Physical urticaria is a heterogeneous group of inducible conditions that includes symptomatic dermographism, cold contact urticaria, heat contact urticaria, delayed pressure urticaria, and others. Symptomatic dermographism is the most common subtype, where mechanical stroking of the skin causes a wheal and flare reaction with itch. Cold contact urticaria is triggered by skin contact with cold stimuli and can be diagnosed using an ice cube test. Treatment involves avoidance of physical triggers as well as antihistamines. For severe cases that are resistant to antihistamines, immunosuppressants or intravenous immunoglobulins may be considered.
This document provides an overview of physical urticarias. It defines physical urticarias as urticarias induced by physical stimuli like pressure, vibration, heat, cold, etc. It describes several types of physical urticarias in detail, including dermographism (pressure urticaria), delayed pressure urticaria, and vibratory angioedema. For each type, it covers epidemiology, clinical features, pathogenesis, diagnostic testing, and treatment approaches. The document is a comprehensive review and classification of physical urticaria subtypes.
This document summarizes information on chronic urticaria, including its prevalence, causes, impact on quality of life, and treatment options. It notes that chronic urticaria affects approximately 1% of people with acute urticaria and has a significant negative impact on quality of life. First-line treatment includes non-sedating antihistamines, sometimes at higher off-label doses. If patients do not respond sufficiently to antihistamines alone, second-line options include doxepin, leukotriene antagonists, short-term corticosteroids, dapsone, sulfasalazine, and narrowband UVB phototherapy. The document reviews evidence on the efficacy and safety of these second-
1. Atopic dermatitis is the most common type of dermatitis, which is a chronic, pruritic inflammatory skin disease that varies in severity. It primarily causes intense itching.
2. The pathogenesis is multifactorial involving genetic predisposition, skin barrier dysfunction, and immune abnormalities.
3. Treatment focuses on managing flares with topical corticosteroids and infections, while remission involves long-term emollient use and trigger avoidance.
Contact dermatitis is a common inflammatory skin disease caused by direct or indirect contact with harmful substances. It can be irritant contact dermatitis from irritants like soaps or allergic contact dermatitis from allergens that cause a delayed hypersensitivity reaction. Symptoms include erythema, vesicles, papules and scaling with itch. Diagnosis involves identifying the causative agent through patient history and patch testing. Treatment focuses on eliminating contact with the irritant or allergen and using topical corticosteroids.
hanifin and rajka criteria, entymology, definition of AD, atopy, etiopathogenesis of AD, genetics in AD, filaggrin, epidermal barrier dysfunction, atopic march, hygiene hypothesis, infantile phase of AD, childhood phase of AD, adult phase of AD, pityriasis alba, denne morgan folds, dirty neck appearence, nipple dermatitis, hanifin and rajka criteria, UK refinement of hanifin and rajka criteria, millenium criteria of AD, japanese dermatological association criteria, management of AD, wet wrap therapy,
The document discusses atopic dermatitis (AD), also known as eczema. It defines AD as a pruritic, chronic inflammatory skin condition characterized by dry skin and itchy rashes. AD is common in childhood and often runs in families with other allergic diseases. The pathogenesis involves genetic predisposition, skin barrier defects, and abnormal immune responses. Clinical manifestations vary depending on the stage of life, from facial rashes in infants to thickened plaques on flexural areas in older patients. Treatment focuses on moisturizing the skin, identifying trigger factors, and using topical corticosteroids or calcineurin inhibitors to control symptoms.
This document provides an overview of contact dermatitis, including its definition, classification, epidemiology, pathology, clinical presentation, investigation, and management. Contact dermatitis can be allergic, caused by an allergen-specific immune response, or irritant, caused by prolonged exposure to irritants. It is a common skin condition worldwide, with prevalence rates varying by region. Diagnosis involves a clinical examination and patch testing to identify potential allergens. Management focuses on avoiding causal allergens or irritants.
Urticaria is characterized by itchy red wheals or plaques on the skin that resolve over hours without marks. It can involve superficial or deep swellings in the dermis or subcutaneous tissues. Urticaria includes common conditions like acute or chronic hives, as well as physical, contact, and vibratory urticarias. Potential triggers include drugs, foods, infections, stress, and systemic diseases. It is a heterogeneous group of disorders distinguished by the transient appearance of wheals that come and go over periods of less than or greater than six weeks.
This document provides an overview of physical urticarias. It defines physical urticarias as urticarias induced by physical stimuli like pressure, vibration, heat, cold, etc. It describes several types of physical urticarias in detail, including dermographism (pressure urticaria), delayed pressure urticaria, and vibratory angioedema. For each type, it covers epidemiology, clinical features, pathogenesis, diagnostic testing, and treatment approaches. The document is a comprehensive review and classification of physical urticaria subtypes.
This document summarizes information on chronic urticaria, including its prevalence, causes, impact on quality of life, and treatment options. It notes that chronic urticaria affects approximately 1% of people with acute urticaria and has a significant negative impact on quality of life. First-line treatment includes non-sedating antihistamines, sometimes at higher off-label doses. If patients do not respond sufficiently to antihistamines alone, second-line options include doxepin, leukotriene antagonists, short-term corticosteroids, dapsone, sulfasalazine, and narrowband UVB phototherapy. The document reviews evidence on the efficacy and safety of these second-
1. Atopic dermatitis is the most common type of dermatitis, which is a chronic, pruritic inflammatory skin disease that varies in severity. It primarily causes intense itching.
2. The pathogenesis is multifactorial involving genetic predisposition, skin barrier dysfunction, and immune abnormalities.
3. Treatment focuses on managing flares with topical corticosteroids and infections, while remission involves long-term emollient use and trigger avoidance.
