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NeuroEndocrine 3 > Hypothalamic pituitary relationships and feedback part 2 > Flashcards

Hypothalamic pituitary relationships and feedback part 2 Flashcards

1
Q

what is found in the Zona glomerulosa and what is its function

A

Mineralcorticoid which produce aldosterone which regulates the salt and volume homeostasis

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2
Q

What is found in the zona fasciculata and what is its function

A

Glucocorticoid which produce cortisol and androgens (DHEAS)

cortisol is a longeracting stress response steroid hormone that regulates glucose utilization, immune and inflammatory homeostasis

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3
Q

WHat is found in the zona reticularis and what is its function

A

glucocortocoid cortisol and androgens DHEAS

androgens are important for secondary sex characteristics

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4
Q

what is the axes of cortisol

A

Hypothalamus releases CRH which acts on the anterior pituitary that releases ACTH which acts on MC2R receptors in the adrenal cortex that releases cortisol

cortisol then serves as negative feedback

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5
Q

What are causes for the release of CRH

A

Emotional stress
Physical stress
Metabolic stress
Infection and inflammation

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6
Q

does the circadian rhythm play a factor in cortisol

A

yes, the secretory rates of cortisol are high in the mornings but are low in the late evenings

ACTH is fairly constant through out the day

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7
Q

what is the pathway and regulation of aldosterone secretion

A

if their is a decrease in BP or decrease in Na+

hypothalamus releases CRH onto the anterior pituitary which releases ACTH which releases Aldosterone from the adrenal cortex

this targets the kidneys to reabsorb Na+ and water that leads to an increase n BP

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8
Q

What is Cushings syndrome and what are some symptoms

A

high cortisol

buffalo hump
truncal obesity
immunosuppression
hypertension
edema
weakness
osteoporosis
acne
purple striae
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9
Q

How does a low dose Dexamethasone suppression test work

A

dexamethasone is a synthetic glucocorticol

at low doses it differentiates patients with Cushings syndrome vs patients who dont have it

if their is no ACTH suppression then it indicates Cushings syndrome

however it doesn’t specify source of ACTH over production

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10
Q

How does a high dose dexamethasone suppression test work

A

Distinguishes patients with cushings disease has a pituitary tumor or a ectopic tumor

if their is a decrease in ACTH levels due to negative feedback then it is a pituitary tumor

if their is no change in ACTH then it is an ectopic tumor

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11
Q

if Cushings syndrome is caused by a adrenal tumor what is the levels of CRH, ACTH, and cortisol

A

decrease in CRH
Decrease in ACTH
and increase in Cortisol

thats because the adrenal cortex is overactive and still get the negative feedback

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12
Q

if cushings syndrome is caused by pituitary disease what is the levels of CRH, ACTH, and cortisol

A

decrease in CRH
increase in ACTH
increase in Cortisol

this is because it is in the anterior pituitary therefore the only thing getting a negative feedback is the hypothalamus

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13
Q

if cushings syndrome is caused by ectopic secreting ACTH tumor what is the levels of CRH, ACTH, and cortisol

A

low CRH
High ACTH
High cortisol

however the pituitary and hypothalamus is inhiibited therefore the release of ACTH is coming not from the pituitary

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14
Q

if cushings syndrome is caused by exogenous glucocorticoids what is the levels of CRH, ACTH, and cortisol

A

low CRH
Low ACTH
Low cortisol

but the exogenous corticoids mimic cortisol actions showing cushings disease symptoms

iatorgenic cushings disease

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15
Q

what is significant about the exogenous glucocorticoids especially on the zona fasciculata and that are some examples of drugs

A

they have the same negative feedback as cortisol
but can cause atrophy to zona fasciculata

Prednisone
methylprednisone
dexamethasone

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16
Q

What is the primary action of aldosterone

A

renal sodium reabsorption and potassium secretion in the distal nephron

does this by altering trnscription of creating new channels in the distal nephraon

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17
Q

what is ACTH derived from

A

made in anterior pituitary and derived from Post translational processing of POMC

is a peptide hormone

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18
Q

what happens when their is a supraphysiological level of ACTH

A

leads to hyperpigmentation

ACTH has a low binding affinity for MC1R which is melanocytes in the skin and increase production of Melanin

causes darkening of the skin and production of MSH

19
Q

what does the cosyntropin stimulation test detect

A

Adrenal gland insufficiency
-high increase of cortisol after 30 min

low levels/normal means secondary or tertiary Adrenal insufficency

elevated levels of ACTH means Primary adrenal insufficency

cosyntropin is a synthetic ACTH

20
Q

what happens to levels of cortisol and aldosterone secretion in primary adrenal insufficiency

A

decrease secretion in both cortisol and aldosteron

21
Q

what happens to levels of cortisol and aldosterone secretion in secondary and tertiary adrenal insufficiency

A

decrease in cortisol

aldosterone still exists due to the renin-angiotensin-aldosterone axis

22
Q

what are the causes and treatments of primary adrenal insufficiency (addisons disease)

A

autoimmune disease
adrenal hemorrhage
waterhose-friedrichsen syndrome

tuberculosis
meningitidis
tumor to the adrenal gland

treatment: replace cortisol and aldosterone
aldosterone: fludrocortisone
cortisol: dexamethasone

23
Q

What is the plasma cortisol, plasma CRH, Plasma ACTH, and pigmentation if you have a disorder of: Primary (excess)

A

high cortisol
low CRH
low ACTH
no hyperpigmentation

24
Q

What is the plasma cortisol, plasma CRH, Plasma ACTH, and pigmentation if you have a disorder of: Secondary excess

A

high cortisol
low CRH
High ACTH
yes pigmentation

25
Q

What is the plasma cortisol, plasma CRH, Plasma ACTH, and pigmentation if you have a disorder of: Primary deficiency

A

low cortisol
high CRH
High ACTH
yes hyperpigmentation

26
Q

What is the plasma cortisol, plasma CRH, Plasma ACTH, and pigmentation if you have a disorder of: Secondary deficiency

A

low cortisol
high CRH
low ACTH
no hyperpigmentation

27
Q

primary Hyperaldosteronism

A

excessive aldosterone from the cortex

conns syndrome: adenoma in the adrenal cortex

hypertension
hypokalemia

28
Q

Secondary hyperaldosteronism

A

excessive renin secretion by the juxtaglomerular cells in the kidney
hypertension
hypokalemia

29
Q

Hypoaldosteronism

A

destruction of the adrenal cortex
defects in aldosterone synthesis
inadequate stimulation of aldosterone secretion

30
Q

what enzymes are used to make androgens

A

17, 20, 3B(to make a minor proust)

31
Q

What enzymes are used to make aldosterone

A

3B, 21, DOC (serves as a mineralcorticoid), 18

32
Q

what enzymes are used to make cortisol

A

3B, 17, 21, 11

33
Q

How is the mineralcorticoid receptor protected from activation via cortisol

A

11B-HSD2 converts cortisol to cortisone

34
Q

All congenital adrenal enzyme deficiencies are chacracterized by what

A

Enlargement of both adrenal glands due to the increase ACTH stimulation due to the decrease of cortisol

35
Q

what is the Mineralcorticoids, cortisol, sex hormones, blood pressure, potassium levels, labs, and other presentations of an enzyme deficiency: 17a

A 
high mineralcorticoids
low cortisol
low sex hormones
high blood pressure
low potassium
decrease in androstenedione
men, undescended testes
women, lack of secondary sexual development
36
Q

what is the Mineralcorticoids, cortisol, sex hormones, blood pressure, potassium levels, labs, and other presentations of an enzyme deficiency: 21B

A 
decrease in mineralcorticoids
low cortisol
high sex hormones
low blood pressure
high potassium
high renin activity
high 17-hydroxy progesterone
salt wasting
precocious puberty
virilization
37
Q

what is the Mineralcorticoids, cortisol, sex hormones, blood pressure, potassium levels, labs, and other presentations of an enzyme deficiency: 11B

A 
decrease in Aldosterone
increase in DOC (increase in BP)
decrease in Cortisol
increase in sex hormones
high BP
Low potassium
decrease in renin activity
Virilization
38
Q

Pheochromocytoma

A 
tumor that increases the secretion of catecholamines that stimulate both alpha and beta receptors
hypertension
sweating
palpitations
headaches
39
Q

synthesis of Catecholamines is under the control of what activity

A

Sympathetics (Acetylcholine) and the CRH-ACTH-cortisol axes

cortisol upregulates the PNMT enzyme
phenylethanolamine N methyl transferase

40
Q

How is norepinephrine and epinephrine synthesized

A

Rate limiting step is the hydroxylation of tyrosine by tyrosine hydroxylase making DOPA

converted to DA then transported into a secretory vesicle (chromaffin granule)

in the granule the DA is converted to NE by dopamine B hydroxylase

then NE diffuses out of chromaffin granule and is methylated via PNMT to form Epinephrine

then transported back to granule via VMATs

41
Q

What are chromogranins

A

Multimolecular complexes thought to decrease the osmotic burden of storing E

these can be used as a biomarker for sympathetic paraganglion derived tumors

42
Q

How are catecholamines degrared

A

COMT: catecholamine O methyltransferase
MAO: monoamine oxidase

43
Q

response of receptors to NE vs E

A

alpha and B3 receptors respond more to NE
B1 responds equally to NE and E
B2 responds more to E

NeuroEndocrine 3 (17 decks)

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