ENDOCRINOLOGY – 2017

The paraventricular nucleus (PVN) is a key part of the hypothalamus and has both neuroendocrine and autonomic functions.

The PVN primarily synthesizes:

• Oxytocin, which:

  • Causes uterine contractions during labor

  • Triggers the milk ejection reflex during breastfeeding

  • Also plays a role in emotional bonding and social behavior

It also produces:

• Some antidiuretic hormone (ADH), though ADH is primarily synthesized in the supraoptic nucleus

After synthesis, these hormones travel via axons down the hypothalamo-hypophyseal tract to be stored and released from the posterior pituitary.

So, while both oxytocin and some ADH are made in the PVN, oxytocin is more definitively and classically associated with this nucleus.

Incorrect Answer Explanations:

Antidiuretic hormone (ADH)

• Incorrect (partially correct)

  • While some ADH is made in the paraventricular nucleus, it is primarily synthesized in the supraoptic nucleus.

  • So it’s not the best or most characteristic choice here.

Gonadotropin-releasing hormone (GnRH)

• Incorrect

  • GnRH is produced in the preoptic area of the hypothalamus, not in the paraventricular nucleus.

  • It controls the release of LH and FSH from the anterior pituitary.

Prolactin

• Incorrect

  • Prolactin is secreted by the anterior pituitary, not the hypothalamus.

  • Its secretion is primarily regulated (inhibited) by dopamine from the hypothalamus.

Adrenocorticotropic hormone (ACTH)

• Incorrect

  • ACTH is produced by the anterior pituitary, stimulated by CRH (corticotropin-releasing hormone) from the hypothalamus.

  • It is not secreted by the paraventricular nucleus.

Conn syndrome, also known as primary hyperaldosteronism, is caused by excess secretion of aldosterone, typically due to an adrenal adenoma or adrenal hyperplasia.

Physiological Role of Aldosterone:

Aldosterone acts on the distal nephron (especially the collecting ducts) of the kidneys to:

• Increase sodium reabsorption (→ water retention → hypertension)

• Increase potassium excretion (→ hypokalemia)

• Increase hydrogen ion excretion (→ metabolic alkalosis)

Why Metabolic Alkalosis?

• The increased loss of hydrogen ions (H⁺) in the urine leads to a rise in blood pH.

• This results in metabolic alkalosis — a key metabolic derangement seen in Conn syndrome.

Incorrect Answer Explanations:

Hyperkalemia

• Incorrect: Aldosterone increases potassium excretion, so Conn syndrome causes hypokalemia, not hyperkalemia.

Hypercalcemia

• Incorrect: Conn syndrome does not affect calcium metabolism directly.

• Hypercalcemia is more characteristic of hyperparathyroidism or vitamin D toxicity.

Metabolic acidosis

• Incorrect: This would occur if hydrogen ions were retained, such as in renal failure or type 1 renal tubular acidosis.

• In Conn syndrome, H⁺ is excessively excreted, leading to alkalosis.

Respiratory acidosis

• Incorrect: This is due to hypoventilation, causing CO₂ retention (e.g., in COPD or CNS depression).

• Conn syndrome is a metabolic, not respiratory, disorder.

When Triglycerides Are Dangerously High (> 1000 mg/dL):

• Pancreatitis becomes a significant risk.

• The excess triglycerides are broken down by pancreatic lipase into free fatty acids (FFAs) in the pancreatic capillaries.

• FFAs are toxic at high concentrations, leading to pancreatic inflammation, ischemia, and cellular injury.

Clinical Relevance:

• Hypertriglyceridemia is one of the top three causes of acute pancreatitis, along with gallstones and alcohol abuse.

• It is particularly common in patients with uncontrolled diabetes, obesity, and familial lipid disorders.

Incorrect Answer Explanations:

Diabetes Type 1

• Type 1 Diabetes Mellitus involves autoimmune destruction of pancreatic beta cells, leading to insulin deficiency.

• While diabetic ketoacidosis (DKA) may transiently elevate triglycerides, severe hypertriglyceridemia is more typical of Type 2 diabetes or metabolic syndrome, not Type 1.

• Not directly linked to pancreatitis unless DKA-induced hypertriglyceridemia occurs, which is rare.

Retinopathy

• Diabetic retinopathy is a microvascular complication of diabetes, primarily related to chronic hyperglycemia, not hypertriglyceridemia.

• Lipid abnormalities may worsen retinal outcomes but retinopathy is not directly caused by hypertriglyceridemia.

Diabetic Foot

• Diabetic foot ulcers are caused by neuropathy, ischemia, and infection.

• There is no direct association with hypertriglyceridemia.

Appendicitis

• Appendicitis is due to inflammation of the appendix, commonly from luminal obstruction (like fecaliths or lymphoid hyperplasia).

• There is no link between triglyceride levels and appendicitis.

Hypothyroidism slows down many of the body’s processes, including metabolism, neuromuscular activity, and cardiovascular function.

Common Signs and Symptoms of Hypothyroidism:

• Weight gain (due to decreased basal metabolic rate)

• Dry skin

• Constipation (slowed gastrointestinal motility)

• Cold intolerance

• Fatigue

• Bradycardia (slow heart rate)

• Depression or cognitive slowing

• Menstrual irregularities

• Delayed relaxation phase of deep tendon reflexes (especially the ankle jerk)—this is a classic clinical finding and considered one of the most specific neuromuscular signs of hypothyroidism.

Why does this happen?

• Delayed relaxation of reflexes is thought to result from impaired calcium reuptake into the sarcoplasmic reticulum of muscle due to thyroid hormone deficiency.

• Weight gain results from decreased energy expenditure.

These signs complement the other findings in hypothyroidism and help solidify the diagnosis.

Incorrect Answer Explanations:

Systolic Hypertension and Hyper-reflexia

• These are typically seen in hyperthyroidism, not hypothyroidism.

• Hyperthyroidism increases sympathetic activity, leading to brisk reflexes and higher systolic pressure due to increased cardiac output.

Palmar Erythema and Tachycardia

• These are signs of hyperthyroidism or liver disease, not hypothyroidism.

• In hyperthyroidism, increased circulation causes palmar erythema and tachycardia due to heightened metabolic demands.

Lid Lag and Lid Retraction

• Classic signs of Graves’ disease (hyperthyroidism) due to sympathetic overactivity affecting the levator palpebrae superioris muscle.

Weight Loss and Bruit

• Seen in hyperthyroidism:

  • Weight loss occurs due to increased metabolism.

  • A thyroid bruit may be heard in Graves’ disease due to increased blood flow in the hyperactive thyroid gland.

Biguanides (Metformin) are the first-line drug for patients with insulin resistance, which is commonly seen in both Type 2 Diabetes Mellitus and Polycystic Ovary Syndrome (PCOS).

Mechanism of Action:

• Reduces hepatic glucose production (gluconeogenesis)

• Increases insulin sensitivity in peripheral tissues (muscle and fat)

• Helps with weight control or mild weight loss, making it ideal for obese patients

Why is Metformin Ideal Here?

• Hyperglycemia: Metformin lowers blood sugar without causing hypoglycemia.

• Obesity: Metformin does not cause weight gain, unlike insulin or sulfonylureas.

• Amenorrhea: In cases like PCOS, Metformin can help restore menstrual cycles by improving insulin sensitivity, which reduces hyperandrogenism and helps normalize ovulation.

Thus, Metformin addresses all three of the patient’s issues in a safe and effective manner.

Incorrect Answer Explanations:

Alpha-glucosidase Inhibitors

• Mechanism: Slow carbohydrate digestion in the intestines, reducing post-meal blood sugar spikes.

• Why Incorrect?

  • They do not affect insulin resistance.

  • No role in correcting amenorrhea or aiding in weight loss.

  • Not first-line for this clinical scenario.

Insulin

• Mechanism: Lowers blood glucose by promoting glucose uptake into cells.

• Why Incorrect?

  • May cause further weight gain, which is counterproductive in an obese, insulin-resistant patient.

  • Does not address amenorrhea or improve insulin resistance directly.

  • Reserved for severe hyperglycemia or treatment failure with oral agents.

Sulphonylureas

• Mechanism: Increase insulin secretion from the pancreas.

• Why Incorrect?

  • Can cause hypoglycemia and weight gain.

  • Do not improve insulin sensitivity.

  • Not preferred in obese patients with insulin resistance.

Thiazolidinediones (TZDs)

• Mechanism: Increase insulin sensitivity in adipose tissue and muscle.

• Why Incorrect?

  • Cause weight gain, including fluid retention and increased fat mass.

  • Potential side effects include cardiovascular risks (e.g., heart failure exacerbation).

  • Although they improve insulin resistance, they are not first-line therapy, especially in an obese patient.

• Steroids (glucocorticoids like prednisone) are commonly prescribed for rheumatoid arthritis and other inflammatory conditions.

• Long-term steroid use can lead to iatrogenic Cushing’s syndrome, which causes:

  • Weight gain (central obesity, “moon face”, “buffalo hump”)

  • Muscle weakness (proximal myopathy due to protein catabolism)

  • Blurry vision (due to steroid-induced cataracts or glaucoma)

  • Hyperglycemia, osteoporosis, skin thinning, and immune suppression are other known side effects.

Why the Other Options Are Incorrect:

Summary:

The patient’s muscle weakness, weight gain, and blurry vision are classic side effects of long-term steroid use, which is a common medication in arthritis management

• Polycystic kidney disease (PKD) is a genetic disorder that leads to the formation of multiple fluid-filled cysts in the kidneys.

• It primarily affects kidney structure and function, leading to:

  • Hypertension

  • Kidney failure

  • Abdominal mass or flank pain

• **PKD is not directly associated with diabetes mellitus or its pathogenesis.

• It does not affect insulin production, insulin resistance, or glucose metabolism.

Conditions Associated with Diabetes Mellitus:

Why the Other Options Are Incorrect:

Summary:

Polycystic kidney disease is not associated with diabetes mellitus, whereas obesity, genetics, heart disease, and atherosclerosis are closely linked to diabetes and its complications.

• Subacute thyroiditis is also called De Quervain’s thyroiditis or granulomatous thyroiditis.

• Often follows viral infections such as mumps, influenza, or coxsackievirus.

• Characterized by:

  • Painful, tender thyroid gland

  • Transient hyperthyroidism (due to release of preformed thyroid hormones)

  • Possible hypothyroid phase before recovery

Treatment of Choice:

• The main goal is to reduce pain and inflammation.

• First-line therapy:

  • Non-steroidal anti-inflammatory drugs (NSAIDs) for mild cases

  • Glucocorticoids (e.g., prednisone) if NSAIDs are not sufficient or if symptoms are severe

• Beta blockers can be used for symptomatic control of hyperthyroidism (e.g., palpitations) but do not treat the inflammation.

• Levothyroxine is not required initially, unless the patient becomes hypothyroid long-term.

• Anti-thyroid drugs (e.g., methimazole) are not indicated, because the hyperthyroidism is due to hormone leakage, not overproduction.

Why the Other Options Are Incorrect:

Summary:

The treatment of subacute (De Quervain’s) thyroiditis is NSAIDs and steroids, with steroids reserved for severe or refractory cases.

Why IV Hydrocortisone is the Treatment of Choice:

• The clinical picture suggests acute adrenal insufficiency (Addisonian crisis) superimposed on chronic adrenal insufficiency.

• Hydrocortisone is the first-line treatment because it provides glucocorticoid replacement, which is essential for:

  • Maintaining blood pressure (by sensitizing vasculature to catecholamines)

  • Maintaining blood sugar (prevents hypoglycemia)

  • Reducing inflammation and stress response

• In high doses, hydrocortisone also has mineralocorticoid activity, helping with sodium retention and potassium excretion.

Standard Emergency Treatment:

1. Immediate IV hydrocortisone

   • Typically, 100 mg IV bolus, followed by continuous infusion or regular doses.

2. IV fluids (normal saline or dextrose) to correct hypotension and dehydration.

3. Glucose correction if needed (due to hypoglycemia).

4. Identify and treat any underlying cause (e.g., infection, stopping steroids abruptly).

Why the Other Options Are Incorrect:

Summary:

In a 16-year-old girl with Addisonian crisis (hypotension, lethargy, hypoglycemia, and flank tenderness), the treatment of choice is intravenous hydrocortisone to correct glucocorticoid deficiency and stabilize the patient.

Why the Short Synacthen Test is Best:

• The Short Synacthen Test (ACTH stimulation test) is the gold standard initial diagnostic test for suspected adrenal insufficiency.

• Synacthen is a synthetic ACTH.

• Procedure:

  • Measure baseline cortisol.

  • Administer Synacthen (250 µg IV or IM).

  • Measure cortisol again at 30 and 60 minutes.

• Normal response: Cortisol rises significantly (>18–20 µg/dL).

• Adrenal insufficiency: Little or no cortisol rise after Synacthen.

Why It’s Important:

• This test directly evaluates the adrenal cortex’s ability to produce cortisol.

• It helps distinguish between:

  • Primary adrenal insufficiency (Addison’s disease) → No cortisol rise

  • Secondary adrenal insufficiency (pituitary cause) → May have a blunted response

Why the Other Options Are Incorrect:

Summary:

The Short Synacthen Test is the most appropriate initial investigation in a patient with suspected adrenal insufficiency, as it directly assesses adrenal cortisol production capacity.

What is Addison’s Disease?

• Addison’s disease is primary adrenal insufficiency—the adrenal glands fail to produce cortisol and aldosterone.

• Common causes include autoimmune destruction, infections (e.g., TB), or adrenal hemorrhage.

Key Clinical Features in This Case:

Lab Findings Typically Seen:

• Low cortisol

• High ACTH (in primary adrenal failure)

• Hyponatremia and hyperkalemia

• Hypoglycemia

Why the Other Options Are Incorrect:

Summary:

A 16-year-old girl with chronic weight loss, fatigue, hypotension, altered mental status, and flank tenderness most likely has Addison’s disease (primary adrenal insufficiency).

What is MEN1?

Multiple Endocrine Neoplasia Type 1 (MEN1) is a hereditary syndrome characterized by tumors in:

Symptoms in This Case:

• Hypoglycemia → Suggests insulinoma (pancreatic islet cell tumor)

• Loose stools → May be due to VIPoma or gastrinoma (also seen in MEN1)

• Renal stones → Due to hyperparathyroidism causing hypercalcemia

• Erectile dysfunction → Could be from pituitary tumor (prolactinoma) affecting gonadal function

Why the Other Options Are Incorrect:

Summary:

The combination of hypoglycemia, diarrhea, renal stones, and erectile dysfunction is characteristic of MEN1, which involves tumors of the parathyroid, pancreas, and pituitary.

Why Parathyroid Gland Removal Is the Most Likely Cause:

• The parathyroid glands regulate calcium levels through the secretion of parathyroid hormone (PTH).

• Neck surgeries, especially thyroidectomy, may accidentally damage or remove the parathyroid glands because of their close anatomical location.

• Hypocalcemia due to parathyroid removal leads to:

  • Tingling (paresthesia) around the mouth, fingers, and toes

  • Muscle cramps

  • Tetany (severe hypocalcemia)

  • Chvostek’s and Trousseau’s signs may be positive on physical exam

Why This Happens:

• Low PTH → Decreased calcium reabsorption from bones, kidneys, and intestines

• Result: Hypocalcemia → Neuromuscular excitability → Tingling and cramps

Why the Other Options Are Incorrect:

Summary:

The most likely cause of tingling after neck surgery is accidental removal or damage to the parathyroid glands, leading to hypocalcemia and neuromuscular symptoms.

Initial Testing for Hypothyroidism:

• The first-line tests for suspected hypothyroidism are:

  • TSH (Thyroid Stimulating Hormone) – assesses pituitary response

  • Free T4 (Thyroxine) – assesses thyroid gland output

Why These Tests?

• TSH is the most sensitive screening test because the pituitary responds to small changes in T4 by adjusting TSH secretion.

• Free T4 tells you whether the thyroid is actually producing enough hormone.

Interpretation:

Why the Other Options Are Incorrect:

Summary:

The initial tests for hypothyroidism are TSH and free T4, as they provide a complete picture of pituitary and thyroid function

• Methimazole is a thionamide anti-thyroid drug used in hyperthyroidism treatment.

• Its mechanism: Inhibits thyroid peroxidase, preventing the organification of iodine and thyroid hormone synthesis.

Serious Side Effect:

• Agranulocytosis is the most feared side effect of methimazole (can also occur with propylthiouracil but is more common with methimazole).

• It involves severe reduction in neutrophils (granulocytes) → very low WBC count.

• Presents as:

  • Sudden onset of sore throat and fever

  • Increased risk of life-threatening infections

Management:

• Immediate discontinuation of the drug is required.

• Perform urgent CBC to check for leukopenia/neutropenia.

Why the Other Options Are Incorrect:

Summary:

Methimazole can cause agranulocytosis, presenting as sore throat, fever, and a low WBC count—a medical emergency requiring immediate attention.

What is Kallmann’s Syndrome?

• Kallmann’s syndrome is a form of hypogonadotropic hypogonadism combined with anosmia (loss of smell).

• It results from defective migration of GnRH-secreting neurons and olfactory neurons during embryonic development.

Pathophysiology:

• Normally, GnRH neurons originate near the olfactory placode and migrate to the hypothalamus.

• In Kallmann’s syndrome, this migration fails → deficient GnRH production.

• This leads to:

  • Low LH/FSH (hypogonadotropic hypogonadism)

  • Undescended testes (cryptorchidism) or underdeveloped genitalia in males

  • Delayed or absent puberty

  • Anosmia or hyposmia (impaired smell)

Why the Other Options Are Incorrect:

Summary:

A 10-year-old boy with anosmia, undescended testes, and hypogonadism most likely has Kallmann’s syndrome, a developmental disorder of GnRH and olfactory neuron migration.

• Sitagliptin is an oral antidiabetic drug used for type 2 diabetes mellitus.

• It belongs to the class of DPP-4 inhibitors (dipeptidyl peptidase-4 inhibitors).

Mechanism of Action:

• DPP-4 normally breaks down incretin hormones (GLP-1 and GIP).

• Incretins increase insulin secretion (glucose-dependent) and decrease glucagon secretion after meals.

• Sitagliptin inhibits DPP-4, leading to:

  • Increased GLP-1 and GIP levels

  • Prolonged insulin secretion

  • Decreased glucagon release

  • Better postprandial glucose control

Why the Other Options Are Incorrect:

Summary:

Sitagliptin is a DPP-4 inhibitor that increases incretin levels, leading to improved insulin secretion and reduced glucagon, helping control blood sugar in type 2 diabetes.

• Sheehan’s syndrome is postpartum hypopituitarism caused by ischemic necrosis of the anterior pituitary due to severe blood loss during or after childbirth (postpartum hemorrhage).

• The anterior pituitary enlarges during pregnancy, making it more susceptible to ischemia in the event of hypotension or hemorrhage.

Clinical Features:

• Failure to lactate (due to prolactin deficiency)

• Amenorrhea or oligomenorrhea (due to gonadotropin deficiency → low LH/FSH)

• Fatigue, weakness, cold intolerance (due to TSH and ACTH deficiency)

• Loss of pubic and axillary hair (optional finding)

Why the Other Options Are Incorrect:

Summary:

A postpartum woman with amenorrhea, inability to lactate, and a history of postpartum hemorrhage is classic for Sheehan’s syndrome (postpartum pituitary necrosis).

Why Prolactin is the Most Important Test:

• Prolactin is the hormone responsible for milk production (galactorrhea).

• Hyperprolactinemia (excess prolactin) can cause:

  • Galactorrhea (milk secretion without pregnancy or breastfeeding)

  • Infertility due to suppression of GnRH, leading to low LH/FSH and anovulation

• The most common cause is a prolactinoma (pituitary adenoma), but other causes include:

  • Hypothyroidism

  • Medications (dopamine antagonists)

  • Chest wall stimulation

Why the Other Options Are Incorrect:

Summary:

In a woman with galactorrhea and infertility, the first lab test to order is serum prolactin to evaluate for hyperprolactinemia, which is the most likely cause.

Why PCOS is the Most Probable Diagnosis:

Polycystic Ovarian Syndrome (PCOS) is the most common endocrine disorder in reproductive-aged women, typically presenting with:

• Oligomenorrhea or amenorrhea (due to anovulation)

• Hirsutism (excess hair growth) from androgen excess

• Weight gain/obesity, often linked to insulin resistance

• Polycystic ovaries seen on ultrasound (multiple peripheral follicles)

Pathophysiology:

• Increased LH:FSH ratio, leading to increased androgen production by the ovaries

• Impaired follicle maturation → anovulation

• Insulin resistance worsens hormonal imbalance

Why the Other Options Are Incorrect:

Summary:

The combination of oligomenorrhea, hirsutism, and weight gain in a young woman is most consistent with Polycystic Ovarian Syndrome (PCOS).

Understanding the Lab Findings:

Primary Hyperparathyroidism:

• Caused by parathyroid adenoma (most common), parathyroid hyperplasia, or rarely parathyroid carcinoma.

• In this condition, the parathyroid glands secrete PTH autonomously, ignoring normal feedback mechanisms.

• High PTH leads to:

  • Increased calcium reabsorption from bone and kidney

  • Increased activation of Vitamin D (but normal Vitamin D here suggests early stage or regulated synthesis)

  • Increased intestinal absorption of calcium (via Vitamin D)

• Result: High calcium, high PTH, and normal renal function (normal creatinine)

Why the Other Options Are Incorrect:

Summary:

High PTH + High Calcium + Normal Creatinine and Vitamin D is classic for Primary Hyperparathyroidism.

• Iodine is essential for the production of thyroid hormones (T3 and T4).

• People living in mountainous or inland areas often have limited access to iodine-rich foods, such as seafood.

• Soil and water in these areas are typically iodine-deficient, leading to iodine deficiency disorders (IDD).

Hypothyroidism from Iodine Deficiency:

• Lack of iodine → Reduced thyroid hormone production

• Leads to hypothyroidism and sometimes goiter (thyroid enlargement as compensation)

• Common in regions without iodized salt programs

Why the Other Options Are Incorrect:

Summary:

In a mountainous region, iodine deficiency is the most common cause of hypothyroidism due to low environmental iodine availability.

• Produced by: Hypothalamus (supraoptic and paraventricular nuclei)

• Stored and released by: Posterior pituitary

Primary Function:

• ADH helps regulate water balance in the body by:

  • Increasing water reabsorption in the collecting ducts of the kidneys

  • It binds to V2 receptors on the kidney tubules

  • This activates adenylyl cyclase → cAMP → insertion of aquaporin-2 water channels

  • Result: more water is reabsorbed, urine becomes concentrated, and plasma osmolality decreases

When is ADH Released?

• High blood osmolality (dehydration, high sodium)

• Low blood volume or pressure (e.g., hemorrhage)

Why the Other Options Are Incorrect:

Summary:

Anti-diuretic hormone (ADH) primarily regulates water balance by increasing water reabsorption in the kidneys, helping to maintain blood pressure and plasma osmolality.

• Glycogenolysis is the process of breaking down glycogen into glucose-1-phosphate for energy production.

• It starts at the non-reducing ends of glycogen, removing glucose residues one at a time.

Role of Glycogen Phosphorylase:

• Glycogen phosphorylase cleaves α-1,4 glycosidic bonds at the peripheral (non-reducing) ends of glycogen.

• It uses inorganic phosphate (Pi) to release glucose-1-phosphate.

• This is the rate-limiting step of glycogenolysis.

What Happens to Branches?

• When glycogen phosphorylase gets close to a branch point, it cannot cleave α-1,6 linkages.

• At that point, the debranching enzyme takes over to handle branch points.

Why the Other Options Are Incorrect:

Summary:

Glycogen phosphorylase is responsible for cleaving glucose-1-phosphate from the peripheral ends of glycogen during glycogenolysis.

• Erythroblastosis fetalis (also known as hemolytic disease of the newborn) occurs when the maternal immune system destroys fetal red blood cells, often due to Rh incompatibility.

• The fetal body responds by overproducing red blood cell precursors to replace the destroyed cells.

Bone Marrow Response:

• Normally, the bone marrow releases mature red blood cells (RBCs).

• In erythroblastosis fetalis, there is massive hemolysis, so the bone marrow becomes hyperactive.

• It starts to release immature red blood cell precursors (blast cells), specifically erythroblasts, into the bloodstream.

• This is why the condition is called erythroblastosis (“erythro-” = red blood cells, “-blastosis” = immature cell proliferation).

Why the Other Options Are Incorrect:

Summary:

In erythroblastosis fetalis, the bone marrow releases blast cells (erythroblasts) into the circulation in excess to compensate for severe red cell destruction.

• Steroid hormones are lipophilic (fat-soluble).

• They easily diffuse through the cell membrane.

• Once inside the cell, they bind to intracellular receptors, primarily located in the cytoplasm (some may be nuclear).

Mechanism of Action:

1. Steroid hormone enters the cell.

2. It binds to a cytoplasmic receptor, forming a hormone-receptor complex.

3. This complex translocates to the nucleus.

4. It binds to specific DNA sequences (hormone response elements) to regulate gene transcription.

5. New proteins are synthesized, leading to long-lasting effects.

Examples of Steroid Hormones:

• Cortisol, Aldosterone, Estrogen, Testosterone, Progesterone, Vitamin D

Why the Other Options Are Incorrect:

Summary:

Steroid hormones bind to cytoplasmic receptors, leading to direct regulation of gene expression.

• The adrenal medulla secretes catecholamines:

  • Epinephrine (adrenaline) – ~80%

  • Norepinephrine (noradrenaline) – ~20%

Function:

• These hormones produce sympathetic system-like effects:

  • Increased heart rate and contractility

  • Vasoconstriction (norepinephrine)

  • Vasodilation in skeletal muscle (epinephrine)

  • Bronchodilation

  • Increased blood glucose (via glycogenolysis and gluconeogenesis)

  • Lipolysis

Essentially, the adrenal medulla acts as a modified sympathetic ganglion, releasing hormones directly into the bloodstream for systemic “fight-or-flight” responses.

Why the Other Options Are Incorrect:

Summary:

The adrenal medulla hormones have sympathetic system-like activity, mediating fight or flight responses.

• Adenylate cyclase is a membrane-bound enzyme that plays a central role in the cAMP second messenger system.

• It is activated by Gs proteins when certain hormones or neurotransmitters bind to their receptors.

• It catalyzes the conversion of ATP to cyclic AMP (cAMP).

Reaction:

ATP→cAMP+PPi (pyrophosphate)ATP→cAMP+PPi (pyrophosphate)

Function of cAMP:

• cAMP activates protein kinase A (PKA)

• PKA phosphorylates various enzymes, leading to cellular responses such as:

  • Glycogen breakdown

  • Increased heart rate

  • Hormone secretion regulation

Why the Other Options Are Incorrect:

Summary:

Adenylate cyclase converts ATP into cAMP, which serves as a second messenger in many hormone signaling pathways.

Mechanism of Action of Steroid Hormones:

Steroid hormones include:

• Glucocorticoids (e.g., cortisol)

• Mineralocorticoids (e.g., aldosterone)

• Sex hormones (e.g., estrogen, testosterone, progesterone)

• Vitamin D (acts like a steroid hormone)

Steroid Hormones Act By:

1. Crossing the cell membrane (lipid-soluble)

2. Binding to intracellular receptors (in the cytoplasm or nucleus)

3. Forming a steroid-hormone receptor complex

4. This complex binds to DNA regulatory elements (hormone response elements, HREs)

5. Regulating gene transcription, leading to new protein synthesis.

Why “Activates adenyl cyclase” is Incorrect:

• Adenylyl cyclase activation → cAMP pathway is used by peptide and catecholamine hormones, not steroids.

• Examples of hormones that use this pathway:

  • Glucagon, ACTH, TSH, FSH, LH, Epinephrine (via beta receptors)

• Steroids do not activate second messenger systems like cAMP directly.

Why the Other Options Are Correct (Characteristics of Steroids):

Summary:

Steroid hormones do not activate adenyl cyclase or use cAMP pathways. They act by binding intracellular receptors and regulating gene transcription, making “Activates adenyl cyclase” the correct answer

The catecholamines include:

• Dopamine

• Norepinephrine (noradrenaline)

• Epinephrine (adrenaline)

All are synthesized from Tyrosine, which is the direct precursor.

Steps in Catecholamine Synthesis:

1. Tyrosine → L-DOPA
   (enzyme: tyrosine hydroxylase; rate-limiting step)

2. L-DOPA → Dopamine

3. Dopamine → Norepinephrine

4. Norepinephrine → Epinephrine
   (in the adrenal medulla, using phenylethanolamine-N-methyltransferase, stimulated by cortisol)

Why the Other Options Are Incorrect:

Summary:

Tyrosine is the precursor of catecholamines, making it the correct answer.

• Increases blood glucose (gluconeogenesis, decreased peripheral glucose uptake)

• Promotes lipolysis (fat breakdown for energy)

• Promotes protein catabolism

• Supports the vascular system (increases responsiveness to catecholamines)

• Suppresses the immune system

How Epinephrine Has Cortisol-like Actions:

• Epinephrine, secreted by the adrenal medulla, shares several metabolic actions with cortisol:

  • Raises blood glucose by:

    • Stimulating glycogenolysis (in liver and muscle)

    • Promoting gluconeogenesis (in liver)

  • Enhances lipolysis via beta-adrenergic receptors

  • Inhibits insulin secretion (via alpha-2 receptors) to prevent glucose storage during stress.

• Both cortisol and epinephrine are critical for the stress response, though they act via different receptors and pathways (cortisol via intracellular receptors, epinephrine via adrenergic receptors).

Why the Other Options Are Incorrect:

Summary:

Epinephrine is the hormone that has cortisol-like actions, especially in terms of increasing blood glucose and promoting lipolysis, making it the correct answer.

• A prolactinoma is the most common type of pituitary adenoma.

• It arises from mammotropes (also called lactotrophs), the prolactin-secreting cells of the anterior pituitary.

Effects of a Prolactinoma:

• Hyperprolactinemia → leads to:

  • Galactorrhea (inappropriate milk production)

  • Amenorrhea (in women)

  • Infertility (in both sexes)

  • Hypogonadism (due to prolactin’s inhibitory effect on GnRH)

• Mass effect symptoms if large (headache, visual field defects from optic chiasm compression)

Why the Other Options Are Incorrect:

Summary:

A prolactinoma is a tumor of the mammotropes (lactotrophs) in the anterior pituitary, which produce prolactin.

Synthesis and Release of Oxytocin and Vasopressin:

• Both oxytocin and vasopressin (antidiuretic hormone, ADH) are synthesized in the hypothalamus, specifically in the:

  • Paraventricular nucleus → mostly oxytocin

  • Supraoptic nucleus → mostly vasopressin

• After synthesis, the hormones are transported down the axons of hypothalamic neurons to the posterior pituitary (neurohypophysis), where they are stored and released into the bloodstream.

Key Concept:

Why the Other Options Are Incorrect:

Summary:

Oxytocin and vasopressin are produced in the hypothalamus, then transported to the posterior pituitary for storage and release.

Hormones Using cAMP as Second Messenger:

The cAMP pathway is one of the most common second messenger systems used by peptide hormones. These hormones bind to G-protein coupled receptors (Gs), activating adenylyl cyclase, which converts ATP to cAMP, triggering downstream effects.

Examples that use cAMP:

Why Oxytocin Is the Correct Answer (Does Not Use cAMP):

• Oxytocin works through the IP₃/DAG pathway, not the cAMP system.

• It binds to Gq protein-coupled receptors, activating phospholipase C (PLC).

• This leads to:

  • Increased intracellular calcium (via IP₃)

  • Activation of protein kinase C (via DAG)

• The rise in calcium causes smooth muscle contraction in the uterus and mammary glands.

Why the Other Options Are Incorrect (They DO Use cAMP):

Summary:

Oxytocin does NOT use cAMP; it works through the IP₃/DAG pathway and calcium-mediated signaling.

The thyroid gland is unique among endocrine glands because it stores its hormone precursors in follicles filled with colloid.

Structure of the Thyroid Gland:

• Thyroid follicles are spherical units lined by follicular (epithelial) cells.

• The central cavity of each follicle is filled with colloid, a protein-rich material.

• Colloid contains thyroglobulin, which is the precursor for thyroid hormones (T3 and T4).

Why is this unique?

• The thyroid is the only endocrine gland that stores large amounts of hormone precursor (thyroglobulin) extracellularly.

• Most other endocrine glands store hormones intracellularly in secretory granules.

Why the Other Options Are Incorrect:

Summary:

The thyroid gland is the only gland with follicles containing colloid, making it histologically unique among endocrine organs.

The anterior pituitary (adenohypophysis) is made up of specialized hormone-secreting cells, each type producing specific tropic hormones that regulate various body functions.

Major Cell Types in the Anterior Pituitary:

Why Melanocytes Are the Correct Answer (Not Present in Anterior Pituitary):

• Melanocytes are pigment-producing cells found in the skin, eyes, and hair follicles, where they produce melanin.

• They are NOT present in the anterior pituitary.

• Melanocyte-stimulating hormone (MSH) is related to pro-opiomelanocortin (POMC) cleavage, but MSH production primarily occurs in the intermediate lobe of the pituitary in some animals, and minimally in humans.

Why the Other Options Are Incorrect (They ARE present in the anterior pituitary):

Summary:

Melanocytes are not found in the anterior pituitary.
They are located in the skin and other peripheral tissues, not in endocrine organs.

• Iodine trapping is the first step of thyroid hormone synthesis.

• It refers to the active transport of iodide (I⁻) from the bloodstream into the thyroid follicular cells (thyrocytes).

Mechanism:

• Sodium-Iodide Symporter (NIS):

  • This transporter on the basolateral membrane of thyrocytes uses the sodium gradient (Na⁺/K⁺ ATPase-driven) to bring iodide into the cell.

  • This process requires ATP to maintain the sodium gradient.

Why Peroxidase is Not Involved in Trapping:

• Thyroid peroxidase (TPO) is involved in the next steps, not in trapping:

  • Oxidation of iodide (I⁻ to I₂)

  • Iodination of tyrosine residues on thyroglobulin (organification)

  • Coupling of iodotyrosines to form T3 and T4

• Since iodine trapping happens before TPO acts, peroxidase is not required for iodine trapping.

Why the Other Options Are Involved in Iodine Trapping:

Summary:

Peroxidase is not required for iodine trapping because it functions in iodide oxidation and organification, not in the initial transport of iodide into the thyroid cell.

The absorption of glucose from the intestine requires the breakdown of complex carbohydrates (like starch and disaccharides) into monosaccharides (glucose, galactose, fructose).

Role of Alpha-Glucosidase:

• Alpha-glucosidase is an enzyme located on the brush border of the small intestine (enterocytes).

• It breaks down oligosaccharides and disaccharides into glucose, which can then be absorbed by intestinal transporters (like SGLT1).

• Without this step, glucose cannot be absorbed, even if large carbohydrate molecules are present.

Clinical Relevance:

• Alpha-glucosidase inhibitors (e.g., acarbose, miglitol) are used to treat diabetes mellitus because they slow carbohydrate digestion, reducing postprandial blood glucose spikes.

Why the Other Options Are Incorrect:

Summary:

Alpha-glucosidase is the enzyme responsible for breaking down carbohydrates into glucose for absorption in the intestine, making it the correct answer.

While deficiencies in many hormones can cause serious problems, cortisol deficiency is the most immediately life-threatening because cortisol is critical for survival, especially in times of stress.

Functions of Cortisol:

• Maintains blood pressure (supports vascular tone and responsiveness to catecholamines)

• Regulates glucose metabolism (increases gluconeogenesis and prevents hypoglycemia during fasting or stress)

• Suppresses excessive inflammation

• Supports cardiovascular function during stress

Why cortisol deficiency is life-threatening:

• In Addison’s disease (primary adrenal insufficiency), lack of cortisol can lead to an Addisonian crisis, characterized by:

  • Severe hypotension or shock

  • Hypoglycemia

  • Hyponatremia and hyperkalemia (due to concurrent aldosterone deficiency in primary cases)

  • Vomiting, abdominal pain, and weakness

• Without immediate corticosteroid replacement, this condition is often fatal.

Why the Other Options Are Incorrect (Less Immediate Risk of Death from Deficiency):

Summary:

Cortisol is the hormone whose deficiency most rapidly leads to life-threatening conditions, especially during stress, illness, or injury.

Sheehan syndrome is a condition resulting from ischemic necrosis of the anterior pituitary, typically following severe postpartum hemorrhage (PPH).

Pathophysiology:

• During pregnancy, the anterior pituitary enlarges, mainly due to increased prolactin-secreting cells to prepare for lactation.

• Despite the enlargement, the blood supply does not increase proportionally, making the pituitary vulnerable to ischemia.

• If a woman experiences massive postpartum hemorrhage, the sudden drop in blood pressure can cause hypoperfusion of the anterior pituitary, leading to necrosis and hypopituitarism.

Key Clinical Features:

• Failure to lactate (due to prolactin deficiency)

• Amenorrhea or oligomenorrhea (due to gonadotropin deficiency)

• Hypothyroidism and adrenal insufficiency may also develop over time due to TSH and ACTH deficiencies.

Why the Other Options Are Correct (True Statements):

Why “It is associated with antepartum hemorrhage” is Incorrect:

• Antepartum hemorrhage occurs before delivery (e.g., placenta previa, placental abruption).

• **Sheehan syndrome is specifically associated with postpartum hemorrhage, meaning bleeding after delivery.

• Therefore, the statement about antepartum hemorrhage is wrong.

The adrenal medulla is the inner part of the adrenal gland, and it functions as a neuroendocrine organ. It secretes catecholamines in response to sympathetic stimulation, especially during stress.

Main Secretory Product: Adrenaline (Epinephrine)

• Approximately 80% of adrenal medulla secretion is adrenaline (epinephrine).

• The remaining 20% is mostly norepinephrine, with very small amounts of dopamine.

Why does the adrenal medulla secrete mostly adrenaline?

• The adrenal medulla contains the enzyme phenylethanolamine-N-methyltransferase (PNMT), which converts norepinephrine into epinephrine.

• This conversion is stimulated by cortisol coming from the adrenal cortex—this is why the adrenal medulla produces so much epinephrine relative to norepinephrine.

Functions of Adrenaline:

• Increases heart rate (positive chronotropy)

• Increases cardiac output (positive inotropy)

• Dilates bronchioles

• Mobilizes energy stores (glycogenolysis, lipolysis)

• Prepares the body for “fight or flight”

Why the Other Options Are Incorrect:

Cortisol

• Cortisol is secreted by the adrenal cortex, not the medulla.

• It plays a role in metabolism and stress response, but it is not part of adrenal medulla secretion.

Adrenocorticotropic hormone (ACTH)

• ACTH is secreted by the anterior pituitary, not the adrenal medulla.

• ACTH stimulates the adrenal cortex, not the medulla.

Aldosterone

• Aldosterone is a mineralocorticoid secreted by the zona glomerulosa of the adrenal cortex.

• It regulates sodium and potassium balance, not part of adrenal medulla output.

Norepinephrine

• The adrenal medulla does secrete norepinephrine, but it makes up only about 20% of its catecholamine output.

• 80% is adrenaline (epinephrine).

Cushing syndrome refers to excess cortisol production, which can result from:

• Exogenous corticosteroid use (most common overall cause)

• Endogenous causes, such as:

  • Pituitary adenoma (Cushing disease)

  • Adrenal tumors

  • Ectopic ACTH production

Best initial diagnostic test: The Dexamethasone Suppression Test

• Dexamethasone is a synthetic glucocorticoid that normally suppresses ACTH production via negative feedback to the pituitary.

• In normal individuals, a low-dose dexamethasone test lowers cortisol levels.

• In Cushing syndrome, cortisol secretion is not suppressed due to:

  • An ACTH-secreting tumor (pituitary or ectopic source)

  • Adrenal tumors autonomously producing cortisol

Why is it the best test?

• The low-dose dexamethasone suppression test is recommended by most guidelines (e.g., Endocrine Society) as the first-line screening test for suspected Cushing syndrome.

• It helps distinguish between physiologic causes of high cortisol (stress, obesity, etc.) and true Cushing syndrome.

Why the Other Options Are Incorrect:

ACTH levels

• ACTH testing is important after confirming Cushing syndrome to determine if the cause is ACTH-dependent or ACTH-independent.

• It is not the first diagnostic step.

Serum cortisol levels

• Single cortisol measurements are not reliable because cortisol has a diurnal rhythm (high in the morning, low at night).

• A random cortisol level can be misleading and does not diagnose Cushing syndrome.

Blood glucose levels

• Hyperglycemia is common in Cushing syndrome due to cortisol-induced insulin resistance.

• However, blood glucose testing is not diagnostic of Cushing syndrome—it just detects a complication.

24-hour urine collection for free cortisol

• 24-hour urinary free cortisol (UFC) is also a valid test for Cushing syndrome, but it is often considered less practical as the first-line test because:

  • It requires strict timing and collection compliance, which is cumbersome.

  • It is often used as a confirmatory or secondary test, not the first step.

Congenital hypothyroidism is a condition where the newborn has low thyroid hormone levels at birth. It is one of the most common preventable causes of mental retardation if not treated early, which is why newborn screening programs universally test for it.

Most Common Cause: Thyroid Dysgenesis

• Thyroid dysgenesis refers to the failure of the thyroid gland to develop properly during fetal life. This can involve:

  • Aplasia (complete absence of the thyroid)

  • Hypoplasia (underdeveloped thyroid)

  • Ectopic thyroid tissue (thyroid tissue located in the wrong place, often along the path of embryonic descent)

• This accounts for about 85-90% of congenital hypothyroidism cases, making it the most common cause.

Why the Other Options Are Incorrect:

Hereditary

• Only 10-15% of cases of congenital hypothyroidism are hereditary.

• Genetic defects in thyroid hormone synthesis (known as dyshormonogenesis) are less common compared to thyroid dysgenesis.

Obesity

• Obesity is not a cause of congenital hypothyroidism.

• While thyroid problems can affect metabolism, obesity is not related to congenital cases.

Iodine deficiency

• Iodine deficiency is a global cause of hypothyroidism, but in developed countries, it is not the most common cause of congenital hypothyroidism due to iodine supplementation in salt and prenatal care.

• In certain endemic regions, iodine deficiency can cause goitrous hypothyroidism in neonates, but thyroid dysgenesis remains more common overall.

Lack of iodine intake in childhood

• Iodine deficiency during childhood can lead to goiter and hypothyroidism, but this affects postnatal development, not congenital (from birth) hypothyroidism.

In this case, the patient is a lean lady with hypotension (90/60 mmHg), irritability, and hyperglycemia (240 mg/dL). These findings suggest an underlying endocrine problem, most likely involving the adrenal glands.

Why test cortisol first?

• Cortisol is the major stress hormone produced by the adrenal cortex.

• It plays a crucial role in:

  • Maintaining blood pressure by enhancing the responsiveness of blood vessels to catecholamines (like adrenaline).

  • Regulating glucose metabolism, typically raising blood glucose levels during fasting or stress.

• Deficiency of cortisol (adrenal insufficiency) leads to:

  • Hypotension due to lack of vascular tone support

  • Blood sugar dysregulation, though typically hypoglycemia is seen, some atypical cases may present with stress-induced hyperglycemia, especially if there is underlying glucose intolerance or diabetes.

• Testing serum cortisol (preferably morning cortisol) is the first diagnostic step when adrenal insufficiency is suspected.

• After cortisol measurement, further tests like ACTH levels or stimulation tests may be performed to pinpoint the cause.

Why the Other Options Are Incorrect:

Electrolytes

• While electrolyte testing (checking for hyponatremia, hyperkalemia) can support adrenal insufficiency diagnosis, it is not the first step.

• Electrolyte changes are secondary findings, whereas cortisol directly addresses the primary issue.

T3

• Triiodothyronine (T3) measures thyroid function.

• Although thyroid dysfunction can cause irritability or fatigue, it is not the main concern here, especially given the presence of hypotension and hyperglycemia.

ACTH

• ACTH (adrenocorticotropic hormone) testing is important but comes after cortisol testing.

• You need to confirm low cortisol first before using ACTH to distinguish between:

  • Primary adrenal insufficiency (high ACTH, low cortisol)

  • Secondary adrenal insufficiency (low ACTH, low cortisol)

T4

• Thyroxine (T4) is another measure of thyroid function but does not explain the low blood pressure and hyperglycemia combination.

• Thyroid problems are not the first suspicion in this scenario.

Steroid hormones are synthesized from cholesterol, making them lipid-derived hormones. Examples include:

• Glucocorticoids (e.g., cortisol)

• Mineralocorticoids (e.g., aldosterone)

• Sex hormones (e.g., estrogen, testosterone, progesterone)

Site of synthesis: Smooth Endoplasmic Reticulum (SER)

• The smooth endoplasmic reticulum is the primary site for steroid hormone synthesis in steroidogenic cells (e.g., adrenal cortex, gonads).

• The mitochondria also participate in the initial and final steps of steroidogenesis, but the bulk of the enzymatic modifications happen in the SER.

• Enzymes such as cytochrome P450 family members located in the SER membranes catalyze the conversion of cholesterol into various steroid hormones.

Why the Other Options Are Incorrect:

Cytoplasm

• Steroid hormones are not synthesized in the free cytoplasm.

• However, cholesterol transport to organelles starts in the cytoplasm, but the enzymatic steps happen in the SER and mitochondria.

Nucleus

• The nucleus is involved in gene transcription but does not synthesize hormones.

• Steroid hormones act on nuclear receptors, but they are not made in the nucleus.

Golgi bodies

• The Golgi apparatus is mainly involved in protein processing, modification, and packaging.

• It is not involved in steroid synthesis, though it processes some peptide hormones.

Rough endoplasmic reticulum (RER)

• The RER is studded with ribosomes and is specialized for protein synthesis, not lipid or steroid metabolism.

• Steroidogenesis occurs in the SER, not the RER.

Glucagon is a catabolic hormone secreted by the alpha cells of the pancreas in response to low blood glucose levels (hypoglycemia). Its primary target is the liver, where it acts to increase blood glucose levels.

Main Action: Hepatic Glycogenolysis

• Glycogenolysis is the breakdown of glycogen into glucose.

• In the liver, glucagon activates glycogen phosphorylase, the key enzyme that liberates glucose-1-phosphate from glycogen, ultimately producing free glucose that enters the bloodstream.

• This process is crucial during fasting, exercise, or hypoglycemia to maintain adequate blood glucose levels.

Additional actions of glucagon:

• Stimulates gluconeogenesis (making new glucose from non-carbohydrate sources like amino acids)

• Promotes lipolysis indirectly, providing energy substrates for the liver

• Inhibits glycogenesis and protein synthesis in the liver

Why the Other Options Are Incorrect:

Amino acid uptake

• Glucagon does increase the availability of amino acids for gluconeogenesis, but it generally does not enhance cellular amino acid uptake for anabolic purposes.

• Instead, it stimulates the liver to convert amino acids into glucose, not to store them.

Protein formation

• Glucagon is a catabolic hormone.

• It inhibits protein synthesis and promotes protein breakdown to supply amino acids for gluconeogenesis.

Lipid oxidation

• While glucagon can indirectly promote lipolysis in adipose tissue, the primary hormone for lipid oxidation is epinephrine.

• Glucagon does not directly stimulate lipid oxidation in the liver or muscle as its main function.

Hepatic glycogenesis

• Glycogenesis is the formation of glycogen from glucose, which is promoted by insulin, not glucagon.

• Glucagon inhibits glycogenesis to prevent glucose storage during fasting.

Glucosidase inhibitors are a class of oral antidiabetic drugs that specifically target the small intestine to inhibit carbohydrate absorption.

How do they work?

• Alpha-glucosidase enzymes, located in the brush border of the small intestine, are responsible for breaking down complex carbohydrates (starches, disaccharides) into simple sugars (glucose) for absorption.

• Glucosidase inhibitors (e.g., Acarbose, Miglitol) block these enzymes, delaying carbohydrate digestion.

• As a result, glucose absorption is slowed down, leading to a blunted postprandial (after-meal) rise in blood sugar levels.

This mechanism is especially helpful in managing postprandial hyperglycemia in type 2 diabetes mellitus.

Clinical effect:

• Decreases post-meal blood glucose peaks

• Minimal risk of hypoglycemia when used alone

• Common side effects: flatulence, bloating, and diarrhea (due to undigested carbs fermenting in the colon)

Why the Other Options Are Incorrect:

Metformin

• Metformin is a biguanide that works by:

  • Inhibiting hepatic gluconeogenesis (decreasing liver glucose production)

  • Increasing insulin sensitivity in peripheral tissues

• It does not inhibit intestinal glucose absorption directly, although it may mildly reduce glucose uptake from the gut in some cases—but this is not its primary mechanism.

Insulin aspart

• Insulin aspart is a rapid-acting insulin analog that helps lower blood sugar by:

  • Promoting glucose uptake into cells

  • Suppressing hepatic glucose output

• It does not affect intestinal glucose absorption.

Rosiglitazone

• Rosiglitazone is a thiazolidinedione (TZD).

• It works by activating PPAR-γ receptors, which increase insulin sensitivity in adipose tissue and muscle.

• It has no effect on glucose absorption in the intestine.

Exogenous glucose

• Exogenous glucose refers to glucose given orally or intravenously.

• It raises blood glucose levels; it is not a drug that inhibits glucose absorption.

Somatostatin is known as the “universal inhibitor” because it suppresses the secretion of multiple hormones across different organ systems.

In the pancreas, somatostatin is secreted by the delta cells of the islets of Langerhans, where it inhibits both insulin and glucagon secretion:

• Insulin (from beta cells) lowers blood glucose by promoting cellular uptake of glucose.

• Glucagon (from alpha cells) raises blood glucose by stimulating glycogenolysis and gluconeogenesis.

• Somatostatin regulates this system by inhibiting both, preventing rapid swings in glucose levels and providing a brake mechanism on pancreatic activity.

Why does this happen?

• Somatostatin prevents overstimulation of both anabolic and catabolic pathways.

• It promotes homeostasis during digestion by slowing nutrient absorption and limiting hormone release, ensuring that blood glucose levels don’t fluctuate wildly.

Somatostatin also inhibits growth hormone (GH), thyroid-stimulating hormone (TSH), and various gastrointestinal hormones, but in the pancreatic context, its key role is to reduce both insulin and glucagon secretion.

Why the Other Options Are Incorrect:

Cortisol only

• Cortisol is produced by the adrenal cortex and is regulated by ACTH from the pituitary.

• Somatostatin does not directly inhibit cortisol secretion.

Cortisol and Insulin

• Again, somatostatin inhibits insulin, but it does not directly inhibit cortisol.

• Cortisol secretion is under the control of the HPA axis, not the pancreas.

Insulin only

• Somatostatin inhibits both insulin and glucagon, not insulin alone.

• This option is partially correct but incomplete.

Glucagon only

• Somatostatin inhibits glucagon, but it also inhibits insulin, so this option is incomplete as well.