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HP Relationships And Biofeedback Pt. 2 Flashcards

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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
What changes in the HP-axis will occur from an ectopic ACTH secreting tumor?
Exogenous ACTH: high Cortisol: high Endogenous ACTH: low CRH: low
26
What is Cushing DISEASE?
HYPERcortisolism with HIGH ACTH bc of pituitary adenoma
27
What are the symptoms of Cushing’s?
``` !!• 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. ```
28
What is the test for Cushing’s syndrome?
Dexamethasone suppression test Will administer synthetic glucocorticoid @ low dose Positive: no acth suppression
29
What will a HIGH dose of Dexamethasone suppression test tell you?
The cause of Cushing’s syndrome - drop in ACTH = pituitary adenoma - no change = non-pituitary adenoma
30
What can cause Cushing syndrome? (Excess cortisol)
Exogenous glucocorticoid adminstration Pseudo Cushing’s Cushing’s DISEASE adrenal adenoma/carcinoma Ectopic ACTH or CRH secreting tumors
31
What is pseudo Cushing’s syndrome caused by?
Depression, anxiety, acute/chronic illness, alcoholism All stressors that could cause release of CRH and increase cortisol
32
How will acth levels change in Cushing syndrome caused by a Pituitary tumor?
High
33
How will acth levels change in Cushing syndrome caused by a Adrenal tumor?
Lower than normal
34
How will acth levels change in Cushing syndrome caused by a Ectopic acth secreting tumor?
Higher than normal
35
What is Addison’s disease?
Primary Adrenal insufficiency | Low in aldosterone and cortisol, yet HIGH ACTH
36
What are the symptoms of Addisons?
``` • Hyperpigmentation ◦ excess ACTH —> MC1R—> increase melanin production • Weakness • Weight loss • Hypotension • Hyponatremia (low Na) ```
37
What are the causes of Addison’s disease?
``` • Autoimmune disease • Adrenal hemorrhage ◦ Waterhouse-Friedrichsen syndrome ◦ hemorrhage from anticoagulant treatment • infection ◦ Tuberculosis ◦ N. Meningitis is • tumor metastasis to adrenal gland ```
38
What is Waterhouse-Friedrichsen syndrome? What can Waterhouse-friedrichsen cause?
‣ Adrenal hemorrhage secondary to N. Meningitis is Can cause Addison’s disease
39
What is low/nonexistent in Addison’s disease? High?
Low: cortisol and aldosterone Non-existent: renin-angiotensin-aldosterone axis High = ACTH
40
What is the test for Addison’s disease?
• Cosyntropin (synthetic ACTH) stimulation test Cortisol = less than 18 ug/dL If ACTH = elevated = pirmary If ACTH = low/normal = secondary/tertiary Adrenal insufficiency
41
What is the treatment for Addison’s?
Steroid replacement for life | Cortisol replaced w/ corticosteroid (Aldosterone replaced w/ mineralcorticoid)
42
What is secondary adrenal insufficiency? How does it differ from primary? How will tx differ?
Low production of cortisol because of NO ACTH Renin-angiotensin-aldosterone axis still exists Cortisol replacement needed but not mineralocorticoid (aldosterone) replacement
43
What regulates the secretion of aldosterone? Where is it secreted from?
Angiotensin II from renin-angiotensin system Zona glomerulosa
44
What activates the renin-angiotensin system? What will this then go and activate?
‣ Activated by decrease in Na or by increase in K == Decrease in BP Angiotensin —> aldosterone
45
What is the primary action of aldosterone?
Renal sodium reabsorption to INCREASE BP
46
How does aldosterone increase BP?
‣ 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
What is primary HYPERaldosteronism?
Excess release of aldosterone bc defect @ adrenal cortex
48
What is COnn’s syndrome? Tx?
Adenoma in adrenal cortex causes Primary HYPERaldosteronism Surgery
49
What is bilateral adrenal hyperplasia? Tx?
Can cause HYPERaldosteronism Spironolactone
50
What are the symptoms of PRIMARY HYPERaldosteronism?
Hypertension (too much Na reabsorption) HYPOkalemia (too much K secretion) Low plasma renin
51
What is secondary HYPERaldosteronism?
Excess aldosterone production bc of excess renin secretion by juxtaglomerular cells in kidney
52
How is Hyperaldosternoism detected?
