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179 Cards in this Set
- Front
- Back
Hypothroidism?
|
-condition in which there is an INADEQUATE amt of circulating thyroid hormones (T3 & T4)
-DECREASE in metabolic rate affects all body systems |
|
Primary Hypothyroidism?
|
--most common
-caused by disease or loss of thyroid gland -EX: iodine deficiency, surgical removal of thyroid gland |
|
Secondary Hypothyroidism?
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--failure of Anteriod Pit. Gland to stimulate gland
-or failure of targe tissues to respond to the thryoid hormones (pituratry tumors) |
|
Teritary Hypothyroidism?
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-failure of hypothalamus to proude thyroid releasing factor
|
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Hyptothroyroidism is calssied by?
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-AGE OF ONSET
|
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Cretinism
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-state of severe hytothryoidsm found in fants
0don't rpdoude normal amts of thyroid hormones -skelttal maturation and CNS decolpment altered = growth retardation of phycial growth & mental growth or both |
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Juveinile hypothyroidism?
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-caued by chronic automimunie thyroididtis
-affectgs: growth & sexual maturation of child -treatment can reverse most cases of disease |
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Disorder of hypothyroidism is most prevelant in?
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-Women
-Persons age 40 - 50 |
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What is LOW during hypothyroidism?
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-T3 and T4
- |
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Serum thyroid-stimulaation hormone (TSH) is?
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-Level is ELEVATED w/Primary Hypothyroidism
-Level is DECREASED w/Secondary hypothyroidism |
|
what is elevated during Thyrotropin-releasing hormone (TRH) stimulation test?
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-Basal
-presence of early hypothyroidism |
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During hypothyroidsm Free thyroxing indexx (FTI) and thyroxing (T4) levels are?
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-DECREASED
|
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What do skull X-rays, CT scans, and MRI's do for hypothyroidsm?
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-Locate pituitary or hypothalmic lesions that may be underlying cause of hypothyroidism
|
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Radioisotope (131 I ) scan and uptake for hypothyroidism will be?
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-less than 10% in 24hr period
-2ndary hypothyroidism intake INCREASES w/admin of exogenous TSH |
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What will a ECG look like for hypothyroidism?
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-SINUS Bradycardia
-flat or inverted T-waves |
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Hypothyroidsm Serum Cholesterol will be?
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-ELEVATED
|
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CBC of hypothyroidism will show?
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-Anemia
|
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Early Symptoms of Hypothyroidsm are?
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-weakeness and fatigue
-intolerance to cold -decreased bowel motility -weight gain Joint or muscle pain -Brittle, thinning hair -Pale Skin -Depression |
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Late symptoms of hypothyroidism are?
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-Slow thought processes and speech
-Thickening of skin -Thinning eyebrows -dry flaky skin -swelling in hands and feet -decreased cardiac output -ineffective breathing pattern -activity intolerance -imbalanced nutrition: more than body requirements -risk factor for constipation -deceased acuity of taste and smell -hoarse, raspy speech -abnormal menstrual periods and decreased libido |
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What drus are CONTRAINDICATED for hypothyroidism?
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-Barbiturate
-Sedatives -CNS depressants!!!! |
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What is most frequently admined for Thyroid hormone therapy? [Hypothyroidism]
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-Levothyroxine(Synthroid)
|
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What should the PT be monitored for during thyroid hormone therapy for Hypothyroidism?
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-risk for cardiac compliactions
-Monitor: for cardio comprimise (palpiations, cehst pain, SOB, rapid heart rate) -usually occurs during early therapy |
|
How does thyroid hormone therapy begin? [Hypothyroidism]
|
-SLOWLY
-dosage Increases every 2 - 3 weeks -Treatment considered LIFELONG |
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S/S of hyperthyroidism with overmedication from Thyroid hormone therapy include?
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-irritability
-termors -tachycardia -palpitations -heat intolerance |
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For Hypothyroidism what should be increased gradually?
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-client's activity level
-provide frequent rest periods to avoid fatigue -Decreasemyocardial oxygen demand |
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For Hypothyroidism, what shoudl be applied to the client's legs?
|
-Antiembolism stockins
-elevate PT's legs to assist venous return |
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For Hypothyroidism, what should be encouraged to precent pumonary complications?
