Endocrine.pdf

Care of Client with Endocrine Disorders Endocrine Disorders Pituitary disorders Thyroid disorders Adrenal disorders Diabetes mellitus Endocrine System Hormones Hormone Overview- Hypothalamus Base of skull Linkes brain to endocrine system connecte...

Care of Client with Endocrine Disorders Endocrine Disorders Pituitary disorders Thyroid disorders Adrenal disorders Diabetes mellitus Endocrine System Hormones Hormone Overview- Hypothalamus Base of skull Linkes brain to endocrine system connected by a stalk containing nerves and blood vessels o This stalk is how hormones made from the hypothalamus travel to the pituitary Hormone Overview – Pituitary and Pineal Glands 1. Anterior Pituitary ACTH (Adrenocorticotropic hormone) o Stress response, stimulates adrenal gland to produce cortisol o Regulates metabolism, bp, blood glucose, reduces inflammation FSH (Follicle Stimulating Hormone) o Sperm production in AMAB and ovaries to produce estrogen and egge development in AFAB GH (growth hormone) o Stimulates growth o Makes you taller as a child o Adults: maintains healthy muscle and bones, impacts fat distribution, metabolism LH (luteinizing/gonadotropin hormone) o Stimulates ovulation and testosterone production o Function of ovaries and testes PRL (prolactin) o Stimulates breast milk production after birth o Affects fertility and sexual function TSH (thyroid stimulating hormone) o Stimulates thyroid hormones T3 and T4 to manage metabolism, energy levels, brain development, cell replication 2. Posterior Pituitary (storage and release) ADH/vasopressin o Regulates water balance and sodium levels in body (serum osmolarity) o e.g. dehydration -> less water -> higher serum osmolarity Oxytocin o Laboring process -> progress labor during childbirth by sending signals to uterus to contract o Parent and child binding o Mobilizing sperm 3. Pineal Melatonin o Sleep o Secretion is connected to time of day o Declines with age Positive feedback loop Infant suckling activates nerves leading to hypothalamus -> tells hypothalamus to make oxytocin -> pituitary releases oxytocin -> oxytocin acts on breast tissue to allow milk to flow Negative feedback loop Increased levels of cortisol in the blood -> trigger stop cortical releasing hormone by hypothalamus - > stop ACTH from being released from pituitary gland (acts on adrenal glands that release cortisol Increase in growth hormone -> triggers hypothalamus (makes and releases growth hormone) -> acts on pituitary gland that releases growth hormone to stop releasing growth hormone Hormones – Ovaries & Testes Ovaries o Estrogen ▪ Peak before ovulation, increase during luteal phase o Progesterone ▪ Peak post ovulation o Fluctuate across 28 day cycle Testes o Estradiol o Testosterone Hormones - Adrenal Gland Cortex: Steroid hormones o Glucocorticoids (cortisol) ▪ Glucose metabolism; impacts glucose, protein, fat metabolism, stress, immune function ▪ Increased cortisol secretion -> increased blood glucose levels ▪ Inhibit inflammatory process ▪ Prevent tissue rejection ▪ SE: diabetes, osteoporosis, peptic ulcer, redistribution of body fat, poor wound healing, muscle wasting  o Mineralocorticoids (aldosterone) ▪ Act on renal tubules and GI epithelium to increase sodium reabsorption and excrete K+ and H+ ▪ Aldosterone is main hormone for long term regulation of sodium balance o Sex hormones (androgens and estrogen) ▪ Androgens associated with start of puberty and reproductive health and body development (i.e. testosterone) Testes and ovaries produce them mostly, but so do adrenal glands Medulla: Catecholamines o Epinephrine ▪ 90% of secretion ▪ Fight or flight response o Norepinephrine o Thyroid Hormone Thyroid hormone Comprised of T3 and T4, calcitonin (secreted in response to high plasma levels of calcium and reduces the plasma level of calcium by increasing its deposition in bone Iodine is essential to create hormones o Get iodine from diet o Secretion of T3 and T4 is controlled by TSH Thyroid hormones impact cell replication which is important for brain development, normal growth, bone health, digestion, metabolism o Effects ever major organ system and tissue function (basal metabolic rate, metabolism, cholesterol levels, vascular resistance Low levels of iodine -> triggers elevated TSH, overproduction of T3 and T4, hypertrophy of thyroid gland -> goiter o Iodized salts help to eliminate goiters Euthyroid = normal functioning thyroid Parathyroid glands Secrete parathyroid hormone -> regulate calcium and phosphorus metabolism o Tends to lower blood phosphorus level o Increased secretion of PH -> increased calcium absorption from kidney, intestines, bones -> raises serum calcium level -> increased calcium results in decreased PH secretion ▪ Negative feedback! Hyper parathyroid results from overproduction of parathyroid mode and causes bone decalcification and the development of renal calculi or kidney stones containing calcium o Symptoms: pain, fatigue, muscle weakness, nausea, vomiting, constipation, HTN, cardiac arrythmias may occur, anorexia o Tx: removing 1 or more glands, minimally invasive, outpatient o Require increase in daily fluid intake (more than 2 liters) to prevent renal calculi formation o Walking is encouraged bc bones that experience stress from walking release less calcium o Bedrest also increases calcium excretion and other risk of kidney stones o Encourage appetite and PO intake ▪ Eat normal levels of calcium o For constipation: prune juice, activity, stool softener Hypo parathyroid caused by removal of thyroid glands o When there is a toxic thyroid that needs to be removed, parathyroid may be partially removed or damaged o Other causes: autoimmune response, vitamin D deficiency o Causes hyperphosphatemia (increased blood phosphate levels) and hypocalcemia (low calcium) ▪ Hypocalcemia is chief symptoms of hypoparathyroidism which is tetany -> muscle tremors and spams in the arms and legs with later signs being numbness and tingling in hands and feet, positive spastic and trousseau signs o Goal of therapy is to increase serum calcium up to 9/10 (normal is 8.5-10.5) ▪ Tx: calcium, magnesium, herbal calciferol, calcitriol (preferred) Pituitary Disorders Acromegaly Diabetes insipidus SIADH Acromegaly Rare disorder of GH in adults o Increase in GH, increase in size of body parts, no height increase Labs, x-rays, cat scans to diagnose Coarse facial features o Enlarged forehead, lips, ears, lower jaw protrusion o Wide spaces between teeth, enlarged tongue o Soft tissue swelling Enlarged hands and feet, thickened skin Deepening of voice, oily skin, excessive sweating, carpal tunnel, sleep apnea, osteoarthritis, HA Severe headaches, sweating, HTN Onset is gradual over years Left untreated -> HTN, diabetes mellitus, heart problems Treatment depends on cause (i.e. tumor) o Surgery, meds, radiation therapy o Surgery: removing pituitary adenoma (trans nasal approach) o Meds: inhibit release of growth hormones o Radiation is used when surgery or meds are not sufficient Rx: oInhibit GH release: octreotide (sandostatin), lanreotide (somatuline) ▪ Significant shrinkage of tumor in 30-50% pts o GH receptor blocker: pegvisomant (somavert) Psychosocial support, medication education  Diabetes Insipidus Deficient ADH Rare, injury caused to hypothalamus or pituitary glands that results in deficiency of ADH (secreted by posterior pituitary) Decreased ADH reduces ability of distal renal tubules and kidneys to collect and concentrate urine - > excretion of large volumes of dilate urine, excessive thirst, excessive fluid intake, electrolyte imbalances Causes: central & nephrogenic o Central: from brain, head trauma, surgery, infection, inflammation, brain tumors, radiation in or around pituitary gland o Nephrogenic: originates in kidneys where renal tubules do not react to ADH; cause is adverse effect from meds like lithium or tetracycline antibiotics or the result of kidney injury/electrolyte imbalances (hyperkalemia or hypercalcemia) Symptoms: dehydration, dry and cracked lips, confusion, weakness Assessment: o Polyuria: 3-20 L/day and consequent polydipsia o Tachycardia, hypotension, loss or absence of skin turgor, dry mucus membranes, weak pulses, decreased cognition, constipation, nocturia, fatigue, weight loss, dilute urine o Labs: ▪ Urine: low specific gravity < 1.005; low osmolality < 200mOsm/L; low urine pH, Na, &K Super dilute ▪ Blood: high blood osmolality > 300 mOsm/L; high Na & K Very concentrated and high osmolarity in blood Care:  o vital signs, urinary output, I/Os, specific gravity, labs (K, Na, BUN, Cr, spec grav, osmolarity), daily weights, IV hydration, electrolyte replacement