The basics Hormones Flashcards
What is Follicle Stimulating Hormone (FSH) function
is a hormone your pituitary gland makes and releases that plays a role in sexual development and reproduction. It affects the function of ovaries and testicles.
What is Lutenizing Hormone (LH) function
- In the pituitary of people designated female at birth (DFAB), LH is released only in the second part of the menstrual cycle. That is, after an initial surge causes the release of an egg (ovulation), LH is released at a constant pace for two weeks. This stimulates ovarian progesterone production.
- In the pituitary of people designated male at birth (DMAB), LH is released at a constant pace over time and testosterone is produced at a constant level, as well.
From https://my.clevelandclinic.org/health/body/22255-luteinizing-hormone
- Ovulation: A surge in LH causes your ovary to release a mature egg around the second week of each menstrual cycle. A high LH level around this time means that you’re at that moment in your cycle when you’re most likely to get pregnant.
What is Progesterone function
Effect:
Prepares the uterus for implantation by thickening the endometrium.
Maintains pregnancy by preventing uterine contractions.
Regulates menstrual cycle by signaling the end of the proliferative phase.
Modulates the immune system to tolerate the fetus.
Promotes the growth of mammary glands during pregnancy for lactation preparation.
Key Role: Known as the “pregnancy hormone,” it is essential for conception and maintaining early stages of pregnancy.
What is Prostaglandins function
Overview
Prostaglandins are bioactive lipid mediators derived from arachidonic acid via the cyclooxygenase (COX) pathway.
- Synthesis Enzymes:
COX-1: Produces prostaglandins involved in physiological functions like gastric protection.
COX-2: Induced during inflammation and contributes to pain and fever.
Mode of Action: They act locally due to rapid breakdown and do not circulate like traditional hormones.
- Pain Sensitization:
Mechanism: Prostaglandin E2 (PGE2) lowers the threshold for pain receptors (nociceptors), amplifying pain signals.
Clinical Impact: Contributes to pain in inflammatory conditions like arthritis and injury.
-Fever Induction:
Mechanism: Prostaglandins, particularly PGE2, act on the hypothalamus, the brain’s thermoregulatory center.
During infections or inflammation, immune cells release cytokines (e.g., interleukin-1, TNF-alpha), which stimulate the production of PGE2 in the hypothalamus.
PGE2 binds to receptors in the hypothalamus, increasing the body’s temperature set point.
Clinical Relevance:
The rise in body temperature (fever) creates an environment less favorable for pathogen survival and enhances immune cell activity.
Antipyretic medications like NSAIDs reduce fever by inhibiting COX enzymes, decreasing PGE2 production.
-Vasodilation and Edema:
Mechanism: Increases blood flow and vascular permeability, allowing immune cells to access tissues.
Clinical Impact: Leads to redness, heat, and swelling in inflammation.
- Fever: Prostaglandins can act on the hypothalamus in the brain, raising the body’s temperature and contributing to the development of fever during infections or inflammatory processes.
- Gastric Protection the Prostaglandins Involved:
PGE2 and PGI2 are key players in maintaining the integrity of the gastric mucosa.
Mechanism:
Stimulate the secretion of protective mucus and bicarbonate, creating a barrier against stomach acid.
Reduce gastric acid secretion by acting on parietal cells.
Enhance mucosal blood flow, supporting tissue repair and maintenance.
Clinical Relevance:
NSAIDs inhibit COX enzymes, decreasing protective prostaglandins and increasing the risk of gastric ulcers and bleeding.
Synthetic prostaglandins (e.g., misoprostol) are used to prevent NSAID-induced ulcers.
- Platelet Aggregation: Prostaglandins can have both pro-aggregatory and anti-aggregatory effects on platelets, depending on the specific type of prostaglandin and the context in which it acts.
Vascular Tone Regulation:
Prostacyclin (PGI2): Promotes vasodilation and inhibits platelet aggregation, reducing thrombosis risk.
Thromboxane A2 (TXA2): Induces vasoconstriction and enhances platelet aggregation for clotting. - Renal Function: Prostaglandins play a role in regulating renal blood flow and glomerular filtration rate (GFR) in the kidneys, particularly through their interactions with the Renin-Angiotensin-Aldosterone System (RAAS).
