., acetazolamide); amphotericin B; high-dose sodium penicillin, nafcillin, ampicillin, or carbenicillin; cisplatin; aminoglycosides, corticosteroids, mineralocorticoids, foscarnet sodium
• Increased mineralocorticoid activity (primary or secondary aldosteronism), Cushing’s syndrome
• Inadequate dietary intake (e.g., anorexia nervosa)
• Hypokalemic periodic paralysis: rare familial disorder manifested by recurrent attacks of flaccid paralysis and hypokalemia
• High dietary sodium intake, excessive use of licorice
• GI loss: vomiting, nasogastric suction, diarrhea, laxative abuse, villous adenoma, fistulas
• Diabetic ketoacidosis (DKA), ureteroenterostomy
• Cutaneous loss (excessive sweating)
• Correction of digoxin intoxication with digoxin antibody fragments (Digibind)
• Chronic metabolic alkalosis from loss of gastric fluid (increased renal potassium secretion)
• Cellular shift (redistribution) and undetermined mechanisms
• Bartter’s syndrome: hyperplasia of juxtaglomerular cells leading to increased renin and aldosterone, metabolic alkalosis, hypokalemia, muscle weakness, and tetany (seen in young adults)
• Barium poisoning, toluene intoxication, verapamil intoxication, chloroquine intoxication
• Alkalosis (each 0.1 increase in pH decreases serum potassium by 0.4 to 0.6 mEq/L)
• β-Adrenergic agonists (e.g., terbutaline), decongestants, bronchodilators, theophylline, caffeine
• Vitamin B12 therapy for megaloblastic anemias, acute leukemias
• Renal tubular acidosis (RTA): distal (type 1) or proximal (type 2)
• Postobstruction diuresis, diuretic phase of tyrosinase-negative oculocutaneous albinism (ATN)
• Osmotic diuresis (e.g., mannitol)
• Magnesium deficiency
• Insulin administration
• Increased renal excretion secondary to medications: diuretics, including carbonic anhydrase inhibitors (e.g., acetazolamide); amphotericin B; high-dose sodium penicillin, nafcillin, ampicillin, or carbenicillin; cisplatin; aminoglycosides, corticosteroids, mineralocorticoids, foscarnet sodium
• Increased mineralocorticoid activity (primary or secondary aldosteronism), Cushing’s syndrome
• Inadequate dietary intake (e.g., anorexia nervosa)
• Hypokalemic periodic paralysis: rare familial disorder manifested by recurrent attacks of flaccid paralysis and hypokalemia
• High dietary sodium intake, excessive use of licorice
• GI loss: vomiting, nasogastric suction, diarrhea, laxative abuse, villous adenoma, fistulas
• Diabetic ketoacidosis (DKA), ureteroenterostomy
• Cutaneous loss (excessive sweating)
• Correction of digoxin intoxication with digoxin antibody fragments (Digibind)
• Chronic metabolic alkalosis from loss of gastric fluid (increased renal potassium secretion)
• Cellular shift (redistribution) and undetermined mechanisms
• Bartter’s syndrome: hyperplasia of juxtaglomerular cells leading to increased renin and aldosterone, metabolic alkalosis, hypokalemia, muscle weakness, and tetany (seen in young adults)
• Barium poisoning, toluene intoxication, verapamil intoxication, chloroquine intoxication
• Alkalosis (each 0.1 increase in pH decreases serum potassium by 0.4 to 0.6 mEq/L)
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Symptoms and Signs – Differential Diagnosis of Hypomagnesemia
• Renal tubular acidosis (RTA)
• Redistribution: hypoalbuminemia, cirrhosis, administration of insulin and glucose, theophylline, epinephrine, acute pancreatitis, cardiopulmonary bypass
• Parenteral therapy without magnesium
• Miscellaneous: sweating, burns, prolonged exercise, lactation, “hungry bones” syndrome
• Inadequate dietary intake (e.g., alcoholics)
