- Published on
Dermatology - Measles
The symptoms of measles, a highly contagious viral illness, include fever, coryza, coughing, mucocutaneous rash, and conjunctivitis. The prevention of infection is greatly enhanced by immunization.
Significant morbidity and mortality are possible. Despite being rare in nations where vaccination is widely practiced, measles kills more than 150,000 people annually worldwide. Recent outbreaks have occurred in the US as vaccination refusal has grown. Aerosolized respiratory droplets from coughing and sneezing transmit the measles. Those who have the infection can spread to others up to five days after the lesions start to show.
A prodrome of fever, malaise, photophobia, conjunctivitis with lacrimation, upper respiratory symptoms (coryza, hacking cough similar to barking dogs), and periorbital edema is present. The rash appears and gets worse before these symptoms start to go away.
Damage
Clusters of tiny, bluish white dots on a red background that occur in the mouth cavity on the buccal mucosa on the second or third day of a feverish illness are known as Koplik spots and are a reliable indicator of measles. Erythematous macules and papules occur on the forehead behind the ears and along the hairline on the fourth febrile day. After that, by the third day, the rash has expanded inferiorly and centrifugally to encompass the face, torso, limbs, palms, and soles of the feet. Confluence of initially separate lesions is possible, particularly on the face, neck, and shoulders. Lesions eventually disappear in the order that they first develop, leaving behind a mild desquamation or a persistent yellow-tan stain.
The measles antigen can, but is not required to, be found in respiratory secretions to confirm the clinical diagnosis. Drug responses, scarlet fever, Kawasaki disease, and other viral exanthems are also included in the differential.
For the majority of cases, measles is a self-limiting infection. As you watch for potential consequences of infections (respiratory, ear), thrombocytopenia, and encephalitis, give supportive and symptomatic therapy.
The symptoms of measles, a highly contagious viral illness, include fever, coryza, coughing, mucocutaneous rash, and conjunctivitis. The prevention of infection is greatly enhanced by immunization.
Significant morbidity and mortality are possible. Despite being rare in nations where vaccination is widely practiced, measles kills more than 150,000 people annually worldwide. Recent outbreaks have occurred in the US as vaccination refusal has grown. Aerosolized respiratory droplets from coughing and sneezing transmit the measles. Those who have the infection can spread to others up to five days after the lesions start to show.
A prodrome of fever, malaise, photophobia, conjunctivitis with lacrimation, upper respiratory symptoms (coryza, hacking cough similar to barking dogs), and periorbital edema is present. The rash appears and gets worse before these symptoms start to go away.
Damage
Clusters of tiny, bluish white dots on a red background that occur in the mouth cavity on the buccal mucosa on the second or third day of a feverish illness are known as Koplik spots and are a reliable indicator of measles. Erythematous macules and papules occur on the forehead behind the ears and along the hairline on the fourth febrile day. After that, by the third day, the rash has expanded inferiorly and centrifugally to encompass the face, torso, limbs, palms, and soles of the feet. Confluence of initially separate lesions is possible, particularly on the face, neck, and shoulders. Lesions eventually disappear in the order that they first develop, leaving behind a mild desquamation or a persistent yellow-tan stain.
The measles antigen can, but is not required to, be found in respiratory secretions to confirm the clinical diagnosis. Drug responses, scarlet fever, Kawasaki disease, and other viral exanthems are also included in the differential.
For the majority of cases, measles is a self-limiting infection. As you watch for potential consequences of infections (respiratory, ear), thrombocytopenia, and encephalitis, give supportive and symptomatic therapy.
- Published on
Dermatology - Seborrheic Keratosis
Benign epithelial tumors most commonly occur from seborrheic keratosis. The onset of lesions is delayed until age thirty and is inherited. Over the course of a lifetime, they continue to develop, ranging in size from a few dispersed lesions to literally hundreds in certain extremely old patients.
Lesions can vary in size from tiny, hardly noticeable papules to plaques that have a warty surface and seem to be "stuck on." The lesions are rarely itchy. If they have secondary infections, they become painful.
Damage
Little, scarcely elevated papules, measuring 1 to 3 mm, develop into bigger plaques, either with or without pigment.
The surface feels oily, the edge is strongly marginated, and fine stippling, resembling a thimble's surface, is frequently visible with a hand lens. By using liquid nitrogen to gently freeze the lesion, elevation can be seen. Late plaques appear "greasy" or "stuck on" and have a warty surface. Horn cysts are frequently visible using a hand lens; however, they are always visible and diagnostic through dermoscopy. These are flat, round, oval, brown, gray, black, or skin-colored nodules that range in size from 1 to 6 cm. Lesions can form on the face, trunk, upper limbs, and in women, usually in the submammary skin folds. They can be localized or widespread. Dermatosis papulosa nigra is the term for a group of tiny, black lesions on the face that appear in people with darker complexion. In sun-exposed areas where dermatoheliosis is present, seborrheic keratoses are most prevalent. They have the potential to congregate when numerous and dense.
In a clinical setting, diagnosis is made with ease. Make sure squamous cell carcinoma is not the cause. Malignant melanoma, pigmented basal cell carcinoma (BCC), squamous cell carcinoma, solar lentigo or spreading pigmented actinic keratosis, and verruca vulgaris (differentiated by the presence of thrombosed capillaries in verrucae) are among the conditions included in the differential.
Treatment is not necessary for benign lesions, unless they are for aesthetic purposes. It is possible to simply rub off the entire lesion with light electrocautery. To stop recurrence, the base can then be gently cauterized. However, this makes histopathologic verification of the diagnosis impossible and should only be carried out by a qualified diagnostician. Liquid nitrogen spray cryosurgery is only effective on flat lesions, and recurrences may be more common.
The optimum method is curettage with cryospray after a brief freezing period, which enables histopathologic analysis.
Benign epithelial tumors most commonly occur from seborrheic keratosis. The onset of lesions is delayed until age thirty and is inherited. Over the course of a lifetime, they continue to develop, ranging in size from a few dispersed lesions to literally hundreds in certain extremely old patients.
Lesions can vary in size from tiny, hardly noticeable papules to plaques that have a warty surface and seem to be "stuck on." The lesions are rarely itchy. If they have secondary infections, they become painful.
Damage
Little, scarcely elevated papules, measuring 1 to 3 mm, develop into bigger plaques, either with or without pigment.
The surface feels oily, the edge is strongly marginated, and fine stippling, resembling a thimble's surface, is frequently visible with a hand lens. By using liquid nitrogen to gently freeze the lesion, elevation can be seen. Late plaques appear "greasy" or "stuck on" and have a warty surface. Horn cysts are frequently visible using a hand lens; however, they are always visible and diagnostic through dermoscopy. These are flat, round, oval, brown, gray, black, or skin-colored nodules that range in size from 1 to 6 cm. Lesions can form on the face, trunk, upper limbs, and in women, usually in the submammary skin folds. They can be localized or widespread. Dermatosis papulosa nigra is the term for a group of tiny, black lesions on the face that appear in people with darker complexion. In sun-exposed areas where dermatoheliosis is present, seborrheic keratoses are most prevalent. They have the potential to congregate when numerous and dense.
In a clinical setting, diagnosis is made with ease. Make sure squamous cell carcinoma is not the cause. Malignant melanoma, pigmented basal cell carcinoma (BCC), squamous cell carcinoma, solar lentigo or spreading pigmented actinic keratosis, and verruca vulgaris (differentiated by the presence of thrombosed capillaries in verrucae) are among the conditions included in the differential.
Treatment is not necessary for benign lesions, unless they are for aesthetic purposes. It is possible to simply rub off the entire lesion with light electrocautery. To stop recurrence, the base can then be gently cauterized. However, this makes histopathologic verification of the diagnosis impossible and should only be carried out by a qualified diagnostician. Liquid nitrogen spray cryosurgery is only effective on flat lesions, and recurrences may be more common.
The optimum method is curettage with cryospray after a brief freezing period, which enables histopathologic analysis.
- Published on
Dermatology - Hereditary Epidermolysis Bullosa ( Koebner Variant)
Hereditary epidermolysis bullosa is a spectrum of rare genodermatoses. Disturbed coherence
of the epidermis and/or dermis leads to blister formation following trauma.
Classification is based on the site of blister formation: epidermolytic or EB simplex (EBS),
junctional EB (JEB), and dermolytic, or dystrophic, EB (DEB). In each of these there are
several distinct types. Epidermolysis bullosus simplex (EBS) Koebner variant is a traumainduced,
intraepidermal blistering form that is dominantly inherited, with onset at birth to
early infancy.
Disease manifestations range from very mild to mutilating. There is generalized blistering
following trauma with a predilection for traumatized body sites such as feet, hands, elbows,
and knees.
Lesions
Blisters are tense or flaccid at first and lead to erosions. There is rapid healing and only
minimal scarring at sites of repeated blistering. Palmoplantar hyperkeratoses may be
present. Nails, teeth, and oral mucosa are usually spared.
Diagnosis is based on clinical appearance and history. Histopathology determines the level
of cleavage, which is further defined by electron microscopy and/or immunohistochemical
mapping. Western blot, Northern blot, restriction fragment length polymorphism (RFLP)
analysis, and DNA sequences may then identify the mutated gene.
Management is tailored to the severity and extent of skin involvement and consists of supportive
skin care, supportive care for other organ systems, and systemic therapies for complications.
Wound management, nutritional support, and infection control are key and the
maintenance of a cool environment and use of soft, well-ventilated shoes are important.
Treat blistered skin with saline compresses and topical antibiotics or, in the case of inflammation,
with topical steroids.
Hereditary epidermolysis bullosa is a spectrum of rare genodermatoses. Disturbed coherence
of the epidermis and/or dermis leads to blister formation following trauma.
Classification is based on the site of blister formation: epidermolytic or EB simplex (EBS),
junctional EB (JEB), and dermolytic, or dystrophic, EB (DEB). In each of these there are
several distinct types. Epidermolysis bullosus simplex (EBS) Koebner variant is a traumainduced,
intraepidermal blistering form that is dominantly inherited, with onset at birth to
early infancy.
Disease manifestations range from very mild to mutilating. There is generalized blistering
following trauma with a predilection for traumatized body sites such as feet, hands, elbows,
and knees.
Lesions
Blisters are tense or flaccid at first and lead to erosions. There is rapid healing and only
minimal scarring at sites of repeated blistering. Palmoplantar hyperkeratoses may be
present. Nails, teeth, and oral mucosa are usually spared.
Diagnosis is based on clinical appearance and history. Histopathology determines the level
of cleavage, which is further defined by electron microscopy and/or immunohistochemical
mapping. Western blot, Northern blot, restriction fragment length polymorphism (RFLP)
analysis, and DNA sequences may then identify the mutated gene.
Management is tailored to the severity and extent of skin involvement and consists of supportive
skin care, supportive care for other organ systems, and systemic therapies for complications.
Wound management, nutritional support, and infection control are key and the
maintenance of a cool environment and use of soft, well-ventilated shoes are important.
Treat blistered skin with saline compresses and topical antibiotics or, in the case of inflammation,
with topical steroids.
- Published on
Dermatology - Infective endocarditis
The endocardium becomes inflamed with infectious endocarditis, which manifests as mucocutaneous symptoms.
During transitory bacteremia, the main cause is bacterial adhesion to damaged valves.
Septic embolization then happens to the brain, kidney, spleen, skin, and other organs.
Anorexia, fever, and malaise are common non-cardiac problems that patients bring with them. It is common to hear a murmur that is unfamiliar or has changed in tone.
Damage
Osler nodes are erythematous, painful nodules that typically develop on the pads of the fingers and toes. 15% of patients have Janeway lesions, which are nontender, erythematous, nodular lesions that are most frequently encountered on the palms and soles. Splinter hemorrhages are tiny, brown-colored, linear subungual hemorrhages that start off red in the middle part of the nail bed. Petechial lesions are tiny, reddish-brown, nonblanching macules that appear in clusters on the upper chest, extremities, and mucous membranes. They disappear in a few days (20–40%).
Roth spots are white patches of retina near the optic disk that are frequently encircled by hemorrhages; they are also associated with leukemia and pernicious anemia. Usually in the acral region, septic emboli are painful hemorrhagic macules, papules, or nodules.
