184: Glucocorticoids Flashcards
1
Q
What are the three main mechanisms of glucocorticoid action?
A
- Direct effects on gene expression: Glucocorticoid receptors bind to glucocorticoid-responsive elements, inducing proteins like annexin I and MAPK phosphatase, which reduce phospholipase A2 activity and limit prostaglandin and leukotriene formation.
- Indirect effects on gene expression: Glucocorticoid receptors interact with other transcription factors, inhibiting AP-1 and nuclear factor κB, which decreases the synthesis of proinflammatory molecules such as cytokines and interleukins.
- Receptor-mediated effects on second messenger cascades: This involves nongenomic pathways like the phosphatidylinositol 3′-kinase (PI3K)-Akt-eNOS pathway.
2
Q
What are the cellular side effects of corticosteroids?
A
- Monocytopenia, eosinopenia, and lymphocytopenia: Greater effect on T cells than B cells.
- Lymphocytopenia: Caused by redistribution of cells to other lymphoid tissues.
- Increase in circulating polymorphonuclear leukocytes: Related to demargination from the bone marrow.
- Decreased macrophage functions: Including phagocytosis and antigen processing, affecting hypersensitivity responses.
- Suppression of monocyte and lymphocyte function: More than polymorphonuclear leukocyte function, clinically significant in granulomatous diseases.
3
Q
What are the indications for glucocorticoid use in dermatology?
A
Short courses of glucocorticoids may be used for:
- Contact dermatitis
- Atopic dermatitis
- Photodermatitis
- Exfoliative dermatitis
- Erythrodermas
The use of glucocorticoids is controversial in treating:
- Erythema nodosum
- Lichen planus
- Cutaneous T-cell lymphoma
- Discoid lupus erythematosus.
4
Q
What factors determine the dosing regimen for systemic glucocorticoids?
A
The dosing regimen for systemic glucocorticoids is determined by:
1. Nature of the disease: The specific condition being treated.
2. Extent of the disease: Severity and spread of the lesions.
3. Route of administration: Options include intralesional, oral, intramuscular, and intravenous.
5
Q
What risks should be considered when prescribing glucocorticoids to a patient with granulomatous tuberculosis?
A
Glucocorticoids suppress monocyte and lymphocyte function, increasing the risk of exacerbation and relapse of granulomatous infectious diseases like tuberculosis.
6
Q
Why is the use of glucocorticoids in erythema nodosum controversial?
A
The use of glucocorticoids in erythema nodosum is controversial due to limited evidence supporting their efficacy in this condition.
7
Q
What is the likely mechanism for steroid-induced hyperglycemia?
A
Steroid-induced hyperglycemia occurs due to increased gluconeogenesis and insulin resistance caused by glucocorticoids.
8
Q
What is the likely mechanism for steroid-induced immunosuppression leading to infection?
A
Glucocorticoids suppress monocyte and lymphocyte function, reducing the immune response and increasing susceptibility to infections.
9
Q
What is the major naturally occurring glucocorticoid?
A
Cortisol (hydrocortisone), synthesized from cholesterol by the adrenal cortex.
10
Q
What percentage of circulating cortisol is unbound and active?
A
Less than 5%.
11
Q
What is the average daily cortisol production?
A
5 to 7 mg/m2, with a diurnal peak around 8:00 am.
12
Q
How do glucocorticoids affect macrophage functions?
A
They decrease macrophage functions, including phagocytosis, antigen processing, and cell killing.
13
Q
What routes can systemic glucocorticoids be administered?
A
Intralesionally, orally, intramuscularly, and intravenously.
14
Q
What is a consideration when using glucocorticoids on the face?
A
Lower concentrations are used to prevent atrophy of the skin.
15
Q
What are the two primary situations in which intravenous glucocorticoids are used?
A
- To provide stress coverage for patients who are acutely ill or undergoing surgery and have adrenal suppression from daily glucocorticoid use.
- For patients with certain diseases such as resistant pyoderma gangrenosum, severe pemphigus, or serious systemic lupus erythematosus, to gain rapid control of the disease and minimize the need for long-term, high-dose oral steroid therapy.
16
Q
What are the fundamental principles to consider before initiating therapy with glucocorticoids?
A
- Weigh the expected benefits against potential side effects.
- Consider alternative or adjunctive therapies, especially for long-term treatment.
- Take into account coexisting illnesses such as diabetes, hypertension, and osteoporosis.
- Assess the patient’s predisposition to side effects as part of the risk evaluation.
17
Q
What dietary recommendations should be followed for patients on glucocorticoids?
A
- Diet should be low in calories, fat, and sodium, and high in protein, potassium, and calcium as tolerated.
- Minimize the use of alcohol, coffee, and nicotine.
- Encourage exercise to help manage side effects.
18
Q
What precautions should be taken regarding infections for patients on glucocorticoids?
A
- Patients receiving glucocorticoid doses of 15 mg or greater for 1 month or longer should be screened for tuberculosis with a tuberculin skin test.
- Pay special attention to patients on high doses with underlying lung disease or low lymphocyte counts, as they are at increased risk for infections such as Pneumocystis pneumonia.
19
Q
What considerations should be made when choosing among glucocorticoids?
A
- Select a preparation with minimal mineralocorticoid effect to decrease sodium retention.
- Prefer long-term use of prednisone or similar drugs with intermediate half-life and weak steroid-receptor affinity to reduce side effects.
- If a patient does not respond to cortisone or prednisone, consider substituting with cortisol or prednisolone.
20
Q
What is the recommended limit for the total monthly dose of Kenalog to avoid HPA axis suppression?
A
20 mg.
21
Q
What serious side effects are associated with intravenous administration of glucocorticoids?
A
Anaphylactic reactions, seizures, arrhythmias, and sudden death.
22
Q
What should be monitored before and after pulse therapy with glucocorticoids?
A
Serum electrolytes.
23
Q
What is the importance of considering coexisting illnesses before starting glucocorticoid therapy?
A
To assess the risk of side effects and tailor treatment accordingly.
24
Q
What should be included in the baseline evaluation before starting glucocorticoid therapy?
A
A personal and family history with attention to predisposition to diabetes, hypertension, hyperlipidemia, glaucoma, and associated diseases.
25
What is the role of protein intake in the diet of patients on glucocorticoids?
To reduce steroid-induced nitrogen wasting.
26
What is the recommendation for immunization with live vaccines for patients on glucocorticoids?
Can be done if glucocorticoid use is less than 2 weeks at any dose or less than 20 mg/day.
27
What precautions should be taken regarding immunization with live vaccines in patients receiving high doses of glucocorticoids?
Immunization with live vaccines should not be done for at least 1 month after receiving high doses of glucocorticoids (>20 mg/day) for more than 2 weeks.
28
What is the recommended calcium and vitamin D supplementation for patients on glucocorticoid therapy for 3 months or longer?
Any patient anticipated to be on glucocorticoid therapy for 3 months or longer should receive calcium 1200 mg/day and vitamin D 800 International Units/day through diet and supplements.
29
What are the symptoms of adrenal insufficiency associated with long-term glucocorticoid therapy?
Symptoms of adrenal insufficiency include lethargy, weakness, nausea, anorexia, fever, orthostatic hypotension, hypoglycemia.
30
What are the symptoms of adrenal insufficiency associated with long-term glucocorticoid therapy?
Symptoms of adrenal insufficiency include lethargy, weakness, nausea, anorexia, fever, orthostatic hypotension, hypoglycemia, and weight loss.
31
What is the relationship between glucocorticoid therapy and cardiovascular disease risk?
Increased risk for ischemic heart disease and heart failure is associated with glucocorticoid therapy, particularly in patients with iatrogenic Cushing syndrome, due to mechanisms like hypercortisolism-induced hypertension and structural changes in the heart.
32
What should be done if a patient on glucocorticoids develops gastrointestinal complications?
If gastrointestinal complications develop, prophylaxis with a proton pump inhibitor should be initiated, especially in patients with 2 or more risk factors for peptic ulcer disease.
33
What is the significance of tapering glucocorticoids in patients with adrenal suppression?
Patients receiving daily glucocorticoid therapy for longer than 3 to 4 weeks must be assumed to have adrenal suppression, requiring a tapering of glucocorticoids to allow for recovery of the HPA axis.
34
A patient on long-term glucocorticoid therapy develops osteoporosis. What preventive measures could have been taken?
Patients on long-term glucocorticoid therapy should receive calcium (1200 mg/day) and vitamin D (800 IU/day) supplementation. Vitamin D levels should be checked and repleted before initiating therapy. Patients at high risk for osteoporosis should be evaluated for secondary causes.
35
A patient undergoing surgery has been on daily glucocorticoid therapy for 6 weeks. What perioperative management is required?
Patients on daily glucocorticoid therapy for longer than 3-4 weeks are assumed to have adrenal suppression. They should be maintained on their regular glucocorticoid dose, and clinicians should monitor for intraoperative hypotension or adrenal insufficiency.
36
A patient on glucocorticoids develops peptic ulcers. What could have been done to prevent this?
Patients on glucocorticoids and NSAIDs should receive prophylaxis with a proton pump inhibitor. Prophylaxis is especially important for patients with risk factors like a history of peptic ulcers.
37
A patient on glucocorticoids for 2 weeks is scheduled for a live vaccine. What should be done?
Live vaccines can be administered if glucocorticoid use is less than 2 weeks at any dose or if the dose is less than 20 mg/day.
38
A patient develops adrenal insufficiency after stopping glucocorticoids abruptly. What tapering strategy should have been used?
Glucocorticoids should be tapered gradually to allow recovery of the HPA axis. A slower taper or temporarily increasing the dose can help manage symptoms of adrenal insufficiency.
39
A patient with steroid withdrawal syndrome experiences lethargy and nausea. What is the cause?
Steroid withdrawal syndrome occurs when patients experience symptoms of adrenal insufficiency despite a normal cortisol response. It is due to the body's adjustment to high glucocorticoid levels.
40
A patient with steroid-induced hypertension is managed for cardiovascular risk. What should be monitored?
Blood pressure, diet, serum lipids, and glucose levels should be monitored serially. Abnormalities should be treated according to current guidelines.
41
A patient with steroid-induced osteoporosis is evaluated. What secondary causes should be considered?
Secondary causes like sarcoidosis or renal stones should be evaluated in patients with steroid-induced osteoporosis.
42
A patient with steroid-induced cataracts is evaluated. What is the likely cause?
Cataracts can develop even with alternate-day dosing of glucocorticoids, likely due to prolonged exposure to the drug.
43
A patient with steroid-induced adrenal suppression is undergoing surgery. What precautions should be taken?
Patients with adrenal suppression should be maintained on their regular glucocorticoid dose, and clinicians should monitor for signs of adrenal insufficiency during surgery.
44
A patient with steroid-induced gastrointestinal bleeding is evaluated. What prophylactic measures could have been taken?
Prophylaxis with a proton pump inhibitor should be initiated in patients on glucocorticoids and NSAIDs, especially those with risk factors for GI bleeding.
45
A patient with steroid-induced avascular necrosis is evaluated. What imaging is recommended?
MRI is recommended for early detection of avascular necrosis, especially if radiographs are normal but suspicion is high.
46
A patient with steroid-induced HPA axis suppression is evaluated. What is the mechanism?
HPA axis suppression occurs due to the body's adjustment to exogenous glucocorticoids, leading to reduced endogenous cortisol production.
47
A patient with steroid-induced hypertension is evaluated. What structural changes may occur?
Structural changes like ventricular hypertrophy and myocardial fibrosis may occur in steroid-induced hypertension.
48
A patient with steroid-induced osteoporosis is managed. What is the mechanism of bone loss?
Bone loss occurs due to decreased osteoblast activity, increased osteoclast activity, and reduced calcium absorption caused by glucocorticoids.
49
What should be avoided for at least 1 month after receiving high doses of glucocorticoids?
Immunization with live vaccines.
50
What is the recommended action for patients receiving glucocorticoid therapy for longer than 3 to 4 weeks?
They must be assumed to have adrenal suppression that requires tapering of the glucocorticoids.
51
What percentage of individuals treated long-term with systemic glucocorticoids develop osteoporosis?
40%.
52
What is a significant risk associated with glucocorticoid therapy and nonsteroidal anti-inflammatory agents?
Increased risk for peptic ulcer disease and GI bleeding.
53
What should patients on glucocorticoid therapy for 3 months or longer receive?
Calcium 1200 mg/day and vitamin D 800 International Units/day.
54
What is a common symptom of adrenal insufficiency due to glucocorticoid therapy?
Lethargy, weakness, nausea, anorexia, fever, orthostatic hypotension, hypoglycemia, and weight loss.
55
What is the recommended management for patients with increased cardiovascular risk due to glucocorticoid therapy?
Cardiovascular risk factors should be aggressively managed, including monitoring blood pressure, diet, serum lipids, and glucose levels.
56
What is the importance of early detection in avascular necrosis (AVN) related to glucocorticoid therapy?
Early intervention may prevent progression to degenerative joint disease requiring joint replacement.
57
What is the steroid withdrawal syndrome?
A condition where patients experience symptoms of adrenal insufficiency despite having a normal cortisol response to adrenocorticotropic hormone.
58
What are the implications of adrenal suppression in patients receiving glucocorticoid therapy for more than 3 to 4 weeks?
Patients receiving glucocorticoid therapy for longer than 3 to 4 weeks must be assumed to have adrenal suppression. This requires a tapering of glucocorticoids to allow recovery of the HPA axis. Clinicians should monitor for intraoperative hypotension and other signs of adrenal insufficiency in at-risk patients undergoing surgical procedures.
59
How should clinicians manage the risk of osteoporosis in patients on long-term glucocorticoid therapy?
Clinicians should evaluate patients anticipated to be on glucocorticoid therapy for 3 months or longer for osteoporosis. Recommendations include: 1. Administer calcium 1200 mg/day and vitamin D 800 International Units/day. 2. Monitor patients with comorbidities closely. 3. Consider checking vitamin D levels and repleting prior to maintenance therapy. 4. Evaluate secondary causes of osteoporosis in all patients.
60
What are the cardiovascular risks associated with long-term glucocorticoid therapy?
Long-term glucocorticoid therapy increases the risk for ischemic heart disease and heart failure, particularly in patients with iatrogenic Cushing syndrome. Contributing factors include hypertension and increased atherosclerosis. Structural changes such as ventricular hypertrophy and myocardial fibrosis may occur. Increased cardiovascular risk may persist for years after normalization of serum cortisol levels. Management should include regular monitoring of blood pressure, diet, serum lipids, and glucose levels.
61
What steps should be taken to prevent gastrointestinal complications in patients taking glucocorticoids?
To prevent gastrointestinal complications such as peptic ulcer disease and GI bleeding in patients taking glucocorticoids, clinicians should: 1. Initiate prophylaxis with a proton pump inhibitor for patients on combined therapy with a nonsteroidal anti-inflammatory agent. 2. Consider prophylaxis in patients with 2 or more risk factors, such as a history of peptic ulceration or advanced malignant disease.
62
What is the significance of the hypothalamic-pituitary-adrenal (HPA) axis suppression in patients on glucocorticoids?
The HPA axis is rapidly suppressed after the onset of glucocorticoid therapy, leading to symptoms of adrenal insufficiency such as lethargy, weakness, nausea, and weight loss. If therapy is limited to 1 to 3 weeks, recovery of the HPA axis is rapid. However, longer therapy can lead to a steroid withdrawal syndrome, where symptoms persist despite normal cortisol response. Management includes slower tapering of glucocorticoids or temporarily increasing the dose.
63
What are the psychiatric effects associated with glucocorticoid therapy?
Mood and cognitive changes are dose dependent and can appear shortly after starting glucocorticoids. Age and gender are risk factors for specific side effects: Women may be more likely to develop depression. Men may be more likely to develop mania. The risk of depression, mania, delirium, confusion, and disorientation increases with age, while the opposite is true for suicidal behavior and panic disorder. The incidence of neuropsychiatric events is highest in the first 3 months of therapy. Prednisone doses greater than 80 mg/day increase the risk for steroid psychosis.
64
What concerns should be considered regarding glucocorticoid use during lactation and pregnancy?
Glucocorticoids cross the placenta but are not teratogenic. They are secreted into breastmilk, but no adverse effects have been reported in breastfed infants of mothers taking glucocorticoids. Using prednisolone instead of prednisone and avoiding breastfeeding for 4 hours after a dose may decrease the amount of drug transferred during breastfeeding.
65
What issues are specific to pediatric patients when using glucocorticoids?
Glucocorticoids can cause growth suppression and early osteoporosis in pediatric patients. They inhibit bone formation, affect calcium and phosphorus metabolism, and interfere with growth hormone through: Effects on growth hormone secretion, growth hormone receptor expression, and signal transduction from growth hormone to target tissues. Osteoporosis can reverse after stopping glucocorticoids.
66
What are the mechanisms of action of topical corticosteroids?
Anti-proliferative effects: Inhibition of DNA synthesis and mitosis, reducing keratinocyte size and proliferation. Inhibition of fibroblast activity and collagen formation. Vasoconstriction: Topical steroids cause capillaries in the superficial dermis to constrict, reducing erythema. The mechanism is thought to involve inhibition of natural vasodilators (e.g., histamine, bradykinins, prostaglandins) and possibly augmentation of vascular tone.
67
What factors influence the pharmacokinetics of topical corticosteroids?
Patient-related factors: Age, extent and location of body surface area, presence or absence of inflammation. Drug-related factors: Concentration, duration of use, vehicle, intrinsic characteristics of the agent. Penetration varies by skin site, related to the thickness of the stratum corneum and vascular supply: Greater penetration through eyelids and scrotum than through forehead, palms, and soles.
68
A patient on glucocorticoids develops mood swings and confusion. What factors could have contributed to this?
Mood and cognitive changes are dose-dependent and can appear shortly after starting glucocorticoids. Prednisone doses >80 mg/day increase the risk of steroid psychosis. Age and gender also influence specific side effects.
69
A patient with steroid-induced psychosis is managed. What dose of prednisone is associated with this risk?
Prednisone doses greater than 80 mg/day are associated with an increased risk of steroid psychosis.
70
A patient with steroid-induced psychiatric effects is evaluated. What factors influence the risk?
Age, gender, and dose influence the risk of psychiatric effects. Women are more likely to develop depression, while men are more likely to develop mania.
71
What psychiatric effects can occur with glucocorticoid use?
Mood and cognitive changes, including depression and mania, can occur and are dose dependent.
72
Which gender is more likely to develop depression when using glucocorticoids?
Women are more likely to develop depression, whereas men may be more likely to develop mania.
73
What is the risk associated with prednisone doses greater than 80 mg/day?
Patients are at increased risk for steroid psychosis.
74
How do glucocorticoids affect lactation?
Glucocorticoids cross the placenta but are not teratogenic; they are also secreted into breastmilk with no reported adverse effects in breastfed infants.
75
What issues do glucocorticoids cause in the pediatric population?
They can cause growth suppression and early osteoporosis.
76
What is the mechanism of action of topical corticosteroids regarding cell proliferation?
They inhibit DNA synthesis and mitosis, reducing keratinocyte size and proliferation.
77
What effect do topical steroids have on dermal capillaries?
They cause capillaries in the superficial dermis to constrict, reducing erythema.
78
What factors influence the pharmacokinetics of glucocorticoids?
Patient-related factors such as age and body surface area, as well as drug-related factors like concentration and vehicle.
79
How does the penetration of topical steroids vary?
It varies according to the skin site and is related to the thickness of the stratum corneum and vascular supply.
80
What are the psychiatric effects associated with glucocorticoid therapy, and how do they vary by age and gender?
Mood and cognitive changes are dose-dependent and can appear shortly after starting glucocorticoids. Women may be more likely to develop depression, while men may be more likely to develop mania. The risk of depression, mania, delirium, confusion, and disorientation increases with age, but the opposite is true for suicidal behavior and panic disorder. The incidence of neuropsychiatric events is highest in the first 3 months of therapy. Prednisone doses greater than 80 mg/day increase the risk for steroid psychosis.
81
What precautions should be taken regarding glucocorticoid use during lactation and pregnancy?
Glucocorticoids cross the placenta, but they are not teratogenic. Although glucocorticoids are secreted into breastmilk, no adverse effects have been reported among breastfed infants of mothers taking glucocorticoids. Prednisolone instead of prednisone and avoiding breastfeeding for 4 hours after a dose may decrease the amount of drug transferred during breastfeeding.
82
What are the specific issues related to glucocorticoid use in the pediatric population?
In pediatrics, glucocorticoids can cause growth suppression and early osteoporosis. They inhibit bone formation, affect calcium and phosphorus metabolism, and interfere with growth hormone.
83
What are the effects of glucocorticoids on breastfed infants?
No adverse effects have been reported among breastfed infants of mothers taking glucocorticoids.
84
How can prednisolone usage affect breastfeeding?
Using prednisolone instead of prednisone and avoiding breastfeeding for 4 hours after a dose may decrease the amount of drug transferred during breastfeeding.
85
What specific issues are related to glucocorticoid use in pediatrics?
Glucocorticoids can cause growth suppression and early osteoporosis, inhibit bone formation, affect calcium and phosphorus metabolism, and interfere with growth hormone.
86
What is the mechanism by which topical corticosteroids exert antiproliferative effects?
Topical corticosteroids inhibit DNA synthesis and mitosis, reduce keratinocyte size and proliferation, and inhibit fibroblast activity and collagen formation.
87
How do topical corticosteroids induce vasoconstriction?
Topical steroids cause capillaries in the superficial dermis to constrict, reducing erythema by inhibiting natural vasodilators and possibly augmenting vascular tone.
88
What patient-related factors should be considered regarding glucocorticoids pharmacokinetics?
Factors include age, extent and location of body surface area, and presence or absence of inflammation.
89
What drug-related factors should be considered regarding glucocorticoids pharmacokinetics?
Factors include concentration, duration, vehicle, and intrinsic characteristics of the agent.
90
How does skin site affect glucocorticoid penetration?
Penetration varies by skin site, with greater absorption through eyelids and scrotum compared to forehead, palms, and soles.
91
What are the recommended methods for treating atopic dermatitis with topical corticosteroids?
Recommended methods include the soak and smear method, using occlusive dressings, and increasing hydration of the stratum corneum.
92
What precautions should be taken when using topical corticosteroids in pediatric patients?
Precautions include recognizing higher absorption in children, cautious application to the diaper area, selecting appropriate strength, and addressing corticosteroid phobia.
93
What is the recommended dosing regimen for topical corticosteroids?
The regimen includes twice-daily application for most, once-daily for superpotent corticosteroids, and awareness of tachyphylaxis with long-term use.
94
What are the potential side effects of topical corticosteroids?
Potential side effects include local irritation, systemic absorption, tachyphylaxis, and the need for monitoring as only 1% remains therapeutically active.
95
What considerations should be made when using topical corticosteroids in elderly patients?
Considerations include thinner skin, preexisting skin atrophy, corticosteroid phobia, and using similar precautions as for infants.
96
What precautions should be taken for pediatric patients prescribed high-potency topical corticosteroids?
Use high-potency corticosteroids for short courses only, guided by body site, extent of involvement, and flare intensity.
97
What precautions should be taken when prescribing topical corticosteroids during pregnancy?
Mild or moderate corticosteroids are generally safe; high-potency steroids should be used cautiously due to a risk of low birth weight.
98
What does the soak-and-smear method involve?
It involves taking a warm bath followed by a generous application of topical corticosteroids.
99
What is tachyphylaxis in the context of topical corticosteroids?
Tachyphylaxis occurs due to diminished vasoconstriction, rebound DNA synthesis, and recovery of histamine wheals after long-term use.
100
What should be done with topical corticosteroids prior to breastfeeding?
Topical corticosteroids should be wiped off prior to breastfeeding.
101
What are the potential side effects of applying corticosteroids to large surface areas?
Increased risk of systemic absorption and subsequent side effects.
102
What is the significance of occlusion when applying topical steroids to the diaper area?
Occlusion results in increased penetration of the steroid, enhancing its effectiveness.
103
What is a common concern among patients regarding corticosteroid use?
Corticosteroid phobia, which can lead to treatment noncompliance.
104
Why is it important to select the appropriate strength of topical corticosteroids?
It is essential for treatment success based on the body site and extent of involvement.
105
What factors should be considered when selecting the strength of topical corticosteroids for pediatric patients?
Consider body surface area to weight ratio, skin thickness, site of application, extent of involvement, and flare intensity.
106
What precautions should be taken when using topical corticosteroids in elderly patients?
Consider skin condition, preexisting conditions, corticosteroid phobia, and apply similar precautions as for infants.
107
What is the recommended dosing regimen for topical corticosteroids, and how does it vary with potency?
General recommendation is twice-daily application; superpotent corticosteroids may be effective once-daily, and tachyphylaxis should be considered.
108
What are the potential side effects of topical corticosteroids and how can they be monitored?
Local side effects, systemic side effects from large surface areas, and monitoring for tachyphylaxis and cutaneous adverse effects.
109
What considerations should be made regarding the use of topical corticosteroids during pregnancy and breastfeeding?
Most topical steroids are category C; mild or moderate steroids are generally safe, while high-potency may pose risks.
110
What are the potential adverse effects of topical corticosteroids related to skin atrophy?
Skin atrophy involves epidermis and dermis, leading to loss of dermal support and increased risk of bruising and ulceration.
111
What are the common cutaneous effects associated with the use of topical corticosteroids?
Decreased pigmentation, hypertrichosis, and burning sensation after withdrawal.
112
How can topical corticosteroids affect the development of infections?
They may exacerbate or mask cutaneous infectious diseases, including tinea versicolor and dermatophytosis.
113
What should be suspected if dermatitis worsens with corticosteroid therapy?
Allergic contact dermatitis from steroids should be suspected.
114
What is a well-known complication of diaper dermatitis during corticosteroid treatment?
Granuloma gluteale infantum, characterized by reddish-purplish granulomatous lesions.
115
What systemic effect can high-potency topical glucocorticoids cause?
HPA axis suppression.
116
What are the potential cutaneous adverse effects of topical corticosteroids, particularly regarding skin atrophy?
Skin atrophy, vascular dilation, purpura, easy bruising, and ulceration.
117
What conditions should be suspected if dermatitis worsens with corticosteroid therapy?
Allergic contact dermatitis from steroids.
118
What are the potential cutaneous adverse effects of topical corticosteroids?
- Skin atrophy is a prominent adverse effect involving the epidermis and dermis.
- It develops from the antiproliferative effects on fibroblasts, inhibiting collagen and mucopolysaccharide synthesis, leading to loss of dermal support.
- Fragmentation and thinning of elastic fibers occur in the upper dermis, while deeper fibers remain compact.
- Atrophy is more likely with high-potency corticosteroids, but can be reversed by reducing potency.
119
How do topical corticosteroids affect the development of infections?
Topical corticosteroids can exacerbate and/or mask cutaneous infectious diseases, including:
- Tinea versicolor
- Disseminated Alternaria infection
- Dermatophytosis
Additionally, they can lead to granuloma gluteale infantum, characterized by reddish-purplish lesions in the diaper area.
120
What steps should be taken if dermatitis worsens with corticosteroid therapy?
1. Patch testing to identify if the vehicle or the steroid is causing the contact dermatitis.
2. If patch testing is unavailable, prescribe a Class C steroid based on cross-reactivity with allergic contact dermatitis.
121
What systemic adverse effects can result from the use of high-potency topical glucocorticoids?
High-potency topical glucocorticoids, especially Class 1 agents, may lead to HPA axis suppression and rarely, other systemic adverse effects.
122
What are the categories of responsiveness of dermatoses to topical corticosteroids?
| Responsiveness Level | Conditions |
|---------------------|------------|
| Highly responsive | Atopic dermatitis (children), Intertrigo, Psoriasis (intertriginous), Seborrheic dermatitis |
| Moderately responsive| Atopic dermatitis (adults), Lichen simplex chronicus, Nummular eczema, Papular urticaria, Parapsoriasis, Psoriasis |
| Least responsive | Allergic contact dermatitis, acute phase, Dyshidrotic eczema, Granuloma annulare, Insect bites, Lichen planus, Lupus erythematosus, Necrobiosis lipoidica diabeticorum, Palmoplantar psoriasis, Pemphigus, Psoriasis of nails, Sarcoidosis |
123
What are the principles to follow when initiating topical steroid therapy?
1. Initiate lowest potency to sufficiently control disease.
2. Avoid topical corticosteroids on ulcerated or atrophic skin, and on skin with coexisting infections.
3. Avoid prolonged use of insufficiently potent agent.
4. Use low to medium potency preparations for large surface areas.
5. Highly responsive diseases usually require weak steroid preparations, while less-responsive diseases need medium- or high-potency topical steroids.
6. Very potent steroid therapy, especially under occlusion, is needed for hyperkeratotic or lichenified dermatoses.
7. High-potency preparations should be avoided in infants and young children, except for short-term application.
124
What are the recommendations for continuing the use of topical steroids?
- Use highly potent formulations for short periods (2 to 3 weeks) or intermittently.
- If disease control is partially achieved, initiate a less-potent compound.
- Reduce frequency of application (e.g., apply only in the morning, alternate-day therapy) once disease control is partially achieved.
- Avoid sudden discontinuation to prevent rebound phenomena.
- Follow special guidelines when treating certain body areas (e.g., intertriginous areas, elderly) to prevent local or systemic adverse effects.
- Monitor closely and evaluate if systemic absorption is suspected; consider adding topical calcineurin inhibitors or other agents.
125
What are potential allergens found in topical corticosteroid vehicles?
- Formaldehyde-releasing preservatives (imidiazolidinylurea, diazolidinylurea)
- Fragrance
- Lanolin
- Methylchloroisothiazolinone/methylisothiazolinone
- Parabens
- Propylene glycol
- Sorbitan sesquioleate
126
What are the characteristics of highly responsive dermatoses to topical corticosteroids?
Highly responsive dermatoses include atopic dermatitis (children), intertrigo, psoriasis (intertriginous), and seborrheic dermatitis.
127
What should be done once disease control is partially achieved with topical steroids?
Reduce frequency of application and consider using a less-potent compound.
128
What is recommended for large surface areas when initiating topical steroid therapy?
Treatment with low to medium potency preparations is recommended.
129
What should be avoided when using topical corticosteroids on ulcerated or atrophic skin?
Topical corticosteroids should be avoided on ulcerated or atrophic skin, and on skin with coexistent infectious dermatoses.
130
What are potential allergens in topical corticosteroid vehicles?
Potential allergens include formaldehyde-releasing preservatives, fragrance, lanolin, and parabens.
131
What is the recommendation for highly responsive diseases when using topical steroids?
Highly responsive diseases will usually respond to weak steroid preparations, while less-responsive diseases require medium- to high-potency topical steroids.
132
What should be monitored when using high-potency topical steroids?
Close monitoring and further evaluation should be conducted if systemic absorption of corticosteroids is suspected.
133
What is the classification of corticosteroids based on cross-reactivity?
Corticosteroids are classified based on structural class and potential cross-reactivity with other substances.
134
What are the recommended practices for initiating topical steroid therapy in patients with various skin conditions?
1. Initiate lowest potency to sufficiently control disease.
2. Avoid topical corticosteroids on ulcerated or atrophic skin and on skin with coexisting infections.
3. Avoid prolonged use of insufficiently potent agents.
4. Use low to medium potency preparations for large surface areas.
5. Highly responsive diseases should use weak steroid preparations; less-responsive diseases may require medium- or high-potency steroids.
6. Very potent steroids should be used with occlusion for conditions like hyperkeratotic or lichenified dermatoses.
7. Caution with high-potency preparations in infants and young children for short-term application.
135
What are the guidelines for the continued use of topical steroids to prevent rebound phenomena?
1. Use highly potent formulations for short periods (2 to 3 weeks) or intermittently.
2. Once disease control is partially achieved, switch to a less-potent compound.
3. Reduce frequency of application (e.g., apply only in the morning, alternate-day therapy) once disease control is partially achieved.
4. Avoid sudden discontinuation to prevent rebound phenomena.
5. Follow special guidelines when treating certain body areas (e.g., intertriginous areas, elderly) to prevent local or systemic adverse effects.
6. Monitor closely and evaluate if systemic absorption of corticosteroids is suspected.
136
What are the potential allergens found in topical corticosteroid vehicles that practitioners should be aware of?
| Potential Allergen | Description |
|-------------------|-------------|
| Formaldehyde-releasing preservatives | Imidazolidinylurea / Diazolidinylurea |
| Fragrance | Common irritant and allergen |
| Lanolin | Potential skin irritant |
| Methylchloroisothiazolinone | Preservative that can cause allergic reactions |
| Parabens | Common preservatives that may cause sensitivity |
| Propylene glycol | Can cause irritation in sensitive individuals |
| Sorbitan sesquioleate | Potential allergen in topical formulations |
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How does the responsiveness of different dermatoses to topical corticosteroids vary?
| Responsiveness Level | Dermatoses |
|---------------------|------------|
| Highly responsive | Atopic dermatitis (children), Intertrigo, Psoriasis (intertriginous), Seborrheic dermatitis |
| Moderately responsive | Atopic dermatitis (adults), Lichen simplex chronicus, Nummular eczema, Papular urticaria, Parapsoriasis, Primary irritant dermatitis, Psoriasis |
| Least responsive | Allergic contact dermatitis, Acute phase, Dyshidrotic eczema, Granuloma annulare, Insect bites, Lichen planus, Lupus erythematosus, Necrobiosis lipoidica diabeticorum, Palmoplantar psoriasis, Pemphigus, Psoriasis of nails, Sarcoidosis |