• Endocrine disturbances (diabetic ketoacidosis [DKA], hyperaldosteronism, hyperthyroidism, hyperparathyroidism), syndrome of inappropriate antidiuretic hormone (SIADH), Bartter’s syndrome, hypercalciuria, hypokalemia
• Diuretics
• Diuretic phase of acute tubular necrosis (ATN)
• Defective GI absorption (malabsorption)
• Cisplatin, alcohol, cyclosporine, digoxin, pentamidine, mannitol, amphotericin B, foscarnet, methotrexate
• Chronic diarrhea, villous adenoma, prolonged nasogastric suction, fistulas (small bowel, biliary)
• Antibiotics (gentamicin, ticarcillin, carbenicillin)
• Renal tubular acidosis (RTA)
• Redistribution: hypoalbuminemia, cirrhosis, administration of insulin and glucose, theophylline, epinephrine, acute pancreatitis, cardiopulmonary bypass
• Parenteral therapy without magnesium
• Miscellaneous: sweating, burns, prolonged exercise, lactation, “hungry bones” syndrome
• Inadequate dietary intake (e.g., alcoholics)
• Endocrine disturbances (diabetic ketoacidosis [DKA], hyperaldosteronism, hyperthyroidism, hyperparathyroidism), syndrome of inappropriate antidiuretic hormone (SIADH), Bartter’s syndrome, hypercalciuria, hypokalemia
• Diuretics
• Diuretic phase of acute tubular necrosis (ATN)
• Defective GI absorption (malabsorption)
• Cisplatin, alcohol, cyclosporine, digoxin, pentamidine, mannitol, amphotericin B, foscarnet, methotrexate
• Chronic diarrhea, villous adenoma, prolonged nasogastric suction, fistulas (small bowel, biliary)
• Antibiotics (gentamicin, ticarcillin, carbenicillin)
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Symptoms and Signs – Differential Diagnosis of Hyponatremia
HYPOTONIC HYPONATREMIA
Isovolemic Hyponatremia
• Syndrome of inappropriate antidiuretic hormone (SIADH)
• Water intoxication (e.g., schizophrenic patients, primary polydipsia, sodium-free irrigant solutions, multiple tap-water enemas, dilute infant formulas). These entities are rare and often associated with a deranged antidiuretic hormone (ADH) axis.
• Renal failure
• Reset osmostat (e.g., chronic active TB, carcinomatosis)
• Glucocorticoid deficiency (hypopituitarism)
• Hypothyroidism
• Thiazide diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), carbamazepine, amitriptyline, thioridazine, vincristine, cyclophosphamide, colchicine, tolbutamide, chlorpropamide, angiotensin-converting enzyme (ACE) inhibitors, clofibrate, oxytocin, selective serotonin reuptake inhibitors (SSRIs), amiodarone. With these medications, various drug-induced mechanisms are involved.
Hypovolemic Hyponatremia
• Renal losses (diuretics, partial urinary tract obstruction, salt-losing renal disease)
• Extrarenal losses: GI (vomiting, diarrhea), extensive burns, third spacing (peritonitis, pancreatitis)
• Adrenal insufficiency
Hypervolemic Hyponatremia
• Congestive heart failure (CHF)
• Nephrotic syndrome
• Cirrhosis
• Pregnancy
ISOTONIC HYPONATREMIA
Normal Serum Osmolality
• Pseudohyponatremia (increased serum lipids and serum proteins). Newer sodium assays eliminate this problem.
• Isotonic infusion (e.g., glucose, mannitol)
HYPERTONIC HYPONATREMIA
Increased Serum Osmolality
• Hyperglycemia: each 100 mg/dL increment in blood glucose level above normal decreases plasma sodium concentration by 1.6 mEq/L
• Hypertonic infusions (e.g., glucose, mannitol)
HYPOTONIC HYPONATREMIA
Isovolemic Hyponatremia
• Syndrome of inappropriate antidiuretic hormone (SIADH)
• Water intoxication (e.g., schizophrenic patients, primary polydipsia, sodium-free irrigant solutions, multiple tap-water enemas, dilute infant formulas). These entities are rare and often associated with a deranged antidiuretic hormone (ADH) axis.