Contact dermatitis is a common inflammatory skin disease caused by direct or indirect contact with harmful substances. It can be irritant contact dermatitis from irritants like soaps or allergic contact dermatitis from allergens that cause a delayed hypersensitivity reaction. Symptoms include erythema, vesicles, papules and scaling with itch. Diagnosis involves identifying the causative agent through patient history and patch testing. Treatment focuses on eliminating contact with the irritant or allergen and using topical corticosteroids.
hanifin and rajka criteria, entymology, definition of AD, atopy, etiopathogenesis of AD, genetics in AD, filaggrin, epidermal barrier dysfunction, atopic march, hygiene hypothesis, infantile phase of AD, childhood phase of AD, adult phase of AD, pityriasis alba, denne morgan folds, dirty neck appearence, nipple dermatitis, hanifin and rajka criteria, UK refinement of hanifin and rajka criteria, millenium criteria of AD, japanese dermatological association criteria, management of AD, wet wrap therapy,
The document discusses atopic dermatitis (AD), also known as eczema. It defines AD as a pruritic, chronic inflammatory skin condition characterized by dry skin and itchy rashes. AD is common in childhood and often runs in families with other allergic diseases. The pathogenesis involves genetic predisposition, skin barrier defects, and abnormal immune responses. Clinical manifestations vary depending on the stage of life, from facial rashes in infants to thickened plaques on flexural areas in older patients. Treatment focuses on moisturizing the skin, identifying trigger factors, and using topical corticosteroids or calcineurin inhibitors to control symptoms.
This document provides an overview of contact dermatitis, including its definition, classification, epidemiology, pathology, clinical presentation, investigation, and management. Contact dermatitis can be allergic, caused by an allergen-specific immune response, or irritant, caused by prolonged exposure to irritants. It is a common skin condition worldwide, with prevalence rates varying by region. Diagnosis involves a clinical examination and patch testing to identify potential allergens. Management focuses on avoiding causal allergens or irritants.
Urticaria is characterized by itchy red wheals or plaques on the skin that resolve over hours without marks. It can involve superficial or deep swellings in the dermis or subcutaneous tissues. Urticaria includes common conditions like acute or chronic hives, as well as physical, contact, and vibratory urticarias. Potential triggers include drugs, foods, infections, stress, and systemic diseases. It is a heterogeneous group of disorders distinguished by the transient appearance of wheals that come and go over periods of less than or greater than six weeks.
Urticaria is a skin problem triggered by reaction to food, medicine or allergic to any other thing. Urticaria leads to red, itchy, and swollen skin. This disease is also known as Hives. Hives formed due to allergy, changes size rapidly and often move around, in different parts of the body.
Eczema is a chronic inflammatory skin condition characterized by dry, itchy, scaly, and sometimes infected skin. The underlying cause is a defective skin barrier that allows too much moisture to escape, resulting in dryness. Proper treatment involves frequent use of emollients to restore the skin barrier, along with intermittent use of topical corticosteroids when flare-ups occur. Patient education is important to ensure correct application of treatments and avoidance of exacerbating factors.
Vitiligo is a common skin condition characterized by loss of pigment cells called melanocytes, resulting in chalky white patches on the skin. It affects around 0.5-2% of the population worldwide and has no known cause, though it may be related to an autoimmune response or genetic factors. The patches of depigmentation are well-defined, often appear on areas exposed to the sun like the face and hands, and may worsen with sun exposure. Treatment options include PUVA therapy which uses psoralen drugs and ultraviolet light to stimulate repigmentation, topical corticosteroids to reduce inflammation, and camouflage creams to hide patches.
This document discusses the management of atopic dermatitis (AD). It covers the epidemiology, risk factors, clinical presentation, conventional therapies, and role of topical corticosteroids in treating AD. Specifically, it notes that AD is a chronic inflammatory skin disease affecting 15-30% of children and 2-10% of adults. Genetic and environmental factors like allergens and irritants play a role. Treatment focuses on eliminating triggers, moisturizing, and using topical corticosteroids in a stepwise approach depending on severity.
This document provides information on atopic dermatitis (AD), including its definition, epidemiology, pathophysiology, clinical manifestations, and treatment. Some key points:
1. AD is a chronic inflammatory skin disease associated with other atopic disorders like asthma. It is characterized by dry skin and sensitization to allergens.
2. The prevalence of AD has increased in recent decades, commonly starting early in life. Genetic factors like mutations in the filaggrin gene contribute to impaired skin barrier function which increases allergen sensitization risk.
3. Clinical features include severe pruritus, chronic relapsing course, and characteristic rash typically located in flexural areas. Complications can include
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by dry, itchy skin lesions. It is associated with elevated IgE levels and a family history of atopic diseases. The causes involve genetic susceptibility and environmental triggers that disrupt the skin barrier and promote a TH2-mediated immune response. Treatment focuses on identifying and avoiding triggers while improving the skin barrier with emollients and controlling inflammation with topical corticosteroids and calcineurin inhibitors. New targeted therapies that block cytokines and immune cells involved in AD pathogenesis are under investigation.
This case involves a 25-year-old woman who presented to the emergency department with shortness of breath and an expanding rash. She has a history of asthma and allergies to aspirin and shellfish. On exam, she was tachypnic, hypertensive, and had periorbital edema and scattered wheals. Her symptoms and history are concerning for anaphylaxis.
Urticaria, commonly known as hives, is a skin rash with pale red, itchy bumps that appear and disappear quickly. It is characterized by transient wheals (swellings) and angioedema (swelling of deeper layers of skin). Urticaria can be caused by allergic reactions, infections, physical stimuli like heat, cold, pressure, or vibrations. It is classified as acute, chronic, physical or contact urticaria. Treatment involves identifying and avoiding triggers, and using antihistamines.
Dr Muhammad Raza's presentation provides information about atopic dermatitis (eczema), including its signs and symptoms, causes, diagnosis, and management. The key points are that it is a chronic skin condition causing red, itchy, cracked skin that is common in children; has genetic and immunological factors; and is typically diagnosed clinically and managed through moisturizers, topical steroids, and other topical or systemic treatments depending on severity. The goal is for participants to understand the basic concepts, diagnosis, management, and appropriate referrals for atopic dermatitis.
The document discusses different types of eczema and dermatitis. It describes acute and chronic eczema and lists various exogenous and endogenous forms of eczema including atopic dermatitis, seborrheic dermatitis, contact dermatitis, and others. Key characteristics, histology, and treatments are mentioned for different conditions. Common sites of involvement and diagnostic criteria are provided for atopic dermatitis. Contact dermatitis can be irritant or allergic in nature.
Exfoliative dermatitis is a condition where more than 90% of the skin surface becomes inflamed and scaly. It can be caused by underlying skin diseases like psoriasis or eczema, drug reactions, or systemic illnesses. Clinically, it presents as generalized redness and scaling of the skin with potential complications involving other organs. Making an accurate diagnosis requires considering the patient's medical history and risk factors, examining skin changes and biopsy findings, and ruling out potential etiologies through laboratory tests and imaging.
