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Physiology 2 > Jan 27 - Adrenal Hormones > Flashcards

Jan 27 - Adrenal Hormones Flashcards

1
Q

Name the two parts of the adrenal gland, from superficial to deep

A

The adrenal cortex

The adrenal medulla

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2
Q

Name the three parts of the adrenal cortex, from superficial to deep

A

The zona glomerulosa
The zona fasciculata
The zona reticularis

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3
Q

What is the common precursor for all adrenal steroid hormones?

A

Cholesterol

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4
Q

What does the zona glomerulosa produce?

A

Aldosterone (the mineralocorticoid pathway)

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5
Q

What does the zona fasciculata produce?

A

Cortisol (the glucocorticoid pathway)

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6
Q

What does the zona reticularis produce?

A

Androstenedione (androgen pathway)

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7
Q

How does the pituitary affect the adrenal cortex?

A

It secretes adrenocorticotropin hormone (ACTH) which converts cholesterol into pregnenolone

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8
Q

What does angiotensin II do in the adrenal cortex?

A

It converts corticosterone into 18-hydroxycorticosterone (mineralocorticoid pathway)

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9
Q

What is cortisol bound to throughout circulation?

A

Transcortin

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10
Q

What are the functions of cortisol?

A

It stimulates protein breakdown to amino acids (especially muscles)
It facilitates lipid breakdown in adipose tissue to fatty acids and glycerol
It promotes hepatic gluconeogenesis (synthesis of glucose) from amino acids, glycerol and fatty acids (via oxaloacetate)
It makes glucose available to the brain by inhibiting utilization by other tissues

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11
Q

What is a permissive action of cortisol?

A

A small amount is required for metabolisms, especially those promoted by catecholamines (e.g. lipolysis, bronchodilation)

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12
Q

What are the anti-inflammatory effects of glucocorticoids?

A

They inhibit local reactions to injury (e.g., capillarie dilation, phagocytosis)
They reduce local release of degradative enzymes
They decrease fibroblast proliferation and collagen deposition

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13
Q

What are the immunosuppressive effects of glucocorticoids

A

They prevent organ/graft rejection and manage allergic disorders by inhibiting IL-1 production by macrophages (decrease T cell recruitment), inhibiting IL-2 production from T helper cells (reduce both T and B cell formation), induces apoptosis (programmed cell death) of T cells

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14
Q

What considerations should be taken into account for patients using glucocorticoids long term?

A

Impaired body’s defence against infections, etc.
Loss of bone mass
Atrophy of the adrenal (negative feedback on pituitary-adrenal axis)
Other metabolic effects (e.g. hyperglycemia)

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15
Q

Explain the negative feedback loop on the pituitary-adrenal axis by synthetic glucocorticoids

A

Synthetic glucocorticoids (e.g. dexamethasone) exert strong negative feedback on the hypothalamus and anterior pituitary. This inhibits ACTH production. The anterior pituitary corticotropes atrophies because no ACTH is required. The adrenal cortex atrophies because of the lack of stimulation by ACTH and there are low levels of cortisol, aldosterone and DHEA production

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16
Q

What is the major form of adrenal mineralocorticoids?

A

Aldosterone

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17
Q

What is the role of aldosterone?

A

It controls body fluid volume by increasing sodium reabsorption by the kidneys

18
Q

What stimulates aldosterone secretion?

A

Mainly by the activation of renin-angiotensin system in response to decreased blood pressure, low plasma sodium and high plasma potassium. Also, ACTH has a minor role

19
Q

What is DHEA?

A

Dehydroepiandrosterone. It’s a major form of adrenal androgens. It is a weak androgen (not important in males), however it is an important source (50%) of androgens in females

20
Q

What is DHEA important for in females?

A

The enhancement of pubertal growth spurt
It maintains secondary sex characteristics - pubic and axillary hair
It’s also important for the libido and some conversion of aromatase to estrogen (via testosterone) in peripheral tissues

21
Q

What is the name for the condition characterized by aldosterone excess? What are the causes? What are the symptoms?

A 
Primary hyperaldosteronism (Conn's syndrome) or Secondary hyperaldosteronism.
Conn's syndrome is caused by hypersecreting tumor of zona glomerulosa. Secondary hyperaldosteronism is caused by high renin-angiotensin.
The symptoms are hypernatremia (high Na), hypokalemia and hypertension
22
Q

What is the name for the condition characterized by cortisol excess? What are the causes? What are the symptoms?

A

Cushing’s syndrom
It is caused by excess CRH/ACTH (hypothalamus disorder, pituitary tumor) or by an adrenal tumor or by ectopic ACTH (e.g. lung cancer)
The symptoms are hyperglycemia, excess protein breakdown, abnormal fat distribution, insulin resistance, decreased immune response, decreased inflammatory response

23
Q

What is the name for the condition characterized by androgen excess? What are the causes? What are the symptoms?

A

Congenital adrenal hyperplasia aka CAH (adrenogenita syndrome in females)
It’s caused by a genetic deficiency in cortisol synthetic enzymes (21- and 11-OH)
The symptoms are inappropriate masculinization, pseudohermaphroditism and virilization in female, and pseudopuberty in boys

24
Q

What happens if the enzymes responsible for converting progesterone and hydroxyprogesterone into deoxycorticosterone and deoxycortisol, respectively, are absent?

A

There won’t be any aldosterone or cortisol, only androstenedione. This is caused by a genetic mutation. Because cortisol regulates the negative feedback loop in the hypothalamus and pituitary, there won’t be any inhibition of ACTH secretion. The adrenal gland will become very large (CAH

25
Q

How is congenital adrenal hyperplasia (CAH) treated?

A

Add cortisol and the regulation becomes normal

26
Q

What is the name for the condition characterized by cortisol and aldosterone deficiency? What are the causes?

A

Primary adrenal insufficiency (Addison’s disease)

It’s caused by the destruction, or atrophy, of the adrenal cortex

27
Q

What is the name for the condition characterized by cortisol deficiency? What are the causes?

A

Secondary adrenal insufficiency

It’s caused by insufficient ACTH (hypothalamus/pituitary failure)

28
Q

What are the symptoms of someone who has a cortisol deficiency?

A

Poor response to stress
Hypoglycemia
Low metabolic activities

29
Q

What are the symptoms of someone who has an aldosterone deficiency?

A

Hyperkalemia, which causes arrhythmia, decreased heart rate and weakness
Hyponatremia, which causes oedema, headache, confusion, muscle cramps, weakness
Hypotension

30
Q

What composes the adrenal medulla?

A

Modified postganglionic neurons without axons

31
Q

What do the cell bodies of the adrenal medulla produce?

A

The major adrenal hormones, epinephrine and norepinephrine

32
Q

How are the actions of the adrenal catecholamines exerted?

A

Their effects in their target organs are mediated by alpha and beta adrenergic receptors; target organ tissues may have one or more receptor types. The actions of one hormone mediated by the two classes of receptors often produce opposite effects (e.g. for epinephrine, alpha = vasoconstriction, beta2 = vasodilation. When exerted through the same type of receptor, epinephrine and norepinephrine exert similar effects

33
Q

What do alpha mediated receptors upregulate? What do they downregulate?

A

It upregulates gluconeogenesis, arterial constriction (renal, cutaneous), muscle contraction (GI, urinary), growth hormone secretion, sweating, dilation of pupils
It downregulates insulin secretion

34
Q

What do beta mediated receptors upregulate? What do they downregulate?

A

It upregulates glycogenolysis, lipolysis & ketosis, arteriolar dilation, cardiac contractility (beta1), heart rate, muscle relaxation (GI, bronchial, urinary; beta2), insulin secretion, renin secretion and thyroid hormone secretion
It downregulates glucose utilization

35
Q

What is a pheochromocytoma? What does it do?

A

A tumor arising from the chromaffin cells in the sympathetic nervous system, mostly in the adrenal gland. Ir releases large quantities of epinephrine and/or norepinephrine (and dopamine in some cases)

36
Q

What are the consequences of a pheochromocytoma?

A

Hypertension, increased heart rate (palpitations), hyperglycemia, anxiety, headache, weight loos, sweating

37
Q

How is a pheochromocytoma treated?

A

Surgery, alpha and beta receptor blockers

38
Q

What is stress? What causes stress?

A

Stress is a generalized, nonspecific response of the body to any factor (stressor) that overwhelms or threatens to overwhelm the body’s compensatory abilities to maintain a state of homeostasis. The factors can be physical, chemical, physiological, psychological/emotional or social, and will stimulate cortisol release

39
Q

What are the three responses to stress?

A

A stressor increases corticotropin-releasing factor secretion, which increases ACTH secretion, which stimulates adrenal cortisol release
A stressor stimulates sympathetic nerves, which stimulates adrenal epinephrine release
A stressor stimulates vasopressin release, which increases water retention

40
Q

What is the result of adrenal cortisol increase in response to stress?

A

Blood glucose, amino acids and fatty acids increase

41
Q

What is the result of adrenal epinephrine increase in response to stress?

A

Increase in blood glucose and fatty acids
Increase in glucagon and decrease in insulin, causing an increase in glucose and fatty acids
Increase in vasoconstriction, which causes a decrease of blood flow in the kidneys
Increase in angiotensin, which causes an increase in aldosterone release
Increase in salt/water retention, which sustains blood pressure

Physiology 2 (19 decks)

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