Nursing 372: Caring of Patients with Gland Disorders, Fractures, and Renal Disorders
Nursing 372: Caring of Patients with Gland Disorders, Fractures, and Renal Disorders 372
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This 47 page Study Guide was uploaded by ndp33 on Wednesday July 6, 2016. The Study Guide belongs to 372 at Niagara University taught by in Summer 2014. Since its upload, it has received 10 views. For similar materials see Nursing Concepts III: Individual w/ Identified Needs in NURSING at Niagara University.
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Date Created: 07/06/16
*UTIs- causes Risk factors: -Inability to empty bladder. Eg neurogenic bladder, urinary obstruction due to tumor, kidney stone, prostatic hyperplasia, or urinary stasis -Being female. This is due to the proximity of the urinary meatus to the vagina and rectum and anus. -Sexually active women. This is due to the increased risk of bacterial contamination from intercourse -Pregnant women. App 2.9-5% women develop asymptomatic bacteriuria; if untreated, app 20- 30% of these infections develop into pyelonephritis. -Diabetes. This is due to the dev of neurogenic bladder, which causes incomplete emptying and urinary stasis. Also, glucose in the urine may support bacterial growth. -Compromised renal function from other renal dis increases the susceptibility. -Instrumentation eg catheterization, cystoscopy, or urologic surgery -Bacteria translocated by the blood -Obstruction -In severe infection, abscesses develop and can lead to necrosis, scarring, and renal failure -Most common causative bacteria: E. coli, Proteus, and Pseudomonas. Other causative bacteria: Enterococcus, S. aureus, Staphylococcus saprophyticus, and Klebsiella. *Nursing Interventions for UTI -Prevention: Avoid indwelling catheters, care of catheters -Personal hygiene -Meds as prescribed: antibiotics, analgesics, and antispasmodics -Application of heat to the perineum to relieve pain and spasm -Increased fluid intake: 2-3L /day - Avoidance of urinary tract irritants such as coffee, tea, citrus, spices, cola, and alcohol -Frequent voiding -Patient edu: don’t stop antibiotics early; plan activities in short increments to allow for rest time in order to prevent fatigue Note: Elderly patients often lack the physical symptoms of UTI and sepsis Pharm therapy for UTI: -antibacterial that eradicates bacteria from the urinary tract w/ minimal side effects on the nl flora affordable and few s/e oral/IV -uncomplicated: antibiotic therapy – shortcourse(3-4 days- 7- 10 days) - complicated (pyelonephritis) Cephalosporins, ampicillin/aminoglycoside (7-10 days) Bactrim, Septra, Macrodantin, ampicillin, amoxicillin -Levoquin short-term therapy-mild- to moderate UTI costly, use only when costly measures are ineffective UTI – Assessment -Assess: -voiding patterns, -association of symptoms w/ sexual intercourse, -contraceptive practices, -personal hygiene -Gerontological considerations: incomplete bladder emptying, indwelling caths, post-menopausal – absence of estrogen, more susceptible to colonization males – decrease amount of prostatic secretions that protect from bacteria -Assessment of urine, urinalysis, and urine cultures Bacterial9 colony counts, color, clarity, odor, I&O -Other diagnostic tests: Dipstick:- WBCs, STDs, CT, U/S, abscesses, pyelonephritis UTIs: pyelonephritis -bacterial infection of the renal pelvis, tubules, interstitial tissue, or one or both kidneys -causes: -upward spread of bact from bladder -obstruction -systemic infections- TB can spread to kidneys and result in abscess -Iv antibiotics may be used initially to control the growth of bacteria in more severe infection; commonly used incl cephalosprons, amoxicillin, and fluroquinolones urinary analgesics if pt is burning when urinary, and frequently and urgently urinating Acute -chills, fever, leukocytosis, bacteriuria, pyruria, low back pain, flank pain, N/V, s/sx of UTI -DX: CT- to locate obstruction MRI – id of sites of inf that may not be seen on CT urine c/s, Cx -Management outpatient tx – 2wk course of antibiotics(Cipro, gentamicin, cephalosporin) pregnancy- 2-3 days IV antibiotics may need antibiotics for up to 6 wks antipyretics if high fever pt teaching of proper technique for urine collecting: clean-catch urine specimen and send urine culture within 20 min of collection to prevent overgrowth of bacteria if urine collecting and urinalysis Chronic -repeated bouts of acute pyelo -may have no s/sx of inf -may have: -fatigue, -poor appetite, -fever, -polyuria, -excessive weight loss, -may lead to renal failure -management: longterm prophylactic antibicrobial therapy may limit attacks and scarring careful monitoring of renal function increased fluids 3-4L/day antipyretics bedrest teaching UTI: Collaborative Prob, Potential -sepsis: -early recognition of UTI Complications -test for bact if chronic infection -teach s/sx -renal failure Urolithiasis and Nephrolithiasis – Risk factors -diet rich in meat, Na, oxalate, and tomatoes -Reduced fluid intake - Increased fluid loss in hot weather -High intake of grapefruit juice -Dehydration -long periods of inactivity -being overweight -fasting -UTI -previous kidney stone -gout -Crohn’s disease -ulcerative colitis -kidney disease -high BP -chronic diarrhea -overactive parathyroid -certain cancers -neurologic conditions affecting the ability of the bladder to empty -Meds: Antacids containing sicilates (calcium) anticonvulsants (topiramate, felbamate, zonisamide) degonestants: guafinesin, ephedrine some diuretics (such as triamterene) some steroids thyroid meds chemotherapy drugs some drugs used to treat HIV (such as indinavir) -men are 4-5x more likely to develop calcium or uric acid stones -women are more likely to develop struvite stones -Genetic factors: family members who have had kidney stones or gout -ethnic background: Caucasians and Asians are more likely than AA, NA, and people from Africa and the Middle East Note: Urolithiasis and nephrolithiasis are calculi (stones) in urinary tract or kidney -pathophysiology -causes; may be unkown inherited conditions bowel conditions hypercalcemia hyperoxaluria hypomagnesiuria hypocitraturia renal tubular acidosis -potential sites: kidneys, ureters, bladder Kidney Stones: Manifestations -depend on loc and presence of obstruction or infection -pain and hematuria -Dx: x-ray, blood chemistries, and stone analysis, strain all urine and save stones Kidney Stones: Methods of Treatment -cystoscopy (w/ optical lens, light source, tubes that infuse irrigant through urethral opening and bladder to take out stone) -shock wave therapy- electromagnic waves over the body -percutaneous lithrolithotomy (w/ alligator forceps) for larger stones Kidney stones – patient teaching -s/sx to report -follow-up care -urine pH monitoring -measures to prevent recurrent stones -importance of fluid intake -dietary teaching -medication teaching as needed *AV fistula -An arteriovenious fistula, AV fistula is a connection, made by a vascular surgeon, from an artery to a vein in forearm or upper arm to make hemodialysis sessions possible -AV fistula causes extra blood and P to grow into the vein, making it grow very strong provides good blood flow for hemodialysis lasts longer than other types of access is less likely to get infected or cause blood clots than other types of access performed in hospital or outpatient setting, with a Doppler setting to map location first, takes 2-3 months to grow Note: fistula in general is an abnormal opening or tract b/w two structures caused by cancer, infection, injury, or surgery Chronic renal failure (CRF) – Causes -DM -hypertension - chronic glomerulonephritis -pyelonephritis or other infections -obstruction of urinary tract -hereditary lesions -vascular disorders -medications or other toxic agents Note: Chronic renal failure is a progressive, irreversible, deterioration of renal fxn that results in azotemia CRF Manifestations -Cardiac: most common cause of death (45% cardiac disease, 20% MI) HTN d/t Na+ and H2O retention HF Pulm edema d/t fluid overload pericarditis -Skin: severe pruritis uremic frost (urea crystal formation) uncommon d/t early treatment -GI: anorexia, N/V, hiccups inadequate dialysis - odor of urine on breath -Neuro: Altered LOC