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143 Cards in this Set
- Front
- Back
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Name the two life-threatening deficiencies that are associated with the endocrine system.
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ACTH - adrenocorticotropic hormone
THS - thyroid stimulating hormone |
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Name the general clinical manifestations of growth hormone deficiency
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-growth below the 3rd percentile - dwarfism
-overcrowded malpostional teeth -normal intelligence -reproduce normal offspring |
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Name the general clinical manifestations of growth hormone excess
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-overgrowth of long bones, viscera and muscles - acromegaly or prepubertal gigantism
-separation of teeth and malocclusion |
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At what age does the epiphyseal plate closes?
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25 years.
Excess of growth hormone prior to 25 years: prepubertal gigantism Excess of growth hormone after 25 years: acromegaly |
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Name some causes of GH deficiency.
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-benign or malignant pituitary tumor
-severe malnutrition or rapid loss of body fats (anorexia nervosa patients) -shock or severe hypotension -head trauma, infections, brain surgery -postpartum hemorrhage (can lead to shock and hormone deficiency) |
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With excessive growth hormone, what general presentation do we look for first?
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-Neuro: first occurs as changes in vision
-temporal headaches, diplopia, occasional muscle paralysis -acromegaly is famous for causing vision problems as the optic chasm sits right above the pituitary gland. If the pt has diplopia, then there is a tumor already. Do a "follow my finger" test to see where the peripheral vision exists. |
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Clinical manifestations of deficient growth hormone
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-decreased bone density
-pathologic fractures (look at gait for sign that pt had a problem with fractures before) -decreased muscle strength -increased serum cholesterol levels |
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Clinical manifestations of deficient gonadotropins (LH and FSH)
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Women
-amenorrhea -anovulation -low estrogen levels -breast atrophy -loss of bone density -decreased axillary and pubic hair -decreased libido Men -decreased facial hair -decreased ejaculate volume -reduced muscle mass -loss of bone density -decreased body hair (look to see if body is hairless and smooth) -decreased libido -impotence |
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Clinical manifestations of deficient thyroid-stimulating hormone (thyrotropin) (TSH)
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-decreased thyroid hormone levels
-weight gain -intolerance to cold (because they're not generating heat) -scalp alopecia -hirsutism -menstrual abnormalities -decreased libido -slowed cognition -lethargy |
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Clinical manifestations of deficient adrenocorticotropic hormone (ACTH)
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-decreased serum cortisol levels
-pale, sallow complexion -malaise and lethargy -anorexia -postural hypotension (brain isn't getting enough oxygen and pt gets dizzy) -headache -hypoglycemia (more dangerous than hypergycemia, pt can die faster, brain doesn't store sugar) -hyponatremia -decreased axillary and public hair (women) |
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Clinical manifestations of deficient vasopressin (ADH)
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Diabetes Insipidus
-greatly increased urine output -low urine specific gravity <1.005 -hypovolemia: hypotension, dehydration -increased plasma osmolarity -increased thirst -output does not decrease when fluid intake decreases |
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What is the therapeutic management for growth hormone deficiency?
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-surgical intervention: remove or irradiation of craniopharyngioma
-endocrine: replacement of GH wit recombinant DNA GH -stop GH therapy when epiphysis closes |
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What is the therapeutic management for growth hormone excess?
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-surgical removal of lesion
-endocrine replacement of all hormones affected |
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What is the concern regarding males and hormone replacement?
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Androgen therapy is avoided in men with prostate cancer.
Side effects of testosterone therapy include gynecomastia (male breast tissue development), acne, baldness, and prostate enlargement. |
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What is the concern regarding females and hormone replacement?
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The risk for hypertension or thrombosis (formation of blood clots in deep veins) is increased with estrogen therapy, especially among women who smoke.
We worry virilization, clots, and smokers. Monitor trending blood pressures and clot formation (Homan's sign, foot flexion). |
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What is the most common cause of hyperpituitarism?
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Adenoma; tumor on the pituitary gland.
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What are the clinical manifestations of excessive prolactin?
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Prolactin (PRL)-secreting tumors are the most common type of pituitary adenoma. Excessive PRL inhibits the secretion of gonadotropins and sex hormones in men and women, resulting in galactorrhea (breast milk production), amenorrhea, decreased libido, impotence, and infertility.
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How do you assess for acromegaly?
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Increase size in hat, gloves, ring, or shoes.
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What is the drug intervention for hyperpituitarism?
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bromocriptinee mesylate (Parlodel)
-stimulates dopamine receptors in brain and inhibit the release of GH and PRL -in acromegaly, it reduces GH levels and decreases tumor size octreotide (Sandostatin) -inhibits GH release through negative feedback -must be given as an injection on daily or weekly schedule |
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What are the side effects of bromocriptine (Parlodel)?
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-orthostatic (postural) hypotension
-gastric irritation -nausea -headaches -abdominal cramps -constipation -give bromocriptine with meal/snack to reduce side effects -if pregnancy occurs, stoop bromocriptine immediately! |
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What is the side effect of octreotide (Sandostatin)?
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-gallbladder disease
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What is the drug alert for bromocriptine (Parlodel)?
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Teach pts taking bromocriptine to seek medical care immediately if chest pain, dizziness, or watery nasal discharge occurs because of the possibility of serious side effects, including cardiac dysrhythmias, coronary artery spasms, and cerebrospinal fluid leakage.
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Name the surgery that removes the pituitary tumor through the nasal cavity.
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Transsphenoidal surgery; hypophysectomy.
Have pt sit up, we don't want the brain to shift when going in. We also worry about hemorrhaging since so close to carotid arteries and sinuses. |
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How long after the transsphenoidal/hypophysectomy operation does the pt have to follow the precautions?
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2 months. Because that bony structure has to take that long to build itself back up. In the meantime, the pituitary will be very vulnerable. Pt will not stay in hospital for 2 months, so we need to educate them.
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What is the post-op care after a hypophysectomy?
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-monitor the pt's neurological status hourly for the first 24 hours and then even 4 hours
-Monitor fluid balance, especially for output greater than intake, because transient diabetes insipidus can occur -encourage pt to maintain pulmonary hygiene through deep-breathing exercises -instruct the pt to not cough, blow nose, or sneeze -instruct pt to use dental floss and oral mouth rinses because brushing teeth is not permitted until the incision heals sufficiently -instruct pt to avoid bending at the waist for any reason because this position increases intracranial pressure -monitor the nasal drip pad for the type and amount of drainage; the presence of the halo sign may indicate CSF leak (A light, yellow color at the edge of the clear drainage on the dressing is called the "halo sign" and indicates CSF.) -monitor bowel movements to prevent constipation and subsequent "straining" -teach the pt self-administration of the prescribed hormones |
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What is the home care assessment for a pt who has undergone transsphenoidal or endoscopic nasal hypophysectomy for hyperpituitarism?
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Assess cardiovascular status:
-vital signs, including apical pulse, pulse pressure, presence or absence of orthostatic hypotension, and the quality/rhythm of peripheral pulses Assess cognition and mental status: -level of consciousness -orientation to time, place, and person -accurate reading of a seven-work sentence containing no words longer than three syllables Assess condition of operative site: -observe nasal area for drainage -if drainage present, not color, clarity, and odor -test clear drainage for the presence of glucose Assess neuromuscular status: -reactivity of patellar and biceps reflex -oral temperature -handgrip strength -steadiness of gait -visual fields -distant and near visual acuity -pupillary responses to light Assess kidney function -observe urine specimen for color, odor, cloudiness, and amount Ask about: -headaches or visual disturbances -ease of bowel movements - 24-hr fluid I&O - 24-hr diet recall - 24-hr activity recall -OTC and Rx drugs taken Assess pt's overall understanding of illness and adherence with treatment -signs and symptoms to report to health care provider -drug plan (correct timing and dose) |
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What is normal urine output per day?