This document provides information on urticaria (hives), including:
- Urticaria is characterized by itchy pink swellings (wheals) that appear on the skin and do not last more than 24 hours. It is classified as acute (<6 weeks) or chronic (>6 weeks).
- Urticaria is caused by mast cell degranulation releasing histamine, causing increased capillary permeability and fluid leakage leading to wheal formation.
- There are different types of physical urticarias triggered by factors like cold, heat, sunlight, pressure, water, etc. Investigation and treatment depends on the identified cause.
- Antihistamines are the main treatment for symptom
Atopic dermatitis is a common inflammatory skin condition characterized by itchy, red lesions. It has a complex pathogenesis involving skin barrier dysfunction, immune dysregulation with Type 2 inflammation, and microbial dysbiosis. Genetic factors like filaggrin mutations contribute to impaired skin barrier function. Colonization by Staphylococcus aureus and Malassezia yeasts further damages the skin and promotes inflammation. Pruritus (itching) activates scratch responses that sustain the condition through additional skin damage and inflammation. Treatment involves managing symptoms, restoring skin barrier function, and controlling inflammation and infection.
Eczema, also known as dermatitis, is a common skin condition affecting 20% of patients referred to clinics. It is characterized by redness, swelling, blistering, crusting, and flaking in areas with poorly defined borders. Histologically, eczema shows inflammation of the epidermis and dermis. The causes include allergic and irritant contact dermatitis. Treatment depends on the severity and includes emollients, topical corticosteroids, wet wrap dressings, systemic antibiotics, and avoidance of exacerbating factors. Atopic eczema, the most common form, has a genetic component and usually starts in childhood.
Atopic dermatitis is a chronic inflammatory skin disease associated with respiratory allergies. It is characterized by recurrent eczematous lesions and intense itch. Genetic factors like filaggrin mutations cause skin barrier defects allowing allergens and microbes to trigger immune responses. The disease involves type 2 immunity cytokines activating neurons to produce itch. Staphylococcus aureus colonization exacerbates inflammation. Clinical features include erythematous patches and plaques with lichenification in chronic cases.
Cutaneous drug reactions are adverse skin reactions caused by medications. They range from mild rashes to potentially life-threatening conditions like toxic epidermal necrolysis. Most cutaneous drug reactions are immune-mediated and occur within a few weeks of starting a medication. Management involves promptly withdrawing the offending drug, providing supportive care, and occasionally systemic corticosteroids for more severe reactions to prevent complications and mortality. The prognosis depends on the specific reaction, with most mild rashes resolving on their own while toxic epidermal necrolysis has a high mortality rate of around 50%.
Vitiligo is a hypopigmentation disorder characterized by depigmented patches on the skin. It is caused by a loss of melanocytes in the affected areas. There are several proposed mechanisms including genetic predisposition, autoimmune attack on melanocytes, and neural mechanisms. Clinically, it presents as well-circumscribed milky white macules that may coalesce. Treatment involves phototherapy with PUVA or narrowband UVB, topical corticosteroids for localized lesions, and systemic corticosteroids for more widespread or rapidly progressive disease. Surgical interventions like melanocyte transplantation can be used for sites resistant to medical therapy.
Drug eruptions can mimic various skin conditions and are often caused by medications. The document defines adverse drug reactions and lists common inducing drugs. It describes several types of drug eruptions like maculopapular eruptions, urticaria, angioedema, DRESS syndrome, erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, fixed drug eruptions, leukocytoclastic vasculitis, photosensitivity, erythroderma, erythema nodosum, acute generalized exanthematous pustulosis, and anticoagulant skin necrosis. It emphasizes the importance of history, physical exam, potential lab tests, identifying the culprit drug
This document discusses systemic retinoids, including their sources, generations, pharmacokinetics, mechanisms of action, uses, and side effects. It focuses on isotretinoin and its use for severe acne. Isotretinoin is well absorbed from the gut and transported to target cells via intracellular proteins. It has a half-life of about 20 hours and is metabolized and eliminated by the liver. Isotretinoin reduces sebum production and inflammation for acne clearance. Strict monitoring and contraceptive measures are required due to its teratogenicity. Common side effects include dryness, cheilitis and hypertriglyceridemia.
Cryotherapy involves the application of cold to induce therapeutic effects by decreasing tissue temperature. It works through mechanisms like conduction, convection, and evaporation to remove heat from the body. While cryotherapy can provide benefits like reduced pain and inflammation, it may exacerbate conditions involving impaired circulation or nerve function and cause issues in sensitive individuals. Precautions should be taken when applying cryotherapy to avoid potential contraindications or side effects.
Cryotherapy involves applying cold to the body and can have therapeutic effects. It works by reducing cell metabolism, inflammation, muscle spasm, and pain while increasing pain tolerance. The appropriate temperature range is between 32-65°F. It provides pain relief and reduces swelling by causing vasoconstriction and decreasing metabolic rate in tissues. Precautions must be taken for patients with poor circulation, open wounds, or nerve damage in the area being treated.
Urticaria is a skin problem triggered by reaction to food, medicine or allergic to any other thing. Urticaria leads to red, itchy, and swollen skin. This disease is also known as Hives. Hives formed due to allergy, changes size rapidly and often move around, in different parts of the body.
Eczema is a chronic inflammatory skin condition characterized by dry, itchy, scaly, and sometimes infected skin. The underlying cause is a defective skin barrier that allows too much moisture to escape, resulting in dryness. Proper treatment involves frequent use of emollients to restore the skin barrier, along with intermittent use of topical corticosteroids when flare-ups occur. Patient education is important to ensure correct application of treatments and avoidance of exacerbating factors.
Vitiligo is a common skin condition characterized by loss of pigment cells called melanocytes, resulting in chalky white patches on the skin. It affects around 0.5-2% of the population worldwide and has no known cause, though it may be related to an autoimmune response or genetic factors. The patches of depigmentation are well-defined, often appear on areas exposed to the sun like the face and hands, and may worsen with sun exposure. Treatment options include PUVA therapy which uses psoralen drugs and ultraviolet light to stimulate repigmentation, topical corticosteroids to reduce inflammation, and camouflage creams to hide patches.
