Dermatology Flashcards
(232 cards)
1
Q
What type of lesions will blanch under pressure?
A
Erythematous
2
Q
What is the size of the following lesions: Macule, Patch, Papule, Plaque, Vesicle, and Bulla?
A
<0.5cm, >0.5cm, <0.5cm, >0.5cm, <0.5cm, and >0.5cm
3
Q
Which of the following lesions are non-palpable and which are palpable?
A
Macule and Patch=non-palpable
Papule and Plaque=palpable
4
Q
What type of primary lesion will not blanch under pressure and why?
A
Purpuric legions: petechia, purpura, and ecchymosis. Won’t blanch due to extravasation of red blood cells (ruptured or leaky blood vessels).
5
Q
What are the sizes of the purpuric lesions and are they palpable or non-palpable?
A
petechia <0.3mm, purpura 3-9mm, and ecchymosis >1cm. They can be either.
6
Q
What is the most common dermatitis in the USA?
A
Eczema (atopic dermatitis)
7
Q
What is the atopic march triad?
A
atopic dermatitis, asthma, and allergic rhinitis.
8
Q
What percentage of children with atopic dermatitis will develop asthma and what percentage will develop allergic rhinitis?
A
50% and 75%
9
Q
What type of skin condition is due to mutation in filaggrin gene leading to defect in skin barrier (“leaky” skin leading to water loss); also, low number of beta defensins leading to infections (S. aureus)?
A
Atopic dermatitis
10
Q
What is lichenification?
A
(thickening of the skin and an increase in skin markings) normally from repeated scratching.
11
Q
What’s the effect on the innate immunity (epidermal barrier) in atopic dermatitis?
A
Water loss and increased penetration.
12
Q
What causes xerosis (water loss) and increased penetration in atopic dermatitis?
A
xerosis=skin barrier is compromised which leads to transepidermal water loss which causes dry skin. It’s worsened by sweating, stress, and prolonged hot showers or bath which further strips the skin of its natural oils.
Increased penetration= defective/compromised skin causes more penetration of allergens and irritants like detergents, dust mites, and hard water which leads to itching (pruritus) and potential skin infection.
13
Q
In what way is adaptive immunity affected in atopic dermatitis?
A
There is an increased number of T helper type 2 (TH-2) cells and elevated levels of Immunoglobulin E (IgE), which are indicative of a skewed adaptive immune response.
This immune dysregulation leads to inflammation in the form of papules and patches and can cause intercellular edema known as spongiosis, which results in the formation of vesicles (small blisters).
IL-13 is a cytokine that is known to contribute to the itch experienced in atopic dermatitis.
14
Q
What cytokine contributes to itchiness in atopic dermatitis?
A
IL-13
15
Q
What are the physical manifestations of atopic dermatitis?
A
Scratching due to intense itchiness causes vesicle to rupture leading to excoriations (scratches or abrasions), oozing of fluid, crusting, and dry scales forming on skin.
16
Q
Which bacteria is associated with changing the skin microbiome in atopic dermatitis?
A
Staphylococcus aureus Colonization due to its release of toxins.
17
Q
How does chronic lesions like plaque arise in atopic dermatitis?
A
arise from resolution of acute flares which causes excess keratin to accumulate and hyperplasia (thickening) of the epidermis and dermis which overtime leads to lichenification which is the thickening of the skin with pronounced lines and margins.
18
Q
How does atopic dermatitis present clinically in infants?
A
widely distributed xerosis (dry/scaly), erythematous patches with exudation and small excoriations (also in face, scalp; cheeks & forehead especially; diaper area is spared).
19
Q
How does atopic dermatitis present clinically in toddlers (ages >/=1)?
A
rash becomes more localized (face/neck/extensor surfaces).
20
Q
How does atopic dermatitis present clinically in children (ages 3-12)?
A
rash in flexor surfaces (wrists, elbows, ankles, and knees). Eczematous and exudative lesions, lichenification (thickening of skin); excoriations and crusting.
21
Q
How does atopic dermatitis present clinically in adults (beyond puberty)?
A
widespread lichenification & xerosis; some have brown macular ring around neck (amyloid deposition); lesions in flexural surfaces (anti-cubital & popliteal fossae).
22
Q
What is contact dermatitis and what causes it?
A
Inflammatory eczematous disease caused by chemicals or metal ions.
23
Q
What skin condition is subdivided into allergic and irritant forms?
A
Contact dermatitis
24
Q
What only produces innate immune response and produce toxic effects without inducing a T-cell response
A
Contact irritants (Examples: direct chemical injury to the skin from hand soap (healthcare providers), hydrofluoric acid exposure (chemical plant) that cause contact dermatitis aka irritant contact dermatitis.
25
What are allergens and what do they do in contact dermatitis?
They are chemicals that modify proteins; haptens (small particles that bind to protiens to create antibody effect) induce innate & adaptive immune responses
26
Which skin condition produces (type IV hypersensitivity; delayed [happens 48-72 hrs after exposure).
Contact dermatitis
27
What are some common causes of allergic contact dermatitis?
Paraphenylenediamine: Found in hair dyes, it can cause reactions on the scalp, face, and ears.
Poison Ivy: Contains urushiol, a potent allergen that can cause severe skin reactions.
Neomycin and Bacitracin: Commonly found in topical antibiotics, they can cause reactions especially in areas of skin breakdown such as stasis dermatitis and leg ulcers.
Topical Neomycin and Corticosteroids: These can cause reactions when used in the ear to treat otitis externa.
Nickel: A metal commonly found in artificial jewelry and coins, and it is the most common cause of allergic contact dermatitis.
28
What is the most common cause of atopic dermatitis?
Nickel
29
What form of contact dermatitis is caused by release of proinflammatory cytokines from keratinocytes in response to chemical stimuli causing skin barrier disruption and further cytokine release?
[irritant contact dermatitis]
30
What are the 2 stages in allergic contact dermatitis?
Sensitization and Elicitation
31
What does the sensitization stage and elicitation stage of allergic contact dermatitis entail?
Sensitization: Dendritic cells in skin take the allergen to the lymph nodes and present it to the helper T-cells there which activates the allergen specific cytotoxic T-cell.
Elicitation: Upon re-exposure to the allergen causes a more vigorous response activating the cytotoxic T-cells which damages tissue causing the symptoms of dermatitis.
32
What is an immediate Type 1 hypersensitivity reaction, IgE mediated, and may progress to anaphylaxis or angioedema (normally swelling around eyes, mouth etc.)?
