Lecture 8 Flashcards

(59 cards)

1
Q

Whata re the layers of the skin?

A
  • Epidermis
  • Dermis
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2
Q

Erythema

A

a type of skin rash or a
change in colour of an area of skin, caused by increased blood flow in certain capillaries

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3
Q

Papules

A

elevated lesions that
frequently appear in groups

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4
Q

Plaque

A

a collection of papules or
nodules

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5
Q

Vesicle

A

a small, fluid-filled blister that is
smaller than 0.5 cm in diameter

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6
Q

Macule

A

a flat, distinct, discoloured
area of skin less than 1cm wide

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7
Q

Nodules

A

elevated lesions on the skin that
are smaller than two millimetres in diameter with slightly hard consistency

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8
Q

Scales

A

lumps of skin cells that pile up and break off the surface of the skin

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9
Q

Crust

A

also known as a scab, is a type of
skin lesion that develops on top of a scratched, damaged, or irritated original skin lesion

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10
Q

Ulcer

A

a break in the skin’s or mucosa’s
continuity

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11
Q

Allergic Contact Dermatitis

A

Immune-mediated skin condition caused by exposure to allergens that trigger a delayed hypersensitivity reaction

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12
Q

What is the etiology of allergic contact dermatitis?

A

Results from the contact of an offending chemical antigen and subsequent T-cell mediated response

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13
Q

Antigens of Contact Dermatitis

A
  • Poison ivy
  • Nickel
  • Rubber gloves
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14
Q

What are the 2 phases of ACD?

A
  • Sensitisation phase
  • Elicitation phase
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15
Q

What is the sensitisation phase of ACD?

A

When the skin is first exposed to an allergen
- contact of the allergen to the skin
* taken up by langerhans cells
* migrate towards regional lymph nodes
* antigens contact with the adjacent T-lymphocytes
* formation of antigen-specific t-lymphocytes

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16
Q

What is the elicitation phase of ACD?

A

Re-exposure to the antigen
- triggers a cytokine-induced proliferation process
- localised inflammatory response

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17
Q

Clinical Presentation of ACD?

A
  • limited to sites of direct contact with triggering agent
  • pruritus (itchiness) is characteristics
  • new lesions take the form of erythematous papules, which ooze and become crusted
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18
Q

Diagnosis ACD

A

Detailed history and physical examination
- Patch testing
- Skin biopsy

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19
Q

Management of ACD

A
  • Avoidance of triggering agents
  • Anti-inflammatory drugs such as topical steroids and oral corticosteroids
  • Topical calcineurin inhibitors
  • Symptomatic
  • Antihistamines
  • Cool water soaks
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20
Q

Erythema Multiforme (EM)

A

An acute condition, sometimes recurrent, of the skin and mucosal membranes
- characterised by a wide array lesions, which may include macules, papules, vesicles and bullae

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21
Q

Aetiology of Erythema Multiforme

A
  • Herpes
  • Mycoplasma pneumoniae
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22
Q

Medications for EM?

A
  • Sulfonamides
  • Penicillin
  • Salicylates
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23
Q

Erythema Multiforme Pathophysiology

A

HSV-associated EM: HSV DNA found in lesions → damage via type IV cell-mediated immunity.

Drug-induced EM: earliest feature = keratinocyte necrosis.

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24
Q

Clinical presentations of erythema multiforme

A

A fever and a feeling of general unwell
- Target lesion
- Trunk is often spared
- Muscosal lesions
- Pulmonary signs

25
Management of EM
- Supportive treatment: oral rinses, topical anesthetics for pain and maintaining hydration - Etiological treatment when a cause is identified: azithromycin & antiviral
26
Psoriasis
- Chronic immune-mediated skin disorder characterised by the rapid growth of skin cells = thick, scaly patches - Up to 10% is associated with arthritis
27
What is the etiology and triggers of psoriasis?
Autoimmune (T-cell mediated), HLA-associated Better in summer, worse in winter Drugs: chloroquine, lithium, β-blockers, steroids, NSAIDs Triggers: infections, stress, alcohol, smoking, obesity, hypocalcemia
28
What are the clinical features of psoriasis?
Well-defined erythematous plaques with silvery scales Sites: scalp, knees, elbows, lumbosacral region (extensors) Koebner phenomenon: trauma → new lesions Nail changes: pitting, dystrophy, “oil drop,” onycholysis ~30%: psoriatic arthritis
29
Management of Psoriasis
Medications: - Drug of choice is methotrexate - Cyclosporine - When patients fail to respond to methotrexate, switch to biological agents Phototherapy
30
Actinic Keratosis
Premalignant skin tumor Usually occurs in skin exposed to: - Sum-damaged - Ionising radiation - Industrial hydrocarbons Skin and exhibits hyperkeratosis
31
Morphology of Actinic Keratosis
Typically tan-brown, red, or skin-coloured and have a rough, sandpaper-like consistency
32
Histology of Actinic Keratosis
The stratum corneum is thickened(hyperkeratosis) and parakeratosis (retain their nuclei) * Basal cell layer atypia (dysplasia)
33
Progression of Actinic Keratosis
Premalignant lesion from sun damage May regress, persist, or progress Risk of progression → squamous cell carcinoma
34
What is squamous cell carcinoma (SCC)?
Malignancy of epidermal keratinocytes
35
Where does SCC commonly occur and in whom?
2nd most common tumor on sun-exposed skin Older adults Male > female
36
What precursor lesions are associated with SCC?
Actinic keratosis Keratinocytic dysplasia SCC in situ (confined to epidermis)
37
What are causes of squamous cell carcinoma
- DNA damage induced by V - Immunosuppression
38
What are the risk factors of squamous cell carcinoma?
- Industrial carcinogens - Chronic ulcers - Old burn scars - Ingestion of arsenicals - Ionising radiation
39
What is the key early genetic event in SCC pathogenesis?
p53 dysfunction from UV-induced DNA damage
40
How does UV light promote SCC?
Causes DNA damage → error-prone repair → mutations passed to daughter cells
41
What other signaling pathways contribute to SCC transformation?
↑ RAS signaling ↓ Notch signaling
42
Morphology of SCC
- Most often in sun exposed areas - Thin = erythematous scaly thin papule or plaque - Thick = erythematous plaque, nodule, ulcer
43
Histopathology of SCC
Cells are atypical involve all levels of epidermis - variable degrees of cell differentiation
44
Treatment of SCC
- Surgical excision with adequate margins - Immunotherapy is inoperable - Curettage, electrodessication, cryotherapy
45
Basal Cell Carcinoma
- Locally aggressive skin malignancy - Associated with mutations that activate the hedgehog signaling pathway
46
Risk factors of basal cell carcinoma
- Sun-exposed sites in lightly pigmented elderly adults - Immunosuppression - Disorders of DNA repair
47
What genetic pathway is central to BCC pathogenesis?
Hedgehog signaling pathway (uncontrolled activation)
48
What is the role of PTCH in normal Hedgehog signaling?
PTCH binds SMO (inhibits it) When SHH binds PTCH → PTCH releases SMO → normal tissue development
49
How do PTCH mutations cause BCC?
Mutated PTCH fails to inhibit SMO SMO stays active → uncontrolled cell division
50
Morphology of BCC
Shiny, skin-colored/translucent nodule with visible vessels Pigmented lesion (brown/black/blue) Flat, scaly patch with raised edge White, waxy, scar-like lesion with ill-defined border
51
Malignant Melanoma
- Arise from melanocyte in the skin - UV exposure is main factor - Greater in male than female
52
Risk Factors for Malignant Melanoma
- Fair skinned populations - Family history - Intense intermittent sun exposure - Increased mole count - Dysplastic nevus phenotype - Immunosuppression
53
What factors contribute to melanoma pathophysiology?
Genomic, environmental, and host interactions Multistep progression
54
Which cell cycle control gene is commonly mutated in melanoma?
CDKN2A
55
Which pro-growth pathways are frequently involved in melanoma?
RAS PI3K/AKT signaling
56
Which telomerase gene mutation contributes to melanoma?
TERT gene
57
What are the key morphological features of malignant melanoma?
Multiple colors: black, brown, red, blue, gray Irregular borders Follows ABCDE rule
58
What does ABCDE stand for in melanoma?
A – Asymmetry B – Border irregularity C – Color variation D – Diameter > 6mm E – Evolving lesion
59
What is the management of melanoma?
- Wide surgical excision - Sentinel lymph node biopsy - Adjuvant/systemic therapy starting - Chemotherapy - Radiotherapy