Endocrine system
Composed of cells and organs that manufacture and secrete hormones.
A system of communication that controls many life-long bodily responses and functions.
relays information and instructions throughout the body
glands, hormones, target cells
The endocrine system responds to stimuli by
releasing hormones from endocrine glands
Hormones regulate 4 major body functions
Reproduction, growth and development, homeostasis, metabolism
All hormones share certain general characteristics
rates and patterns
operate within a feedback system
affects target cells with specific receptors and then initiate specific cell functions
excreted by kidneys or deactivated by the liver or cellular mechanisms
Negative feedback
occurs because the rising hormone levels negates the initiating change that triggered the release of the hormone
3 categories of endocrine disease
hypo secretion, hyper secretion, hyporesponsiveness
Hypo secretion
gland releases an inadequate amount of hormone to meet physiological needs
hyper secretion
increased secretion
Hypo-responsiveness
of the target organ causes the same set of clinical symptoms as hypo secretion
usually caused by deficiency of receptors
Causes of hypo secretion
Congenital, Absence of enzyme needed for synthesis, Disruption of blood flow, Infection, inflammation, immune response, Neoplasms
causes of hyper secretion
excessive stimulation, hyperplasia of the gland, hormone producing tumor of the gland
Hypothalamus
the primary organ of the body concerned with maintaining homeostasis
sends several hormones to anterior or posterior pituitary gland
hypothalamus and pituitary gland
regulates hormone secretion from all major endocrine organs EXCEPT pancreas and parathyroid glands
the hypothalamus synthesizes 2 hormones
ADH and oxytocin
ADH and oxytocin
produced in the hypothalamus and stored in the posterior pituitary until stimulated
oxytocin
protein hormone stored and released from the posterior pituitary
� little effect in non-pregnant women
� increases intensity of labor - stimulates contraction of uterine smooth muscle
Pitocin
a derivative of oxytocin, it is used to initiate and speed labor
� Also, stimulates contraction of the smooth muscle lining of the milk ducts of the breast, causing letdown of stored milk into nipples
ADH
stored and released from the posterior pituitary
Anti-diuretic hormone
water does NOT follow salt in this case
ADH aids in the control of blood volume by acting on the kidneys to absorb more water back in the blood
Also referred to as vasopressin because of its ability to cause vasoconstriction if the plasma levels are extremely elevated
Does ADH make you retain or diurese?
retain water
Diseases of the Posterior Pituitary
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
Diabetes Insipidus (DI)
Too much ADH secretion
SIADH (high levels of ADH)
water intoxication
caused by tumors of the CNS, certain drugs, cancers, common with critical illness and surgery
Too little ADH secretion
DI (insufficiency of ADH)
SIADH is characterized by
water retention
decreased urine output
urine hyperosmolarity (Concentrated)
s/s of hypervolemia: swelling, anxiety, JVD, bounding pulse, crackles
dilution hyponatremia
low serum osmolality (blood is diluted)
Cells swell (confusion, seizures, coma)
Manifestations of SIADH
serum hypo-osmolality and hyponatremia
Na <130: thirst, impaired taste, anorexia, fatigue, dulled sensorium
Where is the water? blood and third space, cells, everywhere except toilet
Na does not follow water in this case
urine hyperosmolaity, high specific gravity, improvement of hyponatremia with water restriction
In SIADH hypervolemia triggers
ANP, it does not help because we don't need to excrete any more salt
SIADH treatment
Fluid restriction
DIURETICS
hypertonic IV saline solution 3%
In SIADH the client is retaining water because they have too much
ADH
urine is concentrated
blood is dilute
Diabetes Insipidus
hyposecretion of ADH or lack of renal response to ADH causes excessive loss of water and results in a disorder call Diabetes Insipidus , (DI)
Caused by injury to pituitary gland, brain tumors, damage to renal tubular cells, pharmacologic agents.
Think diuresis!
worry about dehydration
Polyuria (15 L in 24 hours) excretion of large volumes of dilute urine
Polydipsia (excessive thirst)
Nocturia
Low specific gravity of urine. Urine is diluted
Hypernatremia - high serum osmolarity. Blood is concentrated
Na did not follow water
neuro symptoms due to shrinkage and dehydration of cells
DI treatment
Vasopressin
DOC-DDAVP (Desmopressin)
correct dehydration with hypotonic 1/2 normal saline
prevent clots (at risk due to dehydration of the intravascular compartment)
Vasopressin
Antidiuretic hormone preparation
� Used to normalize urinary water excretion in patients with DI (tx is lifelong)
� Monitor fluid and electrolytes
� Monitor for water intoxication:
� Drowsiness
� Listlessness
� H/A
� Use caution in patients with CAD or PVD because it is a powerful vasopressin (Constrict)
nursing implications
If patient inadvertently takes too much drug, assess for s/s of water intoxication: drowsiness, listlessness, and headache
� Assess for vasoconstrictive effects: angina, hypertension, gangrene of extremities
� Assess compliance - life long administration: delivered by nasal spray. Tablet for enuresis
� Monitor I and O, daily weight
anterior pituitary
Anatomically separate from the hypothalamus, but functionally connected to it via its blood supply
� In response to hormone activation from hypothalamus, anterior pituitary will secrete various hormones
� Anterior pituitary is a major target organ for hypothalamus hormones with release of its own hormones (TROPIC)
anterior pituitary hormones
Somatotropic hormones
� Growth hormone
� Prolactin
� Thyroid stimulating hormone (TSH)
� Thyrotropin controls the release of thyroid hormone from the thyroid gland
� Adrenocorticotropin (ACTH) hormone
� Controls the release of cortisol from the adrenal gland
� Follicle stimulating hormone (FSH) and Lutenizing hormone (LH)
growth hormone
Also called SOMATOTROPIN
hypothalamus releases GHRF
� Released from the anterior pituitary in response to growth-hormone releasing factor (GHRF) from the hypothalamus
� Acts directly on most body tissues, promoting protein deposits that are essential for growth
� Increases the mobilization of fatty acids
� Decreases glucose utilization (insulin resistance is increased)
no specific target organ
too much growth hormone increases blood sugar
deficiency of growth hormone
Caused by decreased secretion of GhRF or GH, tumors, radiation, trauma
� Impairs normal growth and development in infants, children and adolescents (when GH is normally secreted in higher amounts).
� Treated with synthetic GH subcutaneously 3 to 7 days a week. Prior to closure of growth plates (epiphyseal)
� Goal: improved growth velocity and attainment of an adult height that is normal for the individual's genetic background.
