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Exam 2 · Week 5 · Standalone study page

M5 · Endocrine Disorders

This page keeps all of the original course information, while reducing the decision to one module: hormone excess, deficiency and crisis patterns.

🧩 30 study chunks🧬 6 disorders · six sections each🎯 16 practice questions⭐ exam spotlight📱 Foldy-friendly
▸M5Endocrine DisordersWeek 5
📚 Reading: Hinkle ch. 45
💡 The one idea

Compare the gland hormone with its stimulating hormone and the diagnosis appears.

Low T4 + high TSH → the thyroid failed (primary). Low T4 + low TSH → the pituitary failed (secondary). Both moving the same way means the problem is upstream.

 HYPOthyroidHYPERthyroid
MetabolismEverything slowsEverything speeds up
WeightGains, despite poor appetiteLoses, despite eating more
TemperatureCold intoleranceHeat intolerance, sweating
Heart rateBradyTachy, atrial fibrillation
Bowels / moodConstipation, depression, fatigueDiarrhea, anxiety, insomnia
DistinctiveDry skin, hair loss, myxedemaExophthalmos (Graves), goitre
CrisisMyxedema coma — hypothermia, ↓LOCThyroid storm — fever, HR >140
⭐ Levothyroxine teaching — four points, all testable
  • Take in the morning, on an empty stomach, 30–60 min before food
  • Lifelong — do not stop when feeling better
  • Report chest pain or palpitations — the dose is too high
  • Separate from calcium, iron and antacids by 4 hours — they block absorption
 SIADH — “soaks”Diabetes insipidus — “drains”
ADHToo muchToo little
UrineScant, concentratedLiters of dilute, pale urine
Serum sodiumLOW (dilutional)HIGH
WeightGains, fluid retainedLoses, dehydrated
TreatmentFluid restriction, hypertonic saline if severeDesmopressin, replace fluids
🚨 Addison vs Cushing — opposite ends of cortisol

Addison’s (too little) — hypotension, hyperkalemia, hyponatremia, hypoglycemia, weight loss, bronze skin. Crisis is a shock emergency: fluids + steroids now.

Cushing’s (too much) — hypertension, hypokalemia, hypernatremia, hyperglycemia, moon face, buffalo hump, thin skin, easy bruising.

Steroids are always tapered, never stopped abruptly - the adrenals have atrophied.

⭐ High-yield — what the exam actually asks

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  • Addison's = low cortisol and aldosterone → low BP, low glucose, low sodium, high potassium, hyperpigmentation, weight loss. Cushing's is the mirror image plus moon face, buffalo hump, central obesity, thin limbs.
  • Addisonian crisis order: fluids + dextrose first, then IV hydrocortisone. Fix the hyperkalemia with insulin + D50.
  • Cushing's: taper steroids, never stop abruptly — exogenous steroids suppress the body's own cortisol. Sodium restriction, K-sparing diuretics.
  • Pheochromocytoma: catecholamine-secreting adrenal tumor → severe HTN, headache, diaphoresis, tachycardia. Alpha blockers before surgery.
  • DI = "Dry Inside." Too little ADH → massive dilute urine, low specific gravity, dehydration, low BP, high sodium. Fluids + desmopressin.
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  • SIADH = "Soaked Inside." Too much ADH → scant concentrated urine, high specific gravity, overload, high BP, low sodium. Fluid restriction + diuretics + sodium. Low sodium means seizure precautions.
  • Graves'/hyperthyroid: weight loss with a big appetite, heat intolerance, tachycardia, tremor, diarrhea. Methimazole (immunosuppression) or PTU (hepatotoxicity), or radioactive iodine.
  • Thyroid storm: high fever, severe tachycardia, delirium → fluids + dextrose first, then beta blockers for the cardiac symptoms plus PTU/methimazole, plus cooling.
  • Hashimoto's/hypothyroid: fatigue, bradycardia, constipation, cold intolerance, depression. Airway is the priority — lethargic with poor respiratory effort. Myxedema coma: fluids + dextrose first, then IV levothyroxine plus warming.
  • Overtreated hypothyroidism looks exactly like hyperthyroidism — agitation, insomnia, sweating.

🎧 From the LSC exam-prep recording

What the faculty actually said in the review session for this week — their numbers, their worked calculations, their priority rulings. On an exam, this beats the textbook.

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  • Their thyroid model: a dial from 0 to 10, normal sits at 5. Hypo = dial down, every organ slows. Hyper = dial up. They want pattern-matching, not memorized symptom lists — "find the pattern and do not deviate from it."
  • The hypothyroid highlight, cues they scored: tired for weeks, +10 lb without a diet change, dry skin and brittle hair, feels cold most of the time, HR 56, temp 97.2 °F. Constipation would count too. "Denies heat intolerance" was NOT scored — absence of a hyper sign only means normal.
  • Hypo and hyper are opposites in everything except three: fatigue, insomnia and hair loss appear in both. Learn one list and invert it.
  • Primary hypothyroidism = high TSH with low T3/T4 (the gland has failed). Secondary = low TSH with low T3/T4 (the pituitary has). Hashimoto's is roughly 18 of every 20 primary cases, and overwhelmingly female.
  • Hypothyroid symptoms + high TSH + low T4 → levothyroxine. Methimazole would drive them further down; vasopressin is ADH; hydrocortisone is for Addison's.
  • Levothyroxine overdose is iatrogenic hyperthyroidism. Scored findings: temp 104.9 °F, HR 125, RR 42, restlessness, tremor, heat intolerance, weight loss. Not cold intolerance, not constipation — it would be diarrhea.
  • Interventions for that overdose: beta blocker, cooling blanket, low-stimulation room, hold the next dose and notify. Antithyroid drugs are useless here — the excess T4 is already circulating, not being made. Levothyroxine is started low and titrated slowly, especially in older adults.
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  • "DI = dry inside, SIADH = soaked inside." Their other hook: ADH is the anti-pee hormone — no anti-pee means a lot of pee.
  • "Diabetes" is just Latin for a lot of urine. Diabetes insipidus has nothing to do with glucose. On the fluid deprivation test the DI finding is dilute urine continuing despite the restriction; a normal person concentrates it.
  • In DI the serum sodium climbs — you are losing water, not salt. DI is genuinely rare and usually follows brain injury. Stop a fluid deprivation test for hypotension, tachycardia, dizziness or severe dehydration; you have your answer already.
  • SIADH plan of care, their SATA: seizure precautions, daily weights, urine specific gravity, regular neuro assessments. Not a low-potassium diet — potassium is not part of this picture, and they said to leave it rather than guess. Their case sodium was 120.
  • The SIADH story to recognize: cough, weight loss, hemoptysis and a sodium of 120 = a lung cancer secreting ADH. Brain injury and meningitis can do it too.
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  • Cushing's is three hormones, not one: cortisol (breaks down muscle and fat, releases liver sugar → hyperglycemia), aldosterone (holds sodium, dumps potassium → hypertension and hypokalemia) and androgens (hirsutism in women).
  • Cushing's diet: potassium-rich, sodium-restricted, high protein. Not high calorie — steroids stimulate appetite and they are already gaining. Not protein-restricted — cortisol is already breaking down muscle.
  • Addison's diet is the exact mirror: high sodium, low potassium. No aldosterone means salt and water are lost and potassium is retained.
  • Their point about frequency: Cushing's is usually something we cause with prednisone and dexamethasone, so it is common and worth knowing cold — moon face, central obesity, purple striae, thin bruising skin, osteoporosis, new diabetes. Addison's is far rarer.
  • Dexamethasone suppression test: cortisol that stays elevated confirms Cushing's. It is confirmatory because a plain serum cortisol swings high in the morning and low at night.
  • Adrenal crisis: hypotension, confusion, hyperkalemia, plus severe abdominal pain, vomiting and diarrhea (which is why every oral option is wrong). The keyed answer was IV hydrocortisone, but both instructors said fluids first, steroids second — steroids take days to raise a pressure. Do not take orthostatics on a client who is already hypotensive, and do not default to high-flow oxygen when nothing respiratory is described.
  • Pheochromocytoma releases catecholamines — epinephrine and norepinephrine — in bursts: episodic severe hypertension, palpitations, sweating, flushing, then it settles. Treatment is an alpha blocker, the "-osin" drugs (doxazosin, terazosin), because the problem is vasoconstriction. Beta blockers work on the heart, not the vessels. Watch first-dose severe hypotension; the same class treats BPH. Cure is adrenalectomy — one gland is plenty.
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  • Post-thyroidectomy priority is voice change (recurrent laryngeal nerve). But if neck swelling is on the list, it wins — that is an airway. Then hypocalcemia from the parathyroids sitting behind the gland — Chvostek, Trousseau, carpopedal spasm. Never encourage neck extension — that is how you dehisce the wound.
  • Thyroid storm bow-tie vitals: HR 142, BP 168/88, RR 22, SpO₂ 94% RA, temp 103.8 °F, vomiting, diarrhea, new seizures. Priorities: beta blocker + cooling.
  • Two test-taking rules they gave here: if two options say essentially the same thing, both are wrong (they cannot both be right). If two options are exact opposites, one of them is usually the answer.
  • Calc: 5 mcg/kg/min, 132 lb, supplied 100 mg/100 mL → 18 mL/hr. Their mantra: "2.2 always goes with the pounds." Dimensional analysis, formula or ratio — pick one and get the same answer every time.

