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Year 2 semester 4 integration for clinical application > Session 4 > Flashcards

Session 4 Flashcards

1
Q

DERMATOLOGICAL HISTORY

A

• Presenting complaint - • Nature (e.g. rash vs lesion)
• Site
• Duration
• History of presenting complaint - • Initial appearance and evolution*
• Symptoms (particularly itch and pain)
• Aggravating and relieving factors (“triggers”)
• Previous and current treatments (effective or not)
* Indicates points more important with lesions as presenting complaint
• Past medical history -• Systemic diseases
• History of atopy (asthma, hay fever, eczema)
• History of skin cancer or pre-cancer*
• History of sunburn/sunbathing/sun-bed use*
• Skin type*
• Family history - • Family history of skin disease*
• Family history of atopy
• Family history of autoimmune disease
• Social history - • Occupation
• Sun exposure*
• Contactants
• Improvement in PC when away from work
• Drug history and allergies - • Regular and recent
• Systemic and topical
• Get specific with topical treatments!
• Where?
• How much?
• How long for?

  • Impact on quality of life / ICE• Impact of skin complaint on life
  • Ideas
  • Concerns
  • Expectations- • Impact of skin complaint on life
  • Ideas
  • Concerns
  • Expectations
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2
Q

What are the different skin types?

A

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3
Q

EXAMINING THE SKIN and description of physical findings

A

Inspect
describe
palpate
systemic check - whole skin, hair, nails, mucous membranes

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4
Q

How to describe a skin condition?

A 
SCAM
• S - Site, distribution (rash) 
• or Size and Shape (lesion)
• C - Colour (and Configuration)
• A - Associated changes e.g. surface features
• M - Morphology
ABCD FOR PIGMENTED LESIONS
• Asymmetry
• Border (irregular or blurred)
• Colour
• Diameter
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5
Q

How to describe Site & Distribution of a skin condition

A

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6
Q

How to describe Configuration of a skin condtion

A

inser image

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7
Q

How to describe the colour of a skin condition

A

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8
Q

How to describe the Surface Features of a skin condition

A

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9
Q

How to describe the hair findings in a skin condition

A

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10
Q

How to describe nail findings?

A

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11
Q

Case presentation
• A 42 year old man with a background of chronic plaque psoriasis has presented to Accident Emergency feeling unwell.
• Describe the rash?
• Describe which functions of the skin are impaired in this patient?
• What is the name of this clinical presentation?
onsert image

A

panopto

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12
Q

Functions of the skin

A
  • Protective barrier against environmental insults
  • Temperature regulation
  • Sensation
  • Vitamin D synthesis
  • Immunosurveillance
  • Cosmesis
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13
Q

Erythroderma and its complications

A
  • > 90% of body surface area affected, erythematous and exfoliatitive
  • Causes: psoriasis, eczema, drugs, cutaneous T cell lymphoma
  • Symptoms: pruritus, fatigue, anorexia, feeling cold
  • Signs: erythematous, thickened, inflamed, scaly, no sparing
  • ‘Total skin failure’
  • Hypothermia (loss of thermoregulation)
  • Infection (loss of protective barrier)
  • Renal failure (insensible losses)
  • High output cardiac failure (dilated skin vessels)
  • Protein malnutrition (high turnover of skin)
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14
Q

Cells of the Epidermis

A
  • 4 major cell types each with individual function
  • Keratinocytes - protective barrier
  • Langerhan cells- antigen presenting cells
  • Melanocytes- produce melanin which provides pigment to the skin and protects cell nuclei from UV DNA damage
  • Merkel Cells - contain specialised nerve endings for sensation
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15
Q

Layers of the epidermis

A
  • 4 layers of the epidermis
  • Each layer represents a different stage of maturation of the keratinocyte
  • Average epidermal turnover time is about 30 days
  • The 4 layers of the epidermis include: stratum basale (basal layer), stratum spinosum, stratum granulosum, stratum corneum (horny layer- most superficial)
  • Stratum lucidum found in areas of thicker skin such as palms and soles
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16
Q

How might pathology affect the epidermis

A
  • a) Change in epidermal turnover
  • b) Change in surface of the skin
  • c) Changes in pigmentation of the skin
17
Q

Dermis

A
  • Composed of collagen, elastin and glycosaminoglycans
  • Provides strength and elasticity
  • Also contains immune cells, nerve cells, skin appendages, lymphatics and blood vessels
18
Q

Sebaceous gland

A
  • Produce sebum through hair follicles (pilosebaceous unit)
  • Secrete sebum on to skin which lubricates skin
  • Active after puberty
  • Stimulated by conversion of androgen to dihydrotestosterone
  • Increased sebum production and bacterial colonisation in conditions such as acne vulagris
19
Q

Eccrine and Apocrine glands

A
  • Regulate body temperature
  • Innervated by sympathetic system
  • Two types: Eccrine and Apocrine
  • Eccrine are widespread
  • Apocrine are active following puberty and are found in axillae, areolae, genitalia and anus.
20
Q

Hair

A
  • Each hair consists of modified keratin and is divided into hair shaft and hair bulb
  • 3 main types of hair: lanugo hair, vellum hair (short hair all over body), terminal hair (coarse long hair)
  • Each hair follicle enters a growth cycle which has 3 main phases: anagen, catagen, telogen
21
Q

Nails

A
  • Consists of a nail plate which arises from the nail matrix at the posterior nail fold and rests on the nail bed.
  • Nail bed contains blood capillaries
22
Q

⦁ Learn the history and key presenting features of Atopic Eczema

A

GENERALISED SYMMETRICAL rash consisting of ERYTHEMATOUS, SCALY, ILL DEFINED, PATCHES, EROSIONS
•Endogenous vs Exogenous •Acute vs chronic •Epithelial disruption-vesicles, bullae, papules •Pruritus +++ •Clinical diagnosis- personal or family history of atopy(inc.hay fever and asthma) •Complications include heavy bacterial colonization, eczema herpeticum, superimposed contact allergy, reduced quality of life
•Education-National Eczema society •Avoidance of exacerbating factors and use of soap substitute •Generous use of non-perfumed emollient (500g/week) •Topical steroids/calcineurininhibitors •Phototherapy •Systemic therapies

23
Q

⦁ Learn the history and key presenting features of psoriasis

A

Extensor surfaces with Scaly, well defined, Plaques and nail pitting
• Overactive maturation of keratinocytes driven by inflammation • Autoimmune driven- genetic and environmental factors • Made worse by stress, infection and cold weather (improved by sun light) • Patients can also have nail findings and psoriatic arthritis • Management: Steroid creams, Vitamin D3 analogues, UV light therapy and immunosuppressant therapy

24
Q

⦁ Learn the history and key presenting features of Acne Vulgaris

A

Generalised, Erythematous, maculopapular vesciles, pustules and comedones with crusting and excoriation
• Occur when dead skin cells and oil (sebum) clog hair follicles • Often more common in adolescents due to pubertal effects on sebum production • Genetics plays a large role in incidence • Can also be affected by diet, stress and infections • Usually managed in community but if resistant or scarring present then dermatology input advised • Treatment involves lifestyle changes, antibacterial facewash, antibiotics and hormonal therapy

25
Q

Macules and Patches

A

Macules are nonpalpable lesions <1 cm that vary in pigmentation from the surrounding skin. Patches are nonpalpable lesions >1 cm. These lesions are flush with the surrounding skin.

26
Q

Papules

A

Papules are palpable, discrete lesions measuring <1 cm in diameter. They may be isolated or grouped

27
Q

Plaques

A

Plaques are elevated lesions that are >1 cm in diameter. Plaques may be formed by a confluence of papules

28
Q

Nodules

A

Nodules are palpable, solid or cystic, discrete lesions measuring 1-2cm in diameter.

29
Q

Pustules

A

Pustules are small, circumscribed skin papules containing purulent material

30
Q

Vesicles and Bullae

A

Vesicles are small (<1 cm in diameter), circumscribed skin papules containing clear serous or hemorrhagic fluid Bullae are large (>1 cm in diameter) vesicles.

31
Q

Wheals

A

Wheals are irregularly shaped, elevated, edematous skin areas that may be erythematous or paler than surrounding skin. The borders of a wheal are well demarcated but not stable; they may move to adjacent, uninvolved areas over periods of hours.

32
Q

⦁ Learn the history and key presenting features of Urticaria

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A

GENERALISED SYMMETRICAL rash, consisting of WELL DEFINED, ERYTHEMATOUS, URTICATED PAPULES AND PLAQUES Note: if we know they are transient (<24 hours) we can call them WHEALS
• Erythematous, pruritic ‘swellings’ (wheals) • Transient (<24 hours) +/-angioedema • Acute vs chronic (urticarial persisting for over 6 weeks) • Mast cell degranulation and histamine release leading to increased capillary permeability and leakage of fluid into surrounding tissue
• Clinical diagnosis
• Eliminate underlying cause (eg drug related) • High dose anti-histamines –second generation H1 anti histamines eg fexofenadine, cetirizine, loratadine • Acute course of oral steroids, ciclosporin, montelukast, H2 antihistamine, omaluzimab

Urticarial lesions may be rounded (F) or irregular (A) in shape and uniform or mixed (G) in morphology. Individual lesions may be small (H) or large (D). Urticaria are raised plaques, although they may appear flattened in patients taking antihistamines (C). Although lesions are consistently erythematous, this may be difficult to appreciate on darkly pigmented skin (I). Some urticaria show central clearing (E).

33
Q

⦁ Learn the history and key presenting features of Molluscum contagiosum
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A

LOCALISED, UNILATERAL skin condition consisting of MULTIPLE WELL DEFINED*, SHINY, DOME- SHAPED, UMBILICATED PAPULEs *(DISCRETE can be accepted)
•Pox virus infection •2-6 week incubation period •More common in atopic and immunocompromised patients •Most self resolve within 6-9 months •No treatment required

34
Q

⦁ Learn the history and key presenting features of Tinea Capis
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A

BODY- SOLITARY, WELL DEFINED, ERYTHEMA, SCALY, ANNULAR (with central clearing, as opposed to circular/discoid), PLAQUE SCALP- LOCALISED, SOLITARY, ERYTHEMA, SCALE with accompanying HAIR LOSS (PATCH of ALOPECIA)

35
Q

⦁ Learn the history and key presenting features of Drug exanthem

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A

GENERALIZED, MACULAR, PAPULAR, ERYTHEMATOUS (blanching) rash
•Often appear after a latent period required for induction. •Cell mediated immune reaction •Most common reaction is macular-papular (morbilliform) rash •Culprit drug avoidance important • Penicillins • Cephalosporins • Allopurinol • NSAIDs

36
Q

chronology, and morphology and localisation of uticaria, anjioedema, maculopapular exanthem, fixed frug eruption, pustular exanthem and vesicobullous exanthems

A

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37
Q

⦁ Learn the history and key presenting features of Shingles (herpes zoster infection)

A

LOCALISED, DERMATOMAL rash consisting of PAPULE, VESICULE, BULLA, EROSION, CRUST (some due to dry blood and exudate from vesicle content, some with yellow discoloration GOLDEN suggesting infection)
•Herpes virus varicella zoster-dermatomal(unilateral) •Attack usually result of re-activation of virus which has remained dormant in a sensory root ganglion since an earlier episode of chicken pox (varicella) •Elderly and immuno-compromised are at higher risk •Associated with burning pain •Duration is around 2-3 weeks
•Complications include secondary bacterial infection, paralysis (if motor nerve involvement), corneal ulcers and scarring if ophthalmic division of trigeminal nerve involved), neuralgic pain •Systemic acyclovir within 2 days of episode and analgesics

38
Q

⦁ Learn the history and key presenting features of Steven - Johnson syndrome / toxic epidermal necrolysis

A

The oral mucosa and the vermilion border are involved, with painful hemorrhagic erosions covered with a grayish-white membrane
Multiple bullae and areas of denuded epidermis are present.
Dermatologic emergency!
• Severe mucocutaneous reactions, most commonly triggered by medications, characterized by extensive necrosis and detachment of the epidermis. • Mucous membranes are affected in >90% of patients, usually at >2 distinct sites (ocular, oral, and genital) • SJS is the less severe condition, in which skin detachment is <10% of the body surface • TEN involves detachment of >30% of the body surface area • The incidence is much higher in patients with HIV or active cancer • SJS/TEN can occur in patients of any age. Female > Male 2:1 • The overall mortality rate among patients with SJS/TEN is approximately 30% (up to 50% for TEN) • Treatment is mainly supportive +/- steroids, immunosuppressive drugs
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39
Q

skin cancer?

A

research

Year 2 semester 4 integration for clinical application (7 decks)

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