Paediatrics Flashcards
What are the 5 key develomental fields?
Gross motor
Fine motor
Social and self-help
Speech and language
Hearing and vision
What factors influence development?
- Genetics (Family, race, gender)
- Environment
- Positive early childhood experience
- Developing brain vulnerable to insults
–Antenatal
–Post natal
–Abuse and neglect
What are adverse environmental factors for develoment?
•Antenatal
–Infections (CMV, Rubella, Toxo, VZV)
–Toxins (Alcohol, Smoking, Anti-epileptics)
•Postnatal
–Infection (Meningitis, encephalitis)
–Toxins (solvents mercury, lead)
–Trauma (Head injuries)
–Malnutrition (iron, folate, vit D)
–Metabolic (Hypoglycaemia, hyper + hyponatraemia)
–Maltreatment/ under stimulation/ domestic violence
–Maternal mental health issues
•Good (sensitive) histories are therefore important
Who performs developmental assessment?
•Patients
–Child surveillance v.s. developmental screening v.s. developmental assessment
–Specific groups (premature, syndromes, events)
•Assessors
–Parents and wider family
–Health visitors, nursery, teachers
–GPs, A+E, FYs, STs, students
–Paediatricians and community paediatricians
What is used to determine developmental assessment?
Healthy chid programme
Information from parents
Red book
Medical history and examination
What are the recogniased phases of childhood?
- Neonate (<4w)
- Infant (<12m/1y)
- Toddler (~1-2y)
- Pre-school (~2-5y)
- School age
- Teenager/ Adolescent
Examples of normal variation of development
- Early developers
- Late normal
- Bottom shufflers- walking delay
- Bilingual families- apparent language delay (total words may be normal)
- Familial traits
What are developmental red flags?
- Loss of developmental skills
- Parental/ professional concern re. vision (simultaneous referral to paediatric ophthalmology)
- Hearing loss (simultaneous referral for audiology/ ENT)
- Persistent low muscle tone/ floppiness
- No speech by 18 months, esp if no other communication (simultaneous referral for urgent hearing test)
- Asymmetry of movements/ increased muscle tone
- Not walking by 18m/ Persistent toe walking
- OFC > 99.6th / < 0.4th / crossed two centiles/ disproportionate to parental OFC (occipitofrontal circumference)
- Clinician uncertain/ thinks that development may be disordered
Who is responsibe for keeping track of the healthy child programme?
GP,s health visitors and midwives
What are the screening events for babies?
- New-born exam and blood spot screening*
- New-born hearing screening (by Day 28)
- Health Visitor First Visit
- 6-8w Review (Max 12w)
- 27-30 month Review (Max 32m)
- Orthoptist vision screening (4-5y)
- If needed
–Unscheduled review
–Recall review
What diseases are screened for in the child health programme?
The programme includes screening for Phenylketonuria (PKU); Congenital Hypothyroidism (CHT); and Cystic Fibrosis (CF), Medium Chain Acyl-CoA Dehydrogenase Deficiency (MCADD) and Sickle Cell Disorder (SCD).
What is covered in the 6-8 week review?
- Identification data (Name, address, GP)
- Feeding (breast/ bottle/ both)
- Parental concerns (appearance, hearing; eyes, sleeping, movement, illness, crying, weight)
- Development (gross motor, hearing + communication, vision + social awareness)
- Measurements (Weight, OFC, Length)
- Examination (heart, hips, testes, genitalia, femoral pulses and eyes (red reflex))
- Sleeping position (supine, prone, side)
What is covered in the 27-30 month review?
- Identification data (name, address, GP)
- Development
–Social, behavioural, attention and emotional
–Communication, speech and language
–Gross and fine motor
–Vision, hearing
- Physical measurements (height and weight)
- Diagnoses / other issues
What are the health promotion aspects of the healthy child programme?
•Health Promotion
–Smoking
–Alcohol/ Drugs
–Nutrition
–Hazards and safety
–Dental Health
–Support services
•Additional input during immunisations and as issues are identified
When might you postpone a vaccination for a child?
•Postponed if unwell (fever, systemic symptoms)
What are the physical measurements for growth monitoring?
•Physical measurements of 3 key parameters
–Weight (grams and Kgs)
–Length (cm) or height (if >2y)
–Head circumference (OFC) (cm)
What are the values of weight, length and OFC for birth, 4 months, 12 months and 3 years
What is failure to thrive?
•Child growing too slowly in form and usually in function at the expected rate for his or her age
What is the general cause of failure to thrive?
Supply of energy is less than the demand of energy
What are maternal causes of failure to thrive?
–Poor lactation
–Incorrectly prepared feeds
–Unusual milk or other feeds
–Inadequate care
What are infant causes of failure to thrive?
–Prematurity
–Small for dates
–Oro palatal abnormalities (e.g. cleft palate)
–Neuromuscular disease (e.g. cerebral palsy)
–Genetic disorders
Increased metabolic demands
Excessive nutrient loss
Give examples of causes of increased metabolic demands
- Congenital lung disease
- Heart disease
- Liver disease
- Renal disease
- Infection
- Anemia
- Inborn errors of metabolism
- Cystic fibrosis
- Thyroid disease
- Crohn’s/ IBD
- Malignancy
Give examples of causes excessive nutrient loss
- Gastro oesophageal reflux
- Pyloric stenosis
- Gastroenteritis (post-infectious phase)
- Malabsorption
–Food allergy
–Persistent diarrhoea
–Coeliac disease
–Pancreatic insuffiency
–Short bowel syndrome
What are non-organic causes of failure to thrive?
- Poverty/ socio-economic status
- Dysfunctional family interactions (especially maternal depression or drug use)
- Difficult parent-child interactions
- Lack of parental support (eg, no friends, no extended family)
- Lack of preparation for parenting/ education
- Child neglect
- Emotional deprivation syndrome
- Poor feeding or feeding skills disorder
- Feeding disorders (eg, anorexia, bulimia- later years)
What is presentation of eczema?
Itchy, dry inflammatory skin disease.
What are the types of eczema that have endogenous causes?
Atopic – ‘genetic barrier dysfunction’
Seborrheoic – face/scalp – scale associated
Discoid – annular/circular patches
Pomphylx – vesicles affecting palms/soles
Varicose – oedema/venous insufficiency
What are exogenous causes of eczema?
Exogenous (external cause)
Allergic contact dermatitis (sensitised to allergen)
Irritant contact dermatitis (friction, cold, chemicals e.g acids,alkalis, detergents, solvents)
Photosensitive/photoaggravated eczema
What can causes flares of eczema?
