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CRP- Renal > Corticoids and Mineralcorticoids > Flashcards

Corticoids and Mineralcorticoids Flashcards

1
Q

What are glucocorticoids?

A

corticosteroids (produced in the adrenal cortex), which are a class of steroid hormones. They (i.e. cortisol) bind to the glucocorticoid receptor that is present in almost every cell.

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2
Q

What is the major endogenous glucocorticoid?

A

hydrocortisone (aka cortisol)

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3
Q

What type of regulation governs glucocorticoids?

A

negative feedback

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4
Q

What hormone regulates cortisol?

A

pituitary hormone ACTH (corticotropin), which regulates synthesis and secretion of cortisol.

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5
Q

Are glucocorticoids and mineralocorticoids similar to androgens (testosterone and estradiol)?

A

YES

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6
Q

What else does ACTH (corticotropin) do?

A

also a growth factor for adrenal cortex

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7
Q

What happens with a decrease in ACTH (corticotropin)?

A

decrease in hydrocortisone (cortisol) and atrophy of adrenal cortex.

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8
Q
  • Remember, does potency = efficacy?
A

NO. This doesn’t necessarily mean it’s better.

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9
Q

How do you increase the potency of a steroid?

A

add a halogen to it.

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10
Q

** What are the 7 glucocorticoid drugs and their equiv. dose?

A
  1. hydrocortisone= nice balance between anti-inflammatory and salt retention (20 mg).
  2. cortisone= nice balance between anti-inflammatory and salt retention (25 mg).
  3. prednisone= mostly anti-inflammatory (5 mg).
  4. methylprednisolone= only anti-inflammatory (4 mg).
  5. triamcinolone= only anti-inflammatory (4 mg).
  6. dexamethasone= only anti-inflammatory (0.75 mg).
  7. betamethasone= only anti-inflammatory (0.6 mg).
    * So a very small dose of betamethasone is equivalent to a much larger does of cortisone).
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11
Q

** What are the metabolic effects of glucocorticoids?

A
  • INCREASED gluconeogenesis, glycogenolysis, and protein catabolism.
  • DECREASED osteoblast formation and activity, calcium absorption from GI tract, secretion of TSH, and protein synthesis.
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12
Q

** What are the anti-inflammatory effects of glucocorticoids?

A
  • DECREASED production of cytokines, interleukins, prostaglandins, proliferation of lymphocytes and macrophages, and migration of lymphocytes and macrophages.
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13
Q

How much glucocorticoid is required for therapeutic purposes?

A

large (pharmacologic) doses, not physiologic amounts.

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14
Q

*** What are the therapeutic uses of glucocorticoids?

A
  • replacement in adrenal hypofunction
  • anti-inflammatory effect
  • immunosuppressive effect
  • adjunct to myeloproliferative disease and other malignancies.
  • endocrine disorders: primary (at the site) and secondary (pituitary) adrenocortical insufficiency, and congenital adrenal hyperplasia.
  • rheumatic disorder: RA, bursitis, gouty arthrits
  • dermatological: severe psoriasis and severe seborrheic dermatitis.
  • allergic states: severe bronchial asthma, contact dermatitis, and drug hypersensitivity.
  • palliation of neoplasms: leukemias and lymphomas (adult).
  • GI: ulcerative collitis
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15
Q

What are the musculoskeletal ADRs of glucocorticoids?

A
  • muscle weakness
  • loss of muscle mass
  • tendon rupture
  • steroid myopathy
  • osteoporosis
  • bone fracture
  • vertebral compression fractures
  • aseptic necrosis (femoral and humoral heads)
  • decreased metabolic effects: decreased osteoblast formation and activity, and decreased Ca++ absorption form GI (even with high vit. D).
  • hypocalcemia followed by increased PTH, causing further bone degeneration.
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16
Q

What are the fluid/electrolyte ADRs of glucocorticoids?

A
  • Na+ retention, fluid retention, hypertension, and thus CHF in susceptible pts.
  • K+ loss and thus HYPOKALEMIC ALKALOSIS.
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17
Q

What are the GI ADRs of glucocorticoids?

A
  • peptic ulcer with perforation

- perforation of small and large bowel (esp in pts with inflammatory disease).

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18
Q

What are the dermatologic ADRs of glucocorticoids?

A
  • thin fragile skin
  • impaired wound healing
  • erythema
19
Q

What are the psychological ADRs of glucocorticoids?

A
  • acute= euphoria

- chronic= insomnia, depression, psychosis

20
Q

What are the immunological ADRs of glucocorticoids?

