Paeds Flashcards
Discuss the phases of growth in children
Foetal phase: 30% of eventual height
Infantile phase: up to 18mnths, requires good health and thyroid function
Childhood phase: slow and steady prolonged period of growth. Based on genes, good health and thyroid hormones
Pubertal phase: driven by sex hormones. If puberty is early (not uncommon in girls) overall growth will be lower due to earlier fusion of the epiphyseal growth plates
Discuss the pubertal changes seen in females and males
Females:
- Breast development (12.5years)
- Pubic hair growth and rapid height spurt
- Menarche 2.5 yrs after initial breast development
Males:
- Testicular enlargement
- Pubic hair growth
- Height spurt
Both sexes
- Development of acne
- Axillary hair
- Body odour
- Mood changes
Discuss the causes of short stature
Familial: both parents are short Intrauterine growth restriction/prematurity Constitutional delay of puberty Endocrine: Hypothyroidism, GH deficiency Nutritional deficiency Psychosocial deprivation Chromosomal disorders
Discuss the investigations for short stature
Plotting previous and current height and weights X-ray of wrist and hands FBC U&E's Karotype IgA antibodies CPR/ESR MRI
Discuss the causes of tall stature
Familial
Obesity
Secondary : Hyperthyroidism, increase sex steroids, excessive adrenal androgens)
Syndromes: Marfans, Klinefleters, maternal DM
Causes of abnormal head growth
A. Microcephaly
- Familial
- Autosomnal recessive
- Congenital infection
- Acquired insult
B.Macrocephaly
- > 98th centile
- Rapid increase = ICP
- Hydrocephalus
- Tumour
- Neurofibromas
- CNS storgage disorders
C. Craniostanosis
- Premature fusions of sutures (distortion of the head shape)
Define premature sexual development
8 years = female
9 years = males
Growth spurt + pubic hair and breast development
Classify precocious puberty
True PP: premature activation of the hypothalamic-pituitary-gondal axis
Pseudo PP: excess sex steroids
Discuss the causes of precocious puberty
Gonadotrophin-dependent Idiopathic/Familial CNS lesions (postradiation, tumours)
Gonadotrophin-indepedent
McCune-Albright
Tumours of adrenals or gonads
Define congenital adrenal hyperplasia (CAH)
Caused by a defect in pathway that synthesises cortisol to cholesterol
Deficiency in 21-hydroxylase or 11-hydroxylase
Autosomal recessive
Chromosome 6
Clinical features of CAH
Female virilization Salt wasting adrenal crisis (mineralcorticoid deficiency) Cortisol deficiency (hypoglycaemia, hypotension, shock)
Diagnosis and management of CAH
Elevated levels of 17alpha-hydroxylprogesterone
Hyponatraemia
Hypochloridaemia
Management: Females (corrective surgery) Lifelong glucocorticoids Mineralcorticoids Carry a lifelong steroid replacement card
List the four fields of development
Gross motor
Vision + fine motor
Hearing and speech language
Social, emotional and behaviour
List the primitive reflexes
Moro: extension of the head, extension of the arms (drop the baby)
Grasp: flexion of fingers when object placed in hand
Rooting: head turns to stimulus near the mouth
Stepping: Feet step when touching the floor
Discuss the physiology of the change in foetal Hb
Foetus Hb contains 4 alpha chains, higher affinity for oxygen.
HbF is gradually replaced with HbA
Foetus is born with a good store of iron, folic acid and vitb12
Define anaemia
Hb level below the normal limits
neonante < 14g/dL
1-12 months < 10g/dL
1-12years < 11g/dL
Causes of anaemia
Impaired red cell production
Increased red blood cell production
Iron deficiency anaemia
Impaired red cell production Fatigue Poor feeding Pallor Pice
Microcytic, hypochromic anaemia ( decreased MCV, decreased MCH)
Oral intake Iron supplement (sodium iron date)
Red cell aplasia
Impaired red cell production
- Congenital
- Erythoblastema of the new born
- Parovirus B19 infection
Low reticulocyte Low Hb Normal bilirubin Absent RBC precursors on bone marrow -ve antiglobin test
Oral steroids
Blood transfusions
Discuss the pathophysiology of increased red blood cell destruction
Intravascular ( circulation)
Extravascular (liver/spleen)
Red cell membrane disorders
Red cell enzyme disorders
Haemoglobinopathies
Glucose-6-phophate dehydrogenase deficiency
G6PD: rate limiting enzyme pathway (stop oxidative damage)
Neonatal jaundice
Acute haemolysis
Measure G6PD
Avoid triggers ( blood fine outside episodes)
Sickle cell disease
Haemoglobinopathies
Autosomal recessive HbsHbs
HbsC = carrier of the disease
Anaemia Infection Painful crisis Acute anaemia Splenomegaly
Hydroxycarbinamide
Opiates + hydration
B-thalasaemia
Haemoglobinopathies
Decrease production of beta global chain
Two types major and minor
Anaemia
Growth failure
Haemoposis
Blood transfusions
Bone marrow transplant
Immune thrombocytopenia
Most common thrombocytopenia in childhood
Destruction of circulating antibodies by anti platelet IgG autoantibodies
Petechiae
Purpura
Superficial brusing
Epitaxis
Will resolve spontaneously
Severe: oral prednisolone
Causes of anaemia of the newborn
Decrease RBS production
- Red cell aplasia
Bleeding
- Umbilical cord
- Internal haemorrhage
Haemolytic anaemia
- Ab destroying the RBC
- Immune (haemolytic disease of the newborn)
- Red membrane disorders
- Red enzyme disorders
- Abnormal haemoglobin disorders
Blood loss
- Feto-maternal haemorrhage
- Twin to twin transfusions
- Blood loss at delivery
Anaemia of prematurity
- Decreased EPO production
- Decrease RBC lifespan
- Iron and folate acid deficiency
Discuss the traffic light system for identifying a sick child
- Colour
- Activity
- Respiratory
- Circulation/Hydration
Discuss the pathophysiology of septicaemia
Focal infection/proliferation of blood stream
Release of cytokines and endothelial cells
Cause = meninoccal infection ( kids)
Grp B strep ( neonates)
Clinical features of septicaemia
Fever Poor feeding Miserable/ irritable Increase HR/RR Decrease Bp Shock
Management of septicaemia
Antibiotics ( infection specific)
Fluids ( correct hypovolaemia )
Catheter ( regular U/O)
DIC ( FFP/platelet transfusions)
Discuss the pathophysiology of meningitis
Inflammation of the menages covering the brain
Inflammatory cells present in the CSF
Bacterial/ viral
List the microorganisms that cause bacterial meningitis
Neonates - 3 months: Grp B strep, E.coli, Listeria
1 month- 6 years: Nessieria meningitides, strep pneumonia
> 6 years: Nessieria meningitides, strep pneumonia
Clinical features of meningitis
Headache
Photophobia
Neck stiffness
\+ rash vomiting irritable seizures poor feeding shock
Compare the CSF changes in bacterial vs viral meningitis
Bacterial
- increase WCC
- increased protein
- decreased glucose
- polymorphic cells
Viral
- increase in WCC
- normal protein
- normal glucose
- lymphocytes
Treatment of bacterial menigitis
3rd generation cephalosporin ( cefotaxime/ ceftrixone)
Bactericidal
Works on the beta-lactam
Disrupt the synthesis of the peptidoglycan layer forming the bacterial cell wall
Prevents cross linking of the peptidoglycan
Rifampacin to all household contacts
Discuss the causes and the management of viral meningitis
Enterovirus EPV Adenovirus Mumps Herpes zooster virus
Rx: Acyclovir
Meningococcal infection
Septicaemia + purpuric rash
Rash: non blanching, regular size, neurotic centre
Impetigo
Highly contagious strep or staph infection
Erythematous macules = vascular pustular or bulbous
