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Addison's Disease Quiz: Test Your Knowledge Now!

Ready for our adrenal insufficiency quiz? Test your Addison's disease symptom smarts!

Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
Paper cut style adrenal glands with quiz elements pencil notebook question marks on teal background

Curious if your fatigue, weight loss or skin changes signal adrenal insufficiency? Our free do i have Addison's disease quiz tests your knowledge of Addison's disease symptoms and even includes an endocrine disorders quiz angle. In just minutes, you'll tackle questions on adrenal function and common risk factors to see if you need further evaluation. Explore related assessments with our do i have cushing's syndrome quiz or try the do i have an autoimmune disease quiz. Take the adrenal insufficiency quiz now and unlock instant insights - let's get started!

What hormone is primarily deficient in Addison's disease?
Cortisol
Aldosterone
Adrenocorticotropic hormone (ACTH)
Insulin
Addison's disease is characterized by primary adrenal insufficiency leading to inadequate cortisol production. Cortisol is critical for stress response, metabolism, and immune regulation. Loss of cortisol causes many of the systemic symptoms seen in Addison's disease. Mayo Clinic
A common early symptom of Addison's disease is:
Fatigue and weakness
Weight gain
Hyperactivity
Insomnia
Fatigue and muscle weakness are among the most frequent early symptoms due to cortisol deficiency and impaired energy metabolism. These symptoms often precede more specific signs like hyperpigmentation. Early recognition of fatigue can prompt evaluation for adrenal insufficiency. Endocrine Society
Hyperpigmentation in Addison's disease results from increased levels of:
ACTH
Melatonin
Cortisol
Renin
In primary adrenal insufficiency, low cortisol triggers increased production of ACTH from the pituitary. ACTH is derived from POMC, which also yields melanocyte-stimulating hormone (MSH), causing skin hyperpigmentation. This feature is absent in secondary adrenal insufficiency. NCBI Bookshelf
The most common cause of Addison's disease in developed countries is:
Autoimmune adrenal destruction
Tuberculosis infection
Metastatic cancer of the adrenals
Adrenal hemorrhage
Autoimmune adrenalitis is the leading cause of primary adrenal insufficiency in developed nations. The immune system targets enzymes in adrenal cortex cells, impairing hormone synthesis. Tuberculosis remains important globally but is less common in areas with good TB control. UpToDate
Addison's disease primarily affects which gland?
Adrenal glands
Thyroid gland
Pituitary gland
Pancreas
Addison's disease is primary adrenal insufficiency caused by dysfunction of the adrenal cortex. The adrenal glands produce vital hormones like cortisol and aldosterone. When these glands fail, systemic symptoms of adrenal insufficiency appear. Endocrine Society
In primary adrenal insufficiency, serum sodium is typically:
Low
High
Normal
Variable depending on cortisol levels
Aldosterone deficiency in primary adrenal insufficiency leads to sodium loss and hyponatremia. Cortisol deficiency also contributes by increasing ADH secretion and water retention. Hyponatremia is a hallmark electrolyte disturbance in Addison's disease. NCBI PMC
Which test is diagnostic for Addison's disease?
Cosyntropin (ACTH) stimulation test
Dexamethasone suppression test
Insulin tolerance test
Water deprivation test
The cosyntropin stimulation test measures cortisol response to synthetic ACTH. In primary adrenal insufficiency, there is a blunted or absent cortisol rise. This test differentiates primary from secondary or tertiary causes. Mayo Clinic Proceedings
In primary adrenal insufficiency, ACTH levels are:
Elevated
Decreased
Normal
Fluctuating
Loss of cortisol feedback inhibition causes increased CRH and ACTH release from the hypothalamus and pituitary. Elevated ACTH helps distinguish primary from secondary adrenal insufficiency. High ACTH also leads to skin hyperpigmentation. Endocrine Society
Treatment of Addison's disease typically includes:
Glucocorticoid and mineralocorticoid replacement
Beta blockers
Loop diuretics
Insulin therapy
Patients require cortisol replacement (usually hydrocortisone) and often fludrocortisone to replace aldosterone. This combination corrects hormone deficits and normalizes electrolytes and blood pressure. Dosages are adjusted based on stress and illness. UpToDate
One of the hallmark electrolyte disturbances in Addison’s disease is:
Hyperkalemia
Hypokalemia
Hypernatremia
Hypocalcemia
Aldosterone deficiency reduces potassium excretion, leading to hyperkalemia. This is a key diagnostic clue in primary adrenal insufficiency. Concurrent hyponatremia often occurs due to sodium loss. NCBI Bookshelf
After administration of cosyntropin, a patient with primary adrenal insufficiency will exhibit:
Minimal rise in serum cortisol
Marked increase in cortisol
Normal response but delayed
Exaggerated cortisol response
In primary adrenal insufficiency, adrenal cortex damage prevents cortisol synthesis even when stimulated by ACTH analogs like cosyntropin. This blunted cortisol response confirms the diagnosis. In secondary etiologies, a delayed but present response may be seen. Mayo Clinic
Which feature is NOT typical of secondary adrenal insufficiency?
Hyperkalemia
Low ACTH levels
Normal aldosterone production
Absence of skin hyperpigmentation
Secondary adrenal insufficiency involves pituitary failure to secrete ACTH, leading to low cortisol but preserved aldosterone production. As a result, potassium levels remain normal and hyperpigmentation is absent. Elevated potassium is a hallmark of primary adrenal insufficiency only. UpToDate
Waterhouse-Friderichsen syndrome causes adrenal failure due to:
Bilateral adrenal hemorrhage
Autoimmune adrenalitis
Tuberculous infiltration
Adrenal vein thrombosis
Waterhouse-Friderichsen syndrome is acute adrenal failure from hemorrhagic necrosis, often in meningococcal sepsis. Rapid destruction of both adrenal glands leads to adrenal crisis and shock. It is a medical emergency requiring immediate steroid replacement. NCBI PMC
Addison’s disease can be confirmed by finding which autoantibody?
21-hydroxylase antibody
17?-hydroxylase antibody
Thyroid peroxidase antibody
Islet cell antibody
Autoimmune adrenalitis is associated with antibodies against 21-hydroxylase, an enzyme in cortisol synthesis. These autoantibodies indicate an immune-mediated mechanism. They are highly specific for primary adrenal insufficiency. Endocrine Abstracts
Which imaging study is most useful to evaluate adrenal morphology in Addison’s disease?
Abdominal CT scan
Chest X-ray
Head MRI
Abdominal ultrasound
An abdominal CT scan provides detailed images of adrenal size and shape, identifying atrophy, calcification, or hemorrhage. It is the preferred modality for evaluating adrenal morphology in suspected Addison's disease. Ultrasound lacks sufficient resolution for adrenals. NCBI PMC
Mutations in which gene cause congenital adrenal hyperplasia that can mimic Addison's disease?
CYP21A2 (21-hydroxylase)
HSD17B3 (17?-hydroxysteroid dehydrogenase)
MC2R (ACTH receptor)
CYP11A1 (side-chain cleavage enzyme)
Deficiency of 21-hydroxylase due to CYP21A2 mutations leads to congenital adrenal hyperplasia with cortisol and aldosterone deficits. This can present similarly to Addison's disease but often has androgen excess. Genetic testing distinguishes CAH from autoimmune adrenal insufficiency. NCBI PMC
In an acute Addisonian crisis, which is essential immediate treatment?
Intravenous hydrocortisone
Oral fludrocortisone
Intravenous insulin
Oral dexamethasone
Acute adrenal crisis requires prompt IV hydrocortisone to replace both glucocorticoid and some mineralocorticoid activity. Fluid resuscitation and correction of electrolytes follow. Delaying steroid therapy increases risk of shock and mortality. UpToDate
Which cytokine is most implicated in autoimmune destruction of the adrenal cortex in Addison's disease?
Interferon-gamma
Interleukin-4
Interleukin-10
Interleukin-17
Autoimmune adrenalitis involves Th1-mediated immunity with high levels of interferon-gamma driving macrophage activation and tissue damage. IFN-? is a key proinflammatory cytokine in many organ-specific autoimmune diseases. IL-4 and IL-10 are more associated with regulatory or humoral responses. NCBI PMC
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Study Outcomes

  1. Recognize Key Symptoms -

    Identify the hallmark signs ofAddison's disease, including fatigue, weight loss, hyperpigmentation and salt cravings, to enhance your symptom-awareness.

  2. Differentiate Adrenal Insufficiency Types -

    Distinguish between primary and secondary adrenal insufficiency by evaluating underlying causes and hormonal profiles.

  3. Analyze Risk Factors and Causes -

    Assess factors like autoimmune conditions, infections and genetic predispositions that contribute to the development ofAddison's disease.

  4. Interpret Quiz Results -

    Evaluate your quiz score to gauge your current understanding of adrenal function and identify knowledge gaps.

  5. Apply Knowledge to Real-Life Scenarios -

    Use insights from the quiz to recognize when symptoms warrant professional medical evaluation and further testing.

  6. Access Credible Endocrine Resources -

    Locate authoritative sources and guidelines for ongoing education on adrenal disorders and endocrine health.

Cheat Sheet

  1. HPA Axis and Cortisol Synthesis -

    Review the hypothalamic - pituitary - adrenal (HPA) axis: CRH from the hypothalamus stimulates ACTH release, which in turn drives cortisol production in the adrenal cortex. Remember the mnemonic "A-C-T-H" (Amazon's Cloud Talks Hypercortisolism) to recall the cascade. Knowing this pathway is key for any adrenal insufficiency quiz.

  2. Primary vs. Secondary Adrenal Insufficiency -

    Differentiate Addison's disease (primary) from secondary causes by lab values: primary shows ↑ACTH with ↓cortisol, whereas secondary has ↓ACTH and ↓cortisol. A simple chart or table helps - list baseline ACTH and cortisol levels side by side for quick recall. This distinction often trips up even experienced students in an Addison's disease quiz.

  3. Hallmark Clinical Features -

    Memorize classic symptoms: hyperpigmentation, orthostatic hypotension, fatigue, and weight loss. Use the phrase "PAHS" (Pigmentation, Appetite loss, Hypotension, Salt cravings) to lock in these signs. These features frequently appear in Addison's disease symptom quizzes.

  4. Autoimmune Pathophysiology -

    Most Addison's cases are autoimmune, with autoantibodies targeting 21-hydroxylase. Recall "21st birthday" as a cue for 21-hydroxylase autoimmunity. Understanding this mechanism is crucial for both endocrine disorders quiz questions and clinical correlation.

  5. Diagnostic Testing: ACTH Stimulation -

    Learn the cosyntropin stimulation test: measure cortisol at 0 and 30 minutes; a peak <18 µg/dL confirms adrenal insufficiency. Jot down the formula ΔCortisol = Cortisol30min - Cortisol0min to track your expected rise. This protocol is a staple in adrenal function and Addison's disease quizzes.

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