Adrenal Hormones Flashcards Preview

Physio II Exam 3 > Adrenal Hormones > Flashcards

Flashcards in Adrenal Hormones Deck (19)
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1
Q

Medulla

A
  • Secretes epinephrine and norepinephrine

* Functionally related to sympathetic nervous system

2
Q

Cortex

A

Secretes corticosteroids
•Mineralocorticoids
•Glucocorticoids
•Androgenic hormones

3
Q

Corticosteroids

A

Synthesized from cholesterol:
•Provided mostly by LDLs in the plasma
•Most attach to coated pits
•ACTH increases number of LDL receptors
•Cholesterol converted to pregnenolone in mitochondria
•Enzyme for conversion = cholesterol desmolase(rate-limiting step)
•Both ACTH and angiotensin II increase the conversion of cholesterol to pregnenolone.

4
Q

21- carbon steroids

A
  • Progesterone
  • Deoxycorticosterone
  • Aldosterone
  • Cortisol
5
Q

Mineralocorticoids

A

Major: Aldosterone (20 min half-life)
Especially affects the electrolytes (sodium and potassium)
Increases sodium reabsorption by kidney tubules:
•Acts on principal cells in late distal tubule
Hyperkalemia increases aldosterone secretion.
Aldosterone increases potassium secretion by kidneys:
•Acts on principal cells in late distal tubule
Aldosterone increases hydrogen ion secretion by kidneys:
•Acts on intercalated cells in late distal tubule
Secretion is controlled mainly by angiotensin II and K+
Secreted by zona glomerulosa

6
Q

Glucocorticoids

A

Major: Glucocorticoid

Essential in stress response
Secretion is controlled mainly by ACTH (from anterior pituitary):
•ACTH up-regulates it own receptor.
•Under the influence of CRH (corticotropin-releasing hormone from neurosecretory cells located in the paraventricular nuclei.
•Second messenger for both CRH and ACTH is cAMP.

Secreted by zona fasciculata
Cortisol has negative feedback response to both CRH and ACTH

Cortisol oscillates with circadian rhythm:
•Normally highest before waking
•Normally lowest in evening

7
Q

Androgenic Hormones

A

19-carbon steroids have androgenic activity and are precursors to the estrogens.
•DHEA (dehydroepiandrosterone) and androstenedione
•Dehydroepiandrosterone is converted to testosterone in the testes

Adrenal androgens are excreted as 17-ketosteroids in the urine.

18-carbon steroids have estrogenic activity:
•Oxidation of one of the rings occurs in the ovaries to produce estrogens, but not in the adrenal glands or testes.
•Secreted by zona reticularis

8
Q

Lack of Aldosterone

A
  • Total loss causes death in a matter of days unless extensive salt therapy and mineralocorticoid injections are available.
  • Without mineralocorticoids potassium levels in ECF rise markedly and sodium and chloride are lost rapidly from the urine.
  • Total ECF and blood volume become greatly reduced.
  • Person develops diminished cardiac output and progresses to a shock-like state.
  • Hyperkalemia and serous cardiac toxicity
9
Q

Excess of Aldosterone

A
  • Increase in ECF and arterial pressure
  • Small effect on plasma sodium concentration because sodium reabsorption in renal tubules is accompanied by equivalent amount of water reabsorption.
  • Hypokalemia and muscle weakness
  • Stimulates transport of potassium from ECF into most cells of the body.
  • Causes alkalosis (hydrogen ions are secreted in exchange for sodium.
10
Q

Aldosterone increases what and what in the urine?

A

aldosterone increases renal tubular reabsorption of sodium and increases potassium in the urine

11
Q

Cellular Sequence of Events Leading to Sodium Reabsorption (6 steps)

A
  1. Aldosterone is lipid soluble and diffuses readily into the interior of the tubular epithelial cells.
  2. Aldosterone combines with mineralocorticoid receptor proteins.
  3. Aldosterone-receptor complex diffuses into nucleus.
  4. RNA transcription is induced.
  5. Sodium-potassium ATPase pump proteins are among those formed as a result of this induction.
  6. Epithelial sodium channel (ENaC) is also formed
12
Q

Treatment of sodium depleted dogs with ACE for 7 days followed by infusion of AngII=

A

ACE blocks formation of angiotensin.

AngII stimulates aldosterone secretion during sodiuim depletion.

13
Q

Regulation of Aldosterone Secretion

A
  • Almost entirely independent of the regulation of cortisol secretion.
  • Increased potassium ion concentration greatly increases aldosterone secretion.
  • Increased angiotensin II concentration greatly increases aldosterone secretion.
  • ACTH is necessary for aldosterone secretion but has little effect in controlling rate of secretion.
14
Q

Functions of Glucocorticoids

A
  • stimulates gluconeogenesis
  • may lead to adrenal diabetes
  • resists stress
  • resists inflammation
  • causes resolution of inflammation
  • inhibits immune response
  • maintains vascular response to catecholamines
15
Q

Hyperadrenalism–Cushing’s Disease

A
Causes: 
•Administration of glucocorticoids 
•Adenomas of anterior pituitary 
•Abnormal function of hypothalamus 
•Ectopic secretion of ACTH by tumor 
•Adenomas of adrenal cortex 
•Excess ACTH secretion is cause of Cushing’s
Characteristics: 
•Increase in cortisol and androgen levels 
•“Buffalo torso” 
•Moon face 
•Acne and hirsutism 
•Hypertension 
•Increased blood glucose 
•Increase in protein catabolism and muscle wasting
16
Q

Hypoadrenalism–Addison’s Disease

A

Primary- due to injury of adrenal cortex
Secondary- due to impaired function of pituitary gland

Disturbances
•Due to mineralocorticoid deficiency
•Due to Glucocorticoid deficiency
•Melanin pigmentation

17
Q

Mineralocorticoid deficiency

A
  • Decreased extracellular fluid volume
  • Hyponatremia
  • Hyperkalemia
  • Mild acidosis
  • Rise in RBC concentration
  • Decrease in cardiac output
  • Decrease in blood pressure
  • Metabolic acidosis
  • Death from shock
18
Q

Glucocorticoid Deficiency

A
  • Loss of ability to maintain normal blood glucose concentrations between meals → hypoglycemia
  • Reduction in both proteins and fats leading to depression of other bodily functions
  • Weight loss, nausea, vomiting
  • Muscle weakness
  • Highly susceptible to stress
19
Q

Melanin Pigmentation

A
  • May be caused by loss of negative feedback to pituitary, allowing increased amounts of MSH
  • Results in uneven distribution of pigmentation, especially in thin skin areas