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Paediatrics > Infection and Immunology > Flashcards

Infection and Immunology Flashcards

1
Q

What is the incidence of meningococcaemia?

A

2/3 are viral
80% of bacterial cases are in patients younger than 16yo
- 10% mortality
- 10% neurological deficit

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2
Q

What is the pathophysiology of meningococcaemia?

A

N. meningitides causes it
A+C occur in Asia and Africa
B+C occur in Europe, North and South America

Infection is preceded by nasopharyngeal colonisation

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3
Q

What are the virulence factors of N. meningtitides?

A

Polysaccharide capsule
Lipo-oligosacchardie endotoxin (mediates invasion and is protein body responds to)
Immunoglobulin A1 protease (cleaves membranes and helps virus survive intracellularly)

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4
Q

What are other causative organisms of meningitis?

A

Neonates to 3 months - Group B strep, E. coli, Listeria

1 month - 6 years - N. meningitidis, Strep. pneumoniae, H. influenzae

> 6 years - N. meningitidis, Strep. pneumoniae

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5
Q

How does meningitis present in the first 3 months?

A

In neonate period, associated with maternal infection or pyrexia on delivery

Hyper/hypothermia
Irritability
Lethargy
Bulging fontanelle
Quiet at rest but cries when moved
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6
Q

How does meningitis present >3 months?

A

Features more associated with bacterial infection - fever, vomiting, irritability, lethargy

Petechial rash common
Postive Kernig and Brudzinski

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7
Q

What is septicaemia?

A

Activation and stimulation of immune system by cytokines

Capillary leak
Coagulopathy
Metabolic derangement
Myocardial failure

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8
Q

How does capillary leak occur in sepsis?

A

Presentation until day 4

Vascular permeability increases causing protein to enter intravascular space and urine -> severe hypovolaemia

Initial vasoconstriction to compensate but eventually decreased venous return and cardiac output

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9
Q

How does coagulopathy occur in sepsis?

A

Cytokines activate procoagulation factors in blood vessel wall -> endothelial damage

Damaged wall inhibits anticoagulation properties -> intravascular clotting and multiple organ failure

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10
Q

How does metabolic derangement occur in sepsis?

A 
Acidosis with severe abnormalities
Hypokalaemia
Hypocalcaemia
Hypomagnesaemia
Hypophosphataemia
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11
Q

How does myocardial failure occur in sepsis?

A

Function remains impaired after circulating volume is restored
Gallop rhythm with elevated central venous pressure and hepatomegaly

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12
Q

What are differentials of meningococcal septicaemia?

A 
Sepsis
Febrile seizures
Measles
Mumps
HSP
ITP
Reye's syndrome
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13
Q

What is the initial treatment of meningitis?

A

Ceftriaxone or cefotaxime
Dexamethasone reduces risk of long term complications

Rifampicin to eradicate nasopharyngeal carriage in household contacts

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14
Q

What are complications of meningococcal disease?

A 
DIC
Thrombocytopenia
Septic arthritis
Pericarditis
Bacterial endocarditis
Gangrene
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15
Q

What are causative agents of early onset neonatal sepsis?

A

Ascending infection from the birth canal into amniotic fluid –> pneumonia and septicaemia

Group B strep
E. coli
H. influenzae
Listeria

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16
Q

What are causative agents of late-onset neonatal sepsis?

A 
Staph. epidermidis
Staph. aureus
E. coli
Klebsiella
Pseudomonas
Enterobacter
Candida
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17
Q

What are the causes of infant sepsis?

A

H. influenze B
Strep. pneumoniae
N. meningitides
Salmonella

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18
Q

What is the pathophysiology of shock?

A

Inadequate delivery of substrates and oxygen to meet metabolic needs of the tissue

Anaerobic respiration leads to lactic acid accumulation until energy cannot be produced any more

Disruption of cell membrane pumps -> accumulation of intracellular sodium and efflux of potassium

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19
Q

What antibiotics are used for septicaemia?

A

6-8 weeks AMPICILLIN + gent, cefotacime or ceftriaxone

Older infants have cefs

20
Q

What is the pathophysiology of an allergic reaction?

A

Type 1 hypersensitivity
Involves IgE and mast cells which bind together via antigens
Release of inflammatory mediators -> vasodilation, smooth muscle contraction, increased small vessel permeabilty, secretion of mucus

21
Q

How is HIV passed to children?

A

Pregnancy, delivery or breast feeding

22
Q

What are risks of HIV?

A

Opportunistic infections - TB, PCP (give co-trimoxazole), VZV, HSV, candida

Blood problems - thrombocytopenia, anaemia, neutropenia

Kaposi’s sarcoma, non-Hodgkin’s lymphoma

DON’T GIVE BCG VACCINE -> DIC

23
Q

How does infectious mononucleosis present?

A 
1-2 weeks of fatigue and malaise
Sore throat
Headache - retro-orbital
LUQ pain - spleen enlargement (?rupture)
Fever
24
Q

What are complications of mono?

A

Hepatitis
Jaundice
Thrombocytopenia

25
Q

What is the diagnostic criteria for Kawasaki disease?

A 
Fever >30 for >5 days
Conjunctival injection in both eyes
Change to mouth or throat
Chnage to skin on arms or legs
Rash
Swollen lymph nodes of neck
26
Q

What are the three phases of Kawasaki disease?

A 
Phase 1 (acute) - weeks 1+2
Symptoms appear suddenly and severely

Phase 2 (sub-acute) - weeks 3+4
Symptoms are less severe but irritability and pain persist
Complications arise

Phase 3 (convalescent) - weeks 4-6
Child begins to recover but may still lack energy
27
Q

What is the treatment of Kawasaki disease?

A

IV immunoglobulins reduce risk of aneurysm
Aspirin reduces risk of thrombosis
Warfarin and antiplatelets

28
Q

What are complications of Kawasaki disease?

A

Aneurysm

Heart problems

29
Q

What are causes of immunosuppression?

A

Deliberate - bone marrow or organ transplant, treated of autoimmune disease

Non-deliberate - malnutrition, ageing, leukaemia, lymphoma, multiple myeloma

30
Q

What are causes of immunodeficiency?

A

Primary - intrinsic defect of immune defect present from birth, genetic, mainly boys

Secondary (more common) - caused by another disease or treatment such as infection, malignancy, malnutrition, HIV, splenectomy or nephrotic syndrome

31
Q

How do T-cell defects present?

A

Severe and/or unusual viral and fungal infections and failure to thrive in first months of life

Severe combined immunodeficiency (SCID) - defective cellular immunity altering T and B cell lymphocytes
Treated by bone marrow transplant

HIV infection - causes a progressive T cell deficiency

32
Q

How do B-cell defects present?

A

Infants has passive immunity from mother but afterwards up to 2 years, there are severe bacterial infections esp. ear, sinuses, skin and pulmonary
Can lead to failure to thrive, bronchiectasis and impaired hearing

X-linked agammaglobulinaemia - B-cells can’t mature

Common variable immunodeficiency (CVID) - later onset but high risk of autoimmune disorders and malignancies

33
Q

How do neutrophil defects present?

A

Recurrent bacterial infections - abscesses, poor wound healing, perianal disease, peridontal infectiond, aspergillosis, granulomas

Chronic granulomatous disease - X-linked recessive, defect in phagocytosis

34
Q

How do leucocyte function defects present?

A

Delayed separation of umbilical cord
Delyaed wound healing
Chronic skin ulcers
Deep seating infection

Leucocyte adhesion deficiency (LAD) - neutrophils can’t migrate to sites of infection

35
Q

How do complement defects present?

A

Recurrent bacterial infections, SLE like illness, recurrent meningococcal infection

36
Q

How are immunodeficiencies treated?

A

Co-trimoxazole to prevent pneumocystis jiroveci

Antibiotic prophylaxis - azithromycin

37
Q

How does typhoid fever present?

A

Infection with salmonella typhi or paratyphi

Worsening fever
Headache
Cough
Abdo pain
Myalgia
GI symptoms may not appear til second week

May have splenomegaly, bradycardia and rose coloured spots

38
Q

What are complications of typhoid fever?

A

GI perforation
Myocarditis
Hepatitis
Nephritis

Needs cephalosporin or ampicillin

39
Q

How does malaria present?

A

Worst in children 6 months to 5 years
Typical onset 7-10 days after innoculation
Fever, diarrhoea, vomiting, jaundice, anaemia, thrombocytopenia

40
Q

What are complications of malaria?

A

Severe anaemia

Cerebral malaria - rapidly developing encephalopathy becuase of parasite adhering to microvasculature causing blockage

41
Q

How is malaria treated?

A

Quinine

Bed nets

42
Q

What is the immunisation schedule?

A

Newborn - BCG if high risk

2,3 and 4 months - 5 in 1 (diptheria, tetanus, pertussis, Hib, polio)

2, 4 and 12 months - pneumococcal and meningitis B

2 and 3 months - rotavirus

3 months and 1 year - meningitis C

1 year - Hib/men C booster, MMR

pre-school - MMR and 4 in 1 pre-school booster (diptheria, tetanus, pertussis, polio)

13 years - HPV

14 years - 3 in 1 (diptheria, tetanus, polio), men ACWY

43
Q

What is pseudomembranous colitis?

A

Antibiotics wipe out colonising bacteria leaving only C. diff

Watery diarrhoea +/- blood, abdo cramps, fever

44
Q

What presents with a heliotrope rash around the eyes and knuckles?

A

Juvenile dermatomyositis

Elevated CK

45
Q

What is chronic fatigue syndrome?

A 
Infection like onset
>6 months and causes reduction in activity levels
Impaired memory/concentration
Myalgia and arthralgia
Headaches
Sore throat
Tender lymph nodes
46
Q

What investigations are done for CFS?

A 
FBC - rule out anaemia, iron deficiency and leukaemia
ESR/CRP - shouldn't be raised
Blood glucose
U+E
TFT
LFT
Urine dip
47
Q

What is the diagnostic criteria for SLE?

A

4 need to be present

Malar/discoid rash
Photo sensitivity
Oral ulcers
Arthritis
Pleuritis/pericarditis
Renal disorder
Seizures/psychosis
Haemolytic anaemia/leukopenia/thrombocytopenia
Antinuclear antibody positive
Antiphospholipid positive

Paediatrics (14 decks)

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