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-Cough and deep breathe deeply
|
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For Hypothyroidism, what type of diet should be encouraged?
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-HIGH BULK, LOW Calorie diet
-encourage exercise to promote weight loss -Admin: laxatives and stool softners as needed |
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For Hypothyroidism, if person is in bed rest what should you do?
|
-Turn and reposition every 2 hr
-Use alochol free skin care products and emollient lotion after bathing |
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For Hypothyroidism patients with decreased cold tolerance should be taken care of how?
|
-extra clothing and blankets
-Dress client in layers -adjust room temp -encourage warm liquids if possible -Caution against electric blankets and heating devices b/c combo of vasodilation, decreased sensation, decreased alertness may result in unrecognized burns |
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Myxedma Coma
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-life threatening condition occurs when hypothyroidism is UNTREATED
-when strressor such as infection affects individual with hypothyroidism |
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What do PT's with Myxedma Coma experince?
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-Decreaed respirations
-PaCO2 lvls may rise -Decreased cardiac output -Worsening cerebral hypoxia -Stupor -Hypothermia -Bradycardia -Hypotension |
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RN responses to Myxedma Coma?
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-Maintain ariway patency
-Maint cirucalion: IV flurid replacment -Continuous ECG monitoiring -Monitor ABG (arterial blood gases) - detects hypotxia and metabolic acidosis -Warm cleitn w/blankets -Monitor body temp until stable -Replacy thryoid hormone by admin large IV levothyroxine(Synthroid) as ordered -Monitor VS b/c radid correctoin of MC can ause advers Cardiac effects -Wigh daily and montior I&O, with treament Urine output will increase body weight decrease -Provide supplemental glucoses as needed -check of rinfections: wound, |
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The Thyroid gland produces what three hormones?
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--T4 (thyroxine)
-T3 (triiodothyronine) -Thyrocalcionin (calcitonin) |
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What regulates T3 and T4 secretion?
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-Anterior Pit. Gland though (-) feebback mechanism
|
|
What happens when T3 and T4 are decreased?
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-TSH is relased by Anterior Pit. Gland
-stimulates gland to secrete MORE homrones until normal lvl released |
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How does T3 and T4 affect all body systems?
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-Regulate overall body metabolism, energy production, fluid & electrolyte balances, controlling tissue use of fats, proteins and carbohydrates
|
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What does calcitonin inhibit?
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-Mobilization of Ca+ from bone and reduces blood Ca+ levels
|
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Hypterthyroidism?
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-caussed by Excessive circulation thyroid hormones
-Affecte enire body -causes exaggerate state of normal body functios |
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What can hyperthyroidism produce?
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-Hyper metabolic state
|
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Causes of Hypterthyroidism?
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-action of immunboglobulins on thyroid hormones
|
|
Graves disease:
|
-most common cause of HyperT
--automimmune mimic TSH lead to hypersectretion of thyroid hormones |
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Hyperthyroidism Serum TSH test?
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-DECREASED
|
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Hyperthyroidism Free thyroxine index (FTI) & T4?
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-ELEVATED
|
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Hyperthyroidism Thyrotropin-releasing hormone (TRH) stimulation test?
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-failure of expected rise in TSH
|
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Hyperthyroidism radioiodine (131 I ) and thyroid scan
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-clarifies size of gland and detect presence of hot or cold nodules
|
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For Hyperthyroidism why would a medication history be necessary to determine use of Iodines?
|
-Contrast median and OC cause falsely ELEVATED serum TSH lvls
-Severe illness, malnutrition use of aspirin, corticosteroids and phenytoin Na_ cause false decrease in serum TSH lvls |
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S/S of Hyperthyroidism?
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-Nervoussness, irriability, emotianl lability decreased attention span
-weakeness, easy fatibability, exercise intolerance -Heat intolerance -Weight change (usually loss); -increased appetite -Insomnia (interrupted sleep) -Frequent stools (diarrhea) -Mensstural irregulatirites, increased libido -Warm, sweaty flushed skin w?velverly smooth texture -Tremor, hyperknesias, hyperflexia -Vision changes, expohthalmos, treaterace eye lids, staring gaze -Hair loss -Goiter -Bruits over the thyroid gland -Elevated systolic BP, widened pulse pressure, S3 heart sound |
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For Hyperthyroidism Antithyroid medications?
