endocrine 3 & 4

the following are characteristics for what condition:

•Strong, rapid HR

•dysrhythmias

•angina

•CNS stimulation

•nervousness

•insomnia

•rapid thoughts/speech

•muscle weaknesss/atrophy

•increased metabolism

•increased heat production

•increased body temp

•intolerance to heat

•warm & moist skin

•increased appetite

•wt loss

thyrotoxicosis

What is severe hypothyroidism in adults called?

myxedema

what are the common causes of hypothyroidism?

• Hashimoto’s thyroiditis (autoimmune thyroid destruction)

• Insufficient iodine

• Surgical removal of thyroid

• Destruction by radioactive iodine

How does hypothyroidism treatment change in pregnancy?

Increase replacement dose in 1st trimester

What is hypothyroidism in infants called?

Cretinism – requires replacement therapy

What is the most common cause of hyperthyroidism?

Graves’ disease – thyroid-stimulating immunoglobulins (TSIs)

What is Plummer’s disease?

Toxic nodular goiter – hyperthyroidism without exophthalmos

Treatment options for hyperthyroidism?

• Surgical removal of thyroid tissue

• Radioactive iodine destruction

• Suppress hormone synthesis (e.g., methimazole)

• Adjunct: beta-blockers, nonradioactive iodine

What triggers thyrotoxic crisis (thyroid storm)?

Severe thyrotoxicosis + major stressor (surgery, illness)

Symptoms of thyroid storm?

• Hyperthermia ≥105°F

• Severe tachycardia

• Restlessness, agitation, tremor

• Hypotension, heart failure

• Unconsciousness, coma

How is thyroid storm treated?

• Methimazole

• Beta-blocker

• Sedation

• Cooling

• Glucocorticoids

• IV fluids

What is the drug of choice for all hypothyroidism?

Levothyroxine (also Liothyronine, Liotrix, thyroid USP)

How does levothyroxine work?

Synthetic thyroid hormone: T4, T3, or combination

What are symptoms of overmedication with levothyroxine (thyrotoxicosis)?

• Anxiety, tachycardia, chest pain

• Nervousness, tremors, palpitations

• Abdominal cramps, fever

• Heat intolerance, diaphoresis, weight loss

• chronic overmedication: A fib, fracture risk

How should levothyroxine be taken?

Empty stomach, 30–60 min before first meal

What is the half-life of levothyroxine, and how long to reach steady state?

• 7 days half-life

• Steady state ~1 month

What should patients avoid when taking levothyroxine?

• Switching brands without provider approval

• Stopping therapy abruptly (lifelong therapy)

cautions & interactions with levothyroxine

•Caution in: Lactation, following MI, older adults, diabetes

Interactions:

•Increased risk for dysrhythmias

•With catecholamines – epinephrine, dopamine, dobutamine

•May need to increase doses of insulin and digoxin

•Block levothyroxine absorption

•Cholestyramine, colestipol, antiulcer medications, Ca, Fe, Mg, food (ncrease levothyroxine metabolism)

•Many antiseizure and antidepressant medications

•May increase anticoagulant effects of warfarin

•Monitor PT/INR

How do Methimazole and PTU work?

Block thyroid hormone synthesis
(Do not destroy existing hormones—takes 3–12 weeks for effect)

Methimazole & Propylthiouracil (PTU) uses

•Grave’s Disease, before thyroidectomy, with thyroid irradiation, thyrotoxic crisis

•Methimazole is 1^st choice

AE of Methimazole & Propylthiouracil (PTU)

•Hypothyroidism

•Agranulocytosis

•Liver injury / hepatitis  (PTU)

Which thionamide is preferred and why?

Methimazole = first choice (safer, once daily) & avoided in 1st trimester
But PTU preferred in 1st trimester pregnancy

Key nursing considerations for Methimazole & Propylthiouracil (PTU)

• Take same time daily, don’t stop abruptly

• Monitor VS, weight, TSH

• Watch for signs of hypo- and hyperthyroidism

• ↑ Anticoagulant effects → monitor PT/INR, aPTT

• May ↑ digoxin levels

When is caution needed for Methimazole & Propylthiouracil (PTU)

• Bone marrow suppression

• Immunosuppression

• Liver failure risk

What is radioactive iodine (I-131) used for?

• Hyperthyroidism

• Thyroid cancer

What is the half-life and time to full effect for radioactive iodine ( I-131) ?

• Half-life: 8 days

• Full effect: 2–3 months

• <1% radioactivity: ~56 days

What are the main adverse effects of radioactive iodine?

• Radiation sickness (nausea, vomiting, hematemesis, epistaxis)

• Bone marrow depression (anemia, leukopenia, thrombocytopenia)

• Hypothyroidism

Who should not receive radioactive iodine?

• Children

• Pregnancy

• Lactation

What are key nursing instructions for patients receiving radioactive iodine I-131?

• Avoid close contact with others 6 ft apart

• Increase fluid intake

• Dispose of body wastes per protocol

What is nonradioactive iodine (Lugol’s Solution) used for?

• Suppress thyroid hormone before surgery

• Treat thyrotoxicosis

What is iodism?

Toxicity from iodine:

• Metallic taste

• Sore teeth & gums

• Stomatitis

• Frontal headache

• Skin rash

• Severe GI distress (if progresses)

What should patients avoid while taking Lugol’s Solution?

• Iodized salt

• Seafood with iodine

• Potassium-sparing diuretics

• Potassium supplements

• ACE inhibitors

How should Lugol’s Solution be taken?

• Dilute in juice (improves taste)

• Take at the same time every day

• Increase fluid intake

What do the adrenal glands secrete?

• Glucocorticoids

• Mineralocorticoids

• Androgens

What functions do adrenal hormones regulate?

• Glucose availability

• Water & electrolyte balance

• Sex characteristics development

• Stress responses

What are the 4 main effects of glucocorticoids on carbohydrate metabolism?

1. Stimulate gluconeogenesis

2. Reduce peripheral glucose use

3. Inhibit glucose uptake by muscle & fat

4. Promote glycogen storage

What is the main mineralocorticoid and what is its function?

Aldosterone & influence renal processing of sodium, potassium, and hydrogen

What does aldosterone do?

• Conserves sodium & water

• Excretes potassium

• Regulates plasma volume

• regulated by RAAS

What harmful effects occur with high levels of aldosterone?

Cardiovascular damage

How is aldosterone regulated?

Renin–angiotensin–aldosterone system (RAAS)

causes of cushing’s syndrome

•Hypersecretion of adrenocorticotropic hormone (ACTH) by pituitary adenomas

•Hypersecretion of glucocorticoids by adrenal adenomas & carcinomas

•Administration of glucocorticoids in large doses and/or long-term

What are the key clinical features of Cushing’s syndrome?

• Hyperglycemia, glycosuria

• Hypertension, fluid/electrolyte disturbances

• Osteoporosis, muscle weakness, myopathy

• Hirsutism, menstrual irregularities

• Immunosuppression, thin skin, striae, easy injury

• Fat redistribution (moon face, buffalo hump)

• Psych symptoms

How is Cushing’s syndrome treated?

• Surgical removal of adrenal gland (adenoma/carcinoma)

• Replacement therapy (glucocorticoids + mineralocorticoids if bilateral adrenalectomy)

• Adjunct drug: Ketoconazole (Nizoral)

What is primary hyperaldosteronism?

Excessive secretion of aldosterone

What are the main causes of primary hyperaldosteronism?

• Aldosterone-producing adrenal adenoma

• Bilateral adrenal hyperplasia

What are the key clinical effects of primary hyperaldosteronism?

• Hypokalemia

• Metabolic alkalosis

• Hypertension

How is primary hyperaldosteronism treated?

• Surgery (if adenoma)

• Aldosterone antagonist (spironolactone)

common cause of Addison’s disease (primary adrenocortical insufficiency)

autoimmune destruction of adrenal tissue (80%), TB/other infections (15%)

clinical presentation of Addison’s disease (primary adrenocortical insufficiency)

•N/V/D, anorexia, weakness, emaciation, abdominal pain

•hyperkalemia, hyponatremia, hypotension

•Increased pigmentation of skin and mucous membranes

treatment of Addison’s disease (primary adrenocortical insufficiency)

•Replacement therapy with adrenocorticoids

•Hydrocortisone is drug of choice

•Pts should keep some always on hand

What causes secondary adrenocortical insufficiency?

Decreased secretion of ACTH.

What causes tertiary adrenocortical insufficiency?

Decreased secretion of CRH.

In secondary and tertiary insufficiency, which hormone secretion is decreased?

Glucocorticoid secretion.

What is the treatment for secondary and tertiary adrenocortical insufficiency?

Replacement therapy with a glucocorticoid (hydrocortisone).

What are the main symptoms of acute adrenal crisis?

Hypotension, dehydration, weakness, lethargy, nausea, vomiting, diarrhea.

What are common causes of acute adrenal crisis?

Adrenal or pituitary failure, or abrupt withdrawal of corticosteroids.

What are the main components of treatment for adrenal crisis?

Rapid replacement of fluid, salt, glucocorticoids, and glucose.

Describe the emergency management steps for adrenal crisis.

Hydrocortisone bolus, IV normal saline with dextrose, continuous hydrocortisone infusion (100 mg every 8 hours)

How does congenital adrenal hyperplasia present in girls?

Masculinization of external genitalia.

How does congenital adrenal hyperplasia present in boys?

Precocious (early) penile enlargement.

What growth patterns are seen in children and adults with congenital adrenal hyperplasia?

Children: Increased linear growth.
Adults: Diminished final adult height.

What is the treatment for congenital adrenal hyperplasia?

Glucocorticoid therapy (hydrocortisone, dexamethasone, or prednisone)

General statements about corticosteroid medications

•Same mechanism of action

•Same basic adverse effects (dose dependent)

•Indications & AE’s vary by dose, length of use, route of administration

•Well-absorbed, widely distributed to all body tissues

•Highly bound to plasma proteins

•Metabolized by liver

•Excreted by kidneys

•Pregnancy category C

•Secreted in breast milk

Adverse effect of corticosteroids

•Long-term therapy has the potential to cause serious AE’s in multiple body systems.

•Glucose intolerance : hyperglycemia, glucosuria

•Fluid/electrolyte disturbance

•Na+ & H2O retention, K+ loss

•HTN, Edema, Dysrhythmias

•Osteoporosis

•Adrenal Suppression

•Increase doses with stress

•Do not stop abruptly

•Peptic Ulcer / GI Discomfort

•Infection: Immunosuppression, masks S/S infection

•Cushing’s Syndrome

•CNS effects: Insomnia, anxiety, headache, vertigo, depression, confusion

•Cataracts

Preventing adverse effects of corticosteroids

•Lowest possible dose

•Alternate-day dosing to minimize adrenal atrophy

•For acute conditions

•Large doses, then gradually tapered until discontinued

•Administration

•Locally when possible, which rarely produces systemic adverse effects

Nursing Considerations for corticosteroids

•Monitor B/P, blood glucose, mood swings, weight gain

•Monitor for GI bleeding: black or tarry stools, coffee ground emesis, hypotension, lightheadedness

•Monitor for s/s of infection: fever, sore throat

•Monitor for osteoporosis: ensure adequate calcium & Vit D intake, weight-bearing exercises

•***DO NOT STOP ABRUPTLY****

•Take with food, milk, or a meal to prevent GI upset

what are Glucocorticoids (hydrocortisone, prednisone, dexamethasone) used for

•For adrenal insufficiency  (low dose)

•Arthritis, asthma, allergies, transplant rejection, IBD, skin conditions, cancer

caution with Glucocorticoids (hydrocortisone, prednisone, dexamethasone)

Recent MI, gastric ulcer, HTN, kidney disorder, osteoporosis, DM, cirrhosis, hypothyroid, myasthenia gravis, glaucoma, seizures

interactions with Glucocorticoids (hydrocortisone, prednisone, dexamethasone)

•Oral antidiabetics

•NSAIDs, acetaminophen, EtOH

•vaccines

what is Mineralocorticoid (fludrocortisone) used for

Addison’s disease, Primary hypoaldosteronism, Congenital adrenal hyperplasia

AE of Mineralocorticoid (fludrocortisone)

•Fluid & Sodium Retention

•Hypertension

•Edema

•Cardiac enlargement

•Hypokalemia

nursing considerations for Mineralocorticoid (fludrocortisone)

•Pt teaching

•S/S fluid & sodium retention, potassium loss

Interactions:

•Barbiturates & phenytoin  (reduce effects of mineralocorticoid)

•Insulin, sulfonylureas  (reduced glucose control)