Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Paeds > Infection/Immunology > Flashcards

Infection/Immunology Flashcards

1
Q

What organisms cause bacterial meningitis by age?

A

Neonate-3m

  • GBS
  • E.Coli/ other coliforms
  • Listeria

1m-6y

  • N meningitidis
  • Strep pneumoniae
  • HiB

> 6y

  • N meningitidis
  • Strep pneumoniae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What pathogen is meningococci?

A

Neisseria Meningitidis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does meningococcal disease cause?

A

Meningitis 30-50%
Septicaemia 7-10%
Both 40%

  • Neurological consequences in 10%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Peak incidence of meningococcaemia?

A

6-24m

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Meningitis vaccination schedule?

A

Men B –> 8w, 16w, 1y
Men C –> discontinued 2016
Men A –> 14y (Men ACWY)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In UK which N meningitides most common?

A

Men B - vaccine not that effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Features of meningitis? (many)

A
  • Fever
  • Headache
  • Photophobia
  • Neck stiffness
  • Lethargy
  • Poor feeding/vomiting
  • Irritability
  • Hypotonia
  • Drowsiness
  • Loss of consciousness
  • Seizures
  • Petechiae rash
  • → Can be v non-specific in young children/ early stages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Features of meningoccaemia?

A

→ Signs of shock

  • Tachycardia
  • Tachypnoea
  • Prolonged cap refill
  • Hypotension
  • Cold extremities
  • PURPURIC RASH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Features of a purpuric rash? (3)

A
  • Non-blanching on palpation
  • Irregular in size and outline
  • Necrotic centre
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What management if child with purpuric rash + fever?

A

Immediate systemic IV/IM abx eg benzylpenicillin

Immediate transfer to hospital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Ddx for purpuric rash? (3)

A
  • Infections → septicaemia, measles, other meningitis
  • Immune causes → HSP, SLE, RA
  • Thrombocytopaenic → leukaemia, aplastic anaemia, immune thrombocytopaenia, DIC, HUS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ix if petechial rash + fever?

A
  • FBC
  • CRP
  • Coagulation screen
  • Blood culture
  • Whole body PCR for N. Meningitidis
  • Blood glucose
  • Blood gas (for acidosis)
  • U&Es, LFTs
  • Culture of blood, throat, urine, stool
  • LP unless CI (raised ICP, shock)
  • Consider CT/MRI and EEG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which abx to give in confirmed meningococcal disease?

A

IV ceftriaxome for 7d

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Immediate complications of meningococcaemia?

A
  • DIC
  • Coma
  • Thrombocytopaenia
  • Septic arthritis
  • Bacterial endocarditis
  • Peripheral gangrene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Long term complications for meningococcaemia?

A
  • Hearing loss
  • Orthopaedic - damage to bones and joints
  • Skin complications (inc scarring from necrosis)
  • Psychosocial problems
  • Neurological and developmental problems
  • Renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Commonest pathogen overall in sepsis in children?

A

N Meningitidis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Common pathogens in sepsis in neonates?

A

Early onset (<48h) → from mother/birth canal

  • GBS
  • E Coli
  • Coagulase negative staph
  • H influenza
  • Listeria monocytogenes

Late onset (4-90d) → from environment:

  • Coagulase negative staph
  • S. Aureus
  • E. Coli
  • Klebsiella
  • Pseudomonas
  • Candida
18
Q

Sepsis sx?

A
  • Fever
  • Poor feeding
  • Miserable, irritable, lethargy
  • Hx of focal infection, e.g. meningitis, osteomyelitis, gastroenteritis, cellulitis
  • Predisposing conditions, e.g. sickle cell disease, immunodeficiency
19
Q

Signs of sepsis?

A
  • Fever
  • Tachycardia, tachypnoea, low BP
  • Purpuric rash (meningococcal septicaemia)
  • Shock
→ delayed cap refill, widened pulse pressure
  • Multi-organ failure
20
Q

Normal pulse rate by age?

A

<1y –> 110-160
1-5y –> 95-140
5-12y –> 80-120
>12y –> 60-100

21
Q

Upper limit of SBP for

a) 1-5y
b) 6-10y

A

a) <110mmHg

b) <120mmHg

22
Q

Clinical features of shock?

A

Early (compensated)

  • Tachypnoea
  • Tachycardia
  • Decreased skin turgor
  • Sunken eyes and fontanelle
  • Delayed capillary refill (>2 s)
  • Mottled, pale, cold skin
  • Core–peripheral temperature gap (>4°C)
  • Decreased urinary output

Late (decompensated)

  • Acidotic (Kussmaul) breathing
  • Bradycardia
  • Confusion/depressed cerebral state
  • Blue peripheries
  • Absent urine output
  • Hypotension
23
Q

Empirical abx for suspected sepsis in

a) <8w
b) >8w

A

a) ampicillin + gentamicin/cefotaxime/ceftriaxone

b) 3rd gen cephalosporin - cefotaxime/ceftriaxone

24
Q

Initial fluid resus in shock?

A

0.9% saline or blood
20ml/kg

Give 2x if necessary

25
Q

2 types of allergic reactions?

A

Non-IgE mediated

  • Reflux, tummy pain, eczema, diarrhea
  • Delayed onset and variable clinical presentation

IgE mediated (T1 hypersensitivity)

  • Swelling, urticarial, angioedema, sneezing, bronchospasm, anaphylaxis
  • Early phase → caused by histamine release and other mediators from mast cells → urticaria, angioedema, sneezing and bronchospasm
  • Late phase → 4-6 hours later with nasal congestion in upper airway and cough and bronchospasm in lower airway
26
Q

Pathophysiology of IgE mediated allergic reaction?

A

Sensitisation:

  • Antigen of allergen taken up by antigen-presenting cell
  • Antigen is presented on class II MHC to T helper cells
  • T cell produces cytokines to cause B cells to proliferate and differentiate into IgE-producing plasma cells
  • IgE molecules attach via constant regions to Fc receptors on mast cells
  • Once attached IgE molecules can survive for weeks
  • → Now sensitized

Reaction

  • When exposed to antigen 2nd time, antigen binds to IgE antibodies on mast cells
  • To trigger response, 2 IgE molecules must interact with specific antigen
  • This → release of histamine and other inflammatory mediators
  • → Capillary dilation, airway constriction, mucus secretion, pain, itching
27
Q

Management strategies for allergies? (4)

A
  • Antihistamines
  • Steroids
  • Epipen provided for anaphylaxis
  • Possibly systemic desensitisation
28
Q

How does HIV present when there is mild immunosuppression?

A
  • Lymphadenopathy

- Parotitis

29
Q

How does HIV present when there is moderate immunosuppression?

A
  • Recurrent bacterial infections
  • Candidiasis
  • Chronic diarrhea
  • Lymphocytic interstitial pneumonitis (LIP)
  • → This lymphocytic infiltration of lungs may be caused by a response to HIV infection itself, or may be related to EBV infection
30
Q

Name some severe AIDs defining diagnoses?

A
  • Opportunistic infections, e.g. Pneumocystis jiroveci (carinii) pneumonia (PCP)
  • Severe FTT
  • Encephalopathy
  • Malignancy → rare in children
  • > 1 clinical feature often present
  • Unusual constellation of symptoms, esp if infectious, should alert one to HIV infection
31
Q

What interventions are used to reduce mother-baby transmission of HIV?

A
  • Use of maternal antenatal, perinatal and postnatal ARVs to achieve undetectable maternal viral load at time of delivery
  • Avoidance of breast­feeding
  • Active management of labour and delivery, to 
avoid PROM or
unnecessary instrumentation
  • Pre­labour C- section if mother’s viral
load detectable close to delivery
32
Q

Management of HIV?

A

Drugs:

  • As in adults, 3 or 4 dugs used
  • PCP prophylaxis with co-trimoxazole given to all infants with HIV or older children with low CD4

Other aspects:

  • Immunisation → give all routine but not BCG (live), also give additional against influenza, Hep A, B and varicella
  • MDT management with family to ensure compliance and planning for future
  • Regular follow up – weight, neurodevelopment, clinical S+S of disease
33
Q

Clinical features of infectious mononucleosis?

A
  • Fever
  • Malaise
  • Tonsillopharyngitis – often severe, limiting oral ingestion of fluids and food; rarely, breathing compromised
  • Lymphadenopathy – prominent cervical lymph nodes, often diffuse adenopathy
  • Fatigue
34
Q

Treatment of infectious mononucleosis?

A
  • Symptomatic
  • When airway severely compromised, corticosteroids considered
  • In 5%, group A strep grown from tonsils
  • → May be treated with penicillin
  • Ampicillin or amoxicillin may cause florid maculopapular rash in children infected with EBV and should be avoided
35
Q

Complications of infectious mononucleosis?

A
  • Prolonged fatigue (>6m) → >1/10 pts
  • Anaemia/neutropenia/ thrombocytopenia
  • Ruptured spleen – 1/500-1000 cases → avoid contact sports during illness
  • Neurological complications →Guillain Barre, Bell’s palsy, viral meningitis, encephalitis
  • Secondary infection → pneumonia, pericarditis (usually only if immunocompromised)
36
Q

What is Kawasaki disease?

A

Systemic vasculitis (usually in <5yo)

  • Specific cause unknown
  • Important diagnosis b/c aneurysms of coronary arteries are potentially devastating complication
37
Q

Diagnostic criteria of Kawasaki disease?

A

Fever (>38) ≥ 5 days duration + ≥4 of (incomplete if <4):

  • Polymorphous rash (92%) – many different forms, always extensive
  • Changes in extremities
- eg erythema of palms/soles (80%), indurative oedema, desquamation of fingers/toes
  • Bilateral non exudative bulbar conjunctivitis
  • Changes in lips and oral cavity
- eg dryness, erythema, fissuring of lips, strawberry tongue (71%)
  • Cervical lymphadenopathy – least common

RED RED RED

38
Q

Ddx of Kawasaki disease? (7)

A
  • Viral exanthems (e.g. measles, adenovirus, enterovirus, EBV)
  • Scarlet fever
  • Staphylococcal scalded skin syndrome
  • Stevens-Johnson syndrome
  • Juvenile idiopathic arthritis (systemic onset)
  • Toxic shock syndrome
  • Drug hypersensitivity reactions
39
Q

Diagnostic test for Kawasaki disease?

A

No diagnostic test

–> Clinical diagnosis

40
Q

Treatment of Kawasaki disease?

A
  • Self-limiting, treat to reduce coronary aneurysms
  • Coronary arteries affected in 1/3 within 6w, aneurysms can → subsequent narrowing of vessels → myocardial ischaemia and sudden death
  • Mortality = 1-2%
  • IVIG given within 10d – reduce aneurysms
  • Aspirin – reduce thrombosis
  • If giant coronary aneurysms – may need long term warfarin
  • Can use antiplatelet if severe thrombocytosis

Paeds (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions