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Physiology > Endo IV Adrenal Hormones > Flashcards

Endo IV Adrenal Hormones Flashcards

1
Q

is the adrenal cortex essential to life? adrenal medulla?

A

cortex- yes
medulla- no

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2
Q

what does the adrenal cortex secrete

A

-corticosteroids
- mineralocorticoids
- sex hormones

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3
Q

what does the adrenal medulla secrete and in response to what

A

EPI and NE in response to SNS

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4
Q

what are the hormones secreted by the adrenal cortex made from

A

cholesterol

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5
Q

what are the three layers of the cortex from outer to inner

A

-zona glomerulosa
- zona fasciculata
- zona reticularis

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6
Q

what is secreted in the zona glomerulosa

A

mineralocorticoids

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7
Q

what is secretion in the zona glomerulosa regulated by

A

the renin-angiotensin-aldosterone system (RAAS)

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8
Q

what does the zona fasciculata secrete

A

glucocorticoids

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9
Q

what is secretion by the zona fasciculata regulated by

A

the hypothalamic-pituitary-adrenal axis (HPA) - CRH, ACTH

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10
Q

what is secreted by the zona reticularis

A

androgens

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11
Q

what is secretion by the zona reticularis regulated by

A

HPA

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12
Q

what is secreted by the adrenal medulla

A

catecholamines

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13
Q

what secrete EPI and NE from the adrenal medulla

A

chromaffin cells

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14
Q

what enzyme converts cortisol to cortisone

A

HSD11B2

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15
Q

what enzyme converts cortisone to cortisol

A

HSD11B1

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16
Q

what is androstenedione used to make

A

estrogen and testosterone

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17
Q

what part of the cell do pathways for synthesis of steroid hormones in the adrenal cortex occur

A

in the mitochondria or endoplasmic reticulum

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18
Q

what does aldosterone do

A

increases renal tubular reabsorption of Na+ and secretion of K+ leading to an increase in EC fluid volume and Mean Arterial Pressure

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19
Q

what is aldosterone secretion stimulated by

A

-angiotensin II
- high K+ (hyperkalemia)
-low Na+ (hyponatremia)

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20
Q

what is aldosterone’s effect on salivary glands

A

greatly increases reabsorption of sodium and secretion of potassium by gland ducts, same effect as on renal tubules

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21
Q

what is aldosterone’s effect on sweat glands

A

conserves sodium in hot environments

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22
Q

what is aldosterone’s effect on salivary glands during high rates of salivary secretion

A

conserves sodium

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23
Q

describe the renin-angiotensin-aldosterone system and the results of it

A
  • angiotensin gets converted to angiotensin I by renin
  • angiotensin I gets converted to angiotensin II by ACE
    -angiotensin II triggers vasoconstriction, ADH secretion, thirst stimulation, and aldosterone secretion
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24
Q

what is renin released from

A

the kidneys

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25
Q

what is angiotensin converting enzyme (ACE) produced by

A

the endothelium

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26
Q

what is another term for primary hyperaldosteronism

A

Conn’s syndrome

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27
Q

what are the causes of primary hyperaldosteronism

A

-adrenal adenoma (benign)
- adrenal hyperplasia
- adrenal carcinoma (malignant)

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28
Q

what are the signs and symptoms of primary hyperaldosteronism

A

-hypertension
-hypernatremia
- potassium depletion
-low plasma renin
- hypokalemic alkalosis
- polyuria
- weakness
-headaches

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29
Q

what are the treatment options for primary hyperaldosteronism

A

-surgical removal of the tumor or most of the adrenal tissue when hyperplasia is the cause
- pharmacological antagonism of the mineralocorticoid receptor

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30
Q

what is secondary hyperaldosteronism caused by

A

-CHF
-renal artery stenosis

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31
Q

what are the signs and symptoms of secondary hyperaldosteronism

A

-high plasma renin activity
- hypernatremia with extracellular volume expansion
- edema
- decreased cardiac output
- similar clinical findings as primary hyperaldosteronism-hypertension

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32
Q

when is cortisol secreted

A

-with any stress
-trauma
-infection
- intense heat or cold
- injection of norepinephrine
- surgery
- hypoglycemia
- psychological stress
- any disease

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33
Q

what does cortisol cause in general

A

mobilization of the energy stores, suppresses the immune response, gluconeogenesis, protein mobilization, fat mobilization, stabilization of lysosomes

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34
Q

when is cortisol secretion the highest and what is the pattern of cortisol secretion

A

highest in the AM and the pattern is a circadian

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35
Q

what does cortisol negatively inhibit

A

ACTH secretion from anterior pituitary and the hypothalamus

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36
Q

why are other hormones secreted from the AP along with ACTH

A

because the gene for ACTH forms a larger protein- a preprohormone called proopiomelanocortin (POMC)

37
Q

what hormones are secreted with ACTH

A

-MSH
- Beta endorphon
-beta lipotropin

38
Q

what does MSH cause

A

formation of melanin pigment in mucus membranes and skin

39
Q

which has a higher affinity for the mineralocorticoid receptor: cortisol or aldosterone

A

about the same

40
Q

which has a higher circulating concentration: cortisol or aldosterone

A

cortisol, 1000 fold higher circulating concentration

41
Q

with how much cortisol is circulating why doesnt it cause a mineralocorticoid effect

A

11beta hydroxysteroid dehydrogenase (11BetaHSD) converts cortisol to cortisone in aldosterone responsive tissues and cortisone doesnt bind GC or MR receptors with as high of an affinity as cortisol

42
Q

what does a genetic deficiency of 11beta HSD lead to

A

AME (apparent mineralocorticoid excess)

43
Q

what does glycyrrhetinic acid do and what is it

A

a compound in licorice that inhibits the activity of 11 beta HSD

44
Q

what can overwhelm the 11beta HSD enzyme

A

high circulating cortisol levels

45
Q

what are the carbohydrate effects of cortisol on metabolism

A

-stimulation of gluconeogenesis and glycogenolysis in the liver to increase plasma glucose
- anti-insulin action- decreases glucose uptake in muscle and fat but not brain and heart
-makes diabetes worse by increasing glucose levels, lipid levels, ketone body formation and insulin secretion

46
Q

what are the protein effects of cortisol on metabolsim

A

-inhibits protein synthesis and increases proteolysis in skeletal muscle
- cortisol excess leads to muscle weakness, pain, thin skin, and abdominal striae due to protein catabolism

47
Q

what are the lipid effects of cortisol on metabolism

A

-promotes lipolysis; shifts energy system from utilization of glucose to fatty acids during stress
- causes lipid deposition in certain areas (abdomen, buffalo hump, moon face)

48
Q

what are the effects of low glucocorticoid levels

A

-circulatory failure due to loss of permissive action of catecholamines in blood vessels
- prevents mobilization of energy sources (glucose and FFAs) during stress and can result in fatal hypoglycemia

49
Q

what is 95% of glucocorticoid activity of the adrenal cortex due to

A

secretion of cortisol

50
Q

what are the anti-inflammatory actions of cortisol

A

-stabilizes lysosomal membrane
-decreases capillary permeability
-decreases WBC migration and phagocytosis
- suppresses T lymphocytes proliferation
-decreases IL-1 secretion from WBCs

51
Q

what can glucocorticoid treatment in anti-inflammatory diseases cause and why

A

can cause osteoporosis because:
-stimulates bone resorption (via increased RANKL)
- inhibits osteoblastic maturation and activity
-promotes apoptosis of osteoblasts and osteocytes

52
Q

when does the zona reticularis secrete adrenal androgens

A

starts at age 8, peaks in early 20s and decreases with age

53
Q

what adrenal androgens are secreted by the zona reticularis

A

-DHEA
-adrostenedione
- testosterone

54
Q

which gender is more affected by adrenal androgens

A

weak in males, contributes 50% of active androgens in females

55
Q

what do adrenal androgens do in females

A

growth of pubic and axillary hair and libido

56
Q

what are some conditions resulting from excess androgen production

A
  • in pre-pubertal boys it can cause precocious pseudopuberty
  • 12-hydroxylase deficiency can result in virilization in newborn females and pseudo-hermaphroditism
  • androgen secretin tumors producing excess androgen result in virulization and precocious pseudopuberty in females
57
Q

which is secreted in higher quanitties and which is more important: DHEA and androstenedione

A

DHEA is secreted in higher quanitites but androstenedione is more important because it is more readily converted into testosterone

58
Q

where does conversion of androstenedione to 5-dihydrotestoterone and testosterone occur

A

in peripheral tissues

59
Q

what do hormonally active benign adrenal adenomas usually secrete

A

aldosterone or cortisol

60
Q

what are virulizing tumors in women likely to be caused by

A

ovarian tumors instead of adrenal tumors

61
Q

what are some signs and symptoms of virulization

A

-male pattern baldness
- male musculatre
-irregular menses

62
Q

what is primary adrenal insufficiency

A

primary atrophy or injury of adrenal cortex

63
Q

in about 80% of US cases of primary hypoadrenalism atrophy is caused by ____

A

autoimmune destruction of ALL cortical zones

64
Q

what are the levels of ACTH and corticosteroids in primary adrenal insufficiency

A

high ACTH and low corticosteroid production

65
Q

what secretion is lost in primary adrenal insufficiency

A

glucocorticoid, mineralocorticoid, and adrenal androgen secretion

66
Q

what is happening in secondary adrenal insufficiency

A

pituitary gland unable to secrete enough ACTH

67
Q

what is secondary adrenal insufficiency commonly caused by

A

iatrogenic (medication caused) due to abrupt cessation of steroid therapy

68
Q

what are the levels of ACTH and cortisol in secondary adrenal insufficiency

A

low ACTH and cortisol production

69
Q

is mineralocorticoid secretion affected in secondary adrenal insufficiency

A

no

70
Q

what are the signs and symptoms of glucocorticoid deficiency (low cortisol) in primary and secondary

A

-fatigue
- weight loss
- myalgia
- fever
- hypoglycemia
-low BP
- hyponatremia

71
Q

what are the signs and symptoms of mineralocorticoid deficiency (low aldosterone) seen in primary

A

-salt craving
- low BP
- hyponatremia
- hyperkalemia

72
Q

what are the signs and symptoms of adrenal androgen deficiency seen in primary and secondary

A

-lack of energy
- dry and itchy skin
-loss of libido
- loss of axillary and pubic hair

73
Q

what disease causes hyperpigmentation and why

A

primary adrenal insufficiency due to excess POMC

74
Q

what disease causes alabaster colored pale skin and why

A

secondary adrenal insufficiency due to deficiency of POMC

75
Q

what are the oral manifestations of primary adrenal insufficiency

A

skin pigmentation seen in
- mucocutaneous junction lips
- intraoral mucosal surfaces
- buccal mucosa
-palate
-lingual surfaces of tongue

76
Q

what causes skin pigmentation in addisions disease

A

ACTH causes increased MSH

77
Q

what is the treatment for addisons disease

A

corticosteroids

78
Q

what does the treatment for addisons disease cause

A

-immunosuppression
-suscpetibility to oral candidiasis
- recurrent herpes labialis
- herpes zoster infections
-gingival and periodontal diseases
-impaired wound helaing

79
Q

what are the aspects of dental management for addisons patients

A

-treatment in the morning when cortisol is high
-controlling anxiety
-using long acting anesthetics
- treating postoperative pain
-preventing fracture during surgery for patients with history of long term corticosteroid use

80
Q

what is the difference between cushings disease and cushings syndrome

A

disease is a secondary disorder in the brain, syndrome is a primary disorder in the adrenal cortex

81
Q

which is ACTH independent: cushings disease or cushings syndrome

A

cushings syndrome

82
Q

what are the possible causes of cushings disease

A

-adenoma of anterior pituitary secretes large amounts of ACTH
-ectopic secretion of ACTH by non pituitary tumor such as lungs
- ectopic secretion of CRH by non pituitary tumor

83
Q

what are the possible causes of cushings syndrome

A

-adenomas of the adrenal cortex overproducing cortisol
- primary nodular hyperplasia of the adrenal gland causing overproduction of cortisol

84
Q

what are the manifestations of cushings syndrome/disease

A

-redistrubition of body fat (abdomen)
- moon face with erythema and telangiectases of cheeks and forehead
- increased fat deposition in supraclavicular fossa and dorsocervical area (buffalo hump)
- msucle wasting
-thin extremities
-osteoporosis
- androgen ecess
-increased mineralocorticoid effect -> HTN and hypokalemic alkalosis
-DM

85
Q

what are the oral manifestations of cushing sydrome/disease

A

-round moon face (muscle wasting and fat accumulation)
- fragile surface capillaries -> susceptible to hematomas after mild trauma
- acne and excessive facial hair
-delayed growth and development
- increased pigmentation of buccal mucosa if due to ACTH excess
- immunosuppresion

86
Q

what are the 3 adrenal diseases and what causes them

A
  • Conn’s syndrome (mineralocorticoids)
  • Pheochromocytoma (catecholamines)
  • cushing’s syndrome/disease (glucocorticoids)
87
Q

what is pheochromocytoma caused by

A

sudden released of hormone causing sudden attack due to chromaffin cell tumor in the adrenal medulla resulting in excessive secretion of EPI and NE

88
Q

what are the signs and symptoms of excess NE and EPI

A

-HTN
- tachycardia
-palpitations
-headache
-sweating
-tremors
-weight loss
-hyperglycemia
- orthostatic hypotension

89
Q

what is the incidence rate of pheochromocytoma and when is onset

A

2-8 in 1 million person per year with mean age diagnosis of 40 but can occur from childhood to late life

Physiology (41 decks)

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