Inability to concentrate Muscle twitching Agitation, confusion, seizure activity Severe pain Restless leg syndrome Neuropathy Care of Renal Failure – Assessment -Fluid status, -Nutritional status, -PT knowledge, -Activity tolerance, -Self-esteem, -Potential complications Renal failure- Collaborative Prob/Potential -Hyperkalemia: -decreased excretion Complications -cardiac arrhythmias -pericarditis, pericardial effusion: d/t retention of uremic waste and inadequate dialysis -hypertension: d/t Na+ and H2O retention -anemia -bone disease and metastatic calcifications: d/t phosphate retention, low serum Ca++, abn vit D metabolism, elevated albumin *Meds for hyperkalemia -Kayexalate (sodium polysterene sulfonate) Excess fluid volume -assess for s/sx of fluid volume excess, and keep accurate I&O and daily weights -limit fluid to prescribe amounts -id sources of fluid -explain to pt and family the rationale for the restriction -assist pt to cope w/ the fluid restriction -provide or encourage frequent oral hygiene *Dialysis: Acute -high, incr levels of K+, fluid overload, pulm edema, increasing acidosis, pericarditis, severe confusion -removal of meds or other toxins from the blood (poisoning, OD) *Dialysis: Chronic (maintenance dialysis) -ESRD, eremic s/sx affecting all body syst -Pts w/ no renal fxn - Prevents death, does not cure *Hemodialysis -most common method -Goal: extract sub form blood and remove excess H2O -used for both acute and chronic -dialyzer: serves at the kidney(synthetic semipermeable membrane filter for the impaired kidney) -treatments: 3x/wk, 3-4 hrs -should be initiated before s/sx become severe Access devices: hemodialysis cather -access to the pts vascular syst: allow blood to be removed, cleansed and replaced at a rate of 300-550 ml/min -types : double lumen – used in acute dialysis *Peritoneal dialysis -goals are same as hemodialysis -treatment of choice for pts unwilling to undergo renal dialysis or transplant -slower rate of dialysis less F&E complications DM, CV dis, older pts HRF F&E imbalances takes 26-48 hrs -interventions: -enc pt to empty bowel, bladder -decrease risk of puncture -antibiotics pre-procedure Note: peritoneal dialysis: dialysis is infused into peritoneal cavity by gravity, the clamp is on the infusion line is then closed. After a dwelling time, the drainage tube is unclamped, and the fluid drains again by gravity. The abd organs and abd cavity serve as the semipermeable membrane. Note: Failure of permanent (not temporary) dialysis access accounts for most hospital admissions of pts undergoing chronic hemodialysis. *Complications of hemodialysis -hypotension: during treatment due to hypovolemia n/v, diaphoresis, tachycardia, dizziness -muscle cramping: late in dialysis d/t F&E rapid removal from the extracellular space -dysrhythmias: F&E removal changes, removal of antiarrhythmic meds from the syst -air embolism: rare, can occur if air enters the venous syst during dialysis -dialysis disequilibrium: cerebral fluid shifts H/A, N/V, restlessness, LOC changes, restlessness, seizures more likely to occur w/ acute renal failure or when urea blood levels are high *Complications of peritoneal dialysis -peritonitis: most common and serious complication Staph infection, e. coli cloudy dialysate drainage diffuse abd pain rebound tenderness hypotension, shock -leakage: through the cath usu stops spontaneously, dialysis held for a few days treatment: - smaller amt of dialysate -may leak for yrs -bleeding: common and nl in the first few exchanges after a new cath insertion stops in 1-2 days, usu requires no intervention more frequent changes may be needed to prevent clot formation at the site *Nursing Management of the Hospitalized Patient on Dialysis -Protection of vascular assess; assess site for patency and signs of infection; and do not use for BP or blood draws -Monitor for fluid balance indicators and monitor IV therapy carefully: accurate I&O; IV administration pump -Assess for s/sx of uremia and electrolyte imbalance; regularly check lab data -Monitor cardiac and resp status carefully -Hypertension: monitor BP; antihypertensive agents must be held on