Download Diabetes Mellitus

Assessment and Management
of Patients With Endocrine
Disorders
Glands of the Endocrine System
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Hypothalamus
Posterior Pituitary
Anterior Pituitary
Thyroid
Parathyroids
Adrenals
Pancreatic islets
Ovaries and testes
Hypothalamus
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Releasing and inhibiting hormones
Corticotropin-releasing hormone
Thyrotropin-releasing hormone
Growth hormone-releasing hormone
Gonadotropin-releasing hormone
Somatostatin-=-inhibits GH and TSH
Anterior Pituitary
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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
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
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,
• Growth hormone deficiency in childhood will
result in primary dwarfism.
Pituitary Tumors—Assessment and
Diagnostic Findings
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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,
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
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
Thyroid
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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
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
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/preexistent 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
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
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
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
Assessment and Diagnostic
Findings
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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
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
Assessment and Diagnostic
Findings
• 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;
Management of
Hypoparathyroidism
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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
Assessment and Diagnostic
Findings
• 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
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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
Addison’s Disease
• Adrenocortical insufficiency
• Autoimmune or idiopathic atrophy
• Can be caused by inadequate ACTH from
pituitary
• Therapeutic use of steroids
Manifestations
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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
Assessment and Diagnostic
Findings
• 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
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
Assessment and Diagnostic
Findings
• 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
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
Assessment and Diagnostic
Findings
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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
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Hydrocortisone--Cortisol
Cortisone--Cortate
Prednisone--Deltasone
Prednisolone-Prelone
Triamcinolone--Kenalog
Betamethasone--Celestone
Fludrocortisone (contains both
mineralocorticoid and glucocorticoid) Florinef
Indications
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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?
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)
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?
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
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
Diabetes Mellitus
Diabetic Ketoacidosis (DKA)
1. Results from breakdown of fat and overproduction
of ketones by the liver and loss of bicarbonate
2. 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
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Mortality as high as 14%
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
280-300)
Diabetes Mellitus
• DKA
– Signs and symptoms
• Kussmals respirations
– Blow off carbon dioxide to reverse acidosis
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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
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
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
2. 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 greaternormal 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
–
–
–
–
5.
MI
Stroke
Pancreatitis
pregnancy
Slow onset 1 – 14 days
Diabetes Mellitus
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
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
–
•
2.
•
•
3.
Hemorrhage, swelling, decreased vision
b. Leads to retinal ischemia and breakdown of
blood-retinal barrier
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
1.
4.
Should be sent immediately to ophthalmologist upon
diagnosis because may already have damage
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.
•
2.
•
•
•
•
•
Medications
Insulin
1. Sources: standard practice is use of human insulin
prepared by alteration of pork insulin or recombinant DNA
therapy
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
http://www.diabetes.org/nutrition-andreceipes/nutrition/overview.jsp
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