Assessment and Management of Patients With Endocrine Disorders

Assessment and Management of Patients With Endocrine Disorders
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Glands of the Endocrine System
Hypothalamus Posterior Pituitary Anterior Pituitary Thyroid Parathyroids Adrenals Pancreatic islets Ovaries and testes 2

Hypothalamus Releasing and inhibiting hormones
Corticotropin-releasing hormone Thyrotropin-releasing hormone Growth hormone-releasing hormone Gonadotropin-releasing hormone Somatostatin-=-inhibits GH and TSH 3

Anterior Pituitary Growth Hormone-- Adrenocorticotropic hormone
Thyroid stimulating hormone Follicle stimulating hormone—ovary in female, sperm in males Luteinizing hormone—corpus luteum in females, secretion of testosterone in males Prolactin—prepares female breasts for lactation 4

Posterior Pituitary Antidiuretic Hormone
Oxytocin—contraction of uterus, milk ejection from breasts 5

Adrenal Cortex Mineralocorticoid—aldosterone. Affects sodium absorption, loss of potassium by kidney Glucocorticoids—cortisol. Affects metabolism, regulates blood sugar levels, affects growth, anti-inflammatory action, decreases effects of stress Adrenal androgens—dehydroepiandrosterone and androstenedione. Converted to testosterone in the periphery. 6

Adrenal Medulla Epinephrine and norepinephrine
serve as neurotransmitters for sympathetic system 7

Thyroid Follicular cells—excretion of triiodothyronine (T3) and thyroxine (T4)—Increase BMR, increase bone and calcium turnover, increase response to catecholamines, need for fetal G&D Thyroid C cells—calcitonin. Lowers blood calcium and phosphate levels 8

Parathyroid Parathyroid hormone—regulates serum calcium 9

Pancreatic Islet cells
Insulin Glucagon—stimulates glycogenolysis and glyconeogenesis Somatostatin—decreases intestinal absorption of glucose 10

Kidney 1, 25 dihydroxyvitamin D—stimulates calcium absorption from the intestine Renin—activates the RAAS Erythropoietin—Increases red blood cell production 11

Ovaries Estrogen Progesterone—inportant in menstrual cycle,*maintains pregnancy, 12

Testes Androgens, testosterone—secondary sexual characteristics, sperm production 13

Thymus Releases thymosin and thymopoietin
Affects maturation of T lymphocetes 14

Pineal Melatonin Affects sleep, fertility and aging 15

Prostaglandins Work locally Released by plasma cells
Affect fertility, blood clotting, body temperature 16

Assessment Health history—energy level, hand and foot size changes, headaches, urinary changes, heat and cold intolerance, changes in sexual characteristics, personality changes, others Physical assessment—appearance including hair distribution, fat distribution, quality of skin, appearance of eyes, size of feet and hands, peripheral edema, facial puffiness, vital signs 17

Diagnostic Evaluation
Serum levels of hormones Detection of antibodies against certain hormones Urinary tests to measure by-products (norepinephrine, metanephrines, dopamine) Stimulation tests—determine how an endocrine gland responds to stimulating hormone. If the hormone responds, then the problem lies w/hypothalmus or pituitary Suppression tests—tests negative feedback systems that control secretion of hormones from the hypothalamus or pituitary. 18

Disorders of the Pituitary
Pituitary Tumors Eosinophilic tumors may result in gigantism or in acromegaly. May suffer from severe headaches, visual disturbances, decalcification of the bone, endocrine disturbances Basophilic tumors may cause Cushing’s syndrome w/features of hyperadrenalism, truncal obesity, amenorrhea, osteoporosis Chromophobic tumors—90% of pituitary tumors. Present with lowered BMR, obesity, somnolence, scant hair, low body temp, headaches, visual changes 19

Growth hormone deficiency in childhood will result in primary dwarfism.
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Pituitary Tumors—Assessment and Diagnostic Findings
H&P Vision tests CT, MRI Serum levels of pituitary hormones, others 21

Diabetes Insipidus Deficiency of ADH
Excessive thirst, large volumes of dilute urine Can occur secondary to brain tumors, head trauma, infections of the CNS, and surgical ablation or radiation Nephrogenic DI—relates to failure of the renal tubules to respond to ADH. Can be related to hypokalemia, hypercalcemia and to medications (lithium demeocycline) 22

Manifestations Excessive thirst Urinary sp. gr. of 23

Assessment and Diagnostic Findings
Fluid deprivation test—withhold fluids for 8-12 hours. Weigh patient frequently. Inability to slow down the urinary output and fail to concentrate urine are diagnostic. Stop test if patient is tachycardic or hypotensive Trial of desmopressin and IV hypertonic saline Monitor serum and urine osmolality and ADH levels 24

Pharmacologic Tx and Nursing Management
DDAVP—intranasal bid Can be given IM if necessary. Every 24-96h. Can cause lipodystrophy. Can also use Diabenese and thiazide diuretics in mild disease as they potentiate the action of ADH If renal in origin—thiazide diuretics, NSAIDs (prostaglandin inhibition) and salt depletion may help Educate patient about actions of medications, how to administer meds, wear medic alert bracelet 25

SIADH Excessive ADH secretion
Retain fluids and develop a dilutional hyponatremia Often non-endocrine in origin—such as bronchogenic carcinoma Causes: Disorders of the CNS like head injury, brain surgery, tumors, infections or medications like vincristine, phenothiazines, TCAs or thiazide diuretics Meds can either affect the pituitary or increase sensitivity to renal tubules to ADH Management: eliminate cause, give diuretics (Lasix), fluid restriction, I&O, daily wt., lab chemistries 26

