Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endo/Repro Midterm > The Adrenal Gland > Flashcards

The Adrenal Gland Flashcards

1
Q

What is the origin of the adrenal cortex? Hormones?

What is the origin of the adrenal medulla? Hormones?

A

Epidermal (intermediate mesoderm); corticoids and androgens

Ectodermal; catecholamines

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

What are the three regions of the adrenal gland and what do they secrete?

A

Zona glomerulosa: mineralocorticoids (aldosterone)

Zona fasiculata: glucocorticoids (cortisol) androgens

Zona reticularis: glucocorticoids and androgens

Adrenal medulla: catecholamines (N/NE)

*more pronounced

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

What hormones are produced in the adrenal cortex?

A

Mineralocorticoids (aldosterone)

Glucocorticoids (cortisol)

Sex steroids (DHEA, DHEAS)

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

Adrenal enzyme deficiency: 21-hydroxylase causes what symptoms?

Treatment?

A

Decreased cortisol and mineralocorticoid, increased sex hormones

Hypotension (decreased aldosterone), Na and volume loss, hyperkalemia, elevated renin, female virilization (secondary’s male characteristics) of fetus and sexual ambiguity, male precoscious puberty and premature epiphyseal plate closure

Replace glucocorticoids and mineralocorticoids

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

Adrenal enzyme 11 beta-hydroxylase deficiency causes what symptoms?

A

Decreased cortisol and mineralocorticoids, and increased androgens

Virilization of female fetus, increases 11-deoxycorticosterone (builds up because lacks enzyme to convert it to corticosterone)

Hypertension, hypokalemia, suppressed renin secretion

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

Adrenal enzyme 17 alpha-hydroxylase deficiency causes what symptoms?

A

Decreased androgens and cortisol, excess mineralocorticoids

Hypertension, hypokalemia, hypogonadism

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

Describe the genomic and non-gemomic actions of cortisol

Glucocorticoid excess causes what?

Glucocorticoid deficiency causes what?

A

Glucocorticoid response elements (GRE) lead to genomic: glucocorticoid binding to its steroid hormone and affecting GRE directly or indirectly through secondary messenger signaling and affecting transcription or translation
AND
non-genomic actions (endocannabinoids): binding of glucocorticoid to its receptor in a neuron, neuron releases neurotransmitter (glutamate) into synaptic cleft and causes depolarization to nearby neuron

Cushing syndrome/disease

Addison disease

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

What are the effects of cortisol on the liver, muscle, fat, cutaneous, immune system, endocrine, GI?

A

Liver: increase gluconeogenesis

Muscle: breakdown of muscle protein

Fat: promotes lipolysis in extremities, promotes central fat deposition

Cutaneous: skin thins, fragile blood vessels

Immune system: increase infection

Endocrine: insulin resistant or glucose intolerant

GI: interferes with Ca absorption

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

Describe the regulation of cortisol:

What is released from the hypothalamus?

What are stressors that cause this to be released?

What does it bind to?

What does it do?

A

Stressors induce: hypoglycemia, hypotension, fever, trauma, surgery

CRF (CRH) is release from paraventricular nucleus in the hypothalamus

Binds to CRH1 receptor (G-protein receptor)

Stimulates the release of ACTH from the anterior pituitary gland

Stimulates the release of cortisol from the adrenal gland

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

ACTH is derived/cleaved from ____ that is produced in the anterior pituitary.

ACTH can be broken down into ____.

Excess ACTH can lead to disease of _____.

A

POMC

MSH (melanocytes stimulation hormone)

Hyperpigmentation

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

Describe the feedback loops of ACTH

A

Long loop: cortisol inhibiting release of CRH in hypothalamus

Short loop: ACTH inhibits CRH

Ultrashort loop: CRH inhibits itself from being secreted from the hypothalamus

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

ACTH and cortisol is normally released in a _____.

Highest levels of cortisol are in the ____.

A

Rhythm

Morning (arouses you)

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

Describe the negative feedback of cortisol

___ can stimulate the stress response and therefore cortisol pathway

___ is also involved in negative feedback.

A

Glucocorticoids (GC) exert a negative feedback onto CRH and ACTH by inhibiting POMC transcription and mRNA synthesis of CRH and ACTH

Amygdala

Hippocampus

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

What does the dexamethasone suppression test (DST) do? (Exogenous glucocorticoid)

Effects of low dose?

High does?

