NURS 331 EXAM 1 (copy)

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






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)


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


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


- 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



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)


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


a condition produced by hypersecretion of growth hormone during the early years of life; individuals will reach 7-9ft tall


- 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.


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


- 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


- 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


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


- 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)


cortisol; regulates mood, surpresses the immune/inflamm response, increase breakdown of protein/fats, and inhibit insulin release (increased blood sugar)


aldosterone; regulates fluid and mineral balance (kidneys retain Na+ and water and lose K+)


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?


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


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


- 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




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


- 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)


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?


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)


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


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?


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?


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
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


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?


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


Without insulin K+ can __________ in the bloodstream


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_____________


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