• Renal failure
• Reset osmostat (e.g., chronic active TB, carcinomatosis)
• Glucocorticoid deficiency (hypopituitarism)
• Hypothyroidism
• Thiazide diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), carbamazepine, amitriptyline, thioridazine, vincristine, cyclophosphamide, colchicine, tolbutamide, chlorpropamide, angiotensin-converting enzyme (ACE) inhibitors, clofibrate, oxytocin, selective serotonin reuptake inhibitors (SSRIs), amiodarone. With these medications, various drug-induced mechanisms are involved.
Hypovolemic Hyponatremia
• Renal losses (diuretics, partial urinary tract obstruction, salt-losing renal disease)
• Extrarenal losses: GI (vomiting, diarrhea), extensive burns, third spacing (peritonitis, pancreatitis)
• Adrenal insufficiency
Hypervolemic Hyponatremia
• Congestive heart failure (CHF)
• Nephrotic syndrome
• Cirrhosis
• Pregnancy
ISOTONIC HYPONATREMIA
Normal Serum Osmolality
• Pseudohyponatremia (increased serum lipids and serum proteins). Newer sodium assays eliminate this problem.
• Isotonic infusion (e.g., glucose, mannitol)
HYPERTONIC HYPONATREMIA
Increased Serum Osmolality
• Hyperglycemia: each 100 mg/dL increment in blood glucose level above normal decreases plasma sodium concentration by 1.6 mEq/L
• Hypertonic infusions (e.g., glucose, mannitol)
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Symptoms and Signs – Differential Diagnosis of Serum Hypo-osmolality
• Syndrome of inappropriate antidiuretic hormone (SIADH)
• Overhydration
• Hypothyroidism
• Hyponatremia
• Addison’s disease
• Syndrome of inappropriate antidiuretic hormone (SIADH)
• Overhydration
• Hypothyroidism
• Hyponatremia
• Addison’s disease
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Symptoms and Signs – Differential Diagnosis of Urine Hypo-osmolality
• IV hydration with D5W
• Glomerulonephritis
• Excessive water intake
• Diabetes insipidus (DI)
• Acute renal insufficiency
• IV hydration with D5W
• Glomerulonephritis
• Excessive water intake
• Diabetes insipidus (DI)
• Acute renal insufficiency
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Symptoms and Signs – Differential Diagnosis of Hypophosphatemia
• Decreased intake (prolonged starvation, hyperalimentation, or IV infusion without phosphate)
• Malabsorption
• Phosphate-binding antacids
• Renal loss: renal tubular acidosis (RTA), Fanconi’s syndrome, vitamin D–resistant rickets, tyrosinase-negative oculocutaneous albinism (ATN) (diuretic phase), hyperparathyroidism (primary or secondary), familial hypophosphatemia, hypokalemia, hypomagnesemia, acute volume expansion, glycosuria, idiopathic hypercalciuria, acetazolamide
• Transcellular shift into cells: alcohol withdrawal, diabetic ketoacidosis (DKA) (recovery phase), glucose-insulin or catecholamine infusion, anabolic steroids, total parenteral nutrition, theophylline overdose, severe hyperthermia, recovery from hypothermia, “hungry bones” syndrome
• Decreased intake (prolonged starvation, hyperalimentation, or IV infusion without phosphate)
• Malabsorption
• Phosphate-binding antacids
• Renal loss: renal tubular acidosis (RTA), Fanconi’s syndrome, vitamin D–resistant rickets, tyrosinase-negative oculocutaneous albinism (ATN) (diuretic phase), hyperparathyroidism (primary or secondary), familial hypophosphatemia, hypokalemia, hypomagnesemia, acute volume expansion, glycosuria, idiopathic hypercalciuria, acetazolamide