Prostaglandins: Multifunctional Lipid Compounds
Production and Overview
Definition: Prostaglandins are bioactive lipid mediators derived from arachidonic acid via the cyclooxygenase (COX) pathway.
Synthesis Enzymes:
COX-1: Produces prostaglandins involved in physiological functions like gastric protection.
COX-2: Induced during inflammation and contributes to pain and fever.
Mode of Action: They act locally due to rapid breakdown and do not circulate like traditional hormones.
Roles of Prostaglandins in the Body
1. Inflammation and Immune Response
Pain Sensitization:
Mechanism: Prostaglandin E2 (PGE2) lowers the threshold for pain receptors (nociceptors), amplifying pain signals.
Clinical Impact: Contributes to pain in inflammatory conditions like arthritis and injury.
Fever Induction:
Mechanism: PGE2 acts on the hypothalamus to increase the body’s set point temperature.
Clinical Impact: Causes fever, aiding in the immune response to infection.
Vasodilation and Edema:
Mechanism: Increases blood flow and vascular permeability, allowing immune cells to access tissues.
Clinical Impact: Leads to redness, heat, and swelling in inflammation.
- Reproductive System
Uterine Contractions:
Prostaglandins Involved: PGE2 and PGF2α regulate contractions for menstruation and labor.
Clinical Impact: Overproduction leads to dysmenorrhea (painful periods) or preterm labor.
Prostaglandin Involved: PGE2 softens the cervix for labor.
Clinical Use: Administered to induce labor.
Ovulation:
Mechanism:
Prostaglandins are involved in follicular rupture by modulating enzymes that break down the follicle’s outer wall.
Facilitate the release of the oocyte during ovulation.
Clinical Relevance:
Dysregulation of prostaglandins can impair ovulation and contribute to infertility in certain conditions.
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3. Gastrointestinal System
Mucosal Protection:
Prostaglandins Involved: PGE2 and PGI2 stimulate mucus and bicarbonate secretion while reducing gastric acid.
Clinical Impact: Deficiency, such as from NSAID use, increases ulcer risk.
Motility Regulation:
Mechanism: Modulate smooth muscle contraction, influencing digestion and bowel movements.
Clinical Relevance:
A deficiency in prostaglandins, such as from chronic NSAID use, can result in gastrointestinal irritation, ulcers, or impaired motility.
- Cardiovascular System
Vascular Tone Regulation:
Prostacyclin (PGI2): Promotes vasodilation and inhibits platelet aggregation, reducing thrombosis risk.
Thromboxane A2 (TXA2) is not a prostagladin but a thrombaxone: Induces vasoconstriction and enhances platelet aggregation for clotting.
Blood Pressure Modulation:
Balance Impact: Interaction between PGI2 and TXA2 influences vascular resistance and blood pressure.
Clinical Relevance:
Imbalance between PGI2 and TXA2 contributes to cardiovascular diseases like hypertension, atherosclerosis, and thrombosis.
Thromboxane A2 is derived from arachidonic acid, similar to prostaglandins, but it is classified as a thromboxane, not a prostaglandin.
- Kidney Function
Renal Blood Flow:
Prostaglandins Involved: PGE2 and PGI2 maintain renal perfusion, especially under stress (e.g., dehydration).
Sodium and Water Regulation:
Prostaglandins modulate sodium reabsorption in the nephron, influencing fluid balance and blood pressure.
Clinical Relevance:
NSAIDs can impair prostaglandin production, reducing renal blood flow and potentially leading to kidney injury, particularly in patients with compromised renal function.
- Respiratory System
Bronchial Tone Regulation:
Prostaglandins Involved:
PGE2: Relaxes bronchial smooth muscle, aiding airflow.
PGF2α: Constricts bronchi, potentially exacerbating asthma symptoms. - Uterine Contractions Prostaglandins Involved:
PGE2 and PGF2α regulate smooth muscle contractions in the uterus.
Mechanism:
During menstruation, prostaglandins facilitate the shedding of the endometrial lining by inducing contractions.
During labor, prostaglandins increase the frequency and intensity of uterine contractions to aid childbirth.
Clinical Relevance:
Overproduction of prostaglandins can lead to dysmenorrhea (painful menstrual cramps) or premature labor.
Prostaglandin analogs (e.g., dinoprostone, a form of PGE2) are used to induce labor.
8.7. Bone Health
Bone Remodeling:
Prostaglandin Involved: PGE2 stimulates bone resorption by osteoclasts.
Clinical Impact: Chronic overproduction may contribute to osteoporosis.
From https://chat.openai.com/c/f180869f-f8ca-48de-85fc-e4789c6251eb
What is estrogen function in the body
Effect: Promotes development of secondary sexual characteristics (e.g., breasts, wider hips), regulates menstrual cycles, and maintains reproductive tissues.
Key Role: Supports pregnancy, bone health, and cardiovascular health in women.
What is Testosterone function
Effect: Promotes sperm production, libido, and secondary sexual characteristics like increased muscle mass, facial hair, and deeper voice.
Key Role: Vital for male reproductive function and overall anabolic effects on the body.
What is Growth Hormone function
Effect: Stimulates protein synthesis, increases muscle mass, promotes growth of bones and cartilage, and enhances fat metabolism for energy.
Key Role: Important during childhood and adolescence for overall growth and also helps repair tissues in adults.
What is ADH function and what is oxytoxin function and where are they stored in the body?
They are stored in the posterior pituitary
1. ADH- Effect: Increases water reabsorption in the kidneys, reducing urine output and maintaining hydration.
Key Role: Prevents dehydration and regulates blood osmolarity.
2. Oxytocin- Effect: Triggers uterine contractions during labor and milk ejection during breastfeeding. Also linked to emotional bonding.
Key Role: Facilitates childbirth and mother-infant bonding
What is TSH function
✅ Red Flag Conditions of Thyroid are:
- Thyroid Storm – Life-threatening due to severe hyperthyroidism → High mortality if untreated.
🚨 Red flags: High fever, tachycardia, cardiovascular collapse, delirium, seizures.
Immediate treatment needed: Beta-blockers, PTU/methimazole, corticosteroids, iodine (after ATDs).
- Myxedema Coma – Severe hypothyroidism leading to organ failure.
🚨 Red flags: Bradycardia, hypothermia, respiratory failure, altered mental status.
Immediate treatment needed: IV levothyroxine, supportive care (warming, fluids, ventilation).
- Acute Suppurative Thyroiditis – Bacterial thyroid infection (Rare but life-threatening)
🚨 Red flags: Severe neck pain, high fever, swollen/tender thyroid with erythema, dysphagia, airway compromise.
Immediate treatment needed: IV antibiotics, possible surgical drainage if abscess is present. - Invasive (Riedel’s) Thyroiditis – Fibrotic thyroid leading to airway compression
🚨 Red flags: Progressive dysphagia, hoarseness, stridor (suggesting airway compression).
Immediate treatment needed: Surgery if airway obstruction occurs; steroids/immunosuppressants may be used.
Effect: Stimulates the thyroid gland to produce thyroxine (T4) and triiodothyronine (T3), which regulate metabolism.
Key Role: Controls energy usage in cells, body temperature, and metabolic rate.
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Thyroid Storm (✅)
A life-threatening complication of severe hyperthyroidism, often due to untreated Graves’ disease or toxic multinodular goiter.
Triggers: Infection, surgery, trauma, iodine load (contrast media, amiodarone).
Features: High fever, tachycardia, delirium, cardiovascular collapse, agitation, seizures.
Treatment: Beta-blockers (propranolol), antithyroid drugs (PTU/methimazole), corticosteroids, iodine (after antithyroid drugs).
Myxedema Coma (❌)
A severe complication of hypothyroidism, leading to multi-organ dysfunction.
Causes: Untreated hypothyroidism, infection, cold exposure, sedatives (opioids, benzodiazepines).
Features: Bradycardia, hypothermia, respiratory depression, altered mental status, puffy face.