PRN, fall precautions, skin turgor, mucous membranes, high fiber, diet avoid alcohol consumption/caffeine, Complications: o Dehydration, hypernatremia, unconsciousness, CNS damage, seizures, circulatory collapse Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Excess ADH, excess fluid retention Causes: o Tumors, head injury, meningitis, medications (anesthetics, chemotherapy agents, antidepressants (SSRIs, TCAs), opioids, barbiturates). Assessment: o Early: headache, weakness, anorexia, muscle cramps, water weight gain, s/s fluid volume excess (crackles, distended neck veins, HTN) o Late: confusion, lethargy, nausea, vomiting, diarrhea, oliguria, Cheyne-Stokes respirations, seizures ▪ Oliguria = dark, concentrated urine (less output) Care: I/Os and restricting fluid intake, daily weight, urine and blood chemistries, and neurologic status, administer diuretics and hypertonic NaCl (3%) for severe hyponatremia may be Rx o Treat underlying cause and symptom management Complications: water intoxication, severe hyponatremia -> coma -> death o Water intoxication: crackles in lungs, distended neck veins, confusion, HA, disorientation, muscle cramping o Hyponatremia can lead to cerebral edema, pulmonary edema, coma and death Thyroid Disorders Hypothyroidism Decreased levels of thyroid hormone think SLOW o Impacts metabolism so everything will slow down Causes: o Autoimmune thyroiditis (Hashimoto disease), hyperthyroid tx (radioactive iodine or antithyroid meds), thyroidectomy o Myxedema is severe form of hypothyroidism o Hashimoto's is most common Assessment: -> image  o o Fatigue, lethargy, sleep a lot, constipation, cold intolerance, thinning hair/eyebrows, weight gain, swelling of face, hands, feet, enlarged tongue, slow speech/thoughts, bradycardia, deeper voice, etc. o Menorrhagia in menstruating adults o In myxedema: hypothermia, personality and cognitive changes (similar to dementia), sleep apnea, pleural effusion, pericardial effusion, respiratory muscle weakness; sensitive to sedatives, opioids, anesthetics ▪ Coma: hypothyroid, hypothermic, unconscious Develops with undiagnosed hypothyroidism or follows infection/sedatives/opioid analgesics Hyponatremia, hypoglycemia, hyperventilation, hypotension, bradycardia, hypothermia Contribute to cardiovascular shock and collapse and require critical care Care: o levothyroxine 75 – 150 mcg PO daily on empty stomach with full glass of water ▪ Older adults require a lower dose o start low and titrate until desired TSH ▪ For older adults ▪ Prevalence increases with age and signs of hypothyroidism can be confused with signs of aging o Supportive care Complications: o Myxedema (severe deficiency), Myxedema coma (rare, life-threatening condition) Hyperthyroidism Increase in levels of thyroid hormone think FAST From excessive endogenous thyroid hormone or exogenous (from meds) Causes:  o Graves disease (autoimmune), thyroiditis (inflammation), excessive intake of thyroid hormone ▪ Graves is most common cause Assessment: -> image o o Anxious, restless, irritable, muscle weakness and wasting, tremors, emotional lability, decreased attention, sinus tachycardia or arrhythmias, insomnia, diarrhea, weight loss, warm/sweaty/flushed skin, perspiration, big appetite, heat intolerance, fine hair, exophthalmos, goiter, etc. ▪ Oligomenorrhea- irregular and inconsistent period o If left untreated and severe -> enlargement of heart (myocardial hypertrophy) and eventual heart failure o Graves disease will present with exophthalmos, goiter, pretibial myxedema ▪ Exophthalmos: occurs from edema in extra ocular muscles and increased fatty tissue deposits behind eye Blurry vision, double vision, tiring of eyes May not be reversible even with treatment ▪ Pretibial myxedema: dry, waxy, swelling of front surfaces of lower legs that resemble benign tumors Treatment: antithyroid meds, radioactive iodine, beta blockers for symptom management (cardiac), thyroidectomy o Radioactive iodine is effective in 80-90% of pts (1 dose) Care o Antithyroid meds (see next slide), radioactive iodine (131I), beta blockers, surgery Complications: o Thyroid storm (> 101.3oF, > 130 bpm, altered neuro state, & exaggerated hyperthyroid symptoms), hypocalcemia/tetany, nerve damage (vocal disturbances/vocal cord paralysis) ▪ Thyroid storm: life threatening condition of thyroid due to untreated hypothyroidism; triggered by stress (injury/infection/surgery/pregnancy/withdrawal from meds/emotions) Abrupt onset, almost always fatal without prompt treatment High fevers, tachycardia, exaggerated symptoms of hyperthyroidism, change in LOC, psychosis, coma Tx: temperature and cardiac  o Temp: hypothermic blankets with ice packs, acetaminophen , humidified oxygen, IV fluids, dextrose, propylthiouracil or Methimazole to block conversion of T3 and T4, hydrocortisone for shock or adrenal insufficiency, iodine o Cardiac: propranolol, digoxin o NO ASPIRIN, SALICYLATE, SULFATES ▪ They displace thyroid hormone from binding proteins and worsen hypermetabolism Adrenal Disorders Adrenocortical Insufficiency (Addison’s Disease) Damage or dysfunction of adrenal cortex -> decrease steroids in adrenal glands o Decreased aldosterone and cortisol Causes: o Autoimmune, surgery, cancers, steroid withdrawal o Meds that can cause: rifampin, barbituates, ketoconazole, tyrosine kinase inhibitors, sudden stopping of exogenous steroid therapy ▪ Adrenal insufficiency should be considered in any pt who has been treated with corticosteroids o Loss of mineralocorticoid -> increased secretion of NaCl, increased retention of K, hypoglycemia, weakness, fatigue Assessment: o Weakness/fatigue, weight loss, salt craving, hyperpigmentation (knuckles, knees, skin folds, mucus membranes), anorexia, n/v, hyponatremia, hypovolemia, hypoglycemia, hyperkalemia, hypercalcemia Care: o Glucocorticoid replacement: hydrocortisone, prednisone, or cortisone o Mineralocorticoid replacement: fludrocortisone o Hydrocortisone IV, 0.9% NS/D5W IV fluids, vasopressors, antibiotics PRN, monitor/treat hyperkalemia and hypoglycemia Complications  Addisonian crisis (confusion and restlessness, severe hypotension, cyanosis, fever, n/v, signs of shock) o Acute adrenal insufficiency, abrupt onset, medical emergency o If not treated promptly, prognosis is poor o Signs of shock: hypotension, tachycardia that leads to arrythmias, LOC, being unresponsive, pallor, decreased urinary output, rapid and weak pulse, tachypnea o Treatment: lifelong oral replacement of adrenal cortex hormones (hydrocortisone, prednisone, cortisone) o Education! Monitoring! Safety precautions! o Severe cases: prevent and treat circulatory shock that could ensure (restore blood circulation, administer fluids and steroids IV, monitor vitals, lie flat, vasopressors) ▪ Susceptible to infection to abx ▪ Monito labs for hyperkalemia, hypoglycemia Cushing’s Syndrome/Disease Increase in adrenal cortex hormones Causes o Medications, hyperplasia of cortex, pituitary tumor ▪ Can happen more in pts with history of asthma or arthritis from meds Assessment o Classic signs: central obesity, fat around the face (moon face), back of neck (buffalo hump) and abdomen o Weakness, fatigue, sleep disturbances, thin, fragile skin, striae, HTN , hyperglycemia, heart failure, hirsutism, amenorrhea, depression, dark facial hair, poor would healing, muscle wasting, osteoporosis, red cheeks ▪ Risk for falls and fractures o Retain sodium and water as result of increased mineralocorticoid leading to HRN and heart failure o Increase in androgen secretion in AFAB causes excessive facial hair, breast atrophy, cessation of menses o  o Treatment o If med is cause: taper med to minimum dose needed to treat underlying disease o Hypertrophy: adrenalectomy to remove adrenal gland o Pituitary tumor: surgery to remove tumor or pituitary gland (radiation is possible as well) Care o Depends on the cause: surgery or medication dosage adjustment; psychological support; maintaining adequate, cardiac function, decreasing the risk of injury and infection, promoting skin integrity Diabetes Mellitus (DM) Chronic metabolic disorder characterized by hyperglycemia from inadequate production of insulin (Type 1), or cells do not respond to insulin (Type 2) Types: o Prediabetes – blood sugar > normal, not high enough for type 2 diagnosis, aka impaired glucose tolerance or impaired fasting glucose) ▪ 1/3 adults have it ▪ Increase risk of type 2 diabetes, heart disease, stroke ▪ Prevented with lifestyle ▪ https://www.cdc.gov/prediabetes/risktest/index.html Type 1 – inadequate production of insulin (fka insulin-dependent or juvenile diabetes) Type 2 – insulin resistance (fka non-insulin-dependent, adult-onset) o 95% have this Gestational – develops in pregnant people with no history of DM o Onset in 2nd or 3rd trimester o Can lead to macrosomia: babies in higher weight o Managed with diet modification, with exercise, blood glucose monitoring o If hyperglycemia persists, then insulin is prescribed Normal: eat -> insulin secretion increases -> moves glucose from blood and into muscle, liver, fat cells o Insulin transports and metabolizes glucose, tells liver to stop release of glucose, stimulates storage of glucose in liver and muscle in form of glycogen, enhances storage of dietary fat and adipose tissue, accelerates transport of amino acids from protein, inhibits breakdown of stored glucose, protein, and fat  Type 1: beta cells of pancreas is destroyed so that there is decreased insulin production, increased glucose production by liver -> hypoglycemia o Glucose from food cannot be stored in liver, but will remain in bloodstream and contribute to postprandial hypoglycemia o Excess glucose is not reabsorbed by kidneys so passes in urine -> loss of fluid and electrolytes -> osmotic diuresis o Fat breakdown and production of highly acidic ketone bodies -> ketoacidosis (hyperglycemia, ketosis, metabolic acidosis) o Type 2 diabetes: impaired insulin secretion and insulin resistance o Insulin is less effective at glucose uptake by tissues and regulating the release of glucose by the liver o Increased amounts of insulin must be secreted to maintain blood glucose at normal level o Uncontrolled -> HHS hypoglycemic hyperosmolar syndrom o Diabetes Mellitus (DM) Signs and symptoms o Polyuria- increased urination o Polydipsia- increased thirst o Polyphagia- increased appetite o Other: fatigue, sudden vision changes, dry skin, slow healing wounds, recurrent infections Variable Normal Prediabetes Diabetes Fasting plasma glucose level 70 – 99 mg/dL 100 – 125 mg/dL ≥ 126 mg/dL (NPO x 8 hrs) Random blood sugar < 125 mg/dL or < 140 (depends on time of mg/dL ------- ≥ 200 mg/dL last meal) post - prandial Hemoglobin A1C < 5.7% 5.7 – 6.4% ≥ 6.5% Consequences of DM o Neuropathy ▪ Numbness and tingling in hands or feet o Nephropathy ▪ Kidney disease o Retinopathy Treatment o Education o Medication o Diet and nutrition o Physical activity Diabetes Treatment - Education 1. Pathophysiology a. Basic definition of diabetes (having a high blood glucose level) b. Normal blood glucose ranges and target blood glucose levels c. Effect of insulin and exercise (decrease glucose) d. Effect of food and stress, including illness and infections (increase glucose) e. Basic treatment approaches 2. Treatment modalities a. Administration of insulin and oral antidiabetic medications b. Meal planning (food groups, timing of meals) c. Monitoring of blood glucose and urine ketones 3. Recognition, treatment, and prevention of acute complications a. Hypoglycemia  b. Hyperglycemia 4. Pragmatic information a. Where to buy and store insulin, syringes, and glucose monitoring supplies b. When and how to contact the primary provider Diabetes Treatment - Medications Oral Medications o (Separate slide) o Start at low dose adn increase every 2 weeks until maximum dose is reached Insulin injection o Mostly in type 1 o U-100 syringes o Note type of insulin Rx o Note onset, peak, duration of dose o Insulin pens ▪ Prefilled cartridges of 150-300 units of insulin, disposable needles, good for travel or pts with problems with vision/dexterity ▪ TEACH: must use insulin u-100 syringe for administration ▪ o Insulin pump o Continuous infusion of insulin, can give in a bolus as well o Change every 2-3 days to prevent infection o Complications:  ▪ Accidental cessation of insulin administration (turned off before a surgery and never turned back on) ▪ Obstruction of tubing/needle ▪ Pump failure ▪ Infection Insulin Types & Sliding Scale Rapid- give when food is about to be eaten in 10 mins, subq Regular/short acting- give 30 mins before food, subq/IV NPH- 30-60 mins before meals and at night for glycemic control throughout day LA- peak less, lasts 24 hours, subq ONLY Sliding scale is based on glucose reading Antidiabetic agents *GLP1’s, biguanides (metformin), 2nd gen sulfonylureas, Diabetes Treatment Diet and nutrition Plate method o ½ plate is veggies, ¼ is proteins, ¼ is carbs Talk to dietician, consider cultural preferences (american diet?) Diabetes Treatment – Physical Activity ADA Recommendations: o 150+ min/wk of moderate- to vigorous-intensity aerobic activity  ▪ 75 min/wk of vigorous-intensity or interval training o T1 and T2D should engage in 2–3 sessions/wk of resistance exercise on nonconsecutive days o Decrease sedentary behavior ▪ Prolonged sitting should be interrupted every 30 min o Flexibility and balance training recommended 2–3 times/week. ▪ Yoga and tai chi may be included based on individual preferences to increase flexibility, muscular strength, and balance. **Check blood glucose before and after physical activity** Acute Complications of Diabetes Hypoglycemia Diabetic ketoacidosis (DKA) Hyperglycemia hyperosmolar syndrome (HHS) I. Hypoglycemia: < 70 mg/dL Low blood sugar, normal range is 70-99 mg/dL Too much insulin/PO hypoglycemic meds, excess physical activity Mild: sweating, tremors, tachycardia, palpitations, nervousness, hunger Moderate: inability to concentrate, headache, lightheaded, confusion, numb lips/tongues, slurred speech, irritable/combative, double vision, drowsiness Severe: disoriented behavior, seizures, difficult to arouse, loss of consciousness Gerontologic considerations o If living alone, may not recognize the signs/symptoms (time is important in treating this) o Decreased kidney function -> increased time to excrete PO hypoglycemic meds o Skipping meals due to finances or decreased appetite o Decreased vision -> errors in insulin administration Treatment: conscious -> 15-20 g carbs (4-6 oz juice/soda), glucose tabs, glucose gel packets, 6 hard candies; unconscious or < 54 mg/dL-> glucagon (SQ/IM) or 1 ampule of D50 o Glucagon is given outside hospital by family, self, caregiver ▪ After 20 mins of consciousness after glucagon, give a snack of concentrated carbs (juice or soda) to prevent reoccurrence, need to be side lying after glucagon due to nausea and potential nausea o D50 is within mins in hospital ▪ Possible HA after ▪ Recheck glucose every 15 mins after administration ▪ Give carb and protein snack when its normal Hypoglycemia Management Pt education!! Hyperglycemia Management Insulin therapy for levels of 180 Target range should be 140-180, shortened to 110-140 for selected pts where maintaining glucose within those ranges does not cause hypoglycemia  Teach to recognize: thirst, dry mouth, peeing a lot, fatigue, blurred vision, unintentional weight loss, recurrent infections Test for ketones in urine if they have these symptoms, stay hydrated, check sugar/urine, administer insulin, rehydrate, notify provider, potentially go to hospital for follow up treatment Administer insulin, educate on s/s- hot, dry skin; fruity breath, test urine for ketones (notify provider if +), encourage sugar-free fluids to prevent dehydration, if s/s progress, notify provider, call RR Acute Complications of Diabetes II. Diabetic Ketoacidosis (DKA) Absent or very little insulin, more often in Type 1 Caused by: o Reduced or missed dose of insulin: insulin insufficiency o Illness or infection ▪ Infection can cause increased blood glucose levels, may need to increase insulin dose ▪ Association with insulin resistance in response to emotional stress (glucagon, epinephrine, norepinephrine, cortisol, growth hormone) All of these hormones promote glucose production by the liver and interfere with how glucose is used by the muscle and fat tissue (counteracting insulin and causing hypoglycemia) o Undiagnosed or untreated T1D ▪ Someone who does not know they have diabetes Characterized by: o Hyperglycemia o Dehydration & electrolyte loss ▪ Lose several liters of water and electrolytes ▪ 3 fatty acids are converted into ketones from liver -> metabolic acidosis Metabolic acidosis: any process that causes a decrease in the pH of the body as a result of retention of acids, or from the loss of bicarbonate o Acidosis (fruity odor of breath) ▪ Symptoms: polydipsia, polyuria, extreme fatigue, blurred vision, weakness, HA, OH, rapid/weak pulse, anorexia, N/V, abdominal pain, hyperventilation (Kussmaul breathing), mental status changes ▪ Blood glucose levels will be super high (250-800-1,000) Treatment: rehydration, replace electrolytes, reverse acidosis o Need 6-10 liters of fluids (monitor I and O)  o K+ is most important (hyperkalemic in DKA), insulin will pull it into cells (ECG