Adrenal Hormones Flashcards
what are the 3 pathways of that produce adrenal hormones? what structure do they associate with?
glucocorticoid pathway - zona fasciculata
mineralcorticoid pathways - zona glomerulosa
androgen pathway - zona reticularis
what is the zona glomerulosa?
most superficial layer of the adrenal cortex
what is the zona fasciculata?
the middle layer of the adrenal cortex
what is the zona reticularis?
the innermost layer of the adrenal cortex
what hormone(s) is the zona glomerulosa responsible for producing?
aldosterone
what hormone(s) is the zona fasciculata responsible for producing?
cortisol and androgens
what hormone(s) is the zona reticularis responsible for producing?
androgens
what is the medulla responsible for producing?
catecholamines
what is ACTH? what is its function?
adrenocorticotropin hormone
key regulator of conversion of cholesterol to pregnenolone (mineralocorticoid pathway)
what are the hormones/molecules involved in the mineralocorticoid pathway? list them in order of when they appear in the pathway.
1) cholesterol
2) pregnenolone
3) progesterone
4) 11-deoxycorticosterone
5) corticosterone
6) 18-hydroxycorticosterone
7) aldosterone
what hormones/molecules are involved in the glucocorticoid pathway? list them in order of when they appear in the pathway.
1) 17alpha-hydroxypregnenolone
2) 17alpha-hydroxyprogesterone
3) 11-deoxycortisol
4) cortisol
what hormones/molecules are involved in the androgen pathway? list them in order of when they appear in the pathway.
1) dehydroepiandrosterone (DHEA)
2) androstenedione
give two examples of the following:
glucocorticoids
mineralocorticoids
androgens
gluco - cortisol, corticosterone
mineral - aldosterone, deoxycorticosterone
andro - DHEA, androstenedione
what does cortisol bind to in circulation? how does it affect various molecules?
transcortin
effects intermediary metabolism of carbs (makes Glc available to brain by inhibiting other tissues from using it), lipids (breakdown in adipose tissue to FAs and glycerol), and proteins (stimulates breakdown to AA)
What are the anti-inflammatory actions caused by glucocorticoids?
1) inhibit local reaction to injury
2) decrease local release of degradative enzymes
3) decrease fibroblast proliferation and collagen deposition
what are the immunosuppresion actions caused by glucocorticoids?
1) inhibit IL-1 production by macrophages, decreasing T cell recruitment
2) inhibit IL-2 production by T-helper cells, decreasing T and B cell recruitment
3) induce apoptosis of T cells
What is the hypothalamus-pituitary adrenal axis feedback regulation?
1) hypothalamus releases CRH (positive release to pituitary)
2) pituitary releases ACTH (positive release to adrenal cortex)
3) Adrenal cortex releases:
a) DHEA (negative feedback on H-P-G axis)
b) Aldosterone
c) Cortisol
what is involved in the negative feedback on pituitary-adrenal axis by glucocorticoids?
Strong negative feedback on hypothalamus/pituitary
Inhibits ACTH production
Causes atrophy of anterior pituitary corticotropes (no acquired ACTH) and of adrenal cortex (lack of ACTH stimulation)
what is the function of aldosterone?
controls body fluid volume, leading to increased Na reabsorption in kidneys
what stimulates aldosterone secretion?
RAAS activation responding to low BP, low plasma Na, or high plasma K
ACTH (minor)
what is the function of DHEA in females?
1) enhancement of pubertal growth spurt
2) maintains secondary sex characteristics (pubic and axillary hair)
3) libido (sex drive)
4) conversion by aromatose to estrogen via testosterone in peripheral tissue
what two conditions could arise due to excess of aldosterone?
primary aldosteronism (Conn's disease) secondary aldosteronism
what is the difference between primary and secondary aldosteronism?
primary - caused by a hypersecreting tumour of zona glomerulosa
secondary - caused by high renin-angiotensin
what are some symptoms of excess aldosterone?
hypernatremia
hypokalemia
hypertension
what condition could arise due to excess cortisol?
Cushing’s syndrome
what causes cushing’s syndrome? (3pts)
excess CRH/ACTH (hypoth disorder, pituitary tumour)
adrenal tumour
ectopic ACTH (lung cancer)
what are some symptoms of excess cortisol?
hyperglycemia
insulin resistance
decreased immune response
what condition could arise from excess androgen?
congenital adrenal hyperplasia (CAH) (adrenogenita syndrome in females)
what causes congenital adrenal hyperplasia?
genetic deficiency in cortisol synthetic enzymes (21-OH and 11-OH)
what are some symptoms of excess androgen?
inappropriate masculinization
pseudohermaphroditism
virilization in females
pseudopuberty in males
what could cause enzyme deficiencies in CAH?
absence of negative feedback on ACTH and hypothalamus
what condition could arise from a deficiency in cortisol/aldosterone?
addision’s disease (primary adrenal insufficiency)
what causes addison’s disease?
destruction or atrophy of adrenal cortex
what are some symptoms of cortisol/aldosterone deficiency?
poor response to stress
hypoglycemia
low metabolic activities
what condition could arise due to cortisol (only) deficiency?
secondary adrenal insufficiency
what causes secondary adrenal insufficiency?
insufficient ACTH-hypoth/pituitary failure
what are some symptoms of cortisol (only) deficiency? (10pts)
hyperkalemia decreased HR weakness arrhythmias hyponatremia edema headache confusion muscle cramps hypotension
what 2 hormones are produced by the medulla?
norepinephrine
epinephrine
how are NE and E produced in the medulla? identify the hormones/molecules in the order they appear in the pathway.
1) tyrosine
2) hydroxylated to DOPA
3) decarboxylated to DA
4) NE
5) E
what receptors regulate effects of NE and E on target organs?
alpha and beta adrenergic receptors
name 3 catecholamines
DA
NE
E
What is special about the alpha and beta adrenergic receptors?
they exert opposite effects, even if stimulated by the same hormones
if two different hormones stimulate the same receptor, the affect will be similar
name various impacts binding of NE or E to an alpha receptor has on the body (7pts)
1) increase gluconeogenesis
2) increase arterial constriction
3) increase muscle contraction (GI, urinary)
4) decrease insulin secretion
5) increase growth hormone secretion
6) increase sweating
7) increase pupil dilation
name various impacts binding of NE or E to an beta receptor has on the body (10pts)
1) increase glycogenolysis
2) increase lipolysis and ketosis
3) decrease Glc utilization
4) increase arterial dilation
5) increase cardiac contractility (beta1), increase HR
6) increase muscle relaxation (beta2) (GI, bronchial, urinary)
7) increase insulin secretion
8) increase renin secretion
9) increase thyroid hormone secretion
10) increase pupil contraction
what is pheochromocytoma?
tumours arising from chromaffin cells in the SNS (mostly adrenal) that release large quantities of E/NE (sometime DA)
what are some symptoms of pheochromocytoma? (7pts)
hypertension increased HR (palpitations) hyperglycemia anxiety headache wt loss sweating
what are 2 ways to treat pheochromocytoma?
surgery
alpha and beta receptor blockers
what is stress?
generalized, non-specific response of the body to any factor (stressor) that overwhelms/threatens to overwhelm the body’s compensatory abilities to maintain a state of homeostasis
what hormones do stressors promote the release of?
cortisol
what is the pathway for a stressor causing adrenal cortisol release?
Stressor
CRF (corticotropin-releasing hormone)
ACTH
what is the pathway for a stressor causing release of adrenal epinephrine?
stressor
sym nerve
adrenal epinephrine
what are 3 main effects adrenal epinephrine release has on the body?
1) increased blood Glc and FAs
2) increased glucagon and decreased insulin (leading to increased Glc and FAs)
3) increased vasodilation, angiotensin and NaCl/H2O retention (leads to decreased blood flow to kidneys which increases aldosterone)
what is the pathway for a stressor causing increased water retention?
stressor
vasopressin
H2O retention
