CASE 9 - DERMATOLOGY Flashcards
1
Q
Name the 3 layers of the skin
A
Epidermis
Dermis
Subcutaneous fat
2
Q
Name the layers of the epidermis
A
Come, let’s get some beers
Stratum Corneum Stratum Lucidum Stratum Granulosum Stratum Spinosum Stratum Basale
3
Q
Name the 2 major types of skin disease
A
Inflammatory
Neoplastic
4
Q
Name 4 common inflammatory conditions
A
- Eczema
- Psoriasis
- Tinea
- Drug eruptions
5
Q
Outline the questions to ask in a skin history (for history of presenting complaint)
A
- Symptoms (e.g. itchy)
- Site of rash (e.g. chickenpox starts on the trunk)
- Onset of rash/triggers (e.g. started after using this treatment)
- Character of lesions (e.g. raised, flat)
- Course of rash (has it moved?)
- Treatment
- Past medical/family history (e.g. asthma, eczema)
6
Q
Outline the questions to ask in a skin history (for further history)
A
- Are other family members affected?
- Aggravating / relieving factors?
- Overseas travel (some skin diseases are endemic in certain regions)
- Occupation & hobbies (contact with glues, etc.)
- Medications
- Impact on quality of life
7
Q
Outline the features to be observed upon general inspection of a skin lesion
A
SSCAMM:
Size & shape
Colour
Associated secondary change
Morphology, margin (border)
8
Q
What should be examined in a PIGMENTED skin lesion? (ABCD)
A
ABCD
Asymmetry
Border (irregular?)
Colour (two or more?)
Diameter >6mm
9
Q
What should PALPATION of a skin lesion involve? (SCMTT)
A
Surface Consistency Mobility Tenderness Temperature
10
Q
What other examinations should be carried out? (in addition to examination of the skin lesion/rash)
A
Hair, scalp, skin, nails, mucous membranes
11
Q
What is a macule?
A
Flat (wouldn’t be able to notice it if you closed your eyes and felt the area)
<1cm in size
*look up photos
12
Q
What is a patch?
A
Flat (not palpable)
> 1cm in size
13
Q
What is a papule?
A
Raised (palpable)
<1cm
14
Q
What is a nodule?
A
Elevated (usually rounded)
> 1cm
15
Q
What is a plaque?
A
Raised, but flat-topped
> 1cm
Diameter > thickness
e.g. psoriatic plaques
16
Q
What is a vesicle?
A
Fluid-filled
<1cm
17
Q
What is a bullae/blister?
A
Fluid-filled
> 1cm
18
Q
What is a wheal?
A
Transient area of DERMAL oedema (e.g. hives, symptomatic dermographism)
NO EPIDERMAL CHANGES
19
Q
What is a pustule?
A
Pus-filled
<1cm
20
Q
What is an abscess?
A
Pus-filled
> 1cm
21
Q
What is a polypoid?
A
Structures on a stalk (e.g. skin tags)
Classically seen around the neck, groin
22
Q
What are comedones?
A
A plug of keratin and sebum in the opening of a pilosebaceous gland
OPEN = blackheads CLOSED = whiteheads
23
Q
What is a cyst?
A
A closed cavity or sac with epithelial lining containing solids or fluids
24
Q
What is erythema?
A
Redness of the skin produced by vascular congestion or increased blood flow (e.g. rosacea)
25
What is a violaceous skin lesion and what does it imply?
Purple/mauve-coloured discolourations
Usually implies inflammation deeper down (further than blood vessels), e.g. of the blood vessel wall or a tumour
26
What is a scale?
| secondary
Thickened stratum corneum
Flaky, dry, and usually whitish
27
What is atrophy?
| secondary
Thinning of the skin without atrophy
| loss of skin from the epidermis, dermis, or subcutis with loss of normal markings
28
What are purpura?
Bleeding into the dermis that may be macular or papular
e.g. in older patients, where blood vessels are thinned and rubbing or knocking can cause them to burst.
29
What is telangiectasia?
Visible blood vessels in the upper dermis
30
Where is eczema (atopic dermatitis) typically found?