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1.5 liters or 1,500 mL per day
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If normal output is 1500 mL/day, what is the expected output per hour? 8-hr shift? 12-hr shift?
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1500 mL/day / 24 hours = 62.5 mL/hour
1500 mL/day / 3 = 500 mL/8-hr shift 1500 mL/day / 2 = 750 mL/12-hr shift |
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What is the etiology of diabetes insipidus?
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-undersecretion of ADH
-inability of the kidneys to response to ADH -damage or tumor to posterior pituitary gland leads to uncontrolled diuresis -damage may be coup, countercoup, swelling, edema, or even immediate inflammatory response when we didn't even touch the pituitary gland in surgery |
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What is the nursing alert regarding diabetes insipidus?
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Ensure that no pt suspected of having diabetes insipidus is deprived of fluids for more than 4 hours, because they cannot reduce urine output and severe dehydration can result.
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What are the clinical manifestations for diabetes insipidus?
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Cardiovascular
-hypotension -decreased pulse pressure -tachycardia -peripheral pulses weak, easily blocked -hemoconcentration: increased hemoglobin, hematocrit, BUN Kidney/Urinary -increased urine output: dilate, low specific gravity;hypo-osmolar Skin -poor turgor -dry mucous membranes Neurologic -increased sensation of thirst -irritability -decreased cognition -hyperthermia -lethargy to coma -ataxia All S/Sx are related to dehydration related to thirst and urination! |
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How do you monitor and create cardiovascular trends for diabetes insipidus?
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-take BP with pt standing up and sitting down
-always check apical pulse for heart rate, more accurate -7 cardinal pulse points: carotid, apical, brachial, radial, femoral, popliteal, pedal -auscultate heart sounds -worry about heart murmurs: potassium is being lost -know labs to establish pt baseline |
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How do you monitor and create kidney trends for diabetes insipidus?
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Look at BUN – we’re going to bombard the kidneys with fluid, so see if glomerulus stays intact
Output Intake Specific gravity |
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How do you monitor and create neurological trends for diabetes insipidus?
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Assess LOC (mentation), pt needs to be able to track conversation – before you get to severe dehydration.
Monitor hyperthermia. |
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What are the drug therapies for diabetes insipidus?
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desmopressin (DDVAP, Rhinal Tube, Minirin, Stimate)
-synthetic type of ADH that serves as replacement; binds to kidney receptors and enhances the reabsorption of water, thus reducing urine output vasopressin (Pitressin) -exogenous form of ADH that serves as replacement; binds to kidney receptors and enhances the reabsorption of water, thus reducing urine output chlorpropamide (Diabinese, Insulase) -antidiabetic agent drug that also has some antidiuretic activity through an unknown mechanism; decreases urine output |
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What are the nursing interventions regarding desmopressin?
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-teach pt using the inhaled form to blow the nose before taking drug
-teach pt using the inhaled form to sit upright and hold breath when spraying or using the rhinal tube -warn pts not to drink more than 3 L of fluids daily while on this drug -teach pt to weigh themselves daily and to notify health care provider if 2 lbs or more is gained in 24 hours -tell pt to notify health care provider if they experience a persistent headache or acute confusion |
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What are the nursing interventions regarding vasopressin?
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-monitor pt for signs of water intoxication: listlessness, drowsiness, confusion, headache, anuria, and weight gain
-warn pts not to drink more than 3 L of fluids daily while on this drug -teach pt to weigh themselves daily and to notify health care provider if 2 lbs or more is gained in 24 hours -tell pt to notify health care provider if they experience a persistent headache or acute confusion |
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What are the nursing interventions regarding chlorpropamide?
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-ask whether pt has any allergies to sulfa-based drugs
-teach pts the manifestations of hypoglycemia and to always carry candy or concentrated sugar with them The main action of the drug is to lower blood glucose levels; when taken by a person whose blood glucose is normal, hypoglycemia may result. |
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What is the etiology of SIADH?
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-over secretion of ADH, resulting in fluid retention and hypotonicity (dilutional hyponatremia)
-infections, tumors, CNS disease or trauma *know S/Sx of water intoxication |
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What will you assess in a pt with SIADH?
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All assessments and interventions are related to water retention!
GI -loss of appetite, anorexia -nausea -vomiting Neuro (esp. when sodium levels drop < 115 mEq/L) -lethargy -headaches -hostility -disorientation -change in LOC -decreased responsiveness -seizures -coma -assess deep tendon reflexes, which are usually decreased (paresthesia) Vital Signs -full, bounding pulse (due to increased fluid volume) -hypothermia (due to CNS disturbance) -HTN Urine volume decreases, urine osmolarity increases. Plasma volume increases, and plasma osmolarity decreases. Elevated urine sodium levels and specific gravity reflect increased urine concentration. Serum sodium levels are often decreased as low as 110 mEq/L. |
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What is the therapeutic management for a pt with SIADH?
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-restrict fluids; keep at 500-600 mL/24 hr
-use normal saline rather than plain water, which would add to the water intoxication -report weight gain of 2 lbs or more per day A 1-kg weight increase is equal to a 1000 mL fluid retention (i kg = 1 L). |
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What is the drug therapy for a pt with SIADH?
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tolvaptan (Samsca)
conivaptan (Vaprisol) These are vasopressin antagonists that promote water excretion without causing sodium loss. |
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What is the black box warning for tolvaptan (Samsca)?
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Rapid increases in serum sodium levels, those greater than 12 mEq/L increase in 24 hr, has been associated with CNS demyelination that can lead to serious complications and death.
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What are the signs and symptoms of fluid retention getting worse?
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Monitor the pt's response to therapy to prevent the fluid overload from SIADH from becoming worse, leading to pulmonary edema and heart failure.
Possible neurological changes and the risk for seizures increase as a result of osmotic fluid shifts into brain tissue. Assess for subtle changes, such as muscle twitching, before they progress to seizures or coma. |
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Differ between acute adrenal insufficiency vs. adrenal insufficiency.
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Acute adrenal insufficiency
-life-threatening -adrenal crisis; addisonian crisis -need for cortisol and aldosterone is greater than the available supply Adrenal insufficiency -is developing into life-threatening -impaired cortisol secretion results in decreased gluconeogenesis, leading to hypoglycemia. -reduced aldosterone secretion causes hyperkalemia, hyponatremia, and hypovolemia; potassium retention also promotes reabsorption of hydrogen ions, which can lead to acidosis. |
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What are the 3 H's for Addison's Crisis?
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hormone replacement
hyperkalemia hypoglycemia |
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What is the emergency care for hormone replacement in adrenal insufficiency?
