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Endo Repro Midterm > The Adrenal Gland _PV > Flashcards

The Adrenal Gland _PV Flashcards

1
Q

Describe the organization of the adrenal gland in terms of its functional layers and the principal hormones secreted from them.

LO1

A

Adrenal Cortex

1) Zona Glomerulosa
- mineralcorticoids (aldosterone)
2) Zona fasciculata
- glucocorticoids (cortisol)
- androgens (DHEA)
3) Zona reticularis
- glucorticoids (cortisol)
- androgens (DHEA)

Adrenal Medulla
- Catecholamines ( Epi and NE)

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2
Q

What does steroidogenesis start with?

A

cholesterol

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3
Q

Describe the pathways that control steroid hormone production?

LO2

A

Cholesterol-> Prenganglone via desmolase-> progesterone -> 11b deoxycorticosterone via 21 hydroxylase and 17a hydroxyprogesterone via 17 hydroxylase -> androgens via 17,20 lyase

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4
Q

HPA axis is under what type of control?

  • stimulated by
  • target organs and effects (4)
A

negative feedback

stimulatory factors: stress and circadian rhythm

Target Organs

1) immune system- immune suppression
2) liver- gluconeogenesis
3) muscle- protein catabolism
4) adipose tissue- lipolysis

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5
Q

Circadian rhythm of cortisol

A

high in morning

low in late evening

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6
Q

Glucocorticoids

  • what type of control?
  • examples
A

negative feedback

  • cortisone
  • prednisone
  • methylprednisone
  • dexamethasone
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7
Q

21 hydroxylase deficiency

  • describe
  • symptoms

LO2a

A

CYP21A2

  • most common
  • decrease cortisol
  • decrease mineralcorticoid
  • increase sex hormones

Symptoms

  • hypotension
  • decrease aldosterone
  • sodium and volume loss (salt wasting)
  • hyperkalemia
  • elevated renin
  • Female: virilization and sexual ambiguity
  • Male: phenotypically normal, precocious psuedo-puberty, premature epiphyseal plate closure
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8
Q

11B hydroxylase deficiency

  • describe
  • symptoms

LO2a

A

CYP11B1

  • increased androgens
  • virilization of female fetuses
  • increase 11 deoxycorticosterone

Symptoms

  • HTN
  • hypokalemia
  • suppressed renin secretion
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9
Q

17a hydroxylase deficiency

  • describe
  • symptoms

LO2a

A

CYP17A1

  • extremely rare
  • decreased androgens and cortisol
  • excess mineralocorticoids
  • diagnosed at puberty

Symptoms

  • HTN
  • hypokalemia
  • hypogonadism
  • male: undescended testes
  • female: lack of secondary sexual development
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10
Q

Actions of mineralcorticoids

LO3

A

influence sodium and potassium levels

aldosterone

  • kidney fxn
  • secreted in response to low BP or blood volume
  • controlled by RAAS
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11
Q

Actions of Corticosteroids

LO3

A

influence glucose metabolism and immune system

ACTH
- stimulated by stress and mediates glucose metabolism

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12
Q

Actions of Androgens

LO3

A
  • influence secondary sex characteristics
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13
Q

Cortisol

  • describe
  • target organ
  • action
  • diseases
A

target tissue: body wide

Actions: numerous

  • glucocorticoid response elements (GRE)
  • non-genomic actions( endocannabinoids)

Glucocorticoid excess= Cushing syndrome or disease

Glucocorticoid defiency= Addison disease

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14
Q

Effects of cortisol on:

Liver

A

increases gluconeogenesis

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15
Q

Effects of cortisol on:

muscle

A

breakdown of muscle protein

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16
Q

Effects of cortisol on:

fat

A

promotes lipolysis in extremities

promotes central fat deposition

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17
Q

Effects of cortisol on:

cutaneous

A

skin thins

fragile blood vessels

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18
Q

Effects of cortisol on:

immune system

A

increase infection

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19
Q

Effects of cortisol on:

endocrine

A

insulin resistant

glucose intolerant

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20
Q

Effects of cortisol on:

GI

A

interferes with calcium absorption

- risk of osteoporosis

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21
Q

Describe the regulation of cortisol secretion
-steps

LO5

A

1) CRF (CRH)
2) release from PVN
3) brinds CRF1 receptor (GPCR)
4) stimulates release of ACTH

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22
Q

Describe the pattern of ACTH and cortisol release.

  • produced where
  • derived from
  • component
  • type of control

LO4

A

produced in anterior pituitary (PEPTIDE HORMONE)

principle hormone that stimulates adrenal glucocorticoids

derived from POMC

contains MSH activity (excess ACTH= hyperpigmentation)

negative feedback

  • glucocorticoid exert negative feedback onto CTH adn ACTH secretion
  • GC inhibit POMC
  • GC inhbit mRNA synthesis of CRH and ACTH
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23
Q

Dexamethasone suppression test

-types and describe

A

1) Low dose
- determines whether a problem is present
- overnight
- differentiates pts with Cushing of any cause from patients who do not have Cushing
- no ACTH suppression= Cushing
- normal response= suppression of ACTH and cortisol secretion

2) High Dose
- distinguishes patients with Cushing
- help determine source of the problem

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24
Q

Cosyntropin (synthetic ACTH) stimulation tests

  • test for what
  • steps
A

for adrenal gland insufficiency

1) adminster ACTH
2) results
- healthy= cortisol should increase from baseline
- adrenal unresponsive and cortisol remains the same= adrenal insuffiency
- adrenal responds dramatically and cortisol increases too= secondary adrenal insufficiency

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25
Etiologies of Cushing's syndrome
1) exogenous glucocorticoid excess - latrogenic - decrease cortisol but symptoms of excess 2) psuedo cushing syndrome - major depression - anxiety - acute/chronic illness - alcoholism 3) ACTH dependent - cushing disease - ectopic acth- secreting tumors - CRH secreting tumors 4) ACTH- independent - adrenal adenoma/carcinoma
26
Primary action of aldosterone | - steps
Renal sodium absorption 1. Aldosterone combines with cytoplasmic receptor 2. hormone-receptor complex initiates transcription in nucleus 3. translation and protein synthesis makes new protein channels and pumps 4. aldosterone-induced proteins modulate existing channels and pump 5. increase Na reabsorption and K secretion
27
Symptoms and signs of Cushing's syndrome LO7
- truncal obestity - moon face - buffalo hump - easy bruising - HTN - edema - osteoporosis - hirsutism - acne - virilization - diabetes
28
Cushing Syndrome - describe - clinical lab results LO7
hypercortisolism hypersecretion of CORTISOL - adrenal neoplasm elevated cortisol but LOW ACTH * Adrenal problem Test - if inject exogenous glucocorticoid (dexamethasome)-> ACTH undetectable and dexamathasone FAILS to suppress cortisol secretion (negative feedback works but hypercortisolism still persist)
29
Cushing Disease - descrive - clinical lab results LO7
Hypercortisolism *pituitary problem hypersecretion of ACTH - pituitary gland tumor - can be non-pituitary neoplasm (cell carcinoma) overstimulates adrenal cortex and excess cortisol is secreted HIGH ACTH HIGH CORTISOL Test - if inject exogenous glucocorticoid (dexamethasome)-> ACTH normal or slightly elevated and SUCCESSFULLY suppresses cortisol secretion (abnormal negative feedback)
30
Addison Disease - describe - clinical lab results LO7
primary adrenal insufficiency * adrenal problem chronic, progressive destruction of adrenal gland HIGH ACTH LOW CORTISOL - adrenal response is blocked from signal Test - if inject synthetic ACTH (cosyntropin)-> no change in plasma cortisol level (bc adrenals can't respond to ACTH)
31
Secondary Adrenal Insufficiency - describe - clinical lab results LO7
* pituitary problem - caused by exogenous glucocorticoid administration ACTH deficiency LOW ACTH LOW CORTISOL Test - if inject synthetic ACTH (cosyntropin)-> increase in plasma cortisol level (bc adrenals are functional)
32
Primary vs Secondary/ Tertiary adrenal insuffiency
Primary - both cortisol and aldosterone DECREASES - RAAS damafed Secondary/Tertiary - cortisol decreases - but RAAS STILL exists
33
Causes of Primary adrenal insufficiency | - Symptoms
Addison's disease - autoimmune disease Adrenal hemmorhage - can be caused by anticoagulant infection - tuberculosis - meningitidis Tumor metastases to adrenal gland Symptoms: - hyperpigmentation - hypoglycemia - weight loss - muscle weakness - hypotension - hyponatremia - hyperkalemia
34
Treatment for Adrenal insufficiency
cortisol is replaced with corticosteroid aldosterone in replaced with mineralcorticoid hormone (fludrocortisone) * people with secondary adrenal insufficiency normally maintain aldosterone production-> do NOT require mineralcorticoid replacement therapy
35
Primary excess (adrenal) - cortisol - CRF - ACTH - hyperpigmentation?
- cortisol: increase - CRF: decrease - ACTH: decrease - hyperpigmentation: No
36
Secondary excess (pituitary ) - cortisol - CRF - ACTH - hyperpigmentation?
- cortisol: increase - CRF: decrease - ACTH: increase - hyperpigmentation: Yes
37
Primary excess (adrenal) - cortisol - CRF - ACTH - hyperpigmentation?
- cortisol: decrease - CRF: increase - ACTH: increase - hyperpigmentation: yes
38
Secondary deficiency (pituitary) - cortisol - CRF - ACTH - hyperpigmentation?
- cortisol: decrease - CRF: increase - ACTH: derease - hyperpigmentation: no
39
Exogenous glucocorticoid treatment - cortisol - CRF - ACTH - hyperpigmentation?
