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Physiology > HPA Axis and Adrenal Gland > Flashcards

HPA Axis and Adrenal Gland Flashcards

1
Q

What are the components of the HPA axis?

A

Hypothalamus
Pituitary
Adrenal Gland

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2
Q

What are the main functions of the HPA axis?

A
  • Adaptive response to stress

- Regulation of immune function

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3
Q

What are the hormones of the HPA axis?

A

Catecholamines – epinephrine and norepinephrine

Glucocorticoids – cortisol

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4
Q

What enacts short loop inhibition on CRH?

A

ACTH

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5
Q

What enacts long loop inhibition on CRH?

A

Cortisol

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6
Q

Where is CRH made?

A

Parvocellular Neurons of the PVN

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7
Q

What is the release pattern of CRH?

A

Pulsatile so it results in periodic release of ACTH

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8
Q

What receptor does CRH use for the release of ACTH?

A

GPCR

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9
Q

What are the main receptors that bind CRH and what is the binding affinity?

A

CRH R1 - Binds with highest affinity to CRH R1 in anterior pituitary.

CRH R2 - Binds with higher affinity to urocortin.

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10
Q

What is the synergistic effect of CRH and AVP?

A

ACTH release is amplified in the presence of AVP and CRH together

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11
Q

What is POMC?

A

Pro-opiomelanocortin and it is the precursor of ACTH

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12
Q

Where is ACTH made?

A

Anterior PItuitary

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13
Q

What receptors does ACTH bind to and with what affinity?

A

Binds with high affinity to MC2R

Binds with low affinity to MC1R (skin)

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14
Q

How do high levels of ACTH causes hyper pigmentation of the skin?

A

It will increase MC1R binding in the skin

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15
Q

What are the 3 layers of the adrenal gland?

A

Capsule
Cortex
Medulla

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16
Q

What hormones does the cortex secrete??

A

Steroids

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17
Q

What hormones does the medulla secrete?

A

Catecholamines

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18
Q

What is the cell type of cortex and the medulla?

A

Cortex - glandular

Medulla - neural

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19
Q

What are the 3 layers of the adrenal cortex and the hormones that they produce?

A

Zona Glomerulosa - Mineralcorticoids
Zona Fascilculata - Glucocorticoids
Zona Reticularis - Weak Androgens (DHEA)

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20
Q

What is the blood supply of the adrenal cortex?

A

Suprarenal arteries break into subcapsular plexus of capillaries (fenestrated).

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21
Q

What is the blood supply of the adrenal medulla?

A

It has a dual blood supply.

  • Bathes the medullary cells with blood carrying corticosteriods from the cortex – important for conversion of NE to E.
  • Arterioles break into fenestrated capillaries.
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22
Q

What is cortisol released in response to?

A

Acute/chronic stress

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23
Q

Where is cortisol released from?

A

Zona Fasciculata

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24
Q

How is cortisol transported in the blood?

A

90% is bound to corticosteroid binding globulin (CBG)

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25
Q

What converts cortisone into cortisol?

A

11beta-HSD1

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26
Q

What is pleiotropy in cortisol?

A

It has different effects on different tissues.

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27
Q

What is the effect of cortisol on bone?

A

Increases bone resorption and decreases bone formation by decreasing IGF-I receptors.

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28
Q

What is the effect of cortisol on muscle?

A

Decreases muscle mass

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29
Q

What is the effect of cortisol on the immune system?

A

Suppresses immune and inflammatory responses

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30
Q

What are the metabolic actions of cortisol?

A

It is a potent counter-regulatory hormone to insulin.

  • Increase gluconeogenesis and plasma glucose levels
  • Increase lipolysis
  • Increases proteolysis
  • Redistributes fat to the abdominal area
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31
Q

What is the metabolic effect of cortisol in the muscle?

A

Prevents the insertion of GLUT4 on the membrane

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32
Q

How does cortisol inhibit the immune system?

A

It binds to glucocorticoid receptors (GR) which increases IkB transcription.

IkB prevents NFkB from going to the nucleus and the inflammatory response is thus inhibited.

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33
Q

What are the CV effects of cortisol?

A

Increases RBC production

34
Q

What is Cushing Disease?

A

Pituitary adenoma results in excess cortisol that will result in increased abdominal fat, moon face, osteoporosis, hypertension and glucose intolerance.

35
Q

What is Cushing Syndrome?

A

It has the same symptoms as Cushing Disease, but is caused by something other than a pituitary adenoma.

36
Q

What is Addison’s Disease?

A

It is a primary failure of the adrenal glands due to autoimmune destruction of the adrenals.

37
Q

What causes secondary/tertiary adrenal insufficiency?

A

Most common cause = sudden cessation of glucocorticoid therapy with patient failure to secrete CRH or ACTH due to down regulation after chronically being on the glucocorticoid drugs.

38
Q

What is the function of mineralocorticoids?

A

Steroid hormones that regulate sodium/water balance

39
Q

What is the primary mineralocorticoid and where is it made?

A

Aldosterone.

Zona Glomerulosa.

40
Q

Where are the main sites of mineralocorticoid receptor (MR) expression?

A

Distal tubule in kidney
Colon
Salivary ducts
Sweat ducts

41
Q

What is the main target of aldosterone?

