front 1 During nephrectomy exposure, the surgeon identifies endocrine glands
at the ___ pole of each kidney. | back 1 A. Superior pole |
front 2 Each adrenal gland is composed of: | back 2 D. Adrenal cortex and medulla |
front 3 A patient with episodic palpitations has excess
epinephrine/norepinephrine. Which adrenal region produces
these? | back 3 B. Adrenal medulla |
front 4 A CT shows intact medulla but damaged cortex. Which hormone class is
most reduced? | back 4 C. Corticosteroids |
front 5 Which pair correctly lists the two major adrenocortical hormone
classes? | back 5 A. Mineralocorticoids and glucocorticoids |
front 6 The adrenal cortex also secretes small amounts of hormones with
testosterone-like effects. These are: | back 6 D. Androgenic hormones |
front 7 A patient with hyperkalemia needs rapid electrolyte regulation. Which
adrenocortical class chiefly regulates ECF Na+ and K+? | back 7 B. Mineralocorticoids |
front 8 A patient develops fasting hyperglycemia and muscle wasting patterns.
Which hormone class most directly raises blood glucose and alters
protein/fat metabolism? | back 8 C. Glucocorticoids |
front 9 The principal mineralocorticoid and principal glucocorticoid,
respectively, are: | back 9 D. Aldosterone, cortisol |
front 10 A thin cell layer just beneath the adrenal capsule (≈15% cortex)
secretes: | back 10 A. Zona glomerulosa |
front 11 A patient on an ACE inhibitor has reduced signaling. Aldosterone
secretion is normally stimulated by: | back 11 C. Angiotensin II and potassium |
front 12 The middle, widest adrenal cortical zone (≈75% cortex) is: | back 12 B. Zona fasciculata |
front 13 A patient with high ACTH has increased cortisol plus adrenal
androgens/estrogens. Which zone produces this trio? | back 13 D. Zona fasciculata |
front 14 Secretion of cortisol, adrenal androgens, and estrogens is primarily
controlled by: | back 14 C. ACTH |
front 15 The inner zone of the adrenal cortex is the: | back 15 B. Zona reticularis |
front 16 A steroid profile shows high DHEA and androstenedione with small
estrogen output. Which zone fits best? | back 16 A. Zona reticularis |
front 17 LDL receptors on adrenocortical membranes cluster in specialized
structures called: | back 17 A. Coated pits |
front 18 After LDL binds, coated pits are internalized by: | back 18 B. Endocytosis |
front 19 ACTH increases adrenal steroid synthesis partly by: | back 19 C. Increasing LDL receptors and enzymes |
front 20 After cholesterol enters an adrenocortical cell, it is delivered to
mitochondria and cleaved by: | back 20 A. Cholesterol desmolase |
front 21 Cholesterol → pregnenolone via cholesterol desmolase is the: | back 21 B. Rate-limiting step |
front 22 Steps of adrenal cortical steroid synthesis occur mainly in: | back 22 C. Mitochondria and ER |
front 23 A steroid is 1/30 as potent as aldosterone and is secreted in very
small quantities: | back 23 B. Deoxycorticosterone |
front 24 A hormone with slight mineralocorticoid activity is: | back 24 A. Corticosterone |
front 25 A synthetic steroid slightly more potent than aldosterone is: | back 25 B. 9α-fluorocortisol |
front 26 Very slight mineralocorticoid activity but secreted in large
quantity: | back 26 C. Cortisol |
front 27 The glucocorticoid responsible for ~95% of total glucocorticoid
activity is: | back 27 A. Cortisol |
front 28 About 4% of glucocorticoid activity, much less potent than
cortisol: | back 28 C. Corticosterone |
front 29 A steroid almost as potent as cortisol is: | back 29 A. Cortisone |
front 30 A synthetic steroid ~4 times as potent as cortisol is: | back 30 A. Prednisone |
front 31 A synthetic steroid ~5 times as potent as cortisol is: | back 31 C. Methylprednisone |
front 32 A synthetic steroid ~30 times as potent as cortisol is: | back 32 B. Dexamethasone |