• Transcellular shift into cells: alcohol withdrawal, diabetic ketoacidosis (DKA) (recovery phase), glucose-insulin or catecholamine infusion, anabolic steroids, total parenteral nutrition, theophylline overdose, severe hyperthermia, recovery from hypothermia, “hungry bones” syndrome
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Symptoms and Signs – Differential Diagnosis of Hypopigmentation
• Atopic dermatitis
• Chemical leukoderma
• Idiopathic hypomelanosis
• Nevoid hypopigmentation
• Oculocutaneous albinism
• Phenylketonuria (PKU)
• Sarcoidosis
• Scleroderma
• Systemic lupus erythematosus (SLE)
• Tinea versicolor
• Vitiligo
• Atopic dermatitis
• Chemical leukoderma
• Idiopathic hypomelanosis
• Nevoid hypopigmentation
• Oculocutaneous albinism
• Phenylketonuria (PKU)
• Sarcoidosis
• Scleroderma
• Systemic lupus erythematosus (SLE)
• Tinea versicolor
• Vitiligo
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Symptoms and Signs – Differential Diagnosis of Hypopituitarism
• Acquired: the result of destruction of pituitary cells caused by
• Congenital: mutations in transcription factors produce multiple hormonal deficiencies. Mutations in genes produce single hormonal deficiency.
• Infiltrative disease, including sarcoidosis, hemochromatosis, histiocytosis X, Wegener’s granulomatosis, lymphocytic hypophysitis, and infection of the pituitary (tuberculosis,
• Pituitary apoplexy: hemorrhage or infarction of the pituitary gland. Predisposing factors include diabetes mellitus, anticoagulation therapy, head trauma, and radiation therapy. Sheehan’s syndrome: postpartum necrosis, a rare complication after pregnancy.
• Pituitary tumors: classified by size (microadenomas, <10 mm; macroadenomas, >10 mm) and function. Prolactin-secreting tumors and nonfunctioning tumors account for the majority of pituitary adenomas.
• Primary empty sella syndrome: flattening of the pituitary gland caused by extension of the subarachnoid space and filling of cerebrospinal fluid into the sella turcica
• Suprasellar tumors: craniopharyngiomas are the most common.
mycosis, syphilis)
• Acquired: the result of destruction of pituitary cells caused by
• Congenital: mutations in transcription factors produce multiple hormonal deficiencies. Mutations in genes produce single hormonal deficiency.
• Infiltrative disease, including sarcoidosis, hemochromatosis, histiocytosis X, Wegener’s granulomatosis, lymphocytic hypophysitis, and infection of the pituitary (tuberculosis,
• Pituitary apoplexy: hemorrhage or infarction of the pituitary gland. Predisposing factors include diabetes mellitus, anticoagulation therapy, head trauma, and radiation therapy. Sheehan’s syndrome: postpartum necrosis, a rare complication after pregnancy.
• Pituitary tumors: classified by size (microadenomas, <10 mm; macroadenomas, >10 mm) and function. Prolactin-secreting tumors and nonfunctioning tumors account for the majority of pituitary adenomas.
• Primary empty sella syndrome: flattening of the pituitary gland caused by extension of the subarachnoid space and filling of cerebrospinal fluid into the sella turcica
• Suprasellar tumors: craniopharyngiomas are the most common.
mycosis, syphilis)
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Symptoms and Signs – Differential Diagnosis of Hypoproteinemia
• Chronic diseases
• Cirrhosis
• Low-protein diet
• Malabsorption
• Malnutrition
• Neoplasms
• Nephrosis
• Overhydration
• Pregnancy
• Severe burns
• Chronic diseases
• Cirrhosis
• Low-protein diet
• Malabsorption
• Malnutrition
• Neoplasms
• Nephrosis
• Overhydration
• Pregnancy
• Severe burns
