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My Phase 3a Revision > PAEDS - INFECTIOUS DISEASES / ALLERGIES > Flashcards

PAEDS - INFECTIOUS DISEASES / ALLERGIES Flashcards

1
Q

FEBRILE CHILD
What system is used to assess a febrile child?
What are the main components?

A
  • NICE traffic light system for <5
  • Colour (skin, lips, tongue)
  • Activity
  • Respiratory
  • Circulation + hydration
  • Other
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2
Q

FEBRILE CHILD
In terms of the NICE traffic light system, what is considered amber for…

i) colour?
ii) activity?
iii) respiratory?
iv) circulation and hydration?
v) other?

A

i) Pallor
ii) No smile, decreased activity, not responding to social cues, wakes when roused
iii) Nasal flaring, SpO2 ≤95%, crackles in chest RR>50 (6-12m) or >40 (>12m)
iv) Tachy (>160 if <1y, >150 if 1–2y, >140 if 2–5y), CRT ≥3s, dry mucous membranes, reduced urine output
v) 3-6m temp ≥39, fever ≥5d, rigors, joint swelling, non-weight bearing

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3
Q

FEBRILE CHILD
In terms of the NICE traffic light system, what is considered red for…

i) colour?
ii) activity?
iii) respiratory?
iv) circulation and hydration?
v) other?

A

i) Mottled skin
ii) No response to cues, doesn’t wake if roused, weak, high-pitched or constant cry
iii) Grunting, RR>60, mod-severe chest indrawing
iv) Reduced skin turgor, no urine output
v) <3m temp ≥38, non-blanching rash, bulging fontanelle, neck stiffness, status, focal seizures/neuro

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4
Q

FEBRILE CHILD
What are some common and uncommon causes of fever?

A
  • Common = URTI, tonsillitis, otitis media, UTI
  • Uncommon = Meningitis, epiglottitis, kawasaki disease, TB
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5
Q

FEBRILE CHILD
What is the management of a green score?

A
  • Manage at home with safety netting
  • Regular fluids, monitor child, contact if concerned
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6
Q

FEBRILE CHILD
What is safety netting?

A
  • Clear verbal ± written advice about warning signs with plan of action
  • Follow up if required
  • Liaise with other HCPs so direct access if child needs
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7
Q

FEBRILE CHILD
What is the management of an amber score?

A
  • F2F assessment with paeds or specialist for further investigation
  • ?Home with safety net
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8
Q

FEBRILE CHILD
What is the management of a red score?

A
  • Urgent referral to hospital for specialist assessment (?999)
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9
Q

CHICKEN POX
What is chicken pox?

A
  • Primary infection by Varicella zoster virus (human herpes virus 3)
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10
Q

CHICKEN POX
How does it spread?

A

Droplet via resp route

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11
Q

CHICKEN POX
How long is it contagious for?

A

Contagious 4d before rash + until lesions crusted (often 5d)

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12
Q

CHICKEN POX
What are some risk factors for chicken pox?

A
  • Immunocompromised
  • Older age
  • Steroids
  • Malignancy
  • Neonates
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13
Q

CHICKEN POX
What is the clinical presentation of chicken pox?

A
  • Prodromal high fever 38-39 often ceases when rash appears, malaise
  • Very itchy, vesicular rash starts on head + trunk > peripheries
  • Not infective once vesicles have crusted over (5d usually)
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14
Q

CHICKEN POX
What are some complications of chicken pox?

A
  • Secondary bacterial infection
  • Shingles (older children)
  • Ramsay Hunt syndrome (older children)
  • Risk to immunocompromised, neonates + pregnant women
  • Rarer = pneumonia, encephalitis
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15
Q

CHICKEN POX
How does secondary bacterial infection present in chicken pox?
How is it managed?

A
  • Small area of cellulitis or erythema, persistent fever
  • Small risk staph/group A strep infection > necrotising fasciitis
  • NSAIDs may increase risk, Rx with Abx (IV if severe or dehydrated)
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16
Q

CHICKEN POX
What is shingles?

A
  • Reactivation of dormant virus > herpes zoster virus (shingles) in dorsal root ganglia
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17
Q

CHICKEN POX
How does shingles present?

A

Characteristic rash in dermatomal distribution, acute, unilateral, blistering painful rash

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18
Q

CHICKEN POX
What is the management of shingles?

A

PO aciclovir

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19
Q

CHICKEN POX
What is Ramsay Hunt syndrome?

A
  • Herpes zoster oticus > reactivation of varicella zoster virus in geniculate ganglion of CN7
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20
Q

CHICKEN POX
How does Ramsay Hunt Syndrome present?

A
  • Auricular pain,
  • facial nerve palsy,
  • vesicular rash around ear,
  • ?vertigo + tinnitus
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21
Q

CHICKEN POX
What is the management of Ramsay Hunt syndrome?

A

PO aciclovir + corticosteroids

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22
Q

CHICKEN POX
What is the risk of chicken pox to…

i) immunocompromised?
ii) neonates?
iii) pregnant?

A

i) Disseminated disease, DIC, pneumonitis (VZIG if exposed to case)
ii) Mother develops shortly before/after delivery infant > VZIG + aciclovir
iii) Risk of foetal varicella syndrome if <20w

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23
Q

CHICKEN POX
What is the management of chicken pox?

A
  • Camomile lotion to stop itching
  • Avoid high risk groups
  • Trim nails
  • School exclusion until all lesions crusted over (usually 5d after rash)
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24
Q

MENINGITIS
What is meningitis?

A
  • Inflammation of the meninges which line the brain + spinal cord
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25
Q

MENINGITIS
How does it occur?

A

Microorganisms reach meninges by direct extension from ears, nasopharynx or bloodstream spread

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26
Q

MENINGITIS
What are the most common causes of bacterial meningitis?

A
  • Neonates = GBS or listeria monocytogenes
  • 1m–6y = N. meningitidis (gram -ve diplococci), S. pneumoniae (gram + ve cocci chain), H. influenzae
  • > 6y = meningococcus + pneumococcus, rarely TB
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27
Q

MENINGITIS
What are some other causes of meningitis?

A
  • Herpes simplex virus (HSV), enteroviruses, EBV + varicella zoster virus
  • Aseptic/sterile by malignancy or autoimmune diseases
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28
Q

MENINGITIS
What are the symptoms of meningitis?

A
  • Fever, headache, vomiting, drowsiness, poor feeding, irritable/lethargic
  • Later may have seizures, focal neurology, decreased GCS/coma
  • Neonates may have hypothermia, lethargy + hypotonia
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29
Q

MENINGITIS
What are some signs of meningitis?