SIADH Restoration of electrolytes must be gradual
May use 3% NaCl in conjunction with Lasix 27

Thyroid T3 and T4 Need iodine for synthesis of hormones—excess will result in adaptive decline in utilization called the Wolf-Chaikoff mechanism Thyroid is controlled by TSH Cellular metabolism, brain development, normal growth, affect every organ in the body T3 is five times as potent as T4 Calcitonin—secreted in response to high levels of serum calcium, increases deposition in the bone 28

Thyroid Inspect gland Observe for goiter Check TSH, serum T3 and T4
T3 resin uptake test useful in evaluating thyroid hormone levels in patients who have received diagnostic or therapeutic dose of iodine. Estrogens, Dilantin, Tagamet, Heparin, amiodarone, PTU,steroids and Lithium can cloud the accuracy T3 more accurate indicator of hyperthyroidism according to text 29

Thyroid Antibodies seen in Hashimoto’s, Grave’s and other auto-immune problems. Radioactive iodine uptake test measures rate of iodine uptake. Patients with hyperthyroidism exhibit a high uptake, hypothyroidism will have low uptake Thyroid scan—helps determine the location, size, shape and size of gland. “Hot” areas (increased function) and “cold” areas (decreased function) can assist in diagnosis. 30

Nursing Implications Be aware of meds patient is taking (see list in text) that can affect accuracy of testing Also be aware if patient is taking multivitamins and food supplements 31

Hypothyroidism Most common cause is Hashimoto’s thyroiditis
Common in those previously treated for hyperthyroidism Atrophy of gland with aging Medications like lithium, iodine compounds, antithyroid meds can cause Radiation treatments to head and neck Infiltrative diseases like amyloidosis, scleroderma Iodine deficiency and excess Hypothalamic or pituitary abnormality More common in women, especially over age 50 32

Manifestations From mild symptoms to myxedema
Myxedema –accumulation of mucopolysaccharides in sc and interstitial tissues. Is the extreme form of hypothyroidism. Can progress to shock. S/S—fatigue, hair loss, dry skin, brittle nails, numbness and tingling of the fingers, amenorrhea, weight gain, decreased heart rate and temperature, lassitude, cognitive changes, elevated cholesterol levels, constipation, hypotension 33

Pharmacologic Management of hypothyroidism
Levothyroxine is preferred agent Dosage is based on TSH Desiccated thyroid used infrequently due to inconsistent dosing Angina can occur when thyroid replacement is initiated as it enhances effects of cardiovascular catecholamines (in pt. w/pre-existent CAD). Start at low dose. Hypnotics and sedatives may have profound effects on sensorium 34

Management in Myxedema
Cautious fluid replacement Glucose to restore to normal glycemic levels Avoid rapid overheating due to increased oxygen demands but keep warm May give levothyroxine intravenously With recovery, Modify activity High fiber foods Home health for follow-up 35

Hyperthyroidism Extreme form is Grave’s disease
Caused by thyroiditis, excessive amount thyroid hormone, abnormal output by immunoglobulins Is more common in women 36

Manifestations of hyperthyroidism
Thyrotoxicosis—nervousness, irritable, apprehensive, palpitations, heat intolerance, skin flushing, tremors, possibly exophthalmos Have an increased sensitivity to catecholamines Can occur after irradiation or presence of a tumor 37

Assessment and Diagnosis
Thyroid thrill and or bruit may be present Thyroid may be enlarged Decreased TSH, increased free T4 and an increased radioactive iodine uptake 38

Management Reduce thyroid hyperactivity—usually use radioactive iodine, antithyroid meds or surgery) Beta blockers Can be relapse with antithyroid meds 39

Pharmacologic Therapy
Irradiation with administration of radioisotope iodine 131—initially may cause an acute release of thyroid hormones. Should monitor for thyroid storm S/S of thyroid storm—high fever. Tachycardia, delirium, chest pain, dyspnea, palpitations, weight loss, diarrhea, abdominal pain Management of thyroid storm—oxygen, IV fluids with dextrose, hypothermic measures, steroids to treat shock or adrenal deficiency, iodine to decrease output of T4, beta blockers, PTU or Tapazole impedes formation of thyroid hormone and blocks conversion of T4 to T3 40

Antithyroid Medications
PTU—propylthiouracil—blocks synthesis of hormones Tapazole (methimazole)—blocks synthesis of hormones. More toxic than PTU. Sodium Iodide-suppresses release of thyroid hormone SSKI (saturated solution of potassium chloride)– suppresses release of hormones and decreases vascularity of thyroid. Can stain teeth Dexamethazone—suppresses release of thyroid hormones 41

Surgical Management Reserved for special circumstances, e.g. large goiters, those who cannot take antithyroid meds, or who need rapid normalization Subtotal thyroidectomy Before surgery, give PTU until s/s of hyperthyroidism have disappeared Iodine may be used to decrease vascularity 42

Nursing Management Reassurance r/t the emotional reactions experienced
May need eye care if has exophthalmos Maintain normal body temperature Adequate caloric intake Managing potential complications such as dysrhythmias and tachycardias Educate about potential s/s of hypothyroidism following any antithyroid tx. 43

Parathyroid Glands Parathormone maintains sufficient serum calcium levels Excess calcium can bind with phosphate and precipitate in various organs, can cause pancreatitis Hyperparathyroidism will cause bone decalcification and development of renal calculi More common in women Secondary hyperparathyroidism occurs in those with chronic renal failure and renal rickets secondary to excess phosphorus retention (and increased parathormone secretion) 44

Manifestations of Hyperparathyroidism
May be asymptomatic Apathy, fatigue, muscle weakness, nausea, vomiting, constipation, hypertension and cardiac dysrhythmias Excess calcium in the brain can lead to psychoses Renal lithiasis can lead to renal damage and even failure Demineralization of bones with back and joint pain, pain on weight bearing, pathologic fractures Peptic ulcers and pancreatitis can also occur 45

Persistent elevated calcium levels Elevated serum parathormone level Bone studies will reveal decreased density Double antibody parathyroid hormone test is used to distinguish between primary hyperparathyroidism and malignancy Ultrasound, MRI, thallium scan, fine needle biopsy also can be used to localize cysts, adenomas, or hyperplasia 46

Management Recommended treatment for hyperparathyroidism is surgical removal Hydration therapy necessary to prevent renal calculi Avoid thiazide diuretics as they decrease renal excretion of calcium Increase mobility to promote bone retention of calcium Avoid restricted or excess calcium in the diet Fluids, prune juice and stool softeners to prevent constipation Watch for s/s of tetany postsurgically (numbness, tingling, carpopedal spasms) as well as cardiac dysrhythmias and hypotension 47

Hypercalcemic crisis Seen with levels greater than 15mg/dL
Can result in life-threatening neurologic, cardiovascular and renal symptoms Treatments include: hydration, loop diuretics to promote excretion of calcium, phosphate therapy to promote calcium deposition in bone and reducing GI absorption of calcium Give calcitonin or mithramycin to decrease serum calcium levels quickly 48

Hypoparathyroidism Seen most often following removal of thyroid gland, parathyroid glands or following radical neck surgery Deficiency of parathormone results in increased bone phosphate and decreased blood calcium levels In absence of parathormone, there is decreased intestinal absorption of dietary calcium and decreased resorption of calcium from bone and through kidney tubules 49

Clinical Manifestations of Hypoparathyroidism
Irritability of neuromuscular system Tetany—hypertonic muscle contractions , numbnes, tingling, cramps in extremities, laryngeal spasm, bronchospasm, carpopedal spasm ( flexion of the elbows and wrists, dorsiflexion of the feet), seizures 50

Trousseau’s sign—can check with a BP cuff Chvostek’s sign—tapping over facial nerve causes spasm of the mouth, nose and eye Lab studies may reveal calcium levels of 5-6 mg/dL or lower Serum phosphate levels will be decreased 51

Management of Hypoparathyroidism
Restore calcium level to 9-10 mg/dL May need to give IV calcium gluconate for immediate treatment Use of parathormone IV reserved for extreme situations due to the probability of allergic reactions Monitor calcium levels May need bronchodilators and even ventilator assistance Diet high in calcium and low in phosphorus; thus, avoid milk products, egg yolk and spinach. 52

Management of Hypoparathyroidism
Keep calcium gluconate at bedside Ensure has IV access Cardiac monitoring Care of postoperative patients who have undergone thyroid surgery, parathyroidectomy or radical neck surgery. Be watchful for signs of tetany, seizures, and respiratory difficulties 53

Adrenals--Pheochromocytoma
Usually benign tumor Originates from the chromaffin cells of the adrenal medulla Any age but usu. Between years old Can be familial 10% are malignant May be associated with thyroid carcinoma or parathyroid hyperplasia or tumor 54

Clinical Manifestations
Headache, diaphoresis, palpitations, hypertension May have hyperglycemia related to excess epinephrine secretion Tremors, flushing and anxiety as well Blurring of vision Feeling of impending doom BPs exceeding 250/150 have occurred 55

Associated with the 5 H’s—hypertension, headache, hyperhidrosis, hypermetabolism and hyperglycemia Urinary catecholamines and metanephrine are direct and conclusive tests Serum epinephrine and norepinephrine levels will be elevated Urinary vanillymandelic acid also diagnostic Must avoid coffee, tea, bananas, chocolate, vanilla and ASA, nicotine, amphetamines, decongestants before 24h urine testing Clonidine suppression test—in normal individual, would block catecholamine release Imaging studies 56

Management Bedrest Elevated HOB ICU Nipride
Calcium channel blockers and Beta blockers Surgical management (manipulation of the tumor can cause excessive release of catecholamines) Steroid therapy if adrenalectomy performed Hypotension and hypoglycemia can occur post-op 57

Addison’s Disease Adrenocortical insufficiency
Autoimmune or idiopathic atrophy Can be caused by inadequate ACTH from pituitary Therapeutic use of steroids 58

Manifestations Muscle weakness Anorexia Dark pigmentation Hypotension
Hypoglycemia Low sodium levels High potassium levels Can result in Addisonian crisis 59

Addisonian crisis Circulatory shock
Pallor, apprehension, weak&rapid pulse, rapid respirations and low blood pressure Headache, nausea, abdominal pain and diarrhea Can be brought on by overexertion, exposure to cold, acute infection, decrease in salt intake 60

Early morning serum cortisol and plasma ACTH are performed. Will distinguish between primary and secondary adrenal insufficiency. In primary, will have elevated ACTH levels and below normal cortisol levels. If the adrenal cortex is not stimulated by the pituitary, a normal response to doses of exogenous ACTH (see text) Blood sugar levels and electrolyte values 61

Management Restore circulatory status—fluids, steroids
May need antibiotics if infection precipitated crisis May need lifelong steroid therapy and mineralocorticoid therapy May need additional salt intake Check orthostatics Daily weights Aware that stressors can precipitate crises Medic alert bracelet or similar identification of history 62

