Cellulitis; Pressure Sores; Head lice; Folliculitis; Contact Dermatitis Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

What are the different classes of cellulitis

A

Class I:
- There are no signs of systemic toxicity and the person has no uncontrolled co-morbidities

Class II:
- The person is either systemically unwell or systemically well but with a co-morbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection

Class III:
- The person has significant systemic upset such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable co-morbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromize

Class IV:
- The person has sepsis syndrome or a severe life-threatening infection such as necrotizing fasciitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which patients do you admit for cellulitis? [6]

A
  • Has Eron Class III or Class IV cellulitis.
  • Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
  • Is very young (under 1 year of age) or frail.
  • Is immunocompromized.
  • Has significant lymphoedema.
  • Has facial cellulitis (unless very mild) or periorbital cellulitis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe how you manage Eron Class I / II cellulitis [1]

A
  • oral flucloxacillin as first-line treatment for mild/moderate cellulitis
  • oral clarithromycin, erythromycin (in pregnancy) or doxycycline is recommended in patients allergic to penicillin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do you manage Class III/IV Cellulitis? [2]

A

Eron Class III-IV
* admit
* NICE recommend: oral/IV co-amoxiclav, oral/IV clindamycin, IV cefuroxime or IV ceftriaxone

General points
* mark the area of erythema to detect spreading cellulitis
* if possible elevate the leg
* consider paracetamol or ibuprofen for pain or fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
A

Flucoxacillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
A

Co-amoxiclav

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define what is meant by a pressure sore [1]

A

Localised injuries to the skin and underlying tissue due to prolonged pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the pathophysiology of pressure sores [3]

A

sequence of events initiated by unrelieved pressure:
- Ischaemia: when external pressure exceeds capillary closing pressure, it leads to occlusion of blood vessels causing ischaemia in the affected area. This deprives tissues of oxygen and nutrients leading to cell death and necrosis.
- Reperfusion injury: Upon relief from sustained pressure, reperfusion occurs. However, this sudden influx of blood can cause further damage due to oxidative stress and inflammation.
- Tissue distortion: Continuous mechanical stress can distort and damage cells directly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the stages in the development of pressure sores [4]

A

Non-blanchable erythema::
- Initial presentation involves reddening of the skin that does not turn white (non-blanchable) when pressed.
- The affected area may feel differently than surrounding skin – warmer or cooler, firmer or softer.

Partial-thickness skin loss:
- With continued pressure, there is partial-thickness loss involving epidermis or dermis.
- It presents as a shallow open ulcer with a red-pink wound bed without sloughing.

Full-thickness skin loss:
- Prolonged unrelieved pressure results in full-thickness tissue loss exposing subcutaneous fat but not muscle or bone. Slough may be present along with undermining or tunneling.

Full-thickness tissue loss with exposed bone, muscle or tendon:
- This is the most severe form of pressure sore where there is extensive destruction and necrosis extending to underlying structures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Beyond the 4 stages of pressure sores, what two categories of pressure sore exist? [2]

A

Unstageable Pressure Sores:
- This classification is used when the base of the ulcer is covered by slough (yellow, tan, grey, green or brown) and/or eschar (tan, brown or black) in the wound bed, making it impossible to determine its depth.

Suspected Deep Tissue Injury (SDTI):
- SDTI is characterised by a purple or maroon localised area of discoloured intact skin or a blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What investigations do you perform for pressure sores? [3]

A

Wound Swab
FBC; U&E; CRP & albumin levels
Radiological imaging - if ?osteomyelitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which score / scores are used to identify patients at risk of pressure sores? [2]

A

Braden or Waterlow scale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do you prevent / manage pressure sores [4]

A

Regular repositioning every 2 hours for bed-bound patients and hourly for those in chairs.

Maintain skin integrity by keeping skin clean and dry. Use mild soap and warm (not hot) water for cleaning

Dressings:
- Alginate dressings are useful for exuding wounds;
- Hydrocolloid dressings can be used for non-exuding wounds.

Administer analgesics as required. Regularly reassess pain levels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Long-standing pressure sores can occasionally give rise to [] - a type of squamous cell carcinoma.

A

Cancerous changes: Long-standing pressure sores can occasionally give rise to Marjolin’s ulcers - a type of squamous cell carcinoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

In addition to the typical presentations of head lice, there are other possible features associated with head lice infestation:

A

Secondary bacterial infection:
- Persistent scratching can lead to excoriation and subsequent bacterial superinfection, manifesting as impetigo or cellulitis.

Cervical lymphadenopathy:
- Swollen lymph nodes in the neck area may occur due to local inflammatory response or secondary infection.

Psychological distress:
- Patients, particularly children, may experience embarrassment, anxiety or sleep disturbances due to the infestation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

One of the primary challenges in diagnosing head lice (Pediculus humanus capitis) lies in distinguishing it from other conditions that present with similar symptoms, such as itching and visible evidence on the scalp.

What are the main three differential diagnoses? [3]

A

seborrhoeic dermatitis, dandruff, and folliculitis.

17
Q

How do you differentiate head lice to seborrhoeic dermatitis, dandruff, and folliculitis?

A

seborrhoeic dermatitis:
- Redness, greasy or oily areas of skin, white or yellowish crusty scales
- head lice itchier

Dandruff
- White flakes on shoulders of dark clothing, itchy scalp.

Folliculitis
- Red and inflamed hair follicles, pus-filled blisters that break open and crust over.
- Typically more painful than pruritic

18
Q

Which pathogen is the most common cause of follicullitis? [1]

A

Staphylococcus aureus

19
Q

Describe the basic pathophysiology of follicultiis

A
  1. Bacterial colonisation within the hair follicle (especially if there is any damage or disruption to skin barrier)
  2. An inflammatory response is triggered; leads to follicular wall rupture causing it to break down and release its contents (including bacteria) into the surrounding dermis.
  3. Leads to a cycle of ongoing tissue damage and repair
20
Q

Asides from pain, itching and small red inflamed papules, what is a key localised symptom seen in folliculitis? p[1]

A

Follicular hyperkeratosis: This describes thickening or roughness of the skin surrounding the hair follicle, which can be a feature in chronic cases.

21
Q

Name this subtype of folliculitis [1]

A

Pseudofolliculitis barbae: This is a specific type of folliculitis that commonly affects men with curly hair.
- It presents as inflammation and bumps in the beard area due to ingrown hairs.

22
Q

Hot tub folliculitis is associated with an infection from which pathogen? [1]

A

Pseudomonas aeruginosa:
- It typically presents as a sudden onset of widespread follicular-based papules and pustules, often on the trunk and limbs.

23
Q

What is the name for this form of folliculitis? [1]

A

Folliculitis decalvans
- A chronic form of deep folliculitis that leads to scarring and permanent hair loss, usually on the scalp. Patients may present with painful, red plaques containing pustules around hair follicles.

24
Q

How do you differentiate acne vulgaris to folliculitis?

A

Acne vulgaris predominantly affects the face and upper trunk where there is a high density of sebaceous glands.

folliculitis can occur anywhere on the body where hair follicles are present.

25
Q

Treatment algorithm for folliculitis? [2]

A

Topical treatments
* Mild cases can often be managed with topical antiseptics (e.g., chlorhexidine) or antibiotics (e.g., fusidic acid).
* If fungal infection suspected (e.g., Pityrosporum folliculitis), consider antifungal creams or shampoos containing ketoconazole.

Systemtic treatments:
- In severe or recurrent cases, consider oral antibiotics that cover Staphylococcus aureus (e.g., flucloxacillin).

26
Q

Why might reoccurring folliculitis occur? [2]

A

Antibiotic resistance or due to an an underlying disease such as diabetes

27
Q

Name these complications of folliculitis [1]

A
28
Q

Name for this? [1]

A

Sycosis barbae
- A specific type of deep folliculitis affecting the beard area in men, leading to scarring and hair loss if left untreated.

29
Q

A patient has a PMH of HIV.

Present with what appears to be folliculitis.

Which type of folliculitis is this most likely to be? [1]

A

Eosinophilic folliculitis: A variant seen in immunocompromised patients (e.g., HIV/AIDS) presenting with recurrent itchy papules and pustules predominantly on the face and upper body.

30
Q

; Co

Describe the difference between irritant and allergic contact dermatitis

A

Irritant Contact Dermatitis
- The process commences when an irritant breaches the stratum corneum, the outermost layer of the skin. This occurs because of direct physical or toxic damage to skin cells.

Allergic contact dermatitis:
- involves skin inflammation via an underlying allergic process (type 4 delayed hypersensitivity reaction). Allergy usually develops after an initial sensitisation event.

31
Q

Common examples of allergens that can result in dermatitis include [4]

A
  • Metals (e.g. Nickel)
  • Personal care products (e.g. preservatives used in cosmetic products; fragrances used in perfumes and body washes; nail varnish; and hair dyes).
  • Topical medications (e.g. antibiotics and steroids)
  • Plants (e.g. sunflower)
32
Q

What is the gold standard ttest for allergic contact dermatitis?

A

Patch testing:
- It involves the application of allergens to the skin under occlusion for 48 hours, followed by readings at 48 and 96 hours.

33
Q

What clinical sign often helps to distinguish that a patient is suffering from irritant contact dermatitis c.f allergic?

A

the sentinel sign - and is commonly caused by prolonged contact with water.

34
Q

How do you differentiate atopic dermatitis to contact determatitis? [1]

A

Atopic dermatitis frequently has an early onset in childhood and may be associated with a personal or family history of atopy.

Atopic dermatitis typically affects the flexural surfaces such as the antecubital and popliteal fossa; this contrasts with contact dermatitis where lesions tend to localise to areas of direct exposure.

35
Q

Management of contact dermatitis?

A

Avoiding allergens

Topical corticosteroids are first-line treatment for acute flares.

36
Q

Define urticaria [1]

A

Urticaria is a skin rash characterised by red, raised, itchy areas that result from release of chemical mediators such as histamine

Urticaria is due to the release of inflammatory mediators by mast cells and basophils in the upper dermis.

37
Q

What should you ask if a patient has come into contact in if you suspect they have urticaria? [6]

A

Recent illnesses
New medications
Food ingestion
Exercise/physical exertion
Insect bites/stings
Travel history

38
Q

Urticaria is which type HS reaction? [1]

A

Type 1 (IgE mediated)

39
Q

How do you manage urticaria? [3]

A

It is critical that all patients presenting with urticaria are assessed for a more systemic allergic reaction (e.g. anaphylaxis) or angio-oedema affecting the airway due to laryngeal oedema

non-sedating antihistamines (e.g. loratadine or cetirizine) are first-line
- NICE Clinical Knowledge Summaries suggest continuing these for up to 6 weeks following an episode of acute urticaria CKS

a sedating antihistamine (e.g. chlorphenamine) may be considered for night-time use (in addition to day-time non-sedating antihistamine) for troublesome sleep symptoms CKS

prednisolone is used for severe or resistant episodes