- Flares can be associated with:
- Infections/viral illness
- Environment: central heating, cold air
- Pets: if sensitised/allergic
- Teething
- Stress
- Sometimes no cause for flare found
What protein is associated with atopic eczema?
Filaggrin
What is the effect of the loss of barrier functino on the skin?
Loss of water
Irritants may penetrate (soap detergeant, solvents, dirt)
Allergens may penetrate (pollens, dust-mite antigens, microbes)
Where on the body is mainly affected byu seborrheoic dermatitis?
Mainly the scalp and the face
Who is often affected by seborrheoic dermatitis?
Babies under 3 months, usually resolves by 12 months
What is the causative organism for seborrhoeic dermatitis?
Associated with proliferation of various species of the skin commensal Malassezia in its yeast form
Treatment for seborrheoic dermatitis
•Emollients, antifungal creams,
antifungal shampoos, mild topical
steroids
What are the features of varicose eczema?
- Associated with oedema, varicose veins, chronic leg swelling
- Skin often dry and inflamed
- Skin may ulcerate
What is the managment for varicose eczema?
Emollients, topical steroids, compression stockings
What is thre effect of food allergy on eczema?
- Immediate reactions (lip swelling, facial redness/itching, anaphylactoid symptoms)
- Late reactions (worsening of eczema 24/48 hours after ingestion) – especially if pattern with specific food (food diaries encouraged).
- GI problems
- Failure to thrive
- Severe eczema unresponsive to treatment
- Severe generalised itching – even when the skin appears clear
- Atopy can be associated with food allergy
What are the two ways to test for food allergy?
- 2 ways to test for food allergy:
- Blood test for specific IgE antibodies to certain foods
- Skin prick testing
What are the most common food products that you can be allergic to?
•Commonest: milk/dairy, soy, peanuts, eggs, wheat, fish
Give examples of airbourne allergens
•Airborne allergens (can also be tested for in same way)
- house dust mite, pet dander, pollens
What is treatment for eczema?
- Emollients (Lotions, creams or ointments – fragrance free, greasier ointments more effective)
- Topical steroids
- Calcineurin inhibitors (e.g protopic – steroid sparing topical agents)
- UVB light therapy
- Immunosuppressive medication
Give examples of topical steroids
- Very potent (Dermovate)600x
- Potent (Betnovate)100x
- Moderate (Eumovate) 25x
- Mild (Hydrocortisone)
What is the appearance of impetigo?
Pustules and honey coloured crusted erosions
What is the cause of impetigo?
Staph aureus
What is the treatment for Impetigo?
Topical antibacterial (fucidin)
Oral antibiotic (flucloxacillin)
What is the appearance of molluscum contagiousm?
Pearly papules, umbilicated centre
What causes molluscum contagiousm?
Molluscipox virus
What is the treatment for molluscum contagiousm?
Treatment is not usually recommended. If lesions are troublesome or considered unsightly, use simple trauma or cryotherapy, depending on the parents’ wishes and the child’s age:
Squeezing (with fingernails) or piercing (orange stick) lesions may be tried, following a bath. Treatment should be limited to a few lesions at one time
Cryotherapy may be used in older children or adults, if the healthcare professional is experienced in the procedure
Eczema or inflammation can develop around lesions prior to resolution. Treatment may be required if:
→ Itching is problematic; prescribe an emollient and a mild topical corticosteroid (e.g. hydrocortisone 1%)
→ The skin looks infected (e.g. oedema, crusting); prescribe a topical antibiotic (e.g. fusidic acid 2%)
What is the colour of viral warts?
SKin coloured
What causes viral skin warts?
- Common non-cancerous growths of the skin caused by infection with human papillomavirus (HPV)
- Sole foot – verruca
- Transmitted by direct skin
contact
Give examples of viral exanthems
- Chicken pox
- Measles
- Rubella
- Roseola (herpes virus 6)
- Erythema infectiosum (Parvovirus B19, slapped cheek )
What is the presentation of viral examnthems?
- Associated viral illnesses
- Common
- Fever, malaise, headache
Where does damage arise in viral exanthems?
•Either reaction to a toxin produced by the organism, damage to the skin by the organism, or an immune response.
How many times can you get chicken pox?
- One infection is thought to confer lifelong immunity.
- Immunocompromised individuals are susceptible to the virus at all times.
What is the presentation of chicken pox?
- Red papules (small bumps) progressing to vesicles (blisters) often start on the trunk.
- Itchy. Associated with viral symptoms
What is the incubation period of chicken pox?
10-21 days
When is chicken pox contagious?
1-2 days before rash appears and until lesions have crusted
What is the presentation of parovirus (slapped cheek)?
- Viral symptoms.
- Erythematous rash cheeks initially and then also
lace like network rash (trunk and limbs). Can take 6w to full fade.
What are potentiual complications of parovirus (slapped cheek)?
- Very rarely….
- Aplastic crisis (if haemolytic disorders)
- Risk to pregnant women (spontaneous abortion, intrauterine death, hydrops fetalis)
What organism causes hand foot and mouth disease?
- Usually Coxsackie virus A16
- (can also be due to Enterovirus 71 and other coxsackivirus types)
What is the presentation of hand foot and mouth disease?
•Blisters on the hands, feet and in the mouth. Viral symptoms.
What is the presentation of orofacial granulomatosis?
Lip swelling and fissuring
Oral mucosal lesions: ulcers and tages, cobblestone appearance
Crohn’s disease
What is the presentation of erythema nodosum?
- Painful, erythematous subcutaneous nodules
- Over Shins; sometimes other sites
•Slow resolution - like bruise,
6-8 weeks
What are potential causes of erythema nodosum?
- Infections – Streptococcus, Upper respiratory tract
- Inflammatory bowel disease
- Sarcoidosis
- Drugs – OCP, Sulphonamides, Penicillin
- Mycobacterial Infections
- Idiopathic
What skin condition is linked to dermatitis herpetiformis?
Coeliacs disease
What is the presentation of dermatitis Herpetiformis?
- Rare but persistent immunobullous disease that has been linked to coeliac disease
- Itchy blisters can appear in clusters
- Often symmetry
- Scalp, shoulders, buttocks, elbows and knees
What are the investigations for dermatitis herpetiformis?
- Detailed history
- Coeliac screening
- Skin biopsy
What is the treatment for dermatitis Herpetiformis?
•Emollients, gluten free diet, topical steroids, dapsone
What is the presentation of urticaria?
- Wheals/hives
- Associated angioedema (10%)
- Areas of rash can last from few minutes up to 24 hours
What is the definition of acute vs chronic urticaria?
Acute is less than 6 weeks
Chronic is more than 6 weeks
What are the causes of urticaria?