Main aspects are the basis for diagnosis: A single positive blood culture or an IgG antibody titer >1>:800 for Coxiella burnetii;2) two separate or consistently positive blood cultures for typical microorganisms;3) indications of endocardial involvement, new valvular regurgitation, an echo showing an intracardiac mass, abscess, or valve dehiscence, and minor features
1) susceptibility to infective endocarditis; 2) fever; 3) vasculitis symptoms; 4) immunologic factors, such as glomerulonephritis or positive rheumatoid factor; 5) serologic indications of current infection. A diagnosis is deemed to be confirmed in the event where there are two majors, one major, three minors, or five minors. Three minor traits, or one major and one minor, are regarded as clinically suggestive. All other potential causes of mucocutaneous vasculitis are included in the differential.
Most of the time, parenteral antibiotics are administered for 4-6 weeks at a time. Surgery may be necessary in cases with refractive error.
The endocardium becomes inflamed with infectious endocarditis, which manifests as mucocutaneous symptoms.
During transitory bacteremia, the main cause is bacterial adhesion to damaged valves.
Septic embolization then happens to the brain, kidney, spleen, skin, and other organs.
Anorexia, fever, and malaise are common non-cardiac problems that patients bring with them. It is common to hear a murmur that is unfamiliar or has changed in tone.
Damage
Osler nodes are erythematous, painful nodules that typically develop on the pads of the fingers and toes. 15% of patients have Janeway lesions, which are nontender, erythematous, nodular lesions that are most frequently encountered on the palms and soles. Splinter hemorrhages are tiny, brown-colored, linear subungual hemorrhages that start off red in the middle part of the nail bed. Petechial lesions are tiny, reddish-brown, nonblanching macules that appear in clusters on the upper chest, extremities, and mucous membranes. They disappear in a few days (20–40%).
Roth spots are white patches of retina near the optic disk that are frequently encircled by hemorrhages; they are also associated with leukemia and pernicious anemia. Usually in the acral region, septic emboli are painful hemorrhagic macules, papules, or nodules.
Main aspects are the basis for diagnosis: A single positive blood culture or an IgG antibody titer >1>:800 for Coxiella burnetii;2) two separate or consistently positive blood cultures for typical microorganisms;3) indications of endocardial involvement, new valvular regurgitation, an echo showing an intracardiac mass, abscess, or valve dehiscence, and minor features
1) susceptibility to infective endocarditis; 2) fever; 3) vasculitis symptoms; 4) immunologic factors, such as glomerulonephritis or positive rheumatoid factor; 5) serologic indications of current infection. A diagnosis is deemed to be confirmed in the event where there are two majors, one major, three minors, or five minors. Three minor traits, or one major and one minor, are regarded as clinically suggestive. All other potential causes of mucocutaneous vasculitis are included in the differential.
Most of the time, parenteral antibiotics are administered for 4-6 weeks at a time. Surgery may be necessary in cases with refractive error.
- Published on
Dermatology - Splinter Hemorrhages
Psoriasis, atopic dermatitis, and moderate trauma are the most prevalent causes of distal splinter hemorrhages, occurring in up to 20% of the normal population. Trauma, sideropenic anemia, bacterial endocarditis, trichinosis, antiphospholipid antibody syndrome, and altitude sickness are the causes of proximal splinter hemorrhages.
Little linear structures, typically 2-3 mm in length, are positioned along the nail's long axis. When they first form, they are plum in color; after 1-2 days, they deepen to brown or black. With nail growth, local and distant splinter hemorrhages occur.Finding the root cause is the aim of diagnostics.
Determine the underlying illness and treat it.
Psoriasis, atopic dermatitis, and moderate trauma are the most prevalent causes of distal splinter hemorrhages, occurring in up to 20% of the normal population. Trauma, sideropenic anemia, bacterial endocarditis, trichinosis, antiphospholipid antibody syndrome, and altitude sickness are the causes of proximal splinter hemorrhages.
Little linear structures, typically 2-3 mm in length, are positioned along the nail's long axis. When they first form, they are plum in color; after 1-2 days, they deepen to brown or black. With nail growth, local and distant splinter hemorrhages occur.Finding the root cause is the aim of diagnostics.
Determine the underlying illness and treat it.
