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..3 > HP Relationships And Biofeedback Pt. 2 > Flashcards

HP Relationships And Biofeedback Pt. 2 Flashcards

1
Q

What are mineralocorticoids?

Secreted from?

Function?

A

Aldosterone

From zona glomerulosa of adrenal cortex

Regulates salt and volume homeostasis

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2
Q

What are glucocorticoids?

Secreted from?

Function?

A

Cortisol

Form zona Fasciculata of adrenal cortex

longer acting stress response steroid hormone, regulates glucose utilization, immune and inflammatory homeostasis

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3
Q

What does the zona fasciulata and zona reticularis both secrete?

A

Glucocorticoids

Androgens

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4
Q

What are catelcholamines?

Where are they secreted from?

Function?

A

NE and E

Medulla’s chromaffin cells

Rapid responder to stress
(i.e. hypoglycemia, exercise)

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5
Q

What are the hypothalamic hormones released in the HP-Adrenal axis?

A

CRH

Corticotropin releasing hormone

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6
Q

What are the pituitary hormones released in the HP-Adrenal axis?

A

ACTH

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7
Q

What is ACTH derived from?

What does it share a precursor with?

A

From post-translational processing of POMC (proopiomelanocortin)

Melanin

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8
Q

What hormones does the adrenal cortex release in the HP-Adrenal axis?

A

Cortisol (Zona Glom.)
Mineralocorticoid (Zona F and R)
Androgens (Zona F and R)

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9
Q

What regulates teh HP-Adrenal axis?

A

Cortisol will feedback and INHIBIT pituitary and hypothalamus

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10
Q

What is the stimulus for CRH (Corticotropin releasing hormone) from the Hypothalamus?

A
  • emotional stress (fear)
    • physical stress (surgery)
    • metabolic stress (hypoglycemia)
    • infection and inflammation via cytokines
    • Circadian rhythm
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11
Q

What 3 things will cortisol feedback and inhibit?

A

ACTH @ pituitary

CRH @ hypothalmus

Cytokines (in infections and inflammation)

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12
Q

What kind of loop does cortisol act in?

A

Long loop negative feedback

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13
Q

What are the actions of cortisol on the

Immune system?
Liver?
Muscle?
Adipose tissue?

A

◦ Immune system —> immune suppression
◦ Liver —> gluconeogenesis
◦ Muscle —> protein catabolism
◦ Adipose tissue —> lipolysis

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14
Q

When is secretion of cortisol highest?

Lowest?

A

Highest in early morning

Lowest in late evening

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15
Q

What will exogenous glucocorticoid drugs do?

A

mimic cortisol actions

  • longer acting stress response steroid hormone
  • regulates glucose utilization
  • immune and inflammatory homeostasis
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16
Q

What can administration of an excess of exogenous glucocorticoid drugs do?

A

Atrophy adrenal cells that produce cortisol

Show symptoms of XS cortisol (Cushing’s)

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17
Q

What are examples of synthetic glucocorticoids?

A

Prednisone

Methylprednisone

Dexamethasone

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18
Q

If there is increased ACTH levels, what will happen to your skin?

A

Hyperpigmentation due to acth acting on alpha-MSH and inducing melanin synthesis

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19
Q

What is primary hypercortisolism?

How will levels of 
Cortisol
CRH
ACTH 
Change?
A

Xs production of cortisol by adrenal cortex

Cortisol: high
CRH: low (cortisol acts back)
ACTH: Low (cortisol acts back)

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20
Q

What is secondary hypercortisolism?

How will levels of 
Cortisol
CRH
ACTH 
Change?
A

Xs production of cortisol by defect @ pituitary gland

Cortisol: high
CRH: low (cortisol acts back)
ACTH: high (defect @ pituitary)

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21
Q

What is Primary deficiency of cortisol?

How will levels of 
Cortisol
CRH
ACTH 
Change?
A

Deficiency @ adrenal cortex

Cortisol: low
CRH: high (no cortisol to act back)
ACTH: high (no cortisol to act back)

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22
Q

What is secondary deficiency of Cortisol?