- Many causes:
- Viral infection
- Bacterial infection
- Food or drug allergy
- NSAIDS, OPIATES,
- Vaccinations
- Chronic urticaria – idiopathic often no cause found. Likely autoimmune cause.
What is the treatment for urticaria?
- Antihistamines
- Newer generation e.g desloratadine
- 3 x daily (off licence doses)
- Ranitidine
- Montelukast
- Omalizumab
- Ciclosporin
What is the artiology of congenital heart disease?
Genetic susceptibility (6-10% of all CHD have underlying chromosomal problems)
Teratogenic insult (18-60 days post ceonception)
Environmental factors( drgus such as alcohol cocaine, infections such as TORCH and others, maternal factors such as diabetesm SLE)
What heart defects are associated with trisomy 13?
VSD and ASD
What heart defects are assoiciated with trisomy 21?
multiple cardiac problems may be present
endocardial cushion defect (most common, 40%, also known as atrioventricular septal canal defects)
ventricular septal defect (c. 30%)
secundum atrial septal defect (c. 10%)
tetralogy of Fallot (c. 5%)
isolated patent ductus arteriosus (c. 5%)
What do the following conditions cause to happen to the heart?
Turner
Noonan
Williams
Turner = co-arctation of the aorta
Noonan = Pulmonary stenosis
Williams = supravalvular AS
What are the features of still’s murmur
(who is affected, where can you hear it, what type of murmur is it and when can you hear it best?)
Age 2-7 years
Soft systolic; vibratory, musical,”twangy”
Apex, left sternal border
Increases in supine position and with exercise
What are the features of pulmonary outflow murmur?
(who is affected, where can you hear it, what type of murmur is it and when can you hear it best?)
Age 8-10 years
Soft systolic; vibratory
Upper left sternal border, well localised, not radiating to back
Increases in supine position, with exercise
Often children with narrow chest
What are the features of carotid/brachiocephalic arterial bruits?
Age 2-10 years
1/6-2/6 systolic; harsh
Supraclavicular, radiates to neck
Increases with exercise, decreases on turning head or extending neck
What are the features of venous hum?
Age 3-8 years
Soft, indistinct
Continuous murmur, sometimes with diastolic accentuation
Supraclavicular
Only in upright position, disappears on lying down or when turning head
What are the main types of ventricular septal defects?
3 main types : - subaortic
- perimembranous
- muscular
L to R shunt
What is the clinical presentation of VSD?
Pansystolic murmur lower left sternal edge, sometimes with thrill
In very small VSDs, early systolic murmur
In very large VSDs diastolic rumble due to relative mitral stenosis
Signs of cardiac failure in large VSDs, eventually leading to biventricular hypertrophy and pulmonary hypertension
What is the core feature in Eisenmenger syndrome?
Eisenmenger syndrome occurs when the increased pressure of the blood flow in the lung becomes so great that the direction of blood flow through the shunt reverses. Oxygen-poor (blue) blood from the right side of the heart flows into the left side of the heart and is pumped to your body so you don’t receive enough oxygen to all your organs and tissues.
Results from intracardiac communication and causes cyanosis, pulmonary hypertensio and shunt reversal. Erythrocytosis also follows
What is used to close a VSD?
Amplatzer device
Patch closure
What is AVSD?
Singular AV valve with ostium primum ASD and high VSD
What is the presentation for pulmonary stenosis?
Asymptomatic in mild stenosis, in moderate and severe exertional dyspnoea and fatigue
Ejection systolic murmur upper left sternal border with radiation to back
What is the presentation of aortic stenosis?
Mostly asymptomatic, if severe, reduced exercise tolerance, exertional chest pain, syncope
Ejection systolic murmur upper right sternal border, radiation into carotids
What are changes in fetal circulation at birth?
Pulmonary Vascular Resistance Falls
Pulmonary Blood Flow Rises
Systemic Vascular Resistance is increased
Ductus Arteriosus Closes
Foramen Ovale Closes
Ductus Venosus Closes
What is the treatment for patent ductus arteriosus?
fluid restriction/
diuretics, prostaglandin inhibitors
(Indomethacin, Ibuprofen), surgical
ligation
In term babies good chance of spontaneous closure, not prostaglandin sensitive
What is the investigation for coarctation of the aorta?
MRI
What is the management of coarctation of the aorta?
Re-open PDA with Prostaglandin E1 or E2
Resection with end-to-end anastomosis
Subclavian patch repair
Balloon Aortoplasty
What are the 4 components of tetralogy of fallot?
ventricular septal defect (VSD)
right ventricular hypertrophy
right ventricular outflow tract obstruction, pulmonary stenosis
overriding aorta
What is the presentation of tetralogy of fallot?
cyanosis
causes a right-to-left shunt
ejection systolic murmur due to pulmonary stenosis (the VSD doesn’t usually cause a murmur)
a right-sided aortic arch is seen in 25% of patients
chest x-ray shows a ‘boot-shaped’ heart, ECG shows right ventricular hypertrophy
What is managementof tralogy of fallot?
surgical repair is often undertaken in two parts
cyanotic episodes may be helped by beta-blockers to reduce infundibular spasm
WHen is ALT/AST raised?
Elevated in hepatocellular damage (hepatitis)
When is alkaline phosphatase and gamma GT raised?
Elevated in biliary disease
What are tests to assess liver function?
•Coagulation
- •Prothrombin time (PT)/INR
- •APTT
- Albumin
- Bilirubin
- (Blood glucose)
- (Ammonia)
Here are the signs of liver disease in children
Why does jaundice happen?
Discolouration of the skin due to accumulatino of bilirubin
Where is infant jaundce most noticeable?
Sclera
What level of total bilirubin is recquired for jaundice?
•Usually visible when total bilirubin >40-50 umol/l
Here is bilirubin metabolism
Here is where pre-hepatic, hepatic and post hepatic hepatitis happens
What are the causes of early, intermediate and prolonged jaundice?
•Early (<24 hours old)
- Always pathological
- Causes: Haemolysis, Sepsis
•Intermediate (24hrs – 2 weeks)
•Causes: Physiological, Breast milk, Sepsis, Haemolysis
•Prolonged (>2 weeks)
•Causes: Extrahepatic obstruction, Neonatal hepatitis, Hypothyroidism, Breast milk
Why does physiological jaundice happen?
- Shorter RBC life span in infants (80-90 days)
- Relative polycythaemia
- Relative immaturity of liver function
What type of jaundice is physiological jaundice?
- Unconjugated jaundice
- Develops after first day of life
What type of jaundice is breast milk jaundice?
- Unconjugated jaundice
- Can persist up to 12 weeks
It is essentially an extension of physiological jaundice and the exact mechanism of action is unknown
What are causes of early/intermediate unconjugated infant jaundice?
- Sepsis
- Haemolysis
- •ABO incompatibility
- •Rhesus disease
- •Bruising/cephalhaematoma
- •Red cell membrane defects (e.g. spherocytosis)
- •Red cell enzyme defects (e.g. G6PD)
•(Abnormal conjugation)
- •Gilbert’s disease – common, mild
- •Crigler-Najjar syndrome – v. rare, severe
What are the tests for the following conditions?
- Sepsis
- Haemolysis
- •ABO incompatibility
- •Rhesus disease
- •Bruising/cephalhaematoma
- •Red cell membrane defects (e.g. spherocytosis)
- •Red cell enzyme defects (e.g. G6PD)
•(Abnormal conjugation)
- •Gilbert’s disease – common, mild
- •Crigler-Najjar syndrome – v. rare, severe
- Sepsis (urine + blood cultures, TORCH screen)
- Haemolysis
- ABO incompatibility (Blood group, DCT)
- Rhesus disease (Blood group, DCT)
- Bruising/cephalhaematoma (clinical examination)
- Red cell membrane defects (e.g. spherocytosis) (Blood film)
- Red cell enzyme defects (e.g. G6PD) (G6PD assay)
- (Abnormal conjugation)
- Gilbert’s disease (genotype/phenotype)
- Crigler-Najjar syndrome (genotype/phenotype)
What is kernicterus?
Deposits of bilirubin in the brain
- Unconjugated bilirubin is fat-soluble (water insoluble) so can cross blood-brain barrier
- Neurotoxic and deposits in brain
What are tearly signs of kernicterus?
•Early signs – encephalopathy – poor feeding, lethargy, seizures
What are the late consequences of kernicterus?
•Late consequences – severe choreoathetoid cerebral palsy, learning difficulties, sensorineural deafness
What is the treatment for kernicterus?
- Treatment for unconjugated jaundice
- Visible light (450nm wavelength) (not UV) converts bilirubin to water soluble isomer (photoisomerisation)
- Threshold for phototherapy in infants guided by charts
What are causes of prolonged infant jaundice?
Note: • Conjugated jaundice in infants is always abnormal and always requires further investigation
What is the most important test in prolonged jaundice?
Split bilirubin - determines if it is a prolonged / not-prolonged jaundice
What are the causes of biliary obstruction?
These cause prolonged jaundice that are conjugated
•Biliary atresia
- •Conjugated jaundice, pale stools
•Choledochal cyst
- •Conjugated jaundice, pale stools
•Alagille syndrome
- •Intrahepatic cholestasis, dysmorphism, congenital cardiac disease
Prolonged jaundice message 2:
• Always assess stool colour in infants with prolonged jaundice
What is the stool and urine like in biliary artresia?
Pale stools
dark urine
Where does the fibro-inflammatory effect of biliary artresia cause?
Obstruction of extra hepatic bile ducts
What is the surgical procedure for biliary artresia?
Intraoperative cholangiogram is the gold standard for confirming obstruction
Kasai portoenterostomy
Success rate diminishes rapidly with age
Best results if performed before 60 days (<9 weeks)
Potential medication - ursodeoxycholic acid
What are the tests for the following conditions?
- Biliary atresia
- Conjugated jaundice, pale stools
- Choledochal cyst
- Conjugated jaundice, pale stools
- Alagille syndrome
- Intrahepatic cholestasis, dysmorphism, congenital cardiac disease
•Biliary atresia
•(split bilirubin, stool colour, ultrasound, liver biopsy)
•Choledochal cyst
•(split bilirubin, stool colour, ultrasound)
•Alagille syndrome
•(dysmorphism, genotype)
What are causes of neonatal hepatitis?
Causes prolonged jaundice
- Alpha-1-antitrypsin deficiency
- Galactosaemia
- Tyrosinaemia
- Urea cycle defects
- Haemochromatosis
- Glycogen storage disorders
- Hypothyroidism
- Viral hepatitis
- Parenteral nutrition
What are the tests for the following conditions?
- Alpha-1-antitrypsin deficiency
- Galactosaemia
- Tyrosinaemia
- Urea cycle defects
- Haemochromatosis
- Glycogen storage disorders
- Hypothyroidism
- Viral hepatitis
- Parenteral nutrition
- Alpha-1-antitrypsin deficiency (phenotype/level)
- Galactosaemia (GAL-1-PUT)
- Tyrosinaemia (amino acid profile)
- Urea cycle defects (ammonia)
- Haemochromatosis (iron studies, liver biopsy)
- Glycogen storage disorders (biopsy)
- Hypothyroidism (TFTs)
- Viral hepatitis (serology, PCR)
Parenteral nutrition (history
What is the presentation of constipation?
Poor appetite
Irritable
Lack of energy
Abdominal pain or distension
Withholding or straining
Diarrhoea (this is what the symptom they present with)
Why do people become constipated?
Poor appetite
Irritable
Lack of energy
Abdominal pain or distension
Withholding or straining
Diarrhoea
What drugs make people constipated?
Opiates
Gaviscon
Why do children become constipated?
Social
- poor diet
- •Insufficient fluids
- •Excessive milk
- potty training / school toilet
Physical
- intercurrent illness
- medication
Family history
Psychological (secondary)
Organic
Constipation cylce
What is the treatment of constipation?
Dietary
- fibre
- fruit
- vegetables
- fluids
- milk
Psychological elements of therapy:
Reduce aversive factors
Make going to the toilet a pleasant experience
- Correct height
- Not cold
- School toilets
- Soften stool and remove pain
Avoid punitive behaviour from parents
Reward ‘good’ behaviour
General praise
Star charts
Soften stool and stimulate defecation:
- Osmotic laxitives (lactulose)
- Stimulant laxitives (senna, picolax)
- Isotonic laxitives (movicol)
Advantages - non-invasive, given by patients.
Disadvantages - non-compliance, side effects
What can be a complication of constipation?
Megarectum can press on bladder and urethra - can cause poor stream, incomplete voiding and can result in UTI’s
What is the treatment of impaction?
Empty impacted rectum
Empty colon
Maintain regular stool passage
Slow weaning off treatment
(can be movicol disimpaction) - can be messy though
Presentation of Crohn’s vs UC
Histopathology (crohn’s has granulomas)
Crohns has a massive effect of weight loss and growth failure in children.
UC has more diarrhoea and rectal bleeding
What are the laboratory investigations for IBD?
