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exam 2 adrenal hormones (quiz 2 info) Flashcards

1
Q

what is essential for life?
what is not essential for life?

A

is= adrenal cortex
isnt= adrenal medulla

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2
Q

what 3 things does the adrenal cortex secrete

A
  1. corticosteroids (cortisol)
  2. mineralocorticoids (aldosterone)
  3. sex hormones (DHEA)
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3
Q

20-30% of adrenal gland tissue and helps to prepare individual to deal with emergencies

A

adrenal medulla

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4
Q

what does the adrenal medulla secrete in response to sympathetic NS stimulation?

A

EPI and NE

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5
Q

3 layers of cortex from most outer to inner:

A

outer:
1. zona glomerulosa-> mineralocorticoids

  1. zona fasciculata (largest)-> glucocorticoids
  2. zona reticularis-> androgens
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6
Q

what is mineralocorticoids secretion regulated by?

(zona glomerulosa)

A

renin-angiotensin-aldosterone system (RAAS)

(aldosterone)

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7
Q

what is glucocorticoids secretion regulated by?
(zona fasciculata)

A

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

(releasing cortisol)

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8
Q

what is androgens secetion regulated by?

(zona reticularis)

A

HPA also

(DHEA- sex hormones)

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9
Q

what cells secrete catecholamines EPI and NE into the blood?

A

chromaffin cells

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10
Q

adrenal cortex secretes hormones that are made from

A

cholesterol

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11
Q

aldosterone increases renal tubular reabsorption of ____ and secretion of ____.

leads to an increase in EC fluid volume and mean arterial pressure

A

reabsorption of Na+
secretion of K+

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12
Q

aldosterone secretion is stimulated by:

A

angiotensin II (releases when blood pressure is low)
increase K+
decrease Na+

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13
Q

aldosterone has similar effects on sweat glands and salivary glands as renal tubules.
increases Na and secretes K
effect on sweat glands important to:
effects on salivary glands

A

conserve body salt in hot environments

conserve na during high rates of salivary secretion

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14
Q

enzyme released by the cells in the kidneys in response to a variety of stimuli ex. sympathetic nervous system:

what are these cells releasing this enzyme?

A

renin

cells are juxtaglomerular cells

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15
Q

angiotensin II does:

A

-aldosterone secretion
-vasoconstriction
-thirst stimulation
-ADH stimulation

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16
Q

how do we get to angiotensin II?

A

angiotensinogen (inactive) to angiotensin I via renin enzyme

angiotensin I to angiotensin II via ACE enzyme

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17
Q

what is the enzyme converting angiotensin I to angiotensin II and is produced by endothelium

A

ACE (angiotensin converting enzyme)

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18
Q

causes:
-adrenal adenomal (benign)
-adrenal hyperplasia
-adrenal carcinoma (malignment)

INCREASE IN aldosterone (ALD)

A

primary hyperaldosteronism (Conn’s Syndrome)

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19
Q

signs and symptoms of Conn’s syndrom (primary hyperaldosteronism)

A

-hypertension
-hypernatremia (high Na)
-headaches
-potassium depletion (hypokalemia)
^ fatigue and weakness
-polyuria
-hypokalemic alkalosis
-LOW plasma renin (due to negative feedback= hypertension and high ALD)

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20
Q

treatment options of primary hyperaldosteronism (Conn’s Syndrome)

A

-surgical removal of tumor or most adrenal tissue when hyperplasia is caused
-medication antagonism of mineralocorticoid receptor

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21
Q

caused by decreased blood flow and pressure in renal artery

A

secondary hyperaldosteronism

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22
Q

CHF
cirrhosis
nephrosis
renal artery stenosis (decrease in blood flow to a kidney so the kidney thinks blood pressure is low= increase in renin)

A

secondary hyperaldosteronism

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23
Q

what is the cause of secondary hyperaldosteronism

A

high plasma renin activity

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24
Q

signs and symptoms:
-hypernatremia w/ ecf volume expansion
-edema
-decreased cardiac output
-similar to primary hyperaldosteronism
BUT high renin and not low

A

secondary hyperaldosteronism

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25
Q

what is secreted with any stress

A

cortisol

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26
Q

what does cortisol cause

A

mobilization of energy stores and suppresses immune response

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27
Q

when is cortisol peak?
secreted in CIRCADIAN RHYTHME

A

peaks in AM

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28
Q

types of stress that INCREASE cortisol release include:

A

-trauma of almost any kind
-infection
-intense heat or cold
-injection of NE
-surgery
-hypoglycemia
-stress
-debilitating disease

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29
Q

is the regulation of glucocorticoid secretion long or short negative feedback?

A

long bc cortisol is doing the feedback

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30
Q

what key things does cortisol do?
1
2
3
4

A
  1. gluconeogenesis (making new glucose)
  2. protein mobilization (protein catabolism/breakdown)
  3. fat mobilization
  4. stabilizes lysosomes (inhibits immune system activity)
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31
Q

when ACTH is secreted from the anterior pituitary, several other hormones are secreted as well bc the gene for ACTH forms a larger protein:

A

a preprohormone called POMC- Proopiomelanocortin

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32
Q

POMC cleaves into ACTH and:

A

-melanocyte stimulating hormone (MSH)
-B-endorphin
-B-lipotropin

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33
Q

specific proteins produced from POMC depend on processing enzymes found in the cell.
many tissues express the POMC gene besides AP:

melanocytes have processing enzymes that form MSH
which stimulates formation of:

A

hypothalamus and melanocytes

formation of melanin pigment

34
Q

ACTH is high secretion and other hormones are low from POMC, but in addison’s disease, the levels of some other hormones can increase such as MSH. this can cause changes in:

A

pigmentation of mucus membranes and thin skin

35
Q

cortisol is found in 1000-fold higher circulating concentration (compared to aldosterone) which could potentially cause symptoms of:

by why doesn’t it?

A

mineralocorticoid excess

bc of the 11B-HSD2 enzyme which converts cortisol to cortisone in aldosterone-responsive tissues

36
Q

what enzyme converts cortisol to cortisone in aldosterone-responsive tissues? in cells of kidneys

and why?

A

11B-HSD2

bc cortisone does not bind GC or MR receptors with as high affinity as cortisol, so then there wont be high amounts of cortisol excess which is bad!

37
Q

enzymes in kidney.

11B-HSD2:

enzymes in skin:
11B-HSD1:

A

11B-HSD2: converts cortisol to cortisone
11B-HSD1: converts cortisone to cortisol

38
Q

a genetic dificiency of 11B-HSD2 leads to the syndrome:

examples:
1
2

A

AME (apparent mineralocorticoid excess)

glycyrrhetinic acid in black licorice inhibits enzyme

cushing syndrome (high cortisol) can overwhelm enzyme

all leading to hypertension

39
Q

too much aldosterone, too much na reabsorption, too much water retention= BP very high!

A

why need 11B-HSD2 receptor

40
Q

effects of cortisol on metabolism with 3 diff biomolecules:

A

carbohydrates
proteins
lipids

41
Q

effects of cortisol on metabolism with carbohydrates:
1
2
3

A
  1. stimulate gluconeogenesis and glycogenolysis in liver (increase plasma glucose levels)
  2. anti-insulin action =decreases glucose uptake in muscle and fat but not brain and heart
  3. makes diabetes worse by increasing:
    glucose levels
    lipid levels
    ketone body formation
    insulin secretion
42
Q

effects of cortisol on metabolism with proteins:
1
2

A
  1. inhibits protein synthesis and INCREASE proteolysis especially in skeletal muscle (provides AA)
  2. cortisol excess leads to muscle weakness, pain, thin skin, abdominal striae in times of stress
43
Q

effects of cortisol on metabolism with lipids:
1
2

A
  1. lipolysis (lipid breakdown)= shifts energy from utilization of glucose to FA in time of stress
  2. causes lipid deposition in certain areas (abdomen, buffalo hump and MOON FACE)
44
Q

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

A

cortisol

45
Q

absence of cortisol contributes to circulatory failure due to loss of

A

loss of permissive action of catecholamines on blood vessels (EPI and NE)

46
Q

lack of cortisol also prevents mobilization of energy sources (glucose and FFA) during stress and can result in

A

fatal hypoglycemia

47
Q

effects of cortisol on the immune system generates:

A

anti-inflammatory actions of cortisol

48
Q

due to their anti-inflammatory properties, _____________ can be used to treat patients with diseases/conditions that involve an inflammatory process ex. rheumatoid arthritis, glomerulonephritis, rheumatic fever, anaphylaxis

A

GLUCOCORTICOIDS

49
Q

great glucocorticoid can be used to treat inflammation but…. glucocorticoid treatment can cause osteoporosis:
1
2
3

A
  1. stimulate bone resorption (via increase in RANKL expression)
  2. inhibit osteoblastic maturation and activity
  3. promotes apoptosis of osteoblasts and oestocytes
50
Q

adrenal androgens come from the

A

zona reticularis

51
Q

the zona reticularis begins to secrete adrenal androgens around age:
peaking in the early:
and then falling with age

A

8
20s

52
Q

what hormones are released from zona reticularis and are androgens?

A

DHEA
androstenedione
testosterone

53
Q

adrenal androgens have weak effects in:

A

males

contrinbute 50% of active androgens in women

54
Q

what are due to adrenal androgens in females

A

growth of pubic and axillary hair and libido

55
Q

what are conditions resulting from excess androgen production by adrenal gland

A
  1. pre-pubertal boys= cause precocious pseudo puberty (early puberty)
  2. 21-hydroxylase deficiency = can result in virilization in newborn females and pseudo-hermaphroditism
  3. androgen secreting tumors producing excess androgen result in virilzation and precious pseudopuberty in females
56
Q

21-hydroxylase deficiency cant make ______ and cant make ____, so precursors build up and produce excessive amounts of DHEA, DHEA sulfate, but __________ is more important because it is more readily converted to testosterone. (can also make estrogens)

A

aldosterone
cortisol

androstenedione

57
Q

in adults, hormonally active benign adrenal adenomas usually secrete aldosterone or cortisol. virilizing tumors in women are more likely to be caused by:

but are rare and usually due to hypersecretion of adrenal androgens

A

ovarian tumors

58
Q

signs and symptoms of virlization of hypersecretion of adrenal androgens include:

A

hirsutism
male-pattern baldness
acne
deep voice
male musculature
menses
amenorrhea
clitoromegaly
increased libido
-rapid linear growth with advanced bone age common in children

59
Q

excess secretion of adrenal androgens can also occur inwhat other disease

A

cushing’s syndrome (increased cortisol)

60
Q

hypoadrenalism (adrenal insufficiency).
-primary adrenal insufficiency is _____ disease.
caused by:

A

addison’s disease
-primary atrophy or injury of adrenal cortex

61
Q

secondary hypoadrenalism (adrenal insufficiency).
cause by

A

-pituitary gland is unable to secrete ENOUGH ACTH

62
Q

with primary hypoadrenalism, in 80% of US cases, atrophy is caused by

A

autoimmune destruction of all cortical zones->
(loss of glucocorticoid, mineralcorticoid and adrenal androgen secretion)

63
Q

in primary hypoadrenalism,
acth and corticosteroid production:

also aldosterone and androgen production:

A

HIGH ACTH (bc lack negative feedback)
and LOW corticosteroid production

aldosterone: low
androgen: low

64
Q

what is often latrogenic due to abrupt cessation of steroid therapy

A

secondary hypoadrenalism

65
Q

what is low ATCH
low cortisol
and does NOT affect mineralcorticoid secretion

A

secondary hypoadrenalism

66
Q

signs and symptoms of glucocorticoid deficiency (low cortisol levels) both primary and secondary:

