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Neuroendocrine Exam 3 > Hypothalamic And Pituitary Relationsihps and Biofeedback 2 > Flashcards

Hypothalamic And Pituitary Relationsihps and Biofeedback 2 Flashcards

1
Q

Suprarenal Glands

A

Adrenal Glands, since it is above the Kidney

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2
Q

Epi and NorEpi function and Class

A

Rapid response to stress (hypoglycemia, Exercise) Catecholamines

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3
Q

Cortisol Function and class

A

Chronic Stress, regulate glucose breakdown, immune homeostasis Glucocorticoid (steroid)

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4
Q

Aldosterone

A

Regulate salt and volume homeostasis Mineralcorticoid (steroid)

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5
Q

Dehydroepiandrosterone (DHEAS)

A

Androgen Precursor Steroid

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6
Q

Cortisol pathway

A
  1. Hypothalamus: releases CRH from circadian rhythm or stress 2. AP releases ACTH 3. ACTH goes to the Adrenal Gland= release Cortisol CORTISOL: immune suppression, gluconeogenesis, protein catabolism, Lypolysis
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7
Q

Cortisol Regulations

A

+: metabolic, physical, emotional stress, inflammation -: cortisol goes to hypo and AP

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8
Q

Where does ACTH bind on

A

On MC2R receptor on the Zona Fasciculata of the Adrenal Gland = CORTISOL (-feedback on Hypo and AP) If it binds to MC2R receptor on the Zona Reticularis of the Adrenal Gland =ANDROGENS (no negative feedback)

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9
Q

Cortisol and circadian rhythm

A

LOW: late evening HIGH: early morning

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10
Q

How is Aldosterone secretion regulated

A
  1. Low BP = Kidneys secrete RENIN *Liver: makes angiotensinogen 2. Renin converts angiotensinogen to Angiotensin 1 3. ACE: converts Angiotensin 1- Angiotensin 2 4. Angiotensin 2 goes to Adrenal Cortex= release ALDOSTERONE 5. Aldosterone goes to cytoplasmic R. and make proteins for ion channels 6. Causes Resorption of Na+ and H2O + excretion of K+ from kidneys 7. Increase BP
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11
Q

ACE

A

Angiotensin converging enzyme Also inhibits Bradykinin

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12
Q

Crushing syndrome Sx:

A

Truncal obesity (BACK OF NECK FAT+ABD) Moon face (ROUND FACE) Easy bruising PURPLE bruising HTN Edema Weakness Osteoporosis Diabetes Immunosuppressant Cognitive impairment

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13
Q

Dexamethasone Suppression Test LOW DOSE

A

Different pt. With CS and without CS(crushing syndrome) CS= no ACTH suppression

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14
Q

Dexamethasone Suppression Test HIGH DOSE

A

Distinguish pt. Both with CS (feeds back to the AP) CS caused by AP ACTH secretion tumor (is decrease in ACTH) or CS caused by NOT AP ACTH secretion tumor (no decrease in ACTH)

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15
Q

Excess Glucocorticoid causes + exogenous Glucocorticoid

A

Bone resorption Muscle protein breakdown Gluconeogenesis Obesity Decreased growth Insulin resistance And FA production Atrophy of adrenal gland = X cortisol

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16
Q

ACTH made in AP(from POMC)from other not adrenal cortex organs

A

Binds to the alpha-MSK R. that make MELANIN =can cause hyperpigmentation = Addison’s disease

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17
Q

Primary Adrenal insufficiency

A

ADDISONS DISEASE (due to excess ACTH) ACTH and RENIN does not bind effectively to Adrenal Gland *adrenal gland issue LOW CORTISOL AND ALDOSTERONE CAUSE: Autoimmune, Adrenal hemorrhage after meningitis or anticoagulant, TB, or tumor

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18
Q

Secondary/Teritary adrenal insufficiency

A

ACTH is not made by AP (no hyperpigmentation) *AP problem Renin can still bind and make aldosterone No CORTISOL

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19
Q

Adrenal Insufficiency Tx:

A

Replace the H. That Adrenal gland can’t make Cortisol ——> Corticosteroid (Hydrocortisone, prednisone, dexamethasone) Aldosterone——> mineralcorticoid (fludrocortisone) (only in primary)

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20
Q

Primary Adrenal Excess

A

HGIH CORTISOL LOW ACTH, LOW CRH No hyperpigmentation

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21
Q

Secondary Pituitary Excess

A

HIGH CORTISOL, ACTH, LOW CRH (hyperpigmentation)

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22
Q

Primary deficiency

A

LOW CORTIOL, ALDOSTERONE HIGH ACTH, CRH (hyperpigmentation)

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23
Q

Secondary Deficiency

A

LOW ACTH, CORTISOL HIGH CRH, ALDOSTERONE (no hyperpigmentation)

24
Q

Steroid administration other then cortisol

A

LOW CORTISOL, CRH, ACTH (no hyperpigmentation)

25
Q

Primary Hyperaldosteronism

A

Excessive ALDOSTERONE from adrenal cortex CONN’S SYNDOME = tumor (adenoma) in the adrenal glands

26
Q

Secondary Hyperaldosteronism

A

Excessive RENIN from juxtaglomerular cells in kidenys

27
Q

Hypoaldosteronism

A

X adrenal Cortex. Aldosterone synthesis, stimulation to secrete aldosterone

28
Q

Addison’s disease

A

ADRENAL insufficiency, LOW cortisol, and aldosterone , HIGH ACTH (adrenal cortex atrophy) Hypotension, hyponatremia , weakness, weight loss, hyperpigmentation Dx: ACTH stimulation test

29
Q

Primary Hyperaldosteronism

A

CONN’S DISEASE —> surgery Bilateral adrenal hyperplasia—> Spironolactone excess Aldosterone, HTN, Hyperkalemia, LOW Renin Dx: [Aldosterone] vs[Renin]

30
Q

Aldosterone] vs[Renin] Both high

A

secondary hyperaldosteronism

31
Q

Aldosterone] vs[Renin] high low

A

Primary Hyperaldosteronism

32
Q

Aldosterone] vs[Renin] both low

A

Congential Adrenal Hyperplasia Exogenous mineralocorticoid

33
Q

Adrenal Cortex: where in it is Aldosterone made and where is Androgens made and where is cortisol made

A

Cholesterol-> Pregenolone—-> 1. 3B hydroxylase+21B+11B = ALDOSTERONE(zona glomerulosa) 2. 3B+17a+21B +11 = CORTISOL (zona fasciculata) 3. 17a + 3B = DHEA –> ANDROGEN (zona reticularis)

34
Q

Mineralocorticoid response

A

ALDOSTERONE

35
Q

Glucocorticoid response

36
Q

Overview of Adrenal enzyme deficiency

A

LOW Cortisol can be made due to impareid AP HIGH ACTH = adrenal hyperplasia

37
Q

Adrenal enzyme deficiency 17a

A

HIGH Aldosterone, BP LOW cortisol, sex h., K, androgen X sexual development

38
Q

Adrenal enzyme deficiency 21B

A

HIGH sex h. K, Renin LOW cortisol, aldosterone, BP Na wasting, and puberty too soon

39
Q

Adrenal enzyme deficiency 11B

A

HIGH BP, sex h., LOW Aldpsterone, cortisol, K, Renin Virilization (women with make characteristics)

40
Q

Pheochromocytoma

A

dangerous HTN from adrenal tumor Adrenal glands release catecholamines(epi and norepi) = headache HTN, sweating, Palpations HIGH catecholamines

41
Q

Epinephrine

A

responds to stress, exercise,CO, hypoglacimia….

42
Q

how is Epi made

A

Tyr—> L DOPA—-> Dopamine—-> Norepi—[use CORTISOL to simulate PNMT enzyme]—-> Epinephrine

43
Q

how does catecholamines get secreted from the adrenal medulla (like after epi is made)

A

ACH causes the release Epi= acts on far cells (made in cytosol with help of cortisol) NorEpi= acts on cells in that location of release (made in the chromaffin granules) released as chromaffinins

44
Q

circulating chromaffinins

A

can show there is a tumor (paragangliomas)

45
Q

How are catecholamines degraded

A

Epi—[MAO]—> Dihydroxymandelic acid—- [COMT]—->VMA(URINE) ——[COMT]—> Metanephrine—–[MAO]—-> VMA (URINE) NorEpi—[MAO] —>DHMA—–[COMT]—–> VMA (URINE) —–[COMT]—> normetanephrine —-[MAO]——->Vanillymandelic acid(URINE)

46
Q

Epinephrine receptor

A

B2= vasodilation, resp. dilation, glucose breakdown, release glucagon B1 (increase CO)

47
Q

Norepinephrine receptors

A

B3, = lipolysis and glucose breakdown B1 (increase CO) A1, = vasoconstriction, sphincter contraction A2, = inhibit NE release + inhibit insulin release, platelet aggregation

48
Q

SHORT TERM STRESS vs LONG TERM STRESS

A

SHORT TERM= hypo senses stress —-> spinal cord stimulates the adrenal cortex to release CATECHOLAMINES =E and NE LONG TERM= hypo senses stress—–> AP to release ACTH —-> Adrenal cortex to release Mineralcorticoids (aldosterone) + Glucocorticoids (cortisol)

49
Q

CATECHOLAMINES =E and NE

A

increase HR, dilate bronchioles, increase BP, high glucose breakdown

50
Q

Mineralcorticoids (aldosterone)

A

BP raises, Na+ and H2O is retained by kidneys

51
Q

Glucocorticoids (cortisol)

A

Gluconeogenesis, glucose breakdown, immune suppression

52
Q

Zona glomerulosa

A

Mineralcorticoids

= ALDOSTERONE

53
Q

Zona Fasciculata

A

Glucocorticoids

= CORTISOL

(long-term stress response)

54
Q

Zona Reticulata

A

Androgens

= testosterone and androstenedione–> estrogen and progesterone

=DHEA

55
Q

Medulla

A

Catecholamines

= NE and E and Dopamine

(short-term response to stress)

Neuroendocrine Exam 3 (18 decks)

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