Inflammatory Dermatoses Flashcards

1
Q

what kind of cells are found in the stratum corneum?

A

dead keratinocytes which have lost their nuclei

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

what kind of cells are found in the stratum granulosum?

A

cells with keratin granules

much flatter

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

what kind of cells are found in the stratum spinosum?

A
  • living keratinocytes

- dendritic cells (Langerhan cells)

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

what kind of cells are found in the stratum basale?

A
  • melanocyte
  • dividing keratinocyte (stem cell)
  • tactile cell with sensory nerve ending (Merkel cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

where are the youngest and oldest cells found in the epidermis?

A

the youngest cells are near the basement membrane where they freshly differentiate

the older cells are closest to the stratum corneum

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

what are the stages of differentiation of basal cells into keratinocytes?

A

basal cell

  • to prickle/spinous cell (in the spinosum layer)
  • to granular cell (in the granulosum layer)
  • to keratin producing cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the two layers of the dermis layer?

A

papillary dermis

reticular dermis

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

what function does the stratum corneum have and how is this achieved?

A

barrier function:

corneocytes (differentiated keratinocytes) have a glue around them made of lipids (filaggrin)

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

what protein is required for the glue around the corneocytes?
what is the result of a defect in this protein (gene) ?

A

filaggrin

a defect in the protein’s gene predisposes you to eczema

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

what are the 4 main types of eczema/dermatitis?

A
  • atopic
  • seborrhoeic
  • discoid
  • allergic contact

ASDA

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

what is the associated tendency with atopic diseases?

A

the tendency to develop hypersensitivity – includes eczema, hay fever & asthma:

from early life. Many grow out of it

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

what is the cause of atopic dermatitis?

A

defective barrier of skin e.g. filagrin epidermal protein gene mutation

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

what is a sign of filagrin mutation?

A

palmar hyperlinearity

the lines of the palm are more prominent

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

what is the consequence of a defective skin barrier due to the mutation in filagrin?

A

Defective barrier then allows entry of irritants, allergens and pathogens which then cause inflammation.

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

what is the consequence of chronic scratching and rubbing of atopic dermatitis?

A

lichenification where the skin becomes thick and leathery

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

how is severe eczema described?

A

erythroderma

describe intense and usually widespread reddening of the skin due to inflammatory skin disease.

17
Q

what are some microbial infections that lead to severe eczema?

A

staphylococcus, streptococcus and herpes simplex

susceptible to these infection due to eczema

18
Q

what is seborrhoeic eczema?

A

Associated with an overgrowth of malassezia (species of yeast on the skin that causes inflammation) with eczema

19
Q

who does seborrhoeic eczema affect?

A

Common skin condition affecting babies and adults but is NOT itchy.

distinctive distribution involving
– nasolabial folds, eyebrows, scalp, central chest, axilla and groin.

20
Q

in what sort of skin is discoid eczema common?

A

small discrete discs common in overwashed skin due to lack of skin oils

21
Q

what are the types of psoriasis?

A

o Chronic plaque.
o Guttate.
o Palmoplantar pustulosis.
o Generalised pustular psoriasis

22
Q

what is the cause of psoriasis?

A

many genes are implicated including PSOR1 alongside Environmental causes i.e. triggers like
- alcohol, stress, smoking, drugs (antimalarials, beta blockers) infection (strep)

in infection, tonsillectomy can improve psoriasis

23
Q

what is the mechanism resulting in psoriasis?

A
  • T-lymphocytes move out of blood vessels into the dermis
  • initiate release of cytokines (e.g. TNFa)
  • the epidermis thickens in response (produces more keratinocytes)
  • Neutrophils infiltrate the epidermis and lymphocytes infiltrate the dermis.
24
Q

what are the histological features of psoriasis?

A

proliferation effects:

  • hyperkeratosis: thickening due to overproliferation
  • parakeratosis: top layer of keratinocytes have not lost their nuclei
  • acanthosis: thickening
  • inflammation
  • dilated blood vessels
25
Q

info about Guttate psoriasis

A

smaller plaques (papule)
pink and scaly
exacerbated by strep infections

26
Q

info about palmoplantar pustolosis

A

pustules on the hands or feet

exacerbated by smoking, stress and obesity

27
Q

what is acne the disease of?

A

disease of the pilosebaceous unit of the skin involving the hair follicle at its opening

28
Q

what is the process that leads to acne formation?

A

o Hyperkeratinisation of the epidermis in the infundibulum of hair follicles.
- Accumulation of dead keratinocytes in the lumen of the hair follicle.

o Increase sebum production stimulated by androgens.

o Proliferation of Propionibacterium acnes (bacteria) within pilosebaceous unit.

o Rupture of inflamed pilosebaceous unit –> further inflammation of surrounding skin

important drivers: propionibacteria and androgenic stimulation

29
Q

what are the clinical features of acne?

A
  • open (blackhead) comedones
  • closed (whitehead) comedones
  • papules
  • pustules
  • nodules
  • scars on face, chest and back.
30
Q

what is Bullous Pemphigoid?

A

autoimmune bullous inflammatory condition most common in the elderly

31
Q

what are the clinical features of bullous pemphigoid?

A
  • pruritis (itch)
  • deep blistering (tense blisters/bullae) on an erythematous background of skin or mucous membrane

e.g. epidermolysis bullosa

32
Q

what is the autoimmune mechanism of bullous pemphigoid?

A

IgG auto-antibodies against basement membrane antigens

  • BP180 (T17 collagen)
  • BP230

leads to an inflammatory response:
result in cleavage of skin at the dermo-epidermal (between dermis and epidermis) junction leading to sub-epidermal blisters.

(?) antigens: BPAg1 and BPAg2

33
Q

in embryology, where is the epidermis and dermis derived from?

A

epidermis from ectoderm

dermis from mesoderm

34
Q

what is pemphigus vulgaris?

A

uncommon AI bullous inflammatory disease most common in middle-aged people

more likely in Asians than whites (at a younger age group)

35
Q

what are the clinical features of pemphigus vulgaris?

A

flaccid blisters which break easily leaving erosions and crusted lesions

36
Q

what is the autoimmune mechanism in pemphigus vulgaris?

A

IgG auto-antibodies to epidermal cell surface proteins desmogleins 1 & 3 (cadherins)

this results in the loss of cell-cell adhesion (acantholysis) between keratinocytes within the epidermis causing flaccid blisters in the skin or mucous membranes

summary: AI reaction affects intercellular adhesions between keratinocytes at cell-cell junction

NB pemphigoid is to do with basement membrane

37
Q

what is the difference between bullous pemphigoid and pemphigus vulgaris?

A

BP:

  • Affects the junction between the epidermis and dermis.
  • Affects an older age group (elderly)

PV:

  • Effect is within the epidermal layer (due to keratinocyte adhesions)
  • Affects a younger age group (at middle age)