exam 4- ch 51

exocrine glands

secrete enzymes- responsible for digestive system and sweat glands; secretions are protective and functional

endocrine glands

ductless; release hormones directly into the bloodstream

-control regulatory function (cellular metabolism, human growth, fluid and electrolyte balance)

hormones

chemical messengers that travel through the bloodstream to their target organs

-are controlled by negative feedback

pituitary gland

referred to as hypophysis

-controls endocrine glands through negative feedback

anterior pituitary gland hormones

-somatotropin (growth hormone)

-adrenocorticotropic

-thyroid-stimulating

-follicle-stimulating

-luteinizing

-prolactin

posterior pituitary gland hormones

Oxytocin and antidiuretic hormone which are released when hypothalamus is stimulated

thyroid gland + its hormones

-very vascular- receives 80-120 mL of blood per minute

-triiodothyronine and thyroxine hormone (regulate growth and development)

-calcitonin released from gland

parathyroid glands

secrete parathyroid hormone

-regulates amount of phosphorus in the blood

hypocalcemia vs hypercalcemia

-hypo: causes nerve cells to become excited and stimulate muscles with too many impulses; spasm occurs and slows heart rate

-hyper: causes impaired heart function and can result in death

adrenal cortex

-mineralcorticoids: involved in water and electrolyte balance (aldosterone)

-glucocorticoids (cortisol)

-s*x hormones (androgen hormones)

adrenal medulla

Epinephrine and norepinephrine - causes increase in heart rate and blood pressure and liver to release glucose reserves for energy

pancreas

islets of langerhans secrete insulin and glucagon

thymus gland

thymosin plays an active role in the immune system

pineal gland

secretes melatonin which is linked to sleep function and regulation of circadian rhythm

acromegaly

overproduction of somatotropin (growth hormone) after the onset of puberty and closure of growth plates

-s/s: (starts around age 30-40) enlarged cranium and lower jaw, seperated maloccluded teeth, bulging forehead, bulbous nose, thick lips, enlarged tongue, generalized coarsening of facial features- physical changes are irreversible

-enlargement of heart, liver, spleen

-tumor cause cause pressure on optic nerve- visual disturbances are often the first sign

gigantism

results from an oversecretion of GH before the onset of puberty due to hyperplasia of the anterior pituitary

-overgrowth of long bones; patients are very weak

-lab test: glucose solution ingested- in a normal pt GH levels will fall but in this case, will remain elevated (GH suppression test)

dwarfism

caused by genetic mutation, GH deficiency, and other unknown causes; in some cases, pt lack ACTH, TSH, and the gonadotropins

-s/s: short stature, well-proportioned and well-nourished but appear younger than chronological age, problems with dentition when permanent teeth erupt due to underdeveloped jaw, normal but delayed sexual development

diabetes insipidus

metabolic disorder of the pituitary gland and develops when there is a decreased production of ADH or action of ADH is diminished

-decreased ADH causes increased urination and dehydration

-s/s: polyuria, polydipsia (excessive thirst), dilute urine, urine output as high as 5-20 L in 24 hours, hypernatremia, tachycardia, tachypnea, hypotension

-can lead to hypovolemic shock if happens when patient is unconscious

SIADH - syndrome of inappropriate antidiuretic hormone

occurs when pituitary gland releases too much ADH- kidneys reabsorb more water, decreasing urinary output and expanding body’s fluid volume

-s/s: hyponatremia, water retention, water intoxication, nausea, vomiting, irritability, confusion, tremors, seizures, stupor, coma, cramping, anorexia, headaches

-fluid restrictions and monitor I&Os

hyperthyroidism/graves disease

autoimmune disorder of unknown cause; a condition in which there is increased activity of the thyroid gland; overproduction of T3 and T4; exaggeration of metabolic process

-as T3 and 4 increase, TSH stops to secrete

-s/s: exophthalmos (can cause corneal ulcers and loss of vision), visible neck edema, difficulty concentrating, unplanned weight loss, nervous/jittery, insomnia, hypertension, tachycardia

-radioactive iodine to destroy hypertrophied thyroid tissue

-drug therapy- takes 6-8 weeks for symptoms to decrease

postop thyroidectomy

-always have IV calcium gluconate available to treat tetany (low serum calcium)- if not treated, convulsions or lethal cardiac dysrhythmias can occur

thyroid storm

occurs when the thyroid gland is manipulated during surgery and large amounts of thyroid hormones are released into the blood stream; s/s of hyperthyroidism are exaggerated

-other s/s: nausea, vomiting, severe tachycardia, severe hypertension, hyperthermia up to 106 F, increased Ft4 and decreased TSH

three goals of thyroid storm management

-induce a normal thyroid state

-prevent cardiovascular collapse

-prevent excessive hyperthermia

hypothyroidism

occurs when thyroid fails to secrete sufficient hormones slowing the body’s metabolic process

-severe can cause myxedema- edema of hands, face, feet and periorbital tissues

-s/s: decreased body heat, intolerance to cold, weight gain, CAD, decreased cardiac output, decreased exercise tolerance, dyspnea on exertion, difficulty concentrating, constipation

-hormone replacement therapy for life- taken in mornings on empty stomach

simple (colloid) goiter

develops when the thyroid gland enlarge in response to low iodine levels in the blood

-diagnosis is based on physical appearance

-s/s: dysphagia, hoarseness, or dyspnea

cancer of the thyroid

risk factors: diets low in iodine, radiation exposure, obesity, women

-s/s: firm, fixed, small, rounded painless mass or nodule that is felt during palpation of the gland, trouble breathing, hoarseness, difficulty swallowing

-thyroid function test is normal; thyroid scan uses an isotope to test thyroids uptake of the material

thyroid scan for cancer

-papillary thyroid cancer: a “cold” nodule shows decreased uptake of the isotope

-benign adenomas and follicular cancers: a “hot” nodule shows increased uptake of the isotope

hyperparathyroidism

increased production of PTH

-cause can be benign or malignant; can also result from chronic renal failure, pyelonephritis or glomerulonephritis

-s/s: nausea, vomiting, weakness and fatigue, skeletal pain, pain on weight-bearing and pathologic fractures r/t calcium leaving the bones and accumulating in the blood

-assess for hypertension and cardiac dysrhythmias; observe urine for hematuria

hypoparathyroidism

decreased PTH which results in decreased levels of serum calcium and increased serum phosphorus levels

-most common cause is accidental removal or destruction of one of the glands during thyroidectomy

-s/s: neuromuscular hyper-excitability, involuntary and uncontrolled muscle spasms, hypocalcemic tetany, laryngeal spasm, stridor, cyanosis, parkinsonian syndrome

-assess for chvostek sign or trousseau sign

hypoparathyroidism medical management and nursing interventions

-MM: IV administration of calcium gluconate or calcium chloride- push slowly due to irritation of the vein (possibility of cardiac dysrhythmias, EKG monitoring)

-long term therapy: oral calcium supplements, vitamin D, magnesium; daily PTH injections if not able to maintain with oral supplements

-NI: monitor for s/s of hypercalcemia after start of therapies; teach pt about high calcium diet- low fat dairy products, dark green vegetables, canned fish with bones (1000 mg/day)

cushing syndrome

adrenal hyperfunction caused by excess corticosteroids

-can be caused by hyperplasia of adrenal tissue d/t overstimulation by ACTH

-physical characteristics: moon face, buffalo hump, weight gain (accumulation of adipose tissue in trunk, face, and c-spine area), thin arms and legs, possible kyphosis

-hypokalemia and hyperglycemia

-protein in urine, excretion of calcium, kidney stones

s/s of hypercalcemia

vomiting, disorientation, anorexia, abdominal pain, weakness

cushing syndrome diagnostic test and medical management

-tests: based on clinical appearance, elevated serum cortisol levels, skull-xray to assess for pituitary tumor, abdominal ct or MRI to assess for tumor

-tumor removal; mitotane (Lysodren) if surgery is not possible- alters the metabolism of cortisol - given for 3 months but can damage adrenal glands

-low sodium diet

-interventions: gentle handling to prevent skin tears and bruising

addison’s disease

adrenal hypofunction occurring because the adrenal glands do not secrete adequate amounts of cortisol, aldosterone, sex hormones

-most common cause is an autoimmune disease

-assess for electrolyte and fluid imbalances, hypovolemia, and dehydration

-s/s do not usually show up until 90% of adrenal cortex is destroyed; progressive weakness, fatigue, nausea, anorexia, craving salt, vertigo, syncope

addisonian crisis

life-threatening emergency caused by insufficient adrenocortical hormones or a sudden, sharp decrease in these hormones

-precipitating factors: infection, surgery, trauma, hemorrhage, psychological stress, sudden withdrawal of corticosteroid hormone therapy, pituitary gland destruction

pheochromocytoma

tumor of the adrenal medulla that causes excessive secretion of a catecholamine (epi or norepinephrine)

-s/s: anxiety, severe headache, diaphoresis, tachycardia, shortness of breath, feelings of extreme fright, unexplained abdominal pain

-diagnostic test: 24 hours urine collection to measure catecholamine, plasma catecholamine are elevated

-can lead to DM, cardiomyopathy and death if undiagnosed

diabetes mellitus

a systemic metabolic disorder that involves improper metabolism of carbs, fat and proteins

r/t a decrease or absolute lack of insulin production by the beta cells of the islets of langerhans

insulin

a protein that allows the body’s cells to absorb glucose from the bloodstream

-average amount secreted is 40-50 units/day

normal insulin secretion

peaks 30 mins after meals and returns to normal in 2-3 hours

normal blood glucose

70-100 mg/dL

type I DM

an autoimmune disease results in destruction of beta cells and deficient insulin production

-formerly called juvenile diabetes, juvenile-onset diabetes, or insulin-dependent DM

-urine strongly positive for ketones (means that fat is used for energy instead of glucose)

type II DM

abnormal resistance to insulin action

-formerly called adult-onset diabetes, maturity-onset diabetes, or non-insulin dependent DM

symptoms of type I DM

sudden; polyphagia, polydipsia, polyuria, weight loss, weakness, fatigue; glycosuria, hyperglycemia; acidosis progressing to DKA

symptoms of type II DM

gradual; may be asymptomatic at onset; later may develop s/s of type I; other include slow wound healing, blurred vision, pruritus, boils and other skin infections; vaginal infections in women

causes and complications of DM

-exact cause unknown but contributing factors are genetics, viruses, aging process, diet and lifestyle, ethnicity

-damage blood vessels which increases risk for heart disease, hypertension and stroke

-can cause renal failure, erectile dysfunction, neuropathy, and retinopathy

prediabetes

-insulin resistance occurs; the body’s response lessens to the production of insulin

-glucose levels may be initially normal but the pancreas is working overtime

-monitor caloric intake and regular exercise to aid in weight loss

Pathophysiology of type I DM

-when glucose is not available, liver converts fatty acids into ketone bodies which serve as fuel for muscles or energy source for the brain

-lack proper amounts of insulin impairs use of glucose and hyperglycemia and glycosuria can result

diagnostic test for DM

-random glucose level greater than 200 mg/dL

-fasting blood glucose level greater than 126

-oral glucose tolerance test: glucose fluid drink; pt is tested for 3 hrs (not necessary for pts showing overt signs)

-serum insulin: absent in type I; normal-high in type II

-postprandial blood glucose: meal with carbs; blood sample 2 hrs later- more than 160 mg/dL indicates presence of DM

-glycosylated hemoglobin (HbA1c): normal s 4-6%; glucose incorporated into the hemoglobin

-c-peptide test: c-peptide is in the chain of insulin and released into the bloodstream- shows whether insulin is being produced

ADA diet

-45-50% carbs

-10-20% proteins

-no more than 30% fat

-sugars and complex carbs counted together as a total carbohydrate

diabetes and exercise

patient cannot begin exercise unless blood glucose is 100 mg/dL or higher but less than 250 mg/dL

-reduces insulin resistance and increases glucose uptake for as long as 72 hours post-exercise

diabetes and stress

-emotional and physical stress can increase blood glucose levels

-extra insulin may be necessary and food intake is important

-monitor presence of ketones in the urine

-increase fluid intake

-pt should contact hcp when blood glucose exceeds 250 mg/dL

biosynthetic insulin

-produced by genetically altered common bacteria or yeast, using DNA technology

-given subcutaneously or via IV if immediate action is needed- must be mixed in normal saline

rapid acting insulin

lispro (humalog), aspart (novolog), glulisine (apidra)

-human clear

-5-15 mins before meal

-risk time: no meal within 30 mins

-15-30 mins onset of action

-1-2 hours peak action

-3-4 hours duration

short-acting insulin

regular, humalin R, novolin R, ReliOnR

-human clear

-30 mins before meals

-risk time: 3-4 hours

-30-60 mins onset of action

-2-4 hours peak action

-6-8 hours duration

mixed insulin -rapid and intermediate

novolog mix, humalog mix

-human cloudy

-15 mins before meals

-risk time: no meal within 30 mins

-rapid and intermediate

-15-30 mins onset of action

-2-10 hours peak action

-12-16 hours duration

mixed insulin -short and intermediate

NPH/regular mix, novolin mix, ReliOn N mix, NPH/regular, humulin mix

-human cloudy

-30-60mins before eals

-risk time: 3-4 hours

-short and intermediate

-30-60 mins onset of action

-6-12 hours peak action

-18-24 hours duration

intermediate acting insulin

NPH humulin N, novolin N, ReliOn N

-human milky when mixed

-30 mins before meals

-risk time: 4-6 hours

-2-4 hours onset of actin

-6-8 hours peak action

-12-16 hours duration

long acting insulin

glargine (lantus), detemir (levemir)