Laboratory investigations
Full blood count & ESR
- Anaemia
- Thrombocytosis
- Raised ESR
Biochemistry
•Stool calprotectin
- Raised CRP
- Low Albumin
Microbiology
•No stool pathogens
In crohn’s symptoms are not very strong, you should do tests at low threshold.
Who is pancolitis more likely to affect in UC, adults or children?
Children = 60%
Adults = 20%
What is the diagnosis of IBD?
Definitive investigations
Radiology (especially Crohn’s disease)
- MRI - recquires drinking a lot of water, so you can’t put them under GA. Asking a child to sit still for so long is really difficult to this is probably reserved for older children
- Barium meal and follow-through (younger kids)
Endoscopy
- Ileocolonoscopy
- Upper GI endoscopy
- Mucosal biopsy
- Capsule endoscopy
- Enteroscopy
What are the aims of treatment for IBD?
Induce and maintain remission
Correct nutritional deficiencies
Maintain normal growth and development
Methods of treatment of treatment for IBD
Medical
Anti-inflammatory
Immuno-suppressive
Biologicals ( Infliximab)
Nutritional
Immune modulation
Nutritional supplementation
Surgical
Lecture notes:
Crohn’s in childhood is managed by nutrition– child is given milkshakes.
UC – 5 aminosalycilate, distal can give rectal preparations, usually need course of oral corticosteroids. SE = greasy hair, weight gain and spots.
Azathioprine
Crohn’s – chance of disease coming back is really high 5ASA’s don’t work. Put them on azathioprine from the start.
Bottom-up treatment for Crohn’s disease =
Polymeric diet or oral prednisolone
Steroid sparing agents azathioprine/6MP or methotrexate
Biologicals (infliximab/adalibumab)
Surgery
How can you modify body language when talking to a baby/child?
Be friendy and smile
acknowledge child early on
Get down to their level
Utilise play
Ask age appropriate questions
Positioning of baby can be on parents lap
When do you start measuring height as opposed to length?
2 years of age
Why would yo umeasure sitting height?
If there is body disproportion
What bone age indicates that you have stopped growing?
14 years in girls
16 years in boys
What are assessment tools for child growth?
Height, lenght, weight
Growth charts and plotting
MPH and target centiles
Growth velocity Bone age
Pubertal assessment
What are common causes of short stature?
Familial
Constitutional
SGA/IUGR
What are pathological causes of short stature?
Undernutrition
Chronic ilness (JCA, IBD, Coeliac)
Iatrogenic (steoids)
Psychological and social
Hormonal (GHD, hypothyroidism)
Syndromes (Turner, P-W)
(turner is a spectrum of dysmorphia - you need to perform a karyotype)
What are hormone test for short stature?
IGF-1
GH stimulation test (given arginine or insulin growth factor?)
Why might MRI be useful in finding out the cause of short stature?
Look for abnormalities of the pituitary
What are the stages of puberty (tanner staging)?
- B (breast - for girls) 1-5
• G (genital development) 1-5
• PH (pubic hair) 1 to 5
• AH (axilary hair) 1 to 3
• T (2ml to 20ml)
• SO eg statement as B3 PH3 or G2 PH2 6/6
What are the cut offs for early and delayed puberty?
Boys
– early < 9 years (rare)
– delayed >14 (common, especially CDGP)
• Girl
– early <8 years
– delayed >13 (rare)
CDGP = constitutional delay in growth and puberty
What are causes of delayed puberty?
Gonadal dysgenesis (Turner 45X, Klinefelter 47XXY)
- Chronic disease (Crohn’s, asthma)
- Impaired HPG axis (septo-optic dysplasia, craniopharyngioma, Kallman’s syndrome)
- Peripheral (cryptorchidism, testicular irradiation)
What are the features of central precocious puberty?
Pubertal development
– Breast development in girls
– Testicular enlargement in boys
- Growth spurt
- Advanced bone age
What is the mainstage of management for central precocious puberty?
• Need to exclude pituitary lesion—- MRI
What are the featuers of precocious pseudopuberty?
Abnormal sex steroid hormone secretion
- Gonadotrophin independent (low/prepubertal levels of LH and FSH)
- Clinical picture: secondary sexual characteristics
What is the mainstay in investigation for precocious pseudopuberty / ambiguous genitalia
Need to exclude congenital adrenal hyperplasia
What is the management for ambiguous genitalia?
Do not guess the sex of the baby!
Multidisciplinary approach (paed endo, surg,
neonatologist, geneticist, psychologist)
Exam: gonads?/ internal organs
Karyotype
Exclude Congenital Adrenal Hyperplasia!- risk of adrenal crisis is first 2 weeks of life
What is the start of puberty in Tanner stages?
– Breast budding (Tanner Stage B 2) in a girl
– Testicular enlargement (Tanner Stage G2 -T 3- 4 ml) in boy
What are causes of congenital hypothyroidism?
Athyreosis / hypoplastic / ectopic
Dyshormonogenic
What is the most common cause of acquired hypothyroidism?
Hasimotos thyroiditis
What are child issues of acquired hypothyroidism?
Lack of eight gain
Pubertal delay (or precocity)
Poor school performance
What are the comlications of obesity in children?
Main ones:
- Gallstones
- PCOS
- Obstructuve sleep apnoea
- Atherosclerotic cardiocvascular disease
- non-alcoholic steatohepatitis
- SCFE
Metabolic syndrome
Fatty liver disease (nonalcoholic steatohepatitis)
Gallstones
Reproductive dysfunction (eg, PCOS)
Nutritional deficiencies
Thromboembolic disease
Pancreatitis
Central hypoventilation
Obstructive sleep apnea
Gastroesophageal reflux disease
Orthopaedic problems (slipped capital femoral epiphysis, tibia vara)
Stress incontinence
Injuries
Psychological
Left ventricular hypertrophy
Atherosclerotic cardiovascular disease
Right-sided heart failure
What are causes of obesity in children?
SIMPLE OBESITY
• Drugs
• Syndromes (would also have learning difficulties)
• Endocrine disorders (woul dhave growth failure)
• Hypothalamic damage (loss of appetite control)
What are the symptoms of diabetic ketoacidosis?
Nausea and vomitting
Abdominal pain
Sweet smelling breath
Drowsiness
Rapid deep signing respiration
Coma
What is the first thing you do when you suspect DKA?
Immediately test finger prick blood capillary glucose
Result >11mmol/l - Diabetes
Result <11mmol/l - Other cause
What should the weight be of a child in kilograms?
Wt (kg ) = 2 x (Age +4)
How do you calculate the blood volume of a child?
Blood Volume (mls) = 80mls/kg
What is urine output for a child?
0.5 -1 ml/kg/hour
How do you calculate insensible fluid loss in children?
20ml/kg/day
What shold systolic blood pressure be for a child?
80+ (2 x age)
Vital Signs
There was a large slide which made a point that children need analgesia at the earliest opportunity because it will make no difference in the diagnosis, makes them easier to examine and it also makes them more comfortable.
WHO pain management ladder
1 in 5 people don’t have the enzyme to metabolise codein
1 in 10-15000 have hella enzymes which makes the peak dose massive - can cause respiratory depression and even death.
Codein is a prodrug so we might as well give morphine
What is fluid managment for resuscitation?
20ml/kg bolus 0.9% NaCl
What is the fluid managemnt for maintenance fluid?
0.9% NaCl / 5% Dextrose +/- 0.15% KCl
4ml/kg 1st 10kg
2ml/kg 2nd 10 kg
1ml/kg every kg thereafter
10 yrs = 2 x (10+4) = 28kg = 40+20+8 = 68mls/hr
What are general red flags in a baby? (‘sentinel signs’)
Feed refusal
Bile vomits
Colour (sick babies tend to look grey - poorly perfused skin)
Tone (baby is normally quite active, floppy is a bad sign)
Temperature (Low temperature is more worrying than high temperature, high temperature is often jsut normal response to virus)
(green bile vomit is a bowel obstruction until proven otherwise - has to be green)
What is murphys triad for classical appendicitis?
pain
vomiting
fever
Classical appendicitis features tenderness over mcBurney’s point.
Where is McBurney’s point?
McBurney’s point is the name given to the point over the right side of the abdomen that is one-third of the distance from the anterior superior iliac spine to the umbilicus (navel). This point roughly corresponds to the most common location of the base of the appendix where it is attached to the cecum.
What are complications of appendicitis?
Abscess
Mass
Peritonitis
What are features of the pain in appendicitis?
Pain migrates from the centre to the right iliac fossa
Pain is worse on coughing or when going over speed bumps. Children can’t typically hop on their right leg due to the pain
What grade is the fever in appendicitis?
mild pyrexia is common - temperature is usually 37.5-38oC. Higher temperatures are more typical of conditions like mesenteric adenitis
What is the appetite like of someone with appendicitis?
anorexia is very common. It is very unusual for patients with appendicitis to be hungry
How is the diagnosis made of appendicitis?
Raised inflammatory markers with a compatiable history
To exclude pregnancy, renal colic and UTI a urine sample may also be taken, it might show mild leucocytosis but there shouldn’t be any nitrites
USS might be useful to exclude pelvic organ pathology, although the appendix can’t always be seen.
What is the management of appendicitis?
Laparoscopic surgery is the treatment of choice. Open surgery is an alternative
Pre-operative abx to reduce rates of wound infection
Perforated appendicitis requires abdominal lavage
Appendix mass is given broad spectrum abx and consideration is given to performaing an interval appendicectomy.
What are the features of non-specfic abdominal pain?
features:
short duration
central
constant
not made worse by movement
no GIT disturbance
no temperature
site & severity of tenderness vary
What are causes of abdominal pain in children?
Appendicitis
Mesenteric adenits (follows from a symtoms of a cold, high temperature)
Pneumonia (commonly in the right lower lobe - will have a soft abdomen, also has a high respiratory rate and a high CRP)
When does pyloric stenosis present?
In the first 4-16 weeks of life
Usually males (5:1 ratio)
FH is common
What are the features of pyloric stenosis?
Non-bilous vomiting - ‘projectile’
Weight loss
Cap gas (alkalosis, hypochloraemia, hypokalaemia)
What is the management of pyloric stenosis?
Test feed
IV fluid
(0. 45 N Saline/ 5% Dextrose + KCl
0. 9% Saline for NG loss)
US
Periumbilical pyloromyotomy
What is the diagnosis of a baby who presents with bile vomiting (MUST BE GREEN COLOUR)
Malrotation and volvulus
What is the investigation for malrotation?
Upper GI contrast study ASAP
What is management of malrotation volvulus?
Laparotomy ASAP
What is the diagnosis of a baby that is 6-12 months old
- 3 day history of viral ilness then intermittent colic and dying spells
- Bilious vomiting
4 seconds capillary refill
Bloody mucous PR (redcurrant jelly stool)
Dying spells are when the baby goes white and floppy
Intussusception
What is the investigtaion for intussesception?
USS abdomen
looking for a target sign - This is usually when the terminal ileum goes through the ileocecal valve. Bits of odematous bowel inside each other.
What is the management of intussusception?
pneumostatic reduction (air enema)
laparotomy
What increases the risk of umbilical hernia?
LBW
Trisomy 21
Hypothyroidism
Mucopolysaccharidosis
What is the management of umbilical hernia?
Normally self-resolves by the age of 4
Repair if there are compications
Peristance over 4 years, large defect, aesthetic
What is gastroschisis?
When all of the abdomen is born outside the body - abdominal wall defect. Gut is eviscerated and exposed
What is the condition called when there is a large abdominal defect, organs born outside the body but they are covered by viscera?
Exomphalos
What are the associated anomalies of exomphalos?
associated anomalies
25% cardiac
25% chromosomal - Trisomy 13, 18, 21
15% renal, neurological
Beckwith-Weideman syndrome
What is the management of exomphalos?
Primary/delayed closure
Who is most likely to get groin hernias?
Boys (2% of boys get them)
Boys are 9 times more likely to get a hernia than a girl
What type of hernia is most common?
Indirect
What increase the risk of hernias?
Prematurity
What is the main risk attached to hernias?
Incarceration - risk is especially high in children less than 1 year of age
What is the management of hernias?
management
< 1 year
URGENT referral
repair - no place for observation
> 1 year
elective referral and repair
incarcerated
reduce and repair on same admission
What is often contained in a female inguinal hernia?
Ovary
What are the features of hydrocele?
Scrotal swelling
Very common in newborns
Painless
Increase with crying, straining, evening
Bluish colour
Chinese lantern effect
What is the definition of cryptochidism?
testis that cannot be manipulates into the bottom half of the scrotum
What are the subclassifications of cryptorchidism?
true cryptorchidism
retractile
ectopic
(ascending testis)
Retractile = you can pull it down but it can also jump back up inside.
Ectopic – can be somewhere in the canal (superficial femoral pouch or somewhere on the other side)
Ascending – as they grow the cord doesn’t increase at the same rate – usualy normal but then 5 years later they are ascended.
What are the indications for orchidopexy?
fertility
1% loss germs cells / month undescent……
malignancy
- RR 3 x (probably intra-abdominal only)
- lifetime risk - <1%
trauma (increased likelihood of rupture of they are not within the scrotum)
torsion
cosmetic
What are the absolute and relative indications for circumcision?
Absolute: Balanitis Xerotica Obliterans
Relative:
- Balanitis prosthitis
- Religious
- UTI
(circumcision for UTI prevention is only really effective if there is an abnormal urinary tract that is predisposing the person to recurrent urinary tract infections
What are complications of circumcision?
Painful
Bleding
Meatal stenosis
Fistula
Cosmetic (looks different)
What is the differential doagnosis for acute scrotum?
Torsion of the testis (you have 6-8 hours to recover the testis from the onset of symptoms- if in doubt explore)
Torsion appendix testis
Epididymitits
Why is it important to investigate UTI?
Prevent renal scarring
Reflux nephropathy and chronic renal failure, prevent hypertension
Who gets investigated for UTI?
xall <6/12, atypical, recurrent
What is the definition of UTI?
pure growth bacteria > 105
pyuria
systemic upset
fever, vomiting
What are the possible assessments for UTI?
US (looking at the size, position, shape and for hydronephrosis)
Renography:
- MAG3 - drainage, function, reflux
- DMSA - function, scarring
Micturating cystourethrogram (MCUG) (this is good for showing reflux but it is a really uncomfortable test for a child
What is the management of vesicoureteric reflux?
conservative
- voiding advice, constipation (you want to avoid constiaption), fluids
antibiotic prophylaxis
- ? until age 4
- Trimethoprim (2mg/kg nocte)
STING (submucosal teflon injection)
- mild/moderate with symptoms
ureteric reimplantation
Where is the most likely place for hypospadias?
What are the assocaited anomalies with hypospadias?
Upper tract
Intersex
What is the management of hypospadias?
Do not circumsize
One stage or 2 stage procedure
What is the name of the bend of the penis assocaited with hypospadias?
Chordee
What are the functional aspects of a childs development?
Motor
Language
Cognitive
Social
Emotional
Significant delay of skills is when they are 2SD from population
What is global developmental delay?
when 2 or more domains are affected
What is learning disability?
A learning disability is a significant impairment in intellectual functioning and affects the person’s ability to learn and problem-solve in their daily life.It has nearly always been present since childhood.
What are primary care assessment tools for developmental delay/learning dofficulties?
ASQ (ages and stages questionnaire)
PEDS (Parents evaluation of developmental status)
M-CHAT (Checklist for autism in toddlers)
SOGS-2 (Schedule of Growing Skills)
Quantification of developmental abnormalities?
All areas of development are age appropriate
Delay: Global or isolated
Disorder: Abnormal progression and presentation eg Autism
Regression: loss of milestones
What are the facial features of williams?
Broad forehead
Medial eyebrow flare
Strabismus
Flat nasal bridge
Malar flattening
Short nose, long philtrum
Full lips
Wide mouth
What are red flag signs for learning difficulties?
Learning Guide developmental red flags:
- Social smile by two months
- Sitting unsupported at 9 months
- Standing unsupported at 18 months
- No words by 2 years
Positive:
Loss of developmental skills
Concerns re vision
Concerns re hearing
Floppiness
No speech by 18-24 months
Asymmetry of movement
Persistent toe walking
Head circumference >99.6th C or < 0.4th C
Negative:
Sit unsupported by 12 months
Walk by 18months (boys) or 2 years (girls): Check creatinine kinase
Walk other than on tiptoes
Run by 2.5 years
Hold objects in hand by 5 months
Reach for objects by 6 months
Points to objects to share interest by 2 years
What are investigations for learning difficulties?
Based on clinical abnormalities
Diagnostic yield of specific tests
Timing
Genetic testing: chromosomal analysis, Fragile X, FISH, array CGH
Creatine kinase
Thyroid screening
Metabolic testing: amino and organic acids,NH4,Lactate.
Ophthalmological examination
Audiology assessment
Consider congenital infection
Neuroimaging
What are common motor probems in children?
Delayed maturation
Cerebral palsy
Developmental coordination disorder
What are the possible manifestations of cerebral palsy?
abnormal tone early infancy
delayed motor milestones
abnormal gait
feeding difficulties
What are common sensory problems?
deafness
visual impairment
Multisensory impairment
What are the language and cognitive problems?
Specific Language Impairment
Learning Disability
What are common problems of social / communication
Autism
Asperger syndrome
Elective mutism
What is the purpose of investigating developmental problems?
The family gains understanding of the condition, including prognostic information
Lessens parental blame
Ameliorates or prevents co-morbidity by identifying factors likely to cause secondary disability that are potentially preventable
Appropriate genetic counselling
Accessing more support
Address concerns about possible causes e.g. events during pregnancy or delivery
Potential treatment for a few conditions
What are the multidisciplinary teams for developmental issues?
Developmental paediatrician
Speech and Language therapist
OT/ PT: functional impairments and strengths
Psychologist
Social worker
Geneticist
What are additional support needs?
A child or young person is said to have ‘additional support needs’ if they need additional support with their education.
Additional support can mean any kind of educational provision that is more than, or very different from, the education that is normally provided in mainstream schools
What are local services for developmental problems?
Community paediatrics clinics
Child development teams
Multidisciplinary assessment
Therapy services
Why might a child need additional support?
Difficulties with mainstream approaches to learning
Disability or health needs, such as motor or sensory impairment, learning difficulties or autistic spectrum disorder.
Family circumstances e.g. young people who are carers or parents.
What is personal learning planning?
Personal learning planning (PLP) is a way of thinking about, talking about and planning what and how a child learns. It’s also a way of assessing their progress and acting on the results of that assessment.
So this means deciding how a child learns and evaluating on the go.
What is individualised educational plane?
lIEP is a detailed plan for a child’s learning. It contains some specific, short-term learning targets for the child and will set out how those targets will be reached. Targets are:
l Specific ● Measurable ● Achievable ● Relevant
● Timed.
In some areas these plans are called additional support plans or individual support plans.
Not legal documents.
This is essentially just SMART goals
What is the legal document that outlines a childs supprt plan?
CSP - coordinated support plan.
A CSP is a detailed plan of how child’s support will be provided. It is a legal document and aims to ensure all the professionals who are helping the child, work together. It also helps ensure that everyone, including parents and the child, is fully involved in that support.
For children in local authority school education and needing significant additional support.
Complex or multiple needs
Needs likely to continue > 1 year
Support required by > 1 agency.
The parents’ guide to additional support for learning, Enquire (2016)
Why might a child need a childs plan?
If they need extra support
Access to mental health services
Access to respite care
This is part of the children and young people act
Part of the GIFREC approach (getting it right for every child)
What is contained in the childs plan?
Why they need support
What type of support they need
How long they need support for
Who should provide the support
May include IEP or a CSP
Why do children get more easily cold, dehydrated and hypoglycaemic?
Increase area : volume ration
Deceased water content
Decrease metabolic reserves
What is the most common form of hypoglycaemia in a child between 18 months -5 years of age?
Ketotic hypoglycaemia
What is the pulse rates, rr and bp in a child?
BP increase
RR increase
Lower BP
Why is the MMR and the pheumococcal vaccine only given at 12 months
Baby immune system is not fully developed
From 4 months to 5 years - lots of recurrent infections (before 4 months you are leaching off the immunoglobulins from the mother
Why is chicken pox a good example of intact immune function?
Requires both humeral and cellular immunity
What conditions occur in children but not in adults?
- Abdominal migraine
- Bronchiolitis
- Bronchopulmonary dysplasia
- Croup
- Enuresis
- Febrile convulsion
- Glue ear
- Intraventricular haemorrhage
- Necrotising enterocolitis
- Non accidental injury
- Sudden unexplained death of infants
- Toddler’s diarrhoea
- Vesico-ureteric reflux
- Viral induced wheeze
Chronic conditions with childhood onset
- Asthma (COPD)
- Autism
- Cerebral palsy
- Cystic fibrosis
- Gastroschisis
- Hirschsprungs disease
- Spina bifida
What is the main differential for febrile convulsions?
Meningitis
Neorological examination in childhood
- Opportunistic approach and observation skills
- Appearance
- Gait
- Head size
- Skin findings
- Real world examination (depends on age)
- Synthesis of history and clinical findings into a differential diagnosis and investigation plan
Observation is really important before you even do any ‘examination’
Which of these headaches are more likely to have a cause
Isolated acute
Recurrent acute
Chronic progressive
Chronic non-progressive
Isolated acture
Chronic progressive
Chronic non-progressive is likely to be tension type
What are the parts of headache examination?
- Growth parameters, OFC, BP (Craniopharyngioma may affect growth)
- Sinuses, teeth, visual acuity
- Fundoscopy (papilloedema)
- Visual fields (craniopharyngioma)
- Cranial bruit
- Focal neurological signs
- Cognitive and emotional status
- The diagnosis of headache etiology is clinical
What are pointers to childhood migraine?
- Associated abdominal pain, nausea, vomiting
- Focal symptoms/ signs before, during, after attack: Visual disturbance, paresthesia, weakness
- ‘Pallor’
- Aggravated by bright light/ noise
- Relation to fatigue/ stress
- Helped by sleep/ rest/ dark, quiet room
- Family history often positive
Migraine vs Tension headache
- Hemicranial pain
- Throbbing/ pulsatile
- Abdo pain, nausea, vomiting
- Relieved by rest
- Photophobia/ phonophobia
- Visual, sensory, motor aura
- Positive family history
Tension:
- Diffuse, symmetrical
- Band-like distribution
- Present most of the time (but there may be symptom free periods)
- “Constant ache”
What are the red flags for raised intracranial pressure?
- Aggravated by activities that raise ICP eg. Coughing, straining at stool, bending
- Woken from sleep with headache
What are the features of analgesic overuse headache?
- Headache is back before allowed to use another dose
- Paracetamol/ NSAIDs
- Particular problem with compound analgesics eg. Cocodamol
What are indications for neuroimaging?
- Features of cerebellar dysfunction
- Features of raised intracranial pressure
- New focal neurological deficit eg. new squint
- Seizures, esp focal
- Personality change
- Unexplained deterioration of school work
What is managment of migraine?
- Acute attack: effective pian relief, triptans
- Preventative (at least 1/week): Pizotifen, Propranolol, Amitryptyline, Topiramate, Valproate
What is the managment of tension type headaches
- Aim at reassurance: no sinister cause
- Multidisciplinary management
- Attention to underlying chronic physical, psychological or emotional problems
- Acute attacks: simple analgesia
- Prevention: Amitryptiline
- Discourage analgesics in chronic TTH
What causes seizures?
•An abnormal excessive hyper synchronous discharge from a group of (cortical) neurons
Signs of general NM disorders
What are the differences between neuropathy and myopathy?
Developing prefrontal cortex
Potential cancer symptoms in children
Normal Child Values
What makes breast milk good?
Nutritionally best for full term babies
Well tolerated
Less allergenic
Low renal solute load
Ca:PO4, LCP FAs
Improves cognitive development
Reduces infection
Macrophages and lymphocytes
Interferon, lactoferrin, lysozyme
Bifidus factor
Summary of G/O reflux investigations
Differences between osmotic and secretory diarrhoea
Croup vs Epiglottitis
oxygenation, hydration are rubbish in epiglottitis because they are usually septic
What is the mechanism of bacterial bronchitis?
•Disturbed mucociliary clearance
–Minor airway malacia
–RSV/adenovirus
- Lack of social inhibition!
- Bacterial overgrowth is secondary
What is the presentation of bronchiolitis?
- Nasal stuffiness, tachypnoea, poor feeding
- Crackles +/- wheeze
Asthma treatment ladder
What is the purpose of the ductus arteriosus?
Protects lungs against circulatory overload
Allows the right ventricle to strengthen
Carries low oxygen saturated blood
Blood pressure in newborn
Breathing rate of newborn
Heart rate of newborn
Normal values
What are possible pathogens for paediatric sepsis?
What are the organisms for paediatric meningitis?
What various systems does strep pneumoniae affect?
Comparison with candida vs Aspergillus
Maybe just remember that candida has positive blood cultures whereas aspergillus doesn’t
Aso candida assocaited with birth canal
Aspergillus is everywhere
Summary of droooogs
What are side effects of glucocorticoids
spectrum of nephrotic syndrome
Nephroticc vs nephritic syndrome
Comparison between IgA and post - strep GN
Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis
post-streptococcal glomerulonephritis is associated with low complement levels
main symptom in post-streptococcal glomerulonephritis is proteinuria (although haematuria can occur)
there is typically an interval between URTI and the onset of renal problems in post-streptococcal glomerulonephritis
Summary
What are the stages of CKI?
What is the common presentation of UTI in a child?
Good to know that JFN is normotensive whereas the polystic disorders are hypertensive
PKD 1 is more aggressive than PKD 2
STORK MARK
This is a very common flat pink lesion, present at
birth. It is usually located on the forehead, eyelids,
occiput, neck or midline of the back. It may
be V-shaped on the forehead/occiput. Facial lesions
fade, occipital tend not to. The lesions are not pathological
so there is no active management needed.
Here is how heat is lost
