DERMATOLOGY Flashcards

1
Q

a Tzanck showing multinucleated epithelial giant cells?

A

VARICELLA ZOSTER

Tzanck smear is a cytologic technique most often used in the diagnosis of herpesvirus infections (herpes simplex virus [HSV] or varicella-zoster virus [VZV]). Multinucleated epithelial giant cells suggest the presence of HSV or VZV.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

38 year old male developed greasy scales overlying erythematous patches or plaques in the eyebrows, eyelids, glabella, and nasolabial folds, which he described as dandruff. What is the dx? and best management for this case?

A

Seborrheic dermatitis tx:
reatment with low-potency topical glucocorticoids in conjunction with a topical antifungal agent, such as ketoconazole cream or ciclopirox cream, is often effective. High-potency glucocorticoids should not be used on the face because this treatment is often associated with steroid-induced rosacea or atrophy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

A 68 year old female presented with pruritic, erythematous, curvilinear plaques with scaling on the anterior surface of her both legs. She recently went to Northern Mongolia during the winter season. What is the best management of choice?

A

Asteatotic eczema, also known as xerotic eczema or “winter itch,” is a mildly inflammatory dermatitis that develops in areas of extremely dry skin, especially during the dry winter months. Asteatotic eczema responds well to topical moisturizers and the avoidance of cutaneous irritants.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What organism causes the lesion shown below which produces the character

A

Corynebacterium minutissimum

Wood’s lamp will cause erythrasma (a superficial, intertriginous infection caused by Corynebacterium minutissimum) to show a characteristic coral pink color, and wounds colonized by Pseudomonas will appear pale blue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

wounds colonized by _____will appear pale blue under wood’s lamp

A

wounds colonized by Pseudomonas will appear pale blue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

True re: STASIS DERMATITIS

Diuretics may be required to adequately control chronic edema.

Patients with stasis dermatitis and stasis ulceration benefit greatly from leg elevation and the routine use of compression stockings with a gradient of at least 30–40 mmHg.

The typical initial site of involvement is the** medial **aspect of the ankle…

Glucocorticoids should not be applied to ulcers, because they may retard healing…

All are correct

A

ALL ARE CORRECT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A 46 year old male came in your clinic due to progressive sharply demarcated intensely erythematous plaques with secondary pustules and scaling, initially started in the palms and soles before progressing to his arms and legs. He also reported undocumented febrile episodes. He recently used an unrecalled topical skin care product recommended by a friend. What is the best management of choice

A

Diagnosis: pustular psoriasis, patients may have disease localized to the palms and soles, or the disease may be generalized. Regardless of the extent of disease, the skin is erythematous, with pustules and variable scale. When it is generalized, episodes are characterized by fever (39°–40°C [102.2°–104.0°F]) lasting several days, an accompanying generalized eruption of sterile pustules, and a background of intense erythema; patients may become erythrodermic. Local irritants, pregnancy, m tions, infections, and systemic glucocorticoid withdrawal can precipitate this form of psoriasis. Oral retinoids are the treatment of choice in nonpregnant patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Drugs that can cause Pityriasis rosea like

A

Pityriasis rosea–like drug eruptions are seen most commonly with:
* beta blockers,
* angiotensin-converting enzyme (ACE) inhibitors
* metronidazole,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

medications that can produce lichenoid eruptions

A

LICHENOID eruption include:
1. thiazides,
2. antimalarials,
3. quinidine,
4. beta blockers,
5. TNF inhibitors,
6. anti-PD-1/PD-L1 antibodies, and
7. ACE inhibitors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

A 57 year old male presented with opacified and thickened nails and subungual debris. He has hypertension, heart failure, and was recently diagnosed with HIV. Which medications is appropriate for this patient?

A

TERBINAFINE

Two other oral antifungal agents, itraconazole and terbinafine, are sometimes prescribed “off-label” for superficial fungal infections. Oral itraconazole is approved for onychomycosis. Itraconazole has the potential for serious interactions with other drugs requiring the P450 enzyme system for metabolism. Itraconazole should not be administered to patients with evidence of ventricular dysfunction or patients with known CHF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

most common malignancy that is associated with acanthosis nigricans

A

GASTRIC

Acanthosis nigricans can be a reflection of an internal malignancy, most commonly of the gastrointestinal tract, and it appears as velvety hyperpigmentation, primarily in flexural areas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the most common manifestation of patients with Dermatomyositis

A

The most common manifestation is a purple-red discoloration of the upper eyelids, sometimes associated with scaling (“heliotrope” erythema; Fig. 59-3) and periorbital edema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

CLinical feautures of genital ulcers

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Nonscarring alopecia (primary cutaneous disorders)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

key pathway in the pathophysiology of adverse drug reaction in contact dermatitis

A

the key pathway of ADE in contact dermatitis is T-lymphocyte-mediated macrophage inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

A 40 year old male initially presented with cough and fever, and was given Cotrimoxazole by a local physician. He eventually developed high grade fever, sore throat, conjunctivitis, oral ulcerations, and acute onset of painful dusky, atypical, target-like lesions of hands and feet, eventually progressing of abdomen and bilateral legs with 40% desquamation. What is the best management for this case

A

Dx: TEN

The case presented is a case of toxic epidermal necrolysis (TEN). At this time, there is no consensus on the most effective treatment for SJS/TEN. The best outcomes stem from early diagnosis, immediate discontinuation of the suspected drug, and meticulous supportive therapy in an intensive care or burn unit. Early administration of systemic glucocorticoids, intravenous immunoglobulin, cyclosporine, or etanercept may improve disease outcomes, but randomized studies to evaluate potential therapies are lacking and difficult to perform.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

26 year old female patient comes to your clinic for skin eruptions characterized by multiple erythematous plaques with a target morphology, treated for UTI a few days prior given TMPSMX

A

The patient has erythema multiforme. This eruption is characterized by multiple erythematous plaques with a target or iris morphology. It usually represents a hypersensitivity reaction to drugs (e.g., sulfonamides) or infections (e.g., HSV).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

True or falseCyclosporine P 378 UV-light therapy is contraindicated in patients receiving cyclosporine as patients on cyclosporine has an increased risk of developing skin cancer when exposed to phototherapy

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

:

TRUE OR FALSE
Cyclosporine P 378 UV-light therapy is contraindicated in patients receiving cyclosporine as patients on cyclosporine has an increased risk of developing skin cancer when exposed to phototherapy

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

large >2cm FLAT lesion with a color diff from the surrounding skin

A

PATCH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

primary skin lesion described as a large (0.5-5.0 cm) firm lesion raised above the surface of the surrounding skin:

A

Nodule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

a flat colored lesion <2cm not raised above the surrounding skin

A

MACULE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
solid raised growth >5cm in diameter
TUMOR
26
large >1cm flat topped raised may either be distinct
Plaque seen in Psoriasis, eczematous dermatitis
27
small lesion solid, <0.4 cm in diameter RAISED above the surface
Papule | (seen in closed comedone, acne, headache)
28
small fluid lesion less than 0.5 cm in diameter, raised above the plane of surrounding skin
vesicle
29
vesicle filled with leucocytes
PUSTULES
30
a fluid filled, rased often translucent lesion 0.5cm in diameter
BULLA
31
raised, eryhtematous edematous papule or plaque, representing short lived VASO DILATION AND PERMEABILITY
WHEAL
32
violacious to purple polygonal lesions
Lichenoid eruption
33
oval to round plaques with trailing scale, eruption lines up in skinfolds
Pityriasis rosea
34
sharply dermacated, plaques, on knees, elbows, scalps, intertirginous areas
psoriasis
35
purple polygonal papules marked by severe pruritus, lacy white markings, especially associated with mucous membrane lesions
Lichen planus
36
Polymorphous appearance, sharply deifined to ill demarcated scaly plaques, may be associated with hair loss
Dermatophytosis
37
38
benign proliferations of nevomelanocytes characterized by regularly shaped hyperpigmented macules or papules of a uniform color
FIGURE 56-2 Nevomelanocytic nevus. Nevi are benign proliferations of nevomelanocytes characterized by regularly shaped hyperpigmented macules or papules of a uniform color.
39
FIGURE 56-1 Superficial spreading melanoma. This is the most common type of melanoma. Such lesions usually demonstrate asymmetry, border irregularity, color variegation (black, blue, brown, pink, and white), a diameter >6 mm, and a history of change (e.g., an increase in size or development of associated symptoms such as pruritus or pain).
40
secondary lesion- distincitive thickening of the skin
41
secondary lesions?
Lichenification Scale Crust Erosion Ulcer Excoriation Atrophy
42
42
Chalk-white macules, in Periorificial, trunk, extensor surfaces of extremities, flexor wrists, axillae
Vitiligo
42
Indurated and possibly hyperkeratotic lesions often showing ulceration and/or crusting
squamous cell carcinoma
42
42
Papule with pearly, telangiectatic border on sun-damaged skin
basal cell carcinoma
43
Trunk (Christmas tree pattern); herald patch followed by multiple smaller lesions Symmetric erythematous papules and plaques with a collarette of scale
Pityriasis rosea
43
Dermatomal, usually trunk but may be anywhere vesicles
HSV
44
scaly hyper- or hypopigmented macules in chest back abdomen, proximal extremities
Tinea versicolor
44
Brown plaques with adherent, greasy scale; “stuck on” appearance
Seborrheic keratosis
45
Follicular pustules Papules, vesicles, pustules, often with **honey-colored crusts **in any hair bearing area, can occur anywhere as well
Folliculitis Impetigo
46
Patches of erythema and scaling on background of hyperpigmentation associated with signs of venous insufficiency, ankles lower legs over MEDIAL Malleoli
Stasis dermatitis
47
Palpable purpuric papules on the lower legs are seen in this patient with cutaneous small-vessel vasculitis.
Necrotizing vasculitis. Palpable purpuric papules on the lower legs are seen in this patient with cutaneous small-vessel vasculitis. (Courtesy of Robert Swerlick, MD; with permission.)
47
48
Meningococcemia. An example of fulminant meningococcemia with extensive angular purpuric patches.
49
This papulosquamous skin disease is characterized by small and large erythematous papules and plaques with overlying adherent silvery scale.
Psoriasis Pathophysiology Autoimmune Mechanism Dysregulated T-cell mediated immune response (Th1, Th17 pathways). IL-23/IL-17 axis plays a major role. Overproduction of TNF-α, IL-17, IL-22, and IL-23 drives inflammation. Keratinocyte Hyperproliferation Abnormal differentiation and proliferation of keratinocytes, leading to thickened epidermis (acanthosis), parakeratosis (retention of nuclei in stratum corneum), and elongated rete ridges. Angiogenesis & Inflammation Increased vascularization in the dermis due to VEGF activation.
50
Discrete and confluent, edematous, erythematous papules and plaques are characteristic of this whealing eruption
urticaria
51
ERYTHEMA MULTIFORMEThis eruption is characterized by multiple erythematous plaques with a target or iris morphology. It usually represents a hypersensitivity reaction to drugs (e.g., sulfonamides) or infections (e.g., HSV).
52
52
a cytologic technique most often used in the diagnosis of herpesvirus infections (herpes simplex virus [HSV] or varicella-zoster virus [VZV])- placed on a glass slide, air-dried, and stained with Giemsa or Wright’s stain. Multinucleated epithelial giant cells suggest the presence of HSV or VZV; culture, immunofluorescence microscopy, or genetic testing must be performed to identify the specific virus
A Tzanck smear is a cytologic technique most often used in the diagnosis of herpesvirus infections (herpes simplex virus [HSV] or varicella-zoster virus [VZV])
53
Vitiligo Characteristic lesions display an acral distribution and striking depigmentation as a result of loss of melanocytes.
54
Diagnosis? 1. Pruritus and scratching 2. Course marked by exacerbations and remissions 3. Lesions typical of eczematous dermatitis 4. Personal or family history of atopy (asthma, allergic rhinitis, food allergies, or eczema) 5. Clinical course lasting >6 weeks 6. Lichenification of skin 7. Presence of dry skin
atopic dermatitis
55
characterized by circular or oval “coinlike” lesions, beginning as small edematous papules that become crusted and scaly in thr trunk, extensor surfaces
Nummular eczema is characterized by circular or oval “coinlike” lesions, beginning as small edematous papules that become crusted and scaly. The etiology of nummular eczema is unknown, but dry skin is a contributing factor. Common locations are the trunk or the extensor surfaces of the extremities, particularly on the pretibial areas or dorsum of the hands. Nummular eczema occurs more frequently in men and is most common in middle age. The treatment of nummular eczema is similar to that for AD.
55
deep-seated vesicles and scaling on palms and lateral fingers, and the disease is often associated with an atopic diathesis.
Dyshidrotic eczema. This example is characterized by deep-seated vesicles and scaling on palms and lateral fingers, and the disease is often associated with an atopic diathesis.
56
Stasis dermatitis. An example of stasis dermatitis showing erythematous, scaly, and oozing patches over the lower leg. Several stasis ulcers are also seen in this patient.
57
. Central facial erythema with overlying greasy, yellowish scale is seen in this patient.
Seborrheic dermatitis. Central facial erythema with overlying greasy, yellowish scale is seen in this patient. Tx: Treatment with low-potency topical glucocorticoids in conjunc- tion with a topical antifungal agent, such as ketoconazole cream or ciclopirox cream, is often effective. The scalp and beard areas may benefit from antidandruff shampoos, which should be left in place 3–5 min before rinsing. High-potency topical glucocorticoid solutions (betamethasone or clobetasol) are effective for control of severe scalp involvement. High-potency glucocorticoids should not be used on the face because this treatment is often associated with steroid-induced rosacea or atrophy.
58
Type of psoriasis that is most common in children and young adults. It develops acutely in individuals without psoriasis or in those with chronic plaque psoriasis. Patients present with many small erythematous, scaling papules, frequently after upper respiratory tract infection with β-hemolytic streptococci.* The differential diagno- sis should include pityriasis rosea and secondary syphilis.*
Guttate psoriasis (eruptive psoriasis)
58
FDA Approved therapy for psoriasis
58
side effects(Renal dysfunction, hypertension, hyperkalemia, hyperuricemia, hypomagnesemia, hyperlipidemia, increased risk of malignancies) of what psoriasis drug ?
Cyclosporine calcineurin inhibitor
59
PDE4 inhibitor fda approved for Psoriasis
Apremilast
59
59
Adverse effects of Methortrexate
Hepatotoxicity, pulmonary toxicity, pancytopenia, potential for increased malignancies, ulcerative stomatitis, nausea, diarrhea, teratogenicity
60
FDA Approved Biologics for Psoriasis or Psoriatic Arthritis
61
psoriasis medications that work via **Anti-TNF-α**
Etanercept (Ps, PsA; SC) Adalimumab (Ps, PsA; SC) Certolizumab (Ps, PsA; SC) Infliximab (Ps, PsA; IV) Golimumab (PsA; SC)
62
showing multiple flat- topped, violaceous papules and plaques. Nail dystrophy, as seen in this patient’s thumbnail, may also be a feature.
Lichen planus
63
anti IL 12 and IL 23 treatment for psoriasis
Ustekinumab
64
Anti-IL-23 treatment for psoriasis
RISA TILDRA GUSEL 23 Risankizumab (Ps; SC) Tildrakizumab (Ps; SC) Guselkumab (
64
multiple round to oval erythematous patches with fine central scale are distributed along the skin tension lines on the trunk,
Pityriasis rosea. papulosquamous eruption of unknown eti- ology occurring more commonly in the spring and fall. Its first mani- festation is the development of a 2- to 6-cm annular lesion (the herald patch). This is followed in a few days to a few weeks by the appearance of many smaller annular or papular lesions with a predilection to occur on the trunk
65
Anti-IL-17
SE-XE-BRODA == 17 Secukinumab (Ps, PsA; SC) Ixekizumab (Ps; SC) Brodalumab (Ps; SC)
65
with inflammatory papules, pustules, and comedones. (
acne vulgaris Treatment of acne vulgaris is directed toward elimination of come- dones by normalizing follicular keratinization and decreasing seba- ceous gland activity, the population of C. acnes, and inflammation
65
Erythroderma Figure
65
Prominent facial erythema, telangiectasia, scattered papules, and small pustules are seen in this patient with acne rosacea. tx: Acne rosacea can be treated topically or systemically. Mild disease often responds to topical preparations of metronidazole, sodium sulfacetamide, azelaic acid, ivermectin, brimonidine, or oxyme- tazoline. More severe disease requires oral tetracyclines in suban- timicrobial, modified-release preparations. Residual telangiectasia may respond to laser therapy. Topical glucocorticoids, especially potent agents, should be avoided because chronic use of these prep- arations may elicit rosacea. Application of topical agents to the skin is not effective treatment for ocular disease.
66
non-scarring alopecia causes
67
Tx for Upper trunk and neck (shawl- like distribution), groin Young adults Macules have fine white scale when scratched with golden flouroscense, on wood's lamp skin biopsy: hyphal forms and budding yeast in stratum corneum
Pityriasis (tinea) versicolora Tx? Selenium sulfide 2.5% shampoo; topical imidazoles; oral triazoles Pathogenesis: Invasion of stratum corneum by the yeast Malassezia Yeast is lipophilic and produces C9 and C11 dicarboxylic acids, which in vitro inhibit tyrosinase
68
Flaccid bullae are easily ruptured, resulting in multiple erosions and crusted plaques. B. Involvement of the oral mucosa, which is almost invariable, may present with erosions on the gingiva, buccal mucosa, palate, posterior pharynx, or tongue may elicit the separation of the epidermis (Nikolsky’s sign).
Pemphigus vulgaris Histology: acantholytic blister formed in suprabasal layer of epidermis Cell surface deposits of IgG on keratinocytes autoantigens Dsg3 (plus Dsg1 in patients with skin involvement)
69
olymorphic autoimmune subepidermal blistering disease usually seen in the elderly. Initial lesions may consist of urticarial plaques; most patients eventually display tense blisters on either normal-appearing or erythematous skin
BULLOUS PEMPHIGOID The major histocompatibility complex class II allele HLA-DQβ1*0301 is prevalent in patients with BP. Though most cases occur sporadi- cally, BP can be triggered by medications (e.g., furosemide, dipeptidyl peptidase-4 inhibitors, immune checkpoint inhibitors), ultraviolet light, or ionizing radiation. Several studies have shown that BP is associated with neurologic diseases (e.g., stroke, dementia, Parkinson’s disease, and multiple sclerosis).
69
Acute cutaneous lupus erythematosus (LE). A. Acute cutaneous LE on the face, showing prominent, scaly, malar erythema. Involvement of other sun-exposed sites is also common. B. Acute cutaneous LE on the upper chest, demonstrating brightly erythematous and slightly edematous papules and plaques.
70
Gottron’s papules. Dermatomyositis often involves the hands as erythematous flat-topped papules over the knuckles. Periungual telangiectasias are also evident.
71
Dermatomyositis. Periorbital violaceous erythema characterizes the classic heliotrope rash.
72
73
cleroderma showing acral sclerosis and focal digital ulcers.
74
Scleroderma often eventuates in development of an expressionless, masklike facies.
75
76
77
78
79
Adverse drug rxn type Vasculitis, serum sickness, drug- induced lupus
Type III Immune Complex IgG + Antigen
80
Adverse drug reaction type ? SJS/TEN Morbilliform eruption
Type IVc T lymphocyte– mediated cytotoxic T lymphocyte inflammation
81
rare reaction (0.01–0.1%) usu- ally occurs between the third and tenth days of therapy with ___ usually in women. Common sites are breasts, thighs, and buttocks Lesions are sharply demarcated, erythematous, or purpuric, and may progress to form large, hemorrhagic bullae with necro- sis and eschar formation.
Warfarin necrosis
82
Uritcaria Angioedema Anaphylaxis?
Type I IGe Mediated
82
Drug-induced hemolysis, thrombocytopenia (e.g., penicillin)
Type II IgG mediated cytoxicity
82
Tuberculin skin test, contact dermatitis
Type IVa T lymphocyte– mediated macrophage inflammation
82
DIHS Morbilliform eruption
Type 4b T lymphocyte– mediated eosinophil inflammation L-4, IL-5, IL-13 TH2 cells Eosinophils
82
Toxic erythema of chemotherapy.
82
Allergic contact dermatitis (bullous) due to adhesive tape.
82
Morbilliform drug eruption.
82
presents with a prodrome of fever and flu-like symptoms for several days, followed bythe appearance of a diffuse morbilliform eruption, usually involving the face
Drug-induced hypersensitivity syndrome/drug rash with eosinophilia and systemic symptoms (DIHS/DRESS DIHS is a systemic drug reaction also known as DRESS (drug reaction with eosinophilia and systemic symptoms) syndrome; because eosinophilia is not always present, the term DIHS is preferred. Clinically, DIHS presents with a prodrome of fever and flu-like symptoms for several days, followed bythe appearance of a diffuse morbilliform eruption, usually involving the face