front 33 Adrenocortical hormones circulate bound primarily to: | back 33 B. Plasma proteins |
front 34 High cortisol protein binding slows cortisol: | back 34 B. Elimination from plasma |
front 35 Cortisol’s half-life is approximately: | back 35 C. 60–90 minutes |
front 36 Aldosterone has a relatively ___ half-life of about ___. | back 36 A. short; 20 minutes |
front 37 Adrenocortical hormones are metabolized primarily in the: | back 37 B. Liver |
front 38 Adrenal steroids are degraded and conjugated to: | back 38 B. Glucuronic acid |
front 39 About 25% of steroid conjugates are excreted in: | back 39 C. Bile then feces |
front 40 Aldosterone blood concentration depends strongly on dietary: | back 40 A. Sodium and potassium |
front 41 Total loss of adrenocortical secretion may cause death within days
unless treated with extensive: | back 41 A. Salt therapy |
front 42 In total adrenal cortical failure, survival can be supported by
injections of: | back 42 B. Mineralocorticoids |
front 43 Without mineralocorticoids, extracellular potassium
concentration: | back 43 C. Rises |
front 44 Without mineralocorticoids, sodium and chloride are rapidly: | back 44 B. Lost |
front 45 Without mineralocorticoids, total extracellular volume and blood
volume become: | back 45 D. Greatly reduced |
front 46 Renal epithelial cells express 11β-HSD2 to: | back 46 B. Prevent cortisol activating MR |
front 47 Genetic deficiency of 11β-HSD2 causing cortisol mineralocorticoid
effects is: | back 47 D. Apparent mineralocorticoid excess |
front 48 Ingestion of large amounts of ___ can cause AME by blocking
11β-HSD2. | back 48 B. Licorice |
front 49 Aldosterone ___ renal tubular sodium reabsorption and ___ potassium
secretion. | back 49 B. increases; increases |
front 50 Because aldosterone increases Na+ reabsorption, it simultaneously
increases secretion of: | back 50 C. Potassium |
front 51 Aldosterone causes sodium to be ___ in ECF while increasing potassium
loss in urine. | back 51 B. Conserved |
front 52 ECF sodium concentration rises only slightly in hyperaldosteronism
because Na+ reabsorption pulls in: | back 52 B. Water |
front 53 Which hormone enhances water reabsorption in distal and collecting
tubules? | back 53 C. ADH |
front 54 Increased arterial pressure increases renal Na+ and water excretion
called: | back 54 C. Pressure natriuresis/diuresis |
front 55 Normalization of Na+ and water excretion during high aldosterone via
pressure mechanisms is: | back 55 A. Aldosterone escape |
front 56 When aldosterone secretion becomes zero, large amounts of sodium are
lost in: | back 56 B. Urine |
front 57 Loss of sodium in urine during aldosterone absence ___ ECF
volume. | back 57 C. Decreases |
front 58 Excess aldosterone most classically causes: | back 58 B. Hypokalemia |
front 59 Aldosterone deficiency most classically causes: | back 59 A. Hyperkalemia |
front 60 Excess aldosterone increases tubular hydrogen secretion
causing: | back 60 B. Alkalosis |
front 61 Aldosterone stimulates sodium and potassium transport in: | back 61 A. Sweat and salivary glands |
front 62 Aldosterone diffuses ___ into tubular epithelial cells. | back 62 C. Readily |
front 63 In a principal cell, aldosterone binds a cytosolic protein with high
stereospecificity. That protein is the: | back 63 C. Mineralocorticoid receptor |
front 64 After aldosterone binds its receptor, the complex enters the nucleus
and most directly promotes formation of: | back 64 A. mRNA |
front 65 The aldosterone-induced transcript returns to cytoplasm and, with
ribosomes, produces: | back 65 D. Protein enzyme |
front 66 The principal basolateral driver of renal Na+/K+ exchange is: | back 66 B. Na+-K+ ATPase |
front 67 Increased extracellular angiotensin II most strongly: | back 67 D. Increases aldosterone output |
front 68 Increased extracellular sodium concentration will very
slightly: | back 68 B. Decrease aldosterone output |
front 69 A pituitary hormone is necessary for aldosterone synthesis but
usually not rate-controlling. Which is it? | back 69 C. ACTH |
front 70 When RAAS is activated, aldosterone’s key renal effects are: | back 70 A. Excrete K, raise blood pressure |
front 71 A patient starts an angiotensin II receptor blocker. Plasma
aldosterone will: | back 71 D. Decrease |
front 72 Cortisol most directly stimulates hepatic: | back 72 B. Gluconeogenesis |
front 73 Cortisol increases the hepatic components needed to convert amino
acids into glucose, especially: | back 73 C. Enzymes |
front 74 In prolonged fasting, cortisol shifts substrate availability by
causing: | back 74 D. Mobilization from extrahepatic tissues |
front 75 Cortisol counteracts insulin’s suppression of hepatic
gluconeogenesis; it: | back 75 A. Antagonizes insulin |
front 76 Cortisol causes a moderate ____ in glucose utilization by most
cells. | back 76 C. Decrease |
front 77 Reduced GLUT4 translocation to the cell membrane from cortisol leads
to: | back 77 B. Insulin resistance |
front 78 Sustained cortisol-induced hyperglycemia can produce: | back 78 A. Adrenal diabetes |
front 79 Cortisol decreases ____ stores in essentially all cells except
liver. | back 79 D. Protein |
front 80 Cortisol’s net effect on liver and plasma proteins is: | back 80 B. Increases both |
front 81 Cortisol ____ mobilization of fatty acids from adipose
tissue. | back 81 C. Promotes |
front 82 Beyond mobilization, cortisol also directly tends to ____ fatty acid
oxidation in cells. | back 82 A. Enhance |
front 83 Any major stress increases ____ secretion, which increases cortisol
output. | back 83 D. ACTH |
front 84 After major surgery, a patient’s cortisol spikes. Which stimulus is
classically associated with increased cortisol? | back 84 C. Surgery |
front 85 A restrained lab animal develops high cortisol. This is best
classified as: | back 85 A. Physiologic stressor |
front 86 Which exposure is a classic cortisol-raising trigger? | back 86 D. Intense heat or cold |
front 87 A patient receives a norepinephrine injection during shock. This can
increase cortisol as a: | back 87 B. Stress-related trigger |
front 88 Large doses of glucocorticoids can usually block inflammation and may
reverse effects in: | back 88 A. Rheumatoid arthritis |
front 89 Cortisol’s anti-inflammatory effect includes stabilization
of: | back 89 D. Lysosomal membranes |
front 90 Cortisol blocks edema formation partly by decreasing: | back 90 A. Capillary permeability |
front 91 Cortisol decreases leukocyte migration and phagocytosis partly by
reducing: | back 91 B. Prostaglandins and leukotrienes |
front 92 Cortisol suppresses immunity primarily by decreasing: | back 92 C. Lymphocyte reproduction |
front 93 Cortisol attenuates fever mainly by reducing release of: | back 93 A. IL-1 from WBCs |
front 94 Cortisol’s effect on allergic inflammation is best described
as: | back 94 B. Blocks allergic inflammatory response |
front 95 Cortisol also promotes: | back 95 D. Healing |
front 96 Lymphocytopenia or eosinopenia suggests overproduction of: | back 96 C. Cortisol |
front 97 Cortisol is lipid-_____ , enabling membrane passage. | back 97 A. soluble |
front 98 Inside the cell, cortisol binds its receptor in the: | back 98 A. Cytoplasm |
front 99 The cortisol–receptor complex regulates transcription by
binding: | back 99 B. Glucocorticoid response elements |
front 100 ACTH is best described as: | back 100 C. 39–amino acid polypeptide |
front 101 CRF-secreting neuron cell bodies are mainly in the: | back 101 B. Paraventricular nucleus |
front 102 ACTH activates which membrane enzyme to raise cAMP? | back 102 C. Adenylyl cyclase |
front 103 The most important ACTH-stimulated step listed is activation
of: | back 103 A. Protein kinase A |
front 104 Protein kinase A activation most directly promotes cholesterol
conversion to: | back 104 B. Pregnenolone |
front 105 Physiologic stress increases secretion of: | back 105 A. ACTH and cortisol |
front 106 Cortisol exerts direct negative feedback on: | back 106 A. Hypothalamus and anterior pituitary |
front 107 The precursor that yields ACTH, MSH, β-lipotropin, and β-endorphin
is: | back 107 C. POMC |
front 108 Primary adrenal cortical atrophy or injury with low adrenocortical
hormones is: | back 108 B. Addison’s disease |
front 109 Mineralocorticoid deficiency most directly causes: | back 109 A. ECF depletion → shock risk |
front 110 Glucocorticoid deficiency in Addison prevents between-meal glucose
maintenance because it impairs: | back 110 C. Gluconeogenesis |
front 111 A key cause of Addison-associated mucocutaneous hyperpigmentation is
increased: | back 111 A. Melanin |
front 112 Standard chronic therapy for Addison disease is: | back 112 D. Daily mineralocorticoids and glucocorticoids |
front 113 Severe stress-related debility requiring extra glucocorticoids in
Addison is: | back 113 B. Addisonian crisis |
front 114 Hypersecretion by the adrenal cortex causing a complex cascade
is: | back 114 A. Cushing syndrome |
front 115 Cushing syndrome due to excess pituitary ACTH is: | back 115 C. Cushing disease |
front 116 The drug classically administered to differentiate ACTH-dependent vs
ACTH-independent Cushing is: | back 116 D. Dexamethasone |
front 117 With very high-dose dexamethasone, which change can occur in many
patients with Cushing disease? | back 117 B. ACTH becomes suppressed |
front 118 Iatrogenic Cushing syndrome can result from prolonged administration
of: | back 118 A. Glucocorticoids |
front 119 The classic facial appearance in Cushing syndrome is: | back 119 D. Moon face |
front 120 About 80% of patients with Cushing syndrome develop: | back 120 B. Hypertension |
front 121 Cushing hypertension is largely attributed to: | back 121 C. Cortisol mineralocorticoid activity |
front 122 Purplish striae in Cushing syndrome reflect depletion of: | back 122 A. Collagen depletion |
front 123 A correct treatment approach for Cushing syndrome includes: | back 123 D. Tumor removal or steroidogenesis blockade |
front 124 Among listed treatments, the “last resort” option is: | back 124 C. Adrenalectomy |
front 125 A small zona glomerulosa tumor secreting large aldosterone
is: | back 125 A. Primary aldosteronism |
front 126 A diagnostic criterion for primary aldosteronism is: | back 126 D. Decreased plasma renin |
front 127 Treatment for primary aldosteronism is best: | back 127 B. Surgery or MR antagonist |
front 128 An adrenocortical tumor secreting excess androgens causing
masculinization is: | back 128 C. Adrenogenital syndrome |
front 129 Adrenal cortex layers superficial → deep are: | back 129 A. Glomerulosa fasciculata reticularis |
front 130 Which finding best supports primary adrenal insufficiency over
secondary? | back 130 B. Melanin pigmentation present |
front 131 A classic trigger for Addisonian crisis is: | back 131 D. Infection or trauma stress |
front 132 A patient with Addison disease is especially prone to: | back 132 C. Hypoglycemia between meals |
front 133 A patient has persistently high aldosterone, yet after several days
their renal Na+/H2O excretion returns near baseline. This phenomenon
is: | back 133 C. Aldosterone escape |
front 134 The key driver of aldosterone escape is: | back 134 A. Increased BP → natriuresis/diuresis |
front 135 A patient with aldosterone deficiency is at greatest risk
for: | back 135 D. Hyperkalemia with arrhythmias |
front 136 A patient with chronic watery diarrhea and low aldosterone most
directly has impaired: | back 136 B. Intestinal sodium-water absorption |
front 137 In renal tubular epithelial cells, aldosterone initially binds its
receptor in the: | back 137 A. Cytoplasm |
front 138 After aldosterone binds its receptor, the complex: | back 138 D. Translocates to nucleus, alters genes |
front 139 In principal cells, the Na+-K+ ATPase is located on the: | back 139 B. Basolateral membrane |
front 140 In principal cells, the epithelial Na+ channel is located on
the: | back 140 C. Luminal membrane |
front 141 The second messenger system listed for aldosterone is: | back 141 A. cAMP second messenger |
front 142 The most potent regulators of aldosterone secretion are: | back 142 D. Potassium and RAAS |
front 143 When RAAS is activated, aldosterone helps restore homeostasis
by: | back 143 B. Excreting potassium, raising pressure |
front 144 During stress, cortisol raises blood glucose partly by inhibiting
insulin via reduced: | back 144 C. GLUT4 translocation in muscle |
front 145 In a prolonged stress response, cortisol increases blood glucose
by: | back 145 A. Increasing gluconeogenesis and AA mobilization |
front 146 When cortisol inhibits insulin signaling, gluconeogenesis: | back 146 D. Cannot be stopped, causing hyperglycemia |
front 147 A patient on chronic high-dose glucocorticoids develops “adrenal
diabetes.” Insulin therapy is often: | back 147 B. Ineffective due to resistance |
front 148 α-glycerophosphate (from glucose) is required for: | back 148 D. Triglyceride deposition in adipocytes |
front 149 A patient on chronic glucocorticoids shows elevated hematocrit
without bleeding. This aligns with cortisol: | back 149 D. Increasing hematopoiesis |
front 150 CRF is secreted into the primary capillary plexus of the portal
system at the: | back 150 D. Median eminence |
front 151 CRF, ACTH, and cortisol secretion is highest: | back 151 A. In the morning |
front 152 ACTH synthesis/secretion is associated with which peptides? | back 152 D. MSH, lipotropin, endorphin |
front 153 In corticotrophs, which convertase yields ACTH and
β-lipotropin? | back 153 A. Prohormone convertase 1 |
front 154 A pathway produces α-MSH, β-MSH, γ-MSH, and β-endorphin, but not
ACTH. Which enzyme is responsible? | back 154 D. Prohormone convertase 2 |
front 155 Most melanocyte-stimulating hormone is secreted from the: | back 155 B. Pars intermedia |
front 156 In severe primary adrenal failure, ACTH is high and hyperpigmentation
occurs. Best explanation? | back 156 A. ACTH has MSH activity |
front 157 A patient has adrenal insufficiency with very high ACTH and increased
other POMC-derived peptides. Most likely diagnosis? | back 157 D. Addison disease |
front 158 Which constellation best fits primary Addison disease? | back 158 B. Hyponatremia, hyperkalemia, pigmentation |
front 159 Postpartum pituitary infarction causes low ACTH and low cortisol with
intact adrenals. This is: | back 159 C. Secondary hypoadrenalism |
front 160 Metyrapone, ketoconazole, and aminoglutethimide are useful in Cushing
because they: | back 160 B. Block steroid synthesis |
front 161 Serotonin antagonists can reduce hypercortisolism by: | back 161 A. Inhibiting ACTH secretion |
front 162 A small zona glomerulosa tumor secreting aldosterone causes: | back 162 D. Conn syndrome |
front 163 A screening clue for Conn syndrome is: | back 163 C. Low plasma renin |
front 164 A classic clinical feature of Conn syndrome is: | back 164 D. Hypokalemia and muscle weakness |
front 165 An adrenocortical tumor secreting excess androgens with masculinizing
effects is: | back 165 A. Adrenogenital syndrome |
front 166 In females, adrenogenital syndrome most classically causes: | back 166 B. Virilization |
front 167 In prepubertal males, adrenogenital syndrome most classically
causes: | back 167 C. Rapid male sex traits |
front 168 Best diagnostic lab finding for adrenogenital syndrome is: | back 168 A. Urinary 17-ketosteroids high |