dialysis days to avoid hypotension -Monitor all meds and med dosages carefully. Avoid all meds containing Mg and K. -Address pain and discomfort -Stringent infection control measures -Dietary considerations: Maintain good nutritional status Protein restriction, decreases accumulation of nitrogen wastes, may even postpone dialysis for a few months 1.2- 1.3 g/kg/day Na+: 2-3g/kg/day fluid restriction decreases risk of fluid accumulation K+ restriction Skin care: pruritus is a common prob: keep skin clean and well moisturized; and trim nails and avoid scratching *Diabetes insipidus (DI) -water metabolism prob caused by ADH deficiency; inability of kidneys to concentrate urine, resulting from an absolute or relative lack of circulating ADH results from destruction to posterior pituitary, but not alone; destruction to hypothalamus or part of supraoptic hypophyseal tract must also occur classifications: -nephrogenic: generalized defect in V2 class of ADH receptor, aquaporin-2water channel or the renal tubules -primary: acquired, resulting from injury to neurohypophysis, such as head trauma, neoplasms, and infection; can be congential (X-linked disorder) -secondary -drug-related : results from decreased sensitivity to receptors to ADH, and is usually reversible after drug is withdrawn -Assessment: symptoms: of dehydration increase in frequency of urination and excessive thirst dehydration and hypertonic saline tests used for dx urine diluted w/ low specific gravity(<1.005) -DI Interventions: Oral chlorpropamide for treatment of secondary DI desmopressin acetate early detection of dehydration and maintenance of adequate hydration lifelong vasopressin therapy w/ permanent condition teach pts to weigh themselves daily to id weight gain low salt diet to treat nephrogenic DI to reduce amount of urine kidney is producing replace lost fluids, especially for central DI; IV fluids may be nec observe patient closesly for hyponatremia; patient may also be presumed to have anterior pituitary insufficiency and should receive corticosteroid replacement therapy SIADH -vasopressin secreted even when plasma osmolarity is low or normal -feedback mechanisms do not function properly -water is retained, results is hyponatremia, fluid overload (characterized by distended neck veins…) -Assessment – findings: recent head trauma cerebrovascular dis TB or pulmonary dis cancer (esp lung cancer) all past and current drug use decrease in serum Na levels -Interventions: fluid restrictions drug therapy (diuretics, hypertonic saline, democlocyline); monitor for fluid overload safe environment neurologic assessment Adrenal gland hypofunction -adrenocortical steroids may decrease from inadequate secretion of ACTH - dysfunction hypothalamus-pituitary control mechanism -direct dysfunction of adrenal tissue -Addison crisis vs Addison’s dis Addison’s disease -Primary -Secondary sudden cessation of long-term high- dose glucocorticoid therapy Acute Adrenal Insufficiency/Addisonian crisis -Life-threatening event; need for cortisol and aldosterone is greater than available supply -Usu occurs in response to greater event Adrenal gland hyperfunction -Hypersecretion of ACTH by adrenal’s cortex results in Cushing’s syndrome/disease; hypercortisolism, or excessive androgen production *Hypercortisolism (Cushing’s disease)-S/SX -Etiology most common cause is pituitary adenoma tumor can also be due to adrenocortical (tumor of adrenal cortex) or iatrogenic (eg medications, such as prednisone) origin, resulting in excess production of glucocorticoids operation: transphenoidal hypophysectomy postoperatively in removing pituitary tumor, most concern is monitoring neurologic status (eg LOC, mental status, changes in vision, strength) - Incidence/prevalence -Patient-centered collaborative care -Assessment: clinical manifestations elevated BP, hyperglycemia, fatigue, muscle weakness, bruising, acne, dependent edema, weight gain, hirsutism (abnormal hair growth) female balding obesity; truncal obesity w/ thin extremities moon face; Buffalo hump; osteoporosis thinning skin w/ striae GI bleeding depression emotional lability psychosis vertigo