This document discusses the management of atopic dermatitis (AD). It covers the epidemiology, risk factors, clinical presentation, conventional therapies, and role of topical corticosteroids in treating AD. Specifically, it notes that AD is a chronic inflammatory skin disease affecting 15-30% of children and 2-10% of adults. Genetic and environmental factors like allergens and irritants play a role. Treatment focuses on eliminating triggers, moisturizing, and using topical corticosteroids in a stepwise approach depending on severity.
This document provides information on atopic dermatitis (AD), including its definition, epidemiology, pathophysiology, clinical manifestations, and treatment. Some key points:
1. AD is a chronic inflammatory skin disease associated with other atopic disorders like asthma. It is characterized by dry skin and sensitization to allergens.
2. The prevalence of AD has increased in recent decades, commonly starting early in life. Genetic factors like mutations in the filaggrin gene contribute to impaired skin barrier function which increases allergen sensitization risk.
3. Clinical features include severe pruritus, chronic relapsing course, and characteristic rash typically located in flexural areas. Complications can include
Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by dry, itchy skin lesions. It is associated with elevated IgE levels and a family history of atopic diseases. The causes involve genetic susceptibility and environmental triggers that disrupt the skin barrier and promote a TH2-mediated immune response. Treatment focuses on identifying and avoiding triggers while improving the skin barrier with emollients and controlling inflammation with topical corticosteroids and calcineurin inhibitors. New targeted therapies that block cytokines and immune cells involved in AD pathogenesis are under investigation.
This case involves a 25-year-old woman who presented to the emergency department with shortness of breath and an expanding rash. She has a history of asthma and allergies to aspirin and shellfish. On exam, she was tachypnic, hypertensive, and had periorbital edema and scattered wheals. Her symptoms and history are concerning for anaphylaxis.
Urticaria, commonly known as hives, is a skin rash with pale red, itchy bumps that appear and disappear quickly. It is characterized by transient wheals (swellings) and angioedema (swelling of deeper layers of skin). Urticaria can be caused by allergic reactions, infections, physical stimuli like heat, cold, pressure, or vibrations. It is classified as acute, chronic, physical or contact urticaria. Treatment involves identifying and avoiding triggers, and using antihistamines.
Dr Muhammad Raza's presentation provides information about atopic dermatitis (eczema), including its signs and symptoms, causes, diagnosis, and management. The key points are that it is a chronic skin condition causing red, itchy, cracked skin that is common in children; has genetic and immunological factors; and is typically diagnosed clinically and managed through moisturizers, topical steroids, and other topical or systemic treatments depending on severity. The goal is for participants to understand the basic concepts, diagnosis, management, and appropriate referrals for atopic dermatitis.
The document discusses different types of eczema and dermatitis. It describes acute and chronic eczema and lists various exogenous and endogenous forms of eczema including atopic dermatitis, seborrheic dermatitis, contact dermatitis, and others. Key characteristics, histology, and treatments are mentioned for different conditions. Common sites of involvement and diagnostic criteria are provided for atopic dermatitis. Contact dermatitis can be irritant or allergic in nature.
Exfoliative dermatitis is a condition where more than 90% of the skin surface becomes inflamed and scaly. It can be caused by underlying skin diseases like psoriasis or eczema, drug reactions, or systemic illnesses. Clinically, it presents as generalized redness and scaling of the skin with potential complications involving other organs. Making an accurate diagnosis requires considering the patient's medical history and risk factors, examining skin changes and biopsy findings, and ruling out potential etiologies through laboratory tests and imaging.
This document provides information on urticaria (hives), including:
- Urticaria is characterized by itchy pink swellings (wheals) that appear on the skin and do not last more than 24 hours. It is classified as acute (<6 weeks) or chronic (>6 weeks).
- Urticaria is caused by mast cell degranulation releasing histamine, causing increased capillary permeability and fluid leakage leading to wheal formation.
- There are different types of physical urticarias triggered by factors like cold, heat, sunlight, pressure, water, etc. Investigation and treatment depends on the identified cause.
- Antihistamines are the main treatment for symptom
Atopic dermatitis is a common inflammatory skin condition characterized by itchy, red lesions. It has a complex pathogenesis involving skin barrier dysfunction, immune dysregulation with Type 2 inflammation, and microbial dysbiosis. Genetic factors like filaggrin mutations contribute to impaired skin barrier function. Colonization by Staphylococcus aureus and Malassezia yeasts further damages the skin and promotes inflammation. Pruritus (itching) activates scratch responses that sustain the condition through additional skin damage and inflammation. Treatment involves managing symptoms, restoring skin barrier function, and controlling inflammation and infection.
Eczema, also known as dermatitis, is a common skin condition affecting 20% of patients referred to clinics. It is characterized by redness, swelling, blistering, crusting, and flaking in areas with poorly defined borders. Histologically, eczema shows inflammation of the epidermis and dermis. The causes include allergic and irritant contact dermatitis. Treatment depends on the severity and includes emollients, topical corticosteroids, wet wrap dressings, systemic antibiotics, and avoidance of exacerbating factors. Atopic eczema, the most common form, has a genetic component and usually starts in childhood.
Atopic dermatitis is a chronic inflammatory skin disease associated with respiratory allergies. It is characterized by recurrent eczematous lesions and intense itch. Genetic factors like filaggrin mutations cause skin barrier defects allowing allergens and microbes to trigger immune responses. The disease involves type 2 immunity cytokines activating neurons to produce itch. Staphylococcus aureus colonization exacerbates inflammation. Clinical features include erythematous patches and plaques with lichenification in chronic cases.
Cutaneous drug reactions are adverse skin reactions caused by medications. They range from mild rashes to potentially life-threatening conditions like toxic epidermal necrolysis. Most cutaneous drug reactions are immune-mediated and occur within a few weeks of starting a medication. Management involves promptly withdrawing the offending drug, providing supportive care, and occasionally systemic corticosteroids for more severe reactions to prevent complications and mortality. The prognosis depends on the specific reaction, with most mild rashes resolving on their own while toxic epidermal necrolysis has a high mortality rate of around 50%.
Vitiligo is a hypopigmentation disorder characterized by depigmented patches on the skin. It is caused by a loss of melanocytes in the affected areas. There are several proposed mechanisms including genetic predisposition, autoimmune attack on melanocytes, and neural mechanisms. Clinically, it presents as well-circumscribed milky white macules that may coalesce. Treatment involves phototherapy with PUVA or narrowband UVB, topical corticosteroids for localized lesions, and systemic corticosteroids for more widespread or rapidly progressive disease. Surgical interventions like melanocyte transplantation can be used for sites resistant to medical therapy.
Drug eruptions can mimic various skin conditions and are often caused by medications. The document defines adverse drug reactions and lists common inducing drugs. It describes several types of drug eruptions like maculopapular eruptions, urticaria, angioedema, DRESS syndrome, erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, fixed drug eruptions, leukocytoclastic vasculitis, photosensitivity, erythroderma, erythema nodosum, acute generalized exanthematous pustulosis, and anticoagulant skin necrosis. It emphasizes the importance of history, physical exam, potential lab tests, identifying the culprit drug
This document discusses systemic retinoids, including their sources, generations, pharmacokinetics, mechanisms of action, uses, and side effects. It focuses on isotretinoin and its use for severe acne. Isotretinoin is well absorbed from the gut and transported to target cells via intracellular proteins. It has a half-life of about 20 hours and is metabolized and eliminated by the liver. Isotretinoin reduces sebum production and inflammation for acne clearance. Strict monitoring and contraceptive measures are required due to its teratogenicity. Common side effects include dryness, cheilitis and hypertriglyceridemia.
Cryotherapy involves the application of cold to induce therapeutic effects by decreasing tissue temperature. It works through mechanisms like conduction, convection, and evaporation to remove heat from the body. While cryotherapy can provide benefits like reduced pain and inflammation, it may exacerbate conditions involving impaired circulation or nerve function and cause issues in sensitive individuals. Precautions should be taken when applying cryotherapy to avoid potential contraindications or side effects.
Cryotherapy involves applying cold to the body and can have therapeutic effects. It works by reducing cell metabolism, inflammation, muscle spasm, and pain while increasing pain tolerance. The appropriate temperature range is between 32-65°F. It provides pain relief and reduces swelling by causing vasoconstriction and decreasing metabolic rate in tissues. Precautions must be taken for patients with poor circulation, open wounds, or nerve damage in the area being treated.
This document discusses hot and cold applications for therapeutic purposes. Hot applications are used to relieve pain and congestion, provide warmth, and promote healing by increasing blood flow. Cold applications are used to reduce pain, control bleeding and bacteria growth, and decrease inflammation by constricting blood vessels. Both have specific indications and contraindications. Guidelines are provided for safely applying heat or cold to achieve therapeutic benefits while avoiding potential complications like burns or tissue damage.
This document discusses various topics related to thermoregulation including types of temperature, factors affecting thermoregulation, fever, hyperthermia, hypothermia, and frostbite. It defines these conditions and discusses their causes, signs and symptoms, diagnosis, and management. Nursing considerations are provided for assessment and care of patients experiencing fever, hyperthermia, and hypothermia. Current trends in cooling techniques for hyperthermia are also reviewed.
Urticaria, Angioedema, and Anaphylaxis.pptxJwan AlSofi
This document provides an overview of urticaria, angioedema, and anaphylaxis. It defines the conditions, describes their pathophysiology as being related to mast cell degranulation and mediator release, and classifies them as acute, chronic, physical, or hereditary. Epidemiology, clinical manifestations, diagnostic approach, differential diagnosis, treatment involving antihistamines and epinephrine, and prevention are discussed. Anaphylaxis is emphasized as a medical emergency requiring immediate epinephrine injection and supportive care.
This document provides information on urticaria (hives), including definitions, epidemiology, pathogenesis, classification, and specific types. Some key points:
- Wheals are central swellings surrounded by erythema that itch or burn and resolve within 24 hours. Angioedema causes swelling below the skin that takes longer to resolve.
- Urticaria prevalence is 15-25% lifetime and chronic urticaria affects 1% annually, more common in adults and women.
- Pathogenesis involves skin mast cell degranulation in response to triggers like allergens, autoantibodies, neuropeptides.
- Classification includes acute (<6 weeks), chronic (>6 weeks),
This document provides an overview of urticaria and skin allergy tests. It discusses:
1. The goals of understanding the clinical approach to evaluating and treating urticaria, including distinguishing between types of urticaria and treatments.
2. Details on the morphology, pathophysiology, clinical features, diagnosis, and treatment of different types of urticaria such as acute vs chronic urticaria.
3. Descriptions of prick and patch tests used to diagnose allergies, including how they work, what positive and negative results look like, and the testing process.
The document discusses dengue fever, including its origins, epidemiology, transmission, clinical features, diagnosis, and laboratory tests. It provides details on dengue virus serotypes, the disease progression and definitions of dengue fever, dengue hemorrhagic fever, and dengue shock syndrome. Rapid tests and other laboratory diagnostics for dengue are also outlined.
The document discusses Raynaud's disease, including its causes, symptoms, diagnostic evaluation, treatment options, nursing care, and more. Raynaud's disease is a condition characterized by reduced blood flow to the extremities, such as the fingers and toes, causing discoloration, pain, and numbness when exposed to cold or stress. It can be either primary or secondary to other conditions like connective tissue disorders. Treatment involves lifestyle changes to avoid triggers and medications like calcium channel blockers or nitroglycerin to dilate blood vessels. Nurses play an important role in educating patients, preventing complications, and supporting patients psychologically.
NO 1163 AEF Topik 2 and 3 Thermal agents 2023.pptxnhafifi
The document provides information about cold therapy and its application as a thermal agent in physiotherapy. It discusses the physiological effects of cold such as initial vasoconstriction and decreased blood flow, followed by vasodilation and increased blood flow with prolonged application. Cold therapy can help control inflammation, edema, pain, and spasticity. The document outlines different cold application techniques like cold packs, ice packs, and ice massage and provides guidance on their proper use and any contraindications to cold therapy.
The document discusses burns, including:
1. The structure of skin and how burns damage the epidermis and dermis layers.
2. The main causes of burns are thermal, chemical, inhalation, electric, and radiation burns.
3. Burn classification includes depth, extent, location, and patient risk factors which determine prognosis.
4. Burn management has three phases - emergent, acute, and rehabilitative - and the emergent phase focuses on airway management, IV fluids, wound care, drugs, and nutrition to stabilize the patient.
