Derm Flashcards
1
Q
Vesicles vs. Bullae
A
Vesicles: less than 5 mm, easily traumatized and unroofed, leave shallow ulcerations.
Bullae: also fluid filled, but larger than 0.5 cm.
2
Q
Macules
A
- Macules are not raised, flat, less than 0.5cm, distinguished by a difference in color.
- if larger than 0.5cm = patch.
3
Q
Papules vs. nodules
A
- Papule- elevated, less than 0.5cm
- if larger, nodule.
- either may be dome-shaped or flat-topped.
4
Q
Pustules
A
raised, filled with leukocytes (yellow color)
5
Q
3 layers of skin
A
Epidermis-keratinized stratified sq epithelium
Dermis-connective tissue
Hypodermis-subQ tissue, fat (not part of skin!)
6
Q
5 layers of epidermis
A
o stratem basiles (mitotic) o stratem venosum o stratem granulosum o stratem leucederm (clear) o stratem corneum (corn, keratin layer, not present everywhere, found in palm and soles of feet, in thick skin).
7
Q
flat discolored lesion, could be either ___ or ___ based on size.
A
Wheal (hive) – transient (1cm????
8
Q
A fluid filled lesion may be 3 things:
A
Vesicles – fluid-filled lesion, elevated, 1 cm
Pustule – puss-filled lesion, variable size
9
Q
An elevated lesion may be one of 3 things:
A
Papule – elevated (palpable) lesion, 1cm
Nodule – elevated, deep lesion with spherical edge, >1cm (ex if the lesion is in lymph node, not skin)
10
Q
features of Eczemateous Dermatitis lesions (4)
A
Eczema = boil over, Broad class of skin conditions
- Papulovesicular lesions that are oozing/wet/weeping and red.
- Scaling (hyperkeratotis) – extra keratin
- Epidermal hyperplasia (acanthosis) – which makes extra keratin
- Can become superinfected
11
Q
3 key features of Urticaria.
Caused by ___.
Treatment.
A
- IgE-mediated degranulation of mast cells after antigen exposure. Maybe non IgE mediated. Release of vasoactive mediators (Histamine) cause vasodialation and edema.
- Hives/wheals that disappear within 24 hrs, may reappear + Superficial dermal edema + itchiness
- HISTO: appears like gaps in dermis
- histamine causes symptoms, so treatment is antihistamines
12
Q
3 types of eczematous dermatitis
A
1) Contact dermatitis
2) atopic dermatitis
3) primary irritant dermatitis.
13
Q
2 types of contact dermatitis
A
- Allergen induces - immune mediated, delayed type hypersensitivity (poison Ivy, nickel, perfume, latex)
- Irritant induced - nonimmune mediated, direct damage to skin by irritant. More common (acids, bleach, water, cement, diaper rash, etc)
14
Q
Atopic dermatitis
A
- Chronic dermatosis.* Part of allergen triad (asthma, atopic dermatitis, seasonal allergy)
- erythematous plaques in flexure areas
- Spongiosis – fluid bw cells of epidermis = weeping lesions, vesicles. Scales.
- Genetics + immune system + dysfunctional epidermal permeability barrier (skin cant hold onto hydration). family history of eczema, hay fever or asthma.
15
Q
Contact dermatitis
A
- a class of eczematous dermatitis
- itching/burning or both
- requires sensitization on prior exposure (langerhan cells, immune cells of skin, present antigen to T cells
16
Q
All kinds of eczematous dermatitis share one histological feature:_____
A
Spongiotic dermatitis
17
Q
Functions of skin:
A
- protection: secrete chemicals to kill bacteria, uv protection, waterproof barrier, immune cells of skin (Langerhan cells)
- body temp regulation
- sensation – somatic sensory receptors (pressure, pain, temp), hair movement sensed by hair follicle receptors.
- VitaD activation, some waste elimination
18
Q
Layers of the skin:
A
Epidermis – No blood supply
Dermis – inner connective tissue. Sweat glands, hair follicles, blood vessels, touch receptors.
Hypodermis – (NOT part of the skin)—subcutaneous tissue and fat
19
Q
Dermis
A
- inner connective tissue; contains sweat glands, hair follicles, blood vessels, touch receptors.