- Published on
Dermatology - Port Wine Stain
A macular capillary malformation (CM) with an irregular shape, red or violaceous, that is present from birth and never goes away on its own is called a port-wine stain (PWS). It is frequent (affecting 0.3% of infants); the deformity is usually limited to the skin, though it can also be linked to leptomeninges (a condition that causes vascular abnormalities in the eye) and Sturge-Weber syndrome.
Macules that range in color from pink to purple are lesions. Large lesions are typically unilateral (85%), however they are not always, and they follow a dermatomal distribution. Lesions most frequently occur on the face, typically on the superior and middle branches of the trigeminal nerve. Mouth and conjunctival mucosa may become involved. CM might also touch other websites. As the patient ages, rubbery nodules or papules frequently appear, severely deforming the body.
Clinical diagnosis is made.
It is possible to conceal PWS with cosmetics during the macular phase. Treatment with copper vapor lasers or tunable dye is quite successful.
A macular capillary malformation (CM) with an irregular shape, red or violaceous, that is present from birth and never goes away on its own is called a port-wine stain (PWS). It is frequent (affecting 0.3% of infants); the deformity is usually limited to the skin, though it can also be linked to leptomeninges (a condition that causes vascular abnormalities in the eye) and Sturge-Weber syndrome.
Macules that range in color from pink to purple are lesions. Large lesions are typically unilateral (85%), however they are not always, and they follow a dermatomal distribution. Lesions most frequently occur on the face, typically on the superior and middle branches of the trigeminal nerve. Mouth and conjunctival mucosa may become involved. CM might also touch other websites. As the patient ages, rubbery nodules or papules frequently appear, severely deforming the body.
Clinical diagnosis is made.
It is possible to conceal PWS with cosmetics during the macular phase. Treatment with copper vapor lasers or tunable dye is quite successful.
- Published on
Dermatology - Acrodermatitis Enteropathica
An autosomal recessive zinc absorption condition called acrodermatitis enteropathica can strike babies who are breastfed or bottle-fed cow's milk shortly after they are weaned.
Acrodermatitis enteropathica causes growth failure, photophobia, and uncontrollable crying and whining in children. There is anemia, low zinc levels in the serum and plasma, and decreased zinc excretion in the urine.
Dry, scaly, strongly marginated, brilliantly red eczematous dermatitis patches and plaques eventually develop into vesiculobullous, pustular, erosive, and crusted lesions. Lesions first appear in the anogenital and perioral regions, then progress to the scalp, hands, feet, flexural regions, and trunk. Fingertips are shiny, erythematous, and show signs of secondary paronychia and fissures.
Wound healing is compromised when Candida albicans and S. aureus secondary infect lesions. In addition to paronychia, nail loss, and ridging of the nails, diffuse alopecia and graying of the hair also occur. There could be superficial erosions that resemble aphthous and a red, glossy tongue in the oral cavity.
The basis for the diagnosis is the combination of test and clinical data.
Zinc salt supplements taken orally or intravenously (IV) in two to three times the daily requirement can return zinc levels to normal in a matter of days to weeks. Severe erosive and infected skin lesions recover in 1-2 weeks after zinc replacement. Within 24 hours, the diarrhea stops and the irritation and mood sadness go better.
An autosomal recessive zinc absorption condition called acrodermatitis enteropathica can strike babies who are breastfed or bottle-fed cow's milk shortly after they are weaned.
Acrodermatitis enteropathica causes growth failure, photophobia, and uncontrollable crying and whining in children. There is anemia, low zinc levels in the serum and plasma, and decreased zinc excretion in the urine.
Dry, scaly, strongly marginated, brilliantly red eczematous dermatitis patches and plaques eventually develop into vesiculobullous, pustular, erosive, and crusted lesions. Lesions first appear in the anogenital and perioral regions, then progress to the scalp, hands, feet, flexural regions, and trunk. Fingertips are shiny, erythematous, and show signs of secondary paronychia and fissures.
Wound healing is compromised when Candida albicans and S. aureus secondary infect lesions. In addition to paronychia, nail loss, and ridging of the nails, diffuse alopecia and graying of the hair also occur. There could be superficial erosions that resemble aphthous and a red, glossy tongue in the oral cavity.