menstrual disorders decreased libido impotence kidney stones poor wound healing -Psychosocial assessment -Laboratory tests -Imaging assessment - Nonsurgical management: Pt safety Drug therapy: to suppress cortisol production and to inhibit adrenocortical biosynthesis Nutrition therapy Monitoring eg VS, LOC, wound sites and drains, IV sites, pain source - Surgical management: Hypophysectomy postop to monitor for: report any postnasal drip, keep the head of the bead elevated, monitor for a light- yellow color at the edge of clear drainage, have the patient avoid coughing soon after surgery pt will need to take thyroid and glucocorticoid meds for rest of life Adrenalectomy -essential prob to monitor: fluid overload, risk for infection, predisposition to injury Hyperaldosteronism -Increased secretion of aldosterone results in mineralcorticoid excess; most common cause is autonomous aldosterone-producing adenoma -Primary hyperaldosteronism (Conn’s syndrome)- result of excess secretion of aldosterone from one or both adrenal glands - Interventions: Adrenalectomy Drug therapy Glucocorticoid replacement when surgery cannot be performed – spironolactone replacement Hyperthyroidism -thyrotoxicosis: a clinical syndrome that results when tissues are exposed to high levels of circulating TH; an inclusive term that describes severe hypermetabolic conditions caused by the thyroid hormones; varies dependent on the causative factors of the condition -Grave’s dis: most common cause of thyrotoxicosis, is an autoimmune dis of unknown cause, characterized by: goiter (enlargement of thyroid gland), exophtalmos, pretibial myxedema (thickening of skin commonly over anterior and lateral aspects of lower legs); a thrill (palpable increased blood flow in thyroid) may be present in thyroid gland, reflecting increased vascularity in gland) -weight loss, heat intolerance despite increased appetite, nervousness -Assessment -Hx -Physical Assessment -Clinical manifestations -Psychosocial assessment -Lab tests: T3 (70-205 ng/dL) T4 (4-12 mcg/dL) TSH, 0.3-5 unitsT3RU, TSH-Rab Thyroid scan Ultrasonography ECG -Nonsurgical management Monitoring Reducing stimulation Promoting comfort Drug therapy *Surgical management: Total or subtotal thyroidectomy- interventions Postop complications: -Hemorrhage (characterized by tachycardia, hypotension, frequent swallowing, feeling of fullness at incision site, choking and bleeding) -Resp distress - Hypocalcemia and tetany (tetany if paraythyroid glans are destroyed from surgery): hypoparathyroidism -Laryngeal nerve damage -laryngeal edema -Thyroid storm (hyperythyroidism) or storm crisis -Eye and vision prob of Grave’s dis Post op monitoring: -Hoarseness or stridor or airway obstruction (signs of laryngeal damage) -Suture line pressure - Hypocalcemia and tetany -Thyroid storm *Thyroid storm – s/sx --life-threatening conditions characterized by exacerbation of all the s/s of hyperthyroidism -fever (temp >104), diaphoresis, tachycardia, atrial fibrillation, N/V, diarrhea, tremors, agitation and restlessness, and delirium -may be triggered by surgery, trauma, infection, postpartum status, or withdrawal of anti- thyroid drugs, resulting in severe tachycardia, HF, hyperthermia, and shock Hypothyroidism -Causes : when Iodine deficiency occurs, the thyroid is unable to secret sufficient thyroid hormone, and with an underactive thyroid gland, the TSH level (released by pituitary gland in response) will be high Hashimoto’s thyroiditis (a genetic immunological disease characterized by the development of autoantibodies, particularly directly toward thyroglobulin, resulting in lymphocytic infiltration and fibrosis and thyroidal tissue, leading to diminished production of T3 and T4 and the dev of hypothyroidism) Lymphocytic thyroiditis (which may occur after hyperthyroidism) thyroid destruction (From radioactive iodine or surgery) Pituitary or hypothalamic dis (secondary or tertiary hypothyroid disease) Meds Severe iodine deficiency - Differentiating: aging vs hypothyroidism -Decreased metabolism from low TH level -Myxedema -Myxedema coma (Severe hypothyroidism may result in myxedema coma, in which a drastic drop in metabolic rate causes decreased vital signs, hypoventiliation (possibly leading to respiratory acidosis, and nonpitting edema -Assessment: Hx Physical, psychosocial, lab assessments Clinical manifestations *Myxedema coma - Severe hypothyroidism may result in myxedema coma, in which a drastic drop in metabolic rate causes decreased vital signs, hypoventiliation (possibly leading to respiratory acidosis, and nonpitting edema -medical emergency resulting from untreated or inadequately treated hypothyroidism -s/sx include hyperthermia, but these signs will be exacerbated -condition is often precipitated by some event such as infection, trauma, surgery, or neurological disorder in a patient with hypothyroidism -S/s of myxedema incl: facial edema, thick tongue (macroglossia), mental confusion, irritability, severe mood swings, significant hypothermia (91- 95degress F), severely slowed pulse and respirations, decreased BP, profound neuromuscular weakness, anemia, and signs of psychosis Thyroiditis -thyroid gland inflammation -3 types: acute; subacute (granulomatous); chronic (Hashimoto’s – most common type) -thyroiditis vs. hyperthyroidism, hypothyroidism -nonsurgical management, surgical management -drug therapy Hyperparathyroidism -parathyroid glands- calcium and phosphate balance - hypercalcemia and hypophosphatemia -nonsurgical v surgical management Hypoparathyroidism -Decreased fxn of parathyroid gland -Iatrogenic -Idiopathic - Hypomagnesemia -Interventions- correcting hypocalcemia, vit D deficiency, hypomagnesemia *Acromegaly - -GH secretion following epiphyseal fusion (after puberty); rare hormonal syndrome caused in at least 90% of cases by a benign GH-secreting pituitary adenoma -due to slow rate of tumor growth, acromegalic pts are often older than 50 yrs of age; when GH- hypersecretion occurs in teenagers, it may cause gigantism -Manifestations: coarse features; overgrowth of bones, especially in skull and mandible; large hands and feet with thick fingers and toes; no linear growth because of fusion of epiphysis -Dx made based on glucose suppression tests;:pts with GH excess may be hyperglycemic b/c of increased insulin resistance; CT scan or MRI may show pituitary tumor; radiographs may show sella turcica (bony cavity in skull that houses pituitary) -Treatment: surgical intervention, including transphenoidal microsurgery; somatostatin analogus (drugs that are a synthetic versions of the hormone somatostatin) to shrink tumor prior to surgery; radiation if candidate is not good surgical candidate *Type-1 Diabetes -insulin-producing beta cells in the pancreas are destroyed by an autoimmune process - Requires insulin, as little or no insulin is produced -Onset is acute and usu occurs before age 30 -5-10% of per w/ diabetes *Type 2 diabetes -decreased sensitivity to insulin and impaired beta cell production results in decreased insulin production -90-95% of people w/ diabetes -more common in per >30 and in the obese -slow, progressive glucose intolerance -treated initially w/ diet and exercise -oral hypoglycemic agents and insulin may be used Absence of insulin -Hyperglycemia -Polyuria -Polydipsia - Polyphagia -Ketone bodies -Hemoconcentration, hypovolemia, hyperviscosity, hypoperfusion, and hypoxia -Acidosis, Kussmaul respirations -Hypokalemia, hyperkalemia, or normal serum K levels *Complications of DM; Complications of Diabetes: -Acute: -Diabetic ketoacidosis - Hyperglycemic-hyperosmolar state (HHS) -Hypoglycemia from too much insulin or too little glucose -Chronic: -Macrovascular/microvascular dis macrovascular complications: CV dis and cerebrovascular dis microvascular complications: eye and vision complications, diabetic neuropathy, diabetic nephropathy, male erectile dysfunction -Retinopathy (vision prob) -Nephropathy (kidney disfxn) -Neuropathy (nerve disfxn) *Long-term effects of DM -delayed wound healing, -infection, -hearing loss, -foot: loss of sensation in foot, skin dryness, cracking, and calluses -oral: prob w/ teeth and gums -HTN -stroke -neuropathy (loss of sensation of peripheral nerves) -lower extremity ulceration -charcot deformity -gastroporesis *DM- interventions Treatment of DKA: -Rehydration w/ IV fluid -IV continuous infusion of regular insulin -Reverse acidosis and restoration of electrolyte imbalance -Note: rehydration leads to increased plasma volume and decreased K+; insulin enhances movement of K+ from extracellular fluid into the cells - Monitor Treatment of HHNS: -Rehydration -Insulin administration -Monitor fluid volume and electrolyte status -Prevention Assessment of DM: -Hx -Blood tests Fasting plasma glucose (FPG) NL <100 fasting Oral glucose tolerance test (OGTT) < 140 other blood tests screening ongoing assessment – glycosylated hemoglobin assays, glycosylated serum proteins and albumin urine tests, tests for kidney function -HbA1C=4- 6% Treatment Options: -oral therapies -insulin therapies -nutritional considerations - exercise -surgical intervention -foot care -wound care Insulin therapy: -blood glucose monitoring -categories of insulin: rapid-acting short-acting intermediate-acting very long-acting -inhaled insulin Patient education: -insulin storage -dose preparation -syringes -blood glucose monitoring - infection control measures -diet therapy Management of hypoglycemia: -Treatment must be immediate -Give 15g of fast-acting, concentrated carb 3 or 4 glucose tabs 4-6 oz of juice or regular soda 6-10 hard candies 2-3 tbsp of honey -retest blood glucose in 15 min, retreat if <70 mg/dL or if symptoms persist more than 10-15 min and testing is not possible -provide a snack with protein and carb unless the patient plans to eat a meal within 30-60 min Emergency Measures for Hypoglycemia: -If the patient cannot swallow or is unconscious: SQ or IM glucagon 1 mg 25-50 mL dextrose solution IV Meal Planning -consider food preferences, lifestyle, usual eating times, and cultural/ethic background -review diet hx and need for weight loss, gain, or maintenance -consider caloric requirements and caloric distribution throughout the day -carbs: 50- 60% of carbs, emphasize whole grains -fats: 20-30% with >10% from saturated fat and >300 mg cholesterol -fiber -provide exchange lists *Diabetic ketoacidosis (DKA) -Caused by an absence of or inadequate amount of insulin resulting in abnormal metabolism of carb, prot, fat -Clinical features: dehydration hyperglycemia Acidosis -Manifestations incl: polyuria, polydipsia, blurred vision, weakness, HA, anorexia, abdominal pain, N/V, acetone breath, hyperventilation w/ Kussmaul ventilations, and mental status changes -Assessment: blood glucose levels vary b/t 300 and 800 mg/dL severity of DKA is not related to blood glucose level ketoacidosis is reflected in low serum bicarbonate pH; low pCO2 reflects respiratory compensation ketone bodies in blood and urine electrolytes vary according to water loss and level of hydration *Hypoglycemia s/sx Manifestations: CNS symptoms incl: -sweating, -tremors, -tachycardia, - palpitations, -nervousness, and -hunger -inability to concentrate, -HA, -confusion, -memory lapses, -slurred speech, -numbness of lips and tongue, - irrational or combative behavior, -double vision, and -drowsiness Severe hypoglycemia may cause disorientation, seizures, and LOC Note: Hypoglycemia is abnormally low blood glucose level. -Causes incl too much insulin or oral hypoglycemic agents, too little food, and excessive physical activity *Hyperglycemia s/sx -Hyperosmolality and hyperglycemia occur due to lack of effective insulin; ketosis is minimal or absent -Hyperglycemia causes osmotic diuresis with loss of water and electrolytes; hypernatremia and increased osmolality occur -Manifestations: hypotension, profound dehydration, tachycardia, and variable neurologic signs due to cerebral dehydration -high mortality Muscles: changes in older adult -loss of bone mass in older women -joint and disk cartilage dehydrates causing loss of flexibility contributes to degenerative joint disease (osteoarthritis); joints stiffen, lose ROM -cause stooped posture, changing center of gravity - elderly at risk for falls -endocrine changes cause skeletal muscle atrophy -muscle tone decreases Assesment of muscles -Health hx -Chief
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