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mineralcorticoids (fluid balance) and glucocorticoids (hypoglycemia)
-start rapid infusion of normal saline or dextrose 5% in normal saline -initial dose of hydrocortisone sodium succinate (Solu-Cortef) is 100-300 mg or dexamethasone 4-12 mg as an IV bolus -infuse additional 100 mg of hydrocortisone sodium succinate by continuous IV drip over the next 8 hours -give hydrocortisone 50 mg IM concomitantly every 12 hours -initiate an H2 histamine blocker (e.g. ranitidine) IV for ulcer prevention |
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What is the emergency care for hyperkalemia in adrenal insufficiency?
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monitor for arrythmias, monitor labs (potassium and sodium and see for balance between two, look at completely panel)
-administer insulin (20-50 units) with dextrose (20-50 mg) in normal saline to shift potassium into cells -administer potassium binding and excreting resin (e.g. Kayexalate) -give loop or thiazide diuretics -avoid potassium-sparing diuretics -initiate potassium restriction -monitor I&O -monitor heart rate, rhythm, and ECG for manifestations of hyperkalemia (slow heart rate, heart block, tall peaked T waves, fibrillation, asystole) |
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What is the emergency care for hypoglycemia in adrenal insufficiency?
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monitor blood glucose (related to glucocorticoids), for someone in a crisis then monitor every half hour and do needle stick b/c hypoglycemia will kill brain
The max you can go without monitoring is 15-30 min because brain will die -administer IV glucose -administer glucagon -maintain IV access -monitor blood glucose level hourly |
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What are the clinical manifestations of adrenal insufficiency?
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Neuromuscular
-muscle weakness -fatigue -joint/muscle pain Gastrointestinal -anorexia -nausea, vomiting -abdominal pain -bowel changes (constipation/diarrhea) -weight loss -salt craving Skin: -vitiligo -hyperpigmentation Cardiovascular -anemia -hypotension -hyponatremia -hyperkalemia -hypercalcemia Neuro: fatigue, muscle weakness, which can cause pt to fall and crack head open; look at sensorium and mentation GI: report bowel sounds x4, if you hear hypo sounds indicate which quadrant Listen 5 minutes before reporting hypo sound, also a good time to confirm everything else Palpate or chart may say no palpation on abdomen because of adrenal tumor and pheochromocytoma Pt will be vocal about wanting potato chips, salty foods Skin: see hyperpigmentation on hands, at everything RN is responsible for assessing everything Cox has pt with vitiligo on labia Decreased hair, look at race CV: Have to know the normals, labs, VS, trends Anemia: pink in hands, Hct is 35, Hgb is 12 Apical pulse, listen minimum of 1 minute |
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In Addison's disease, why do we monitor?
-sodium and potassium -glucose -calcium -BUN, cortisol -stimulation tests |
Sodium 136-145 mEq/L
Potassium 3.5-5.9 mEq/L -in balance with sodium potassium pump, look at them together and make sure we’re not hypo or hyper condition Glucose 70-115 mg/dL -avoid hypoglycemia, most vulnerable organ is brain, s/s include dizziness, LOC loss -look at 70 for s/s of hypoglycemia -60 – you can still recover it -50 – you’re in crisis mode and you’re worried about pt dying Calcium 9-11 mg/dL -we want to protect heart and conduction system, EKC monitoring and know basics of what rhythm strip looks like, ventricle reaction, etc. -Ca has everything to do with neuro, monitor sensation and mentation BUN 10-20 mg/dL Cortisol 6am-8am: 5-23 mcg/dL 4pm-6pm: 3-13 mcg/dL -low corticol, without this glucocorticoid then we are dead -Corticol must be a certain level all the time -Addison will have low cortisol level -Draw corticol level at AM and PM -must have monitoring equipment, know where crash card is, keep airway/ABCs going, |
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What is the drug therapy for Addison's disease?
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cortisone
hydrocortisone (Cortef) prednisone fludrocortisone (Florinef) |
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What are the pt instructions regarding cortisone?
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Instruct the pt to take the drug with meals or snacks. GI irritation can occur.
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What are the s/sx of toxicity regarding hydrocortisone?
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Instruct the pt to report these signs or symptoms of excessive drug therapy:
-rapid weight gain -round face -fluid retention |
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When administering fludrocortisone, what are we going to monitor for?
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Monitor pt's blood pressure; HTN is a potential side effect. Instruct the pt to report weight gain or edema; sodium-related fluid retention is possible.
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Describe adrenal hyperfunction in the cortex and medulla.
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Hypersecretion by adrenal cortex:
-hypercortisolism (Cushing's disease or C syndrome) -hyperaldosteronism (excessive mineralcorticoid or excessive androgen) Hyperstimulation of adrenal medulla: -excessive secretion of catecholamines (epinephrine for short responses, norepinephrine for long responses) |
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What are the clinical manifestations of Cushing's disease or Cushing's syndrome?
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Excess glucocorticoids results in metabolic problems and affects all systems.
General Appearance -fat redistribution: moon face, buffalo hump, truncal obesity -weight gain Cardiovascular -hypertension -increased risk for thromboembolic events -frequent dependent edema -capillary fragility: bruising, petechiae Musculoskeletal -muscle atrophy (most apparent in extremities -osteoporosis (bone density loss): pathologic fractures, decreased height and vertebral collapse, aseptic necrosis of the femur head, slow or poor healing of bone fractures Skin -thinning skin ("paper-like" appearance, especially on the back of the hands) -striae -increased pigmentation (with ectopic or pituitary production of ACTH) Immune System -increased risk for infection -decreased immune function: decreasing circulating lymphocytes, decreased production of immunoglobulins (antibodies) -decreased inflammatory responses: decreased eosinophil count, slight increased in neutrophil count but activity is reduced -decreased production of pro-inflammatory cytokines, histamine, and prostaglandins -manifestations of infection/inflammation may be masked |
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Describe the laboratory assessment for Cushing's disease or Cushing's syndrome.
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-cortisol levels: blood, urine, saliva
-Dexamethasone suppression test -glucose, CBC, sodium, potassium, calcium -imaging -xray, MRI, CT scan, arteriography Xray can look for adenoma or pheochromocytoma. |
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What is the therapy for Cushing's disease or Cushing's syndrome?
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-restoring fluid balance and monitor for s/sx of fluid overload
-drug therapy: drugs that interfere wih ACTH production or adrenal hormone synthesis, decreases cortisol production. - we need to monitor for glucose, CBC, sodium, potassium calcium -nutrition therapy may involve restriction of both fluid and sodium intake to control fluid volume. -monitor I&O and daily weights -radiation and surgical interventions |
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Name the three P's of hyperaldosteronism.
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polidipsia
polyuria paresthesia Increased aldosterone levels affect the kidney tubules and cause sodium retention with potassium and hydrogen ion excretion. Hypernatremia, hypokalemia, and metabolic alkalosis result. Sodium retention increases blood volume, which raises blood pressure but usually does not cause peripheral edema. The elevated blood pressure may cause strokes, heart attacks, and kidney damage. |
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How do you assess for hyperaldosteronism?
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-polydipsia
-polyuria -paresthesias (sensations of numbness or tingling) may occur if potassium depletion is severe -hypokalemia -elevated BP (looks at trends, sitting up and laying down, check again in 30 minutes if you suspect hyperaldosteronism) -muscle weakness -fatigue (watch pt safety, keep bedrails up, BSC nearby) -headache -nocturia -loss of stamina Brain become ischemic or has thrombus, or a rupture, type of strokes Can’t say “they’ll stroke out” you need to be specific: ischemic stroke, thrombotic stroke, hemorrhagic stroke |
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What labs will you look at regarding hyperaldosteronism?
