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Year 3 Paeds > Paediatric LOs > Flashcards

Paediatric LOs Flashcards

1
Q

Asthma

How common is it in children

Explain the pathophysiology (5)

A

Most common respiratopry illness in children

  • IgE type 1 hypersensitivity reaction against foreign proteins detected as antigens
  • Th2, eosinophils, mast cells and CD4+ neutrophils form inflammatory infiltrate in the airway epithelium and smooth muscle, leading to airway remodeling (i.e. desquamation, subepithelial fibrosis, angiogenesis, smooth muscle hypertrophy).
  • Hypertrophy of airways causes narrowing of lumen and hyperreactivity
  • Loss of bronchoconstriction factors (e.g., prostaglandin E2)
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2
Q

How to most patients overcompensate for acute asthma?

resp/ met alkalosis/ acidosis?

if untreated leads to what failure

A
  1. hyperventilation
  2. Resp and metabolic acidosis- CO2 can’t be blown off + increased lactic acid production by respiratory muscles due to prolonged and increased work of breathing, tissue hypoxia secondary to reduced cardiac output and ventilation-perfusion mismatch
  3. cardiac and respiratpry failure
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3
Q

Assessment of asthma (4)

A
  1. Clinical evaluation- history and physical respiratory examination
  2. Confirmation via pulmonary function testing- stop bronchodilators before test. Spirometry is then done before and after inhaling a SABA bronchodilator. (Signs of airflow limitation prior- low FEV1 and reduced FEV1/FVC ratio) improvement by 12% shows reversibility
  3. Exclude other possible causes of wheeze- e.g., via volume-flow loop to remove vocal chord dysfucntion
  4. Provocative testing
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4
Q

Short term treatment of asthma (5)

A
  1. Control of triggers- e.g., exposure to dog dander, change job, don’t run on cold mornings
  2. Drug therapy- bronchodilators (B2-agonists, Anticholinergics), corticosteroids, leukotriene modifiers, mast cell stabilizers, methylxanthines, immunomodulators
  3. Monitoring
  4. Patient education
  5. Treatment of acute exacerbations-relieve symptoms and return patient’s lung function. Use inhaled bronchodilators (B2 agonists and anticholinergics)
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5
Q

Long term management of asthma (2)

A
  1. stepwise increase of medication until appropriate control is found (patient adherence to previous stage is crucial before moving on)
  2. address comorbid factors like obesity
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6
Q

How long does a reliever last?

how many puffs are you allowed per 4 hours?

A

lasts 2-4 hours

up to 10 puffs per 4 hours

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7
Q
  1. Stridor is stypically what kind of breath sound?
  2. it indicates airflow obstruction where?
  3. obstruction may be due to?
A
  1. Insipiratory breath sound
  2. due to partial obstruction of the upper airway
  3. in the lumen (foreign. body), in the wall (e.g., tumour or cord palsy) or extrinsic (e.g., goitre)
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8
Q

What is bronchiectasis?

main symptoms

A
  • Chronic inflammation of the bronchi and bronchioles leasind to permanent dilatation and thinning of these airways
  • persistent cough, copious purulent sputum, haemoptysis
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9
Q
  1. What is bronchiolitis
  2. what is the most common causative agent
  3. what are the initial symptoms
  4. what symptoms follow
  5. symptomatically worst after how many days of infection
A
  1. paediatric condition that results in inflammation of the bronchioles
  2. RSV in 80% of cases (respiratory syncytial virus)
  3. coryzal (nasal discharge, nasal obstruction, sneezing, sore throat, general malaise and cough)
  4. dry cough, increased breathlessness
  5. 4-5 days
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10
Q

How would you diagnose bronchiolitis

A

Clinical diagnosis:

  1. Winter months
  2. Initial coryza, then cough and breathlessness
  3. Subcostal and intercostal recessions as they struggle to breathe
  4. hyperinflation of the chest
  5. fine end respiratory crackles

Pulse oximetry

Other features include:

  1. wheeze (episodes of apnoea) expiratory>inspiratory
  2. Liver displaced downwards
  3. resultant feeding difficulties due to respiratory distress
  4. encephalopathy due to hyponatraemia
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11
Q

Signs to suggest differential diagnosis

A
  1. High grade, persistemt fever: bacterial pneumonia
  2. Associated lactic acidosis, hepatomegaly or persistemt tachycardia: suggets possible decompensation of cardiac disease
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12
Q

Investigations for bronchiolitis

A
  • SpO2
  • CXR- if other disease suspected. In bronchiolitis, expect signs of hyperinflation, atelectasis (partioal or complete collapse of lobe/ lung) and consolidation
  • ABG- CO2 retention sign of late stage
  • Nasopharyngeal aspirate or throat swab- looking for viral cause
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13
Q

Admit to hospital for bronchiolitis if any of the following (4)