⚠️ Exam traps

  • Addison's low / Cushing's high on nearly every parameter except potassium, which inverts. That one flip is the whole question.
  • DI vs SIADH: sort it by urine concentration and serum sodium and it falls out immediately.
  • Both thyroid crises start with fluids + dextrose before the definitive drug.

⚠️ What it turns into — the complication for each one

The disorder cards below run definition, causes, signs, diagnostics, management and nursing. This is the part they do not have, and it is where the exam lives: so what happens if this is missed or left? Each of these has a crisis state at the far end of it, and the crisis is what the exam asks about.

DisorderWhat it turns into
Hypothyroidism and myxedema comaMyxedema coma — hypothermia, hypotension, hypoventilation and falling consciousness. Heart failure, pericardial effusion, and dangerous sensitivity to sedatives and opioids
Hyperthyroidism and thyroid stormThyroid storm — fever, extreme tachycardia, agitation, and death if untreated. Atrial fibrillation, heart failure, osteoporosis, and exophthalmos leaving the cornea exposed and ulcerating
Thyroidectomy careAirway obstruction from hemorrhage or edema — why a tracheostomy set stays at the bedside. Hypocalcaemia and tetany if the parathyroids were bruised or removed: check Chvostek and Trousseau. Laryngeal nerve damage causing hoarseness, and thyroid storm
Cushing syndromeHypertension, hyperglycaemia and diabetes, osteoporosis with fragility fractures, infection with the usual signs masked by the steroid, poor wound healing, GI bleeding, and mood change or psychosis
Addison disease and adrenal crisisAdrenal crisis — profound hypotension, hyperkalaemia, hyponatraemia, hypoglycaemia, shock and cardiac arrest. Triggered by stress, infection, or stopping the steroid abruptly
SIADH and diabetes insipidusSIADH: hyponatraemia causing cerebral edema and seizures. DI: severe dehydration, hypernatraemia and hypovolaemic shock. Opposite problems, opposite fixes — get them the wrong way round and you make it worse

🩸 The endocrine disorders, section by section

Thyroid first, then the adrenals, then the two opposite ADH problems. Almost every one of these is a pair — too much and too little of the same hormone — so learn them together.

Hypothyroidism and Myxedema ComaOpenClose
Definition and Overview

Too little thyroid hormone, so everything in the body runs slow. Primary hypothyroidism is a failure of the thyroid gland itself and is by far the commonest; secondary hypothyroidism is a failure of the pituitary to make TSH. Myxedema coma is the extreme, decompensated end — hypothermia, hypotension, hypoventilation and altered consciousness — and it is a medical emergency.

Causes and Risk Factors

Hashimoto autoimmune thyroiditis is the leading cause in iodine-sufficient countries. Then treatment for hyperthyroidism — thyroidectomy or radioactive iodine — iodine deficiency worldwide, amiodarone and lithium, external radiation to the neck, and pituitary disease. More common in women and with increasing age. Myxedema coma is usually precipitated by infection, cold, surgery, sedatives or stopping the replacement.

Clinical Manifestations

Fatigue, cold intolerance, weight gain, constipation, dry coarse skin, brittle hair and hair loss including the outer third of the eyebrow, bradycardia, hoarseness, slowed thinking and depression, heavy menstrual periods, and delayed deep tendon reflexes. Non-pitting edema of the face, hands and periorbital tissue. In older adults it is easily mistaken for depression or dementia. Myxedema coma adds hypothermia without shivering, hypotension, hypoglycaemia, hyponatraemia, hypoventilation with CO2 retention and stupor — and it is fatal if missed.

Assessment and Diagnostic Findings

TSH is the screening test and the one that matters. In primary hypothyroidism TSH is high and free T4 is low. A high TSH with normal T4 is subclinical disease. In secondary disease both are low. Thyroid peroxidase antibodies confirm Hashimoto. Check lipids (cholesterol is high), sodium, glucose, CBC for anemia, and an ECG for bradycardia and low voltage. Recheck TSH about 6 weeks after any dose change.

Medical Management

Levothyroxine, once daily, for life, titrated to a normal TSH. Start low and go slowly in older adults and in anyone with coronary disease, because raising the metabolic rate too quickly can precipitate angina, infarction or a dysrhythmia. Myxedema coma is treated in intensive care with intravenous levothyroxine, intravenous corticosteroids, passive warming, fluids and ventilatory support, and by treating the precipitating cause.

Nursing Management and Client Education

Teach that levothyroxine is taken on an empty stomach, first thing in the morning, with water, at least 30 to 60 minutes before food and other drugs, and that calcium, iron, antacids and coffee block its absorption — separate them by at least 4 hours. It is lifelong and must not be stopped when the client feels well, and doses must never be doubled up to catch up. Teach the signs of too much — palpitations, tremor, weight loss, insomnia, heat intolerance — and to report chest pain immediately. Warm the client with blankets rather than a heating pad, since the skin is fragile and sensation blunted. Expect constipation and manage it with fiber and fluids. Take care with sedatives and opioids, which this client is extremely sensitive to. Be patient with the slowed thinking and give instructions in writing.

Hyperthyroidism and Thyroid StormStorm is an emergencyOpenClose

🖼️ InfographicsHyperaldosteronism & Pheochromocytoma

Definition and Overview

Too much thyroid hormone, so everything runs fast. Graves disease is the commonest cause: an autoimmune antibody that stimulates the TSH receptor, driving the gland and also causing the eye disease. Thyroid storm (thyrotoxic crisis) is an abrupt, life-threatening exaggeration of it — fever, tachycardia, agitation and organ failure.

Causes and Risk Factors

Graves disease, toxic multinodular goitre, a toxic adenoma, thyroiditis, excessive levothyroxine, and amiodarone, which can cause either too much or too little. Far more common in women, typically 20 to 40. Thyroid storm is precipitated by infection, surgery (especially thyroid surgery on an unprepared client), trauma, childbirth, iodine contrast or abrupt withdrawal of antithyroid drugs.

Clinical Manifestations

Weight loss despite a big appetite, heat intolerance, sweating, tremor, palpitations, tachycardia and atrial fibrillation, anxiety and irritability, insomnia, frequent stools, and warm moist skin. Graves adds a diffuse goitre and exophthalmos — protruding eyes with lid lag, which does not resolve when the hormone is corrected. Thyroid storm: temperature above 102°F (38.9°C), heart rate over 130, severe hypertension then hypotension, delirium, vomiting and diarrhea — treat it before waiting for confirmatory labs.

Assessment and Diagnostic Findings

TSH is low and free T4 and T3 are high. Thyroid-stimulating immunoglobulin confirms Graves. Radioactive iodine uptake scan distinguishes Graves and toxic nodules (high uptake) from thyroiditis (low uptake). ECG for atrial fibrillation. Weight, vital signs, sleep and, for Graves eye disease, visual acuity and corneal integrity.

Medical Management

Antithyroid drugs — methimazole, or propylthiouracil in the first trimester of pregnancy and in thyroid storm. Beta blockers for the tachycardia, tremor and anxiety while waiting for those to work. Then definitive treatment: radioactive iodine, which usually leaves the client hypothyroid and needing lifelong replacement, or thyroidectomy. In storm: propylthiouracil first, then iodine at least an hour after it, plus beta blockers, corticosteroids, cooling without aspirin, fluids and treatment of the trigger.

Nursing Management and Client Education

Cool, quiet, calm room — noise and heat make this client worse. High-calorie, high-protein diet with several meals and snacks; no caffeine. Daily weight and vital signs. For the eyes: artificial tears, sunglasses, elevate the head of the bed, and tape the lids at night if they do not close. On antithyroid drugs, teach that agranulocytosis is the dangerous side effect — report sore throat, fever or mouth ulcers at once and stop the drug — and watch for jaundice. Never use aspirin to cool a client in thyroid storm; it displaces thyroid hormone from its binding protein and makes the crisis worse. After radioactive iodine, teach the radiation precautions for a few days: sleep alone, flush twice, separate laundry and utensils, and avoid close contact with children and pregnant people. After thyroidectomy, see the surgical card below.

