ENDOCRINOLOGY – 2024

Propylthiouracil (PTU) acts by:

1. Inhibiting thyroid peroxidase (TPO)
   → This blocks:

   • Oxidation of iodide

   • Iodination of tyrosine

   • Coupling of MIT + DIT → T3, and DIT + DIT → T4 ✅

2. Inhibiting peripheral conversion of T4 → T3
   → Unique to PTU (methimazole does not do this)

❌ Why the Other Options Are Incorrect:

• Reuptake of iodine by thyroid
  ❌ That’s blocked by perchlorate or thiocyanate, not PTU.

• Increase valence of iodine
  ❌ This is not a pharmacological mechanism; iodine oxidation is actually blocked by PTU.

• Reducing thyroxine-binding globulin (TBG)
  ❌ PTU does not affect TBG. TBG controls circulating hormone levels, not production.

• Reducing thyroglobulin
  ❌ Thyroglobulin is the storage protein for thyroid hormone, and PTU doesn’t reduce its synthesis.

Peptide hormones (like insulin, glucagon, ACTH, TSH):

• • Are hydrophilic (water-soluble)

  • Cannot cross the lipid-rich plasma membrane

  • Therefore, they bind to membrane-bound receptors (e.g., G-protein coupled, tyrosine kinase)

This triggers second messenger pathways inside the cell, such as:

• cAMP

• IP₃/DAG

• Tyrosine kinase cascade

🔄 Contrast with Other Hormones:

Metacognition = “thinking about thinking”
It involves:

1. Planning – choosing strategies

2. Monitoring – checking progress during the task

3. Evaluating – assessing performance and strategy effectiveness

So when the student:

• Uses strategies ✅ (planning)

• Analyzes how he is doing while solving ✅ (monitoring)

→ He is engaging in metacognition.

❌ Why the Other Option Is Incorrect:

• Seeing at the end whether he has done right or wrong
  ❌ This is just evaluation of outcome, not metacognitive monitoring or strategy adjustment.

The adrenal cortex is divided into three layers, each with distinct cellular arrangements and hormone functions:

❌ Why the Other Options Are Incorrect:

• Zona fasciculata
  ❌ Cells arranged in long straight columns separated by sinusoidal capillaries.

• Zona reticularis
  ❌ Has a net-like (reticular) or anastomosing cord pattern of small, deeply stained cells.

• Medulla
  ❌ Contains chromaffin cells, arranged in irregular clumps or cords, not rounded clusters.

cAMP (cyclic AMP) is a second messenger generated by the enzyme adenylyl cyclase, which is activated by G-protein-coupled receptors (GPCRs) in response to hormones like:

• Glucagon

• TSH

• ACTH

• Epinephrine (via β-receptors)

➡️ Adenylyl cyclase converts ATP → cAMP
➡️ cAMP activates Protein Kinase A (PKA) → intracellular signaling cascade

❌ Why the Other Options Are Incorrect:

• Tyrosine kinase
  ❌ Works via phosphorylation of tyrosine residues on receptors (e.g., insulin), not via cAMP.

• Phosphodiesterase
  ❌ Breaks down cAMP into AMP — it terminates the signal, not generates it.

Lorain Dwarfism is a form of Laron Syndrome, a type of GH insensitivity caused by:

• A mutation in the GH receptor

• Normal or elevated GH levels ✅

• Low IGF-1 levels ✅ (GH can’t stimulate its production)

Key clinical features:

• Short stature

• Delayed growth

• Low IGF-1 despite normal or high GH

• Poor response to GH therapy (needs IGF-1 replacement instead)

❌ Why the Other Option Is Incorrect:

• Cretinism
  ❌ Due to congenital hypothyroidism
  ❌ Features: mental retardation, coarse facial features, macroglossia, umbilical hernia
  ❌ Not related to GH or IGF-1 pathways

Osteomalacia is the adult counterpart of rickets (which occurs in children). It’s caused by defective mineralization of osteoid due to vitamin D deficiency or phosphate metabolism disorders.

Typical lab findings in osteomalacia:

• ↓ Calcium ✅

• ↓ Phosphate ✅

• ↑ Alkaline Phosphatase ✅ (due to increased osteoblastic activity trying to mineralize bone)

Clinical signs:

• Diffuse bone pain

• Muscle weakness

• Fragility fractures (especially in spine, pelvis, and ribs)

❌ Why the Other Options Are Incorrect:

• Osteoporosis
  ❌ Normal calcium, phosphate, and ALP levels. It’s due to decreased bone mass, not defective mineralization.

