ECZEMA
If it’s not Itch It’s not Eczema
Eczema is a group of medical conditions which
causes inflammation and irritation to skin.
It is also called as Dermatitis
Dr. Ayesha Fatima, Pharm D
Assistant Professor
Department of Pharmacy Prctice
Eczema is an itchy consisting of ill defined
erythremotous patches. The skin surface is usually
scaly and As time progress, constant scratching leads
to thickened lichenified skin.
Lichenified Skin
Classification of Eczema
Several classifications of eczemas are available based on Etiology,
Pattern and chronicity
Aetiology
According to aetiology Eczema are classified as:
• Endogenous eczema: Where constitutional factors predispose the
patient to developing an eczema.
• Family history (maternal h/o eczema) is often present
• Strong genetic predisposition (Filaggrin gene mutations are often
present).
• Filaggrin is responsible for maintaining moisture in skin (hence all
AD patients have dry skin.
• Immunilogical factor-Th-2 disease, Type I hypersensitivity (hence
serum IgE high)
e.g., Seborrheic dermatitis, Statis dermatitis, Nummular
dermatitis, Dyshidrotic Eczema
•Exogenous eczema: Where external stimuli trigger
development of eczema,
e.g., Irritant dermatitis, Allergic Dermatitis,
Neurodermatitis,
• Combined eczema: When a combination of
constitutional factors and extrinsic triggers are
responsible for the development of eczema
e.g., Atopic dermatitis
Extrinsic triggers
1. Extremes of Temperature
2. Irritants : Soaps, Detergents, Shower gels,
Bubble baths and water
3. Stress
4. Infection either bacterial or viral,
Bacterial infections caused by
Staphylococcus aureus and Streptococcus
species.
Viral infections such as Herpes Simplex,
Molluscum Contagiosum
5. Contact allergens
6. Inhaled allergens
7. Airborne allergens
Allergens include
• Metals eg. Nickle, Cobalt
• Neomycin, Topical
ointment
• Fragrance ingredients such
as Balsam of Peru
• Rubber compounds
• Hair dyes for example p-
Phenylediamine
• Plants eg. Poison ivy
Atopic Dermatitis
AD is a chronic, pruritic inflammatory skin
disease characterized by itchy inflamed skin
Types of Eczema
Allergic Dermatitis
A red itchy weepy reaction where the skin has come
in contact with a substance That immune system
recognizes as foreign substances.
Ex: Poison envy, Preservatives from creams and
lotions
Contact Irritant Dermatitis
A Localized reaction that include redness, itching and burning where the skin
has come In contact with an allergen or with irritant such as acid, cleaning
agent or chemical
Dyshidrotic Eczema
Irritation of skin on the palms and soles by
clear deep blisters that itch and burn
Nummular Eczema / Discoid Eczema
Coin shaped patches of irritant skin common on
ARMS, BACK, BUTTLOCKS, LOWER LEGS
that may be crusted scaling and extremely itch
Seborrheic Eczema
Yellowish, oily and scaly patches
on the scalp and face
Stasis Dermatitis
A skin irritation to lower legs, generally related
to circulatory problems
Pathogenesis
•Endogenous eczema:
Clinical Features
Acute Eczema:- Acute eczema is characterized
by an erythematous and edematous plaque,
which is ill-defined and is surmounted by
papules, vesicles, pustules and exudate that
dries to form crusts. A subsiding eczematous
plaque may be covered with scales.
Chronic Eczema:- Chronic eczema is
characterized by lichenification, which is a
triad of hyperpigmentation, thickening
markings. The lesions are less exudative and
more scaly. Flexural lesions may develop
fissures.
❖ Pruritus
❖ Characteristic Rash
❖ Chronic or repeatedly occurring symptoms
❖ Family history
Diagnosis
The diagnosis of eczema is based on following Features:
Acute eczema: Itchy exudative plaques, surmounted by
papulovesicles.
Chronic eczema: Lichenified scaly plaques.
It is important to differentiate between endogenous and exogenous eczema.
Endogenous eczema:
● Symmetrical distribution.
● Well-set patterns like atopic dermatitis or seborrheic dermatitis.
Exogenous eczema:
● Asymmetrical distribution; sometimes linear or rectilinear
configuration.
● Known contact with irritants and allergens.
● Well-set pattern like airborne contact dermatitis.
Investigations to Find Cause of Eczema
Some eczemas need to be investigated extensively while others can be treated
without investigations.
The rule of the thumb is to treat acute eczemas without investigations while chronic
and recurrent eczema should be investigated.
Patch Tests: Patch tests are very useful in finding the cause of allergic but not
irritant dermatitis, i.e., they detect allergens responsible for type IV allergy.
Prick Tests: Type I hypersensitivity is detected by prick tests.Relevance of positive
prick tests in determining the cause of eczema (atopic dermatitis) andurticaria,
however, is debatable.
Serological Tests: Total serum IgE levels and IgE antibodies specific to certain
antigens (measured using radioallergosorbent test or RAST) may be useful in
diagnosis in atopic states.
RAST help to identify specific (dietary and environmental) allergens which may be
perpetuating dermatitis in an atopic patient. Most dermatologists, however, doubt
the relevance of this test.
Goals of treatment for eczema:-
1. Control Itching
2. Identify and when possible minimize triggering
factors
3. Identify and minimize predisposing factors for
exacerbations
4. Minimize the adverse effects from medications
5. Prevent future exacerbations
6. Provide social and Psychological Support
Treatment
Non Pharmacological Measures
1. Use of moisturizers :- To improve hydration. The active ingredient used as
mineral oil, petroleum jelly, ceramide and urea
● Mineral oil: Blocks the loss of water from skin allowing greater
hydration.
● Petroleum jelly: Modulator of antimicrobial activity on the skin
preventing infections.
● Ceramide: Enhances skin barrier by preventing water loss by reducing
permeability and optimising pH for endogenous biosynthesis of
proteins.
● Urea: Dissolves intracellular matrix of cells of St. Corneum,
promoting desquamation of scaly skin resulting in softening of
hyperkeratotic area.
Types of moisturizers :-
1. Occlusives :- Provide oily layer on the surface to slow
transepidermal water loss thus increases moisture
content.
2. Humectants:- Increases the water holding capacity in
stratum corneum, thus increases the moisture. It gives
stinging effect
3. Emollients:- Smooth out the surface of the skin by
filling the spaces with droplets of oil.
2. Banding/ wet wrap therapy :-
● Occlusion with bandage is useful to prevent scratching and
potentiate the action of the ointment or cream on the lesion.
● Wet wrapping involve application of emollients and steroids
under double layer to keep inner layer moist, promotes skin
hydration reducing disease severity.
3. Wear cotton fabrics, non polyesters
4. Avoid overheating
5. Identify and remove irritants
6. Use sedating antihistamines at bedtime to reduce scratching
Pharmacological Therapy
1. Topical Therapy
i. Topical Corticosteroids
ii. Topical Calcineurin inhibitors
iii.Coaltar
iv. Topical Imidazoles
2. Phototherapy
3. Systemic Therapy
i. Systemic Corticosteroids
ii. Cyclosporin
iii.Azathioprine
iv. Methotrexate
v. Antihistamines
vi. Mycophenolate mofetil
vii.IV Immunoglobulins
1. Topical corticosteroids
❖ First line treatment for eczema.
❖ Produces anti inflammatory effect by binding to intracellular corticosteroid
receptor and gene regulation which codes for proinflammatory cytokines.
❖ The choice depends on the site and severity of infection.
❖ Low potent, Potent TCs i.e Hydrocortisone 1% are suitable for face, genitals
and flexures.
❖ Medium potent i.e Betamethasone 0.1% used for other parts of body.
❖ Twice daily application till inflammatory lesion significantly improves and can
continue upto 1 week to several weeks.
❖ Once control is achieved stop the use and use of moisturizers until next flare up.
❖ AE-
❖ Local - Skin atrophy, periorbital dermatitis, acne, focal hypertrichosis,
allergic contact dermatitis.
❖ Systemic - Hypothalamic pituitary adrenal suppression, Cataract,
glaucoma, growth retardation
2. Topical Calcineurin inhibitors
❖ MOA: Inhibit activation of T cells and most cells by
blocking the production of cytokines and its mediators.
❖ Tacrolimus ointment and Pimecrolimus cream reduce
severity, extend and symptoms of disease in children and
adult.
❖ Tacrolimus ointment : Derived from oral medicine FK506.
0.1% and 0.03% preparation used in treatment of moderate to
severe Eczema.
❖ Pimecrolimus cream - 1% : Indicated for short term,
intermittent use for mild to moderate eczema.
❖ AE - Burning, stinging, increases risk for malignancy.
3. Coal Tar
❖ Tar cream and ointment is used in the management of
hyperkeratotic lichenified eczema, by acting as an
antipruritic agent.
❖ Not recommended on acutely inflamed skin lesion.
❖ Less cosmetically acceptable due to staining and
malodorous.
3. Topical Imidazoles
❖ Ketoconazole shampoo or cream is effective in reduction of
Pityrosporum ovale on skin.
❖ Useful in the management of Seborrhoeic dermatitis.
Phototherapy
➔ Phototherapy can be effective second line therapy, when the
disease is not controlled by TCS or Topical calcineurin inhibitors.
➔ Used to treat acute or maintenance therapy in adults and children.
➔ It consist of UV light alone or Along with UV light systemic or
topical agent.
➔ UV A + Psoralances or NBUVB + Coal tar is the effective
treatment for acute eczema
➔ Contraindicated in Photosensitive eczema
➔ AE -
◆ Short term - Erythema, skin pain, skin burn, Sunburn,
Pruritus, Pigmentation
◆ Long term - Premature aging of skin, folliculitis, Photo
Onycholysis, facial hypertrichosis, skin cancer.
Systemic therapy - Used when Topical and phototherapy do not
adequately control the disease
1. Systemic corticosteroids
❖ Short term - Oral prednisolone used in management of severe acute
eczema which require rapid control.
❖ Long term - Rarely used due to adverse effects and risk of HTN and
osteoporosis.
1. Azathioprine
❖ It is a purine analogue that inhibits DNA synthesis and can be
effective as monotherapy in Adult eczema
1. Methotrexate
❖ Used as second line agent for moderate to severe atopic dermatitis.
4. Cyclosporin
❖ It is a systemic immunosuppression that blocks activation of T-
lymphocytes
❖ It is effective for short term therapy for severe chronic adult eczema
with rapid onset of action.
❖ Intermittent doses of 2.5 - 5 mg/kg/day are effective with maximum
benefit observed after 2 to 6 weeks of therapy and relapse may occur
quickly after cessation of therapy.
❖ AE - Dose related nephrotoxicity - hence monitoring of Sr.
Creatinine is essential, HTN, Increases risk for cancer.
❖ DFI - Grapefruit juice - Increases blood levels of cyclosporine
increasing risk for nephrotoxicity.
4. Antihistamines
❖ No direct impact on pruritis, main effect is sedation.
1. Illustrated Synopsis of Dermatology and Sexually Transmitted
Diseases, Fourth Edition.
Neena Khanna, MD
Professor
Department of Dermatology and Venereology
All India Institute of Medical Sciences
New Delhi, India
2. Review of Dermatology, Fourth Edition
Saurabh Jindal, MD, DNB, DDV
Department of Dermatology and Venereology
Dr.Jindal Clinic
New Delhi, India
3. Dipiro
Reference:-
Scabies
Impetigo
Psoriasis
Psoriasis
Psoriasis Vulgaris
Guttate Psoriasis
Scalp Psoriasis
Nail Psoriasis
Palmoplantar Psoriasis
Erythrodermic Psoriasis
Generalized Pustular
Psoriasis

ECZEMA 3rd year notes with images .pptx

  • 1.
