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Altered hormonal function - Coggle Diagram

- - - - connected with
      - connected with
      - connected with
- - - - pathophysiology
        
        impaired hypothalamic osmoreceptors due to trauma or surgery, leading to insufficient ADH levels that results in inability to concentrate or retain water
      - diagnostic criteria
        
        history of recent brain surgery or head trauma, signs of dehydration, enlarged bladder due to over-filling, highly dilute urine with low specific gravity, hyperosmolality
      - clinical manifestations
        
        polyuria (large volume urine output), excessive thirst, shock, death
      - treatment
        
        drinking enough water to replace fluid loss, IV hypotonic solution, antidiuretics (e.g. desmopressin)
- - - - pathophysiology
        
        excessive secretion of ectopic ADH due to a tumor; high levels of ADH stimulate water retention and lead to hypotonic hyponatremia
      - treatment
        
        water restriction, isotonic or hypertonic IV saline, drugs to block effects of ADH or to increase urine output, surgery to remove tumor
      - clinical manifestations
        
        anorexia, nausea/vomiting, headache, irritability, disorientation, muscle cramps, weakness, psychosis, gait disturbances, seizers, coma
      - diagnostic criteria
        
        hyponatremia, hypotonicity, decreased urine output, concentrated urine with high sodium content, absence of renal, adrenal, or thyroid abnormalities
- - - - pathophysiology
        
        impaired ability to metabolize or eliminate hormones, leading to excess circulation levels of hormones
- - - - pathophysiology
        
        excessive thyroid hormone due to excessive stimulation of thyroid gland (e.g. Graves disease), diseases of thyroid gland, or excessive production of TSH by pituitary adenoma
      - clinical manifestations
        
        enlarged thyroid gland (goiter), protrusion of the eyeballs (exophthalmos), signs and symptoms of excessive metabolic rate: weight loss, agitation, restlessness, sweating, heat intolerance, diarrhea, tachycardia, palpitations, tremors, fine hair, oily skin, irregular menstrual cycle, weakness
      - diagnostic criteria
        
        family history of autoimmune disease, thyroid disease, or emigration from iodine-deficient location, enlarged and slightly firm thyroid, protrusion of the eyes, TSH levels and serum/free thyroxine levels, increased uptake of radioactive iodine by the thyroid gland
      - treatment
        
        goal is to reduce thyroid hormone levels through gland destruction via radioactive iodine, drugs that block thyroid hormone production, or surgery to remove all or part of the gland, thyroid replacement therapy if the glad is fully removed
    - - pathophysiology
        
        condition of prolonged exposure to elevated levels of either endogenous or exogenous glucocorticoids
        
        long-term administration of corticosteroid medication
        
        pituitary gland tumors that stimulate excess ACTH production
        
        adrenal grand tumors that stimulate excess cortisol production
        
        ectopic production of ACTH or CRH from tumor at a distant site (e.g. small cell lung carcinoma)
      - diagnostic criteria
        
        24-hour urine collection to check if cortisol levels are elevated, imagining studies to locate tumors
      - clinical manifestations
        
        obesity of the trunk, face ("moon face") and upper back ("buffalo hump"), stretch marks, weakness and muscle wasting, thin skin, osteoporosis, increased infections, skin ulcerations, poor wound healing, glucose intolerance that may lead to diabetes mellitus, euphoria, emotional disturbances, psychosis; sometimes hypertension, hypokalemia, excessive body and facial hair (hirsutism)
      - treatment
        
        surgery or radiation to remove tumors, gradual withdrawal of corticosteroid medications
- - - - pathophysiology
        
        deficient thyroid hormone due to congenital causes (lack of thyroid gland development, lack of appropriate synthesis of thyroid hormone, or problems with TSH secretion)
        
        deficient thyroid hormone due to acquired causes (deficient thyroid hormone synthesis, destruction of thyroid gland, impaired TSH or THR secretion) due to autoimmunity, iodine deficiency, surgical removal or radiation therapy to thyroid gland, medications that destroy thyroid gland, or genetic defects that affect thyroid hormones
      - diagnostic criteria
        
        TSH assay, free T4, total T4, and T3 uptake, thyroid autoantibodies, and antithyroglobulin tests are used to confirm diagnosis (serum thyroid hormone is typically decreased while TSH is often elevated)
      - clinical manifestations
        
        fatigue, cold intolerance, weakness, weight gain, dry skin, coarse hair, constipation, lethargy, impaired reproduction, impaired memory, enlarged gland (goiter), nonpitting edema of face, mucous membranes, hands, feet (myxedema)
      - treatment
        
        goal is to replace deficient hormone with thyroid hormone replacement therapy (e.g. levothyroxine)
    - - pathophysiology
        
        adrenal cortical insufficiency
        
        lack of ACTH production from the pituitary due to destruction of the pituitary gland from tumors, hemorrhage, trauma, radiation, or surgical removal
        
        lack of hormones secreted from the adrenal cortex
        
        autoimmune destruction of adrenal cortex leading to inability of the adrenal glands to produce any glucocrticosteroids
        
        adrenal gland destruction due to tuberculosis
      - clinical manifestations
        
        if deficient glucocorticoids
        
        hypoglycemia, weakness, poor stress response, fatigue, anorexia, nausea/vomiting, weight loss, personality changes
        
        if deficient mineralocorticoids
        
        dehydration, hyponatremia, hyperkalemia, hypotension, weakness, fatigue, shock
        
        if deficient androgens
        
        sparse axillary and pubic hair in women
      - diagnostic criteria
        
        clinical presentation combined with hyponatremia and hyperkalemia, depressed corticosteroid levels after ACTH administration
      - treatment
        
        isotonic IV fluids with hydrocortisone, oral replacement of glucocorticoid and mineralocorticoid hormones, increased salt intake in hot weather to correct excessive sodium excretion, antibiotics to treat tuberculosis
- - - - decreased number of receptors
      - lack of receptor sensitivity to hormone
      - antibodies that block receptor sites or occupy receptor sites and mimic hormone
      - tumor cells with receptor activity that deprives the unaffected cells of hormone