Thyroidectomy CareAirway and calciumOpenClose
Definition and Overview

Surgical removal of part or all of the thyroid, for cancer, a large goitre causing compression, or hyperthyroidism that drugs cannot control. The two things that make this operation dangerous are anatomical: the airway lies right underneath it, and the parathyroid glands sit on the back of it.

Causes and Risk Factors

Risk of complication rises with a large vascular gland, an inadequately prepared hyperthyroid client, previous neck surgery or radiation, and total rather than partial removal. Postoperative hypocalcaemia is much more likely after a total thyroidectomy.

Clinical Manifestations

What to watch for after surgery: hemorrhage and a neck haematoma — check behind and under the neck, where blood pools by gravity; airway obstruction from swelling or haematoma, showing as stridor, a choking sensation or difficulty breathing; laryngeal nerve damage, showing as hoarseness or a weak voice; hypocalcaemia from parathyroid injury, showing as tingling around the mouth and in the fingers, muscle twitching, and positive Chvostek and Trousseau signs, progressing to tetany and laryngospasm; and thyroid storm.

Assessment and Diagnostic Findings

Preoperatively, the client should be euthyroid before going to theatre — check that the antithyroid drugs and any iodine preparation were actually given. Postoperatively: voice check every hour, respiratory assessment, dressing and neck inspection front and back, vital signs, and serum calcium. Assess for Chvostek (facial twitch on tapping the cheek) and Trousseau (carpal spasm with a blood pressure cuff) signs.

Medical Management

Calcium gluconate for symptomatic hypocalcaemia, then oral calcium and vitamin D, sometimes permanently. Lifelong levothyroxine after a total thyroidectomy. Evacuation of a haematoma in theatre, or at the bedside if the airway is closing. Analgesia and voice rest.

Nursing Management and Client Education

Keep a tracheostomy tray, oxygen and suction at the bedside — that is the standard, and it is a common exam item. Semi-Fowler's position, supporting the head and neck with pillows and hands when moving, and no hyperextension of the neck. Ask the client to speak every hour; increasing hoarseness or a weak voice must be reported. Check the back of the neck and the pillow for blood. Report tingling around the mouth immediately — that is hypocalcaemia and it precedes laryngospasm. Do not let a client with a tight, swelling neck wait for the next round — a haematoma here closes the airway. Teach voice rest, humidification, wound care, and that lifelong hormone replacement after total removal is not negotiable.

Cushing SyndromeOpenClose

🖼️ InfographicsAddison's vs. Cushing's

Definition and Overview

Too much cortisol. Cushing syndrome is the clinical picture from any cause; Cushing disease specifically means a pituitary adenoma secreting ACTH. Cortisol raises glucose, breaks down protein, redistributes fat centrally, retains sodium and water, wastes potassium and suppresses immunity — and every sign follows from that list.

Causes and Risk Factors

The commonest cause by far is exogenous: long-term corticosteroid therapy for asthma, COPD, autoimmune disease or transplantation. Endogenous causes are a pituitary adenoma (Cushing disease), an adrenal tumor, or ectopic ACTH from a tumor, classically small cell lung cancer.

Clinical Manifestations

Central obesity with thin arms and legs, a rounded 'moon' face, a dorsocervical fat pad, thin fragile skin that bruises easily, purple striae on the abdomen, poor wound healing, muscle wasting and weakness in the proximal limbs, osteoporosis and fractures, hypertension, hyperglycaemia, hirsutism and menstrual irregularity, and mood swings, depression or psychosis. Labs show high sodium, low potassium and high glucose. Infection may present without fever, because the cortisol suppresses the inflammatory response that produces one.

Assessment and Diagnostic Findings

24-hour urinary free cortisol, late-night salivary cortisol, and the low-dose dexamethasone suppression test to establish excess cortisol. Then plasma ACTH to find the source: high or normal ACTH points to a pituitary or ectopic source, suppressed ACTH to an adrenal one. Imaging of the pituitary or adrenals follows. Monitor glucose, electrolytes, blood pressure, weight, bone density and skin integrity.

Medical Management

Remove the cause. Transsphenoidal resection of a pituitary adenoma, adrenalectomy for an adrenal tumor, or treatment of the ectopic tumor. If the cause is prescribed steroids, taper to the lowest effective dose — never stop abruptly — and consider alternate-day dosing. Drugs such as ketoconazole, metyrapone or mifepristone block cortisol when surgery is not possible. Lifelong glucocorticoid replacement after bilateral adrenalectomy.

Nursing Management and Client Education

Protect the skin and the bones: careful handling, minimal tape, pressure relief, assistance with mobility, and fall prevention, because these bones fracture easily. Protect against infection: hand hygiene, screen visitors, and report any subtle change — malaise, a slightly raised pulse, a small wound that is not healing — because there may be no fever. Diet high in protein, calcium and vitamin D, and low in sodium and refined carbohydrate. Daily weight and blood pressure, and monitor glucose. Acknowledge the appearance changes directly; they distress people deeply and are largely reversible when the cause is treated. For clients on long-term steroids: never stop suddenly, carry medical identification, take with food, and report black stools, mood change or signs of infection. After surgery, teach lifelong replacement and sick-day dose increases.

Addison Disease and Adrenal CrisisCrisis is an emergencyOpenClose
Definition and Overview

Too little cortisol and aldosterone. In primary adrenal insufficiency (Addison disease) the adrenal cortex itself fails, so both hormones are lost and ACTH rises. In secondary insufficiency the pituitary fails or steroids have been withdrawn, so cortisol is lost but aldosterone is largely preserved. Adrenal (Addisonian) crisis is acute, profound deficiency — shock, hypoglycaemia and hyperkalaemia — and it kills quickly.

Causes and Risk Factors

Primary: autoimmune destruction in most cases, then tuberculosis, adrenal hemorrhage, metastases and HIV-related infection. Secondary: abrupt withdrawal of long-term corticosteroids is the commonest cause of all, plus pituitary tumors and surgery. Crisis is precipitated by infection, trauma, surgery, dehydration, vomiting, or stopping replacement steroid — or by failing to increase it during illness.

Clinical Manifestations

Fatigue and profound weakness, anorexia and weight loss, nausea, vomiting, abdominal pain, hypotension and orthostatic dizziness, salt craving, and hypoglycaemia. Primary disease adds hyperpigmentation — bronzing of the skin, palmar creases, scars, gums and pressure areas — because the high ACTH stimulates melanin; that sign is absent in secondary disease. Labs: low sodium, high potassium, low glucose, high calcium. Crisis: sudden severe hypotension and shock, high fever, vomiting, severe abdominal or flank pain and confusion — give hydrocortisone before the confirmatory test comes back.

Assessment and Diagnostic Findings

Early-morning serum cortisol, low, with the ACTH level separating primary (high) from secondary (low). The ACTH (cosyntropin) stimulation test confirms it: in Addison disease cortisol fails to rise. Electrolytes, glucose, renal function, CBC and adrenal imaging. Continuous vital signs, orthostatic blood pressure, daily weight and strict intake and output.

Medical Management

Lifelong replacement: hydrocortisone for cortisol and, in primary disease, fludrocortisone for aldosterone, with doses doubled or tripled during illness, injury or surgery. Adrenal crisis: immediate intravenous hydrocortisone, plus rapid volume replacement with normal saline with dextrose, correction of hyperkalaemia and hypoglycaemia, and treatment of the precipitating cause.

Nursing Management and Client Education

In crisis, hydrocortisone and fluids come first, and everything else waits. Continuous monitoring, cardiac monitoring for the hyperkalaemia, hourly urine output, and minimising every stress in the environment. Then the teaching, which is what keeps this client alive: the replacement steroid is never stopped and never missed — stopping it causes the crisis. Teach sick-day rules: double or triple the dose for fever, vomiting, injury or dental work, and go to hospital if unable to keep tablets down. Teach the client and a family member to give intramuscular hydrocortisone at home, and make sure the emergency kit exists and is in date. Medical identification bracelet, always. Teach that a liberal salt intake is allowed and often needed, to weigh daily, to rise slowly because of the orthostatic drop, and to tell every clinician, including the dentist, about the diagnosis before any procedure.

