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BAHS-504 PHARMACOLOGY EXAM 2 > Tx – ADRENAL AND THYROID DISEASE > Flashcards

Tx – ADRENAL AND THYROID DISEASE Flashcards

1
Q

what class of steroid hormones does the zona glomerulosa of the adrenal cortex produce?

A

mineralocorticoids – aldosterone

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2
Q

what class of steroid hormones does the zonae fasciculata/reticularis of the adrenal cortex produce?

A

glucocorticoids – hydrocortisone (cortisol)

adrenal androgens (converted to testosterone in other tissues)

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3
Q

what is the primary function of glucocorticoids?

A

carbohydrate (glucose) metabolism

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4
Q

what is the primary function of mineralocorticoids?

A

electrolyte-fluid (salt-water) homeostasis (balance)

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5
Q

name the three adrenal cortical steroids

1.

2.

3.

A
  1. glucocorticoids
  2. mineralocorticoids
  3. adrenal androgens
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6
Q

what enzyme in the zona glomerulosa converts pregnenolone to aldosterone?

A

aldosterone synthase

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7
Q

what are the two enzyme responsible for the conversion of pregnenolone to cortisol in the zona fasciculata/reticularis?

A

P450 17-alpha converts prenenolone to 17-alpha-OH-pregnenolone which is converted to cortisol by P450 11-beta

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8
Q

what are the five prototype synthetic corticosteroids?

A

predninosone

prednisolone

dexamethasone

betamethasone

fludrocortisone

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9
Q

what are the two events of glucocorticoid-mediated transcription and anti-inflammation

A

DNA-dependent regulation (upregulation of anti-inflammatory proteins)

Protein inference mechanisms (downregulation of inflammatory proteins)

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10
Q

what adrenal cortical steroid receptor has wide-spread expression and broad effects, as well as a low affinity for aldosterone?

A

glucocorticoid receptor

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11
Q

what adrenal cortical steroid receptor is expressed abundantly in renal distal tubules and collecting ducts, and is equally sensitive to both cortisol and aldosterone?

A

mineralocorticoid receptors

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12
Q

how does stress affect the hypothalamus-pituitary-adrenal axis?

A

CRH (corticotropin-releasing hormone) is released onto the anterior pituitary by the hypothalamus in release to stress. ACTH (adrenocorticotropic hormone) is released, stimulating the production of cortisol

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13
Q

how are adrenal insufficiency and addison’s disease diagnosed?

A

ACTH IV test.

ACTH is administered to assess the functioning of the adrenal glands stress response by measuring the adrenal response to ACTH

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14
Q

how is pituitary function evaluated during the recovery from prolonged glucocorticoid exposure?

A

morning ACTH level assessment

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15
Q

what percentage of circulating cortisol does corticosteroid-binding-globulin (CBG) bind?

A

80% of circulating cortisol is bound by CBG (unavailable)

< 20% of cortisol is free or loosely bound to albumin (available)

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16
Q

what affinity does corticosteroid-binding globulin (CBG) have for aldosterone and dexamethasone?

A

CBG has no affinity for either aldosterone nor dexamethasone

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17
Q

what are the short-acting corticosteroids that have considerable salt-retaining activity?

A

cortisol and cortisone

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18
Q

what are the intermediate-acting corticosteroids responsible for intermediate anti-inflammatory and salt-retaining activities?

A

prednisone

prednisolone

methylprednisolone

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19
Q

what are the long-acting corticosteroids responsible for maximal anti-inflammatory and minimal salt-retainning activities?

A

dexamethasone

betamethasone

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20
Q

how do glucocorticoids affect gluconeogensis and glucose utilization in the periphery?

A

promote gluconeogensis in liver

inhibit peripheral glucose utilization

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21
Q

do glucocorticoids promote catabolism/ anabolism of protein and fat?

A

increase protein and fat catabolism

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22
Q

how do glucocorticoids affect calcium absorption, osteoblast formation and activity?

