CASE 9 - DERMATOLOGY Flashcards

1
Q

Name the 3 layers of the skin

A

Epidermis
Dermis
Subcutaneous fat

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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
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3
Q

Name the 2 major types of skin disease

A

Inflammatory

Neoplastic

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4
Q

Name 4 common inflammatory conditions

A
  1. Eczema
  2. Psoriasis
  3. Tinea
  4. Drug eruptions
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5
Q

Outline the questions to ask in a skin history (for history of presenting complaint)

A
  1. Symptoms (e.g. itchy)
  2. Site of rash (e.g. chickenpox starts on the trunk)
  3. Onset of rash/triggers (e.g. started after using this treatment)
  4. Character of lesions (e.g. raised, flat)
  5. Course of rash (has it moved?)
  6. Treatment
  7. Past medical/family history (e.g. asthma, eczema)
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6
Q

Outline the questions to ask in a skin history (for further history)

A
  1. Are other family members affected?
  2. Aggravating / relieving factors?
  3. Overseas travel (some skin diseases are endemic in certain regions)
  4. Occupation & hobbies (contact with glues, etc.)
  5. Medications
  6. Impact on quality of life
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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)

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8
Q

What should be examined in a PIGMENTED skin lesion? (ABCD)

A

ABCD

Asymmetry
Border (irregular?)
Colour (two or more?)
Diameter >6mm

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9
Q

What should PALPATION of a skin lesion involve? (SCMTT)

A
Surface
Consistency
Mobility
Tenderness
Temperature
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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

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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

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12
Q

What is a patch?

A

Flat (not palpable)

> 1cm in size

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13
Q

What is a papule?

A

Raised (palpable)

<1cm

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14
Q

What is a nodule?

A

Elevated (usually rounded)

> 1cm

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15
Q

What is a plaque?

A

Raised, but flat-topped

> 1cm

Diameter > thickness

e.g. psoriatic plaques

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16
Q

What is a vesicle?

A

Fluid-filled

<1cm

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17
Q

What is a bullae/blister?

A

Fluid-filled

> 1cm

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18
Q

What is a wheal?

A

Transient area of DERMAL oedema (e.g. hives, symptomatic dermographism)

NO EPIDERMAL CHANGES

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19
Q

What is a pustule?

A

Pus-filled

<1cm

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20
Q

What is an abscess?

A

Pus-filled

> 1cm

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21
Q

What is a polypoid?

A

Structures on a stalk (e.g. skin tags)

Classically seen around the neck, groin

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22
Q

What are comedones?

A

A plug of keratin and sebum in the opening of a pilosebaceous gland

OPEN = blackheads
CLOSED = whiteheads
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23
Q

What is a cyst?

A

A closed cavity or sac with epithelial lining containing solids or fluids

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24
Q

What is erythema?

A

Redness of the skin produced by vascular congestion or increased blood flow (e.g. rosacea)

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25
Q

What is a violaceous skin lesion and what does it imply?

A

Purple/mauve-coloured discolourations

Usually implies inflammation deeper down (further than blood vessels), e.g. of the blood vessel wall or a tumour

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26
Q

What is a scale?

secondary

A

Thickened stratum corneum

Flaky, dry, and usually whitish

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27
Q

What is atrophy?

secondary

A

Thinning of the skin without atrophy

loss of skin from the epidermis, dermis, or subcutis with loss of normal markings

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28
Q

What are purpura?

A

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.

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29
Q

What is telangiectasia?

A

Visible blood vessels in the upper dermis

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30
Q

Where is eczema (atopic dermatitis) typically found?

A

On flexor surfaces (for older children, adolescents, and adults)

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31
Q

Outline the histopathology of psoriasis

A

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)

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32
Q

What is the difference between a primary vs. secondary skin lesion?

A

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.

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33
Q

What is a lichenification? What is it caused by?

A

Thickened skin with accentuated skin markings.

Caused by rubbing or scratching itchy skin (e.g. eczema)

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34
Q

What is an excoriation?

A

Signs of the patient picking at or scratching their skin (e.g. pimples)

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35
Q

What is an erosion?

A

Partial loss of the epidermis

Heals WITHOUT scarring

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36
Q

What is an ulceration?

A

Full thickness of the epidermis lost

Heals WITH scarring

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37
Q

What is an annular lesion?

A

Rounded

38
Q

What is psoriasis?

A

An inflammatory skin disease resulting from a combination of genetic and environmental factors.

It is primarily T-cell mediated and chronic.

39
Q

What is the typical demographic of psoriasis patients?

A

Male (almost twice as common than in women)

Age 20-40 years

40
Q

Describe the appearance of psoriasis

A

Erythematous, well-demarcated silvery-white scaling plaques and papules

41
Q

Where do psoriatic plaques typically manifest?

A

Scalp, back, elbows, knees (extensor surfaces)

42
Q

Is pruritus commonly present in psorasis?

A

Yes (in ~80% of cases)

43
Q

What is responsible for the scaly appearance of psoriasis?

A

Build-up of keratinocytes in the epidermis

44
Q

Is there a genetic contribution to psoriasis?

A

YES

~40% of individuals with psoriasis or psoriatic arthritis have a family history of the disease

45
Q

What are common environmental triggers of psoriasis? Give 4 examples.

A

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
Q

Name the 4 major clinical subtypes of psoriasis and briefly describe their appearance

A
  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
Q

Name 3 differential diagnoses for psoriasis and the features which set them apart from psoriasis

A
  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
Q

How many psoriasis patients get psoriatic arthritis?

A

5-30%

49
Q

When does psoriatic arthritis typically occur in relation to psoriasis?

A

Psoriatic arthritis typically manifests years AFTER psoriasis

50
Q

What is the most common type of psoriatic arthritis?

A

Oligoarthritis (accounts for ~70%) asymmetrically affecting the DIP and PIP

51
Q

How is psoriasis diagnosed?

A

Clinically

Skin biopsy is not routinely performed, but can be used to rule out other causes or for challenging cases

52
Q

Describe the physical exam findings in psoriasis (assume it is chronic large-scale psoriasis, the most common kind)

A

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
Q

What is Koebner phenomenon? Why does it occur in individuals with psoriasis?

A

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
Q

What is Auspitz sign?

A

Pinpoint bleeding which occurs after removal of the scaly part of a psoriatic plaque

55
Q

Name 3 lifestyle risk factors linked with psoriasis

A
  1. Smoking
  2. Alcohol
  3. Obesity
56
Q

Outline the treatment regime for psoriasis

A
  1. Emollients (adjunct) - softens skin to minimise itching and tenderness
  2. Topical corticosteroids
  3. Tar preparations and/or calcipotriol?
57
Q

What is the largest barrier to treatment success with topical therapies?

A

Patient adherence / education / information

58
Q

When are biological agents used for psoriasis? Give some examples of biological agents.

A

Moderate - severe disease

E.g. monoclonal antibodies, TNF-alpha inhibitors

59
Q

When does someone qualify for PBS funding of biologic treatments for psoriasis?

A
  • 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
Q

What is the fingertip unit?

A

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
Q

List 2 predisposing factors for tinea infection

A
  • Contact w/infected individuals or animals

- Moist environments (e.g. public swimming pools)

62
Q

Describe the lesions seen in tinea corporis (ringworm)

A

Annular, pruritic, erythematous plaques that grow centrifugally

Develops into round, pruritic plaque with central clearing and a scaling, raised border

63
Q

Describe the lesions seen in tinea pedis (athlete’s foot)/tinea manuum

A

Interdigital (most common): chronic, pruritic, erythematous scaling and erosions between the toes/fingers

Can also manifest on the soles and medial foot

64
Q

How are dermatophyte infections diagnosed?

A

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
Q

Name 3 skin infections that can cause annular lesions

A

Erythema migrans (Lyme disease)

Plaque psoriasis

Nummular eczema (one of 7 types of eczema)

66
Q

What are dermatophyte infections?

A

Tinea

Caused by fungal species that infect keratinised tissue

67
Q

How is tinea classified?

A

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
Q

Atopy is a Type I hypersensitivity reaction. Briefly describe the pathophysiology behind Type I hypersensitivity reactions.

A

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
Q

Allergic contact dermatitis is a Type IV hypersensitivity reaction. Briefly describe the pathophysiology behind Type IV hypersensitivity reactions.

A
  1. T cell sensitisation upon first contact with the antigen

2. Presensitised T cell response upon repeat contact with the antigen

70
Q

Atopic individuals are also more susceptible to…?

A

Atopic individuals are also more susceptible to irritant dermatitis (skin isn’t good - epidermal barrier dysfunction)

71
Q

What is promethazine used for?

A

Promethazine is a sedating antihistamine used for:

  • allergic conditions
  • itch
  • nausea & vomiting
  • short-term sedation
72
Q

Why were antihistamines ineffective against Mr Farmer’s irritant dermatitis?

A

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
Q

Discuss 1 similarity and 2 differences between Type I and Type IV hypersensitivity reactions

A

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
Q

Name 3 functions of skin

A
  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
Q

Which type of hypersensitivity reaction is NOT antibody-mediated?

A

Type IV is cell-mediated.

Types I-III are antibody-mediated.

76
Q

What are common exposures that can lead to irritant contact dermatitis?

A
Soaps
Detergents
Physical irritants (e.g. friction, abrasive grains)
Alcohol
Workplace exposures
77
Q

What considerations must be taken into account if corticosteroids are used on the face?

A

Can cause skin atrophy - use sparingly

Skin atrophy is less of a concern on the trunk and thicker areas

78
Q

Betamethasone is a commonly-used topical corticosteroid. What is its mechanism of action?

A

Has anti-inflammatory & immunosuppressive effects
Causes vasoconstriction
Antimitotic activity against cutaneous fibroblasts and epidermal cells

79
Q

What is the MOA of corticosteroids for the skin?

A

Anti-inflammatory, immunosuppressive, and antimitotic activity against cutaneous fibroblasts and epidermal cells.

They are also vasoconstrictive.

80
Q

Give an example of a Type I Hypersensitivity reaction

A

Atopic dermatitis (eczema)

Allergic rhinitis (hay fever)

Allergic conjunctivitis

81
Q

Give an example of a Type IV Hypersensitivity reaction

A

Allergic contact dermatitis

Type IV drug reactions (e.g. SJS)

Type I Diabetes Mellitus

Rheumatoid arthritis

Multiple sclerosis

82
Q

List 5 eczema/atopic dermatitis triggers

A
  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
Q

Compare irritant contact dermatitis and allergic contact dermatitis

A

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
Q

Describe the clinical manifestations of psoriatic arthritis

A
  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
Q

What happens when the offending agent comes in contact with the skin in irritant contact dermatitis?

A

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
Q

Outline the management of Irritant vs. allergic contact dermatitis

A

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
Q

management in general

A

.

88
Q

Describe the differences in appearance between irritant contact dermatitis and allergic contact dermatitis

A

IRRITANT CONTACT DERMATITIS:

  • Eczema
  • Erythema
  • Desquamation
  • Fissures
  • Well-demarcated

ALLERGIC CONTACT DERMATITIS

  • Eczema
  • Erythema
  • Oedema
  • Bullar
  • Vesicles
  • Ill-defined
89
Q

Outline the pathophysiology behind psoriasis

A

(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
Q

How do corticosteroids enter the nucleus to influence gene transcription?

A

Binds to a cytoplasmic receptor that moves to the nucleus

91
Q

Compare Type I and Type II collagen

A

TYPE I: most common, makes up 90% of hair, skin nails, organs, bones, and ligaments

TYPE II: cartilaginous tissues