ENDOCRINOLOGY – 2020

Cushing disease is a specific condition where there is excessive secretion of ACTH from the pituitary gland — usually due to a pituitary adenoma (benign tumor).

Here’s what happens:

• Excess ACTH stimulates the adrenal cortex

• This causes overproduction of cortisol

• The result is Cushing syndrome (the collection of signs and symptoms due to high cortisol), but since it’s caused by high ACTH from the pituitary, it’s specifically called Cushing disease

🧬 Key features include:

• Moon face

• Central obesity

• Hypertension

• Muscle weakness

• Skin thinning and striae

❌ Why the Other Options Are Wrong (Simple):

• Addison disease
  ❌ This is primary adrenal insufficiency, where the adrenal glands fail.

  • ACTH may be high (due to low cortisol), but it’s a response, not the cause.

  • The issue is not ACTH overproduction, but adrenal failure.

• Thyrotoxicosis
  ❌ Involves excess thyroid hormone (T₃/T₄) — not related to ACTH at all.

• Myxedema
  ❌ This is severe hypothyroidism, involving low thyroid hormones, again unrelated to ACTH.

• Pheochromocytoma
  ❌ A tumor of the adrenal medulla, producing excess catecholamines (adrenaline and noradrenaline) — ACTH has no role here.

The parathyroid gland has two main types of cells:

1. Chief cells (also called principal cells)

2. Oxyphil cells

In this case, the pathologist sees:

• Small cells

• Rounded central nuclei

• Pale eosinophilic or clear cytoplasm

• Arranged in clusters

• And they form about 80% of the gland in adults

These features match perfectly with the description of chief (principal) cells.

🔬 Function of Chief Cells:

• They are the main functional cells of the parathyroid.

• They synthesize and secrete parathyroid hormone (PTH), which regulates calcium and phosphate balance in the blood.

❌ Why the Other Options Are Wrong (Simple):

• Follicular cells
  ❌ These are found in the thyroid gland, not the parathyroid. They line thyroid follicles and produce thyroid hormones (T₃, T₄).

• Clear cells
  ❌ This is a vague term. Chief cells can appear clear, but the term “clear cells” alone is non-specific and not the best answer here.

• Oxyphil cells
  ❌ These are larger, have acidophilic (pink) cytoplasm, and appear later in life. They are less numerous and their function is not fully clear.

• C cells
  ❌ Also called parafollicular cells, they are found in the thyroid, not the parathyroid. They secrete calcitonin.

Addison disease is caused by the failure of the adrenal cortex itself — meaning the adrenal glands cannot produce enough cortisol, and often aldosterone too.

This is called primary adrenal insufficiency, or primary adrenocortical hypofunction.

Common causes include:

• Autoimmune destruction (most common in developed countries)

• Tuberculosis (common in developing countries)

• Infections, cancer, or adrenal hemorrhage

The key point is:
👉 The problem starts in the adrenal gland itself.

Because the adrenal cortex fails:

• Cortisol and aldosterone levels drop

• ACTH levels rise (trying to stimulate the failing gland)

• This leads to symptoms like:

  • Fatigue

  • Weight loss

  • Hypotension

  • Hyperpigmentation (due to high ACTH)

❌ Why the Other Options Are Wrong (Simple):

• Secondary adrenal hypofunction
  ❌ This is due to pituitary failure (low ACTH), so it’s not Addison disease — Addison is primary.

• Tertiary disorder of the cortisol hormone system
  ❌ Tertiary refers to hypothalamic failure (low CRH → low ACTH → low cortisol). Again, this is not primary, so not Addison.

• Abnormal growth of the thyroid gland
  ❌ That relates to thyroid disease, not the adrenal glands.

• Functional disability of the hormone cortisol
  ❌ Cortisol dysfunction might be a result, but Addison disease refers to adrenal gland failure, not cortisol resistan

The thyroid gland makes T₃ (triiodothyronine) and T₄ (thyroxine), and for that, it needs iodine in a specific active form.

Here’s how it works step-by-step:

1. Iodide ions (I⁻) are absorbed from the blood into thyroid follicular cells.

2. These iodide ions must first be oxidized to elemental iodine (I⁰) by the enzyme thyroid peroxidase (TPO).

3. Only oxidized iodine can attach to tyrosine residues on thyroglobulin to form:

   • MIT (mono-iodotyrosine)

   • DIT (di-iodotyrosine)
     → Which then combine to form T₃ and T₄

✅ So the oxidation of iodide to iodine is an essential and rate-limiting step in thyroid hormone formation.

❌ Why the Other Options Are Wrong (Simple):

• Thyroxine

  • This is the final product (T₄), not a step in the formation process.

• Iodide to chloride

  • ❌ Not part of thyroid hormone synthesis. This reaction doesn’t happen.

• Thyroglobulin

  • Yes, it’s important, as the scaffold for hormone formation — but the oxidation of iodide must occur before iodination of thyroglobulin.

• Iodide to sodium iodide

  • Sodium iodide is how iodide is absorbed from the gut, not how it’s activated in the thyroid.

A diabetogenic effect means the hormone causes the body to act in a way that resembles diabetes, especially by:

• Raising blood glucose levels

• Reducing insulin sensitivity

• Promoting lipolysis and gluconeogenesis

That’s exactly what Growth Hormone (GH) does!

➡️ GH increases:

• Glucose production by the liver

• Fat breakdown (lipolysis)

• Insulin resistance in peripheral tissues

Because of these effects, GH raises blood sugar — making it diabetogenic (can lead to high blood sugar or even diabetes if in excess, like in acromegaly).

❌ Why the Other Options Are Wrong (Simple):

• Oxytocin

  • Helps in uterine contraction and milk ejection. No role in glucose metabolism.

• Thyroid hormone

  • Increases metabolic rate, but doesn’t directly cause insulin resistance or a diabetic-like state.

• Vasopressin (ADH)

  • Regulates water balance and blood pressure, not blood glucose.

• Insulin

  • Does the opposite — it lowers blood sugar by promoting glucose uptake into cells.

📋 Case Summary:

• Elderly male with weight gain and lethargy → common signs of hypothyroidism

• Known case of hypertension and ischemic heart disease

• TSH = 21 mIU/L (↑ high)

• Free T4 = 0.02 ng/dL (↓ low)
  → This is primary hypothyroidism (thyroid gland failure)

Since he is taking heart-related medications, we suspect drug-induced hypothyroidism.

💊 Why Amiodarone is the Correct Answer:

Amiodarone is a class III antiarrhythmic drug used to treat atrial fibrillation, ventricular arrhythmias, etc.

• It contains iodine — each 200 mg tablet has ~75 mg iodine.

• This iodine overload can disrupt thyroid hormone synthesis via the Wolff–Chaikoff effect, leading to:

  • Hypothyroidism (more common)

  • Hyperthyroidism (less common, but possible)

Since the patient has ischemic heart disease, amiodarone is likely in use — making it the most common cause in this context.

❌ Why the Other Options Are Wrong (Simple):

• Phenylbutazone

  • An old anti-inflammatory drug (NSAID-like). Rarely used now, and not linked to thyroid dysfunction.

• Interferon

  • Can affect the thyroid, especially in autoimmune patients, but is mainly used in hepatitis and cancer, not heart disease.

• Sulphasalazine

  • Used in inflammatory bowel disease and rheumatoid arthritis — not a likely drug in this cardiac patient.

• Interleukin blockers

  • Used in autoimmune conditions (like rheumatoid arthritis), but thyroid dysfunction is rare, and not common in heart patients.

Insulin is a protein hormone made by β-cells of the pancreas and plays a key role in lowering blood glucose levels.

Its mature, active form consists of:

• Two separate chains:

  • A (alpha) chain = 21 amino acids

  • B (beta) chain = 30 amino acids

• These chains are connected by two disulfide bonds (and one intrachain disulfide bond in the A chain).

Together, the total is 51 amino acids — but the structure is not one continuous chain, it is two separate chains held together by bonds.

This structure forms after processing of preproinsulin inside the β-cell:

1. Preproinsulin → 108 amino acids (includes signal sequence)

2. Proinsulin → 86 amino acids (after signal is cleaved)

3. Insulin → final hormone with A and B chains + C-peptide is removed

❌ Why the Other Options Are Wrong (Simple):

• Preproinsulin having 108 amino acids and proinsulin having 86 amino acids

  • ✅ This is true about the precursors, but the question is asking about the final composition of insulin.

