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Endocrine > 2-9-16-The Adrenal Gland (Lopez) > Flashcards

2-9-16-The Adrenal Gland (Lopez) Flashcards

1
Q

What types of hormones does the adrenal cortex secrete?

What types of hormones does the adrenal medulla secrete?

A

Steroids–> aldosterone, cortisol, androgens

AA derived –> epinephrine and norepinephrine

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2
Q

What are the 3 zones of the adrenal cortex from outer to inner layer?

A

Glomerulosa, fasciculata, reticularis

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3
Q

What does the zona glomerulosa secrete?

What does the zona fasciculata secrete?

What does the zona reticularis secrete?

A

Mineralocorticoids (aldosterone)

Glucocorticoids (cortisol) and androgens

Glucocorticoids (cortisol) and androgens

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4
Q

What does the adrenal medulla secrete?

A

Catecholamines (Epi and norepi)

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5
Q

___ is a transport protein that regulates cholesterol transfer within the mitochondria, which is the rate-limiting step in the production of steroid hormones

A

StAR (Steroidogenic Acute Regulatory Protein)

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6
Q

__ stimulates synthesis and secretion of adrenal cortical hormones such as glucocorticoids (cortisol) and mineralocorticoids (aldosterone)

A

ACTH

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7
Q

ACTH is a peptide hormone produced in the anterior pituitary and is derived from post-translational processing of ___

A

POMC (pro-opiomelanocortin)

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8
Q

The HPA axis is under negative feedback control by ___

A

Cortisol

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9
Q

List the effect of cortisol secretion on the following:

A-Immune system
B-Liver
C-Muscle
D-Adipose tissue

A

A-Immune suppression
B-Gluconeogenesis
C-Protein catabolism
D-Lipolysis

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10
Q

The secretory rates of cortisol are highest during ___ and lowest in the ___

A

Early morning

Late evening

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11
Q

Cushing’s disease is caused by a pituitary tumor or an adrenal tumor and is an example of ____-cortisolism

A

Hyper-

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12
Q

Addison’s disease can be caused by autoimmune disease of the adrenal gland and is an example of ____-cortisolism

A

Hypo-

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13
Q

Secondary adrenal insufficiency can be caused by glucocorticoid drugs suppressing the hypothalamus and Pituitary and is an example of ___-cortisolism

A

Hypo

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14
Q

Rounding of the face, excess fat on the back of the neck, excess weight gain in abdomen, and dark red or purple stretch marks are symptoms of ___

A

Cushing’s syndrome

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15
Q

Primary hypercortisolism (Cushing’s syndrome) is due to what?

A

Adrenal tumor that autonomously secretes cortisol (adrenal excess)

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16
Q

Secondary hypercortisolism (Cushing’s disease) is due to what?

A

Pituitary tumor that autonomously secretes ACTH (pituitary excess)

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17
Q

A pituitary tumor that autonomously secretes ACTH is known as ____

A

Cushing’s DISEASE –> secondary hypercortisolism, pituitary excess

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18
Q

Describe primary adrenocortical insufficiency

A

Addison’s disease –> hyposecretion of all adrenal steroid hormones (hypocortisolism)

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19
Q

Describe secondary adrenocortical insufficiency

A

ACTH deficiency–> chronic exogenous glucocorticoid treatment (hypocortisolism)

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20
Q 
Describe the levels of the following in Primary (adrenal) excess:
Plasma cortisol-
Plasma CRH-
Plasma ACTH-
Hyperpigmentation-
A

Plasma cortisol=increase
Plasma CRH=decrease
Plasma ACTH=decrease
Hyperpigmentation=no

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21
Q 
Describe the levels of the following in Secondary (pituitary) excess:
Plasma cortisol-
Plasma CRH-
Plasma ACTH-
Hyperpigmentation-
A

Plasma cortisol=increase
Plasma CRH=decrease
Plasma ACTH=increase
Hyperpigmentation=Yes

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22
Q 
Describe the levels of the following in Primary cortisol deficiency:
Plasma cortisol-
Plasma CRH-
Plasma ACTH-
Hyperpigmentation-
A

Plasma cortisol=decrease
Plasma CRH=increase
Plasma ACTH=increase
Hyperpigmentation=Yes

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23
Q 
Describe the levels of the following in Secondary cortisol deficiency:
Plasma cortisol-
Plasma CRH-
Plasma ACTH-
Hyperpigmentation-
A

Plasma cortisol=decrease
Plasma CRH=increase
Plasma ACTH=decrease
Hyperpigmentation=No

24
Q 
Describe the levels of the following after steroid administration (synthetics other than cortisol)
Plasma cortisol-
Plasma CRH-
Plasma ACTH-
Hyperpigmentation-
A