The basis for the diagnosis is the combination of test and clinical data.
Zinc salt supplements taken orally or intravenously (IV) in two to three times the daily requirement can return zinc levels to normal in a matter of days to weeks. Severe erosive and infected skin lesions recover in 1-2 weeks after zinc replacement. Within 24 hours, the diarrhea stops and the irritation and mood sadness go better.
- Published on
Dermatology - Nail Psoriasis
The most prevalent dermatosis that affects the nail apparatus is psoriasis, which affects the nails in >50% of cases, up to 80–90% of cases over the course of a lifetime.
Elkonyxis, also known as pitting, will be present in the nail matrix. These small, shallow punctate depressions come in a variety of sizes and shapes. Though they can also occur as regular lines (transverse; long axis) or in grid-like patterns, their characteristics are isolation and depth.
Lesions in the toenails are rare. The nail is rough, brittle, and dull. Proximal nail matrix destruction is linked to sandpaper nails, or twenty-nail dystrophy; however, this is general and can also be observed in alopecia areata, lichen planus, and atopic dermatitis.
Repeated transverse depressions may resemble the "washboard" nails of tic habits, where the cuticle is pushed back.
Longitudinal ridging, akin to melted wax, could exist. One or two millimeter white spots in the nail plate called punctate leukonychia are sometimes misdiagnosed as injuries.
An oval, salmon-colored nail bed called "oil" patches may be present, and onycholysis may develop as a result, affecting the hyponychium medially or laterally.
There could be secondary infections. Subungual hyperkeratosis, or raising of the nail plate off the hyponychium, is possible.
A clinical exam and history are used to make a diagnosis. Onycholysis, onychomycosis, trauma (toenail), eczema, and alopecia areata are among the differential diagnoses.
Intralesional triamcinolone 3-5 mg/mL may be useful for matrix involvement. Topical steroid (occluded) decreases hyperkeratosis in nail bed psoriasis. Nail apparatus psoriasis is frequently improved by systemic therapy, such as methotrexate, acitretin, or "biologics," though results may not show up for some months after treatment has finished.
The most prevalent dermatosis that affects the nail apparatus is psoriasis, which affects the nails in >50% of cases, up to 80–90% of cases over the course of a lifetime.
Elkonyxis, also known as pitting, will be present in the nail matrix. These small, shallow punctate depressions come in a variety of sizes and shapes. Though they can also occur as regular lines (transverse; long axis) or in grid-like patterns, their characteristics are isolation and depth.
Lesions in the toenails are rare. The nail is rough, brittle, and dull. Proximal nail matrix destruction is linked to sandpaper nails, or twenty-nail dystrophy; however, this is general and can also be observed in alopecia areata, lichen planus, and atopic dermatitis.
Repeated transverse depressions may resemble the "washboard" nails of tic habits, where the cuticle is pushed back.
Longitudinal ridging, akin to melted wax, could exist. One or two millimeter white spots in the nail plate called punctate leukonychia are sometimes misdiagnosed as injuries.
An oval, salmon-colored nail bed called "oil" patches may be present, and onycholysis may develop as a result, affecting the hyponychium medially or laterally.
There could be secondary infections. Subungual hyperkeratosis, or raising of the nail plate off the hyponychium, is possible.
A clinical exam and history are used to make a diagnosis. Onycholysis, onychomycosis, trauma (toenail), eczema, and alopecia areata are among the differential diagnoses.
Intralesional triamcinolone 3-5 mg/mL may be useful for matrix involvement. Topical steroid (occluded) decreases hyperkeratosis in nail bed psoriasis. Nail apparatus psoriasis is frequently improved by systemic therapy, such as methotrexate, acitretin, or "biologics," though results may not show up for some months after treatment has finished.
- Published on
Dermatology - Drug Induced Pustular Rash
Pustular Rash Caused by Drug (Adverse Cutaneous Drug Reactions)
Acute generalized exanthematous pustulosis (AGEP) is a febrile eruption with an estimated yearly frequency of 1-2 million cases. It is frequently linked to leukocytosis. Skin lesions may not show for one to three weeks following drug administration; in patients who have already been sensitized, skin signs may manifest in two to three days.
Elevated blood neutrophils and fever are frequent. After less than 15 days, there is spontaneous resolve, which is followed by generalized desquamation around two weeks later.
Damage
Nonfollicular sterile pustules can be randomly distributed or aggregated, typically beginning in the skin folds and/or on the face, and they appear on a diffuse, edematous erythema.
Clinical diagnosis and differential diagnosis include subcorneal pustular dermatosis (Sneddon-Wilkinson disease), pustular psoriasis, and the hypersensitivity syndrome reaction with pustulation. Iodides, bromides, adrenocorticotropic hormone (ACTH), glucocorticoids, isoniazid, androgens, lithium, actinomycin D, and phenytoin are linked to acneiform pustular eruptions. The EGFR tyrosine kinase inhibitors erlotinib, gefitinib, cetuximab, and panitumumab cause non-acneiform pustules that typically appear on the face but can also occur in unexpected locations including the arms and legs. These pustules are also typically monomorphous. Usually, comedones are not present.
Stop using the offending medication and give the patient supportive treatment.
Pustular Rash Caused by Drug (Adverse Cutaneous Drug Reactions)
Acute generalized exanthematous pustulosis (AGEP) is a febrile eruption with an estimated yearly frequency of 1-2 million cases. It is frequently linked to leukocytosis. Skin lesions may not show for one to three weeks following drug administration; in patients who have already been sensitized, skin signs may manifest in two to three days.
Elevated blood neutrophils and fever are frequent. After less than 15 days, there is spontaneous resolve, which is followed by generalized desquamation around two weeks later.
Damage
Nonfollicular sterile pustules can be randomly distributed or aggregated, typically beginning in the skin folds and/or on the face, and they appear on a diffuse, edematous erythema.
Clinical diagnosis and differential diagnosis include subcorneal pustular dermatosis (Sneddon-Wilkinson disease), pustular psoriasis, and the hypersensitivity syndrome reaction with pustulation. Iodides, bromides, adrenocorticotropic hormone (ACTH), glucocorticoids, isoniazid, androgens, lithium, actinomycin D, and phenytoin are linked to acneiform pustular eruptions. The EGFR tyrosine kinase inhibitors erlotinib, gefitinib, cetuximab, and panitumumab cause non-acneiform pustules that typically appear on the face but can also occur in unexpected locations including the arms and legs. These pustules are also typically monomorphous. Usually, comedones are not present.
Stop using the offending medication and give the patient supportive treatment.
- Published on
Dermatology - Candidal Infection of the Nail
Nail infection caused by Candida
Candida spp. infections of the nail can cause the immune-compromised host's nail to fall off. Rarely are environmental fungus primary infections; instead, they produce secondary colonization of damaged nails.
Nail candidiasis can result in a persistent, severe, and sporadic infection of the paronychia, accompanied by erythema, pus, and discomfort. The nail may develop transverse furrows, areas of opacification, and discolorations of white, yellow, green, or black as it becomes dystrophic. Diabetes patients may develop subungual candidiasis and an onycholytic space abscess. Children with HIV/AIDS frequently develop paronychia and onychia, which are frequently linked to mucosal candidiasis.
Tinea unguium, psoriasis, eczema, chronic paronychia, and lichen planus are among the differential diagnoses made using direct microscopy and potassium hydroxide.
Use oral antifungal medications to treat.
Nail infection caused by Candida
Candida spp. infections of the nail can cause the immune-compromised host's nail to fall off. Rarely are environmental fungus primary infections; instead, they produce secondary colonization of damaged nails.
Nail candidiasis can result in a persistent, severe, and sporadic infection of the paronychia, accompanied by erythema, pus, and discomfort. The nail may develop transverse furrows, areas of opacification, and discolorations of white, yellow, green, or black as it becomes dystrophic. Diabetes patients may develop subungual candidiasis and an onycholytic space abscess. Children with HIV/AIDS frequently develop paronychia and onychia, which are frequently linked to mucosal candidiasis.
Tinea unguium, psoriasis, eczema, chronic paronychia, and lichen planus are among the differential diagnoses made using direct microscopy and potassium hydroxide.
Use oral antifungal medications to treat.