A

Kidney

42
Q

What is the effect of aldosterone on the kidney?

A

Aldosterone stimulates sodium and water reabsorption in the kidney; increases potassium secretion

43
Q

What triggers renin release from the kidney?

A

Decrease in BP

44
Q

What is the function of renin and its relation to aldosterone?

A

Renin cleaves angiotensinogen into AT I
AT I is cleaved by ACE into AT II
AT II is a vasoconstrictor and it stimulates aldosterone release

45
Q

What is the effect of aldosterone?

A

It is the primary regulator of extracellular volume.

  • Stimulates sodium and water reabsorption in kidney
  • Stimulates potassium excretion
46
Q

What is the effect of AVP?

A

It is the primary regulator of free water balance.

  • Stimulates distal nephron water permeability which increases water retention
  • Decreases plasma osmolality which secondarily affects sodium concentration in the blood
47
Q

What is the main difference in the effects of aldosterone/AVP?

A

ADH has no direct effect on Na -> Aldosterone does

48
Q

What happens to cortisol as it enters an MR targeted cell?

A

It is converted to cortisone.

49
Q

What converts cortisol to cortisone?

A

11beta-HSD2

50
Q

What is the function of cortisone?

A

It is the deactivated form of cortisol

51
Q

What is the main function of the zona reticularis?

A

DHEA - androstendione (weak androgen) synthesis

52
Q

What delivers free cholesterol to the cell for the synthesis of steroid hormones?

A

HDL and LDL

53
Q

What transports the free cholesterol from the cytoplasm into the mitochondria?

A

StAR

54
Q

What is the function of CYP11A1 (desmolase)?

A

Converts free cholesterol into pregnenlone, the precursor of all steroid hormones

55
Q

Where is 17alpha-hydroxylase found?

A

Zona Fasciculata and Reticularis

Sites of cortisol and DHEAS production

56
Q

What is the defect in congenital adrenal hyperplasia?

A

21alpha-hydroxylase deficiency

57
Q

What is the effect of CAH (21alpha-hydroxylase deficiency)?

A

It results in excess DHEA, with no mineralocorticoids or glucocorticoids

It is needed in the zona glomerulosa and fasciculata.

58
Q

What are some clinical presentations of 21alpha-hydroxylase deficiency?

A 
Hypotension
Hyperkalemia
High plasma renin
Masculinization
High ACTH
59
Q

What is the effect of 11alpha-hydroxylase deficiency (CYP11B1)?

A

It results in no cortisol with increased androgens (DHEAS) and low aldosterone

It is needed in the zona fasciculata

60
Q

What are the clinical presentations of 11alpha-hydroxylase deficiency?

A

Hypertension* due to excess 11-deoxycorticosterone exerting mineralocorticoid effects

Hypokalemia
Masculinization
High ACTH

61
Q

Where is 11alpha-hydroxylase found (CYP11B1)?

A

Zona Fasciculata

62
Q

What is the effect of 17alpha-hydroxylase deficiency?

A

No cortisol
Decreased DHEAS
High MR activity

63
Q

What are the clinical presentations of 17alpha-hydroxylase?

A

Hypertension
Hypokalemia
Feminization/ pseudohermaphroditism
High ACTH

64
Q

What is CYP11B2 also known as?

A

11beta-hydroxylase OR aldosterone synthase

65
Q

What is the effect of ACTH on cholesterol?

A

It stimulates the conversion of cholesterol to pregnenolone by activating StAR

66
Q

What are the effects of ACTH in the adrenal cortex (four)?

A

Stimulates cellular hypertrophy
Stimulates biosynthesis of cortisol
Stimulates biosynthesis of DHEA (CYP17)
Stimulates 11beta-hydroxylase (CYP11B1)

67
Q

What is the effect of ACTH in the adrenal medulla?

A

It stimulates the conversion of dopamine to norepinephrine

68
Q

What is the effect of cortisol in the adrenal medulla?

A

Stimulates the conversion of norepineprhine into epinephrine

69
Q

What is the function of epinephrine?

A

Response to acute stress and it occurs rapidly

70
Q

What are the 3 main targets of E?

A

Muscle
Liver
Fat

71
Q

What is the effect of E in muscle?

A

Glycogenolysis to generate ATP for local energy

72
Q

What is the effect of E in liver?

A

Releases glucose into the blood

73
Q

What is the effect of E in fat?

A

Increases release of FFAs

74
Q

What are the arousal effects of E?

A

Pupil dilation

Sweating

75
Q

What are the CV effects of E?

A

Vasoconstriction

Tachycardia

76
Q

What is the main enzyme in the metabolism of catecholamines?

A

MAO

77
Q

What can be assessed in the urine for excess NE or E production?

A

VMA - it is a product of MAO metabolism of the catecholamines

78
Q

What is the main cause of catecholamine overproduction?

A

Pheochromocytomas – tumors originating from chromaffin cells.

79
Q

What are some of the symptoms of pheochromocytomas?

A

Hypertension with no response to medication
Tachycardia
Headaches

80
Q

What are pheochromocytomas also known as?

A

The 10% Tumor

Physiology (81 decks)

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