Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

26 Clinical Use of Hormones: Focus on Steroids Mak Flashcards

1
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the steps in the HPA axis?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the short acting corticosteroids?

A

Cortisone. Hydrocortisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the intermediate acting corticosteroids?

A

Prednisone. Prenisolone. Triamcinolone. Methyl-prednisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the long acting corticosteroids?

A

Dexamethasone. Betamethasone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the Mineralcorticoids?

A

Fludrocortisone. Aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which corticosteroids have the highest potency?

A

Long acting > intermediate > short

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which corticosteroids have the highest anti-inflammatory potency?

A

Long acting > intermediate > short

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How often do long acting corticosteroids need to be taken?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How often do intermediate acting corticosteroids need to be taken?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the half-life of short acting corticosteroids?

A

half-life: 8-12 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does Cortisol do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What can Cortisol deficiency cause?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What can excess Cortisol cause?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Cortisol products based on?

A

Diurnal cycle. Stress and feedback mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does Aldosterone (mineralcorticoid) do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does Aldosterone (mineralcorticoid) deficiency do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are oral glucocorticoids classified by?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What will exogenous administration of glucocorticoids lead to?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

Daily or alternate day regimen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

When are Glucocorticoids usually taken?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How can you decrease the ADRs with Glucocorticoids?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How can you prevent disease flare-ups with Glucocorticoids?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

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

A

Inhaled. Nasal. Ocular. Parenteral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

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

A

Flunisolide ~ TMC < Beclomethasone ~ Budesonide < Fluticasone ~ Mometasone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the PO PK of Glucocorticoids?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the Topical PK of Glucocorticoids?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the Inhaled PK of Glucocorticoids?

A

Work like poor PO absorption and extensive first-pass metabolism

31
Q

What is the Nasal PK of Glucocorticoids?

A

Rapid absorption in respiratory and GI tract; undetectable in plasma

32
Q

What is the Eye PK of Glucocorticoids?

A

Some systemic absorption, infrequent systemic ADRs

33
Q

What is the IV and IM PK of Glucocorticoids?

A

Based on solubility of agents

34
Q

How do the effects of topical Glucocorticoids differ?

A

By concentrations, dressings, vehicle

35
Q

What are the local skin effects of topical Glucocorticoids?

A

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

36
Q

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

A

Aerosol sprays and foams

37
Q

What are the early symptoms of Addison Crisis?

A

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

38
Q

What is the main problem causing Addison Crisis?

A

Adrenal glands not functioning

39
Q

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

A

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

40
Q

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

A

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

41
Q

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

A

Tuberculosis, tumors, lymphomas, histoplasmosis, medications

42
Q

What medications can possibly cause Addison’s Disease?

A

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

43
Q

What are the treatments for Addison’s Disease?

A

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

44
Q

What are the functions/implications of decreased GH?

A

Inadequate growth or development. Fatigue, weakness in adults

45
Q

What are the functions/implications of decreased ACTH?

A

Lower cortisol secretion. Adrenal deficiency

46
Q

What are the functions/implications of lower FSH?

A

Inadequate sexual development. Hypoganodism

47
Q

What are the functions/implications of lower LH?

A

Lower secretion of testosterone/estrogen/progesterone

48
Q

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

A

Inadequate breast development and milk production

49
Q

What are the functions/implications of lower ADH?

A

Diabetes Insipidus with polyuria and polydipsia

50
Q

What is the treatment option for low GH?

A

Growth Hormone

51
Q

What is the treatment option for low ACTH?

A

Hydrocortisone

52
Q

What is the treatment option for low FSH?

A

Estrogen/Testosterone

53
Q

What is the treatment option for low LH?

A

Estrogen/Testosterone

54
Q

What is the treatment option for low ADH?

A

Vasopressin/ADH

55
Q

What are Glucocorticoids mainly used for?

A

Adrenal insufficiency (Enhance metabolic effects. Modify immune response)

56
Q

What is Hydrocortisone used for?

A

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

57
Q

What is the DOC for maintenance therapy for GLucocorticoids?

A

Prednisone

58
Q

What do Thyroid hormones do?

A

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

59
Q

What are ADH replacements that can be used?

A

Vasopressin. Desmopressin

60
Q

What is Vasopressin therapy for?

A

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

61
Q

What is Desmopressin therapy for?

A

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

62
Q

What do growth hormones do?

A

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

63
Q

What does Testosterone do?

A

Promotes and maintains secondary sex characteristics for androgen deficiency

64
Q

What does Estrogen do?

A

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

65
Q

What are some complications from HPA suppression?

A

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

66
Q

What is the Etiology of Cushing’s Syndrome?

A

Adrenal tumors. Adrenal hyperplasia. Pituitary dysfunction. Latrogenic

67
Q

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

A

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
Q

What are the treatment choices for Cushing’s Disease?

A

Surgery. Medical

69
Q

What are the medical options for Cushing’s Disease?

A

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
Q

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

A

Worsen hypokalemia

71
Q

What should be avoided while using steroids?

A

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

72
Q

What are the monitoring parameters for steroid use?

A

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

73
Q

What should you educate patients on who are using steroids?

A

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

Thera VI (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions