26 Clinical Use of Hormones: Focus on Steroids Mak Flashcards Preview

Thera VI > 26 Clinical Use of Hormones: Focus on Steroids Mak > Flashcards

Flashcards in 26 Clinical Use of Hormones: Focus on Steroids Mak Deck (73):
0

How much cortisol is released in a normal person every day?

Non-stressed patients secrete cortisol amount equivalent to 5mg prednisone daily (>5mg considered supraphysiologic, may cause HPA (hypothalamus, Pituitary, Adrenal axis) suppression)

2

What are the steps in the HPA axis?

Hypothalamus releases CRH (corticotropin releasing hormone) which acts on the Anterior pituitary which releases ACTH (adrenocorticotropic hormone) which acts on the Adrenal cortex which releases Cortisol (which has a negative feedback function on H and P)

3

What are the short acting corticosteroids?

Cortisone. Hydrocortisone

4

What are the intermediate acting corticosteroids?

Prednisone. Prenisolone. Triamcinolone. Methyl-prednisone

5

What are the long acting corticosteroids?

Dexamethasone. Betamethasone

6

What are the Mineralcorticoids?

Fludrocortisone. Aldosterone

7

Which corticosteroids have the highest potency?

Long acting > intermediate > short

8

Which corticosteroids have the highest anti-inflammatory potency?

Long acting > intermediate > short

9

How often do long acting corticosteroids need to be taken?

Once a day or every other day (half-life: 36-54 hours)

10

How often do intermediate acting corticosteroids need to be taken?

Once a day (half-life: 12-36 hours)

11

What is the half-life of short acting corticosteroids?

half-life: 8-12 hours

12

What does Cortisol do?

Regulates metabolism of proteins, CHO, and lipids. Breakdown protein and fat. Promote gluconeogenesis (can cause glucose intolerance)

13

What can Cortisol deficiency cause?

Severe fatigue, weakness, weight loss, hyperpigmentation, nausea, loss of appetite

14

What can excess Cortisol cause?

Weight gain, fatigue, easy bruising, muscle weakness, redness in the face, pink stretch marks, mood swings

15

What is Cortisol products based on?

Diurnal cycle. Stress and feedback mechanism

16

What does Aldosterone (mineralcorticoid) do?

Sodium and water retention. Increases potassium excretion. Increases circulating blood volume (HTN, edema, exertional HA)

17

What does Aldosterone (mineralcorticoid) deficiency do?

Reduced blood pressure, dizziness on standing, salt craving, muscle cramps

18

What are oral glucocorticoids classified by?

Duration of action. Generally QD dosing except for replacement therapy (Addison's). Longer acting agents have greater glucocorticoid activities

19

What will exogenous administration of glucocorticoids lead to?

Suppression of HPA axis (dose and duration related, administration time, routes, hence ADRs)

20

What is the dosing strategy for Glucocorticoids in chronic long-term suppression of immune response?

Daily or alternate day regimen

21

What is the dosing strategy for glucocorticoids to break an acute immune response?

IVP for emergency cases. Pulse therapy = high dose for a short period. Should consider tapering off

22

When are Glucocorticoids usually taken?

QD between 6-8am. BID for larger doses to reduce GI irritation

23

How can you decrease the ADRs with Glucocorticoids?

Alternate dose (e.g. 5mg prednisone one day, 2.5mg the other). Intermediate acting agents appropriate. May not minimize risk of osteoporosis or cataract formation

24

How can you prevent disease flare-ups with Glucocorticoids?

Tapering. Supraphysiologic doses x short duration (< 2 weeks) may be stopped without tapering. Individualize schedule. May switch to shorter acting agents when ~5mg prednisone for further tapering

25

What type of disease state could cause a higher risk of ADRs with Glucocorticoids?

Diseases causing lower serum albumin (e.g. Hypothyroidism)

26

What are some other Non-PO routes of Glucocorticoid administration?

Inhaled. Nasal. Ocular. Parenteral

27

How do the different Glucocorticoids compare in potency for inhaled and nasal products?

Flunisolide ~ TMC < Beclomethasone ~ Budesonide < Fluticasone ~ Mometasone

28

What is the PO PK of Glucocorticoids?

Completely absorbed. Peak levels in 30-100 minutes, delayed by food; bound to proteins. Hepatic metabolism and renally eliminated (Prednisone --> Prednisolone. Cortisone --> Hydrocortisone)

29

What is the Topical PK of Glucocorticoids?

Absorption increased by skin temperature, hydration, integrity of skin, occlusive dressing. Ointment > cream delivery. Enter systemic circulation and metabolized

30

What is the Inhaled PK of Glucocorticoids?

Work like poor PO absorption and extensive first-pass metabolism

31

What is the Nasal PK of Glucocorticoids?

Rapid absorption in respiratory and GI tract; undetectable in plasma

32

What is the Eye PK of Glucocorticoids?

Some systemic absorption, infrequent systemic ADRs

33

What is the IV and IM PK of Glucocorticoids?

Based on solubility of agents

34

How do the effects of topical Glucocorticoids differ?

By concentrations, dressings, vehicle

35

What are the local skin effects of topical Glucocorticoids?

Face most sensitive, more susceptible to systemic absorption. Fluorinated agents may produce a rosacea-like eruption

36

What type of topical Glucocorticoids forms are preferred for intertriginous and hair-bearing skin?

Aerosol sprays and foams

37

What are the early symptoms of Addison Crisis?

Fatigue, weight loss, hyperpigmentation, NVD, muscle/joint pain, depression

38

What is the main problem causing Addison Crisis?

Adrenal glands not functioning

39

In Addison Crisis, what are some of the steps when Cortisol (hydrocortisone, cortisone acetate, prednisone, or dexamethasone) are very low or absent?

Liver function decreases, extremely low sugar, leads to COMA and DEATH

40

In Addison Crisis, what are some of the steps when Aldosterone (Florinef) is very low or absent?

Kidney (water and sodium loss), leads to low fluid volume and low blood pressure, leads to SHOCK, then COMA and DEATH

41

In Addison's Disease, what can gland destruction be due to?

Tuberculosis, tumors, lymphomas, histoplasmosis, medications

42

What medications can possibly cause Addison's Disease?

Steroid withdrawal. Adrenal antagonists (metyrapone/aminoglutethamide). Heparin and warfarin, excessive causing adrenal hemorrhage. Rifampin and other CYP inducers with pre-existing problems

43

What are the treatments for Addison's Disease?

Chronic replacement: 1) Glucocorticoids (cortisone, prednisone. Avoid dexamethasone (more ADRs, no mineralcorticoid effects)). 2) Mineralcorticoids (fludrocortisone). Pre-op and stress supplements necessary

44

What are the functions/implications of decreased GH?

Inadequate growth or development. Fatigue, weakness in adults

45

What are the functions/implications of decreased ACTH?

Lower cortisol secretion. Adrenal deficiency

46

What are the functions/implications of lower FSH?

Inadequate sexual development. Hypoganodism

47

What are the functions/implications of lower LH?

Lower secretion of testosterone/estrogen/progesterone

48

What are the functions/implications of lower Prolactin (PRL)?

Inadequate breast development and milk production

49

What are the functions/implications of lower ADH?

Diabetes Insipidus with polyuria and polydipsia

50

What is the treatment option for low GH?

Growth Hormone

51

What is the treatment option for low ACTH?

Hydrocortisone

52

What is the treatment option for low FSH?

Estrogen/Testosterone

53

What is the treatment option for low LH?

Estrogen/Testosterone

54

What is the treatment option for low ADH?

Vasopressin/ADH

55

What are Glucocorticoids mainly used for?

Adrenal insufficiency (Enhance metabolic effects. Modify immune response)

56

What is Hydrocortisone used for?

Replacement in adrenocortical deficiency. Anti-inflammatory effects. IV for acute situation

57

What is the DOC for maintenance therapy for GLucocorticoids?

Prednisone

58

What do Thyroid hormones do?

Influence growth and maturation of tissues (normal growth, normal metabolism, normal development)

59

What are ADH replacements that can be used?

Vasopressin. Desmopressin

60

What is Vasopressin therapy for?

Replace Vasopressin (IM/SQ). Vasopressor effect (promotes vascular smooth-muscle contractino). ADH activity (increases water resorption at the distal renal tubular epithelium)

61

What is Desmopressin therapy for?

Longer acting ADH derivative (nasal). Increases cellular permeability of collecting ducts and resorb water

62

What do growth hormones do?

Stimulates growth of linear bone, skeletal muscle, organs. Stimulates erythropoietin. Maintain adequate functionality (decrease central obesity, maintain muscle mass, improve attention and memory)

63

What does Testosterone do?

Promotes and maintains secondary sex characteristics for androgen deficiency

64

What does Estrogen do?

Promotes and maintains female reproductive system and secondary sex characteristics and organs

65

What are some complications from HPA suppression?

Musculoskeletal (osteoporosis, myopathy, avascular necrosis). Ophthalmic (cataracts, glaucoma). GI. Cardiovascular. Dermatological. CHO and lipid metabolism. CNS (anxiety, depression, insomnia, euphoria, psychosis). Infection

66

What is the Etiology of Cushing's Syndrome?

Adrenal tumors. Adrenal hyperplasia. Pituitary dysfunction. Latrogenic

67

What is the mnemonic (CUSHING) for the symptoms of Cushing's Syndrome?

C: Central obesity. U: Urinary cortisol/glucose. S: Striae, Suppressed immunity. H: Hyper-cortisol, tension, glycemia, lipidemia, hisurtism. I: Iatrogenic causes. N: Noniatrogenic causes, neurological symptoms. G: Growth retardation in children

68

What are the treatment choices for Cushing's Disease?

Surgery. Medical

69

What are the medical options for Cushing's Disease?

Inhibition of ACTH (cyproheptadine, bromocriptine). Inhibition of cortisol synthesis (aminoglutethamide, ketoconazole). Inhibition of cortisol/block synthesis (metyrapone). Destruction of adrenal cells that synthesize cortsiol (mitotane)

70

What is a drug interaction when using steroids and diuretics and amphotericin?

Worsen hypokalemia

71

What should be avoided while using steroids?

Live attenuated or bacterial vaccines, or tuberculin skin tests. Contact with others with chickenpox or measles. NSAIDs, ASA, EtOH

72

What are the monitoring parameters for steroid use?

BP. Weights in CHF. Glucose, lipid levels. UA. BMD. Slit lamp eye exams. IOP

73

What should you educate patients on who are using steroids?

Signs of myopathy, avascular necrosis, infection, and CNS effects