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S&F IV: Exam Two- European Gigalo > Adrenal Glands > Flashcards

Adrenal Glands Flashcards

1
Q

Steroid Hormone Synthesis

A

Cholesterol is transported to the inner mitochondrial membrane via StAR and converted to pregnenolone by P450cc (found on membrane); synthesis of the steroid then proceeds in an unregulated fashion inside the mitochondria

*Transport across the mitochondrial membrane= rate-limiting

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2
Q

Cholesterol Esters

A

Storage form of the substrate (cholesterol) for steroid hormones that are formed by cholesterol acyltransferase

*Necessary because steroid hormones cannot be stored

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3
Q

3 types of steroid binding proteins

A
  1. Corticosteroid binding globulin
  2. Sex-steroid binding globulin
  3. Vitamin D binding globulin
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4
Q

Steroid Hormone Metabolism

A

Are broken down to glucuronic acid and sulfate by the liver and further excreted by the kidneys

*Conjugation increases the steroid’s water solubility and decreases its affinity for binding protein

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5
Q

Steroid Hormone Receptors

A

When bound to a steroid, it releases its complex of HSPs and activates its NLS to travel to the nucleus and activate transcription

=>Binds to HRE as two homodimers and recruits CoAs and HAT to induce action

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6
Q

Aldosterone Synthase

A

Expressed in the zona glomerulosa; converts DOC to aldosterone

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7
Q

17a-hydroxylase

A

Leads to the formation of 11-dehydroxy cortisol and w/ the fnxn of 11B-hydroxlase it forms cortisol

*Absent in the zona glomerulosa

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8
Q

P450c17

A

Assists the fnxn of 17a-hydroxylase and 17,20-lyase in the zona fasciculata and reticularis

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9
Q

17,20-lyase

A

Fnxns to produce androgens; found in high concentration in the zona reticularis

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10
Q

Transcription of StAR

A

Zona glomerulosa: Induced by A-II (Gq)
*Hyperkalemia will also induce

Zona fasciculata and reticularis: Induced by ACTH (Gs)

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11
Q

Aldosterone

A

Mostly found unbound; therefore, it has a very short half-life

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12
Q

11B-hyrdoxysteroid dehydrogenase II

A

Converts cortisol to the physiologically inactive cortisone; present in mineralcorticoid tissues

  • DOC and Aldosterone react similarly w/ receptors. This prevents cortisol from influencing
  • 11B-hydroxysteroid dehydrogenase I is found in corticoid tissues and converts cortisone back to cortisol
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13
Q

DHEA

A

Secreted bound to sulfate, is slowly metabolized due to strong binding to albumin, and good indicator of adrenal fnxn

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14
Q

Fetal zone

A

Secretes large amounts or DHEA sulfate that is converted to estrogen by the placenta

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15
Q

Adrenarche

A

Rise in DHEA secretion during puberty; is not involved in initiating puberty

*Females use DHEA to grow axillary and pubic hair; males dont really need it

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16
Q

Most accurate measurement of cortisol production

A

24 hour urine cortisol excretion

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17
Q

Synthetic glucocorticoids

A

Have enhanced stimulation due to their increased affinity for the glucocorticoid receptor and decreased plasma clearance

*Dexamethasone

18
Q

Effects of ACTH

A

Acute: Increased transcription of StAR, increased activity of cholesterol esterase

Chronic: Proliferation of the zona fasciculata and reticularis, increased steroidogenic enzymes, increased LDL receptors

19
Q

AVP

A

Secrete into the hypothalamophyseal system during times of stress; induces ACTH secretion via a Gq pathway

20
Q

Regulation of cortisol release

A

Regulated by the SCN sending neurons to the PVN; induces a diurnal rhythm w/ increased levels in the morning

21
Q

Stress and glucocorticoid release

A

Can override the SCN and cause release of cortisol

22
Q

Glucocorticoid Actions

A

Permissive Effects: Helps glucagon by increasing glycogen synthase activity
*More glycogen to be broken down when needed

Synergistic: Inhibits fasting hypoglycemia by promoting gluconeogenesis and antagonizing the action of insulin =>Increased FFAs
-Promotes protein catabolism in muscle, decreases GLUT-4, inhibits Ca2+ uptake,

*When present in excess, actually PROMOTES fat deposition in adipocytes

23
Q

Alveolar Maturation

A

Stimulated by cortisol; also promotes surfactant production

*Glucocorticoids are used to accelerate fetal lung maturation in premies

24
Q

Anti-inflammatory actions of glucocorticoids

A
  • Inhibits production of TNF-a and IL-1
  • Produces lipocortin => inhibitor of Phospholipase A2 => Decreased prostaglandin synthesis
  • Inhibits NO synthase
  • Glucocorticoids also suppress immune fnxn
25
Q

Cholesterol source

A

LDLs are compartmentalized and undergo lysosomal degradation to generate free cholesterol

*Cholesterol esterase also produces some new cholesterol from stored lipids

26
Q

Addison’s Disease

A

Adrenocortical insufficiency usually caused by an AI disorder

Aldosterone deficiency => Hyponatremia, polyuria, hypotension, hyperkalemia

Cortisol deficiency => Hypoglycemia, weakness, hyperpigmentation (ACTH accumulation)

*Kennedy had this

27
Q

Secondary Adrenocortical Insufficiency

A

Decreased ACTH from pituitary; common to see w/ superphysiological concentrations of synthetic glucocorticoids used as anti-inflammatories

-Inhibits prod. of ACTH => Adrenal atrophy

28
Q

Pseudohypoaldosteronism

A

Loss of the mineralcorticoid receptor leading to hyperkalemia, salt wasting, and metabolic acidosis (decreased H+ secretion)

29
Q

Cushing’s Syndrome

A

Mostly caused by abuse of glucocorticoids; also can be ectopic ACTH secreting tumor

*Assoc. w/ obesity, hypertension, hirsutism, purple stria on abdomen, moon face, acne, and decreased healing capability (anti-Wolverine)

30
Q

Cushing’s Disease

A

Disease of excess production of ACTH by the pituitary; same symptoms as Cushing’s Syndrome

31
Q

Conn’s Syndrome

A

Usually due to an adenoma of the zona glomerulosa

=>Mild hypertension, metabolic alkalosis, hypokalemia

32
Q

Congenital Adrenal Hyperplasia

A

Genetically inherited deficiency for the synthetic enzymes of the steroid pathway

*Most commonly block of the 21a-hydroxylase enzyme

Symptoms include: build-up of steroid intermediates, adrenal hypertrophy, excess ACTH
(M)Early maturation of genitalia and appearance of secondary sexual characteristics, early closure of the epiphyseal plate
(F)Fusion of labia [if prior to 12 weeks] and clitoral hypertrophy; absence of breast development and period

33
Q

Chromaffin Cells

A

Cells of the adrenal medulla that secrete catecholamines directly into the bloodstream; only source of epinephrine in the body

34
Q

Catecholamine Synthesis

A

TH converts tyrosine to DOPA which then becomes dopamine

=> Dopamine transported into a chromaffin (secretory) granule via VMAT and converted to NER

=>NER diffuses out and is converted to ER by PNMT; transported back into granule via VMAT

35
Q

Catecholamine release

A

Stored in chromaffin granules w/ Ca2+, ATP, and chromogranin; released after Ach (sympathetic depolarization) or Cortisol stimulation (increases PMNT fnxn and prevents chromafffin cells from becoming post-ganglionic fibers)

36
Q

Catecholamine Degrading Enzymes

A

MAO and COMT; work rapidly in the liver, heart, and kidney

*Rapid degradation => no good serum assay

37
Q

Catecholamine metabolites

A

Metanephrines (formed by COMT) and Vanillylmandelic acid (formed by MAO)

38
Q

Adrenergic Receptor Actions

A

a1- Increased IP3, intracellular Ca2+

a2- Decreased cAMP

B1,2,3- Increased cAMP

39
Q

Pheochromocytoma

A

Tumor of the chromaffin cells causing tachycardia, tremors, sweating, increased BMR

40
Q

21B-hydroxylase

A

Forms DOC from progesterone

41
Q

11B-hydroxylase

A

Converts DOC to corticosterone or cortisol

S&F IV: Exam Two- European Gigalo (14 decks)

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