2/19: Adrenal Hormones Flashcards

1
Q

What does the adrenal hormone consist of?

A

Outer cortex
Inner medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the adrenal cortex essential for?

A

Life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does the adrenal cortex secrete?

A

Corticosteroids (ex. Cortisol)
Mineralocorticoids (ex. Aldosterone)
Sex hormones (ex. DHEA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is 20-30% of gland tissue?

A

Adrenal medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does the adrenal medulla secrete?

A

Epinephrine and norepinephrine in response to sympathetic NS stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What hormones are not essential for life, but help to prepare the individual to deal with emergencies?

A

Adrenal medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Adrenal cortex secretes hormones that are made from __________

A

Cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the three layers of the cortex?

A

Zona Glomerulosa (~15%), Zona Fasciculata (~75%), Zona Reticularis (~10%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does the zona glomerulosa secrete?

A

Mineralocorticoids
- Secretion regulated by the
renin-angiotensin-
aldosterone system (RAAS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does the zona fasciculata secrete?

A

Glucocorticoids
- Secretion regulated by the
hypothalamic-pituitary-adrenal axis (HPA) – CRH, ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does the sona reticularis secrete?

A

Androgens
- secretion regulated by the HPA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does the adrenal medulla secrete?

A

Catecholamines
- related to the sympathetic nervous system and
chromaffin cells secrete the catecholamines epinephrine (EPI) and norepinephrine (NE) into the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are steroid hormones derived from?

A

Cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does aldosterone do?

A

Increases renal tubular reabsorption of Na and secretion of K
Increase ECF Na+
Decrease ECF K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does increases of Na+ reabsorption and K+ secretion lead to?

A

An increase in EC fluid volume and mean arterial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is aldosterone secretion stimulated by?

A

Angiotensin II
Increase K+
Decrease Na+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Aldosterone has similar effect on _______ and ________ as renal tubules

A

Sweat glands; salivary glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does aldosterone increase reabsorption of?

A

Sodium by gland ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does aldosterone increase secretion of?

A

Potassium by gland ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the effect of aldosterone on sweat glands important for?

A

To conserve body salt in hot environments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the effect of aldosterone on salivary glands conserve?

A

Sodium during high rates of salivary secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What causes secretion of aldosterone?

A

Angiotensin II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is renin?

A

an enzyme released by the cells in the kidneys in response to a variety of stimuli (ex. Sympathetic Nervous system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is angiotensin converting enzyme (ACE) produced by?

A

Endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What cells make up renin?

A

Juxtaglomerular cells in kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the pathway of angiotensinogen to aldosterone

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does angiotensin II cause?

A

Vasoconstriction
ADH secretion
Thirst stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What enzyme converts angiotensinogen to angiotensin I?

A

RENIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What enzyme converts angiotensin I to angiotensin II?

A

ACE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are causes of primary hyperaldosteronism (Conn’s syndrome)?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are signs and symptoms of primary hyperaldosteronism (conn’s syndrome?

A
  • Hypertension
  • Hypernatremia
  • Headaches
  • Potassium depletion
  • Weakness
  • Fatigue
  • Polyuria
  • Hypokalemic alkalosis
  • Low plasma renin!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are tx options of primary hyperaldosternosim?

A

– Surgical removal of the tumor or most of the adrenal tissue when hyperplasia is
the cause.
– Pharmacological antagonism of the mineralocorticoid receptor (ex: spironolactone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is secondary hyperaldosteronism caused by?

A

Decreased blood flow and pressure in renal artery
– CHF
– Cirrhosis
– Nephrosis
– Renal artery stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are signs and symptoms of secondary hyperaldosteronism?

A
  • High plasma renin activity
  • Hypernatremia w/extracellular volume expansion
  • Edema
  • Decreased cardiac output
  • Similar clinical findings as Primary Hyperaldosteronism-hypertension
    etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the cause of the pathology of secondary hyperaldosteronism?

A

High plasma renin activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

When is cortisol secreted?

A

With any stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What does cortisol cause?

A

mobilization of energy stores and suppresses the immune response

38
Q

What are types of stress that increase cortisol?

A
  • Trauma of almost any type
  • Infection
  • Intense heat or cold
  • Injection of norepinephrine
  • Surgery
  • Hypoglycemia
  • Psychological stress
  • Almost any debilitating disease
39
Q

When does cortisol secretion peak?

A

In the AM - it is secreted in circadian

40
Q

What are the functions of cortisol?

