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459 Cards in this Set
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what does the thyroid gland do?
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1.It controls metabolic rate by
2.It stores T3 and T4 3.It takes Iodide from blood and turns it in to T3 and T4 |
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What is metabolic rate?
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energy expenditure, oxygen consumption, and heat production. all can go either up or down depending on activity of thyroid.
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What is the deal with the follicles inside the thyroid gland?
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the follicles are filled with thyroglobulin proteins which store T3 and T4. These hormones are synthesized because thyroid is highly vascular, and Iodide is removed from GI, converted to Iodine, and formed into T3 and T4 which is stored in follicles.
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what are the METABOLIC activities that the thyroid gland controls?
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causes the BMR to increase or decrease, thus increasing or decreasing the energy and oxygen used, and the amount of heat produced.
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do thyroid hormones have local or widespread effects?
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systemic, because it effects all cells.
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thyroxine (T4)
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lasts longer and there's more of it.
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tri-iodothyronine (T3)
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has a shorter duration, but more of it is activated.
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what are the functions of thyroid HORMONES?
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1. increase BMR (heat, energy, O2)
2. affects protein metabolism (increases synthesis of proteins essential for growth and dev) 3. affects carb metabolism (increasing synthesis of glucose, cellular uptake of glucose, and absorption of glucose from GI) 4. sensitizes tissues to SNS stim (E & NE) |
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how do T3 and T4 work in a feedback mechanism?
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low T3 and T4--> hypotal secretes TRH--> pituitary release TSH--> TSH causes T3 and T4 release & increase size, number, activity of thyroid gland--> increase absorption of iodide.
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what does TSH do? where is it released?
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released by pituitary.
1. causes thyroid hormones to be released 2. stimulates increase in size, #, and activity of thyroid gland cells-->absorption of Iodide |
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Abnormal function of thyroid gland can either be...
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hyperthyroidism or hypothyroidism.
HYPERthyroidism = thyrotoxicosis/ overproduction of hormones HYPOthyroidism = deficiency of hormones |
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hyperthyroidism can either be what? what does it cause?
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exogenours or latrogenic (drug induced from too much synthetic hormone).
causes metabolic activities to be increased! |
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SIGNS AND SYMPTOMS OF HYPERTHYROIDISM
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skin= warm, sweaty
heat intolerance = basal temp 99 Wt loss = thin quickly, but eat a lot Tremors = cells sensitive to E & NE Cardiac = increased HR, HB force, RR Restlessness = mood swings Eyes = bulging; exophalmus Enlarged Thyroid gland = goiter; palpable |
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Diagnosis for Hyperthyroidism
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1. serum T3 and T4 levels
2. plasma TSH (not TSI) 3. BMR increased 4. more uptake of Radio-labeled Iodide |
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Graves Dz is a type of what?
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Hyperthyroidism
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Graves Dz characteristics
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most common. women age 30-50. pos family hx or autoimmune. pituitary secretes TSI (not TSH)
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What's the deal with TSI?
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It mimics TSH. TSI stim thyroid to make T3 & T4, but doesn't participate in feedback, so it doesn't signal thyroid to terminate TSH release. SO end result of TSI is hypersecretion of T3 & T4
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the pituitary releases what hormones?
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TSI and TSH
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The thyroid releases what hormones?
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T3 and T4
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The hypothalamus releases what hormones?
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TRH
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What does TRH do?
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secreted by hypothalamus, it stimulates the pituitary to release TSH which acts on thyroid to secrete or stop hormone (T3 and T4) release.
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What is the Patho of Graves Dz?
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T3 and T4 levels are high, but TSH is low since TSH because TSI has taken the place. You will see low levels of TSH, but high levels of T3 and T4 and know something is wrong (because TSH usually stimulates release of T3 and T4).
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Treatment for Graves Dz
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Goal: reduce T3 and T4 production. First: anti-thyroid drugs (last 1 yr)
Second: surgery (partial thyroidectomy if goiter is large) Tx will be based on how active thyroid is. Will give RADIOACTIVE I-131 to destroy part of thyroid gland. |
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What is the complication that can arise when a combination of surgery and anti-thyroid drugs is sued to treat hyperthyroidism?
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Hypothyroidism can result. will then give replacement tx of synthetic hormones, because thyroid was too destroyed.
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What is hypothyroidism caused by?
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1. TSH or TRH aren't being RELEASED (by hypothal or pituit)
2. T3 and T4 production is impaired (thyroid is damanged) 3. Iodide deficiency (causes decrease in T3 & T4 synthesis) |
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TSH role in hypothyroidism
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stimulates T3 and T4 release and Increases absorption of Iodine, which increases T3 & T4 creation. It's supposed to stop when levels of T3 & T4 are high, but if TSH isn't being released at all, then T3 & T4 won't be released and you will see effects of hypothyroidism.
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TRH role in hypothyroidism
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stimulates TSH release, which causes T3 and T4 release and production. IF TRH isn't being released, then there will be no stimulation or release of T3 and T4 and you will see hypothyroidism.
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In general, manifestations of hypothyroidism will look like what?
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a decrease in metabolism and a general slowing of bodily functions.
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Specifically, manifestations of hypothyroidism will look like what?
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fatigue, slow mvmt, decreased mental alertness, cold intolerance, decreased sweating, decreased body temp, cool dry skin, constipation, bloating, weight gain, decreased pulse, cardiac output peripheral blood flow to tissues, non-pitting edema of hands feet face, decreased GFR.
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What's the deal with adult hypothyroidism?
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happens in adulthood. slow onset, same symptoms, goiter can develop from overactivity of thyroid gland to try and produce more hormones.
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Toxic Nodular Goiter is a form of what?
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HYPERthyroidism
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what's the deal with toxic nodular goiter?
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happens in elderly. goiter produces T3 and T4. will see more CARDIOVASCULAR symptoms in addition to other hyperthyroid sx. it's milder than graves, and has slow onset.
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How does hyperthyroidism work?
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it's an overproduction of thyroid hormones due to TSI being released in place of TSH. TSH is secreted by pituitary and increases synthesis and release of T3 and T4 by increasing size, activity and number of thyroid cells and stimulating release of thyroid hormones. TSI is the antibody that acts like TSh, but doens't partake in feedback mechanism.
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When T3 and T4 are high...
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TSH stimulates thyroid to STOP releasing T3 and T4
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When T3 and T4 levels are low...
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TSH stimulates synthesis and release of thyroid hormones.
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If TSI takes the place of TSH in receptors...
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T3 and T4 will be synthesized and released, but won't stop when levels are high.
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Adrenal Function is controlled by what?
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adrenal medulla and adrenal cortex
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adrenal medulla does what?
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extension of SNS; middle portion of adrenal gland that secretes Epinephrine and Norepinephrine
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adrenal cortex does what?
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deals with corticoids and androgens. secretes glucocorticoids, mineralcorticoids, and adrenal sex hormones.
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glucocorticoids
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steroids. controlled by ACTH. cortisol is main one.
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mineralcorticoids
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controlled by RAA. aldosterone is main one.
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adrenal sex hormones
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androgens. controlled by ACTH.
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ACTH controls what two adrenal cortex hormones?
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cortisol and androgens (sex hormones)
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RAA controls what adrenal cortex hormone?
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aldosterone. it's a mineral corticoid.
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effects of adrenal cortex hormones
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1. pubertal growth of hair
2. increase in blood volume 3. regulation of blood glucose |
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what hormone controls pubertal growth of hair?
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adrenal sex hormones regulated by ACTH.
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what controls increase in blood volume.
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aldosterone which is regulated by RAA.
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aldosterone is essential for
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K+, Aa+, and H2O regulation. IT's regulated by renin angiotensin and K+.
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patho for aldosterone
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decreased blood flow to kidneys --> rennin to be secreted from juxtaglomerulus apparatus--> angiotensinogen-->angiotensin 1-->angiotensin 2 __>stimulates aldosterone release-->reabsorption of Na+ and H2O and secretion of K+-->decreased RAA
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Aldosterone is released when
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K+ levels are elevated or when blood volume is low
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CRF negative feedback mechanism
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Corticotropin Releasing Factor. Secreted by Hypothalamus. stimulates anterior pituitary to release ACTH. ACTH goes to adrenal cortex to release cortisol. If cortisol is high, CRF production is stopped.
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effects of cortisol
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1. gluconeogenesis
2. cells use fatty acids for energy 3. fat accumulates in trunk 4. anti-inflammatory effects 5. (in excess) Na+ and fluid retention and K+ excretion |
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Gluconeogenesis and cortisol: 1st way they're related...
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1. cortisol release--> protein breakdown + AA transported to liver-->AA and proteins turned to glucose
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gluconeogenesis and cortisol: 2nd way they're related..
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cortisol release-->movement of FA to liver-->liver converts FA to glucose
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anti-inflammatory effects of cortisol
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increased cortisol levels (prednisone)--> decreased capillary permeability and decreased release of histamine-->inflammatory response blocked
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what's the problem with the anti-inflammatory effects of cortisol?
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along with the inflammatory response being blocked, SO IS THE ANTIBODY RESPONSE. could be an infection and not know it.
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Abnormal adrenal gland dz
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cushings syndrome (hypersecretion)
addisons dz (hyposecretion) |
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cushing's syndrome
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hyperfunction of adrenal gland produces hypersecretion of hormones.
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cushing's can be caused by what?
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1. tumor that secretes cortisol
2. hypersecretion of ACTH 3. long term steroid use |
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if a tumor is causing increase in cortisol levels what can you expect to see?
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it won't be under feedback, so increased cortisol levels won't signal hypothalamus to stop secreting CRF; pituitary will release ACTH, which will stimulate cortex to secrete more cortisol
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if hypersecretion of ACTH is causing cushing's then what can you expect to see?
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ACTH secretion will cause cortisol secretion from a. cortex, along with androgenic hormones from adrenal gland-->hair growth, glucose metab, etc???
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latrogenic cushing's
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caused by long term steroid use (like prednisone). it's drug induced hyper function of adrenal gland and hyper secretion of hormones.
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in general the manifestations of cushing's deal with...
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breakdown of proteins and fats
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specifically, manifestations of cushing's will look like...
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1. increased blood glucose
2. muscle wasting 3. decreased immunity 4. thin skin 5. bone fractures and osteoporosis 6. truncal obesity; buffalo hump 7. striae (stretch marks) 8. moon/ round face 9. facial hair in females, acne, menstruation changes 10. psychological disturbances 11. hypertension 12. GI ulcers |
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addison's dz happens because of...
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hypofunction of adrenal cortex. it's because cortisol and aldosterone production is decreased.
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causes for decreased production of aldosterone and cortisol in relation to addison's dz are...
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1. destruction of adrenal gland (autoimmune or TB)
2. not enough ACTH (so not enough cortisol) 3. atrophy of adrenal gland (d/t quick withdrawl of steroid therapy) |
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signs and symptoms of addison's dz
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1. hypoglycemia: wont' be able to tolerate food deprivation
2. inability to handle stress: surgery, illness, trauma, psych stress |
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hypoglycemia and addisons
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decreased cortisol levels --> decreased glucose production --> low blood glucose.
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inability to handle stress and addisons
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will develop vascular collapse because decreased aldosterone will affect blood cell production and blood volume.
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posterior pituitary problems are r/t..
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either an ADH deficiency or an ADH excess
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ADH deficiency
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no ADH--> no reabsorption of water-->poly dipsia, poly uria (10/L day urine output)
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diabetes insipidus
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IS AN ADH DEFICIENCY. think: inSIPidus, SIP water, if you're thirsty you're dehyrated-->no ADH
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treatment of ADH deficiency
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ADH nasal spray (vasopressin)
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ADH excess
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ADH is constantly released and not in r/t blood volume or osmolarity--> no feedback to turn it off-->increased blood volume.
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SIADH
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is an excess of ADH. Syndrome of Inappropriate ADH.
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patho of SIADH
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hypothalamus or pituitary trauma cause from oat cell carcinoma in lungs that produces ADH.
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how do you diagnose SIADH?
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urine sample, or blood Na+ sample.
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diaphysis
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MIDDLE section of long bone. CONTAINS MARROW. made of fat tissue.
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epiphysis
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ROUNDED EDGE of long bone AT JOINT. contains epiphyseal plate.
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epiphyseal growth plate
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made of haylene cartlidge in metaphysis (end of long bone)
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osteoBLASTS
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bone building cells. synthesize and secrete bone matrix.
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osteoCYTES
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"cyteeee" the old janior. mature bone cells. release ca+ in blood.
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osteoCLASTS
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"bone chewing" reabsorb and release Ca+ P+ from bone. phagocytic.
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periosteum
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membrane that covers bone (except at joint ends)
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tendon
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connects muscle to bone
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ligament
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connects bone to bone.
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an assessment of the musculoskeletal system should include what?
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bony skeleton, articular system, muscular system, gait assessment, skin and peripheral circulation.
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assessment: bony skeleton: look for
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deformities, alignment, ab norm growth, symmetry, spine alignment
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articular sys: assessment: look for
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think joints: ROM (active/passive), deformities, stability, pain/swelling in joints.
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muscular system: assessment: look for
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strength, coordination, size, tone of muscles and girth of extremity.
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gait assessment: look for
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smoothness, rhythm, steadiness of walk and presence/absence of limping
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skin and peripheral circulation:assessment: look for
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neurological damage to tissues. think blood vessels: circulation in fx extremity, edema, cuts, bruises, parasthesias, skin color, decreased circulation (cap refil, bp), infection, skin temp, peripheral pulses.
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diagnostic procedures for musculoskeletal system
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XR, CT, MRI, Arteriogram, myelogram, arthrography, arthrocentesis, arthroscopy, bone scan, EMG, lab work
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lab work for muscluoskeletal diagnosis
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(ca, p, spk, sgot, alk phosphatase, pth, calcitonin, and ca in urine).
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x ray will show (MS)
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density and shape changes in bone relationship
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(MS) arteriogram would be used to...
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determine wheter or not to amputate. shows circulation to extremity, and assesses potential for healing.
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(MS) myelogram would show...
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bulging disc (herniation). injects contrast medium into space in lumbar spine to show bulging area.
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MS; arthrography would be used to..
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assess tears and contours of joint. assessment done by injection of dye into joint.
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MS; arthrocentisis would be used to...
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show presence of WBC RBC< bacteria or clot formation in joint fluid (synovial fluid). NORMAL: clear, straw colored, scanty.
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MS; arthroscopy would give...
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visualization of joint. happens under general anestheisa. post-op: wrap in bandage and elevate to reduce swelling.
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MS; bone scan would check for...
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uptake of isotope over 4-6 hrs. encourage fluid after test.
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MS; EMG (electromyography) would be used to...
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determine problems with innervation of muscle and see how muscle responds to electrical stimuation.
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MS; Ca+ levels in urine
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bone destruction. Ca+ lost from bone is filtered into urine.
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MS; high alk phosphatase levels...
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metastatic bone tumors d/t osteoblasts indicating bone building.
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MS; high Ca+ and Phospate in blood
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it's in blood if it's coming out of bone
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trauma to MS can come in the form of...
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contusion (bruise), strain, sprain, avulsion FX, dislocation, fracture
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soft tissue trauma involves
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muscles, skin, blood vessels, nerves
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hard tissue trauma involves
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skeleton: bones, ligaments and tendons
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contusion
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injury to soft tissue. happens with blunt force. may see ecchimosis or bleeding in tissues.
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strain
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muscle pull from overuse. microscopic muscle tears. heals on own, but causes pain.
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sprain
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twisting injury to ligaments. ligaments give structure and strength to joint, so if they tear you can lose stability in joint.
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avulsion fracture
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when bone fragment is pulled away from rest of bone by ligament or tendon.
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dislocation
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joint surfaces are not longer in contact. can see and feel changes in contour of joint. involves soft tissue damage.
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full dislocation
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joint surfaces are not longer touching
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if trauma from dislocation is not recognized or reduced
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can lead to avascular necrosis. no blood to tissue--> no O2
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two joints at greatest risk of dislocation
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hip and shoulder
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signs and symptoms of dislocation
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change in contour (bump or dent), change in length (arm longer or shorter), pain (soft tissue damage), decreased mobility.
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interventions for dislocation
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check neuro-vascular function, immobilize during transport, reduce it, immobilize after reduced.
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if you reduce a joint
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you put it back in to alignment
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when you check nuero-vascular function you look at...
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capillary refil, temp, parastesias, pulse, blood pressure
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normal neuro vascualr check should look like
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able to wiggle extremity, minimal discomfort, dignits are pink, warm, sensations intact, rapid capillary refil
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abnormal neuro vascualr check would look like
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coolness, decreased pulse, pain, pallor, parastesias, sluggish capillary refil. ALWAYS COMPARE BILATERALLY.
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danger signals for neurovascualr check
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blue tinged, white, cold, decreased pulse, parasthesias, decreased movement. be prepared to splint or cast.
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the more dislocated a joint is...
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the more stretched out it will be. so pt may need surgery to prevent habitual dislocation.
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fractures
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soft and hard tissue damage. it's a break in the CONTINUITY of bone d/t greater stress than bone can absorb.
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soft tissue damage related to fracture can lead to
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swelling
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fractures often accompanied by
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bleeding into joints, dislocations, nerve damage, blood vessel damage, tendon and ligament damage
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fractures are classified by
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LTD: location, type, direction/pattern
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classification of fracutres by direction
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complete or incomplete; open or closed (also called simple or compound); displaced or non-displaced
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complete fracture
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break across entire section of bone (eg oblique)
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incomplete fracture
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break goes part way across bone (eg greenstick)
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closed or simple fracture
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no break in skin or mucous membrane
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open or compound fracture
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break in skin or mucous membrane. greater risk of contamination because skin is damaged.
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displaced
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bone is no longer in alignment
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non-displaced
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bone is still in alighment
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specific types of fractures
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GOT CDC PAS: greenstick, oblique, transverse, comminuted, depressed, compression, pathological, avulsion, spiral
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clinical manifestations of fractures involve
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pain and muscle spasms (because muscle fibers torn above and below muscles will spasm). soft tissue damage, loss of funcion and deformity (compare bilaterally), and crepitus (feel bone fragments with palpation. also localized swelling, or discoloration (immediate or progressing to different colors).
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4 R's of fracture management
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Recognition, Reduction, Retention (of reduction), and Rehabilitation
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2st step in tx of fracture
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reduction. can be closed or open. restore fragments to alignment, before edema sets in (because it will make it hard to palpate fracture). give meds to relax muscles and relieve pain.
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1nd step in tx of fracture
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recognition of fracture through XR or MRI.
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closed reduciton of fx
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manual traction or manipulation brings bone fragments back to alignment. exerts pull on extremity.
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immobilizing devices
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maintain reduction and stabilize extremity for healing.
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open reduction of fracture
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surgical incision brings bone fragments into alignment. internal fixating devices used to stabilize fracture.
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internal fixating devices
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pins, screws, nails, plates. maintain alignment while fracture heals.
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3rd step in tx of fracture
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retention (of reduction). wan tot immobilize it. can use plaster cast or fiberglass cast or traction.
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casts
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include joints distal and proximal to fx. eg if your ankle breaks you cast kee, ankle and foot.
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plaster casts
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take up to 72 hrs to dry. are bendable until plaster is dry, and if they get wet they're moveable.
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fiberglass casts
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most commonly used. get hard in matter of minutes. doesn't get soft if wet. cotton inside, so you don't want it to get wet.
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traction
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used if person is not candidate for surgery. uses force to pull body part to prevent spasming of muscle.
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complications from casts
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vascualr insufficiency and nerve compression and compartment syndrome.
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vascular insufficiency and nerve compression from casts
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maximal swelling not yet occurred when cast was put on, and cast is non yielding.
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prevention of vascular insufficiency and nerve compression complications from casting
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elevate limb (change fluid direction), apply ice (vasoconstriction reduces blood flow), neurovascular check bilaterally (make sure they can wiggle tows, pain, pallor, parasthesias, pulses, temp)
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signals of vascular insufficiency from casting
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blue tinged, white, cold, decreased pulse, parasthesias, decreased mvmt, slow cap refil, can't wiggle toes.
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bi-valve
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splitting along entire length of cast to relieve pressure. may lose reduction of fx, but better than losing limb d/t decreased blood flow.
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compartment syndrome
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increased tissue pressure from swelling. happens inside muscle and fasica. forms compartment. increased pressure leads to occlusion of blood supply. blood supply cut off to tissues will cause death of nerve and severe muscle tissue damage.
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anoxia
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no blood supply
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signs and symptoms of compartment syndrome
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worst pain you've ever felt: unrelieved pain is most common sx. doesn't go away even with meds because it's nerve damage. also see parasthesias, motor and sensory loss, cold, pale, decreased capillary refil.
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tx for compartment syndrome
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Goal: relieve pressure. open cast or fasciotomy (cutting open tissue to relieve pressure).
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pint specific pain
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burning pain cause by irritation at pressure point when cast is on. can point to it and say it's the exact place they feel pain.
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when casting be aware to
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pad bony prominences
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long cast
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over upper arm or knee
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spika cast
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trunk and one or more extremity. bar to hold integrity of cast.
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short cast
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below arm or knee
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external fixators
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used for open fx and severely comminuted fx. pins are attached to frame and inserted through bone fragments after fx is reduced and immobilized.
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in external fixators the pins are
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possible source for infection. they go through skin. benefit is that ppl can bear wt on them faster, which decreases DVT.
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traction
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applying pulling force to either skin or bone.
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skin traction is
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pull on skin transmits to MS structures. LIMITED BY SHEARING FORCE ON SKIN. can be take 4-7 lbs for extremity or 10-20 lbs for pelvis.
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tx for compartment syndrome
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Goal: relieve pressure. open cast or fasciotomy (cutting open tissue to relieve pressure).
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pint specific pain
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burning pain cause by irritation at pressure point when cast is on. can point to it and say it's the exact place they feel pain.
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when casting be aware to
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pad bony prominences
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long cast
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over upper arm or knee
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spika cast
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trunk and one or more extremity. bar to hold integrity of cast.
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short cast
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below arm or knee
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external fixators
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used for open fx and severely comminuted fx. pins are attached to frame and inserted through bone fragments after fx is reduced and immobilized.
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in external fixators the pins are
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possible source for infection. they go through skin. benefit is that ppl can bear wt on them faster, which decreases DVT.
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traction
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applying pulling force to either skin or bone.
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skin traction is
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pull on skin transmits to MS structures. LIMITED BY SHEARING FORCE ON SKIN.
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skeletal traction and limitations
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pull is on bone by pins or wires distal to fx. wts overcome strength of muscle. allows up to 25 lbs to be applied, but pins possible source for infection.
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|
|
purposes of traction
|
overcome muscle spasm, reduces, aligns, immobilizes fx. increases space between joint surfaces for compression fracture.
|
|
|
subluxation
|
parital dislocation. joints still touching, but not aligned. eg. ball and socket where ball is still in socket, but askew.
|
|
|
treatment for ms system trauma: RICE
|
Rest extremity; Ice intermittently for 20-30 min/hr for 1st 24 hr; Compress with bandage to reduce swelling; Elevate above heart to reduce swelling.
|
|
|
in addition to RICE tx you would
|
check neurovascular status frequently. alllow for rest and repair. after swelling goes down apply moist heat 15-30 min 4x/day. gradual resumption of activity.
|
|
|
complications that can result from fractures are...
|
hemorrhage/shock
compartment syndrome fat embolism thromboembolus infection avascular necrosis slowed healing (delayed union) bones heal out of alignment (malunion) * HCF damit * |
|
|
fx complicaton: hemorrhage shock
|
always a possibility. associated with initial injury. common with pelvis fx.
|
|
|
fx complication: compartment syndrome
|
tissue perfusion impaired by swelling causes ischemia of tissue. Think: deep pain unrelieved by meds. Look for: neurovascular impairment signs.
|
|
|
fx complication: fat embolism
|
think: petecchae, sudden dyspnea, anxiety, change in mental status. happens a lot with fx of femur or crushed pelvis.
|
|
|
fx complication: thromboembolus
|
check: homan's sign and circumference of calf. happens in lower legs when wt bearing activity is minimized.
|
|
|
fx complication: infection
|
infection d/t wires, pins, tissue trauma. can be 1. wound related: at sight of pins or 2. osteomyelitis: infection of bone. increased risk: diabetes, steroid use, RA
|
|
|
prevention of osteomyelitic infection due to fracture
|
irrigation, debridement with delayed closure. if not, could lead to bone death (hard to get antibiotics to bone where there's not a lot of blood vess.)
|
|
|
fx complication: avascular necrosis
|
most common: dislocations. happens when bone and tissues die d/t lack of O2.
|
|
|
fx complication: delayed union
|
slow healing. common: older adults, d/t decreased osteoblasts. corticosteroids decrease healing speed.
|
|
|
fx complication: malunion
|
bones heal out of alignment.
|
|
|
complications that can result from fractures are...
|
hemorrhage/shock
compartment syndrome fat embolism thromboembolus infection avascular necrosis slowed healing (delayed union) bones heal out of alignment (malunion) * HCF damit * |
|
|
fx complicaton: hemorrhage shock
|
always a possibility. associated with initial injury. common with pelvis fx.
|
|
|
fx complication: compartment syndrome
|
tissue perfusion impaired by swelling causes ischemia of tissue. Think: deep pain unrelieved by meds. Look for: neurovascular impairment signs.
|
|
|
fx complication: fat embolism
|
think: petecchae, sudden dyspnea, anxiety, change in mental status. happens a lot with fx of femur or crushed pelvis.
|
|
|
fx complication: thromboembolus
|
check: homan's sign and circumference of calf. happens in lower legs when wt bearing activity is minimized.
|
|
|
fx complication: infection
|
infection d/t wires, pins, tissue trauma. can be 1. wound related: at sight of pins or 2. osteomyelitis: infection of bone. increased risk: diabetes, steroid use, RA
|
|
|
prevention of osteomyelitic infection due to fracture
|
irrigation, debridement with delayed closure. if not, could lead to bone death (hard to get antibiotics to bone where there's not a lot of blood vess.)
|
|
|
fx complication: avascular necrosis
|
most common: dislocations. happens when bone and tissues die d/t lack of O2.
|
|
|
fx complication: delayed union
|
slow healing. common: older adults, d/t decreased osteoblasts. corticosteroids decrease healing speed.
|
|
|
fx complication: malunion
|
bones heal out of alignment.
|
|
|
site of hip fx
|
head of femur. hip fx d/t osteoporosis. mostly in elderly population. tx determined by bone strength: THR or ORIF
|
|
|
manifestations of hip fx
|
external rotation, shortening of extremity d/t muscle spasms, severe pain and tenderness.
|
|
|
open reduction of hip fx
|
plates and pins hold femur head fx together. NO ARTHRITIS. bone and joint must be healthy for wt bearing.
|
|
|
total hip replacement d/t hip fx
|
femur head sawed off and replaced with metal implant. DO FOR ARTHRITIS. bone must be healthy enough for healing.
|
|
|
what is rheumatic dz is all about?
|
connective tissue damage: affects bones, muscles, joints. collagen, elastin and reticulin are connective tissues. when there's loose connective tissue (reticulin) you will see changes in blood vessels.
|
|
|
rheumatoid arthritis, think:
|
bilateral. symmetric. systemic implications (ill, fever, wt loss fatigue), exacerbations and remissions. cloudy synovial fluid, increased ESR. RF positive. Ulnar drift.
|
|
|
RA is described as...
|
chronic, systemic, progressive, and inflammatory. destorys lining of joint (synovial membrane)-->pain, stiffness, decreased mobility.
|
|
|
synovitis is...
|
inflammation of synovial membrane. happens with RA.
|
|
|
RA is most common in what population?
|
women ages 30-50, and after age 70
|
|
|
Anaclitic depression: What is Anaclitic depression?
|
Depression in an infant due to continued separation from caregiver, can result in failure to thrive. Results in withdrawal and unresponsiveness.
|
|
|
patho of RA
|
antibodies are formed against Rheumatoid Factor--> antibody is produced that releases enzymes-->enzymes cause inflammation of synovial membrane-->joint swelling and edema.
|
|
|
pannus
|
thickening of synovial membrane.
|
|
|
manifestations of RA
|
joint pain, swelling, warm and red (erythema), decreased function, systemic sx (ill, fever, wt loss, fatigue, anemia), rheumatoid nodules over bony prominences (can be referred), neuropathies, scleritis, pericarditis, arteritis
|
|
|
onset of RA
|
insidious. starts out as stiff joints and leads to redness and swelling. begins in hands, fingers, wrists, feet but may progress to knees, shoulders, hips, elbows. occurs bilaterally and symmetrically.
|
|
|
patho of RA
|
antibodies are formed against Rheumatoid Factor--> antibody is produced that releases enzymes-->enzymes cause inflammation of synovial membrane-->joint swelling and edema.
|
|
|
pannus
|
thickening of synovial membrane.
|
|
|
deformities caused by RA
|
ulnar drift: swan neck, hands and feet. spindle shaped joints. tendons stick out. partial subluxations and contractures can result.
|
|
|
diagnosis of RA
|
80% of ppl will be RF positive. elevated ESR rate d/t inflammation caused by antibodies. thick, cloudy synovial fluid. positive for antibodies: CRP and ANA (affects bone marrow).
|
|
|
manifestations of RA
|
joint pain, swelling, warm and red (erythema), decreased function, systemic sx (ill, fever, wt loss, fatigue, anemia), rheumatoid nodules over bony prominences (can be referred), neuropathies, scleritis, pericarditis, arteritis
|
|
|
patho of RA
|
antibodies are formed against Rheumatoid Factor--> antibody is produced that releases enzymes-->enzymes cause inflammation of synovial membrane-->joint swelling and edema.
|
|
|
onset of RA
|
insidious. starts out as stiff joints and leads to redness and swelling. begins in hands, fingers, wrists, feet but may progress to knees, shoulders, hips, elbows. occurs bilaterally and symmetrically.
|
|
|
management of RA
|
reduce and suppress inflammatory response, provide comfort, preserve joint function.
|
|
|
pannus
|
thickening of synovial membrane.
|
|
|
deformities caused by RA
|
ulnar drift: swan neck, hands and feet. spindle shaped joints. tendons stick out. partial subluxations and contractures can result.
|
|
|
manifestations of RA
|
joint pain, swelling, warm and red (erythema), decreased function, systemic sx (ill, fever, wt loss, fatigue, anemia), rheumatoid nodules over bony prominences (can be referred), neuropathies, scleritis, pericarditis, arteritis
|
|
|
ASA
|
asprin
|
|
|
patho of RA
|
antibodies are formed against Rheumatoid Factor--> antibody is produced that releases enzymes-->enzymes cause inflammation of synovial membrane-->joint swelling and edema.
|
|
|
onset of RA
|
insidious. starts out as stiff joints and leads to redness and swelling. begins in hands, fingers, wrists, feet but may progress to knees, shoulders, hips, elbows. occurs bilaterally and symmetrically.
|
|
|
diagnosis of RA
|
80% of ppl will be RF positive. elevated ESR rate d/t inflammation caused by antibodies. thick, cloudy synovial fluid. positive for antibodies: CRP and ANA (affects bone marrow).
|
|
|
deformities caused by RA
|
ulnar drift: swan neck, hands and feet. spindle shaped joints. tendons stick out. partial subluxations and contractures can result.
|
|
|
NSAIDS
|
non-steroidal anti inflammatory drugs
|
|
|
pannus
|
thickening of synovial membrane.
|
|
|
management of RA
|
reduce and suppress inflammatory response, provide comfort, preserve joint function.
|
|
|
ASA
|
asprin
|
|
|
Meds for RA
|
NSAIDS first to reduce inflammation. then DMARDS (disease modifying anti rheumatoid drugs) <-- have lots of side effects. tx with prednisone (increases blood glucose levels, makes skin thin, redistributes fat: SO IT LOOKS LIKE CUSHINGS.
|
|
|
manifestations of RA
|
joint pain, swelling, warm and red (erythema), decreased function, systemic sx (ill, fever, wt loss, fatigue, anemia), rheumatoid nodules over bony prominences (can be referred), neuropathies, scleritis, pericarditis, arteritis
|
|
|
diagnosis of RA
|
80% of ppl will be RF positive. elevated ESR rate d/t inflammation caused by antibodies. thick, cloudy synovial fluid. positive for antibodies: CRP and ANA (affects bone marrow).
|
|
|
NSAIDS
|
non-steroidal anti inflammatory drugs
|
|
|
management of RA
|
reduce and suppress inflammatory response, provide comfort, preserve joint function.
|
|
|
onset of RA
|
insidious. starts out as stiff joints and leads to redness and swelling. begins in hands, fingers, wrists, feet but may progress to knees, shoulders, hips, elbows. occurs bilaterally and symmetrically.
|
|
|
deformities caused by RA
|
ulnar drift: swan neck, hands and feet. spindle shaped joints. tendons stick out. partial subluxations and contractures can result.
|
|
|
ASA
|
asprin
|
|
|
Meds for RA
|
NSAIDS first to reduce inflammation. then DMARDS (disease modifying anti rheumatoid drugs) <-- have lots of side effects. tx with prednisone (increases blood glucose levels, makes skin thin, redistributes fat: SO IT LOOKS LIKE CUSHINGS.
|
|
|
diagnosis of RA
|
80% of ppl will be RF positive. elevated ESR rate d/t inflammation caused by antibodies. thick, cloudy synovial fluid. positive for antibodies: CRP and ANA (affects bone marrow).
|
|
|
NSAIDS
|
non-steroidal anti inflammatory drugs
|
|
|
management of RA
|
reduce and suppress inflammatory response, provide comfort, preserve joint function.
|
|
|
ASA
|
asprin
|
|
|
Meds for RA
|
NSAIDS first to reduce inflammation. then DMARDS (disease modifying anti rheumatoid drugs) <-- have lots of side effects. tx with prednisone (increases blood glucose levels, makes skin thin, redistributes fat: SO IT LOOKS LIKE CUSHINGS.
|
|
|
NSAIDS
|
non-steroidal anti inflammatory drugs
|
|
|
Meds for RA
|
NSAIDS first to reduce inflammation. then DMARDS (disease modifying anti rheumatoid drugs) <-- have lots of side effects. tx with prednisone (increases blood glucose levels, makes skin thin, redistributes fat: SO IT LOOKS LIKE CUSHINGS.
|
|
|
what is SLE (systemic lupups erythematosus)
|
"the great imitator." chronic, inflammatory, autoimmune, collagen-vascular dz. affects blood vessels. autoimmune regulation problem causes extra T LYMPHOCYTE production --> inflammation.
|
|
|
onset of SLE
|
women, over age 30. can follow pregnancy or life altering situation. more common in african americans and asians.
|
|
|
what does SLE look like?
|
musculoskeletal pain, skin issues, pericardium issues, lung issues, vascualr issues, lymph renal and neuropsych issues. comes in EXACERBATIONS AND REMISSIONS.
|
|
|
musculoskeletal sx of SLE
|
joint pain, poly arthritis with pain and swelling.
|
|
|
arthralgias
|
joint pains
|
|
|
skin sx of SLE
|
butterfly rash (looks like butterfly wings with bumps. sun sensitivity.
|
|
|
pericardial sx of SLE
|
pericarditis: inflamm of pericardial sac. may be asymptomatic or lead to pericardial effusion.
|
|
|
lung sx of SLE
|
can cause inflamm of peural sac: pleuritis.
|
|
|
vascular sx of SLE
|
inflammation of terminal arterioles: arteritis. causes purpuric lesions in fingers, toes, elbows.
|
|
|
lymph sx of SLE
|
inflammation of lymph tissues: lymphadenopathy.
|
|
|
renal sx with SLE
|
glomular damage to kidney. worst part, b/c alters efficacy of kidneys. doesn't have to be severe, but can cause kidney damage.
|
|
|
neuropsych sx of SLE
|
behavior changes
|
|
|
diagnosis of SLE
|
is hard, because it's great imitator. based on symptoms. no definitive lab work. will see elevated ESR, ANA (antibody) positive. elevated IgA, IgM, IgG (but they're elevated in all autoimmune dz). anemia, decreased platelets and decreased WBC.
|
|
|
management of SLE involves...
|
Goal: prevent loss of organ function, minimize disability, prevent complications from drug treatments. protect joints with splints, heat/cold, rest, ROM (active/passive). 1. NSAIDs to control inflammation. 2. prednisone is main tx: high or low doses depending on exaccerbations and remissions and dz activity.
|
|
|
what is osteoarthritis?
|
DJD. it's local, not systemic. develops in ppl with arthritis: degeneration/thinning of cartilage--> bones rub together-->bone spurs. no cartilage = space in between joints is gone.
|
|
|
onset of OA, and patho...
|
insidious. inflammation and pain with weight bearing-->decreased joint use--> decreased ROM--> leads to muscle atrophy
|
|
|
common sites for OA
|
hips, knees, vertebral column, distal finger joints. other joints may get DJD if traumatized.
|
|
|
DJD: definition
|
degenerative joint disorder
|
|
|
contributing (predisposing) factors for OA
|
genetics. obesity. trauma or injury or fracture.
|
|
|
Substance abuse (p. 128): Greater safety margin, amnesia, ataxia, somnolesence, minor respiratory effects, and addictictive effects with alcohol are the characteristics of which drug?
|
Benzodiazepines
|
|
|
when you think about OA, think:
|
radial deviation. localized, not systemic. no specific lab work. morning stiffness with dull pain and decreased ROM. thin joint cartilage-->djd-->bones rub-->bone spurs. hips knees, proximal and distal finger joints, vertebral column.
|
|
|
treatment of OA involves...
|
Goal: minimize joint damage and maintain mobility. NAIDS, muscle relaxants (spasms), heat/ice, ROM, wt loss, assistive devices, THR, TKR, PT
|
|
|
what is osteoporosis?
|
loss of bone mass and density. imbalance between bone production and bone reabsorption.
|
|
|
when you think about OA, think:
|
radial deviation. localized, not systemic. no specific lab work. morning stiffness with dull pain and decreased ROM. thin joint cartilage-->djd-->bones rub-->bone spurs. hips knees, proximal and distal finger joints, vertebral column.
|
|
|
treatment of OA involves...
|
Goal: minimize joint damage and maintain mobility. NAIDS, muscle relaxants (spasms), heat/ice, ROM, wt loss, assistive devices, THR, TKR, PT
|
|
|
patho for osteoporosis
|
happens as you age, because androgens and estrogens maintain osteoblast and osteoclast activity. age = less osteoblasts (less bone building).
|
|
|
osteoporosis is common in what population?
|
women, after menopause: age 50. can lose up to 30% of bone mass in next 20 yrs. Men = much later, no sharp decrease in androgens.
|
|
|
what is osteoporosis?
|
loss of bone mass and density. imbalance between bone production and bone reabsorption.
|
|
|
what are the symptoms of osteoporosis?
|
usually none until fx occurs. may see kyphosis (loss of ht). happens from immobility and disuse (no wt bearing = low bone density).
|
|
|
patho for osteoporosis
|
happens as you age, because androgens and estrogens maintain osteoblast and osteoclast activity. age = less osteoblasts (less bone building).
|
|
|
osteoporosis is common in what population?
|
women, after menopause: age 50. can lose up to 30% of bone mass in next 20 yrs. Men = much later, no sharp decrease in androgens.
|
|
|
kyphosis
|
loss of height d/t leaning forward.
|
|
|
what are the symptoms of osteoporosis?
|
usually none until fx occurs. may see kyphosis (loss of ht). happens from immobility and disuse (no wt bearing = low bone density).
|
|
|
what are the common sites for fx with osteoporosis?
|
vertebrae: compression fx. colle's fx: radial fx. femoral neck hip fx.
|
|
|
how would you diagnose osteoporosis?
|
with bone density test. advised for women over 50, and every 5-10 yrs after.
|
|
|
kyphosis
|
loss of height d/t leaning forward.
|
|
|
what's the treatment for osteoporosis?
|
goal: prevention. wt bearing activity, high Ca+ and Vit D intake.
|
|
|
what are the common sites for fx with osteoporosis?
|
vertebrae: compression fx. colle's fx: radial fx. femoral neck hip fx.
|
|
|
how would you diagnose osteoporosis?
|
with bone density test. advised for women over 50, and every 5-10 yrs after.
|
|
|
what's the treatment for osteoporosis?
|
goal: prevention. wt bearing activity, high Ca+ and Vit D intake.
|
|
|
what do you assess when looking for neurological disorders?
|
mental status, LOC, cerebral function, cranial nerves, motor function, reflexes, sensory response.
|
|
|
to check mental status for neuro disorder you would look for what?
|
ability to plan, reason, remember and interpret. count backwards from 100 by 7's.
|
|
|
when testing LOC, you should...
|
describe behavior and responses. don't just label "confused" or "delerious."
|
|
|
when checking for cerebral function in neuro disorders, what would you look for?
|
speech, vision, calculations, auditory isses.
|
|
|
what changes in speech could be related to neuro disorders?
|
dysarthia, dysphonia, apasias (sensory or global). usually related to the function of the dominant hemisphere.
|
|
|
dysphonia
|
HOARSENESS. damage to laryngeal nerve causes hoarseness.
|
|
|
dysarthia
|
difficulty with PRONUNCIATION. happens with stroke.
|
|
|
aphasias
|
can be motor or expressive. decreased ability to express verbally or in writing.
|
|
|
expressive aphasia
|
motor problems: writing?
|
|
|
receptive aphasia
|
sensory. decreased ability to UNDERSTAND written or verbal language.
|
|
|
if you were assessing motor function for a neuro disorder what would you look at?
|
gait, coordination, and muscle strength.
|
|
|
what reflexes would be assessed for neuro disorders?
|
deep tendon reflexes like babinski reflex.
|
|
|
if you were checking sensory response for neuro disorder, what would you look at?
|
ability to feel pain, temperature, motion and position.
|
|
|
what diagnostic testing would you use for neurodisorders?
|
cerebral angiogram, lumbar puncture, MRI, CAT, EMG, EEG
|
|
|
a cerebral angiogram would show you what?
|
blood flow to brain. contrast medium is injected into cerebral circulation. wouldn't do it for someone with brain bleed.
|
|
|
what would a lumbar puncture tell you?
|
spinal tap at L3 and L4 would check pressure in CSF and presence of bacteria, or glucose if it was a viral problem.
|
|
|
what would an MRI or a CAT show you?
|
a cross section of brain to LOCATE the problem.
|
|
|
what would and EMG show you?
|
the neuro-muscular innervation. it could tell you what the loss of a limb was due to.
|
|
|
what would an EEG show you?
|
the brain wave activity. electroencephalogram.
|
|
|
what is increased intracranial pressure all about (ICP)?
|
increase in cranial pressure due to increased brain tissue, fluid or blood. NOT A DZ IN ITSELF, HAPENS WITH LOTS OF DZ. happens temporarily with valsalva or coughing, but if sustained can cause brain damage.
|
|
|
what can ICP result from?
|
tumor, injury (with cerebral edema), obstruction of CSF flow.
|
|
|
what are the compensatory mechanisms for increased intracranial pressure?
|
body will shunt CSF down spinal cord and away from brain. veins dilate, systolic BP rises, but pulse and RR drop.
|
|
|
what happens if ICP increases? what would you see?
|
increase in pulse pressure: the difference between systolic and diastolic BP will widen. systolic BP will rise, but HR AND RR WILL DROP.
|
|
|
what are the most common causes of ICP?
|
cerebral edema r/t fluid and electrolye imbalance, hypoxia (no O2 in blood), ischemia (no O2 to tissue), infection, injury, hemorrhage.
|
|
|
what would an Increase in Intracrainal pressure look like?
|
changes in LOC: 1st sign is behaviors and responsiveness. headache due to lining of brain being stretched (dura). papilledema: pressure on optic disc causes eyes to bulge. projectile vomiting, increase in pulse pressure, decrease in HR, RR, seizures, motor or sensory changes.
|
|
|
what is the glascow coma scale?
|
it is a standardized method of consciousness that gives behaviors a number.
|
|
|
if you're checking the pupil for suspected ICP what would you look for?
|
size, symmetry, shape and reaction to light.
|
|
|
what is a CVA?
|
stroke. it's an interruption in the blood: brain flow.
|
|
|
how is blood supplied to brain?
|
via internal carotid, vertebral arteries, vessels branch over surface, arteries branch inward.
|
|
|
does a CVA happen quickly or slowly?
|
slowly. blood is gradually decreased to brain. blood vessels will sense this and try to autoregulate. eg increased pCO2 and decreased pO2 will be sensed by receptors and vasodilation and increased blood flow will happen.
|
|
|
risk factors for CVA?
|
atherosclerosis, hypertension, valvar dz (embolism), diabetes and smoking (compound risks), congenital aneurysms.
|
|
|
3 types of CVAs
|
TIA, progressive stroke, completed stroke. classified by chronological sequence.
|
|
|
TIA transient ischemic attack
|
mini-stroke. BRIEF INTERRUPTION in brain:blood flow. lasts few min to hrs. reversible ischemia, no perm damage. (d/t arteriosclerotic plaque or thrombus).
|
|
|
symptoms of TIA
|
paralysis, weakness, balance difficulty, slurring speech or forgetting words. may not even know they're having a TIA.
|
|
|
progressing stroke
|
stroke in evolution. begins with weakness (paresis) and leads to paralysis over hrs or days. reversed by thrombolytic drugs. will affect the function of whatever part of brain it hits.
|
|
|
completed stroke
|
has prolonged or perm damage
|
|
|
symptoms of CVA
|
vary with location of issue. weakness, paralysis, parasthesias, ataxia, dysphagia, visual disturbances (pin-point vision), expressive aphasia (broca) or receptive aphasia (wernicke) or global. confusion and emotional changes.
|
|
|
hemi-paresis or hemi-plegia
|
weakness or paralysis
|
|
|
ataxia
|
loss of balance or coordination
|
|
|
dysphagia
|
difficulty swallowing
|
|
|
dysphagia
|
difficulty swallowing
|
|
|
patho of stroke
|
thrombus is most common. also can be embolus or hemorrhage.
|
|
|
a thrombus related stroke is...
|
r/t artherosclerosis and hypertension. PEAKS AGE 60-70.
|
|
|
onset of thrombus related stroke is...
|
GRADUAL ONSET: weak on one side in AM and as clot gets bigger it may lead to paralysis. may have had TIA in past.
|
|
|
what age is embolism related stroke most common?
|
30's, 40's, 50's. common in YOUNGER population.
|
|
|
the patho of a embolism related stroke is...
|
embolism originating from thrombus in LEFT SIDE OF HEART. SUDDEN ONSET. clot leaves atrium-->carotid-->blood vessel in brain that's smaller than it is-->wedges
|
|
|
cerebral hemorrhage related stroke is...
|
NOT AGE SPECIFIC. ruptured vessel of an aneurysm.
|
|
|
most common site for cerebral hemorrhage related stroke is...
|
circle of wilis. lots of damage to brain with no warning sign.
|
|
|
manifestations of cerebral hemorrhage related stroke are..
|
violent HA, nuchal rigidity (stiff neck), vomiting, convulsions, coma, death. rapid downhill decline.
|
|
|
to diagnose a CVA you would...
|
determine location of lesion by symptoms, CAT, brain scan, EEG, angiogram.
|
|
|
what's the preventative surgery for a CVA?
|
carotid endarterectomy: for ppl with decreased blood flow d/t plaque. clean out carotid to increase blood perfusion to brain.
|
|
|
how do you prevent a CVA?
|
control hypertension especially in conjunction with risk factors like diabetes high blood lipids, smoking, and heart dz. give ASA for thrombus induced CVA. prevent progression of TIA to CVA.
|
|
|
2 types of vascular headaches
|
migraines and cluster headaches.
|
|
|
vascular headaches involve...
|
changes in blood flow to brain that originate in blood vessels.
|
|
|
characteristics of migraines
|
unilateral, throbbing headache. prodromal symptoms (warning signs): visual changes or numbness. + fam hs. women. associated with period of fatigue, stress, alcohol.
|
|
|
pathology of migraines
|
1st: vasoconstriction (causes numbness and visual changes) 2nd: vasodilation (throbbing pain). may also involve neurotransmitter changes (inflamm response)
|
|
|
a person having a migraine might want to...
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lie down
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symptoms of a migraine are...
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HA accompanied by nausea, vomiting, light sensitivity, peripheral vascular changes (cold hands, feet, pallor), and tend to feel ill.
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treatment for migraines involves...
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medications that reverse vasoconstriction/vasodilation phase. beta blockers block vasoconstriction.
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what's up with cluster headaches?
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the occur frequently and last for a few days or weeks. constant. common: men.
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a person having a cluster headache might tend to want to...
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walk around
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symptoms of cluster headaches
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constant, severe, unilateral pain. localizes to one eye: tearing or redness. start when person is asleep, precipitated by alcohol or stress.
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do vascular headaches run in families?
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yes. sister may have migraines while brother has cluster headaches.
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how are seizures defined?
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convulsions. abnormal activity caused by sudden discharge of neuronal firing.
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what causes seizures?
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vascular insufficiency, fever, head injury, hypertension, infection (CNS), metabolic disturbances (like hypoglycemia), drug and alcohol withdrawal, stroke, tumor, or it can be idiopathic.
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how is epilepsy defined?
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recurrent seizures
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2 classifications of seizures
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1. partial (also called jacksonian or focal)
2. generalized seizures |
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what is a partial seizure is characterized by?
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NO LOSS OF CONSCIOUSNESS. unilateral twitching that may start in face and progress to entire side of body.
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what is a general seizure characterized by?
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A LOSS IN CONSCIOUSNESS. can also get muscle tone loss sometimes.
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3 types of generalized seizures
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1. petit mal (or absence)
2. drop seizure (or atonic) 3. grand mal (or tonic-clonic) |
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what population is a petit mal usually seen in?
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children
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what do petit mal seizures look like?
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short, may progress, vacant stare, rapid blinking, short lapses in consciousness. usually lasts about 30 sec-1 min.
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what does a drop seizure look like?
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loss of muscle tone. 30 sec-1 min. children, may fall out of chair.
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aura
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a warning sign for seizure. could be smell, ringing, flashing lights.
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what does a grand mal seizure look like?
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sudden loss of consciousness often preceded by aura.
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what are tonic-clonic contractures and what type of seizure are they associated with?
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grand mal. when flexors and extensors contract at same time. preceded by muscle rigidity.
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what might happen to a person that was having a grand mal seizure?
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may bite tongue, become incontinent, fall into period of deep sleep after. saliva may collect in mouth.
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how long does a grand mal usually last?
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3-5 min
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how would you diagnose a seizure?
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CT, EEG locates where neurons are misfiring.
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how do you treat epilepsy?
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constant meds and med management to control seizure activity.
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what is status epilepticus?
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2 or more seizures without period of recovery. can be fatal, since brain doesn't have time to replenish O2 or Glucose.
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what is multiple sclerosis?
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"multiple scarring." myelin sheath surrounding nerves (that cary impulses) is scarred.
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what might you see in someone with MS?
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jerky movements d/t jerky nerve impulses.
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what population is the most commonly affected by MS?
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females. age 20-40. autoimmune dz.
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what does MS look like?
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exacerbations and remissions that are prolonged, unpredictable, and variable.
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early symptoms of MS are...
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fatigue, muscle weakness, numbness (paresthesias), visual changes (dbl vision).
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as MS progresses, what symptoms would you see?
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ataxia and loss of bladder control
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ataxia
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loss of coordinated mvmts.
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what's the goal of managing MS?
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to control the symptoms and prevent damage (by keeping in remission) corticosteroids (prednisone) to reduce inflammation during exacerbations helps prevent scar tissue from forming around myelin sheath. meds for incontinence and muscle relaxants.
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how is parkinson's defined?
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progressive neurological dz that affects part of brain which controls movement regulation and control.
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substantia nigra
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part of brain that controls muscle mvmt
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what is the pathology of parkinson's dz?
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dopamine deals with muscle mvmt and control. substantia nigra is part of brain that controls muscle mvmt. a lesion in substantia nigra decreases dopamine production, which leads to BRADYKINESIS, TREMORS, MUSCLE RIGIDITY
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bradykinesis
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slowed mvmts
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what age group does parkinson's generally affect? what causes it?
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age 60+
unknown etiology, NOT autoimmue |
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what would you see in someone with parkinson's?
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muscle rigidity and weakness. ratchet mvmts, difficulty initiating motor activities. supination/pronation and pill rolling tremors. gait is forward leaning, shuffling, and bent knees. depression sometimes. lose ability for spontaneous expression = mask like face. drool.
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how do you treat parkinson's?
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no treatment. in crease their dopamine.
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what are the 4 studies you can do to diagnose urologic disorders
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1. urinalysis
2. C&S 3. Residual flow 4. 24 hour urine collection |
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what does a urinalysis tell you?
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general screening. urine should contain waste products but little to no blood cells or glucose.
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what is a urine C&S?
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culture tests for bacteria and sensitivity tells you what abtibiotics you need. done with clean catch voiding.
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what is residual urine and how do you get it?
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urine left in bladder after voiding. in and out cath.
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what is a 24 hr urine collection and what does it tell you?
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how well kidneys are functioning. measures creatine clearance.
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what does creatine clearance tell you?
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GFR. how well kindeys are working, by their ability to clear creatine from blood.
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what would you expect to see in someone with kidney dz?
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urine creatine will go down, serum creatine will go up.
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bun
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5-25 mg/dL
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creatine
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0.5-1.5 mg/dL
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K+
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3.5-5.5
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what happens with K+ levels if kidney is diseased?
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since kidneys excrete K+ if kidney is dz then blood will have elevated K+ levels.
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what XR diagnostic tests are used for urologic disorders?
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KUB, IVP, ultrasound, endoscopy, renal biopsy, voiding cystogram.
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what will KUB show you?
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Kidney Ureters Bladder. shows GROSS ABNORMALITIES.
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what will IVP show you?
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Intravenous Pyelogram. shows outline of structures and indicates where strictures, tumors and stones are.
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what will an ultrasound show you?
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distinguishes between fluid and solid. 1st test, non-invasive.
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what will an endoscopy show you?
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cytoscopy done for bladder. takes tissue sample for cancer testing. under local or general anesthesia something is inserted through urethra to bladder.
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what will a voiding cystogram show you?
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checks for reflux from bladder back to ureters.
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what will a renal biopsy show you?
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tissue of kidney taken by insertion of needle through flank and into kidney. checks for kidney dz??
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what are the urologic disorders?
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infections, cystitis, pyelonephritis, obstructions, bladder cancer, BPH, prostate cancer.
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what causes urinary tract infections?
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mainly E. Coli that travels up sterile urethra.
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what keeps urethra sterile?
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pH of urine, valves at bladders neck, flushing urine through when voiding.
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what population do UTIs affect the most?
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women. short urethra and close proximity to rectum.
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what causes UTI?
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if person can't completely empty their bladder, instrumentation, kidney stones or other obstructions, contamination of urethra from rectum.
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what can an untreated UTI lead to?
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chronic kidney dysfunction
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what is cystitis?
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bladder infection usually due to ascending bacteria.
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what are the symptoms of cystitis?
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frequency, urgency, dysuria, foul smelling urine, hematuria, suprapubic pain, cloudy urine from bacteria and white blood cells.
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how would you diagnose cystitis?
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urinalysis, C&S, if recurrent check for incompetent valves through IVP.
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how do you treat cystitis?
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7-10 day antibiotics (or 3 day). make sure to take all of them otherwise infection will come back. INCREASE FLUIDS TO 3000cc/day.
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what is pyelonephritis?
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inflammation of kidney pelvis and parenchyma.
Kidney Inflammation. |
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what causes pyelonephritis?
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E.coli ascending infection following cystitis. could be r/t stones, obstructions, reflux.
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how would you diagnose pyelonephritis?
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urinalysis: cloudy, foul smelling urine with PYURIA
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pyuria
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pus in urine/dead white blood cells.
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what are symptoms of pyelonephritis?
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malaise, fever, chills, FLANK PAIN, dysuria, frequency, N&V
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what is treatment for pyelonephritis?
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antibiotics for 10-14 days and increase fluid intake. check for blood bacterial cultures!
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2 classifications of obstructions
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congential or aquired.
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what happens with congenital obstruction?
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strictures of ureters.
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strictures
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narrowing of pathways of body.
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what happens with acquired obstructions?
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tumors in prostate or bladder or scar tissue cause urinary calculi to form (stones).
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patho for obstruction
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normal urine flow obstructed in urinary tract. kidneys still produce urine--> obstruction in ureter-->decreased urine output--> increases pressure in kidney--> causes kidney dilation--> kidney destruction.
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what will the labs work show if kidneys are having issues?
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increased BUN and creatine.
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Hydronephrosis
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kidney dilation
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increase in retention of urine or urine stasis puts someone at risk for what?
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infection!!
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what happens with acquired obstructions?
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tumors in prostate or bladder or scar tissue cause urinary calculi to form (stones).
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oliguria
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100-400 cc Urine/day
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patho for obstruction
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normal urine flow obstructed in urinary tract. kidneys still produce urine--> obstruction in ureter-->decreased urine output--> increases pressure in kidney--> causes kidney dilation--> kidney destruction.
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anuria
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less than 100 cc urine/day
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what will the labs work show if kidneys are having issues?
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increased BUN and creatine.
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if an obstruction progresses it can lead to..
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oliguria or anuria
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Hydronephrosis
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kidney dilation
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what population is most frequently affected by stones (renal calculi/nephrolithiasis)?
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men ages 20-55. tend to be recurrent.
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what are risk factors for stones?
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decreased fluid intake, decreased urinary output, elevated serum Ca+, family history sedentary lifestyle?
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increase in retention of urine or urine stasis puts someone at risk for what?
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infection!!
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oliguria
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100-400 cc Urine/day
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anuria
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less than 100 cc urine/day
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if an obstruction progresses it can lead to..
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oliguria or anuria
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what population is most frequently affected by stones (renal calculi/nephrolithiasis)?
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men ages 20-55. tend to be recurrent.
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what are risk factors for stones?
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decreased fluid intake, decreased urinary output, elevated serum Ca+, family history sedentary lifestyle?
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what are symptoms of a kidney stone?
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depends on the location of stone. INTENSE, COLICKY PAIN THAT MOVES DOWN URETER, N&V, chills, fever, UTI sx (frequent urination, urgency, dysuria, foul smelling urine, hematuria, suprapubic pain cloudy urine)
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how would you diagnose kidney stones?
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1st-ultrasound. KUB or IVP. surgery to break stone: cytoscopy (10% of people). lithotripsy (uses water pressure to break stone).
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in what population is bladder cancer most common?
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men ages 50-70. highly correlated to smoking.
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what are sx of bladder cancer?
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painless gross hematuria (lots of bleeding in urine).
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how would you diagnose and treat bladder cancer?
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cytoscopy to obtain biopsy and remove lesion. could put chemo in bladder. curable if caught early.
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in what population will you find BPH, Benign Prostatic Hypertrophy?
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75% of men, very common, especially by age 65-70.
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patho for BPH
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small nodules on prostate (medial and lateral lobes) that grow and press on urethra and obstruct urinary flow.
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what are the symptoms of BPH?
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nocturia, hesitancy, small or narrowed urinary stream, dribbling. UTI can develop from urinary retention. can lead to renal failure.
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how would you diagnose BPH?
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through DRE or biopsy to rule out cancer.
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how would you treat BPH?
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temporarily cath them to bypass obstruction. give antibiotics for UTI.
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whats the most common surgery for BPH?
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transurethral resection of prostate (TURP or TUR)
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what is a TUR or TURP
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transurethral resection of prostate. enter bladder with resectoscope to shave off extra prostate tissue. 3-way foley provides drainage, flushing of bladder, and irrigation to prevent blood clots from urine obstruction.
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how would you detect prostate cancer?
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DRE, 75% have already metastasized by time detected.
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what are the symptoms of prostate cancer?
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UNILATERAL ENLARGEMENT. sx similar to BPH (nocturia, hesitancy, small or narrowed urinary stream), UTI, urinary retention.
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