A
  • signs of infection may be masked

- immunosuppression with large doses (Chx pox and measles can be fatal in children).

21
Q

What are the endocrine ADRs of glucocorticoids?

A
  • suppression of growth in children
  • menstrual irregularities and anovulation in women.
  • decreased testosterone in men.
  • Cushingoid state= hypercortisolemia, moon face, buffalo hump.
  • hypothalamic suppression, and thus pituitary adrenal axis suppression (most common side effect of chronic glucocorticoid use).
22
Q

What are the ophthalmic ADRs of glucocorticoids?

A

cataracts or increased intraocular pressure

23
Q

What are some drug interactions with glucocorticoids?

A
  • enzyme inducers= phenytoin, phenobarbital, rifampin

* Thus you may need an increased dose if on any of these.

24
Q

What is a glucocorticoid antagonist?

A
  • mifepristone= synthetic compound used to reverse Cushing’s syndrome
  • Mitotane= synthetic adrenal cytotoxic agent that directly suppresses adrenal cortex. Used to treat inoperable adrenal cortical carcinoma.
25
Q

What are mineralocorticoids?

A

class of corticosteroids (produced in the adrenal cortex) that influence salt and water balances.

26
Q

** What is the primary mineralocorticoid?

A

aldosterone (which acts at the collecting tubules/ducts of the nephron to increase both Na+ and water reabsorption, while excreting K+ and H+). This has a short duration.

27
Q

What system regulates aldosterone secretion?

A
  • RAAS and K+ concentration

- ACTH (corticotropin) secondarily

28
Q

Are the pharmacologic actions of mineralocorticoids (aldosterone) more powerful on carbohydrate metabolism and electrolyte balance?

A

YES

29
Q

What is the ultimate effect of mineralocorticoids?

A

increased BP

30
Q

What will large doses of mineralocorticoids do to adrenocortical secretion, pituitary corticotropin secretion, and thymus activity?

A

DECREASE all due to negative feedback.

31
Q

Will large doses of mineralocorticoids increase or decrease deposition of liver glycogen?

A

INCREASE, due to increase in glucose levels.

32
Q

What will large doses of mineralocorticoids do to protein catabolism?

A

INCREASE it (except in presence of adequate protein intake).

33
Q

*** What do we use mineralocorticoids to treat?

A
  • Addison’s disease as replacement therapy for primary and secondary adrenocortical insufficiency. Glucocorticoids are also given for this.
  • treatment of salt-losing adrenocongenital syndrome/ hypoaldosteronism.
34
Q

** What are the mineralocorticoid drugs?

A
  • fludrocortisone= synthetic compound similar to hydrocortisone, but very powerful mineralocorticoid actions. Also has strong glucocorticoid actions.
35
Q

What is important to do when on chronic fludrocortisone therapy?

A
  • check serum electrolyte levels diligently.
  • restrict dietary salt
  • provide K+ therapy (if needed).
36
Q

What will large doses of mineralocorticoids inhibit?

A
  • adrenal cortical secretions
  • pituitary corticotropin excretion
  • thymic activity
  • Due to negative feedback.
37
Q

Will large doses of mineralocorticoids induce negative N balance?

A

YES, so you need to eat plenty of protein.

38
Q

What are the ADRs of mineralocorticoids related to Na+ and water retention?

A
  • edema
  • hypertension
  • CHF
  • cardiac enlargement
  • K+ loss (thus hypokalemic alkalosis)
39
Q

What are the musculoskeletal ADRs of mineralocorticoids?

A
  • muscle weakness
  • steroid myopathy
  • loss of muscle mass
  • osteoporosis
  • vertebral compression
  • spontaneous fractures
40
Q

What are the GI ADRs of mineralocorticoids?

A
  • peptic ulcer with potential for perforation or hemorrhage.
  • ulcerative esophagitis
41
Q

What are the dermatologic ADRs of mineralocorticoids?

A
  • impaired healing of wounds
  • bruising, petechiae, and ecchymoses
  • thin fragile skin
  • acneiform eruptions
42
Q

What are the endocrine ADRs of mineralocorticoids?

A
  • suppression of growth in children
  • development of cushingoid state
  • decreased in secondary adrenocortical and pituitary response
43
Q

What are the metabolic ADRs of mineralocorticoids?

A
  • hyperglycemia (especially diabetics)
  • glycosuria
  • negative N balance
44
Q

What drugs interact with mineralocorticoids?

A
  • barbiturates
  • digoxin
  • furosemide
  • phenytoin
  • rifampin

CRP- Renal (19 decks)

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