Cushing’s Syndrome Results from excessive adrenocortical activity
May be related to excessive use of corticosteroid medications or due to hyperplasia of the adrenal cortex Oversecretion of corticosteroids can also be caused by pituitary tumor Can be caused by bronchogenic carcinoma or other malignancy 63

Manifestations of Cushing’s syndrome
Cataracts, glaucoma Hypertension, heart failure Truncal obesity, moon face, buffalo hump, sodium retention, hypokalemia, hyperglycemia, negative nitrogen balance, altered calcium metabolism Decreased inflammatory responses, impaired wound healing, increased susceptibility to infections Osteoporosis, compression fractures Peptic ulcers, pancreatitis Thinning of skin, striae, acne Mood alterations 64

Overnight dexamethasone suppression test frequently used for diagnosis Administered at 11pm and cortisol level checked at 8am Suppression of cortisol to less than 5mg/dL indicates normal functioning Measurement of plasma ACTH (radioimmunoassay) in conjunction with dexamethasone suppression test helps distinguish pituitary vs. ectopic sites of ACTH. MRI, CT and CT also help detect tumors of adrenal or pituitary 65

Medical Management If pituitary source, may warrant transphenoidal hypophysectomy Radiation of pituitary also appropriate Adrenalectomy may be needed in case of adrenal hypertrophy Temporary replacement therapy with hydrocortisone or Florinef Adrenal enzyme reducers may be indicated if source if ectopic and inoperable. Examples include: ketoconazole, mitotane and metyrapone. If cause is r/t excessive steroid therapy, tapering slowly to a minimum dosage may be appropriate. 66

Primary Aldosteronism or Conn’s Syndrome
Excessive aldosterone secondary to adrenal tumor retain sodium and excrete potassium Results in alkalosis Hypertension—universal sign of hyperaldosteronism Inability of kidneys to concentrate the urine Serum becomes concentrated Excessive thirst Hypokalemia interferes with insulin secretion thus will have glucose intolerance as well 67

High sodium Low potassium level High serum aldosterone level Low renin level Aldosterone excretion rate after salt loading is diagnostic for primary aldosteronism Renin-aldosterone stimulation test 68

Management Surgical removal of tumor Correct hypokalemia
Usual postoperative care with abdominal surgery Administer steroids Fluids Monitoring of blood sugar Control of hypertension with spironolactone 69

Corticosteroid Therapy
Hydrocortisone--Cortisol Cortisone--Cortate Prednisone--Deltasone Prednisolone-Prelone Triamcinolone--Kenalog Betamethasone--Celestone Fludrocortisone (contains both mineralocorticoid and glucocorticoid) Florinef 70

Indications RA Asthma MS COPD exacerbations Lupus
Other autoimmune disorders Dermatologic disorders 71

Dosing Lowest dose Limited duration
Best time to give dose is in early morning between 7-8 am Need to taper off med to allow normal return of renal function 72

Side Effects of Steroids
Hypertension, thrombophlebitis, accelerated atherosclerosis Increased risk of infection Glaucoma and corneal lesions Muscle wasting, poor wound healing, osteoporosis, pathologic fractures Hyperglycemia, steroid withdrawal syndrome Moon face, weight gain, acne 73

Case Study 1 35 year old male presents with BP of 188/112 at a yearly physical exam. Previous exams noted blood pressures of 160/94 and 158/92. On questioning, patient admits to twice a month episodes of apprehension, severe headache, perspiration, rapid heartbeat, and facial pallor. These episodes had an abrupt onset and lasted minutes. Routine hematology and chemistry studies are wnl and chest xray and ECG are normal. What is your impression? What labs would you draw? 74

Case Study 2 50 year old woman presents with enlargement of left anterior neck. She has noted increased appetite over the past month with no weight gain, and more frequent bowel movements over the same period. Patient feels jittery at times, experiences palpitations and feels “hot” a lot recently. She is 5’8” tall and weighs 150#. Heart rate is 110 and blood pressure is 110/76. What might be this patient’s problem? What lab tests might you draw? 75

Case study 3 48 year old woman with a past history of mental illness presents with a new onset of bizarre psychotic behavior. She had been well over the past two years. She is 5’5” tall and weighs 138#. Her heart rate is 65, irreg and BP is 130/75. Exam is normal except that she is confused to place, time and year. Patient c/o joints aching and of feeling fatigued. Lab tests reveal serum calcium level of 13.8mg/dL (reference range is ) Phosphorus is 2.4 (reference range is ) What is your diagnosis? 76

Case Study 4 40 year old deeply tanned woman presents with a 6 month history of increasing fatigue. For the past three months she has suffered from recurrent URIs, poor appetite, abdominal cramps, fatigue and diarrhea. She has lost 25#. She has noted joint pains, muscle weakness, and has not menstruated for the past 3 months. Labs reveal blood glucose of 59, Na+ 130, K+ 6.0. What disorder do you expect? 77

Case Study #5 27 year old woman presents with depression, insomnia, increased facial fullness and recent increase in acne. She had an episode of depression and acute psychosis following uncomplicated delivery of normal baby boy 9 months previously. Her menses have been irregular since their resumption after the birth (she is not breast feeding). Patient relates has had several vaginal yeast infections recently. Heart rate is 90bpm, BP is 146/100. Her face is puffy and has acne vulgaris. Thin extremities and with truncal obesity. What are your suspicions? What labs will you draw? 78

Diabetes Mellitus Definition: metabolic disorder characterized by hyperglycemia due to an absolute or relative lack of insulin or to a cellular resistance to insulin Major classifications 1. Type 1 Diabetes 2. Type 2 Diabetes