• Paget’s disease
  ❌ Typically has elevated ALP, but normal calcium and phosphate. Bones are thickened, not softened.

• Primary hyperthyroidism
  ❌ Doesn’t fit lab findings. Might cause hypercalcemia, not low calcium.

• Rickets
  ❌ Same pathology as osteomalacia but occurs in children, not adults.

The most common cause of hypoparathyroidism is accidental removal or damage to the parathyroid glands during thyroid surgery (e.g., total thyroidectomy).

• The parathyroid glands are very small and closely related to the thyroid gland, making them vulnerable to removal or vascular compromise.

• Loss of parathyroid hormone (PTH) leads to hypocalcemia, presenting with tetany, muscle cramps, carpopedal spasm, and Chvostek’s/Trousseau’s signs.

Why the Other Options Are Incorrect

• Adenoma ❌
  Parathyroid adenoma is the most common cause of hyperparathyroidism, not hypo.

• Carcinoma in situ ❌
  Not a recognized cause of hypoparathyroidism.

• Parathyroid hyperplasia ❌
  Leads to primary hyperparathyroidism, not hypoparathyroidism.

• Renal insufficiency ❌
  Causes secondary hyperparathyroidism (due to chronic hypocalcemia and phosphate retention), not primary hypoparathyroidism.

Cell signaling is categorized based on distance and target:

In the stomach:

• ECL cells secrete histamine

• It diffuses locally to bind H₂ receptors on parietal cells

• This stimulates HCl secretion → paracrine signaling

❌ Why the Other Options Are Incorrect:

• Juxtacrine
  ❌ Requires direct cell-to-cell contact — not applicable here.

• Endocrine
  ❌ Involves hormones traveling via bloodstream to distant organs — not local like histamine.

• Merocrine
  ❌ Refers to mechanism of secretion, not cell signaling.

• Autocrine
  ❌ Would mean histamine acts on the same ECL cell — which it doesn’t.

Subclinical hypothyroidism is defined by:

• Elevated TSH ✅

• Normal free T4 ✅

• No obvious symptoms, or very mild (fatigue, cold intolerance, etc.)

Why?

• The pituitary detects early thyroid underactivity and increases TSH to compensate.

• But the thyroid gland still maintains adequate T4 levels, keeping them in the normal range.

❌ Why the Other Options Are Incorrect:

• Normal free T4, low TSH
  ❌ This suggests subclinical hyperthyroidism, not hypothyroidism.

• High free T4, high TSH
  ❌ Suggests secondary hyperthyroidism (like TSH-secreting pituitary adenoma), not subclinical hypo.

• High free T4, low TSH
  ❌ Suggests primary hyperthyroidism (like Graves’ disease or toxic adenoma).

Calcitonin is a hormone secreted by parafollicular (C) cells of the thyroid gland. It lowers blood calcium by:

• Inhibiting osteoclast activity → less bone resorption

• Increasing calcium excretion in urine

• Slightly reducing intestinal calcium absorption

It is used in:

• Acute management of hypercalcemia

• Paget’s disease

• Osteoporosis (less preferred today)

❌ Why the Other Options Are Incorrect:

• Vitamin D
  ❌ Increases calcium absorption from the gut — would worsen hypercalcemia.

• Hydrochlorothiazide
  ❌ A thiazide diuretic that reduces calcium excretion in urine — can cause or worsen hypercalcemia.

• Teriparatide
  ❌ A recombinant PTH analog used to increase bone formation in osteoporosis — raises serum calcium.

Anti-thyroid drugs, particularly the thioamides group, act by inhibiting thyroid peroxidase (TPO) — the enzyme that catalyzes:

1. Oxidation of iodide to iodine

2. Iodination of tyrosine residues on thyroglobulin (→ MIT, DIT)

3. Coupling of MIT + DIT → T₃, and DIT + DIT → T₄ ✅

Thus, inhibition of the coupling reaction is the critical step by which free T₃ and T₄ levels decrease.

PTU also has an additional effect: it inhibits peripheral conversion of T₄ to T₃ (methimazole does not).

❌ Why the Other Options Are Incorrect:

• Oxidation of iodide
  ❌ Also inhibited by thioamides, but not the main answer in the context of reducing T₃/T₄ levels directly — coupling is the key step.