Semorelin
Synthetic growth hormone-releasing factor
� Acts like natural GhRH: acts on the anterior pituitary to stimulate release of GH
� Use for treatment in GH deficiency in children to normalize growth and development
� Contraindicated after epiphyseal closure
� Must have a functioning anterior pituitary. Why? Because if you don't, it will not make the growth hormone
� Monitor height/weight and blood glucose
growth hormone excess
almost all cases caused by pituitary adenomas
gigantism and acromegaly
gigantism
before puberty
causes bones to grow large and long
acromegaly
after puberty
usually occurring in 4th or 5th decade of life
? bone density and width of bones enlarge: lower jaw, hands, face, and feet
� Has a diabetogenic effect:
� The increase in mobilization of fatty acids predisposes to ketoacidosis and the decrease in the utilization of glucose tends to increase blood sugar.
manifestations of acromegaly
Enlarged tongue
� Interstitial edema
� Coarse skin and body hair
� Enlargement facial bones, hands, feet
� Profusion of the jaw and forehead
� Barrel chest with arthralgia and arthritis
� Nerve damage: weakness, muscular atrophy, footdrop, and sensory changes
� Hypertension, left heart failure, CNS disturbances
� Enlarged & overactive sebaceous and sweat glands
� Impaired glucose tolerance
acromegaly treatment
Remove Adenoma
� Resection of Anterior Pituitary tumor
� Possible radiation therapy
� Pharmocologic
� Octreotide (Sandostatin)
� Synthetic Somatostatin used to decrease Growth Hormone Release
thyroid produces 3 hormones
t3, t3, and calcitonin
The principal hormones produced are Triiodothyronine (T3) Thyroxine (T4)
� Many tissues in the body convert T4 to T3. T3 is the more active form of thyroid hormone.
We need an adequate supply of iodine in our diet for thyroid hormone to be produced because the thyroid gland takes iodine from the blood to make thyroid hormones
Thyrotropin-releasing hormone (TRH)
� When thyroid hormone levels get low, TRH is released from the hypothalamus. TRH Stimulates thyroid-stimulating hormone (TSH) release from the anterior pituitary. For TSH, the target organ is the thyroid gland which secretes thyroid hormones.
� TSH stimulates all aspects of thyroid function, including release of T3 and T4
� Works on a negative feedback system. T3 and T4 act on the pituitary to suppress further TSH release and inhibit TRH
function of thyroid hormones
Important in the regulation of:
� protein synthesis
� basal metabolic rate (BMR), which is the rate of heat production and energy expenditure in the body
� gluconeogenesis and cellular uptake of glucose
� the force and rate of cardiac contractions
� normal development of CNS
� the responsiveness of target cells (beta-receptors) to catecholamines, thus increasing heart rate and causing heightened emotional responsiveness
goiter
Enlarged thyroid glands
� Appears in both hypo or hyperfunction of the thyroid
� The gland enlarges in an attempt to produce sufficient amounts of thyroid hormones or in response to overproduction of hormones
� Goiter can be due to other causes:
� one cause is iodine deficiency in diet
low iodine
when iodine availability is low, production of thyroid hormones decreases. This promotes the release of TSH which causes thyroid size to increase (goiter)
high iodine
when iodine levels are high, uptake of iodine is suppressed and synthesis and release of thyroid hormones decline
Serum T4 test
� measures total (bound plus free) thyroxine
� reflects overall thyroid activity
� used for initial screening of thyroid function
� T4 low in hypothyroid (primary)
� T4 high in hyperthyroid
serum T3 test
� Measures total (bound plus free) triiodothyronine
� Useful in diagnosing hyperthyroidism
Serum TSH
Most sensitive test for diagnosis of hypothyroidism because small reductions in T3 and T4 cause dramatic increase in TSH
hypothyroidism
Most common thyroid disorder
� Results from decreased levels of circulating thyroid hormone
� Caused by:
� autoimmune diseases (Hashimoto's), most common
� insufficient iodine in the diet
� surgical removal of the thyroid
� destruction of the thyroid by radiation
� neoplasms
� severe trauma
� Infections
� congenital
Primary hypothyroidism
Results from pathologic process that destroys thyroid gland (high TSH, low thyroid hormone)
secondary hypothyroidism
Caused by deficiency of pituitary TSH secretion (low TSH, low thyroid hormone)
� May be med induced:
� Iodide, PTU
� Sulfonamides, Amiodarone,
� Inteluekin 2, Interferon alpla
congenital hypothyroidism (cretinism)
causes mental retardation and derangement of growth
short stature, failure to thrive, massive CNS deficiency, mentally slow
decrease in BMR
Lowers BMR-results in a general slowing down of body processes (cold, dry skin) weight gain
� Lowers heat production cold intolerance, lethargy, fatigue. Mentality may be impaired.
� Goiter if reduced levels of T3 and T4 promote excessive release of TSH
� myxedema -altered composition of dermis and separation of connective fibers
� Nonpitting, boggy edema around eyes, hands,feet
� Thickened tongue hoarseness, slurred speech
hypothyroidism diagnosis
Decreased levels of T3 and T4
Serum TSH may be high or low
everything goes down except weight increases because of the lower basal metabolic rate
S&S include:
� hypothermia
� hypoventilation
� hypotension
� bradycardia
myxedema coma
rare, usually seen in elderly women with chronic hypothyroidism
a medical emergency: a diminished level of consciousness associated with severe hypothyroidism.
hypothyroidism pharmacologic treatment
Thyroid deficiency - treat with hormone replacement therapy
� Synthetic Thyroxine (T4):
� Levothyroxine (Synthroid) is DOC
� Usual dose: 100-150mcg/day for life
� Increases levels of T3 and T4 because most T4 is converted to T3
� Also used for simple goiter and Hashimoto's Disease
� Other Pharmacologic options:
� Liothyronine (Cytomel)
� Synthetic T3
� Not recommended for long-term use
� Liotrix (Thyrolar)
� combination of Levothyroxine and Liothyronine
� No advantage over Levothyroxine
thyroid replacement nursing implications
Adverse reactions are rare if dose is appropriate
� Use caution if patient has C/V disease - hormone can increase responsiveness to catecholamines and sympathetic stimulation
� So what can occur?
arrhythmias, increase HR and BP, hyperthyroidism them thyroid storm
� If dosage is excessive or if you have a decrease in excretion, thyrotoxicosis and thyroid storm may occur
� Treatment ............ forever!
� Teach S/S of thyrotoxicosis and not to d/c abruptly
hyperthyroidism
increased thyroid hormone
� Diagnosis: excessive levels of circulating TSH
� Caused by:
� Dysfunction of the thyroid gland, the pituitary, or the hypothalamus (Overactive)
� Excessive intake of thyroid hormones
Because increased amounts of thyroid hormones reach the cells, all metabolic activities are increased; the BMR rises, energy expenditure is increased, and heat production rises
Everything goes up except weight decreases - why?
