assessment and management of patients with diabetes mellitus

Assessment and Management of Patients With Endocrine

Disorders

Glands of the Endocrine System

• Hypothalamus

• Posterior Pituitary

• Anterior Pituitary

• Thyroid

• Parathyroids

• Adrenals

• Pancreatic islets

• Ovaries and testes

Hypothalamus

• Releasing and inhibiting hormones

• Corticotropin-releasing hormone

• Thyrotropin-releasing hormone

• Growth hormone-releasing hormone

• Gonadotropin-releasing hormone

• Somatostatin-=-inhibits GH and TSH

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

Posterior Pituitary

• Antidiuretic Hormone

• Oxytocin—contraction of uterus, milk ejection from breasts

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.

Adrenal Medulla

• Epinephrine and norepinephrine

serve as neurotransmitters for sympathetic system

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

Parathyroid

• Parathyroid hormone—regulates serum calcium

Pancreatic Islet cells

• Insulin

• Glucagon—stimulates glycogenolysis and glyconeogenesis

• Somatostatin—decreases intestinal absorption of glucose

Kidney

• 1, 25 dihydroxyvitamin D—stimulates calcium absorption from the intestine

• Renin—activates the RAAS

• Erythropoietin—Increases red blood cell production

Ovaries

• Estrogen

• Progesterone—inportant in menstrual cycle,*maintains pregnancy,

Testes

• Androgens, testosterone—secondary sexual characteristics, sperm production

Thymus

• Releases thymosin and thymopoietin

• Affects maturation of T lymphocetes

Pineal

• Melatonin

• Affects sleep, fertility and aging

Prostaglandins

• Work locally

• Released by plasma cells

• Affect fertility, blood clotting, body temperature

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

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.

Disorders of the PituitaryPituitary 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

• Growth hormone deficiency in childhood will result in primary dwarfism.

Pituitary Tumors—Assessment and Diagnostic Findings

• H&P

• Vision tests

• CT, MRI

• Serum levels of pituitary hormones, others

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)

Manifestations

• Excessive thirst

• Urinary sp. gr. of 1.001.1.005

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

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

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

SIADH

• Restoration of electrolytes must be gradual

• May use 3% NaCl in conjunction with Lasix

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

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

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.

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

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

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

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

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

Hyperthyroidism

• Extreme form is Grave’s disease

• Caused by thyroiditis, excessive amount thyroid hormone, abnormal output by immunoglobulins

• Is more common in women

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

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

Management

• Reduce thyroid hyperactivity—usually use radioactive iodine, antithyroid meds or surgery)

• Beta blockers

• Can be relapse with antithyroid meds

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

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

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

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.

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)

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


• 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

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

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

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

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


• 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

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.

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

Adrenals--Pheochromocytoma

• Usually benign tumor

• Originates from the chromaffin cells of the adrenal medulla

• Any age but usu. Between 40-50 years old

• Can be familial

• 10% are malignant

• May be associated with thyroid carcinoma or parathyroid hyperplasia or tumor

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


• 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

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

Addison’s Disease

• Adrenocortical insufficiency

• Autoimmune or idiopathic atrophy

• Can be caused by inadequate ACTH from pituitary

• Therapeutic use of steroids

Manifestations

• Muscle weakness

• Anorexia

• Dark pigmentation

• Hypotension

• Hypoglycemia

• Low sodium levels

• High potassium levels

• Can result in Addisonian crisis

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


• 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

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

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

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


• 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

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.

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


• 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

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

Corticosteroid Therapy

• Hydrocortisone--Cortisol

• Cortisone--Cortate

• Prednisone--Deltasone

• Prednisolone-Prelone

• Triamcinolone--Kenalog

• Betamethasone--Celestone

• Fludrocortisone (contains both mineralocorticoid and glucocorticoid) Florinef

Indications

• RA

• Asthma

• MS

• COPD exacerbations

• Lupus

• Other autoimmune disorders

• Dermatologic disorders

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

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

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 10-15 minutes.

• Routine hematology and chemistry studies are wnl and chest xray and ECG are normal.

• What is your impression?• What labs would you draw?

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?

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 8.4-10.1)

• Phosphorus is 2.4 (reference range is 2.5-4.5)• What is your diagnosis?

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?

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?

Diabetes MellitusDiabetes 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


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 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)


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


Manifestations

1.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


Diabetic Ketoacidosis (DKA)1. Results from breakdown of fat and overproduction of

ketones by the liver and loss of bicarbonate2. 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

1. 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)


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

280-300)

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


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 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

Diabetes Mellitus

Pathophysiology

• 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


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


Manifestations1. 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


Hypersomolar Hyperglycemic Nonketotic Syndrome (HHNS)

1. Potential complication of Diabetes Type 22. Life threatening medical emergency, high

mortality rate, as high as 50%3. Enough insulin is secreted to prevent

ketosis, but not enough to prevent hyperglycemia

4. High blood sugar causes an extreme diuresis with severe electrolyte and fluid loss

• Characterized by– Plasma osmolarity 340 mOsm/l or greater-

normal 280-300– Blood glucose severely elevated, 800-1000 – 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


Pathophysiology• 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


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 MellitusDiabetes MellitusComplications of Diabetes A. Alterations in blood sugars: hyperglycemia and hypoglycemiaB. Macrocirculation (large blood vessels)• 1. Atherosclerosis occurs more frequently, earlier in

diabetics• 2. Involves coronary, peripheral, and cerebral arteriesC. Microcirculation (small blood vessels)• 1. Affects basement membrane of small blood vessels and

capillaries• 2. Involves tissues affecting eyes and kidneysD. Prevention of complications • 1. Managing diabetes• 2. Lowering risk factors for conditions• 3. Routine screening for complications• 4. Implementing early treatment

Diabetes MellitusDiabetes MellitusComplications of Diabetes: Alterations in blood sugarsA. 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 MellitusDiabetes MellitusSpecific 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


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


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


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

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• 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


Diabetic Retinopathy1. Definition• a. Retinal changes related to diabetes

– Hemorrhage, swelling, decreased vision • b. Leads to retinal ischemia and breakdown of blood-

retinal barrier2. Leading cause of blindness ages 25 – 74• a. Affects almost all Type 1 diabetics after 20 years• b. Affects 60 % of Type 2 diabetics3. Diabetics should be screened for retinopathy and receive

treatment (laser photocoagulation surgery) to prevent vision loss

1. Should be sent immediately to ophthalmologist upon diagnosis because may already have damage

4. Diabetics also have increased risk for cataract development


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


Collaborative CareA.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. ExerciseC.Management of diabetes with pancreatic transplant,

pancreatic cell or Beta cell transplant is in investigative stage


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 MellitusDiabetes MellitusDiagnostic 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

)


• 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 complications6.Serum electrolytes in clients with DKA or

HHNS

Diabetes MellitusDiabetes MellitusMedications

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 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


• 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


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 MellitusDiabetes MellitusClassifications and actiona.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 MellitusDiabetes MellitusThizaolidinediones (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


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

http://www.diabetes.org/nutrition-and-receipes/nutrition/overview.jsp

Diabetes MellitusDiabetes MellitusCare 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


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 MellitusDiabetes MellitusCommon Nursing Diagnoses and Specific Teaching InterventionsA. 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 blistersB. 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 dysfunctionE.Ineffective coping• 1. Assisting clients with problem-solving

strategies for specific concerns


• 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 diabetes mellitus

Health & Medicine