Propplthiouracil(PTU) Methiimazol(Tpazole) |
-blocks thyroid hormone synthesis
|
|
For Hyperthyroidism Antithyroid medications?
Beta-Adrengergic blockers |
-Treats sympathetic nervous systems effects (tachycardia, palpiations)
|
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For Hyperthyroidism Antithyroid medications?
Iodine containing meds |
-inhibit release of stored thyroid hormone and retard hormone synthesis
-Use of these meds is CONTRAINDICATED in pregnancy |
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What should PT's receiving antithyroid meds for Hyperthyroidism be monitored for?
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-Hypothyroidism, occurs with OVERMEDICATION
|
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If PT is unresponsive to antithroid meds what should be done?
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-Prepare PT for total/subtotal thyroidectomy or has airway obstruction goiter
|
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What should be monitored during anitthyroid med therapy?
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-Vital Signs
-Hemodyanmic parameters for sings of HF |
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What should be provided for a patient with exopthalmos (hyperthyroidism)?
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-Eye protection(patches, eye lubricant, taping eyelids closed)
|
|
Thyroid Storm [Thyrotoxic crisis}?
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-large amts of thrydoid hromones into bloodstream
-causes greater increased body metabolism -this is a MED emergency w/high mortality rate |
|
Thyroid Storm precipiating factors?
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-Inefection, anemia, trauma, emotional stress = all increase demond on body metabolism
-Can occur with subtoal thyroidectome b/c manipulaion of gland during surgery |
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Thyroid Storm symptoms?
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-hyperthermia, hypertension, delirium, vomiting, abdominal pain, tachdysrhthmias
|
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RN response to Thyroid Storm?
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-Maintain patent airway
-Montor for dyshrthmias -Admin ASA (acetominophen) to decrease temp DONT USE ASPRIN -Cool sponge baths: or ice packs to client's axilla an graoin to decrease fever -Admin Propylthiouracil (PTU) : to prevent synthesis & release of thyroid hormones -Admin Propanol (inderal) to block sympathetic nervous system effects -Admin IV fluids -Admin Sodium Iodine 1 hr after admin of PTU -Admin small doses of Insulin to control hyperglcemia -Admin supplemental O2 |
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Thyroidectomy?
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-surgical removal of part/all of thyroid gland
|
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Thyroidectomy?
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-performed for treatment of hyperthyroidism when drug therapy FAILS, & radiaion contraindicated
-used to correct diffuse goiter & thyroid cancer |
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LIfelong thyroid replacement therapy is required for?
|
-client who has total thyroidectomy
|
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Steps taken before thyroidectomy?
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-4 - 6 weeks before surgery pt placed on PTU or methimazol(tapazole)
-client should receive IODINE 10 - 14 weeks before -Helps reduce size of gland & prevent excess bleeding -Propanol (inderal) may be given to block adrengeric effects |
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Why is it important to collect serum thyroid hormones before a thyroidectomy?
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-Determination to check for Euthyroidism preoperatively
|
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ECG before thyroidectomy?
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-To evaluate cardiac status
|
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Complications of Thyroidectomy include?
|
-Hemorrhage: surgical dressing and incision need to be assessed for excessive drainage and bleeding
-Tell PT to avoid neck flexion or extension - avoids pressure on suture line -Suport head and neck with pillow/sandbags -Thyroid storm (tachycardia, diaphoreses, increase BP, anxiety) -Airway Obstruction: trach tray kept near client at ALL times -Bed in HIGH fowler's postion to decrease edema and swelling of neck -Hypocalcemia and tetany (due to damage of parathyroid glands) -Monitor for signs of hypocalcemia (tingle of fingers and toes, carpopedal spams and convulsions) -have Calcium gluconate available -maintain seizure precautions -Nerve Damage -led to vocal cord paralysis and vocal disturbances -PT will be able to speak rarely and to rst voice for several days, should also expect it to be hoarse -Monitor clients ability to speak -Asses client' voice tone and quality pre/post op |
|
Diabetes Insipiduse
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-results from deficiency of ADH hormone
|
|
Antidiuretic Hormone (ADH)?
