| Condition | Description | Cause | Manifestation | Treatment |
|---|---|---|---|---|
| Hypopituitarism | Decrease secretions of one or more of the 8 hormones normally produced by the pituitary gland at the base of the brain | ACTH: life threatening, nausea, vomiting, anorexia, fatigue, weakness – this hormone is lost last TSH : cold intolerance, skin dryness, myexedma, lethargy – lost second last FSH and LH: ammennorhea, atrophy of reproductive organs – lost second and third GH: growth failure in children, social withdrawal, fatigue, decrease in well being for adults – lost first | find underlying cause | |
| Hyperpituitarism | Pituitary gland too active in the secretion of hormones | Benign tumours | Headaches, fatigue, neck pain, stiffness, seizures, acromegaly | treat underlying cause |
| Acromegaly | Excess production of GH in adults | Benign tumour | Small bones continue to grow, soft tissue continues to grow, organ enlargement, excessive sweating, oily skin, heat intolerance, parenthesis | remove tumour, radiation, medication to inhibit GH |
| Diabetes Inspidus | Insufficient ADH due to neurogenic, nephrogenic or psychogenic causes resulting in diluted urine, polydispia and polyuria | Neurogenic: disruption of synthesis, transportation or release of ADH in the brain Nephrogenic : damage at nephron causes the ADH to not reach the target cells, leading to no reabsorption of water Psychogenic: from extreme consumption of water | Excessive urination, excessive thirst, dry skin, muscle weakness, electrolyte, imbalance | treat underlying cause, injections of ADH |
| SIADH | Excess ADH Urine is concentrated and urination is infrequent, blood is thin and dilute | Head trauma, brain tumour, any surgery, infection, pain and stress | Watery blood, concentrated urine, equal output and input of sodium, lack of peripheral edema | Treat underlying problem |
| Addison’s Disease | Lack of cortisol and aldosterone secretions | Auto-immune destruction of glandular tissue, infections, metastasis from lung and breast cancer, surgery and trauma to area around the adrenals | symptoms occur after 80% of functional tissue is present. Hyper-pigmentation of skin, vitiligo, postural hypotension | Treat underlying cause, drug replacement therapy, salt tablets |
| Secondary Adrenal Cortex Insufficiency/Secondary Hypocortisolism | Little of no ACTH is present. Adrenals, as a result of not being stimulated, atrophy and corticosteroids become depleted | Tumour on the pituitary or hypothalamus, removal of pituitary gland, sudden withdrawal from corticosteroid medication | Similar to Addison’s but aldosterone and potassium levels remain normal | Treat underlying cause |
| Cushing’s Disease | Excess ACTH that leads to excess in cortisol | Exogenous administration of corticosteroids over a long period of time, pituitary tumour, tumour in adrenals, autoimmune hyperplasia | Weight gain, muscle weakness, altered fat metabolism, thin skin, back pain, hirsutism in females, electrolyte imbalance | Treat underlying cause |
| Primary Aldosteronsim | Excessive Secretion of aldosterone | Aldosterone producing benign adenoma of adrenal cortex, idiopathic adrenal hyperplasia | Hypertension, hypokalemia, pseudohypocalcemia | Treat underlying cause |
| Hypothyroidism | Under-active thyroid | Injury, progressive loss of functional thyroid tissue, thyroid gland removal, iodine deficiency, lack of thyroid | Gradual weakness and fatigue, unexplained weight gain, loss of appetite, cold intolerance, dry, cold, pale, yellow skin, puffy face, husky voice | |
| Hyperthyroidism | Over-active thyroid | Grave’s Disease, excessive thyroid hormone replacement for hypothyroidism | Hunger, weight loss, moist, warm skin, increased perspiration to rid body of excessive heat | Anti-thyroid drugs, radioactive iodine therapy, surgery |
| Diabetes Mellitus | Chronic disorder of carb, fat and protein metabolism. Classification: Type 1: Insulin dependent diabetes mellitus Type 2: Non-insulin dependent Gestational Pre-Diabetes | Type 1: anti-islet cell antibodies attack Beta-cells, onset occurs usually before 20, often related to genetics and keto-acidosis Type 2: adult onset after 30, insulin resistance occurs, number of beta cells decreases | Increase urination, increased thirst, increased appetite, hyperglycaemia, extreme fatigue, weight change, tingling/numbness in hands | Insulin pump, monitor sugar instake |
Dylan Crake RMT & R.KIN 
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