Child Health 4 Flashcards

1
Q

What are the features of Autism Spectrum Disorder? (triad +1) (4) and their factors.

A
  1. IMPAIRED SOCIAL INTERACTION:
    - Does not seek comfort, share pleasure or form close relationships
    - prefers own company, no interest or ability in interacting with peers (play or emotions)
    - gaze avoidance
    - lack of joint attention
    - socially and emotionally inappropriate behaviour
    - does not appreciate that others have thoughts and feelings
    - lack of appreciation of social cues.
  2. SPEECH AND LANGUAGE DISORDER
    - delayed development, may be severe
    - limited use of gestures and facial expression
    - formal pedantic language, monotonous voice
    - impaired comprehension with over-literal interpretation of speech
    - echoes questions, repeats instructions, refers to self as ‘you’
    - can have superficially good expressive speech.
  3. RIGIDITY - IMPOSITION OF ROUTINES WITH RITUALISTIC AND REPETITIVE BEHAVIOUR
    - on self and others, with violent temper tantrums if disrupted
    - unusual stereotypical movements such as hand flapping and tiptoe gait
    - concrete play
    - poverty of imagination in play and general activities
    - peculiar interests and repetitive adherence
    - restriction in behaviour repertoire
  4. COMORBIDITIES
    - general learning and attention difficulties (2/3)
    - seizures (1/4)
    - affective disorders (moods, feelings and attitudes) [sleep and anxiety]
    - mental health disorders [attention deficit hyperactivity disorder]`
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2
Q

What is Asperger syndrome?

What has it been replaced with?

A
  1. mild social impairment
  2. narrow, unusual intense interests
  3. stilted way of speaking
  4. clumsy

Autistic Spectrum Disorder with description of strengths and weaknesses.

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3
Q

What are DSM5 or ICD?

A

Diagnostic and Statistical manual in the US

International Classification of Diseases

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4
Q

When does Autism become apparent?

can they be independent?

A

2 - 4 years when there is the greatest increase in language and social skills.

incidence of 3-6 live births per 1000

Fewer than 10% of children with autism are independent as adults.

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5
Q

What is palivizumab?

A

a monoclonal Ab for RSV given by monthly IM to prevent RSV in preterm infants. NNT 17.

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6
Q

What different organisms cause pneumonia in difference age groups?

A
  1. Viruses more common in younger children
  2. Bacteria most common in older chldren

NEWBORN - organisms from mothers genital tract: group B streptococcus, Gram-negative enterococci and bacilli

INFANTS AND YOUNG CHILDREN - respiratory viruses (RSV). Bacteria: Strep pneumoniae or Haemophilus influenzae [reduced since Hib A], Bordetella Pertusssis and Chylamydia trachomatis.

CHILDREN OVER 5 - Mycoplasma penumoniae, Strep pneumoniae and Chlamydia pneumoniae

IN ALL AGES - mycobacterium tuberculosis.

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7
Q

What are the clinical features of pneumonia in children?

What features are there on examination?

A
  1. Fever (38C)
  2. Cough
  3. Tachypnoea
  4. Lethargy
  5. poor feeding

Typically precede with a URTI

ON EXAMINATION

  1. Tachypnoea - key clinical sign (over 60)
  2. Nasal flaring, chest indrawing (subcostal recession)
  3. End-inspiratory coarse crackles over the affected area. though the classic consolidation with dullness to percussion, decreased breath sounds and bronchial breathing may be absent
  4. May have decreased SpO2
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8
Q

What investigations may be useful in pneumonia?

A
  1. CXR

2. Nasopharyngeal aspirate

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9
Q

How should you manage children with pneumonia?

A

Most children can be managed at home:

Criteria for admission:
1. Spo2 <92% on air

  1. Recurrent Apnoea
  2. Grunting/ resp distress
  3. inability to maintain 50% of feeds/fluids

Oxygen and analgesia for pain (alternate paracetamol and ibuprofen for pain not for fever).

Physiotherapy has no proven role.

ANTIBIOTICS;

Newborns - IV - broad spectrum

Children oral amoxicillin/erythromycin

Complicated children - co-amoxiclav.

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10
Q

What education should be provided to parents for caring for a child with a chest infection?

A

PARENT AND FAMILY EDUCATION.

