During nephrectomy exposure, the surgeon identifies endocrine glands at the ___ pole of each kidney.
A. Superior pole
B. Inferior pole
C. Medial hilum
D. Lateral surface

A. Superior pole

Each adrenal gland is composed of:
A. Capsule and cortex
B. Medulla only
C. Cortex only
D. Adrenal cortex and medulla

D. Adrenal cortex and medulla

A patient with episodic palpitations has excess epinephrine/norepinephrine. Which adrenal region produces these?
A. Zona glomerulosa
B. Adrenal medulla
C. Zona fasciculata
D. Zona reticularis

B. Adrenal medulla

A CT shows intact medulla but damaged cortex. Which hormone class is most reduced?
A. Catecholamines
B. Peptide hormones
C. Corticosteroids
D. Thyroid hormones

C. Corticosteroids

Which pair correctly lists the two major adrenocortical hormone classes?
A. Mineralocorticoids and glucocorticoids
B. Catecholamines and steroids
C. Aldosterone and catecholamines
D. Insulin and glucagon

A. Mineralocorticoids and glucocorticoids

The adrenal cortex also secretes small amounts of hormones with testosterone-like effects. These are:
A. Estrogenic hormones
B. Thyroid hormones
C. Progestin hormones
D. Androgenic hormones

D. Androgenic hormones

A patient with hyperkalemia needs rapid electrolyte regulation. Which adrenocortical class chiefly regulates ECF Na+ and K+?
A. Glucocorticoids
B. Mineralocorticoids
C. Androgens
D. Estrogens

B. Mineralocorticoids

A patient develops fasting hyperglycemia and muscle wasting patterns. Which hormone class most directly raises blood glucose and alters protein/fat metabolism?
A. Mineralocorticoids
B. Catecholamines
C. Glucocorticoids
D. Androgenic hormones

C. Glucocorticoids

The principal mineralocorticoid and principal glucocorticoid, respectively, are:
A. Cortisol, aldosterone
B. DHEA, cortisol
C. Aldosterone, DHEA
D. Aldosterone, cortisol

D. Aldosterone, cortisol

A thin cell layer just beneath the adrenal capsule (≈15% cortex) secretes:
A. Zona glomerulosa
B. Zona fasciculata
C. Zona reticularis
D. Adrenal medulla

A. Zona glomerulosa

A patient on an ACE inhibitor has reduced signaling. Aldosterone secretion is normally stimulated by:
A. ACTH and cortisol
B. Sodium and glucose
C. Angiotensin II and potassium
D. Epinephrine and norepinephrine

C. Angiotensin II and potassium

The middle, widest adrenal cortical zone (≈75% cortex) is:
A. Zona reticularis
B. Zona fasciculata
C. Zona glomerulosa
D. Adrenal medulla

B. Zona fasciculata

A patient with high ACTH has increased cortisol plus adrenal androgens/estrogens. Which zone produces this trio?
A. Zona reticularis
B. Zona glomerulosa
C. Adrenal medulla
D. Zona fasciculata

D. Zona fasciculata

Secretion of cortisol, adrenal androgens, and estrogens is primarily controlled by:
A. Potassium
B. Angiotensin II
C. ACTH
D. Sodium

C. ACTH

The inner zone of the adrenal cortex is the:
A. Zona fasciculata
B. Zona reticularis
C. Zona glomerulosa
D. Adrenal medulla

B. Zona reticularis

A steroid profile shows high DHEA and androstenedione with small estrogen output. Which zone fits best?
A. Zona reticularis
B. Zona fasciculata
C. Zona glomerulosa
D. Adrenal medulla

A. Zona reticularis

LDL receptors on adrenocortical membranes cluster in specialized structures called:
A. Coated pits
B. Tight junctions
C. Desmosomes
D. Gap junctions

A. Coated pits

After LDL binds, coated pits are internalized by:
A. Exocytosis
B. Endocytosis
C. Diffusion
D. Oxidation

B. Endocytosis

ACTH increases adrenal steroid synthesis partly by:
A. Blocking LDL receptor recycling
B. Decreasing LDL receptor number
C. Increasing LDL receptors and enzymes
D. Inhibiting cholesterol release from LDL

C. Increasing LDL receptors and enzymes

After cholesterol enters an adrenocortical cell, it is delivered to mitochondria and cleaved by:
A. Cholesterol desmolase
B. 11β-hydroxylase
C. Aldosterone synthase
D. 17α-hydroxylase

A. Cholesterol desmolase

Cholesterol → pregnenolone via cholesterol desmolase is the:
A. Terminal step
B. Rate-limiting step
C. Coupling step
D. Storage step

B. Rate-limiting step

Steps of adrenal cortical steroid synthesis occur mainly in:
A. Nucleus and Golgi
B. Cytosol only
C. Mitochondria and ER
D. Lysosomes only

C. Mitochondria and ER

A steroid is 1/30 as potent as aldosterone and is secreted in very small quantities:
A. Cortisol
B. Deoxycorticosterone
C. Corticosterone
D. 9α-fluorocortisol

B. Deoxycorticosterone

A hormone with slight mineralocorticoid activity is:
A. Corticosterone
B. Prednisone
C. Dexamethasone
D. Cortisone

A. Corticosterone

A synthetic steroid slightly more potent than aldosterone is:
A. Cortisol
B. 9α-fluorocortisol
C. Deoxycorticosterone
D. Corticosterone

B. 9α-fluorocortisol

Very slight mineralocorticoid activity but secreted in large quantity:
A. Aldosterone
B. Deoxycorticosterone
C. Cortisol
D. 9α-fluorocortisol

C. Cortisol

The glucocorticoid responsible for ~95% of total glucocorticoid activity is:
A. Cortisol
B. Corticosterone
C. Cortisone
D. Prednisone

A. Cortisol

About 4% of glucocorticoid activity, much less potent than cortisol:
A. Dexamethasone
B. Cortisone
C. Corticosterone
D. Methylprednisone

C. Corticosterone

A steroid almost as potent as cortisol is:
A. Cortisone
B. Prednisone
C. Dexamethasone
D. Aldosterone

A. Cortisone

A synthetic steroid ~4 times as potent as cortisol is:
A. Prednisone
B. Methylprednisone
C. Dexamethasone
D. Corticosterone

A. Prednisone

A synthetic steroid ~5 times as potent as cortisol is:
A. Prednisone
B. Dexamethasone
C. Methylprednisone
D. Cortisone

C. Methylprednisone

A synthetic steroid ~30 times as potent as cortisol is:
A. Methylprednisone
B. Dexamethasone
C. Prednisone
D. Cortisone

B. Dexamethasone

Adrenocortical hormones circulate bound primarily to:
A. Platelets
B. Plasma proteins
C. RBC membranes
D. Albumin-free fraction only

B. Plasma proteins

High cortisol protein binding slows cortisol:
A. Filtration by kidneys
B. Elimination from plasma
C. Synthesis in cortex
D. Transport into cells

B. Elimination from plasma

Cortisol’s half-life is approximately:
A. 5 minutes
B. 20 minutes
C. 60–90 minutes
D. 6 hours

C. 60–90 minutes

Aldosterone has a relatively ___ half-life of about ___.
A. short; 20 minutes
B. long; 20 minutes
C. short; 90 minutes
D. long; 90 minutes

A. short; 20 minutes

Adrenocortical hormones are metabolized primarily in the:
A. Kidney
B. Liver
C. Lung
D. Spleen

B. Liver

Adrenal steroids are degraded and conjugated to:
A. Sulfuric acid
B. Glucuronic acid
C. Hydrochloric acid
D. Carbonic acid

B. Glucuronic acid

About 25% of steroid conjugates are excreted in:
A. Sweat then skin
B. Urine then bladder
C. Bile then feces
D. CSF then blood

C. Bile then feces

Aldosterone blood concentration depends strongly on dietary:
A. Sodium and potassium
B. Calcium and phosphate
C. Iron and folate
D. Iodine and selenium

A. Sodium and potassium

Total loss of adrenocortical secretion may cause death within days unless treated with extensive:
A. Salt therapy
B. Glucose infusion
C. Thyroxine therapy
D. Beta-blockade

A. Salt therapy

In total adrenal cortical failure, survival can be supported by injections of:
A. Catecholamines
B. Mineralocorticoids
C. Calcitonin
D. Thyroxine

B. Mineralocorticoids

Without mineralocorticoids, extracellular potassium concentration:
A. Falls rapidly
B. Remains unchanged
C. Rises
D. Cycles unpredictably

C. Rises

Without mineralocorticoids, sodium and chloride are rapidly:
A. Retained
B. Lost
C. Converted to bicarbonate
D. Stored in bone

B. Lost

Without mineralocorticoids, total extracellular volume and blood volume become:
A. Increased
B. Unchanged
C. Diluted
D. Greatly reduced

D. Greatly reduced

Renal epithelial cells express 11β-HSD2 to:
A. Enhance cortisol mineralocorticoid effects
B. Prevent cortisol activating MR
C. Convert aldosterone into cortisol
D. Block aldosterone binding MR

B. Prevent cortisol activating MR

Genetic deficiency of 11β-HSD2 causing cortisol mineralocorticoid effects is:
A. Cushing syndrome
B. Conn syndrome
C. Addison disease
D. Apparent mineralocorticoid excess

D. Apparent mineralocorticoid excess

Ingestion of large amounts of ___ can cause AME by blocking 11β-HSD2.
A. Grapefruit
B. Licorice
C. Caffeine
D. Ethanol

B. Licorice

Aldosterone ___ renal tubular sodium reabsorption and ___ potassium secretion.
A. decreases; decreases
B. increases; increases
C. decreases; increases
D. increases; decreases

B. increases; increases

Because aldosterone increases Na+ reabsorption, it simultaneously increases secretion of:
A. Calcium
B. Hydrogen
C. Potassium
D. Bicarbonate

C. Potassium

Aldosterone causes sodium to be ___ in ECF while increasing potassium loss in urine.
A. Excreted
B. Conserved
C. Oxidized
D. Chelated

B. Conserved

ECF sodium concentration rises only slightly in hyperaldosteronism because Na+ reabsorption pulls in:
A. Glucose
B. Water
C. Phosphate
D. Urea

B. Water

Which hormone enhances water reabsorption in distal and collecting tubules?
A. Aldosterone
B. Cortisol
C. ADH
D. ANP

C. ADH

Increased arterial pressure increases renal Na+ and water excretion called:
A. Osmotic diuresis
B. Countercurrent multiplication
C. Pressure natriuresis/diuresis
D. Tubuloglomerular feedback

C. Pressure natriuresis/diuresis

Normalization of Na+ and water excretion during high aldosterone via pressure mechanisms is:
A. Aldosterone escape
B. Mineralocorticoid resistance
C. Addison crisis
D. Conn crisis

A. Aldosterone escape

When aldosterone secretion becomes zero, large amounts of sodium are lost in:
A. Sweat
B. Urine
C. Stool
D. Saliva

B. Urine

Loss of sodium in urine during aldosterone absence ___ ECF volume.
A. Increases
B. Does not change
C. Decreases
D. Doubles

C. Decreases

Excess aldosterone most classically causes:
A. Hyperkalemia
B. Hypokalemia
C. Hypercalcemia
D. Hypocalcemia

B. Hypokalemia

Aldosterone deficiency most classically causes:
A. Hyperkalemia
B. Hypokalemia
C. Hypernatremia
D. Hypomagnesemia

A. Hyperkalemia

Excess aldosterone increases tubular hydrogen secretion causing:
A. Acidosis
B. Alkalosis
C. Respiratory alkalosis
D. Lactic acidosis

B. Alkalosis

Aldosterone stimulates sodium and potassium transport in:
A. Sweat and salivary glands
B. Sweat and pancreas
C. Saliva and thyroid
D. Liver and spleen

A. Sweat and salivary glands

Aldosterone diffuses ___ into tubular epithelial cells.
A. Poorly
B. Slowly via carriers
C. Readily
D. Only by endocytosis

C. Readily

In a principal cell, aldosterone binds a cytosolic protein with high stereospecificity. That protein is the:
A. Glucocorticoid receptor
B. Angiotensin II receptor
C. Mineralocorticoid receptor
D. ACTH receptor

C. Mineralocorticoid receptor

After aldosterone binds its receptor, the complex enters the nucleus and most directly promotes formation of:
A. mRNA
B. cAMP
C. IP3
D. DAG

A. mRNA

The aldosterone-induced transcript returns to cytoplasm and, with ribosomes, produces:
A. Steroid hormone
B. Second messenger
C. Glycogen polymer
D. Protein enzyme

D. Protein enzyme

The principal basolateral driver of renal Na+/K+ exchange is:
A. Na+-H+ exchanger
B. Na+-K+ ATPase
C. NKCC cotransporter
D. ENaC channel

B. Na+-K+ ATPase

Increased extracellular angiotensin II most strongly:
A. Decreases aldosterone output
B. Abolishes aldosterone output
C. Does not change output
D. Increases aldosterone output

D. Increases aldosterone output

Increased extracellular sodium concentration will very slightly:
A. Increase aldosterone output
B. Decrease aldosterone output
C. Greatly increase aldosterone output
D. Not affect aldosterone output

B. Decrease aldosterone output

A pituitary hormone is necessary for aldosterone synthesis but usually not rate-controlling. Which is it?
A. ADH
B. TSH
C. ACTH
D. GH

C. ACTH

When RAAS is activated, aldosterone’s key renal effects are:
A. Excrete K, raise blood pressure
B. Excrete Na, lower blood pressure
C. Retain K, raise blood pressure
D. Retain water, lose sodium

A. Excrete K, raise blood pressure

A patient starts an angiotensin II receptor blocker. Plasma aldosterone will:
A. Increase
B. Remain unchanged
C. Oscillate widely
D. Decrease

D. Decrease

Cortisol most directly stimulates hepatic:
A. Glycolysis
B. Gluconeogenesis
C. Glycogenesis
D. Ketolysis

B. Gluconeogenesis

Cortisol increases the hepatic components needed to convert amino acids into glucose, especially:
A. Transporters
B. Receptors
C. Enzymes
D. Ribosomes

C. Enzymes

In prolonged fasting, cortisol shifts substrate availability by causing:
A. Storage of amino acids
B. Oxidation of amino acids
C. Sequestration in connective tissue
D. Mobilization from extrahepatic tissues

D. Mobilization from extrahepatic tissues

Cortisol counteracts insulin’s suppression of hepatic gluconeogenesis; it:
A. Antagonizes insulin
B. Enhances insulin
C. Mimics insulin
D. Replaces insulin

A. Antagonizes insulin

Cortisol causes a moderate ____ in glucose utilization by most cells.
A. Increase
B. No change
C. Decrease
D. Complete blockade

C. Decrease

Reduced GLUT4 translocation to the cell membrane from cortisol leads to:
A. Hypoglycemia
B. Insulin resistance
C. Mineralocorticoid excess
D. Increased glucose sensitivity

B. Insulin resistance

Sustained cortisol-induced hyperglycemia can produce:
A. Adrenal diabetes
B. Type 1 diabetes
C. Diabetes insipidus
D. Pancreatic failure

A. Adrenal diabetes

Cortisol decreases ____ stores in essentially all cells except liver.
A. Glycogen
B. Triglyceride
C. Phosphate
D. Protein

D. Protein

Cortisol’s net effect on liver and plasma proteins is:
A. Decreases both
B. Increases both
C. No net change
D. Denatures both

B. Increases both

Cortisol ____ mobilization of fatty acids from adipose tissue.
A. Inhibits
B. Blocks
C. Promotes
D. Converts

C. Promotes

Beyond mobilization, cortisol also directly tends to ____ fatty acid oxidation in cells.
A. Enhance
B. Suppress
C. Prevent
D. Randomize

A. Enhance

Any major stress increases ____ secretion, which increases cortisol output.
A. TSH
B. ADH
C. GH
D. ACTH

D. ACTH

After major surgery, a patient’s cortisol spikes. Which stimulus is classically associated with increased cortisol?
A. High dietary sodium
B. Hypercalcemia
C. Surgery
D. Increased sunlight exposure

C. Surgery

A restrained lab animal develops high cortisol. This is best classified as:
A. Physiologic stressor
B. Primary thyroid failure
C. Mineralocorticoid excess
D. Paraneoplastic syndrome

A. Physiologic stressor

Which exposure is a classic cortisol-raising trigger?
A. Low ambient light
B. High carbohydrate meal
C. Mild dehydration only
D. Intense heat or cold

D. Intense heat or cold

A patient receives a norepinephrine injection during shock. This can increase cortisol as a:
A. Paracrine reflex
B. Stress-related trigger
C. Thyroid feedback effect
D. Renal compensation

B. Stress-related trigger

Large doses of glucocorticoids can usually block inflammation and may reverse effects in:
A. Rheumatoid arthritis
B. Graves disease
C. Type 1 diabetes
D. Myxedema

A. Rheumatoid arthritis

Cortisol’s anti-inflammatory effect includes stabilization of:
A. Nuclear pores
B. Tight junctions
C. Microtubules
D. Lysosomal membranes

D. Lysosomal membranes

Cortisol blocks edema formation partly by decreasing:
A. Capillary permeability
B. Venous compliance
C. Lymphatic pumping
D. Erythrocyte rigidity

A. Capillary permeability

Cortisol decreases leukocyte migration and phagocytosis partly by reducing:
A. Histamine and bradykinin
B. Prostaglandins and leukotrienes
C. Interferons and antibodies
D. Renin and angiotensin

B. Prostaglandins and leukotrienes

Cortisol suppresses immunity primarily by decreasing:
A. Neutrophil degranulation
B. Monocyte differentiation
C. Lymphocyte reproduction
D. Platelet aggregation

C. Lymphocyte reproduction

Cortisol attenuates fever mainly by reducing release of:
A. IL-1 from WBCs
B. IL-2 from T cells
C. TNF from endothelium
D. IFN-γ from NK cells

A. IL-1 from WBCs

Cortisol’s effect on allergic inflammation is best described as:
A. Potentiates histamine release
B. Blocks allergic inflammatory response
C. Increases mast-cell numbers
D. Prolongs late-phase wheeze

B. Blocks allergic inflammatory response

Cortisol also promotes:
A. Hemolysis
B. Necrosis
C. Calcification
D. Healing

D. Healing

Lymphocytopenia or eosinopenia suggests overproduction of:
A. Aldosterone
B. ACTH
C. Cortisol
D. TSH

C. Cortisol

Cortisol is lipid-_____ , enabling membrane passage.
A. soluble
B. charged
C. insoluble
D. anchored

A. soluble

Inside the cell, cortisol binds its receptor in the:
A. Cytoplasm
B. Extracellular fluid
C. Nucleus
D. Mitochondria

A. Cytoplasm

The cortisol–receptor complex regulates transcription by binding:
A. TATA boxes
B. Glucocorticoid response elements
C. Thyroid response elements
D. Estrogen response elements

B. Glucocorticoid response elements

ACTH is best described as:
A. Tripeptide amide
B. Steroid hormone
C. 39–amino acid polypeptide
D. Catecholamine precursor

C. 39–amino acid polypeptide

CRF-secreting neuron cell bodies are mainly in the:
A. Supraoptic nucleus
B. Paraventricular nucleus
C. Median eminence
D. Arcuate nucleus

B. Paraventricular nucleus

ACTH activates which membrane enzyme to raise cAMP?
A. Phospholipase C
B. Guanylyl cyclase
C. Adenylyl cyclase
D. Tyrosine kinase

C. Adenylyl cyclase

The most important ACTH-stimulated step listed is activation of:
A. Protein kinase A
B. 11β-HSD2
C. LDL endocytosis
D. Aldosterone synthase

A. Protein kinase A

Protein kinase A activation most directly promotes cholesterol conversion to:
A. Cortisol
B. Pregnenolone
C. Aldosterone
D. Corticosterone

B. Pregnenolone

Physiologic stress increases secretion of:
A. ACTH and cortisol
B. TSH and calcitonin
C. ADH and aldosterone
D. Renin and insulin

A. ACTH and cortisol

Cortisol exerts direct negative feedback on:
A. Hypothalamus and anterior pituitary
B. Thyroid and parathyroids
C. Posterior pituitary and pineal
D. Adrenal medulla and kidney

A. Hypothalamus and anterior pituitary

The precursor that yields ACTH, MSH, β-lipotropin, and β-endorphin is:
A. Angiotensinogen
B. Thyroglobulin
C. POMC
D. Albumin

C. POMC

Primary adrenal cortical atrophy or injury with low adrenocortical hormones is:
A. Cushing syndrome
B. Addison’s disease
C. Conn syndrome
D. Graves disease

B. Addison’s disease

Mineralocorticoid deficiency most directly causes:
A. ECF depletion → shock risk
B. RBC hemolysis → anemia
C. Hypercalcemia → tetany
D. SIADH → hyponatremia

A. ECF depletion → shock risk

Glucocorticoid deficiency in Addison prevents between-meal glucose maintenance because it impairs:
A. Glycogenolysis
B. Ketogenesis
C. Gluconeogenesis
D. Lipolysis

C. Gluconeogenesis

A key cause of Addison-associated mucocutaneous hyperpigmentation is increased:
A. Melanin
B. Bilirubin
C. Hemosiderin
D. Carotene

A. Melanin

Standard chronic therapy for Addison disease is:
A. High-dose dexamethasone
B. Beta-blocker monotherapy
C. Aldosterone alone
D. Daily mineralocorticoids and glucocorticoids

D. Daily mineralocorticoids and glucocorticoids

Severe stress-related debility requiring extra glucocorticoids in Addison is:
A. Thyroid storm
B. Addisonian crisis
C. Conn syndrome
D. Cushing syndrome

B. Addisonian crisis

Hypersecretion by the adrenal cortex causing a complex cascade is:
A. Cushing syndrome
B. Addison disease
C. Graves disease
D. Hashimoto disease

A. Cushing syndrome

Cushing syndrome due to excess pituitary ACTH is:
A. Conn syndrome
B. Addison disease
C. Cushing disease
D. Adrenogenital syndrome

C. Cushing disease

The drug classically administered to differentiate ACTH-dependent vs ACTH-independent Cushing is:
A. Aldosterone
B. Cortisol
C. ACTH
D. Dexamethasone

D. Dexamethasone

With very high-dose dexamethasone, which change can occur in many patients with Cushing disease?
A. Renin rises markedly
B. ACTH becomes suppressed
C. Cortisol rises further
D. Aldosterone becomes undetectable

B. ACTH becomes suppressed

Iatrogenic Cushing syndrome can result from prolonged administration of:
A. Glucocorticoids
B. Mineralocorticoids
C. Thyroxine
D. Insulin

A. Glucocorticoids

The classic facial appearance in Cushing syndrome is:
A. Butterfly rash
B. Masklike facies
C. Myxedematous facies
D. Moon face

D. Moon face

About 80% of patients with Cushing syndrome develop:
A. Hypotension
B. Hypertension
C. Bradycardia
D. Syncope

B. Hypertension

Cushing hypertension is largely attributed to:
A. Autoantibodies stimulating AT1 receptors
B. Catecholamine excess
C. Cortisol mineralocorticoid activity
D. Low aldosterone signaling

C. Cortisol mineralocorticoid activity

Purplish striae in Cushing syndrome reflect depletion of:
A. Collagen depletion
B. Keratin excess
C. Elastin overgrowth
D. Melanin accumulation

A. Collagen depletion

A correct treatment approach for Cushing syndrome includes:
A. Iodine ablation only
B. Beta-blocker only
C. Salt therapy only
D. Tumor removal or steroidogenesis blockade

D. Tumor removal or steroidogenesis blockade

Among listed treatments, the “last resort” option is:
A. High-dose dexamethasone
B. Methimazole therapy
C. Adrenalectomy
D. Pheochromocytoma resection

C. Adrenalectomy

A small zona glomerulosa tumor secreting large aldosterone is:
A. Primary aldosteronism
B. Addison disease
C. Cushing syndrome
D. Adrenogenital syndrome

A. Primary aldosteronism

A diagnostic criterion for primary aldosteronism is:
A. Increased plasma renin
B. Increased TSH
C. Decreased cortisol
D. Decreased plasma renin

D. Decreased plasma renin

Treatment for primary aldosteronism is best:
A. Levothyroxine replacement
B. Surgery or MR antagonist
C. Radioiodine ablation
D. Dopamine agonist therapy

B. Surgery or MR antagonist

An adrenocortical tumor secreting excess androgens causing masculinization is:
A. Conn syndrome
B. Cushing disease
C. Adrenogenital syndrome
D. Addisonian crisis

C. Adrenogenital syndrome

Adrenal cortex layers superficial → deep are:
A. Glomerulosa fasciculata reticularis
B. Fasciculata reticularis glomerulosa
C. Reticularis glomerulosa fasciculata
D. Medulla glomerulosa fasciculata

A. Glomerulosa fasciculata reticularis

Which finding best supports primary adrenal insufficiency over secondary?
A. No ACTH present
B. Melanin pigmentation present
C. Moon face present
D. Hypertension present

B. Melanin pigmentation present

A classic trigger for Addisonian crisis is:
A. High sodium diet
B. Cold adaptation
C. Exercise training
D. Infection or trauma stress

D. Infection or trauma stress

A patient with Addison disease is especially prone to:
A. Hyperglycemia after meals
B. Hypertension after meals
C. Hypoglycemia between meals
D. Polycythemia between meals

C. Hypoglycemia between meals

A patient has persistently high aldosterone, yet after several days their renal Na+/H2O excretion returns near baseline. This phenomenon is:
A. Mineralocorticoid resistance
B. Adrenal diabetes
C. Aldosterone escape
D. Apparent mineralocorticoid excess

C. Aldosterone escape

The key driver of aldosterone escape is:
A. Increased BP → natriuresis/diuresis
B. Decreased ADH → water loss
C. Increased GFR → glucosuria
D. Decreased RAAS → low aldosterone

A. Increased BP → natriuresis/diuresis

A patient with aldosterone deficiency is at greatest risk for:
A. Hypocalcemia and tetany
B. Metabolic alkalosis only
C. Hypernatremia and edema
D. Hyperkalemia with arrhythmias

D. Hyperkalemia with arrhythmias

A patient with chronic watery diarrhea and low aldosterone most directly has impaired:
A. Gastric acid secretion
B. Intestinal sodium-water absorption
C. Pancreatic enzyme release
D. Hepatic bile acid synthesis

B. Intestinal sodium-water absorption

In renal tubular epithelial cells, aldosterone initially binds its receptor in the:
A. Cytoplasm
B. Nucleus
C. Luminal membrane
D. Basolateral membrane

A. Cytoplasm

After aldosterone binds its receptor, the complex:
A. Activates MAPK at membrane
B. Opens ENaC directly
C. Blocks potassium secretion
D. Translocates to nucleus, alters genes

D. Translocates to nucleus, alters genes

In principal cells, the Na+-K+ ATPase is located on the:
A. Luminal membrane
B. Basolateral membrane
C. Nuclear envelope
D. Apical tight junctions

B. Basolateral membrane

In principal cells, the epithelial Na+ channel is located on the:
A. Basolateral membrane
B. Mitochondrial membrane
C. Luminal membrane
D. Nuclear membrane

C. Luminal membrane

The second messenger system listed for aldosterone is:
A. cAMP second messenger
B. IP3-DAG signaling
C. cGMP signaling
D. JAK-STAT pathway

A. cAMP second messenger

The most potent regulators of aldosterone secretion are:
A. Sodium and chloride
B. ACTH and cortisol
C. ADH and osmolality
D. Potassium and RAAS

D. Potassium and RAAS

When RAAS is activated, aldosterone helps restore homeostasis by:
A. Excreting sodium, lowering pressure
B. Excreting potassium, raising pressure
C. Retaining potassium, lowering pressure
D. Retaining water, lowering pressure

B. Excreting potassium, raising pressure

During stress, cortisol raises blood glucose partly by inhibiting insulin via reduced:
A. Glycogen synthase activity
B. GLUT2 insertion in hepatocytes
C. GLUT4 translocation in muscle
D. Pyruvate kinase in erythrocytes

C. GLUT4 translocation in muscle

In a prolonged stress response, cortisol increases blood glucose by:
A. Increasing gluconeogenesis and AA mobilization
B. Decreasing hepatic enzyme production
C. Increasing insulin-mediated glucose uptake
D. Blocking amino acid mobilization

A. Increasing gluconeogenesis and AA mobilization

When cortisol inhibits insulin signaling, gluconeogenesis:
A. Becomes fully suppressed
B. Requires thyroid hormone first
C. Stops after meals only
D. Cannot be stopped, causing hyperglycemia

D. Cannot be stopped, causing hyperglycemia

A patient on chronic high-dose glucocorticoids develops “adrenal diabetes.” Insulin therapy is often:
A. Curative at low doses
B. Ineffective due to resistance
C. Always contraindicated
D. Unnecessary due to hypoglycemia

B. Ineffective due to resistance

α-glycerophosphate (from glucose) is required for:
A. Ketone body formation
B. Cholesterol ester storage
C. Hepatic urea synthesis
D. Triglyceride deposition in adipocytes

D. Triglyceride deposition in adipocytes

A patient on chronic glucocorticoids shows elevated hematocrit without bleeding. This aligns with cortisol:
A. Decreasing hematopoiesis
B. Causing hemolysis
C. Blocking erythropoietin release
D. Increasing hematopoiesis