• Reduced uptake of iodide
  ❌ Seen with iodide transporter blockers (e.g., perchlorate, thiocyanate), not thioamides.

• Reduced release of thyroid hormones
  ❌ This is the effect of high-dose iodine (Wolff-Chaikoff effect) or lithium, not thioamides.

• Reduced binding to TBG
  ❌ TBG binding affects total hormone levels, not free T₃/T₄ synthesis. Also, antithyroid drugs do not influence TBG.

All steroids share a common cyclopentanoperhydrophenanthrene ring structure, which consists of:

• 3 six-membered rings (A, B, C)

• 1 five-membered ring (D)

This 4-ring carbon skeleton is the signature feature of all steroids, including:

• Cholesterol

• Cortisol

• Testosterone

• Estrogen

• Aldosterone

• Progesterone

• Vitamin D (modified steroid structure)

❌ Why the Other Options Are Incorrect:

• At least 1 fatty acid
  ❌ Steroids are not fatty acids or triglycerides — they are lipid-derived but do not contain fatty acid chains.

• Glycerol group
  ❌ Found in triglycerides and phospholipids, not in steroid structures.

• Soluble in water
  ❌ Steroids are lipophilic, not water-soluble — they need carrier proteins in the bloodstream.

• Made in liver
  ❌ Not all — for example, cortisol and aldosterone are made in the adrenal cortex, sex steroids in gonads. The liver metabolizes them but doesn’t synthesize all of them.

A patient with:

• High ACTH

• Low cortisol

• Elevated 11-deoxycorticosterone (DOC)

…points to 11β-hydroxylase deficiency.

🧪 Biochemical Pathway:

Normally:

• 11-deoxycorticosterone (DOC) → Corticosterone via 11β-hydroxylase

• 11-deoxycortisol → Cortisol via 11β-hydroxylase

When 11β-hydroxylase is deficient:

• DOC and 11-deoxycortisol accumulate

• Cortisol and corticosterone are low

• Low cortisol → ↑ ACTH via negative feedback

• DOC (a mineralocorticoid) builds up → hypertension (not salt-wasting)

❌ Why Others Are Wrong:

• 21-hydroxylase deficiency → ↓ DOC, ↓ aldosterone, ↓ cortisol → salt-wasting, not elevated DOC

• 17α-hydroxylase deficiency → ↓ sex steroids and cortisol, ↑ DOC and aldosterone, but ambiguous genitalia and low androgens are more prominent

• 18α-hydroxylase → not classically involved in congenital adrenal hyperplasia (CAH)

• CYP → too vague (refers to cytochrome P450 enzymes broadly)

Reference : https://www.wikidoc.org/index.php/11%CE%B2-hydroxylase_deficiency_pathophysiology

Hormones bind to different receptor types depending on their chemical nature:

• Cortisol is a lipophilic steroid hormone secreted by the adrenal cortex (zona fasciculata).

• It freely crosses the cell membrane, binds to cytoplasmic glucocorticoid receptors, and the complex then enters the nucleus to regulate gene transcription.

❌ Why the Other Options Are Incorrect:

• Insulin
  ❌ Peptide hormone — too large and hydrophilic to enter cells; acts via membrane-bound tyrosine kinase receptors.

• Glucagon
  ❌ Also a peptide hormone; uses G-protein coupled receptors on the plasma membrane to increase cAMP.

The Heisenberg Medical Dossier: Prognostic Timelines

In the cold, hard numbers of oncology, when we’re tracking a patient like, say, our very own Mr. White after his “diagnosis” of an aggressive malignancy, what do we call the crucial span from the moment his condition is identified to the final fade-out, directly attributable to the disease’s grim work?

• Survival refers to the duration a patient lives after being diagnosed with a disease like cancer.

  • It’s usually expressed as 5-year survival, median survival, or overall survival.

  • It’s a key indicator of prognosis and effectiveness of treatment.

❌ Why the Other Options Are Incorrect:

• Incubation
  ❌ Time between exposure to an infectious agent and appearance of first symptoms — applies to infections, not cancer.

• Latent period
  ❌ Time between exposure and the disease becoming clinically detectable — more relevant to environmental or occupational carcinogens, not the post-diagnosis phase.

• Serial interval
  ❌ Time between onset of symptoms in one case and onset in a secondary case — used in tracking infectious disease transmission, not cancer.

The OGTT involves:

1. Fasting overnight

2. Measuring fasting glucose

3. Giving 75g oral glucose (or 100g in some protocols)

4. Measuring glucose levels at 1, 2, and sometimes 3 hours

It’s primarily used to screen for and diagnose gestational diabetes mellitus (GDM) during 24–28 weeks of pregnancy, when insulin resistance increases.

🧬 Summary:

❌ Why the Other Options Are Incorrect:

• Type 1 Diabetes
  ❌ Autoimmune — presents acutely, not ideal for OGTT. Usually diagnosed with blood glucose, ketones, and autoantibody testing.

• Type 2 Diabetes
  ❌ OGTT can be used, but is not the first-line test — fasting glucose and HbA1c are more commonly used in routine screening.

This situation describes a classic fight-or-flight response, which is triggered by the sympathetic nervous system and supported by hormones released from the adrenal medulla.

➡️ Adrenaline (epinephrine) is the fast-acting hormone released within seconds in response to sudden fear, activating:

• ↑ Heart rate

• ↑ Blood glucose

• ↑ Blood flow to skeletal muscle

• Pupil dilation

• Bronchodilation

Perfectly suited for immediate escape actions like running down 12 floors!

❌ Why the Other Options Are Incorrect:

• Aldosterone
  ❌ Maintains blood pressure long-term via sodium reabsorption — no role in acute stress escape.

• Cortisol
  ❌ Helps manage stress but acts hours later, not instantaneously.

The adrenal gland has a rich vascular network adapted for rapid hormone release, especially in the cortex, which produces steroid hormones. The key zone relationships are:

➡️ Zona fasciculata is the widest layer, packed with lipid-laden cells producing cortisol, which needs to enter the blood rapidly. Hence, it’s richly supplied with fenestrated capillaries, allowing easy hormone passage into circulation.

❌ Why the Other Options Are Incorrect:

• Zona glomerulosa
  ❌ Makes aldosterone, but not as richly fenestrated as fasciculata.

• Zona reticularis
  ❌ Some fenestrations may exist, but it’s not the primary zone for fenestrated capillaries.

• Medulla
  ❌ Supplied by sinusoidal capillaries, not fenestrated — facilitates release of catecholamines (epinephrine, norepinephrine).

• Exophthalmos is due to inflammatory enlargement of extraocular muscles and orbital fat, pushing the eye forward.

• Seen classically in Graves’ orbitopathy, and can be measured with an exophthalmometer.

• Lid lag is a different clinical sign — the upper eyelid fails to follow the eyeball promptly when the patient looks downward, but the eye itself remains in the socket.

❌ Why Lid Lag Is Incorrect:

• Lid lag is commonly present in hyperthyroidism, but it is a neuromuscular response, not a structural protrusion.

• You may have lid lag without exophthalmos.

Glucocorticoids vary in potency depending on their anti-inflammatory strength, duration of action, and mineralocorticoid activity.

➡️ Dexamethasone is a synthetic glucocorticoid with:

• Very high glucocorticoid potency

• Minimal mineralocorticoid effect

• Long duration of action

That’s why it’s often used in:

• Cerebral edema

• Severe inflammation

• Dexamethasone suppression test (for Cushing’s)

❌ Why the Other Options Are Incorrect:

• Cortisol
  ❌ Natural hormone, but much weaker (potency = 1).

• Corticosterone
  ❌ Weak glucocorticoid, more involved in mineralocorticoid function.

• Prednisolone
  ❌ Moderate potency (≈4× cortisol), but far less potent than dexamethasone.

🔹 Timeline of Fasting Metabolism

When food intake stops, the body switches through several stages of fuel use:

1. 0–24 hours (Early fasting)

   • Primary energy source: Glycogenolysis (liver glycogen → glucose)

   • Fat breakdown starts slowly.

2. 1–3 days (Short-term fasting)

   • Liver glycogen stores are depleted (~24 hrs).

   • Gluconeogenesis becomes the main source of blood glucose (from amino acids, glycerol, lactate).

   • Lipolysis increases to provide fatty acids.

3. >3–5 days (Prolonged fasting/starvation)

   • Brain adapts to using ketone bodies (β-hydroxybutyrate, acetoacetate) to spare protein breakdown.

   • Ketogenesis in the liver becomes the main energy source for the brain and much of the body.

   • Lipolysis fuels ketogenesis.

🔹 Why Ketogenesis Is Correct Here

• After one week without food, the primary energy supply for most tissues, especially the brain, comes from ketone bodies.

• This adaptation reduces protein degradation, preserving muscle mass.

• Gluconeogenesis continues at a low rate for tissues that must have glucose (RBCs, renal medulla), but it’s not the primary energy source at this point.

❌ Why the Other Options Are Wrong:

• Glycogenolysis → Only lasts about 24 hours; long gone by one week.

• Gluconeogenesis → Still occurs but is secondary; ketones have taken over most of the energy supply.

• Protein degradation → Reduced during prolonged starvation to spare muscle; not the main energy source now.

• Lipolysis → Still ongoing, but fatty acids from lipolysis are mainly used by muscle; the primary energy source overall is ketones derived from this fat.

There are three ketone bodies, but not all are ketones chemically or detectable in urine:

➡️ Acetoacetate is the only major ketone body that:

• Is a true ketone

• Is detectable in urine with common clinical dipstick tests (like nitroprusside reaction)

Beta-hydroxybutyrate is the most abundant in DKA, but cannot be detected by urine dipsticks — blood-specific tests are required for that.

❌ Why the Other Options Are Incorrect:

• Acetone
  ❌ Volatile and exhaled through lungs — not excreted significantly in urine.

• Beta-hydroxybutyric acid
  ❌ Technically not a ketone (no ketone group) and not detected on standard urine tests.

• Acetaldehyde
  ❌ Byproduct of alcohol metabolism — not a ketone body.

• Acetoacetyl-CoA
  ❌ A fatty acid intermediate — too large to be excreted in urine and not a circulating ketone body.

The thyroid gland originates from the foramen cecum at the base of the tongue (near the root) and migrates downward along the thyroglossal duct to reach its final position in the anterior neck (below the cricoid cartilage, at the level of the 2nd–4th tracheal rings).

During this descent, ectopic (aberrant) thyroid tissue can be found anywhere along this path:

Note: Although thyroid goiters or carcinoma can extend into the superior mediastinum, ectopic (aberrant) thyroid tissue does not originate there developmentally.

❌ Why the Other Options Are Incorrect:

• Root of tongue
  ✅ True site — this is where the thyroid begins (lingual thyroid is the most common ectopic site).

• In the neck
  ✅ True — includes pre-tracheal, para-tracheal, and midline neck regions.

• Along the descent of thyroglossal duct
  ✅ True — classic migration pathway.

• Just inferior to the hyoid
  ✅ True — most thyroglossal duct cysts are found here.

• Superior mediastinum
  ❌ Not part of the thyroid’s embryological migration path — therefore not a site for ectopic thyroid origin.

The adrenal gland is derived from two embryonic origins:

• Chromaffin cells are modified postganglionic sympathetic neurons.

• They migrate into the developing adrenal gland from the neural crest, the same origin as peripheral neurons and melanocytes.

❌ Why the Other Options Are Incorrect:

• Coelomic mesothelium
  ❌ Forms the adrenal cortex, not chromaffin cells.

• Splanchnic mesoderm
  ❌ Involved in gut and visceral organ development — not adrenal medulla.

• Notochord
  ❌ Induces neural tube formation but does not give rise to adrenal structures.

• Endoderm
  ❌ Gives rise to gut epithelium and glands, not adrenal tissues.

Amine hormones are derived from one of two amino acids:

• Tyrosine → gives rise to:

  • Dopamine ✅

  • Norepinephrine

  • Epinephrine

  • Thyroid hormones (T₃/T₄)

• Tryptophan → gives rise to:

  • Serotonin

  • Melatonin

So, dopamine is a catecholamine, and it is the first product in the tyrosine → dopamine → norepinephrine → epinephrine pathway.

❌ Why the Other Options Are Incorrect:

• Bradykinin
  ❌ It’s a peptide, not an amine, and is not derived from tyrosine.

• Serotonin
  ❌ Derived from tryptophan, not tyrosine.

• Histamine
  ❌ Derived from histidine, not tyrosine.

• Melatonin
  ❌ Also derived from tryptophan → via serotonin, not tyrosine.

• The pituitary gland (hypophysis) sits in a small depression of the sphenoid bone known as the sella turcica.

• Within the sella turcica lies the hypophyseal fossa, which directly houses the gland.

• It is covered superiorly by the diaphragma sellae, a fold of dura mater.

❌ Why the Other Options Are Incorrect:

• Clivus
  ❌ A sloped bony surface behind the sella turcica — supports the brainstem, not the pituitary.

• Anterior cranial fossa
  ❌ Houses the frontal lobes of the brain. Pituitary sits lower and more posterior.

• Posterior cranial fossa
  ❌ Contains the cerebellum and brainstem, not the pituitary gland.

Peptide hormones (like insulin, glucagon, ACTH, etc.) are:

• Hydrophilic (water-soluble)

• Large, charged molecules

• Cannot cross the lipid bilayer of cell membranes

Therefore, their receptors must be located on the plasma membrane surface, triggering second messenger systems like cAMP, IP₃/DAG, or tyrosine kinase pathways to carry the signal inside the cell.

❌ Why the Other Options Are Incorrect:

• Hydrophobic
  ❌ Hydrophobic molecules (like steroid hormones) can cross the cell membrane and bind to intracellular receptors, not surface receptors.

• Effector system
  ❌ That refers to the mechanism activated after receptor binding — not the reason receptors are on the surface.

• Lipophilic
  ❌ Lipophilic = fat-loving = membrane-permeable → applies to steroids & thyroid hormones, not peptides.

• High affinity for cAMP
  ❌ Peptide hormones trigger cAMP via membrane receptors, but don’t bind directly to cAMP. That’s part of the downstream signaling — not the reason for receptor location.

The adrenal cortex has three distinct zones in adults, each with a specific function:

During fetal life:

• The fetal adrenal cortex contains two major regions: an outer definitive cortex (which becomes glomerulosa + fasciculata) and a large fetal zone (which degenerates after birth).

• The zona reticularis forms gradually after birth, especially around age 3–4, and matures by the time of adrenarche (pre-puberty androgen production).

❌ Why the Other Options Are Incorrect:

• Zona fasciculata
  ❌ Present before birth and actively secretes cortisol important for fetal lung development.

• Zona glomerulosa
  ❌ Also develops prenatally, and is functional at birth.

• Zona pellucida
  ❌ Not a real layer of the adrenal cortex — this term is used in oocyte biology, not adrenal histology.

The adrenal gland develops from two embryological sources:

• The fetal adrenal cortex is the first to develop, beginning in the 5th week as cells from the coelomic epithelium (mesothelium) proliferate.

• The neural crest-derived cells later invade this tissue to form the medulla, which produces catecholamines like epinephrine.

❌ Why Other Options Are Incorrect:

• 3rd week
  ❌ Too early — basic germ layers just formed, no organ-specific differentiation yet.

• 4th week
  ❌ Slightly early — limb buds and early facial features begin, but adrenal cortex starts just after this.

• 8th week
  ❌ This is when the adrenal medulla begins forming, not the cortex.

• 12th week
  ❌ By this time, both adrenal regions are more defined — development is well underway.

The pituitary gland has a dual embryological origin:

• The anterior pituitary develops from an upward invagination of oral ectoderm known as Rathke’s pouch.

• The posterior pituitary arises from a downward extension of the hypothalamus (neuroectoderm).

❌ Why the Other Options Are Incorrect:

• Mesoderm
  ❌ Gives rise to muscle, bone, blood — not pituitary structures.

• Neuroectoderm
  ❌ This forms the posterior pituitary, not anterior.

• Oral endoderm
  ❌ Endoderm contributes to gut lining and organs — not pituitary.

In SIADH (Syndrome of Inappropriate Antidiuretic Hormone secretion):

• ADH (vasopressin) promotes water reabsorption from the kidneys, especially in the collecting ducts.

• This leads to water retention without proportional sodium retention.

• The result is a dilutional hyponatremia: total body water increases, but total body sodium stays the same or decreases → plasma sodium concentration drops.

Patients are often euvolemic (normal body fluid volume) because of compensatory natriuresis (kidneys excrete sodium to get rid of some water).

❌ Why Other Options Are Incorrect:

• Hypernatremia
  ❌ Seen in diabetes insipidus (ADH deficiency), not SIADH.

• Hypokalemia
  ❌ Not characteristic of SIADH. More common in conditions with excessive aldosterone.

• Hyperkalemia
  ❌ No direct link with SIADH. Seen in renal failure, hypoaldosteronism, etc.

• Hypochloremia
  ❌ Might occur secondarily but not the defining feature. Hyponatremia is the key lab abnormality.

Insulin preparations vary by onset, peak, and duration. Here’s a quick comparison:

➡️ Glargine is a long-acting insulin analog designed to mimic basal insulin secretion, maintaining steady glucose levels over a full day without a peak.

❌ Why the Other Options Are Incorrect:

• Glulisine
  ❌ Rapid-acting; ideal for meals, not for 24-hour coverage.

• Lispro
  ❌ Also rapid-acting; short duration of action.

• NPH insulin
  ❌ Intermediate-acting; doesn’t last full 24 hours, and has a significant peak (risk of hypoglycemia).

• Aspart
  ❌ Rapid-acting; used just before meals, not for basal control.

The anterior pituitary (pars distalis) contains five main hormone-secreting cell types, each targeting different organs. Their relative abundance is:

Somatotrophs dominate in quantity and are responsible for producing growth hormone, which plays a major role in development, metabolism, and linear growth.

❌ Why Other Options Are Incorrect:

• Lactotroph
  ❌ Less abundant than somatotrophs; numbers increase in pregnancy but not under normal conditions.

• Thyrotroph
  ❌ Among the least numerous cell types in the anterior pituitary.

• Corticotroph
  ❌ Moderate in number, but not more than somatotrophs.

• Gonadotroph
  ❌ Secrete LH and FSH, but make up only a small portion (~10%).

The anterior pituitary contains three main types of cells based on how they stain with dyes:

Acidophilic cells are those that absorb acidic dyes like eosin and appear pink or reddish under the microscope. These include:

• Somatotrophs → secrete Growth Hormone (GH)

• Lactotrophs → secrete Prolactin (PRL)

❌ Why the Other Options Are Incorrect:

• Luteinizing hormone (LH) and Follicle-stimulating hormone (FSH)
  ❌ Both are secreted by gonadotrophs, which are basophils, not acidophils.

• Luteinizing hormone (LH) and Growth hormone (GH)
  ❌ LH is from basophils, GH is from acidophils. The question asked only about acidophilic cells.

• Growth hormone (GH) and Adrenocorticotropic hormone (ACTH)
  ❌ GH is from acidophils (✔), but ACTH is secreted by corticotrophs, which are basophils (❌).

• Growth hormone (GH) and Thyroid-stimulating hormone (TSH)
  ❌ GH is from acidophils (✔), but TSH is secreted by thyrotrophs, which are basophils (❌).

https://www.researchgate.net/figure/Galli-Curci-A-in-1919-before-any-trace-of-the-goiter-is-visible-B-showing-clear_fig1_12031497

A diffusely enlarged thyroid with normal free T4 and normal TSH is a euthyroid (nontoxic) goiter. “Diffuse” + “nontoxic” basically means the gland is enlarged without hyperthyroidism and without nodules.

Why this is correct ✅

• Diffuse enlargement + no masses/nodules on exam

• Normal free T4 and normal TSH → thyroid hormone production is adequate (so it’s not toxic and not hypothyroid)

• Most common physiology: TSH-driven hypertrophy/hyperplasia over time due to mild iodine deficiency or dietary goitrogens (classically seen in settings where iodine intake can be variable).

Why the other options are wrong ❌

❌ Subacute granulomatous thyroiditis (de Quervain)

• Typically painful/tender thyroid + recent viral illness

• Often shows transient hyperthyroid phase (↑T4, ↓TSH)

• Your stem: painless, chronic, euthyroid labs

❌ Toxic multinodular goiter

• Usually nodular/irregular thyroid rather than smooth diffuse enlargement

• Causes hyperthyroidism: ↓TSH with ↑T3/T4

• The stem: normal TSH/T4, no nodules

❌ Hashimoto’s thyroiditis

• Often progresses to hypothyroidism: ↑TSH (early) and later ↓T4

• Frequently firm/rubbery gland + anti-TPO positive

• The patient is perfectly euthyroid and doesn’t suggest autoimmune disease in this case

❌ Papillary carcinoma

• Classically a discrete nodule (not diffuse symmetric enlargement)

• May have cervical lymph nodes

• Thyroid function tests usually normal, but the exam would show a mass

Clinical Presentation: This patient presents with a diffuse, painless goiter (gradual enlargement). Hashimoto’s is the most common cause of hypothyroidism in iodine-sufficient areas and frequently presents as an asymptomatic diffuse enlargement of the thyroid in middle-aged women.

Laboratory Findings: The labs show subclinical hypothyroidism (Normal Free T4, but elevated TSH). This indicates primary thyroid failure; the pituitary is secreting more TSH to maintain normal T4 levels due to the autoimmune destruction of the thyroid follicles.

Epidemiology: It is most commonly seen in women between 30 and 50 years of age.

Why the other options are incorrect

• Subacute granulomatous thyroiditis (De Quervain’s): This condition is typically painful and often follows a viral illness. It usually presents with a tender thyroid, which contradicts this patient’s painless enlargement.

• Toxic multinodular goiter: This would present with signs of hyperthyroidism (suppressed TSH, elevated T3/T4) and a nodular (bumpy) thyroid exam, rather than a diffuse enlargement with elevated TSH.

• Diffuse nontoxic goiter: While this presents with a diffuse goiter, it is typically defined by euthyroid status (normal TSH and T4). The elevated TSH in this patient points toward a failing thyroid (hypothyroidism), which favors the autoimmune etiology of Hashimoto’s.

• Papillary carcinoma: This usually presents as a palpable thyroid nodule rather than a diffuse enlargement. Furthermore, patients with thyroid cancer are typically euthyroid (normal TSH and T4).

https://www.netterimages.com/meningococcemia-labeled-anderson-endocrinology-frank-h-netter-64512.html

This autopsy description is classic for Waterhouse–Friderichsen syndrome: fulminant meningococcemia causing endotoxemia → DIC → shock, with massive bilateral adrenal cortical hemorrhage leading to acute adrenal insufficiency and sudden death (often after a brief “viral-like” prodrome like sore throat).

Why Neisseria meningitidis fits ✅

• Sudden deterioration after a mild upper-respiratory–type symptom

• Bilateral adrenal hemorrhage

• Mechanism: LOS (endotoxin) triggers cytokine storm + DIC, causing hemorrhage/infarction in multiple organs, classically the adrenals.

Why the other options are wrong ❌

❌ Mycobacterium tuberculosis

• Causes chronic adrenal destruction (Addison disease) with granulomas/caseation, not sudden hemorrhage.

❌ Streptococcus pneumoniae

• Can cause meningitis/sepsis, but Waterhouse–Friderichsen is classically meningococcal (exam favorite). Pneumococcus doesn’t typically present with the “adrenal hemorrhage + DIC” signature as the classic association.

❌ Histoplasma capsulatum

• Opportunistic/chronic disseminated infection; can involve adrenals but not with abrupt bilateral cortical hemorrhage and sudden death in a previously healthy person.

❌ Cytomegalovirus (CMV)

• Usually in immunocompromised patients; can cause adrenalitis, but again not the classic fulminant DIC picture in a healthy adult.

Conscientiousness in the Big Five model describes traits related to self-discipline, organization, and dependability.

The “Desi” Context: In a culture where “Inshallah time” (being late) and chaotic paperwork are common tropes, the person who pays bills early and arrives on time is the ultimate example of high conscientiousness.

Why the others are wrong:

• Wide interest: This describes Openness to Experience.

• Energetic: This falls under Extraversion.

• Anxious / Tense: These are traits of Neuroticism.

Young patient, mild fasting hyperglycemia (120 mg/dL), mild glucosuria, no ketones, no insulin autoantibodies, and a strong family history at a similar young age → this screams MODY (autosomal dominant monogenic diabetes).
The classic gene here is glucokinase (GCK) → MODY 2.

Why Glucokinase is correct ✅

• Glucokinase is the glucose sensor in pancreatic β-cells (and also in liver).

• Mutation → β-cells “think” blood glucose is lower than it is → higher threshold for insulin release.

• Result: stable, mild fasting hyperglycemia from a young age; usually no ketosis, often doesn’t need aggressive treatment.

Why the other options are wrong ❌

❌ Glucagon

• Glucagon defects don’t classically cause this inherited mild fasting hyperglycemia picture.

❌ Insulin

• Insulin gene mutations can cause rare neonatal diabetes or severe phenotypes, not the classic familial mild fasting hyperglycemia pattern described.

❌ MHC DR

• Associated with type 1 diabetes risk (autoimmune). But she has no insulin autoantibodies and has a clear autosomal dominant-style family history.

❌ GLUT4

• GLUT4 is the insulin-responsive transporter in muscle/adipose (type 2 physiology/insulin resistance). Wouldn’t give this classic young-onset, mild, inherited presentation.