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-sodium is elevated
-potassium is decreased -plasma renin is low -aldosterone level is high -low UA specific gravity -MRI -CT |
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What are the therapies for hyperaldosteronism?
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surgery: head vs. adrenal gland
drugs: spironolactone (Aldactone) -potassium-sparing and aldosterone antagonist Because spironolactone is a potassium-sparing diuretic, hyperkaleia can occur in pts who have impaired kidney function or excessive potassium intake. Advise the pt to avoid potassium supplements and food rich in potassium. Hyponatremia can occur with spironolactone therapy, and the pt may need increased dietary sodium. Instruc the pt to report symptoms of hyponatremia, such as dryness of the mouth, thirst, lethargy, or drowsiness. Teach pts to report any additional side effects of spironolactone therapy, including gynecomastia, diarhea, drowsiness, headache, rash, urticaria (hives), confusion, erectile dysfunction, hirsutism, and amenorrhea. |
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Tell me about pheochromocytoma.
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-catecholamine producing tumor in adrenal medulla (norepi and epi)
-assess: BP, HA, palpitations, diaphoresis, flushing, apprehension, pain. Nursing Alert: Do not palpate the abdomen because this action could stimulate a sudden release of catecholamines and trigger severe HTN. Dx: 24-hr urine will show elevated levels of vanillylmandelic acid, metanephrine, and catecholamines. MRI CT scan Surgery Post-op: monitor BP, as HTN is the hallmark of the disease. |
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What are the possible disorders involving thyroid function?
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hyperthyroidism
hypothyroidism hyperparathyroidism hypoparathyroidism |
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What is the etiology of hyperthyroidism?
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-autoimmune disease
-immunoglobulins attach to TSH receptors -glandular cells enlarge, resulting in goiter -leading to thyrotoxicosis -leads to Graves' disease The most common cause of hyperthyroidism is Graves' disease. Graves' disease is an autoimmune disorder in which antibodies (thyroid-stimulating immunoglobulins [TSI]) are made and attach to the thyroid-stimulating hormone (TSH) receptors on the thyroid tissue. The thyroid gland responds by increasing the number and size of glandular cells, which enlarges the gland, forming a goiter, and overproduces thyroid hormones (thyrotoxicosis). |
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What is the incidence rate for hyperthyroidism?
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Occurs 10 times more often in women. Common in ages 20-40 yr.
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Name the clinical manifestations of hyperthyroidism.
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The hallmark sign is heat intolerance; the pt may have diaphoresis (increased sweating) even when the environmental temperatures are comfortable for others. Also, visual changes.
Clinical manifestations are caused by hyper metabolism! Increases in SNS, HR, SV, CO, SBP, and blood flow. Protein synthesis (buildup) and degradation (breakdown) are increased, but breakdown exceeds buildup, causing a net loss of body protein known as negative nitrogen balance. Glucose tolerance is decreased, and the pt has hyperglycemia. Fat metabolism is increased, and body fat decreases. Although the pt has increased appetite, the increased metabolism causes weight loss and nutritional deficiency. Skin -diaphoresis (excessive sweating) -fine, soft, silky body hair -smooth, warm, moist skin -thinning of scalp hair Pulmonary -SOB with or without exertion -rapid, shallow respirations -decreased vital capacity Cardiovascular -palpitations -chest pain -increases systolic BP -widened pulse pressure -tachycardia -dysrhythmias Gastrointestinal -weight loss -increased appetite -increased stools -hypoproteinemia Musculoskeletal -muscle weakness -muscle wasting Neurological -blurred or double vision (diplopia) -eye fatigue -corneal ulcers or infections -increased tears -injected (red) conjunctiva -photophobia -eyelid retraction -eyelid lag (Graves' disease only) -globe lag (Graves' disease only) -hyperactive deep tendon reflexes -tremors -insomnia Metabolic -increased basal metabolic rate -heat intolerance -low-grade fever -fatigue Psychological/Emotional -decreased attention span -restlessness -irritability -emotional lability -manic behavior Reproductive -amenorrhea -decreased menstrual flow -increased libido Other -goiter -wide-eyed or startled appearance (exophthalmos) (Graves' disease only) -decreased total WBC count -enlarged spleen |
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How is hyperthyroidism diagnosed?
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Blood values for T3 (triiodothyronine) and T4 (thyroxine. Labs will show increased in T3 and T4, but almost nil TSH.
Thyroid scan uses radioactive iodine [123I]; however radioactive iodine destroys thyroid cells, so assess for S/Sx of hypothyroidism. Pregnancy should be ruled out before thyroid scan is performed. Child-bearing age: 11-50 yr, or puberty to menopause. |
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What is the drug therapy for hyperthyroidism?
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propylthiouracil (PTU)
methimazole (MTZ) (Tapazole) These drugs block thyroid hormone production by preventing iodide binding in the thyroid gland. PTU also prevents T4 from being converted to the active and more powerful T3 in the tissues. These responses are delayed because the pt may have large amounts of stored thyroid hormones to continue the release. |
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What is the black box warning regarding PTU and MTZ?
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Suppress rate of hormone secretion and safe guarding CV.
Both propylthiouracil (PTU) and methimazole (MTZ) (Tapazole) are effective but dangerous drugs. Propylthiouracil now has a black box warning because it is associated with an incidence of serious liver injury and liver failure. Methimazole can cause birth defects. The FDA recommends that unless a pt is pregnant or allergic to methimazole, propylthiouracil should be avoided. Assess any pt taking propylthiourcal for manifestations of liver problems (e.g. yellowing of the sclera and skin, dark urine, clay-colored stools, elevated liver enzymes). |
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What is the non-surgical nursing care for a pt?
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VS, rest, diet, medications, emotional & hygiene support, quite environment. Increase temperature sould indicate thyroids storm.
Radioactive iodine is given to destroy the thyroid cells. -use a toilet that is not used by others for at least 2 weeks after receiving the radioactive iodine. -sit to urinate to avoid splashing seat, walls, and floor. -flush the toilet 3 times after each use. -if urine is spilled on the toilet seat or floor, use paper tissues or towels to clean it up, bag them in sealable plastic bags, and take them to the hospital's radiation therapy department. -men with urinary incontinence should use condom catheters and a drainage bag rather than absorbent gel-filled briefs or pads. -women with urinary incontinence should use facial tissue layers in their clothing to catch the urine rather than absorbent gel-filled briefs or pads. -using a laxative on the 2nd or 3rd day after receiving the radioactive drug helps you excrete the contaminated stool faster (this also decreases the exposure of your abdominal organs to radiation). -wear only machine-washable clothing, and wash these items separately from others in your household. -after washing your clothing, run the washing machine for a full cycle on empty before it is used to wash the clothing for others. -avoid close contact with pregnant women, infants, and young children for the first week after therapy. Remain at least 3 feet (about 1 meter) away from these people, and limit your exposure to them to no more than 1 hour daily. -some radioactivity will be in your saliva during the first week after therapy. Precautions to avoid exposing others to this contamination (both household members and trash collectors) include: -not sharing toothbrushes or toothpaste tubes -using disposable tissues, rather than cloth handkerchiefs, and either flushing used ones down the toilet or keeping them in a plastic bag and turning them in to the radiation department of the hospital for disposal -use disposable utensils, plates, and cups -selecting foods that can be eaten completely and do not result in saliva-coated remnant (foods to avoid are fruit with a core that can be contaminated, meat with a bone [e.g., chicken wings or legs, ribs]) |
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Tell me about propylthiouracil (PTU).
