Adrenocorticosteroids (Sandini) Flashcards
Which of the following correctly matches a zone of the adrenal cortex with its primary hormone?
A) Zona glomerulosa – Cortisol
B) Zona fasciculata – Aldosterone
C) Zona reticularis – Androgens
D) Adrenal medulla – Cortisol
Zona reticularis – Androgens
Answers:
Zona glomerulosa-aldosterone
Zona faci- cotrisol glucocortcoids
Zona reticularis: androgens
What is the role of the medula and the cortex?
Medulla - secretes epinephrine and NE
Cortex(outer layer) secretes mineralcorticoids, lgucocorticoidsm and androgens
Which hormone is most directly responsible for stimulating cortisol synthesis in the adrenal cortex?
A) Renin
B) CRH
C) ACTH
D) Angiotensin II
C
Explanation: ACTH from the anterior pituitary stimulates cortisol release from the adrenal cortex.
Which of the following statements about the circadian secretion of cortisol is CORRECT?
A) Cortisol levels peak around midnight and are lowest at midday.
B) The circadian rhythm of cortisol is independent of ACTH secretion.
C) Cortisol secretion follows both circadian and ultradian rhythms, peaking in the early morning.
D) Cortisol levels remain constant throughout the day in healthy individuals.
Cortisol secretion follows both circadian and ultradian rhythms, peaking in the early morning.
Which of the following correctly represents the sequence of events leading to aldosterone secretion in the RAAS pathway?
A) Angiotensin-converting enzyme (ACE) → Renin → Angiotensin I → Angiotensin II → Aldosterone
B) Angiotensinogen → Renin → Angiotensin I → ACE → Angiotensin II → Aldosterone
C) Aldosterone → Renin → ACE → Angiotensin I → Angiotensin II
D) Renin → ACE → Angiotensinogen → Angiotensin II → Aldosterone
The correct sequence is:
Renin is released from the juxtaglomerular cells of the kidney in response to low blood pressure or sodium.
Renin converts angiotensinogen (from the liver) into angiotensin I.
ACE (mostly in the lungs) converts angiotensin I into angiotensin II (ATII).
Angiotensin II stimulates the adrenal cortex (zona glomerulosa) to release aldosterone.
B
An enzyme responsible for processing angiotensin 2 into ATI
A. Renin
B. Ace
C. AT2
D. Aldosterone
Renin
An enzyme responsible for converting ATI into Angiotensin 2
A. Renin
B. Ace
C. AT2
D. Aldosterone
Ace
What is the primary outcome of the RAAS pathway?
A) Increase in cortisol secretion
B) Decrease in Na+ reabsorption
C) Release of aldosterone from zona reticularis
D) Increased sodium and water retention via aldosterone
E) control blood pressure and fluid balance
D and E
Which of the following correctly represents the sequence of events following the release of a steroid hormone (e.g., cortisol) from its carrier protein in the blood?
A) Steroid diffuses into cell → Binds DNA directly → Enters nucleus → Activates receptor → Alters mRNA transcription
B) Steroid binds to cytosolic receptor → Diffuses into cell → Enters nucleus → Binds DNA → Changes protein synthesis
C) Steroid dissociates from CBG → Passively diffuses into target cell → Binds intracellular receptor → Hormone-receptor complex translocates to nucleus → Binds hormone response element (HRE) on DNA → Regulates transcription
D) Steroid binds to cell surface receptor → Activates G-protein → Increases cAMP → Activates transcription factor → Enters nucleus
Correct answer: C
Explanation:
1. Steroid binds to corticosteroid CBG and carried in blood
2. Enters the cell as a free steroid and binds to target receptor
3. Hormone binding causes a dissociation form Hsp and it goes into the nucleus
4. Receptor steroid complex becomes a dimer and becomes activated
5. Dimer attatches to GRE (glutocorticoid receptor element in DNA promotor region) and leads to protein synthesis and biological responses
Which of the following is true? GC=glucocorticoids
A. Receptors for corticosteroids are Gs
B. Receptors for corticosterouds are GCs
B
Which is true between endogenous GCs and synthetic GCs?
A. Endogenous glutocorticoids have different affinities for GR and MR receptors
B. Endogenous glutocorticoids activate both GR and MR
C. Synthetic glutocorticoids activate both GR and MR
D. SYnthetic glutocorticoids have different affinities for GR and MR
GR=glutocorticoid receptor (cortisol)
MR= mineralcorticoid receptor (aldosterone)
Recall that GCs are receptors for corticosteroids
The correct statements are B and D
What is the role of 11β-HSD1 in tissues like liver and adipose?
A) Inactivates cortisol to cortisone
B) Converts cortisone into active cortisol
C) Stimulates aldosterone secretion
D) Synthesizes cholesterol
Converts cortisone into active cortisol
Whats the difference between 11β-HSD1 And 11β-HSDII
11b-HSD1 is an enzyme used to convert cortisone into active cortisol
11B-HSD11 is an enzyme expressed by the kidney cells to turn cortisol inactiuve
Which of the following BEST describes the effect of dexamethasone on cortisol production in the body?