  1. Nature of illness and suspected clinical course
  2. Call the GP or return to ED if the following RED FLAGS are present:
    - Increasing RR/work of breathing, grunting, nasal flaring, marked chest recession
    - Apnoea/ Cyanosis
    - Inability to maintain hydration: <50%-75% of feeding
    - no wet nappies in more than 8 hours
    - worsening general appearance
    - exhaustion/ not responding to social cues
    - if they are unable to cope themselves
    - worsening of fever, or if the fever does not settle within 48 hours of initial ABX.
  3. Don’t try and cool the child down by under-dressing or use of tepid sponging.
  4. Give regular feeds/fluids
  5. Use paracetamol / alternative ibuprofen to alleviate pain but not as an antipyretic - don’t give both simultaneously.
  6. Check on the child regularly, including through the night.
  7. importance of hand washing before and after contact
  8. avoid exposure to environmental smoking
  9. avoid exposure to sick contacts
  10. provide PIL
  11. Arrange an appropriate follow up.
  12. Check understanding, especially with language and competent and confidence for caring for them at home.
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11
Q

What is Whooping Cough? What is it caused by?

How does Whooping Cough present?

A

Pertussis - caused the bacteria Bordetella pertussis. It is highly contagious and endemic causing epidemics every 3-4 years.

  1. Catarrhal Phase
  2. Paroxysmal Phase
  3. Convalescent phase

A week of coryza (catarrhal phase) is followed by a characteristic paroxysmal or spasmodic cough followed by a inspiratory whoop (paroxysmal phase).

The cough is often worse at night and may culminate in vomiting.

During a paroxysm, the child can go red or blue int he face, and mucus flows from the nose and mouth.

NOTE: the whoop may be absent in infants, but apnoea is common.

Epitaxis and subconjunctival haemorrhages can occur after vigorous coughing.

The paroxysmal phase can last up to 3 months. With the symptoms gradually decreasing (convalescent phase)

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12
Q

How can organisms be identified in suspected pertussis?

What would a FBC show?

What is the management?

Is vaccination helpful?

A

Pernasal swab. - By culture/PCR

A marked lymphocytosis >15 x 10^9 /L

Management is via a macrolide ABX (azithromycin/erythromycin) which is only effective a decreasing symptoms if used in the catarrhal phase.

Close contacts should receive prophylaxis.

Vaccination reduces the risk and severity but does not guarantee protection - it declines slowly over childhood and is why pregnant mothers should be re-immunized to protect their infants.

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13
Q

How can TB present? _ what is the pathophysiology?

A
  1. Asymptomatic (latent)
  2. Symptomatic
    - Local immune response fails and the bacteria spread to the local lymph nodes.
    The lung lesion + lymph node are the Ghon focus.

In 3 - 6 weeks the host responds to the infection, reducing M. tuberculosis replication but resulting in systemic symptoms of:

    • Fever (prolonged)
    • Anorexia and Weight loss
    • Cough
    • Malaise
    • Chest X-ray changes.

The primary complex usually heels and may calcify - inflammatory enlargement of peribronchial lymph nodes may cause bronchial obstruction with collapse and consolidation of the affected lung.

Other organs may be affected.

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14
Q

If TB reactivates what can happen?

How does this relate to child health?

A

Post-primary TB dissemination (military TB), to site such as bones, joints, kidneys, pericardium and CNS.

infants and young children are particularly prone to tuberculous meningitis.

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15
Q

What tests are suitable for TB?

A

Gastric washings in children - acid fast staining (Ziehl-Neelsen or auramine)#

  • culture
  • Tuberculin Skin Test (mantoux)
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16
Q

What is the treatment of TB?

A
  1. TRIPLE OF QUADRUPLE THERAPY

RIFAMPICIN

ISONIAZID (needs B6 -pyridoxine, given weekly for adolescents, not in young children)

PYRAZINAMIDE

ETHAMBUTOL

Then RIFAMPICIN + ISONIAZID for 2 months.

treatment is usually 6 months for pulmonary TB.

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17
Q

What is the aetiology of CF?

A

CF results from a defect in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR). Where the defect occurs alters how severe the disease is.

It is a cAMP-dependent chloride channel found in the membrane of cells.

UK most common mutation: deltaF508

Carrier rate of 1 in 25

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18
Q

What is the pathophysiology of CF?

A

Abnormal ion transport:

Airways: reduced airway liquid layer - mucociliary dysfunction and retention of mucopurulent secretions

    • chroninc infection with Pseudomonas aeruginosa.
    • Impaired immunity

Intestine: Thick viscid meconium. (10-20% ileus)

Pancreatic duct: blockage - enzyme deficiency and malabsorption

Sweat gland: excessive concentration of sodium chloride in the sweat.

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19
Q

How is CF normally diagnosed?

A

Heel Prick Test for Immunoreactive Trypsin (IRT).

Then screening for common CFTR mutations

Two mutations -> Sweat Test

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20
Q

Is a child isn’t identified by the Heel Prick Test how might they present?

Long term sequelae?

A
  1. Recurrent chest infections
    - S. Aureus - H. Influenzae. P. Aeruginosa
    - - Wet cough - purulent sputum
  2. Faltering Growth
  3. Malabsorption - steatorrhoea.

O/E

  • Hyper-inflated chest
  • Coarse inspiratory crepitations
  • +/- expiratory wheeze
  • Finger clubbing

Sequelae - Bronchiectasis and abscess.

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21
Q

What is the management of CF?

A

By the multidisciplinary team.

  1. Daily physiotherapy at least twice per day.
  2. Continuous prophylactic antibiotics +/- acute IVI for 14 via a PIC.
  3. Nebulised DNase or Hypertonic saline.
  4. Azithromycin
  5. 150% calories - + CREON - pancreatic enzymes + fat soluble vitamin supplements
  6. CFTR potentiators [Ivacaftor] and correctors [Lumicaftor]
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22
Q
  1. What is tonsillitis?
  2. What are the common pathogens?
  3. How might it present? (+ common age)
  4. Rx?
  5. What should you avoid?
  6. What disease can become a problem in association with a common cause of tonsillitis? - features?
A
  1. A form of pharyngitis.
    - intense inflammation of the tonsils
    - purulent exudate
  2. COMMON PATHOGENS:
    - - Group a beta-haemolytic [ Strep pyogenes]

– Epstein-Barr Virus [infectious mononucleosis]

  1. Presents with (most commonly in 5 - 15 year olds)
  • fever (>38)
  • throat pain
  • headache
  • apathy
  • abdominal pain
  • white tonsillar exudate
  • tonsillar erythema
  • cervical lymphadenopathy
  1. Although only 1/3 caused by bacteria:

Pen V or erythromycin for 10 days to prevent rheumatic fever.

  1. Avoid Amoxicillin as can cause a maculopapular rash if due to EBV
  2. Scarlet fever (5 - 12 years) Fever usually precedes headache and tonsillitis by 2 - 3 days

[ maculopapular rash with flushed cheeks and perioral sparing - tongue is white coated and red.]

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23
Q

What is a prediction score to determine the likelihood of streptococcal infection?

A

FeverPAIN

Fever = over 38C
P-urulence (phargyngeal/tonsillar exudate)
A-ttend rapidly (3 days or less)
I-nflamed tonsils (severely)
N-o cough or coryza

4/5 = ABX probably a good idea. ( remember throat culture )

  • though reduce symptoms less than 1 day.. (delayed script)
24
Q

Advice on how to care for a child with tonsilitis?

A
  1. It normally clears up on its own in 3 to 4 days.
  2. most sore throats aren’t serious
  3. You should contact GP or another health service if your child has difficulty swallowing, breathing , a temperature more than 38.3C, very tender or swollen glands in the neck, painful sinuses or a cough with mucus. Doesn’t improve after 3 days. One sided throat swelling.
  4. Antibiotics usually aren’t useful. as most are caused by viruses.
  5. Paracetamol or ibuprofen - talk to your pharmacist.
  6. adequate fluid intake.
  7. try salt water gargling, medicate lozenges or anaesthetic sprays.
    - avoid hot drinks
  8. children can return to school or daycare after fever has resolved and they are not longer feeling unwell, and/or taking ABX for 24 hours.
  9. routine follow up not required.
25
Q

What is the aetiology of acute nephritis?

A

AETIOLOGY:
Nephritis develops as a result of abrupt onset of glomerular injury and inflammation that leads to a decline in glomerular filtration rate with sodium and water retention.
[ The increased glomerular cellularity restricts glomerular blood flow. ]

    • 80% are Post-Streptococcal GlomeruloNephritis (APSGN)
    • Vasculitis (Henoch-Schonlein Purpura (HSP)) / SLE / ANCA (antineutrophil cytoplasmic antibody) +ve
    • IgA nephropathy (normal C3)
    • Goodpasture’s
26
Q

What are the clinical features of acute nephritis?

At what ages?

What is the management?

Prognosis?

A
  • Decreased urine output {
27
Q

What are the features to look for of fluid overload?

A

tachycardia

hypertension

respiratory distress

warm peripheries

hepatomegaly

raised JVP

28
Q

What are ASOT and Anti-Dnase B tests for?

what other tests would you do?

A

Recent infection with group A strep. strep pyogenes

OTHERS:

urinalysis

urine culture

urine microscopy

urine PCR

Blood for renal profile
FBC
C3 and C4 levels
ANA level

Throat swab
??CXR if overloaded.

29
Q

What are the features of Henoch-Schonlein Purpura (HSP)

When does it commonly occur? - who?

A

It’s a small vessel vasculitis

  1. Characteristic skin rash [ maculopapular and purpuric] on extensor surface of arms and legs & buttocks [ can be trunk sparing]
  2. Arthralgia ( knees and ankles) (66% (2/3)
  3. Periarticular oedema
  4. Abdominal Pain (75% - 3/4)
  5. Glomerulonephritis (80%)ww
  6. Fever
  7. Haematuria +/- proteinuria
  8. EXCLUSION OF OTHER CAUSES OF PURPURIC RASH - meningococcal septicaemia, NIC, TTP etc.

Occurs between 3 - 10 years and has a 2:1 ratio boys to girls. Peaking during winter.

More common in Asian and Caucasian, least in Afro

30
Q

What is the management of HSP?

Prognosis?

A

Provide parents with
1. infoKID.org.uk

  1. Supportive:
    - - Hydration and simple analgesia
  2. Severe abdo pain may warrant roid - surg rev first
  3. ? Nephrology ref
  4. follow up 1 week (give bottle for urine collection at 1 week)

PROG:

Long term follow up for 6 months to 1 year - to detect HSP nephritis. 50% develop it within the first 6 weeks up to 6 months.

31
Q

What disease has the same histology and management as HSP?

A

IgA Nephropathy

32
Q

What is the cause of nephrotic syndrome?

A

90% due to minimal change disease

Secondary to HSP / other vasculitides (SLE)

Infection (malaria)

allergens (bee sting)

33
Q

What is the definition of nephrotic syndrome?

A
  1. Heavy proteinuria (3+/4+ on dipstrick or urine protein [PCR] >250mg/mmol creatinine)
  2. Hypoalbuminaemia (< 20g/L (<25 g/L))
  3. Oedema
34
Q

What is the incidence of nephrotic syndrome?

what can it be associated with?

A
  1. In the UK 2 per 100,000 children per year
  2. in south Asia 16 per 100,000

May be associated with atopy and precipitated by a resp infection.

35
Q

What are clinical signs of nephrotic syndrome?

What importantly might the GP do?

A
  1. Periorbital oedema (particularly on waking)
  2. Scrotal, vulva, leg and ankle oedema
  3. Ascites
  4. Breathlessness due to pleural effusions and abdominal distension
  5. infection due to loss of immunoglobulin
  6. thrombosis risk.

THE GP MIGHT DIAGNOSE ALLERGY FIRST AND TRY PRITION - WHILE THE PERIORBITAL OEDEMA MAY GET BETTER OVER THE DAY.

DIP THE URINE FOR PROTEIN

36
Q

What investigations are a good baseline for nephrotic syndrome?

A
  1. Renal profile (U+Es and Bone profile)
  2. FBC
  3. Varicella immunity status
37
Q

What features are consistent with typical nephrotic syndrome?

How do these contrast to a typical nephrotic?

A

———————-TYPICAL—————————

AGE: 1 - 11 years

RENAL FUNCTION: normal creatinine

HAEMATURIA: Microscopic may occur

HYPERTENSION: normotensive

FHx OF NEPHROTIC: Absent

———————ATYPICAL—————————-

AGE: <1/ >11

RENAL FUNCTION: Elevated creatinine

HAEMATURIA: Macroscopic

HYPERTENSION: Elevated

FHX OF NEPHROTIC: May be present

38
Q

What is the initial management of children with nephrotic syndrome?

A

Aiming to induce remission with steroids (most respond in 7 - 14 days) and promote diuresis.

ORAL PREDNISOLONE

39
Q

What are the common causes of UTI?

What is the incidence?

A
E. Coli (75%)
Klebsiella
Proteus mirabilis
Staph Saprophyticus
strep faecalis

3-7 % of girls and 1-2% of boys have atleast 1 symptomatic UIT before the age of 6.

More common in girls apart from during the first 6 months.

40
Q

What are categories of haematuria?

List causes of the categories

A
  1. Glomerular (brown, casts,+/- proteinuria)
  2. Non-glomerular (red, at beginning or end)

GLOMERULAR:

  • Acute glomerulonephritis
  • Chronic glomerulonephritis
  • IgA nephropathy
  • Familial nephritis
  • Thin basement membrane disease

NON-GLOMERULAR

  • Infection - viral, bacterial, TB, schistosomiasis
  • Trauma
  • Stones
  • Tumours
  • Sickle cell disease
  • Bleeding disorders
  • Renal vein thrombosis
  • Hypercalciuria
41
Q

How do UTIs present in

  1. Infants
  2. Preverbal Children
  3. Verbal Children
A

INFANT <3 months:

  • unexplained fever, vomiting, lethargy, irritability
  • poor feeding, faltering growth
  • abdominal pain, jaundice, haematuria, offensive urine

PREVERBAL <3 months [same]

  • fever, vomiting, lethargy, irritability
  • poor feeding, faltering growth
  • abdominal pain, loin tenderness, haematuria, offfensive urine

VERBAL CHILD

  • frequency, dysuria
  • dysfunctional voiding, changes to continence, abdominal pain, loin tenderness
  • fever, malaise, vomiting, haematuria, offensive urine, offensive urine, cloudy urine
42
Q

How is UTI defined in children?

A
  1. Clinical suspicion

2. Growth of 10^5 organisms (10^8/L) of a single bacteria on CCU or MSU.

43
Q

What differentiates upper urinary tract infection from lower?

A
  1. Acute pyelonephritis
    - significant bacteriuria and fever >38C +/- loin tenderness/pain (or similar without temperature)
  2. Cystitis
    - significant bacteriuria without systemic features
44
Q

How should a child be treated with.

Leucocyte and nitrite +ve dipstik

Nitrite only +ve

Leucocyte +ve only

Leucocyte/ Nitrite -ve

A
  1. Treat and await culture
  2. treat and await culture
  3. Treat if strong clinical suspicion, look for another source.
  4. do not culture, unless highly suspicious of UTI. look for another focus of infection.
45
Q

What investigations are required in atypical and recurrent UTI?

A

USS in the acute phase and 4 -6 week follow up DMSA (tracer) test.

46
Q

What are atypical features of a UTI in children?

A
  • seriously ill
  • poor urine flow
  • abdominal or bladder mass
  • raised creatinine
  • septicaemia
  • failure to respond to treatment with suitable antibiotics within 48 hours
  • infection with non E.coli organisms
47
Q

What are the features of recurrent UTI in children?

A
  • 2 or more episodes of UTI with acute pyelonephritis OR
  • 1 episoe of UTI with APye + 1 more episode of LUTI or
  • 3 or more cystitis
48
Q

What is the incidence of Vesicoureteric reflux in the general population and in those with UTI?

A

In general:
8% in girls
2% in boys

Out of all children with UTI
- 25-40% of them with have VUR

49
Q

Diagnostic tests for VUR?

A

USS > if features consistent with VUR then

Voiding Cystourethrogram (Radiation)

50
Q

Rx for pyelonephritis?

A

7- 10 day ABX

< 3 months sepsis cover (broad spectrum)

> 3 mo - Ciprofloxacin (PO) Cefuroxime (IV)

51
Q

Rx for vulvovaginitis in a child?

A

In infants: nappy rash - ammonical dermatitis

candida infection

can be caused by group A strep.

  • amoxicillin 5 days PO TDS
52
Q

what is AKI?

A

A sudden, potentially reversible inability of the kidney to maintain normal body chemistry and fluid balance.

53
Q

What are the presenting features of AKI in children?

A

Often asymptomatic Consider with acute illness or those with a background of chronic disease.

Hypotension, oedema,

NICE:

Investigate for AKI by measuring creatinine and comparing with baseline in those with acute illness associated with:

  • CKD
  • Heart failure
  • Liver disease
  • AKI hx
  • Oliguria (<0.5 ml/kg/hr) for more than 8 hours
  • young age or disability
  • hypovoaemia
  • urological obstruction
  • severe diarrhoea
  • deteriorating PEWS
  • nephritis - oedema, haematuria
  • hypotension

Also consider in those without acute illness

  • fall in eGFR >25%
  • 50% or greater rise in serum creatinine in the past week.
54
Q

What is haemolytic uraemic syndrome and what organism most commonly causes it?

A

HUS is a triad of

  1. AKI
  2. Microangiopathic Haemolytic Anaemia (MHA)
  3. Thrombocytopenia

Typically secondary to gastrointestinal infection with verocytotoxin producing
– E Coli O157:H7 –
(farm animals and uncooked beef)

[the toxin enters the G.I. tract, localises to the kidney endothelial cells and causes intravascular thrombogenesis (AKI) - Platelets are consumed in the process (thrombocytopenia) and blood traveling via the occluded circulation are damaged (MHA)

OR

Shigella

55
Q

What are the symptoms/Signs of typical HUS?

what is the prognosis?

What about with atypical?

A

Blood diarrhoea - good prognosis with early therapy (Dialysis + support), though they require long term follow up as persistent proteinuria, hypertension and progressive CKD may develop

Atypical has no diarrhoeal symptoms, may be familial and frequently relapses.

  • High risk of CKD
  • Hypertension
  • Mortality