83
60-5 Fixed drug eruption
83
characterized by blisters and mucosal/epider- mal detachment resulting from full-thickness epidermal necrosis in the absence of substantial dermal inflammation with >30% detachment
TEN
83
10–30% epidermal detachment
SJS TEN overkap
83
medications that cause DIHS /DRESS
** allopurinol** classically induces DIHS with renal involvement; cardiac and lung involvement are more common with **minocycline**; gastrointestinal involvement is almost exclusively seen with **abacavir**; and some medications typically do not induce eosinophilia (**abacavir**, **dapsone**, **lamotrigine**). The cutaneous reaction usually begins 2–8 weeks after the drug is started and persists after drug cessation. Signs and symptoms may continue for several weeks, especially those associated with hepatitis. The eruption recurs with rechallenge, and cross-reactions among aromatic anticonvulsants, including **phenytoin**, **carbamazepine**, and **phenobarbital**, are com- mon. Other drugs causing DIHS include antibacterial sulfonamides and other antibiotics. Hypersensitivity to reactive drug metabolites, **hydroxylamine** for **sulfamethoxazole** and arene oxide for aromatic anticonvulsants, may be involved in the pathogenesis of DIHS. R
83
describes cases in which the total body surface area of blistering and eventual detachment is <10%
SJS Patients with SJS/TEN initially present with fever >39°C (102.2°F); sore throat; conjunctivitis; and acute onset of painful dusky, atypical, target-like lesions (Intestinal and upper respiratory tract involvement are associated with a poor prognosis, as are older age and greater extent of epidermal detachment. A
83
Drugs that most commonly cause SJS/TEN
Drugs that most commonly cause SJS/TEN are **sulfonamides, allopurinol, antiepilep- tics (e.g., lamotrigine, phenytoin, carbamazepine), oxicam NSAIDs, β-lactam and other antibiotics, and nevirapine.** Frozen-section skin biopsy may aid in rapid diagnosis.
84
Target like lesion in SJS Patients with SJS/TEN initially present with fever >39°C (102.2°F); sore throat; conjunctivitis; and acute onset of painful dusky, atypical, target-like lesions
85
Tx for SJS TEN
immediate discontinuation of the suspected drug, and meticulous supportive ther- apy in an intensive care or burn unit. Fluid management, atraumatic wound care, infection prevention and treatment, and ophthalmologic and respiratory support are critical. Early administration of systemic glucocorticoids, intravenous immunoglobulin, cyclosporine, or etaner- cept may improve disease outcomes, but randomized studies to evalu- ate potential therapies are lacking and difficult to perform
86
87
four (4) main questions to answer regarding a suspected drug eruption:
There are four main questions to answer regarding a suspected drug eruption: 1. Is the observed rash caused by a medication? 2. Is the reaction severe or evolving with systemic involvement? 3. Which drug or drugs are suspected, and should they be withdrawn? 4. What recommendation can be made for future medication use?
87
drugs that causes Drug-induced hypersensitivity syndrome/drug rash with eosinophilia and systemic symptoms (DIHS/DRESS))
Anticonvulsants, sulfonamides, allopurinol, minocycline
87
Cutaneous small-vessel vasculitis (CSVV, leukocytoclastic vasculitis
87
88
Dx? diffuse, deep red morbilliform eruption with facial involvement; facial and acral swelling Fever, lymphadenopathy, hepatitis, nephritis, myocarditis, eosinophilia, atypical lymphocytosis drinking allopurinol
Drug-induced hypersensitivity syndrome/drug rash with eosinophilia and systemic symptoms (DIHS/DRESS)
89
Fritzpatrick classification of skin type and sunburn sensitivity
89
Monitoring for methotrexate tx
LFTs, CBC, renal function (every 4-8 weeks)
89
Algorithm for the diagnosis of a patient with photosensitivity
89
89
Cyclosporine
BP, renal function (every 2-3 months)
89
Biologics monitoring labs?
TB testing before initiation
90
CASPAR Criteria
91
pathophysiology of psoriasis
1. Autoimmune Mechanism * Dysregulated T-cell mediated immune response (Th1, Th17 pathways). * IL-23/IL-17 axis plays a major role. * Overproduction of TNF-α, IL-17, IL-22, and IL-23 drives inflammation. 2. Keratinocyte Hyperproliferation * Abnormal differentiation and proliferation of keratinocytes, leading to thickened epidermis (acanthosis), parakeratosis (retention of nuclei in stratum corneum), and elongated rete ridges. 3. Angiogenesis & Inflammation * Increased vascularization in the dermis due to VEGF activation.
91
Epidemiology of psoriasis
* Prevalence: Affects 2-3% of the global population. * Age of Onset: Bimodal peaks at 15-30 years (early onset) and 50-60 years (late onset). * Gender: Equal prevalence in males and females. * Genetics: Strong genetic component; associated with HLA-Cw6.
92