A
  1. Apnoea
  2. Peristent oxygen sat of (50-75%)
  3. Inadequate oral fluid intake
  4. Severe respiratory distress (grunting, marked chest recessions, resp rate over 70/min)
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14
Q

Other causes of bronchiolitis include:

A
  1. Viruses: parainfluenza, influenza, adenovirus, rhinovirus
  2. Chlamydia
  3. M. pneumoniea
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15
Q

bronchiolitis typically affects children aged

should stop by age

A

3-6 months

2 years

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16
Q

Hospital treatment of bronchiolitis (6)

A

Mainly supportive and will resolve itself in 2 weeks

  1. O2 to achieve Sp02 of >92%
  2. If significant resp distress—– NGT feeding
  3. bronchodilators for wheeze
  4. mucolytic therapy
  5. non-invasice therapy- CPAP and humidified high flow nasal cannula
  6. antiviral therapy e.g., oseltamavir
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17
Q

prophylaxis for bronchiolitis:

A

palivuzimab monoclonal antibody

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18
Q

Causes of acute respiratory distress (9)

A
  1. Bronchiolitis
  2. Viral episodic wheeze
  3. Pneumonia
  4. Heart failure
  5. Foreign body
  6. Anaphylaxis
  7. Pneumothorax or pleural effusion
  8. Metabolic acidosis
  9. Severe anaemia
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19
Q
  • Croup is also known as
  • what is croup
  • commonly caused by which 3 organisms
  • peak incidence age is
  • affects which ages
  • which season is it most common in
A
  • viral laryngotracheobronchitis
  • croup is a mucosal inflammation affecting anywhere from the nose to lower respiratory airways
  • parainfluenza, rhinovirus and RSV
  • 2 years old
  • 6 months- 6 years old
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20
Q

the typical features of croup are:

2 initial-

followed by (5) -

A

coryza and fever

followed by:

  1. hoarseness (inflammation of the coal cords)
  2. barking cough (tracheal oedema and collapse)
  3. harsh stridor
  4. variable difficulty of breathing w chest recessions
  5. symtpoms starting and being worse at night
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21
Q

treatment of croup

A
  1. airway protection- do not startle child. let otolaryngologist and anaesthetist know emergency airway support may be needed
  2. treat at home unless recessions, stridor at rest
  3. steroids- PO dexamthosone or nebulised budesonide
  4. nebulized adrenaline- transient relief of symptoms
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22
Q

differentiating between viral croup and acute epiglotitis

A

Croup*** ***Epiglottitis

Time course. Days. Hours

Prodrome. Coryza. None

Cough. Barking. slight iof any

Feeding. Can drink No

Mouth. Closed Drooling saliva

Fever. <38.5. >

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23
Q

Pneumonia

at what ages does pneuemonia incidence peak

most common newborn cause

infant and young child

children over 5

all ages

A

extremens of age- young and old

  • group B strep
  • RSV and other resp viruses
  • mycoplasma pneumoniae
  • mycobacterium tuberculosis at all ages should be considered
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24
Q

Diagnosis of pneumonia

A

Symptomatic- presence of

  • Cough w increasing sputum production
  • Dyspnoea
  • Pleuritic chest pain
  • Rigors or night sweats
    • Myalgia
  • malaise
  • anorexia
  • lethargy
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25
Q

Investigations for pneumonia

A
  • CXR- consildation with dullness on percussion
  • Pulse oximetry
  • ABG
  • Urea and electrolyteS
  • Blood culture
  • Sputum culture
  • Urinary antigen testing for legionella and pneumococcus
  • PCR
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26
Q

Community acquired pneumonia causes

typical

atypical

A

Typical:

  • Streptococcus pneumoniae (commonest)
  • Haemophileus influenzae
  • Moraxella catarrhalis

Atypical:

  • Mycoplasma pneumoniae
  • Staphylococcus aureus
  • Legionella
  • Chlamydia
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27
Q

pneumonia hiospital acquired causes

A

Gram negative enterobacteriae (commonest)

Staph aureus

Pseudomonas

Krebsiella

Clostridia

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28
Q

management (8)

A

most can be treat at home

  1. consider CURB-65
  2. antibiotics- usually amoxicillin or clarithromycin
  3. O2 to keep sats >92%
  4. IV fluids (shock, dehydration and anorexia)
  5. VTE prophylaxis
  6. Analgesia if pleurisy
  7. Possible chest drain for effusions
  8. Follow up w CXR at 6 weeks
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29
Q

CURB-65

A

Use CURB-65 to identify severity and whether it should be treat in the community

  • Confusion
  • Urea (>7mmol/L)
  • Respiratory rate (>30)
  • BP (<90/60)
  • Age >65

1 point for every category

  • 0-1 outpatient
  • 2 inpatient
  • 3+ ICU
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30
Q

Cystic fibrosis

mendelian inheritcance pattern

which defective gene

what is useful in treating

A
  • Most common life-threatening autosomal recessive condition in Caucasians
  • Defective protein called CF (CF transmembrane conductance receptor CFTR)
  • cAMP reliant channel found in the membrane of cells.
  • Most frequent change (78%) is to the F508 gene

CFTR correctors (Lumicafitor) and CTFR potentiators (Ivacaftor) are useful in treating

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31
Q

cystic fibrosis presentation

newborn

infant

young child

older child and adolescent

A

Newborn

Diagnosed through newborn screening

Meconium ileus

Infancy

Prolonged neonatal jaundice

Constant chest infections

Malabsorption, steatorrhoea

Young child

Bronchiectasis

Rectal prolapse

Nasal polyp

Sinusitis

Older child and adolescent

Diabetes mellitus

Cirrhosis and hypertension

Distal intestinal obstruction

Pneumothorax or recurrent haemoptysis

Sterility in males

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32
Q

What is meningitis

Causative organisms- which is more severe and which is more common

A

Inflammation of the meninges covering the brain

Bacterial (more severe)

Neonates

Group B streptococcus

E.Coli

Listeria monocytogenes

1m – 6 years

Neisseria meningitides

Streptococcus pneumoniae

Haemophilus influenza

>6 years

Neisseria meningitides

Strep. pneumoniae

Fungal meningitis (very rare)

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33
Q

meningitis presentation

A
  • Fever
  • Headache
  • Photphobia
  • Lethargy
  • Poor feeding/ vomiting
  • Irritability
  • Hypotonia
  • Drowsiness
  • Loss of consciousness
  • Seizures
  • Positive for Bruzinkis and kernigs signs
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34
Q

what does a positive bruzinki’s and Kernig’s sign present as?

A

bruzinki’s sign-

(flexion of neck while supine causes flexion of the knees and hips)

kernig’s sign-

child lying supine and with hips and knees flexed, there is back pain and extension of the knee)

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35
Q

diagnosis of meningitis

A
  • Lumbar puncture to obtain CSF to:
    • Confirm diagnosis
    • Identify possible organism
    • Identify antibiotic sensitivity
  • Typical changes in CSF
    • Bacterial- appears turbid, white cell polymorphs increased, protein very high, glucose very low
    • Viral- appears clear, lymphocytes increased, protein normal/ increased, glucose normal/ decreased
  • Blood culture or PCR in those who can’t have a lumbar puncture
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36
Q

Presentation of otitis media

on examination with otoscope?

A
  • Pain- child may tug or cradle ear that hurts, or appear irritable or become disinterested with food
  • Malaise
  • Fever
  • Coryzal symptoms

tympanic membrane will look erythematous and may be bulging. If the fluid pressure has perforated the TM there may be a small tear visible with purulent discharge in the auditory canals.

Conductive hearing loss or cervical lymphadenopathy.

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37
Q

explanation of otitis media

A

Bacterial infection of the middle ear results from nasopharyngeal organisms migrating via the eustachian tube.

Anatomy of Eustachian tube in younger children is immature, typically being shorter, straighter and wide (only becoming oblique as the child grows), meaning infection is more likely.

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38
Q

management of otitis media

A
  • Majority of acute cases will resolve spontaneously within 24 hours, nearly all within 3 days “Watch and wait”.
  • Treat all patients with simple analgesics at first
  • Grommets can be used in some cases
  • Abx management

Abx should be avoided unless significant deterioration or disease progression is seen. Oral abx can be considered if:

  • Systemically unwell children not requiring admission
  • Known risk factors for complications- e.g., congenital heart disease or immunosuppression
  • Unwell for 4 days or more
  • Discharge
  • Children younger than 2 years with bilateral infection
  • Systemically unwell adult

Manegement of chronic OM

  • Non-surgical- hearing aid insertion
  • Surgical- myringotomy and grommet insertion (grommet if >3 months of bilateral OME
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39
Q

Impetigo

cause

age group

features

infectivity

antibiotics

A

cause- staphylococcal/ streptococcal skin infectino

age group- infants and young children

features- erythematous macules on face, neck and hands

infectivity- nasal carriage is often source of infection

antibiotics- PO antibiotics e.g., amoxicillin

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40
Q

impetigo

  1. is it localised
  2. how contagious is it
  3. more common in children who
  4. rupture of vesicles gices characteritic ____ appearance
  5. infection spreads along the host via
  6. Which antibiotics used
A
  1. localised
  2. highly contagious
  3. more common in children with eczema
  4. rupture of vesicles gices honey-coloured crusted lesions
  5. infection spreads rapidly to adjacent areas via autoinoculation
  6. topical Abxs like mupirocin nad narrow spectrum like fluclox
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41
Q

