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Pathophysiology > Skin Disorders > Flashcards

Skin Disorders Flashcards

1
Q

Inflammatory Skin Disorders

A

are Inflammatory conditions that often manifest as visible skin lesions.

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2
Q

Atopic Dermatitis: Aetiology and Pathophysiology

A

Chronic skin condition linked to genetic factors and an overactive immune response.
“Inside-out” theory: immune dysfunction damages the skin barrier.
“Outside-in” theory: skin barrier damage triggers immune response.
Characterized by increased production of proteases, which break down skin tissue.
Exacerbated by factors raising skin’s pH, Staphylococcus aureus, or dust mites.

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3
Q

Atopic Dermatitis: Clinical manifestations

A

Presents as itchy, red, and scaly lesions, commonly on cheeks, scalp, and limbs.
Severe cases may develop weepy, crusty lesions; affected areas may thicken over time.
Disease course involves flare-ups and remission periods.

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4
Q

Atopic Dermatitis: Diagnosis

A

Primarily clinical, based on visual inspection, patient history, and age consideration.
No specific lab tests, though secondary infections may be detected microbiologically.

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5
Q

Atopic Dermatitis: Management

A

Proper skin hygiene with pH-neutral cleansers and fragrance-free moisturizers.
Topical corticosteroids are key during flare-ups; antihistamines manage itching.
Systemic immunomodulators may be required in severe cases.
Preventing secondary infections through meticulous hygiene is crucial.

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6
Q

Contact Dermatitis: Aetiology and Pathophysiology

A

Occurs when skin reacts to an exposure to an irritant, allergen, or photosensitizing substance, leading to inflammation.
Three types:
Irritant contact dermatitis: Caused by direct skin damage from a substance.

Allergic contact dermatitis: Delayed hypersensitivity reaction following allergen exposure after initial sensitization.

Photo contact dermatitis: Ultraviolet light activates a substance on the skin, causing a reaction.

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7
Q

Contact Dermatitis: clinical manifestations

A

Irritant contact dermatitis: Redness and scalded appearance in exposed areas.
Allergic contact dermatitis: Delayed reaction with redness, small raised bumps, and sometimes blisters.
Photo contact dermatitis: Redness, itching, and in severe cases, burning pain or eczema-like lesions in sun-exposed areas.

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8
Q

Contact Dermatitis: Diagnosis

A

Mainly clinical, based on patient history and visual examination.
Skin patch testing can identify specific allergens in allergic contact dermatitis

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9
Q

Contact Dermatitis: Management

A

Identify and remove the causative agent.
Irritant contact dermatitis: Use barrier creams and pH-balanced cleansers to reduce inflammation.
Allergic contact dermatitis: Treated with topical corticosteroids; systemic corticosteroids for severe cases.
Photo contact dermatitis: Strict sun protection and avoidance of triggering substances.

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10
Q

Stasis Dermatitis: Aetiology and Pathophysiology

A

Linked to chronic venous insufficiency, particularly in older adults with heart or liver failure.
Dysfunctional venous valves decrease blood flow, leading to inflammation, hypoxia, and skin damage due to impaired circulation.

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11
Q

Stasis Dermatitis: Clinical Manifestations

A

Typically presents as swollen, reddish-brown skin, often on the lower legs.
Discoloration is due to the buildup of blood cell breakdown byproducts.
Increases the risk of secondary infections in affected areas.

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12
Q

Stasis Dermatitis: Diagnosis

A

Based on clinical assessment, including visual inspection and patient history focusing on venous insufficiency.
No specific lab tests; microbiological analysis may identify secondary infections.

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13
Q

Stasis Dermatitis: Management

A

Aim to improve venous circulation through limb elevation, compression therapy, and wound care.
Use topical corticosteroids to reduce inflammation.
Good hygiene is crucial to prevent infections.

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14
Q

Incontinence-associated Dermatitis: Aetiology and Pathophysiology

A

Caused by prolonged skin exposure to urine or feces, leading to chemical irritation, increased microbial activity, and physical damage.
Ammonia from urine raises skin pH; enzymes in feces further irritate the skin.
Friction from cleaning or incontinence products worsens inflammation and weakens the skin’s barrier.

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15
Q

Incontinence-associated Dermatitis: clinical manifestations

A

Early symptoms include redness and tenderness in the perineal area.
Progression may lead to white, wrinkled, and weepy skin.

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16
Q

Incontinence-associated Dermatitis: Diagnosis

A

Based on visual examination and patient history of incontinence.
Testing for bacterial or fungal infections is possible but not necessary for diagnosis.

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17
Q

Incontinence-associated Dermatitis: Management

A

Prevention is key, with barrier creams and proper hygiene practices.
Use pH-balanced cleansers and moisturizers to protect the skin and reduc e redness.
Address underlying causes of incontinence to prevent recurrence.

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18
Q

Psoriasis Vulgaris: Aetiology and Pathophysiology

A

Chronic inflammatory skin condition caused by an autoimmune disorder.
About 30% of individuals have a family history, indicating a genetic component.

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19
Q

Psoriasis Vulgaris: Clinical Manifestations

A

Appears as red, inflamed patches of skin covered with silvery-white scales.
Often accompanied by itching, pain, and discomfort.

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20
Q

Psoriasis Vulgaris: Diagnosis

A

Primarily based on visual inspection and patient history; no specific lab tests.
Microbiological analysis may identify infections contributing to the lesion.

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21
Q

Psoriasis Vulgaris: Management

A

Topical corticosteroid creams reduce inflammation.
Moisturizers are helpful and more affordable.
Antibacterial agents and anti-itch treatments provide additional relief.
Topical vitamin D analogues may be used with corticosteroids for positive results.

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22
Q

Superficial Skin Infections

A

Caused by bacteria, viruses, parasites, or fungi.
Complexity depends on the type of organism, immune function, and skin condition.

23
Q

Acne Vulgaris - Bacterial skin infection: Aetiology and Pathophysiology

A

Caused by blocked hair follicles and sebaceous glands with sebum and dead skin cells.
Blockage leads to colonization by skin bacteria, triggering an inflammatory response.

24
Q

Acne Vulgaris - Bacterial skin infection: Clinical Manifestations

A

Presents as two types of lesions: blackheads and whiteheads.

25
Q

Acne Vulgaris - Bacterial skin infection: Diagnosis

A

Primarily based on visual inspection of lesions.
Microbiological testing generally unnecessary, considered in severe cases.

26
Q

Acne Vulgaris - Bacterial skin infection: Management

A

Proper hygiene is essential.
Cleansing agents reduce infection and inflammation.
Antibiotics may be prescribed for severe cases.
Retinoid treatments reduce sebum production, bacterial colonization, and inflammation.

27
Q

Tinea - Fungal skin infection: Aetiology and Pathophysiology

A

Tinea infections are caused by dermatophyte fungi that thrive on keratin in nails, hair, and the stratum corneum.

28
Q

Tinea - Fungal skin infection: clinical manifestations

A

Scalp: Scaly, itchy lesions.
Groin (jock itch): Small, scaly, red patches on inner and upper thighs, worsen in heat and humidity.
Feet (athlete’s foot): Scaly, white, wrinkled skin between toes, often causing pain.
Hands: Dry, scaly, and red lesions.
Nails: Yellow or brown brittle keratin accumulation across the nail.
Other body areas: Circular, red, and scaly lesions.

29
Q

Tinea - Fungal skin infection: Diagnosis

A

Visual examination and patient history assessment.
Samples from affected skin, hair, or nails can be examined using direct microscopy`.

30
Q

Tinea - Fungal skin infection: Management

A

topical or oral antifungal medications based on infection location.
Emphasize proper hygiene practices in management.

31
Q

Candidiasis/Thrush - Fungal skin infection: Aetiology and Pathophysiology

A

Thrush is caused by an overgrowth of yeast, typically Candida albicans.

Candida normally resides harmlessly on skin and mucous membranes, but environmental changes can trigger overgrowth.

Candida infection occurs when multiple immune and non-immune defenses are compromised.

32
Q

Candidiasis (Thrush) - Fungal skin infection: Clinical Manifestations

A

Presents as a soft, red rash or a thick, white coating or discharge, depending on the affected area.
Commonly causes itching and may result in redness.

33
Q

Candidiasis (Thrush) - Fungal skin infection: Diagnosis

A

Involves visual examination and review of patient history and risk factors.
Samples from affected areas may be taken for direct microscopy.
Pathology tests and blood cultures assess systemic infection; serology detects Candida antibodies.

34
Q

Candidiasis (Thrush) - Fungal skin infection: Management

A

In immunocompetent individuals, proper hygiene and antifungal treatments restore the skin barrier.
In immunosuppressed individuals, a longer treatment course may be necessary.

35
Q

Human Papillomavirus (HPV) - Viral skin infection: Aetiology and Pathophysiology

A

Warts are caused by the human papillomavirus (HPV), with over 100 strains leading to different types of warts.
Some HPV strains are linked to cancer, but most do not contribute to malignancies.

Common warts –> hands and knees;
flat warts –> hands, face, and lower legs.
Genital warts –> penis, vulva, or anus
plantar warts –> soles of the feet.

36
Q

Human Papillomavirus (HPV) - Viral skin infection: clinical manifestations

A

The appearance of warts varies based on location and virus strain.
Most warts are painless, except plantar warts, which can cause discomfort due to walking pressure.

37
Q

Human Papillomavirus (HPV) - Viral skin infection: Diagnosis

A

Based on visual inspection, considering wart morphology and location.
Histological and serological confirmation of HPV is generally unnecessary.

38
Q

Human Papillomavirus (HPV) - Viral skin infection: Management

A

Treatment options for non-genital warts include no intervention or removal techniques.

Removal methods: freezing with liquid nitrogen, laser treatment, or scraping with electrical current to stop bleeding.

Topical treatments may be effective depending on wart type and location.

39
Q

Herpes Simplex Virus (HSV) - viral skin infection: Aetiology and Pathophysiology

A

HSV-1 typically causes cold sores on the mouth, tongue, and lips.
HSV-2 is responsible for genital herpes.

40
Q

Herpes Simplex Virus (HSV) - viral skin infection: clinical manifestations

A

HSV-1: Painful lesions cluster around the mouth, highly contagious, dry out and form a crust within days.
- Inflammation, redness, and swelling are common; viral shedding occurs during active infections and asymptomatically.

HSV-2: Painful lesions cluster around the genital area, buttocks, and legs; affected area becomes swollen and red.

41
Q

Herpes Simplex Virus (HSV) - viral skin infection: Diagnosis

A

Primarily based on visual inspection and patient history; serological tests can confirm the virus but may not impact management.

42
Q

Herpes Simplex Virus (HSV) - viral skin infection: Management

A

Lesions are usually self-limiting; over-the-counter topical or oral antiviral medications are most effective when used early (before virus replicates extensively)

In immunocompromised individuals, intensive treatment may be required, including hospitalization, antiviral medications, pain management, and IV fluids for hydration.

43
Q

Chronic Wounds: Aetiology and Pathophysiology

A

Chronic wounds do not heal within the expected timeframe, remaining unhealed for over 3 months.
Linked to conditions like diabetes, venous insufficiency, arterial disease, or prolonged pressure.
Involves persistent inflammation, tissue hypoxia, bacterial colonization, and impaired cellular responses.
Disruption in the balance between tissue repair and breakdown leads to non-healing wounds.

44
Q

Chronic Wounds: Clinical Manifestations

A

Venous ulcers: Located on the lower legs, irregular edges, shallow depth, significant exudate, surrounding skin may show brown discoloration and stasis dermatitis.

Arterial ulcers: Found on toes, feet, or pressure points, well-defined edges, pale base, minimal exudate, surrounding skin is shiny, cool, and hairless, with diminished or absent pulses.

Diabetic ulcers: Occur on feet, often over pressure points, deep with high infection risk, surrounded by calloused skin.

Pressure ulcers: Develop over bony prominences in immobile patients, range from superficial redness to deep tissue damage extending to muscle or bone.

45
Q

Chronic Wounds: Diagnosis

A

Clinical assessment of wound appearance, location, characteristics, and patient history.

Identify wound type (venous, arterial, diabetic, or pressure ulcer) based on location and characteristics.

Assess for infection signs: increased pain, redness, warmth, or purulent exudate.

Evaluate underlying conditions (diabetes, vascular disease, immobility).

Diagnostic tests: wound cultures, blood tests, imaging studies like Doppler ultrasound.

46
Q

Chronic Wounds: Management

A

Wound care: Regular cleaning, debridement, appropriate dressings for exudate

management and moist healing.
Infection control: Topical or systemic antibiotics based on wound culture results.

Relieving pressure for diabetic and pressure ulcers: Specialized footwear, mattresses, repositioning techniques.

Enhancing blood flow for venous or arterial ulcers: Compression therapy or revascularization procedures.

Managing underlying conditions (e.g., diabetes), ensuring adequate nutrition and hydration.

Advanced therapies: Negative pressure wound therapy, hyperbaric oxygen therapy, growth factors, or skin substitutes for challenging chronic wounds.

47
Q

Burns

A

Injury to the skin caused by extreme heat, cold, chemicals, radiation, or electricity.
Severity and outcome depend on burn size, depth, location, and age of the affected person.

48
Q

Superficial Burns: Aetiology and Pathophysiology

A

Affect only the epidermis (outer skin layer), minimal damage.
Typically heal within 3–6 days without scarring; sunburn is a common example.

49
Q

Partial-thickness Burns: Aetiology and Pathophysiology

A

Divided into superficial and deep partial-thickness burns.
Superficial: Impact epidermis and part of the dermis, healing within about two weeks without scarring.
Deep: Extend further into the dermis, may take over three weeks to heal, often result in scarring.

50
Q

Full thickness Burns: Aetiology and Pathophysiology

A

Destroy both epidermis and dermis, may extend into subcutaneous tissue, muscle, or bone.
Do not heal without medical intervention, always result in scarring.
Common causes include flames, chemicals, or high-voltage electricity

51
Q

Burns: clinical Manifestations

A

Burns cause redness, increased blood flow, and swelling; skin may blanch when pressed.

Superficial burns: Initially painful, may become itchy as the skin peels.
Superficial partial-thickness burns: Moist, red, blistered, with pain that worsens with air or temperature changes
.
Deep partial-thickness burns: Pale, mottled, or dry, with deeper burns being drier and paler.

Full-thickness burns: White, yellow, brown, or charred, numb due to nerve damage, with surrounding areas possibly still painful.

52
Q

Burns: Diagnosis

A

Visual inspection and patient history are key; estimating burn size is crucial for treatment planning.
Blistering suggests superficial partial-thickness burns; deeper burns show less blanching and varied appearance.
Full-thickness burns identified by waxy, avascular appearance, possibly charred or leathery tissue.

53
Q

Burns: Management

A

Control pain, prevent infection, protect against hypothermia and dehydration, support metabolic needs.

Superficial burns: Basic pain relief, fluid intake, moisturizers; IV fluids for large burns in vulnerable people.

Partial-thickness burns: Treat in specialized burn units if >10% of the body is affected; clean, debride, and dress wounds; deep burns may need skin grafting.

Full-thickness burns: Complex, extended treatment, high risk of complications, including infection and graft rejection, requiring ongoing medical care.

54
Q

Scarring: Aetiology and Pathophysiology

A

Viewed as a pathology (function of the body) related to the wound healing process.
Keloid scars: Result from excessive cellular activity, disrupting balance between tissue formation and apoptosis; scar tissue extends beyond original wound margins, with thicker epidermal layer and disorganized collagen.
Hypertrophic scars: Caused by excessive collagen accumulation, but scar growth remains confined to the original injury site.
Widened scars: Occur due to excess tension on wound edges during healing, leading to gaping wounds; often associated with secondary intention healing and infection.

Pathophysiology (9 decks)

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