BMR goes up
Causes: Graves disease (more common)
� Autoimmune dx.: Exopthalmus: eyes popping out
� Toxic nodular goiter
� Plummers dx
graves disease
autoimmune disease in which developed antibodies stimulate TSH production and inappropriately activate production of thyroid hormones (T3 & T4)
� Symptoms: Adrenergic stimulation- BMR increased
� Tachycardia and palpitations
� Heat intolerance-excessive sweating
� Nervousness
� Thin hair and skin
� Tremor
� Large and protruding eyeballs-exophthalmos
� Weight loss with hunger
� Diffuse thyroid enlargement (goiter), may auscultate bruit
thyrotoxic crisis
Also called thyroid storm
� Life-threatening complication
� sudden increase in thyroid hormone levels
� uncontrolled fever - 100 to 106 degrees
� significant tachycardia, dysrhythmias
� profuse diaphoresis
� shock
� vomiting
� dehydration
� CNS: hyperkinesis, anxiety, and confusion
thiomides (treatment of hyperthyroidism)
hyroid inhibitors
PTU, Tapazole
� Stops the thyroid from making thyroid hormone!
� Does not destroy existing thyroid stores
� Overuse converts to hypothyroid state
� Monitor levels of T4 and T3
� Goiter associated with prolonged use
� PTU is preferred treatment during pregnancy and breast feeding
iodine compounds (treatment of hyperthyroidism)
Decrease the size and vascularity of the gland
� Radioactive Iodine (131I) - DOC for Graves Dx
� Used to destroy thyroid tissue (goal is to avoid destroying too much)
� Does not affect surrounding tissue
� Monitor bone marrow
� Usually 1-3 treatments, full effects may take 2-3 months
� Contraindicated with pregnancy
� Lugol's solution, SSKI (Potassium iodide) -NONRADIOACTIVE
� Used preoperatively to decrease vascularity and decrease bleeding risk
� Dilute in fruit juice for taste, stains teeth
� Report symptoms of iodism: brassy taste, mouth burning, sore gum & teeth
� Report and discontinue if severe abdominal distress develops from toxicity
beta blockers (treatment of hyperthyroidism)
Inderal (Propanlol)
� Beta blockers won't let you release ADRENALIN
� Decreases HR and BP
� Decreases anxiety
� Slows everything down, you remain calm?
� Who shouldn't take Beta Blockers?
patients with low BP and HR
thyroidectomy
May be partial or complete
� What will they need to take for life after surgery?
Synthroid or some sort of thyroid replacement
� Important to teach to take the same time everyday to maintain constant hormone level.
adrenal glands
Located above the kidneys
� 2 parts: inner medulla (secretes Epi and NE) and outer cortex
� Adrenal cortex synthesizes three important classes of hormones
� Glucocorticoids (Cortisol) sugar
� Mineralocorticoids (primarily aldosterone) salt
� Androgens sex
� Total loss of adrenal cortical function is fatal in 3 to 10 days if untreated
� Referred to as the three S's : Sugar, Salt, Sex
� More than 30 hormones are produced by the adrenal gland. Of these hormones:
� Aldosterone is the principal mineralocorticoid - Salt
� Cortisol (hydrocortisone) the major glucocorticoid -Sugar
� Estrogens and Androgens, the Sex hormones
what regulates hormone release?
Glucocorticoids are regulated by the hypothalamic-pituitary-adrenal negative feedback
� Secretion of Aldosterone is regulated by renin-angiotensin mechanism
glucocorticoids
Essential for survival
� cortisol (hydrocortisone) is the major glucocorticoid
� Major actions:
� Regulate mood
� Suppress the immune and inflammatory response
� Increase breakdown of Protein and Fats
� Inhibit insulin release
mineralocorticoids
Play an essential role in regulating fluid and mineral balance (sodium and potassium)
� Aldosterone stimulates kidneys to retain Na and water and lose K+
androgens
chief sex hormones
Addison's disease
Hypofunction of Adrenals (low secretion)
� Chronic adrenal insufficiency
� Caused by destruction of adrenal glands
� Autoimmune response - most common
� Deficient cortisol secretion, may have ? aldosterone and androgen production
Addison's disease clinical manifestations
Not enough aldosterone, will lose Na+ and water and retain K+. Most of the S&S will initially come from HYPERKALEMIA
� Cortisol insufficiency causes diminished gluconeogenesis, decreased liver glycogen, and increased sensitivity of peripheral tissues to insulin.
� Blood sugar is going to go down
� Symptoms are often vague & may not be apparent until 80-90% of the adrenals have been destroyed
commonly complain of: Chronic fatigue, muscle weakness
� N & V
� Anorexia and weight loss
� Occasional acute abdominal distress
� Salt cravings (dt ? aldosterone and resulting hyponatremia)
� Hypoglycemia
� Hyperpigmentation
� With persistent insufficient amts. of cortisol and aldosterone the body becomes:
� Weak, Dehydrated and unable to maintain BP
Addison disease treatment
Combat the fluid volume deficit
� Why are they losing volume?
because they have no aldosterone which loses salt and then water
� Hormone replacement therapy
� Oral corticosteroids (Replace cortisol)
� Prednisone, Cortisone, Hydrocortisone
� Sometimes mineralcorticoids (Replace aldosterone)
� Fludrocortisone
� Maintains Na+/K+ balance
� Increase salt in the diet
� Treatment generally reverses symptoms
� Lifelong treatment
addisonian crisis
Adrenal crisis acute adrenal insufficiency
� Most commonly seen following abrupt withdrawal of long-term corticosteroid therapy
� **Currently pts. are treated with replacement steroid doses that are often less than half of the dose that was administered in the 1960-70s. This prevents some of the symptoms associated with excess steroids, however, pts. have less reserve and are more likely to go into Addison Crisis when stressed
� Recommended that pts. carry an emergency prefilled steroid syringe in case of crisis due to illness or stress
Addison's disease:
Cushing's syndrome:
Corticosteroid excess (secreting too much)
� Result of pituitary or adrenal tumor
� Excess intake of cortisol
� or Corticosteroid drugs
? Glucocorticoids
� Breakdown of Fat and Protein
� Thin extremities, growth arrest
� Increased risk of infection
� Hyperglycemia
� Depression to Psychosis
� ? Mineralcorticoids
� Retain Na+ and Water, To much fluid
� Lose K+
� ? Sex hormones
� Acne, oily skin
� Hirsuitism
Cushing's treatment
Removal of tumor
� Will need replacement therapy for life
� Adjunct to surgical removal of tumor
� Drugs that ? corticosteroid production
� Aminoglutethimide (Cytadren)
� Can expect resolution within one year after removal of tumor.
� Striae will persist
pheochromocytoma
A rare cause of secondary hypertension
� It is an adrenal medullary tumor that releases excessive amounts of catecholamines (epi and norepi) generally in an intermittent manner.
� Will have surges of epi and norepi
� Are benign in 95% of cases
� Diagnosis
� Vanylmandelic Acid Test
� 24 hour Urine test looking for increased levels of epi and norepi
� Clinical manifestations:
� severe HTN: 250/140 mm Hg) lasting minutes to hours
� pounding headaches
� palpitations, dysrhythmias
� diaphoresis
� Treatment is surgical resection of pheochromocytoma
parathyroid glands
Four in number, lie posterior and adjacent to the thyroid gland
� Function:
� regulate the serum levels of calcium
� control rate of bone metabolism
� regulates phosphorus levels
PTH (parathyroid hormone)
Parathyroid glands secrete PTH (parathyroid hormone)
� PTH is released and acts on bones, renal tubules, and intestinal mucosa.
� Directly regulated by negative feedback system of the circulating blood levels of calcium
� As calcium levels fall, more PTH is secreted; as calcium levels rise, hormone secretion is reduced
PTH maintains extracellular calcium
� Bone-
� PTH increases the rate at which calcium is released from the bone which leads to an overall loss of bone mass: osteoporosis
� GI system
� PTH indirectly controls the rate at which calcium is absorbed from the GI tract by increasing vitamin D activation
� Kidneys
� PTH causes tubular calcium reabsorption and increases phosphate excretion
hyperparathyroidism
Do not have normal feedback mechanism
� Too much PTH in spite of Ca level
� Will see:
� increase Ca levels
� decrease Phos levels
Does the ? serum Ca help?
No
� Too much PTH causes Ca to be removed from bone into serum, therefore serum calcium level rises (hypercalcemia)
� What happens to the bone?
gets brittle, increased risk fractures
hyperparathyroidism caused by
Failure of the normal feedback system
� Adenoma (benign) 75-80%
� Primary hyperplasia 10-15%
� Carcinoma <5%
� As a compensatory response to low levels of calcium
� low calcium diet
� PTH continues to be secreted in the presence of normal levels of calcium
� Remember: You don't have the normal negative feedback and the gland is out of control!
hyperparathyroidism clinical manifestations
Multiple pathological fractures r/t bone demineralization (serum level is high, draws from bone)
� Kyphosis and compression fractures
� Fatigue and weakness
� Calcium-based renal stones (due to high levels in serum)
� EKG abnormalities (ST and PVC's) -due to unstable cardiac muscle depolarization
� Constipation
� N/V, anorexia
� Bone pain
hyperparathyroidism treatment
Remove parathyroid gland
� Drug therapy may work initially,
� 1) Calcitonin (Miacalcin) - decreases serum calcium by driving Ca back into bones
� 2) oral phosphate - inhibit bone reabsorption, decreases calcium level (indirect relationship)
� 3) glucocorticoids - reduce intestinal absorption of calcium
� 4) several miscellaneous agents act directly on bone to prevent calcium removal
� Surgical excision of parathyroid tumor
Hypoparathyroidism
Lack of normal feedback regulation
� Too little PTH in spite of Ca level
� Will see:
� low Ca levels
� high Phos levels
Usually iatrogenic - caused by removal of all viable parathyroid tissue during total thyroidectomy
� In 70% of cases of hypoparathyroidism, tetany is major clinical manifestation.
� Other S/S: laryngeal spasms, carpopedal spasms, seizures
� Positive Chvostek or Trousseau's sign
Positive Chvostek
� Facial nerve irritability/spasms, elicited by tapping the nerve
Trousseau's sign
� Carpal spasm induced by arterial occlusion of the arm with a blood pressure cuff
Hypoparathyroidism treatment
calcitrol (Rocaltrol)
� Vitamin D analogue
� Promotes calcium secretion from the bone to bloodstream
� Promotes calcium uptake from the GI tract
� Phosphorus binding drugs (PhosLo)
� Binds with Phosphorus
� Phosphorus decrease, Calcium increase
� With continued use, assess for s/s of hypercalcemia
DM
disorder of carb metabolism
glucose metabolism in the body
Most cells, including brain and the nervous system rely on glucose as a fuel source.
Because the brain cannot synthesize or store more than a few minutes' supply of glucose, normal cerebral function requires a continuous supply from the circulation.
Severe or prolonged hypoglycemia can cause brain death and dysfunction. Thus the coma associated with diabetes.
regulation of blood glucose levels
About 2/3 of the glucose that is ingested with a meal
is removed from the blood and stored as glycogen.
Blood glucose levels reflect the difference between
the amount of glucose released into the bloodstream by the liver and the amount of glucose taken up by the cell for energy
body tissues
obtain glucose from the blood
non-diabetic fasting blood glucose
70-100 mg/dL
After a meal, blood glucose levels rise, and insulin is secreted in response to this rise in glucose.
glucose is ingested through the diet
Between meals, the liver releases glucose as a means of maintaining blood glucose within normal range.
The liver regulates blood glucose through three processes:
Glycogenesis - glycogen synthesis
Glycogenolysis - glycogen breakdown
Gluconeogenesis - synthesis of glucose from noncarbohydrate sources
glucose is an optimal fuel for tissues
muscles, adipose tissue, and the liver
glucose that is not needed for energy
stored as glycogen or converted to fat
when glucose levels rise
glucose is removed from the blood and converted to glycogen
when glucose levels fall
the liver glycogen stores are broken down and released into the circulation
role of the liver
In addition to mobilizing its glycogen stores, the liver synthesizes glucose from noncarbohydrate sources such as amino acids, lactic acid, and the glycerol part of triglycerides.
When blood glucose levels fall below normal, glycogen is broken down by a process called glycogenolysis and glucose is released.
In addition to mobilizing its glycogen stores, the liver synthesizes glucose from amino acids, glycerol, and fatty acids in a process called gluconeogenesis
role of pancreatic hormones
The endocrine portion of the pancreas, the islets of Langerhans, is embedded between exocrine units like small "islands"
The islets contain 3 major types of cells which empty their secretions into the bloodstream
alpha, beta, delta
alpha
secrete glucagon
beta
secrete insulin
delta
secrete somatostatin
islets of langerhans
responsible for insulin production
insulin
A Protein
Essential for normal carbohydrate, fat, and protein metabolism
Helps produce energy and plays a role in the storing of excess energy as glycogen
For example, in the liver and muscles
output of insulin
regulated mainly by blood glucose levels through a negative feedback mechanism
Begin to rise within minutes after a meal, reaches a peak in 3 to 5 minutes, and then returns to baseline within 2-3 hours
Secretion of insulin
The principal stimulus for insulin release is increased blood glucose
Insulin stimulates cellular transport (uptake) of glucose, amino acids, nucleotides, and potassium. Hyperkalemic goes with hyperglycemic
Insulin deficiency puts the body into a catabolic mode - glycogen is converted into glucose, proteins into amino acids, and fats to glycerol and fatty acids.
Insulin's function
Insulin works to decrease blood glucose levels by:
facilitating transport of glucose across cell membranes into the muscle and adipose tissues
inhibiting gluconeogenesis
An insulin receptor and a specific glucose transporter (GLUT 4) are involved. This transporter removes insulin from the blood and shuttles it across the cell membrane.
Insulin increases as blood glucose levels rise and decreases when blood glucose levels decline
glucagon
Hormone secreted by the Alpha cells of the pancreas, important in the regulation of carbohydrate metabolism
The action of glucagon is opposite to that of insulin, and its secretion results in an increase in blood glucose concentrations
Glucagon maintains blood glucose by increasing the release of glucose from the liver into the blood and promotes gluconeogenesis
other hormones that affect blood glucose
Catecholamines
Growth Hormone
Glucocorticoid Hormones
Cortisol
Catecholamines (epinephrine and norepinephrine)
help to maintain blood glucose levels during periods of stress.
During exercise and types of stress, epinephrine inhibits insulin release and thereby decreases the movement of glucose into muscle cells, it stays in the blood
Exercising muscle has increased insulin sensitivity, which facilitates glucose uptake for as long as 16 hours after exercise (therefore, insulin demand is lowered).
growth hormone (DM)
Increases available glucose from the liver
Growth hormone: has many metabolic effects. It increases protein synthesis in all cells of the body, mobilizes fatty acids and antagonizes effects of insulin.
Exercise, stresses, including anesthesia, fever, and trauma, increase growth hormone
? Growth hormone = blood glucose
glucocorticoid hormones
The glucocorticoid hormones are critical to survival during periods of fasting and starvation.
But, prolonged elevation of glucocorticoid hormones can lead to hyperglycemia and development of diabetes mellitus.
Cortisol (accounts for 95% of all glucocorticoid activity) increases during periods of stress, such as infection, pain, trauma, surgery, exercise, and acute anxiety.
Cortisol stimulates gluconeogenesis and interferes with the action of insulin
? Glucocorticoids = blood glucose
diabetes mellitus
Diabetes is a disorder of carbohydrates, protein, and fat metabolism resulting from an imbalance between insulin availability and insulin need.
It can represent:
1. an absolute insulin deficiency,
2. impaired release of insulin,
3. inadequate or defective insulin receptor, or
4. the production of inactive insulin
A person with uncontrolled diabetes is unable to transport glucose into fat and muscle cells; as a result the body cells are starved, and the breakdown of fat and protein is increased.
Diagnosed by the presence of chronic hyperglycemia.
DM= 3rd leading cause of death.
diabetes classification system
New system in 1997 - eliminates use of "insulin-dependent" and "noninsulin dependent" DM.
Based on disease etiology rather than "drugs needed"
Uses Arabic instead of Roman numeral system
Type 1 diabetes - autoimmune destruction of pancreatic cells.
1A - immune-mediated diabetes; majority of cases
1B - idiopathic diabetes (unknown cause)
Type 2 diabetes - describes a condition of fasting hyperglycemia that occurs despite the availability
of insulin
Type 1 (will also see referred to as "IDDM" or "Type I" )
Type 1 diabetes is characterized by an absolute lack of insulin, an elevation in blood glucose, and a breakdown of body fats and proteins. In the absence of insulin, ketosis develops when fatty acids are released from fat cells and converted to ketones in the liver. These individuals , are prone to developing diabetic keto acidosis.
All persons with Type 1 require exogenous insulin replacement to control blood glucose levels and prevent ketosis.
Thought to be caused by a genetic predisposition. Type 1 patients have autoimmune markers (HLAs), including islet cell auto-antibodies. Auto-antibodies build up in the blood, and attack pancreatic beta cells.
In most cases, onset is abrupt
Because of loss of beta cell function and complete lack of insulin, all people with Type 1A diabetes require insulin replacement to reverse the catabolic state, control blood levels, and prevent ketosis.
Caucasians have the highest rate of Type 1
Type 1 develops more in the winter months and colder climates. Possible trigger? Viruses
Accounts for 10% of all DM
Generally diagnosed after 90% of the beta cell mass has been destroyed
DM metabolic acidosis
No insulin, glucose builds up in the blood
The cells are starving, so they breakdown: protein and fat
When you breakdown fat the byproduct is: ketones
What is the acid/base imbalance that occurs from the breakdown of fat? Metabolic acidosis
If I am acidotic do I want to keep or blow off CO2? Blow off
So, I'm going to breathe fast or slow? Fast
We call these respirations Kussmaul Respirations
Type 2 (used to be called NIDDM or Type II)
Onset insidious
Usually occurs after 30, and 70-80% of those with Type 2 diabetes are obese and older
Currently are seeing an ? in Type 2 DM in children and teens d/t obesity
U.S. ethnic groups most at risk:
African Americans, Mexican Americans, Pima Indians
Family history and obesity are strong risk factors.
Type 2 DM is caused by factors contributing to:
1) inadequate insulin secretion - the pancreas "gives out"
2) insulin resistance - defect in the response of peripheral tissues to insulin
3) increased hepatic glucose production
type 2 DM path
Glucose receptors in cell walls that are normally opened by insulin fail to function properly. As a result of receptor failure, glucose levels in the blood rise
Insulin "Opens the Door"
Islet cells make more insulin in an attempt to lower glucose levels
With Type 2 DM approximately 50% of the Beta cells are destroyed at time of diagnosis, and approximately 4-10% are destroyed each year thereafter unless lifestyle changes/ treatment
? insulin production can be maintained for years, but eventually the islet cells "burn out" and the patient requires exogenous insulin
During the several year period when glucose levels are elevated but partially compensated for, the patient may be relatively symptom free. BUT organ damage is already occurring
More difficult to diagnose than Type 1 on the basis of symptoms b/c their body tries to compensate
They still have some insulin
Type 2 diabetes describes a condition of fasting hyperglycemia that occurs despite the availability of insulin. Not associated with HLA markers or autoantibodies.
Both hereditary and environmental factors are thought to contribute to the pathogenesis of the disorder.
Some drugs are thought to elevate blood glucose:
thiazide diuretics
Diazoxide, glucocorticoids, levodopa, oral contraceptives, sympathomimetics, phenothiazines, phenytoin, and total parenteral nutrition
Gestational diabetes
State of carbohydrate intolerance that is first detected during pregnancy (2-5% of pregnancies)
Pregnancy causes changes in metabolism (because of hormonal changes)
Resembles Type 2 diabetes: weight gain contributes to insulin resistance
Normally during pregnancy, need 2 to 3 times as much insulin
Women with gestational diabetes are unable to produce sufficient amounts of insulin
Cortisol is 3X higher with pregnancy
gestational diabetes screening
Should be screened for diabetes between 24th and 28th week of pregnancy.
Do not need to be screened, if under 25 years, of normal body weight before pregnancy, have no history of diabetes, and not a high-risk ethnic group (Hispanic, Native American, Asian, African American)
Complications to fetus:
Increased birth weight - WHY? Getting all the extra sugar from mom leads to fat
Neonatal hypoglycemia - WHY? Once the baby is born it gets its own nutrition. Pancreas is used to secreting high insulin from mom, no longer receiving extra glucose.
These women have higher tendency to develop type 2 diabetes 5-10 years after delivery.
Diagnosis of Diabetes
Hyperglycemia!