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-suppresses TH synthesis
-rapidly absorbed -1/2 life is 90 min, requiring multi/day doses -side effects: rash, agranulocytosis Reduces manifestations of hyperthyroidism by preventing the new formation of thyroid hormone by inhibiting thyroid binding of iodide and by preventing the conversion of T4 to T3 in the tissues. Drug reduces blood cell count and the immune response, increasing the risk for infection. Manifestations of dark urine, yellowing of skin or eyes, and increased tendency to bruise/bleed may indicate liver toxicity or failure, a possible side effect of the drug. PTU does not prevent the release of hormone already stored in thyroid. |
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Tell me about methimazole (MTZ).
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-suppresses TH synthesis
-rapidly absorbed -1/2 life is 6-13 hrs -single dose/day -side effects: rash, agranulocytosis -crosses placenta, appears in breast milk Reduces manifestations of hyperthyroidism by preventing the new formation of thyroid hormones by inhibiting thyroid binding of iodide. This drug causes birth defects and should not be taken during pregnancy. Drug reduces blood cell count and the immune response, increasing the risk for infection. Manifestations of weight gain, slow heart rate, and cold intolerance may indicate hypothyroidism and require a lower drug dose. MTZ does not prevent the release of hormone already stored in thyroid. |
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Tell me about Iodine (131 I).
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-destroys thyroid tissue
-therapeutic effect in 2-3 months -side effect: hypothyroidism -used in post pubertal adolescents |
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Describe the nursing interventions for hyperthyroidism surgery pre-op.
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If the drugs and radioactive iodine didn't work, surgery is indicated or if the goiter is pressing on trachea.
-give anti-thyroid drugs that decrease secretion of thyroid hormones; iodine preparations used to decrease thyroid size and vascularity and reduces the risk for hemorrhage and potential for thyroid storm during surgery -HTN, dysrhythmias, and tachycardia must be controlled before surgery -teach pt to perform coughing and deep-breathing exercises -stress the importance of supporting the neck when coughing or moving by placing both hands behind the neck; this action reduces the strain on the suture line |
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Describe the nursing interventions for hyperthyroidism surgery post-op.
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Monitor for
-hemorrhage -resp distress -damage to parathyroid gland -damage to laryngeal nerves -thyroid storm Humidifying the air promotes easier respiration and things respiratory secretions. Assist the pt to cough and deep-breathe every 30 minutes to 1 hour. Hemorrhage is likely to occur during the first 24 hours after surgery. Inspect neck dressing and behind pt's neck for blood. Respiratory distress can results from swelling, tetany, or damage to laryngeal nerve resulting in spasms. Hypocalcemia and tetany may occur if the parathyroid glands are removed, damaged, or their blood supply is impaired during surgery, resulting in decreased PTH levels. Assess for Chvostek's (facial nerve; 'C' for cheek) and Trousseau (hand) signs, indicated hypocalcemia. Thyroid storm, or thyroid crisis, is a life-threatening event that occurs in pts with uncontrolled hyperthyroidism and often with Graves' disease. Key manifestations include fever, tachycardia, and systolic HTN. Pt may have GI problems such as abdominal pain, nausea, vomiting, and diarrhea. Often they're very anxious and has tremors. As the crisis progresses, the pt may become restless, confused or psychotic and may have seizures, leading to coma. |
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What are some nursing alerts regarding hyperthyroidism post-op care?
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When stridor, dyspnea, or other symptoms of obstruction appear after thyroid surgery, notify the Rapid Response Team. In some agencies, nurses can remove clips or sutures when medical assistance is not immediately available and swelling at the surgical site is obstructing the airway.
When caring for a pt with hyperthyroidism, even after a partial thyroidectomy, immediately report a temperature increase of even 1˚F because it may indicate an impending thyroid crisis. |
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What is the emergency care for a pt during a thyroid storm?
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-maintain a patent airway and adequate ventilation.
-give anti-thyroid drugs as prescribed: methimazole (Tapazole), up to 60 mg daily; propythiouracil (PTU), 300-900 mg daily -administer sodium iodide solution, 2 g IV daily as prescribed -give propranolol (Inderal), 1-3 mg IV as prescribed. Give slowly over 3 minutes. The pt should be connected to a cardiac monitor, and a central venous pressure catheter should be in place. -give glucocorticoids as prescribed: hydrocortisone, 100-500 mg IV daily; prednisone, 4-60 mg IV daily, or dexamethasone, 2 mg IM every 6 hours. -monitor continually for cardiac dysrhythmias. -monitor vital signs every 30 minutes. -provide comfort measures, including a cooling blanket. -give non-salicylate antipyretics as prescribed. -correct dehydration with normal saline infusions. -apply cooling blanket or ice packs to reduce fever. |
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How does hypothyroidism manifest?
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Primary hypothyroidism will manifest as elevated TSH levels.
Decreased metabolism from low levels of thyroid hormone (TH). This causes the pituitary gland to secrete more TSH, in an attempt to trigger hormone release from the poorly responsive thyroid gland. *Remember, hyperthyroidism shows low to no TSH. Hypothyroidism has elevated TSH. Low levels of T4 and T3 may not occur until later in the course of the disease, due to storage of hormone. Hypothalamic-pituitary dysfunction results in low levels of TSH and T4. |
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What is the etiology for hypothyroidism?
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Most cases of hypothyroidism in the USA occur as a result of thyroid surgery and radioactive iodine (RAI) treatment of hyperthyroidism.
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What is the incidence of hypothyroidism?
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Women are 10 times more likely to get it. Common age is 30-60 years.
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What are the clinical manifestations of hypothyroidism?
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Skin
-cool, pale or yellowish, dry, coarse, scaly skin -thick, brittle nails -dry, coarse, brittle hair -decreased hair growth, with loss of eyebrow hair -poor wound healing Pulmonary -hypoventilation -pleural effusion -dyspnea Cardiovascular -bradycardia -dysrhythmias -enlarged heart -decreased activity tolerance -hypotension Metabolic -decreased basal metabolic rate -decreased body temperature -cold intolerance Musculoskeletal -muscle aches and pains -delayed contraction and relaxation of muscles Neurological -slowing of intellectual functions: -slowing or slurring of speech -impaired memory and cognition -inattentiveness -lethargy or somnolence -confusion -hearing loss -paresthesia (numbness and tingling) of the extremities -decreased tendon reflexes Psychological/Emotional -apathy -depression -paranoia -withdrawal Gastrointestinal -anorexia -weight gain -constipation -abdominal distention Reproductive Women -changes in menses (amenorrhea or prolonged menstrual periods) -anovulation -decreased libido Men -decreased libido -impotence Other -periorbital edema -facial puffiness -nonpitting edema of the hands and feet -hoarseness -goiter (enlarged thyroid gland) -thick tongue -increased sensitivity to opioids and tranquilizers -weakness, fatigue -decreased urine output -anemia -easy bruising -iron deficiency -folate deficiency -vitamin B12 deficiency |
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What labs do you expect from hypothyroidism?
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Laboratory findings for hypothyroidism are the opposite for those with hyperthyroidism. Triiodothyronine (T3) and thyroxine (T4) serum levels are decreased. TSH levels are high in primary hypothyroidism (problem with thyroid tissue or thyroid hormone, pituitary gland is ok and secretes TSH).
