Endocrine Flashcards
(39 cards)
hormone: corticosteroids
secreted by: ___________
disorder: ______________
secreted by: adrenal cortex
hypersecretion: Cushing syndrome
hyposecretion: Addison disease
hormone: insulin
secreted by: _______________
disorder: _______________
drug therapy: _______________
secreted by: Pancreatic islets
hyposecretion: diabetes mellitus
drugs: insulin & oral antidiabetic drugs
hormone: antidiuretic hormone
secreted by:_______________
hypoactive disorder:________
drug therapy:_______________
secreted by: pituitary
hyposecretion: diabetes insipidus
drugs: desmopressin and vasopressin
hormone: growth hormone
secreted by: ________________
hypoactive disorder: _______
drug therapy: _______________
secreted by: pituitary
hyposecretion: small stature
drugs: somatropin
hormone: thyroid hormone
secreted by: ___________________
hyperactive disorder: _______________
drug therapy: ___________________
secreted by: thyroid
hypersecretion: Graves disease
drugs: propylthiouracil
hormone: thyroid hormone
secreted by: ___________________
hypoactive disorder: ___________________
drug therapy: ___________________
secreted by: thyroid
hyposecretion: hypothyroidism - myxedema (adults) & cretinism (children)
drugs: thyroid hormone and levothyroxine
what’s the hypothalamus & what’s it do?
*“master gland”
*Hypothalamus secretes “releasing hormones”
which tell pituitary gland which hormones should be released
antidiuretic hormone prototype, MOA, side effects, interventions
*desmopressin
*Promotes reabsorption of h20 by kidneys
*Vasoconstriction to raise BP
*used for: Diabetes Insipidus, cardiac arrest and nocturnal enuresis (nasal spray form)
*side effects: Hyponatremia, seizures, coma
*intervention: Monitor urine specific gravity, BP, urinary output, Na levels
growth hormone
*somatropin
use: to treat growth hormone deficiency
**Use discontinued before epiphyseal closure (long bones)
*Contraindicated in obese clients
*Adverse: Hyperglycemia, Hypothyroidism
*Interventions: Dose is individualized, given SQ, monitor growth patterns
thyroid agent for hypothyroidism
*levothyroxine
*MOA: replaces (so same as) thyroid hormones
*Take 30 minutes before food in AM
*Take with plenty of water
*Adverse: hyperthyroidism, palpitations, dysrhythmias, anxiety, insomnia, weight loss, heat intolerance, menstrual irregularities and osteoporosis in women, *ONSET 1-3 weeks
*Interventions: Monitor cardiac system, start low dose (increase as needed), *Monitor: T4 and TSH levels
s/s of hypothyroidism (AKA _____)
*“Myxedema”
*Early symptoms: weakness, muscle cramps, and dry skin
*severe symptoms (Myxedema):
Slurred speech, bradycardia, weight gain (slowed metabolism), intolerance to cold environments, low body temp
S/s of hyperthyroidism (AKA: ______)
*Graves disease
*Hypersecretion of thyroid hormone, increased body metabolism, tachycardia, weight loss, increased body temperature, anxiety, bulging eyes
thyroid agent for hyperthyroidism (= “antithyroid agent”)
*propylthiouracil (PTU) & Methimazole
*Educate: Taken with food same time each day, increase fluids to 3L daily to avoid constipation, avoid OTC products w/ iodine, taper off if discontinuing
*Interventions: Monitor pulse, report dizziness, palpitations, intolerance to temp changes, monitor thyroid levels, monitor weekly weight
*Overdose signs: periorbital edema, cold intolerance, mental depression.
what is Addison’s disease?
*Primary adrenocortical insufficiency, deficiency of both mineralocorticoids and glucocorticoids
*s/s: N & V, lethargy, bronze skin, confusion, and coma
*treatment: steroids (do not skip doses)
*Intervention: Monitor BP, fluid, electrolytes and weight. Monitor for signs of bleeding or GI issues.
*Teach: client to take calcium supplements and maintain Vitamin D levels, taper off dose, protect the immune system
primary adrenocorticol insufficiency = _________(short answer)
secondary adrenocorticol insufficiency = __________ (long answer)
primary: For some reason your adrenal glands aren’t working
secondary: Results from long-term therapy with glucocorticoids. The pituitary receives a message through the negative feedback mechanism to stop secreting adrenocorticotropic hormone (ACTH).
Without stimulation from ACTH, the adrenal cortex shrinks in size and stops secreting endogenous glucocorticoids.
Cushing’s syndrome: cause, s/s
cause: Overuse and long term use of steroids.
s/s: Increased risk of infections, delayed wound healing, peptic ulcers, increased appetite, mood & personality changes, retention of sodium and water, Adrenal atrophy, osteoporosis, hypertension, acne, general obesity, redistribution of fat: (moon face, buffalo hump)
Cushing’s syndrome: pharmacotherapy
*Treat cause of excess corticosteroid
*Discontinue use of corticosteroid drugs
hypoglycemia: what is it?
*hormone and organs involved
*a very low level of glucose in the blood which can cause neurological side effects and arousal of sympathetic NS
*blood glucose is low so pancreas secretes glucagon. Liver breaks down glycogen, returning glucose to the blood. Homeostasis restored
hyperglycemia: what is it?
*hormone and organs involved
*Insufficient production or ineffective use of insulin causing an elevated blood glucose level
*blood glucose is high so pancreas secretes insulin. Cells take up glucose for energy/storage. Homeostasis restored.
what is Type 1 Diabetes Mellitus?
*Lack of insulin from pancreas, autoimmune disease
*Treatment: diet restrictions (carbs raise blood sugar/glucose levels) exercise (after exercise, your body doesn’t need as much insulin to process carbohydrates), insulin
*Weight loss, fatigue, Polyuria (excessive urination)
Polyphagia (increased hunger)
Polydipsia (increased thirst), fasting hyperglycemia on 2+ occasions
**Excess glucose attacks nerves = neuropathy
*they don’t heal well due to high blood sugars
labs to look at for diabetes
*Blood Sugar (normal = 70-110)
*Hemoglobin A1C (HA1C)
What’s Type 2 Diabetes Mellitus?
*Insulin resistance
Target cells become unresponsive to insulin; blood glucose levels rise, Pancreas secretes more insulin; hypersecretion leads to beta cell exhaustion and death (which eventually leads to deficiency in insulin secretion + insulin resistance)
*can be reversed w/ diet & exercise
*If untreated, type 2 DM results in same chronic conditions as type 1 DM
Rapid acting insulin
*aspart & lispro
*onset: less than 15 minutes (-30 minutes)
*peak: 1-3 hours (30-60 min. for lispro)
*duration: 3-5 hours
*SubQ
*give when food is in front of patient
Short acting insulin
*Regular insulin
*onset: 30 min - 60 min
*peak: 2-4 hours
*duration: 5-8 hours
*SubQ and IV (ONLY insulin given IV)