Diagnostic Tests
Oral glucose tolerance test - OGTT
Fasting plasma glucose - FBG
Casual plasma glucose test
HA1C
gestational diabetes diagnosis
oral glucose tolerance test, fasting plasma glucose, impaired fasting glucose, casual plasma glucose, HbA1C
oral glucose tolerance test
important screening test for DM. Measures the body's ability to remove glucose from the blood. Administration of a glucose load after a 12 hour fast followed by measurement of serum glucose levels at specified intervals. OGTT > 200mg/dl after 2 hours on at least 2 occasions = Diabetes
fasting plasma glucose levels
blood is drawn at least 8 hour after the last meal. If FPG is greater than 126 mg/dl, on at least 2 occasions = Diabetes.
impaired fasting glucose
Those individuals with a FPG > 110mg/dl but < 126 mg/dl, or
OGTT > 140mg/dl but < 200mg/dl in the 2 hour sample
*At risk for diabetes
casual plasma glucose test
blood is drawn anytime, without regard to meals. > 200 mg/ml or higher suggests diabetes.
HbA1C
5% or less = No Diabetes
5.7% - 6.4% = Pre-diabetes
6.5% or more = Diabetes
SS of Diabetes
3 P's: polyuria, polydipsia, polyphagia
Fatigue
Glucosuria
Blurred vision
Dehydration / hyperkalemia/ hyponatremia with diuresis
Hypovolemia
Skin infections/yeast infections
Why do the clinical manifestations appear? Sugar, bacteria eats sugar
Also seen with: hypercortisolemia, high dose glucocorticoids; or excess in growth hormone
All of these cause the blood glucose to increase or decrease? Increase
When there is "no insulin", glucose cannot enter into muscle and adipose tissue. So the serum glucose level is increased, but there is functional cell starvation because: energy is not getting to cells
The brain and RBC's are spared from glucose deprivation since they do not need insulin for glucose entry.
Polydipsia
(excessive drinking/thirst)
Glucose accumulates in blood - the blood becomes hypersomolar and pulls water from the intracellular compartment. Intracellular dehydration stimulates thirst in the hypothalamus
polyuria
(frequent and excessive voiding)
When the maximum tubular absorptive capacity of the kidney is exceeded (about 180), glucose is lost in the urine, resulting in osmotic diuresis (water moves toward high solute concentration)
Hypovolemia results because: peeing everything out, osmotic diuresis
polyphagia
excessive hunger
Tissues do not have glucose available
Neural tissue in the brain responds to this emergency by promoting eating behavior
weight loss (cell starvation)
despite normal or increased appetite is a common occurrence in a person with uncontrolled Type 1 diabetes.
2 reasons:
1) loss of body fluids and
2) body tissue is lost because the lack of insulin forces the body to use fat stores and cellular proteins as sources of energy.
hyperglycemia
acts as an osmotic diuretic. This means the amount of glucose filtered by the kidneys exceeds that which can be reabsorbed by the renal tubules (exceeds renal threshold). This leads to "spilling sugar" in the urine.
What happens to urine output? Increase
What happens to sodium and potassium during diuretic phase? Decrease, but still hyperkalemic because potassium can't get into cells. Hyponatremic because osmotic diuresis (peeing)
What is the management for Hyperglycemia/Diabetes? Control blood glucose levels
lab values to monitor for glycemic control
glycosylated hemoglobin- HgbA1C, capillary blood glucose levels, urine glucose monitoring, urine albumin
Glycosylated hemoglobin - Hgb A1C
Glucose interacts with hemoglobin to form glycosylated derivatives, the most prevalent of which is named "hemoglobin A 1c".
Glucose entry into RBC is not insulin dependent
Glucose attaches to the hemoglobin molecule. Once attached, it cannot dissociate. The higher the blood glucose levels have been the higher the glycosylated hemoglobin. Since RBC live 120 days, the Hgb A 1c reflects average glucose levels over a three month period of time.
HgbA1c
Glycosylation is essentially irreversible, and the level of glycosylated hemoglobin present in the blood provides an index of blood glucose levels over the previous 2-3 months.
Without diabetes, HgbA1c levels are 5%. If diabetics can keep their level at 7% or less, significantly fewer complications.
capillary blood glucose levels
Can test glucose with a drop of blood - important in self-monitoring - limited for health care practitioner in evaluating long-term compliance
Drop of blood on a chemically treated strip, read by machine
For Type 1, should be done 3 or more times a day
Target value: 80-120 mg/dl before meals and 100-140 mg/dl at bedtime
urine glucose monitoring
Used to monitor for ketones -not accurate reflection of glucose in blood. If negative for glucose, only tells you that blood glucose is below 180 mg/dl, the typical threshold for spilling glucose from blood to urine.(will start having positive urine test for glucose at 180 mg/dl)
urine albumin
If protein in urine, may indicate early signs of chronic renal failure
Why would they develop renal failure? Kidneys aren't being perfused correctly because of thick sugar in blood.
Type 1 DM overview of treatment
goal is to maintain glucose levels within an acceptable range
Glycemic control is accomplished with an integrated program of diet, exercise, and insulin replacement
Exercise increases cellular responsiveness to insulin (need less insulin for glucose control)
Diet should be 55-60% carbohydrates (complex not simple), 30% fat (mostly unsaturated) to 12% proteins
Why is PRO decreased? Potential kidney failure
type 2 DM overview of treatment
oal is to maintain glucose levels within an acceptable range
Control with oral antidiabetic agents, diet and exercise
Often the patient's initial medication will become less effective and have to be modified. Possibly insulin. What factors contribute to this? The body is still being burnt out, illnesses, stressors, cortisol.
anti diabetic medications
Two categories of antidiabetic agents: insulin and oral medications.
Type 1 will need exogenous insulin replacement therapy
Type 2 will be on one or more agents (including insulin if needed)
Oral hypoglycemics
principles of insulin therapy
Insulin cannot be given orally because digestive enzymes in the stomach will break it down. "No pill" - must be given by injection, pump or inhaled
Insulin works by promoting the uptake of glucose into cells
Concentration: - most common concentration is U-100 (100 units/ml)
Most given SC
Regular Insulin can be given IV because it is a "true solution" - most other preparations consist of particles in suspension
Use insulin syringes that correspond to units
Regular insulin is clear- others may be clear or cloudy
Suspensions are absorbed more slowly - peak times are longer than regular insulin
Keep in cool areas and away from sunlight
Gently mix by rolling between palms of hands - to prevent "foaming of suspensions"
To avoid contaminating regular insulin vial with other types of insulin, ALWAYS withdraw regular insulin first - draw up "clear to cloudy"
Rotate injection sites (same area?) to avoid lipohypertrophy
Give at room temperature
Goal is tight glucose control (80-120 mg/dl)
Dose for specialized needs:
increase dosage for infection, stress, obesity, adolescent growth spurt, and 2nd and 3rd pregnancy
decrease dosage for exercise and first trimester
Given to all diabetic type 1 and some type 2 diabetics
insulin injection sites
Abdomen considered ideal site for absorption
Rotate sites
If not rotated, a continuously used site will develop a fatty lump and absorption will be erratic
Dosing Conventional therapy
Insulin is given 15-30 minutes before breakfast and supper. Typically two thirds of the total daily dose is given in the morning and remainder in the pm. Disadvantage is no adjustment is made on daily basis
Dosing Intensified Conventional Control
Injection of intermediate-acting insulin in the morning and evening (basal level of insulin) and also injects regular insulin prior to each meal (for acute needs). Advantage is that you get tight control because the dose of regular insulin is based on capillary glucose levels.
Dosing Continuous SC Insulin Infusion
Accomplished using a portable infusion pump connected to an indwelling SC catheter. Uses regular insulin, infused at slow and steady rate to maintain a basal level. Additionally may take insulin before eating
types of insulin
Rapid -Acting
Short-Acting
Intermediate-Acting
Long-Acting
insulin is classified according to
how it works in the body
Onset is how soon the insulin starts working
Peak is when insulin is working most effectively
Duration is how long the insulin lasts in the body
Rapid-Acting insulin
Lispro (Humalog), Novolog (Aspart), Apidra (Glulisine)
Onset
10-30 minutes
Peak
1-3 hours
Duration
3-5 hours
There is NO defense in a court of law for administering rapid-acting insulin without food immediately available!!!! Cannot be administered more than 5 minutes before a meal
Short-Acting Insulin
Regular (Humulin R, Novolin R, Exubera) - unmodified human insulin
Fast acting agent and has short duration
Regular
onset: 0.5-1 hour
peak: 2-4 hour
duration: 6-8 hours
Commonly used insulin, also used for control with Sliding Scale dosing in patients admitted to hospital
often hospitalization and illness is a source of stress, which increases cortisol release, which increases blood glucose.
Also used for patients on high dose glucocorticoid therapy
Only form of insulin that can be given IV
Intermediate-acting
NPH, Lente, Humulin N, Novolin N
Onset: 1-2 hr
Peak: 6-12 hr
Duration: 18-24 hr
Only longer acting insulin that is suitable for mixing with short acting insulin. Mixing insulins may alter utilization rates
Usual dose: Injected twice daily to provide control between meals and at night
Long-acting 24 hour coverage
Clear insulins
Cannot be mixed with other insulins
Delays onset
Lantus (Glargine)
Advantage
Avoids peaks and valleys.
Onset 1 hour
Peakless (no peak)
Duration: 24 hours
Levemir (Detemir)
Onset: 3-4 hours
Peak: 6-8 hours
Duration: 12-24 hours
premixed insulin
2 types of insulin mixed together in one vial. Usually one insulin is short-acting and the other is long-acting.
Examples:
Humalog Mix 75/25
Humulin 70/30
Jet injectors
devices shoot directly through skin (no needle)
pen injectors
needle that looks like fountain pen
Has pre-filled syringe
portable insulin pumps
Deliver basal (constant) and mealtime boluses (additional doses)
Match metabolic rate
Needle moved every 1-3 days
implantable insulin pumps
external telemetry
CCSI-Continuous subQ insulin infusion
Implantable pump with refillable reservoir
Programmable delivery system
Generally refilled every 3 months thru direct injection
Hypoglycemia: an Adverse Effect of Insulin Therapy
Referred to as "insulin reaction" or "insulin shock"
Caused by excess insulin
(other causes of hypoglycemia: reduced intake of food, V/D, alcohol, increased exercise)
S/S: tachycardia, palpitations, sweating, and nervousness
If severe, brain damage, coma and death occur
If conscious, give oral carbohydrate supplements (food or glucose tablets)
If gag reflex is suppressed or unconscious, give IV glucagon or D50
clinical manifestations of hypoglycemia
Defined as blood glucose less than 50 mg/dL
Abrupt decline in blood glucose
Can be caused by
Fasting coupled with exercise,
Exercise increases the usage of glucose by skeletal muscle
Insulin overdose
Hypoglycemia causes activation of the sympathetic nervous system. S&S related to adrenergic stimulation
Diaphoresis
Weakness
Nervousness
Sudden onset of hunger
Headache, as a result of alteration in blood flow (hypoperfusion) and changes in water balance
If Hypoglycemia occurs gradually, symptoms are CNS in origin: H/A, confusion, drowsiness, and fatigue
In cases of severe hypoglycemia, neurologic function can be severely impaired
confusion
disorientation
bizarre behavior
stupor
Convulsions
Death
hypoglycemia treatment
The most effective treatment of an insulin reaction is the immediate ingestion (if alert) of a concentrated carbohydrate source, such as glucose, honey, candy, or orange juice.
If unconscious, give Glucagon IM or subQ or glucose IV, D50W
Follow this simple sugar with a: complex carb AND protein
Diabetic Ketoacidosis (DKA)
Type 1 diabetics most prone to DKA: Continued insulin deficiency results in lipolysis (breakdown) of body tissues. Both Pro and Fat are metabolized. As fat stores are metabolized, fatty acids are produced. The resulting fatty acids undergo transformation in the liver to keto acids
Anything that increases BS can throw a pt. into DKA
Illness, skipping insulin
A blood glucose level above 240 mg/dl and ketones in the urine are warning signs of DKA
Under normal conditions, ketoacids can be utilized by neural and muscle tissue in energy metabolism. But if continually produced: pt. develops metabolic acidosis accompanied by hyperkalemia
In an attempt to compensate for metabolic acidosis (ketoacidosis), respirations will increase (characterized by prolonged expiratory period) to blow off CO2 . Breathing is deep and labored, known as Kussmaul respirations
Breath is "fruity" or "sweet smelling due to acetone formed during ketosis
Ketouria develops (acetone (ketones) in urine
major problems in DKA
Hyperglycemia
leads to osmotic diuresis, dehydration, and a critical loss of electrolytes
Na and K, which leads to
Cerebral edema
Can progress to Coma
treatment of DKA
IV insulin
What type of insulin? Regular
IV fluids
2 lines, one for fluids one for insulin
What type of fluid? Isotonic
After BS is < 300mg/dl, may switch to D5W for fluids. Why? Don't want to make them hypoglycemic.
What electrolyte might you add to the fluids? Potassium
Hourly BS
Hourly I & O
Polyuria?Oliguria?Anuria
ABG's - What acid/base imbalance? Metabolic acidosis
EKG?, Na Bicarb? Yes
Hyperglycemic, Hyperosmolar, Nonketotic Coma (HHNK)
Looks like DKA, but minimal ketosis
Who gets this? Type 2, Why? The body still produces some insulin
Characterized by extreme hyperglycemia (800-2000 mg/dL) and hyperosmolality (>350 mOsm/kg)
Combined with osmotic diuresis, eventually leads to hyperosmolar dehydration
Cellular dehydration can lead to altered consciousness (coma)
If any Ketoacidosis, it is much less severe compared to diabetic ketoacidosis (DKA)
Why?
