Endo IV Adrenal Hormones Flashcards
is the adrenal cortex essential to life? adrenal medulla?
cortex- yes
medulla- no
what does the adrenal cortex secrete
-corticosteroids
- mineralocorticoids
- sex hormones
what does the adrenal medulla secrete and in response to what
EPI and NE in response to SNS
what are the hormones secreted by the adrenal cortex made from
cholesterol
what are the three layers of the cortex from outer to inner
-zona glomerulosa
- zona fasciculata
- zona reticularis
what is secreted in the zona glomerulosa
mineralocorticoids
what is secretion in the zona glomerulosa regulated by
the renin-angiotensin-aldosterone system (RAAS)
what does the zona fasciculata secrete
glucocorticoids
what is secretion by the zona fasciculata regulated by
the hypothalamic-pituitary-adrenal axis (HPA) - CRH, ACTH
what is secreted by the zona reticularis
androgens
what is secretion by the zona reticularis regulated by
HPA
what is secreted by the adrenal medulla
catecholamines
what secrete EPI and NE from the adrenal medulla
chromaffin cells
what enzyme converts cortisol to cortisone
HSD11B2
what enzyme converts cortisone to cortisol
HSD11B1
what is androstenedione used to make
estrogen and testosterone
what part of the cell do pathways for synthesis of steroid hormones in the adrenal cortex occur
in the mitochondria or endoplasmic reticulum
what does aldosterone do
increases renal tubular reabsorption of Na+ and secretion of K+ leading to an increase in EC fluid volume and Mean Arterial Pressure
what is aldosterone secretion stimulated by
-angiotensin II
- high K+ (hyperkalemia)
-low Na+ (hyponatremia)
what is aldosterone’s effect on salivary glands
greatly increases reabsorption of sodium and secretion of potassium by gland ducts, same effect as on renal tubules
what is aldosterone’s effect on sweat glands
conserves sodium in hot environments
what is aldosterone’s effect on salivary glands during high rates of salivary secretion
conserves sodium
describe the renin-angiotensin-aldosterone system and the results of it
- 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
what is renin released from
the kidneys
what is angiotensin converting enzyme (ACE) produced by
the endothelium
what is another term for primary hyperaldosteronism
Conn’s syndrome
what are the causes of primary hyperaldosteronism
-adrenal adenoma (benign)
- adrenal hyperplasia
- adrenal carcinoma (malignant)
what are the signs and symptoms of primary hyperaldosteronism
-hypertension
-hypernatremia
- potassium depletion
-low plasma renin
- hypokalemic alkalosis
- polyuria
- weakness
-headaches
what are the treatment options for primary hyperaldosteronism
-surgical removal of the tumor or most of the adrenal tissue when hyperplasia is the cause
- pharmacological antagonism of the mineralocorticoid receptor
what is secondary hyperaldosteronism caused by
-CHF
-renal artery stenosis
what are the signs and symptoms of secondary hyperaldosteronism
-high plasma renin activity
- hypernatremia with extracellular volume expansion
- edema
- decreased cardiac output
- similar clinical findings as primary hyperaldosteronism-hypertension
when is cortisol secreted
-with any stress
-trauma
-infection
- intense heat or cold
- injection of norepinephrine
- surgery
- hypoglycemia
- psychological stress
- any disease
what does cortisol cause in general
mobilization of the energy stores, suppresses the immune response, gluconeogenesis, protein mobilization, fat mobilization, stabilization of lysosomes
when is cortisol secretion the highest and what is the pattern of cortisol secretion
highest in the AM and the pattern is a circadian
what does cortisol negatively inhibit
ACTH secretion from anterior pituitary and the hypothalamus
why are other hormones secreted from the AP along with ACTH
because the gene for ACTH forms a larger protein- a preprohormone called proopiomelanocortin (POMC)
what hormones are secreted with ACTH
-MSH
- Beta endorphon
-beta lipotropin
what does MSH cause
formation of melanin pigment in mucus membranes and skin
which has a higher affinity for the mineralocorticoid receptor: cortisol or aldosterone
about the same
which has a higher circulating concentration: cortisol or aldosterone
cortisol, 1000 fold higher circulating concentration
with how much cortisol is circulating why doesnt it cause a mineralocorticoid effect
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
what does a genetic deficiency of 11beta HSD lead to
AME (apparent mineralocorticoid excess)
what does glycyrrhetinic acid do and what is it
a compound in licorice that inhibits the activity of 11 beta HSD
what can overwhelm the 11beta HSD enzyme
high circulating cortisol levels
what are the carbohydrate effects of cortisol on metabolism
-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
what are the protein effects of cortisol on metabolsim
-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
what are the lipid effects of cortisol on metabolism
-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)
what are the effects of low glucocorticoid levels
-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
what is 95% of glucocorticoid activity of the adrenal cortex due to
secretion of cortisol
what are the anti-inflammatory actions of cortisol
-stabilizes lysosomal membrane
-decreases capillary permeability
-decreases WBC migration and phagocytosis
- suppresses T lymphocytes proliferation
-decreases IL-1 secretion from WBCs
what can glucocorticoid treatment in anti-inflammatory diseases cause and why
can cause osteoporosis because:
-stimulates bone resorption (via increased RANKL)
- inhibits osteoblastic maturation and activity
-promotes apoptosis of osteoblasts and osteocytes
when does the zona reticularis secrete adrenal androgens
starts at age 8, peaks in early 20s and decreases with age
what adrenal androgens are secreted by the zona reticularis
-DHEA
-adrostenedione
- testosterone
which gender is more affected by adrenal androgens
weak in males, contributes 50% of active androgens in females
what do adrenal androgens do in females
growth of pubic and axillary hair and libido
what are some conditions resulting from excess androgen production
- 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
which is secreted in higher quanitties and which is more important: DHEA and androstenedione
DHEA is secreted in higher quanitites but androstenedione is more important because it is more readily converted into testosterone
where does conversion of androstenedione to 5-dihydrotestoterone and testosterone occur
in peripheral tissues
what do hormonally active benign adrenal adenomas usually secrete
aldosterone or cortisol
what are virulizing tumors in women likely to be caused by
ovarian tumors instead of adrenal tumors
what are some signs and symptoms of virulization
-male pattern baldness
- male musculatre
-irregular menses
what is primary adrenal insufficiency
primary atrophy or injury of adrenal cortex
in about 80% of US cases of primary hypoadrenalism atrophy is caused by ____
autoimmune destruction of ALL cortical zones
what are the levels of ACTH and corticosteroids in primary adrenal insufficiency
high ACTH and low corticosteroid production
what secretion is lost in primary adrenal insufficiency
glucocorticoid, mineralocorticoid, and adrenal androgen secretion
what is happening in secondary adrenal insufficiency
pituitary gland unable to secrete enough ACTH
what is secondary adrenal insufficiency commonly caused by
iatrogenic (medication caused) due to abrupt cessation of steroid therapy
what are the levels of ACTH and cortisol in secondary adrenal insufficiency
low ACTH and cortisol production
is mineralocorticoid secretion affected in secondary adrenal insufficiency
no
what are the signs and symptoms of glucocorticoid deficiency (low cortisol) in primary and secondary
-fatigue
- weight loss
- myalgia
- fever
- hypoglycemia
-low BP
- hyponatremia
what are the signs and symptoms of mineralocorticoid deficiency (low aldosterone) seen in primary
-salt craving
- low BP
- hyponatremia
- hyperkalemia
what are the signs and symptoms of adrenal androgen deficiency seen in primary and secondary
-lack of energy
- dry and itchy skin
-loss of libido
- loss of axillary and pubic hair
what disease causes hyperpigmentation and why
primary adrenal insufficiency due to excess POMC
what disease causes alabaster colored pale skin and why
secondary adrenal insufficiency due to deficiency of POMC
what are the oral manifestations of primary adrenal insufficiency
skin pigmentation seen in
- mucocutaneous junction lips
- intraoral mucosal surfaces
- buccal mucosa
-palate
-lingual surfaces of tongue
what causes skin pigmentation in addisions disease
ACTH causes increased MSH
what is the treatment for addisons disease
corticosteroids
what does the treatment for addisons disease cause
-immunosuppression
-suscpetibility to oral candidiasis
- recurrent herpes labialis
- herpes zoster infections
-gingival and periodontal diseases
-impaired wound helaing
what are the aspects of dental management for addisons patients
-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
what is the difference between cushings disease and cushings syndrome
disease is a secondary disorder in the brain, syndrome is a primary disorder in the adrenal cortex
which is ACTH independent: cushings disease or cushings syndrome
cushings syndrome
what are the possible causes of cushings disease
-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
what are the possible causes of cushings syndrome
-adenomas of the adrenal cortex overproducing cortisol
- primary nodular hyperplasia of the adrenal gland causing overproduction of cortisol
what are the manifestations of cushings syndrome/disease
-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
what are the oral manifestations of cushing sydrome/disease
-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
what are the 3 adrenal diseases and what causes them
- Conn’s syndrome (mineralocorticoids)
- Pheochromocytoma (catecholamines)
- cushing’s syndrome/disease (glucocorticoids)
what is pheochromocytoma caused by
sudden released of hormone causing sudden attack due to chromaffin cell tumor in the adrenal medulla resulting in excessive secretion of EPI and NE
what are the signs and symptoms of excess NE and EPI
-HTN
- tachycardia
-palpitations
-headache
-sweating
-tremors
-weight loss
-hyperglycemia
- orthostatic hypotension
what is the incidence rate of pheochromocytoma and when is onset
2-8 in 1 million person per year with mean age diagnosis of 40 but can occur from childhood to late life