How will levels of 
Cortisol
CRH
ACTH 
Change?
A

Deficiency of cortisol bc of defect @pituitary gland

Cortisol: low
CRH: high (bc no cortisol to act back)
Pituitary: low (bc problem @ pituitary)

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23
Q

How will steroid administration of glucocorticoids change levels of

Cortisol
CRH
ACTH

A

Cortisol: low
CRH: low
ACTH: low

No need to produce naturally when provided synthetically

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24
Q

What changes in the HP-adrenal axis would an

Adrenal tumor secreting cortisol cause?

A

Increased cortisol

Lower ACTH and CRH (bc of feedback)

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25
Q

What changes in the HP-axis will occur from an ectopic ACTH secreting tumor?

A

Exogenous ACTH: high

Cortisol: high

Endogenous ACTH: low
CRH: low

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26
Q

What is Cushing DISEASE?

A

HYPERcortisolism with HIGH ACTH bc of pituitary adenoma

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27
Q

What are the symptoms of Cushing’s?

A 
!!• Rounding in of face = moon face
!!• Excess fat on back of neck = buffalo hump
!!• Excess weight gain in abdomen 
!!• Dark red or purple stretch marks 
• Osteoporosis
!!• Easy bruising, hypertension
• Hirsuitism (bc androgens also made) 
• Acne
• Etc.
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28
Q

What is the test for Cushing’s syndrome?

A

Dexamethasone suppression test

Will administer synthetic glucocorticoid @ low dose

Positive: no acth suppression

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29
Q

What will a HIGH dose of Dexamethasone suppression test tell you?

A

The cause of Cushing’s syndrome

  • drop in ACTH = pituitary adenoma
  • no change = non-pituitary adenoma
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30
Q

What can cause Cushing syndrome? (Excess cortisol)

A

Exogenous glucocorticoid adminstration

Pseudo Cushing’s

Cushing’s DISEASE

adrenal adenoma/carcinoma

Ectopic ACTH or CRH secreting tumors

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31
Q

What is pseudo Cushing’s syndrome caused by?

A

Depression, anxiety, acute/chronic illness, alcoholism

All stressors that could cause release of CRH and increase cortisol

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32
Q

How will acth levels change in Cushing syndrome caused by a

Pituitary tumor?

A

High

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33
Q

How will acth levels change in Cushing syndrome caused by a

Adrenal tumor?

A

Lower than normal

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34
Q

How will acth levels change in Cushing syndrome caused by a

Ectopic acth secreting tumor?

A

Higher than normal

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35
Q

What is Addison’s disease?

A

Primary Adrenal insufficiency

Low in aldosterone and cortisol, yet HIGH ACTH

36
Q

What are the symptoms of Addisons?

A 
• Hyperpigmentation
		◦ excess ACTH —> MC1R—> increase melanin production
• Weakness
• Weight loss
• Hypotension
• Hyponatremia (low Na)
37
Q

What are the causes of Addison’s disease?

A 
• Autoimmune disease
• Adrenal hemorrhage 
		◦ Waterhouse-Friedrichsen syndrome
		◦ hemorrhage from anticoagulant treatment
• infection
		◦ Tuberculosis
		◦ N. Meningitis is
• tumor metastasis to adrenal gland
38
Q

What is Waterhouse-Friedrichsen syndrome?

What can Waterhouse-friedrichsen cause?

A

‣ Adrenal hemorrhage secondary to N. Meningitis is

Can cause Addison’s disease

39
Q

What is low/nonexistent in Addison’s disease?

High?

A

Low: cortisol and aldosterone

Non-existent: renin-angiotensin-aldosterone axis

High = ACTH

40
Q

What is the test for Addison’s disease?

A

• Cosyntropin (synthetic ACTH) stimulation test

Cortisol = less than 18 ug/dL

If ACTH = elevated = pirmary

If ACTH = low/normal = secondary/tertiary Adrenal insufficiency

41
Q

What is the treatment for Addison’s?

A

Steroid replacement for life

Cortisol replaced w/ corticosteroid
(Aldosterone replaced w/ mineralcorticoid)

42
Q

What is secondary adrenal insufficiency?

How does it differ from primary?

How will tx differ?