A
  1. Gluconeogenesis
  2. Protein mobilization
  3. Fat mobilization
  4. Stabilizes lysosomes
41
Q

When ACTH is secreted from the AP, _____________ are secreted as well

A

Several other hormones because the gene for ACTH forms a larger protein - a preprohormone called Proopiomelanocortin (POMC)

42
Q

What doesn’t express the POMC gene?

A

Anterior pituitary (hypothalamus, melanocytes)

43
Q

What do melanocytes have?

A

Processing enzymes that form MSH which stimulates formation of melanin pigment

44
Q

In Addison’s disease, high levels of MSH can cause what in the oral mucosa?

A

Pigmentation of the mucus membranes and thin skin

45
Q

Cortisol has a similar affinity for the mineralocorticoid receptor (MR) as __________

A

aldosterone

46
Q

Cortisol is found in a higher circulating concentration, what does this cause?

A

Symptoms of mineralocorticoid excess

47
Q

What converts cortisol to cortisone in aldosterone responsive tissues?

A

11betaHSD

48
Q

Cortisone doesn’t bind _____ or _____ receptors with as high of an affinity as cortisol

A

GC; MR

49
Q

What does a genetic dificiency of 11beta-HSD leads to?

A

AME Syndrome (Apparent Mineralocorticoid Excess)

50
Q

What inhibits the activity of 11beta-hydroxysteroid dehydrogenase?

A

Glycyrrhetinic acid - a compound of licorice

51
Q

What can overwhelm the 11beta-HSD enzyme?

A

High circulating cortisol levels (cushing’s syndrome)

52
Q

What do carbohydrates stimulate?

A

Gluconeogenesis and glycogenolysis in liver (increase plasma glucose)

53
Q

What are anti-insulin actions of carbohydrates?

A

Decreases glucose uptake in muscle and fat but not
brain and heart

54
Q

How do carbohydrates make diabetes worse?

A

by increasing glucose levels, lipid levels, ketone
body formation and insulin secretion

55
Q

What do proteins inhibit?

A

Protein synthesis and increases proteolysis especially in skeletal muscle (provides source of AA for gluconeogenesis)

56
Q

What does excess cortisol lead to?

A

muscle weakness, pain due, thin skin and abdominal
striae due to protein catabolic effect

57
Q

What do lipids promote?

A

lipolysis; shifts energy system from utilization of glucose to fatty acids in times of stress

58
Q

What do lipids cause?

A

lipid deposition in certain areas (abdomen, interscapular “buffalo hump” and a rounded “moon face”

59
Q

What does absence of cortisol contribute to?

A
  • Circulatory failure due to loss of permissive action of catecholamines on blood vessels
  • prevents mobilization of energy sources (glucose & free fatty acids) during stress &
    can result in fatal hypoglycemia
60
Q

What can glucocorticoids be used to treat?

A

Patients with diseases/conditions that involve an inflammatory process (ex: rheumatoid arthritis, glomerulonephritis, rheumatic fever, anaphylaxis)

61
Q

What can glucocorticoid treatment cause?

A

Osteoporosis

62
Q

If glucocorticoid treatment causes osteoporosis, what can this cause?

A

1) Stimulates bone resorption (via increased RANK-L expression)
2) Inhibits osteoblastic maturation and activity
3) Promotes apoptosis of osteoblasts and osteocytes

63
Q

What are the three adrenal androgens?

A
  1. Dehydroepiandrosterone (DHEA)
  2. Androstenedione
  3. Testosterone
64
Q

What effect do adrenal androgens have on males and females?

A

Weak effects in males, 50% active androgens in females

65
Q

Conditions resulting from excess androgen production by the adrenal gland are?

A

– In pre-pubertal boys, it can cause precocious pseudopuberty (not
due to the hypothalamic- pituitary-adrenal axis)
– 21-hydroxylase deficiency can result in virilization in newborn
females and pseudo-hermaphroditism
– Androgen secreting tumors producing excess androgen result in virilization and precocious pseudopuberty in females

66
Q

What is androstenedione converted to?

A

Testosterone

67
Q

Where does converstion to testosterone and 5-dihydrotestosterone occur in?

A

Peripheral tissues

68
Q

In adults, hormonally active benign adrenal adenomas usually secrete

A

Aldosterone or cortisol

69
Q

Virilizing tumors in women are more likely to be caused by

A

Ovarian tumors

70
Q

What are signs and symptoms of virilization?