But TSH levels can be decreased or near normal in pts with secondary hypothyroidism (problem with pituitary gland). |
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What are the priority problems for a pt with hypothyroidism?
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-decreased oxygen related to decreased energy, obesity, muscle weakness, and fatigue
-hypotension related to altered heart rate and rhythm as a result of decreased myocardial metabolism -altered cognition functioning related to impaired brain metabolism and edema -potential for myxedema coma #1 should be to have these pts rest. Even though they're lethargic and not moving around, we still want them to rest. |
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What is the nursing alert regarding myxedema coma?
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Myxedema coma can lead to shock, organ damage, and death. Assess the pt with hypothyroidism at least every 8 hours for changes that indicate increasing severity, especially with changes in mental status, and report these promptly to the health care provider.
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What is the drug therapy for hypothyroidism?
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Pt with hypothyroidism requires lifelong thyroid hormone replacement. The most common is levothyroxine sodium (Synthroid, T4).
Be sure to measure heart rate and rhythm prior to giving levothyroxine. Starting at too high of a dose or increasing the dose too rapidly can cause severe HTN, HF, and MI. When the pt requires more sleep and is constipated, the dose of replacement hormone may need to be increased. When the pt has difficulty getting sleep and has more bowel movements than normal for them, the dose may need to be decreased. |
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Name the disorders of parathyroid function.
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Hyperparathyroidism:
-hypercalcemia -hypophasphatemia Hypoparathyroidism -hypocalcemia -hyperphosphatemia Calcium is the most closely regulated element in our body. It is the only element that has its own regulatory system (the parathyroid glands). |
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How do we diagnose hyperparathyroidism?
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Increased serum calcium and decreased serum phosphate, renal panel, ECG, and bone surveys.
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What is the therapy for hyperparathyroidism?
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Primary is HPT surgery.
Secondary HPT tx underlying cause. |
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What are the nursing care interventions before and surgical removal of parathyroid glands?
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Same as hyperthyroidism / thyroidectomy.
Post care: as per protocol for airway Post surgery monitor for polydipsia and polyuria, renal impairment. PTH actually has influence on pituitary and can induce temporary DI. Always check calcium with phosphorus. "stones, bones, moans, groans and psychiatric moans" |
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How do we diagnose hypoparathyroidism?
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Decreased serum calcium and increased serum phosphorus in labs.
Urine cAMP (cyclic adenosine monophosphate) Chvostek's and Trousseau's signs |
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What is the therapy for hypoparathyroidism?
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Focuses on correcting hypocalcemia, vitamin D deficiency, and hypomagnesemia.
Calcium gluconate IV/PO Vitamin D Labs: Ca, Pho, Mg twice/day then q 6 months |
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What are the nursing interventions for hypoparathyroidism?
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Seizure precautions (protect the head), laryngo spasms (have treach set at bedside), IV calcium gluconate
Pt education, med administration, renal impairment. Stress that therapy for hypocalcemia is lifelong. |
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Differ between beta cells and alpha cells in the pancreas.
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Beta cells produce insulin during high levels of blood glucose. Prevents hyperglycemia.
Alpha cells produce glucagon during low levels of blood glucose and triggers the release of glucose from cell storage sites. Prevents hypoglycemia. |
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What is the etiology of secondary DM?
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Secondary diabetes mellitus develops when the pancreatic tissue responsible for the production of insulin is absent. It's is often destroyed by chronic pancreatitis, trauma, or surgical removal of the pancreas.
Can also come from acromegaly and cushing's syndrome. Steroids and estrogen can "mask" DM S/Sx. |
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Tell me about the hormonal regulation of glucose metabolism.
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Glucose – controlled in a narrow range
In the fasting state, glucose is produced by glycogenolysis and gluconeogenesis while insulin secretion falls to basal level Glucagon is responsible for most glucose production in fasting state Counterregulatory hormones (corticosteroids, growth hormone, catecholamines) augment glucose production |
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What protein transporters help glucose cross the cell membrane?
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GLUT transporters.
The total amount of sugar present in the blood can support resting activity (sleep) for no more than 40 minutes. |
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What is the etiology of DM 1?
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HLA: autoantibodies (T cells) destroy pancreatic beta cells.
Insulin- absent |
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What is the etiology of DM 2?
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Obese + genetic susceptible person = DM2
Metabolic abnormalities: -insulin resistance -decreased beta cell activity -inappropriate glucose production by liver -altered function of adipokines |
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What is the etiology and pathology of metabolic syndrome?
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Metabolic syndrome, aka syndrome X, is the simultaneous presence of metabolic factors known to increase risk for developing type 2 DM.
A heart attack and stroke waiting to happen. A - abdominal girth H - hyperglycemia H - HTN H - hyperlipidemia |
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How can a pt get diagnosed with metabolic syndrome?
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Any three of the five measures are needed:
Waist circumference: > 40'' in men > 35'' in women Triglycerides: > 150 mg/dL HDL < 40 mg/dL BP > 135/85 mmHg Fasting Blood Glucose 110-125 mg/dL |
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What is the prevalence of DM?
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57 million in U.S. have pre-diabetes
25.8 million have DM 7th leading cause of death (Heart disease is #1) Long term complications: -adult blindness -ENRD diabetic nephropathy -nontraumatic LE amputations Major contributing factors: -cardiac disease, stroke, HTN Predicted to become the leading cause of morbidity and death in the coming decade. |
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What are the priority problems for a pt with DM?
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1. Potential for injury related to hyperglycemia.
2. Potential for impaired wound healing related to endocrine and vascular effects of diabetes. 3. Potential for injury related to diabetic neuropathy. 4. Pain related to diabetic neuropathy. 5. Potential for injury related to diabetic retinopathy - induced reduced vision 6. Potential for kidney disease related to impaired renal circulation 7. Potential for hypoglycemia 8. Potential for diabetic ketoacidosis 9. Potential for hyperglycemic-hyperosmolar state and coma |
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How can we diagnose DM?
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Glycosaylated hemoglobin A1C test - we want it to be less than 7%.
Hgb A1C measured the amount of glycosylated hemoglobin as a percentage of the total hemoglobin. Hgb A1C gives the level of blood glucose of a time period of 120 days. A1C is the gold standard endorsed by ADA for glycemic control. |
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What factors can affect the Hbg A1C test results?
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-artificial heart valves
-renal failure -blood transfusions -anemia: sickle cell anemia -anemia: hemolytic anemia (hemophiliacs have this, or someone with sepsis) -anemia: iron deficiency anemia -anemia: significant blood loss |
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What are the symptoms of DM type 1?
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-rapid with impending or actual ketoacidosis
-Hx of sudden wt loss. Three Ps. -Polyuria-Frequent urination -Polydipsia-Excessive thirst -Polyphagia -Extreme hunger w/ unexplained wt loss -Without insulin, a Type 1 DM wastes away and eventually dies from diabetic ketoacidosis (DKA) Should not got into ketoacidosis in type 2 because there is still some insulin production. DM type 2 s/sx are gradual and found during routine lab testing. |
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What are the acute complications of DM?
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-hypoglycemia
-hyperglycemia -DKA -HHNS |
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What are the chronic complications of DM?