On flexor surfaces (for older children, adolescents, and adults)
31
Outline the histopathology of psoriasis
Epidermal hyperplasia that is regular or uniform
Parakeratosis (nuclei in the stratum corneum)
Neutrophils in the stratum corneum and epidermis
Thinned or absent stratum granulosum
Thickening of the stratum spinosum
Dilated dermal papillary capillaries
(look up a pic)
32
What is the difference between a primary vs. secondary skin lesion?
Primary skin lesions develop as a result of the disease process.
Secondary lesions evolve FROM primary skin lesions later on in the disease process, or develop as a result of the patient's activities.
33
What is a lichenification? What is it caused by?
Thickened skin with accentuated skin markings.
Caused by rubbing or scratching itchy skin (e.g. eczema)
34
What is an excoriation?
Signs of the patient picking at or scratching their skin (e.g. pimples)
35
What is an erosion?
Partial loss of the epidermis
Heals WITHOUT scarring
36
What is an ulceration?
Full thickness of the epidermis lost
Heals WITH scarring
37
What is an annular lesion?
Rounded
38
What is psoriasis?
An inflammatory skin disease resulting from a combination of genetic and environmental factors.
It is primarily T-cell mediated and chronic.
39
What is the typical demographic of psoriasis patients?
Male (almost twice as common than in women)
Age 20-40 years
40
Describe the appearance of psoriasis
Erythematous, well-demarcated silvery-white scaling plaques and papules
41
Where do psoriatic plaques typically manifest?
Scalp, back, elbows, knees (extensor surfaces)
42
Is pruritus commonly present in psorasis?
Yes (in ~80% of cases)
43
What is responsible for the scaly appearance of psoriasis?
Build-up of keratinocytes in the epidermis
44
Is there a genetic contribution to psoriasis?
YES
~40% of individuals with psoriasis or psoriatic arthritis have a family history of the disease
45
What are common environmental triggers of psoriasis? Give 4 examples.
Infection (e.g. streptococcal tonsilitis)
Skin trauma or mechanical irritation (Koebhner phenomenon)
Psychological stress
Smoking
Drugs (e.g. beta-blockers, lithium, sudden withdrawal of corticosteroids)
Pregnancy
46
Name the 4 major clinical subtypes of psoriasis and briefly describe their appearance
1. Chronic large plaque: symmetrically-distributed thick, well-demarcated, scaly erythematous plaques
2. Guttate: teardrop-shaped papule across the trunk and limbs. Most commonly in children and adolescents.
3. Pustular: widespread sterile white pustules. Can have life-threatening complications. Relapsing course with pronounced malaise, fever, weakness, chills.
4. Erythrodermic: generalised erythema and scaling ('top to toe')
(look @ pictures)
47
Name 3 differential diagnoses for psoriasis and the features which set them apart from psoriasis
1. Atopic dermatitis/eczema (not well-demarcated, usually on flexor surfaces)
2. Basal cell carcinoma (won't be on other parts of the body)
3. Tinea (circular lesion, feet affected, infectious)
48
How many psoriasis patients get psoriatic arthritis?
5-30%
49
When does psoriatic arthritis typically occur in relation to psoriasis?
Psoriatic arthritis typically manifests years AFTER psoriasis
50
What is the most common type of psoriatic arthritis?
Oligoarthritis (accounts for ~70%) asymmetrically affecting the DIP and PIP
51
How is psoriasis diagnosed?
Clinically
Skin biopsy is not routinely performed, but can be used to rule out other causes or for challenging cases
52
Describe the physical exam findings in psoriasis (assume it is chronic large-scale psoriasis, the most common kind)
Well-demarcated, erythematous, silvery-white lesions with plaques
Symmetrical distribution
Affects the scalp, back, gluteal clefts, and extensor surfaces (knees, elbows)
Pruritus
Nails, ear canal, palms, and soles can also be involved
53
What is Koebner phenomenon? Why does it occur in individuals with psoriasis?
The development of skin lesions in sites of trauma (common in psoriasis, but can also be found in other skin diseases)
Psoriasis can be induced by trauma in susceptible individuals, presumably because trauma sets in motion a local inflammatory response that becomes self-perpetuating.
54
What is Auspitz sign?
Pinpoint bleeding which occurs after removal of the scaly part of a psoriatic plaque
55
Name 3 lifestyle risk factors linked with psoriasis
1. Smoking
2. Alcohol
3. Obesity
56
Outline the treatment regime for psoriasis
1. Emollients (adjunct) - softens skin to minimise itching and tenderness
2. Topical corticosteroids
3. Tar preparations and/or calcipotriol?
57
What is the largest barrier to treatment success with topical therapies?
Patient adherence / education / information
58
When are biological agents used for psoriasis? Give some examples of biological agents.
Moderate - severe disease
E.g. monoclonal antibodies, TNF-alpha inhibitors
59
When does someone qualify for PBS funding of biologic treatments for psoriasis?
- A Psoriasis Area and Severity Index (PASI) greater than 15, due to widespread disease
- Significant involvement of hands/feet/face
Such patients must have failed 3 out of 4 treatments (ie methotrexate, phototherapy, acitretin, ciclosporin) to be eligible for funding.
60
What is the fingertip unit?
A guide for the amount of ointment to use.
Squeeze ointment from one fingertip to the first finger crease. This is ONE unit. It is enough for 2 hand areas.
61
List 2 predisposing factors for tinea infection
- Contact w/infected individuals or animals
| - Moist environments (e.g. public swimming pools)
62
Describe the lesions seen in tinea corporis (ringworm)
Annular, pruritic, erythematous plaques that grow centrifugally
Develops into round, pruritic plaque with central clearing and a scaling, raised border
63
Describe the lesions seen in tinea pedis (athlete's foot)/tinea manuum
Interdigital (most common): chronic, pruritic, erythematous scaling and erosions between the toes/fingers
Can also manifest on the soles and medial foot
64
How are dermatophyte infections diagnosed?
KOH preparation is the best initial test: potassium hydroxide is added to a sample of the skin and viewed under a microscope. Should show branched, segmented hyphae.
Confirmatory testing: fungal culture (but antifungals should be started before these results come back)
65
Name 3 skin infections that can cause annular lesions
Erythema migrans (Lyme disease)
Plaque psoriasis
Nummular eczema (one of 7 types of eczema)
66
What are dermatophyte infections?
Tinea
Caused by fungal species that infect keratinised tissue
67
How is tinea classified?
Based on location
Tinea capitis = hair and scalp
Tinea pedis = feet
Tinea corporis/ringworm = a location other than feet, scalp, nails, and groin; mostly the arms and upper body.
68
Atopy is a Type I hypersensitivity reaction. Briefly describe the pathophysiology behind Type I hypersensitivity reactions.
IgE is formed from prior sensitisation to the antigen --> coats mast cells and basophils
Subsequent encounter --> degranulation of cells --> histamine release --> symptoms
Type I is FAST
https://www.amboss.com/us/knowledge/Hypersensitivity_reactions
69
Allergic contact dermatitis is a Type IV hypersensitivity reaction. Briefly describe the pathophysiology behind Type IV hypersensitivity reactions.
1. T cell sensitisation upon first contact with the antigen
| 2. Presensitised T cell response upon repeat contact with the antigen
70
Atopic individuals are also more susceptible to...?
Atopic individuals are also more susceptible to irritant dermatitis (skin isn't good - epidermal barrier dysfunction)
71
What is promethazine used for?
Promethazine is a sedating antihistamine used for:
- allergic conditions
- itch
- nausea & vomiting
- short-term sedation
72
Why were antihistamines ineffective against Mr Farmer's irritant dermatitis?
It was NOT a Type I hypersensitivity reaction. Type I involves mast cells.
Irritant contact dermatitis is not immunologically-mediated; it results from cytotoxic effects of the agent.
73
Discuss 1 similarity and 2 differences between Type I and Type IV hypersensitivity reactions
SIMILARITIES:
Both require sensitisation (Type I = IgE sensitisation, Type IV = T cell sensitisation)
DIFFERENCES:
Type I is IMMEDIATE (minutes for first reaction. Secondary/delayed reaction after about 24-48 hours) and antibody-mediated
Type IV is DELAYED (12-48 hours) and cell-mediated
74
Name 3 functions of skin
1. Temperature regulation
2. Protective barrier (against mechanical, thermal, and physical injury)
3. Prevents moisture loss
4. Immunity
5. Secretory (sweat)
6. Touch
7. Absorption
75
Which type of hypersensitivity reaction is NOT antibody-mediated?
Type IV is cell-mediated.
Types I-III are antibody-mediated.
76
What are common exposures that can lead to irritant contact dermatitis?
```
Soaps
Detergents
Physical irritants (e.g. friction, abrasive grains)
Alcohol
Workplace exposures
```
77
What considerations must be taken into account if corticosteroids are used on the face?
Can cause skin atrophy - use sparingly
Skin atrophy is less of a concern on the trunk and thicker areas
78
Betamethasone is a commonly-used topical corticosteroid. What is its mechanism of action?
Has anti-inflammatory & immunosuppressive effects
Causes vasoconstriction
Antimitotic activity against cutaneous fibroblasts and epidermal cells
79
What is the MOA of corticosteroids for the skin?
Anti-inflammatory, immunosuppressive, and antimitotic activity against cutaneous fibroblasts and epidermal cells.
They are also vasoconstrictive.
80
Give an example of a Type I Hypersensitivity reaction
Atopic dermatitis (eczema)
Allergic rhinitis (hay fever)
Allergic conjunctivitis
81
Give an example of a Type IV Hypersensitivity reaction
Allergic contact dermatitis
Type IV drug reactions (e.g. SJS)
Type I Diabetes Mellitus
Rheumatoid arthritis
Multiple sclerosis
82
List 5 eczema/atopic dermatitis triggers
1. Airborne: dust, animal dander, pollen, fragrances
2. Food allergens: fish, nuts, soy, milk
3. Infections/microbes (bacteria, virus, fungi)
4. Irritants: prolonged water immersion, cosmetics, pools, laundry detergent
5. Environment: low humidity, temp extremes
83
Compare irritant contact dermatitis and allergic contact dermatitis
IRRITANT dermatitis is NOT an immune reaction. It is concentration-dependent, repeated exposure is necessary, often caused by things such as cosmetics (soap, shampoo), detergents, chlorine, etc. Borders are well-defined.
ALLERGIC contact dermatitis is a Type IV hypersensitivity reaction. It is NOT concentration-dependent and common triggers are nickel jewellery, perfume, cosmetics, leather, and latex. Onset is usually rapid. Borders are ill-defined.
84
Describe the clinical manifestations of psoriatic arthritis
1. Asymmetric polyarthritis of small joints (DIP, PIP)
2. Dactylitis
3. Arthritis mutilans (telescoping fingers)
4. Nails: onycholysis, pitting, oil drop sign
5. Uveitis
6. Morning stiffness
85
What happens when the offending agent comes in contact with the skin in irritant contact dermatitis?
The agent has a direct cytotoxic effect on skin cells and the inflammatory response is secondary to cutaneous damage, not to the agent itself.
Cytotoxic effect --> skin damage --> inflammatory response
86
Outline the management of Irritant vs. allergic contact dermatitis
IRRITANT CONTACT DERMATITIS:
- Avoid causative agent
- Local reactions: wet dressings w/saline solution, moisturisers, topical corticosteroids
- Consider oral corticosteroids if severe or widespread
ALLERGIC CONTACT DERMATITIS:
- Avoidance of the allergen
- Acute phase: saline dressings, moisturisers, oatmeal baths. Oral corticosteroids if severe.
87
management in general
.
88
Describe the differences in appearance between irritant contact dermatitis and allergic contact dermatitis
IRRITANT CONTACT DERMATITIS:
- Eczema
- Erythema
- Desquamation
- Fissures
- Well-demarcated
ALLERGIC CONTACT DERMATITIS
- Eczema
- Erythema
- Oedema
- Bullar
- Vesicles
- Ill-defined
89
Outline the pathophysiology behind psoriasis
(Note: not entirely understood)
The culprit antigen / cause from the immune response is not well-understood.
Sensitised populations of CD4+ TH1 and TH17 cells and activated CD8+ cytotoxic effector T cells enter the skin and accumulate in the epidermis.
Cytokines and growth factors stimulate keratinocyte proliferation --> characteristic lesions.
90
How do corticosteroids enter the nucleus to influence gene transcription?
Binds to a cytoplasmic receptor that moves to the nucleus
91
Compare Type I and Type II collagen
TYPE I: most common, makes up 90% of hair, skin nails, organs, bones, and ligaments
TYPE II: cartilaginous tissues