Diabetes Mellitus Impact on health of American population
1. Sixth leading cause of death due to cardiovascular effects resulting in atherosclerosis, coronary artery disease, and stroke 2. Leading cause of end stage renal failure 3. Major cause of blindness 4. Most frequent cause of non-traumatic amputations

Diabetes Mellitus 5. Diabetes affects estimated 15.7 million people (10.3 million are diagnosed; 5.4 million are undiagnosed) 6. Increasing prevalence of Type 2 Diabetes in older adults and minority groups (African American, American Indian and Hispanic populations) 7. Estimated 11 % of older U. S. population (65 – 74) have diabetes

Diabetes Mellitus Diabetes Type 1 Definition
1. Metabolic condition in which the beta cells of pancreas no longer produce insulin; characterized by hyperglycemia, breakdown of body fats and protein and development of ketosis 2. Accounts for 5 – 10 % of cases of diabetes; most often occurs in childhood or adolescence 3. Formerly called Juvenile-onset diabetes or insulin-dependent diabetes (IDDM)

Diabetes Mellitus Pathophysiology
1. Autoimmune reaction in which the beta cells that produce insulin are destroyed 2. Alpha cells produce excess glucagons causing hyperglycemia Risk Factors 1. Genetic predisposition for increased susceptibility; HLA linkage 2. Environmental triggers stimulate an autoimmune response a. Viral infections (mumps, rubella, coxsackievirus B4) b. Chemical toxins

Diabetes Mellitus Manifestations
Process of beta cell destruction occurs slowly; hyperglycemia occurs when 80 – 90% is destroyed; often trigger stressor event (e. g. illness)

Diabetes Mellitus 2. Hyperglycemia leads to
a. Polyuria (hyperglycemia acts as osmotic diuretic) b. Glycosuria (renal threshold for glucose: 180 mg/dL) c. Polydipsia (thirst from dehydration from polyuria) d. Polyphagia (hunger and eats more since cell cannot utilize glucose) e. Weight loss (body breaking down fat and protein to restore energy source f. Malaise and fatigue (from decrease in energy) g. Blurred vision (swelling of lenses from osmotic effects)

Diabetes Mellitus Diagnosis Patient is symptomatic plus
Casual plasma glucose (non-fasting) is 200 mg/dl OR Fasting plasma glucose of 126 mg/dl or higher OR Two hour plasma glucose level of 200 mg/dl or greater during an oral glucose tolerance test

Diabetes Mellitus Diabetic Ketoacidosis (DKA)
1. Results from breakdown of fat and overproduction of ketones by the liver and loss of bicarbonate Occurs when Diabetes Type 1 is undiagnosed or known diabetic has increased energy needs, when under physical or emotional stress or fails to take insulin Mortality as high as 14% 3. Pathophysiology a. Hypersomolarity (hyperglycemia, dehydration) b. Metabolic acidosis (accumulation of ketones) c. Fluid and electrolyte imbalance (from osmotic diuresis)

Diabetes Mellitus Diagnostic tests
a. Blood glucose greater than 250 mg/dL b. Blood pH less than 7.3 c. Blood bicarbonate less than 15 mEq/L d. Ketones present in blood e. Ketones and glucose present in urine f. Electrolyte abnormalities (Na, K, Cl) G. serum osmolality < 350 mosm/kg (normal )

Diabetes Mellitus DKA Signs and symptoms Kussmals respirations
Blow off carbon dioxide to reverse acidosis Fruity breath Nausea/ abdominal pain Dehydration Lethargy Coma Polydipsia, polyuria, polyphagia

Diabetes Mellitus Treatment
a. Requires immediate medical attention and usually admission to hospital B .Frequent measurement of blood glucose and treat according to glucose levels with regular insulin (mild ketosis, subcutaneous route; severe ketosis with intravenous insulin administration) c. Restore fluid balance: initially 0.9% saline at 500 – 1000 mL/hr.; regulate fluids according to client status; when blood glucose is 250 mg/dL add dextrose to intravenous solutions

Diabetes Mellitus DKA d.Correct electrolyte imbalance: client often is initially hyperkalemic As patient is rehydrated and potassium in pushed back into the cell they become hypokalemic Monitor K levels e. Monitor cardiac rhythm since hypokalemia puts client at risk for dysrrhythmias f. Treat underlying condition precipitating DKA G. Acidosis is corrected with fluid and insulin therapy and rarely needs bicarb

Diabetes Mellitus Diabetes Type 2
A. Definition: condition of fasting hyperglycemia occurring despite availability of body’s own insulin B. Was known as non-insulin dependent diabetes or adult onset diabetes Both are misnomers, it can be found in children and type II DM may require insulin

1. Sufficient insulin production to prevent DKA; but insufficient to lower blood glucose through uptake of glucose by muscle and fat cells 2. Cellular resistance to insulin increased by obesity, inactivity, illness, age, some medications

Diabetes Mellitus Risk Factors
1. History of diabetes in parents or siblings; no HLA 2. Obesity (especially of upper body) 3. Physical inactivity 4. Race/ethnicity: African American, Hispanic, or American Indian origin 5. Women: history of gestational diabetes, polycystic ovary syndrome, delivered baby with birth weight > 9 pounds 6. Clients with hypertension; HDL cholesterol < 35 mg/dL, and/or triglyceride level > 250 mg/dl.

Diabetes Mellitus Syndrome X or Metabolic Syndrome
Chronic, low grade inflammatory process Gives rise to diabetes type 2, ischemic heart disease, left ventricular hypertrophy Group of disorders with insulin resistance as the main feature Includes Obesity especially around the waist and abdomen Low levels of physical activity High blood pressure Increased blood cholesterol (high LDL, low HDL, high triglycerides

Diabetes Mellitus Manifestations 1. Client usually unaware of diabetes
a. Discovers diabetes when seeking health care for another concern b. Most cases aren’t diagnosed for 5-6 years after the development of the disease c. Usually does not experience weight loss

Diabetes Mellitus 2. Possible symptoms or concerns
a. Hyperglycemia (not as severe as with Type 1) b. Polyuria c. Polydipsia d. Blurred vision e. Fatigue f. Paresthesias (numbness in extremities) g. Skin Infections

Diabetes Mellitus Hypersomolar Hyperglycemic Nonketotic Syndrome (HHNS) 1. Potential complication of Diabetes Type 2 Life threatening medical emergency, high mortality rate, as high as 50% Enough insulin is secreted to prevent ketosis, but not enough to prevent hyperglycemia High blood sugar causes an extreme diuresis with severe electrolyte and fluid loss

Characterized by Plasma osmolarity 340 mOsm/l or greater- normal Blood glucose severely elevated, Altered level of consciousness

Diabetes Mellitus 4. Precipitating factors a. Infection (most common)
pneumonia b. Therapeutic agent or procedure c. Acute or chronic illness MI Stroke Pancreatitis pregnancy 5. Slow onset 1 – 14 days

a. Hyperglycemia leads to increased urine output and dehydration b. Kidneys retain glucose; glucose and sodium rise c. Severe hyperosmolar state develops leading to brain cell shrinkage Manifestations a. Altered level of consciousness (lethargy to coma) b. Neurological deficits: hyperthermia, motor and sensory impairment, seizures c. Dehydration: dry skin and mucous membranes, extreme thirst, tachycardia, polyuria, hypotension

Diabetes Mellitus Treatment
a. Usually admitted to intensive care unit of hospital for care since client is in life-threatening condition: unresponsive, may be on ventilator, has nasogastric suction b. Correct fluid and electrolyte imbalances giving isotonic or colloid solutions and correct potassium deficits c. Lower glucose with regular insulin until glucose level drops to 250 mg/dL Monitor for renal failure d. Treat underlying condition

Diabetes Mellitus Complications of Diabetes
A. Alterations in blood sugars: hyperglycemia and hypoglycemia B. Macrocirculation (large blood vessels) 1. Atherosclerosis occurs more frequently, earlier in diabetics 2. Involves coronary, peripheral, and cerebral arteries C. Microcirculation (small blood vessels) 1. Affects basement membrane of small blood vessels and capillaries 2. Involves tissues affecting eyes and kidneys D. Prevention of complications 1. Managing diabetes 2. Lowering risk factors for conditions 3. Routine screening for complications 4. Implementing early treatment

Diabetes Mellitus Complications of Diabetes: Alterations in blood sugars A. Hyperglycemia: high blood sugar 1.DKA (mainly associated with Diabetes Type 1) 2.HHS (mainly associated with Diabetes Type 2) 3.Dawn phenomenon: rise in blood sugar between 4 am and 8 am, not associated with hypoglycemia Glucose released from the liver in the early AM secondary to growth hormones Altering the time and dose of the insulin (NPH or Ultralente) by 2-3 units stabilizes the blood sugar

Diabetes Mellitus 4. Somogyi effect: combination of hypoglycemia during night with a rebound morning hyperglycemia that may lead to insulin resistance for 12 to 48 hours

Diabetes Mellitus B. Hypoglycemia (insulin reaction, insulin shock, “the lows”): low blood sugar 1.Mismatch between insulin dose, carbohydrate availability and exercise 2.May be affected by intake of alcohol, certain medications

Diabetes Mellitus Specific manifestations a. Cool, clammy skin
b. Rapid heartbeat c. Hunger d. Nervousness, tremor e. Faintness, dizziness f. Unsteady gait, slurred and/or incoherent speech g. Vision changes h. Seizures, coma 5. Severe hypoglycemia can result in death 6. Clients taking medications, such as beta-adrenergic blockers may not experience manifestations associated with autonomic nervous system 7. Hypoglycemia unawareness: clients with Diabetes Type 1 for 4 or 5 years or more may develop severe hypoglycemia without symptoms which can delay treatment

Diabetes Mellitus Treatment for mild hypoglycemia
a. Immediate treatment: client should take 15 gm of rapid-acting sugar (half cup of fruit juice; 8 oz of skim milk, 3 glucose tablets, 3 life savers b. 15/15 rule: wait 15 minutes and monitor blood glucose; if still low, client should eat another 15 gm of sugar c. Continue until blood glucose level has returned to normal d. Client should contact medical care provider if hypoglycemia occurs more that 2 or 3 times per week

Diabetes Mellitus Treatment for severe hypoglycemia is often hospitalization a. Client is unresponsive, has seizures, or has altered behavior; blood glucose level is less than 50 mg/dL b. If client is conscious and alert, administer 15 gm of sugar c. If client is not alert, administer 1. 25 %– 50% solution of glucose intravenously, followed by infusion of 5% dextrose in water 2. Glucagon 1 mg by subcutaneous, intramuscular, or intravenous route; follow with oral or intravenous carbohydrate d. Monitor client response physically and also blood glucose level

Diabetes Mellitus Complications Affecting Cardiovascular System, Vision, and Kidney Function A. Coronary Artery Disease 1. Major risk of myocardial infarction in Type 2 diabetics Increased chance of having a silent MI and delaying medical treatment 2. Most common cause of death for diabetics (40 – 60%) 3. Diabetics more likely to develop Congestive Heart Failure

