Corticosteroids Flashcards

1
Q

What is the function of the adrenal glands in regards to steroid production?

A

Secrete mineralcorticoids, glucocorticoids, and sex hormones

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2
Q

Where are the adrenal glands located?

A

Sit on top of the kidneys

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3
Q

What are the two main areas of the adrenal glands?

A

Cortex and Medulla

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4
Q

What composes the cortex of the adrenal glands?

A

Zona Glomerulosa
Zona Fasciculata
Zona Reticularis

(GFR on top of kidneys)

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5
Q

Describe the pathway of hormone synthesis in the zona Glomerulosa?

A

Cholesterol –> Desoxycorticosterone –> Corticosterone –> 18-Hydroxyxosterone –> Aldosterone

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6
Q

What is the main steroid product of the zona glomerulosa?

A

Aldosterone

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7
Q

Describe the pathway of hormone synthesis zona fasci?

A

Cholosterol –> Prenolene –> Progesterone –> 17-Hydroxyprogesterone –> 11-Deoxycortisol –> Cortisol

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8
Q

What is the main steroid product of the Zona Fasci?

A

Cortisol

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9
Q

Describe the pathway of hormone synthesis in the zona reticularis?

A

Cholesterol –> 17-Hydroxypregnenolone –> Dehydroepiandrosterone –> Androstenedione –> Testosterone

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10
Q

What cholesterol is used for steroid synthesis?

A

LDL Cholesterol

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11
Q

Where is testosterone mainly produced? In Who?

A

Testosterone can be produced in the Zonba reticularis; however, in males, most testosterone is synthesized in the testes
- Little testosterone production in the female ovaries

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12
Q

What does cortisol regulate in the body?

A
  • Mediate the stress response
  • Help regulate metabolism
  • Help regulate the inflammatory process
  • Help regulate the immune system
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13
Q

When is cortisol released? What does it help restore?

A

Cortisol is released in response to stress and also helps to restore hormone levels when stress resolves

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14
Q

Describe the physiologic pathway of short term stress?

A

Hypothalmus –> Nerve Impulse –> Spinal Cord –> Preganglionic Symapthetic Fibres –> adrenal Medulla (Secretes amino-acid based hormones) –> Catecholamines (epinephrine and norepinephrine)

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15
Q

What is the physiologic response of short term stress?

A
  • Increased heart rate
  • Increased blood pressure
  • Liver converts glycogen to glucose and releases glucose to blood
  • Changes in blood floe patterns leading to decreased digestive system activity and urine output
  • Increased metabolic rate
  • bronchodilation
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16
Q

Describe the physiologic pathway of prolonged stress?

A

Stress –> Hypothalamus –> CRH (corticotropin-releasing hormone) –> Corticotroph cells of anterior pituitary –> ACTH –> Adrenal Cortex ( secretes steroid hormones) –> Releases Mineralcorticoids and Glucocorticoids

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17
Q

In the long term stress response, mineralcorticoids function to:

A

Retention of sodium and water by kidneys
Increased blood volume and blood pressure

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18
Q

In long term stress, glucocorticoids function to:

A
  • Proteins and fats converted to glucose or broken down for energy (muscle wasting)
  • Increased blood glucose
  • Suppression of the immune system
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19
Q

What controls the production and secretion of cortisol?

A

HPA Axis

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20
Q

What is the main function of the HPA axis?

A

Control the production and secretion of cortisol by the hypothalamus-pituatary-adrenal (HPA) axis

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21
Q

Describe the HPA axis pathway?

A

Circadian Regulation and/or stressors (hypoglycemia, hypotension, surgery, fever, injury)

V

Hypothalmus

V

Pituatary (acted on by vasopressin and pro-inflammatory cytokines)

V

ACTH

V

Adrenals

V

Cortisol (exhibits negative inhibition on the hypothalamus and pitautary to inhibit cortisol release)

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22
Q

In the HPA axis pathway, cortisol exhibits ________ on the pitauatary and hypothalmus to…..

