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4th year Paediatrics Placement > Rash > Flashcards

Rash Flashcards

1
Q

What is HSP?

A
  • ANCA negative small vessel vasculitis
  • This is a generalized vasculitis involving the small vessels of the skin, the GI tract, the kidneys and joints (rarely the lungs and CNS) and it is due to deposition of IgA complexes in these places
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2
Q

Who tends to get HSP?

A
  • About 75% of cases occur in children aged 2-11
  • More than 75% of patients have had a preceding URTI. Pharyngeal or GI infection (1-3 weeks before)
  • Commonly infection with group A strep
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3
Q

Presentation of HSP?

A
  • Purpuric rash over buttocks and lower limbs
  • Colicky abdo pain
  • Bloody diarrhea
  • Joint pain with or without swelling
  • Renal involvement – 55% will have renal involvement but it is usually not serious ranging from microscopic haematuria and proteinuria to nephrotic and nephritic syndrome and renal failure
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4
Q

Investigations for HSP?

A
  • Diagnosis is clinical – investigations are usually ruling out other conditions
  • Urinalysis to check for renal involvement
  • FBC may show raised counts
  • Raised ESR
  • Serum IgA is often raised
  • Autoantibodies
  • Abdo US
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5
Q

Management of HSP?

A
  • There is no proven treatment of benefit
  • It is usually self limiting with symptoms resolving in 8 weeks
  • Relapses can occur for months to years
  • MUST PERFORM URINE ANALYSIS TO SCREEN FOR RENAL INVOLVEMENT AS HENOCH SCHONLEIN CAN POTENTIALLY CAUSE RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS
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6
Q

What is anaphylaxis?

A
  • Severe life-threatening generalised hypersensitivity reaction involving the airway and circulation
  • Clinical emergency
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7
Q

Aetiology of anaphylaxis?

A
  • Food triggers are common in children
  • Other triggers include drugs, radiocontrast dyes, venom
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8
Q

Presentation of anaphylaxis?

A
  • Generally ABCDE examination
  • Stridor, swollen airway, struggling to breathe
  • Tachypnoea, wheezing, cough, chest tightness, dyspnoea, hypoxia, acute airway obstruction
  • Dizziness, pallor, tachycardia, collapse, hypotension
  • Confusion, loss of consciousness
  • Feeling of impending doom
  • Urticaria, angioedema
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9
Q

Management of anaphylaxis?

A
  • IM adrenaline – 1:10 000 into anterolateral thigh
  • High flow oxygen and establish airway
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10
Q

Investigations and further management of anaphylaxis?

A
  • Take a blood sample for mast cell tryptase
  • Follow up in allergy clinic
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11
Q

Explain what leukaemia is and most common type in childhood?

A
  • Leukaemia is cancer where there are malignant white cells in the bone marrow and blood
  • Acute lymphocytic leukaemia is the main leukaemia that occurs in children
  • Disruptions in proliferation of lymphoid precursor cells in the bone marrow leads to excessive production of imature blast cells and subsequent drop in the numbers of functional RBCs, WBCs and platelets
  • This is the most common childhood cancer
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12
Q

Incidence of ALL peaks at ____________ patients with some genetic conditions ______ are at increased risk _______

A

age 2-5 years
e.g. Downs

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13
Q

Presentation of leukaemia?

A
  • Specific symptoms are essentially due to deficiencies in functional blood cells:
  • Anaemia – pallor, fatigue, breathless
  • Thrombocytopaenia – easy bruising and bleeding
  • Leukopenia – fevers and infections
  • Children may also complain of bone pain as increased pressure from hyperplastic marrow
  • Weight loss and malaise are also common
  • ALL can also infiltrate the CNS causing seizures and headaches as well as infiltrating the testes
  • Examination may show pallor, easy bruising, lymphadenopathy and hepatosplenomegaly
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14
Q

Investigations for leukaemia?

A
  • FBC likely to show a pancytopenia
  • Blood film likely to show presence of blast cells
  • CXR to exclude mediastinal mass
  • Immunophenotyping is required for a definitive diagnosis with peripheral blood or can also be done on bone marrow
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15
Q

Management of leukaemia?

A
  • Treatment usually involves cycles of chemotherapy, the cycles are of varying intensity and treatment can last for 2-3 years
  • Sometimes patients are given steroids along with the chemotherapy to improve effectiveness
  • Targeted therapies can be used in certain subtypes
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16
Q

Prognosis of leukaemia?

A
  • Over 90% of children are now expected to survive ALL but many suffer complications as a result of treatment or initial diagnosis
  • Infertility, avascular necrosis, peripheral neuropathy and anxiety are all relatively common
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17
Q

What is JIA?

A
  • Autoimmune arthritis that primarily affects children (typical onset before 16)
  • Causes pain and swelling in joints
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18
Q

3 major types of JIA?

A
  • Oligoarticular JIA (fewer than 6 joints)
  • Polyarticular JIA (multiple joints)
  • Systemic JIA (wild variety of systemic symptoms)
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19
Q

What type of JIA tends to cause fevers and a rash?

A

systemic

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20
Q

Presentation of JIA?

A
  • Joint pain
  • Morning stiffness or stiffness after still for a period (gelling)
  • Limp
  • 25% may report no pain, only swelling is observed, massage doesn’t help
  • Systemic symptoms with systemic JIA e.g. rash, daily fevers, hepatosplenomegaly and lymphadenopathy
21
Q

Diagnosis of JIA?

A
  • No one lab is totally diagnostic
  • Elevated ESR, CRP, WBC, platelets
  • Most children do not have positive rheumatoid factor
  • RF positive predicts chronic erosive joints in polyarticular JIA
  • ANA positive is associated with increased risk of uveitis (refer these patients to ophthalmologist)
  • HLAB27 increases risk of enthesitis associated JIA
22
Q

Management of JIA?

A
  • NSAIDs should be tried first
  • Steroids (joint injections)
  • Methotrexate in some children if other treatments not working (follow CBC and LFTs every few months for neutropenia, transaminitis)
23
Q

Complications of JIA and mangement?

A
  • Leg length discrepancy – special shoes or operative
  • Uveitis – requires frequent ophthalmologist screening if ANA pos
  • Contractures – physical therapy, Botox injections and muscle relaxants
  • Growth problems – careful monitoring
24
Q

Prognosis of JIA?

A
  • Oligoarticular – highest rate of remission
  • RF pos oligoarticular has lowest likelihood of remission persist into adulthood as other forms of arthritis
  • Prognosis for systemic depends on extent of arthritis and systemic symptoms after 6 months
25
Q

Measles virus is a type of _____ spread by ________

A

paramyxovirus
highly contagious spread by droplet infection

26
Q

Presentation of measles?

A
  • Prodromal cough, conjunctivitis and coryza (cold like symptoms)
  • Also get characteristic Koplik spots (white spots on a reddened background that occur on the inside of cheeks early in the course of measles)
  • Eruptive Exanthem phase – red blotchy maculopapular rash that spreads from the head downwards to eventually involve the whole body
  • Recovery phase- final symptom persistent cough
27
Q

Diagnosis and Management of measles?

A
  • Most cases are diagnosed clinically but detection of measles specific IgM in blood or oral fluid or genome or antigen detection from nasopharyngeal aspirates or throat swabs can be used to confirm the diagnosis
  • Management is supportive
  • Prevention with vaccine
28
Q

Complications of measles?

A
  • Most worrying complication in an immunocompetent person is risk of encephalitis
  • Other complications include pneumonia and risk of super infections as the virus suppresses the immune system
  • Complications worse amongst young infants
  • In children under 2 there is the risk of rare subacute sclerosing panencephalitis which occurs 7-10 years after initial infection where there is persistence of the virus, reactivation and progressive mental deterioration with a fatal outcome
29
Q

Mumps is caused by infection with ________ it is spread by _______ and humans _________

A

paramyxovirus, spread by droplet infection or direct contact or through fomites, humans only known natural hosts

30
Q

Presentation of mumps?

A
  • Primarily a disease of school aged children and young adults, uncommon before age 2
  • Prodromal symptoms are fever, malaise, headache and loss of appetite
  • Usually followed by severe pain over the parotid glands with either unilateral or bilateral parotid swelling
  • Side note: the parotid glands sit just in front of the ears on each side of the face
  • These enlarged glands obscure the angle of the mandible and may elevate the ear lobe (differentiate from cervical lymph node enlargement as that wouldn’t elevate the ear lobe)
  • Trismus is common at this stage (restriction of the range of motion of the jaw, can be painful)
31
Q

Complications of mumps?

A
  • Can cause meningitis and encephalitis
  • Can infect the testicles and epididymis in males, and then cause inflammation resulting in testicular atrophy, decreased sperm count and motility, although rarely issues are large enough to cause infertility
  • Glomerulonephritis, arthritis, myocarditis, hepatitis, pancreatitis and polyarthritis can also occur
  • Should note that mumps in pregnancy does not increase the risk of congenital defects
32
Q

Diagnosis and management of mumps?

A
  • Diagnosis is on basis of clinical features but can be confirmed using serology and swabs
  • Treatment is supportive
  • Prevention should be mainstay with vaccine available for all children in UK
33
Q

Describe AML in children?

A

second most common leukaemia - vast majority are ALL
tends to have a worse prognosis

34
Q

Rubella is caused by infection with ______

A

RNA virus

35
Q

What is the main worry with rubella?

A
  • Major complication is congenital rubella syndrome if there is maternal infection during pregnancy which causes: cataracts (or other eye abnormalities), hearing impairment and congenital heart abnormalities
36
Q

Presentation of rubella?

A
  • Prodromal phase of fever, headache, mild conjunctivitis and rhinorrhoea
  • Then rash develops initially pink discrete macules that coalesce starting from behind ears to face, and then down
  • Lymphadenopathy often occurs
  • Constitutional symptoms are usually mild
  • In adults arthralgia is common
  • There may be petechiae on the soft palate (Forchheimer’s sign but this is not diagnostic)
37
Q

Investigations for rubella?

A
  • Clinical diagnosis is unreliable as presentation is mimicked by other viruses
  • Serological and/ or PCR is diagnostic
38
Q

Management of rubella?

A
  • Supportive treatment
  • Isolate child
39
Q

Complications of rubella?

A
  • These are rare
  • Encephalopathy
  • Arthritis and arthralgia
  • Thrombocytopenia
  • GBS
  • Panencephalitis
  • Rubella in pregnancy – mother may be offered a termination if there is confirmation that they have been infected
40
Q

What is viral xanthema?

A

eruptive widespread rash, generally caused by a virus. Used to be called diseases 1-6

  1. measles
  2. scarlet fever
  3. rubella
  4. dukes disease
  5. parvovirus B19
  6. roseola infantum
41
Q

Difference between allergy and intolerance?

A

Allergy is overreaction of your immune system, intolerance is the direct effect of food on the GI system
Allergy is immune mediated, intolerance is not

42
Q

Types of food allergy?

A

Two main types: immediate hypersensitivity reactions and delayed
Immediate is IgE mediated and comes on instantly to within 2 hours
Can be hard to tell difference between delayed reactions and an intolerance

43
Q

Treatment of an immediate food allergy?

A
  • Treatment: avoid allergen, antihistamine plus minus adrenaline, ?immunotherapy, see if grow out of it
  • ?immunotherapy – food currently only peanuts, beestings, wasp stings and grass pollen – protects against accidental exposure, doesn’t allow you to eat peanuts – for people who are anaphylactic
44
Q

Is allergy testing helpful in urticaria always?

A

no - some children may just have chronic urticaria - tests can only be done in a context of a history - if not a pattern with food it probably isn’t a food allergy

45
Q

How do you test for delayed onset allergic reactions?

A

no real test, just have to remove the food and see if gets better, common groups are dairy, soy, wheat and eggs

46
Q

Presentation of delayed onset allergies?

A

can cause eczema
GI symptoms
sometimes hard to tell difference between intolerance

47
Q

Presentation of cows milk protein allergy?

A

can present immediately as an IgE mediated reaction (urticaria, lip swelling, nausea, vomiting, diarrhoea etc)

or delayed non IgE mediated (atopic eczema, abdominal symptoms)

IgE mediated can be measured by RAST but with delayed reaction you just have to exclude it from diet on suspicion and see if it gets better

48
Q

What formula do you use for CMPA?

A

extensively hydrolysed formula

49
Q

Management of CMPA?

A

if babies are breastfed then Mum needs to exclude dairy from her diet
if they are formula fed then they need to go on extensively hydrolysed formula
most children outgrow CMPA by 3 years of age (many before)
introduce milk using the milk ladder trialling every 6 months and gradually moving up or down rungs depending on reaction

4th year Paediatrics Placement (11 decks)

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