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MTP > Exam 5: Adrenal Corticosteroid Part 2 > Flashcards

Exam 5: Adrenal Corticosteroid Part 2 Flashcards

1
Q

What are the therapeutic applications of GC agonists?

A
  1. Adrenal insufficiency (Addisons)
  2. Inflammatory disorders
  3. Autoimmune (Rheumatoid arthritis, IB, MS)
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2
Q

What are the therapeutic applications of GC antagonists?

A

Cushing’s syndrome and disease

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3
Q

What is the principal naturally occurring steroid?

A

Hydrocortisone (cortisol)

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4
Q

Describe the properties of hydrocortisone?

A
  1. Often taken orally
  2. A soluble salt can be given IV for rapid effect in an emergency
  3. A suspension (hydrocortisone acetate) can also be given directly into a joint
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5
Q

What is prednisone?

A

A prodrug that is converted into prednisolone in the liver

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6
Q

What is the therapeutic use for prednisolone?

A

An anti-inflammatory glucocorticoid, biologically active that has little sodium-retaining activity

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7
Q

What is an example of flurinated GC?

A

Triamcinolone

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8
Q

What is the use for Triamcinolone?

A

No sodium retaining (mineralocorticoid) effect, but has the disadvantage that muscle wasting may occasionally be severe and anorexia and mental depression may be more common when used at higher doses

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9
Q

What is Dexamethasone and Betamethasone?

A
  1. Powerful anti-inflammatory steroid
  2. Longer acting than prednisolone used for oral, otic, injectable, and topical
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10
Q

What are replacement glucocorticoid therapy used to treat?

A
  1. Acute adrenal insufficiency
  2. Chronic adrenal insufficiency (Addisons)
  3. Gongenital adrenal hyperplasia (autosomal)
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11
Q

How can glucocorticoid pharmacotherapy used for non-endocrine diseases?

A

Dramatic improvements but produce severe adverse effects

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12
Q

What is the primary mineralocorticoids?

A

Aldosterone

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13
Q

What is aldosterone used for?

A

Salt-retaining, rapidly inactivated by first-pass metabolism in the liver, and no place in routine therapeutics

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14
Q

What is fludrocortisone used for?

A
  1. Mineralcorticoid
  2. Long-acting fluorinated steroid that has a large sodium-retaining effect in relation to its anti-inflammatory action
  3. Replaces aldosterone where the adrenal cortex is destroyed and hydrocortisone is not sufficient to normalize sodium and water
  4. Used in patients with autonomic neuropathy
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15
Q

What is an adrenal or Addison crisis?

A

An acute adrenocortical insufficiency which may represent an endocrine emergency

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16
Q

What causes an adrenal crisis?

A

HPA-axis suppression brought on by chronic use of exogenous glucocorticoids and abrupt withdrawal

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17
Q

What is the treatment for Addison?

A

Hydrocortisone, cortisone, prednisone

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18
Q

What is the goal for Addison’s drug treatment?

A

Mimick normal diurnal adrenal rhythm

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19
Q

Why is hydrocortisone used for Addison?

A

It has both glucocorticoid and mineralocorticoid activity

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20
Q

What is Cushing’s?

A

Too much cortisol is made over a long period of time

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21
Q

What is the difference between exogenous and endogenous Cushing’s?

A

Ex: long term treatment with corticosteriod
En: Caused by tumors or adenoma (excessive ACTH)

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22
Q

How can pituitary tumors or adenomas cause Cushing?

A

noncancerous growths on the pituitary gland which make excessive ACTH, causing the adrenals to make too much cortisol

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23
Q

How can ectopic ACTH syndrome cause Cushing?

A

Tumors in other tissues that make ACTH. Tumors most commonly occur in the lungs

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24
Q

How can adrenal tumors cause Cushing’s?

A

Too much cortisol

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25
Q

How can we diagnose Cushing’s?

A
  1. 24 hr urinary free-cortisol test
  2. Low-dose dexamethasone suppression test
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26
Q

What is the 24 hr urinary free-cortisol test?

A
  1. Collect urine over a 24-hour period and test cortisol levels.
  2. Higher than normal cortisol levels suggest Cushing’s syndrome.
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27
Q

What is the Low-dose dexamethasone suppression test?

A

Cortisol levels in the blood should be suppressed after taking dexamethasone. Elevated cortisol levels suggest Cushing’s syndrome.

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27
Q

What are the treatments of Cushing’s?

A
  1. Surgery
  2. Radiation therapy
  3. Steroidogenic inhibitors
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28
Q

What are steroidogenic inhibitors?

A
  1. Inhibit enzymes required for the synthesis of corticosterone and cortisol
  2. Inhibition of the mitochondrial enzyme, 11-beta-hydroxylase is the most common drug target
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29
Q

What is metyrapone?

A
  1. Drug treatment for Cushing’s that inhibits cortisol synthesis
  2. Inhibits 11-beta-hydroxylase, inhibiting synthesis of cortisol from 11-deoxycortisol and corticosterone from desoxycorticosterone in the adrenal gland
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30
Q

What are the side effects of Metyrapone?

A

Nausea and vomiting, vertigo, headache, dizziness, abdominal discomfort, and allergic rashes

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31
Q

What is Osilodrostat?

A

Potent cortisol synthesis inhibitor that blocks the enzyme 11-beta-hydroxylase to interrupt the last step of the cortisol synthesis pathway (Cushing)

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32
Q

How does ketoconazole treat Cushing?

A
  1. Used to treat fungal infections too
  2. inhibitor of mitochondrial P450 enzymes systems (The 11-hydroxylase step is carried out by P450-dependent mitochondrial enzymes)
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33
Q

How does Mitotane treat Cushing’s?

A
  1. a steroid inhibitor and antineoplastic agent used for adrenocortical carcinoma and Cushing’s syndrome
  2. Inhibits 11-hydroxylation and pregnenolone synthesis from cholesterol in the adrenal cortex
  3. Reduces synthesis of cortisol and corticosterone
  4. Mitotane may cause serious, life-threatening adverse reactions
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34
Q

What is Pasireotide?

A

Somatostatin analog that acts via somatostatin receptors to inhibit the secretion of corticotropin from pituitary adenomas in patients with Cushing’s syndrome

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35
Q

What are the side effects of Pasireotide?

A

Hyperglycemia

36
Q

What is atopic dermatitis?

A

Condition that makes skin red and itchy

37
Q

What is seborrheic dermatitis?

A

Scaly patches, red skin and stubborn dandruff of the scalp

38
Q

What is Lichen simplex chronicus and lichen planus?

A

Swelling and irritation of skin, hair, nails and mucous membranes. On skin, appears as purplish, itchy, flat bumps

39
Q

What is Pruritus ani?

A

Chronic itching affecting perianal skin

40
Q

What is Allergic contact dermatitis?

A

Itchy rash caused by direct contact with a substance or an allergic reaction to it

41
Q

What is psoriasis?

A

Skin cells build up and form scales and itchy, dry patches

42
Q

What is Pityriasis rosea?

A

Rash that begins as a large circular or oval spot on your chest, abdomen or back

43
Q

What is vitiligo?

A

Loss of skin color in blotches

44
Q

What are examples of topical corticosteroid?

A

Hydrocortisone
Prednisolone and Methylprednisolone
Dexamethasone and Betamethasone
Triamcinolone
Fluocinonide

45
Q

How are topical steroids ranked?

A

Class I (very potent) -> Class VII (lowest potency)

46
Q

What are the types of steroid vehicles?

A
  1. Ointments
  2. Creams
  3. Lotions and gels
  4. Foams, mouses, and shampoos
47
Q

What are ointments?

A

More lubrication and occlusion than other preparations, and are the most useful for treating dry or thick hyperkeratotic lesions

48
Q

What are creams?

A

Mixes of water suspended in oil which have good lubricating qualities and ability to vanish into skin

49
Q

What are lotions and gels?

A

are the least greasy and occlusive of the topical steroid vehicles

50
Q

What are foams, mousses, and shampoos?

A

effective vehicles for delivering steroids to the scalp

51
Q

What are the special considerations for topical steroids?

A
  1. Face
  2. Intertriginous areas
  3. Children
  4. Effect of occlusion
  5. Infection and combination formulas
52
Q

What are the contraindications of topical steroids?

A
  1. Acne vulgaris
  2. ulcers
  3. Scabies
  4. Warts
  5. Fungal infections
53
Q

What can cause topical steroid side effects?

A

Potency of preparation used
Frequency of application
Duration of use
Anatomic site of application
Individual patient factors

54
Q

What are the local side effects of topical steroids?

A

Telangiectasia (widened blood vessels cause threadlike red lines on the skin)
Purpura (skin hemorrhages)
Epidermal, dermal and subcutaneous atrophy
Cutaneous striae
Folliculitis (inflamed hair follicles)
Allergic reactions
Hypopigmentation
Facial Hypertrichosis (excessive facial hair growth)
Delayed wound healing
Alterations in skin elasticity

55
Q

What is asthma?

A

a Chronic inflammatory disease of the airways (bronchials) in which there is an increased responsiveness of the bronchi to various stimuli

56
Q

What are features of asthma?

A
  1. Inflammation of bronchial walls and inflammatory cell infiltration
  2. Constriction of bronchial smooth muscle leading to a reversible airflow obstruction
  3. Increased mucous secretion
57
Q

What are the symptoms of asthma?

A
  1. Coughing
  2. Shortness of breath
  3. Chest tightness
  4. Wheezing
58
Q

What are the immuno-histopathologic features of asthma?

A
  1. Inflammatory cell infiltration
  2. Mast cell activation
  3. Edema
  4. Denudation of airway epithelium
  5. Collagen deposition beneath the basement membrane
    6.Airway inflammation contributes to airflow limitation, hyperresponsiveness, symptoms, & chronicity
  6. Atopy
59
Q

How can airway inflammation trigger asthma?

A

an initial triggering agent causes release of inflammatory mediators from mast cells, macrophages and epithelial cells

60
Q

How can chemotactic inflammation trigger asthma?

A

These mediators cause infiltration of eosinophils and neutrophils resulting in release of pro-inflammatory mediators, epithelial injury and abnormal neural regulation of airway tone

61
Q

What are the development stage of asthma?

A
  1. Inhales allergens which are digested by mucosal lysozymes to which plasma cells produce and release a specific IgE immunoglobulins
  2. The IgE attaches to mast cells, basophils and macrophages and upon subsequent exposure to the antigen, the IgE sensitized mast cells + antigen causes release of mediators by the mast cells
  3. vasodilation, secretion of thick mucous, inflammation, mucosal edema, and bronchial constriction
62
Q

What are interleukins?

A

Secreted by Type 2 helper T cells that promote the allergic interactions

63
Q

What is IL4?

A

Stimulates B cells to increase the production of IgE

64
Q

What is IgE?

A

Induces growth and degranulation of mast cells

65
Q

What are IL3 and 5?

A

Released by TH2 and mast cells increases eosinophil recruitment and activation

66
Q

What is immediate phase inflammation?

A

IgE/Antigen crosslinking to mast cells leads to degranulation and release of primary mediators (histamine) and secondary mediators (leukotrienes and prostaglandins)

67
Q

What are fasting acting medications?

A
  1. SABA
  2. Systemic steroids
68
Q

What are examples of systemic steroids?

A

Prednisone and prednisolone

69
Q

What are systemic steroids primarily for?

A
  1. Airflow obstruction
  2. Reduce rate of relapse in severe asthma
  3. may help gain prompt control of disease when initiating inhaled (ICS) treatment
70
Q

What are example controllers for maintenance therapy?

A
  1. Inhaled/oral glucocorticosteroids (Mometasone and fluticasone)
  2. LABA (Salmeterol, formoterol, vilanterol)
71
Q

What are inhaled corticosteroids?

A
  1. Preferred treatment alone or in combination with LABAs, for all persistent categories of asthma
  2. Reduces asthma symptoms, bronchial hyperreactivity
  3. Reduces dependence on short acting beta-2 agonists (SABAs) for symptomatic relief
  4. Improves pulmonary function
  5. Improves quality of life
72
Q

What is the MAO for ICS?

A

Suppresses cytokine production by reducing eosinophil infiltration and function, inhibits macrophages and release of chemical mediators of inflammation and stabilizes endothelial membranes

73
Q

What are examples of ICS?

A
  1. Budesonide
  2. Beclomethasone dipropianoate
  3. Ciclesonide
  4. Mametasone
74
Q

What is the MAO of Fluticasone propionate?

A

Undergoes rapid metabolism in the liver by CYP 450 3A4 into FP-17ß-carboxylic acid derivative
Prevention of systemic side effects

75
Q

What are the side effects of ICS?

A

Deposition in mouth and throat may promote oral candidiasis

76
Q

What are the side effects of short term systemic corticosteroid?

A

Reversible increases in glucose, decreased potassium, fluid retention with weight gain, mood alterations (including rare psychosis), hypertension, and peptic ulcers

77
Q

What are the side effects of long term systemic corticosteroid?

A

Iatrogenic Cushing’s syndrome that May also see height and growth suppression and cataracts

78
Q

What is COPD?

A

chronic airflow limitations caused by Chronic bronchitis and/or emphysema, most commonly associated with long term tobacco smoking

79
Q

What are the symptoms of COPD?

A

Airway inflammation, fibrosis, and luminal plugs leading to increased resistance to airflow
Loss of elastic recoil of lungs and alveoli
Loss of alveolar attachments
Decreased expiratory flow rate
Overinflation of the lung

80
Q

What are cell types for asthma?

A

Mast cells, eosinophils, CD4+ Tcells, macrophages

81
Q

What are the mediators for asthma?

A

LTD4, histamine, IL-4, IL-5

82
Q

What are the effects of asthma?

A

Effects bronchials, epithelial shedding (airways remodeling)

83
Q

How do we respond to asthma?

A

Steroids (+++), β-Agonists (+++), Antimuscarinics (+)

84
Q

What are the cell types of COPD?

A

Neutrophils, CD8+ T-cells, macrophages (++++)

85
Q

What are the mediators of COPD?

A

IL-8, TNG-, -1 antitrypsin deficiency, Reactive Oxygen Species

86
Q

What are the effects of COPD?

A

Effects bronchials and alveoli, lung destruction, fibrosis

87
Q

How do we respond to COPD?

A

Antimuscarinics (+/++), β-Agonists (+), Steroids (+/-)

MTP (15 decks)

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