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Year 4 Derm > Emergencies > Flashcards

Emergencies Flashcards

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1
Q

What may be the cause of urticuria (hives), angioedema, anaphylaxis?

A 
Idiopathic 
Food- nuts, sesame seeds, shellfish, dairy 
Drugs- penicillin, contrast media, NSAIDS, morphine, ACE-I 
Insect bites 
Contact- latex 
Viral or parasitic infections 
Auto-immune 
Hereditary
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2
Q

What is urticuria due to?

A

A local increase in permeability of capillaries and small venules
A large no. of inflammatory mediators- prostaglandins, leukotrienes, chemotactic factors play a role but histamine derived from skin mast cells is the major mediator.
Local mediator release from mast cells can either be induced by immunological or non immunological mechanisms

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3
Q

How does urticuria present?

A

itchy wheals- swelling involving the superficial dermis, raising the epidermis

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4
Q

How does angio-oedema present?

A

This is a deeper swelling involving the dermis and subcutaneous tissues, it causes swelling of the tongue and lips

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5
Q

How does anaphylaxis present?

A

This is also known as anaphylactic shock
Results in-
Bronchospasm
Facial and laryngeal oedema
Hypotension
can present initially with urticaria and angioedema

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6
Q

What is the management for urticaria, angio oedema and anaphylaxis?

A

Urticuria- antihistamine ie: cetirizine
Angio-oedema- corticosteroids (these can also be used in sever acute urticaria)

Adrenaline, corticosteroids and antihistamines are all used for anaphylaxis.

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7
Q

What are the complications of urticaria, angio-oedema and anaphylaxis?

A

Urticaria is normally uncomplicated

Angio-oedema and anaphylaxis can lead to asphyxia, cardiac arrest and death

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8
Q

What is erythema nodosum?

A

A hypersensitivity response to a variety of stimuli

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9
Q

What are the causes of erythema nodosum?

A 
Group A beta haemolytic streptococcus 
Primary tuberculosis 
Pregnancy 
Malignancy 
Sarcoidosis 
IBD 
Chlamydia 
Leprosy (chronic progressive bacterial infection)
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10
Q

What is the presentation of erythema nodosum?

A

Discrete tender nodules which may become confluent
Lesions continue to appear 1-2 weeks and leave bruise like discolouration as they resolve
Lesions do not ulcerate and resolve without atrophy or scarring

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11
Q

What are the main site for erythema nodosum?

A

The shins are the main site!

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12
Q

What is erythema multiforme?

A

An cute self limiting inflammatory condition
Herpes simplex virus is the main precipitating factor
Other infections and drugs are also causes
Mucosal involvement is absent or limited to only one mucosal surface

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13
Q

What is Stevens-Johnson syndrome?

A

Rare but serious disorder that affects the skin, mucous membrane, genitals and eyes
It is usually caused by an unpredictable adverse reaction to certain meds and sometimes can be caused by an infection

The syndrome begins with flu like symptoms, followed by a red or purple rash that spreads and forms blisters, the affected skin eventually dies and peel off.

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14
Q

What are the causes of steven johnson syndrome?

A

In children it is usually triggered by a viral infection..

  • mumps
  • flu
  • herpes simplex virus
  • coxsackie virus
  • epstein barr virus (causes glandular fever)

Less commonly bacterial infections can trigger the syndrome

In adults, steven johnson syndrome is often caused by an adverse reaction to medicine
- allopurinol, carbamazepine, lamotrigine, nevirapine, phenytoin, sertraline, sulfasalazine

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15
Q

How does steven johnson syndrome typically present?

A

Flu like symptoms present during the initial stages
Aftera few days a rash appears, which consists of indicidual blemishes, that may look like a target

The rash isn’t usually itchy and spreads over a number of hours or days

Large blisters develop on the skin after the rash which leave painful sores after bursting

Facial swelling and swollen lips covered in crusty sores are common features

The mucous membranes inside your mouth, throat, eyes and genital tract may also become blistered and ulcerated (this can lead to dehydraton :(

The surface of the eyes can also be affected, which can cause corneal ulcers and vision problems if they are not treated quickly.

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16
Q

How do you manage steven johnson syndrome/toxic epidermal necrosis?

A

First step is to stop taking the mediations causing steven johnson syndrome

Analgesia- help ease raw areas of skin

Cool, moist compresses held against the skin

Regularly applying a plain (unscented) moisturiser to the skin

Replacement fluids

Mouthwashes with anaesthetic or antiseptic to make swallowing easier

Short course of corticosteroids (topical)

Abx (if sepsis)

Eyedrops or eye ointment (for eye symptoms)

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17
Q

What is toxic epidermal necrolysis?

A

This is usually drug induced,
causes full skin thickness separation
It is a variant of the steven johnson syndrome

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18
Q

How does staphylococcus scalded skin syndrome present?

A

Usually affects infants 3-7 days old
presents with erythematous bullae all over containing clear fluid which frequently rupture
Preceded by a staph aureus infection

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19
Q

What anti-epileptic is most likely to cause Steven Johnson syndrome?

A

Phenytoin

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20
Q

What is meningococcal disease?

A

This is an illness caused by the bacteria neisseria meningitidis

The two common presentations are meningococcal meningitis (infection of the membranes surrounding the brain and spinal cord) and meningococcemia (infection of the bloodstream)

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21
Q

What are the features of meningitis?

A

Headache, fever, neck stiffness
symptoms of septicaemia- hypotension, fever, myalgia, typical rash
Non blanching purpuric rash on the trunk and extremities

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22
Q

What is the management of acute meningococcaemia?

A

Ceftriaxone
For children- Treat children younger than 3 months with suspected bacterial meningitis without delay using intravenous cefotaxime plus either amoxicillin or ampicillin.

Prophylactic abx (rifampicin) for close contacts (ideally within 14 days of exposure

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23
Q

What are the complications of meningococcaemia?

A

Septicaemia shock
DIC
Multi organ failure
Death :(

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24
Q

What is erythroderma? (Red skin)

A

Inflammatory skin disease with erythema and scaling which affects nearly all the cutaneous surface.

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25
Q

What are the causes of erythroderma?

A

Previous skin disease- eczema, psoriasis
Lymphoma
Drugs (Sulphonamides, gold, sulphonylureas, penicillin, allopurinol, captopril) and idiopathic

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26
Q

What is the presentation of erythroderma?

A

Skin appears inflamed, oedematous and scaly

Systemically unwell with lymphadenopathy and malaise

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27
Q

What is the management of erythroderma?

A

Treat underlying cause, if known
Emollients and wet wraps to maintain skin moisture
Topical steroids to relieve inflammation

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28
Q

What are the complications of erythroderma?

A 
secondary infection 
fluid loss and electrolyte imbalance 
Hypothermia 
High output cardiac failure 
Capillary leak syndrome  (most severe)
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29
Q

What is the prognosis for erythroderma?

A

largely depends on the underlying cause

the overall mortality rate ranges from 20-40%

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30
Q

What is eczema herpeticum?

A

This is a widespread eruption- serious complication of atopic eczema or less commonly other skin conditions
Caused by herpes simplex virus

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31
Q

What is the presentation of eczema herpeticum?

A

Extensive crusted papules
blisters
erosions
systemically unwell with fever and malaise

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32
Q

How do you manage eczema herpeticum?

A

Antivirals (Aciclovir)

Antibiotics for bacterial secondary infection

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33
Q

What are the complications for eczema herpeticum?

A

Herpes hepatitis
Encephalitis
DIC
rarely death

34
Q

What is necrotising fasciitis?

A

A rapidly spreading infection of the deep fascia with secondary tissue necrosis

35
Q

What are the causes of necrotising fasciitis?

A

Group A haemolytic streptococcus

Mixture of anaerobic and aerobic

36
Q

What are the risk factors for necrotising fasciitis?

A

Abdominal surgery

medical co-morbidities- diabetes and malignancy

37
Q

What is the presentation of necrotising fasciitis?

A

Whilst some cases may have a recognisable precipitating event of skin breach (e.g. recent trauma, animal bite or scratch, or recent surgery), this is not always the case.

Clinical features will progress rapidly. Patients will complain of severe pain, often out of keeping with the overt clinical signs. Patients will often be haemodynamically unstable and may show signs of multi-organ dysfunction.

Examination signs are variable, often not representative of the degree or severity of infection present; indeed, overlying skin may appear normal in the early stages. Progression can reveal skin erythema, oedema and signs of skin ischaemia. Late signs include skin crepitus, vesicles / bullae, and obvious skin necrosis.

38
Q

What may you see on x-ray when a patient has necrotising fasciitis?

A

Soft tissue gas

39
Q

What is the management of necrotising fasciitis?

A

Urgent referall for extensive surgical debridement

IV abx

40
Q

What is the prognosis for necrotising fasciitis?

A

poor prognosis! mortality rate is up to 76%

41
Q

What are the 3 main types of skin infections?

A

Bacterial- staphylococcal and streptococcal
Viral- HPV, herpes simplex, herpes zoster
Fungal- tine, candida, and yeasts

Infestations like scabies and cutaneous leishmaniasis can also occue

42
Q

What is the difference between cellulitis and erysipelas?

A

Cellulitis- deep subcutaneous tissue

Erysipelas- acute superficial form of cellulitis and involves the dermis and upper subcutaneous tissue

43
Q

What are the causes of erysipelas and cellulitis?

A

strep pyogenes and staph aureus

44
Q

What are the risk factors for erysipelas and cellulitis?