D. Increasing hematopoiesis

CRF is secreted into the primary capillary plexus of the portal system at the:
A. Arcuate nucleus
B. Supraoptic nucleus
C. Posterior pituitary
D. Median eminence

D. Median eminence

CRF, ACTH, and cortisol secretion is highest:
A. In the morning
B. At midnight
C. After lunch
D. During REM sleep

A. In the morning

ACTH synthesis/secretion is associated with which peptides?
A. ADH, oxytocin, prolactin
B. Renin, angiotensin, aldosterone
C. TSH, TRH, growth hormone
D. MSH, lipotropin, endorphin

D. MSH, lipotropin, endorphin

In corticotrophs, which convertase yields ACTH and β-lipotropin?
A. Prohormone convertase 1
B. Prohormone convertase 2
C. Tyrosine hydroxylase
D. Catechol-O-methyltransferase

A. Prohormone convertase 1

A pathway produces α-MSH, β-MSH, γ-MSH, and β-endorphin, but not ACTH. Which enzyme is responsible?
A. Prohormone convertase 1
B. 21-hydroxylase
C. Protein kinase A
D. Prohormone convertase 2

D. Prohormone convertase 2

Most melanocyte-stimulating hormone is secreted from the:
A. Pars distalis
B. Pars intermedia
C. Posterior pituitary
D. Infundibulum

B. Pars intermedia

In severe primary adrenal failure, ACTH is high and hyperpigmentation occurs. Best explanation?
A. ACTH has MSH activity
B. Increased bilirubin deposition
C. Increased carotene absorption
D. Hemosiderin accumulates in skin

A. ACTH has MSH activity

A patient has adrenal insufficiency with very high ACTH and increased other POMC-derived peptides. Most likely diagnosis?
A. Conn syndrome
B. Cushing syndrome
C. Secondary hypoadrenalism
D. Addison disease

D. Addison disease

Which constellation best fits primary Addison disease?
A. Hypernatremia, hypokalemia, pallor
B. Hyponatremia, hyperkalemia, pigmentation
C. Hyponatremia, hypokalemia, pallor
D. Hypernatremia, hyperkalemia, pallor

B. Hyponatremia, hyperkalemia, pigmentation

Postpartum pituitary infarction causes low ACTH and low cortisol with intact adrenals. This is:
A. Conn syndrome
B. Cushing disease
C. Secondary hypoadrenalism
D. Primary aldosteronism

C. Secondary hypoadrenalism

Metyrapone, ketoconazole, and aminoglutethimide are useful in Cushing because they:
A. Block mineralocorticoid receptors
B. Block steroid synthesis
C. Increase ACTH secretion
D. Raise cortisol-binding globulin

B. Block steroid synthesis

Serotonin antagonists can reduce hypercortisolism by:
A. Inhibiting ACTH secretion
B. Activating aldosterone synthase
C. Activating 11β-hydroxylase
D. Blocking cortisol protein binding

A. Inhibiting ACTH secretion

A small zona glomerulosa tumor secreting aldosterone causes:
A. Addison disease
B. Cushing disease
C. Adrenogenital syndrome
D. Conn syndrome

D. Conn syndrome

A screening clue for Conn syndrome is:
A. High ACTH level
B. High urinary ketosteroids
C. Low plasma renin
D. Low free thyroxine

C. Low plasma renin

A classic clinical feature of Conn syndrome is:
A. Hyperkalemia and fatigue
B. Hyponatremia and pigmentation
C. Hypotension and weight loss
D. Hypokalemia and muscle weakness

D. Hypokalemia and muscle weakness

An adrenocortical tumor secreting excess androgens with masculinizing effects is:
A. Adrenogenital syndrome
B. Conn syndrome
C. Addison disease
D. Cushing syndrome

A. Adrenogenital syndrome

In females, adrenogenital syndrome most classically causes:
A. Galactorrhea
B. Virilization
C. Exophthalmos
D. Myxedema

B. Virilization

In prepubertal males, adrenogenital syndrome most classically causes:
A. Delayed puberty
B. Gynecomastia
C. Rapid male sex traits
D. Loss of secondary traits

C. Rapid male sex traits

Best diagnostic lab finding for adrenogenital syndrome is:
A. Urinary 17-ketosteroids high
B. Plasma renin low
C. Serum TSH high
D. Free T4 low

A. Urinary 17-ketosteroids high