3 parts of endocrine system
glands, hormones, and target cells
How does the endocrine system respond to stimuli?
releases hormones from endocrine glands; target cells then read and follow the hormone's instructions, sometimes building a protein or releasing another hormone
Hormones regulate which body functions?
reproduction, growth/development, homeostasis, and metabolism
General characteristics all hormones share
1. rates/patterns
2. use a feedback system
3. affect target cells with specific receptors which initiate cell function/activity
4. excreted by kidneys or deactivated by the liver/cellular mechanisms
Hyposecretion
#NAME?
Hypersecretion
#NAME?
Hyporesponsiveness
cause the same set of clinical symptoms as hyposecretion; usually caused by deficiency of receptors (Type 2 DM)
Hypothalamus Function
regulates hormone secretion from major endocrine organs (not pancreas or parathyroid); primary organ concerned with homeostasis; sends hormones to anterior or posterior pituitary
Hypothalamus synthesizes
ADH and oxytocin
Oxytocin and ADH are produced by the __________ and stored in the __________.
hypothalamus; posterior pituitary
Oxytocin (OT)
increases intensity of labor (contraction of uterine smooth muscle)
Pitocin
derivative of oxytocin; initiates and speeds labor as well as stimulates contraction of milk ducts causing milk to flow into nipples
What stimulates the release of ADH?
increased plasma osmolality sensed by osmoreceptors in hypothalamus
ADH makes you ___ water
retain
Why is ADH also called vasopressin?
ADH increases peripheral resistance by vasoconstriction
How does ADH aid in the control of blood volume?
acts on kidneys to absorb more water back in the blood
SIADH
- Patho: Excessive ADH secretion=excessive water retention; characterized by decreased urine output with concentrated urine hyperosmolality while blood is diluted and serum osmolaity is low
- Causes: tumors of the CNS, certain drugs, cancers, common with critical illness and surgery
- Symptoms: cells swell (confusion, seizures, coma), hyponatremia, thirst, edema, anorexia, impaired taste, crackles, fatigue, and dulled sensation
- Treatment: fluid restriction, diuretics, hypertonic IV 3% saline (for hyponatremia); usually resolves in 2-3 days
Hypervolemia triggers what compensatory mechanism?
Release of ANP which causes urination with concentrated sodium
Diabetes Insipidus (DI)
-Patho: decreased ADH secretion or decreased response to ADH = excessive water excretion as dilute urine and the retention of sodium (blood is concentrated)
- Causes: injury to pituitary gland, brain tumors, damage to renal tubular cells, or pharmacologic agents
- Sympoms: polyuria (15L in 24hrs), thirst, nocturia, low specific gravity of urine (dilute), hypernatremia, neuro symptoms from dehydration of cells
- Treatment: Vasopressins (DDAVP- Desmopressin) BID as nasal spray for rest of life, correct dehydration with hypotonic IV fluid, prevent clots
Nursing Implications of Vasopressin
#NAME?
Vasopressin
Used to normalize urinary water excretion in pts with DI or used for childhood enuresis; caution with CAD or PVD b/c its a strong vasoconstrictor
Anterior Pituitary secretes
somatotropin hormones, growth hormone, prolactin, TSH, ACTH, FSH, and Lutenizing hormone (LH)
Growth Hormone
released from anterior pituitary in response to GHRF from the hypothalamus; promotes protein deposits that are essential for growth; increases mobilization of fatty acids; decreases glucose utilization and increased insulin resistance(increase blood sugar); has no specific target organ
Growth Hormone Deficiency
- Causes: decreased secretion of GHRF/GH, tumors, radiation, or trauma
- Symptoms: impairs normal growth and development in infants, children, and adolescents
- Treatment: synthetic GH subq injections 3-7 days a week prior to closure of the growth plate (epiphyseal plate)
Sermorelin
medication that acts like natural GhRF; used for treatment in GH deficiency in individuals with a functioning pituitary; height and weight and glucose should be monitored
Types of GH Excess
gigantism and acromegaly
Gigantism
a condition produced by hypersecretion of growth hormone during the early years of life; individuals will reach 7-9ft tall
Acromegaly
- Patho: GH excess occuring in the 4th-5th decade of life with increased bone density and width of bones enlarge; has diabetogenic effect that tends to increase blood sugar
- Symptoms: enlarged tongue, interstsitual edema, HTN, left sided HF, course skin/body hair, enlarged facial bones/hands/feet, profusion of jaw and forehead, barrel chest with arthritis, nerve damage, enlarged sebaceous/sweat glands
- Treatment: remove adenoma, radiation therapy, pharmocologic (sandostatin)
Octreotide (Sandostatin)
synthetic somatostatin used to stop GH release
Hormones produced by the thyroid
T3, T4, calcitonin
Many tissues in the body convert ____ to ____
T4 to T3 because T3 is the more active form of thyroid hormone
Need adequate __________ supply in diet for thyroid hormone production d/t thyroid gland needing this in blood to MAKE thyroid hormone.
iodine
Thyrotropin-releasing hormone (TRH)
released from hypothalamus when thyroid levels are low then promotes secretion of thyroid-stimulating hormone (TSH) and prolactin (PRL) from anterior pituitary
Thyroid Stimulating Hormone (TSH)
stimulates all aspects of thyroid function, including release of T3 and T4 while working on a negative feedback loop (increased T3/T4 decrease TSH release)
Function of Thyroid Hormones
1. protein synthesis
2. Basal metabolic rate (BMR) = rate of BODY'S heat production & energy expenditure
3. Gluconeogenesis & cellular uptake of glucose
4. Force & rate of cardiac contractions
5. Normal CNS development
6. Target cell/beta-receptors responsiveness to catecholamines, increases HR & causes heightened emotional response
Goiter
- Patho: enlarged thyroid gland; appears in hypo or hyper function of the thyroid
- Causes: enlarges in attempt to produce sufficient ammounts of thyroid hormones or in response to overproduction of hormones; iodine deficiency
Iodine and the Thyroid
Low iodine: production of thyroid hormones decreases, promoting the release of TSH which makes thyroid size increase (goiter)
High iodine: uptake of iodine is supressed and synthesis and release of thyroid hormones decline
Serum T4 test
measures total thyroxine (T4); used for initial screening of thyroid function; reflects overall thyroid activity; T4 high in hyperthyroid and low in hypothyroid
Serum T3 test
measures total triiodothyronine (T3); useful in diagnosing hyperthyroidism
Serum TSH
sensitive test for hypothyroidism diagnosis d/t small reductions in T3 & T4 causing dramatic TSH increase
Hypothyroidism
- Patho: results from decreased levels of circulating thyroid hormone; 3 classifications
- Causes: autoimmune disease (Hashimoto's-most common), insufficient iodine, surgical thyroid removal, destruction of thyroid by radiation, infections, congential, severe trauma, and neoplasms
- Symptoms: cold intolerance, lethargy, weight gain, impaired mentality, fatigue, overall decreased BMR
- Diagnosis: decreased T3/T4 levels; serum TSH may be high or low, weight increases due to slowed metabolism
- Pharm Treatment: synthetic T4 (synthroid), synthetic T3 (cytomel), or thyrolar
Levothyroxine (Synthroid)
DOC; taken for life; synthetic T4 that increases levels of T3 & T4 d/t most T4 being converted into T3; also used for simple goiter & Hashimoto's Disease
Liothyronine (Cytomel)
Synthetic thyroid hormone T3 that is not recommended for long-term use
Liotrix (Thyrolar)
combo of levothroxine and liothyronine
Nursing Implications of Thyroid Replacement
- Use caution with C/V disease (hormone can increase responsiveness to catecholamines and sympathetic stimulation leading to arrythmias)
- If dosage is excessive or a decrease in excretion is noted watch for thyrotoxixosis or thyroid storm
- do not d/c abruptly
Primary hypothyroidism
results d/t pathologic process that destroys thyroid gland (high TSH, low thyroid hormone); goiters can form
Secondary hypothyroidism
deficiency of pituitary TSH secretion (low TSH, low thyroid hormone); may be med induced
Congenital hypothyroidism (cretinism)
If deficiency occurs during embryonic & neonatal life, (causes mental retardation & derangement of growth); babies will be small and have intellectual disabilities, goiter (if reduced T3/T4 promote excessive release of TSH) or myxedema; everything slows
Myxedema
altered composition of dermis & separation of connective fibers (Non-pitting, boggy edema around eyes, hands, feet & thickened tongue, hoarseness, slurred speech)
Myxedema coma
Medical emergency; diminished level of consciousness associated with severe hypothyroidism; usually seen in elderly women with chronic hypothyroidism; symptoms include hypothermia without shivering, hypoventilation, hypotension, and bradycradia
