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Endo Repro Exam > Adrenal Gland Basics > Flashcards

Adrenal Gland Basics Flashcards

1
Q

adrenal anatomy - overview

A
  1. outer adrenal cortex
    -3 layers, each producing its own distinct hormone
    -derived from mesoderm
  2. inner adrenal medulla
    -chromaffin cells derived from neural crest cells
    -modified postganglionic nerves: secrete epi/norepi in response to sympathetic stimulation; neurotransmitter is acetylcholine
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2
Q

what cells are the adrenal medulla derived from

A

*derived from NEURAL CREST CELLS

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3
Q

what cells are the adrenal cortex derived from

A

mesoderm

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4
Q

3 layers of adrenal cortex - mnemonic

A

GFR:
1. zona Glomerulosa (produces aldosterone)
2. zona Fasciculata (produces cortisol)
3. zona Reticularis (produced androgens: DHEA)

*GFR corresponds with salt (mineralocorticoids: aldosterone), sugar (glucocorticoids: cortisol), and sex (androgens: DHEA); “gets better the deeper you go”

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5
Q

adrenal cortex - outermost layer

A

*Zona Glomerulosa
*responsible for producing mineralocorticoids: ALDOSTERONE
*action of aldosterone: sodium retention in DCT and collecting ducts, increasing blood pressure

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6
Q

adrenal cortex - middle layer

A

*Zona Fasciculata
*responsible for producing glucocorticoids: CORTISOL
*action of cortisol: coordinating the body’s response to stress through altering metabolism, blood pressure, immune response

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7
Q

adrenal cortex - inner layer

A

*Zona Reticularis
*responsible for producing androgens: DHEA-S
*action of DHEA-S: source of > 50% of the androgens in females; much less in males

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8
Q

Zona Glomerulosa

A

*outermost layer of adrenal cortex
*responsible for producing mineralocorticoids: ALDOSTERONE
*action of aldosterone: sodium retention in DCT and collecting ducts, increasing blood pressure

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9
Q

Zona Fasciculata

A

*middle layer of adrenal cortex
*responsible for producing glucocorticoids: CORTISOL
*action of cortisol: coordinating the body’s response to stress through altering metabolism, blood pressure, immune response

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10
Q

Zona Reticularis

A

*innermost layer of adrenal cortex
*responsible for producing androgens: DHEA-S
*action of DHEA-S: source of > 50% of the androgens in females; much less in males

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11
Q

dual control of adrenal cortex

A
  1. cortisol and DHEA-S secretion are controlled by ACTH secretion from the pituitary
  2. aldosterone secretion is controlled by Renin-Angiotensin system from the kidney (RAAS)
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12
Q

stimulation & suppression of aldosterone release

A

*aldosterone release is stimulated by:
1. RAAS system (activated by low renal BP, decreased NaCl detected by macula densa, sympathetic activation of beta1 receptors)
2. direct stimulation by hyperkalemia

*aldosterone release is suppressed by:
1. renin suppression (increased BP, high sodium diet)
2. hypokalemia

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13
Q

aldosterone - action

A

*aldosterone binds to mineralocorticoid receptors (MR) in nephron → increased expression of ENaC channels → sodium reabsorption
*potassium and H+ ions are EXCRETED in the urine due to change in transmembrane potential

overall: reabsorbs Na+; wastes K+ and H+
(too much aldosterone → hypokalemia & metabolic alkalosis)

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14
Q

cortisol - regulation of release

A
  1. corticotropin-releasing hormone (CRH) is released from hypothalamus and goes to pituitary
  2. CRH stimulates transcription of pro-opiomelanocortin (POMC)
  3. POMC is cleaved into corticotropin (ACTH) and melanocyte stimulating hormone (MSH)
  4. ACTH stimulates cortisol production /& secretion from adrenal gland

note - in disease states where ACTH production is significantly increased, pts can become hyperpigmented due to MSH

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15
Q

diurnal variation of cortisol

A

*peaks around 8am
*nadir (lowest point) around midnight
*this becomes important when ordering and interpreting tests for disease states

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16
Q

cortisol - functions

A
  1. metabolism: increase blood glucose through gluconeogenesis, lipolysis, and muscle catabolism; induces insulin resistance in peripheral tissues
  2. skin, muscle, connective tissue: decreased fibroblast atrophy and collagen; muscle atrophy
  3. bone: inhibits osteoblast function
  4. blood pressure: increased sensitivity to catecholamines and Ang II, decreases nitric oxide → increased BP
  5. immune system: immunosuppression
  6. mood: important for normal mood
  7. endocrine effects: downregulates other axes, esp. gonadal
17
Q

adrenal androgens - overview

A

*DHEA, DHEA-S, and androstenedione are the primary androgens from adrenal gland
*these are converted to testosterone → dihydrotestosterone and estrogen in peripheral tissues
*serve as an important pool of potential androgens, particularly in females
*production is under control of ACTH

18
Q

steroid synthesis pathway - general principles

A

*adrenal steroids are derived from cholesterol
*rate limiting step: first step - conversion of cholesterol to pregnenolone via StAR; blocked by ketonazole
*each layer of adrenal cortex produces its own specific steroid due to differential expression of enzymes
*when there is a genetic deficiency in one enzyme, this results in: 1) buildup of precursors; 2) diversion to other, unaffected pathways; 3) congenital adrenal hyperplasia (CAH)

19
Q

congenital adrenal hyperplasias (CAHs) - overview

A

*autosomal RECESSIVE group of disorders characterized by deficient cortisol synthesis due to mutations in one of the enzymes in the steroidogenesis pathway
*results in either partial or complete blockage at the level of the enzyme → shunting of precursors to the other 2 pathways (androgens and/or mineralocorticoids)
*reduced cortisol synthesis → reduced negative feedback on pituitary → increased ACTH → adrenal hyperplasia
*due to ACTH increase, pts can be hyperpigmented (due to increased MSH)

20
Q

CAH: 21-hydroxylase deficiency - overview

A

*most common congenital adrenal hyperplasia (90-95% of CAH)
*due to increased androgens in utero, females experience virilization (clitoral enlargement, labial fusion) and can have ambiguous genitalia (even with inappropriate sex assignment)
*included in the newborn screening labs now

21
Q

CAH: 21-hydroxylase deficiency - 2 forms

A
  1. classic CAH: salt-wasting or simple virilizing
  2. nonclassical (late-onset)
22
Q

CAH: 21-hydroxylase deficiency - SALT-WASTING form

A

*loss of CORTISOL and ALDOSTERONE (adrenal crisis)
*infants present at 2 weeks of life with severe hypotension, low Na+, high K+
*symptoms include failure to thrive, lethargy, vomiting, sepsis-like syndrome
*mortality is high

23
Q

CAH: 21-hydroxylase deficiency - SIMPLE VIRILIZING form

A

*experience excess androgens, but still able to make some aldosterone, so do not present with adrenal crisis
*females may have ambiguous genitalia, but males are phenotypically normal
*can present with early puberty, growth accelaration
*if untreated, excess androgens lead to premature epiphyseal closure, not reaching adult height

24
Q

CAH: 21-hydroxylase deficiency - diagnosis

A

*test for elevated levels of precursor: 17-hydroxyprogesterone

25
Q

CAH: 21-hydroxylase deficiency - treatment

A

*replace missing cortisol and/or aldosterone with medications
*reduce adrenal androgen synthesis by suppressing ACTH (crinecerfont: oral CRH antagonist)
*surgery to correct ambiguous genitalia

26
Q

CAH: 11-beta hydroxylase deficiency - overview

A

*less common than 21-hydroxylase
*in addition to virilization, patients are hypertensive due to buildup of 11-deoxycortisol
*lab diagnosis: 11-deoxycortisol levels are elevated

27
Q

CAH: 17-alpha hydroxylase deficiency - overview

A

*pts present with low cortisol and low androgens
*often have severe HTN due to excess aldosterone
*inability to make androgens also occurs in gonads, resulting in hypergonadotropic hypogonadism

28
Q

memory aid for congenital adrenal hyperplasias

A

*if the deficient enzyme STARTS with 1, it causes HYPERTENSION: 11-beta hydroxylase; 17-alpha hydroxylase

*if the deficient enzyme ENDS with 1, it causes VIRILIZATION: 21-hydroxylase, 11-beta hydroxylase

29
Q

steroid replacement options

A

*hydrocortisone
*prednisone
*dexamethasone

30
Q

in a patient with hypothyroidism and adrenal insufficiency, which hormone should you replace first?

A

*must give the STEROID prior to the thyroid replacement because the thyroid hormone could otherwise precipitate an adrenal crisis

Endo Repro Exam (31 decks)

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