- cortisol: decrease - CRF: derease - ACTH: decrease - hyperpigmentation: no
40
Aldosterone - describe - regulator - overall results LO9
principal mineralcorticoid controlling Na/K exchange in distal nephrin Major regulator of K body storage increases synthesis and activity of : - Na channels in APICAL membrane - Na/K ATPAse in basolateral membrane in distal tubule Overall result: increase in Na reabsorption and increase in K excretion
41
Actions of aldosterone in kidney (3)
1. increases Na reabsorption 2. Increases K+ secretion 3. Increases H+ secretion
42
Aldosterone pathologies - Hyperaldosteronism - Hypoaldosteronism LO10
Hyperaldosteronism 1. Primary - excessive release of aldosterone from adrenal cortex - exm. Conn's syndrome: adenoma in adrenal cortex 2. Secondary - excessive renin secretion by juxtaglomerular cells in kidney Hypoaldosteronism - destruction of adrenal cortex - defects in aldosterone synthesis - inadequate stimulation of aldosterone secretion
43
High-dose dexamethaosone | - two paths
1) decrease ACTH-> pituitary tumor - effect mediated by negative feedback on pituitary 2) no change in ACTH-> ectopic tumor - no negative feedback effect on ectopic source of ACTH
44
All congenital adrenal enzyme deficiencies are characterized by what?
enlargement of both adrenal gland bc increase ACTH stimulation due to low cortisol
45
Cortisol-cortisone shunt
11B HSD2 metabolizes cortisol to cortisone in kidney protects the MR from cortisol binding keeps MR available for aldosterone 11B HSD2 is inhibited by glcyrrhizic acid (licorice) - cortisol has free access to MR - MR is overwhelemed by cortisol, especially in hypercortisomelic conditions (Cushing)
46
Primary Hyperaldosteronism | - describe
aka Conn Syndrome - hypersecretion of aldosterone - adrenal neoplasm * adrenal problem
47
Secondary Hyperaldosteronism - describe LO10
hypersecretion of rennin excess renin from juxtaglomerular cells of the kidney KIDNEY problem
48
Primary hypoaldosteronism - describe LO10
hyposecretion of aldosterone destruction of adrenal cortex defects in aldosterone synthesis ADRENAL problem
49
Secondary hypoaldosteronism - describe LO10
hyposecretion of renin deficient renin from juxtaglomerular cells of kidney inadequate stimulation of aldosterone KIDNEY problem
50
Primary adrenal failure | -general characteristics
deficient cortisol AND aldosteron
51
ACTH deficiency | - general characterisitc
cortisol deficiency but NOT change in Aldosterone
52
Adrenal androgen - hormone - precursor
DHEA precursor to human sex steroids relies on 3B hsd superfamily to exert androgenic and estrogenic activities adrenal carcinomas that secrete androgens - females may feature virilization, hirsutism, clitoromegaly, acne
53
Cathecholamines - produced where - breakdown
produced in adrenal medulla 80% epinephrine - responder to stress (hypoglycemia/exercise) -influence energy metabolism and cardiac output 20% noepinephrine
54
Epi and NE pathway
1. SNS release Ach 2. Ach binds nicotinic receptor 3. ACH increases synthesis of tyrosine hydroxylase and activity of dopamine 4. VMAT moves EPi into specialized storage vesicles in chromaffin cells
55
Synthesis of catecholamines | -controlled by
under the control of CRH-ACTH-cortisol axis 1. ACTH stimulate synthesis of DOPA 2. Cortisol increase PNMT enzyme 3. release is triggered by CNS control
56
Rate limiting step of NE/E synthesis
tyrosine hydroxylase
57
degradation of catecholamines | - describe enzymes
1) monoamine oxidase -oxidizes stuff - used to treat neuropsychiatric disorders NE or E=> dihydroxymandelic acid 2) COMT - methylates - primary enzymes that inactivates catecholamines released from the adrenal gland both enzymes located in CNS and peripheral tissue
58
Pheochromocytoma - describe - symptoms - receptors
benign, unilateral tumor on chromaffin tissue -produces excess catecholamines Symptoms - HTN - orthostatic hypotension - headaches, sweat, palpitation, chest pain - anxiety Catecholamines secreted by pheochromocytoma stimulate both a & B adrenergic receptors
59
Adrenergic receptors | - which one responds better to NE than E? vice versa? same?
a receptors and B3 respond better to NE than E B1 receptors respond equally to NE and E E is more potent than EN for B2 receptors
60
a1 receptor - primary mechanism - action
ip3/ca/dag increase vascular SM contraction
61
a2 receptor - primary mechanism - action
decrease camp inhibit NE and insulin
62
b1 receptor - primary mechanism - action
increase camp increase CO
63
b2 receptor - primary mechanism - action
increase camp increase hepatic glucose output dilation for bronchioles,, uterus, vessels
64
b3 receptor - primary mechanism - action
increase camp increase hepatic glucose output increase lipolysis
65
Stress Response and HPA axis - short term - long term
``` 1) short term nerve impulse catecholamines (Epi/NE) - increase HR, BP - dilate bronchioles - BMR increase - glycogen to glucose ``` ``` 2) long term mineralocorticoid and glucocorticoid - sodium and h2o retentin - increase BP, BV - immune system suppressed - blood glucose increase ```

Endo Repro Midterm (12 decks)

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