PATHO FINAL

what is SIADH?
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Terms in this set (45)
what is SIADH?
high levels of ADH without a normal physiologic stimulus to release
symptoms of SIADH
water intoxication due to renal water retention or increased total body water --> dilutional hyponatremia, serum hypoosmolarity, urine hyperosmolarity-concentrated (in relation to serum), urine Na excretion = Na intake, normal adrenal and thyroid function, absence of conditions that alter volume status
causes of SIADH
ectopically produced ADH by cancer cells (small cell CA of Lung*, CA pancreas/duodenum; leukemia, lymphoma), brain injury or infection, postoperative fluid volume shifts, & medications
ADH triggers
dehydration stimulates renal tubular reabsorption of sodium and water, low BP, low salt & water concentration in the blood
diabetes insipidus
insufficient activity of ADH
causes of diabetes insipidus
neurogenic/central: absence of ADH
brain tumors, aneurysms, thrombosis, closed head injury

nephrogenic: inadequate response of renal tubules to ADH
pyelonephritis & some medications
signs/symptoms of diabetes insipidus
continuous thirst (polydipsia), polyuria, nocturia, low urine specific gravity, hypernatremia, hyperosmolality, low urine osmolality, dehydration develops without fluid replacement
Graves Disease
stimulation of thyroid by autoantibodies (TSI) present against the TSH receptor, antibodies stimulate T3 and T4, TH elevated & TSH suppressed, most common cause of thyrotoxicosis
signs/symptoms of Graves Disease
fatigue, goiter (thyroid enlargement), heat intolerance, increased GI motility, muscle weakness, weight loss with increased appetite, anxiety, depression, irritability, nervousness, atrial fibrillation, palpitations, systolic ejection murmur, eyelid retraction, lid lag, globe lag, enlargement of the ocular muscles, periorbital edema --> exophthalmos, stare, pruritus, smooth skin, sweating, warm/moist skin, pretibial myxedema, hyperactive deep tendon reflex, tremor, erectile dysfunction, gynecomastia, irregular menses
lab tests for graves disease
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hypothyroidismdeficient production of TH by thyroid glandsigns/symptoms of hypothyroidismtiredness, weakness, fatigue, social withdrawal, depression, weight gain, hoarseness, cold intolerance, raynaud's phenomenon, decreased sweating, thick/coarse hair, facial myxedema, loss of lateral third of the eyebrows, cold dry thickened skin, constipation, slowed speech, confusion, lethargy, anemia, hypoventilation, slow movement/reflexes, decrease in TH: slows metabolism/lowers BMR/leads to increased TSH production & goiterlab values for hypothyroidismincreased levels of TSH and decreased levels of TH, decreased serum TSH levels and BMRdiabetes mellitus type 1autoimmune destruction of beta cells of the pancreas (most common) - T cell mediated; affects metabolism of fats, PRO, and CHOsigns/symptoms of DM type 1polyuria (with glycosuria), polydipsia, polyphagia (increase in eating), weight loss: osmotic diuresis; loss of body tissues as fats & proteins are used for energy --> high levels of circulating ketones --> DKA; fatigue due to altered metabolism of food products, & wide fluctuations in blood glucose levelscauses of DM type 1?????lab tests for DM type 1??????Cushing's disease/syndromeexcessive anterior pituitary secretion of ACTH; secretion of cortisol and adrenal androgens is increased, cortisol-releasing hormone is inhibitedsigns/symptoms of cushing's syndrome**weight gain (trunk, facial, and cervical area), glucose intolerance, protein wasting, muscle wasting, loss of collagen in skin, hyperpigmentation of skin, HTN, suppression of immune system, mental status changes, hair growth (face, acne)diagnosis of addison's diseaseinadequate corticosteroid and mineralocorticoid synthesis; elevated serum ACTH due to a loss of negative feedback; caused by an autoimmune mechanism that destroys adrenal cortical cellsosteoblastsbone-forming cellsosteocytesosteoblasts that become imprisoned within the mineralized bone matrixosteoclastsreabsorb bone during growth and repairosteophytesbone spurs that occur in osteoarthritis; grow outward from the underlying bone --> bone deformitiesrhabdomyolysisCK (creatinine kinase) level - elevated; rapid breakdown of muscle with release of intracellular components into the blood and extracellular space including myoglobinsigns/symptoms of rhabdomyolysisclassic triad: muscle pain, dark urine, weakness9 fractureslinear, occult, oblique, spiral, transverse, complete, incomplete, open (compound), closedlinear fractureparallel to the long axis of the boneoblique fractureoblique angle to the shaft of the bonespiral fractureencircles the boneoccult fracturehidden or not readily discernabletransverse fracturestraight across the bonecomplete fracturebone broken all the way throughincomplete fracturedamage but bone is still in one pieceopen/compound fracturebreak through the skinclosed fracturenot through the skinosteoporosisdecrease in bone densityrisk factors of osteoporosisgenetic, anthropometric, hormonal and metabolic, dietary, lifestyle, co-morbidities, medicationspathology of osteoporosischildhood/teenage years: new bone is added faster (formation) than old bone is removed (reabsorption) peak bone mass: reached at age 30 after 30: reabsorption > formation women: most rapid first years after menopause men: also at risk, but start with high bone densityosteoarthritis (OA) - degenerative joint diseasedisorder of synovial jointspathology of OAlocal loss/damage of articular cartilage, narrowing of the joint space due to cartilage loss, formation of bone spurs (osteophytes): grow outward from the underlying bone --> bone deformities; changes in subchondral bone: sclerotic bone & cyst formationsigns/symptoms of OAjoint pain (usually weight bearing), nocturnal pain, referred pain, stiffness, enlargement/swelling, tenderness on palpation, limited ROM, deformityrheumatoid arthritissystemic inflammatory autoimmune diseasecause of rheumatoid arthritisinflammation starts in the synovial membrane which lines the joint cavity, then spreads to the articular cartilage, fibrous joint capsule, surrounding ligaments, tendonspathology of rheumatoid arthritis1. neutrophil activation in the synovial fluid --> degrades articular cartilage surface 2. cytokines (TNF-alpha) stimulates synthesis of proinflammatory (IL-6, IL8) chondrocytes attack cartilage 3. synovium digest nearby cartilage