SIADH and Diabetes InsipidusOppositesOpenClose

🖼️ InfographicsSIADH vs. DI (Diabetes Insipidus)SIADH vs. DI IIDiabetesDiabetes IISIADH 2DI - Diabetes Insipidus 2

Definition and Overview

Two opposite disorders of antidiuretic hormone, and holding them side by side is the easiest way to keep them straight. SIADH is too much ADH: water is retained, so the client is fluid-overloaded and dilute — concentrated urine, dilute blood, low sodium. Diabetes insipidus is too little ADH (or kidneys that ignore it): water pours out, so the client is dehydrated and concentrated — dilute urine, concentrated blood, high sodium.

Causes and Risk Factors

SIADH: small cell lung cancer and other tumors, head injury, stroke, meningitis, pneumonia, and drugs — carbamazepine, SSRIs, chemotherapy agents, desmopressin. DI: central DI from head trauma, pituitary surgery, tumor or infection; nephrogenic DI from lithium, hypercalcaemia, hypokalaemia and chronic kidney disease.

Clinical Manifestations

SIADH: urine output down and dark, weight up with no edema, and the symptoms of hyponatraemia — headache, nausea, muscle cramps, confusion, and at low levels seizures and coma. DI: enormous volumes of pale dilute urine — 4 to 20 liters a day — with intense thirst, especially for cold water, nocturia, weight loss and the signs of dehydration: tachycardia, hypotension, dry mucous membranes, poor turgor. A client who cannot get to water — unconscious, restrained, confused or very young — becomes dangerously hypernatraemic fast.

Assessment and Diagnostic Findings

The lab pattern is the answer to most questions. SIADH: serum sodium and osmolality low, urine sodium and osmolality high, urine specific gravity above 1.030. DI: serum sodium and osmolality high, urine osmolality low, urine specific gravity below 1.005. A water deprivation test distinguishes central from nephrogenic DI. For both: strict hourly intake and output, daily weight at the same time on the same scale — weight is the most reliable measure of fluid balance, neurological checks, and vital signs.

Medical Management

SIADH: fluid restriction, often 800–1000 mL a day, is the mainstay; hypertonic 3% saline for severe symptomatic hyponatraemia, given slowly; loop diuretics; tolvaptan; and treatment of the underlying cause. DI: desmopressin for central DI, orally, intranasally or by injection; free access to water; and for nephrogenic DI, stopping the offending drug plus thiazide diuretics and a low-sodium diet.

Nursing Management and Client Education

SIADH: enforce the fluid restriction and make it liveable — spread the allowance across the day, use ice chips (counted as half their volume), hard sweets and frequent mouth care. Daily weight, seizure precautions when sodium is low, and frequent neurological checks. Correct hyponatraemia slowly — raising sodium too fast causes irreversible brain injury. DI: keep water within reach at all times and replace losses; watch for a client who cannot ask for a drink. Daily weight, hourly output, and report urine output over 200 mL/hr for two consecutive hours. Teach desmopressin technique and that it is lifelong, to weigh daily, to wear medical identification, and to report either extreme — sudden weight gain and headache means too much drug, and a return of thirst and huge urine volumes means too little.

🧠 Mind maps 4

One per disorder, built from the structure of your ATI chapter.

Pituitary Disorders
🎯 Who gets it
  • Acromegaly risk: genetics, onset in the 30s-40s, and pituitary adenomas.
  • Central DI (AVP deficiency) risk: head injury, brain tumor, CNS infection, or autoimmune disease.
  • Nephrogenic DI (AVP resistance) risk: hereditary factors, kidney disease, hypercalcemia, hypokalemia.
  • Lithium and demeclocycline are common drug causes of nephrogenic DI.
👀 What you see
  • Acromegaly: enlarged hands/feet, deepened voice, coarse facial features, thick lips, large nose.
  • Acromegaly: headaches, visual field deficits, carpal tunnel syndrome, joint pain, hyperhidrosis.
  • Acromegaly can also cause hypertension, cardiac murmur, and hyperglycemia.
  • DI mnemonic DILUTE: dehydration, increased serum osmolality, low urine osmolality, diuresis, thirst, electrolyte imbalance.
🧪 What confirms it
  • Acromegaly screening: elevated IGF-1 confirms excess growth hormone.
  • GH suppression test: acromegaly shows little or no GH drop after a glucose load.
  • DI urine: specific gravity <1.005, osmolality <300 mOsm/kg after water deprivation.
  • DI: urine sodium <40 mg/day; blood osmolality >300 mmol/kg, sodium >145 mEq/L.
🩺 What you do
  • GH suppression test: recheck GH and glucose at 10, 60, 120 min after the glucose dose.
  • Client drinks only water for 6-8 hr before GH suppression testing.
  • Assess self-concept related to acromegaly's physical changes; explain treatment options.
  • DI: track LOC, vital signs, strict I&O, specific gravity, and daily weight.
💊 Drugs
  • Acromegaly first line: somatostatin analogs (octreotide, lanreotide, pasireotide) suppress GH release.
  • Bromocriptine or cabergoline (dopamine agonists) also lower GH; watch for psychosis or fibrosis.
  • Pegvisomant (second line) blocks GH receptors and cuts IGF production.
  • Desmopressin (DDAVP) treats DI via intranasal, oral, subQ, or IV routes to cut urine output.
💬 What you teach
  • Acromegaly: hormone replacement therapy may be lifelong; report vision or mental status changes.
  • Acromegaly: avoid lifting or straining postop; report nasal bleeding or watery discharge.
  • Clients with sleep apnea should skip CPAP use right after hypophysectomy.
⚠️ What goes wrong
  • Untreated SIADH can cause water intoxication, cerebral or pulmonary edema, and severe hyponatremia.
  • Without prompt treatment, these SIADH complications can progress to coma and death.
  • Watch for lung crackles, distended neck veins, and neuro changes signaling complications.
  • Maintain seizure precautions and monitor blood sodium closely in SIADH.

Read left to right: who gets it → what you see → what confirms it → what you do → what goes wrong. Cover a column and rebuild it out loud.

Hypothyroidism
🎯 Who gets it
  • Women develop hypothyroidism about 7 times more often than men.
  • Risk rises with older age and history of thyroid surgery.
  • Amiodarone, lithium, immune modulators, and chemotherapy can trigger hypothyroidism.
  • Inadequate iodine intake and autoimmune disease raise hypothyroidism risk.
👀 What you see
  • Classic signs: fatigue, cold intolerance, constipation, and weight gain.
  • Mood/cognitive changes: depression, anxiety, psychosis, and trouble concentrating.
  • Joint stiffness, muscle pain, and carpal tunnel syndrome can occur.
  • Cardiac: hypotension, bradycardia, elevated diastolic BP, dysrhythmias, prolonged QT, and heart failure risk.
🧪 What confirms it
  • T4 is decreased; TSH rises in primary hypothyroidism but is normal or low in secondary/tertiary.
  • Cholesterol, lipids, liver enzymes, and glucose are typically elevated.
  • Antithyroid antibodies may be present; hemoglobin and hematocrit are often decreased.
  • Thyroid scan shows low radioactive iodine uptake in hypothyroidism.
🩺 What you do
  • Monitor heart rate, blood pressure, ECG, and weight closely in hypothyroidism.
  • Increase activity gradually with rest periods to limit myocardial oxygen demand.
  • Apply anti-embolism stockings and elevate legs to support venous return.
  • Encourage coughing and deep breathing to prevent pulmonary complications.
💊 Drugs
  • Levothyroxine is the most commonly prescribed synthetic thyroid hormone replacement.
  • Levothyroxine increases warfarin's effect and raises insulin or digoxin needs.
  • Start levothyroxine at a low dose in older adults or CAD clients to avoid coronary ischemia.
💬 What you teach
  • Report chest pain right away; treatment with thyroid hormone is typically lifelong.
  • Never change levothyroxine's timing, dose, or brand without consulting the provider.
  • Lab work is repeated every 4-6 weeks until thyroid hormones stabilize.

Read left to right: who gets it → what you see → what confirms it → what you do → what goes wrong. Cover a column and rebuild it out loud.