|
-Also known as vasopressin
-Secreted by posterior lobe of Pituitary gland (neurohpophysis) |
|
What does DECREASED adh do?
|
-reduces ability of distal and collection renal tubules in kideny to concentrate urine
-results in EXcessive diluted urination, excessive thirst, excessive fluid intake |
|
What is Neurogenic diabetes insipidus?
|
-Known as Primary or Central-
-caused by: defect in hypothalamus or Pit. Gland as in trauma, irradiation, or cranial surgery |
|
What is Nephrogenic diabetes insipidus?
|
-Inherited
-renal tubules do not respond to ADH |
|
What is drug-induced diabetes insipidus?
|
-From certain medications
|
|
Urine Chemistry for Diabetes Insipidus will be?
|
-think DILUTE
-Decreased specific grav. ( < 1.005) -Decreased urine osmalit (50 - 200 mOsm/kg) -Decreased Urine pH -Decreased urine Na+ & K+ As urine vol. INCREASES, Osmoalty DECREASES |
|
Serum Chemistry for Diabetes Insipidus will be?
|
-Think CONCENTRATED
-Increased serum Osmality -Increased serum Na+ and K+ -as serum volume INCREASES, serum osmality DECREASES |
|
Diabetes insipidus Radioimmunoassay will have?
|
-Decreased ADH
|
|
Water deprivation test for diabetes insipidus?
|
-Simplest and most reliable test
-inablilty of kidneys to concentrate urine despite increased plasma osmolaity and low plasma vasopression level |
|
Vasopression test for diabetes insipidus?
|
-subQ injection of vasopression produces output with increaesd urine specific gravity if client has CENTRAL diabetes
-Helps diffrentiate between Central and Nephrogenic diabetes |
|
S/S of diabetes insipidus?
|
-Polyuria (abrupt onset of exsessive urine)
-Urinary output of 5 to 20L/day of dilute urine -Polydipsia (excessive thirst, consumption of 4 to 30L/day) -Nocturia -Fatigue -Dehydration: EV by: exterme thirst, weight loss, muscle weakness, headache, tachycardia, hypotension, poor skin turgor, dry mucous membranes, constipation, dizziness |
|
What can untreated diabetes insipidus produce?
|
-Hypovolemia, hyperosmality, circulatory collapse, unconsciousness, and CNS damage
|
|
Meds for Diabetes Insipdius?
ADH replacment agent? |
-Desmopression acetate (DDAVP)
-Aquaeous Vasopressin (Pitression) admined intranasally, orally or parentreally |
|
Meds for Diabetes Insipdius?
ADH stimulant |
-Carbamzepine (Tegretol)
|
|
Why should Vasopression be given caustiously for a PT with CAD & diabetes insipdius?
|
-Med causes vasoconstriction
|
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What shoud you tell a DI patient the reason for lifelong vasopressin therapy?
|
-Daily weight, and importance of reporting weight gain, polyuria and polydipsia to primary care provider
|
|
SIADH?
|
-Syndrome of inappopriate ADH
-excessive release of ASD [vasopressin] |
|
[SIADH ] Excess ADH ?
|
-leads to renal absorption of water an disruptions of angiotension mech
-causes renal exreciotn of sodium leading to water intoxication, cellular edema, and dillutional hyponatermia, -Fluid shifts within compartments caused decreased serum osmality |
|
What conditions stimulate the hyptothamlus to hypersecrete ADH?
|
-Malignant tumors( commosn cause is oat-cell lung cancer)
-increasing intrathoracic pressure -head injury -Meningitis -Cardiovascular accident -Meds (alcohol, lithium carbonate, phenytoin) -Trauma -Pain -Stress |
|
[SIADH] Urine Chemistry?
|
-Think CONCENTRATED
-Increased urine Na+ -Increased urine osmolaity -urine vol. DECREASES, urine osmolality INCREASES |
|
[SIADH] blood chemistry?
|
-Think DILUTE
-Decreased serum Na+ (110mEq/L) -Decreased osmolality (< than 270 mEq/L) -As serum vol increases, serum osomlality decreaess |
|
[SIADH] Radioimmunoassay will show?