A

Determines if there is a glucocorticoid problem; give a high does of dexamethasone; ACTH and cortisol secretion should decrease due to the negative feedback

Cushing disease has no suppression

Helps determine which type of Cushing disease

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

What is the cosyntropin (synthetic ACTH) stimulation tests (CST)?

Effects?

A

Tests adrenal gland insufficiency

Administer synthetic ACTH

Normal person, cortisol should increase from baseline

If adrenals are unresponsive, cortisol remains the same or rises in small amount (adrenal insufficiency)

If adrenal respond dramatically and cortisol increases substantially, consider secondary adrenal insufficiency

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

Four cortisol related pathologies

A

Cushing syndrome

Cushing disease

Addison disease

Secondary adrenal insufficiency

17
Q

Hypercortisolism causes what two diseases?

Explain

A

Cushing syndrome: hypersecretion of cortisol; usually adrenal neoplasm; HIGH cortisol but LOW ACTH (negative feedback from cortisol); adrenal problem because primary endocrine disorder

Cushing disease: hypersecretion of ACTH; usually pituitary gland tumor; can be non-pituitary neoplasm like a non-small cell carcinoma; overstimulates the adrenal cortex and excess cortisol is secreted; HIGH ACTH and HIGH cortisol; pituitary problem because secondary endocrine disorder

18
Q

If a pt with Cushing syndrome was injected with exogenous glucocorticoids (dexamethasone), what would happen to their ACTH levels and cortisol suppression?

Why?

A

ACTH would be undetectable and dexamethasone fails to suppress cortisol secretion

Negative feedback loop is functional yet hypercortisolism continues (abnormal feedback at level of adrenal gland)

19
Q

If a pt with Cushing disease was injected with exogenous glucocorticoids (dexamethasone), what would happen to their ACTH levels and cortisol suppression?

Why?

A

ACTH would be normal or slightly elevated and dexamethasone would successfully suppress cortisol secretion

Abnormal negative feedback at level of pituitary

20
Q

Hypercortisolism

Symptoms of moon face, hirsutism, bruising, abdomen adiposity, stretch marks, buffalo hump

A

Cushing’s

21
Q

Hypocorticolism causes what two diseases?

Explain

A

Addison disease: primary adrenal insufficiency; chronic; progressive destruction of adrenal gland; HIGH ACTH but LOW cortisol; adrenal response is blocked from signal; adrenal problem

Secondary adrenal insufficiency: caused by exogenous glucocorticoid administration; ACTH deficiency; LOW ACTH, LOW cortisol; pituitary problem

22
Q

If a pt with Addison disease (primary adrenal insufficiency) is injected with synthetic ACTH (cosyntropin) what would happen to plasma cortisol levels?

If a pt with secondary adrenal insufficiency is injected with synthetic ACTH (cosyntropin) what would happen to plasma cortisol levels?

A

No change (adrenals can’t respond to ACTH)

Increase cortisol (adrenals are functional)

23
Q

Causes of Addison disease

Addison disease causes hyposecretion of all ______.

What is an adrenal crisis?

A

Autoimmune disease of adrenal gland
Adrenal hemorrhage (secondary to infection, secondary to anticoagulant treatment)
Infection (TB, N. menigitidis)
Tumor

Adrenal steroids

Acute change in hypocortisolism (more profound effects)

24
Q

Signs and symptoms of Addison disease

A

Hyperpigmentation (MSH) if elevated ACTH

Weight loss

Muscle weakness

Hypoglycemia

Hypotension

Hyponatremia and hyperkalemia (because loss of aldosterone)

25
Q

Actions of aldosterone

What does a lack of aldosterone cause?

A

Principle mineralocorticoid controlling Na and K exchange in distal nephron

Major regulator of body stores of K

Increase synthesis and activity of Na channels in apical membrane

Increases synthesis and activity of Na/K ATPase in the basolateral membrane of the distal tubule

Increases Na reabsorption and increases K secretion and H secretion

Hyponatremia and hyperkalemia

26
Q

Cortisol-cortisone shunt:

MR has equal affinities for ____ and _____.

____ metabolizes the conversion of cortisol to cortisone

Protects the mineralocorticoid receptor (MR) from binding to ____ and keeps MR available for ____.

This enzyme is inhibited by ______ causing _____.