Cushing Disease and Syndrome
🎯 Who gets it
  • Most common in women aged 50-60 years.
  • Cushing disease (endogenous): adrenal hyperplasia, adrenocortical carcinoma, or an ACTH-secreting pituitary tumor.
  • Lung, GI, or pancreatic tumors can also secrete ACTH and cause Cushing disease.
  • Cushing syndrome (exogenous): long-term glucocorticoids for transplant, chemo, autoimmune disease, asthma, or allergies.
👀 What you see
  • Classic build: moon face, truncal obesity, and a buffalo hump (fat on the back of neck).
  • Skin: thin, fragile, easily bruised, with purple-red striae on abdomen, arms, thighs.
  • Infection risk rises but without usual fever, swelling, or redness (blunted immune response).
  • Hypertension, gastric ulcers, and hyperglycemia are common findings.
🧪 What confirms it
  • Elevated cortisol (blood, urine, or saliva) without illness or stress confirms Cushing's.
  • Labs show low potassium, low lymphocytes, and high blood glucose and sodium.
  • ACTH is elevated with pituitary hypersecretion but decreased with adrenal-source disease.
  • Dexamethasone suppression test: cortisol stays high (nonsuppressed) in Cushing disease.
🩺 What you do
  • Monitor daily weight, I&O, vital signs, and ECG for fluid overload.
  • Watch for fluid overload signs: swelling, neck vein distention, breathlessness, high BP, fast pulse.
  • Protect skin and prevent falls; reposition at least every 2 hr; use surgical asepsis for dressings.
  • Ketoconazole: monitor liver enzymes for toxicity (yellow sclera, dark urine).
💊 Drugs
  • Cushing syndrome treatment: taper glucocorticoids gradually and manage symptoms.
  • Ketoconazole (an antifungal) inhibits adrenal corticosteroid synthesis at high doses.
  • Mitotane selectively destroys adrenocortical cells to treat inoperable adrenal carcinoma; watch for shock.
  • Hydrocortisone replaces cortisol after Cushing treatment and is often paired with ketoconazole.
💬 What you teach
  • Report weight gain over 2 lb in 24 hr or 3 lb in a week.
  • Eat foods high in calcium and vitamin D; avoid high-risk activities to prevent fractures.
  • Ketoconazole relief is temporary; take with food to reduce GI upset.

Read left to right: who gets it → what you see → what confirms it → what you do → what goes wrong. Cover a column and rebuild it out loud.

Addison Disease and Acute Adrenal Insufficiency (Addisonian Crisis)
🎯 Who gets it
  • Primary Addison disease: autoimmune adrenal destruction is the most common cause
  • Primary causes also include TB, histoplasmosis, adrenalectomy, or abdominal radiation
  • Metastatic cancer (breast, lung, colon, melanoma) can destroy adrenal tissue
  • Secondary Addison disease follows steroid withdrawal, hypophysectomy, or pituitary tumors
👀 What you see
  • Chronic Addison disease develops slowly; acute adrenal insufficiency develops rapidly
  • GI/constitutional symptoms: fatigue, weakness, anorexia, nausea, vomiting, diarrhea, abdominal pain
  • Weight loss, salt craving, and skin/mucous membrane hyperpigmentation are classic signs
  • Female clients may notice reproductive or menstrual cycle changes
🧪 What confirms it
  • Electrolytes show high K+, high WBC, low Na+, high BUN/creatinine, high calcium
  • Glucose stays normal or drops in Addison disease
  • Blood or salivary cortisol level drops in Addison disease
  • ACTH stimulation test: cortisol is measured at baseline, 30 min, and 1 hr after IV ACTH
🩺 What you do
  • Top priority in Addison disease care is preventing circulatory shock
  • Give 0.9% NaCl IV to restore volume; watch for dehydration and daily weights
  • Give IV hydrocortisone bolus, then continuous infusion or intermittent IV boluses
  • For hyperkalemia: check potassium, get an ECG, watch for dysrhythmias
💊 Drugs
  • Hydrocortisone, prednisone, cortisone: glucocorticoids replace adrenal hormones and fight inflammation
💬 What you teach
  • Never stop steroid medication abruptly; report Cushingoid signs like moon face or edema
  • Take glucocorticoids with food and report acute illness right away
  • Report adrenal insufficiency signs: fever, fatigue, weakness, dizziness, poor appetite

Read left to right: who gets it → what you see → what confirms it → what you do → what goes wrong. Cover a column and rebuild it out loud.

🎥 Lecture recordings 4

Tap a card to open that recording in Google Drive. The same list lives in the lecture library.

Day 1HaleckaDay 2HaleckaDay 1WagnerDay 2Wagner
All NUR 258 recordings →

🖼️ Infographics 22

Tap a card to open the matching graphics in your infographic library.

🖼️DI - Diabetes Insipidus 2Open matching infographics →🖼️Hormone List 1 of 3Open matching infographics →🖼️Hormone List 2 of 3Open matching infographics →🖼️Hormone List 3 of 3_v2Open matching infographics →🖼️Hyper & Hypothyroid - Patho, s_s causesOpen matching infographics →🖼️Hyper & Hypothyroid - PharmacologyOpen matching infographics →🖼️Hyperaldosteronism & PheochromocytomaOpen matching infographics →🖼️Hypo & HyperpituitarismOpen matching infographics →🖼️Parathyroid - Hyper & HypoOpen matching infographics →🖼️Pituitary DisordersOpen matching infographics →
The pituitary drawn with its anterior and posterior lobes and the hormones each releases, then a table setting SIADH against diabetes insipidus value by value.
ADH holds water. Too much of it is SIADH, none of it is diabetes insipidus, and every value flips. — tap it to open full size.
🖼️Thyroid Function & PathoOpen matching infographics →

📄 Simple Nursing handouts for this module — 10 of them, straight from your Drive.

DI - Diabetes Insipidus 2Simple Nursing handout — opens in Drive →Hormone List 1 of 3Simple Nursing handout — opens in Drive →Hormone List 2 of 3Simple Nursing handout — opens in Drive →Hormone List 3 of 3 2Simple Nursing handout — opens in Drive →Hyper & Hypothyroid - Patho, s s causesSimple Nursing handout — opens in Drive →Hyper & Hypothyroid - PharmacologySimple Nursing handout — opens in Drive →Hyperaldosteronism & PheochromocytomaSimple Nursing handout — opens in Drive →Parathyroid - Hyper & HypoSimple Nursing handout — opens in Drive →Pituitary DisordersSimple Nursing handout — opens in Drive →SIADH 2Simple Nursing handout — opens in Drive →

🖼️ See all 49 NUR 258 handouts in the visual library →

📋 Active Learning Templates 4

One per disorder. Every row is filled from that section of the ATI chapter — print it, cover the right, rebuild it.

Jump to a template📋 Pituitary Disorders📋 Hypothyroidism📋 Cushing Disease and Syndrome📋 Addison Disease and Acute Adrenal Insufficiency (Addisonian Crisis)
📋 Pituitary Disorders6 parts

🖼️ InfographicsPituitary Disorders

ATI Active Learning Template — System DisorderPituitary Disorders

Filled from ATI chapter 77, row by row from that chapter’s own sections — 12 of 12 rows have content.

🧭 What it isAlterations in Health (Diagnosis) · Health Promotion & Disease Prevention
Alterations in Health (Diagnosis)
  • Covers pituitary gland anatomy, anterior/posterior hormones, and three disorders: acromegaly (excess GH), arginine vasopressin disorder (ADH deficiency), and SIADH (excess ADH) with their fluid/electrolyte effects.
Health Promotion & Disease Prevention

From this module — built from the notes above on this page, not a section of the ATI chapter.

  • Lifelong hormone replacement where the gland has been removed or destroyed — and a taper is never skipped for the steroid component.
  • Medical alert identification and sick-day dosing where the adrenal axis is involved.
  • Report early visual change — a growing adenoma presses on the optic chiasm and causes bitemporal hemianopsia.
  • After transsphenoidal surgery: no nose blowing, straws, sneezing with the mouth closed, or straining — all raise pressure on the repair.
  • Report clear nasal drainage that tests positive for glucose — that is cerebrospinal fluid.
👀 How it shows upAssessment — Risk Factors · Assessment — Expected Findings
Assessment — Risk Factors
  • Acromegaly risk: genetics, onset in the 30s-40s, and pituitary adenomas.
  • Central DI (AVP deficiency) risk: head injury, brain tumor, CNS infection, or autoimmune disease.
  • Nephrogenic DI (AVP resistance) risk: hereditary factors, kidney disease, hypercalcemia, hypokalemia.
  • Lithium and demeclocycline are common drug causes of nephrogenic DI.
  • SIADH's most common cause is a malignant tumor, especially small cell lung cancer.
  • SIADH also linked to pulmonary disease, head injury, infection, surgery, and hormone imbalance.
  • Antidepressants, anticonvulsants, antipsychotics, chemo, and pain medications are frequent SIADH triggers.
Assessment — Expected Findings
  • Acromegaly: enlarged hands/feet, deepened voice, coarse facial features, thick lips, large nose.
  • Acromegaly: headaches, visual field deficits, carpal tunnel syndrome, joint pain, hyperhidrosis.
  • Acromegaly can also cause hypertension, cardiac murmur, and hyperglycemia.
  • DI mnemonic DILUTE: dehydration, increased serum osmolality, low urine osmolality, diuresis, thirst, electrolyte imbalance.
  • DI causes polyuria over 3 L/day of dilute urine, plus polydipsia and nocturia.
  • DI also brings tachycardia, hypotension, poor skin turgor, dry mucous membranes, weak pulses.
  • Older adults face higher dehydration risk in DI from blunted thirst and more diuretic use.
  • SIADH early signs: weakness, fatigue, nausea/vomiting, anorexia, muscle cramps.
🧪 How it is confirmedLaboratory Tests · Diagnostic Procedures
Laboratory Tests
  • Acromegaly screening: elevated IGF-1 confirms excess growth hormone.
  • GH suppression test: acromegaly shows little or no GH drop after a glucose load.
  • DI urine: specific gravity <1.005, osmolality <300 mOsm/kg after water deprivation.
  • DI: urine sodium <40 mg/day; blood osmolality >300 mmol/kg, sodium >145 mEq/L.
  • ADH level >5 ng/L suggests central DI; <1 ng/L suggests nephrogenic DI.
Diagnostic Procedures
  • Acromegaly imaging: skull X-ray checks the sella turcica; MRI (or CT) confirms a pituitary tumor.
  • Cerebral angiography rules out vascular malformation or aneurysm in acromegaly workup.
  • MRI evaluates hypothalamus or pituitary damage in suspected DI.
  • Water deprivation test withholds fluids to stimulate ADH, then gives subcutaneous desmopressin.
  • Central DI: urine osmolality rises after desmopressin; nephrogenic DI shows no rise.
🩺 What you doNursing Care · Medications · Therapeutic Procedures
Nursing Care
  • GH suppression test: recheck GH and glucose at 10, 60, 120 min after the glucose dose.
  • Client drinks only water for 6-8 hr before GH suppression testing.
  • Assess self-concept related to acromegaly's physical changes; explain treatment options.
  • DI: track LOC, vital signs, strict I&O, specific gravity, and daily weight.
  • DI: give IV fluids to balance I&O correct electrolytes cautiously, avoid overcorrecting sodium.
  • DI: institute fall precautions and monitor skin turgor and mucous membranes.
  • Vasopressin dose is adjusted by urine output; use cautiously with coronary artery disease.
  • Watch for water intoxication: headache or confusion during vasopressin therapy.
  • SIADH priority: restrict oral fluids first to limit hemodilution; offer thirst comfort measures.
Medications
  • Acromegaly first line: somatostatin analogs (octreotide, lanreotide, pasireotide) suppress GH release.
  • Bromocriptine or cabergoline (dopamine agonists) also lower GH; watch for psychosis or fibrosis.
  • Pegvisomant (second line) blocks GH receptors and cuts IGF production.
  • Desmopressin (DDAVP) treats DI via intranasal, oral, subQ, or IV routes to cut urine output.
  • Desmopressin risk: dilutional hyponatremia, palpitations, tachycardia, headache; limit extra fluid intake.
  • Carbamazepine can stimulate ADH release, reducing urine output in DI.
  • Thiazide diuretics are sometimes used to lower urine output in central DI.
  • Indomethacin (an NSAID) can increase urine concentration in DI.
Therapeutic Procedures
  • Hypophysectomy removes the pituitary via a minimally invasive transnasal transsphenoidal approach; craniotomy if needed.
  • Postop: monitor neurologic status, vision, and vital signs closely (watch for hypotension).
  • Postop: watch the nasal drip pad for epistaxis.
  • Postop: report clear watery nasal drainage - may signal a CSF leak.
  • Postop: encourage deep breathing but limit coughing to avoid raising ICP or a CSF leak.
  • Postop: assess for sinusitis and meningitis; nasal packing is removed on postop day 1.
💬 Around the patientClient Education · Interprofessional Care
Client Education
  • Acromegaly: hormone replacement therapy may be lifelong; report vision or mental status changes.
  • Acromegaly: avoid lifting or straining postop; report nasal bleeding or watery discharge.
  • Clients with sleep apnea should skip CPAP use right after hypophysectomy.
  • Report any increase in urine output after pituitary surgery.
  • DI: drink fluids based on thirst, matching urine output volume; weigh daily.
  • DI: reduce protein and sodium intake to help lower urine output.
  • SIADH: avoid taking demeclocycline with calcium, iron, magnesium, aluminum antacids, or milk.
Interprofessional Care
  • DI and SIADH may need home health support for fluids, meds, and diet management.
⚠️ What goes wrongComplications
Complications
  • Untreated SIADH can cause water intoxication, cerebral or pulmonary edema, and severe hyponatremia.
  • Without prompt treatment, these SIADH complications can progress to coma and death.
  • Watch for lung crackles, distended neck veins, and neuro changes signaling complications.
  • Maintain seizure precautions and monitor blood sodium closely in SIADH.
  • Teach clients to follow fluid restriction strictly to prevent worsening SIADH.
📋 Hypothyroidism6 parts

🖼️ InfographicsHyperthyroid / HypothyroidHyperthyroid / Hypothyroid IIHyper & Hypothyroid - Patho, s s causesHyper & Hypothyroid - Pharmacology

ATI Active Learning Template — System DisorderHypothyroidism

Filled from ATI chapter 79, row by row from that chapter’s own sections — 12 of 12 rows have content.

🧭 What it isAlterations in Health (Diagnosis) · Health Promotion & Disease Prevention
Alterations in Health (Diagnosis)
  • Explains hypothyroidism's primary, iatrogenic, and central (pituitary or hypothalamic) causes, why older adults are often underdiagnosed, and covers its risk factors, findings, labs, levothyroxine therapy, and the emergency of myxedema coma.
Health Promotion & Disease Prevention

From this module — built from the notes above on this page, not a section of the ATI chapter.

  • Take levothyroxine on an empty stomach, in the morning, with water, and wait 30–60 minutes before eating.
  • Separate from calcium, iron, antacids and soya by at least 4 hours — they block absorption.
  • Take it every day, for life, and do not switch brands without a repeat TSH.
  • Newborn screening detects congenital hypothyroidism before it causes harm.
  • Report palpitations, tremor, weight loss or insomnia — those mean the dose is too high.
👀 How it shows upAssessment — Risk Factors · Assessment — Expected Findings
Assessment — Risk Factors
  • Women develop hypothyroidism about 7 times more often than men.
  • Risk rises with older age and history of thyroid surgery.
  • Amiodarone, lithium, immune modulators, and chemotherapy can trigger hypothyroidism.
  • Inadequate iodine intake and autoimmune disease raise hypothyroidism risk.
  • Prior radiation therapy to the head or neck is a risk factor.
Assessment — Expected Findings
  • Classic signs: fatigue, cold intolerance, constipation, and weight gain.
  • Mood/cognitive changes: depression, anxiety, psychosis, and trouble concentrating.
  • Joint stiffness, muscle pain, and carpal tunnel syndrome can occur.
  • Cardiac: hypotension, bradycardia, elevated diastolic BP, dysrhythmias, prolonged QT, and heart failure risk.
  • Sleep apnea and disrupted sleep patterns are common.
  • Skin/hair changes: hair loss, dry skin, and a deepened voice.
  • Reproductive effects: abnormal menstrual cycles and decreased fertility.
🧪 How it is confirmedLaboratory Tests · Diagnostic Procedures
Laboratory Tests
  • T4 is decreased; TSH rises in primary hypothyroidism but is normal or low in secondary/tertiary.
  • Cholesterol, lipids, liver enzymes, and glucose are typically elevated.
  • Antithyroid antibodies may be present; hemoglobin and hematocrit are often decreased.
Diagnostic Procedures
  • Thyroid scan shows low radioactive iodine uptake in hypothyroidism.
  • Fine-needle aspiration evaluates thyroid nodules; ECG can show sinus bradycardia or dysrhythmias.
🩺 What you doNursing Care · Medications · Therapeutic Procedures
Nursing Care
  • Monitor heart rate, blood pressure, ECG, and weight closely in hypothyroidism.
  • Increase activity gradually with rest periods to limit myocardial oxygen demand.
  • Apply anti-embolism stockings and elevate legs to support venous return.
  • Encourage coughing and deep breathing to prevent pulmonary complications.
  • Add dietary fiber and laxatives as needed for constipation.
  • Keep the client warm: extra clothing, blankets, layered dressing, warm liquids.
  • Watch for myxedema coma: lethargy, LOC changes, low cardiac output, hypoventilation, abdominal pain.
  • Levothyroxine: watch for chest pain, palpitations, rapid heart rate, or shortness of breath.
  • Myxedema coma: secure the airway with ventilator support and continuous ECG monitoring.
Medications
  • Levothyroxine is the most commonly prescribed synthetic thyroid hormone replacement.
  • Levothyroxine increases warfarin's effect and raises insulin or digoxin needs.
  • Start levothyroxine at a low dose in older adults or CAD clients to avoid coronary ischemia.
Therapeutic Procedures

From this module — built from the notes above on this page, not a section of the ATI chapter.

  • Levothyroxine replacement, titrated by TSH every 6–8 weeks until stable, then annually.
  • Start low and go slow in older adults and anyone with cardiac disease — a fast increase can precipitate angina or a dysrhythmia.
  • Warm environment, and check for constipation and skin dryness.
  • Myxedema coma: IV levothyroxine, passive warming, ventilatory support, corticosteroids.
  • Do not warm a myxedema client actively — it causes vasodilation and cardiovascular collapse.
💬 Around the patientClient Education · Interprofessional Care
Client Education
  • Report chest pain right away; treatment with thyroid hormone is typically lifelong.
  • Never change levothyroxine's timing, dose, or brand without consulting the provider.
  • Lab work is repeated every 4-6 weeks until thyroid hormones stabilize.
  • Levothyroxine dose increases every 2-3 weeks based on TSH monitoring.
  • Take levothyroxine on an empty stomach, 1 hr before or 3 hr after eating.
  • Space levothyroxine 4 hr apart from other medications to avoid impaired absorption.
  • Report hyperthyroid signs: fever, tremors, tachycardia, palpitations, heat intolerance, weight loss.
Interprofessional Care
  • Home health may monitor for adverse effects during the first weeks of therapy.
  • Refer to an endocrinologist for comorbidities or treatment failure; pharmacists can review drug interactions.
⚠️ What goes wrongComplications
Complications

From this module — built from the notes above on this page, not a section of the ATI chapter.

  • Myxedema coma — hypothermia, hypotension, hypoventilation, hyponatremia and reduced consciousness. High mortality.
  • Cardiac: bradycardia, pericardial effusion, raised cholesterol and accelerated atherosclerosis.
  • Depression and cognitive slowing, easily mistaken for dementia in older adults.
  • Infertility and, in pregnancy, impaired fetal neurodevelopment if untreated.
  • Over-replacement causes atrial fibrillation and bone loss.
📋 Cushing Disease and Syndrome6 parts
ATI Active Learning Template — System DisorderCushing Disease and Syndrome

Filled from ATI chapter 80, row by row from that chapter’s own sections — 12 of 12 rows have content.

🧭 What it isAlterations in Health (Diagnosis) · Health Promotion & Disease Prevention
Alterations in Health (Diagnosis)
  • Distinguishes Cushing disease (pituitary or adrenal oversecretion of ACTH/cortisol) from Cushing syndrome (long-term glucocorticoid therapy), covering adrenal cortex hormones, risk factors, findings, labs, treatment, and surgical care.
Health Promotion & Disease Prevention
  • After adrenalectomy, hormone replacement therapy is lifelong; get an annual flu shot.
  • Wear a medical alert bracelet listing Cushing disease and current medications.
  • Monitor blood glucose and blood pressure at home; report abnormal results.
👀 How it shows upAssessment — Risk Factors · Assessment — Expected Findings
Assessment — Risk Factors
  • Most common in women aged 50-60 years.
  • Cushing disease (endogenous): adrenal hyperplasia, adrenocortical carcinoma, or an ACTH-secreting pituitary tumor.
  • Lung, GI, or pancreatic tumors can also secrete ACTH and cause Cushing disease.
  • Cushing syndrome (exogenous): long-term glucocorticoids for transplant, chemo, autoimmune disease, asthma, or allergies.
Assessment — Expected Findings
  • Classic build: moon face, truncal obesity, and a buffalo hump (fat on the back of neck).
  • Skin: thin, fragile, easily bruised, with purple-red striae on abdomen, arms, thighs.
  • Infection risk rises but without usual fever, swelling, or redness (blunted immune response).
  • Hypertension, gastric ulcers, and hyperglycemia are common findings.
  • Musculoskeletal: osteoporosis with fracture risk, bone pain, and muscle wasting in the limbs.
  • Hirsutism, acne, red cheeks, and irregular scant menses can occur.
  • Weakness, fatigue, sleep disturbance, back/joint pain, and memory impairment are common.
  • Mood changes include irritability, depression, and emotional lability.
🧪 How it is confirmedLaboratory Tests · Diagnostic Procedures
Laboratory Tests
  • Elevated cortisol (blood, urine, or saliva) without illness or stress confirms Cushing's.
  • Labs show low potassium, low lymphocytes, and high blood glucose and sodium.
  • ACTH is elevated with pituitary hypersecretion but decreased with adrenal-source disease.
  • Dexamethasone suppression test: cortisol stays high (nonsuppressed) in Cushing disease.
  • Acute illness or alcohol use disorder can cause false-positive suppression test results.
Diagnostic Procedures
  • Imaging (X-ray, MRI, CT, arteriography) locates lesions in the pituitary, adrenal gland, lung, GI tract, or pancreas.
  • Imaging also distinguishes a tumor from adrenal atrophy as the cause.
🩺 What you doNursing Care · Medications · Therapeutic Procedures
Nursing Care
  • Monitor daily weight, I&O, vital signs, and ECG for fluid overload.
  • Watch for fluid overload signs: swelling, neck vein distention, breathlessness, high BP, fast pulse.
  • Protect skin and prevent falls; reposition at least every 2 hr; use surgical asepsis for dressings.
  • Ketoconazole: monitor liver enzymes for toxicity (yellow sclera, dark urine).
  • Hydrocortisone: watch potassium/glucose; report weight gain over 2.3 kg (5 lb)/week.
  • Post-hypophysectomy: check nasal drainage for glucose or a halo sign (CSF leak).
  • Post-hypophysectomy: neuro checks hourly for the first 24 hr, then every 4 hr.
  • Give glucocorticoids before, during, and after pituitary or adrenal surgery to prevent a cortisol drop.
  • Post-adrenalectomy: watch for adrenal crisis - hypotension, tachycardia, tachypnea, nausea, headache.
Medications
  • Cushing syndrome treatment: taper glucocorticoids gradually and manage symptoms.
  • Ketoconazole (an antifungal) inhibits adrenal corticosteroid synthesis at high doses.
  • Mitotane selectively destroys adrenocortical cells to treat inoperable adrenal carcinoma; watch for shock.
  • Hydrocortisone replaces cortisol after Cushing treatment and is often paired with ketoconazole.
Therapeutic Procedures
  • Chemotherapy with cytotoxic agents can treat tumor-driven Cushing disease.
  • Hypophysectomy (pituitary removal) or adrenalectomy (one or both adrenal glands) may be needed.
💬 Around the patientClient Education · Interprofessional Care
Client Education
  • Report weight gain over 2 lb in 24 hr or 3 lb in a week.
  • Eat foods high in calcium and vitamin D; avoid high-risk activities to prevent fractures.
  • Ketoconazole relief is temporary; take with food to reduce GI upset.
  • Mitotane: report visual changes or blood in urine; use caution driving.
  • Hydrocortisone: never skip a dose; carry emergency corticosteroid ID.
  • Hydrocortisone: report abdominal pain, black tarry stools, or infection signs to the provider.
  • Post-hypophysectomy: breathe through the mouth, avoid coughing, nose-blowing, or sneezing.
Interprofessional Care
  • Arrange frequent endocrinologist follow-up and home care for mobility and fall prevention.
⚠️ What goes wrongComplications
Complications

From this module — built from the notes above on this page, not a section of the ATI chapter.

  • Osteoporosis and fragility fractures, including vertebral collapse.
  • Poorly controlled diabetes and hypertension.
  • Infection with muted signs — steroids blunt fever and inflammation, so a serious infection can look mild.
  • Fragile skin, poor wound healing, easy bruising.
  • Adrenal insufficiency after treatment or abrupt steroid withdrawal — the pendulum swings the other way.
  • Mood disturbance, psychosis and cognitive change.
📋 Addison Disease and Acute Adrenal Insufficiency (Addisonian Crisis)6 parts
ATI Active Learning Template — System DisorderAddison Disease and Acute Adrenal Insufficiency (Addisonian Crisis)

Filled from ATI chapter 81, row by row from that chapter’s own sections — 12 of 12 rows have content.

🧭 What it isAlterations in Health (Diagnosis) · Health Promotion & Disease Prevention
Alterations in Health (Diagnosis)
  • Addison disease is chronic adrenocortical insufficiency from adrenal cortex damage, causing low aldosterone and cortisol; acute adrenal insufficiency (Addisonian crisis) is a rapid, life-threatening emergency requiring immediate treatment, especially in older adults.
Health Promotion & Disease Prevention

From this module — built from the notes above on this page, not a section of the ATI chapter.

  • Never stop corticosteroids abruptly. Abrupt withdrawal is itself a cause of crisis. Taper always.
  • Sick-day dosing — the dose is increased, usually doubled, during illness, injury, or before surgery and dental work.
  • Medical alert identification and an emergency injectable hydrocortisone kit at home, with someone trained to give it.
  • Report vomiting that prevents oral steroids — that needs the injection, not a wait.
  • Annual influenza vaccination and prompt treatment of infection.
👀 How it shows upAssessment — Risk Factors · Assessment — Expected Findings
Assessment — Risk Factors
  • Primary Addison disease: autoimmune adrenal destruction is the most common cause
  • Primary causes also include TB, histoplasmosis, adrenalectomy, or abdominal radiation
  • Metastatic cancer (breast, lung, colon, melanoma) can destroy adrenal tissue
  • Secondary Addison disease follows steroid withdrawal, hypophysectomy, or pituitary tumors
  • High-dose radiation to the pituitary or whole brain causes secondary disease
  • Acute adrenal insufficiency occurs when cortisol need exceeds the body's supply
  • Untreated acute adrenal insufficiency can be rapidly fatal
  • Triggers include infection, trauma, and intense physical exertion
Assessment — Expected Findings
  • Chronic Addison disease develops slowly; acute adrenal insufficiency develops rapidly
  • GI/constitutional symptoms: fatigue, weakness, anorexia, nausea, vomiting, diarrhea, abdominal pain
  • Weight loss, salt craving, and skin/mucous membrane hyperpigmentation are classic signs
  • Female clients may notice reproductive or menstrual cycle changes
  • Adrenal crisis presents with severe hypotension and shock
  • Crisis findings include confusion, hypovolemia, hyponatremia, and hyperkalemia
  • Crisis can also cause severe hypoglycemia and hypercalcemia
🧪 How it is confirmedLaboratory Tests · Diagnostic Procedures
Laboratory Tests
  • Electrolytes show high K+, high WBC, low Na+, high BUN/creatinine, high calcium
  • Glucose stays normal or drops in Addison disease
  • Blood or salivary cortisol level drops in Addison disease
  • ACTH stimulation test: cortisol is measured at baseline, 30 min, and 1 hr after IV ACTH
  • Primary insufficiency: cortisol stays flat after ACTH; secondary: cortisol rises
Diagnostic Procedures
  • ECG checks for dysrhythmias caused by electrolyte imbalance
  • X-ray, CT, and MRI locate the source of adrenal insufficiency (tumor or atrophy)
🩺 What you doNursing Care · Medications · Therapeutic Procedures
Nursing Care
  • Top priority in Addison disease care is preventing circulatory shock
  • Give 0.9% NaCl IV to restore volume; watch for dehydration and daily weights
  • Give IV hydrocortisone bolus, then continuous infusion or intermittent IV boluses
  • For hyperkalemia: check potassium, get an ECG, watch for dysrhythmias
  • Give insulin plus glucose, calcium, sodium bicarbonate, or sodium polystyrene sulfonate for hyperkalemia
  • Watch for and treat hypoglycemia; maintain a safe environment
  • Monitor weight, blood pressure, and electrolytes with glucocorticoid therapy
  • Increase steroid dose during illness or stress; taper before stopping
  • Give glucocorticoids with food to limit GI upset
Medications
  • Hydrocortisone, prednisone, cortisone: glucocorticoids replace adrenal hormones and fight inflammation
Therapeutic Procedures

From this module — built from the notes above on this page, not a section of the ATI chapter.

  • Crisis: high-dose IV hydrocortisone and aggressive isotonic fluid, immediately and together.
  • Treat hypoglycemia with dextrose; correct hyperkalemia.
  • Continuous cardiac monitoring; hourly vital signs and strict intake and output.
  • Daily weights — the most reliable measure of fluid status.
  • Identify and treat the trigger: infection, missed doses, surgery, trauma.
💬 Around the patientClient Education · Interprofessional Care
Client Education
  • Never stop steroid medication abruptly; report Cushingoid signs like moon face or edema
  • Take glucocorticoids with food and report acute illness right away
  • Report adrenal insufficiency signs: fever, fatigue, weakness, dizziness, poor appetite
  • Fludrocortisone (mineralocorticoid replacement) can cause hypertension as a side effect
  • Mild peripheral edema is expected with fludrocortisone; report sudden weight gain
  • Vasopressors treat persistent low blood pressure; antibiotics treat active infections
  • Avoid alcohol and caffeine; watch for GI bleeding signs like black tarry stool
Interprofessional Care
  • Home health can help manage fluids, medications, and diet after discharge
⚠️ What goes wrongComplications
Complications

From this module — built from the notes above on this page, not a section of the ATI chapter.

  • Addisonian crisis — profound hypotension, shock, hypoglycemia, hyperkalemia. Life-threatening within hours.
  • Hyperkalemia with cardiac dysrhythmia.
  • Hypoglycemia and hyponatremia.
  • Hypovolemic shock and acute kidney injury.
  • Over-replacement in the long term produces iatrogenic Cushing features.

📝 Notes & key concepts

The lines from this module that carry a number, a dose or an absolute rule — the ones that decide questions. Everything else is on the cards above.

  • Addisonian crisis order: fluids + dextrose first, then IV hydrocortisone. Fix the hyperkalemia with insulin + D50.
  • Cushing's: taper steroids, never stop abruptly — exogenous steroids suppress the body's own cortisol. Sodium restriction, K-sparing diuretics.
  • Thyroid storm: high fever, severe tachycardia, delirium → fluids + dextrose first, then beta blockers for the cardiac symptoms plus PTU/methimazole, plus cooling.
  • Hashimoto's/hypothyroid: fatigue, bradycardia, constipation, cold intolerance, depression. Airway is the priority — lethargic with poor respiratory effort. Myxedema coma: fluids + dextrose first, then IV levothyroxine plus warming.
  • Their thyroid model: a dial from 0 to 10, normal sits at 5. Hypo = dial down, everything slows. Hyper = dial up. They want pattern-matching, not memorized symptom lists.
  • Primary hypothyroidism = high TSH with low T3/T4. Secondary = low TSH with low T3/T4. Hashimoto's is roughly 18 of every 20 primary cases.
  • Levothyroxine overdose is iatrogenic hyperthyroidism: temp 104.9°F, HR 125, RR 42, restless, heat intolerant. Antithyroid drugs are useless here — the excess T4 is already circulating, not being made. Beta blocker, cooling, low-stimulation room, hold the next dose, notify.
  • Levothyroxine is started low and titrated slowly, especially in older adults. Judge the dose on symptoms plus T4.
  • "DI = dry inside, SIADH = soaked inside." Their SIADH case sodium was 120: fluid restriction, urine specific gravity, seizure precautions and neuro checks — low sodium is a neuro problem. Classic cause is lung cancer secreting ADH.
  • Adrenal crisis: hypotension, confusion, hyperkalemia, plus severe abdominal pain, vomiting and diarrhea (which is why every oral option is wrong). The keyed answer was IV hydrocortisone, but both instructors said what they wanted was a 0.9% NS bolus.
  • Pheochromocytoma: alpha-1 blockers, the "-osin" drugs (doxazosin, terazosin). Watch first-dose severe hypotension. Same class treats BPH.
  • Post-thyroidectomy priority is voice changes (recurrent laryngeal nerve). Then hypocalcemia — Chvostek, Trousseau, carpopedal spasm — then neck swelling. Avoid neck extension.
  • Thyroid storm bow-tie vitals: HR 142, BP 168/88, RR 22, SpO2 94% RA, temp 103.8°F, vomiting, diarrhea, new seizures. Priorities: beta blocker + cooling.
  • Calc: 5 mcg/kg/min, 132 lb, 100 mg/100 mL = 18 mL/hr. Their mantra: "2.2 always goes with the pounds."

🎯 Module quiz

Questions for this module. They also feed the Mega Quiz.

Nothing here yet — drop it in when you have it