If a person is able to secrete some insulin, then it prevents mobilization of fat from tissues and the release of ketone bodies
HHNK
Will they develop Metabolic Acidosis? NO
Will they develop Kussmaul Respirations? NO
What is the Treatment? INSULIN
HHNK vulnerable patients
Older patients with Type 2 diabetes and an acute problem
Undiagnosed with acute problem
Persons on TPN
Symptoms
Similar to DKA without fruity breath.
Why? Not blowing off CO2 (metabolic acidosis)
long term complications of diabetes
Long-term sequelae of diabetes takes years or even decades to develop.
The long-term vascular complications of diabetes involve:
microangiopathy - small vessels, and
macroangiopathy - middle and large-size vessels
Vascular lesions are a hallmark of diabetes. Vessels of all sizes are affected. The sclerosis and capillary basement membrane thickening are related to hyperglycemia
kidney disease
neuropathy
retinopathy
micro aneurysms
diabetic retinopathy
glaucoma and cataracts
infection
CVA
microangiopathy
A specific lesion of diabetes that affects capillaries and arterioles of the retina (diabetic retinopathy), peripheral nerves (diabetic neuropathy), and muscles and skin.
Since the chemical components of the basement membrane can be derived from glucose, hyperglycemia causes an increased rate of formation of basement membrane cells. These cells do not require insulin for glucose use.
macrovascular disease
Leading cause of death
increased risk of hypertension, MI, CAD, and stroke
caused by atherosclerosis
result from alterations in lipid metabolism, rather than hyperglycemia
microvascular disease
Basement membrane of capillaries thickens, causing blood flow in the microvascular to decline
Poor circulation can be prominent in the lower limbs, resulting in chronic skin ulcers and even gangrene
kidney disease
Renal failure caused by glomerular lesions, renal vascular atherosclerosis, and renal tubular alterations from glycogen and fatty changes
Early manifestations of nephropathy are proteinuria and hypertension. As the loss of functioning nephrons progresses, patients develop renal insufficiency and uremia. Patients may require dialysis or renal transplantation.
PRO in the urine = kidney disease
Native Americans and African Americans are at higher risk for CRF.
Risk is higher in Type 1 diabetics
neuropathy
Nerve degeneration results in tingling sensations in the fingers and toes, pain, loss of sensation.
retinopathy
Leading cause of blindness in US
Damage to the retina resulting from lack of oxygen
With hypoxia, scarring and microaneurysm formation occurs
micro aneurysms
Earliest clinical sign of diabetic retinopathy
Diabetic retinopathy: leading cause of new blindness in persons between 20-70 years
cataracts and glaucoma
caused by increased accumulation of sorbitol due to lack of insulin
high levels of sorbitol
Involvement of the autonomic nervous system may be accompanied by nocturnal diarrhea, delayed gastric emptying, erectile dysfunction (caused by nerve tissue damage - high levels of sorbitol)
infection
ability to inspect skin for intactness?
tissue hypoxia
many pathogens proliferate in glucose
decreased blood supply - decreased WBC to site
CVA (stroke)
twice as common in diabetics as non diabetics
glucose elevating medication
Glucagon (Glucagen)
D50W
Glucagon (glucagen)
Action: promotes breakdown of glycogen in liver (glycogenolysos) and converts amino acids to glucose (gluconeogenesis)
Route: IM, SubQ, IV
Use: Emergency treatment of severe hypoglycemia in patients who are unconscious or unable to swallow
Side effects: N/V, hypersensitivity, hyperglycemia, hypokalemia
Nursing implications: Do not reconstitute glucagon with NS, use D5W instead. Do not mix glucagon with any other medications. Patient usually responds in 5-20 mins after administered. After patient awakens, follow with complex carbohydrates.
D50W
Action: Increases circulating blood glucose
Route: IV
Use: Emergency treatment of severe hypoglycemia in patients who are unconscious or unable to swallow
Side effects: N/V, hypersensitivity, hyperglycemia, hypokalemia
Nursing implications: Do not reconstitute glucagon with NS, use D5W instead. Do not mix glucagon with any other medications. Patient usually responds in 5-20 mins after administered. After patient awakens, follow with complex carbohydrates.
Sulfonylureas
First generation: Chlorpropamide (Diabinese)
Second generation: Glipizide (Glucotrol)
Action: stimulate release of insulin from pancreatic islets in type 2 diabetes
Side Effects: GI distress (nausea, heartburn), neurological: dizziness, drowsiness, HA
alcohol may cause a disulfiram-like (Antabuse) reaction: flushing, palpitations, nausea, hypoglycemia
nursing implications: oral dosing 1-3 times a day, may be used alone or in combination with insulin, contraindicated during pregnancy, nursing, or allergies to sulfa and urea
non-sulfonyureas
biguanides, alpha-glucosidase inhibitors, thiazolidinediones, metiglinides, incretin enhancers
Overview: all decrease BG levels after meals in type 2 DM not controlled by diet and exercise. Given orally 1-3 times day. alcohol may increase risk of hypoglycemia. biguanides and alpha glucosidase inhibitors should not be taken together
side effects: all groups have risk of hypoglycemia (tremors, palpitations, sweating) except biguanides;
common GI symptoms include N/V, diarrhea, abd discomfort or flatuence;
decreased b12 levels with biguanides and incretin enhancers,
lactic acidosis may occur with biguanides,
upper respiratory symptoms may occur with metglinides, thiazolidendiones, and incretin enhancers,
anaphylaxis and pancreatitis with metglinides, hepatotoxicity, bone fractures, heart failure, and MI with thiazolidinediones,
angioedema, Stevens-johnson syndrome with sitagliptin
nursing implications: assess vital signs, weight, skin and nails, BG levels, hgbA1C levels, electrolytes
assess renal function and liver function studies
assess for early signs of lactic acid (hyperventilation, myalgia, malaise) and notify provider immediately
IVP dye check renal function studios and hold biguanides for 48 hours following admin of dye
Biguanides
Metformin (Glucophage)
action: decrease production and release of glucose by liver, increase glucose uptake by cells, and lower lipid levels
Alpha-glucosidase inhibitors
Acarbose (Precose)
Action: interfere with carb breakdown and absorption, act locally in GI tract with little systemic absorption
Contraindicated with GI disorders such as bowel inflammatory disease, bowel obstruction, and cautiously with GI distress or liver disease
Thiazolidinediones
Pioglitazone (Actos)
Rosiglitazone (Avandia)
action: inhibit glucose production in liver and increase cellular sensitivity to insulin
use cautiously with liver disease (may cause liver damage)
Metiglinides
nateglinide (starlit)
Repaglinide (prandin)
action: stimulate the release of insulin from the pancreas
incretin enhancers
Exenatide (Byetta)
Sitagliptin (Januvia)
Action: increase synthesis and release of insulin, decrease glucagon production and glucose secretion, and increase satiety