|
-Increased ADH
|
|
Early symtpoms for SIADH?
|
-Headache, weakeness, anorexias, muscle cramps, weight gain (w/o edema b/c wat not Na+ is retatined)
- |
|
For SIADH as serum Na+ decreased the patient will?
|
-experience personality changes, hostility, sluggish deep tendon reflexes, nausea, vomiting, diarrhea, and oliguria
-experience confusion, lethargy, Cheynes-Stokes respirations |
|
For SIADH as serum Na+ is extremly decreased patient will?
|
-seizures, cooma, death may occur
|
|
SIADH?
|
-Syndrome of inappopriate ADH
-excessive release of ASD [vasopressin] |
|
[SIADH ] Excess ADH ?
|
-leads to renal absorption of water an disruptions of angiotension mech
-causes renal exreciotn of sodium leading to water intoxication, cellular edema, and dillutional hyponatermia, -Fluid shifts within compartments caused decreased serum osmality |
|
What conditions stimulate the hyptothamlus to hypersecrete ADH?
|
-Malignant tumors( commosn cause is oat-cell lung cancer)
-increasing intrathoracic pressure -head injury -Meningitis -Cardiovascular accident -Meds (alcohol, lithium carbonate, phenytoin) -Trauma -Pain -Stress |
|
[SIADH] Urine Chemistry?
|
-Think CONCENTRATED
-Increased urine Na+ -Increased urine osmolaity -urine vol. DECREASES, urine osmolality INCREASES |
|
[SIADH] blood chemistry?
|
-Think DILUTE
-Decreased serum Na+ (110mEq/L) -Decreased osmolality (< than 270 mEq/L) -As serum vol increases, serum osomlality decreaess |
|
[SIADH] Radioimmunoassay will show?
|
-Increased ADH
|
|
Early symtpoms for SIADH?
|
-Headache, weakeness, anorexias, muscle cramps, weight gain (w/o edema b/c wat not Na+ is retatined)
- |
|
For SIADH as serum Na+ decreased the patient will?
|
-experience personality changes, hostility, sluggish deep tendon reflexes, nausea, vomiting, diarrhea, and oliguria
-experience confusion, lethargy, Cheynes-Stokes respirations |
|
For SIADH as serum Na+ is extremly decreased patient will?
|
-seizures, cooma, death may occur
|
|
[SIADH] Restrict Oral fluids to?
|
-500 - 1000mL ro prevent further hemodiluation
-privide oral hysteopine as well as ice chips, lozenges or hard candy and scheduled water intake |
|
[SIADH] Monitor VS for?
|
-Increased BP, tachycardia, and hypothermia
|
|
Cushing's disease/Syndrome?
|
-characterized by adrenal glands hyperfunction excess production of glucocoritocid coritsol
|
|
What do high levels of corisold reduce?
|
-Lymphocyte activity which creates immunosuppression
|
|
What is endogenous causes of Cushing's disease include?
|
-Adrenal hyperplasia
-Adrenocoritcal neoplasm -Pituitary neoplasm that secreated adrennocoricopropic horomone (ACTH) -Carincoma: lung, GI tract, pancreas (these tumors can secrete ACTH) - |
|
When does Cushing's disease usually occur?
|
-in women between 25 - 40 years old
|
|
What is endogenous causes of Cushing's disease therapeutic uses of glucocoricoids for?
|
-Chronic fibrosis
-Allergies -Cancer chemotherapy -Organ transplantation -Autoimmune disorders -Asthma |
|
[Cushing's Syndrome/Disease]
Dexamethasone suppression test |
-24hr urine collection reveal suppression of cortisol exertion in clients' w/o cushing's
-Nonsuppriession of coritsol excretion = Cushing's - |
|
[Cushing's Syndrome/Disease]
Diagnostic for Serum Na+, K+, glucose |
-Serum Na+ lvl = INCREASED
-Serum K+ & Ca+ = DECREASED -Serum glucose lvl = INCREASED |
|
[Cushing's Syndrome/Disease]
Urine corisol levels? |
-Elevated lvls of free coritsol
|
|
Therapeutic procedures for engodneous hyptercorisolism include?