A
  • Meningism = neck stiffness (not always present), photophobia
  • Bulging fontanelle, opisthotonos, signs of shock
  • +ve Kernig’s + Brudzinski
  • Non-blanching petechial/purpuric rash = later sign in meningococcal septicaemia (endotoxin causes DIC + subcut haemorrhages)
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30
Q

MENINGITIS
What is the difference between Kernig’s and Brudzinski signs?

A
  • Kernig = pain/unable to extend leg at knee when it’s bent
  • Brudzinski = involuntary flexion of hips/knees when neck flexed
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31
Q

MENINGITIS
What investigations would you do for meningitis?

A
  • Blood cultures + serology (before LP + Abx unless undesirable delay)
  • FBC, U+E, LFTs, CRP, blood glucose
  • LP for MC&S with protein, cell count, glucose + viral PCR
  • ?CT head if other signs like papilloedema
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32
Q

MENINGITIS
When would you not perform a lumbar puncture?
Why?

A
  • Signs of increased ICP, focal neurology, local infection, unduly delay starting Abx or coagulopathies
  • Coning of cerebellar tonsils via foramen magnum
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33
Q

MENINGITIS
You suspect a diagnosis of bacterial meningitis. How would a lumbar puncture confirm the diagnosis for…

i) appearance?
ii) protein?
iii) glucose?
iv) white cell count?
v) other?

A

i) Cloudy/turbid
ii) ++ (make protein)
iii) –– (eat glucose)
iv) ++ neutrophil polymorphs
v) Gram stain

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34
Q

MENINGITIS
You suspect a diagnosis of viral meningitis. How would a lumbar puncture confirm the diagnosis for…

i) appearance?
ii) protein?
iii) glucose?
iv) white cell count?
v) other?

A

i) Clear
ii) Normal/+
iii) Normal/-
iv) + lymphocytes
v) PCR

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35
Q

MENINGITIS
You suspect a diagnosis of TB meningitis. How would a lumbar puncture confirm the diagnosis for…

i) appearance?
ii) protein?
iii) glucose?
iv) white cell count?
v) other?

A

i) Turbid/viscous
ii) +++
iii) –––
iv) + lymphocytes
v) Acid fast bacilli

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36
Q

MENINGITIS
What are some complications of meningitis?

A
  • Hearing (sensorineural) loss is key complication
  • Seizures + epilepsy, cerebral abscess, encephalitis + hydrocephalus
  • Cognitive impairment, cerebral palsy + LD
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37
Q

MENINGITIS
What is the management of bacterial meningitis?

A
  • Supportive = correct shock with fluids, oxygen if needed
  • <3m = IV cefotaxime + amoxicillin (cover listeria from ?pregnancy)
  • > 3m = IV ceftriaxone + IV dexamethasone to reduce frequency + severity of hearing loss + neuro damage (NOT before 3m)
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38
Q

MENINGITIS
What is the management of viral meningitis?

A
  • Milder so supportive + aciclovir if HSV or VSZ
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39
Q

MENINGITIS
You see a child with a non-blanching petechial rash in GP and are concerned about meningococcal septicaemia so call for an ambulance.
What immediate treatment should you give if possible?

A
  • IM benzylpenicillin
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40
Q

MENINGITIS
What shoudl be given to close contacts?

A
  • Single dose ciprofloxacin or rifampicin
  • Ciprofloxacin is prefered as can use for any age, pregnant ladies + does not interfere with OCP
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41
Q

MENINGITIS
What are the drawbacks with giving ciprofloxacin to a close contact?

A
  • Do not give in myasthenia gravis or previous sensitivity,
  • can cause tendinitis
  • can trigger seizures
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42
Q

MENINGITIS
What are the drawbacks with giving rifampicin to a close contact?

A
  • Affect hormonal contraception,
  • not advised in pregnancy
  • have to monitor LFTs + renal function
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43
Q

MENINGITIS
What Public Health aspects are important in terms of meningitis?

A
  • Meningitis B vaccine at 8w, 16w + 1y (men C at 1y too) and ACWY offered to teenagers + uni students
  • Bacterial meningitis + meningococcal = notifiable diseases
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44
Q

ENCEPHALITIS
What is encephalitis?

A
  • Inflammation of the brain parenchyma
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45
Q

ENCEPHALITIS
What causes it?

A
  • Mostly viral – herpes viruses (HSV 1 if child or 2 if neonate from birth, VZV), enteroviruses, EBV, resp viruses
  • Non viral = any bacterial meningitis, TB, lyme disease
  • Non-infective = autoimmune antibodies against brain
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46
Q

ENCEPHALITIS
What is the clinical presentation of encephalitis?

A
  • Similar to meningitis = fever, headache, photophobia, neck stiffness
  • KEY difference = altered mental state (behavioural change, confusion)
  • Acute onset focal neurology (hemiparesis, dysphasia, focal seizures)
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47
Q

ENCEPHALITIS
What are the investigations for encephalitis?

A
  • FBC, U+Es, blood cultures + serology for viral PCR
  • LP for MC&S with protein, cell count, glucose + viral PCR
  • CT/MRI head to visualise brain as ?focal changes, particularly temporal lobes
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48
Q

ENCEPHALITIS
What would the CSF analysis show in encephalitis for…

i) appearance?
ii) protein?
iii) glucose?
iv) white cell count?

A

i) Clear
ii) Normal/+
iii) Normal/–
iv) + lymphocytes

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49
Q

ENCEPHALITIS
What is the management of encephalitis?

A
  • IV aciclovir to cover HSV, Abx in case bacterial meningitis
  • Supportive therapy in HDU/ICU if needed
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50
Q

SEPTICAEMIA
What is septicaemia?

A
  • Bacteria proliferates into bloodstream as host response includes release of inflammatory cytokines + activation of endothelial cells which can lead to septic shock
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51
Q

SEPTICAEMIA
What are the causes of septicaemia?

A
  • Most common = N. meningitidis
  • Neonates = GBS or gram -ve organisms from birth canal
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52
Q

SEPTICAEMIA
What are some risk factors?

A
  • Sickle cell disease
  • immunodeficiency
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53
Q

SEPTICAEMIA
What are the symptoms and signs of septicaemia?

A
  • Fever, poor feeding, irritable/lethargic, Hx of focal infection
  • Fever, purpuric non-blanching rash, multi-organ failure
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54
Q

SEPTICAEMIA
How does shock present?

A
  • Tachycardia + tachypnoea
  • Cold peripheries
  • Capillary refill >2s
  • Hypotensive
  • Oliguria
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55
Q

SEPTICAEMIA
What is the management of septicaemia?