Contact Urticaria (hives at site of contact with allergen)
33
Which Immunoglobulin is associated with allergies?
IgE antibodies
34
What are the most common symptoms of contact dermatitis?
burning, itching, stinging, soreness, and pain (at the beginning).
35
Which symptom is more common in allergic contact dermatitis?
Pruritus
36
How does acute phase of contact dermatitis present clinically?
erythema, edema, oozing, crusting, tenderness, vesicles or pustules.
37
What phase of contact dermatitis presents clinically as crusts, scales, and hyperpigmentation? acute, subacute, or chronic?
Subacute phase
38
How does chronic phase of contact dermatitis present?
Lichenification
39
Which appears and peaks sooner and improves faster, irritant or allergic contact dermatitis?
Irritant
40
What is a Chronic proliferative and inflammatory skin condition (may have systemic manifestations; eyes, joints, depression)?
Psoriasis
41
What induces Psoriasis lesions?
Trauma (mechanical [friction or pressure], chemical [irritants], and radiations [sunburn)
secondary inducers: psychological stress, alcohol, smoking, obesity, and hypocalcemia
42
What worsens Psoriasis lesions?
chloroquine [used for malaria and autoimmune condition], lithium [used for bipolar], beta-blockers [used for high blood pressure], steroids, and NSAIDs
43
What skin condition improves during summer season but worsens in winter seasons?
Psoriasis
Summer provides Vitamin D and antiinflammatory effects from sunlight
44
What does type 1 and type 2 Psoriasis invove?
Type 1: This type is associated with a positive family history, typically affects individuals younger than 40, and is associated with the HLA-Cw6 gene.
Type 2: This type has no family history, usually affects individuals older than 40, and is not associated with the HLA-Cw6 gene.
45
What influences and exacerbates Psoriasis?
Drugs (NSAIDs, lithium, beta-blockers); inflammatory bowel disease, smoking, alcohol, obesity, diet, changing seasons, humidity, HLA Cw6.
46
What skin conditions involves regulatory T-cell defect leading to inflammation in the dermis due to TH-17 immune response which then causes T-cells, dendritic cells, macrophages to migrate to epidermis via IL-8 which attract immune cells to sites of inflammation?
Psoriasis
47
What causes the silver scales and thickened skin commonly seen in Psoriasis?
Keratinocytes proliferate increasedly causing silver appearance and accumulates in excess causing thickened skin.
48
What is the most common type of Psoriasis?
Plaque Psoriasis (80-90%)
49
What is Plaque Psoriasis?
well defined erythematous plaques with silvery scales over scalp, extensor surfaces (knees, elbows, lumbosacral region). May produce blepharitis, conjunctivitis, and corneal dryness.
50
What can blepharitis lead to?
Blepharitis may lead to cicatricial trichiasis (eyelashes grow wrong direction like inward) and ectropion (lower eye lid droops away from eye and turns outward).
51
What is the auspitz sign and which skin condition is it associated with?
pinpoint bleeding on removal of plaque scales.
Plaque Psoriasis
52
What is the Koebner sign and what skin condition is it associated with?
psoriasis lesions appear at sites of trauma (cuts, sutures, etc.).
53
Which skin condition is common in children after upper respiratory tract infection (Streptococcus). Involves Erythematous & scaly papules (droplet pattern) in trunk and back.
Guttate Psoriasis
54
Which condition is associated with hypocalcemia; sterile pustules (small non-infectious pus-filled lesions (palms and soles; may be in whole body).
Pustular Psoriasis
55
What is Inverse Psoriasis and what areas of the body does it affect?
smooth, erythematous, sharply demarcated patches in intertriginous areas (groins, armpits, intergluteal, inframammary region). Moist and macerated skin; may have fissures (painful, malodorous, pruritic). Affects flexor or intertriginous areas.
56
What results in exacerbation of unstable plaque psoriasis after abrupt withdrawal of systemic steroids. Presents with severe itching, swelling, and pain and widespread inflammation, erythema, and exfoliation of more than 90% of skin?
Erythrodermic Psoriasis
56
What related to Psoriasis is associated with skin and nail psoriasis (pitting, oil spots, subungual hyperkeratosis, and dystrophy). Affects joints of fingers and toes leading to sausage-shaped swelling of fingers and toes (dactylitis). Also affects hips, knees, spine (spondylitis) and sacroiliac joints (sacroiliitis)?
Psoriatic arthritis (30%)
57
What are some complications of Psoriasis?
impaired skin barrier ( due to infection or dehydration), increased cutaneous vasodilation and circulation, or high output heart failure (treated as emergency).
58
What is Parakeratosis?
Retention of nuclei in stratum corneum.
59
What is Acanthosis?
Greatly thickened epidermis with elongations into the dermis.
60
What type of Psoriasis presents clinically with erythematous scaly plaques on the trunk and extensor surfaces of the limbs.
Psoriasis Vulgaris
61
What are 2 types of pustular psoriasis and how do they present?
C: generalized pustular psoriasis.
D: pustular psoriasis localized to the soles of the feet.
This variant typically affects the palms of the hands as well; hence, psoriasis pustulosa palmoplantaris.
62
What type of Psoriasis affects the folds of the skin (axillary, intergluteal, inframammary, and genital involvement)?
Inverse Psoriasis. E and F pic
63
What is a clinical presenting of psoriasis on nails and on reddened skin?
Onycholysis (nail separating from nail bed) and Erythrodermic Psoriasis (red rash, rare)
64
Erythrodermic Psoriasis pic
65
Psoriasis presentation pic
66
What is an uncommon inflammatory condition that manifests with characteristic pruritic (severe and insatiable) lesions on wrists, ankles, and mucous membranes.
Unknown etiology; more common in females and it is associated with hepatitis C (especially when mucous membranes are involved)?
Lichen planus
67
What skin conditions is 5 times more likely to test positive for hepatitis C?
Lichen planus
68
What are the 6 P's of Lichen Planus lesions clinical presentation?
Lesions are pruritic, planar, polygonal, purple, plaques, and papules.
May have vesicles or bullae and produce scarring alopecia.
Nails may be dystrophic.
69
What is the mucosal clinical presentation of Lichen Planus?
white, lacy, reticulated patches in oral mucosa = diagnostic of lichen planus (known as Wickham striae).
70
What is Wickham Striae and what skin condition is it associated with?
fine, white, lacy, reticulated patches/lines in oral mucosa = diagnostic of lichen planus (known as Wickham striae).
71
What skin condition progresses from oral lesions to squamous cell carcinoma in <5% of cases?
Lichen Planus
72
Why is Lichen Planus called a T-cell-mediated autoimmune disease?
T-cells that are normally to protect from pathogens mistakenly target and destroy body's own cells.
73
In Lichen Planus, how does exogenous agent (virus, drug, or contact allergen) affect body's own cells?
alters epidermal self-antigens leading to activation of CD8+ T cells (cytotoxic T-cell). Protein on surface of body's own cells are altered making it look foreign to immune system.
74
In Lichen Planus, why do cytotoxic T-cells attack basal keratinocyte in epidermis?
cross reactivity where immune system can't distinguish between normal and altered self-antigens/cells.
75
What are some agents that can trigger Lichen Planus?
Metals used in dental restoration: Mercury, copper, and gold used in dental fillings and crowns can sometimes provoke an immune response, leading to autoimmune reactions.
Drugs: Certain medications, such as antimalarials, ACE inhibitors (ACEIs), thiazide diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), quinidine, beta-blockers, and tumor necrosis factor (TNF)-alpha inhibitors, have been implicated in triggering autoimmune responses, potentially by altering self-antigens or affecting immune regulation.
76
What are some common treatments for Psoriasis or Lichen Planus?
topical corticosteroids, vitamin D analogs, and retinoids
77
What is a common, acute, mucocutaneous disease with classic target-shaped lesions in a symmetric distribution.
Affects young people (18 - 30 years old)?
Erythema Multiforme
78
What triggers cell destruction in the hypersensitive skin reaction called erythema multiforme?
Fragments of herpes simplex virus remaining in keratinocytes after infection subsides are recognized and targeted by cytotoxic T-cells who believe them to be still infected/abnormal.
79
What are the most common viral/bacterial causes of erythema multiforme?
Herpes simplex (HSV-1>HSV-2), Mycoplasma pneumonia (respiratory infection)
Less common causes: drugs (sulfonamides, β-lactams [antibiotic], phenytoin [anticonvulsant], vaccines).
80
What is the name of a type of Erythema Multiforme (EM) that occurs in patients with Systemic Lupus Erythematosus (SLE)?
Rowell Syndrome
It is characterized by a specific set of symptoms, including EM-like lesions, positive lupus erythematosus tests, and speckled pattern of antinuclear antibodies.
81
What skin disorder is the following a description of?
Skin lesions: raised (papular), target lesions with multiple rings and dusky center (in contrast to annular lesions of urticaria). Lesions are asymptomatic (some may be itchy).
Erythema Multiforme
82
What are the most common site of erythema multiforme?
palms/soles, backs of hands and feet, extensor aspects of forearms and legs.
May involve mucous membranes.
May have systemic signs.
83
What is a Negative Nikolsky sign and which skin disorder exhibits it?
Negative Nikolsky sign (rubbing of skin does not cause sloughing – splitting of epidermis from dermis).
Erythema Multiforme
84
What are the 3 concentric zones of an erythema multiforme lesion from inner to outer ring?
Center is dusky/dark and can be crust/vesicle (blistered), next is surrounding pale pink or erythematous zone, next is peripheral red/dark ring.
85
Which skin disorders are flatter, more tender, and ALWAYS involve mucous membrane with +Nikolsky sign compared to Erythema Multiforme?
Steven's Johnson Syndrome (SJS) or Toxic Epidermal Necrolysis (TEN)
86
What is Steven Johnson syndrome/toxic epidermal necrolysis? and how do you classify them separately?
Spectrum of severe, febrile, blistering diseases of the skin and mucous membranes with skin detachment.
Classification:
SJS: < 10% of body surface area
TEN: > 30% of body surface area (high mortality).
SJS/TEN overlap: 10-30% of body surface area
87
Which skin disorder is mainly triggered by drugs such as penicillin, sulfonamides, phenytoin, carbamazepine, lamotrigine, NSAIDs?
Etiology: penicillin, sulfonamides, phenytoin, carbamazepine, lamotrigine, NSAIDs.
Less common cause: infections (Mycoplasma pneumoniae).
88
How does widespread blistering and skin detachment occur in Steven Johnson syndrome/toxic epidermal necrolysis?
Drugs are metabolized but body fails to clear the metabolites properly so they form a complex with proteins in keratinocytes that the immune system recognizes as foreign. The cytotoxic T-cells then mistakenly attack the body's own keratinocytes leading to widespread blistering and skin detachment.
89
What presents with Very painful skin (vs in EM, very mild), systemic signs (fever, dehydration, hypotension) that starts within 1 to 3 weeks after initiating an offending drug?
Steven Johnson syndrome/toxic epidermal necrolysis?
90
Which skin disorder involves Prodromal period [period between appearance of initial symptoms and full development of rash or fever] with malaise, fever, headache, cough, and keratoconjunctivitis, followed by atypical target lesions that suddenly appear on the face, neck, and upper trunk.
Steven Johnson Syndrome/toxic epidermal necrolysis
91
Which skin disorder involves Lesions coalescing into large flaccid bullae, and sloughing over a period of 1 to 3 days.
Nails and eyebrows may be lost along with epithelium?
Steven Johnson Syndrome/toxic epidermal necrolysis
92
Which skin disorder involves skin lesion with initially dusky red macules or patches (not raised) that progress to tense bullae and eventual skin sloughing (unlike those in EM which are typically papular)?
Steven Johnson Syndrome/toxic epidermal necrolysis
93
What are the mucous membrane normally involved in SJS/TEN?
Mucous membranes always involved (bullae and erosions in oral, genital, [ocular], anal mucosa).
94
What is a positive Nikolsky sign and which skin disorder normally have it?
Nikolsky sign positive (rubbing of skin easily causes sloughing – splitting of epidermis from dermis).
SJS/TEN
95
What are some complication that may present with SJS/TEN?
Respiratory distress syndrome, gastrointestinal symptoms [diarrhea, nausea, malabsorption, colonic perforation, and melena], and renal complications [proteinuria, hematuria, and microalbuminuria].
96
What skin disorder happens in 30% of Erythema Multiforme cases and has no recurrence?
SJS
97
Which skin disorder have a 50% mortality rate?
Toxic Epidermal Necrolysis (TEN)
98
What is an Autoimmune blistering disorder characterized by bullae (> 1 cm large, fluid-containing blister) and severe pruritus that affects mostly people older than 70-year-old?
Bullous Pemphigoid
99
Which skin disorder is Associated with loop diuretics, metformin, neuroleptics, and neurologic conditions (multiple sclerosis, dementia, Parkinson disease)?
Bullous Pemphigoid
100
In Bullous Pemphigoid, what does the inflammatory reaction involve?
Auto-antibodies attach to hemidesmosomes which are at the epidermal-dermal junction, this activates compliment immune system which triggers inflammatory reaction which causes skin to separate and blisters to form.
101
Why is Nikolsky sign negative in Bullous Pemphigoid?
bullae are tense so they do not break easily; Nikolsky sign negative.
102
What skin disorder presents with Numerous tense bullae with severe pruritus and may have a history of eczematous or urticarial lesions before the formation of the bullae?
Bullous pemphigoid
103
What skin disorder presents with the following on Physical Exam: tense bullae (may have vesicles too) with a clear exudate (may be hemorrhagic); bullae symmetrically distributed on trunk and extremities. The mucous membranes are spared. Negative Nikolsky sign (no separation of skin layers or blister formation or extension with blunt pressure or lateral traction (dragging finger on skin)?
Bullous Pemphigoid
104
Which skin disorder is distinguished by mucous membrane sparing and Negative Nikolsky sign?
Bullous pemphigoid
105
Which autoantibody target the hemidesmosome proteins at the basement membrane zone in a linear fashion where the epidermis meets the dermis?
IgG
106
Which skin disorder is a Severe and potentially fatal autoimmune blistering disease characterized by painful mucocutaneous lesions that most commonly presents in people from Mediterranean or Jewish descent from 40-60 years of age?
Pemphigus Vulgaris
107
Which skin disorder is Associated with drugs (like penicillamine, benzylpenicillin, captopril, cephalosporin), thymoma, myasthenia gravis, systemic lupus erythematosus?
Pemphigoid Vulgaris
108
What is the underlying cause of Pemphigoid Vulgaris regarding hypersensitivity class and autoantibodies?
It's a type II hypersensitivity reaction where immune system produces autoantibody IgG against desmogleins which are proteins of the desmosome which connects the keratinocytes in epidermis. This causes epidermis to slough off= +Nikolsky sign.
109
Which skin condition has a 75% mortality rate if untreated and a +Nikolsky sign?
Pemphigoid Vulgaris
110
Which skin disorder has Extremely painful progressive blistering involving whole body (including mouth). May have nonhealing and nonscarring ulcers persisting for at least 1 month?
Pemphigoid Vulgaris
111
How would you describe Pemphigoid Vulgaris Bullae on physical exam?
Physical exam: flaccid bullae that are easily ruptured with clear exudate.
112
For Pemphigoid vulgaris, where are the ruptured bullae normally located?
Many superficial erosions of skin (ruptured bullae) often on scalp, face, and trunk, and mucosal ulcers (mouth).
113
What is Leukocytoclastic vasculitis (aka Cutaneous Small Vessel Vasculitis)
a single-organ (skin), skin-isolated leukocytoclastic vasculitis (LCV) (inflammation limited to only the skin and no other organs) or angiitis without systemic vasculitis or glomerulonephritis.
114
How is the inflammation triggered in Leukocytoclastic vasculitis (LCV)?
It's triggered/mediated by immune complexes which are formed when antigens like drugs, infections or endogenous proteins bind to antibodies. The complexes deposit into the walls of small blood vessels like dermal capillaries and venules leading to inflammation and damage.
115
How long does it take Leukocytoclastic vasculitis (LCV) to resolve?
Most cases are self-limited (90% resolve within weeks to months of onset).
However, about 10% may have a chronic course of the disease, lasting for 2 to 4 years. Mortality rate is 2% (related to systemic involvement).
116
Though Leukocytoclastic vasculitis (LCV) involve only the skin, 30% of cases may have symptoms outside of the skin, what are some of these symptoms?
they can include joint pain, abdominal pain, or kidney involvement.
117
What does Leukocytoclasis in histology refer to?
destruction of neutrophils which can be seen under a microscope in a biopsy.
118
Leukocytoclastic vasculitis (LCV) typically happens in adults but a similar condition happens in children and is slightly more common in males, what is this called?
Henoch-Schönlein purpura (aka IgA Vasculitis)
119
What is the primary cause of Leukocytoclastic vasculitis (LCV)?
In 50% of cases, the cause of the condition is unknown or not attributable to an external factor (aka IDIOPATHIC). This is commonly seen in medical conditions where despite extensive evaluation, the precise cause cannot be determined.
120
What are some secondary triggers or causes of Leukocytoclastic vasculitis?
Post-Infectious: Certain infections can trigger the condition. These include infections by Streptococcus (often linked to upper respiratory tract infections), Mycobacterium species, Staphylococcus aureus, Chlamydia, Neisseria, and viruses like HIV, chronic hepatitis B and C, and syphilis.
Drugs: Various medications can induce the condition, typically 1 to 3 weeks after initiation of the drug. These include beta-lactam antibiotics, erythromycin, clindamycin, vancomycin, sulfonamides, the diuretic furosemide, the gout medication allopurinol, various NSAIDs, the antiarrhythmic agent amiodarone, gold salts used in rheumatoid arthritis, thiazide diuretics, the anticonvulsant phenytoin, beta-blockers, TNF-alpha inhibitors used in inflammatory diseases, selective serotonin reuptake inhibitors (antidepressants), the diabetes drug metformin, the anticoagulant warfarin, and the anticonvulsant and mood-stabilizing drug valproic acid.
Neoplasia: Certain types of cancer such as lymphomas, leukemias, intestinal adenocarcinomas, and lung cancer can be associated with the condition, likely due to complex immune interactions and paraneoplastic phenomena.
Systemic Diseases: A range of systemic diseases can be associated with this condition, including systemic lupus erythematosus (SLE), Sjogren's syndrome [autoimmune, immune system attacks the glands that make moisture in the eyes, mouth, and other parts of the body like salivary and tear glands], various inflammatory bowel diseases, Behcet's disease [inflammation of blood vessels and tissues], rheumatoid arthritis, cryoglobulinemic vasculitis, and Henoch-Schönlein purpura (HSP), which is a form of vasculitis that often affects children.
121
Why is leukocytoclastic vasculitis (LCV) called a type III hypersensitivity reaction?
Because it involves deposition of immune complexes (antigen-antibody complexes) within the walls of small blood vessels. These complexes activate the complement system which is used to clear pathogens and damaged cells.