monitoring) o GIVE INSULIN slowly to inhibit fat breakdown ▪ Measure blood glucose hourly ▪ Regular insulin only Acute Complications of Diabetes – Prevention as Treatment Sick day rules Never eliminate insulin when N/V occur Pts should take usual insulin and consume small portions of carbs, juice, soda, jello-o (NOTHING DIET) Drink fluids to avoid dehydration Check urine and glucose every 3-4 hours Eat 50g carbs every 4 hours or soft foods 6-8 times a day  Acute Complications of Diabetes III. Hyperglycemia Hyperosmolar Syndrome (HHS) Most often in older adults with Type 2 or no history of diabetes Insulin resistance (lack of effective insulin) Caused by: o Physiologic stress (infection, surgery, stroke, MI), medications (thiazides), treatments (dialysis) o Evolves over several days (much slower than DKA which is less than 24 hours) Characterized by: o Hyperglycemia > 600 mg/dL Insulin is low, but not low enough that fat breakdown occurs (no ketone GI symptoms) o Increased osmolality > 320 mOsm ▪ Normal serum osmolality: 275-290 mOsm o Pts will report days-weeks of polyuria with adequate fluid intake o Neurologic changes, polyuria, hypotension, dehydration, tachycardia, seizures, hemiparesis, high glucose levels and osmolality, hallucinations, OH o BUN and creatinine levels are elevated ▪ Cerebral dehydration from extreme hyperosmolarity causes mental status changes, neuro deficits, hallucinations Treatment (similar to DKA): fluid replacement, correct electrolyte imbalances, and insulin administration o Close monitoring of volume and electrolytes to prevent fluid overload, heart failure, cardiac arrhythmias (older pts) o May take 3-5 days for neurologic symptoms to clear (are reversible) Long-term complications of diabetes Many people with metabolic syndrome have diabetes, cardiovascular disease, obesity, hyperlipidemia, HTN, hyperglycemia Macrovascular complications (vessel walls thicken and sclerosis and blood flow is blocked)  o Coronary artery disease ▪ Diminished peripheral pulses and intermittent claudication (pain in thigh, calf, butt when walking) Can lead to gangrene and amputations ▪ CAD in diabetes is 2-3 times likely to have a heart attack and death o Cerebrovascular disease ▪ Atherosclerotic can lead to TIA or stroke, and increased death from stroke o Peripheral vascular disease ▪ Lower extremities Microvascular complications: capillary wall thickening (impact smaller vessels in retina, kidneys) o Retinopathy ▪ Damage to small vessels that feed the retina, causing visual impairments ▪ Leading cause of blindness 20-74 years in USA ▪ In type 1 and 2 ▪ Can also lead to micro aneurysms, intracranial hemorrhage, hard exudates and capillary collapse leading to closure of vessels (decrease perfusion and visual acuity, blindess, cataracts, glaucoma) ▪ o Nephropathy ▪ Diabetes pts account for almost half of new stages of end stage kidney disease ▪ Ability of kidneys to filter has been stressed so proteins (albumin) leak into urine -> pressure in kidneys increase -> nephropathy ▪ As kidney failure progresses, breakdown of exogenous and endogenous insulin -> hypoglycemia Diabetic neuropathy o Peripheral neuropathy ▪ Affects distal portions of nerves, moves proximal ▪ Paresthesia: prickling, tingling, heightened sensations, burning in feet/hands/fingers ▪ Decreased feeling in feet -> risk for falls and undetected foot infections Foot and leg problems o Poor wound healing ▪ Hyperglycemia -> risk of infection (impairs ability of leukocytes to destroy bacteria) ▪ Injury to foot undetected -> can progress to osteomyelitis where the infection spreads to the bone and needs to be amputated o Amputations o Joint deformities (Charcot foot) ▪ Result of neuropathy  ▪ Broken foot (warmth, redness, swelling); unilateral; may not report pain ▪ Bones have fractured and collapsed onto each other ▪ Nonsurgical and surgical approaches to fix ▪ Feet need to be examined daily ▪ Foot Care Take care of diabetes first (diet, nutrition, activity, insulin) Inspect feet everyday Wash feet everyday in warm water (NO SOAKING) Lotion on top and bottom of feet, but not between toes Smooth corns and callus’s Trim toenails each week straight across Shoes and socks at all times Break shoes in slowly to avoid blisters Protect from hot and cold temps Do not cross legs, No smoking (vasoconstriction)