adrenal gland physilogy Flashcards
1
Q
1. Where are the adrenal glands located?
A
On top of the kidneys. Also known as suprarenal glands.
2
Q
- How many layers does the adrenal cortex have, and what are they?
A
The adrenal cortex has three layers: Zona glomerulosa, Zona fasciculata, and Zona reticularis.
3
Q
- What is the composition of the adrenal medulla?
A
The adrenal medulla is made up of neural tissue.
4
Q
- What is the role of the juxtaglomerular cells (JG cells) in response to low blood pressure?
A
JG cells produce renin, which acts on angiotensinogen to produce angiotensin I, leading to the formation of angiotensin II (ATII).
5
Q
- What is the primary effect of ATII on the adrenal cortex?
A
ATII stimulates the zona glomerulosa of the adrenal cortex, activating an intracellular cascade that leads to aldosterone synthesis.
6
Q
- What are the two conditions that constitute a strong stimulus for aldosterone synthesis?
A
Hyponatremia (low sodium levels) and hyperkalemia (high potassium levels).
7
Q
- What is the role of ACTH in the stimulation of the adrenal cortex?
A
ACTH, produced by the corticotropes in the adenohypophysis, stimulates the adrenal cortex, particularly the zona glomerulosa, to produce aldosterone.
8
Q
- What is the role of CRH in the hypothalamic-pituitary-adrenal axis?
A
Corticotropin-releasing hormone (CRH) is produced by the paraventricular nucleus of the hypothalamus and stimulates the release of ACTH from the adenohypophysis.
9
Q
- What is the primary effect of ACTH on the adrenal cortex at the cellular level?
A
ACTH activates an intracellular cascade, leading to the production of aldosterone in the zona glomerulosa.
10
Q
- What are the three layers of the adrenal cortex and their respective locations?
A
Zona glomerulosa (most superficial), Zona fasciculata (in the middle, thickest), and Zona reticularis (the deepest).
11
Q
- What inhibits the synthesis of aldosterone and under what conditions is it secreted?
A
Atrial natriuretic peptide (ANP) inhibits aldosterone synthesis and is secreted when blood pressure is high.
12
Q
- What is the role of ANP in inhibiting aldosterone synthesis?
A
ANP binds to specific receptors, activating a G inhibitory pathway that results in potassium efflux out of the cell.
13
Q
- What is the basic unit required for the synthesis of steroid hormones in the adrenal cortex?
A
Cholesterol serves as the basic unit for the synthesis of steroid hormones in the adrenal cortex.
14
Q
- What is the enzyme responsible for converting cholesterol to pregnenolone in aldosterone synthesis?
A
21-hydroxylase converts cholesterol to pregnenolone in aldosterone synthesis.
15
Q
- How is cortisol transported in the bloodstream, and what proteins does it bind to?
A
Cortisol is transported by binding to corticosteroid binding globulin (CBG or transcortin) and sometimes to albumin, a protein synthesized by the liver.
16
Q
- What is the function of sodium-potassium ATPase in the cells of the distal convoluted tubule (DCT)?
A
Sodium-potassium ATPase pumps 3Na+ out of the cell and 2K+ into the cell, utilizing ATP.
17
Q
- What is the role of protein channels for Na+ in the luminal membrane of the DCT cells?
A
These channels bring Na+ from the filtrate into the cell, and from the cell, it goes into the blood in response to the hyponatremia stimulus.
18
Q
- How does aldosterone influence water reabsorption in the DCT?
A
Aldosterone, in response to the strongest synthesis, causes “water follows sodium,” enhancing water reabsorption.
19
Q
- What is the function of protein channels for K+ in the luminal membrane of the DCT cells?
A
These channels move potassium from the blood into the filtrate to be lost in the urine in response to the hyperkalemia stimulus.
20
Q
- What are the effects of aldosterone on the distal convoluted tubule (DCT) cells at the molecular level?
A
Aldosterone activates specific gene sequences, leading to the production of proteins such as sodium-potassium ATPase and ion channels for Na+ and K+.
21
Q
- What are the two main parts of the adrenal gland, and where are they located in the body?
A
The two main parts of the adrenal gland are the cortex and the medulla. They sit on top of the kidneys in the abdominal cavity below the diaphragm.
22
Q
- How many layers does the adrenal cortex have, and what are their names?
A
The adrenal cortex has three layers: Zona glomerulosa (most superficial), Zona fasciculata (in the middle and thickest), and Zona reticularis (the deepest).
23
Q
- What type of tissue makes up the adrenal cortex layers?
A
All layers of the adrenal cortex are mostly composed of glandular cuboidal epithelial tissue.
24
Q
- What is the adrenal medulla made of, and how many layers does it have?
A
The adrenal medulla is made up of neural tissue and has only one layer.
25
5. What hormone is secreted by the paraventricular nucleus in the hypothalamus to stimulate cortisol synthesis?
Corticotropin-releasing hormone (CRH) is secreted by the paraventricular nucleus in the hypothalamus to stimulate cortisol synthesis.
26
6. What cells in the adenohypophysis are stimulated by CRH to release a hormone into the bloodstream?
Corticotropes in the adenohypophysis are stimulated by CRH to release adrenocorticotropic hormone (ACTH) into the bloodstream.
27
7. What is the role of ACTH in cortisol synthesis, and how does it exert its effects on the adrenal cortex?
ACTH binds to a G protein-coupled receptor, triggering an intracellular cascade that activates adenylate cyclase. This leads to an increase in cAMP and the activation of protein kinase A (pkA), stimulating cortisol synthesis in the adrenal cortex.
28
8. What is the basic unit required for cortisol synthesis, and how is it converted to pregnenolone?
Cholesterol serves as the basic unit for cortisol synthesis, and it is converted to pregnenolone by the enzyme 21-hydroxylase.
29
9. What proteins transport cortisol in the bloodstream, and what percentage binds to each?
Cortisol is transported by binding to corticosteroid binding globulin (CBG or transcortin) (~75%) and albumin (~25%), a protein synthesized by the liver.
30
10. What stimulates cortisol synthesis, and how does the activation of pkA influence this process?
Cortisol synthesis is stimulated by ACTH, and the activation of pkA by phosphorylation influences the enzymes catalyzing the pathway, enhancing cortisol synthesis.
31
1. What is the primary effect of cortisol on skeletal muscles, and how does it achieve this effect?
Cortisol stimulates protein catabolism in muscles, breaking down proteins into amino acids. This is achieved by activating specific genes in the nucleus, leading to the production of proteases that break peptide bonds inside proteins.
32
2. What is the process called when cortisol stimulates protein breakdown in muscles, and what is the fate of the amino acids released?
The process is called protein catabolism. Amino acids released into the bloodstream go to the liver.
33
3. How does cortisol influence catabolism within bones?
Cortisol stimulates catabolism within the bones.
34
4. What is the primary effect of cortisol on adipose tissue, and what process does it stimulate?
Cortisol stimulates lipolysis in adipose tissue, breaking down triglycerides into fatty acids and glycerol.
35
5. What happens to the fatty acids released during cortisol-induced lipolysis?
Fatty acids can be utilized by the muscles or redistributed and relocated to different parts of the body.
36
6. What process in the liver does cortisol stimulate, and what are the two main components of this process?
Cortisol stimulates gluconeogenesis and glycogenesis in the liver. Gluconeogenesis is the production of glucose from non-carbohydrate sources, including amino acids, lactic acid, glycerol, and odd-chain fatty acids. Glycogenesis is the conversion of glucose into glycogen, a storage molecule for glucose.
37
7. How does cortisol influence the sympathetic nervous system, and what is its effect on the adrenergic receptors in the liver?
Cortisol enhances the sympathetic nervous system and acts on tissues sensitive to norepinephrine. There are adrenergic receptors on the liver that bind norepinephrine.
38
8. What is the overall effect of norepinephrine on the vessels in response to cortisol's influence on adrenergic receptors?
The overall effect of norepinephrine on the vessels is glycogenolysis, the conversion of glycogen into glucose
39
9. What are the direct and indirect effects of cortisol on glycogenesis and glycogenolysis in the liver?
Cortisol directly stimulates glycogenesis (conversion of glucose into glycogen) and indirectly stimulates glycogenolysis (conversion of glycogen into glucose) by increasing the sensitivity of adrenergic receptors for norepinephrine.
40
10. How does cortisol influence blood vessels, and what is its effect on adrenergic receptors in smooth muscle cells?
Cortisol enhances the sympathetic nervous system and acts on adrenergic receptors in smooth muscle cells within the tunica media of vessels. It increases the sensitivity of these receptors, leading to vasoconstriction and amplifying the effects of norepinephrine on the vessels.
41
11. What is the overall effect of cortisol on blood vessels, and how does it relate to the sympathetic nervous system?
The overall effect of cortisol on blood vessels is vasoconstriction, and it amplifies the vasoconstriction initiated by the sympathetic nervous system.
42
12. How does cortisol affect the immune system, and which immune cells and processes does it inhibit?
Cortisol can inhibit specific processes inside immune cells. It inhibits basophils from secreting histamines, leukotrienes, and prostaglandins, and it inhibits lymphocytes and monocytes from secreting interleukins and cytokines involved in the inflammatory immune response.
43
13. What are the main stimuli for cortisol release, and how does cortisol respond to hypoglycemia?
Hypoglycemia (low blood glucose levels) is one of the main stimuli for cortisol release. In response to hypoglycemia, cortisol indirectly stimulates glycogenolysis and directly stimulates gluconeogenesis and glycogenesis, helping to raise blood glucose levels.
44
14. What is another stimulus for cortisol release, and how does cortisol respond to long-term stress?
Long-term (chronic) stress is another stimulus for cortisol release. In response to long-term stress, cortisol increases the sensitivity of adrenergic receptors in smooth muscle cells, enhances muscle catabolism to provide nutrients, and depresses the immune system.
45
What is the impact of long-term stress, such as preparing for finals, on the immune system?
Long-term stress, like preparing for finals, can depress the immune system, making individuals more susceptible to infections. Microorganisms can cause damage due to the weakened immune response, often leading to illness before finals.
46
How is cortisol utilized in the treatment of leukemia?
Cortisol is employed in leukemia treatment by depressing the bone marrow and inhibiting white blood cells. It also prevents already formed cells from producing inflammatory cytokines, contributing to its therapeutic effects.
47
What feedback mechanism is triggered by elevated cortisol levels in the blood?
Elevated cortisol levels initiate a negative feedback loop on the hypothalamus and inhibit the adenohypophysis from producing ACTH. This negative feedback helps regulate cortisol levels in the blood.
48
What happens when cortisol levels decrease in the blood?
When cortisol levels decrease, there's insufficient inhibition on the hypothalamus and adenohypophysis. This leads to stimulation of the nuclei to produce more CRH, which, in turn, stimulates the pituitary to produce more ACTH. Ultimately, this increased ACTH stimulates the synthesis of cortisol.
49
What are the main parts of the adrenal gland?
The adrenal gland consists of the cortex and the medulla. The cortex is further divided into three layers: Zona glomerulosa (superficial), Zona fasciculata (middle and thickest), and Zona reticularis (deepest). The medulla is composed of neural tissue.
50
Describe the synthesis of androstenedione.
Androstenedione synthesis begins with the secretion of corticotropin-releasing hormone (CRH) from the paraventricular nucleus of the hypothalamus. CRH stimulates corticotropes in the adenohypophysis to release adrenocorticotropic hormone (ACTH). ACTH, in turn, triggers a cascade involving G-proteins, adenylate cyclase, and protein kinase A (pkA). In the zona reticularis of the adrenal cortex, steroid hormones, including androstenedione, are synthesized from cholesterol. This process is regulated by enzymes and involves the activation of pkA through phosphorylation.
51
What is the role of ACTH in androstenedione synthesis?
Adrenocorticotropic hormone (ACTH) plays a crucial role in androstenedione synthesis. It is released in response to corticotropin-releasing hormone (CRH) and binds to a G-protein coupled receptor on the adrenal cortex cells. This binding triggers an intracellular cascade involving adenylate cyclase, GTPase, and protein kinase A (pkA), ultimately leading to the synthesis of androstenedione and other steroid hormones in the zona reticularis.
52
What alternative pathway exists in androstenedione synthesis?
An alternative pathway involves the conversion of cholesterol to pregnenolone, with subsequent synthesis of weak sex hormones, DHEA (dehydroepiandrosterone), and androstenedione. These gonadocorticoids are produced in the zona reticularis of the adrenal cortex and contribute to the overall synthesis of androstenedione.
53
What is the general function of androstenedione?
Androstenedione is a weak sex hormone classified as a gonadocorticoid. Its general function involves contributing to the synthesis of other sex hormones.
54
What are the effects of androstenedione in males?
In males, androstenedione goes to the testes, where it gets converted to testosterone in minimal amounts. It increases libido (sex drive), stimulates the development of secondary sex characteristics, including pubic, axillary, and facial hair growth, and stimulates the secretions of the sebaceous glands of the skin.
55
What are the effects of androstenedione in females?
In females, androstenedione goes to the theca cells in the ovaries, where it gets converted to estrogen in minimal amounts. It increases libido (sex drive), stimulates the development of secondary sex characteristics, including the growth of mammary glands (breasts) and pubic and axillary hair growth, and stimulates the secretions of the sebaceous glands of the skin. Excessive DHEA and androstenedione production in females can lead to clitoral enlargement resembling a small penis.
56
What is the outer layer of the adrenal cortex?
Zona glomerulosa
57
What is the middle layer of the adrenal cortex?
Zona fasciculata
58
What tissue is the adrenal medulla made of?
Neural
59
What does the paraventricular nucleus secrete?
CRH (Corticotropin-releasing hormone)
60
What is the basic unit required for androstenedione synthesis?
Cholesterol
61
Where does androstenedione convert to testosterone in males?
Testicles
62
Where does androstenedione convert to estrogen in females?
Theca cells of the ovaries
63
What are the effects of testosterone in males?
Libido, facial hair growth, deep voice
64
What are the effects of estrogen in females?
Stimulates the growth of the breasts
65
Where do the adrenal glands sit, and what is their shape?
The adrenal glands sit on top of the kidneys and have a roughly pyramid shape.
66
2. How many layers does the adrenal cortex have, and what are their names?
The adrenal cortex has three layers: Zona glomerulosa (most superficial), Zona fasciculata (in the middle and thickest), and Zona reticularis (the deepest).
67
3. What is the composition of the adrenal medulla?
The adrenal medulla is made up of neural tissue - chromaffin cells, which are the cell bodies of the postganglionic motor neurons of the sympathetic nervous system.
68
4. What is the primary stimulus for the sympathetic nervous system (SNS), and in what situations does it activate?
Short-term (acute) stress is the primary stimulus for the SNS, activating in "fight or flight" situations, such as escaping from a threat.
69
5. How does the hypothalamus contribute to activating the SNS?
The hypothalamus, a strong regulator, sends presynaptic potentials through descending fibers to the lateral gray horn (LGH) of the spinal cord (Th1 to L2), activating the SNS.
70
6. Describe the anatomy of preganglionic and postganglionic neurons in the adrenal medulla.
In the adrenal medulla, preganglionic motor neurons are long and reach postganglionic cell bodies. Postganglionic neurons are very short, with cell bodies located inside the adrenal medulla, forming an intramural ganglion.
71
7. What neurotransmitter is released by preganglionic motor neurons in the SNS, and what receptors does it bind to?
Preganglionic motor neurons in the SNS are cholinergic and release acetylcholine. It binds to nicotinic receptors on chromaffin cells.
72
8. What is the primary pathway for preganglionic and postganglionic neurons in the sympathetic nervous system?
In most cases, preganglionic neurons are short and go to the chain ganglia, while postganglionic neurons are long and begin from the chain ganglia. However, in the adrenal medulla, preganglionic motor neurons are long and reach postganglionic cell bodies inside the organ, forming an intramural ganglion.
73
9. What is the building block of catecholamine synthesis, and what are the successive conversions in this pathway?
Tyrosine is the building block. It is converted to L-DOPA by tyrosine hydroxylase. L-DOPA is then converted to dopamine by DOPA decarboxylase. Dopamine is further converted to norepinephrine and, finally, to epinephrine by phenylethanolamine n-methyltransferase (PNMT).
74
10. How does the sympathetic nervous system respond to short-term stress?
The SNS responds to short-term (acute) stress, such as "fight or flight" situations, by being the primary stimulus. It is activated by the hypothalamus, leading to the release of catecholamines (epinephrine and norepinephrine) from the adrenal medulla.
75
1. What are the proportions of epinephrine and norepinephrine secreted at the synapse of postganglionic motor neurons?
80% epinephrine and 20% norepinephrine.
76
2. How are epinephrine and norepinephrine normally stored in the presynaptic terminal?
They are presynthesized, put into vesicles, and located in the terminal bulb of the axon.
77
3. What happens when Na+ enters the cell in the postganglionic motor neuron?
Action potentials are produced down the axon. When they reach the terminal bulb and the potential reaches +30 mV, Ca++ channels open, allowing Ca++ to flow in.
78
4. How does Ca++ act as a bridge in catecholamine release?
Ca++ causes the vesicles to merge with the cell membrane, releasing epinephrine and norepinephrine into the bloodstream.
79
5. What is the primary effect of epinephrine on the liver?
It activates a G stimulatory protein, leading to the activation of adenylate cyclase on the cell membrane. This activates a cascade, ultimately resulting in glycogenolysis and gluconeogenesis, leading to hyperglycemia.
80
6. Describe the process of glycogenolysis in the liver stimulated by catecholamines.
Catecholamines stimulate the breakdown of glycogen (polymer of glucose) in the liver into individual monomers (glucose) through enzymes like glycogen phosphorylase and debranching enzymes.
81
7. What is the overall result of glycogenolysis and gluconeogenesis in the liver?
The overall result is glucose production, leading to hyperglycemia. Glucose can be utilized by the muscles for contraction.
82
8. How do catecholamines affect adipose tissue?
Catecholamines bind to a G protein-coupled receptor, activating hormone-sensitive lipase (HSL), which breaks down triglycerides into fatty acids and glycerol. Glycerol goes to the liver and is converted to glucose, while fatty acids go to the muscles, undergo beta-oxidation, and produce ATP, aiding in muscle contraction.
83
9. What is the role of catecholamines in the heart?
Catecholamines stimulate the expression of beta-1-adrenergic receptors in cardiomyocytes, and these receptors bind catecholamines. They also affect non-contractile muscle cells of the SA node and the AV node, stimulating the expression of beta-1-adrenergic receptors, which also bind catecholamines.
84
1. What is the effect of catecholamines on blood vessels?
Catecholamines also bind to alpha-1-adrenergic receptors on some blood vessels, causing vasoconstriction, which increases blood pressure to deliver nutrients quickly to vital tissues.
85
2. How do catecholamines affect the smooth muscle of bronchi?
Catecholamines act on the smooth muscle surrounding the bronchi by binding to alpha-2-adrenergic receptors, causing bronchioles to dilate.
86
3. What happens to the blood vessels going to the GI tract in response to catecholamines?
The vessels going to the GI tract constrict, diverting blood to skeletal muscles, brain, heart, etc., resulting in decreased GI tract activity.
87
4. What occurs in the blood vessels going to the kidneys in response to catecholamines?
The blood vessels going to the kidneys constrict and divert blood.
88
5. What happens to the blood vessels in the skin in response to catecholamines?
The blood vessels in the skin constrict and divert blood.
89
6. Which layer of the adrenal cortex is innermost?
Zona reticularis
90
7. What tissue is the adrenal medulla made of?
Neural
91
8. True statement about the adrenal medulla?
Has one layer
92
9. Primary stimulus of the sympathetic nervous system (SNS)?
Acute stress
93
10. What is the building block of the epinephrine pathway?
Tyrosine
94
11. Which enzyme converts dopamine to norepinephrine?
Dopamine beta hydroxylase
95
12. Effects of catecholamines on the liver?
Stimulating glycogenolysis and gluconeogenesis, leading to hyperglycemia.
96
13. Effects of catecholamines on the heart?
All of the above (↑ heart rate, ↑ cardiac output, ↑ stroke volume).
97
14. Effects of catecholamines on the lungs?
Bronchodilatation
98
15. What is wrong regarding the effects of catecholamines?
Stimulating lipogenesis (The correct effects are ↑ blood pressure, stimulating glycogenolysis, and ↓ GI tract activity).
99
1. What hormone does the paraventricular nucleus secrete?
Corticotropin-releasing hormone (CRH)
100
2. Where does CRH go after secretion?
CRH goes into the hypophyseal portal system, the vascular connection between the hypothalamus and the anterior pituitary (adenohypophysis).
101
3. What do corticotropes in the adenohypophysis secrete?
Corticotropes secrete α-MSH and adrenocorticotropic hormone (ACTH) into the bloodstream.
102
4. What is the main stimulus for the zona glomerulosa?
Other stimuli for the zona glomerulosa include Angiotensin 2 (ATII), hyponatremia (low plasma Na+ ions), and hyperkalemia (high plasma K+ ions).
103
5. What inhibits the zona glomerulosa?
The atrial natriuretic peptide (ANP) inhibits the zona glomerulosa.
104
6. What does the zona fasciculata secrete?
Zona fasciculata secretes glucocorticoids, chemicals responsible for quick control over metabolic activities related to glucose, with cortisol being the main one.
105
7. What chemicals does the zona reticularis secrete?
Zona reticularis secretes gonadocorticoids, including dehydroepiandrosterone (DHEA) and andostenedione, collectively called androgens.
106
8. What is the adrenal medulla made of?
The adrenal medulla is made up of neural tissue and contains postganglionic motor neurons stimulated by the sympathetic nervous system (SNS).
107
9. What hormones does the adrenal medulla secrete?
The adrenal medulla secretes catecholamines, including epinephrine and norepinephrine.
108
10. What are the effects of catecholamines?
Catecholamine effects include increasing blood pressure, glycogenolysis, gluconeogenesis, and lipolysis.
109
11. What does aldosterone stimulate in the kidneys?
Aldosterone stimulates Na+ reabsorption, pulling sodium from the glomerular filtrate and putting it into the blood. It also promotes K+ excretion.
110
1. What are the effects of cortisol on white blood cells?
Inhibits the release of cytokines and other chemicals.
111
2. How does cortisol affect skeletal muscles?
Stimulates protein catabolism, which is the breakdown of proteins into amino acids.
112
3. What effect does cortisol have on adipose tissue?
Stimulates lipolysis, the breakdown of triglycerides into fatty acids and glycerol.
113
4. What does cortisol do in the liver?
Stimulates gluconeogenesis, the conversion of non-carbohydrate sources (amino acids, glycerol, etc.) into glucose.
114
5. How does cortisol enhance the sympathetic nervous system?
Increases the adrenergic receptors.
115
6. What are the primary effects of androgens?
Control the libido, the sex drive.
116
7. What is the mechanism of feedback for cortisol?
↑ levels of cortisol exert a negative feedback on the hypothalamus, inhibiting the adenohypophysis production of ACTH. ↓ levels of cortisol result in the stimulation of CRH and ACTH production.
117
8. What is an effect of cortisol on the human body?
d) All of the above (Protein breakdown, ↑ lipolysis, Immunosuppression)
118
9. What does the zona reticularis secrete?
d) Androgens
119
10. What tissue is the adrenal medulla made of?
d) Neural
120
11. What is the inner layer of the adrenal cortex?
d) Zona reticularis
121
12. What does the adrenal medulla secrete?
b) Epinephrine
122
13. What does the zona fasciculata secrete?
c) Cortisol
123
14. Which is the WRONG effect of aldosterone?
c) Increase in serum potassium level
124
15. What is an effect of catecholamines?
c) Stimulating glycolysis
125
16. How does a high level of cortisol affect ACTH?
b) Inhibits ACTH production
126
17. What is the effect of cortisol on the liver?
c) Stimulation of gluconeogenesis
127
1. How does cholesterol convert to pregnenolone in adrenal corticosteroid biosynthesis?
Cholesterol → pregnenolone via P-450scc (rate limiting).
128
2. Where is aldosterone synthesized in the adrenal cortex?
Aldosterone is synthesized in the zona glomerulosa.
129
3. In which region of the adrenal cortex is cortisol synthesized?
Cortisol is synthesized in the zona fasciculata.
130
4. What hormones are synthesized in the zona reticularis?
DHEA and androstenedione are synthesized in the zona reticularis, convertible to testosterone and dihydrotestosterone by 5⍺ reductase in peripheral tissues.
131
5. What clinical conditions are associated with defective corticosteroid synthesis?
Disorders are associated with defects in the enzymes of corticosteroid synthesis pathways.
132
6. What is the primary regulatory axis for cortisol and androgen production in the adrenal glands?
The primary regulatory axis is the HPA (Hypothalamus-Pituitary-Adrenal) axis.
133
7. How is cortisol and androgen production regulated in the HPA axis?
Cortisol and androgen production in the HPA axis is regulated by hormones produced by the hypothalamus and anterior pituitary gland.
134
8. What system regulates aldosterone in the adrenal glands?
Aldosterone is regulated by the renin-angiotensin-aldosterone system (RAAS).
135
9. What activates the RAAS system and what are its effects?
The RAAS system is activated in response to decreased blood pressure, leading to the production of angiotensinogen II causing vasoconstriction and aldosterone release.
136
10. Where can DHEA and androstenedione be converted into testosterone and dihydrotestosterone?
They can be converted in peripheral tissues by 5⍺ reductase.
137
What is the mechanism of action for corticosteroids?
Corticosteroids bind to intracellular receptors, primarily nuclear. The receptor/ligand complex then binds to DNA, affecting transcription.
138
2. Name the classes of steroid receptors.
Glucocorticoid, Mineralocorticoid, Progestin, Oestrogen, Androgen, Vitamin D.
139
3. List major actions of cortisol in the circulatory/renal system.
- Increases cardiac output. - Raises blood pressure. - Enhances renal blood flow and glomerular filtration rate (GFR).
140
4. What are the CNS effects of cortisol?
- Mood lability. - Euphoria/psychosis (in excess). - Decreased libido.
141
5. How does cortisol affect bone/connective tissue?
- Accelerates osteoporosis. - Decreases serum calcium. - Inhibits collagen formation. - Delays wound healing.
142
6. What immunological effects does cortisol have?
- Decreases capillary dilation/permeability. - Inhibits leucocyte migration. - Suppresses macrophage activity. - Reduces inflammatory cytokine production.
143
7. What metabolic changes occur with cortisol?
- Carbohydrate: Increases blood sugar. - Lipid: Increases lipolysis, central redistribution. - Protein: Increases proteolysis.
144
8. What are the three main principles of clinical corticosteroid use?
- Suppress inflammation. - Suppress the immune system. - Replacement treatment.
145
9. In what forms can corticosteroids be administered?
Orally, IV (intravenous), IM (intramuscular), and topically.
146
10. Mention some clinical applications of corticosteroids.
- Allergic disease (e.g., asthma/anaphylaxis). - Inflammatory disease (e.g., rheumatoid arthritis, IBD). - Malignant disease.
147
1. What is the primary mechanism of action for aldosterone?
Aldosterone exerts its effects via the mineralocorticoid receptor, primarily expressed in the kidneys, as well as in the salivary glands, gut, and sweat glands.
148
2. Name the tissues/organs where mineralocorticoid receptors are expressed.
Primarily in the kidneys, as well as in the salivary glands, gut, and sweat glands.
149
3. What are the main actions of aldosterone?
- Sodium/potassium balance. - Blood pressure regulation. - Regulation of extracellular volume.
150
4. How are adrenaline and noradrenaline synthesized in the adrenal medulla?
Adrenaline and noradrenaline are derived from dopamine, which, in turn, is derived from tyrosine.