Chicken pox

  1. How long does it last
  2. How many organs does it affect
  3. Usually affects which stage of life
  4. Usually caused by which virus
  5. Chicken pox is which stage of the virus
A
  1. Acute
  2. Systemic
  3. Childhood
  4. Caricella-zoster virus (human herpes virus type 3)
  5. Acute invasive phase
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42
Q
  1. What is shingles
  2. How are the lesions of chicken pox characterised
  3. There is a severe risk of neurological complications in which groups
  4. cHICKENPOX IS SPREAD VIA
A
  1. The reactivation of the latent phase
  2. Macules, papules, vesicles and crusting
  3. Adults and neonates
  4. Airborne droplets or aerosolizing particles and direct contact
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43
Q

Signs anf symptoms of chickenpox

describe the initial rash

A
  • mild headache
  • moderate fever
  • malaise

all appear 34-36 hours of lesions

  • macular eruption with evanescent flush
  • lesions progress to papules and then teardrop vesicles on intensely itchy red base
  • lesions start on face and trunk and erupt in successive crops
44
Q

diagnosis of chicken pox

treatment of chicken pox

A
  1. clinical evaluation
  2. PCR
  3. serological testing
  4. immunofluorescent tagging of antigen

symptomatic in mild or child e.g., put oatmeal on lesions

antivirals

45
Q

interpretatino of urine investigations

methods of urine testing (2)

WBC esterase and nitrite +ve

WBC esterase -ve and nitrite +ve

WBC esterase +ve and nitrite -ve

WBC and nitrite -ve

Blood, protein and glucose present on stick

A

nitrate stick testing

leukocyte esterase stick (testing for WBC’s)

  • WBC esterase and nitrite +ve———- UTI
  • WBC esterase -ve and nitrite +ve —- Start abx treatment if clinical evidence
  • WBC esterase +ve and nitrite -ve —- Only start abx if clincal evidence
  • WBC and nitrite -ve———————– UTI unlikely, repeat or semd urine for culture if clinical history is suggestive
  • Blood, protein and glucose present on stick—suspect other comorbidity e.g., nephritis or diabetes mellitus
46
Q

treatment of UTI

A

Oral abx use alongside trimethoprim

47
Q

Immunisation schedule

Babies <1 year

8 weeks

12 weeks

16 weeks

A

8 weeks

  • 6 in 1 vaccine
  • Rotavirus vaccine
  • MenB

12 weeks

  • 6 in 1 vaccine (2nd dose)
  • PCV (pneumoccal)
  • Rotavirus (2nd dose)

16 weeks

  • 6 in 1 (3rd dose)
  • MenB (2nd dose)
48
Q

Immunisation schedule

Children 1-15

1 year

2-10 years

3 years and 4 months

12-13 years

14 years

A

1 year

  • Hib/ men C (1st dose)
  • MMR (1st dose)
  • PCV (2nd)
  • Men B (3rd)

2-10 years

  • Flu vaccine (every year)

3 years and 4 months

  • MMR (2nd dose)
  • 4 in 1 preschool booster

12-13 years

  • HPV vaccine

14 years

  • 3 in 1 teenage booster
  • MenACWY
49
Q

adults immunisation schedule

65 years

65 years (and every year after)

70 years

A

65 years

  • PPV (pneumococcal)

65 years (and every year after)

  • Flu vaccine

70 years

  • Shingles vaccine
50
Q

which vaccines should a pregnant woman be offered (2)

A

flu and whooping cough

51
Q
  1. Gastroenteritis is usually bacterial or viral?
  2. What are the presentation for viral?
  3. What additional presentations are there for bacterial gastro?
  4. common viral causes
  5. common bacterial causes
A
  1. usually viral
  2. watery diarrhoea (rarely bloody), vomiting, cramping, abdo pain, fever, dehydration, electrolyte disturbanec, upper resp problems associated with rotavirus
  3. malaise, dystentery (blood and mucous in stools), abdo pain may mimic appendicitis
  4. rotavirus, enteric adenovirus etc.
  5. salmonella spp, campylobacter jejuni, shigella, E.coli, C. difficile
52
Q
  1. investigations for viral gastroenter
  2. investigations for bacterial
  3. treatment of viral gastro
  4. treatment for bacterial gastro
A

Stool EM or immunoassay

stool and blood culture, stool C.diff toxin, endoscopy if stool samples negative and suspect IBD

supportive rehydration PO/ NGT, IV glucose

rehydration as for viral, be careful with abxs???

53
Q

fluid management

  1. no clinical dehydration
  2. clinical dehydration
  3. shock
  4. deterioration after initial rehab
  5. after rehydration
A

if no clinical dehydration- prevent dehydration. E.g., encourage breast feeding to balance out gastrointestinal losses.

If clinical dehydration- give fluid deficit replacement (50ml/kg) over 4 hoursas well as maintenance fluid as required. If frequent vomiting consider giving ORS via nasogastric tube.

Shock- IV therapy. Give bolus of 0.9% sodium chloride solution. Repeat if necessary.

If deterioration after prior treatment-IV therapy for rehabilitation

After rehydration-Give full strength milk and reintroduce usual solid food. Avoid fruit juices and carbonated drinks. Advise patients about hygiene to prevent reinfection.

54
Q

diagnosis of GORD

management

A

endoscopy- look for evidence of gastritis or metaplasia, ambulatory pH probe

management

  • sleeping upright
  • eeating less spicy foods and drinking less alcohol
  • antacids, PPIs and no NSAIDs
  • fundoplication surhgery
55
Q

coeliac disease

presentation (11)

stools are (4)

A
  1. Chronic diarrhoea
  2. Abdominal distension
  3. Abdominal pain
  4. Vomiting
  5. Failure to thrive
  6. Apathy
  7. Anorexia
  8. Pallor
  9. Generalised hypotonia
  10. Muscle wasting
  11. anaemia
  • soft
  • clay coloured
  • bulky
  • offensive
56
Q

investigations for coeliacs (3)

A
  1. Use serological markers first:
    1. Anti-tissue transglutaminase antibody (tTG)
    2. Anti-endomysial antibody

Then if both are present definitely go for a

  1. Small-bowel biopsy- taken from the 2nd portion of the duodenum. Findings show villous atrophy, increased intraepithelial cells and crypt hyperplasia. Repeat a few months after gluten free diet started.
  2. Gluten challenge in later life to determine whether gluten intolerance has continued.
57
Q

management of coeliacs

A
  • Diet- remove all products containing wheat, rye, and barley. This should be adhered to for life.
  • Supervision by a dietician
  • Join a coeliac support group
  • Supplementary vitamins and minerals
  • Corticosteroids in refractory period if they don’t tolerate gluten withdrawal well
58
Q

BMI measurement for obesity in children

what is the bmi centile?

what is the equation

what value is the obese range

A

The BMI centile is a simple and reliable indicator of a healthy body weight in childhood.

BMI = kg/m2

30.0 or higher is in the obese range

59
Q

what is faultering weight gain

if prolonged and severe it may affect their ____

causes general

A

Sustained drop sown 2 centile spaces. Has a significant interruption in the expected rate of growth compared with other children of a similar age and sex during early childhood.

If prolonged and severe, it will result in a reduction of height and growth which may be associated with delayed development.

  1. Inadequate intake (environmental, psychosocial deprivation, underlying pathology)
  2. Inadequate retention (vomiting, GORD)
  3. Malabsorption (coeliac, CF, milk allergy)
  4. Failure to utilise nutrients (metabolic disorders, down’s, extreme prematurity, storage disorders)
  5. increased requirements (CF, malignancy, CKD, congenital heart defect)
60
Q
A
61
Q

hepatomegaly

what is it

causes (7)

A

Liver easily palpated 1-2 cm below rib line in children. Rarely presents alone and usually accompanies other clinical signs and symptoms.

  1. infection (congenital, infectious mononucleosis, hepatitis, malaria)
  2. haematological (sickle cell, thalassaemia)
  3. liver disease (portal hypertension, hepatitis)
  4. malignancy
  5. cardiovascular
  6. apparent (chest hyperexpansion from bronchiolitis or asthma)
62
Q

what is appendicitis

typically results in (3)

if left untreated can lead to

pathophysiology

A

Acute inflammation of the appendix. Included in an acute abdomen (pain that has come on quickly).Most common cause of abdo pain in childhood that requires surgery.

typically results in; necrosis, gangrene and perforation

patho caused by:

  1. luminal obstruction (usually secondary to faecoliths- like rocks)
  2. lymphoid hyperplasia
  3. apendicael or caecal tumour
  • obstructed commensal flora in the appendix multipy resulting in acute inflammation
  • reduced venous drainage and inflam increase pressure in the appendix causing ischaemia
63
Q

risk factors for appendicitis (3)

presentation (6)

Signs (5)

A

fhx, ethnicity caucasian, summer

presentation:

  • abdo pain- periumbilical, dull and poorly localised (visceral peritoneum), but later migrates to RIF where it is well localised and sharp (parietal), aggravated by movement
  • anorexia
  • vomiting
  • nausea
  • diarrhoea
  • constipation

signs

rebound tenderness

percussion pain (persistent guarding over McBurney’s point)

fever

+ve Rovsings sign

Psoas sign

64
Q

what is rovsigs sign- RIF pain on palpation of the LIF

Psoas sign- RIF pain with extension of the right hip

A
65
Q

differential diagnoses for appendicitis

  • gynae
  • renal
  • urological
  • in children
A
  • gynae- ovarian cyst rupture, ectopic pregnancy, pelvic inflammatory disease
  • renal- ureteric stones, urinary tract infection, pyelonephritis
  • urological- testicular torsion, epididymo-orchitis
  • in children- acute mesenteric adenitis, gastroenteritis, constipation, intussusception, UTI
66
Q

investigations for appendicitis

management

A

usually clinical

  • urinalysis (exclude renal or urological cause, preg test for women)
  • routine bloods- FBC, CRP and serum B-hcg for preg women
  • ultrasound- gynae differential
  • CT

management

laprascopic appendicetomy

67
Q

Intussuception

  1. what is it
  2. epidemiology
  3. patho
A
  1. The “telescoping” of one part of the bowel into another.
  2. -5-7 months peak incidence. Rare to occur after 2. Boys twice as likely to be affected.
  3. Telescoping can lead to intestinal blockage. 90% that occur are the ileo-colic type, whereby the distal ileum passes into the caecum via the ileo-caecal valve.
68
Q

intussuception

  • history
  • examination
A

History

  • Sudden onset inconsolable crying episodes
  • Pallor
  • Draw knees up to chest to alleviate pain
  • Later stages, stools may be red stained with blood and mucous
  • In older children blockage more evident via vomiting and abdo pain

Examination

distension

palpable sausage shaped abdominal mass found in RUQ usually

peritonism

presence of bowel sounds

69
Q

intussuception

diagnosis and invetsigation (2)

A

AXR:

Distended bowel loops

A curvilinear outline of the intussuception

Absence if bowel gas in colon distal to site

If perforated Rigler’s sign

Ultrasound better

70
Q

pyloric stenosis

presentation

A
  • Vomiting which increases in frequency and forcefulness over time ultimately becoming more projectile. Milky
  • dehydration
  • hunger after feeding
  • weight loss if prolonged
71
Q

Autistic spectrum disorder

  • when do presenting features appear?
  • what are they (4)
A

appears 2-4 years

1) Impaired social interactions (gaze avoidance, own company, does not seek comfort or close friends, doesn’t appreciate social cues)
2) Speech and language interactions (delayed development, limited use of facial gestures and facial expression, formal pedantic language)
3) imposition of routines with ritualistic and repetitive behaviour (on self and others and breech leads to temper, poverty of imagination, concrete play)
4) comorbidities (general learning and attention difficulties, seizures, affective disorders)

72
Q

ADHD

presenting features- 3 categories

A
  1. inattentive
  2. hyperactive-impulsive
  3. combined

inattentive

  • Fails to give close attention to details or males careless mistakes
  • Has difficulty sustaining attention
  • Does not appear to listen
  • Struggles to follow instructions

hyperactive-impulsive

  • Talks excessively
  • Blurts out answers
  • Difficulty waiting or taking turns
  • Fidgets with or feet or squirms in chair

Combined

meets the cirteria for both prior

73
Q

kawasaki disease

  • example of what kind of disease
  • what is a severe complication
  • symptoms preceded by
  • diagnositic criteria (symptoms) (5)
A

systemic vasculitis

aneurysm of the cerebral arteries

fever

diagnositic criteria

  1. conjunctival infection- bilateral, non-exudative, painless
  2. rash- erthymatous polymorphous rash occuring in the first few days, involving trunk and extremities, maculopapular
  3. oral changes- strawberry tongue, erythema, dryness, cracking and bleeding of lips
  4. extremity changes- hyperaemia and painful oedema of hands and feet that progresses to desquamation
  5. lymphadenopathy- cervical, most commonly unilateral, tender

74
Q

what is a febrile seizure

what are suspected causes (2)

simple FS (3)

A

a seizure associated with a febrile illness that is not caused by an infection of the CNS that does not fit the descritption of other seizures

  • reaction to fever in a devloping brain
  • viral infections may be triggering

simple FS:

  • should not be >15 mins
  • should not involve focal or asymmetrical activity
  • should not recur within 15 mins
75
Q

diagnosis of febrile seizure

management

call for medical emergency attention if:

A
  • history
  • EEG in complex seizure
  • MRI as an extra

most stop in a couple minutes. during you can:

  • Place child on their side on a soft surface
  • Start timing the seizure
  • Stay close and comfort
  • Remove hard or sharp objects nearby
  • Loosen or remove restrictive clothing
  • Don’t restrain their movements

seizure lasts more than 5 mins

repeated seizures less than 5 mins apart

76
Q

Classification of seziures (2)

A

generalised

focal

77
Q

generalised seizure classifications (5)

A
  1. absence
  2. myoclonic
  3. tonic
  4. tonic-clonic
  5. atonic
78
Q

absence seizure

A

example of generalised seizure

  • transient loss of consciousness,
  • an abrupt onset termination
  • unaccompanied by motor phenomena apart from some flickering of the eyelids and minor alteration in muscle tone
  • hyperventilation prior to absences
79
Q

mycolonic seizures

clonic seizures

A

mycolonic seizures

  • brief
  • repetitive jerking movements of the limbs neck or trunk

tonic seizures

generalised increase in tone

80
Q

tonic-clonic seizures

A

Rhythmical contraction of muscle groups following the tonic phase

Rigid tonic phase: children may fall to ground injuring themselves, presence of apnoea (lackof breathing) sp become cyanosed (blue)

-Clonic phase: jerking of the limbs, irregular breathing, there may be tongue biting and urinary incontinence. Seizure lasts seconds to minutes and is followed by up to hours of unconsciousness

example of generalised seizure

81
Q

atonic seizure

A

example of generalised seizure

often combined w myoclonic jerk, followed by transient loss of muscle tone causing a sudden fall

82
Q

What is a focal seizure?

how many categories of it are there?

what are they?

A

focal seizure- where seizures arise from one or part of one hemisphere- presentation is dependent on functional localisation. In focal seizures, the level of consciousness may be retained, lost or progress into a secondary generalised tonic-clonic

4

  • frontal lobe
  • temporal lobe
  • occipital
  • parietal
83
Q

frontal lobe seizures

A

focal seizure

  • Motor + pre-motor involvement
  • -May lead to clonic movements, which may travel proximally (Jacksonian march)
  • -May lead to a tonic seizure w both upper limbs raised high briefly
  • -grunting
  • -Asymmetrical tonic seizures can be seen (bizarre presentation?)
84
Q

temporal lobe seizure

A

focal seizure

  • may have auras present (warning feelings) such as smell+ taste+ sound+ shape abnormalities
  • strangeness and anxiety
  • lip smacking
  • pulling at clothing
  • walking in a non-purposeful manner (automatisms)
  • Deja-vu sensation
  • Consciousness can be impaired
85
Q

occipital lobe seizure

A

focal seizure

multi-coloured bright lights spread from one area of the homonymous visual field to another

86
Q

parietal lobe seizure

A

focal seizure

cause contralateral dysesthesias (altered sensation), or distorted body image

87
Q

differential diagnosis for seizures (10)

A
  1. Syncope with secondary jerky movements
  2. Primary cardiac or repiratory abnormalities presenting with secondary anoxic seizures
  3. Hyperkplexia (excessive shock recation to suprises)
  4. Focal motor seizures (facial muscle and eye movements)
  5. Tics (transient focal motor attacks)
  6. Transient cerebral ischaemia
  7. Partial seizures
  8. Hypoglycaemia (loss of consciousness)
  9. Nonconvulsive status epilepticus (prolonged confusional states)
  10. Transient global amnesia (prolonged confusional states)
88
Q

cerebral palsy

  • what is it
  • cardinal features (4)
  • associations
  • types (5)
A

Chronic movement disorder of movement and/or posture that presents early (before the age of 2y) and continues throughout life. It is caused by static injury to a developing brain.

Cardinal features

  1. Delay in motor development milestones
  2. Abnormalities of muscle tone
  3. Reduction in normal movement
  4. Presence of abnormal movements

Associations

Children with CP are at a higher risk of impairments, including vision, hearing, speech, learning, nutrition and psychiatric problems

types of cerebral palsy:

  1. spastic- (hypertonic) increased muscle tone, jerky movements (spasticity), contractures, hyperreflexia
  2. mixed-
  3. athetoid- involuntary movement in the face, torso, and limbs, affects basal ganglia and cerebellum, problems with posture, stiff or rigid body
  4. hypotonic- floppy muscles, lack of head control, trouble walking
  5. ataxic- cerebllum—ataxia: balance, co-ordination, speech. shakiness, tremors
89
Q

what is puberty?

how is it mediated?

what classification system do we use to classify the satges?

A
  • Well-defined sequence of physical and physiological changes occurring during the adolescent years that culminates in attainment of full physical and sexual maturity.
  • Nocturnal pulsatile secretions of gonadotrophin-secreting hormone by the hypothalamus is the first step in the imitation of puberty. This in turn causes the pulsatile secretions of LH and FSH (gonadotrophins). LH stimulates sex hormone secretion from the hormones.

The normal stages of puberty can be classed into the Tanner stages, they are passed through in an orderly sequential way:

90
Q

tanner stages of development

boys:

stage, genitalia, pubic hair, other events

A

Stage

Genitalia

Pubic hair

Other events

I

Pre-pubertal

Vellus not thicker than on abdomen

TV <4mL

II

Enlargement of testes and scrotum

Sparse, long pigmented strands at base of penis

TV 4-8mL; voice starts to change

III

Lengthening of penis

Darker and curlier

TV 8-10mL; axillary hair

IV

Increase in penis length and breadth

Adult type hair but covering a small area

TV 10-15mL; upper lip hair, peak height velocity

V

Adult shape and size

Spread to medial thighs (stage VI spread to linea alba)

TV 15-25mL, facial hair spreads to cheeks, adult voice

91
Q

tanner stages of development

girls:

stage, genitalia, pubic hair, other events

A

Stage

Genitalia

Pubic hair

Other events

I

Elevation of papilla only

Vellus not thicker than on abdomen

II

Breast bud stage; elevation of breast and papilla

Peak height velocity

III

Further elevation of breast and areola together

Darker and curlier

IV

Areola forms a second mound on top of breast

Adult type hair but covering a small area

Menarche

V

Mature stage: areola recedes and only papilla projetcs

Spread to medial thighs (stage VI spread to linea alba)

92
Q

diabetic ketoacidosis presenting features

A
  • Dehydration
  • Lethargy, confusion
  • Polyuria, confusion
  • Weight loss
  • Abdominal pain +/- vomiting (may mimic a surgical abdomen)
  • Rapid, deep sighing (Kussmaul’s respirations)
  • Ketotic breath- fruity, pear drop smell
  • Fever- not normal for DKA and a source of sepsis must be sought
  • Drowsiness, shock, coma (assess GCS)
  • Any evidence of cerebral oedema
93
Q

hypothyroidism- newborn screening

which 3 mesurements are taken?

A

1) primary TSH measurement with backup thyroxine (T4) determination for infants with high TSH.
2) Primary T4 measurements with backup TSH assessment in infants with low T4 level.
3) Simultaneous measurement of T4 and TSH

94
Q

iron deficiency anaemia

causes (6)

presenting features (4)

A

Causes

  • Dietary (most common) e.g., exclusive consumption of breast milk, with late introduction of iron containing solids
  • Infancy and early childhood- low level of dietary iron, GI blood loss
  • ↑ demand in rapid growth- e.g., after immaturity or growth spurt
  • Malabsorption- coeliac disease, IBD
  • Rarely blood loss: Meckel’s diverticulum, oesophagitis, bleeding may be occult in cysts, tumours or drug use e.g., NSAID’s
  • Intestinal parasites- e.g, hookworm in less developed countries

presenting features

Onset is usually insidious

  • Pallor
  • Lethargy
  • Poor feeding
  • Breathless
95
Q
  • What does ITP stand for
  • what is it
  • presentation
A
  • immune thrombocytopaenia
  • immune destruction of platelets by antibodies

presentation

mostly insidious and most are subclinical

  • Petechiae (<5mm)
  • Purpura (purple spots)
  • Superficial bruising
  • Epistaxis (nose bleed)
  • Uncommon to get profuse bleeding

96
Q

Ivestigations for ITP

Treatment for ITP

A
  • FBC- look for low platelets
  • blood film
  • bone marrow biopsy

Treatment for ITP

  • Observation. Self resolves in 6-8 weeks
  • May need steroids or IV. Ig
97
Q

Henoch Scholein purpura

presentation

onset

more common in which gender

often preceded by

A

presentation

  • Characteristic skin rash on the extensor surfaces (back of legs, buttocks and arms)
  • Arthralgia
  • Periarticular oedema
  • Abdominal pain
  • Glomerulonephritis
  • Bloody diarrhoea
  • Onset between 3-10 years. Twice as common in boys as it is in girls.
  • Incidence peaks in Winter months
  • Often preceded by URTi (usually Group A streptococci)
98
Q

eczema

age of onset

patho basic

A
  • <6 months onset
  • fundamental problem is a barrier defect—- water is lost easily, dry skin that may itch. Irritants, allergens, and microbes penetrate the skin more easily., often causing flares.
99
Q

eczema clinical features

A

Acute:

  • Erythamatous
  • Weeping

Chronic:

  • Lichenified
  • Dry

Infant:

  • Cheeks
  • Elbows
  • Knees with crawling
  • Childhood:*
  • Flexural, wrists and ankles
  • Adolescent and adult:*
  • Flexural but may also affect head and neck, nipples, palms and soles
100
Q

management of eczema

A
  • Explain diagnosis and provide education for the family and patient.
  • Treat flares
  • Maintain skin integrity
  • General measures

Soap avoidance

Short showers and baths not too hot

Avoidance of irritancies- don’t overdress, avoid fragranced products, keep fingernails short

Moisturise

Avoid lotions

Creams are good moisturisers but sting on open excoriated skin

Treat itch and inflammation with topical corticosteroids daily until the eczema is clear

Treat infection if present

101
Q

Heel prick test

when is it done?

how many diseases is it screening for?

what are those diseases?

A

AKA newborn blood spot screening

done at 5 days old

1/9 rare but serious health conditions

  • sickle cell disease
  • cystic fibrosis
  • congenital hypothyroidism
  • inherited metabolic diseases ((phenylketonuria (PKU), medium-chain acyl-CoA dehydrogenase deficiency (MCADD), maple syrup urine disease (MSUD), isovaleric acidaemia (IVA), glutaric aciduria type 1 (GA1), homocystinuria (pyridoxine unresponsive) (HCU))
  • severe combined immunodeficiency (SCID)
102
Q
A
103
Q

at what spinal level should you do a lumbar puncture

A

L3/4

104
Q

what are the 4 measurements we use to track a childs growth

A

weight

height

head circumference

BMI

105
Q

head circumference measurement

what is it an indirect measuremnt of

important in children who

A
  • occipitofrontal circumference
  • head and brain growth
  • developmental delay or suspected hydrocephalus

Year 3 Paeds (4 decks)

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