Treatment: IV levothyroxine + supportive care (warming, fluids, mechanical ventilation if needed).
Addison’s Crisis (Adrenal Crisis) (❌)
A life-threatening emergency due to adrenal insufficiency, leading to severe cortisol deficiency.
Triggers: Infection, surgery, stopping steroids abruptly.
Features: Severe hypotension, shock, hypoglycemia, hyponatremia, hyperkalemia.
Treatment: IV hydrocortisone, IV fluids, glucose replacement.
Hashitoxicosis (❌)
A temporary hyperthyroid phase in early Hashimoto’s thyroiditis, due to thyroid cell destruction releasing stored hormone.
Not a severe emergency like thyroid storm.
Features: Mild hyperthyroid symptoms (palpitations, weight loss, sweating), then progresses to hypothyroidism.
Treatment: Beta-blockers for symptoms; no antithyroid drugs needed.
What is cortisol function
Red Flags
1. Addison’s Crisis (Adrenal Crisis) – Acute cortisol deficiency → Shock & death if untreated.
🚨 Red flags: Severe hypotension, shock, hypoglycemia, hyponatremia, hyperkalemia.
Immediate treatment needed: IV hydrocortisone, IV fluids, glucose replacement.
- Pheochromocytoma Crisis – Adrenal tumor secreting excess catecholamines
🚨 Red flags: Extreme hypertension (hypertensive crisis), severe headache, palpitations, diaphoresis, anxiety, risk of stroke.
Immediate treatment needed: IV alpha-blockers (phenoxybenzamine/phentolamine), beta-blockers (AFTER alpha blockade), IV fluids. - Waterhouse-Friderichsen Syndrome – Adrenal hemorrhage leading to adrenal failure
🚨 Red flags: Sudden shock, purpuric rash (meningococcemia), fever, DIC (disseminated intravascular coagulation), coma.
Immediate treatment needed: IV hydrocortisone, aggressive IV fluids, treat underlying infection (commonly meningococcal sepsis).
Effect: Increases blood glucose levels, suppresses immune responses, and aids in metabolism of fats, proteins, and carbohydrates.
Key Role: Critical for responding to stress and maintaining energy balance during prolonged challenges.
What is insulin function? It is a pancreatic hormone
Effect: Lowers blood glucose by facilitating glucose uptake into cells, especially in muscles and fat. Encourages glycogen storage in the liver.
Key Role: Maintains normal blood sugar levels and prevents hyperglycemia.
What is the role of glucagon in the body? It is a pancreatic hormone
Effect: Stimulates the breakdown of glycogen in the liver into glucose, increasing blood sugar levels during fasting or low energy states.
Key Role: Prevents hypoglycemia by ensuring steady glucose supply.
What is epinephrine function
Effect: Increases heart rate, dilates airways, and enhances blood flow to muscles. Mobilizes energy by breaking down glycogen and fat stores.
Key Role: Prepares the body for “fight or flight” during acute stress.
What is the key difference between primary and central hypothyroidism?
A) In primary hypothyroidism, TSH is elevated and T4 is low.
B) In central hypothyroidism, TSH is elevated and T4 is low.
C) Primary hypothyroidism has normal TSH levels.
D) Central hypothyroidism results in an elevated TSH and T4 levels.
✅ Correct Answer: A) In primary hypothyroidism, TSH is elevated and T4 is low.
🔹 Primary hypothyroidism is caused by thyroid dysfunction, which leads to low T4 and elevated TSH levels as the body tries to stimulate the thyroid.
❌ B) In central hypothyroidism, TSH is elevated and T4 is low. – Central hypothyroidism is caused by pituitary or hypothalamic dysfunction, leading to low TSH and low T4.
❌ C) Primary hypothyroidism has normal TSH levels. – TSH is elevated in primary hypothyroidism due to the lack of thyroid hormone production.
❌ D) Central hypothyroidism results in an elevated TSH and T4 levels. – Central hypothyroidism leads to low TSH and low T4 due to pituitary or hypothalamic failure.
Which laboratory findings suggest primary hypothyroidism?
A) Low T4, low TSH
B) High T4, high TSH
C) Normal T4, low TSH
D) Low T4, high TSH
Answer:
✅ D) Low T4, high TSH – In primary hypothyroidism, low thyroid hormone levels lead to compensatory elevation of TSH.
❌ A) Low T4, low TSH – This pattern suggests central (secondary) hypothyroidism.
❌ B) High T4, high TSH – This pattern is not typical of hypothyroidism; it could suggest TSH-secreting pituitary adenoma.
❌ C) Normal T4, low TSH – This is not a hypothyroid pattern.
Which of the following is a potential cause of acquired hypothyroidism?
A) Maternal iodine deficiency
B) Hashimoto’s thyroiditis
C) Congenital thyroid hypoplasia
D) Thyroid agenesis
In a newborn screening program, what is the next step if an abnormal T4 or TSH result is found?
A) Repeat the screening test in one year
B) Start levothyroxine immediately
C) Confirm with venous T4 and TSH levels
D) Perform a thyroid ultrasound
Answer:
✅ C) Confirm with venous T4 and TSH levels – This is the standard protocol to verify newborn screening results.
❌ A) Repeat in one year – Waiting too long can lead to developmental delays.
❌ B) Start levothyroxine immediately – Treatment should be started only after confirmation.
❌ D) Perform a thyroid ultrasound – Imaging is not necessary for diagnosis.
What is the most common cause of hyperthyroidism in children?
A) Hashimoto’s thyroiditis
B) Toxic multinodular goiter
C) Grave’s disease
D) Subacute thyroiditis
Answer:
✅ C) Grave’s disease – The most common cause due to autoantibodies stimulating the TSH receptor.
❌ A) Hashimoto’s thyroiditis – This typically leads to hypothyroidism.
❌ B) Toxic multinodular goiter – More common in adults.
❌ D) Subacute thyroiditis – Often transient and not the most common cause.
Conditions & Associations
Type 2 Diabetes (❌)
Not associated with Hashimoto’s thyroiditis.
Hashimoto’s is an autoimmune condition, while Type 2 diabetes is primarily related to insulin resistance and metabolic syndrome.
Type 1 diabetes, an autoimmune disease, has a stronger link to Hashimoto’s.
Marfan Syndrome (❌)
A genetic connective tissue disorder caused by FBN1 gene mutations.
Features: Tall stature, long limbs, joint hypermobility, lens dislocation, aortic aneurysm risk.
No direct association with Hashimoto’s or other autoimmune thyroid disorders.
Klinefelter Syndrome (❌)
A chromosomal disorder (XXY karyotype) in males.
Features: Small testes, infertility, gynecomastia, tall stature, learning difficulties.
Not strongly associated with Hashimoto’s thyroiditis.
Graves’ Disease (✅)
The most common cause of hyperthyroidism.
Autoantibodies stimulate the TSH receptor, leading to excessive thyroid hormone production.
Features: Goiter, exophthalmos, tachycardia, heat intolerance, weight loss.
Hashimoto’s Thyroiditis (❌)
Autoimmune hypothyroidism, NOT hyperthyroidism.
Features: Fatigue, weight gain, dry skin, cold intolerance, bradycardia.
Toxic Multinodular Goiter (❌)
Hyperfunctioning thyroid nodules cause hyperthyroidism, but more common in older adults, NOT the most common cause of hyperthyroidism in children.
Subacute Thyroiditis (❌)
De Quervain thyroiditis: Viral infection causes inflammation and transient hyperthyroidism.
Features: Neck pain, fever, malaise, thyroid tenderness.
Not the most common cause of hyperthyroidism.
What is the preferred first-line treatment for Grave’s disease?
A) Beta-blockers
B) Methimazole
C) Radioactive iodine
D) Surgery
Answer:
✅ B) Methimazole – First-line antithyroid drug for controlling hyperthyroidism.
❌ A) Beta-blockers – Used to manage symptoms, but they do not treat the underlying disease.
❌ C) Radioactive iodine – Used when antithyroid drugs fail or in specific cases.
❌ D) Surgery – Reserved for large goiters, nodules, or refractory cases.
What is a serious complication of untreated hyperthyroidism?
A) Myxedema coma
B) Thyroid storm
C) Addison’s crisis
D) Hashitoxicosis
Answer:
✅ B) Thyroid storm – A life-threatening complication of severe hyperthyroidism.
❌ A) Myxedema coma – A complication of severe hypothyroidism.
❌ C) Addison’s crisis – Related to adrenal insufficiency, not hyperthyroidism.
❌ D) Hashitoxicosis – A transient hyperthyroid phase of Hashimoto’s thyroiditis, not a severe complication.
Which of the following is TRUE about congenital hypothyroidism?
A) Early treatment leads to normal neurocognitive outcomes
B) It is usually acquired rather than congenital
C) It is usually diagnosed in adulthood
D) Imaging is always required for diagnosis.
✅ A) Early treatment leads to normal neurocognitive outcomes – Treatment within the first month is critical for normal brain development.
❌ B) It is usually acquired rather than congenital – Congenital hypothyroidism is present from birth, often due to thyroid agenesis or dysgenesis.
❌ C) It is usually diagnosed in adulthood – Newborn screening detects congenital hypothyroidism early.
❌ D) Imaging is always required for diagnosis – Imaging is not necessary for diagnosis, as blood tests (T4, TSH) confirm it.
Which of the following conditions is NOT associated with an increased risk of Hashimoto’s thyroiditis?
A) Marfan Syndrome
B) Turner Syndrome
C) Celiac Disease
D) Type 1 Diabetes
✅ A) Marfan Syndrome – A connective tissue disorder, not autoimmune.
❌ B) Turner Syndrome – Increased risk due to its association with autoimmune diseases.
❌ C) Celiac Disease – Hashimoto’s is more common in people with celiac disease due to shared autoimmune mechanisms.
❌ D) Type 1 Diabetes – Strongly linked to Hashimoto’s due to common autoimmune pathways.
Which of the following statements about subacute (De Quervain) thyroiditis is TRUE?
A) It is caused by viral infections
B) It leads to lifelong hypothyroidism – It is usually self-limiting and transient.
C) It is caused by autoantibodies attacking the thyroid
D) It is best treated with methimazole
✅ A) It is caused by viral infections – Commonly associated with mumps, influenza, coxsackievirus, EBV.
❌ B) It leads to lifelong hypothyroidism – It is usually self-limiting and transient.
❌ C) It is caused by autoantibodies attacking the thyroid – Unlike Hashimoto’s, subacute thyroiditis is inflammatory rather than autoimmune.
❌ D) It is best treated with methimazole – Methimazole treats hyperthyroidism, while subacute thyroiditis often resolves on its own with supportive care.
What lab findings are expected in Addison’s crisis?
A) Hyponatremia, hyperkalemia, hypoglycemia.
B) Hypernatremia, hypokalemia, hyperglycemia.
C) Normal sodium and potassium levels.
D) Hypercalcemia and low TSH.
✅ A) Hyponatremia, hyperkalemia, hypoglycemia – Due to low cortisol and aldosterone deficiency.
❌ B) Hypernatremia, hypokalemia, hyperglycemia – This describes Cushing’s syndrome (excess cortisol).
❌ C) Normal sodium and potassium levels – Addison’s affects electrolytes significantly.
❌ D) Hypercalcemia and low TSH – Addison’s does not typically cause thyroid dysfunction.
Which of the following differentiates Hashitoxicosis from Graves’ disease?
A) Hashitoxicosis is a temporary phase, while Graves’ disease is a sustained autoimmune disorder.
B) Both have positive TSH receptor antibodies.
C) Both require long-term antithyroid drug therapy.
D) Radioactive iodine uptake is high in Hashitoxicosis.
✅ A) Hashitoxicosis is a temporary phase, while Graves’ disease is a sustained autoimmune disorder.
❌ B) Both have positive TSH receptor antibodies. – Only Graves’ disease has TSH receptor antibodies.
❌ C) Both require long-term antithyroid drug therapy. – Hashitoxicosis resolves on its own, while Graves’ requires treatment.
❌ D) Radioactive iodine uptake is high in Hashitoxicosis. – RAIU is low in Hashitoxicosis because thyroid cells are being destroyed, not stimulated.
Why is Peripheral Precocious Puberty Considered “Independent”?
The key distinction between central (gonadotropin-dependent) and peripheral (gonadotropin-independent) precocious puberty is where the signal to start puberty originates:
Central (gonadotropin-dependent):
Issue originates from the brain (hypothalamus or pituitary).
The hypothalamus releases GnRH, stimulating the pituitary to release FSH & LH, which then act on the gonads to produce sex hormones.
Examples: CNS tumors, brain lesions, idiopathic cases.
Peripheral (gonadotropin-independent):
Issue originates outside the brain—the gonads or adrenal glands produce excessive sex hormones independently of pituitary control.
The hypothalamus and pituitary are NOT the primary cause; instead, the excess hormones are produced directly by the ovaries, testes, or adrenal glands.
Since the pituitary senses high hormone levels, it reduces FSH & LH secretion (negative feedback).
Examples: Congenital adrenal hyperplasia (CAH), ovarian cysts, gonadal tumors, adrenal abnormalities.
In summary:
“Dependent” means puberty is driven by the normal pathway (brain → pituitary → gonads).
“Independent” means excess hormones are coming from another source, bypassing the normal brain signaling.
Which of the following is the primary cause of Cushing DISEASE?
A) Adrenal adenoma
B) Pituitary adenoma
C) Ectopic ACTH-producing tumor
D) Chronic glucocorticoid use
Adrenocorticotropic Hormone (ACTH)
Answer: ✅ B) Pituitary adenoma
Cushing disease refers specifically to pituitary overproduction of ACTH, usually from a pituitary adenoma.
This leads to excessive cortisol secretion from the adrenal glands.
❌ A) Adrenal adenoma → This causes Cushing Syndrome, not Cushing Disease (since it’s an adrenal cause, not a pituitary cause).
❌ C) Ectopic ACTH-producing tumor → Causes ACTH-dependent Cushing Syndrome (e.g., small cell lung cancer), but not Cushing Disease.
❌ D) Chronic glucocorticoid use → Exogenous corticosteroids cause iatrogenic Cushing Syndrome, but not Cushing Disease.
What is the best initial test for suspected Cushing Syndrome?
A) Random serum cortisol
B) Dexamethasone suppression test
C) ACTH stimulation test
D) MRI of the brain
Answer: ✅ B) Dexamethasone suppression test
First-line screening test → If cortisol fails to suppress after low-dose dexamethasone, Cushing Syndrome is likely.
❌ A) Random serum cortisol → Cortisol levels fluctuate, so a random test is unreliable.
❌ C) ACTH stimulation test → Used for adrenal insufficiency, not Cushing Syndrome.
❌ D) MRI of the brain → Done after biochemical confirmation to check for a pituitary tumor.
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Why is this true, is it because dexamethasone is a glucocorticoid and it should reduce the GnRH and if it does not then it is an adrenal or gonad issue probably or adrenal or will I not be able to tell until
The dexamethasone suppression test works because dexamethasone is a synthetic glucocorticoid that mimics cortisol. Here’s why it helps identify Cushing Syndrome and differentiate its causes:
Why is the Dexamethasone Suppression Test Used?
Normally, cortisol follows a negative feedback loop:
The hypothalamus releases CRH → stimulates the pituitary to release ACTH → stimulates the adrenal glands to release cortisol.
When cortisol levels are high, negative feedback suppresses CRH & ACTH production, preventing excess cortisol.
Dexamethasone is a potent glucocorticoid that should act like cortisol and suppress ACTH secretion.
If it fails to suppress cortisol, it suggests Cushing Syndrome (excess cortisol production).
How to Interpret the Dexamethasone Suppression Test?
Step 1: Low-Dose Dexamethasone Suppression Test (1 mg overnight)
Normal response: Cortisol suppresses (negative feedback working).
Abnormal (Cushing Syndrome): Cortisol remains high (something is causing excessive cortisol).
✅ If abnormal, we move to Step 2 to find the cause.
What About GnRH?