|
-Surgical removal of Pit. or Adr. Gland (depending on cause)
Hypophysectomy: Intervene for risk ass. with cranial surgery -Adrenlaectomy: intervene for risks assoc. with flank or abdominal surgery. provide glucocoritcoid replacement as needed Chemothearpy w/cytotoxic agents: Monitor AE example thrombocytopenia Radiation Therapy: Intervene for skin and alopecia effects |
|
S/S of [Cushing's Syndrome/Disease]
|
-Decreased immune fucntion
-Decreased inflammatory resonse -HTN (Na+ and H20 retention) -Changes in fat distrubution: moon face, truncal obestity, fat collection on back of next (buffalo hump) -Emotional lability -Fractures (osteoporosis) -Impaired glucose tolerance -Hirsutism -Bruising and petechiae (fragile blood vessels) -Muscle wasting |
|
Addison's disease:
|
-adrenocortical insufficieny
-caused by damge or dysufntion of adrenal cortex |
|
What does the adrenal cortex produce?
|
-Mineralcoricoids, Gluccoritcoids, Sex hormones
|
|
Mineralcorticoids:
[Addison's disease] |
-Aldosterone: Increases na absorption, causes K+ secretion
|
|
Glucocoricoids:
[Addison's disease] |
-Corisole -affects glucose, protein and fat metabolism and body's resonse to stress and body's immune function
|
|
Sex hormones:
[Addison's disease] |
-ANdrogens and Estrogen
|
|
Production of what is diminshed in Addison's disease?
|
-Mineralcoritcoids and glucocoritcoids, resulting in decreased aldosterone and cortisol
|
|
Adrenal Crisis:
[Addison's disease] |
-also knowsn as acute adrenal insufficency
-is a MED emergency |
|
Majority causes of [Addison's disease]
|
-Idopahtics autoimmune dysfunction
-Tuberculosis |
|
Adrenal crises [Addison's disease] caused by
|
-acute chronic insufficiency due to:
-sepsis -trauma -stress -adrenal hemmorrhage -steroid withdrawal |
|
Diagnostic procedures and expected findings for [Addison's disease]:
Serum electrolytes? |
-increased K+ & Ca+, decreased Na+,
|
|
Diagnostic procedures and expected findings for [Addison's disease]:
BUN, Creatinine? |
-Increased
|
|
Diagnostic procedures and expected findings for [Addison's disease]:
ECG? |
-Dysrhythmias
|
|
Diagnostic procedures and expected findings for [Addison's disease]:
Serum glocuose and cortisol? |
-Decreased
|
|
Diagnostic procedures and expected findings for [Addison's disease]:
ACTH |
-ACTH infused and cortisol lvl measured
-Plasma cortisol lvls don't rise |
|
S/S [Addison's disease]:
|
-Hyperpigmentation
-Weakness and fatigue -Nausea and vomiting -Dizziness w/orthostatic hypotension -Dehydration -Hyponatremia -Hyperkalemia -Hypoglycemia -Hypercalcemia |
|
Pheochromocytoma
|
-tumor of the adrenal gland
-rare tumor -about 10% of pheochromocytomas are malignant |
|
Pheochromocytoma produced and stored?
|
-catecholamines, such as epinephrine and norepinephrine
-excess epi and nonepi, produce sympathetic nervous system effects |
|
Preciptating factors of a catecholamine surge by peochromoocytome in a PT may be?
|
-Anesthesia
-Opiates and opiate antagonists (ex: naloxone) -Dopamine antagonist (droperidol, phenothizines) -Drugs that inhibit catecholamie reputake (TCA) -Childbirth -Radograhic contrast media -Foods high in tyramine (wine, aged cheese) |
|
Diagnostic tests for Pheochromocytoma:
Vanillymandelic acid testing (VMA) |
-24 hour urine collection for catecholamines, metanephrine, and VMA
-Normal: 2 - 7mg/24hr -High levels @ rest indicate pheochromocytoma |
|
Diabetes mellitus is characterized by?
|
-Chronic hyperglycemia due to problems w/insulin secregoin or effectiveness of endogenous insulin
|
|
Diabetes mellitus is a contributing factor to?
|
-Cardiovascular disease, hypertension, renal failure, blindness, and stroke
-Due to impact on larg and small blood vessels |
|
Hallmark symptoms assoc. with Diabetes Mellitus? 3P's!
|
-Polyuria
-Polydipsia -Polyphagia |
|
Normal Range for Diabetes mellitus
|
-70 - 120 mg/dL
|
|
Type 1 diabetes characterized by?
|
-autoimmune disorder characterized by beta cell destruction
-Occurs genetically suspectiple ppl before the age of 30 |
|
Type 2 diabetes characterized by?
|
-development of resistance to endogenous insulin
-occurs frequently in individuals with family disposition who are Obese and over the age of 40 |
|
Hallmark risk factors for development of insulin resistance include?
|
-Obesity, physical inactivity, high triglycerides (.250 mg/dL) and hypertension
|
|
Secondary causes of diabetes mellitus include?
|
-Pancreatitis
-Cushing's syndrome |
|
Iatrogenic causes of diabetes mellitus include?
|
-Glucocorticoid usage
|
|
Diagnostic criteria for diabetes mellitus two findings (separate days) of one of the following:
|
-Sym. of diabets + casual plams glucose concentration of greater than 200mg/dL (w/o regard to time since last meal)
-Fasting blood glucose greater than 126 mg/dL (8 hr fasting) -Two-hour glocse greater than 200mg/dL with an oral glucose tolerance test (10 - 12 hr fasting) |
|
Fasting blood glucose
|
-Ensure pt has fasted for 8 hr period prior to blood draw
-Antibidabetic meds should be postponed |
|
Pre-meal glucose:
|
-Target is 90 - 130 mg/dL
- |
|
Oral glucose tolerance test:
|
-Instruct client to consume balnced diet for 3 days prior to test
-Than instruct client to fast for 10 - 12 hrs prior to test -Fasting blood glucose drawn at start of test -Client than instructed to consume specified amt of glucose -Blood glucose levels than taken every 30 min for 2 hrs -Client must be assessed for hyperglycemia throughout procedure |
|
Glycosylated hemoglobin (HbA1c)
|
-Target is 4 - 6%
-best indicator of average blood glucose level for past 120 days |
|
S/S of Type 1 Diabetes:
|
-Polyurida, Polydipsia, Polyphagia
-weight loss -fatigue -Increased frequency of infections -Rapid onset -controlled by exogenous insulin |
|
S/S of Type 2 Diabetes:
|
-Polyurida, Polydipsia, Polyphagia
-Obesity -fatigue -Increased frequency of infections -Gradual onset -controlled by oral antidiabetic meds and insulin |
|
S/S by Glucose alteration:
Hypoglycemia |
- ( < 50mg/dL)
-Cool, clammy skin -Diaphoresis -Anxiety, irritability, confusion, blurred vision -Hunger -General weakness, seizures, (severe hypoglycemia) |
|
S/S by Glucose alteration:
Hyperglycemia |
- ( > 250mg/dL)
-Hot, dry skin - Absence of diaphoresis -Alert to coma (varies) -N/V, abdominal pain (w/ketoacidosis) -Rapid deep respirations (acetone/frutiy odor due to ketones) |
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Appropriate Assessments for PT with diabetes mellitus include?
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-Blood glucose lvls
-I & O, weight -Skin integerity and healing status of wounds -Sensory alterations (tingling, numbness) -Condition of feet and foot care practices Dietary practices -Exercise patterns -Client's self montior of blood glucose skill profeicency -Client's self med admin proficiency -Pain levels |
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Instructions for proper foot care for patient with diabetes mellitus?
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-Insepect feet daily wash with warm water & mild soap
-Pat feet dry, especially between toes -Use mild foot powder (powder with cornstartch) on sweaty feet -Don't use commercial remedies to remove calluses or corns -Cut toenails even with rounded contour of toes; don't cut corners -Best time to cut nails = after shower/bath -Cusult podiatrist for trimming thick, malformed toenails -Avoid open-toed, open heel shoes. Leather shoes are perferred over plastic ones. Wear slippers with traction. Never go barefoot. Shake shoes upside down before putting them on -Wear clean abosorbent socks or stockings -Don't apply exernal heat to warm feet. wear socks for warmth -avoid extensive periods of sitting, standing, and avoid crossing legs |
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Nutritional Management for a patient with diabetes mellitus?
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-Count grams of carbohydrates consume (Dosage of insulin determined by this consumption; 1 unit/15 g carbohydrates)
-Restric calories and increased physical activity for clients that are obese -Include fiber in diet to increase carbohydrate metabolism and help control cholesterol levels -use artificial sweetners -Use fat replacers within guidelines |
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Rapid-Acting (Humalog, Lispro)
Onset: Peak: Duration: Administer: |
Onset: < 15 mins
Peak:0.5 - 1.5 hr Duration: 2 - 6 hr Administer: 5 - 15 min ac |
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Intermediate-Acting (Lente)
Onset: Peak: Duration: |
Onset: 3 -4 hrs
Peak:4 - 12 hrs Duration: 12 - 20 hrs |
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Short-Acting (Humulin R, Regular)
Onset: Peak: Duration: Administer: |
Onset: 30 - 60 min
Peak: 2 - 3 hrs Duration: 3 - 10 hrs Administer: 30 min ac |
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Intermediate-acting: Humulin N, NPH, 70/30, 70/25)
Onset: Peak: Duration: Administer: |
Onset: 2 - 4 hrs
Peak: 4 - 10 hrs Duration: 10 - 18 hrs |
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Long-acting: Ultralente
Onset: Peak: Duration: |
Onset: 6 - 10 hrs
Peak: 8 - 20 hrs Duration: 18 - 24 hr |
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Long Acting: Lantus
Peak: Duration: |
Peak: none
Duration: 24 hrs |
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Why is it important to rotate injection site for pt with diabetes mellitus?
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-prevents liphohypertrophy
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How to inject insulin for patient with diabetes mellitus?
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-90 degree angle for obese patient
-45 degree angle for thin patient -Aspiration of blood not necessary |
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How to mix rapid or short acting insulin with long acting insulin?
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-1st draw up shorter acting insulin into syringe
-Than draw up longer acting insulin |
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Diabetic ketoacidosis (DKA):
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-acute, life threatening condition
-characterized by hyperglycemia (> 300mg/dL) -results in breakdown of body fat for energy and accumulation of ketones in blood and urine -Onset = rapid -Moratly rate 1 - 10% |
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Hyperglycemic-hyperosmolar nonketotic syndrome (HHNS)
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-acute, life thretening condiong
-characterized by profound hyperglycemia (>600 mg/dL) |
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DKA & HHNS both result in sever hyperglycemia from:
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-lack of sufficient insulin (new onset diabetes, lack of compliance of diabetes plan)
-increased need for insulin (stress, illness, infection, surgery, trauma) |
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DKS more common in:
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-individuals with type 1 diabetes mellitus
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HHNS more common in?
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-older adult clients and individuals with untreated or undiagnosed type 2 diabetes mellitus
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Diagnostic Procedures: DKA
Serum Glucose lvls |
- > 300 mg/dL
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Diagnostic Procedures: DKA
Serum Electrolytes |
-Na+ increased due to water loss
-K+ initally low due to diuresis, may increase due to acidosis |
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Diagnostic Procedures: DKA
Serum Renal studies |
-BUN & Cretinine: Increased seocndary to dehydration
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Diagnostic Procedures: DKA
Ketone Levels |
-Serum and Urine: both present
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Diagnostic Procedures: DKA
Serum Osmolarity |
-High
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Diagnostic Procedures: DKA
Serum pH (ABG) |
-Metabolic acidosis with respiratory compensation (Kussmaul respirations)
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Diagnostic Procedures: HHNS
Serum pH (ABG) |
-Absence of acidosis
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Diagnostic Procedures: HHNS
Serum osmolarity |
-very high
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Diagnostic Procedures: HHNS
Ketone levels |
-Serum & Urine: Both absent
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Diagnostic Procedures: HHNS
Serum Renal studies: |
-BUN and Creatinine: Increased secondary to dehydration
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Diagnostic Procedures: HHNS
Serum electrolytes |
-Na+ increased due to water loss
-K+ initially low due to diuresis |
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Diagnostic Procedures: HHNS
Serum glucose levels |
- ( > 600 mg/dL)
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