A

inhibit calcium absorption, osteoblast formation/activity

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23
Q

describe the anti-inflammatory effects of glucocorticoids

  1. (T cells/ cytokines)
  2. (inflammatory mediators)
  3. (lymphocytes, monocytes, eosinophils, basophils)
  4. (leukocytes and macrophages)
A
  1. suppress T cell activation/ cytokine production
  2. inhibit inflammatory mediator release
  3. reduce circulating lymphocytes, monocytes, eosinophils, basophils
  4. inhibit function of leukocytes and macrophages
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24
Q

how do glucocorticoids effect gastric acid and pepsin?

A

stimulate production of gastric acid and pepsin

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25
Q

what are the three therapeutic uses of glucocorticoids?

A
  1. hormone replacement therapy for adrenocortical insufficiency
  2. anti-inflammation and immunosuppression
  3. evaluate the function of the HPA-axis (hypothalamus-pituitary-adrenal)
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26
Q

what are the primary and secondary therapeutic indications for HRT?

A
  • Primary indication: Addison’s disease

(all adrenal steroids are low)

  • Secondary indication: suppression of the HPA-axis

(low cortisol and androgens, but normal aldosterone)

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27
Q

what is the therapeutic treatment for acute Addison’s disease?

A

hydrocortisone (cortisol) IV

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28
Q

what is the glucocorticoid therapeutic treatment for chronic Addison’s disease?

A

hydrocortisone (cortisol) replacement therapy mimicing the natural circadian secretion

29
Q

what is the clinical indicator for addison’s disease vs suppression of HPA-axis?

A

addison’s disease = reduced production of all adrenal steroids

HPA-axis suppression = low cortisol and androgens, but normal aldosterone

30
Q

what are the therapeutic anti-inflammatory/immunosuppression indications of glucocorticoids?

1.

2.

3.

4.

A
  1. allergy: bee sting, drug rxns, contact dermititis
  2. bronchial asthma, infant respiratory distress
  3. inflammation and autoimmune disorders: arthritis, multiple sclerosis, systemic lupus
  4. prevent organ refection in transplantation
31
Q

what is the glucocorticoid therapeutic treatment for anti-inflammation and immunosuppression?

A

intermediate-acting corticosteroids (predinsone, prednisolone, methylprednisolone) and long-acting corticosteriods (dexamethasone, betamethasone)

32
Q

how does cushing’s syndrome present on a HPA-axis evaluation?

A

increased urine cortisol level

failure of low-dose dexamethasone suppression test

33
Q

how does a pt with cushing’s syndrome present physically?

A

full moon face, trunk obesity, buffalo hump, muscle waste and thinning of skin, osteoporosis

(excessive exposure to glucocorticoids)

34
Q

definition:

used to assess adrenal gland function by measuring how cortisol levels change in response to an injection to dexamethasone. typically used to diagnose cushing’s syndrome (increased cortisol production)

A

dexamethasone suppression test (DST)

35
Q

what are the adverse effects and clinical problems that present upon withdrawal of steroids?

A

acute adrenal insufficiency due to suppression of HPA axis, and flare up of underlying disease

36
Q

what are the pharmacological effects of mineralocorticoid administration?

A

salt-retaining activity: promoting reabsorption of sodium, secretion of potassium

37
Q

what are the therapeutic uses of mineralocorticoids?

A

tx of adrenal insufficiency

38
Q

what is the most widely used therapeutic mineralocorticoid?

A

fludrocortisone

39
Q

what adverse effects can mineralocorticoids produce?

A

increased salt-retention and hypertension

40
Q

how does aminoglutethimide block adrenal corticol steroid synthesis?

A

inhibits the conversion of cholesterol to pregnenolone

41
Q

how is aminoglutethimide used as a therapeutic?

A

in the case of andrenal and/or pituitary adenoma

42
Q

how does spironolactone inhibit the action of aldosterone?

A

spironolactone is an antagonist for mineralocorticoid receptors, thus inhibiting activation by aldosterone

43
Q

how is spironolactone used therapeutically?