Plasma cortisol=decrease (but symptoms of excess)
Plasma CRH=decrease
Plasma ACTH=decrease
Hyperpigmentation=no

25
Q

___ test can be used to detect adrenal gland insufficiency

A

Cosyntropin (synthetic ACTH) stimulation test

26
Q

The primary action of aldosterone is ___

A

Renal sodium reabsorption

27
Q

List the steps that result in increased Na reabsorption and K secretion due to the action of aldosterone in the DCT

A

1) aldosterone combines with a cytoplasmic receptor –> 2) hormone-receptor complex initiates transcription in the nucleus –> 3) translation and protein synthesis makes new protein channels and pumps –> 4) aldosterone-induced proteins modulate existing channels and pumps –> 5) result is increase Na reabsorption and K secretion

28
Q

___ is characterized by excessive release of aldosterone from the adrenal cortex

A

Primary hyperaldosteronism

29
Q

__ is due to an adenoma in the adrenal cortex

A

Conn’s syndrome

30
Q

___ is due to excessive renin secretion by the juxtaglomerular cells in the kidney

A

Secondary hyperaldosteronism

31
Q

___ is due to destruction of the adrenal cortex and leads to defects in aldosterone synthesis and inadequate stimulation of aldosterone secretion

A

Hypoaldosteronism

32
Q

What is a possible treatment for Addison’s disease?

A

Steroid replacement therapy for life

33
Q

What is a likely treatment for Conn’s dyndrome (adrenal adosteronoma)?

A

Surgery

34
Q

WHat is a likely treatment option for bilateral adrenal hyperplasia?

A

Spironolactone (K-sparing diuretics)

35
Q

___ responds to stress such as hypoglycemia/exercise and influences energy metabolism and cardiac output

A

Epinephrine

36
Q

What is the initial substrate (amino acid) in the formation of norepi and epi?

A

Tyrosin

37
Q

In order for tyrosine hydroxylase to convert Tyrosine to DOPA, what else needs to happen?

A

Sympathetic stimulation with Ach

38
Q

In order for Dopamine to be converted to Norepinephrine via dopamine-beta-hydroxylase, what needs to happen?

A

Sympathetic stimulation via Ach

39
Q

The synthesis of catecholamines is under the control of the __ axis

A

CRH-ACTH-Cortisol axis

40
Q

___ stimulates synthesis of DOPA

___ increases PNMT enzyme

A

ACTH

Cortisol

41
Q

This enzyme catalyzes the formation of epinephrine from norepinephrine

A

PNMT plus cortisol

42
Q

Where is Epi synthesized?

A

In the cytosol from NE

43
Q

What is the rate-limiting step in the formation of catecholamines?

A

Tyrosine hydroxylase catalyzing TYROSINE –> DOPA

44
Q

DOPA is converted to DOPAMINE by the cytoplasmic enzyme ___ and is then transported into this secretory vesicle ___

A

Aromatic Amino Acid Decarboxylase

Chromaffin granule

45
Q

Within the chromaffin granule, dopamine is converted to NE by the enzyme ___

A

Dopamine-beta-hydroxylase

46
Q

Epinephrine gets transported back into the chromaffin granule by ___

A

Vesicular monoamine transporters (VMAT)

47
Q

___ are multimolecular complexes, thought to decrease the osmotic burden of storing individual molecules of epinephrine within chromaffin granules.

A

Chromogranins

48
Q

Circulating ___ can be used as a marker of sympathetic paraganglion-derived tumors (paragangliomas)

A

Chromogranins

49
Q

Epinephrine –> dihydroxymandelic acid

A

MAO

50
Q

Epi –> metanephrine is catalyzed by ____

NE –> normetanephrine is catalyzed by ___

A

COMT

COMT

51
Q

Metanehprine –> Vanillylmandelic acid (in urine)

A

MAO

52
Q

The adrenal medulla is of ___ origin

The adrenal cortex is of ___ origin

A

Ectodermal

Epidermal

53
Q

___ receptor(s) respond better to norepi than epi

___ receptor(s) respond equally to norepi and epi

Epi is more potent than norepi for the ___ receptor(s)

A

Alpha and beta3

Beta1

Beta2

54
Q

List which adrenergic receptor types result with an increase in cAMP

List which adrenergic receptor types result with a decrease in cAMP

List which adrenergic receptor types result in an increase in IP3 and Ca, and DAG

A

Beta1/2/3

Alpha2

Alpha1

55
Q

___ is a tumor of chromaffin tissue and results in an excess production of catecholamines. Symptoms include hypertension, orthostatic hypotension, headaches, sweating, anxiety, palpitations, chest pain, and flushing

A

Pheochromocytoma

Endocrine (14 decks)

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