• A single polypeptide chain of 84 amino acids

  • ❌ Incorrect — insulin is two chains, not one.

• An α chain having 108 amino acids and a β chain having 30 amino acids

  • ❌ Wrong — no such structure exists. 108 is the preproinsulin total, not a single chain.

• A single polypeptide chain of 51 amino acids

  • ❌ Insulin has 51 amino acids total, yes — but it is not a single chain, it’s two chains joined by disulfide bonds.

The hypophyseal portal system is a special blood vessel network that connects the hypothalamus to the anterior pituitary (adenohypophysis).

Its job is to:

• Carry releasing and inhibiting hormones from the hypothalamus directly to the anterior pituitary.

• This allows for rapid and targeted hormone regulation without dilution in the general bloodstream.

Now, which artery forms this portal system?

👉 The superior hypophyseal artery, a branch of the internal carotid artery, supplies the median eminence and infundibulum, forming the capillary network that becomes the hypophyseal portal system.

❌ Why the Other Options Are Wrong (Simple):

• Ophthalmic artery

  • Also a branch of the internal carotid artery, but it supplies the orbit and eye, not the pituitary.

• Basilar artery

  • Supplies the brainstem and cerebellum, not involved in pituitary circulation.

• Anterior inferior cerebellar artery (AICA)

  • Branch of the basilar artery — supplies the cerebellum and inner ear, not the pituitary.

• Posterior communicating artery

  • Connects the posterior cerebral and internal carotid arteries in the Circle of Willis, but doesn’t directly supply the pituitary portal system.

In Type 1 Diabetes Mellitus, the body doesn’t make insulin (due to autoimmune destruction of pancreatic beta cells).

Insulin normally suppresses gluconeogenesis, which is the process where the liver produces new glucose from non-carbohydrate sources (like amino acids and glycerol).

So in the absence of insulin:

• The liver keeps making glucose, even when there’s already too much in the blood.

• This leads to increased gluconeogenesis, making hyperglycemia worse.

This is one of the most prominent metabolic changes in T1DM.

❌ Why the Other Options Are Wrong (Simple):

• Decreased lipolysis
  ❌ Incorrect — in fact, lipolysis increases in T1DM due to lack of insulin. Fat is broken down for energy.

• Increased lipogenesis
  ❌ Wrong — lipogenesis (fat creation) requires insulin. In T1DM, lipogenesis is reduced, not increased.

• None of these
  ❌ Incorrect — one of the changes is clearly true, and that’s increased gluconeogenesis.

• Decreased ketogenesis
  ❌ Incorrect — ketogenesis increases in T1DM due to unopposed fat breakdown, leading to ketoacidosis.

The thyroid gland is made up of many round follicles — think of them as tiny bubbles filled with colloid, which stores thyroid hormones (T₃ and T₄).

These follicles are lined by a single layer of cuboidal cells:

• “Simple” means: one layer

• “Cuboidal” means: the cells are square-shaped with a central round nucleus

These follicular cells:

• Absorb iodine

• Make thyroglobulin

• Help form thyroid hormone

• Reabsorb colloid when needed

📌 During active hormone production, the cells may become taller (columnar), and when inactive, they can become flatter (squamous) — but in the normal state, the lining is simple cuboidal epithelium.

❌ Why the Other Options Are Wrong (Simple):

• Pseudostratified columnar

  • Found in respiratory epithelium (like trachea), not in thyroid.

• Transitional

  • Found in the urinary system (bladder, ureters) — designed to stretch. Not in the thyroid.

• Simple squamous

  • Found in blood vessels and alveoli — not involved in hormone production.

• Stratified cuboidal

  • Means multiple layers of cuboidal cells — this is rare and seen in ducts (like sweat glands), not in thyroid follicles.

Steroid hormones (like cortisol, estrogen, testosterone, aldosterone) are lipid-soluble — which means they can easily pass through the cell membrane.

Once inside the cell:

1. They bind to intracellular receptors (either in the cytoplasm or nucleus).

2. This hormone-receptor complex moves into the nucleus (if it wasn’t already there).

3. It then binds to specific DNA sequences and acts like a transcription factor.

4. It turns certain genes on or off, which means it increases or decreases the production of specific proteins.

🧬 This is how steroid hormones bring about long-lasting effects — by changing gene expression.

❌ Why the Other Options Are Wrong (Simple):

• It causes the formation of cyclic GMP

  • Cyclic GMP is a second messenger used by some peptide hormones (like nitric oxide), not steroid hormones.

• It causes the formation of releasing hormones

  • Releasing hormones come from the hypothalamus, not from steroid hormone action.

• It causes the formation of cyclic AMP

  • cAMP is a second messenger used by non-steroid hormones (like adrenaline, glucagon), which can’t enter the cell and use membrane receptors.

• It is converted into cholesterol, which acts as a second messenger

  • ❌ Wrong direction. Steroid hormones are made from cholesterol, not the other way around. Cholesterol is not a second messenger.

Parathyroid hormone (PTH) is released when blood calcium levels are low. One of the ways PTH helps raise calcium is by acting on the kidney to activate vitamin D.

Here’s how it works:

• In the kidney, PTH stimulates the enzyme called 1-alpha-hydroxylase.

• This enzyme converts inactive vitamin D (25-hydroxycholecalciferol) into its active form, called 1,25-dihydroxycholecalciferol, or calcitriol.

• Calcitriol then helps increase calcium absorption from the intestines.

So, the process enhanced by 1-alpha-hydroxylase is:
👉 Vitamin D synthesis — specifically, the activation of vitamin D to its biologically active form.

❌ Why the Other Options Are Wrong (Simple):

• Calcium metabolism

  • This is a broad term. PTH affects calcium metabolism, but 1-alpha-hydroxylase specifically helps make active vitamin D, not directly regulate calcium itself.

• Calcitonin synthesis

  • Calcitonin is made by the thyroid gland, not affected by PTH or 1-alpha-hydroxylase.

• Vitamin D catabolism

  • Catabolism means breakdown, but 1-alpha-hydroxylase is doing the opposite — it’s activating vitamin D.

• Vitamin D absorption

  • Vitamin D is absorbed from the gut, but this enzyme acts in the kidney, not in the intestines.

Gigantism occurs when there is too much growth hormone (GH) before the growth plates close (in childhood or adolescence). This leads to:

• Excessive height

• Large hands and feet

• Enlarged organs (viscera)

• It’s caused by a pituitary gland problem, most often a GH-secreting tumor

The specific cells that make growth hormone in the anterior pituitary are called somatotrophs.

So, when these somatotrophs over-secrete GH, it leads to gigantism in children and acromegaly in adults.

❌ Why the Other Options Are Wrong (Simple):

• Mammotrophs

  • Secrete prolactin, which is involved in milk production — not growth hormone.

• Gonadotrophs

  • Secrete LH and FSH, which affect the reproductive organs — not growth.

• Thyrotrophs

  • Secrete TSH (thyroid-stimulating hormone) — they control thyroid function, not growth hormone.

• Corticotrophs

  • Secrete ACTH, which stimulates cortisol production from the adrenal glands — not related to gigantism.

Tetany refers to involuntary muscle spasms and cramps — especially in the hands, face, and feet. It’s caused by low calcium levels in the blood (hypocalcemia).

Now, what keeps calcium levels in the blood normal?

👉 The hormone called parathyroid hormone (PTH), which is made by the parathyroid glands.

PTH raises blood calcium by:

• Increasing calcium absorption from the intestines

• Releasing calcium from bones

• Reducing calcium loss in urine

So if PTH is low (as in hypoparathyroidism), then calcium levels drop, leading to tetany.

❌ Why the Other Options Are Wrong (Simple):

• Hypothyroidism

  • Can cause fatigue, weight gain, and cold intolerance — but not tetany. Calcium levels are usually normal.

• Hyperparathyroidism

  • PTH is too high, so calcium is also high.

  • You may see bone pain or kidney stones, but not tetany.

• Pseudohypoparathyroidism

  • A rare condition where PTH is normal or high, but the body doesn’t respond to it.

  • It can cause tetany, but it is much less common than hypoparathyroidism — so not the best answer here.

• Hyperthyroidism

  • Causes high metabolism, heat intolerance, weight loss — not tetany.

A pituitary adenoma is a benign (non-cancerous) tumor that arises from the anterior pituitary gland. It is the most common pituitary disease, making up the majority of all pituitary disorders.

These tumors can be:

• Functioning (produce excess hormones):

  • Example: Prolactinoma (most common subtype)

  • Others: GH-secreting → acromegaly, ACTH-secreting → Cushing disease

• Non-functioning (do not produce hormones but cause symptoms by mass effect):

  • These can compress surrounding structures like the optic chiasm (causing visual problems) or reduce hormone secretion (hypopituitarism).

❌ Why the Other Options Are Wrong (Simple):

• Empty sella syndrome

  • It’s a radiological finding where the pituitary gland looks flattened.

  • It can be asymptomatic and is less common than adenomas.

• Sarcoidosis

  • A systemic disease that can affect many organs, including the pituitary (rarely).

  • Much less common as a pituitary disorder.

• Pituitary metastatic tumors

  • Very rare — the pituitary is not a common site for cancer spread.

• Pituitary apoplexy

  • A sudden hemorrhage or infarction of the pituitary gland.

  • It’s an emergency, but far less common than adenomas.

The Five-Factor Model (also known as the Big Five Personality Traits) is a widely accepted model in psychology. It includes:

1. Openness – creative, curious

2. Conscientiousness – disciplined, reliable ✅

3. Extraversion – outgoing, energetic

4. Agreeableness – kind, cooperative

5. Neuroticism – anxious, moody

👉 Conscientiousness refers to how organized, dependable, and goal-directed a person is.
People who score high in conscientiousness are:

• Responsible

• Detail-oriented

• Hard-working

• Reliable

• Self-disciplined

That’s why “Reliable, responsible” is the best fit.

❌ Why the Other Options Are Wrong (Simple):

• Tense – This relates more to Neuroticism, not conscientiousness.

• Anxious – Also part of Neuroticism. People high in conscientiousness are usually calm and in control.

• Energetic – Fits with Extraversion, not conscientiousness.

• Wide interest – This belongs to Openness to experience, not conscientiousness.

A hormone is a chemical messenger produced by specialized cells — usually in endocrine glands — that travels through the bloodstream to target cells in other parts of the body.

➡️ It allows one cell (the sender) to communicate with another cell (the receiver), even if they are far apart.

Examples:

• Insulin is released from pancreatic cells and acts on muscle and fat cells to absorb glucose.

• Thyroid hormones are released from thyroid cells and act on cells all over the body to increase metabolism.

So, the hormone’s job is to send cell-to-cell messages using the bloodstream as the delivery system.

❌ Why the Other Options Are Wrong (Simple):

• From one artery to another

  • Arteries carry blood, not messages. Hormones travel in blood, but they don’t signal from one artery to another.

• From one muscle to another

  • Muscles aren’t hormone messengers. Hormones may act on muscles, but they are not sent from muscle to muscle.

• From one membrane to another

  • Membranes are parts of cells. This is not how hormones signal.

• From one tissue to another

  • This might sound close, but it’s too vague. Hormones work by signaling cell to cell, even if those cells are in different tissues.

In a hyperglycemic emergency like Diabetic Ketoacidosis (DKA) or Hyperosmolar Hyperglycemic State (HHS), the patient’s blood sugar is dangerously high and needs to be lowered quickly and safely.

That’s where regular insulin comes in.

✔️ Regular insulin is the only insulin that can be given intravenously (IV).

• When given IV, it acts very quickly — this is critical in emergencies where you need to drop glucose levels fast.

• It has a short half-life and predictable action, making it easy to control and adjust during continuous infusion.

❌ Why the Other Options Are Wrong (Simple):

• It does not form antibody

  • This is more relevant to older animal insulins. Regular human insulin may still lead to minor antibody formation, but that’s not the reason it’s used in emergencies.

• Human insulin is not allergic

  • True, allergic reactions are rare with human insulin — but that’s not the reason for its emergency use.

• It has a delayed onset of action

  • ❌ Wrong — in fact, the whole point of IV regular insulin is that it has a fast onset when used this way.

• None of these

  • ❌ Incorrect, because one of the choices (IV use for rapid action) is clearly correct.

The anterior pituitary produces several hormones, but some of them directly control other endocrine glands.

ACTH (Adrenocorticotropic hormone) does exactly that.

• It travels through the blood to the adrenal cortex, which is part of the adrenal glands.

• There, it stimulates the release of cortisol, a steroid hormone essential for stress response, metabolism, and immune regulation.

So, ACTH is a classic example of a tropic hormone — meaning it acts on another endocrine gland, regulating its function.

❌ Why the Other Options Are Wrong (Simple):

• Prolactin

  • It stimulates milk production in the breast (a non-endocrine organ).

  • It does not regulate another endocrine gland.

• Growth hormone (GH)

  • GH mainly acts on bones, muscles, and liver to promote growth.

  • While it does stimulate the liver to make IGF-1, the liver is not a classical endocrine gland under pituitary control.

• Antidiuretic hormone (ADH)

  • This is made by the hypothalamus and released by the posterior pituitary, not the anterior pituitary.

  • It acts on kidneys, not an endocrine gland.

• Melanocyte-stimulating hormone (MSH)

  • It affects melanocytes in the skin, increasing pigmentation.

  • It’s not a regulator of another endocrine gland.

Adenylyl cyclase is an enzyme that plays a central role in many hormone signaling pathways, especially those that use G-protein coupled receptors (GPCRs).

When a hormone like glucagon, epinephrine, or ACTH binds to its receptor, it activates a G protein → which then stimulates adenylyl cyclase.

What does adenylyl cyclase do?
👉 It converts ATP (adenosine triphosphate) into cAMP (cyclic adenosine monophosphate).

🔁 cAMP acts as a second messenger, which goes on to activate other enzymes inside the cell, like protein kinase A (PKA), which then triggers various cellular effects.

❌ Why the Other Options Are Wrong (Simple):

• Conversion of ATP to cGMP

  • That’s done by guanylyl cyclase, not adenylyl cyclase.

• Conversion of cAMP to ATP

  • This is not possible — once ATP becomes cAMP, it’s not reversed like that.

• Activation of G protein

  • G proteins are activated by hormone-receptor binding, before adenylyl cyclase is involved.

  • Adenylyl cyclase is downstream, not responsible for G protein activation.

• Conversion of ATP to AMP

  • That can happen in other pathways, but adenylyl cyclase makes cAMP, not AMP.

Hyperthyroidism means the thyroid gland is producing too much thyroid hormone (T₃ and T₄).

These hormones act like the body’s accelerator pedal — they speed up metabolism, increase oxygen use, and stimulate many body systems.

The most consistent and defining feature of hyperthyroidism is:

👉 Increased Basal Metabolic Rate (BMR)

This leads to:

• Weight loss despite increased appetite

• Heat intolerance (they feel hot easily)

• Sweating

• Anxiety, tremors, and fast heart rate

• Hyperactivity

• Warm, moist skin

❌ Why the Other Options Are Wrong (Simple):

• Brittle hair

  • More commonly seen in hypothyroidism, not hyper.

  • In hyperthyroidism, hair may thin, but it’s not typically brittle.

• Increase in body weight

  • Opposite! In hyperthyroidism, metabolism is faster, so patients usually lose weight even if they eat more.

• Decrease in sweating

  • Sweating actually increases because the body is generating more heat.

• Cold intolerance

  • This is seen in hypothyroidism.

  • Hyperthyroid patients have heat intolerance, not cold.

The clue in the question is very clear and classic for one particular endocrine gland:

“Round and oval structures lined by cuboidal epithelium.”

These structures are called follicles, and they are filled with colloid, which stores thyroid hormones (T₃ and T₄) in an inactive form.

Here’s what makes the thyroid gland special:

• It is the only endocrine gland with follicles.

• These follicles are spherical, and lined with simple cuboidal epithelial cells.

• The center contains colloid, a pink-staining protein material (mainly thyroglobulin).

So, when you see round follicles + cuboidal lining cells, think thyroid.

❌ Why the Other Options Are Wrong (Simple):

• Pancreas

  • Has islets of Langerhans (lighter patches) and acini (exocrine part).

  • No follicles. Gland is mixed exo-endocrine.

• Pituitary

  • Has acidophils, basophils, and chromophobes (in anterior pituitary), and nerve fibers + Herring bodies (in posterior pituitary).

  • No follicular structure.

• Adrenal

  • Has cortex (3 layers: glomerulosa, fasciculata, reticularis) and medulla (chromaffin cells).