A

Negative Inhibition

  • Inhibits its own release, when cortisol levels are high, the cortisol inhibits further production
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23
Q

What are the main actions of glucocorticoids?

A

They suppress inflammatory and immunological responses

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24
Q

Describe the basics of inflammation? What are its purposes?

A
  • Inflammation is a process whereby WBC’s and other mediators protect against foreign substances
  • The inflammatory process serves several purposes initially (e.g. removal of damaged cells) but may eventually become counterproductive (e.g. edema impedes blood flow)
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25
Q

Describe the inflammatory response

A

Stimulus –> Antigen-Antibody Response
V V
Release of Inflammatory Mediators

and

Cell Mobilization –> Increased Capillary Permeability
V V

Edema, Erythema, and Pruritis

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26
Q

How do corticosteroids exert an anti-inflammatory effect? (Specific)

A
  • Alter cytokine release
  • Blocking increased capillary permeability
  • Causing less vasoactive substance release
  • Inhibits leukocyte and macrophage migration/adhesion
  • Interfering with phagocytosis
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27
Q

When corticosteroids are used pharmacologically, they exert an anti-inflmmatory response by….. (Basic)

A
  • Impede the inflammatory process
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28
Q

How do corticosteroids exhibit immunosuppressive effects? (specific)

A
  • Alter the cell function of specific genes
  • Affect the function of WBC’s
  • Inhibit T-cell activation
  • Inhibit IL’s, cytokines, gamma-interferon, and TNF-alpha synthesis
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29
Q

What are the actions of corticosteroids?

A

Anti-inflammatory
Immunosuppressive
Anti-mitotic
Anti-tumour
Anti-emetic

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30
Q

How do corticosteroids exhibit anti-mitotic activity? When is this useful?

A

Inhibit DNA synthesis and epidermal cell turnover
- Useful in psoriasis

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31
Q

How do corticosteroids exhibit anti-tumour effects? When is this useful?

A

May be related to inhibition of glucose transort or induction of cell death in immature lymphocytes

  • useful in cancer (used in certain chemo regimens)
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32
Q

How do corticosteroids exhibit anti-emetic effects? When would this be beneficial?

A

May be due to a blockade of cerebral innervation of the emetic center
- Block the emetic effects of chemo therapeutic agents

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33
Q

In asthma, what is the standard of care?

A

Inhaled corticosteroids

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34
Q

In atopic dermatitis, what is the standard of care?

A

Topical corticosteroids

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35
Q

In transplant induction, what is standard of care?

A

All will use a corticosteroid

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36
Q

In rheumatoid arthritis, how many in % will a corticosteroid?

A
  • 30-40% will use (up to 75% will use at some time in their life)
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37
Q

What are the two types of corticosteroid dosage forms? Examples?

A

Local Agents:
- Otic
-Opthalmic
-Inhaled
-Topical

Systemic Agents:
- Injectables
-Oral

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38
Q

Why would you want to use an agent locally as opposed to systemically?

A

Fewer side effects

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39
Q

Opthalmic and Otic corticosteroids are available as…..

A

Drops, ointments, emulsions and intravitreal implants

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40
Q

In regards to the eyes and ears, corticosteroids often come in combination with…..

A

Anti-biotics

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41
Q

Opthalmic/Otic corticosteroids are used for:

A

Redness, itching, swelling and pain

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42
Q

What is the main issue with opthalmic and otic eye drops?

A

Correct delievery technique

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43
Q

Nasal Inhaled steroids uses:

A

Rhinitis
Polyps
Sinusitis

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44
Q

What is an issue with inhaled nasal corticosteroids?

A

Installation technique

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45
Q

What are the pros and cons of metred-dose inhalers?

A

Pros - Portability
Cons - Inhalation technique

  • Always guessing how many doses are left
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46
Q

What are some device pros and cons with dry powders for inhalation?

A

Pros:
Actuation
Portable
Shows remaining doses

Cons:
Powder despostion in mouth
requires good lung function
Age restrictions (large strong deep breth, children often can’t do this)

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47
Q

What is a combo inhaled product composed of? When are they often used?

A

Corticosteroid and Beta-2 Adrenergic Agonist (LABA)
- Often used in COPD

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48
Q

Solutions for inhalation are referred to as:

A

Nebulizers

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49
Q

What is an example of a solution for inhalation?

A

Budesonide

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50
Q

What are some pros of nebulizers?

A

Reasonable lung delievery when cannot generate sufficient flow rate
Easy for infants (mask)
Young Children

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51
Q

What are some cons of nebulizers?

A

Time consuming (10-15 min/dose)
Expensive
Non-portable equipment
False sense of superiority

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52
Q

What are the topical corticoidsteroids dosage forms? What is the rating of their strengths/potency?

A

Lotions < Creams < Gels < Ointments

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53
Q

When are lotions most useful?

A

Least occlusive, non-greasy
- Useful for axillia, foot, groin, large, hairy areas and acute weeping lesions

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54
Q

When are creams useful?

A

Medium occlusion
- Cosmetically most acceptable
Suitable for non-acute/wet lesions, intertriginous areas (skin folds)

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55
Q

When are gels useful?

A

Non-greasy, non-occlusive
- Quick drying, can apply to face, hairy areas
- Do not leave residue, useful on scalp or hairy areas
- Irritating

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56
Q

When are ointments useful?

A

Most occlusive
- Greasy; for very dry, scaly or hyperkeratized skin area, palms and soles

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57
Q

What is the rating scale of corticosteroids? What does each category indicate for usage?

A

Potency - Scale of 1 -7

Group 1 - Ultra-high Potency
Group 2,3 - High Potency
–> Generally limit to daily-BID dosing and limit length of therapy
–> Avoid use on large areas, thin skin areas, skin folds, and face
–> Caution in young children/infants
–> Suitable for short term intermittent usage (< 2-4 week usage)

Group 4,5 - Mid-potency
–> Suitable for intermittent long-term usage
–> Chronic use in thick skin areas is suitable
–> Avoid on thin skin areas (e.g. face)

Group 6,7 - Low potency
–> Safest in infants, children and elderly or for larger areas or higher risk areas (e.g. face, perianal, eyelids)
–> Caution still required
–> Suitable for maintenance of chronic conditions after initial control obtained
–> often applied BID-QID, less frequent (OD -BID) if ongoing

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58
Q

What are the main corticosteroid creams and their respective potency?

A

Clobetasol propionate 0.05% - 1

Betamethasone Dipropionate 0.05% - 3

Betamethasone Valerate 0.1% (Fucibet: beta 0.1% + fuscidic acid 2%) - 5

Hydrocortisone 2.5% (1% and 0.5% OTC) - 7

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59
Q

What are the main corticosteroid ointments and their respective potency?

A

Clobetasol propionate 0.05% - 1

Betamethasone dipropionate 0.05% - 2

Betamethasone Valerate 0.1% - 3

Betamethasone Valerate 0.05% - 5

Hydrocortisone (1% or 0.5 % OTC) - 7

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60
Q

What are the main corticosteroid lotions/solutions and their respective potency?

A

Clobetasol Propionate (0.05% Scalp Lotion, 0.05% topical spray) - 1

Betamethasone Dipropionate 0.05% Lotion - 3-5

Betamethasone Valerate (0.1% Scalp lotion, 0.1% lotion, 0.05% lotion) - 5-6

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61
Q

Non-steroidal corticosteroids:

A

Tacrolimus, Pimecrolimus - Calcineurin Inhibitor

Crisaborole 2% oint - PDE0- 4 Inhibitor

Roflumilast 0.3% - PDE0-4 Inhibitor

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62
Q

What factors influence the cutaneous penetration of corticosteroids?

A
  • Moisture of skin (more absorbed when wet)
  • Heat
  • Potency of the steroid
  • Dosage form
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63
Q

What are some forms of dosage forms used for rectal usage? What factor is important in considering what dosage form to use? What sx are they used to tx?

A

Enemas, Rectal ointments, supposoitories, rectal foams

  • Depends on how far you need to go into the colon (ulcerative cholitis vs hemmrhoids)
  • For inflammation, itching and discomfort
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64
Q

What are the common corticosteroids for enemas?

A
  • Betamethasone
  • Budesonide
  • Hydrocortisone
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65
Q

What is the common corticosteroid for rectal ointments?

A

Hydrocortisone

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66
Q

What is the common corticosteroid for suppositories?

A

Hydrocortisone

67
Q

What is the common corticosteroid rectal foams?

A

Hydrocortisone

68
Q

What are the different types of injectable systemic corticosteroids?

A

Intravenous, Intramuscular, Intralesional, Intra-articular

69
Q

What are examples of intravenous corticosteroids?

A

Hydrocortisone

Methylprednisolone

70
Q

When is an IV corticosteroid used over another dosage form?

A

Used when a faster onset or high doses are required

71
Q

What are some examples of intramuscular corticosteroids?

A

Betamethasone Acetate/sodium phosphate
Dexamethasone Sodium phosphate
Methylprednisolone
Triamcinolone

72
Q

What are the two PK effects of intramuscular corticosteroids?

A
  • Have a delayed onset
  • Provide depot effects (sustained action) –> Pain relief varies from person to person
73
Q

What is an example of an intralesional corticosteroids?

A

Triamcinolone Acetonide

74
Q

What are some examples of an intra-articular corticosteroids?

A

Triamcinolone
Betamethasone
Methylpredinsolone

75
Q

What is the main difference between intra-articular and intramuscular corticosteroids?

A

Intra-articular corticosteroids have a quicker onset of action and shorter duration of action

76
Q

What are the usual sites of intra-articular corticosteroid administration?

A

Hip, knee, ankle, shoulder, elbow, wrist

77
Q

What technique should be used when administering an intra-articular corticosteroid?

A

Aseptic technique very important

78
Q

How frequently can a joint be injected? Why?

A
  • No firm answer
  • No more than 2-4x per year
  • Anymore and mechanical disruption in site can cause more damage
79
Q

Describe oral corticosteroid absorption. Result in regards to doasge form?

A

Exhibit rapid and complete absorption from the gut
Oral doses are equivalent to IV

80
Q

What is the conversion of an IV corticosteroid dose to an oral dose? Why?

A

Oral doses are equivalent to IV
Exhibit rapid and complete absorption from the gut

81
Q

What are the corticosteroids found in tablets?

A

Betamethasone
Cortisone
Dexamethasone
Hydrocortisone
Methylprednisolone
Prednisone
Triamcinolone

82
Q

What commercially oral solutions of corticosteroids are available?

A

Prednisolone (pediapred)

83
Q

What type of oral dosage form is Budesonide found in? What is each one used to treat?

A

Tablets –> Ulcerative colitis
Capsules –> Chron’s Disease

84
Q

Define a physiologic dose. What is a physiological dose used for?

A

Used to replace deficiencies (what the body will normally produce in a day)
- A dose equivalent to the amount of cortisol excreted by the adrenal cortex per day

85
Q

The amount of cortisol excreted by the adrenal cortex per day is equivalent to _______ prednisone

A

5 mg of prednisone per day

86
Q

Define pharmacological dose

A

a dose used to treat disease states and provide supportive therapy

87
Q

What is considered a “low dose” or “maintenance dose”of prednisone?

A

5-15 mg per day

88
Q

What is considered a “moderate dose” of prednisone?

A

0.5 mg/kg/day

89
Q

What is considered a high dose of prednisone?

A

1-3 mg/kg/day

90
Q

What is considered a “high or massive dose” of prednisone?

A

15-30 mg/kg/day

91
Q

What are the common adverse effects of opthalmic corticosteroids?

A
  • Stinging, redness
  • Tearing, burning
  • Secondary infection (immune-suppressant, more at risk of infection)
92
Q

What is a more serious a/e of opthlamic corticosteroids?

A

Formation of cataracts or glaucoma

93
Q

What are some adverse effects of oral inhalation corticosteroids? How can they be minimized?

A

Oral Thrush
Dry Mouth
Difficulty Swallowing
Dysphoria (voice change)

–> Rinse your mouth out

94
Q

What are some common adverse effects of nasal corticosteroids? How can they be minimized?

A

Rhinorhhea
Burning
Sneezing
Bloody Nose

–>Point away from nasal septum

95
Q

What are some adverse effects of topical corticosteroids?

A
  • Burning
  • Irritation
  • Skin atrophy
  • Tachyphylaxis (use for long time, effect starts to wear off)
  • Telangiectasia (spider veins)
96
Q

What are some systemic complications and adverse effects of oral corticosteroids?

A

Euphoria
Beign Intercranial HTN
Cataracts
Moon Face with red plethoric cheeks
Buffalo Hump
HTN
Thinning of skin
Increased abdominal fat
Avascular necrosis of femoral head
Easy Bruising
Poor Wound Healing
Thin arms and legs; muscle wasting

97
Q

CNS effects of corticosteroids are real and depend on the ________ (main factor). They may be ______ or _______.

A

Dose Related

May be Chronic or Acute

98
Q

What are the manifestations of CNS effects of corticosteroids?

A

Early Phase:
- Euphoria
- Insomnia
- Restlessness
- Memory Impairment

Late Phase: –>: Chronic Usage
- Altered Mood
- Depression
- Mania
- Psychosis

99
Q

Are CNS effects of corticosteroids permanent?

A

No - When you discontinue this meds, these manifestations will often abide/disappear

100
Q

What are the two worrisome opthalmic adverse effects? Why do these occur? What dosage forms do they occur with?

A

Cataracts and Glaucoma

–> Corticosteroids cause an increase in intraoccular pressure that may cause or worsen cataracts and glaucoma

  • Adverse effects of both topical and oral; however, worse with topical
101
Q

The risk cataracts and glaucoma depend on…..

A

The dose, strength and length of treatment

102
Q

What are the risk factors for cataracts with corticosteroids? There is an increased risk at what dose and duratio of prednisone? Counselling tip?

A
  • Daily dose, cumulative dose, duration, age
  • Increased risk with oral prednisone > 15 mg/d x 1 year
  • Long term corticosteroid users should have routine eye exams as damage is irreversible
103
Q

What is the difference between corticosteroid inducaed glaucoma and cataracts?

A

Cataract damage is irreversible whereas glaucoma (goes away) subsides when agent is d/c

104
Q

What are the risk factors for glaucoma induced by corticosteroids?

A
  • Pre-existing POAG (Glaucoma)
  • Diabetes
  • Family hx of glaucoma
  • RA (Rheumatoid Arthritis)
105
Q

When does glaucoma due to corticosteroids occur? Is the damage irreversible?

A
  • Typically occurs within the first few weeks
  • Subsides when agent is d/c
106
Q

Hypercortisolism presents with ___________ features because__________

A

Cushingoid Features

  • Alters normal fat distribution
107
Q

In regards to hypercortisolism, fat distribution presents as……

A
  • Fat redistribution from the periphery to the trunk
108
Q

Can hyperocortilosim occur with corticosteroids?

A

YES

  • Exogenous steroids increase steroid levels
109
Q

Hypercortisolism fat redistribution presents as_________ such as…….

A

Centripetal Obesity

  • Moon Face
  • Buffalo Hump
  • Protuberant Abdomen
110
Q

Face/Back (Cushingoid Features) occurs when? What does it depend on? Is it permanent?

A
  • Can occur in the first couple months; dose and duration dependent
  • Discontinued –> Will often resolve
111
Q

What is a common G.I. adverse effect of corticosteroids? Counselling tip?

A

Causes G.I. Upset

  • Take with food
112
Q

What are some common G.I. adverse effects of oral corticosteroids? Any drug interactions important to realize?

A
  • Dyspepsia
  • GI upset
  • Increased risk of peptic ulcer disease when used in conjunction with NSAID’s (more at increased risk, not uncommon to use both together)
113
Q

What are the main endocrine adverse effects of corticosteroids?

A

Glucose intolerance
Sodium/water retention
Increased Appetite

114
Q

What is glucose intolerance in regards to corticosteroids? Describe the physiology of how corticosteroids can cause glucose intolerance?

A

Use of corticosteroids can cause an increase in blood glucose

  • Mainly by: increased gluconeogenesis and decreased ultilization of glucose by the tissues
  • Also has effects on glucagon (increases) and catecholamines (increases)
115
Q

Glucose intolerance effects severity? Typically are related to what?

A
  • Increases in blood glucose are normally mild
  • Typically are dose related
116
Q

Increases in blood glucose are seen with what dose of prednisone?

A

Doses > or = to 15 mg/day

117
Q

Does corticosteroids only cause an increase in blood glucose in people with diabetes?

A
  • Increase in blood glucose can occur in those with or without diabetes
118
Q

How long does corticosteroid induced elevated BG last for?

A
  • Elevated BG may persist for months upon d/c
119
Q

How does sodium/water retention occur with corticosteroids?

A
  • Occurs due to a variety of actions corticosteroids have on the kidney and vasculature
120
Q

Sodium/water retention is a more common a/e of what corticosteroids?

A
  • corticosteroids with greatest mineralcorticoid activity are most likely to cause fluid retention
121
Q

What are some factors that pre-dispose someone on corticosteroids to sodium/water retention?

A
  • Age
  • History of high blood pressure
122
Q

Are sodium/water retention adverse effects permanent?

A
  • Usually resolves upon d/c of corticosteroids
123
Q

Increased appetite due to corticosteroid usage is usually seen with what dose?

A

High dose therapy

124
Q

In children, what is a primary concern of corticosteroids? What determines these effects?

A
  • All CS’s can affect growth patterns in children; the effects are dose-dependent and mainly with oral dosage forms
125
Q

All CS’s can affect growth patterns. True or False

A

True

126
Q

CS’s have many effects which could have an effect on growth. Examples include:

A

Decreasing osteoblasts
Decreased GH secretion
Competitively inhibiting insulin receptors

127
Q

What type of CS’s have the most pronounced affect on final height?

A
  • Oral Therapy
128
Q

Are the studies for growth retardation in CS’s usage in children profound? What should a pharmacist consider?

A
  • Can occur in kids but good studies are lacking
  • Consider the risk:benefit ratio
  • Another good reason to use the lowest dose for the shortest duration
129
Q

Compare growth retardation in oral CS’s to inhaled CS’s. Is inhaled progressive?

A
  • Oral - 4 cm in one study
  • Inhaled - Cochran review - 0.5 cm less growth in the first year –> less so in subsequent years, not cumulative, and may not affect final adult height
130
Q

Is CS’s growth retardation permenant?

A

Not necessarily

  • May catch up when come off of the steroid
131
Q

What is the HPA axis? What does it do?

A
  • A connection between the brain and adrenal glands
  • The body’s main stress system
  • It releases cortisol to activate a response to stress
132
Q

The human body’s main stress system is:

A

HPA-axis

133
Q

What is the physiologic secretion of the HPA-axis?

A

Normal Secretion: 10-20 mg/day of cortisol

134
Q

Cortisol secretion follows a ________ cycle

A

Diurnal

135
Q

When are endogenous levels of cortisol the highest? When is it the lowest?

A
  • Endogenous levels of cortisol are highest at 7-8 am
  • Decreases throughout the day and lowest at midnight
136
Q

Does cortisol cortisol secretion fluctuate? If so, when?

A
  • Yes
  • In periods of acute stress, there will be increased release (up to 10 fold release)
  • i.e. illness, stress, surgery
137
Q

Describe the process of HPA axis suppression.

A
  • The HPA axis is under negative feedback control by endogenous cortisol
  • Hence, when exogenous corticosteroids are administered, these cause negative feedback of CRH and ACTH
  • Result is the suppression of the HPA axis
138
Q

What is a main counselling tip for oral CS usage?

A

A patient who is taking enxogenous CS –> This cortisol is being ingested orally –> Disrupts this cycle. –> Inhibits this loop here –> No more CRH and ACTH telling the adrenals to release cortisol –> That is okay as long as people continue to take their corticosteroids

If suddenly under stress, body will not have the capability t produce more when they need more

CANNOT STOP TAKING THE MEDICATION SUDDENLY

Stressful situation –> May require more corticosteroid

139
Q

If HPA-axis suppression is present, what will happen if the steroids are abruptly stopped or if the patient becomes severely ill?

A
  • Hypotension
  • Hypoglycemia
  • Flue like sx: fatigue, N/V, chills, fever, myalgia
  • Weight loss
  • Confusion
140
Q

What are some of the factors that predict the occurrence of HPA-axis supression?

A
  • Dose
  • Type of steroid
  • Interval (10 mg QID does not equal 40 mg OD)
  • Duration
    -Route
  • Time of rhythym (want to follow circadian rhythym - dose it in the morning)
141
Q

In regards to interval of dosing, what is an important point to understand in regards to dosing of CS’s?

A
  • There is more HPA axis suppression if dosed throughout the day than once daily
142
Q

When should oral CS’s be dosed? Why?

A
  • IN THE MORNING (when endogenous cortisol levels are the highest)
143
Q

In regards to HPA axis supresison, at what doses does it occur for maintenance doses? How long does suppresion last for?

A

Maintenance Dosing = Long term use

Prednisone:
5-15 mg/day = variable
>15 mg/day = invariably (suppression) occurs

May take weeks to >1 year for HPA-axis to return to normal when d/c chronic steroids

144
Q

In regards to HPA-axis suppression, at what doses does it occur for short term doses?

A

Maybe:
1 mg/kg/day x 2 weeks
15-40 mg/day x1-4 weeks

No:
15-40mg/day x 5-7 days

145
Q

When is screening for HPA-axis suppression recommended?

A
  • Screening has been recommended for those who take oral CS’s for > 2 consecutive weeks or >3 cumulative weeks in the previous 6 months
146
Q

If HPA axis suppression occurs, how long till it fully recovers?

A
  • Between 1 to 3 years after cessation of exogenous steroids
  • In order to determine if HPA-axis suppression/recovery, a blood test can be performed: the SST (short Synacthen test) –> Synthetic ACTH given and plasma cortisol levels measured at 0, 30, 60 mins to see if it rises
  • NO CLEAR GUIDANCE ON WHEN TO PERFORM HPA-AXIS TESTING –> BASED OFF CLINICAL JUDGEMENT
147
Q

What is the occurence of adrenal insufficiency? Is it easy to predict? What is a recommendation for testing a pt for HPA-axis suppression?

A
  • CS’s used by 15 of the population and risk of adrenal insufficiency is 1 to 60%
  • Difficult to predict who will be insufficient or not
  • Sx’s of mild insufficiency are often non-desriptive
  • Options; Test, taper and see what happens, or stop and see what happens
  • Therefore: pt’s with unexplained sx’s after steroid withdrawal should be tested for HPA axis suppression
148
Q

In regards to immune system a/e of CS’s, what is the main worry? At what doses does this occur?

A
  • Increased susceptibility to infections
  • May see increased susceptibility to:
    i) Viral Infections (variecella zoster)
    ii) Bacterial Infections (Cellulitis)
    iii) Fungal infections (candida)
  • Typically does not occur in doses <10 mg/day (prednisone) or cumulative dose <700 mg
149
Q

What are some a/e associated with the skin/connective tissue with oral CS’s? How does CS’s cause these sx?

A
  • Acne (topical and oral)
  • Bruising
  • Thin Skin - typically rversible (chronic effecr, but will resolve)
  • Striae - Not reversible
  • Impaired wound healing
  • CS’s inhibit epidermal cell division and DNA synthesis
150
Q

What are some a/e of CS’s associated with bone? When do these a/e occur?

A

OSTEOPOROSIS

  • CS’s have multiple effects on bones:
    i) Protein catabolism
    ii) Osteoblast Inhibition
    iii) GH inhibition
    iv) Decreased Ca2+ absoprtion
    v) Decreased renal calcium reabsorption
  • Bone loss with CS’s occurs most rapidly in first 3 months and peaks at 6 months
151
Q

Bone loss associated CS’s a/e correlate to ________ and ________

A

Dose and Duration

152
Q

At what doses does risk of bone fracture increase? Duration?

A

Risk of fracture increases with doses as low as 2.5-7.5 mg/day

Systemic therapy >2-3 months is a major risk factor for bone loss (and fracture)

153
Q

What % of pt’s will develop osteoporosis with chronic tx?

A
  • 30-50% will develop osteoporosis with chronic tx
154
Q

In regards to bone health, what is a clinical practice tip that should be brought up to the pt and physician?

A
  • A fracture risk assesment should be performed on all adults initiating or continuing glucocorticoid therapy > or = to 2.5 mg/day for > 3 months
155
Q

What counselling tips should be provided to a pt about protecting bone health? What population?

A

Adults > or = 40 yrs old at moderate or high risk:

  • Optimize Calcium/Vit.D/Lifestyle
  • Strongly recommend osteoporosis tx (e.g. with a bisphosphonate - preventative tx)
156
Q

CS’s can also cause ________ along with osteoporosis

A

OSTEONECROSIS

157
Q

What is osteonecrosis? What Increases the risk? When do Sx occur? Counselling?

A
  • Death of bone tissue due to impaired blood supply
  • Risk increases with both dose and duration of CS’s
  • Symptoms usually develop after a few months to a few years
  • Long term users should be asked about joint pain/range of motion
158
Q

CS’s a/e of muscle? Dose? Sx?

A

Muscle (myopathy)

  • Muscle weakness may occur which may be due to dcreased protein synthesis in the muscle (CS’s have catabolic effects)
  • More common with prolonged courses of high dose CS’s (at prednisone doses > or = to 10 mg/day
  • Characterized by arm and leg weakness after several weeks to months of use
159
Q

What are some long term s/e’s in kids? When do they occur? What is the most common and serious a/e?

A

Weight gain (most common)
Growth retardation
Cushingoid features

Infection –> Most serious a/e

At least 15 days of tx

160
Q

What are some short course s/e of CS’s in kids? Are serious a/e’s common?

A
  • Vomitting (most common a/e for quitting)
  • Behavioural changes
  • Sleep disturbances

Serious AE’s are uncommon

161
Q

Short term use of CS’s is most commonly used for:
However, short term use is associated with…..

A
  • Most commonly for: URTI, spinal conditions, allergies, LRTI
  • Associated with higher rates of sepsis, VTE, and fracture (even though low dose, low time)
162
Q

Does short term use of CS’s mitigate all the risks of them?

A

NO

163
Q

Do CS’s have a role in COVID-19/ If so, which one?

A

Systemic CS’s improve clinical outcomes and decrease mortality in hospitalized patients requiring oxygen

Recommended Dose: DEX 6 mg od for up to 10 days