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Macrovascular
-CAD (coronary artery disease) -CVD (cardiovascular disease) -HTN -PVD (peripheral vascular disease) -Infection Microvascular (tender, delicate capillaries) -retinopathy -nephropathy -neuropathy (sensorimotor and autonomic) |
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Tell me about the importance of foot care in DM pts.
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-Highest % of amputations
-Determine the risk profile: ie HbA1c >10% -Foot pain = foot problems -Foot numbness = foot problems -Daily inspections -Appropriate foot wear -PMH (primary medical hospital admission) inspection with each visit -Any vascular insufficiency needs further workup; usually pulse is diminished to show vascular insufficiency Poorly controlled blood sugar; evidence of vascular insufficiency in DM, poor glucose control increases infection and decreases wound healing. 0 = Absent 1 = Barely palpable 2 = Easily palpable (normal) 3 = Full 4 = Aneurysmal or Bounding pulse |
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How do you completely a foot assessment for DM pts?
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Sensory examination with Semmes-Weinstein monofilaments is the most practical measure of the risk of foot ulcers. The nylon monofilament is mounted on a holder standardized to exert a 10-g force. A person who cannot feel the 10-g pressure at any point is at increased risk for ulcers.
A fungal infection is a diabetic is a red flag! Always check between toes and bilateral pedal pulses. Also need to assess gait. |
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What is the Tx for DM type 1?
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-insulin!
-diet control / carb count (look at Pg. 1440, Table 67-11) -exercise |
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What is the Tx for DM type 2?
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-diet control!
-exercise! -oral hypoglycemics -eventually insulin maybe |
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Summarize the pathophysiology of type 2 DM.
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Postprandial hyperglycemia
-Delayed & inadequate postprandial insulin secretion -Decreased peripheral glucose uptake & failure to suppress hepatic glucose output Fasting hyperglycemia -Progressive loss of Beta cell function -“insulinopenic” by the time FPG>200 -Increased nocturnal hepatic glucose output |
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What are the symptoms of hypoglycemia?
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-weakness
-fatigue -difficulty thinking -confusion -behavior changes -emotional instability -seizures -loss of consciousness -brain damage -death Adrenergic: -shaky/tremulous -heart pounding -nervous/anxious Cholinergic: -sweaty -hungry -tingling -cool, clammy skin -double vision -blurred vision -tachycardia -palpitations < 70 mg/dL blood glucose *nervousness, confusion, weakness = classic symptoms |
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What are the symptoms of hyperglycemia?
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-polyphagia despite weight loss, polyuria, polydipsia
-warm, moist skin -dehydration -rapid, deep breaths: Kussmaul type -"fruity" odor in breath Acidosis -hypercapnia -abdominal cramps -nausea -vomiting Dehydration -decreased neck filling -orthostatic hypotension -tachycardia -poor skin turgor -positive for ketones > 250 mg/dL blood glucose |
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Tell me about DKA, or diabetic ketoacidosis.
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DKA is characterized by hyperglycemia, metabolic acidosis, and increased production in ketones. It usually occurs in Type 1 diabetics.
Classic Sx: -polyuria, polydipsia, polyphagia -weight loss -vomiting -abdominal pain, dehydration -weakness -altered mental status -shock -coma -Kussmaul respirations (very deep and rapid) cause respiratory alkalosis -fruity breath Blood pH decreases and acidosis occurs. |
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Tell me about HHNKS, or hyperglycemic-hyperosmolar nonketotic syndrome
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In HHNKS, the pt secretes just enough insulin (Type 2) to prevent ketosis but not enough to prevent hyperglycemia.
-levels of ketones is very low or absent -blood glucose are very high, may exceed 600 mg/dL -onset is gradual -altered CNS function with neurologic symptoms -dehydration or electrolyte loss -polyuria, polydipsia, polyphagia -weight loss -dehydration -dry skin -sunken eyes -soft eyeballs -lethargy -coma Blood serum is greater than 7.4 (alkaline). |
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How will you rehydrate a diabetic pt with DKA or HHNKS?
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Large bore catheter in emergency situation to hurry and get fluids in them.
Hour one: -take vital signs and blood glucose -15-20 mL/kg of hypotonic solution -we don't expect any urine output since fluid is going into vascular space to hydrate pt Hour two: -take vital signs and blood glucose -4-14 mL/kg of D5W with 1/2 strength NS (0.45%) -if client has CHF Within 24 hours, pt will receive 6-10 L of fluids. Adjust fluid intake to meet clinical need. Consider urine output rate in calculation. |
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Tell me about potassium replacement therapy in DKA.
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Potassium levels can fluctuate severely during the treatment of DKA, because insulin decreases potassium levels in the blood by redistributing it into cells. A large part of the shifted extracellular potassium would have been lost in urine because of osmotic diuresis. Hypokalemia (low blood potassium concentration) often follows treatment. This increases the risk of dangerous irregularities in the heart rate. Therefore, continuous observation of the heart rate is recommended, as well as repeated measurement of the potassium levels and addition of potassium to the intravenous fluids.
-frequent hourly assessment of urine output <0.5 mL/kg/hr or an abrupt decrease -assess for signs of hyperkalemia: cardiac dysrhythmias -plan to start K administration 1-2 hrs after insulin is started and urine output is normal. The K level may be normal or elevated in a DKA pt once insulin is given because the K hitches the ride back into the cell along with glucose. |
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When can you start to administer IV potassium?
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Make sure the pt produces at least 30 mL/hr of urine.
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Tell me about insulin replacement therapy in DKA pts.
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-Insulin is always given IV in DKA or HHNKS
-Low dose continuous therapy 5 – 10 units/hr or 0.1 units/kg/hr -Monitor BG every 15-30 minutes -When BG is 250 or less need to ↓ insulin -Always keep D50 ampule in the room -use a sliding scale; we don't want to send pt into hypoglycemia or shock by giving too much insulin -if pt becomes hypoglycemic, don't use glucagon because it isn't fast enough. |
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What are the three components in the diabetic triad?
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-diet
-exercise -medications Optimal care requires balance of all three. |
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How should you educated a diabetic to go about health eating and meal planning?
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-5 fruits and vegetables
-Low fat to prevent heart disease -Whole grain, fiber rich food controlled for carbohydrate portions, calorie reduction, and consistent CHO -Reduced calories for weight reduction -Reduce FPG and PPG -The right time” - about every four hours -Sugar is allowed |
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How should you educated a diabetic about recommended exercise??
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-Enhances tissue sensitivity to insulin increases cell membrane receptors.
-Assists in weight management and preservation of lean body mass -Improves risk factors for cardiovascular disease -After meals: Safe intensity, duration (consider complications) -Carry glucose tablets, may not always have time to eat. -Any activity counts -Adults – 30 min. Moderate preferably everyday of the week -Children – 60 min. But sure to look at pt comoridities; may not expect pt to keep up with rigidity with HF, etc. If they lose 2 pounds, celebrate that. We're trying to save that end organ from damage. |
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What are the ACDEFGHIJK of DM patients?
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A A1C
B Blood Pressure C Cholesterol D Diet/Diabetes Ed/Dental Exam (if we have vascular problems, it may first show up as gingiva) E Eye Exam/Exercise (have eye exam every 6 months) F Foot Exam G Glucose monitoring H Heart Health (can pt walk same distance without problems?) I Indications for specialties (endocrinologist, cardiologist, etc.) K Kidney |
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Describe the three oral diabetes medications.