Diabetes Mellitus B. Hypertension
1. Affects 20 – 60 % of all diabetics 2. Increases risk for retinopathy, nephropathy

Diabetes Mellitus C. Stroke:
Type 2 diabetics are 2 – 6 times more likely to have stroke as well as Transient Ischemic Attacks (TIA) or mini stroke

Diabetes Mellitus D. Peripheral Vascular Disease
1. Increased risk for Types 1 and 2 diabetics 2. Development of arterial occlusion and thrombosis resulting in gangrene 3. Gangrene from diabetes most common cause of non-traumatic lower limb amputation

Diabetic Foot Ulcer

Diabetes Mellitus Diabetic Retinopathy 1. Definition
a. Retinal changes related to diabetes Hemorrhage, swelling, decreased vision b. Leads to retinal ischemia and breakdown of blood-retinal barrier 2. Leading cause of blindness ages 25 – 74 a. Affects almost all Type 1 diabetics after 20 years b. Affects 60 % of Type 2 diabetics Diabetics should be screened for retinopathy and receive treatment (laser photocoagulation surgery) to prevent vision loss Should be sent immediately to ophthalmologist upon diagnosis because may already have damage 4. Diabetics also have increased risk for cataract development

Diabetes Mellitus Diabetic Nephropathy
1. Definition: glomerular changes in kidneys of diabetics leading to impaired renal function 2. First indicator: microalbuminuria 3. Diabetics without treatment go on to develop hypertension, edema, progressive renal insufficiency a. In type 1 diabetics, 10 – 15 years b. May occur soon after diagnosis with type 2 diabetes since many are undiagnosed for years 4. Most common cause of end-stage renal failure in U.S. 5. Kimmelstiel-Wilson syndrome: glomerulosclerosis associated with diabetes

Diabetes Mellitus Male erectile dysfunction
Half of all diabetic men have erectile dysfunction

Diabetes Mellitus Collaborative Care
A. Based on research from 10-year study of Type 1 diabetics conducted by NIH focus is on keeping blood glucose levels as close to normal by active management interventions; complications were reduced by 60% B. Treatment interventions are maintained through 1. Medications 2. Dietary management 3. Exercise C. Management of diabetes with pancreatic transplant, pancreatic cell or Beta cell transplant is in investigative stage

Diabetes Mellitus Other Complications from Diabetes
A. Increased susceptibility to infection 1. Predisposition is combined effect of other complications 2. Normal inflammatory response is diminished 3. Slower than normal healing B. Periodontal disease C. Foot ulcers and infections: predisposition is combined effect of other complications

Diabetes Mellitus Diagnostic tests to monitor diabetes management
1. Fasting Blood Glucose (normal: 70 – 110 mg/dL) 2. Glycosylated hemoglobin (c) (Hemoglobin A1C) a. Considered elevated if values above 7% b. Blood test analyzes excess glucose attached to hemoglobin. Since rbc lives about 120 days gives an average of the blood glucose over previous 2 to 3 months Not a fasting test, can be drawn any time of the day % of glycated (glucose attached) hemoglobin measures how much glucose has been in the bloodstream for the past 3 months )

Diabetes Mellitus 3. Urine glucose and ketone levels (part of routine urinalysis) a. Glucose in urine indicates hyperglycemia (renal threshold is usually 180 mg/dL) b. Presence of ketones indicates fat breakdown, indicator of DKA; ketones may be present if person not eating 4. Urine albumin (part of routine urinalysis) a. If albumin present, indicates need for workup for nephropathy b. Typical order is creatinine clearance testing

Diabetes Mellitus 5. Cholesterol and Triglyceride levels
a. Recommendations 1. LDL < 100 mg/dl 2. HDL > 45 mg/dL 3. Triglycerides < 150 mg/dL b. Monitor risk for atherosclerosis and cardiovascular complications 6. Serum electrolytes in clients with DKA or HHNS

Diabetes Mellitus A. Insulin
Medications A. Insulin 1. Sources: standard practice is use of human insulin prepared by alteration of pork insulin or recombinant DNA therapy 2. Clients who need insulin as therapy: a. All type 1 diabetics since their bodies essentially no longer produce insulin b. Some Type 2 diabetics, if oral medications are not adequate for control (both oral medications and insulin may be needed) c. Diabetics enduring stressor situations such as surgery, corticosteroid therapy, infections, treatment for DKA, HHNS d. Women with gestational diabetes who are not adequately controlled with diet e. Some clients receiving high caloric feedings including tube feedings or parenteral nutrition

Diabetes Mellitus Injection sites
Abdominal areas is the most preferred because of rapid absorption Do not aspirate insulin injections Administration covered in the lab

Diabetes Mellitus

Diabetes Injection Sites

Diabetes Mellitus When rapid acting or short acting insulin is mixed with longer acting insulin, draw the short acting insulin into the syringe first. Prevents contamination of the shorter acting insulin with the longer acting insulin Draw up clear, then cloudy Insuling glargine (Lantus) should not be mixed with any other insulin

Diabetes Mellitus Mixing insulin

Diabetes Mellitus Alternative insulin administration Insulin pump
Continuous subcutaneous infusion of a basal dose with increases at meal times Implanted pumps Implanted into the peritoneal cavity Inhaled insulin Under development

Insulin Pump

Internal Insulin Pump

Diabetes Mellitus Oral Hypoglycemic Agents
1. Used to treat Diabetes Type 2 2. Client must also maintain prescribed diet and exercise program; monitor blood glucose levels 3. Not used with pregnant or lactating women 4. Several different oral hypoglycemic agents and insulin may be prescribed for the client 5. Specific drug interactions may affect the blood glucose levels 6. Must have some functioning beta cells

Diabetes Mellitus Classifications and action a. Sulfonylureas
1. Action: Stimulates pancreatic cells to secrete more insulin and increases sensitivity of peripheral tissues to insulin 2. Used: to treat non-obese Type 2 diabetics 3. Example: Glipizide (Glucotrol), Chlorpropamide (Diabinese), Tolazamide (Tolinase)

Diabetes Mellitus b. Meglitinides
1. Action: stimulates pancreatic cells to secret more insulin 2. Taken just before meals, rapid onset, limited duration of action 3. Major adverse effects is hypoglycemia 4. Used in non-obese diabetics 5. Example: Repaglinide (Prandin), Nateglinide (Starlix)

Diabetes Mellitus c. Biguanides
1. Action: decreases overproduction of glucose by liver and makes insulin more effective in peripheral tissues 2. Used in obese diabetics 3. Does not stimulate insulin release 4. Metabolized by the kidney, do not use with renal patients 5. Example: Metformin (Glucophage

Diabetes Mellitus d. Alpha-glucoside Inhibitors
1. Action: Slow carbohydrate digestion and delay rate of glucose absorption 2. Take with first bite of the meal or 15 min. after 3. Adjunct to diet to decrease blood glucose levels 4. Example: Acarbose (Precose), Miglitol (Glyset)

Diabetes Mellitus Thizaolidinediones (Glitazones)
1. Action: Sensitizes peripheral tissues to insulin 2. Used in obese diabetics 3. Inhibits glucose production 4. Improves sensitivity to insulin in muscle, and fat tissue 5. Example: Rosiglitazone (Avandia), Pioglitazone (Actos)

Diabetes Mellitus Patients with Type 2 DM who are obese have insulin resistance, they produce enough insulin Should use Glucophage, Actos or Avandia Enhances insulin secretion in tissue, but does not increase amount of insulin secreted

Diabetes Mellitus Patients with Type 2 DM who are thin do not produce enough insulin, they are not insulin resistant Need sulfonylurea agents like Diabinese, Tolinase, Glucotrol, Diabeta

Diabetes Mellitus Role of Diet in Diabetic Management
A. Goals for diabetic therapy include 1. Maintain as near-normal blood glucose levels as possible with balance of food with medications 2. Obtain optimal serum lipid levels 3. Provide adequate calories to attain or maintain reasonable weight

Diabetes Mellitus B. Diet Composition
1. Carbohydrates: 60 – 70% of daily diet Carbohydrates convert quickly to sugars Advice patient to consume a similar amount of carbs at each meal Medications can work on a consistent glucose response from foods 2. Protein: 15 – 20% of daily diet 3. Fats: No more than 10% of total calories from saturated fats

Diabetes Mellitus 4. Fiber: 20 to 35 grams/day; promotes intestinal motility and gives feeling of fullness 5. Sodium: recommended intake 1000 mg per 1000 kcal 6. Sweeteners approved by FDA instead of refined sugars 7. Limited use of alcohol: potential hypoglycemic effect of insulin and oral hypoglycemics

Diabetes Mellitus Diet
Look for more dietary information online at

Diabetes Mellitus Care of diabetic older clients
A. 40% of all clients with diabetes are over age of 65 B. Need to include spouse, members of family in teaching who may assist with client meeting medical needs C. Diet changes may be difficult to implement since client has established eating habits D. Exercise programs may need adjustment to meet individual’s abilities (such as physical limitations from other chronic illnesses) Obesity worsens diabetes Minimum of 30 minutes of moderate exercise like walking or swimming most days of the week

Diabetes Mellitus E. Individual reluctance to accept assistance to deal with chronic illness, assist with hygiene F. Limited assets for medications, supplies, dietary G. Visual deficits or learning challenges to learn insulin administration, blood glucose monitoring

Diabetes Mellitus Nursing Care
A. Assessment, planning, implementation with client according to type and stage of diabetes B. Prevention, assessment and treatment of complications through client self-management and keeping appointments for medical care C. Client and family teaching for diabetes management D. Health promotion includes education of healthy life style, lowering risks for developing diabetes for all clients E. Blood glucose screening at 3 year intervals starting at age 45 for persons in high risk groups

Diabetes Mellitus Common Nursing Diagnoses and Specific Teaching Interventions A. Risk for impaired skin integrity: Proper foot care 1. Daily inspection of feet 2. Checking temperature of any water before washing feet 3. Need for lubricating cream after drying but not between toes 4. Patients should be followed by a podiatrist 5. Early reporting of any wounds or blisters B. Risk for infection 1. Frequent hand washing 2. Early recognition of signs of infection and seeking treatment 3. Meticulous skin care 4. Regular dental examinations and consistent oral hygiene care

Diabetes Mellitus C. Risk for injury: Prevention of accidents, falls and burns D. Sexual dysfunction 1. Effects of high blood sugar on sexual functioning, 2. Resources for treatment of impotence, sexual dysfunction E. Ineffective coping 1. Assisting clients with problem-solving strategies for specific concerns

Diabetes Mellitus 2. Providing information about diabetic resources, community education programs, and support groups 3. Utilizing any client contact as opportunity to review coping status and reinforce proper diabetes management and complication prevention

Assessment and Management of Patients With Endocrine Disorders

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Assessment and Management of Patients With Endocrine Disorders

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