Hyperthyroidism
- Patho: increased thyroid hormone
- Dx: excessive levels of circulating TSH
- Causes: dysfunction of thyroid/pituitary/hypothalamus, excessive intake of thyroid hormones, Grave's disease, Toxic nodular goiter
Graves Disease
- Patho: autoimmune disease in which developed antibodies stimulate TSH production & wrongly activate thyroid hormones production (T3 & T4)
- Symptoms: increased BMR, tachycradia/palpitations, heat intolerance, nervousness, thin hair/skin, tremors, weight loss (increased metabolism), protruding eyeballs, goiter (bruits may be present)
Thyroid Storm (Thyrotoxic Crisis)
life-threatening complication; symptoms include sudden increase in TH levels, uncontrolled fever (100-106), tachycardia & dysrhythmias, profuse diaphoresis & shock, vomiting & dehydration, CNS (hyperkinesis, anxiety, & confusion)
Thiomides: PTU and Tapazole
- Action: stop thyroid storm from making TH without destroying existing thyroid stores
- Use: hyperthyroidism
- Reactions: overuse converts to hypothyroid state, goiter with prolonged use
- Interventions: monitor T3 and T4 levels; PTU preferred during pregancy and breast feeding
What is the drug of choice for Graves disease?
Radioactive Iodine
Radioactive Iodine
- Action: decrease size and vascularity of gland; destroys thyroid tissue w/o affecting surrounding tissue
- Use: hyperthyroidism
- Contraindications: pregnancy
- Interventions: monitor bone marrow, 1-3 treatments with full effects taking 2-3 months
Lugol's solution, SSKI ( Potassium iodine)
-Use: nonradioactive; pre op to decrease vascularity and decrease bleeding risk and hyperthyroidism
- Interventions: dilute in fruit juice for taste (stains teeth); report symptoms of iodism (brassy taste, mouth burning, sore gums/teeth); report and discontinue if severe abdominal distress develops from toxicity
After a thyroidectomy a patient must take...
thyroid hormones for life
Adrenals synthesize what classes of hormones?
1. Mineralocorticoid-Alosterone (salt)
2. Glucocortocoids-Cortisol (sugar)
3. Androgens and Estrogens (sex)
Glucocorticoids
cortisol; regulates mood, surpresses the immune/inflamm response, increase breakdown of protein/fats, and inhibit insulin release (increased blood sugar)
Mineralocorticoids
aldosterone; regulates fluid and mineral balance (kidneys retain Na+ and water and lose K+)
Androgens
chief sex hormones
Addison's disease
- Patho: hypofunction of Adrenals/ chronic adrenal insufficiency
- Causes: destruction of adrenal glands; autoimmune response (most common); deficient cortisol secretion, may have ? aldosterone & androgen production
- Symptoms: vague until 80-90% of adrenal destroyed; N/V, salt cravings, hyperkalemia, chronic fatigue, hypoglycemia, hyperpigmentation (orange), weight loss
- Treatment: lifelong; combat fluid volume deficit, hormone replacement therapy (oral corticosteriods), mineralcorticoids (fludrocortisone-maintain Na+/K+ balance), increase salt
Does blood sugar drop in addison's disease & why?
yes, d/t Cortisol insufficiency = low gluconeogenesis, low liver glycogen, & high insulin sensitivity
What are symptoms of Addison's Disease initially from?
hyperkalemia
Why does Addison's Disease make pt's crave salt?
d/t ? aldosterone & resulting hyponatremia
How does lack of cortisol & aldosterone affect addison's disease?
With persistent insufficient amounts of cortisol & aldosterone body becomes: Weak, Dehydrated & Unable to maintain BP
Addisonian crisis
acute adrenal insufficiency; most commonly seen following abrupt withdrawal of long-term corticosteriod therapy
What should pts with Addison's Disease carry with them?
an emergency, prefilled steroid syringe in case of crisis d/t sickness or stress
Cushing's syndrome
#NAME?
Cushing's syndrome symptoms related to increased Glucocorticoids
breakdown of fat & protein (thin extremities, growth arrest), increased risk of infection, hyperglycemia, and depression to psychosis
Cushing's syndrome symptoms related to increased Mineralcorticoids
retain Na+ and Water, too much fluid, and lose K+
Cushing's syndrome symptoms related to increased sex hormones
acne, oily skin, and hirsutism
Pheochromocytoma
- Patho: adrenal medullary tumor that releases excessive amounts of catecholamines (epi and noepi) in an intermittent manner; are benign in 95% of cases; rare cause of secondary HTN
- Dx: Vanylmandelic Acid test
- Symptoms: severe HTN (250/140 mmHg), pounding headaches, palpitations/dysrhythmias, and diaphoresis
- Treatment: surgical resection of tumor
Vanylmandelic Acid Test
24hr Urine test for increased levels of epi & norepi
Parathyroid gland Function
regulates calcium levels in the blood, controls rate of bone metabolism, and regulates phorphorus levels
PTH (parathyroid hormone)
secreted by parathyroid gland; released when plasma calcium levels are low; targets bone, kidneys, and intestines to increase plasma calcium levels
Low calcium = ______ PTH; High calcium = ______ PTH
high; low
PTH in bone
increases rate of calcium release from bone, leading to overall loss of bone mass
PTH in GI tract
indirectly controls rate of calcium absorbtion from GI tract by increasing vitamin D activation
PTH in kidneys
causes tubular calcium reabsorption and increases phosphate excretion
Calcium vs. Phosphorus levels in Hyperparathyroidism
increased calcium; decreased phosphorus
Hyperparathyroidism
#NAME?
Calcitonin
lowers blood calcium levels by driving Ca+ back into bones
Hyperparathyroidism- Oral Phosphate/Glucocorticoids
oral phospahte: inhibit bone reabsorption, decreases Ca+ levels
glucocorticoids: reduce intestinal absorbtion of Ca+
Calcium vs. Phosphorus levels in Hypoparathyroidism
calcium is low; phosphorus is high
Hypoparathyroidism
- Patho: too little PTH produced
- Cause: excision of viable parathyroid tissue during thyroidectomy
- Symptoms: tetany (70% of cases), seizures, positive chvostek/trousseau sign
- Treatment: calcitriol or phosphate binders
Calcitriol (Rocaltrol)
Vitamin D analog; promotes calcium secretion from bone to bloodstream, & promotes calcium uptake from GI tract
Positive Chvostek's sign
facial nerve irritability/spasms, elicited by tapping nerve
Positive Trousseau's sign
carpal spasm induced by arterial occlusion of arm with blood pressure cuff
Why are beta blockers used in hyperthyroid patients?
they are used as symptom control
Total loss of adrenal cortical function is fatal in ___ to ___ days if untreated
3 to 10 days
Severe or prolonged ________________ can cause brain death and dysfunction (diabetic coma)
hypoglycemia
Blood glucose levels reflect the difference between....
the amount of glucose released into the blood stream by the liver and the amount of glucose taken up by the cell for energy
About 2/3 of the glucose that is ingested with a meal is removed from the blood and stored as __________
glycogen or converted to fat
A non diabetic fasting blood sugar should be?
70-100mg/dl
After eating blood glucose levels _____, and _________ is secreted in response
rise; insulin
What is glucose ingested through?
your diet
The liver regulates blood glucose through what processes?
Glycogenesis (glycogen synthesis)
Glycogenolysis (glycogen breakdown)
Gluconeogenesis (synthesis of glucose from fats or proteins)
When glucose levels rise what occurs? falls?
Rise: glucose in converted to glycogen
Fall: liver glycogen stores are broken down and released into cirulation
How does the liver synthesize glucose?
from noncarbohydrate sources like amino acids, lactic acid, and the glycerol part of triglycerides
Islets of Langerhans
responible for insulin production in pancreas; includes alpha cells (secrete glucagon), beta cells (secrete insulin), and delta cells (secrete somatostatin)
Insulin
protein essential for normal carb, fat, and protein metabolism; helps produce energy and plays a role in storing excess energy as glycogen; stimulates uptake of glucose, amino acids, nucleotides, and potassium
What is the principal stimulus for the release of insulin?
increased blood glucose levels
Catabolic mode
glycogen is converted into glucose, proteins into amino acids, and fats into glycerol and free fatty acids; brought on by insulin deficinecy
How does insulin lower blood glucose levels?
insulin facilitates transport of glucose from blood into cells/tissues and inhibiting gluconeogeneis; an insulin receptor and GLUT4 glucose transporter is used to remove insulin from the blood and shuttles it across the cell membrane into tissues
As blood glucose levels rise, insulin levels________. As blood glucose levels decline, insulin levels________.
increases; decreases
Glucagon
secreted by alpha cells; acts the opposite of insulin and its secretion results in an increase in blood glucose by promoting gluconeogenesis
What additional hormones affect blood glucose?
1. catecholamines (released in times of stress/exercise and inhibits insulin release so you don't become hypoglycemic)
2. growth hormone (increases blood glucose)
3. glucocorticoid or cortisol (increases blood glucose)
Diabetes Mellitus Patho
disorder of carbs, protein, and fat metabolism resulting from an imbalance between insulin availability and insulin need; can be absolute insulin deficiency, an impaired release of insulin, an inadequate or defective insulin receptor, or the production of inactive insulin
How is DM diagnosed?
oral glucose tolerance test, fasting blood glucose, casual plasma glucose test, HB A1C
Uncontrolled DM
unable to transport glucose into fat & muscle cells, as a result, body cells are starved, & breakdown of fat & protein is increased
Type 1 DM
- Patho: autoimmune destruction of pancreas; characterized by an absolute lack of insulin, an elevation in blood glucose, and a breakdown of body fats and proteins
- Causes: genetic predisposition, auto-antibodies build up in the blood and attack pancreatic beta cells (HLA markers), possible trigger from viruses in winter months
- Dx: usually found after 90% of beta cells have been destroyed; most common in caucasians
- Symptoms: sudden onset, hyperglycemia, metabolic acidosis, diabetic ketoacidoisis, kussmaul respirations
- Treatment: insulin replacement, diet (55-60% carb, 30% fat, and 12% protein), exercise
Type 1A vs Type 1B DM
Type 1A: immune-mediated diabetes; most common
Type 1B: idiopathic diabetes (unknown cause)
In Type 1 DM, cells starve and breakdown ______ and _______ which has the byproduct ________
protein and fats; ketones are a fat breakdown byproduct
What acid/base imbalance occurs from the breakdown of fat in Type 1 DM?
metabolic acidosis or diabetic ketoacidosis (patient wants to blow off CO2)
Type 2 DM
- Patho: glucose receptors in cell walls that are normally opened by insulin fail to function properly and glucose levels in the blood rise; islet cells make more insulin in attempt to lower glucose levels but will eventually burn out
- Causes: inadequate insulin secretion, insulin resistance, increased hepatic glucose production, drugs, environmental factors, obesity, family history
- Dx: usually found after 50% of beta cells are destroyed; more difficult to dx b/c body tries to compensate
- Symptoms: slow onset, usually symptom free when glucose levels are being compensated for but organs are being damaged
- Treatment: insulin when beta cells burnout and cannot compensate, diet, exercise
T or F insulin is naturally available in Type 2 DM
True; beta cells continue to produce insulin until they burnout
Gestational Diabetes Mellitus (GDM)
- Patho: state of carbohydrate intolerance that is detected during pregnancy, resembles type 2 DM
- Causes: weight gain can contribute, change in metabolism, cortisol is 3x higher when pregnant
- Dx: hyperglycemia, oral glucose tolerance test (OGTT), fasting plasma glucose (FBG), casual plasma glucose test, HbA1C
- Complications: affects baby, have higher risk of developing type 2 DM 5-10 years after delivery
- Treatment: 2-3x insulin
When should pregnant women be screened for gestational diabetes?
24-28 week; high risk group ( hispanic, native american, asian, african american)
Complications in fetuses with mothers who have gestational diabetes
increased birth weight and neonatal hypoglycemia
What type of drugs are thought to elevate blood glucose?
thiazide diuretics, Diazoxide, glucocorticoids, levodopa, oral contraceptives, sympathomimetics, phenothiazines, phenytoin, and total parenteral nutrition
Oral Glucose Tolerance Test (OGTT)
important screening test for DM especially in pregnant women; 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 greater than 200mg/dl after 2 hours on at least 2 occasions = Diabetes
At risk of DM if greater than 140mg/dl but less than 200mg/dl in the 2 hr sample
Fasting Plasma Glucose
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
At risk of DM if greater than 110mg/dl but less than 126mg/dl
Casual Plasma Glucose
blood is drawn anytime, without regard to meals. If greater than 200 mg/ml or higher on two occassions suggests diabetes.
Hb A1C
5% or less = No Diabetes
5.7% - 6.4% = Pre-diabetes
6.5% or more = Diabetes
provides an index of blood glucose levels over the previous 2-3 months
What are common symptoms of DM?
polyuria, polydipsia, polyphagia, fatigue, glucosuria, blurred vision, dehydration/hyperkalemia/hyponatremia, hypovolemia, skin infections/yeast infections
Polydipsia in DM
excessive thirst; occurs in DM due to the blood being hyperosmolar and pulling water from the intercellular compartment and intercellular dehydration stimulates thirst in the hypothalamus
Polyuria in DM
excessive urination; occurs in DM due when the maximum tubular absorptive capacity of the kidney is exceeded (about 180 of glucose), glucose is lost in the urine, resulting in osmotic diuresis (water moves toward high solute concentration)
Polyphagia in DM
excessive hunger; occurs in DM because neural tissues in the brain respond to the lack of glucose in tissues by promoting eating behavior
Why is weight loss common in those with Type 1 DM?
loss of body fluids and loss of body tissues due to lack of insulin which forces the body to use fat stores and cellular proteins as sources of energy
What happens to urine output with hyperglycemia?
it increases with sodium being excreted and potassium being retained
The higher blood glucose levels, the ____________ HbA1C
higher; glucose attaches to hemoglobin and cannot dissociate (shows for 120 days)
Capillary Blood Glucose Levels
tests glucose with a drop of blood on a chemically treated strip, and read by machine; important in self-monitoring
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; if negative for glucose, only tells you that blood glucose is below 180 mg/dl (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 (scarred blood vessels in kidneys)
Important Principals of Insulin Therapy
1. Insulin cannot be given orally because digestive enzymes in the stomach will break it down
2. Suspensions are absorbed more slowly - peak times are longer than regular insulin
3. Give at room temperature
4. Keep in cool areas and away from sunlight
5. Gently mix by rolling between palms of hands - to prevent "foaming of suspensions
What type of insulin should be drawn up first?
REGULAR (clear to cloudy)
What is the only type of insulin that can be given as an IV?
regular insulin (true solution)
Is regular insulin clear or cloudy?
clear
When should insulin doses be increased?
increase dosage for infection, stress, obesity, adolescent growth spurt, and 2nd and 3rd pregnancy
When should insulin doses be decreased?
decrease dosage for exercise and first trimester of pregnancy
What is the ideal injection site for insulin?
abdomen (make sure to rotate sites)
Insulin Dosing Schedule: Conventional Therapy
Insulin is given 15-30 minutes before breakfast and supper. Typically 2/3 of the total daily dose is given in the morning and remainder in the pm. Disadvantage is no adjustment is made on daily basis
Insulin Dosing Schedule: 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.
Insulin Dosing Schedule: Continuous SC 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
Rapid-Acting Insulin
Lispro (Humalog), Aspart (Novolog), Glulisine (Apidra)
Onset: 10-30 minutes
Peak: 1-3 hours
Duration: 3-5 hours
Rapid-Acting Insulin cannot be administered more than _____________ before a meal
5 minutes
Short-Acting (Regular) Insulin
Humulin R, Novolin R, Exubera
onset: 0.5-1 hour
peak: 2-4 hour
duration: 6-8 hours
most commonly used insulin; also used for cortisol
Intermediate-acting Insulin
NPH, Humulin N, Novolin N, Lente
Onset: 1-2 hr
Peak: 6-12 hr
Duration: 18-24 hr
What type of insulin is the only longer acting insulin that is suitable for mixing with short acting insulin?
intermediate-acting
Long-Acting Insulin
Lantus (glargine), Levemir (detemir)
24 hour coverage
Lantus (glargine)
Avoids peaks and valleys. Can give without food. Cannot be mixed with other insulins.