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Secretagogues - drugs that stimulate the pancrease to release more insulin: sylfonylureas, meglitinides
Sensitizers - drugs that help the body use insulin by increasing receptors sensitivity: biguanides, thiazolidinediones Alpha-glucosidase inhibitors - drugs that block the breakdown of starches and sugars in the small intestine |
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How do sulfonylureas (secretagogues) work?
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MOA: close ATP/K channel in the beta cells, which leads to insulin release
-can cause hypoglycemia, check glucose and observe pt -weight gain, take daily weights -metabolic affected by renal/hepatic impairment -Glyburide should be avoided: not tolerated well with renal insufficiency, blocks ischemic preconditioning -glimepiride -glipiZIDE |
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Name the types of sulfonylurea medications (secretagogues).
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First generation (you may still see these):
-tolazamide (Tolinase) -tolbutamide (Orinase) Second generation: -glyburide (DiaBeta, Micronase) -glipizide (Glucotrol) -glimepride (Amaryl) |
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What are the side effects of sulfonylureas (secretagogues)?
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Hypoglycemia:
-pt will have frequent meals q 4 hr -ensure snacks are available -pt must eat within an hour of taking the medication -make rounds and check for hypoglycemia (fatigue, weakness, difficulty thinking, confusion, loss of consciousness, seizures, coma) Drugs: -react adversely with alcohol - Antabuse effect -beta blocks suppress insulin release -sulfur allergies i.e., sufla ABX -NSAIDs and H2 blockers enhance hypoglycemia |
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When should you administer sulfonylureas (secretagogues)?
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-Generally once or twice daily
-Glipizide 30 minutes before meals, shorter acting, duration 12 hrs -Glyburide - longer acting, duration 24 hours caution in the elderly -(glimepride) Amaryl - once daily with the first main meal, duration 24 hrs |
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Name the types of meglitinides (secretagogues)?
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Meglitinides
-repaglinide (Prandin) Amino Acide Derivatives -nateglinide (Starlix) |
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Tell me about repaglinide (Prandin), which is a meglitinide (secretagogoues)?
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Action
-Rapidly stimulates insulin release in the presence of glucose. Onset 15 - 30 min. Dosage & Frequency -0.5 to 4 mg. Before each meal, max 16 mg/day Special Considerations -Synergistic with metformin (hypoglycemia) -Can be used with caution in patients with renal and hepatic insufficiency. Good choice for the elderly -Duration 2 - 3 hours (shortest duration). -Potential for accumulation is minimal. -Dosing frequency dependent on frequency of meals. 2nd slide? Mode of Action(MOA): Increases insulin release from the pancreas is glucose dependent and diminishes at low blood glucose levels Binds at different beta cell sites than sulfonylureas Helps control hyperinsulinemia |
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What are the side effects of meglitinides (secretagogues)?
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-You will have to calculate the dosage for the day. Give before each meal, max 16 mg/day
-Check labs: caution in patients with renal and hepatic -Patient rounds: check for s/s of hypoglycemia. Adjust assessment for patient’s age. -Daily wts -Check on availability of snacks |
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Tell me about biguanides (Metformin), which is a sensitizer.
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Mode of Action(MOA):
-Improves sensitivity to insulin in the liver. -Decreases production of glucose (gluconeogenesis) in the liver -Enhances glucose uptake and utilization in the muscle. Benefits: -Can cause weight loss. -Does not stimulate insulin therefore does not cause hypoglycemia Adverse side effects: -Caution with ETOH. -Lactic Acidosis(rare), nausea, diarrhea, decreased absorption of vitamin B12 and folic acid. -Half life is 6 – 17 hrs, not metabolized. This is the #1 drug we use with pts. Need to be careful of lactic acidosis from hypoperfusion. Definitely avoid pts with any kidney disease/impairment. Lactic acidosis Sx: -fatigue -unusual muscle pain -difficulty breathing -unusual or unexpected stomach discomfort -dizziness -lightheadedness -irregular heartbeats |
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What are the nursing interventions of biguanides (Metformin), which is a sensitizer?
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Check labs: Renal-metformin rapidly excreted by kidneys!
Caution: ETOH while inpatient caution family on bringing ETOH to pt. SE: Observe for diarrhea-may have been admitted r/t lactic acidosis, elec imbalance brought on by diarrhea Daily wt. |
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Tell me about thiazolidineones Pioglitazone (Actos), which is a sensitizer.
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MOA:
-Decreases peripheral insulin resistance in skeletal muscle w/o stimulating insulin secretion. Inhibits hepatic glucose output Dosage -Monotherapy 15 - 45 mg -30 mg once daily in combination therapy SE: -Hepatic Impairment-monitor ALT (don’t initiate if ALT>2.5 normal -Expands blood volume -Concerns for increased fluid retention aka weight gain and peripheral edema |
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What are the nursing interventions of thiazolidineones Pioglitazone (Actos), which is a sensitizer?
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Check labs:
-Liver function-Monitor ALT some of the early thiazolidineones were removed from use because they induced hepatic failure. This is why we keep a close watch on patients on tdz -UA-specific gravity r/t fluid retention Daily wts (?how much does a liter of water weigh?) 1 L of water = 1 kg = 1,000 grams |
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Tell me about the alpha-glucosidase inhibitor, acarbose (Precose).
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MOA:
-Slows carbohydrate breakdown and glucose absorption in small intestine - inhibits intestinal enzymes Dosage -Start 25 mg with first bite of each meal -Titrate every 4 - 8 weeks Special Considerations -Caution - renal dysfunction, bowel disease (GI related side effects, also rare liver toxicity) -If combination therapy - treat hypoglycemia with monosaccharide (dextrose, glucose) |
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For what reasons would we use a combination therapy?
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-Additional effect, different mechanisms of action
-Diabetes is a progressive disease -Lower insulin resistance -Lower amount of exogenous or endogenous insulin needed -Combination therapy at lower than maximum doses may decrease side effects |
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What factors influence insulin absorption?
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Injection site:
2 in from navel, rotate site but same anatomical area. Usually abdomen and thigh. Absorption/Type of insulin: The longer the duration of action the more unpredictable is the absorption. Scars, heat, massage and exercise(leg vs abdomen) 90ᵒ vs 45ᵒ angle *Subcut: 90 vs. 45: depends on amount of adipose tissue there. You pinch skin and fold comes at half of needle, go 45%. If fold of skin goes to almost whole needle, go 90 degrees. Timing: Lispro, aspart and glulisine 10 min before meal Regular 20 to 30 min before meal "Logs Are (G)Quick faster." |
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What are some complications of insulin therapy?
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Hypoglycemia
70 mg/dL neurogenic and neuroglycopenic symptoms. Neurogenic: -weakness -fatigue -difficulty thinking -confusion -behavior changes -emotional instability -seizures -loss of consciousness -brain damage -death Adrenergic: -shaky/tremulous -heart pounding -nervous/anxious Cholinergic: -sweaty -hungry -tingling Lipoatrophy |
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Name the four general types of hypoglycemia.
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Chronic hypoglycemia - a symptom of a medical problem not related to DM (very rare), maybe a nursing student who hasn't eaten for a while.
Reactive hypoglycemia - caused by diet Fasting hypoglycemia - caused by missing a meal Diabetic hypoglycemia caused by an overdose of insulin or dropping the glucose load too fast in DM 300mg/dL to 150 mg/dL! Watch that sliding scale! |
