Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Derm > conditions > Flashcards

conditions Flashcards

(74 cards)

Start Studying
1
Q

What is Dermatitis Herpetiformis

A

chronic immunobullous condition associated with coeliac disease

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

Dermatitis Herpetiform epidemiology

A
  • Young adults (15-40year olds)
  • Caucasians
  • More common in males
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Dermatitis Herpetiform

Aetiology

A
  • Autoimmune disease in pxs with gluten intolerance
  • Risk factors: coeliac disease, family hx of autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Dermatitis Herpetiform

Pathophysiology

A
  • Intolerance to gliadine part of gluten causes autoimmune reaction in patient
  • IgA molecules are released into circulation before migrating to skin and creating the appearance of this disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Dermatitis Herpetiform

Histophysiology

A
  • Papillary dermal micro abscesses
  • Subepidermal blisters
  • Neutrophil + eosinophil infiltrates in the dermal papillae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where is gluten found

A
  • barley
  • rye
  • wheat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Dermatitis Herpetifrom

presentation

A

Small clusters of vesicles +/or papules:
- Present on knee + elbow extensor surfaces, scalp + buttocks
- Symmetrical distribution
- Extreme pruritus

GI Symptoms of coeliac disease
- Fatigue
- Steatorrhea
- Diarrhoea
- Bloating
- Weight loss
- Pale stools

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

Dermatitis Herpetiform

Diagnosis

A
  • Skin biopsy (direct immunofluorescence shows granular IgA deposits in dermal papillae)
  • tTG IgA antibody testing
  • Duodenal biopsy (if coeliac disease suspected)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Dermatitis Herpetiform Managment

A
  • GF diet
  • Topical steroids (symptomatic relief)
  • Dapsone (for rash + pruritis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Type of cancer associated with dermatitis herpetiform

A

Small bowel lymphoma

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

PEMPHIGUS VULGARIS

Definition

A

Autoimmune condition characterised by intraepithelial blistering of skin + mucous membranes

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

PEMPHIGUS VULGARIS

epidemiology

A
  • 50-60yr olds
  • Ahkenazi Jews + Indians
  • Ppl affected by other autoimmune conditions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

PEMPHIGUS VULGARIS

Aetiology

A
  • Idiopathic aetiology, occurs spontaneously
  • Genetic influence
  • Speicifc triggers (Drugs, malignancy, infection, Trauma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PEMPHIGUS VULGARIS

Pathophysiology

A
  • Circulating IgG molecules attack (the protein desmoglein 3) found within desmosomes holding keratinocytes together at the bottom of the epidermis
  • Separating keratinocytes from eachother
  • Fluid-filled blister appears
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

PEMPHIGUS VULGARIS

Histopathology

A
  • Intra-epidermal blistering (basal layer stays stuck to dermis)
  • Supra basal clefts + blisters containing acantholytic cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PEMPHIGUS VULGARIS

Diagnosis

A
  1. Positive Nikolsky Sign
  2. Skin biopsy
    - Acantholytic cells present
    - Immunofluorescnes shows intracellular deposits of IgG on surface of keratinocytes throughout epidermis (chicken wire pattern)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

PEMPHIGUS VULGARIS

Management

A
  1. Local (topical steroids + topical anaesthetics)
  2. Systemic (prednisolone)
  3. May need other specialties invovled (eg. opthamology)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

PEMPHIGUS VULGARIS

prognosis

A
  • relapsing + remitting course
  • Stop treatment during inactive disease periods + restart during flare ups
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

BULLUS PEMPHIGOID

Definition

A

A rare, subepidermal blistering disease of autoimmune aetiology.

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

BULLUS PEMPHIGOID

EPIDEMEOLOGY

A
  • Elderly (rare <50)
  • Common in elderly w neurological conditions (like parkinsons, stroke and dementia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

BULLUS PEMPHIGOID

aetiology

A
  • HLA associations (Suggesting genetic element)
  • Idiopathic + spontaneous cause
  • Possible triggers (medication, Injury, Skin infection)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

BULLUS PEMPHIGOID

Pathophysiology

A
  • IgG (IgE + Tcells also involved) attacks BP180 + BP230 proteins in BM of epidermis causing an acute inflam response (incl. neutrophil recruitment, complement activaation + release of proteolytic enzymes)
  • This causes destruction of hemidesmosomes + later formation of subepidermal blisters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

BULLUS PEMPHIGOID

histopathology

A
  • Eosinophils prominent
  • Subepidermal cleft w. obvious inflam infiltrates (eg. neutrophils + T cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

BULLUS PEMPHIGOID

presentation

A
  1. Pruritus and erythema - (may precede blistering onset by months)
  2. Large, tense bullae.
    - few or many
    - located anywhere (often flexures)
    - may burst and become crusted erosions
  3. Sparing of mucosal surfaces.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
BULLUS PEMPHIGOID diagnosis
1. Negative Nikolsky sign 2. Skin biopsy => Subepidermal blistering (full thickness epidermis as blister roof) 3. Antibody testing - Indirect IMF for circulating BP180/BP230 antibodies - Direct IMF shows antibodies along basement membrane
25
BULLUS PEMPHIGOID Management
1. Oral Prednisolone (MAIN TREATMENT) 2. Antibiotic therapy (Tetracyclines) 3. Topical steroids (potent or v potent) 4. Antihistamines (for pruritus)
26
BULLUS PEMPHIGOID Why are tetracycline antibiotics used
They have anti-inflam effect + are steroid sparing agents
27
What is negative Nikolsky sign
Rub skin, top layer will not shear off
28
Hair types
- Lanugo - Vellus - Terminal
29
What is scarring alopecia
follicles lost
30
What is non-scarring alopecia
Hair follicles still present (Can regrow)
31
Examples of non-scarring localised hair loss
- Alopecia areata - Androgenetic (pattern alopecia) - Trichotillomania - Traction Alopecia (due to hair stlying) - Tinea capitis (Scalp fungal infection)
32
Examples of localised scarring alopecia
- Burns/Trauma -Chronic discoid lupus (CDLE) - Lichen Planus - Frontal fibrosing alopecia
33
Causes of generalised hair loss
- Telogen effluvium (eg. sever illness, stress, childbirth) - Endocrine (eg. thyroid disease) - Drugs - Dietary deficiency (eg. iron, zinc, vit D) - Diffuse alopecia areata - Malnutrition - Androgenetic alopecia
33
Is generalised hair loss normally scarring or non-scarring
Non-scarring
34
Investigations for hair loss
1. for fungal exam: - Skin scraping - Hair plucking - Woods lamp examination (some fungal species flourescent) 2. general look at hair folicles - Dermoscopy - Scalp biopsy +/- Immunofluorescence - Blood tests (FBC, TFTs, Iron/Zinc levels, Hormone profile)
35
What is this
alopecia areata - circular areas of hair loss - preservation of hair follicles - Broken hair, tapering hair
36
Process of alopecia areata
- Autoimmune - normal recovers itself (takes months to years to recover) - recurrent episodes/extensive involvement = less likely to regrow
37
What is it called when alopecia areata affects: - whole scalp - Whole body
1. Alopecia totalis 2. Alopecia universalis
38
Pharmacological treatment for alopecia areata
- Topical steroids - IL steroids - Wig provision
39
what is this?
Trichotillomania - self-induced hair loss (hair pulling) - Asymmetrical - Associated with psychological issues
40
What is this
Tinea capitis fungal infection of scalp
41
Tinea Capitis investigations
skin scraping hair plucking woods lamp
42
Tinea capitis treatment
oral anti-fungal agent
43
Tinea capitis epidemeology
pre-pubertal kids areas of poverty/overcrowded living
44
What is kerion
Dramatic tinea capitis - big immune response to fungal infection
45
Kerion identifiers
- Abscess formation - More inflamed - Localised scarring hair loss
46
What is this
Chronic Discoid Lupus Erythematosus
47
DCLE Diagnosis
clinical + biopsy with DIF
48
DCLE treatment
1. Potent topical steroids 2. hydroxychloroquine always - photoprotection
49
Androgenetic/Pattern hair loss stages in men + women
- Localised problem Males: Generally starts at resection at temples then vertex of scalp then it joins together) Women: front of hair margin preserved, general thinning across scalp)
50
Androgenetic hair loss investigation
hormone levels iron zinc
51
Androgenetic hair loss treatment
- Minoxidil (regaine) (vasodilator, stops when not in use) - Anti-androgens (common for females with PCOS) - If extensive, wig
52
Hair excess broad categories
- Hirsutism - Hypertrichosis
53
Hirsuitism - Definition
- Excess hair growth in females in male distribution due to ^ androgen levels or ^ end organ response to normal androgen levels
54
Causes of hirsutism
1. Familial/constitutional - associated w seborrhoea, acne, androgenetic alopecia 2. Hormonal - eg.PCOS/Androgen secreting tumour
55
Hirsutism investigation
1. History + exam - Ask about other signs of androgen excess (eg. irregular menstrual cycle, acne, difficulty conceiving) 2. Hormone profile 3. Ovarian US if indicated
56
What is hypertrichosis
Excessive hair growth in a non-adrogenic distribution
56
Hypertrichosis causes 1. Local 2. General
1. Naevi (moles), occult spina bifida (indicated by faun tail sign), Chronic scarring/inflammation 2. Malnutrition, Anorexia, Prophyria, occult malignancy, drugs (eg. minoxidil, phenytoin, cyclosporin)
57
What causes Beau's line
caused by transient arrest in nail growth which occurs during acute stress/illness
58
What condition may they have
Psoriasis - Nail pitting - Dystrophy - Subungual hyperkeratosis - Onikolysis - Oil drop sign
59
Normal nail label
60
What causes acute paronychia
Staph aureus Strep pyogenes
61
What is this
Acute paronychia
62
Acute paronychia treatment
- drain it - oral Antibiotics
63
What causes chronic paronychia where is it commonly seen
- Candida / can be mould-related - people who commonly deal with water
64
Chronic paronychia
topical or oral antifungals protect skin from being wet all the time
65
What is this
fungal nail infection - onicholysis - subungual hyperkeratosis
66
Investigations for fungal nail infection
Nail clipping
67
Treatment for fungal nail infection
- Topical anti-fungal nail varnish - Oral antifungal agent used for 3-6months if extensive disease (eg.Terbinafine)
68
What is this
Subungual haematoma - normally due to trauma
69
Subungual haematoma treatment
- Let it grow out over time - hole can be bore in nail to relieve pressure which is source of pain
70
what is this
malignant melanoma NB - Hutchinson's sign (spreading pigmentation)
71
What is this
myxoid cyst - at proximal nail fold - accumulation of synovial fluid - gutter effect in nail due to (pressures growing nail)

Derm (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions