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103 Cards in this Set
- Front
- Back
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Hypopituitarism
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Decreased secretion of pituitary hormone; 70-90% of anterior pituitary destroyed before symptoms develop; causes: tumors, surgery, lesions, infections, genetic disease; ACTH deficience is most serious deficiency with hypopituitarism
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Hypofunction of Endocrine
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Under secretion; congenital defects, infection, inflammation, autoimmune, neoplasms, altered blood flow to gland, aging, atrophy secondary to drug therapy, defective receptor sites
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Hyperfunction of Endocrine
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Over secretion; excessive hormone production, hyperplasia of gland, tumor
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Growth Hormone
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Somatotropin hormone; necessary for growth and metabolic functions, secreted during lifespan, contributes to growth of epiphyseal plates in long bones, stimulated by: hypoglycemia, fasting, starvation, stress, exercise
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GH Excess (adults)
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Acromegaly; most common cause is adenoma (tumor); enlargement of small bones in hands and feet; enlargment of soft tissues (pronounced brow, nose, jaw); enlarged heart usually leads to death
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Hyperthyroidism
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Excessive thyroid hormone delivery to tissue; causes: autoimmune disorders, excess secretion of TSH from pituitary gland, neoplasms, excessive intake of thyroid medications
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Manifestations of Hyperthyroidism
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Increased metabolism, restlessness, diarrhea, weightloss, heat intolerance
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Grave's Disease
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Antibodies stimulate thyroid hormone via TSH receptors; cause unknown; seen more in women 20-40; goiter and exophthalmos
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Control of Thyroid
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Secretion of thyroid hormone is controlled by hypothalmic-pituitary-thyroid feedback system; TRH controls release of TSH which promotes release of TH from thyroid gland; increased levels of TH inhibit secretion of TRH, thus inhibiting the release of TSH
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Actions of Thyroid Hormone
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Increases metabolism, protein synthesis
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Goiter
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Hyperplasia of thyroid gland
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Hypothyroidism
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Congenital: results in mental retardation (cretinism- disease associated with untreated hypothyroidism) Acquired: thyroidectomy, radiation, antithyroid meds, iodine deficience, autoimmune disorder (Hashimoto's Thyroiditis)
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Manifestations of hypothyroidism
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Decreased metabolic state, weakness/fatigue, weight gain, cold intolerance, dry skin, constipation, mental dullness, lethargy, myxedematous coma
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Thyroid Storm
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life threatening coma, rare, precipitated by: stress, trauma, manipulation; fever, tachycardia, heart failure, angina, agitation, restlessness
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Adrenal Cortex
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Outer portion of the gland, steroid hormones, hormones are all synthesized from cholesterol, cells of the adrenal cortex are stimulatied by ACTH from anterior pituitary
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Hormones of Adrenal Cortex
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Essential for survival; play a role in stress, metabolism, and inflammatory (reduce inflammation) process. Glucocorticoids, Mineralcorticoids, Mineral Corticoids
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Glucocorticoids
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ex. cortisol - Have direct effects on carbohydrate metabolism; they increase blood glucose concentration by promoting stimulating glucose production (gluconeogenesis) in the liver and decreasing use of glucose in muscle, adipose tissue, and lymphatic tissue; contribute to emotional state
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Cortisol
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most potent occurring glucocorticoid; regulated by the hypothalamus and interior ptuitary gland; ACTH is the main regulator of cortisol secretion
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Mineralcorticoids
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Aldosterone: regulated by RAAS
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Hypothalamus>Pituitary>Adrenal Cortex>Adrenal Medulla
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Hypothalamus (CRH)> Anterior Pituitary (ACTH)> Adrenal Cortex (corticosteroids, mineralcorticoids, androgens)> Adrenal Medulla (catecholemines)
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Adrenal Medulla
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Secretes epinephrine and norepinephrine *disorders of the adrenal cortex or adrenal medulla result in changes in the production of adrenocorticotropic hormone (ACTH)
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Congenital Adrenal Hyperplasia
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Autosomal recessive trait; deficiency in cortisol synthesis; increased levels of ACTH and adrenal hyperplasia; may have Na loss; may have enlarged genitalia
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Cushing's Syndrome
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Chronic disorder in which hyperfunction of the adrenal cortex produces excessive amounts of circulating cortisol or ACTH; more common in females 30-50; Patho: Pituitary tumor (ACTH excess causes excess adrenal hormone), adrenal cortex tumor (stimulate corticoids/mineralcorticoids),long term glucocorticoid therapy
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Manifestations of Cushing's
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BOHEMI: Buffalo hump, obesity, hairy, emotional, moonface, increase susceptibility; SSSS-sugar, salt, sex, stria..sugar causes liver to release glucogen, salt-excess aldosterone, decreased libido, stretch marks
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Addison's Disease
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Chronic deficiency of cortisol, aldosterone, adrenal androgens; more common in women
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Pathophysiology of Addison's
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autoimmune destruction of adrenal; cancer, fungal, cytomegalovirus; bilateral adrenal hemorrhage from anticoagulant therapy; ACTH def. from pituitary tumor/surgery/irradiation; abrupt withdrawal from long-term high-dose steroid therapy
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Manifestations of Addison's
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slow onset; hyponatremia, hyperkalemia, fluid volume loss, hypotension, hypoglycemia, hyperpigmentation *opposit man. of Cushing's
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Addisonian Crisis
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life threatening response to acute adrenal insufficiency; primary symptoms are high fever, weakness, abdominal pain, severe hypotension, circulatory collapse, shock, coma; treat-rapid fluid replacement and glucocorticoids
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Energy Metabolism (Alpha Cells)
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Alpha- Glucogen: stimulates breakdown of glycogen in the liver (glycogenolysis), formation of carbs in liver (glyconeogenesis) and the breakdown of lipids; primary function is to increase blood glucose levels; acts when blood glucose levels falls below app. 70mg/dl
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Energy Metabolsism (Beta cells)
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Insulin- transports glucose into cells and transports potassium; decreases blood glucose levels by assisting glucose into the cells; release is regulated by blood glucose levels- levels rise within minutes of eating; inhibit breakdown of stored fat
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Energy Metabolism (Delta cells)
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Somatostatin-inhibits production of glucagon and insulin
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Glycogenolysis
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breakdown of glycogen stores to produce glucose
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Glyconeogenesis
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formation of glycogen in the liver from non-carbohydrate sources such as amino acids and lactates
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Catecholamines
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help to maintain blood glucose levels during periods of stress by inhibiting insulinrelease and promoting glycogenolysis
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Growth Hormone (blood glucose regulation)
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increases level of blood glucose by decreasing cellular uptake of glucose
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Glucocorticoid Hormone (Glucose level relation)
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Increase blood glucose levels by stimulating gluconeogenesis
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Glucose for Cellular Metabolism
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all organs require insulin for glucose uptake except brain, liver, intestines, and renal tubules
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Diabetes Mellitus
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Leading cause of renal failure; contributes to CAD
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Type I DM
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autoimmune reaction that destroys beta cells; beta cells of pancreas no longer produce insulin (absolute deficiency); genetic/environmental
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Type II DM
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Inadequate or insufficient amount of insulin secretion; enough insulin to prevent ketones
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Hyperglycemia
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Polyuria, Polydipsia, Polyphagia, glycosuria, dry/flushed skin, fruity breath, Kussmaul respirations, vision problems, fatiques, parethesias, skin infection
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Diabetic Ketoacidosis
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Ketone production by the liver exceeds cellular use and renal excretion; blood glucose>250 mg/dL-600; pH <7.3
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Hyperglycemic Hyperosmolar Nonketotic Syndrome
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serum osmolality >340; blood glucose >600
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Hypoglycemia
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excess insulin in blood; error in insulin dose; failure to eat; increased exercise; rapid onset; altered cerebral function
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what releases insulin and glucagon
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pancreas
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what releases T3/T4
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thyroid gland
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what is responsible for metabolism & protein synthesis
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T3/T4
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what releases cortisol and aldosterone |
adrenal cortex
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what releases epi and norepinephrine
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adrenal cortex
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what releases ADH and oxytocin
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hypothalamus
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what releases PTH
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parathyroid
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what controls calcium levels
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parathyroid
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what do high cortisol levels do to corticotropin
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inhibits it
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what can low calcium cause
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seizures
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what can high calcium cause
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cardiac arrythmias, muscle bone weakness, renal calculi
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how does low/absent cortisol liver
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decreased glucose output in liver --> hypoglycemia --> profound hypoglycemia --> coma and death
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how does low cortisol affect stomach
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decrease in digestive enzymes --> vomiting, cramps, diarrhea --> hypoglycemia --> shock --> coma/death
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how does low aldosterone affect kidneys
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sodium/water loss --> hypoglycemia --> shock --> coma/death potassium retention--> arrythmias & decr. cardiac output-->hypotension --> shock --> coma/death |
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s/s that may indicate Addison's disease
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* confusion, fatigue * GI disturbances / weight loss * hyperkalemia (potassium) * hyperpigmentation * hypoglycemia *hyponatremia (sodium) *hypotension (BP) * muscle weakness |
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tests that determine Addison's disease
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Plasma and urine tests (which detect decr. corticosteroid concentrations high level corticotropin levels = primary low " " = secondary |
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treatment for Addison's disease
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lifelong corticosteroid replacement
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3 forms of Cushing's syndrome
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* primary - caused by adrenal cortex disease *secondary (most common 70% of cases) caused by hyperfunction of ant. pituitary gland (corticotropin secreting cells) * tertiary - cause by hypothalamic dysfunction/injury |
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complications of Cushing's
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*osteoporosis (b/c of incr. calcium resorption from bone) * peptic ulcer *lipidosis (fat metab. disorder) * impaired glucose tolerance |
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percent of population with DM I
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5-10%
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what electrolytes are decreased with HHNK
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NA - sodium (normal: 135-145) K - Potassium (3.5 - 5.0) P - phosphorus (2.5-4.5) |
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why are electrolytes decreased with HHNK
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because of excessive ostomic diuresis |
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what contributes to hyperosmolarity in HHNK
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(water loss > glucose/electrolyte loss)
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define hyperosmolarity
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extremely high blood sugar levels
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why do pts have osmotic diuresis with HHNK conditions
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b/c all the glucose in kidneys cannot be reabsorbed, so it gets urinated out as an alternative
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what is effect of decreased Na, K in HHNK?
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low K - Heart dysrhythmia (Use defibrillator!) Causes a rise in the ECG’s U wave. Skeletal and Smooth Muscle Weakness/paralysis; weak pulse, shallow/ ineffective respirations d/t weakness of skeletal muscles low Na - confusion, headache, increased urine output, decreased specific gravity, nausea, |
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when you see hyperosmolality (high blood sugar levels), what labs would be evident
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sodium (normals: 135-145) BUN ( 10-20) creatinine (0.5 - 1.5) |
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what levels are considered pre-diabetes
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fasting glucose: 100-125 2 hr glucose: 140-199 AIC: 5.7 - 6.4% |
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what are classic symptoms of hyperglycemia
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polyuria polydipsia polyphagia |
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what numbers are considered diabetes
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FPG: >126 0r hyperglycemia signs and casual plasma glucose > 200 or 2 hr plasma glucose >200 or AIC > 6.5% (confirmation required: repeat testing on diff. day) |
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what is normal AIC
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<5.7%
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complications of persistent hyperglycemia
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stroke/CAD/PAD retinopathy nephropathy neuropathy |
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s/s hypoglycemia
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dizzy hungry anxiety headache sweating, trembling mood changes blurred vision tired/pale |
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s/s hyperglycemia
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dry mouth thirsty oliguria drowsy bed wetting stomach pains |
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s/s hypothyroid
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HYPOMETABOLIC (TOO LITTLE T3 / T4) Decreased BMR Hypothermia, Cold Intolerance anorexia (late sign: weight gain) Bradycardia (WeaknessLethargyMental impairment) Constipation Coarse Hair , receding hair line dull-blank expression , facial / eyelid edema (myxedema) |
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s/s hyperthyroid
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HYPERMETABOLIC (TOO MUCH T3 / T4) Increased BMR HyperthermiaHeat intolerance Weight loss Tachycardia (TremorSleeplessAnxiety) DiarrheaThin Hair |
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what is disease associated with hyperthyroid
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GRAVES DISEASE
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what does T3/T4 and TSH levels look like in GRAVES DISEASE
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HIGH T3/ T4 low TSH |
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what do GRAVES DISEASE pts look like
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goiters protruded eyes eye swelling |
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patho behind GRAVES DISEASE
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autoantibodies stimulate TSH receptors on thyroid gland totrigger thyroid to release T3 and T4. |
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late clinical manifestations of HYPOTHYROID (HASHIMOTO)
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subnormal temp bradycardia weight gain low LOC thick skin cardiac complications |
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patho of HASHIMOTO
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autoimmune destruction of thyroid
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what happens to T3/T4 and TSH levels with HASHIMOTO
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T3/T4 (low) and thyroid stimulating hormone (high) |
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why do we need T4 / T3?
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necesary for normal growth development acts on many tissues to: INCR. metabolic activites and protein synthesis |
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why do we need cortisol
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helps w/ stress response - maintains BP/cardio function - breaks down proteins / mobilizes FFA - stimulates gluconeogenesis in fasting states - suppreses immune response / anti inflammatory -alters mood / behavior |
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why do we need aldosterone
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helps reabsorb Na helps excrete K by kidneys |
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what disease associated with hypocortisol
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addison's disease
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manifestations of Addison's disease
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(decreased cortisol and aldosterone) Weakness Hypotension Hypoglycemia Hyperpigmentation Hyperkalemia Weight Loss |
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causes of Addison's disease
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Destruction of the adrenal cortex Idiopathic or autoimmune Trauma (hemorrhage) Fungal disease or TB Neoplasia Long-term use of Steroids |
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effect of long term use of steroids with Addison's disease
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secondary disease (affecting pituitary gland)
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how are levels affected with Addison's disease
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decreased: aldosterone cortisol |
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what can Addison's disease lead to
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adrenal crisis (critical deficiency of aldosterone and cortisol affects liver, stomach, kidneys) |
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most important issue with hypopituitarism / cortisol
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don't abruptly stop long term corticosteroid therapy bc therapy has already suppressed pituitary corticotropin secretions and causes AG atrophy thus, must taper off instead. |
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effect of low aldosterone on kidneys and heart in Addison's disease
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(kidneys: Na/H20 loss/K retention --> hypoglycemia --> shock --> coma/death heart: decreased C.O. & arrythmias -> hypotension --> shock --> coma/death |
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effect of low cortisol ON LIVER AND STOMACH in Addison's disease
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Liver: decreased output -> hypoglycemia --> profound hypoglycemia --> coma / death stomach: decreased digestive enzymes --> vomiting/cramps/diarrhea --> hypoglycemia --> shock |
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normal levels for T3 , T4 AND TSH
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normals: T3: 60-80 T4: 4.5-11.5 TSH: 0.5-4.5 |
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S/S CUSHINGS DISEASE
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Hyperglycemia Muscle wasting fat redistribution (truncal, moon, dorsocervical)Hypertension hypokalemia Hirsutism |
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s/s ADDISON'S DISEASE
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Hypotension hyperkalemia Hyperpigmentation Weakness weight loss |
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IMPORTANT ISSUE WITH ADRENAL CRISIS
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When pts take meds (prednisone) for cortisol insufficiency, ant pituitary turns off ACTH. Over time --> adrenal cortex atrophy. If meds suddenly discontinued, and the adrenal cortex cannot synthesize cortisol, acute adrenal insufficiency occurs (a med. emergency) instead, taper pts off prednisone so adrenal gland has time to recover ability to synthesize cortisol. |