A) Dexamethasone stimulates ACTH release, increasing endogenous cortisol production
B) Dexamethasone mimics aldosterone and increases cortisol secretion through MR activation
C) Dexamethasone activates GRs, decrease CTH and ACTH secretion, and decreases endogenous cortisol production
D) Dexamethasone increases cortisol levels by converting cortisone to cortisol in the adrenal cortex
Dexamethasone is used by glutocorticoids to provide negative feedback
Dexamethasone activates GRs, decrease CTH and ACTH secretion, and decreases endogenous cortisol production
dexamethasone is a drug that reduces inflammatory responses
What are the long-term metabolic effects of glucocorticoids?
A) Increased insulin sensitivity, decreased glucose production, and lean body mass retention
B) Increased glucose uptake by peripheral tissues, decreased lipolysis, and decreased appetite
C) Insulin resistance, altered fat distribution, hyperglycemia, and features of metabolic syndrome
D) Increased glycogen storage in muscle, enhanced protein synthesis, and lower blood glucose
Correct answer: C
🧠 Explanation:
Long-term exposure to glucocorticoids (e.g., cortisol or synthetic GCs) leads to:
Insulin resistance
Increased hepatic gluconeogenesis → hyperglycemia
Altered fat distribution (e.g., truncal obesity, moon face)
Overall features of metabolic syndrome
How do glucocorticoids regulate the immune response via the arachidonic acid pathway?
A) They activate phospholipase A2 to stimulate prostaglandin synthesis
B) They increase COX1 expression to promote thromboxane formation
C) They inhibit phospholipase A2, reducing arachidonic acid release and downstream inflammatory mediators
D) They block lipoxygenase directly, preventing leukotriene B4 production only
Correct answer: C
🧠 Explanation:
Glucocorticoids inhibit phospholipase A2, which prevents the release of arachidonic acid from membrane phospholipids.
This blocks both:
Prostaglandin synthesis (via COX1 and COX2)
Leukotriene synthesis (via lipoxygenase)
→ Resulting in broad anti-inflammatory effects
Why is COX-2 important in the anti-inflammatory action of glucocorticoids?
A) COX-2 increases cortisol synthesis, which is necessary for the stress response
B) COX-2 promotes anti-inflammatory prostaglandins that enhance glucocorticoid activity
C) Glucocorticoids induce COX-2 to increase lipoxin production
D) Glucocorticoids suppress COX-2 expression, reducing prostaglandin-mediated inflammation
Glucocorticoids suppress COX-2 expression, reducing prostaglandin-mediated inflammation
COX-2 is an inducible enzyme that generates pro-inflammatory prostaglandins during injury or infection.
Glucocorticoids suppress COX-2 gene expression, reducing the production of these inflammatory mediators.
This is distinct from COX-1, which is constitutively active and not significantly affected by GCs.
which is true about glucocorticoids? a. they release adrenaline and noradrenaline
b. they supress COX 1 and lead to prolonged COX1 expression
c. they supress COX 2 and lead to prolonged COX2 expression
d. they inhibit cyclooxygenase activity
e. they do not inhibit cyclooxygenase activity
they supress COX 2 and lead to prolonged COX2 expression AND they do not inhibit cyclooxygenase activity
how does glucocorticoids inhibit phospholipase A2
glucocorticoids cause the production of lipocortins/annexins which inhibit phopholipase A2
recall that glucocorticoids like cortisol supress the immune system
Which of the following BEST explains why Annexin A1 plays a key anti-inflammatory role in glucocorticoid action?
A) It suppresses prostaglandin synthesis by directly inhibiting COX-2 and blocking leukocyte migration.
B) It reduces cytokine production and promotes vasoconstriction at inflammation sites.
C) It inhibits leukocyte tissue infiltration and blocks phospholipase A2 activity, reducing arachidonic acid and prostanoid synthesis.
D) It prevents histamine release and enhances glucocorticoid receptor translocation into the nucleus.
It inhibits leukocyte tissue infiltration and blocks phospholipase A2 activity, reducing arachidonic acid and prostanoid synthesis.
these effects are early in the immune responefor inflammation
a disease in which the adrenal cortex is unable to produce glucocorticoids and mineralcorticoids (low cortisol and aldosterone)
a. addisons disease
b. cushings syndrome
addisons disease
how is addisons disease treated?
a. surgery, depending on the cause
b. radiation therapy
c. hypercortisol drugs
d. GC/MC supplement
GC/MC supplement (hydrocortisone/cortisol)
a disease caused by hypercortisolemia. caused by high amounts of cortisol and acth production, and long term treatment with a high dose of GC
a. addisons disease
b. cushings syndrome
cushings disease
how is cushings disease treated?
treatment depends on cause but includes surgery, chemotherapy and cortisol reducing medications
