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Physiology PHM > Endocrinology: Adrenal gland > Flashcards

Endocrinology: Adrenal gland Flashcards

1
Q

Composition of adrenal gland

A

An outer cortex and an inner medulla. both secrete different types of hormones
Outer cortex made of 3 layers: zona glomerulosa, zona fasciculata, and zona reticularis
MNEMONIC: Go For Red!

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2
Q

Secretions of adrenal cortex vs adrenal medulla

A

Adrenal cortex secretes corticosteroids (mineralcorticoids, glucocorticoids, and adrenal androgens)

Adrenal medulla secretes epinephrine and norephinephrine

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3
Q

True or false: The adrenal medulla is functionally related to the parasympathetic nervous system.

A

False: Adrenal medulla is functionally related to sympathetic nervous system

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4
Q

Adrenal androgens have the same effects as which other hormone?

A

Testosterone

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5
Q

Name the principal mineralcorticoid and the principal glucocorticoid

A

Mineralcorticoid –> aldosterone

Glucocorticoid–> cortisol

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6
Q

Compare and contrast glucocorticoids and mineralcorticoids.

A

Glucocorticoids

  • affect glucose metabolism
  • manage pain
  • antiinflammatory
  • stress management
  • secretion controlled by ACTH
  • secreted by zona fasciculata

Mineralcorticoids

  • affect electrolyte and water balance
  • secreted by zona glomerulosa
  • regulated by renin-angiotensin system

BOTH STIMULATE GLUCONEOGENESIS

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7
Q

Zona glomerulosa makes up ____ % of the adrenal gland cells.

A

15%

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8
Q

Why zona glomerulosa is the only layer capable of secreting aldosterone

A

it has aldosterone synthase

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9
Q

Factors that control secretion of zona glomerulosa.

A

Potassium and Angiotensin II; if they increase, they stimulate its production

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10
Q

Which layer of adrenal gland DOES NOT secrete estrogens and androgens?

A

Zona glomerulosa

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11
Q

Name a hormone involved in regulation of androgens.

A

Cortical androgen-stimulating hormone

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12
Q

All steroid hormones synthesized from ___

A

cholesterol

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13
Q

Majority of cholesterol used to synthesize hormones comes from ____

A

LDLs

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14
Q

Mechanism of cholesterol uptake from LDLs

A

LDLs bind to receptors in coated pits
Are taken in by receptor mediated endocytosis
Fuse with lysosomes; enzymes cleave LDLs to release cholesterol

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15
Q

State the rate-limiting step in formation of adrenal steroid hormones.

A

Where CHOLESTEROL DESMOLASE cleaves cholesterol to form –> pregnenolone

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16
Q

Site of cholesterol cleavage

A

mitochondria and endoplasmic reticulum (but some steps occur only in one of them)

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17
Q

True or false: Cortisone has more mineralcorticoid activity than cortisol.

A

True. But just slightly

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18
Q

The most potent mineralcorticoid is

A

Aldosterone

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19
Q

Glucocorticoids with minealcorticoid activity

A

Cortisol
Cortisone
Corticosterone

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20
Q

Which glucocorticoid is 30 times as potent as cortisol?

A

Dexamethasone

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21
Q

List the glucocorticoids in order of increasing potency.

A 
Corticosterone 
Cortisone 
Cortisol 
Prednisone 
Methylprednisone 
Dexamethasone

*MNEMONIC: See, See, See, People Made Dollars!

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22
Q

Which mineralcorticoid is slightly more potent than aldosterone?

A

9alpha-Flourocortisol

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23
Q

Plasma protein to which cortisol binds

A

Transcortin/Cortisol-binding globulin
Albumin
but has stronger affinity for transcortin

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24
Q

Aldosterone and cortisol transported in which fluid compartment?

25
Physiological importance of binding of adrenal steroids to plasma proteins.
1. Prevents flactuations ex: during brief periods of stress | 2. Ensures uniform distribution throughout the body
26
Major site of adrenocortical steroid degradation
liver
27
The liver converts adrenocotical steroids to
Glucuronic acid | Sulfates
28
Difference in effect of adrenocortical steroids when liver is not working. When kidney is not working.
If liver is not working, the active steroids can't be deactivated. If kidney is not working, the already-deactivated steroids can't be excreted
29
Normal aldosterone concentration in blood is
6 nanograms in 100 mL
30
Consequences of total loss of adrenocortical secretion
Within 3 days to 2 weeks patients die because they are no longer able to reabsorb water and sodium leading to loss of water = decrease in ECF and therefore plasma volume = reduced cardiac output and blood pressure = shock
31
What stops cortisol from binding to mineralcorticoid receptors?
The enzyme 11-beta-hydroxysteroid type 2 converts cortisol to cortisone which binds less avidly and also interrupts redox reaction that occurs for cortisol to bind to the mineralcorticoid receptors
32
Apparent Mineralcorticoid Excess syndrome
When 11 beta hydroxysteroid type 2 enzyme is not working so cortisol is free to bind to mineralcorticoid receptors resulting in effects similar to those if mineralcorticoids bound, yet patient presents with low mineralcorticoid levels.
33
Part of kidney in which Aldosterone has greatest effect
Principal cells in collecting tubules
34
Aldosterone escape
In which the body is able to escape from effects of excess aldosterone (excess sodium reabsorption) since water is stimultaneously reabsorbed by osmosis and increase in angiotensin 2 increases thirst leading to greater water intake. The result is ECF concentration of sodium doesn't change, but ECF volume increases = hypertension
35
Mechanism of aldosterone
Easily diffuses through cell membrane Binds to mineralcorticoid receptor (MR) in cytoplasm Aldosterone-receptor complex diffuses into nucleus Bind to specific hormone response elements to increase transcription of certain genes mRNA goes to cytoplasm to be translated increase in sodium potassium ATPase on basal side and sodium ion channels into lumen side
36
Non-genomic effects of Aldosterone
Activates cAMP messenger system in some cells and phosphatidyl messenger system in other cells
37
Factors that have greatest effect on Aldosterone concentrations.
concentration of potassium | concentration of angiotensin 2 and renin
38
Cortisol is also called
Hydrocortisone
39
How cortisol causes insulin resistance
Inhibits actions of insulin by reducing transcription of their receptors Reduces amount of GLUT3 transporters on cell membranes
40
Adrenal diabetes
Caused by excess cortisol which makes cells insulin resistant = high levels of glucose in blood since cells not taking them up while gluconeogenesis is promoted further increasing glucose stores Unlike diabetes mellitis, administration of insulin does not help
41
How does cortisol increase lipid mobilization?
glucose required to form alpha-glycerophosphate which promotes lipid deposition and maintains lipids. cortisol decreases transport of glucose into cells resulting in insufficient alpha-glycerophosphate = lipids in adipocytes start breaking down and being released
42
Enumerate how cortisol helps body to cope with stress.
By increasing protein breakdown, releases amino acids to go to synthesis of needed compounds By promoting gluconeogenesis, enables glucose to be enough to provide cells with energy for recovery Prevents early stages of inflammation by stabilizing lysozymes and preventing WBCs from causing inflammation
43
Enumerate 5 main stages of inflammation
1. Chemicals like histamine released from damaged tissues 2. Cause vasodilation = increase in blood flow (Erythema) 3. non-pitting edema due to plasma leaking into area 4. WBCs phagocytose 5. Fibrous tissue to help in healing process
44
Erythema
increased in blood flow to damaged area caused by chemicals released by the damaged tissue
45
Cortisol's effect on inflammation process
Stabilizes lysozymes to prevent release of chemicals that cause erythema = reduction of WBCs to area Reduces hyperthermia by preventing release of interleukin 1 which would otherwise go to hypothamus temperature center Prevents leakage of plasma by preventing capillary wall breakdown due to preventing lysozymes from releasing their chemicals Prevents proliferation of leukocytes
46
Normal levels of cortisol
There's no one level. Can range from 5-20 micrograms/deciliter It varies, being highest in the morning and lowest in the evening
47
ACTH precursor is
POMC (Pro-opiomelanocortin)
48
Why Addison's disease causes hyperpigmentation
Addison's disease is also called hypocortisolism. When the adrenal glands stop producing enough cortisol, there is no longer feedback to inhibit ACTH production. POMC is needed for ACTH and is also a precursor of MSH (melanocyte-stimulating hormone). So due to high POMC levels, there is stimultaneous high secretion ACTH with MSH and other hormones
49
Effect of POMC on 1.pituitary corticotroph cells. 2. hypothalamus
EFfect of POMC based on the enzymes present in a cell. In pituitary cells, there is prohormone convertase 1, resulting in formation of ACTH and Beta lipotropin Hypothalamus cells have prohormone convertase 2 instead of 1 resulting in conversion of POMC into melanocyte stimulating hormone and beta endorphin
50
Most clinically significant adrenal androgen is
dehydroepiandrosterone
51
Regulation of zona glomerulosa is by
Renin-angiotensin II | Potassium concentration
52
Purpose of using dexamethasone in hyperadrenalism disorders
Dexamethasone works to inhibit ACTH secretion. It can be used to distuinguish ACTH independent Cushing's Syndrome from ACTH-dependent Cushing's Syndrome (Cushing's disease). When dexamethasone is administered to paients with Cushing's syndrome, there is no effect on the already low ACTH levels. But when administered to those with Cushing's disease, there is a decrease in ACTH levels. BUT there are non-pituitary tumors that don't respond to ACTH inhibition, so this is not an accurate test. Also some pituitary tumors do respond to dexamethasone to reduce ACTH inhibition which can lead to misdiagnosis.
53
Cushing's syndrome caused by disorder of which hormone
Excess cortisol secretion
54
Causes of Cushing's syndrome
``` Pituitary adenoma (=a form of Cushing's syndrome called Cushing's disease) Glucocorticoid drug longterm administration ```
55
Why is there 'moon face' and 'buffalo torso' in Cushing's?
Excess cortisol together with aldosterone results in increased protein breakdown and fat mobilization (=increased appetite), and increase in sodium and water retention (=edema) respectively. The increased appetite is far greater than the fats being mobilized leading to excess fat deposition = buffalo torso. The edema results in moon face
56
Treatment of Cushing's syndrome
Drugs that block steroidogenesis Drugs that block binding of ACTH Partial removal of part of adrenal Drugs that prevent ACTH secretion
57
Drugs that block steroidogenesis
Ketoconazole Metyrapone Aminoglutethimide
58
Increased renin concentration in plasma is a sign of
High levels of aldosterone secretion is called Primary Aldosteronism / Conn's syndrome
59
Diagnosis of Adrenogenital syndrome
high levels of 17-ketosteroids in urine

Physiology PHM (19 decks)

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