A
  • hirsutism,
  • male-pattern baldness,
  • acne,
  • deep voice,
  • male musculature,
  • irregular menses or
    amenorrhea,
  • clitoromegaly,
  • increased libido.
  • rapid linear growth with
    advanced bone age is
    common in children
71
Q

What is primary adrenal insufficiency?

A

Addison’s

72
Q

In about 80% of cases, what is atrophy caused by?

A

Autoimmune destruction of all cortical zones

73
Q

What is primary adrenal insufficency due to glucocorticoid, mineralcorticoid, and androgen secretion?

A

Loss of glucocorticoid, mineralcorticoid and adrenal androgen secretion

74
Q

What is secondary adrenal insufficiency?

A

Pituitary gland unable to secrete enough ACTH

75
Q

Secondary adrenal insufficiency is often _______ due to abrupt cessation of steroid therapy

A

Latrogenic

76
Q

How does secondary adrenal insufficiency affect mineralcorticoid secretion?

A

Not affected

77
Q

What are signs and symptoms of glucocorticoid deficiency?

A
  • fatigue
  • weight loss, anorexia
  • myalgia
  • fever
  • anemia
  • increased TSH
  • hypoglycemia
  • low BP
  • hyponatremia
78
Q

What are signs and symptoms of mineralcorticoid deficiency?

A
  • abdominal pain, nausea, vomiting
  • dizziness
  • salt craving
  • low BP
  • hypotension
  • increased serum creatine
  • hyponatremia
  • hyperkalemia
79
Q

What are symptoms of adrenal androgen deficiency?

A
  • lack of energy
  • dry and itchy skin
  • loss of libido
  • loss of axillary and pubic hair
80
Q

What are orofacial features of adrenal insufficiency (addison’s)?

A

skin pigmentation
o mucocutaneous junctions lips
o intraoral mucosal surfaces
o buccal mucosa
o palate
o lingual surface of the tongue

81
Q

What is treatment for adrenal insufficiency?

A

Corticosteroids
o immunosuppression
o susceptibility to oral candidiasis
o recurrent herpes labialis
o herpes zoster infections
o gingival and periodontal diseases
o impaired wound healing

82
Q

What is ACTH-dependent cushing’s disease?

A
  1. Adenoma of anterior pituitary secretes large
    amounts of ACTH
  2. “Ectopic secretion” of ACTH by non-pituitary
    tumor such as the lungs
  3. “Ectopic secretion” of corticotropin-releasing
    hormone (CRH) by non-pituitary tumor
83
Q

What is ACTH-independent cushing’s syndorme?

A
  1. Adenomas of the adrenal cortex overproducing
    Cortisol
  2. Primary nodular hyperplasia of the adrenal
    gland causing overproduction of Cortisol
84
Q

What are manifestations of cushings syndrome/disease?

A
  • Moon facies with erythema
    and telangiectases of cheeks
    and forehead
  • Increased fat deposition in
    the supraclavicular fossae
    and dorsocervical area
    (buffalo hump)
85
Q

What are orofacial features of hypercortisolism (Cushing’s syndrome/disease)?

A
  • Round, moon face (muscle wasting & fat accumulation)
  • Fragile surface capillaries  susceptible to hematomas after
    mild trauma
  • Acne and excessive facial hair (hirsutism)
  • Delayed growth and development (skeletal and dental structures)
  • Increased pigmentation of buccal mucosa if due to ACTH
    excess
86
Q

What are immunosuppressions of hypercortisolism?

A
  • oral candidiasis
  • Recurrent herpes labialis
  • herpes zoster infections
  • gingival and periodontal diseases
  • impaired wound healing
87
Q

What are the three types of adrenal diseases and what they’re associated with

A

Conn’s syndrome - mineralocorticoids
Pheochromocytoma- catecholamines
Cushing’s syndorme/disease - glucocorticoids

88
Q

What is pheochromocytoma?

A

Sudden releases of hormone causing sudden “attack” due to chromaffin cell
tumor in the Adrenal Medulla resulting in excessive secretion of EPI and NE

89
Q

What are signs and symptoms of excess NE and EPI?

A

Hypertension, Tachycardia, Palpitations, Headache, Sweating, Tremors, Weight
Loss, Hyperglycemia, Orthostatic
Hypotension

90
Q

What is termed”the great masquareder”?

A

Pheochromocytoma