A

aldosteronism, such as adrenal adenoma

44
Q

how does mifepristone (RU486) inhibit adrenal cortical steroid

A
45
Q

describe the action of thyroid hormones:

A

T4:T3 = 4:1 → converted to T3 → Bind surface receptor → internalize and bind nuclear receptor

46
Q

what are the physiological effects of thyroid hormones?

A

increased metabolic activity, appetite, activity of sympathetic nervous system, blood flow and heart rate

decreased body weight

47
Q

describe the control of TH release by the CNS

A

hypothalamus produces thyrotropin releasing hormone (TRH)

pituitary produces thyroid-stimulating hormone (TSH) (thyrotropin)

thyroid produces thyroxin (T4) and thiiodothyronine (T3)

48
Q

hypothyroidism is caused by what?

A

destruction of the thyroid by either an autoimmune disease (hashimoto’s thyroiditis), surgery or lithium overdose

49
Q

how does hypothyroidism present clinically in adults?

A

myxedema/myxedema coma

50
Q

symptoms include:

dry waxy sweelin skin and edema

reduced metabolic rate and appetite with weight gain

reduced cardiac output, slow pulse

A

myxedema

51
Q

how does hypothyroidism present clinically in infants?

A

cretinism

52
Q

symptoms include:

impaired CNS development/ mental retardation

short stature and coarse facial features

A

cretinism

53
Q

what hormones are used in replacement therapy for hypothyroidism?

A

levothyroxine (synthroid, L-T4) – most widely used

liothyronine (L-T3) – for acute severe hypothyroidism (myxedema coma)

54
Q

what two disease states causes hyperthyroidism?

A

grave’s disease

hyperfunction goiter

55
Q

how does grave’s disease cause hyperthyroidism?

A

autoimmune antibody binds TSH receptor and mimics hormone

56
Q

symptoms:

increased metabolic rate

irregular heart beat/rapid pulse

increased appetite with dramatic weight loss

protruding eyes (bug eye) and goiter

A

hyperthyroidism

57
Q

what is the treatment for hyperthyroidism?

A

thiourea drugs

iodide or KI (lugol’s) solution/tablet (>6mg/d)

radioactive iodide (131I) and surgery

beta adrenergic blockers for acute thyroid storm

58
Q

which antithyroid/thiourea drug is contraindicated for pts with liver dysfunction?

A

propylthiouracil (PTU)

59
Q

which antithyroid/thiourea drug is contraindicated for pts in the early stages of pregnancy?

A

methimazole (tapazol)

60
Q

describe the mechanism of action of thiourea drugs

A

inhibits peroxidase rxns in iodination of the thyroid gland and coupling of MIT/DIT (to form T3)

PTU also inhibits the conversion of T4 to T3

61
Q

what is the most common application of thiourea drugs?

A

control of hyperthyroididic symptoms prior to surgery

62
Q

describe the mechanism of action of iodide/KI (Lugol’s) solution

A

inhibits TH formation and release

63
Q

what are the most common applications of iodide/Lugol’s solution?

A

thyroid storm

preoperative administration before thyroidectomy to reduce intraoperative blood loss

64
Q

describe the mechanism of action of radioactive iodide

A

131I emits beta-rays that kills surrounding thyroid cells

65
Q

what is the most common application of radioactive iodide?

A

severe hypothyroidism/thyroid tumor combined with life-long synthroid (levothyroxine) therapy

66
Q

definition:

life-threatening crisis characterized by tachycardia, fibrillation, shock, and heart failure

A

acute thyroid storm

67
Q

what is the drug of choice for acute thyroid storm?

A

propranolol

68
Q

what is the mechanism of action of propranolol?

A

blocks activation of sympathetic nervous system and reverses tachycardia

69
Q

what is the most common application of propranolol?

A

administered in combination with thiourea drugs and a large dose of iodide for rapid treatment of acute thyroid storm

BAHS-504 PHARMACOLOGY EXAM 2 (6 decks)

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