A 
Immunosuppression 
Wounds 
Leg ulcers 
Toe web intertrigo (burning sensation between toes)
Minor skin injury
45
Q

What is the presentation for erysipelas and cellulitis?

A

Most common in lower limb
You will get local signs of inflammation- swelling, erythema, pain, warmth, may be associated with lymphangitis
They may be systemically unwell with fever, malaise, rigors (particularly in erysipelas)

46
Q

how can you distinguish erysipelas from cellulitis?

A

Erysipelas has a well defined, red raised border

47
Q

What is the management of cellulitis/erysipelas?

A

Abx- flucloxacillin/benzylpencillin

Supportive care- rest, leg elevation, sterile dressings, analgesia

48
Q

What are the complications of cellulitis/erysipelas?

A

Local necrosis
abscess
Septicaemia

49
Q

What is a superficial fungal infection?

A

A common and mild infection of the superficial layers of the skin, nails and hair
It can be severe in immunocompromised individuals

50
Q

What is the cause of superficial fungal infections?

A

There are three main groups…

1) Dermatophytes (tinea/ringworm)
2) Yeasts (candidiasis, malassezia)
3) moulds (Aspergillus)

51
Q

What is the presentation of superficial fungal infections?

A

It varies with the site of infection

Superficial fungal infections are usually unilateral and itchy

52
Q

What is the pathophysiology behind superficial fungal infections?

A

Fungi metabolize keratin on the skin, nails and hair

this leads to lesions, scarring, brittleness, dryness

53
Q

Tinea infections are named on where they affect the body, what would tinea which infect the following body parts be named….

1) Trunk
2) feet
3) head
4) Groin
5) nails

A

1) Trunk= tinea corporis
2) Feet= tinea pedis
3) Head= tinea capitis
4) Groin= tinea cruris
5) Nail= tinea unguium

54
Q

What is tinea pedis also known as?

A

Atheletes foot!

The most common dermatophyte infection

55
Q

How does tinea pedis present?

A

Interdigital (most common presentation)
- pruritic, itchy, scaly

Hyperkeratotic
- erythematous and affects soles of feet

Vesiculobullous eruption
- Pruritic, painful on medial foot

56
Q

What is tinea corporis also known as? How does it present?

A

Ringworm
Pruritic
Scaling patch/plaque
It is circular or oval in shape

57
Q

What is tinea capitis?

A

Fungal infection of the head, leads to hair loss, pruritic and scaling

58
Q

What is tinea cruris?

A 
This is a fungal infection of the groin area, it is also known as jock itch 
More common in men than women 
Starts on the medial thigh and has a centrifugal spread 
It is erythematous and raised 
Associated factors= 
- excessive sweating
- obesity
- diabetes 
- immunodefficiency
59
Q

What is the aetiology of erythema nodosum thought to be?

A

Hypersensitivity to a variety of stimuli

60
Q

What is the likely stimuli of erythema nodosum?

A

There are many triggers…

  • Streptococcal throat infection
  • TB
  • Leprosy
  • Chlamydia
  • Sarcoidosis
  • IBD
  • Pregnancy
  • Malignancy
  • Drugs (sulphonamides/contraceptive pill)
61
Q

What ix would you do if a patient had erythema nodosum and had a sore throat over the last week?

A

Throat swab
This could also be supplemented by an ANTI STREPTOLYSIN O TITRE (ASOT) a blood test to measure antibodies against streptolysin O, a substance produced by group A streptococcus bacteria

62
Q

What is the difference between tonsilitis and strep throat?

A

Tonsilitis is inflammation of the tonsils and it has both viral and bacterial causes
Strep pyogenes is the most common cause of bacterial tonsilitis (group A strep)
strep throat is infection of the throat and tonsils by group A strep

63
Q

How would you manage a patient who has erythema nodosum secondary to strep throat?

A

Abx for the streptococcal throat infection- penicillin is the first line treatment
Symptomatic treatment for the erythema nodosum- analgesia

64
Q

How would you explain erythema nodosum secondary to strep throat to a patient?

A

This is a condition called erythema nodosum which is a reaction to the throat infection you have had. The infection will be treated with abx and the erythema nodosum will start to settle once the throat infection is treated
Pain killers can be given for the erythema nodosum.

65
Q

What happens to the skin lesions in erythema nodosum as they get better?

A

Similar to a bruise they go through colour changes as they resolve ie: they go from red to brown to yellow
Eventually they will fade and leave no mark

66
Q

What is an exanthem?

A

A name given to a widespread rash which is usually accompanied by systemic symptoms- fever, headache, malaise
It is usually caused by an infectious condition- like a virus and represents either a reaction to a toxin produced by the organism, damage to the skin by an organism or an immune response

67
Q

What are viral exanthems due to?

A 
Chickenpox (varicella)
Measles (morbillivirus)
Rubella (rubella virus)
Roseola (herpes virus 6B)
Erythema infectiosum (parvovirus B19).
68
Q

What are bacterial exanthems due to?

A

Staphylococcal toxin infections
Toxic shock syndrome (TSS)
Staphylococcal scalded skin syndrome (SSSS)
Streptococcal toxin infections
Scarlet fever
Streptococcal toxic shock-like syndrome (STSS)

69
Q

In rubella and measles, where do the lesions begin?

A

The lesions begin on the face and spread downwards!

70
Q

What are the things which characterise an exanthema?

A
  • erythema
  • maculopapular
  • morbilliform (resembles measles)
  • blisters (less common)- either vesicles or bullae
71
Q

What causes drug induced exanthems? (Exanthematous drug eruption)

A

Abx- sulphonamides, ampicillin, isoniazid
Anti- convulsants- phenytoin, carbamazepine
antimalarials- chloroquine

72
Q

What is the treatment of drug induced exanthema?

A

Stop the drug immediately

Antihistamines, topical steroids

73
Q

Why is it important to differentiate whether a patient has streptococcal infection or infectious mononucleosis?

A

Because it affects the treatment!
Patients with streptococcal infections will need antibiotics whereas patients with epstein barr virus do not, when patients with EBV are given amoxicillin or ampocillin then it is common for them to get a reaction- exanthem.

74
Q

What advice should be given to patients who have had a drug reaction?

A 
Avoid the drug and drugs of the same class 
Make sure that the allergy is recorded in the patients notes and communicated to their GP

Encourage the patient to inform the next of kin

Re-exposure may result in a more severe reaction. In patients who have had a severe adverse cutaneous drug reaction eg: Steven Johnson Syndrome then consider getting a medic alert bracelet.

75
Q

Can a patient be tested for a drug allergy?

A

It depends on the type of reaction! Maculopapular reaction are mediated by type 4 hypersensitivity reactions and therefore there are no widely available, reliable, routine diagnostic tests

Patch tests can be helpful but a negative result doesn’t exclude the diagnosis

Lymphocyte proliferation assays are a research tool which can be helpful

76
Q

What is the emergency treatment of anaphylaxis?

A

500mcg injected prefarably into the anterolateral aspect of the middle 1/3rd of the thigh

May be repeated several times if necessary at 5 minute intervals according to blood pressure, pulse, resp function.

77
Q

How do you get meningococcal disease?

A

Neisseria meningitides bacteria are spread from person to person by inhaling airborne droplets when an infected person coughs or sneezes or just by close contact.

Rarely exposure to neisseria meningitides will lead to meningococcal disease where bacteria spreads to the blood and brain causing meningoccemia and/or meningococcal meningitis, this occurs if the body has not had enough time to build up an antibody defence or in those with defective immune systems.

78
Q

What are the systemic signs and symptoms of meningococcal disease?

A

Meningococcal meningitis in children >1 year and asults…

  • neck stiffness
  • headache
  • photophobia
  • N and V
  • fever and chills
  • irratibility and confusion
Infants...
Refusing feeds 
Increased irritability 
Sleeping all the time 
Fever 
Bulging fontanelle
Inconsolable crying 
Epileptic fits (seizures)
79
Q

What are the signs of the skin of meningococcemia?

A

Petechiae
Blanching or maculopapular rash may also occur
The rash may progress to larger red patches or purple lesions
Most often found in the trunk and extremities but may progress to involve any part of the body
In severe cases lesions may burst and lead to necrosis

80
Q

How is meningococcal disease diagnosed?

A

Blood culture and/or lumbar puncture are used to confirm the diagnosis

An increased no. Of white cells would be seen under the microscope and a diagnosis of meningitis is confirmed when the leukocyte count in the CSF is >5 cells/uL
Microscopy culture and PCR showing gram negative diplococci will confirm the diagnosis

Patients who are suspected of having a raised ICP or with focal neurological deficit may undergo CT scanning

81
Q

How do you treat suspected bacterial meningitis or meningococcal disease?

A

Treat children and young people aged 3 months or older with suspected bacterial meningitis without delay using IV ceftriaxone

Treat children younger than 3 months with suspected bacterial meningitis without delay using IV cefotaxime plus either amoxicillin or ampicillin

Do bot use corticosteroids in children younger than 3 months with suspected or confirmed bacterial meningitis

Give dexamethasone (0.15mg/kg to a max dose of 10mg, four times daily for 4 days) for suspected or confirmed bacterial meningitis as soon as possible if lumbar puncture reveals any of the following…

  • frankly purulent CSF
  • CSF WBC greater than 1000/microlitre
  • raised CSF WBc cot with protein concentration greater than 1g/ litre
  • bacteria on gram stain

Year 4 Derm (11 decks)

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