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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?

A

ECF

25
Q

Physiological importance of binding of adrenal steroids to plasma proteins.

A
  1. Prevents flactuations ex: during brief periods of stress

2. Ensures uniform distribution throughout the body

26
Q

Major site of adrenocortical steroid degradation

A

liver

27
Q

The liver converts adrenocotical steroids to

A

Glucuronic acid

Sulfates

28
Q

Difference in effect of adrenocortical steroids when liver is not working. When kidney is not working.

A

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
Q

Normal aldosterone concentration in blood is

A

6 nanograms in 100 mL

30
Q

Consequences of total loss of adrenocortical secretion

A

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
Q

What stops cortisol from binding to mineralcorticoid receptors?

A

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
Q

Apparent Mineralcorticoid Excess syndrome

A

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
Q

Part of kidney in which Aldosterone has greatest effect

A

Principal cells in collecting tubules

34
Q

Aldosterone escape

A

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
Q

Mechanism of aldosterone

A

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
Q

Non-genomic effects of Aldosterone

A

Activates cAMP messenger system in some cells and phosphatidyl messenger system in other cells

37
Q

Factors that have greatest effect on Aldosterone concentrations.

A

concentration of potassium

concentration of angiotensin 2 and renin

38
Q

Cortisol is also called

A

Hydrocortisone

39
Q

How cortisol causes insulin resistance

A

Inhibits actions of insulin by reducing transcription of their receptors
Reduces amount of GLUT3 transporters on cell membranes

40
Q

Adrenal diabetes

A

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
Q

How does cortisol increase lipid mobilization?

A

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
Q

Enumerate how cortisol helps body to cope with stress.

A

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
Q

Enumerate 5 main stages of inflammation

A
  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
Q

Erythema

A

increased in blood flow to damaged area caused by chemicals released by the damaged tissue

45
Q

Cortisol’s effect on inflammation process

A

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
Q

Normal levels of cortisol

A

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
Q

ACTH precursor is

A

POMC (Pro-opiomelanocortin)

48
Q

Why Addison’s disease causes hyperpigmentation

A

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
Q

Effect of POMC on 1.pituitary corticotroph cells. 2. hypothalamus

A

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
Q

Most clinically significant adrenal androgen is

A

dehydroepiandrosterone

51
Q

Regulation of zona glomerulosa is by

A

Renin-angiotensin II

Potassium concentration

52
Q

Purpose of using dexamethasone in hyperadrenalism disorders

A

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
Q

Cushing’s syndrome caused by disorder of which hormone

A

Excess cortisol secretion

54
Q

Causes of Cushing’s syndrome

A 
Pituitary adenoma (=a form of Cushing's syndrome called Cushing's disease) 
Glucocorticoid drug longterm administration
55
Q

Why is there ‘moon face’ and ‘buffalo torso’ in Cushing’s?

A

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
Q

Treatment of Cushing’s syndrome

A

Drugs that block steroidogenesis
Drugs that block binding of ACTH
Partial removal of part of adrenal
Drugs that prevent ACTH secretion

57
Q

Drugs that block steroidogenesis

A

Ketoconazole
Metyrapone
Aminoglutethimide

58
Q

Increased renin concentration in plasma is a sign of

A

High levels of aldosterone secretion is called Primary Aldosteronism / Conn’s syndrome

59
Q

Diagnosis of Adrenogenital syndrome

A

high levels of 17-ketosteroids in urine

Physiology PHM (19 decks)

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