A

Aldosterone; glucocorticoids

11 beta-HSD2

Cortisol; Aldosterone

Glycyrrhizic acid (licorice); cortisol to have free access to the MR, MR becomes overwhelmed by cortisol especially in hypercortisolemic conditions like Cushings

27
Q

Two diseases caused by hyperaldosteronism

Explain

A

Primary (Conn syndrome): hypersecretion of aldosterone usually from an adrenal neoplasm; adrenal problem (primary endocrine disorder)

Secondary: hypersecretion of renin; excess renin from juxtaglomerular cells of the kidney; kidney problem (secondary endocrine disorder)

28
Q

Two disease caused from hypoaldosteronism

Explain

A

Primary: hyposecretion of aldosterone, destruction of the adrenal cortex, or defects in aldosterone synthesis; adrenal problem (primary endocrine disorder)

Secondary: hyposecretion of renin; deficient renin from juxtaglomerular cells of the kidney; therefore inadequate stimulation of aldosterone; kidney problem (secondary endocrine disorder)

29
Q

How does ACTH affect aldosterone?

A

ACTH had a modest effect on aldosterone secretion

Primary adrenal failure -> deficient cortisol and aldosterone

ACTH deficiency -> cortisol deficiency but no change in aldosterone

30
Q

What are adrenal androgens?

What enzyme do they rely on?

What do adrenal carcinomas that secrete androgens cause?

A

DHEA (dehydroepiandrosterone) and DHEAS (DHEA sulfate)

Precursors to human sex steroids

Relies on 3beta-HSD superfamily to exert androgens and estrogenic activities

Females: virilization, hirsutism, clitoromegaly, breast atrophy, deepening of voice, temporal recession, severe acne

31
Q

E and NE are from sympathetic nerve terminals that release ____.

ACh binds to ____ receptors.

ACh increases synthesis of ____ and activity of ____.

A

ACh

Nicotinic

Tyrosine hydroxylase; dopamine

32
Q

Describe the pathway from L-tyrosine to epinephrine

A

Begin with L-tyrosine -> L DOPA by tyrosine hydroxylase (Rate limiting step)

L-DOPA -> dopamine: dopamine gets stored in secretory vesicles called chromaffin granules by VMAT

Dopamine -> NE by dopamine beta-hydroxylase

NE diffuses out of the granules

NE -> Epi in the cytosol

Epi gets stored in vesicles by VMAT

33
Q

How does sympathetic stimulation affect the conversion of tyrosine to epinephrine?

How does cortisol affect it?

A

Sympathetic terminals release ACh which binds to nicotinic receptors

Nicotinic receptor cell signaling increases expression of tyrosine hydroxylase (RLS) and activity of dopamine beta hydroxylase

Cortisol stimulates the conversion of norepinephrine to epinephrine

34
Q

What is contained in a chromaffin granule?

A

Epinephrine can be re-shunted back into the chromaffin granule; combines with leftover NE, and chromogranins (contain Ca and ATP), and create a storage complex

NE, E, Ca, ATP

Chromogranins are released when catecholamines are stimulated during fight or flight

35
Q

Two enzymes involved in the metabolism of catecholamines

Function?

Location?

What is VMA? (vanillylmandelic acid, metanephrines, catecholamines)

A

MAO (monoamine oxidase): oxidizes; treat neuropsychiatric disorders

COMT (catechol-O-methyltransferase): primary enzyme that inactivates catecholamines released from the adrenal gland

Both in CNS and peripheral tissues

VMA: measurement of breakdown products that are used to determine catecholamines production (elevated VMA = elevated catecholamines)

36
Q

What is pheochromocytoma?

Symptoms?

A

Tumor of the chromaffin tissue; produces excess catecholamines

Hypertension, orthostatic hypotension, HA, sweating, palpitations, CP, flushing, anxiety

37
Q

Stress response and the hypothalamus-pituitary-adrenal axis:

Short-term

Long-term stress

A

HR increases, BP increass, bronchioles dilates, liver converts glycogen to glucose and releases glucose to blood, blood flow changes and reduces digestive system activity and urine output, metabolic rate increase

Kidneys retain Na and water, blood volume and BP rise, protein and fat converted to glucose and broken down for energy, blood glucose increases, immune system suppressed

38
Q

What is the function of renin?

Where is it secreted from?

When is it secreted?

What inhibits it?

A

Converts angiotensinogen to angiotensin I

Kidneys

During times of decreased renal arterial pressure, increased beta-adrenergic action, increased prostaglandins

ANP, dopamine

38
Q

What are the catecholamines?

What do they come from?

Where are they produced?

A

Epinephrine and norepinephrine

L-tyrosine

Adrenal medulla

Endo/Repro Midterm (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions