Immunology, Allergy + Derm Flashcards

1
Q

Anaphylaxis represents the most severe end of the allergy spectrum and can potentially have fatal results.

What are the clinical features of anaphylaxis?

A
  • Respiratory → Laryngeal oedema, leading to upper airway obstruction + stridor, and bronchospasm leading to lower airway obstruction and wheeze
  • GI → Abdo cramping, nausea, vomiting, diarrhoea
  • CVS → Hypotension, tachycardia, shock
  • Skin → Urticaria, agioedema
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2
Q

How is diagnosis of anaphylaxis made?

A
  • Life-threatening emergency requiring prompt treatment
  • Diagnosis based on history + clinical presentation
  • Levels of tryptase, proteinase contained in mast cell, can support the diagnosis
  • It is measured as treatment begins and again within 1 to 4 hrs
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3
Q

What is the acute management of anaphylaxis?

A
  • Resuscitate the patient using ABCDE approach
  • Remove offending allergen if possible
  • Adrenaline should be administered immediately + repeated after 5 minutes if no response
    • Child >12yrs → 500 micrograms IM (0.5mL of 1:1000)
    • Child 6-12yrs → 300 micrograms IM (0.3mL of 1:1000)
    • Child <6yrs → 150 micrograms IM (0.15mL of 1:1000)
  • Following resuscitation, for all established cases of anaphylaxis, give:
    • Chlorpheniramine → anti-histamines important for ameliorating rapid release of histamine by mast cells
    • Hydrocortisone → use of a corticosteroid will suppress immune response + may prevent late-phase response
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4
Q

What is the long-term management of anaphylaxis?

A
  • Allergen avoidance is key in preventing future episodes
  • The patient should undergo skin prick testing + immunoassay testing for IgE to specific allergics if there is doubt
  • Prescription of an Epipen (under supervision of allergy clinic) will provide some security in case of further anaphylaxis
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5
Q

Eczema refers to a group of conditions characterised by itchy, dry and inflammed skin. Atopic eczema is the most common type in children, affecting 20% of children in the UK. It results from impaired barrier function and usually starts in infancy. In those with atopic eczema, the risk of later developing asthma and hay fever is increased.

What are the clinical features of eczema and its two patterns/types?

A
  • Presents w/ dry, erythematous, itchy skin
  • Increased skin temp, oedema, weeping + crusting
  • Infantile eczema → affects face, neck, scalp + extensor surfaces; nappy mostly spared; majority clear within few months but may progress
  • Childhood eczema → favours flexural surfaces, antecubital + popliteal fossae, volar aspect of wrists, necks + ankles; less weepy + wet than infantile; marked lichenification
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6
Q

What is the management of eczema?

A
  • Establish diagnosis, severity + extent of disease
  • Good education vital: give written + verbal advice to parents, explain atopic eczema is a chronic condition + aim of treatment is adequate control, explain recognition + management of flare ups
  • Determine + avoid exacerbating factors: stress, environment allergens, irritants
  • Maintain skin hydration w/ generous + repeated applications of emollients
  • Stop soaps + shower gels and use substitutes
  • Topical corticosteroids to minimise inflammation - steroid phobia major issue
  • Treat pruritus using antihistamines
  • Initiate prompt + aggressive treatment of secondary infection w/ Abx or antivirals as appropriate
  • 2nd line Rx → topical calcineurin inhibitors, bandages + stockinette garments
  • 3rd line → phototherapy, methotrexate, cyclosporine, azathioprine
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7
Q

What are the complications of eczema?

A
  • Post-inflammatory hypo/hyperpigmentation
  • Bacterial infection (common) → staph aureus + strep pyogenes; cause golden crust + pulsation (impetiginized eczema); mild localised infection treated w/ antiseptic washes + topical antibacterial ointments
  • Viral → chickenpox infection widespread + severe; molluscum contagiosum more common in children w/ eczema + spread by scratching
    • Eczema herpeticum serious complication of HSV - presents w/ monomorphic clusters of vesicles that erode + crust; prompt diagnosis + Rx w/ systemic aciclovir is paramount; same day dermatology referral highly recommended
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8
Q

What are causes of nappy rash?

A
  • Irritant dermatitis
  • Candida dermatitis
  • Seborrhoeic dermatitis
  • Psoriasis
  • Atopic eczema
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9
Q

What are general management points for nappy rash?

A
  • Disposable nappies preferrable to towel nappies
  • Expose napkin area to air when possible
  • Apply barrier cream (eg Zinc + castor oil)
  • Mild steroid cream (eg 1% hydrocortisone) in severe cases
  • Candidal nappy rash → topical imidazole; cease use of barrier cream until candida settled
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10
Q

Irritant contact dermatitis

  • Causes?
  • Clinical features?
  • Treatment?
A
  • Caused by: prolonged contact of urine w/ skin, diarrhoea, infrequent changing, using non-disposable nappies
  • Moist erythematous patches
  • Blisters + ulcers in severe cases
  • Affect butocks, perineum, top of thighs + lower tummy
  • Inguinal folds spared

Rxfreq nappy changing + use of disposable nappies; protective emollients; topical corticosteroids

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11
Q

CANDIDA INFECTION

  • Causes?
  • Clinical features?
  • Management?
A
  • Organsim = Candida albicans causing candida dermatitis
  • Precipitated by compromise of cutaneous barrier eg. irritant dermatitis
  • Erythematous patches, may involve inguinal creases + flexures
  • Characteristic satellite lesions
  • Scaling at the margins of lesions

Rx → topical antifungals eg. imidazole

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12
Q

ATOPIC DERMATITIS

  • Causes?
  • Clinical features?
  • Management?
A
  • Genetic predisposition to develop hypersensitivity reactions to common env allergens
  • Presents after first 2 months of life
  • ITCHY!
  • Excoriated areas → erythematous, weeping, crusted
  • Face + trunk predominantly affected
  • Child’s skin tends to be dry

Rx → avoid irritants (soap, bio detergents); liberal application of emollients; topical corticosteroids

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13
Q

INFANTILE SEBORRHEIC DERMATITIS

  • Causes?
  • Clinical features?
  • Management?
A
  • Unknown cause
  • Normally presents in first 2 months
  • Erythematous, non-itchy, scaly eruption on scalp
  • develops into thick, yellow adherent layer AKA cradle cap
  • scaly rash can spread to face, behind ears, flexures + napkin area

Rxemollients; topical corticosteroids if widespread body eruptiion; ointment containing low conc of sulphur + salicylic acid for scalp; antifungals may be of some use

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14
Q

What is Henoch-Schonlein purpura?

A
  • IgA vasculitis
  • an IgA mediated autoimmune disease
  • overlap w/ IgA nephropathy (Berger’s disease)
  • precipitated by infections + vaccinations
  • classically affects children 3-10yrs old
  • more common in boys
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15
Q

What are clinical features of Henoch-Schonlein purpura?

A
  • Purpuric rash → characteristic raised purpuric rash, over buttocks + extensor surfaces of limbs; child usually clinically very well
  • Arthralgia → pain, particularly in knees + ankles, occasionally associated w/ periarticular oedema; usually responds well to simple analgesia
  • Abdo pain → this can also be due to intussusception, which is a complication of the disease

Usually seen in children following an infection and may be features of IgA nephropathy also eg. haematuria, renal failure

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16
Q

What investigations are done for HSP?

A
  • BP → hypertension associated w/ renal impairment
  • Urine dipstick → haematuria/proteinuria
  • Renal fxn
  • Albumin → hypoalbuminaemia associated w/ renal dysfunction
17
Q

What is the management of HSP?

A

General symptomatic w/ simple analgesia for pain (avoiding NSAIDs if renal involvement), children should be discussed w/ a paediatric nephrologist if there is:

  • nephrotic range proteinuria
  • renal dysfunction
  • hypertension
  • macroscopic haematuria
18
Q

The prognosis of HSP is usually excellent, it’s a self-limiting condition, especially in children without renal involvement.

What are complications of HSP?

A
  • Glomerulonephritis → commonest; important to check BP, urine dip + renal fxn
  • GI involvement → intussusception, protein-losing enteropathy, ileus, haemorrhage
  • CNS involvement → can range from self-limiting headaches + mild behavioural changes to CNS vasculitis
  • Orchitis
  • Pulmonary vasculitis
19
Q

What is a capillary hemangioma?

A
  • AKA strawberry naevi
  • benign tumours of vascular endothelium
  • Occur within first few months of life
  • Grow rapidly in first year of life + then gradually regress
  • Involution occurs in around half by 5 years and in majority by 9 years
20
Q

What is erythema toxicum neonatorum?

A
  • migratory raised erythematous rash
  • overlying papules or pustules
  • normally appears on day 2 or 3 of life
  • resolves spontaneously after three to five days
21
Q

What is milia?

A
  • AKA milk spots
  • White papules present at birth
  • Nose + cheeks
  • Caused by build-up of keratin + sebaceous material in skin follicles
  • Benign skin lesions + resolve in first few weeks of life
22
Q

What is a mongolian blue spot?

A
  • Blue pigmented macules that present at birth
  • Most commonly occur in the sacral gluteal region
  • Lesions can be large
  • Have higher incidence in darker pigmented skin
  • Benign lesions + tend to fade within first 2 years of life
23
Q

What is naevus simplex?

A
  • Benign pink, blanching macule present in newborns
  • AKA “salmon patch” or “storker’s bite/mark”
  • Typically found on glabella, eyelid or nape of neck
  • Majority fade within first 2 years of life
24
Q

What is a port wine stain?

A
  • Results from low-flow vascular malfortmations of dermal capillaries
  • Flat, blanching, pink-red lesions
  • Present from birth
  • Found anywhere on body - mostly unilateral w/ midline demarcation
  • They do NOT regress + may become darker and thicker w/ age
25
Q

What is a melanocytic naevi?

A
  • Benign proliferations of subtype of melanocyte known as naevus cell
  • Congenital or acquired
  • Congenital → grow rapidly in infancy, start as flat lesions w/ even pigment but surface later becomes uneven, developing pebbled appearance
26
Q

What is a primary immunodeficiency?

A
  • Result from inherited defect of the immune system
  • Can be isolated defect in a component of immune system or a combination
27
Q

What is a secondary immunodeficiency?

A
  • More common
  • May be related to:
    • systemic disease (SLE, malignancy)
    • malnutrition
    • splenectomy
    • drugs
    • infections
28
Q

What are the clinical features of immunodeficiencies?

A
  • Recurrent infections (hallmark of an immunodeficiency)
  • Concurrent infections at multiple sites
  • Persistent and/or recurrent infections resistant to Abx
  • Atypical, opportunistic, or unusual organisms
  • Accompanying faltering growth
  • Recurrent severe infections in sterile sites eg. meningitis
29
Q

Many primary immunodeficiencies result from gene mutations on recessive genes.

Therefore, what features in the (family) history should you be vigilant for?

A
  • X-linked FHx
  • FHx of early infant deaths
  • Consanguineous FHx
  • Infections apparent at around 6 months old, when protection from transplancentally acquired maternal immunoglobulins diminishes
30
Q

What is severe combined immunodeficiency?

A
  • Arises from severe defects in both humoral and cellular immunity
  • Due to molecular defects
  • Result in defective development and/or functioning of T + B cells
  • Recurrent severe infections typically begin to present at 6 months old, as maternal IgG persists up to this point
31
Q

What is chronic granulomatous disease (CGID)?

A
  • Recurrent + severe bacterial and fungal infections
  • With granuloma formation due to defects in phagocyte NADPH oxidase
  • Diagnosis suggested by recurrent + persistent infections, and infections caused by catalase-producing organisms (eg. staph aureus)
32
Q

What is cyclical neutopenia?

A
  • Regular oscillations in neutrophil count
  • On avg, each cycle lasts 21 days
  • Duration of neutropenia lasts 3-6 days
  • Majority of causes appear to be sporadic, but 1/3rd are inherited in an autosomal dominant pattern
33
Q

What is pancytopenia?

A
  • Simultaneous decrease in number of RBC, WBC + platelets
  • Caused by: aplastic anaemia, chemo, SLE, hypersplenism, HIV