A
  • Septic screen (FBC, U+Es, blood cultures, urine MC&S, LP/CSF, CXR, acute phase reactant like CRP)
  • Aggressive fluid resus, ?ICU
  • Broad-spec Abx until cultures back
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56
Q

KAWASAKI DISEASE
What is Kawasaki disease?
What is the epidemiology?

A
  • Idiopathic medium-sized vessel systemic vasculitis, mainly affects 6m–5y
  • More common in children of Japanese or Afro-Caribbean ethnicity
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57
Q

KAWASAKI DISEASE
What is the diagnostic criteria for Kawasaki disease?

A

Fever + 4 (MyHEART) –

  • Mucosal involvement (red/dry cracked lips, strawberry tongue)
  • Hands + feet (erythema then desquamation)
  • Eyes (bilateral conjunctival injection, non-purulent)
  • lymphAdenopathy (unilateral cervical >1.5cm)
  • Rash (polymorphic involving extremities, trunk + perineal regions
  • Temp >39 for >5d
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58
Q

KAWASAKI DISEASE
What are the 3 phases of Kawasaki disease?

A
  • Acute (1–2w) = child most unwell, fever, rash, lymphadenopathy
  • Subacute (2–4w) = acute Sx settle, desquamation + Risk of coronary artery aneurysms
  • Convalescent (2–4w) = remaining Sx settle, blood markers normalise slowly
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59
Q

KAWASAKI DISEASE
What is a key complication of Kawasaki disease?

A
  • Coronary artery aneurysm + sudden death
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60
Q

KAWASAKI DISEASE
What are some investigations for Kawasaki disease?

A
  • FBC (raised WCC), raised ESR + CRP, raised platelets (week 2)
  • Echocardiogram with close follow up (6w) to rule out aneurysm
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61
Q

KAWASAKI DISEASE
What is the management of Kawasaki disease?

A
  • Prompt IVIg to reduce risk of aneurysm + aspirin to reduce risk of thrombosis
  • If fever persists = infliximab, steroids or ciclosporin
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62
Q

KAWASAKI DISEASE
What are the side effects of IVIG in the management of Kawasaki disease?

A
  • anaphylaxis,
  • aseptic meningitis,
  • organ dysfunction
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63
Q

KAWASAKI DISEASE
Why is the management of Kawasaki disease unique?
Prognosis?

A
  • Aspirin normally contraindicated in children due to risk of Reye’s syndrome (swelling of the liver + brain)
  • 50% evidence of cardiac impairment + mild MR, long-term follow up
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64
Q

MEASLES
What is measles?

A
  • Infection with measles virus (Morbillivirus) via droplets (highly contagious)
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65
Q

MEASLES
What is a risk factor?

A

Avoidance of MMR vaccine

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66
Q

MEASLES
What is the clinical presentation of measles?

A
  • Prodromal Sx for 3–5d (CCCK) – Cough, Coryza, Conjunctivitis, Koplik spots
  • Maculopapular rash starts on forehead, neck + behind ears > down to limb, trunk
  • Fever, marked malaise
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67
Q

MEASLES
What are Koplik spots?

A
  • White spots on buccal mucosa = pathognomonic
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68
Q

MEASLES
What are the investigations for measles?

A

Clinical Dx with serological (blood or saliva) testing for epidemiology

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69
Q

MEASLES
What are some important complications of measles?

A
  • Otitis media (commonest complication)
  • Pneumonia (commonest cause of death)
  • Diarrhoea
  • Febrile convulsions, encephalitis
  • Subacute sclerosing panencephalitis rare where 5-10y after primary measles > loss of neuro function, dementia + death
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70
Q

MEASLES
What is the management of measles?

A
  • Notifiable disease
  • Best treatment is prevention with MMR vaccine
  • Viral illness so supportive (fluids, isolate if in hospital)
  • Antivirals in immunocompromised
  • School exclusion for 4d from rash onset
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71
Q

RUBELLA
What is rubella?
How does it spread?

A
  • Mild notifiable disease occurring in winter + spring
  • Spreads via respiratory route, often from known contact, prevention via vaccine
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72
Q

RUBELLA
What is the clinical presentation of rubella?

A
  • Mild prodrome (low-grade fever, sore throat, coryza)
  • Pink maculopapular rash starts on face then spreads down to cover whole body
  • Rash not itchy in children but is in adults
  • Suboccipital + postauricular lymphadenopathy
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73
Q

RUBELLA
What are the investigations for rubella?

A
  • Clinical Dx
  • Serological confirmation if any risk of exposure of a non-immune pregnant woman
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74
Q

RUBELLA
What are some complications of rubella?
How can it be reduced?

A
  • Rare but > encephalitis, arthritis, myocarditis + thrombocytopenia
  • Congenital rubella syndrome > cataracts, CHD + sensorineural deafness
  • Avoid pregnant women, school exclusion 4d from rash, ensure vaccinated
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75
Q

MUMPS
What is mumps?
How does it occur?

A
  • RNA paramyxovirus, occurs in winter + spring, spreads via resp droplets where virus replicates in epithelial cells
  • Virus accesses parotid glands before further dissemination
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76
Q

MUMPS
What marker may be raised?

A

Raised amylase

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77
Q

MUMPS
What is the clinical presentation of mumps?

A
  • Fever, malaise + parotitis
  • Parotitis often unilateral initially then bilateral > uncomfortable + may have earache or pain when eating/drinking
  • May have hearing loss but often unilateral + transient
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78
Q

MUMPS
What are some complications of mumps?

A
  • Viral meningitis + encephalitis
  • Orchitis (usually unilateral, may reduce sperm count + lead to infertility)
  • Pancreatitis
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79
Q

MUMPS
What is the management of mumps?

A
  • Notifiable disease
  • Prophylaxis via vaccine
  • Clinical Dx, manage Sx as viral
  • School exclusion for 5d of onset of parotid swelling
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80
Q

HAND, FOOT + MOUTH
What is hand, foot and mouth disease caused by?

A
  • Caused by coxsackie A16 virus
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81
Q

HAND, FOOT + MOUTH
How does it present?

A
  • Mild viral URTI (sore throat, cough, fever)
  • Painful red vesicular lesions on hands, feet, mouth + tongue (often buttocks too)
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82
Q

HAND, FOOT + MOUTH
What is the management of hand, foot and mouth disease?

A
  • Subsides within few days, supportive with fluids, analgesia
  • Very contagious, avoid sharing towels + bedding, good handwashing
  • Only exclude from school if unwell
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83
Q

GLANDULAR FEVER
What is glandular fever, or infectious mononucleosis, caused by?

A
  • Epstein-Barr virus (EBV), particular tropism for B lymphocytes + epithelial cells of pharynx
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84
Q

GLANDULAR FEVER
How is it spread?

A

Oral contact ‘kissing disease’

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85
Q

GLANDULAR FEVER
What is the clinical presentation of glandular fever?

A
  • Triad of severe sore throat (tonsillopharyngitis can limit oral intake), lymphadenopathy (cervical) + pyrexia
  • May have petechiae on soft palate, splenomegaly + headache
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86
Q

GLANDULAR FEVER
What are the investigations for glandular fever?

A
  • FBC (lymphocytosis)
  • positive Monospot test with heterophile antibodies
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87
Q

GLANDULAR FEVER
What are the complications of glandular fever?

A
  • Splenic rupture,
  • haemolytic anaemia,
  • chronic fatigue,
  • EBV associated with Burkitt’s lymphoma
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88
Q

GLANDULAR FEVER
What is the management of glandular fever?

A
  • Conservative (fluids, analgesia)
  • Avoid alcohol + contact sports for 8w after to reduce risk of splenic rupture
  • Avoid amoxicillin as can cause florid, pruritic maculopapular rash
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89
Q

SCARLET FEVER
What is scarlet fever?

A
  • Reaction to strep pyogenes (group A beta haemolytic) toxin - strep A
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90
Q

SCARLET FEVER
How is it spread?

A
  • Via respiratory droplets
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91
Q

SCARLET FEVER
What is the clinical presentation of scarlet fever?

A
  • Prodrome = sore throat, fever, vomiting + abdo pain
  • Red-pink diffuse rash that is ‘rough sandpaper-like’ + ‘pinhead’, starts on trunk + spreads outwards
  • May have exudative tonsils + strawberry tongue
  • Tender cervical lymphadenopathy
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92
Q

SCARLET FEVER
What is the investigation of choice for scarlet fever?

A
  • Throat swab (but start Abx)
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93
Q

SCARLET FEVER
What are some complications of scarlet fever?

A
  • Otitis media (#1),
  • quinsy,
  • post-strep glomerulonephritis,
  • rheumatic fever
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94
Q

SCARLET FEVER
What is the management of scarlet fever?

A
  • Notifiable disease
  • Phenoxymethylpenicillin for 10d to prevent rheumatic fever
  • Supportive (fluids, pain relief)
  • School exclusion until 24h after Abx
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95
Q

SLAPPED CHEEK
What is slapped cheek syndrome, or erythema infectiosum?

A
  • Caused by parvovirus B19, outbreaks common during spring months
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96
Q

SLAPPED CHEEK
What is important to note in slapped cheek syndrome?

A

Infects red cell precursors in bone marrow which can cause complications

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97
Q

SLAPPED CHEEK
How is it spread?

A
  • Respiratory secretions,
  • vertical transmission
  • transfusions
98
Q

SLAPPED CHEEK
What is the clinical presentation of slapped cheek syndrome?

A
  • Prodromal Sx = fever, malaise, headache, myalgia
  • Followed by classic rose-red rash on face week later (slapped-cheek)
  • Progresses to maculopapular, ‘lace-like’ rash on trunk + limbs
99
Q

SLAPPED CHEEK
What are some complications of slapped cheek syndrome?

A
  • Aplastic crisis (most serious) more common in chronic haemolytic anaemias like sickle cell, thalassaemia + in immunocompromised
  • Vertical transmission can lead to foetal hydrops + death due to severe anaemia
100
Q

STAPH + STREP INFECTION
What are the different ways that staph can cause diseases?

A
  • Direct invasion of bacteria = abscess, cellulitis, impetigo
  • Toxin-mediated (indirect) = toxic shock, food poisoning
  • Toxin-mediated (direct) = SSS
101
Q

STAPH + STREP INFECTION
What is a boil?
How are they managed?

A
  • Infections of hair follicles or sweat glands by s. aureus
  • Systemic Abx + occasionally surgery
102
Q

IMPETIGO
What is impetigo?

A
  • Localised, highly contagious infection by S. aureus or Strep pyogenes
103
Q

IMPETIGO
Who is it common in?

A

Children with pre-existing skin disease (atopic eczema)

104
Q

IMPETIGO
How is it spread?

A

Rapidly by autoinoculation by infected exudate

105
Q

IMPETIGO
What are the 2 types of impetigo?

A
  • Non-bullous + bullous
106
Q

IMPETIGO
What is non-bullous impetigo?

A
  • Pustules or vesicles typically around nose or mouth
  • Exudate dries > golden crust, itchy but usually not unwell
107
Q

IMPETIGO
What is bullous impetigo?
Who is it seen in?

A
  • Epidermolytic toxins breakdown proteins that hold skin cells together > fluid-filled vesicles (bullae)
  • Rupture + fluid exudation > classic golden/honey crusted lesions
  • More common in neonates or <2y, commonly systemically unwell
108
Q

IMPETIGO
What are some complications of impetigo?

A
  • Risk of SSSS
  • Post-strep glomerulonephritis
109
Q

IMPETIGO
What is the management of impetigo?

A
  • Swab vesicles, avoid sharing towels, cutlery, try not to scratch
  • Hydrogen peroxide 1% cream (or mupirocin)
  • PO flucloxacillin if severe + systemically unwell
  • School exclusion until lesions crusted + healed or 48h after Abx
110
Q

STAPH SCALDED SKIN
What is staphylococcal scalded skin syndrome (SSSS)?

A
  • Caused by type of S. aureus that produces epidermolytic toxins that breakdown proteins that hold skin together
111
Q

STAPH SCALDED SKIN
Who is it more common in?

A

Children <5y as when older they develop immunity to toxins

112
Q

STAPH SCALDED SKIN
What is an important differential?

A

Steven-Johnson’s syndrome

113
Q

STAPH SCALDED SKIN
What is the clinical presentation of SSSS?

A
  • Starts as generalised patches of erythema on the skin, skin looks thin + wrinkled
  • Bullae formation which burst + leave very sore, erythematous skin below (like a burn/scald)
  • Nikolsky sign = gentle rubbing causes peeling
  • Systemic Sx = fever, lethargy, dehydration > sepsis
114
Q

STAPH SCALDED SKIN
What is the management of SSSS?

A
  • Most need admission for IV flucloxacillin, fluid balance + analgesia
115
Q

TOXIC SHOCK SYNDROME
What is toxic shock syndrome?

A
  • Toxin producing S. aureus + group A strep released from infection
116
Q

TOXIC SHOCK SYNDROME
What is the pathophysiology?

A
  • Toxin producing S. aureus + group A strep released from infection acts as a superantigen to cause multi-organ dysfunction
117
Q

TOXIC SHOCK SYNDROME
What can it be caused by?

A
  • Tampons being left in,
  • female barrier contraceptive
118
Q

TOXIC SHOCK SYNDROME
What is the clinical presentation of toxic shock syndrome?

A
  • Fever ≥39
  • Hypotension (shock)
  • Diffuse erythematous rash
  • Desquamation of rash (esp. palms + soles) 1-2w after
  • Multi-organ dysfunction
119
Q

TOXIC SHOCK SYNDROME
Give some examples of multi-organ dysfunction in toxic shock syndrome

A
  • GI = D+V
  • CNS = confusion
  • Thrombocytopenia
  • Renal failure
  • Hepatitis
  • Clotting abnormalities
120
Q

NECROTISING FASCIITIS
What is necrotising fasciitis?

A
  • Severe subcutaneous infection with severe pain + systemic illness
121
Q

NECROTISING FASCIITIS
What causes it?

A

Staph aureus or strep pyogenes ± another synergistic anaerobic organism
May be complication from cellulitis infection in soft tissues

122
Q

NECROTISING FASCIITIS
What is the clinical presentation of necrotising fasciitis?

A
  • Acute onset, painful erythematous lesion
  • Necrotic skin affecting all skin layers down to fascia + muscle
123
Q

NECROTISING FASCIITIS
What is the management of necrotising fasciitis?

A
  • IV Abx (flucloxacillin) PLUS surgical debridement
  • ?ICU, ?IVIg
124
Q

HERPES SIMPLEX
What are the two types of herpes simplex virus?

A
  • HSV1 = lip + skin lesion,
  • HSV2 = genital lesions
125
Q

HERPES SIMPLEX
How is it spread?

A
  • Enters via mucous membranes or skin (kissing, genital contact, vertical transmission at birth)
126
Q

HERPES SIMPLEX
What are the various manifestations of herpes simplex infection?

A
  • Gingivostomatitis
  • Cold sores on lip
  • Eczema herpeticum
  • Herpetic whitlows
  • Eyes = blepharitis or conjunctivitis
  • CNS = aseptic meningitis, encephalitis
127
Q

HERPES SIMPLEX
What is gingivostomatitis?
How may it present?

A
  • Vesicular lesions on lips, gums, tongue which can lead to painful ulceration + bleeding
  • High fever, miserable child, oral intake may hurt
128
Q

HERPES SIMPLEX
How is gingivostomatitis managed?

A

Supportive but PO aciclovir if severe, chlorhexidine mouthwash

129
Q

HERPES SIMPLEX
What is eczema herpeticum?
How does it present?

A
  • Widespread vesicular lesions with pus developing on eczematous skin
  • Fever, lethargy, lymphadenopathy
130
Q

HERPES SIMPLEX
What is a complication of eczema herpeticum?

A

Secondary bacterial infection + septicaemia

131
Q

HERPES SIMPLEX
How is eczema herpeticum managed?

A

IV aciclovir as life-threatening, bacterial infection will need Abx

132
Q

HERPES SIMPLEX
What are herpetic whitlows?
How can they occur?

A
  • Painful pustules on site of broken skin on fingers
  • Infected adult kissing a child’s finger
133
Q

HIV
How is HIV spread?

A
  • Mainly vertical
  • Rarely = sexual abuse, needles
134
Q

HIV
What are some symptoms of immunosuppression in HIV?

A
  • Mild = lymphadenopathy or parotitis
  • Mod = recurrent bacterial infections, candidiasis, recurrent diarrhoea
  • Severe = pneumocystis jiroveci, severe failure to thrive, encephalopathy
135
Q

HIV
When should HIV be suspected?

A
  • Persistent lymphadenopathy
  • Hepatosplenomegaly
  • Recurrent fever
  • Parotitis
  • Serious, persistent, unusual, recurrent (SPUR) infections
136
Q

HIV
How is HIV investigated?

A
  • <18m cannot use antibody (transplacental HIV IgG if exposed anyway)
  • 2x HIV DNA PCR blood test (double negative to exclude) for viral load
    – Within first 3m + at least 2w after completion of postnatal antiretroviral
137
Q

HIV
How should HIV be managed?

A
  • Antiretrovirals based on viral load + CD4 count
  • Co-trimoxazole prophylaxis (PCP)
  • ?Additional vaccines but not BCG as live
  • Regular follow up, check development, psychological support
  • Safe sex education when older
138
Q

TUBERCULOSIS
What is the pathophysiology of tuberculosis (TB)?

A
  • Lung lesion + (mediastinal) lymph nodes = Ghon or primary complex
  • Primary infection > caseating granulomas followed by period of dormancy with ?reactivation (secondary TB)
  • If immune system unable to cope it disseminates > miliary TB
139
Q

TUBERCULOSIS
Where can miliary TB affect?

A
  • Pleura,
  • CNS,
  • pericardium,
  • lymph nodes,
  • GI/GU tract
140
Q

TUBERCULOSIS
What are some risk factors for TB?

A
  • Immunocompromised,
  • overseas contact,
  • homeless,
  • IVDU,
  • alcoholics
141
Q

TUBERCULOSIS
What is the epidemiology for TB?

A

Majority cases are in Africa + Asia (India, China)

142
Q

TUBERCULOSIS
What is the clinical presentation of TB?

A
  • Prolonged fever
  • Haemoptysis
  • Cough
  • Malaise
  • Anorexia
  • Weight loss
143
Q

TUBERCULOSIS
What are some investigations for TB?

A
  • Mantoux ‘tuberculin’ test
  • Interferon gamma release assays
  • 3x samples of sputum MC&S = gold standard
  • CXR
144
Q

TUBERCULOSIS
When diagnosing TB, what would you see on Mantoux test?

A
  • > 15mm suggests active TB,
  • 6-15mm ?previous exposure (may be BCG)
145
Q

TUBERCULOSIS
When diagnosing TB, what would you see on interferon gamma release assays?

A

Confirms latent TB + differentiates from BCG

146
Q

TUBERCULOSIS
When diagnosing TB, what would you see on sputum MC&S?

A

Acid fast bacilli stain red with Ziehl-Neelson stain on Lowenstein-Jenson culture medium

147
Q

TUBERCULOSIS
When diagnosing TB, what would you see on CXR?

A
  • Patchy consolidation,
  • pleural effusions,
  • hilar lymphadenopathy
148
Q

TUBERCULOSIS
What are some complications of TB?

A
  • Pleural + pericardial effusions
  • Lung collapse
  • Lung consolidation
149
Q

TUBERCULOSIS
What management of TB is necessary to prevent the spread?

A
  • BCG for high risk neonates (FHx, relatives from countries with high TB rate)
  • Contact tracing
  • Notifiable to PHE
150
Q

TUBERCULOSIS
What is the management of TB?

A

RIPE
- Rifampicin (6m)
- Isoniazid (6m)
- Pyrazinamide (2m)
- Ethambutol (2m)

151
Q

TUBERCULOSIS
What are the side effects of rifampicin?

A

Red urine

152
Q

TUBERCULOSIS
What are the side effects of isoniazid? How can it be prevented?

A
  • Peripheral neuropathy (I’m-so-numb-azid)
  • co-prescribe pyridoxine (vit B6) after puberty as prophylaxis
153
Q

TUBERCULOSIS
What are the side effects of pyrazinamide?

A
  • Gout due to hyperuricaemia,
  • rash
154
Q

TUBERCULOSIS
What are the side effects of ethambutol?

A

Optic neuritis, reduced acuity + colour (eye-thambutol)

155
Q

TUBERCULOSIS
What is the management of latent TB?

A
  • Isoniazid (+ vit B6) for 6m
  • Isoniazid (+vit B6) + rifampicin for 3m
156
Q

VACCINATIONS
What is the process of vaccinations?

A
  • Induce T + B cell (antibody) immunity
  • Induce immunological memory
  • Herd immunity to protect those who haven’t been immunised
157
Q

VACCINATIONS
How should vaccinations be given in those who are premature?

A
  • Not adjusted for prematurity, give chronologically
  • Babies born <28w should receive first set in hospital due to risk of apnoea
158
Q

VACCINATIONS
What are the two types of immunity?

A
  • Active = give part of pathogen either non-living or attenuated (live but weak)
  • Passive = give them antibodies to pathogen (natural = cross-placental transfer, artificial = treated with human IgG)
159
Q

VACCINATIONS
What vaccines are attenuated?

A
  • MMR, BCG, nasal flu, rotavirus + Men B
160
Q

VACCINATIONS
What advise is given for vaccines that are attenuated?

A

Can give fever, advise normal + administer paracetamol

161
Q

VACCINATIONS
Which vaccines are included in the 6-in-1 injection?

A
  • diphtheria
  • tetanus
  • pertussis DTaP (whooping cough)
  • polio IPV
  • Haemophilus influenza B (HiB)
  • Hepatitis B
162
Q

VACCINATIONS
What vaccines are given at…

i) 2m?
ii) 3m?
iii) 4m?

A

i) 6-in-one, rotavirus + men B
ii) 6-in-one, rotavirus + PCV
iii) 6-in-one, men B

163
Q

VACCINATIONS
What vaccines are given at…
i) 1y?
ii) 3y + 4m?
iii) 12-13y?
iv) 14y?

A

i) Men B, PCV, Hib/Men C + MMR
ii) MMR, 4-in-one preschool booster = DTaP + IPV
iii) HPV
iv) 3-in-1 teenage booster = tetanus, diphtheria + IPV, men ACWY

164
Q

VACCINATIONS
What extra vaccines may be considered?

A
  • Babies born to mothers with hepatitis B = hep B
  • Neonates at TB risk = BCG
  • Children 6m-17y with chronic health conditions get yearly flu vaccine (nasal yearly flu normally 2–10y)
165
Q

VACCINATIONS
When in the vaccination schedule would at risk individuals get…

i) hep B vaccine?
ii) BCG?

A

i) Neonate, 1m and 1y (as well as 2m, 3m, 4m as normal schedule)
ii) Neonate

166
Q

ALLERGY
What is an allergy?
Give examples

A
  • Hypersensitivity reaction initiated by specific immunoglobulins
  • Food allergy, eczema, allergic rhinitis, asthma, urticaria, insect sting, drugs, latex + anaphylaxis
167
Q

ALLERGY
Define hypersensitivity

A

Objectively reproducible symptoms/signs following a defined stimulus at a dose tolerated by a normal person

168
Q

ALLERGY
Define atopy

A

Personal/familial tendency to produce IgE in response to ordinary exposures to allergens (triad = eczema, asthma + rhinitis)

169
Q

ALLERGY
What are two theories of allergy and briefly explain them?

A
  • Hygiene hypothesis = high microbial exposure means less allergy
  • Skin sensitisation theory = regular exposure via food + preventing exposure via breaks in skin before food means less allergies
170
Q

ALLERGY
What are 2 broad categories of allergens?

A
  • Inhalant = house-dust mite, plant pollens, moulds in asthma
  • Ingestant = nuts, cow’s milk, eggs, seafood
171
Q

ALLERGY
What are the 2 broad types of allergy?

A
  • IgE mediated (some food allergies, allergic asthma)
  • Non-IgE mediated (coeliac disease, some food allergies)
172
Q

ALLERGY
How does IgE mediated allergies present?

A
  • Early phase within minutes where release of histamines from mast cells > urticaria, angioedema, sneezing + bronchospasm with a late response 4-6h later with nasal congestion, cough + bronchospasm of lower airway
  • Urticaria can be trigger if in sun or if child gets hot/cold
173
Q

ALLERGY
How does non-IgE mediated allergies present?

A
  • Typically, delayed onset of Sx + a more varied clinical course
174
Q

ALLERGY
What is the Gell and Coombs hypersensitivity classification?

A
  • Type 1 = IgE trigger mast cells + basophils to release histamines + cytokines
  • Type 2 = IgG/M bind to cell-surface antigens which is a host cell but activates immune system as considers foreign > cytotoxic
  • Type 3 = immune complex mediated with activation of complement/IgG
  • Type 4 = T-cell mediated delayed type hypersensitivity
175
Q

ALLERGY
what is the pathophysiology of a type 1 hypersensitivity reaction?

A

IgE trigger mast cells + basophils to release histamines + cytokines

176
Q

ALLERGY
what is the pathophysiology of a type 2 hypersensitivity reaction?

A

IgG/M bind to cell-surface antigens which is a host cell but activates immune system as considers foreign > cytotoxic

177
Q

ALLERGY
what is the pathophysiology of a type 3 hypersensitivity reaction?

A

immune complex mediated with activation of complement/IgG

178
Q

ALLERGY
what is the pathophysiology of a type 4 hypersensitivity reaction?

A

T-cell mediated delayed type hypersensitivity

179
Q

ALLERGY
Give an example of a type 1hypersensitivity reaction

A
  • acute anaphylaxis,
  • hayfever
180
Q

ALLERGY
Give an example of a type 2 hypersensitivity reaction

A
  • autoimmune disease,
  • haemolytic disease of newborn,
  • transfusion reaction
181
Q

ALLERGY
Give an example of a type 3 hypersensitivity reaction

A
  • SLE,
  • RA,
  • HSP,
  • post-strep glomerulonephritis
182
Q

ALLERGY
Give an example for of a type 4 hypersensitivity reaction

A
  • TB,
  • contact dermatitis
183
Q

ALLERGY
What are some investigations that can be done in allergy?

A
  • Skin prick test = test a patch + compare the size of wheals with controls
  • Patch test = useful in allergic contact dermatitis where place a patch of allergens + assess the skins’ reaction
  • RAST test = measures total + allergen specific IgE in blood
  • Food challenge test = slowly increase exposure to allergen + measure response
184
Q

ALLERGIC RHINITIS
What is allergic rhinitis?

A
  • T1 hypersensitivity reaction that is IgE mediated, can be non-atopic where environmental allergens cause allergic inflammatory response in nasal mucosa
185
Q

ALLERGIC RHINITIS
What can trigger it?

A

Tree pollen or grass (hayfever), house dust mites + pets, mould

186
Q

ALLERGIC RHINITIS
What are the types of allergic rhinitis?

A
  • Seasonal (hayfever)
  • Perennial (year-round) e.g. house dust mite allergy
  • Occupational
187
Q

ALLERGIC RHINITIS
What is the clinical presentation of allergic rhinitis?

A
  • Runny, blocked + itchy nose, sneezing
  • Red + swollen eyes
  • Post-nasal drip may cause cough
  • Associated with personal or FHx of atopy
188
Q

ALLERGIC RHINITIS
What investigations for allergic rhinitis?

A
  • Skin prick testing for pollen, animals + house dust mite
189
Q

ALLERGIC RHINITIS
What is the management of allergic rhinitis?

A
  • Avoid trigger, hoover + Change pillows regularly, good ventilation
  • PO antihistamines taken prior to exposure to reduce allergic Sx
  • Nasal corticosteroid sprays like mometasone to suppress local Sx
  • PO Montelukast or specific immunotherapy if poor control
190
Q

ALLERGIC RHINITIS
What are the different types of antihistamines that can be taken for allergic rhinitis?

A
  • Non-sedating = cetirizine, loratadine
  • Sedating = chlorphenamine (Piriton) + promethazine
  • Nasal may be good option for rapid onset Sx in response to trigger
191
Q

ANAPHYLAXIS
What is anaphylaxis?

A
  • Severe T1 hypersensitivity reaction where IgE stimulates mast cells to rapidly release histamine + other pro-inflammatory chemicals (mast cell degranulation)
192
Q

ANAPHYLAXIS
What is a consequence of anaphylaxis?
What can trigger it?

A
  • Compromise in ABC = life-threatening medical emergency
  • Foods (peanuts), insect stings, drugs, latex
193
Q

ANAPHYLAXIS
What is the clinical presentation of anaphylaxis?

A
  • Rapid onset allergic Sx = urticaria, itching, angioedema with swelling around lips + eyes
  • Anaphylaxis Sx = SOB, wheeze, stridor (larynx swelling), tachycardia, light-headed + collapse
194
Q

ANAPHYLAXIS
What investigation confirms anaphylaxis?

A
  • Serum mast cell tryptase within 6h of event = mast cell degranulation
195
Q

ANAPHYLAXIS
What is the acute management of anaphylaxis?

A
  • Airway = secure
  • Breathing = oxygen, salbutamol to help wheeze, monitor SpO2, RR
  • Circulation = IV fluid bolus with collapse, monitor BP, ECG
  • Disability = lie pt flat to improve cerebral perfusion
  • Exposure = look for flushing, urticaria + angioedema
196
Q

ANAPHYLAXIS
What medications can be given in anaphylaxis?

A
  • IM adrenaline (EpiPen if community), repeat after 5m if necessary
  • Antihistamines like chlorphenamine or cetirizine
  • Steroids like IV hydrocortisone
197
Q

IMMUNE DEFICIENCY
What are the 2 broad types of immune deficiency?

A
  • Primary (uncommon) = intrinsic defect in the immune system
  • Secondary = due to another disease or treatment (HIV, nephrotic syndrome)
198
Q

IMMUNE DEFICIENCY
When would you suspect immune deficiency?

A

Severe, prolonged, unusual or recurrent (SPUR) infections

199
Q

IMMUNE DEFICIENCY
What are the 6 types of immune deficiency?

A
  • T-cell defects
  • B-cell defects
  • Combined B- + T-cell defects
  • Neutrophil defect
  • Leucocyte function defect
  • Complement defects
200
Q

IMMUNE DEFICIENCY
What are T-cell defects?

A
  • Severe/unusual viral + fungal infections + failure to thrive in first 2m
201
Q

IMMUNE DEFICIENCY
Give some examples of T-cell defects

A
  • DiGeorge syndrome
  • HIV
  • Duncan syndrome (X-linked lymphoproliferative disease)
  • Ataxic telangiectasia
  • Wiskott-Aldrich
202
Q

IMMUNE DEFICIENCY
What are B-cell defects?
Give some examples

A
  • Present beyond infancy as passively acquired maternal antibodies, severe bacterial infections, esp. (lower) RTIs.
  • Selective IgA deficiency (#1)
  • X-linked (Bruton) agammaglobulinaemia
  • Common variable immune deficiency
203
Q

IMMUNE DEFICIENCY
Give some examples of combined B- and T-cell disorders

A
  • Severe combined immunodeficiency = group of inherited disorders of profound defective cellular + humoral immunity
  • Hyper IgM syndrome = B cells produce IgM but prevented from IgG/A
204
Q

IMMUNE DEFICIENCY
What do neutrophil defects lead to?
Give an example

A
  • Recurrent bacterial infections
  • Chronic granulomatous disease = X-linked recessive, defect in phagocytosis as fail to produce superoxide after ingestion
205
Q

IMMUNE DEFICIENCY
What are leucocyte function defects?
Give an example

A
  • Delayed separation of umbilical cord, wound healing, chronic skin ulcers
  • Leucocyte adhesion deficiency = deficiency of neutrophil surface adhesion molecules so inability to migrate to sites of infection
206
Q

IMMUNE DEFICIENCY
What are complement defects?
Examples

A
  • Recurrent bacterial infections (meningococcal, HiB, pneumococcus), SLE-like illness
  • Hereditary angioedema (measure C4 levels)
  • Mannose-binding lectin deficiency
207
Q

IMMUNE DEFICIENCY
What are some investigations for immune deficiency?

A
  • FBC (WCC, lymphocytes, neutrophils)
  • Blood film
  • Complement
  • Immunoglobulins
208
Q

IMMUNE DEFICIENCY
What prophylaxis should be given in immune deficiency?

A
  • T-cell + neutrophil = co-trimoxazole for PCP, fluconazole for fungal
  • B-cell = azithromycin for recurrent bacterial infections
209
Q

IMMUNE DEFICIENCY
What is the management of immune deficiency?

A
  • Prompt, appropriate + longer Abx courses
  • Screen for end-organ disease (CT scan)
  • Ig replacement therapy if antibody deficient
  • Bone marrow transplantation for SCID, chronic granulomatous disease
210
Q

WHOOPING COUGH
What is it?

A
  • Highly contagious form of bronchitis caused by Bordetella pertussis > gram -ve aerobic coccobacillus
211
Q

WHOOPING COUGH
What is the clinical presentation of pertussis?

A
  • Week of coryza (catarrhal phase)
  • Paroxysmal spasmodic coughing bouts (attacks)
  • Followed by classic inspiratory whoop (infants may have apneoa not whoop, paroxysmal phase)
  • Spasms of cough > vomiting, epistaxis, subconjunctival haemorrhage
212
Q

WHOOPING COUGH
How long does the cough last?

A
  • Can last for months = ‘100 day cough’
213
Q

WHOOPING COUGH
What are the investigations?

A
  • Nasopharyngeal swab with bacterial culture or PCR
  • Marked lymphocytosis on blood film (predom high lymphocytes)
  • Test for anti-pertussis toxin IgG if cough >2w
214
Q

WHOOPING COUGH
What are some complications of pertussis?

A
  • Pneumonia
  • Convulsions
  • Bronchiectasis
215
Q

WHOOPING COUGH
What is the management of pertussis?

A
  • Notify PHE
  • Prophylaxis = vaccine (esp. infants + pregnant women) or if close contact macrolide (erythromycin)
  • PO macrolides (azithromycin, clarithromycin) 1st line if onset <21d
  • School exclusion for 48h following Abx or 21d from onset if no Abx
216
Q

WHOOPING COUGH
When should you admit a child to hospital with pertussis?

A
  • Suffering from cyanotic attacks
  • <6m
217
Q

POLIO
what is the cause?

A

poliovirus type 1

218
Q

POLIO
what is the pathophysiology?

A
  • transmitted via faecal-oral route
  • incubation period is 3-30 days + can be excreted for up to 6 weeks
  • replicates in nasopharynx + GI tract and can spread to CNS where it can affect anterior horn cells, motor neurons and the brainstem
219
Q

POLIO
what is the clinical presentation?

A

90-95% of cases are asymptomatic
fatigue
fever
nausea and vomiting
diarrhoea
sore throat
headache
photophobia

220
Q

POLIO
what are the clinical features of a more serious polio infection?

A

acute flaccid paralysis (AFP)
- initially fatigue, fever N+V
- asymmetrical lower limb weakness and flaccidity

can progress to life-threatening bulbar paralysis and respiratory compromise

221
Q

POLIO
what are the investigations?

A
  • virus culture from stool, CSF or pharynx
  • CSF analysis
  • serum antibodies to poliovirus
  • MRI of spinal cord
  • EMG of affected limb(s)
222
Q

POLIO
what is the management?

A
  • supportive care with rehydration and neurological monitoring
  • physiotherapy
  • intubation and ventilation for respiratory paralysis
223
Q

POLIO
what are the complications?

A

post-poliomyelitis syndrome (PPS) - this usually occurs years after the initial infection
- demonstrates the same features as polio infection
- treated in the same way as polio

224
Q

DIPHTHERIA
what is the cause?

A

Corynebacterium diphtheriae

225
Q

DIPHTHERIA
what is the pathophysiology?

A
  • it infects the epithelium of the skin and the mucosa of the upper resp tract
  • it forms a grey pseudomembrane
226
Q

DIPHTHERIA
what is the clinical presentation?

A
  • sore throat
  • low grade fever
  • dysphagia, dysphonia, dyspnoea and croupy cough can occur in serious illness
227
Q

DIPHTHERIA
what are the investigations?

A
  • throat + nose swabs, microscopy and culture
  • diphtheria antibodies
  • PCR
228
Q

DIPHTHERIA
what is the management?

A
  • hospitalisation, isolation
  • diphtheria anti-toxin
  • antibiotic (procaine benzylpenicillin)
229
Q

DIPHTHERIA
what is the management for close-contacts?

A

prophylactic antibiotics - erythromycin

diphtheria toxoid immunisation

230
Q

CANDIDIASIS
what is the cause?

A

candida albicans fungus

231
Q

CANDIDIASIS
what are the predisposing factors?

A
  • moist body folds
  • treatment with broad spectrum antibiotics
  • immunosuppression
  • diabetes mellitus
232
Q

CANDIDIASIS
where can it occur?

A
  • skin folds
  • vagina
  • penis
  • mouth
  • corners of mouth
  • nail beds (paronychia)
233
Q

CANDIDIASIS
what is the clinical presentation?

A
  • rash/scaling
  • white/yellow vaginal discharge
  • white patches on tongue
  • cracks at the corner of mouth
  • white/yellow nail that separates from the nail bed
234
Q

CANDIDIASIS
what are the investigations?

A

skin scrapings for microscopy and culture

235
Q

CANDIDIASIS
what is the management?

A

oral or topical anti-candidial drugs e.g. nystatin, fluconazole

236
Q

UTRICARIA AND ANGIOEDEMA
what is urticaria?

A

It is a red itchy bumpy rash which can occur anywhere on the body.
It is common - affects at least 20% of people at some stage in their lives
The swelling and redness often improves in one area and then appears in another
It can tingle and itch but is not usually painful.
It is also called nettle rash, welts or wheals.

237
Q

URTICARIA AND ANGIOEDEMA
what is angioedema?

A

It is a swelling deep in the skin which occurs in a minority of people with urticaria or sometimes on its own.
It frequently involves the eyelids, lips and sometimes the mouth.
Sometimes the swelling can be very obvious making it difficult to open the eyes for example.

238
Q

UTRICARIA AND ANGIOEDEMA
what is the pathophysiology?

A

Mast cells release histamine in response to a perceived irritant

239
Q

URTICARIA AND ANGIOEDEMA
what are the causes?

A
  • viral infection
  • idiopathic
  • cold
  • heat
  • exercise
  • stress
  • medications - NSAIDS, antihypertensives
  • thyroid function
240
Q

URTICARIA AND ANGIOEDEMA
is it an allergy?

A
  • single episode could be allergy but there needs to be an obvious link and occur within one hour of food consumption
  • most of the time it is not an allergy
241
Q

URTICARIA AND ANGIOEDEMA
how long does it last for?

A
  • single episode can last a few days
  • can get several episodes over a 4-6 week period = viral
  • recurrent angioedema + urticaria can last for 16-18 months
242
Q

URTICARIA AND ANGIOEDEMA
what is the management?

A
  • antihistamines - cetirizine, loratadine and fexofenadine
  • leukotriene receptor antagonists - montelukast, ranitidine, tranexamic acid
  • prednisolone for severe attacks

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