-synthetic clear

-injection time - 9pm

-risk time: starting dose should be 20% less than total daily dose of NPH

-1-2 hours onset of action

-no peak

-24 hour duration

ultra long acting insulin

degludec

-synthetic clear

-flexible injection time

-no risk time

-1 hour onset of action

-no peak action

-42 hours or longer duration

insulin injection

-inject only into subcutaneous tissue

-should be injected at room temperature

-must be co-signed by another licensed person

-self-injection should be taught prior to discharge

hypoglycemia s/s

faintness, sudden weakness, excessive perspiration, irritability, hunger, palpitations, trembling, drowsiness

-can be similar to that of a stroke

insulin pump

continuous subcutaneous insulin infusion using an external infusion pump

-computerized device - battery operated

-releases small amounts of rapid-acting insulin every few minutes

-clear dressing changed every other day

treatments other than insulin

-pramlintide (symlin): subcutaenous; adjunct to insulin; decreases gastric emptying, glucagon secretion, glucose output from liver

-glucagon 0.5-1 mg; subcutaneous; stimulates liver to change stored glycogen into glucose

pancreas transplant

-ONLY pt with type I

-pancreas and kidney transplants usually done at the same time

-lifelong immunosuppression therapy to prevent rejection

nursing interventions for patient with diabetes

-accurate monitoring of blood glucose levels

-arrange for dietician consult

-proper skin care

-report new cuts

-instruct patient to get eye exam every 6-12 months

-always monitor for s/s of hypoglycemia

foot care for patient with DM

-wash feet daily with soap and warm water

-examine feet daily

-do not cleanse cuts with iodine, rubbing alcohol, or strong adhesives

-report skin infections or nonhealing lesions to the HCP immediately

-avoid open toe, open heel and high heel shoes

-exercise feet daily either by walking or flexing and extending feet

DKA- diabetic ketoacidosis

-type I

-glycosuria and ketonuria

-polyuria and polydipsia

-telltale sign: kussmaul respirations (deep, rapid breathing), fruity breath

-potassium is shifted out of the cells

hypoglycemic reaction

-type I or type II

-absent glycosuria and ketonuria

-absent polyuria and polydipsia

HHNC - hyperglycemic hyperosmolar nonketotic coma

-type II

-glycosuria present; absent ketonuria

-polyuria and polydipsia

hypoglycemic reaction treatment (unconscious pt)

-administer glucose gel tube between cheek and gums

-give glucagon injection

-administer IV of bolus of 20-50 mL of dextrose 50% in water

tx during hyperglycemic reaction

-start IV of normal saline, when BS gets to 250 mg/dL, add 5% dextrose

-give regular insulin as a piggyback infusion in 500 mL of normal saline

-IV replacement of potassium to help move insulin into cells

-administer oxygen

-monitor cardiac status

nursing interventions during and after DKA

-keep patent airway

-maintain patent IV infusion

-accurate I&Os

-test blood for glucose and urine for acetone

-assess cardiac status, breath sounds, LOC, cause of DKA

-infection prevention

chronic complications of DM

-end-organ disease

-blindness, diabetic retinopathy, cataract development

-cardiovascular problems

-renal failure

-diabetic neuropathy- causes pain and decreased sensation

-delayed gastric emptying

pathophysiology of type II DM

-decreased tissue responsiveness to insulin

-overproduction in the early stages, but eventual decrease

-abnormal hepatic glucose regulation

-result in peripheral insulin resistance

Biguanides

-oral medication with a blood-glucose lowering effect

-works by reducing hepatic glucose production and lowers fasting blood glucose levels

-enhances tissue response to insulin and improves glucose transport into cells

*metformin (glucophage)

gestational diabetes

-complications: respiratory distress syndrome, hypoglycemia in infant after delivery, risk for mother to develop type II later in life

-s/s same as type II

-glucose tolerance test done around 26 weeks