Ratio of Plasma aldosterone contention to plasma renin activity ratio ratio > 20 PAC >15 = primary aldosteronism
53
What is hypoaldosternoism?
Inadequate release of aldosterone due to defects in aldosterone synthesis or destruction of adrenal cortex
54
How are steroid hormones produced?
Cholesterol —> Cholesterol desmolase —> Pregnenolone
55
How is aldosteron produced?
``` Pregnenolone —3b—> Progesterone —21–> DOC —11–> Corticosterone —18–> 18-OH Corticosterone —18-oxidase—> ``` Aldosterone
56
How is cortisol produced?
Pregnenolone —3b—> Progesterone —17–> 17-OH Progesterone —21–> 11-Deoxycortisol —11–> Cortisol
57
What is DOC?
A weak mineralocorticoid (aldosterone)
58
How are androgens produced?
Pregnenolone —3b—> Progesterone —17, 20 —> Dehydroepiandrosterone (DHEA) —3B—> Androstenedione
59
What is the function of 11-beta-HSD2? What can inhibit it??
Protects mineralocorticoid receptor from activation by cortisol Inhibited by black licorice
60
How will enzyme deficiencies in steroid biosynthesis pathways ALL present?
Enlargement of adrenal glands (adrenal hyperplasia) Bc of increased ACTh stimulation and low cortisol = no negative feedback
61
How will an enzyme deficiency of | 17alpha present?
``` 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
How will an enzyme deficiency of | 21-beta present?
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
-what is the most common enzyme deficiency in the steroid biosynthesis pathway?
21-beta
64
How will an enzyme deficiency of | 11-beta present?
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
How much Epinephrine is produced c0mpared to norepinephrine?
E: 80% NE: 20%
66
What is the synthesis of catecholamines under? | 2 things
Sympathetic activity CRH-ACTH-Cortisol axis
67
How does cortisol control the synthesis of Catecholamines?
Cortisol upregulates PNMT enzyme that causes NE—> E
68
What is the synthesis pathway for catelcholamines?
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
What is the rate limiting step of catelcholamine synthesis?
Step 1. Tyrosine —tyrosine hydroxylase —> DOPA
70
How are molecules of E and NE stored?
in Chromaffin granule w/ ATP, Ca, and chromogranin proteins
71
What are chromogranins?
multimolecule complexes | ‣ Decrease osmotic burden of storing E w/in chromaffin granules
72
What can circulating chromogranins be used as a marker for?
sympathetic paragnglion derived tumor (paragangliomas)
73
What signals for secretion of catelcholamines?
Sympathetic innervation via ACh
74
How long do catelcholamines act for?
~10 secodns
75
How are NE and E degraded?
Via COMT or MAO
76
If NE or E are degraded by MAO, what are the next steps?
Makes them into dihydroxymandelic acid —> COMT —> Vanyllylmandelic acid in urine
77
If E gets degraded by COMT, what is its byproduct?
Metanephrine —> MAO —> Vanillylmandelic acid in urine
78
If NE gets degraded by COMT, what is its byproduct?
Normetanephrine —> MAO —> Vanillylmandelic acid in urine
79
What can be measured in urine to asses catelcholamine production?
Vanillylmandelic acid
80
What can elevated levels of metabolic byproducts and catecholamines diagnose?
Pheochromocytoma
81
What are the actions of epinephrine? What receptor does it prefer?
◦ 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
What receptors does NE prefer? Actions?
Higher affinity for alpha receptors and beta 3 receptors Increase gluconeogenesis, glycogenolysis, cardiac contractility, arteriolar vasoconstriction, blood pressure, sphincter contract Decrease insulin secretion
83
What is pheochromocytoma?
Tumor of chromaffin cells that secrete xs catelcholamines Most tumors = benign, unilateral adrenal tumors
84
What can pheochromocytoma cause?
Hypertension Headaches Palpitation Sweating Due to catelcholamines stimulating both alpha and beta adrenergic receptors
85
How does short term stress act on the HP-Adrenal axis?
Sympathetic innervation —> medulla Will secrete catecholamines Increasing BP, HR, glycogenolysis, metabolic rate Dilation of bronchioles, reduced blood flow to digestive system
86
How does long term stress act on the HP-Adrenal axis?
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)

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