Onset: 1 hour
Peakless
Duration: 24 hours
Levemir (detemir)
Onset: 3-4 hours
Peak: 6-8 hours
Duration: 12-24 hours
Premixed Insulins
2 types of insulin mixed together in one vial. Usually one insulin is short-acting and the other is long-acting; example: Humalog mix 75/25, Humulin 70/30
Portable Insulin Pumps
deliver basal (constant) and mealtime boluses (additional doses); match metabolic rate; needle moved every 1-3 days
Insulin Shock (hypoglycemia)
- Patho: blood glucose less than 50mg/dl; abrupt decline in blood glucose
- Causes: fasting coupled with exercise, insulin overdose
- Symptoms: tachycardia, palpitations, sweating, and nervousness, brain damage/coma (if severe)
- Treatment: give oral carbohydrate supplements or food like glucose, honey, candy, or orange juice, if gag reflex is suppressed or unconscious, give IM glucagon or IV D50
S&S of Hypoglycemia related to adrenergic stimulation
diaphoresis, weakness, nervousness, drowsiness/fatigue, sudden onset of hunger, H/A
S/S of severe hypoglycemia
confusion, disorientation, bizarre behavior, stupor, convulsions, death
Diabetic Ketoacidosis (DKA)
- Patho: most common in Type 1 DM; continued insulin deficiency results in breakdown of body tissues; fats and proteins are metabolized and ketoacids are eventually formed
- Causes: increased blood glucose, skipping meals, illness
- Symptoms: dehydration, loss of Na+, cerebral edema, coma, fruity breath, kussmaul respirations
- Dx: blood glucose level above 240mg/dl, ketones in urine
- Treatment: regular insulin, normal saline IV, K+ supplements, Na Bicarb
- Interventions: hourly I & O, hourly BS; note that after BS is < 300mg/dl, may switch to D5W for fluids, order EKG and ABGs
Hyperglycemic, Hyperosmolar, Nonketotic Coma (HHNK)
- Patho: most common in Type 2 DM; extreme hyperglycemia (800-2000 mg/dL) and hyperosmolality (>350 mOsm/kg); combined with osmotic diuresis, eventually leads to hyperosmolar dehydration
- Symptoms: coma from cellular dehydration, similar to DKA without fruity breath (no ketones)
- Treatment: insulin and IV fluids
- Vulnerable Patients: older patients with Type 2 diabetes and an acute problem, undiagnosed with acute problem, persons on TPN
Long term complications of diabetes
#NAME?
What is a hallmark physical sign of diabetes?
vascular lesions; all vessels are affected; the sclerosis and capillary basement membrane thickening are related to hyperglycemia
Diabetes Complication: Kidney Disease
renal failure caused by glomerular lesions, renal vascular atherosclerosis, and renal tubular alterations from glycogen and fatty change; proteinuria and HTN are early signs; risk is higher for type 1 diabetics, native americans, and african americans; may require dialysis or transplants
Diabetes Complication: Neuropathy
nerve degeneration results in tingling sensations in the fingers and toes, pain, loss of sensation
Diabetes Complication: Diabetic Retinopathy
leading cause of blindness in people 20-70 in the US; damage to the retina resulting from lack of oxygen, with hypoxia, scarring and microaneurysm formation occurs
What is the earliest clinical sign of diabetic retinopathy?
microaneurysms
What two prominent eye conditions are associated with diabetes?
Cataracts and Glaucoma, caused by increased accumulation of sorbitol due to lack of insulin
A stroke is _____ as common in diabetics than in non diabetics
twice
Without insulin K+ can __________ in the bloodstream
increase
HLA markers
seen in type 1 diabetes and not in type 2 diabetes
Why do the clinical manifestations of DM appear?
insulin deficiency, insulin resistance, or hyporesponsiveness
What two things in the body do not need insulin for glucose entry?
the brain and RBCs
What is the goal % of HbA1C for people with diabetes?
at or below 6.5-7%
With insulin use, the peak is the biggest risk for_____________
hypoglycemia
If hypoglycemia occurs gradually, symptoms are ________ in origin
CNS; H/A, confusion, drowsiness, and fatigue
Sulfonylureas (Glipizide)
oral anti diabetic agent used do decrease blood glucose; if you drink alcohol and take this you will be violently ill (Antabuse rxn); do not take if pregnant or nursing
Biguanides (Metformin)
oral anti diabetic agent used to decrease blood glucose; can give nausea and diarrhea; cannot take for 48hrs prior to a procedure involving dye; can cause lactic acid build up; does not cause hypoglycemia like other anti diabetic meds