    ECZEMA If it’s notItch It’s not Eczema Eczema is a group of medical conditions which causes inflammation and irritation to skin. It is also called as Dermatitis Dr. Ayesha Fatima, Pharm D Assistant Professor Department of Pharmacy Prctice
  • 2.
    Eczema is anitchy consisting of ill defined erythremotous patches. The skin surface is usually scaly and As time progress, constant scratching leads to thickened lichenified skin. Lichenified Skin
  • 3.
    Classification of Eczema Severalclassifications of eczemas are available based on Etiology, Pattern and chronicity
  • 4.
    Aetiology According to aetiologyEczema are classified as: • Endogenous eczema: Where constitutional factors predispose the patient to developing an eczema. • Family history (maternal h/o eczema) is often present • Strong genetic predisposition (Filaggrin gene mutations are often present). • Filaggrin is responsible for maintaining moisture in skin (hence all AD patients have dry skin. • Immunilogical factor-Th-2 disease, Type I hypersensitivity (hence serum IgE high) e.g., Seborrheic dermatitis, Statis dermatitis, Nummular dermatitis, Dyshidrotic Eczema
  • 5.
    •Exogenous eczema: Whereexternal stimuli trigger development of eczema, e.g., Irritant dermatitis, Allergic Dermatitis, Neurodermatitis, • Combined eczema: When a combination of constitutional factors and extrinsic triggers are responsible for the development of eczema e.g., Atopic dermatitis
  • 6.
    Extrinsic triggers 1. Extremesof Temperature 2. Irritants : Soaps, Detergents, Shower gels, Bubble baths and water 3. Stress 4. Infection either bacterial or viral, Bacterial infections caused by Staphylococcus aureus and Streptococcus species. Viral infections such as Herpes Simplex, Molluscum Contagiosum 5. Contact allergens 6. Inhaled allergens 7. Airborne allergens Allergens include • Metals eg. Nickle, Cobalt • Neomycin, Topical ointment • Fragrance ingredients such as Balsam of Peru • Rubber compounds • Hair dyes for example p- Phenylediamine • Plants eg. Poison ivy
  • 7.
    Atopic Dermatitis AD isa chronic, pruritic inflammatory skin disease characterized by itchy inflamed skin Types of Eczema
  • 8.
    Allergic Dermatitis A reditchy weepy reaction where the skin has come in contact with a substance That immune system recognizes as foreign substances. Ex: Poison envy, Preservatives from creams and lotions
  • 9.
    Contact Irritant Dermatitis ALocalized reaction that include redness, itching and burning where the skin has come In contact with an allergen or with irritant such as acid, cleaning agent or chemical
  • 10.
    Dyshidrotic Eczema Irritation ofskin on the palms and soles by clear deep blisters that itch and burn
  • 11.
    Nummular Eczema /Discoid Eczema Coin shaped patches of irritant skin common on ARMS, BACK, BUTTLOCKS, LOWER LEGS that may be crusted scaling and extremely itch
  • 12.
    Seborrheic Eczema Yellowish, oilyand scaly patches on the scalp and face
  • 13.
    Stasis Dermatitis A skinirritation to lower legs, generally related to circulatory problems
  • 14.
  • 16.
    Clinical Features Acute Eczema:-Acute eczema is characterized by an erythematous and edematous plaque, which is ill-defined and is surmounted by papules, vesicles, pustules and exudate that dries to form crusts. A subsiding eczematous plaque may be covered with scales. Chronic Eczema:- Chronic eczema is characterized by lichenification, which is a triad of hyperpigmentation, thickening markings. The lesions are less exudative and more scaly. Flexural lesions may develop fissures. ❖ Pruritus ❖ Characteristic Rash ❖ Chronic or repeatedly occurring symptoms ❖ Family history
  • 17.
    Diagnosis The diagnosis ofeczema is based on following Features: Acute eczema: Itchy exudative plaques, surmounted by papulovesicles. Chronic eczema: Lichenified scaly plaques. It is important to differentiate between endogenous and exogenous eczema. Endogenous eczema: ● Symmetrical distribution. ● Well-set patterns like atopic dermatitis or seborrheic dermatitis. Exogenous eczema: ● Asymmetrical distribution; sometimes linear or rectilinear configuration. ● Known contact with irritants and allergens. ● Well-set pattern like airborne contact dermatitis.
  • 18.
    Investigations to FindCause of Eczema Some eczemas need to be investigated extensively while others can be treated without investigations. The rule of the thumb is to treat acute eczemas without investigations while chronic and recurrent eczema should be investigated. Patch Tests: Patch tests are very useful in finding the cause of allergic but not irritant dermatitis, i.e., they detect allergens responsible for type IV allergy. Prick Tests: Type I hypersensitivity is detected by prick tests.Relevance of positive prick tests in determining the cause of eczema (atopic dermatitis) andurticaria, however, is debatable. Serological Tests: Total serum IgE levels and IgE antibodies specific to certain antigens (measured using radioallergosorbent test or RAST) may be useful in diagnosis in atopic states. RAST help to identify specific (dietary and environmental) allergens which may be perpetuating dermatitis in an atopic patient. Most dermatologists, however, doubt the relevance of this test.
  • 19.
    Goals of treatmentfor eczema:- 1. Control Itching 2. Identify and when possible minimize triggering factors 3. Identify and minimize predisposing factors for exacerbations 4. Minimize the adverse effects from medications 5. Prevent future exacerbations 6. Provide social and Psychological Support Treatment
  • 20.
    Non Pharmacological Measures 1.Use of moisturizers :- To improve hydration. The active ingredient used as mineral oil, petroleum jelly, ceramide and urea ● Mineral oil: Blocks the loss of water from skin allowing greater hydration. ● Petroleum jelly: Modulator of antimicrobial activity on the skin preventing infections. ● Ceramide: Enhances skin barrier by preventing water loss by reducing permeability and optimising pH for endogenous biosynthesis of proteins. ● Urea: Dissolves intracellular matrix of cells of St. Corneum, promoting desquamation of scaly skin resulting in softening of hyperkeratotic area.
  • 21.
    Types of moisturizers:- 1. Occlusives :- Provide oily layer on the surface to slow transepidermal water loss thus increases moisture content. 2. Humectants:- Increases the water holding capacity in stratum corneum, thus increases the moisture. It gives stinging effect 3. Emollients:- Smooth out the surface of the skin by filling the spaces with droplets of oil.
  • 22.
    2. Banding/ wetwrap therapy :- ● Occlusion with bandage is useful to prevent scratching and potentiate the action of the ointment or cream on the lesion. ● Wet wrapping involve application of emollients and steroids under double layer to keep inner layer moist, promotes skin hydration reducing disease severity. 3. Wear cotton fabrics, non polyesters 4. Avoid overheating 5. Identify and remove irritants 6. Use sedating antihistamines at bedtime to reduce scratching
  • 23.
    Pharmacological Therapy 1. TopicalTherapy i. Topical Corticosteroids ii. Topical Calcineurin inhibitors iii.Coaltar iv. Topical Imidazoles 2. Phototherapy 3. Systemic Therapy i. Systemic Corticosteroids ii. Cyclosporin iii.Azathioprine iv. Methotrexate v. Antihistamines vi. Mycophenolate mofetil vii.IV Immunoglobulins
  • 24.
    1. Topical corticosteroids ❖First line treatment for eczema. ❖ Produces anti inflammatory effect by binding to intracellular corticosteroid receptor and gene regulation which codes for proinflammatory cytokines. ❖ The choice depends on the site and severity of infection. ❖ Low potent, Potent TCs i.e Hydrocortisone 1% are suitable for face, genitals and flexures. ❖ Medium potent i.e Betamethasone 0.1% used for other parts of body. ❖ Twice daily application till inflammatory lesion significantly improves and can continue upto 1 week to several weeks. ❖ Once control is achieved stop the use and use of moisturizers until next flare up. ❖ AE- ❖ Local - Skin atrophy, periorbital dermatitis, acne, focal hypertrichosis, allergic contact dermatitis. ❖ Systemic - Hypothalamic pituitary adrenal suppression, Cataract, glaucoma, growth retardation
  • 25.
    2. Topical Calcineurininhibitors ❖ MOA: Inhibit activation of T cells and most cells by blocking the production of cytokines and its mediators. ❖ Tacrolimus ointment and Pimecrolimus cream reduce severity, extend and symptoms of disease in children and adult. ❖ Tacrolimus ointment : Derived from oral medicine FK506. 0.1% and 0.03% preparation used in treatment of moderate to severe Eczema. ❖ Pimecrolimus cream - 1% : Indicated for short term, intermittent use for mild to moderate eczema. ❖ AE - Burning, stinging, increases risk for malignancy.
  • 26.
    3. Coal Tar ❖Tar cream and ointment is used in the management of hyperkeratotic lichenified eczema, by acting as an antipruritic agent. ❖ Not recommended on acutely inflamed skin lesion. ❖ Less cosmetically acceptable due to staining and malodorous. 3. Topical Imidazoles ❖ Ketoconazole shampoo or cream is effective in reduction of Pityrosporum ovale on skin. ❖ Useful in the management of Seborrhoeic dermatitis.
  • 27.
    Phototherapy ➔ Phototherapy canbe effective second line therapy, when the disease is not controlled by TCS or Topical calcineurin inhibitors. ➔ Used to treat acute or maintenance therapy in adults and children. ➔ It consist of UV light alone or Along with UV light systemic or topical agent. ➔ UV A + Psoralances or NBUVB + Coal tar is the effective treatment for acute eczema ➔ Contraindicated in Photosensitive eczema ➔ AE - ◆ Short term - Erythema, skin pain, skin burn, Sunburn, Pruritus, Pigmentation ◆ Long term - Premature aging of skin, folliculitis, Photo Onycholysis, facial hypertrichosis, skin cancer.
  • 28.
    Systemic therapy -Used when Topical and phototherapy do not adequately control the disease 1. Systemic corticosteroids ❖ Short term - Oral prednisolone used in management of severe acute eczema which require rapid control. ❖ Long term - Rarely used due to adverse effects and risk of HTN and osteoporosis. 1. Azathioprine ❖ It is a purine analogue that inhibits DNA synthesis and can be effective as monotherapy in Adult eczema 1. Methotrexate ❖ Used as second line agent for moderate to severe atopic dermatitis.
  • 29.
    4. Cyclosporin ❖ Itis a systemic immunosuppression that blocks activation of T- lymphocytes ❖ It is effective for short term therapy for severe chronic adult eczema with rapid onset of action. ❖ Intermittent doses of 2.5 - 5 mg/kg/day are effective with maximum benefit observed after 2 to 6 weeks of therapy and relapse may occur quickly after cessation of therapy. ❖ AE - Dose related nephrotoxicity - hence monitoring of Sr. Creatinine is essential, HTN, Increases risk for cancer. ❖ DFI - Grapefruit juice - Increases blood levels of cyclosporine increasing risk for nephrotoxicity. 4. Antihistamines ❖ No direct impact on pruritis, main effect is sedation.
  • 30.
    1. Illustrated Synopsisof Dermatology and Sexually Transmitted Diseases, Fourth Edition. Neena Khanna, MD Professor Department of Dermatology and Venereology All India Institute of Medical Sciences New Delhi, India 2. Review of Dermatology, Fourth Edition Saurabh Jindal, MD, DNB, DDV Department of Dermatology and Venereology Dr.Jindal Clinic New Delhi, India 3. Dipiro Reference:-
  • 31.
  • 34.
  • 36.
  • 37.
  • 38.
  • 39.
  • 40.
  • 41.
  • 42.
  • 43.