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APP Part 2 > Derm > Flashcards

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.

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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.
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3
Q

Papules vs. nodules

A
  • Papule- elevated, less than 0.5cm
  • if larger, nodule.
  • either may be dome-shaped or flat-topped.
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4
Q

Pustules

A

raised, filled with leukocytes (yellow color)

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5
Q

3 layers of skin

A

Epidermis-keratinized stratified sq epithelium
Dermis-connective tissue
Hypodermis-subQ tissue, fat (not part of skin!)

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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).
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7
Q

flat discolored lesion, could be either ___ or ___ based on size.

A

Wheal (hive) – transient (1cm????

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8
Q

A fluid filled lesion may be 3 things:

A

Vesicles – fluid-filled lesion, elevated, 1 cm — 

Pustule – puss-filled lesion, variable size — 

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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)

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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
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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
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12
Q

3 types of eczematous dermatitis

A

1) Contact dermatitis
2) atopic dermatitis
3) primary irritant dermatitis.

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13
Q

2 types of contact dermatitis

A
  1. Allergen induces - immune mediated, delayed type hypersensitivity (poison Ivy, nickel, perfume, latex)
  2. Irritant induced - nonimmune mediated, direct damage to skin by irritant. More common (acids, bleach, water, cement, diaper rash, etc)
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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.
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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
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16
Q

All kinds of eczematous dermatitis share one histological feature:_____

A

Spongiotic dermatitis

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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
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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

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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.
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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.
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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
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22
Q

Spongiosis is associated with ___

A

eczema

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23
Q

Disruption of epidermal/dermal junction is associated with ___

A

vulgaris

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24
Q

superficial dermal edema is associated with

A

hives

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25
Q

acantholysis

A

loss of intercellular adhesion.

26
Q

Spongiosis

A
  • 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
Q

With ___, problem is dermal layer, epidermis is normal

A

hives

28
Q

plaque psoriasis

A
  • Pink plaques covered in Silver scales
  • most common on knees, elbow, scalp, lower back.
  • Auspitz sign, multiple bleeding pts when scale is removed.
29
Q

Classic eczema

A

Classic eczema = weeping wet lesion, with scaling on top

30
Q

Pathophysiology of eczema

A

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
Q

Primary vs. secondary lesions

A

– 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
Q

Pathophysiology of contact hypersensitivity

A
  • 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
Q

itchy rash on the trunk and extremities that started to appear 2 days after camping (exposure)
- diagnosis? lesion?

A
  • contact dermatitis/hypersensitivity

- blisters over an erythematous, edematous base.

34
Q

What causes reddening of the skin in contact dermatitis/hypersensitivity?

A

increased blood flow/vasodilation mediated by prostaglandins and nitric oxide

35
Q

Histological feature of eczema

A

Spongiosis = fluid accumulation in intercellular space of epidermis. Keratinocytes move apart. Vesicles. Scales.

36
Q

Histology of Psoriasis:

A
  • 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
Q

____ often occurs with metabolic syndrome and other autoimmune diseases.

A

Psoriasis

38
Q

What histo feature of psoriasis implicates immune cell pathology in psoriasis?

A

neutrophil microabsesses = collection of immune cells in superficial epidermal layers

39
Q

Acute vs. chronic Inflammatory Dermatoses:

A

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
Q

Presentation of eczema:

A

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
Q

Treatment of eczema:

A
  • 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
Q

Pathophysiology of Urticaria/Hives

A
  • 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
Q

Urticaria/Hives: KEY FEATURE OF HIVES:

A
  • episodes of wheals that fade within 24 hrs and pop up elsewhere. Can be erythematous (red)
  • Lesions may coalesce and form larger plaques.
44
Q

Histology of Urticaria/Hives

A

gaps in dermis = superficial dermal edema (fluid)

45
Q

Treatment of Urticaria/Hives

A

antihistamine.

46
Q

Eczemateous Dermatitis:

A 
Eczema = boil over
Broad class of skin conditions: 
Can become superinfected
47
Q

Histology of Eczemateous Dermatitis:

A

◦ 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
Q

in pemphigus vulgaris, immunoglobulins react with which epidermal antigen? how does this present clinically?

A

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
Q

In bullous pemphigoid, the primary lesions are ____ . When they rupture, resulting lesions become ____.

A
  • tense bullae, often in an erythematous background.

- become crusted after rupture.

50
Q

patients with bullous pemphigoid are usually ____ yrs old

A

generally older individuals, 50-70 years old.

51
Q

loss of epidermal component vs. dermal component is called ___

A

epidermal component = erosion

dermal component = ulceration

52
Q

with Hives the problem is___, ___ is normal.

A

dermis is a problem

epidermis is normal

53
Q

see a rash in ___ and ___

A

eczematous dermatitis, contact dermatitis.

54
Q

acanthosis

A

Epidermal hyperplasia, dont confuse with acantholysis!!

55
Q

histology of bullous pemphigoid shows ___

A

subepidermal blister with acantholysis

56
Q

histology of pemphigus vulgaris shows ___, base of the blister consists of ___

A
  • 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
Q

Lime’s disease lesion:

A

bullseye distribution, a rash, flat, large, red, erythematous, 3-4 inch. Confluent, not spread apart.

58
Q

Shingles lesion:

A

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
Q

lupus lesions:

A

Malar rash/flush (check bone = malar), along the cheeks only. Erythematous, not raised.

60
Q

impetigo

A

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
Q

Dermatophyte skin lesions:

A

tenia versicolor, superficial fungal infection, hypopigmentation

62
Q

lesions for Autoimmune throbocytic purpura

A

petechiae, small macules, autoimmune ab attack a/g platelets. Platelets depositing under the skin. Sign of larger issue.

APP Part 2 (9 decks)

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