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Medicine year 1 semester 2 > Case 8- skin diseases > Flashcards

Case 8- skin diseases Flashcards

1
Q

Impetigo pathogen

A

Staphylococcus aureus and occasionally Streptococcus pyogenes.

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2
Q

Impetigo- general

A

An acute, superficial skin infection that mainly affects people 0-4 and to a lesser extent 5-14yrs. It is either a primary condition or secondary to eczema, scabies and trauma. Transmission is via close contact or through infected objects like toys. There are two types bullous (70%) and non-bullous. Bullous refers to 1cm filled blister

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3
Q

Impetigo- presentation

A

Thin pustules or vesicles which break, forming a honey coloured crust. There will be mild erythema (reddening of the skin) and will heal without scarring. It is most commonly on exposed area like face and hands. Individuals can have associated lymphadenopathy, malaise and a mild fever.

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4
Q

Impetigo- treatment for localised non-bullous impetigo

A

Use hydrogen peroxide (1% cream), if it doesn’t work use a short course of topical antibiotics. If impetigo becomes widespread offer a short course of topical or oral antibiotics

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5
Q

Impetigo - treatment for widespread non-bullous impetigo

A

A short course of topical or oral antibiotics (fuisidic acid 2% cream)

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6
Q

Impetigo- treatment for Bullous impetigo / systemically unwell / high risk of complications

A

Offer a short course of oral antibiotics

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7
Q

Example of a topical antibiotic

A

Fusidic acid (2%) cream

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8
Q

Complications of impetigo

A

Impetigo can be serious in neonates and immunocompromised patients leading to life threatening complications. The complications; Cellulitis, Guttate psoriasis, Scarlet fever and Septicaemia

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9
Q

Cellulitis pathogen

A

Staphylococcus aureus

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10
Q

Cellulitis

A

A spreading bacterial infection of the deeper dermis and subcutaneous tissue

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11
Q

Cellulitis risk factors

A

Previous cellulitis, skin breaks, immunocompromised, oedema and obesity

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12
Q

Cellulitis presentation

A

pain, swelling (slightly raised), warmth, erythema (usually more diffuse)- infection is deeper in the dermis. It causes blisters or bullae. You may be systemically unwell with fever, malaise, rigors indication a deep seated infection, abscess or source of sepsis.

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13
Q

Pereorbital cellulitis

A

Inflammation and infection of the eyelid and skin around the eye anterior to the orbital septum. You should admit these patients to hospital to rule out orbital cellulitis which is a serious condition which can result in visual loss and meningitis

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14
Q

Cellulitis treatment systemically well

A

At home you receive a high dose of oral flucloxacillin. You draw around the erythema and add a date so you can see the progression or recession when examining the area again.

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15
Q

Cellulitis treatment- systemically unwell or comorbidities

A

At hospital you receive IV flucloxacillin. You draw around the erythema and add a date so you can see the progression or recession when examining the area again.

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16
Q

What does antibiotic choice depend on for a skin infection

A

If it is a recurrent infection, contamination levels (i.e. by seawater), the site e.g. eyes and nose, if it is an atypical infection.

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17
Q

Erysipelas pathogen

A

Streptococcus pyogenes

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18
Q

Erysipelas

A

A superficial form of cellulitis in the upper dermis. It is typically on the face or a butterfly pattern on the lower limbs

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19
Q

Erysipelas risk factors

A

Previous erysipelas, skin breaks, being immunocompromised, oedema and obesity

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20
Q

Erysipelas presentation

A

Pain, swelling (raised), warmth, erythema (well demarcated), infection is more superficial when compared to cellulitis. There will be blisters or bullae. More likely to be systemically unwell when compared to cellulitis with fever, malaise and rigors. Well bordered.

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21
Q

Treatment for erysipelas

A
  • First choice antibiotic- Flucloxacillin 500mg
  • If allergic to penicillin- Clarithromycin 500mg
  • If near eyes or nose- Co-amoxiclav
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22
Q

Preventing cellulitis or erysipelas

A

You should not routinely offer antibiotic prophylaxis to prevent cellulitis or erysipelas. If you do offer phenoxymethylpenicillin 250mg twice a day or erythromycin 250mg twice a day for penicillin allergy.

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23
Q

Necrotising fasciitis pathogen

A

Group A haemolytic streptococcus, Polymicrobial, Clostridium and marine organisms.

24
Q

Necrotising fasciitis

A

A rapidly spreading infection of the deep fascia

25
Q

Necrotising fasciitis risk factors

A

Abdominal surgery, diabetes and malignancy. 50% of infections are in previously healthy individuals

26
Q

Types of necrotising fasciitis

A
  • Fournier’s gangrene- affecting the perineal, genital and perianal region
  • Ludwig’s angina- affecting submandibular space
27
Q

Presentation of necrotising fasciitis

A

Severe pain which stops when the nerves are destroyed, purple rash, blisters filled with dark fluid, necrosis, oedema, crepitus (gas in tissue) and as critically unwell (fever, hypotension and tachycardia).

28
Q

Treatment for necrotising fasciitis

A

Intravenous antibiotics, make sure blood cultures have been taken. You will also need fluid resuscitation, urgent referral for extensive debridement by plastic surgeons. Hyperbaric oxygen chambers can be used with Clostridium infections to stop toxin production. Mortality is up to 76% and it will require reconstruction and skin grafts. The most serious skin infection.

29
Q

Hair follicle infection pathogen

A

S.aureus

30
Q

Hair follicle infection risk factors

A

Male, adolescent, contact sport, poor personal hygiene, pre-existing skin conditions, steroids, immunosuppression, obesity and malnutrition.

31
Q

Folliculitis

A

Superficial infection of the hair follicles causing papules and pustules

32
Q

Furuncles (boils)

A

Deeper infection of the hair follicle extending through the dermis and into the subcutaneous tissue where abscess’s form

33
Q

Carbuncles

A

The furuncles join into a mass with purulent drainage from multiple follicles

34
Q

Pseudofolliculitis

A

Inflammation due to ingrown hair

35
Q

Treatment for a hair follicle infection

A

Apply heat to the area, Analgesia (pain killers), good personal hygiene measured. May need IV antibiotics and admission if systemically unwell or oral antibiotics at home. In fluctuant furuncle or carbuncle refer to surgeons for incision and drainage.

36
Q

Maculopapillary rash

A

Consists of macules which are flat lesion less then 1.5cm and papules, a solid raised lesion smaller than 05cm.

37
Q

Measles

A

In the Paramyxoviridae family, early symptoms of high fever and the 3 C’s cough, coryza an conjunctivitis. Coryza is inflammation and irritation of the mucus membrane in the nose. You then get a Maculopapular rash.

38
Q

Vesicles

A

A raised, clear, fluid filled lesion which is less than 0.5cm

39
Q

Rubella

A

In the Paramyxoviridae family. Early symptoms of Lymphadenopathy (disease affecting the lymph nodes) in the head and neck. You then get a Maculopapular rash, it spreads from the face to the trunk and to the limbs.

40
Q

Parvovirus

A

Other name for the infection is Erythema infectiosum, fifth disease and slapped cheek disease. Its early signs are fever, coryza and nausea. You then get a slapped cheek rash, a Maculopapular rash to the trunk and arthritis.

41
Q

Herpes simplex virus

A
  • HSV1- oral or genital herpes.

* HSV2- genital herpes

42
Q

Varicella zoster virus (VSV)

A

1) Chickenpox- usually in children

2) Shingles- more common in adults who are immunosuppressed. There is reactivation of the virus after initial infection

43
Q

Causes of Vesicular rash

A

A rash caused by a viral infection. Caused by chicken pox, shingles, Enterovirus and Poxvirus

44
Q

Vasculitis

A

Inflammation of blood vessels, either arteries or veins. It is due to an autoimmune disease. It can be divided on the size of the vessel affected

45
Q

Types of vasculitis

A
  • Small- Granulomatosis with polyangiitis (GPA), microscopic polyangiitis, Henoch-Schonlein purpura (HSP).
  • Medium= Kawasaki disease, Polyarteritis nodosa
  • Large= Giant cell arteritis, Takayasu arteritis.
46
Q

Vasculitis pathology

A

Blood vessels become damaged leaving them prone to aneurysm, increases the chance of coagulation and produces fibrous vessel wall. The difference between the types of vasculitis are their triggers and where they cause pathology. Generalised symptoms are due to inflammation on the body. The specific symptoms depend on the location i.e. affected vessels can cause ischaemic damage to the organs they supply.

47
Q

Henoch-Schonlein purpura

A

Usually occurs in childhood. IgA immune complexes are present in the small blood vessels which trigger inflammation

48
Q

Presentation of Henoch- Schonlein purpura

A
  • Skin- purpuric rash (red or purple, non-blanching) usually to the back of legs.
  • Joints- knees and ankles
  • GI tract- abdominal pain, bloody diarrhoea, nausea and vomiting
  • Kidneys- proteinuria and haematuria
49
Q

Kawasaki disease

A

Occurs in children, thought to be due to an infection triggering an autoimmune response. It presents with a fever higher at 39 degree, a rash- red palms and soles with skin peeling away (desquamation). You get conjunctivitis and inflammation of the lips, tongue and mouth. It presents with Lymphadenopathy. It can affect the coronary arteries so suspected cases should present to hospital.

50
Q

Polyarteritis Nodosa

A

Peak incidence is at 10 years and between 40-50 years. You can have a systemic or cutaneous (less severe forms). Can be associated with a Hepatitis B infection. Cutaneous signs include tender papules and plaques, purpura (purple, non-blanching lesions), livedo reticularis (net-like mottled appearance to the skin), skin necrosis and ulceration.

51
Q

What does Polyarteritis Nodosa effect?

A
  • Peripheral nerves.
  • Kidneys- hypertension or acute kidney injury.
  • GI tract- abdominal pain after eating
  • Skin- legs and feet.
52
Q

Endocrine infection- diabetic dermopathy

A

Unknown cause, it is associated with damage to small blood vessels and nerves which occurs in diabetes. Dermopathy forms oval, light brown patches. It occurs over bony areas, it can form in response to injury in these areas. There is no treatment.

53
Q

Endocrine infection- Acanthosis Nigricans

A

Visualisation of insulin resistance, it also occurs due to certain medications or due to Malignancy’s (GI cancers). There is hyperpigmentation of skin especially in creases- neck, armpits and groin. Skin can become thicker.

54
Q

Endocrine infection- Eruptive xanthomotosis

A

A firm, yellow, pea like enlargement of the skin. It has a red halo and may be itchy. It is a sign of uncontrolled type 1 diabetes, often in young and people with raised triglycerides. Treatment would be diabetes management.

55
Q

Endocrine infection- Necrobiosis lipoidica diabeticorum (NLD)

A

NLD starts as a dull, red lesion then becomes a shiny scar with a violet border. It occurs on the shin and is a rare condition which is mainly seen in women. No treatment is recquired unless there are open sores.

56
Q

Connective tissue infection- Systemic lupus erythematosus (SLE)

A

Autoimmune condition with an unknown cause. Anti-nuclear antibodies (ANA) are present in most cases. It is more common in woman. Is relapsing and remitting in nature

57
Q

Presentation of systemic lupus erythematosus (SLE_

A
  • Skin- sun sensitivity, butterfly shaped rash to the face.
  • MSK- peripheral, symmetrical joint pain and stiffness.
  • Fatigue
  • Raynaud’s phenomenon- temporary reduction in blood supply to fingers and toes,
  • Kidney- nephritis
  • Heart- pericarditis
  • Lungs- pleuritis

Medicine year 1 semester 2 (61 decks)

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