- rupture of the vesicles = honey crusted lesions
Rx: Mild ( topical antiB’s: muciporin)
Narrow ( flucloaxicllin)
May require board spec ( co-amiclav)
Tuberculosis
Caused by mycobacterium tuberculosis
A. Unsymptomatic
- Local inflammation
- Latent disease
- Mantoux test +ve
- Hilar lymphadenopathy on CXR
B. Symptomatic
- Spread to the lymph system
- Lung lesion + infected lymph node = Ghon’s complex
- Fever, Anorexia, Cough, CXR changes
Dx of TB
Acid fast bacili and zieh neslon’s stain +ve
Mantoux test +ve
Rx of Tb
8/52: Rifampain, Isonazid, Pyrazinamide and Ethabutamol
Further 8/52: Rifampicin, Isoniazid
Kawasaki’s disease
Systemic vasculitis
4-6 years old
Asian (Japanese)
Cx: Likely to be immune hyperactivity. Associated with ITPKC gene ( decrease T cells)
Clinical features of Kawasaki’s disease
\+ 5 day fever Bilateral non purulent conjunctivitis Oral mucositis Cervical lymphadenopathy Polymorphic rash Extremity change ( erythema dactlylisis) Coronary artery aneurysms
Rx of Kawasaki’s disease
IV-IgG immunogloblins
High dose aspirin
Must do echo and cardio F/up
Discuss the transmission of HIV
Mother to child ( in vitro)
@ delivery (intrapartum)
Breast feeding (post partum)
Vertical transmission
Dx of HIV in kids
> 18 months: antibodies
<18 months: +ve will only confirm exposure not infection due to transplacental maternal abs
Clinical features of HIV
Persistent lymphadenopathy Hepatosplenomegaly Recurrent fever Parotid swelling Thrombocytopenia
Rx of HIV
Antiviral treatment
- Clinical load
- HIV viral load
- CD4 count
Discuss the ways to reduce vertical transmission
Reduce the viral load of the mother
Avoidance of breast feeding- reduce transmission
Active management of labour and delivery
Causes of prolonged fever
Infective
- Localized infection
- Bacterial infections
- Deep abscess
- Infective endocarditis
- TB
- Viral infections
Non-Infective
- Systemic juvenille arthritis
- SLE
- Vasculitis
- Inflammatory bowel disease
- Sacrodoisis
- Malignancy ( leukamia, lymphoma)
- Drug fever
Discuss the mechanism of action of vaccines
Induce immunity via T-cellss
Induce immunological memory
Herd immunity
Active: Live attenuated (MMR,BCG,Rotavirus)
Passive: Inactivated ( whopping cough, tetanus)
Conjugate virus: Polysacchride coat of bacteria ( pneuma, Hib, MenC)
Improvement of the protein carrier
Generates immunological memory
List the types of immunological memory
- Primary: Intrinsic defect in the immune system
2. Secondary: Caused by a disease or a treatment
List the types of primary immune deficiency
T-cell defects
- Failure to thrive
- Oral thrush
- PCP
Examples:
SCID
HIV infection
B-cell defects
- Bacterial infections
- Recurrent diahorrae
- Failure to thrive
Define wheeze and list the different types
Whistling sounds, breathlessness or persistent troublesome cough severely affecting the wellbeing of the infant
- Transient early wheeze
- Persistent and recurrent wheeze
Causes of a wheeze
Transient early wheeze Atopic asthma (IgE mediated) Non atopic asthma Recurrent aspiration of feeds Inhaled foreign body Cystic fibrosis Recurrent anaphylaxis Congenital abnormality
Discuss the prevalence of wheeze in childhood
Transient early wheeze (0-3yrs)
Viral episodic wheeze (3-5yrs)
IgG associated wheeze (5+)
Clinical features of viral episodic wheeze
No interval symptoms
No excess atopy
Improvement with age
No benefit from inhaled steroids
Clinical features of asthma
Wheeze (polymorphic) Symptoms worse at night or early morning Triggers Family hx to atopy \+ve response to asthma therapy
Investigations for asthma
Clinical dx
Record PEFR ( peak expiratory flow rate)
CXR will be normal ( avoid scanning kids)
Skin prick test for common allergies
Management of asthma
Stepwise approach
1. Inhaled SABA (Salbutamol)
2. Inhaled SABA + inhaled steroids
3. Inhaled LABA ( must be with a corticosteroid) Seretide
Consider adding in leukotriene receptor agents ( <5yrs) or oral theophylline (>5yrs)
4. Increase steroids to the max dose
5. Oral steroids (prednisolone)
Reason for failure to respond to treatment
Adherence
Bad disease pathology
Choice of drugs/devices
Environment (smoke/pets)
Long-term side effects of steroids
Adrenal suppression
Growth suppression
Osteoporosis
Clinical features of a child with chronic asthma
Growth and nutrition may be below normal
Chest: Hyperinflation, harrisons sulci, wheeze
Atopic Hx: Allergic rhinitis, Eczema
Time off school
Presentation of acute asthma attack
Wheeze + tachypnoea Tachycardia Use of accessory muscles and recession \+ve pulse paradoxus Breathlessness prevents talking
Life threatening
- Cyanosis
- Fatigue
- Drowsiness
- Silent chest
- Decreased consciousness
Management of an acute asthma attack
Nebulised B2 agonist
Oral or IV steroids
Nebulised ipratropium
Oxygen
List the common pathogens that cause respiratory infection
VIRUSES
- RSV ( respiratory synctical virus)
- Rhinovirus
- Parainfluenza virus
- Adenovirus
BACTERIAL
- Strep pneumonia
- Haemophilus influenza
- Moxerella catarhalis
Pharyngitis
Pharynx and soft palate are inflamed
Local lymph nodes are enlarged and tender
Grp A Beta-haemolytic streptococus ( must do throat swab in case of further renal complications)
Tonsillitis
Intense inflammation of the tonsils
Caused by Grp A Beta-haemolytic streptococcus and EBV
Bacterial tonsillitis = pencillins
Avoid amoxicillin as will cause maculopapular rash
Acute otitis media
6mnths- 12mnths
Tympanic membrane will be bright and bulging ( loos of normal light reflection
Caused by RSV, Rhinovirus, H.Influenza, Moraxella
Analgesics
Give Abs if severe
Clinical features of laryngeal and tracheal infections
Stridor
Hoarseness due to inflammation
Barking cough
Degree of dyspnoea
Croup
Mucosal inflammation and increased secretions affecting the airway
Narrowing of the trachea
Clinical features of croup
Preceding factors
- Fever
- Coryza
- Chest recession @ activity
Hoarseness
Barking cough
Treatment of croup
Oral dexamethasone (0.15mg) Oral prednisalone (2mg)
Nebulised steroid (Budesomide) Reduce severity, duration and need for admission
Nebulised epinephrine (adrenaline) + O2 facemask (Beware of rebound affects)
Acute epiglottis
Life threatening emergency
Caused by H.Influenza type B
Intense swelling of the epiglottis and surrounding tissues
Clinical features of acute epiglottis
High grade fever
Painful throat
Soft inspiratory stridor
Increasing respiratory difficulty
Treatment of acute epiglottis
Managed in a resuscitation room Examination under anaesthetic Secure the airway Blood for culture IV abs = cefuoxime ( 3rd generation cephalosporin)
Whopping cough
Highly contagious respiratory infection
Caused by bordetella pertussi ( ID via PCR)
An effective vaccine does exist as part of diphtheria, tetanus and pertussis
Infective 7 days post exposure to 3 weeks after cough
Clinical features of whopping cough
Catarrhal phase: Coryzal
Paroxysmal phase: Cough ( inspiratory whoop) can last for 3-6 weeks
Treatment of whopping cough
Erythromycin given early disease reduces infectivity but does not shorten the course of the illness
Cause of bronchiolitis
RSV respiratory syncytial virus
Clinical features of bronchiolitis
Corysal symptoms
Dry cough
Increased work of breathing
Feeding difficulty ( increase dyspnoea)
O/E Increased RR Subcostal/Intercostal recession Hyperinflation of the chest Fine-end inspo crackles Increase HR Cyanosis/Pallor
Treatment of bronchiolitis
Supportive care
Humidified oxygen
Fluids if needed
Admit if
Resp distress
Chronic lung pathology
Feeding difficulties
Causes of pneumonia
Newborn: Grp B strep
Infants: RSV, strep pneumoniae, Bordetella pertussis, Chylamydia
Children: Mycoplasma pneumonia, strep pneumoniae, chlymadia pneuomia
Clinical features of pneumonia
Fever Breathing difficulties Cough Lethargy Poor feeding Unwell child
O/E Tachypnoea Nasal flaring Chest indrawing Increased respiratory rate Dullness to percuss Bronchial breathing
Management of pneumonia
ADMISSION Increase RR Increase WOB Grunting Decreased feeding
Broad spec abs ( amoxicillin)
Clinical features of UTI
Miserable Temperature Vomiting Abdo pain Fever Poor feeding
Cause of UTI
E.Coli or Kleibsiella
Treatment of UTI
Trimethoprim ( if well) IV cefuroxime ( if unwell)
Neonates will require an ultrasound of the kidneys to rule out malformation.
Beware of ESBL:
Extended spectrum beta-lactamase producers
Resistant to all penicillins and cephalosporins
Rx: Meropenem
Treatment for osteomyelitis
Commonly caused by staph aureus
Rx: IV cefuroxime
Differential Dx of MSK pain
- Life threatening pain
- Pain (-ve swelling)
- Pain (+ve swelling)
LIFE THREATENING
Malignancy (leukaemia, bone tumour, lymphoma)
Sepsis (septics arthritis, osteomyelitis)
Non-accidental injury
PAIN -VE SWELLING
Hypermobile joints
Metabolic disease (hypothyroidism)
Tumour (benign)
PAIN +VE SWELLING Trauma Infection JIA Arthritis SLE CF Sarcoidosis
List the types of JIA
- Oligoarthritis:
- 1-4 joints
- ANA+/ANA- - Polyarticular RF-Ve:
- Symmetrical
- Low grade fever
- Anterior uveitis - Polyarticular RF+Ve:
- Symetrical large and small joints
- Rheumatoid +ve
- Poor prognosis - Psoriatic arthritis
- Asymetrical arthritis
- Psoriasis
- Dactylitis
- Nail pitting - Enthesistis related arthritis
- Lower limb large joint arthritis
- Lumbar spine involvement
- Anterior uveitis
- Reiter syndrome
- HLA B27+ - Systemic JIA
- Arthritis ( + daily fever for >3 days)
- Evanscant rash (salmon pink)
- Lymphadenopathy
- Hepatomegaly +/- splenomegaly
- Serositis
- Link with MAS
What is Macrophage Activation Syndrome
Potentially fatal Dysregulation of T-lymphocytes, Natural killer cells activation Excessive cytokine production Abnormal proliferation of macrophages
Clinical features of MAS
Unrelenting fever HSM CNS dysfunction Purpuric rash Cytopenia Increase ferritin
Rx: Steroids, cyclosporin and supportive care
Treatment for JIA
NSAID’s
Steroids
DMARD’s (methotrexate)
Biologics (TNF-alpha- inhibitor)
Define osteoporosis
A disease characterised by low bone mass and micro architectural detonation of bone tissue, leading to enhanced fragility and an increase in fracture risk.
Causes of osteoporosis in children
INHERITED
- Osteogenesis imperfecta
- Inborn errors
- Idiopathic
ACQUIRED
- Drug induced
- Endocrinopathies
- Malabsorption
Aetiology of osteogenesis imperfecta
Autodominat condition which results in defects in the typeI collagen genes
Clinical features of osteogenesis imperfecta
Bone fragility Fractures Deformity Bone pain Impaired mobility Poor growth
Types of osteogenesis imperfecta
I: mild
II: lethal
III: progressively deforming
IV: moderate
Management of osteogenesis imperfecta
Bisphosphonates
Pain management
IV pamidronate
Define rickets
Failure of mineralisation of growing bone or osteoid tissue
Causes of rickets
Nutritional
- Dark skin
- Lack of maternal Vit D
- Diets low in calcium
- Strict vegan diet
Intestinal absorption
- Small bowel enteropathy ( coeliac disease)
- Pancreatic insufficiency
- Cholestatic liver disease
Defective production of 25(OH)D2
-Chronic liver disease
Target organ resistance to 1,25 (OH)D2
- Mutations in the D receptor gene
Clinical features of rickets
Misery Failure to thrive Frontal bossing of the skull Bowing of the weight bearing bones Seizures Hypotonia
Treatment of rickets
Balanced diet
Correction of the predisposing risk factors
Treatment of the underlying cause
Define nephrotic syndrome
Proteinuria
Decreased albumin
Oedema
Types of nephrotic syndrome
Congenital
Steroid sensitive
Steroid resistant
List the investigations of nephrotic syndrome
Urine protein FBC CRP/ESR Complement leves Antistreptolysin O and Anti-DNASE B Throat swab Hep B and Hep C
Steroid sensitive nephrotic syndrome
MACROSCOPIC HAEMATURIA
Rx: Oral corticosteroids (60g/m2) 4/52 Decrease to 40g/m2 Gradually decrease steroids Dipstick urine for 10 days to check decreasing protein levels
1/3 will resolve directly
1/3 frequent relapse
1/3 infrequent relapse
Steroid resistant nephrotic syndrome
Refer to nephrologist Rx: Diuretic Fluid management Salt restriction ACE inhibitors
Congenital nephrotic syndrome
Poor prognosis
High mortality
Causes of acute nephritis
Post infection
Vasculitis
IgA nephrology
Goodpastures (antiglomerular basement membrane)
Clinical features of acute nephritis
Decrease urine output HTN Oedema Proteinuria Haematuria
Treatment of post strep infection nephritis
Increased ASOT
Increased antiDNASE B
Reduced C3 and C4
Rx HTN
Dialysis
Penicillin
Why would a UTI require further investigations
If
- Male
- Recurrent
- Unusual organism grown
A. USS: size and drainage of the bladder and kidneys
B. Micturating cytourethrogram ( vesicoureteric reflux)
C. DMSA scan: radionucleotide imaging renal function