  • No follicles or colloid.

• Testes

  • Has seminiferous tubules with spermatogenic cells and Leydig cells in between.

  • Not an endocrine gland with follicles.

Let’s look at the key clues in this woman’s case:

• Heavy bleeding after delivery

• Poor lactation (can’t breastfeed)

• Loss of pubic hair

• Fatigue

All of these suggest that the woman is suffering from a condition where her pituitary gland has stopped working properly after childbirth.

🩸 What happens in Sheehan syndrome?

• During pregnancy, the pituitary gland grows bigger, but it doesn’t get extra blood supply.

• If a woman has severe blood loss during delivery, it can lead to pituitary infarction (death of the gland tissue due to low blood flow).

• This causes hypopituitarism (loss of pituitary hormones).

🧠 That explains all her symptoms:

• No prolactin → poor lactation

• No LH/FSH → loss of pubic hair (sex hormones drop)

• No ACTH or TSH → fatigue due to low cortisol and thyroid hormone

❌ Why the Other Options Are Wrong (Simple):

• Pituitary adenoma

  • Usually causes too much hormone, not too little.

  • Also, symptoms don’t appear right after delivery with bleeding.

• Prolactinoma

  • A tumor that makes too much prolactin.

  • It would cause galactorrhea (milk discharge) — not poor lactation.

• Empty sella syndrome

  • A condition where the sella turcica (pituitary space) looks empty on imaging.

  • It may cause mild pituitary dysfunction, but it’s not linked to childbirth or bleeding.

• Acromegaly

  • Caused by excess growth hormone in adults.

  • Leads to large hands, jaw, and feet, not the symptoms seen here.

Growth hormone (GH) is a hormone made by the anterior pituitary gland. It helps the body grow, especially during childhood and adolescence.

But GH doesn’t do all the work directly — instead, it stimulates the liver and other tissues to produce a substance called somatomedin, also known as Insulin-like Growth Factor 1 (IGF-1).

🧬 Somatomedin (IGF-1) is responsible for:

• Bone growth

• Muscle growth

• Protein synthesis

• Cell division

So, one of the main functions of growth hormone is to increase the synthesis of somatomedin — and that’s the correct answer!

❌ Why the Other Options Are Wrong (Simple):

• Increase the release of somatostatin

  • Somatostatin actually inhibits growth hormone release.

  • GH does not promote somatostatin — it’s regulated by it.

• Decrease amino acid uptake

  • GH actually increases amino acid uptake by cells to help build proteins.

• Block the formation of somatomedin

  • This is the opposite of what GH does. It stimulates somatomedin production, not blocks it.

• Decrease protein synthesis

  • GH promotes protein building, especially in muscles.

  • It helps the body grow and repair — so it increases, not decreases, protein synthesis.

Vasopressin is another name for antidiuretic hormone (ADH).

Its main job is to:

• Help the kidneys hold onto water (reduce urine output)

• And constrict blood vessels (raise blood pressure in emergencies)

🧪 In Central Diabetes Insipidus, the problem is:

• The pituitary gland doesn’t make enough ADH (vasopressin)

• So, the body loses a lot of water through urine

• This causes frequent urination and dehydration

👉 In this case, giving vasopressin (or desmopressin) replaces the missing hormone and helps the kidneys conserve water.

❌ Why the Other Options Are Wrong (Simple):

• Hypertension

  • Vasopressin can raise blood pressure, so using it in high BP would make it worse. It’s not indicated.

• Diabetes mellitus

  • This is high blood sugar, not related to vasopressin or water balance.

  • The treatment involves insulin or oral sugar-lowering meds, not vasopressin.

• Tachycardia

  • Fast heart rate. Vasopressin does not directly treat this and might actually increase BP, worsening tachycardia in some cases.

• Bronchospasm

  • Seen in asthma or COPD. Vasopressin has no effect on the lungs or bronchi, so it’s not used here.

Diabetes insipidus (DI) is a condition where the body can’t properly retain water.

This usually happens because of either:

• Low levels of antidiuretic hormone (ADH), or

• The kidneys don’t respond to ADH.

ADH helps the kidneys reabsorb water, so when there’s a problem with ADH, the body loses too much water in the urine.

👉 This leads to:

• Very frequent urination (called polyuria)

• And often increased thirst (called polydipsia)

The urine is dilute and pale, and the person can lose liters of fluid per day if untreated.

❌ Why the Other Options Are Wrong (Simple):

• Infertility

  • Not a direct feature of diabetes insipidus.

  • Might be seen in other hormonal problems (like prolactin or gonadotropin issues), but not typical of DI.

• Sexual dysfunction

  • Again, not characteristic of DI.

  • More common in hormonal issues like low testosterone or prolactin excess.

• No urine

  • The opposite of diabetes insipidus!

  • In DI, the person makes too much urine — not none at all.

• Acromegaly

  • A condition caused by too much growth hormone.

  • It leads to large hands, jaw, facial features, not frequent urination.

This woman has several signs that point toward excess cortisol in the body:

• Excess facial hair (hirsutism)

• Irregular menstrual cycles

• Truncal obesity

• Moon facies (rounded face)

These are hallmark features of Cushing syndrome, which is a general term for any condition with too much cortisol.

However, the CT scan shows a pituitary mass — and that’s the key clue.

This makes the diagnosis Cushing disease, which is:

Cushing syndrome caused by a pituitary tumor that secretes too much ACTH, which stimulates the adrenal glands to produce too much cortisol.

❌ Why the Other Options Are Wrong (Simple):

• Waterhouse-Friderichsen syndrome

  • This is a medical emergency caused by adrenal gland bleeding due to severe bacterial infection (often meningococcal).

  • It leads to low cortisol (adrenal insufficiency), not high cortisol.

  • The patient would be acutely sick, not gradually developing symptoms.

• Polycystic ovarian syndrome (PCOS)

  • PCOS can cause irregular periods and hirsutism, but:

    • It does not cause moon face or truncal obesity

    • There is no pituitary mass in PCOS.

    • PCOS also shows enlarged ovaries, not cortisol-related changes.

• Cushing’s syndrome

  • This term refers to high cortisol levels, but not necessarily from the pituitary.

  • Since the CT shows a pituitary mass, the correct term is Cushing disease, a specific subtype of Cushing’s syndrome.

• Prolactinoma

  • A pituitary tumor that makes prolactin, not ACTH.

  • It causes galactorrhea (milk production), infertility, and low estrogen, but not moon face or truncal obesity.

The boy is showing classic signs of Cushing syndrome, which is caused by too much cortisol in the body. Let’s go through the key clues in the question:

🧩 Symptoms:

• Backache → Suggests muscle weakness or bone problems (cortisol causes bone breakdown).

• Moon face & truncal obesity → Very characteristic signs of excess cortisol.

• High blood pressure → Cortisol increases blood pressure.

• Delayed reflexes → Seen in cortisol excess or associated electrolyte issues.

• High cortisol levels in labs → Confirms hypercortisolism.

Now, the question is: What is the cause of this excess cortisol?

🧠 What is Cushing disease?

• Cushing disease is a specific cause of Cushing syndrome — it means the pituitary gland is producing too much ACTH, which then stimulates the adrenal glands to produce too much cortisol.

• Common in adolescents, especially with the pattern of moon face, central obesity, and elevated cortisol.

So, this is the most likely diagnosis based on age, symptoms, and labs.

❌ Why the Other Options Are Wrong (Simple):

• Pheochromocytoma

  • A tumor of the adrenal medulla (not cortex) that makes adrenaline, not cortisol.

  • It causes sudden high blood pressure, palpitations, and sweating — not moon face or obesity.

• Addison disease

  • This is adrenal insufficiency, meaning low cortisol, not high.

  • It causes weight loss, low blood pressure, hyperpigmentation — opposite of what we see here.

• Adrenal cortex tumor

  • This can cause high cortisol, but it’s rare in children and usually does not cause elevated ACTH (it’s ACTH-independent).

  • Cushing disease is much more common in this age group and fits better.

• Pseudo-Cushing syndrome

  • Happens in alcoholism, depression, or severe obesity, where cortisol might be temporarily elevated, but symptoms are not as classic or consistent.

  • This child has clear Cushingoid features, so this is unlikely.

Insulin is a protein hormone that helps control blood sugar levels.

Structurally, insulin is made up of two different chains:

• A chain (21 amino acids)

• B chain (30 amino acids)

These two chains are linked together by disulfide bonds.

Since insulin is made of two different chains that come together to work as one unit, we call it a heterodimer:

• Hetero = different

• Dimer = two units

So, heterodimer means it has two different parts working together, which fits insulin perfectly.

❌ Why the Other Options Are Wrong (Simple):

• Tertiary – This refers to the 3D folding of a single protein chain, not to how insulin is structured as two chains joined together.

• Polymeric – Means many repeating units (like plastics or starch). Insulin is not made of repeating subunits, so it’s not a polymer.

• Monomeric – A monomer is a single unit, but insulin has two chains, so it’s not a monomer.

• Homodimer – That means two identical chains working together. Insulin’s two chains (A and B) are different, so it’s not a homodimer.

The hypothalamus is a part of your brain that controls many important things like hunger, thirst, sleep, and body temperature.

The lateral nucleus of the hypothalamus is known as the “hunger center.”

• When this part is active, it makes you feel hungry and want to eat or drink.

• If it’s damaged, a person or animal may stop eating or drinking completely.

It helps the body respond when energy is low (like when you haven’t eaten or had water in a while), so you feel the urge to eat or drink.

❌ Why the Other Options Are Wrong (Simple):

• Paraventricular nucleus – Helps control hormones and stress, not mainly hunger or thirst.

• Supraoptic nucleus – Makes ADH, a hormone that helps save water in the body, but doesn’t make you feel thirsty.

• Ventromedial nucleus – This is the “fullness center”. When it’s working, you feel satisfied and stop eating. It’s the opposite of the lateral nucleus.

• Suprachiasmatic nucleus – This is your body’s clock. It controls your sleep-wake cycle, not hunger or thirst.

The adrenal cortex is classically divided into three zones, each with a distinct hormone output:

GFR = Salt, Sugar, Sex

• Glomerulosa → Aldosterone (salt)

• Fasciculata → Cortisol (sugar)

• Reticularis → Androgens (sex)

Option-wise Explanation

• Zona pellucida ❌
  ❌ Incorrect. There is no such zone in the adrenal gland.

• Zona glomerulosa ❌
  ❌ Secretes aldosterone, not cortisol.

• Zona reticularis ❌
  ❌ Primarily secretes androgens (DHEA, androstenedione), not cortisol.

• Zona fasciculata and reticularis ❌
  ❌ Tempting but incorrect.
  Cortisol synthesis is restricted mainly to the zona fasciculata.

• Zona fasciculata ✅ (Correct)
  ✔️ This is the principal site of cortisol synthesis and secretion.

A cervical cyst (also called a branchial cyst) typically presents as a painless swelling located anterior to the sternocleidomastoid muscle, often in the lower one-third of the neck.

• It is a congenital cyst arising from the incomplete obliteration of the second branchial cleft during embryological development.

• The cyst is filled with fluid and may enlarge slowly.

• Usually, there are no sinus tracts or fistulas unless infected or complicated.

❌ Why the Other Options Are Incorrect:

• Piriform fistula: A tract arising from the piriform sinus (third or fourth branchial pouch anomaly), typically presenting near the thyroid region, not usually as a cystic neck swelling.

•  External cervical sinus: An opening on the skin surface due to incomplete branchial cleft closure but presents with discharge, not just swelling.

•  Cervical fistula: Has both an internal and external opening; would usually present with persistent discharge.

•  Internal cervical sinus: Opens into the pharynx and not usually palpable as an external swelling.

Pancreatic beta cells begin to increase insulin secretion rapidly when blood glucose levels rise above approximately 100 mg/dL. This is around the normal upper fasting glucose level.

• At glucose levels below 100 mg/dL, insulin secretion is low but sufficient for basal metabolic needs.

• Once glucose reaches or surpasses ~100 mg/dL, beta cells respond by increasing insulin release to promote glucose uptake by tissues.

• This helps maintain glucose homeostasis, preventing hyperglycemia after meals.

❌ Why the Other Options Are Incorrect:

• A. 200 mg/dL and B. 150 mg/dL: These are higher than the threshold where insulin secretion starts to increase rapidly.

• C. 50 mg/dL: Hypoglycemic level; insulin secretion is suppressed here.

• D. 500 mg/dL: Very high glucose; insulin secretion increases much earlier.

The outermost layer of the adrenal gland (the adrenal cortex) originates from mesenchymal cells of the intermediate mesoderm. In embryology, mesenchyme refers to loosely organized embryonic connective tissue derived from mesodermal layers.

• The adrenal cortex develops from mesenchymal cells which arise from the intermediate mesoderm.

• This mesenchyme condenses to form the steroidogenic cortex.

• The inner adrenal medulla is derived from neural crest cells (ectodermal origin).

❌ Why the Other Options Are Incorrect:

•  Neural crest cells: Form the adrenal medulla, not the cortex.

•  Epiblast cells: Early embryonic layer; not specific enough.

•  Intermediate mesoderm: While the adrenal cortex arises from intermediate mesoderm, it is the mesenchymal cells derived from this mesoderm that actually form the cortex.

• Ectoderm: Gives rise to neural crest cells and surface ectoderm; not adrenal cortex.

Insulin, being a peptide hormone, is degraded by digestive enzymes in the gastrointestinal tract when taken orally. Therefore:

• Oral ingestion of insulin does not deliver active insulin into the bloodstream.

• As a result, blood glucose levels remain elevated (persistent hyperglycemia) because the insulin never reaches systemic circulation to lower glucose.

• This is why insulin is administered via subcutaneous injections, bypassing the digestive tract.

❌ Why the Other Options Are Incorrect:

• B. Diarrhea: Not a typical consequence of oral insulin.

• C. Transient ischemic attack: No direct relation.

• D. Uremia: Related to kidney failure, not insulin ingestion.

• E. Nausea: Possible side effect but not the primary expected outcome.

NPH insulin (Neutral Protamine Hagedorn) is a widely used intermediate-acting insulin preparation.

• It contains insulin combined with protamine, which delays absorption and prolongs the duration of action to about 12-16 hours.

• NPH is typically used to provide basal insulin coverage between meals.

❌ Why the Other Options Are Incorrect:

•  Insulin lispro: Rapid-acting insulin analogue; onset within 15 minutes.

•  Protamine zinc insulin: Long-acting insulin preparation.

•  Regular insulin: Short-acting insulin; onset within 30 minutes.

•  Insulin aspartate (Aspart): Rapid-acting insulin analogue.

The adrenal gland has two distinct parts with different embryological origins:

• Adrenal cortex: Derived from the mesoderm, specifically from the mesodermal cells of the urogenital ridge.

• Adrenal medulla: Derived from neural crest cells, which are ectodermal in origin.

The cortex is responsible for producing steroid hormones such as glucocorticoids, mineralocorticoids, and androgens.

❌ Why the Other Options Are Incorrect:

•  Epiblast cells: Early embryonic layer; specific organ structures derive from specialized germ layers.

•  Neural crest cells: Form the adrenal medulla (not cortex) and other structures like peripheral neurons.

•  Endoderm: Gives rise to internal linings of the gut and associated organs, not adrenal cortex.

•  Surface ectoderm: Forms skin and related structures, not adrenal cortex.

In diabetes mellitus, gangrene of the lower extremities typically results from macrovascular disease, which refers to atherosclerosis of large and medium-sized arteries supplying the limbs.

• Macrovascular complications include peripheral arterial disease (PAD), which reduces blood flow and oxygen delivery.

• This ischemia leads to tissue necrosis and gangrene.

• Although microvascular disease (affecting small vessels) contributes to other diabetic complications (like retinopathy and nephropathy), it is less responsible for gangrene.

❌ Why the Other Options Are Incorrect:

• None of these: Incorrect; macrovascular disease is a well-established cause.

•  Microvascular disease: Primarily affects capillaries and small vessels, less commonly causing gangrene.

•  Skin disease: May complicate diabetes but is not the primary cause of gangrene.

•  Trauma: Can precipitate ulcers but underlying ischemia from macrovascular disease is the main cause.

Cortisol is a glucocorticoid hormone secreted by the zona fasciculata of the adrenal cortex. Its secretion is primarily regulated by the anterior pituitary gland via the hormone:

• Adrenocorticotropic hormone (ACTH)

When the anterior pituitary is hyperactive, it secretes excessive ACTH, which stimulates the adrenal cortex to increase cortisol production and secretion.