This document discusses temperature and humidity. It begins by defining temperature and explaining different methods of temperature measurement, including mercury thermometers, resistance thermometers, and thermistors. It then discusses measuring body temperature, factors that influence body temperature, and methods of heat transfer from the body. The document also covers thermoregulation, causes of hyperthermia, temperature changes during surgery, effects of hypothermia, and methods for preventing hypothermia, including through the use of humidity.
This document provides an overview of burns, including definitions, epidemiology, classification, pathophysiology, evaluation, treatment and management. It begins with defining burns as destruction of skin layers through coagulative necrosis. Globally, an estimated 180,000 deaths occur annually from burns, most in low and middle income countries. Burns are classified based on depth and degree of injury. Initial management focuses on ABCs, estimating burn size, preventing infection, and providing wound care and nutrition. Complications can include shock, infection, pulmonary, gastrointestinal and renal issues.
Clinical management of heat related illness, mohLee Oi Wah
Heat-related illnesses range from mild to life-threatening. Heat stroke is the most severe form and occurs when the core body temperature rises above 40.5°C. It can cause damage to the central nervous system and other organs. Immediate cooling through methods like ice packs and cold water is critical for survival, as mortality from heat stroke can be as high as 70% without prompt treatment. Factors like extreme heat, strenuous physical activity, age, and medical conditions increase the risk of developing heat stroke.
The document discusses various types of environmental injuries including injuries from heat, cold, altitude changes, envenomation, dehydration, and burns. It provides information on the physiological changes that occur with these injuries and their typical signs and symptoms. Guidelines are given for assessment and management of these conditions, focusing on stabilization of vital functions and gradual rewarming or cooling as needed. Prevention strategies are also outlined, such as acclimatization procedures for altitude illness and rehydration for dehydration.
Heat and cold applications are used for local and systemic effects. Heat promotes healing, reduces swelling and pain by increasing blood flow. It can increase inflammation and risk of burns. Cold decreases temperature, constricts blood vessels, reduces inflammation and acts as a local anesthetic but can cause pain, burns or cyanosis. Various methods deliver heat or cold including hot packs, electrical pads, ice, compresses and baths. Care must be taken with certain patients and conditions.
This document discusses burn injuries, including:
1) It describes the different types of burns - thermal, chemical, electrical, radiation, and cold injuries. Thermal burns are further divided into flame, scald, and contact burns.
2) It explains the pathophysiology of burns, including the zones of injury and the systemic inflammatory response. Management of burns is also covered, focusing on airway control, fluid resuscitation, wound care, and infection prevention.
3) The severity of burns is classified based on depth and total body surface area affected. Deep partial thickness and full thickness burns require specialized wound care and skin grafting.
Chronic urticaria lasts longer than 6 weeks and presents as recurrent hives and angioedema occurring more than 3 days a week. It can be classified as inducible or spontaneous. Inducible types are triggered by specific physical stimuli like pressure, cold, heat, or vibration. Chronic urticaria is considered after ruling out look-alike conditions such as urticarial vasculitis and other autoinflammatory syndromes. Its evaluation involves considering potential systemic triggers or underlying causes.
Urticaria, also known as hives, is a skin condition characterized by raised, itchy bumps on the skin called wheals. It is caused by an allergic reaction or response of the immune system. Urticaria can be classified as acute (lasting less than 6 weeks) or chronic (lasting 6 weeks or longer). Common triggers include food, medications, insect bites, or physical stimuli like pressure, heat, cold, or vibration. Treatment involves the use of antihistamines as first-line therapy, with corticosteroids, leukotriene inhibitors, or immunosuppressants as second- or third-line options depending on severity and response to initial treatment.
Similar to Diagnosis and treatment of physical urticaria (20)
- Cat and dog allergens such as Fel d 1 and Can f 1 are major allergens found in fur, dander, and saliva that can become airborne and cause sensitization in a large percentage of allergic individuals.
- Lipocalins make up many mammalian allergens and show cross-reactivity between species due to structural similarities, explaining co-sensitizations between cats, dogs, horses, and other animals.
- Higher levels of IgE antibodies to specific dog lipocalins are associated with more severe asthma in children with dog allergy.
1) DRESS syndrome is a severe cutaneous drug reaction characterized by fever, lymphadenopathy, hematologic abnormalities, multisystem involvement, and viral reactivation. It has a delayed onset of 2-3 weeks after starting the culprit drug.
2) The skin manifestations are typically a polymorphous maculopapular eruption and facial edema. Systemic involvement can include the liver, kidneys, lungs and other organs.
3) Diagnosis is based on clinical criteria including the RegiSCAR scoring system which evaluates morphology, timing of onset, organ involvement, hematologic abnormalities and viral reactivation.
Wheat is one of the most important global food sources and wheat allergy prevalence varies from 0.4-4% depending on age and region. Several wheat proteins have been identified as major allergens, including omega-5-gliadin, alpha-amylase inhibitors, and glutenins. Studies have found that serum testing for IgE antibodies to specific wheat allergens, such as omega-5-gliadin, glutenins, and alpha-amylase inhibitors, can help diagnose wheat allergy and distinguish between mild and severe cases. Sensitization to different wheat allergens is associated with wheat-dependent exercise-induced anaphylaxis versus occupational baker's asthma. Proper diagnosis and
Major indoor allergens include dust mites, domestic animals like cats and dogs, insects like cockroaches, mice, and fungi. Dust mites thrive in warm, humid environments like mattresses, bedding, and upholstered furniture, where they feed on human skin scales and excrete allergenic fecal particles. Cat allergens like Fel d 1 accumulate in fur and can become airborne, causing worse asthma outcomes in sensitized individuals. Minimizing exposure involves removing carpets, frequent washing of bedding, humidity control, HEPA filtration and ventilation.
This document provides information on Hymenoptera, focusing on the families Apidae and Vespidae. It discusses the epidemiology and prevalence of insect venom allergy. It also covers the taxonomy, venom composition, and clinical manifestations of common stinging insects like honeybees, hornets, wasps and yellow jackets. Key allergens are identified for different species.
- NSAIDs hypersensitivity can present with distinct clinical phenotypes based on organ system involvement and timing of symptoms. It is estimated that less than 20% of reported adverse reactions to NSAIDs are true hypersensitivities.
- AERD/NERD involves eosinophilic rhinosinusitis, asthma, and nasal polyps. Exposure to aspirin or other NSAIDs exacerbates bronchospasms and rhinitis. Management involves lifelong avoidance of culprit and cross-reacting NSAIDs.
- Various phenotypes are described beyond the EAACI classification, including blended reactions involving multiple organs, food-dependent NSAID-induced anaphylaxis, and NSAID-selective immediate reactions. Proper diagnosis relies
The document discusses food immunotherapy for treating food allergies. It provides definitions and outlines immune mechanisms and efficacy evidence from studies on peanut, cow's milk, egg, and wheat oral immunotherapy (OIT). Peanut OIT studies showed 67-78% of children achieved desensitization and 21-46% achieved sustained unresponsiveness. Cow's milk and egg OIT also demonstrated desensitization in 50-75% of children. Wheat OIT studies found 52-69% achieved desensitization. OIT was effective at increasing tolerance but also increased rates of adverse events during treatment.
This document summarizes X-linked agammaglobulinemia (XLA), an inherited primary immunodeficiency caused by mutations in the Bruton's tyrosine kinase (Btk) gene. XLA is characterized by absent B cells and low immunoglobulin levels, leading to recurrent bacterial infections starting in infancy. Management involves immunoglobulin replacement and antibiotic therapy. With treatment, life expectancy has improved dramatically though complications can include lung disease. The document also briefly discusses other forms of agammaglobulinemia caused by defects in genes important for early B cell development.
This document discusses histamine and anti-histamines. It provides information on:
1. The structure and function of histamine and its receptors in immune response regulation. Histamine plays a role in processes like antigen presentation and influencing T and B cell responses.
2. The classification and structures of different types of anti-histamines, including first and second generation anti-histamines from different chemical classes.
3. Some anti-histamines have the potential to cause hypersensitivity in rare cases, even those from different chemical classes with no structural similarity.
The document discusses beta-lactam allergy, including penicillin and cephalosporin allergies. It covers the epidemiology, classifications, structures, mechanisms, and investigations of beta-lactam allergies. Specifically, it notes that penicillin is the most commonly reported antibiotic allergy. It describes the hapten concept of small molecules like beta-lactams binding covalently to proteins to form antigen complexes. Skin testing and in vitro tests are used to investigate immediate IgE-mediated allergies, while patch testing is used for delayed reactions.
This document provides an overview of intravenous immunoglobulin (IVIG) therapy. It discusses the structure and classes of immunoglobulins, mechanisms of action including neutralization, opsonization, and modulation of immune cells. It also covers the manufacturing process, pharmacokinetics, indications for use in primary immunodeficiencies and autoimmune diseases, dosing, administration, and adverse effects. The differences between IVIG products are also reviewed.
More from Chulalongkorn Allergy and Clinical Immunology Research Group (20)
5. Physical Triggers
• Symptomatic dermographism / Urticaria factitia : mechanical
stroking
• Cold contact urticaria : skin contact with cold air/water/solids
• Heat contact urticaria : skin contact with hot air/water/solids
• Delayed pressure urticaria: vertical sustained pressure
• Vibratory urticaria/angioedema : vibration (e.g. pneumatic
hammer)
• Solar urticaria : UV and/or visible light
• Aquagenic urticaria : water contact at any temperature
• Contact urticaria : contact with an allergic or nonallergic
stimulus
• Exercise induced urticaria /anaphylaxis : physical exercise
• Cholinergic urticaria : increased core body temperature
Allergy 2009; 64 (12): 1715-1721
6. Epidemiology
• Urticaria
- The life-time prevalence of any subtype is 20%
• Physical urticaria
- prevalence 20% of chronic urticaria
- In children prevalence ranges from 6.2-25.5%
Allergy 2009;64: 1417-1426
Ann Allergy 1993:71:205-12
Ann Allergy 1992; 69: 61-65
7.
8. Aim: To study the prevalence, type, clinical data &
natural history of physical urticaria including
prognostic factors for remission
Material & Methods :
- A retrospective study
- The Dermatologic Unit, Siriraj Hospital
- Jan 2003-Dec 2008
- Patients aged above 18 years
- Demographic data, causes of
urticaria, associated diseases, physical
exammination, lab etc.
JEADV 2011 ; 25: 1194-1199.
9. • Tests to categorize type
- Dermographometer ( pressure at 4900 g/cm2 )
- Delayed-pressure ( sandbags 15 lbs over one
shoulder for 15 min) then observe 2-8 hr. later
- Cold urticaria ( Ice-cube test, place ice inside plastic bag on
forearm 10 min then observe 15 min later
- Cholinergic ( run until exhausted & sweaty ) then
observe within 15 min
- Adrenergic ( ID noradrenalin 3-10 ng in 0.02 ml saline
observe erythematous papule & halo )
JEADV 2011 ; 25: 1194-1199.
10. • Tests to categorize type
- Solar urticaria ( photo test with visible light
UVA, UVB )
- Others ; CBC, UA, ESR, ANA, cryoglobulin
HBsAg, anti-HCV Ab etc.
Remission: non-urticarial wheal for at least 6
months after stop medication & negative test
JEADV 2011 ; 25: 1194-1199
15. • From chronic urticaria: physical urticaria was 7.2%
• The most common type is symptomatic dermographism
• Only 13.9% associated with chronic spontaneous urticaria
• No multiple types of physical urticaria
• ESR was the most common abnormal labs
• The median time after onset before 50% remission
- Cholinergic urticaria took the shortest course
- Delayed-pressure took the longest period
- After 1 y & 5 y from onset of symptom, 13 % & 50%
of physical urticaria were free of symptoms
16. Symptomatic Dermatographism
• Syn : urticaria factitia, dermographic urticaria
• The most common subtype of physical urticaria
• Has to be differentiated from simple
Dermographism where wealing, but not
pruritus, occurs after moderate stroking of the
skin
• Develope itching & wealing at a lower force
than that required to induce simple
dermographism
• Other types of dermographism such as white
dermographism (in atopic patients) are
unrelated to symptomatic dermographism
Immunol Allergy Clin North Am2004;24:225–246.
17. Symptomatic Dermatographism
• Provocation testing
- A dermographometer : to apply a rubbing stimulus to a subject’s skin
using predefined and reproducible pressures
- A calibrated dermographometer is commercially available (HTZ
Limited, Vulcan Way, New Addington, Croydon, Surrey, UK)
- It has a spring-loaded smooth steel tip 0.9 mm in diameter. The
pressure on the tip can be varied by turning a screw at the top of the
instrument.
- The scale settings from 0 to 15 ( tip pressures from 20 to 160 g/mm2 )
Immunol Allergy Clin North Am2004;24:225–246.
18. Figure 3 Dermatographism. Linear stroking of skin
elicits a wheal within several minutes.
The American Journal of Medicine 2008; 121 ( 5) : 379 - 384
19. Symptomatic Dermatographism
• Diagnosis of symptomatic dermographism
-the smooth blunt object should be held
perpendicular to and used to apply a light
stroking pressure to the skin of the upper back
or volar forearm
- The skin at the test site should be unbroken
and free of obvious signs of infection
-Three parallel lines (up to 10 cm long)
should be made with dermographometer
settings equivalent to 20, 36 and 60 g/mm2.
Immunol Allergy Clin North Am2004;24:225–246.
20. Symptomatic Dermatographism
• The positive reaction : showing a wheal
response & report pruritus at the site of
provocation at 36 g/mm2 (353 kPa) or less
• A wheal response without itch on provocation
at 60 g/mm2 (589 kPa) or higher indicates
simple dermographism
• The test response should be read 10 min after
testing
J Am Acad Dermatol2008;59:752–757.
21. Management of Symptomatic
Dermatographism
• Diphenhydramine or hydroxyzine 25-50
mg. qid for severe patient
• Non-sedating antihistamine in mildly to
moderately severe cases, can be triple
the usual dose
Middleton’s Allergy 7TH Edition
22.
23.
24. Conclusion
• Cyclosporin may be worth trying for
antihistamine-resistant DU, especially in
those patient cases characterized by
severe itching
. Further studies on a larger scale are
expected to be conducted in order to
generate stronger levels of clinical
evidence.
25. Cold Urticaria & Related
Disorders
• Trigger by a cold stimulus ; wind, liquid
holding cold objects
• Total body exposure can lead to hypotension
( swimming)
• Disease begin in any age group, young adult
• “Ice-cube Test” placing a plastic containing ice
cube inside on patient’s forearm for 4 min, then
observe 10 min
Middleton’s Allergy 7th Edition
26. Cold Urticaria
• Positive : a palpable & clearly visible weal & flare reaction
with itchy and/or burning sensation
• In a positive test reaction, threshold testing should be
performed
• Threshold level may help patients to avoid risky situations and
their physician to optimize treatment
• Determining the stimulation time threshold, which is the
shortest duration of cold exposure required to induce a
positive test reaction
• Temperature thresholds, i.e. the highest temperature sufficient
to induce a positive test reaction, can be assessed with
TempTest
J Allergy Clin Immunol1986;78:417–423.
29. Management of Cold Urticaria
• Avoidance
• Cyproheptadine is the drug of choice
• Non-sedating H1 antihistamine
• For patient where IgE has a
role, monoclonal IgG anti-IgE may be
effective
Middleton’s Allergy 7th Edition
30. Atopic dermatitis and skin disease
High-dose desloratadine decreases wheal
volume and improves cold provocation
thresholds compared with standard-dose
treatment in patients with acquired cold
urticaria
: A randomized, placebo-controlled, crossover
study
Frank Siebenhaar, MD, Franziska Degener, MD,Torsten
Zuberbier, MD, Peter Martus, PhD,andMarcus Maurer, MD
Berlin, Germany
J Allergy Clin Immunol 2009;123:672-9
31. - Aim: assess the effects of 5 and 20 mg of
desloratadine and placebo on cold-induced
urticarial reactions in patients with acquired
cold urticaria (safety & efficacy)
- A prospective, double-
blind, randomized, placebo-controlled
crossover study
J Allergy Clin Immunol 2009;123:672-9
32. • Materials & Methods
- OPD of urticaria specialty clinic of the Allergie-
Centrum-Charite´ of the Charite´-
Universita¨tsmedizin, Berlin, Germany
- Patients aged 18 to 75 years with a confirmed
diagnosis of Acquired Cold Urticaria , made at least
6 week before
- Signs/symptoms were assessed by using the
Acquired Cold Urticaria Severity Index (ACUSI), &
triggering stimuli, previous medication use, and
concomitant disease
J Allergy Clin Immunol 2009;123:672-9
37. B, Example of thermographic images of the cold-induced wheal response over
20 minutes in a patient with ACU treated with placebo, 5 mg/d and 20 mg/d
desloratadine for 7 days
J Allergy Clin Immunol 2009;123:672-9
42. Conclusion
Treatment with desloratadine at doses of
5 and 20 mg daily significantly
decreased wheal volume/size
, improved CTTs & CSTTs in patients with
ACU
Treatment with the higher dose of
desloratadine yields higher outcomes in
wheal volume and CTTs and CSTTs
comparing with standard-dose
desloratadine
43. Solar Urticaria Treated With
Intravenous Immunoglobulins
HenriAdamski,MD, Christophe Bedane, MD, Annie
Bonnevalle, MD, Pierre Thomas, MD, Jean-Louis Peyron, MD, Bernard
Rouchouse, MD, Frederic Cambazard, MD, Michel
Jeanmougin, MD,and Manuelle Viguier, MD
Rennes, Limoges, Lille, Montpellier, Saint-Etienne, and Paris, France
J Am Acad Dermatol 2011;65:336-40
44. Solar urticaria treated with
intravenous immunoglobulins
• To report the effectiveness of intravenous immunoglobulins
(IVIG) in severe solar urticaria ( SU)
• A retrospective multicentric study via the mailing of a
questionnaire to the French Photodermatology Units
• Severe SU was defined as having a poor response to
antihistamine use and impairment of the quality of life
(impact on daily and professional life)
• Collected age, sex, medical history, medications, clinical
features, pho-tobiological characteristics, laboratory
investiga-tions, and clinical response to IVIG
J Am Acad Dermatol 2011;65:336-40
49. Solar Urticaria
- A rare idiopathic photodermatosis
- Sun avoidance and antihistamine
- Severe solar urticaria needs more modality
such as
intravenous immunoglonulins
- Further trials are needed