A

-hypoglycemia
-low blood pressure
-hyponatremia (lack of feedback)
-weight loss
-joint pain

67
Q

signs and symptoms of mineralcorticoid deficiency (primary only aka addison’s disease):

A

-salt craving
-hyponatremia
-hyperkalemia
-low blood pressure
-vomiting

68
Q

adrenal androgen deficiency

A

-lack of energy
-dry and itchy skin (in women)
-loss of libido (in women)
-loss of axillary and pubic hair (in women)

69
Q

hyperpigmentation (primary adrenal insufficiency only) due to

A

excess of POMC which increases ACTH which increases MSH (melaonocytes form for pigment)

70
Q

alabaster-colored pale skin (secondary adrenal insufficiency only) due to

A

deficiency of POMC which decreases ACTH which decreases MSH

71
Q

oral manifestations of adrenal insufficiency (addison’s disease)

A

1 .skin pigmentation
(-mococutaneous junction lips
-intraoral mucosal surfaces
-buccal mucosa
-palate
-lingual tongue)

72
Q

treatment for oral manifestations of adrenal insufficiency (addison’s disease)

A
  1. corticosteroids

(what would occur:
-immuonsuppreison
-recurrent herpes
-IMPAIRED WOUND HEALING
-herpes zoster infections
-susceptibility to oral candidiasis
-gingival and periodontal diseases)

73
Q

hyperadrenalism aka

A

cushing’s disease

74
Q

ACTH dependent Cushing’s disease is a secondary disorder. the adenoma of anterior pituitary secretes

A

large amounts of ACTH

75
Q

when would you want to conduct a patient’s appt who has addison’s disease?

A

in the morning bc that is when their cortical levels are the highest

76
Q

manifestations of cushing’s syndrome/disease:

A

-moon face with erythema and telangiectases of cheeks and forehead
-abdominal striae
-thick neck
-thin extremities
-thinning of bones
-acne
-buffalo hump-increased fat deposition in supraclavicular fossae and dorsocervical area
-central obesity
-hypertension
-ADROGEN excess
-DIABETES MELLITUS (cortisol is insulin antaongist- it raises blood glucose)

77
Q

cushing syndrome (primary hyperadrenalism) acth and cortisol levels:

A

HIGH cortisol
LOW acth

cortisol only syndrome

78
Q

in cushings SYNDROME (primary),
1. ______ of the adrenal cortex overproducing cortisol. this is a benign working tumor of glandular tissue.

  1. ___________ of the adrenal gland causing overproduction of cortisol
A

adenomas

primary nodular hyperplasia of adrenal gland

79
Q

oral manifestations/orofacial of hypercortisolism (cushing’s syndrome/disease)

A

-round moon face
-fragile surface capillaries(hematomas)
-acne and excess facial hair (increase androgens)
-delayed growth and development
-increased pigmentation if due to increase of ACTH
-immunosuppression (impaired wound healing)

80
Q

3 adrenal diseases.
conn’s syndrome:
cushings syndrome/disease:
pheochromocytome:

A

conn’s syndrome: mineralocorticoid excess (aaldosterone)
cushings syndrome/disease: glucocorticoid excess (cortisol)
pheochromocytome: excess catecholamines (EPI and NE)

81
Q

sudden releases of hormone causing sudden attack due to chromaffin cell tumor in the _________ resulting in excess secretion of EPI and NE (tumor!)

A

adrenal medulla

82
Q

signs and symptoms of excess EPI and NE:

(classic triad)

A

hypertension
tachycardia
!!!palpitations!!!!!
!!!!headache!!!!!
!!!sweating!!!!!!
trmoes
weight loss
hyperglycemia
orthostatic
hypotension

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