A

Low production of cortisol because of NO ACTH

Renin-angiotensin-aldosterone axis still exists

Cortisol replacement needed but not mineralocorticoid (aldosterone) replacement

43
Q

What regulates the secretion of aldosterone?

Where is it secreted from?

A

Angiotensin II from renin-angiotensin system

Zona glomerulosa

44
Q

What activates the renin-angiotensin system?

What will this then go and activate?

A

‣ Activated by decrease in Na or by increase in K == Decrease in BP

Angiotensin —> aldosterone

45
Q

What is the primary action of aldosterone?

A

Renal sodium reabsorption to INCREASE BP

46
Q

How does aldosterone increase BP?

A

‣ 1. Aldosterone combines w/ a cytoplasmic receptors

‣ 2. Hormone receptor complex initiates transcription in teh nucleus

‣ 3. Translation and protein synthesis makes new protein channels and pumps

‣ 4. Aldosterone induced proteins modulate existing channels and pumps

‣ 5. Result = increased Na reabsorption and K+ secretions—> increased BP

47
Q

What is primary HYPERaldosteronism?

A

Excess release of aldosterone bc defect @ adrenal cortex

48
Q

What is COnn’s syndrome?

Tx?

A

Adenoma in adrenal cortex causes Primary HYPERaldosteronism

Surgery

49
Q

What is bilateral adrenal hyperplasia?

Tx?

A

Can cause HYPERaldosteronism

Spironolactone

50
Q

What are the symptoms of PRIMARY HYPERaldosteronism?

A

Hypertension (too much Na reabsorption)

HYPOkalemia (too much K secretion)

Low plasma renin

51
Q

What is secondary HYPERaldosteronism?

A

Excess aldosterone production bc of excess renin secretion by juxtaglomerular cells in kidney

52
Q

How is Hyperaldosternoism detected?

A

Ratio of Plasma aldosterone contention to plasma renin activity ratio

ratio > 20
PAC >15
= primary aldosteronism

53
Q

What is hypoaldosternoism?

A

Inadequate release of aldosterone due to defects in aldosterone synthesis or destruction of adrenal cortex

54
Q

How are steroid hormones produced?

A

Cholesterol —> Cholesterol desmolase —> Pregnenolone

55
Q

How is aldosteron produced?

A 
Pregnenolone —3b—> 
Progesterone —21–> 
DOC —11–> 
Corticosterone —18–> 
18-OH Corticosterone —18-oxidase—>

Aldosterone

56
Q

How is cortisol produced?

A

Pregnenolone —3b—>
Progesterone —17–>
17-OH Progesterone —21–>
11-Deoxycortisol —11–>

Cortisol

57
Q

What is DOC?

A

A weak mineralocorticoid (aldosterone)

58
Q

How are androgens produced?

A

Pregnenolone —3b—>
Progesterone —17, 20 —> Dehydroepiandrosterone (DHEA) —3B—>

Androstenedione

59
Q

What is the function of 11-beta-HSD2?

What can inhibit it??

A

Protects mineralocorticoid receptor from activation by cortisol

Inhibited by black licorice

60
Q

How will enzyme deficiencies in steroid biosynthesis pathways ALL present?

A

Enlargement of adrenal glands (adrenal hyperplasia)

Bc of increased ACTh stimulation and low cortisol = no negative feedback

61
Q

How will an enzyme deficiency of

17alpha present?

A 
High aldosterone 
HIGH BP (See above) 
LOW K (see above) 
Low cortisol  
Low sex hormones

Low androstenedione (precursor to androgens)

Males - in descending testes
Females - lack of secondary sexual development

62
Q

How will an enzyme deficiency of

21-beta present?

A

LOW aldosterone
—> low BP
—> high K

High sex hormones
Low cortisol
Increased renin activity (trying to get BP up)
Increased 17-hydroxy-progesterone (step in cortisol production that requires 21 next)

Salt wasting in infants
Precocious puberty
Virilization

63
Q

-what is the most common enzyme deficiency in the steroid biosynthesis pathway?

A

21-beta

64
Q

How will an enzyme deficiency of

11-beta present?

A

Affects all pathways

Low aldosterone
HIGH DOC (precursor to aldosterone)
—> HIGH BP
—> LOW K

Low cortisol
High sex hormones
Decreased renin activity (bc BP is high)

Virilization

65
Q

How much Epinephrine is produced c0mpared to norepinephrine?

A

E: 80%

NE: 20%

66
Q

What is the synthesis of catecholamines under?

2 things

A

Sympathetic activity

CRH-ACTH-Cortisol axis

67
Q

How does cortisol control the synthesis of Catecholamines?

A

Cortisol upregulates PNMT enzyme that causes NE—> E

68
Q

What is the synthesis pathway for catelcholamines?

A
  1. hydroxylation of Tyrosine by tyrosine hydroxylase
    ◦ Produces DOPA
  2. DOPA —> DA (via Aromatic amino acid de Carboxylase - AADC)
  3. DA transported into secretory vesicle (chromaffin granule)
  4. DA —> NE (via Dopamine beta-hydroxylase - DBH) INSIDE CELL
    • Most of the NE diffuses out by facilitated transport
  5. NE —> E (via methylation by PNMT)
    OUTSIDE CELL
  6. E transported back into granule by VMATS (Vesicular monoamine transporters)
69
Q

What is the rate limiting step of catelcholamine synthesis?

A

Step 1.

Tyrosine —tyrosine hydroxylase —> DOPA

70
Q

How are molecules of E and NE stored?

A

in Chromaffin granule w/ ATP, Ca, and chromogranin proteins

71
Q

What are chromogranins?

A

multimolecule complexes

‣ Decrease osmotic burden of storing E w/in chromaffin granules

72
Q

What can circulating chromogranins be used as a marker for?

A

sympathetic paragnglion derived tumor (paragangliomas)

73
Q

What signals for secretion of catelcholamines?

A

Sympathetic innervation via ACh

74
Q

How long do catelcholamines act for?

A

~10 secodns

75
Q

How are NE and E degraded?

A

Via COMT or MAO

76
Q

If NE or E are degraded by MAO, what are the next steps?

A

Makes them into dihydroxymandelic acid

—> COMT —> Vanyllylmandelic acid in urine

77
Q

If E gets degraded by COMT, what is its byproduct?

A

Metanephrine

—> MAO —> Vanillylmandelic acid in urine

78
Q

If NE gets degraded by COMT, what is its byproduct?

A

Normetanephrine

—> MAO —> Vanillylmandelic acid in urine

79
Q

What can be measured in urine to asses catelcholamine production?

A

Vanillylmandelic acid

80
Q

What can elevated levels of metabolic byproducts and catecholamines diagnose?

A

Pheochromocytoma

81
Q

What are the actions of epinephrine?

What receptor does it prefer?

A

◦ Reponder to stress
‣ I.e. hypoglycemia/exercise
◦ influences energy metabolism and cardiac output
-increases lipolysis, Ca Lori genesis, insulin secretion, glucagon secretion, muscle potassium uptake, cardiac contractility, heart rate, conduction velocity,

Decrease BP, glucose utilization

◦ Higher affinity for Beta -2 receptor

82
Q

What receptors does NE prefer?

Actions?

A

Higher affinity for alpha receptors and beta 3 receptors

Increase gluconeogenesis, glycogenolysis, cardiac contractility, arteriolar vasoconstriction, blood pressure, sphincter contract

Decrease insulin secretion

83
Q

What is pheochromocytoma?

A

Tumor of chromaffin cells that secrete xs catelcholamines

Most tumors = benign, unilateral adrenal tumors

84
Q

What can pheochromocytoma cause?

A

Hypertension
Headaches
Palpitation
Sweating

Due to catelcholamines stimulating both alpha and beta adrenergic receptors

85
Q

How does short term stress act on the HP-Adrenal axis?

A

Sympathetic innervation —> medulla Will secrete catecholamines

Increasing BP, HR, glycogenolysis, metabolic rate

Dilation of bronchioles, reduced blood flow to digestive system

86
Q

How does long term stress act on the HP-Adrenal axis?

A

ACTH —> Adrenal cortex
Release of steroid hormones

Aldosterone: raises BP by retaining Na and H20

Cortisol: proteins and fat broken down for energy, increase in blood glucose, suppression of immune system (cytokines)

..3 (16 decks)

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