122
In leukocytoclastic vasculitis (LCV) what does activation of the complement system cause?
It leads to a series of inflammatory responses which involeves recruitment of neutrophils to site of immune complexes.
123
In Leukocytoclastic Vasculitis LCV, how does Neutrophil recruitment lead to the exudation (leakage) of erythrocytes (red blood cells), fibrin (a protein involved in blood clotting), and serum into the surrounding tissue?
Once neutrophils reach site of immune complexes they release enzymes and reactive oxygen species which damage the vessel walls
124
What is fibrinoid necrosis and how is it caused?
A type of damage. Neutrophil enzymes like collagenases and elastases along with reactive oxygen species cause the destruction of small vessel walls causing fibrinoid necrosis.
125
In Leukocytoclastic vasculitis (LCV), what cytokines are circulating during the inflammatory process causing further inflammation and tissue damage?
IL-1, IL-6, IL-8, and TNF (a multifunctioning cytokine)
126
What body part does vasculitis typically affect?
Legs due to factors such as turbulence in blood flow and increased venous pressure in the lower extremities.
127
How is superficial dermal involvement seen in biopsy of affected skin?
Deposits of IgG, IgM, IgA, and complement component C3 along the vessel walls.
128
What is Henoch-Schönlein Purpura and how is it distinguished in biopsy compared to Leukocytoclastic vasculitis (LCV)?
A small vessel vasculitis that often affects children and can lead to a rash, joint pain, and gastrointestinal symptoms.
A strong deposition of immunoglobulin A (IgA) without significant deposition of other antibodies is characteristic of Henoch-Schönlein purpura
129
What skin condition involves Skin lesions that typically appear within 1 to 3 weeks after a triggering event, which might be an infection, medication, or another immune stimulus?
Leukocytoclastic vasculitis (LCV)
130
How do you describe the appearance of Leukoctoclastic vasculitis legions including size and distribution etc?
The lesions vary in size from 1 mm to 1 cm and manifest as erythematous (red) macules (flat lesions) with palpable purpura. Palpable purpura refers to small, raised, purple spots or patches on the skin caused by bleeding under the skin. These lesions are bilaterally symmetrical and commonly located on the lower extremities and buttocks.
They can appear all at once or in crops (clusters), with different clusters at various stages of development.
131
What type of sensation does Leukocytoclastic vasculitis (LCV) lesions cause?
While the lesions are generally asymptomatic, they may cause sensations of itching, burning, or stinging.
132
What are the different lesion types of Leukocytoclastic vasculitis (LCV)?
The skin condition can present with a range of lesion types, including hemorrhagic vesicles (small blisters with bleeding), bullae (larger fluid-filled blisters), pustules, nodules, crusted ulcers, or livedo reticularis (a mottled purplish discoloration of the skin).
133
What are some systemic symptoms of Leukocytoclastic vasculitits (LCV)?
Systemic symptoms are uncommon but can include low-grade fevers, general feelings of discomfort or unease (malaise), weight loss, muscle pains (myalgias), and joint pains (arthralgias). Arthralgia occurs in about 30% of cases.
If systemic symptoms are present, which can indicate a more serious or widespread disease, further investigation into the differential diagnosis is necessary to guide management.
134
What skin disorder is a common, chronic, inflammatory skin disease associated with Malassezia furfur (a yeast fungus formerly called Pityrosporum ovale); Involves scalp and eyebrows; aka, dandruff (adults), cradle cap (infants)?
Seborrheic dermatitis
135
Which type of disease is Seborrheic dermatitis more severe in?
neurologic disease (traumatic brain injury, Parkinson’s disease, stroke) & HIV patients.
136
How does Seborrheic dermatitis present clinically on on physical exam?
Clinical features: “dandruff” in hair and face, burning, itchy, & scaling.
Physical exam: scaly, greasy, flaky (dandruff) skin on scalp margins and face (can be erythematous).
137
What are the most common areas of body affected by seborrheic dermatitis?
Scalp, eyebrows, face, and hair.
138
What causes Malassezia colonies to overgrow on the skin, irritate it, and cause scaliness?
The yeast Malassezia thrives in oily environment and the skin releases sebum which is a form of oil/lipid to prevent the skin from losing too much water and drying out. Malassezia secretes lipase to break down the lipids into free fatty acids (FFA) and lipid peroxidase. These 2 byproducts triggers the immune system to produce inflammatory cytokines and TNF-alpha which triggers inflammation which stimulates keratinocytes to proliferate and differentiate disrupting the normal maturation of skin cells and disrupting skin barrier which is what causes the itchiness (pruritus), redness (erythema), and scaliness.
139
What are the 2 byproducts Malassezia produces that triggers inflammation in Seborrheic dermatitis?
Lipase peroxidase and free fatty acids
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True of false Malassezia is a part of the normal skin flora?
True
141
What is a common chronic or recurrent cutaneous disorder that manifests with inflammatory and non-inflammatory lesions and can lead to disfigurement or psychologic distress?
Acne vulgaris
142
What are the typical types of lesions for acne vulgaris and where are they normally located?
papules (small, raised, solid bumps), pustules (pus-filled lesions), and nodules (larger, solid lesions). These can occur on the face, neck, trunk (chest and back), and proximal upper extremities.
143
How is acne vulgaris developed in the skin?
1. Follicular hyperproliferation happens where cells in the hair follicles are overproduced.
2. abnormal desquamation where cell lining the follicles abnormally sheds, clogging the pores.
3. Increased sebum production where sebaceous gland produce excess oil which causes acne lesions to develop.
4. Bacterial proliferation where bacterium cutibacterium acne (aka propionibacterium acnes) proliferates in the oily sebaceous gland leading to inflammation.
5. Inflammation triggered by immune system as a result of the above factors causing redness, swelling, and pain associated with acne due to recruitment of immune cells like neutrophils and macrophages which rupture comedo.
144
What bacteria is associated with acne vulgaris?
cutibacterium acne (aka propionibacterium acnes)
145
What is the age of onset of acne vulgaris and why?
Acne can present at any age but is typically more common and more severe during puberty (teenagers) due to hormonal changes that stimulate sebum production.
146
What is Post inflammatory hyperpigmentation?
A potential complication of acne vulgaris. After the inflammatory lesions of acne have healed, they can leave behind darkened areas on the skin, known as post-inflammatory hyperpigmentation. This is more common in individuals with darker skin tones.
147
True or false: Acne can significantly affect a person's self-esteem and can be associated with depression and anxiety, especially if the acne is severe or persistent?
True
148
What are some risk factors and triggers for acne vulgaris?
Risk factors: menstrual cycle, emotional stress, occlusion of skin with greasy products, excessive sweating, pregnancy, milk consumption.
Etiology: multifactorial, androgen production, medications (steroids).
Menstrual Cycle: Hormonal fluctuations related to the menstrual cycle can lead to acne flares.
Emotional Stress: Stress can exacerbate acne through various mechanisms, including hormone level changes and inflammatory pathways.
Occlusion: Using greasy or comedogenic products can clog pores and worsen acne.
Excessive Sweating: Sweat, especially when combined with friction from clothing, can irritate the skin and contribute to acne.
Pregnancy: Hormonal changes during pregnancy can lead to the development of acne.
Milk Consumption: Some studies suggest that dairy, particularly skim milk, may be associated with acne, possibly due to hormones present in milk.
Etiology: Acne's causes are multifactorial and can include:
Androgen Production: Increased androgen levels stimulate the sebaceous glands to produce more sebum, which can lead to clogged pores and acne lesions.
Medications: Certain medications, especially steroids, can induce or aggravate acne by affecting hormone levels or immune responses.
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What is an inflammatory disorder of the pilosebaceous unit (hair follicle and sebaceous gland) due to interaction of multiple factors that result in the formation of comedones and the development of inflammation?
Acne Vulgaris
150
What are closed and open comedones?
closed comedone (follicle opening is blocked to skin surface/whitehead), open comedones (follicle opening open to skin surface causing sebum to oxidize and turn black/brown due to melanin/blackhead)
151
What are the main factors involved in acne vulgaris?
Androgen-mediated stimulation of sebaceous glands
Androgens like testosterone increase the size and activity of sebaceous glands leading to excess sebaceous production which will clog hair follicles.
Dysbiosis within the microbiome of the pilosebaceous follicle
Dysbiosis refers to an imbalance in the microbial community on the skin. For acne sufferers, this often means an overgrowth of certain bacteria, such as Cutibacterium acnes (formerly Propionibacterium acnes), which can trigger inflammation and contribute to acne development.
Innate and cellular immune responses
Innate immune system is first line of defense against microbial invaders, with acne the immune system overreacts to bacteria and sebum in follicle leading to inflammation and acne lesions.
May be influenced by factors such as genetics
Most likely to have acne if close relatives suffered from it. Genetics can influence factors such as sebum production rates, skin cell turnover, and immune responses.
and, possibly, diet.
High glycemic index food and dairy exacerbates it.
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Does the following describe mild, moderate, or severe acne?
Scattered, small (<5 mm), comedonal or inflamed papules or pustules without associated scarring.
Limited skin involvement (one body area or relatively few lesions in more than one body area).
Absence of nodules (no deeper skin involvement).
Absence of near confluent skin involvement (lesions are not densely packed together).
mild
153
Does the following describe mild, moderate, or severe acne?
Visually prominent acne consisting of many comedonal or inflamed papules or pustules
Presence of nodules (deeper skin involvement)
Involvement of multiple body areas with more than a few, scattered lesions
Associated scarring (includes atrophic scares [depressions in skin] and hypertrophic scars [raised scarring].
moderate to severe
154
Example of severe acne
Acne conglobata
155
What skin disorder is a Reactive skin condition characterized by facial flushing and a spectrum of clinical signs like erythema, telangiectasia, coarseness of skin (eg. rhinophyma), and an inflammatory papulopustular eruption resembling acne?
Acne Rosacea
156
What environmental factors trigger acne rosacea and is genetics involved in rosacea?
Sun, heat, and alcohol consumption.
Rosacea is an interplay between genetics and environmental factors
157
How do environmental factors trigger symptoms of acne rosacea?
These factors may lead to the dysregulation of the vascular system, causing increased blood flow and inflammation (due to abnormal reaction of immune system). This increased blood flow leads to characteristic redness.
158
What is rhinophyma?
Nose is coarse, red, bumpy, bulbous as a result of untreated or severe rosacea. Predominantly in males.
159
Which skin condition exhibits the following:
Typically, in women of middle age.
Redness in central face (cheeks, nose, and sometimes forehead and chin) with small erythematous papules surmounted by pinpoint pustules (pus filled).
History of flushing (heat, red wine, stress).
Telangiectasias (can be difficult to distinguish from erythematous background)?
Papulo-pustular rosacea (classic)
160
Ocular rosacea example
161
What skin condition is a form of panniculitis (inflammation of the subcutaneous fat) with features of a delayed-type hypersensitivity reaction.
Occurs in women in the second to fourth decade of life but may occur at any age and in males?
Erythema Nodosum
162
What are some triggers of erythema nodosum?
Triggers: infection, drug exposures, sarcoidosis, inflammatory bowel disease, pregnancy, and malignancy.
Many cases are idiopathic.
May follow a prodrome of fever, malaise, and symptoms of upper respiratory infection.
163
Which skin disorder has legions that present as erythematous, tender nodules on the shins. Less often on the thighs, arms, calves, buttocks, or face. Lesions are symmetric and with poorly defined margins.
Erythema Nodosum
164
What concurrent symptoms does erythema nodosum present with?
Patients may have concurrent fever and arthralgias.
165
How long does it take erythema nodosum to resolve?
Usually resolves spontaneously within a few weeks.
166
What type of hypersensitivity is erythema nodosum?
Type IV hypersensitivity with deposition of immune complexes in venules of subcutaneous adipose tissue causing inflammation.
Unlike Type I, II, and III reactions, which involve antibodies, Type IV hypersensitivity is mediated by T cells.
167
What causes Erythema Nodosum?
Infections: Such as coccidioidomycosis (also known as "desert bumps" due to the nodules that form under the skin), histoplasmosis, tuberculosis, infections caused by streptococcal bacteria, and leprosy. These infections can cause the body to form immune complexes as part of the immune response to the pathogens.
Inflammatory Bowel Disease: Conditions like Crohn's disease and ulcerative colitis can be associated with panniculitis as an extraintestinal manifestation.
Sarcoidosis: A multi-system inflammatory disease that can also cause granulomatous panniculitis, which is a type of panniculitis characterized by granuloma formation in the subcutaneous tissue.
168
What skin disorder can be caused by coccidioidomycosis (also known as "desert bumps"? and what are desert bumps?
Erythema Nodosum.
Nodules that form under the skin
169
what disease is an Idiopathic condition characterized by granulomatous inflammation of multiple organs (lungs most involved organ). Non-caseous granulomas (no necrotic tissue in center with macrophages)
Commonly causes restrictive lung disease (may cause obstructive or mixed pattern).
Sarcoidosis
170
How is the inflammation process initiated in Sarcoidosis?
CD4 T-helper cell secretes IFN-gamma a cytokine that promotes inflammation and activates other immune cells.
171
What's the most common organ affected in sarcoidosis?
Lungs.
secondarily: While the lungs are the most commonly affected organs, sarcoidosis can also involve the liver, spleen, bones, heart, and other organs.
172
What inflammatory disease is often presents in Black women during their 3rd or 4th decade of life.
Sarcoidosis
173
What other disorder is sarcoidosis associated with?
May be associated with diabetes insipidus due to granulomatous infiltration of the pituitary. A condition characterized by excessive thirst and large volumes of urine.
174
Which condition Presents with Bilateral hilar lymphadenopathy, elevated ACE (not always), and hypercalcemia (hypervitaminosis D due to increased activity of alpha 1 hydroxylase which converts vitamin D into its active form).
Sarcoidosis
175
Why doesn't sarcoidosis respond to skin test PPD?
Individuals with sarcoidosis may not react to skin tests such as the tuberculin skin test (PPD test) because the immune response is concentrated in the granulomas and is less active in the peripheral circulation.
176
What will the biopsy of affected tissue in sarcoidosis show?
A biopsy of affected tissue will show the characteristic non-caseating granulomas with multinucleated giant cells, which are large cells with several nuclei that form from the fusion of macrophages in an attempt to contain the perceived foreign body.
177
How does sarcoidosis present? Hint. remember mnemonic
May be asymptomatic (50% of cases were incidental chest radiograph findings), or have cough, fever, malaise, arthritis (ankle and legs).
Mnemonic: can be GRUELING
Granulomas
Rheumatoid arthritis
Uveitis
Erythema nodosum
Lymphadenopathy
Interstitial fibrosis
Negative TB
Gammaglobulinemia (polyclonal [not specific to one type of antibody)
178
How does cutaneous sarcoidosis present?
Cutaneous lesions may present with a variety of morphologies, including papules, nodules, plaques, and infiltrated scars.
179
What is Lupus pernio?
A manifestation of sarcoidosis that presents with violaceous or erythematous papules, plaques, or nodules predominantly involving the central facial skin (nose and cheeks).
180
What manifestation of sarcoidosis is associated with more chronic and severe form and often correlates with involvement of the upper respiratory tract and lungs?
Lupus Pernio
181
What is known as "scar sarcoidosis" or "tattoo sarcoidosis" and is the first sign of sarcoidosis for some ?
sarcoidosis appearing in areas of the skin that have been injured or where tattoos are present. The granulomatous reaction may occur many years after the skin has been damaged or the tattoo ink has been injected.
182
What might it be if patients has persistent or unusual inflammatory lesions that change over time or do not heal as expected?
Sarcoidosis
183
What is the most common nonspecific manifestations of sarcoidosis and is normally found on lower legs?
erythema nodosum
184
What type of sarcoidosis present with Well demarcated, erythematous plaques on the cheek with numerous telangiectasias?
Angiolupoid sarcoidosis
184
What type of sarcoidosis present with Multiple indurated nodules are present on the forearm?
Subcutaneous sarcoidosis
185
What type of sarcoidosis presents with Multiple round papules are present on the eyelids and central face?
Papular sarcoidosis
186
what type of sarcoidosis presents with large, confluent, geometric erythematous plaques covering most of the body?
Erythrodermic sarcoidosis
187
what type of sarcoidosis presents Firm papules that are present within the tattooed areas?
tattoo/scar sarcoidosis
188
what type of sarcoidosis present with discrete hyperkeratotic, thick, hyperpigmented plaques. These types of lesions may be misdiagnosed as lichenified psoriasis, prurigo nodularis, or hypertrophic lichen planus?
Verrucous sarcoidosis
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oral sarcoidosis example
Oral sarcoidosis. Diffused granulomatous infiltration of lips, with gross enlargement of the upper lip is present. Honeycomb, postinflammatory pigmentary changes are present on the superior portion of the upper lip.
190
Sarcoidal dactylitis example
Sarcoidal dactylitis. Swelling and deformity of all fingers are present. Some fingers demonstrate erythema and swelling of the nail folds and beds. Marked onychodystrophy is present.
191
what skin conditions is a common benign skin growths that appear in older adults. They look like waxy, tan-brown "stuck on" lesions and can be found on various parts of the body?
Seborrheic keratosis
Although benign, a rapid onset of many seborrheic keratoses, known as the sign of Leser-Trélat, may be a marker of an internal malignancy.
192
What is Leser-Trélat sign?
Sudden appearance of multiple seborrheic keratoses is associated with underlying malignancy
193
What is Melanocytic nevi (mole)?
Benign neoplasm composed of melanocytes; can occur anywhere on the body and can mimic melanoma.
194
What is acrochordon (skin tags)?
These are small, benign, skin-colored growths (pedunculated papules) that typically appear on the neck, in the armpits, and other areas where skin rubs together or in skin folds. They are more common in people who are overweight or have diabetes, which is associated with insulin resistance.
195
What is cherry angioma?
This is a common, benign vascular lesion. It appears as small, bright red to purple (violaceous) spots on the skin and is caused by an overgrowth of capillaries. Cherry angiomas are often found on the torso and increase in number with age.
196
What is Dermatofibroma?
This is a benign fibrous nodule that typically occurs on the lower extremities, more often in women. They are firm and may appear tan to brown. When pinched, they can create a dimple, a characteristic known as the "dimple sign".
197
what is the name of a fibrous nodule that's more common in women and dimples when pinched?
Dermatofibroma
198
what is the most common skin cancer?
basal cell carcinoma (BCC)
199
what skin cancer is primarily caused by chronic exposure to ultraviolet (UV) light. It is characterized by its appearance as a pearly nodule, often with visible blood vessels ( arborizing telangiectasias) on the surface, and it can ulcerate or look like an open sore?
Basal cell carcinoma
While BCCs rarely spread to other parts of the body (metastasize), they can lead to significant destruction of the surrounding tissue if not treated.
200
which skin cancer is a precancerous lesion that occurs due to long-term/lifetime sun exposure. It usually appears as transparent or yellow rough, scaly/crusty/horny, or "sandpaper-like" patches on the skin, often pink in color?
Actinic keratosis
201
Why is actinic keratosis considered precancerous?
These lesions are considered precancerous because a small percentage can eventually develop into squamous cell carcinoma (SCC) if left untreated. (<5% progress to squamous cell carcinoma)
202
Which skin cancer can actinic keratosis progress to?
Squamous cell carcinoma
203
What is the second most common type of skin cancer and is mainly caused by UV light exposure?
Squamous cell carcinoma
204
which skin cancer presents as scaly, pink papules, plaques, or nodules that can become ulcerated and bleed. They may form over an area of chronic skin inflammation or injury, which is known as a Marjolin's ulcer?
Squamous cell carcinoma
205
What is marjolin ulcer and which skin cancer does it present in?
a cutaneous malignancy that arises in the setting of previously injured skin, longstanding scars, and chronic wounds.
SCC
206
What are some risk factors for squamous cell carcinoma besides the sun?
Additional risk factors include exposure to certain chemicals (coal, soot, arsenic), infection with certain types of Human Papillomavirus (HPV), and immunosuppression, such as that which occurs in organ transplant recipients.
207
Which skin cancer commonly happens in fair skinned elderly patients on sun exposed areas like face, head, neck, dorsal hands, forearm, BALD SCALP, shoulders, and ears and is normally asymptomatic?
actinic keratosis
lifetime sun exposure leading to keratinocyte damage
208
which skin cancer grows the slowest?
Basal cell carcinoma
209
which skin cancer is the Most common type of facial BCC; Shiny or pearly nodule with a smooth surface; May have central depression or ulceration, so its edges appear rolled; Blood vessels cross its surface?
Nodular BCC
210
Which skin cancer is most common in young people?
Superficial BCC
211
Which skin cancer is Most common type in younger adults; Most common type on upper trunk and shoulders; Slightly scaly, irregular plaque; Thin, translucent rolled border; Multiple micro erosions?
Superficial BCC
212
which skin cancer Present as enlarging scaly or crusted lumps.; usually within pre-existing actinic keratosis or intraepidermal carcinoma.
Grow over weeks to months; may ulcerate; often tender or painful.
Located on sun-exposed sites, particularly the face, lips, ears, hands, forearms and lower legs.
Size varies from a few millimeters to several centimeters in diameter?
Squamous cell carcinoma
Intraepidermal carcinoma ((also known as Bowen's disease, a form of SCC that is confined to the outer layer of the skin).
Bowen's disease is also called squamous cell carcinoma in situ and is early stage of skin cancer that's very treatable.
213
Which skin cancer is associated with human papillomavirus?
Squamous cell carcinoma
especially those in the genital area or on the mucous membranes
214
which skin cancer is the Most deadly skin cancer; very aggressive; high risk of metastasis; lifetime risk is 1 in 50 individuals?
Malignant Melanoma
215
how does melanoma present clinically? Hint remember mnemonic.
ABCDE:
Asymmetry: One half of the mole doesn't match the other.
Border: Edges are irregular, ragged, notched, or blurred.
Color: Includes different shades of black, brown, or tan, and may also include areas of white, gray, red, pink, or blue.
Diameter: The spot is larger than 6 mm across (about ¼ inch – the size of a pencil eraser), although melanomas can sometimes be smaller than this.
Evolution: The mole is changing in size, shape, or color.
216
which skin cancer is the most common subtype, accounting for about 70% of cases. It usually presents as a flat or slightly raised lesion with a varied pigmentation and irregular borders?
superficial spreading Melanoma
217
which subtype of melanoma is normally located on the back in men but on the posterior legs in women?
superficial spreading melanoma
218
which subtype of melanoma Comprises 15–30% of cases, often presenting as a darkly pigmented, raised lesion that can resemble a berry?
nodular melanoma
219
which subtype of melanoma accounts for 10–15% of cases, characterized by flat and atypical pigmented areas, typically on chronically sun-damaged skin of older adults?
Lentigo maligna melanoma
220
which subtype of melanoma is The most common subtype in individuals with dark skin, this type appears as dark brown areas on the palms, soles, or under the nails?
Acral lentiginous
221
which subtype of melanoma is A type of melanoma that affects parts of the eye such as the iris, ciliary body, or choroid?
Uveal melanoma
222
which subtype of melanoma is A rare form that occurs on mucosal surfaces like the gastrointestinal tract, genitourinary tract, or respiratory tracts?
Mucosal Melanoma
223
Ungual melanoma example
224
Amelanotic melanoma example
225
What is Type I hypersensitivity and can you provide an example?
Type I hypersensitivity is an immediate allergic reaction mediated by IgE antibodies. It occurs within minutes to an hour after exposure to an antigen. An example of this reaction is anaphylaxis, which is a severe, potentially life-threatening allergic reaction.
226
How does Type II hypersensitivity differ from Type I?
Type II hypersensitivity is a cytotoxic reaction mediated by IgG or IgM antibodies that lead to the destruction of cells. It has a slower onset, ranging from hours to days, and examples include conditions like hemolytic anemia, where the immune system attacks red blood cells.
227
What is the main mechanism behind Type III hypersensitivity?
Type III hypersensitivity is caused by immune complex-mediated reactions. It involves the formation of antibody-antigen complexes that can deposit in various tissues, leading to complement activation and an inflammatory response. This type takes 1-3 weeks to develop and includes diseases such as serum sickness and systemic lupus erythematosus (SLE).
228
Can you explain what Type IV hypersensitivity is and give an example?
Type IV hypersensitivity, also known as delayed-type hypersensitivity, is mediated by T cells rather than antibodies. The reaction typically occurs days to weeks after antigen exposure. An example of this type of hypersensitivity is contact dermatitis from poison ivy, where the skin reacts to an irritant with inflammation.
229
Why is Type I hypersensitivity reaction considered immediate?
Type I hypersensitivity is considered immediate because it involves IgE antibodies that trigger mast cells to release histamine and other inflammatory mediators quickly upon exposure to an allergen, leading to rapid onset of symptoms.
230
In which type of hypersensitivity reaction is the skin test typically negative, and why?
The skin test is typically negative in Type IV hypersensitivity reactions because this type involves T-cell mediated immune responses, which take longer to develop. In conditions like sarcoidosis, there is reduced peripheral T-cell activity, making skin tests like the tuberculin skin test (PPD) unresponsive.