- Dermal papillary ridges give you traction, junction between epi/dermis.
20
Q
Epidermis
A
- Keratinized stratified squamous epithelium—extra layer of keratin protein on top.
- Protection from abrasion.
- Waterproof.
- Contains melanocytes in basale layer. Basale layer mitotic
- No blood supply, nutrients by diffusion.
21
Q
Dermis has 2 layers:
A
- Papillary layer – areolar connective tissue, loose connective tissue for cushioning purposes.
- Reticular layer – deeper layer, bulk of it. Made up of dense irregular connective tissue
22
Q
Spongiosis is associated with ___
A
eczema
23
Q
Disruption of epidermal/dermal junction is associated with ___
A
vulgaris
24
Q
superficial dermal edema is associated with
A
hives
25
acantholysis
loss of intercellular adhesion.
26
Spongiosis
- fluid accumulation in intercellular space of epidermis, bc keratinocytes moved apart. Causes vesicles in eczema.
- Not much of a cap to this lesion, easy to burst open, cause oozing wet lesions.
- skin responds by producing more keratin (simultaneously or later)--> causes scaling
27
With ___, problem is dermal layer, epidermis is normal
hives
28
plaque psoriasis
- Pink plaques covered in Silver scales
- most common on knees, elbow, scalp, lower back.
- Auspitz sign, multiple bleeding pts when scale is removed.
29
Classic eczema
**Classic eczema = weeping wet lesion, with scaling on top**
30
Pathophysiology of eczema
Probably multifactorial, two things may be involved:
1) immune system
2) problem within skin itself-- problem maintaining hydration mayb. Ppl with eczema often have dry skin, which has trouble maintaining physical barrier.
31
Primary vs. secondary lesions
– what happened first and did something occur on top, like a lichenification, scratching, superinfection (if skin breaks open, easier for bacteria to get in).
32
Pathophysiology of contact hypersensitivity
- When an allergen comes into contact with skin, Langerhans cell, principal antigen-presenting cells of epidermis, internalizes it and expresses it on its membrane.
- The Langerhans cells migrate to lymph nodes through lymphatics, where they present the antigen to naive lymphocytes (CD4+ T cells, TH1), which then proliferate into memory and effector cells. These cells enter the circulation and home into the dermis in the elicitation phase. They secrete the cytokines IL-2, which causes T cells to proliferate, and IFN-γ, which activates monocytes-macrophages. The monocytes damage the cells in the epidermis.
33
itchy rash on the trunk and extremities that started to appear 2 days after camping (exposure)
- diagnosis? lesion?
- contact dermatitis/hypersensitivity
| - blisters over an erythematous, edematous base.
34
What causes reddening of the skin in contact dermatitis/hypersensitivity?
increased blood flow/vasodilation mediated by prostaglandins and nitric oxide
35
Histological feature of eczema
Spongiosis = fluid accumulation in intercellular space of epidermis. Keratinocytes move apart. Vesicles. Scales.
36
Histology of Psoriasis:
- inflammation of epidermis causes scales on top
- growth of keratinocytes (cells of epi), amount of cells in epidermis DEC, but that thickness is replaced by scales.
- Under the scale dermal papillae are raised closer to the surface than usual, that's why bleeds if you take scale off (Auspitz sign). Dermal papillae/dermis is where the blood vessels are.
- Neutrophil microabsesses-- collection of immune cells in superficial epidermal layers
37
____ often occurs with metabolic syndrome and other autoimmune diseases.
Psoriasis
38
What histo feature of psoriasis implicates immune cell pathology in psoriasis?
neutrophil microabsesses = collection of immune cells in superficial epidermal layers
39
Acute vs. chronic Inflammatory Dermatoses:
Acute: lasts days-weeks, local inflammation, ex: Hives/Urticaria, Eczematous dermatitis
Chronic: months-years, altered skin growth and fibrosis, ex: Psoriasis, Seborrheic dermatitis, Atopic dermatitis
40
Presentation of eczema:
First in early childhood, before 5.
Most cases improve with age, older ppl have lesions in hands and feet.
Characteristic lesions occur on flexure surfaces, around bends of skin.
41
Treatment of eczema:
- try to maintain skin hydration, prevent damage to barrier. Avoid low humidity, excess washing, hydrate with thick cream (low water content).
- Active lesions can be treated with topical steroid cream. But too much steroids even topically may be absorbed systemically, and these dry skin.
- antihistamines for the itching.
42
Pathophysiology of Urticaria/Hives
- Can occur as part of an allergic response: allergen exposure leads IgE to degranulate mast cells → histamine release causes blood vessels to dilate, makes them leaky→ superficial dermal edema (in histo: gaps in dermis). Histamine also causes itchiness!
- May be related to angioedema (of deeper dermis and subcutenous tissue), can block airways = anaphylaxis!!
- Mast cell may not be involved. Other causes: sunlight, cold, NSAIDs/other drugs, hormones, infections (parasitic), transfusion, insect bites (nonallergenic/allergenic).
* * Most of the time cause is UNKNOWN. May be chronic.
43
Urticaria/Hives: KEY FEATURE OF HIVES:
- episodes of wheals that fade within 24 hrs and pop up elsewhere. Can be erythematous (red)
- Lesions may coalesce and form larger plaques.
44
Histology of Urticaria/Hives
gaps in dermis = superficial dermal edema (fluid)
45
Treatment of Urticaria/Hives
antihistamine.
46
Eczemateous Dermatitis:
```
Eczema = boil over
Broad class of skin conditions:
Can become superinfected
```
47
Histology of Eczemateous Dermatitis:
◦ Papulovesicular lesions – oozing/wet/weeping
◦ Scaling (hyperkeratotis) – extra keratin
◦ Epidermal hyperplasia (acanthosis)
◦ Spongiosis = Vesicles, fluid accumulation in intercellular space of epidermis. Keratinocytes move apart. lead to Scales.
48
in pemphigus vulgaris, immunoglobulins react with which epidermal antigen? how does this present clinically?
desmoglein 3 present in desmosomes in the lower layers of the epidermis. This causes an intraepidermal blister just above the basal layer of epidermis.
49
In bullous pemphigoid, the primary lesions are ____ . When they rupture, resulting lesions become ____.
- tense bullae, often in an erythematous background.
| - become crusted after rupture.
50
patients with bullous pemphigoid are usually ____ yrs old
generally older individuals, 50-70 years old.
51
loss of epidermal component vs. dermal component is called ___
epidermal component = erosion
| dermal component = ulceration
52
with Hives the problem is___, ___ is normal.
dermis is a problem
| epidermis is normal
53
see a rash in ___ and ___
eczematous dermatitis, contact dermatitis.
54
acanthosis
Epidermal hyperplasia, dont confuse with acantholysis!!
55
histology of bullous pemphigoid shows ___
subepidermal blister with acantholysis
56
histology of pemphigus vulgaris shows ___, base of the blister consists of ___
- histology of pemphigus vulgaris shows an intraepidermal blister.
- dermal collagen, covered by one layer of basal keratinocytes.
- individual basal keratinocytes have separated from the upper layer of epidermis and from each other, due to acantholysis.
57
Lime's disease lesion:
bullseye distribution, a rash, flat, large, red, erythematous, 3-4 inch. Confluent, not spread apart.
58
Shingles lesion:
Dermatomal rash – papillovesicular, raised, some have fluid inside, others don’t.
Distribution= dermatome.
Reactivation of the chicken pox virus; sits in your nerves and reactivates in a dermatomes distribution.
59
lupus lesions:
Malar rash/flush (check bone = malar), along the cheeks only. Erythematous, not raised.
60
impetigo
Eczematous rash, suprainfection: Primary lesion is eczema, secondary lesion on top = superinfection--vesicular like lesions that broke open, giving rise to honeycomb crusted lesions (typical for superinfections)
61
Dermatophyte skin lesions:
tenia versicolor, superficial fungal infection, hypopigmentation
62
lesions for Autoimmune throbocytic purpura
petechiae, small macules, autoimmune ab attack a/g platelets. Platelets depositing under the skin. Sign of larger issue.