❌ Why the Other Options Are Incorrect:

• A. Parathyroid gland: Regulates calcium metabolism, not cortisol.

• B. Pancreas: Secretes insulin and glucagon; unrelated to cortisol.

• C. Pineal gland: Secretes melatonin; unrelated.

• D. Posterior pituitary gland: Releases oxytocin and vasopressin; does not regulate cortisol.

In glandular histology, the term “compound” refers specifically to the duct system of the gland:

• A simple gland has an unbranched duct.

• A compound gland has a branched duct system, meaning multiple ducts merge into larger ducts.

For the pancreas:

• It is a compound gland because it has a branched duct system (interlobular and intralobular ducts).

• It is tubuloacinar because its secretory units are a mix of tubular and acinar structures.

❌ Why the Other Options Are Incorrect:

• Interlobular ducts: These are part of the compound duct system but do not alone define “compound”.

•  All of them: Not all options accurately define “compound”.

•  Branched secretory portion: Refers to secretory units, not the meaning of “compound”.

•  Exocrine and endocrine parts: This describes the pancreas but does not define the term “compound”.

Hashimoto thyroiditis is a common cause of hypothyroidism, which leads to a characteristic type of non-pitting edema called myxedema.

• The edema in hypothyroidism is due to accumulation of mucopolysaccharides, especially hyaluronic acid and chondroitin sulfate, in the interstitial spaces.

• These glycosaminoglycans are hydrophilic, attracting and trapping water, which results in fluid retention and swelling.

• This is a hallmark feature of hypothyroid-related edema.

❌ Why the Other Options Are Incorrect:

• B. Increase in acetic acid: No relation to edema in hypothyroidism.

• C. Hives: Are allergic skin reactions, not related to hypothyroid edema.

• D. Abscess: Localized infection with pus; unrelated.

• E. Hyperglycemia: Characteristic of diabetes; not the cause of hypothyroid edema.

Oxytocin is a hormone secreted by the posterior pituitary gland (neurohypophysis) and plays a crucial role in the milk ejection reflex (let-down reflex) during breastfeeding.

• When the infant suckles, sensory nerves in the nipple send signals to the hypothalamus.

• This triggers oxytocin release into the bloodstream.

• Oxytocin causes contraction of myoepithelial cells surrounding the alveoli of the mammary glands.

• This contraction forces milk from the alveoli into the ducts, allowing milk to be ejected.

❌ Why the Other Options Are Incorrect:

• B. Prolactin: Stimulates milk production (synthesis), but not ejection.

• C. Progesterone: Involved in breast development but inhibits milk production during pregnancy.

• D. Luteinizing hormone (LH): Regulates ovulation and steroidogenesis; unrelated to milk ejection.

• E. Somatomammotroph: Refers to a type of anterior pituitary cell that secretes growth hormone and prolactin, not a hormone itself.

In the neurohypophysis (posterior pituitary):

• Supporting cells are called pituicytes. These are specialized glial-like cells that provide structural and metabolic support to the unmyelinated nerve fibers.

• The dilated terminal ends of axons store neurosecretory products such as vasopressin and oxytocin in structures called Herring bodies (or neurosecretory bodies).

Together, these structures are characteristic features of the neurohypophysis on histology.

❌ Why the Other Options Are Incorrect:

•  Mammophytes and Herring body: Mammophytes are not related to neurohypophysis; likely a confusion with “mammotrophs” (anterior pituitary cells).

•  Neurophysin and Herring body: Neurophysin is a carrier protein bound to oxytocin and vasopressin, not a cell type.

•  Neurohypophysis and Pars nervosa: These are names for the region itself, not specific cell types or structures.

•  Vasopressin and Oxytocin bodies: These hormones are stored in Herring bodies but are not names of cells or structures.

Tetany is a clinical syndrome characterized by muscle cramps, spasms, and increased neuromuscular excitability.

• In hypoparathyroidism, there is decreased secretion of parathyroid hormone (PTH).

• PTH normally increases blood calcium levels by promoting bone resorption, increasing renal calcium reabsorption, and stimulating vitamin D activation.

• Deficiency of PTH leads to low serum calcium levels (hypocalcemia).

• Hypocalcemia increases the excitability of nerves and muscles, resulting in tetany.

❌ Why the Other Options Are Incorrect:

• A. Parathyroid hyperplasia: Usually leads to hyperparathyroidism, not hypoparathyroidism.

• C. Vitamin D deficiency: Can cause hypocalcemia and tetany but is a separate condition from hypoparathyroidism.

• D. Hyperkalemia: High potassium levels affect cardiac and muscle function but are unrelated to tetany.

• E. Neuropathy: Refers to nerve damage; not directly related to tetany caused by hypocalcemia.

The brain primarily relies on glucose as its main energy source under normal physiological conditions because:

• Glucose can readily cross the blood-brain barrier via specific glucose transporters (GLUT1 and GLUT3).

• It is efficiently metabolized by neurons and glial cells to generate ATP, essential for maintaining ion gradients, neurotransmission, and other cellular functions.

• Although the brain can adapt to use ketone bodies during prolonged fasting or starvation, glucose remains the primary and preferred fuel.

❌ Why the Other Options Are Incorrect:

•  Fatty acids: Do not cross the blood-brain barrier efficiently and are not used as a primary energy source by the brain.

•  Glutamine: Amino acid involved in neurotransmission and nitrogen transport, but not a primary energy substrate.

•  Creatine: Involved in short-term energy storage in muscles and brain but not a main energy substrate.

• Alanine: Amino acid; can serve as a substrate for gluconeogenesis but not a primary energy source for the brain.

Parathyroid hormone (PTH) plays a crucial role in maintaining blood calcium levels by:

• Increasing osteoclastic activity in bones, leading to bone resorption, which releases calcium (and phosphate) into the bloodstream.

• Increasing renal calcium reabsorption (thus decreasing calcium excretion).

• Increasing renal phosphate excretion (promoting phosphate loss in urine).

• Enhancing intestinal absorption of calcium indirectly by stimulating calcitriol (active vitamin D) production in the kidneys.

❌ Why the Other Options Are Incorrect:

• A. Decreases renal phosphate excretion: Incorrect; PTH increases phosphate excretion in urine.

• B. Decreases intestinal absorption of calcium: Incorrect; PTH increases calcium absorption indirectly.

• C. Decreases the blood calcium level: Opposite of PTH’s function; it raises blood calcium.

• E. Increases renal calcium excretion: Incorrect; PTH decreases calcium excretion by kidneys.

In primary hyperthyroidism, such as Graves’ disease or toxic multinodular goiter, the thyroid gland overproduces thyroid hormones (free T₃ and T₄). These elevated hormone levels exert negative feedback on the hypothalamus and anterior pituitary, leading to:

• ↓ TSH (Thyroid Stimulating Hormone)

Thus, the hallmark lab pattern in hyperthyroidism is:

• ↑ Free T₃ and T₄

• ↓ TSH

❌ Why the Other Options Are Incorrect:

• A. TSH levels increased: Seen in hypothyroidism or secondary hyperthyroidism (rare).

• B & C. Parathyroid hormone levels (PTH): Not directly related to thyroid hormone production; PTH regulates calcium levels.

• D. Free T₃ and T₄ levels decreased: Suggestive of hypothyroidism, not hyperthyroidism.

The tail of the pancreas contains a high concentration of the islets of Langerhans, which are endocrine cell clusters responsible for hormone secretion into the bloodstream.

🔹 Key Features:

• Fenestrated capillaries allow efficient hormone diffusion.

• The islets contain four main cell types:

  • Alpha cells – secrete glucagon

  • Beta cells – secrete insulin

  • Delta cells – secrete somatostatin

  • PP (F) cells – secrete pancreatic polypeptide

These characteristics match the histological description in the question.

❌ Why the Other Options Are Incorrect:

•  Follicles of thyroid: Have spherical colloid-filled follicles with a single epithelial lining; do not have four distinct endocrine cell types.

•  Head of pancreas: May contain islets, but fewer than the tail, which is richer in endocrine tissue.

•  Medulla of adrenal gland: Contains chromaffin cells that secrete catecholamines, but not four distinct types of endocrine cells.

•  Sinusoids of liver: Contain hepatocytes and Kupffer cells; not grouped secretory endocrine cells with distinct hormone profiles.

The thyroid gland produces thyroxine (T₄) and triiodothyronine (T₃), both of which are essential for normal growth and development, especially during childhood.

🔹 Key Functions of Thyroid Hormones:

• Stimulate protein synthesis and cellular metabolism

• Promote growth of bones and tissues by enhancing the effect of growth hormone (GH)

• Crucial for brain development in the fetal and early postnatal period

• Regulate basal metabolic rate (BMR)

Thus, thyroid hormones are vital for overall body growth and development, particularly during early life.

❌ Why the Other Options Are Incorrect:

• B. Glandular development: Not a direct function of thyroid hormones; more influenced by sex hormones and local growth factors.

• C. Breast development: Regulated mainly by estrogen, progesterone, and prolactin.

• D. Blood pressure: May be indirectly influenced by thyroid status (e.g. hyperthyroidism → increased heart rate and systolic BP), but not a primary function.

• E. Uterine muscle contraction: Controlled primarily by oxytocin, not thyroid hormones.

Aldosterone is a steroid hormone produced by the zona glomerulosa of the adrenal cortex. Like all steroid hormones, it is lipid-soluble and easily crosses cell membranes to enter the cytoplasm and nucleus of target cells.

🔹 Mechanism of Action:

• Inside the cell, aldosterone binds to intracellular receptors, forming a hormone-receptor complex.

• This complex enters the nucleus and binds to specific DNA sequences, altering gene transcription.

• This leads to synthesis of new proteins, such as:

  • Na⁺/K⁺ ATPase

  • Epithelial sodium channels (ENaCs)
    → Result: Increased sodium reabsorption and potassium secretion in the distal nephron.

Thus, aldosterone exerts its effects directly on the genetic machinery.

❌ Why the Other Options Are Incorrect:

• A. Follicle-stimulating hormone (FSH): Acts via G-protein-coupled receptors and cAMP; does not directly affect gene transcription.

• B. Adrenaline: Acts via adrenergic receptors (G-protein-coupled); causes rapid, non-genomic effects.

• C. Glucagon: Also works via cAMP and second messengers, not direct gene activation.

• E. Insulin: Acts via tyrosine kinase receptors and activates intracellular signaling cascades; may influence gene expression indirectly, but not as directly or primarily as steroid hormones.

Glucagon is a peptide hormone secreted by the alpha cells of the pancreatic islets in response to low blood glucose. Its primary function is to increase blood glucose levels during fasting or between meals.

🔹 Primary Target: Liver

• The liver is the main target of glucagon.

• Glucagon binds to its receptors on hepatocytes, activating adenylate cyclase, increasing cAMP, and promoting:

  • Glycogenolysis (breakdown of glycogen)

  • Gluconeogenesis (synthesis of glucose from non-carbohydrate sources)

  • Inhibition of glycogenesis (formation of glycogen)

These actions work together to raise blood glucose levels.

❌ Why the Other Options Are Incorrect:

• B. Brain: The brain is a consumer of glucose, not a target for glucagon’s action.

• C. Kidney: Plays a role in glucose handling but not a primary target of glucagon.

• D. Skeletal muscle: Lacks glucagon receptors; glycogen breakdown here is regulated by epinephrine, not glucagon.

• E. Adipose tissue: Has secondary involvement (e.g., mild lipolysis), but liver is the main site of glucagon’s metabolic effects.

Hyperthyroidism is a clinical condition caused by excess thyroid hormones (T₃ and T₄), which increase basal metabolic rate and sensitize the body to catecholamines (e.g., epinephrine).

🔹 Key Neuromuscular Sign:

• A fine muscle tremor, especially noticeable in the outstretched hands, is a classic and early sign.

• This tremor is due to increased β-adrenergic activity and enhanced neuromuscular excitability.

❌ Why the Other Options Are Incorrect:

• A. Bradycardia: Seen in hypothyroidism; hyperthyroidism causes tachycardia.

• B. Slow reflexes: Suggest hypothyroidism; in hyperthyroidism, reflexes are brisk.

• C. Jerky reflexes: Not a standard clinical term or recognized pattern in thyroid disease.

• E. Coarse tremor of muscles: More associated with hypothyroidism or neuromuscular disorders, not hyperthyroidism.

Glucocorticoids (primarily cortisol) have complex metabolic effects that help the body respond to stress and maintain energy homeostasis. Their effects can be summarized as:

🔹 Anti-Insulin Effects (Peripheral):

• Decreased glucose uptake in peripheral tissues (muscle, adipose), leading to insulin resistance

• Increased protein catabolism in muscles

• Increased lipolysis in adipose tissue
  → These contribute to hyperglycemia, muscle wasting, and fat redistribution.

🔹 Anabolic Effects (Liver):

• Stimulate gluconeogenesis and glycogen synthesis
  → Promotes increased glucose output

Thus, glucocorticoids are catabolic in peripheral tissues and anabolic in the liver—helping to increase blood glucose levels, especially during fasting or stress.

❌ Why the Other Options Are Incorrect:

•  Enhances energy provision: Partially true, but too vague and nonspecific.

•  Causes the synthesis of significant proteins: Actually, they cause protein breakdown, especially in muscles.

•  Insulin function enhancement: Glucocorticoids oppose insulin action.

•  Excessive catabolism of proteins, fats, and carbohydrates: Glucocorticoids are catabolic in protein and fat metabolism, but not carbohydrates directly—they promote gluconeogenesis and glucose sparing, not breakdown of carbs.

Thyroid hormones (T₃ and T₄) are synthesized in the thyroid gland and are derived from the amino acid tyrosine.

• Tyrosine residues on thyroglobulin undergo iodination to form monoiodotyrosine (MIT) and diiodotyrosine (DIT).

• Coupling of these iodinated tyrosines forms:

  • T₃ (triiodothyronine) = MIT + DIT

  • T₄ (thyroxine) = DIT + DIT

Thus, thyroid hormones are iodinated derivatives of tyrosine, making tyrosine their biochemical precursor.

❌ Why the Other Options Are Incorrect:

• . Testosterone,  Estrogen,  Progesterone: These are steroid hormones, derived from cholesterol, not amino acids.

• Growth hormone (GH): A protein hormone composed of amino acid chains, but not derived from tyrosine—it is synthesized as a gene product by the anterior pituitary.

Pheochromocytoma is a rare, catecholamine-secreting tumor that arises from chromaffin cells of the adrenal medulla.

• These tumors secrete excessive amounts of catecholamines, primarily:

  • Epinephrine (adrenaline)

  • Norepinephrine (noradrenaline)

  • Occasionally dopamine

🔹 Clinical Effects:

The excess catecholamines lead to symptoms of sympathetic overactivity, such as:

• Episodic hypertension

• Palpitations

• Sweating

• Tremors

• Anxiety or panic-like episodes

❌ Why the Other Options Are Incorrect:

• Tyrosinase: An enzyme involved in melanin synthesis; not secreted by pheochromocytomas.

•  Androgen: Secreted by adrenal cortex (zona reticularis) or gonads, not medullary tumors.

•  Insulin: Produced by pancreatic beta cells, not adrenal tumors.

•  Oxytocin: Produced by the hypothalamus and released by the posterior pituitary, unrelated to adrenal function.

A thyroglossal cyst is a congenital midline neck cyst resulting from the persistence of the thyroglossal duct, which normally disappears after the descent of the thyroid gland during embryonic development.

• The thyroid gland originates at the foramen cecum (at the base of the tongue) and descends to its final position in the neck, passing anterior to the hyoid bone.

• The most common site for a thyroglossal cyst is just below the hyoid bone, typically near its lower border in the midline of the neck.

These cysts are midline, move upward with tongue protrusion and swallowing, and are most commonly detected in children or young adults.

❌ Why the Other Options Are Incorrect:

• B. In front of trachea: This describes the general location of the thyroid gland, not the most common site of the cyst.

• C. Base of tongue: While this is the origin of the thyroglossal duct, it is a less common site for cyst formation.

• D. Near laryngeal cartilages: Not typically associated with thyroglossal duct remnants.

• E. Near the lower border of mandible: Too high; not on the thyroglossal duct’s path.

The most common and clinically significant autoantibodies in autoimmune hypothyroidism (Hashimoto’s thyroiditis) are:

• Anti-thyroid peroxidase antibodies (anti-TPO antibodies)

  • Target the enzyme thyroid peroxidase (TPO), essential for thyroid hormone synthesis.

  • Highly sensitive and specific markers for autoimmune thyroid disease.

• Anti-thyroglobulin antibodies are also present but less specific.

❌ Why the Other Options Are Incorrect:

• Antifollicular: Non-specific term; not commonly used clinically.

•  Antinuclear: Present in systemic autoimmune diseases like lupus, but not specific for thyroid autoimmunity.

•  Anticytoplasmic: More relevant to certain vasculitides (ANCA-associated), not thyroid.

•  Anti-membrane: Not a recognized antibody in thyroid autoimmune disease.

Growth hormone (GH) secretion is regulated by a balance between stimulatory and inhibitory factors. One of the strongest natural stimulators of GH release is deep sleep, especially during stages 3 and 4 of non-REM sleep (also called slow-wave sleep).

🔹 Other Physiological Stimuli for GH Release:

• Deep sleep

• Exercise

• Hypoglycemia

• Fasting

• High protein meals

• Stress (acute)

These conditions often reflect states where anabolism or tissue repair is needed, which GH supports.

❌ Why the Other Options Are Incorrect:

• A. Aging: GH secretion declines with age, so aging reduces, not stimulates GH release.

• B. Increased blood glucose: Hyperglycemia suppresses GH secretion; hypoglycemia stimulates it.

• C. Increased free fatty acid level in blood: Suppresses GH secretion; low FFA levels stimulate it.

• D. Somatomedins (IGF-1): These are GH-induced hormones that provide negative feedback to inhibit GH secretion.

The neurohypophysis (posterior pituitary) does not synthesize hormones itself. Instead, it stores and releases hormones produced by hypothalamic nuclei, specifically:

• ADH (vasopressin) – synthesized by the supraoptic nucleus

• Oxytocin – synthesized by the paraventricular nucleus

These hormones are transported down axons through the hypothalamo-hypophyseal tract and stored in the axon terminals of the neurohypophysis until released into circulation.

❌ Why the Other Options Are Incorrect:

• A. ACTH: Synthesized and secreted by the anterior pituitary (adenohypophysis).

• B. FSH: Secreted by the anterior pituitary.

• C. Prolactin: Produced by lactotrophs in the anterior pituitary.

• D. LH: Another anterior pituitary hormone regulated by GnRH.

Only ADH (and oxytocin) are secreted by the posterior pituitary (neurohypophysis).

Pheochromocytoma is a catecholamine-secreting tumor that arises from chromaffin cells of the adrenal medulla. It is a known cause of secondary hypertension.

• While most pheochromocytomas are unilateral, bilateral pheochromocytomas can occur, especially in association with familial syndromes like:

  • Multiple Endocrine Neoplasia (MEN) type 2

  • Von Hippel–Lindau disease

  • Neurofibromatosis type 1 (NF1)

• Symptoms include episodic hypertension, headaches, palpitations, sweating, and anxiety—due to surges in epinephrine and norepinephrine.

❌ Why the Other Options Are Less Likely:

• A. Renal tumor: Can cause hypertension via renin secretion, but does not explain adrenal enlargement.

• B. Hyperplasia of suprarenal medulla: Not a commonly diagnosed or well-defined clinical condition.

• D. Renal cyst: Usually asymptomatic and not related to hypertension or adrenal changes.

• E. Hyperplasia of suprarenal cortex: Causes cortical hormone excess (aldosterone, cortisol) but pheochromocytoma better explains medullary involvement with catecholamine-related symptoms.

Hyperparathyroidism is characterized by excessive secretion of parathyroid hormone (PTH), which plays a key role in calcium and phosphate homeostasis.

🔹 PTH effects:

• Increases plasma calcium by:

  • Stimulating bone resorption

  • Increasing renal calcium reabsorption

  • Promoting activation of vitamin D, enhancing intestinal calcium absorption

• Decreases plasma phosphate by:

  • Inhibiting phosphate reabsorption in the renal proximal tubules, leading to increased urinary phosphate excretion

❌ Why the Other Options Are Incorrect:

• B. Sodium: Not significantly affected by PTH.

• C. Calcium: Actually increased, not decreased, in hyperparathyroidism.

• D. Calcitonin: May be elevated as a counter-regulatory response, but not consistently or significantly decreased.

• E. Potassium: PTH has no direct effect on potassium homeostasis.

• The pituitary gland sits in the sella turcica of the sphenoid bone, which is located just inferior to the optic chiasma.

• The optic chiasma is the point where the optic nerves partially cross.

• A pituitary adenoma, by expanding upward, compresses the optic chiasma from below, causing characteristic bitemporal hemianopia (loss of peripheral vision in both visual fields).

• This is because the crossing nasal fibers in the chiasma, responsible for temporal visual fields, are affected.

❌ Why Other Positions Are Incorrect:

• Anteriorly: The pituitary is not located in front of the optic chiasma.

• Superiorly: The optic chiasma lies above the pituitary, not vice versa.

• Laterally: The pituitary lies centrally, not on the sides of the chiasma.

• Posteriorly: The pituitary lies in front and below the chiasma, not behind it.

Gluconeogenesis is the metabolic process of producing glucose from non-carbohydrate sources (like amino acids and glycerol), primarily in the liver.

• Insulin is the key hormone that decreases gluconeogenesis. It promotes glucose uptake and utilization, suppresses glucose production, and favors storage pathways like glycogenesis and lipogenesis.

• On the other hand, glucagon, cortisol, epinephrine, and other glucocorticoids stimulate gluconeogenesis to increase blood glucose levels, especially during fasting or stress.

❌ Why the Other Options Increase Gluconeogenesis:

• Glucagon: Activates gluconeogenesis and glycogenolysis to increase blood glucose.

• Cortisol (a glucocorticoid): Stimulates gluconeogenesis during stress and fasting.

• Epinephrine: Promotes gluconeogenesis and glycogenolysis during “fight or flight” response.

• Glucocorticoids: A class that includes cortisol, promoting gluconeogenesis.

• The thyroid gland is composed of spherical follicles, which are functional units.

• Each follicle is lined by follicular cells that can vary in shape depending on activity:

  • Active thyroid follicles have tall columnar epithelium indicating active synthesis and secretion of thyroid hormones.

  • Inactive follicles are lined by low cuboidal or squamous cells.

• The follicle lumen contains colloid, a gelatinous substance rich in thyroglobulin (a glycoprotein), which is the precursor of thyroid hormones.

❌ Why the Other Options Are Incorrect:

• Suprarenal gland: Has distinct zones but no follicles with glycoprotein-filled cavities.

•  Parathyroid gland: Made of chief and oxyphil cells; no follicles or colloid.

•  Inactive thyroid gland: Follicles lined by low cuboidal or squamous epithelium, not tall columnar.

•  Cortex of the kidney: Contains renal corpuscles and tubules, no follicles with glycoprotein.

Adenylate cyclase is an enzyme that converts ATP into cyclic AMP (cAMP), a critical second messenger involved in many hormone signaling pathways.

• Glucagon binds to its G protein-coupled receptor (GPCR) on liver and fat cells.

• This activates the Gs protein, which stimulates adenylate cyclase.

• Activation of adenylate cyclase leads to increased cAMP production, triggering downstream effects like glycogen breakdown and gluconeogenesis.

❌ Why the Other Options Do Not Activate Adenylate Cyclase:

• Insulin: Signals via tyrosine kinase receptors, not adenylate cyclase.

• Ca²⁺ ions: Act as intracellular messengers but do not directly activate adenylate cyclase.

• K⁺ ions: Regulate membrane potential; no role in adenylate cyclase activation.

• Prostaglandin E1: Though it can activate adenylate cyclase in some contexts, it is less classic compared to glucagon in this pathway and often not emphasized in basic physiology contexts.

The parathyroid gland is mainly composed of two types of parenchymal cells:

• Chief cells: The most numerous cells; responsible for producing parathyroid hormone (PTH).

• Oxyphil cells: Larger, acidophilic cells; function is not fully clear but appear after puberty.

Additionally, adipose cells and lymphocytes may be present within the parathyroid gland as part of the supporting tissue or due to infiltration but are not functional parenchymal cells.

🔍 Why C cells are NOT present:

• C cells (parafollicular cells) are found in the thyroid gland, not the parathyroid gland.

• C cells produce calcitonin, which lowers blood calcium.

• Their presence is specific to the thyroid’s follicular epithelium and they are absent in the parathyroid gland.

❌ Why Other Cells May Be Present: