Ch40 Endocrine disorders

Primary: intrinsic malfunction of the hormone producing target gland

Secondary: malfunction of the hypothalamus pituitary cells that control the hormone -producing target gland

Primary target is the liver 

-Increase lean body mass, reduce fat mass, and induces the liver to release glucose under conditions of hypoglycemia

• -Decrease GH secretion 
• -defective GH action 
• -defective IGF-1 (somatomedin) generation

• birth history of labor or breech delivery 
• midline craniocerebral defects 
• congenital malformation/chromosomal anomaly 
• mystagmus, retinal abnormalities, midline of midfacial abnormalities (cleft lip/palate)

• diminished lean body mass 
• hypercholesterolemia 
• decreased bone density 
• treatment w/ individualized therapy

• uncontrolled production by a tumor in the pituitary (somatotropic tumor) 
• stimulates liver to produce IGF-1
• together cause up-regulated growth of soft and bony tissue

• occurs in childhood before skeletal epiphyses are closed 
• Acromegaly: occurs in adults

GH excess that occurs in adults

• surgical removal of tumor 
• counteracting effects of GH (octreotide, synthetic somatostatin)
• may be radiation

• TSH that are secreted from the anterior pituitary
• regulators of metabolism

• congenital/acquired 
• majority are primary due to intrinsic dysfunction of the thyroid gland 
• congenital hypothyroidism (cretinism) due to thyroid dysgenesis

• defects in TSH production 
• results from: head trauma, cranial neoplasms, brain infections, cranial irradiation, neurosurgical procedures

• dull appearance, thick, protuberant tongue, thick lips (=feeding difficulties)
• prolonged neonatal jaundice
• poor muscle tone 
• bradycardia, mottled extremities 
• umbilical hernia 
• hoarse cray

• weakness, lethargy, cold intolerance, decreased appetite 
• bradycardia, mild/moderate wt gain 
• elevated serum cholestrol and triglycerides 
• enlarged thyroid, dry skin, constipation 
• depression, difficulties with concentration/memory 
• menstrual irreg.

• will manifest as elevated TSH 
• hypothalamic-pituitary dysfunction results in low levels of TSH and T4

• levothyroxine 
• intravenous levothyroxine used for myxedema coma

• increased T4 and T3 (Graves disease) 
• thyroid follicular cell destruction with release of preformed T4 and T3 (Hashimoto thyroiditis)
• ingestion of excessive thyroid hormone/iodide preparation

autonomous

mediated thru stimulation of TSH receptors by substances such as TSH 

Autoimmune - related to S=TSH receptor antibodies

• pituitary adenoma
• thyroid carcinoma
• inflammation of thyroid follicular cells 
• ingestion of thyroid hormone preparations/excessive iodides 
• toxic goiter 
• common in women

will manifest as undetectable TSH levels and serum T4 and T3

• from hyperthyroidism 
• -a form of life-threatening thyrotoxicosis that occurs when excessive amts of thyroid hormones are acutely released into circulation

• B-blockers 
• antithyroid drugs, thioamides
• radioactive iodine treatment 
• surgical removal of thyroid gland (for tumors)
• pituitary adenoma surgically removed

• achieve metabolic balance 
• antithyroid drugs, follow by iodine adm.
• B-blockers for symptoms and control blood pressure 
• antipyretic therapy
• fluid replacement
• glucocorticoids

synthesizes glucocortiocoids, mineralocorticoids, and androgens 

cortisol is primary glucocorticoid and negative feedback suppresses ACTH release

• primary: hyposecretion due to disease of adrenal cortex (Addison disease) 
• Seconardy: inadequate secretion of ACTH from anterior pituitary
• Tertiary: lack of CRH secretion from hypothalamus due to hypothalamic malfunction or injury

caused be destruction of adrenal gland

• hypothalamic-pituitary dysfunction 
• related to corticosteroid therapy, which suppresses ACTH, CRH

life threatening condition caused by inadequate levels of glucocorticoids and mineralocorticoids in circulation

replace absent/deficient hormones - to mimics natural production

• intraenous glucocorticoids 
• volume replacement

• congenital adrenal hyperplasia 
• enzyme needed for cortisol production lacking due to gene defect

glucocorticoids

• primary adrenocortical hyperfunction (due to adrenal adenoma) 
• secondary: cause by hyperfunction of anterior pituitary ACTH secreting cells 
• Tertiary: by injury

• type of hypercortisolism 
• -used to describe the clinical features of hypercortisolism, regardless of cause

diagnosis reserved for pituitary dependent conditions of hypercortisolism

• excessive production of pituitary ACTH
• exogenous steroid - common cause of Cushing syndrome

• round face w/ flushed cheeks, 'moon facies'
• wt gain w/ excess total body fat (esp in abdomen)
• decreased muscle mass, muscle weakness
• glucose intolerance, hyperglycemia
• hypertension 
• osteoporosis
• ^ androgen production = excessive hair prod., acne, menstrual irreg.

• ACTH measurement: 
• --primary = low ACTH 
• --seconardy = high ACTH 
• urinary free cortisol levels 
• dexamethasone suppression test

treat based on etiology

primary - Conn syndrome; usually due to aldosterone-secreting tumors 

Secondary - associated with poor kidney perfusion that stimulates the RAAS cascade (heart failure, reduced kidney perfusion, liver cirrhosis)

• salt and water retention 
• low K+ level

• spironolactone to increase sodium excretion and potassium retention 
• sodium restriction and K+ replacement may be

• part of the adrenal medulla 
• secretes catecholamines, norepinephrine and epinephrine 
• a tumor of chromaffin tissue - excessive production and release of catecholamines

• hypertension 
• headache, tachycardia, diaphoresis
• tremor nervousness, 
• hypermetabolic state with fever, wt loss, polyuria, and polydipsia

• sympathetic blocking meds to manage bp 
• surgical removal of tumor 
• meds to block catecholamine prod

• detect [Ca+] and help maintain constant levels thru regulation of Ca+ absorption and resorption from bone
• absorption of Ca+ from intestine and renal tubules is vitamin D dependent and may be impaired in conditions in which vitamin D is deficient (renal failure)

• serum Ca+ levels provide the feedback to regulate PTH
• decrease in Ca+ causes PTH release 
• elevated Ca+ levels lead to suppression of PTH secretion

PTH increases osteoclastic activity, and increases renal Ca+ reabsorption

• produced by thyroid parafollicular cells of parathyroid hormone 
• controls calcium content of blood by increasing bone formation by osteoblasts and inhibit bone breakdown by osteoclasts 
• decrease blood Ca+ levels and promotes conservation of hard bone matrix

• despite ^ Ca+ level, PTH cont. to be secreted 
• -genetic origin
• -parathyroid adenoma
• -hyperplasmia of parathyroid glands

can result from reduced production of active Vita D (impairs Ca absorption)

• kidney stones 
• osteoporosis
• polyuria and dehydration 
• anorexia, nausea, vomit, constipaton 
• bradycardia, heart block ,and cardiac arrest

serum Ca+ levels are elevated wtih low to normal phosphorus levels

surgically remove parathyroid gland

• serum Ca+: low 5-7 mg/dl 
• Phosphorus Lvl: high 7-12 mg/dl 
• levels of antibodies to parathyroid glands are high if autoimmune mechanism is present

oral calcium supplement with Vita D

• are vasopressin secreted by posterior pituitary gland - response to blood osmolality 
• acts directly on renal collecting ducts and distal tubules, ^ membrane permeability to and reabsorption of H2O

disorder of insufficient ADH activity = excessive loss of water in urine

• excessive ADH due to tumors, tb
• results in hyponatremia

• hyponatremia
• high urine osmolality
• low serum osmolality
• weakness, muscle cramps,

• free water restriction 
• if severe, IV adm of saline with diuretics 
• hyponatremia corrected slowly to avoid rapid changes in brain cell volume