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Endocrine & Metabolism > Week 4 - Adrenal > Flashcards

Week 4 - Adrenal Flashcards

1
Q

What is the action of Amiloride?

A

Blocks ENaC channels –> K+ sparing diuretic

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2
Q

What is the action of Spironolactone?

A

Antagonist of mineralocorticoid (aldosterone) and androgen receptors –> K+ sparing diuretic

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3
Q

What is the screening test for Cushing’s Syndrome?

A
  • ACTH level

- Overnight dexamethasone suppression test

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4
Q

What is the test for differentiating Cushing’s Disease from other causes of Cushing’s syndrome?

A

Petrosal sinus sampling

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5
Q

What lab tests are required to rule out Pheochromocytoma?

A

Urine catecholamines and catecholamine metabolites (ex. metanephrine)

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6
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism due to aldosterone-secreting adenoma

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7
Q

What test is useful to rule out Conn’s syndrome?

A

Aldosterone:renin ratio

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8
Q

What is the first investigation for adrenal insufficiency?

A

Rapid ACTH stimulation test (with baseline ACTH and cortisol measurements)

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9
Q

For ACTH stimulation test, what does it mean if there is blunted cortisol response with high ACTH?

  • with low ACTH?
  • what about normal ACTH and normal cortisol response?
A

High ACTH, Low cortisol response ==> Primary Adrenal Insufficiency (Addison’s disease)

Low ACTH, Low cortisol response ==> Secondary Adrenal Insufficiency or Chronic Steroid Use

Normal ACTH, Normal cortisol response ==> Not Addison’’s

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10
Q

What are the cells in the adrenal medulla called?

- what do they secrete?

A

Chromaffin cells

- secrete catecholamines

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11
Q

What does MEN stand for?

A

Multiple Endocrine Neoplasia

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12
Q

What are the types and subtypes of MEN?

A

MEN-1

MEN-2: subclassified to

  • MEN-2a
  • MEN-2b
  • MCT (Medullary carcinoma of the thyroid)
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13
Q

What are the main symptoms associated with MEN-2?

A
  1. Medullary carcinoma of the thyroid (>95%)

2. Pheochromocytoma (50%)

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14
Q

What are the main symptoms associated with MEN-1?

A

“P-P-P triad”

  1. Parathyroid
  2. Pancreatic Islet cell (usually insulin or gastrin secreting)
  3. Pituitary (anterior)
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15
Q

What’s the difference in clinical presentation between MEN-2a & MEN-2b?

A

MEN-2a has hyperparathyroidism.

MEN-2a is more common than 2b.

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16
Q

How is the presentation of medullary carcinoma of the thyroid different than other MEN-2 presentations?

A

MCT is not a/w pheos.
MCT and MEN-2b do not have hyperPTH, but Men-2a does.

ie. the only symptom a/w MCT is MCT.

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17
Q

How is dx of MEN-2 confirmed?

A
  • Bx of mass in neck (most important early finding).

- Measure for elevated calcitonin

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18
Q

What is a marker for MCT?

A

elevated calcitonin

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19
Q

What is the rate of secretion of cortisol under physiological conditions?

A

10mg/day

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20
Q

What is the normal range for K+ in the blood?

A

3.5-5mmol/L

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21
Q

List the types of corticosteroids and state their main function.

A

Glucocorticoids - regulate carbohydrate metabolism (& anti-inflammatory)
Mineralocorticoids - regulate electrolyte balance (mainly Na+ retention)

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22
Q

What is the transport protein for cortisol in the blood?

A

CBG (Corticosteroid binding globulin)

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23
Q

Name a short-acting glucocorticoid.

- what is the approximate half life of this?

A

Hydrocortisone (cortisol) or cortisone

- t(1/2) = 8-12 hrs

24
Q

Name a intermediate-acting glucocorticoid.

- what is the approximate half life of this?

A

Prednisone

- t(1/2) = 12-36 hrs

25
Q

Name a long-acting glucocorticoid.

- what is the approximate half life of this?

A

Dexamethasone

- t(1/2) = 36-72 hrs

26
Q

What synthetic corticosteroid has much more potent mineralocorticoid action (as opposed to glucocorticoid action)

A

Fludrocortisone

27
Q

What is the benefit of taking steroids in the inhaled form?

A

Prevents systemic effects of the drug

28
Q

What are the pharmacokinetics of ingested cortisol (ADME)?

A

A: well absorbed via GI
D: binds to CBG or albumin in blood
M: hepatic metabolism
E: excreted by kidneys

29
Q

Of the alpha and beta type catecholamine receptors, which one has a much higher affinity for Epi over NE?

A

beta-2 receptors

30
Q

How does cortisol act in catecholamine production?

A

Induces PNMT (enzyme that converts NE –> Epi

31
Q

What is the rate-limiting step in catecholamine synthesis?

A

Tyrosine –> DOPA

enzyme = Tyrosine hydroxylase

32
Q

What is the enzyme that catalyzes the rate-limiting step in cholesterol synthesis?

A

HMG-CoA reductase

33
Q

Why does the adrenal medulla get stained dark brown?

A

Due to conversion of catechols to melanin (occurs in granules)

34
Q

Is the adrenal medulla necessary for life?

A

no.

35
Q

What are the pathways for the metabolism of Epi & NE?

(include enzymes)

A

Epi –(COMT)–> metanephrine –(MAO)–> VMT

NE –(COMT)–> normetanephrine –(MAO)–> VMT

36
Q

Why is dexamethasone given after surgery?

A

To prevent nausea/vomiting

37
Q

What are some of the main complications of long-term glucocorticoid tx?

A

Adrenal atrophy –> iatrogenic Cushing’s (due to too much synthetic glucocorticoid action)

Glucocorticoid withdrawal –> acute adrenal insufficiency

38
Q

What is the similarity between the following drugs?

  • Aminoglutethimide
  • Metyrapone
  • Ketoconazole
  • Etomidate
A

CYP 450 inhibitors

  • affect the production of corticosteroids and androgens
39
Q

What is the molecular action of finasteride?

A
  • 5-alpha-reductase inhibitor

- prevents conversion of T –> DHT

40
Q

What is the action of Mifepristone?

A

Progesterone receptor blocker

41
Q

What cells are in the adrenal medulla to support the spindle cells?

A

Sustentacular cells

42
Q

Where are the spindle cells?

A

At periphery of the nests of chromaffin cells.

43
Q

What is the most common adrenal mass in children?

A

Neuroblastoma

44
Q

What is the DDx for bilateral adrenal masses?

A
  • pheo
  • cushing’s disease (excess ACTH stimulation)
  • ectopic ACTH/CRH production
  • mets
  • hemorrhage
  • adrenal nodular hyperplasia
  • lymphoma
45
Q

In Addison’s disease, what percent of the adrenal cortex has to be destroyed before symptoms present?

A

90% compromised

46
Q

What are some causes of Addison’s disease?

A
  • autoimmune
  • infections (TB, histoplasmosis, coccidiodes)
  • mets/lymphomas
  • hemorrhage
  • HH (hemochromatosis)
47
Q

What virus is common in adrenal glands of AIDS patients?

A

CMV

48
Q

Where are steroid receptors when not activated?

A

In cytoplasm, bound to HSD (heat shock protein)

49
Q

What are fibrates used to treat?

- what receptor do they bind to?

A

Treat dyslipidemia

- bind PPAR-alpha receptor

50
Q

What is Vit D used to prevent?

- which receptor does it bind?

A

Prevents rickets & ostemalacia, diabetes, CA

- binds VDR (Vit D receptor)

51
Q

What are thiazolidinediones used to treat?

- what receptor does it bind?

A

Diabetes

- binds PPAR-gamma receptor

52
Q

How are blood glucose levels related to serum K+?

A

Hypokalemia causes inhibition of insulin secretion, thus leading to hyperglycemia

53
Q

How does cortisol affect GFR?

A

Cortisol increases GFR –> increases free water clearance

54
Q

What’s associated with mutations in the RET proto oncogene?

A

MEN-2a
MEN-2b
MCT
Hirschprung’s syndrome

55
Q

What happens in Addisonian Crisis?

A

hypotension, hyperkalemia, hyponatremia

Endocrine & Metabolism (5 decks)

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