You asked if dexamethasone should suppress GnRH. The answer is indirectly, yes, but that’s not why we use this test for Cushing Syndrome.
Chronically high cortisol (from Cushing Syndrome) inhibits GnRH release, which can cause low FSH & LH and result in irregular periods or infertility.
However, we use dexamethasone suppression to assess the cortisol feedback loop, not GnRH directly.
When Can You Tell If It’s Adrenal vs. Pituitary vs. Ectopic?
1️⃣ Low-dose dexamethasone test:
Cortisol suppresses → No Cushing Syndrome.
Cortisol remains high → Cushing Syndrome confirmed.
2️⃣ ACTH level measurement:
High ACTH → Likely Cushing Disease (pituitary) or ectopic ACTH tumor → Do high-dose dexamethasone test.
Low ACTH → Likely adrenal tumor (ACTH-independent Cushing Syndrome).
3️⃣ High-dose dexamethasone test (if ACTH is high):
Partial suppression → Pituitary tumor (Cushing Disease).
No suppression → Ectopic ACTH-producing tumor.
4️⃣ Imaging (MRI or CT):
Pituitary MRI → If Cushing Disease suspected.
Adrenal CT → If adrenal tumor suspected.
Chest CT → If ectopic ACTH tumor (e.g., small cell lung cancer) suspected.
Summary
Dexamethasone suppression test is used because it mimics cortisol and should suppress ACTH (and therefore cortisol) in a normal person.
If cortisol is not suppressed, it indicates Cushing Syndrome.
Further tests (ACTH levels, high-dose dexamethasone, imaging) are needed to pinpoint the exact cause (pituitary vs. adrenal vs. ectopic).
A female newborn presents with ambiguous genitalia, salt-wasting crisis, and elevated 17-hydroxyprogesterone. What is the most likely diagnosis?
A) Turner Syndrome
B) Congenital Adrenal Hyperplasia
C) Androgen Insensitivity Syndrome
D) Klinefelter Syndrome
Answer: ✅ B) Congenital Adrenal Hyperplasia (CAH)
CAH is the most common cause of ambiguous genitalia in newborn females.
21-hydroxylase deficiency leads to:
Excess androgens → Virilization (ambiguous genitalia).
Mineralocorticoid deficiency → Salt wasting, hyponatremia, hyperkalemia.
Elevated 17-hydroxyprogesterone (diagnostic marker).
❌ A) Turner Syndrome → Causes primary amenorrhea, but NOT virilization or salt wasting.
❌ C) Androgen Insensitivity Syndrome → 46 XY karyotype with female external genitalia, but no uterus.
❌ D) Klinefelter Syndrome → 47 XXY karyotype, causes infertility and gynecomastia, but does not affect genital development at birth.
Which treatment is used to suppress excess androgens in Congenital Adrenal Hyperplasia (CAH)?
A) Spironolactone
B) Hydrocortisone
C) Fludrocortisone
D) Estrogen therapy
Answer: ✅ B) Hydrocortisone
First-line treatment → Suppresses ACTH secretion, reducing excess androgen production.
❌ A) Spironolactone → Used for hirsutism in PCOS, not for CAH treatment.
❌ C) Fludrocortisone → Used for salt-wasting CAH (mineralocorticoid replacement), but doesn’t suppress androgens.
❌ D) Estrogen therapy → Used for delayed puberty, not CAH.
What is the best test to differentiate between central vs. peripheral precocious puberty?
A) Bone age X-ray
B) GnRH stimulation test
C) Serum estradiol/testosterone
D) ACTH stimulation test
Answer: ✅ B) GnRH stimulation test
Gold standard to determine if puberty is central or peripheral.
Central → FSH & LH will rise after GnRH stimulation.
Peripheral → FSH & LH will remain low due to negative feedback from excess sex hormones.
❌ A) Bone age X-ray → Helps confirm precocious puberty but doesn’t determine central vs. peripheral.
❌ C) Serum estradiol/testosterone → Can confirm puberty but doesn’t differentiate causes.
❌ D) ACTH stimulation test → Used for adrenal insufficiency, not precocious puberty.
