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4th Year Paeds > Essential Conditions (2) > Flashcards

Essential Conditions (2) Flashcards

1
Q

Causes of constipation?

A

Idiopathic - low fibre, lack of mobility and exercise, poor colonic motility

GI - Hirschsprung’s, anal disease, partial intestinal obstruction, food hypersensitivity, coeliac disease

Non-GI - hypothyroidism, hypercalcaemia, neuro disease, chronic dehydration (diabetes insipidus), drugs, sexual abuse

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2
Q

Red flag symptoms in constipation?

A

Failure to pass meconium - Hirschsprung’s

FTT - hypoT, coeliac

Gross distension - Hirchsprung, GI dysmotility

Perianal fistulae, abscesses or fissures - perianal Crohn’s disease

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3
Q

History features in constipation?

A 
	Straining and/or infrequent stools
	Anal pain on defecation (Crying)
	Fresh rectal bleeding (anal fissure)
	Abdominal pain
	Anorexia
	Growth failure
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4
Q

Management of constipation?

A

DIETARY
Increase fluid intake, increase fibre, natural laxatives (prune juice)

BEHAVIOUR
Toilet footrests, regular toilet time, don’t show concern to child

MEDICATION
Disimpaction and maintenance - consistency and adherence, treat for at least 3 months.

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5
Q

Disimpcation regieme?

A

 Regular oral faecal softeners e.g. Movicol
 Oral stimulant laxatives e.g. Senna
 Marcogel laxative e.g. Polyethene glycol (PEG)
 Escalating dose for 1-2 weeks until impaction resolves.

Long term treatment allows rectum to return to normal size –> sphincter function regained

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6
Q

Causes of gastroenteritis?

A

Viral - ROTAVIRUS, adenovirus, norovirus, coronavirus, astrovirus

Bacterial - CAMPYLOBACTER JEJUNI, shigella, salmonella, E.coli, cholera

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7
Q

Indications for stool sample in gastroenteritis?

A

blood in stools
dysentery (mucous + blood), immunocompromised child
recent foreign travel
uncertain diagnosis

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8
Q

Advice in gastroenteritis?

A

Little and often fluids better than regular
Appropriate hand hygiene
Avoid antidiarrhoeals

SAFETY NET = weeing/drinking <50% normal or difficulty in waking

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9
Q

Management of dehydration in gastroenteritis?

A

Mild (<5%) = oral rehydration

Moderate (5-10%) = ORS 50ml/kg over 4 hours –> IV therapy if necessary

Severe (>10%) = boluses 20ml/kg then IV therapy for rehydration (100ml/kg)

AND MAINTENANCE

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10
Q

When does GORD usually resolve by?

A

12 months

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11
Q

Presentation of GORD?

A

GI - Vomiting (non-billious), Faltered growth , Oesophagitis

Resp - Apnoea, hoarseness/cough/stridor, lower RT disease

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12
Q

Complications of GORD?

A

Failure to thrive

Oesophagitis - Haematemesis, Discomfort on feeding/heartburn, Iron deficiency anaemia (chronic blood loss)

Recurrent pulmonary aspiration - Recurrent pneumonia, Cough or wheeze, Apnoea in preterm infants

Dystonic neck posturing - Sandifer Syndrome

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13
Q

Investigations in GORD?

A

Usually none - of uncertain, complications or not responding to treatment

24-hour oesophageal pH monitoring - Can quantify degree of acid reflux – GORD = acid in oesophagus for >4% of day

24-hour impedance monitoring

Endoscopy and biopsy - Identify oesophagitis and exclude other causes of vomiting

Fluoroscopy - Barium swallow. Can identify things like – achalasia, oesophageal strictures, malrotation

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14
Q

Management of GORD?

A

GENERAL
• Sit baby upright when possible (30o head-up prone position post-feeding) – encourage papoose slings
• Small regular feeds – avoid feeds before sleep, avoid fatty foods, citrus juices, caffeine and carbonated drinks.
• Do not overfeed (stomach = child’s fist)
• Add gaviscon to feeds and thicken feeds

MEDICAL
GORD - gaviscon, omeprazole, ranitidne, domperidone - reassess after 4-6 weeks

SURGICAL
Nissen’s fundoplication - failed intensive treatment, Barrett’s oesophagus, stricture, severe oesophagitis, recurrent apnoea, LRT disease, FTT

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15
Q

Red flag symptoms of vomiting

A

Bile stained - obstruction

Haematemesis - oesophagitis, peptic ulcer, oral/nasal bleeding

Projectile in first weeks - pyloric stenosis

Vomiting at end of paroxysmal coughing - whooping cough

Abdo tenderness - surgical abdomen

Abdo distension - obstruction, strangulated hernia

Organomegaly - chronic liver disease

Bloody stool - Intussception, bacterial gastroenteritis

Severe dehydration/shock - severe gastroenteritis, systemic infection, DKA

Bulging fontanelle/seziures - raised ICP

FTT - GORD, coeliac

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16
Q

Presentation of TIDM?

A

Thirsty
Toilet
Thinner
Tired

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17
Q

Diagnosis of TIDM?

A

Symptomatic AND

Random BM of >11.1 mmol/L

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18
Q

Other tests you should do in T1DM?

A

U&Es

Blood pH (to exclude DKA)

Diabetes antibodies (Anti-islet cell, Anti-insulin, Anti-GAD)

Autoimmune disease screen (TFTs, Tissue Transglutaminase (TTG), anti-gliadin and anti-endomysial)

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19
Q

Education on T1DM?

A

Pathophysiology

Injection (site rotation)

Sick day rules - extra monitoring when unwell, may need dose changing, maintain carbohydrate/fluid intake as much as possible - call diabetes team if vomiting/diarrhoea

Recognition of hypos

Voluntary groups (Diabetes UK)

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20
Q

Diet in T1DM?

A

o Reduced refined carbohydrates (low glycaemic index)
o No more than 30% fat intake
o Carbohydrate counting (1 unit per 20g of carbs)

Complex carbohydrates Adjustments of diet and insulin for exercise

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21
Q

BM monitoring in T1DM?

A

Regular monitoring when blood levels suspected to be high or low – adjust insulin regimen.

Aim = keep blood glucose as near to normal as possible (4-10 mmol/L in children, 4-8 mmol/L in adolescents)

Minimal testing 4 times a day (can be done with subcutaneous continuous glucose monitoring - CGM)

HbA1c to be checked at least 3 times a year.

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22
Q

Sites for insulin injection?

A

Injection sites – 45 degree angle – site rotation essential.

o Upper arm
o Anterior/lateral thigh
o Buttocks
o Abdomen

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23
Q

Management of hypos?

A

Hunger, sweatiness, faint/dizzy, irritability/ confusion, pallor

• Oral glucose
o Buccal gels
o Drinks (Lucozade)
o Tablets

If unconscious – IM glucagon injection..

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24
Q

What is mild and severe FTT?

A

Mild = falls across 2 centile lines

Severe = falls across 3 centile lines

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25
Q

Management of non-organic FTT?

A

MDT - carried out in primary care by increasing energy intake

Healthcare visitor - can assess eating behaviour and provide support
Dietary advice, behavioural modification, monitoring growth

Dietician, SALT, social services, nursery placement

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26
Q

Management of extreme cases of FTT?

A

Admission if <6 months requiring active refeeding - can observe and improve mother’s feeding skills and demonstrate that child will gain weight when fed appropriately.

If it continues despite dietary input - investigations for organic cause

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27
Q

Causes of FTT?

A

INADEQUATE INTAKE

Non-organic = inadequate availability of food, psychosocial deprivaiton, neglect or child abuse
Organic = impaired suck/swallow, chronic illness --> anorexia

OTHERS

Inadequate retetnion (vomiting, severe GORD)
Malabsorption (coeliac, CF, CM intolerance)
Failure to utilise nutrients
Increased requirements (thyroid, CF, malignancy, infection, CHD)
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28
Q

Why is vesico-ureteric reflux bad?

A

Can cause renal scarring –> HTN

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29
Q

Risk factors for UTI?

A 
Constipation
Female gender
VUR
CAKUT (posterior urethral valves, boys only)
Previous UTIs
Encopresis
Nephrolithiasis
Uncircumcised boys
30
Q

Organisms causing UTI?

A

E.coli = most common

Klebsiella, proteus, pseudomonas, strep faecalis

31
Q

Methods of urine collection?

A

Clean catch
MSU
Catheter (transurethral or suprapubic)
Urine bag

32
Q

Definition of recurrent UTIs?

A

2 or more upper
1 upper and 1 lower
3 lower

33
Q

Definition of atypical UTI?

A 
Seriously ill
Poor urine flow
Raised creatinine
Septicaemia
Non-E.coli
Failure to respond in 48 hrs
34
Q

Criteria for UTI investigations?

A

<6 months - USS in 6 weeks (during infection if atypical), DMSA/MCUG if atypical/recurrent

6m - 3y - USS in 6 weeks if recurrent, DMSA 4-6 months if atypical/recurrent

3y + - USS in 6 wks if recurrent, DMSA in 4-6 months if recurrent

35
Q

Prevention of UTIs?

A
  • High fluid intake
  • Regular voiding – ensure complete bladder emptying and encourage child to try second empty
  • Perineal hygiene
  • Prevent/treat constipation
36
Q

Treatment of UTIs?

A

Oral = trimethoprim, cephalexin, co-amoxiclav
IV = cefuroxime, gentamicin
Repeat urine culture on completion of abx.

<3 months = Admit to hospital. IV abx until temperature settled then oral abx.

> 3 months upper = Oral abx for 7-10 days OR IV abx for 2-4 days then oral Abx for total treatment duration 10 days (i.e. 6 days oral)

> 3 months lower = Oral abx for 3 days. If still unwell after 24-48 hours –> reassess.

37
Q

Where does infantile eczema affect?

A

Affects the face, neck, behind ears, scalp (cradle cap) and extensor surfaces. Nappy area mostly spared. Majority of cases clear within a few months but may progress.

38
Q

Where does childhood eczema affect?

A

Mostly flexor surfaces – antecubital and popliteal fossae, volar aspect of wrists, neck and ankles. Less weepy and wet than infantile eczema but there is marked lichenification.

39
Q

Complications of eczema?

A

Bacterial
• Golden crust and sometimes postulation (impetiginized eczema)
• Mild cases can be treated with antiseptic washes and topical antibacterial ointments. Oral abx and topical steroids for widespread infections.

Viral
• Chickenpox can be widespread and severe. Molluscum contagiousum more common.
• Eczema herpeticum = serious HSV complication. Monomorphic clusters of vesciles that erode and crust. Systemic acyclovir and same day dermatology referral.

40
Q

General management of eczema?

A

Avoid irritants like soap and biological detergents. Clothing next to skin should be pure cotton where possible – avoid nylon and pure woollen garments.

Cut nails short to reduce damage from scratching.

Mittens at night in the very young

If specific allergen such as cow’s milk proven to be a precipitant –> avoid.

Can use antihistamines to stop itching

41
Q

Emolients and steroids in eczema?

A

EMOLIENTS
Mainstay of treatment – apply liberally two or more times a day and after a bath. Can also use emollient oil as a soap substitute in bath - apply in direction of hair.

STEROIDS
Use with care – explain that benefits outweigh risks when used correctly. Prescribe lowest effective strength.
Apply thinly and use on the face should be avoided – excessive use can cause skin thinning and systemic side effects – should not deter from their use in exacerbations though.

42
Q

Examples of topical steroids?

A 
Mild = 1% hydrocortisone
Moderate = 2.5% hydrocortisone
Strong = Betnovate/dermovate
43
Q

Most common cause of septic arthritis?

A

Staph aureus

Streptococci in neonates

Haematogenous spread
Direct innoculation from wound
Direct invasion from adjacent focus of infection (osteomyelitis)

44
Q

Presentation of septic arthritis?

A

Warm, erythematous, swollen and acutely tender joint
Severely restricted joint movement (pseudoparalysis)
Joint effusion
Inability to weight bear – if hip involvement, leg is held flexed and abducted.

75% lower limb – Hip > knee > ankle
<10% will have more than one joint affected

Systemic features = Fever, rigors, tachycardia

45
Q

Investigations in septic arthritis?

A

BLOODS
FBC - ↑WCC
CRP/ESR – both elevated
Blood cultures – take before abx commenced

IMAGING
X-ray
USS - effusion and can guide aspiration

ASPIRATION
Carried out under aseptic conditions by orthopaedic surgeon with US guidance  can culture organisms  guides Abx therapy.

46
Q

Management of septic arthritis?

A

IV ABX
Start after joint aspirate and blood cultures taken – splint joint and start empirical broad-spectrum IV abx.
• Flucloxacillin – 3 weeks – until inflammatory markers normalise.
• Followed by oral abx for 4-6 weeks – tailor according to culture results.

SURGICAL
Irritgation/drainage/debridement – if resolution does not occur rapidly.

47
Q

Prognosis and complicaitons of septic arthritis?

A

Prognosis is good with prompt recognition and treatment. <10% recurrence and develop chronic infection. Hip joint has worst prognosis.

  • Joint stiffness – secondary to cartilage damage
  • Septic dislocation – secondary to damage to the joint capsule and bone
  • Osteonecrosis – secondary to ischaemia
  • Shortening of limb – secondary to dislocation and osteonecrosis
  • Secondary osteoarthritis – secondary to damage to joint capsule
48
Q

Causes of cerebral palsy?

A 
Foetal
Structural abnormalities (e.g. cerebral malformation), maternal hypothyroidism, chorioamnionitis.

Neonatal
Premature delivery, birth hypoxia, congenital infections.
Intraventricular haemorrhage, hyperbilirubinemia, hypoglycaemia, cerebral infarcts, meconium aspiration syndrome.

Infant
Hydrocephalus, hypoglycaemia, head injury secondary to non-accidental injury, CNS infection

Child
Hypoxic events (e.g. drowning), head trauma, lead poisoning, CNS infections
49
Q

Pathophysiology of spastic CP?

A

UMN lesion –> nerve receptors in spine don’t respond to GABA (inhibitory) properly –> hypertonia

Velocity dependent –> weakness, increased tone, brisk reflexes, clonus, bulbar palsy (dysphagia/dribbling)

50
Q

Three types of spastic CP?

A

Spastic hemiplegia

Spastic diplegia

Spastic quadriplegia

51
Q

How does spastic hemiplegia present?

A

Arm and leg on one side, arms affected more, sparing of face. Spasticity greatest in antigravity muscles.

Affected Arm = flexed, pronated, fisting of hand.

Affected leg = circumduction gait, toe-heel (tip toe) gait. Delayed walking.

May have growth arrest in extremities. Moderate incidence of seizure disorders and intellectual impairment.

52
Q

How does spastic diplegia present?

A

Common in ex-prems (intra-ventricular haemorrhage)

Lower limbs (some involvement of ULs). ‘Paraplegia’ if no involvement of ULs.

Commando crawl (dragging legs)
Scissoring of lower legs
Severely delayed walking
Toe-heel gait with feet held in equinovarus position. Legs severely underdeveloped compared to arms.

Disuse atrophy, impaired growth of lower extremities. Usually have normal intellectual development. Other learning difficulties and deficits in other neuro pathways (e.g. hearing). Minimal risk of seizures.

53
Q

How does spastic quadriplegia present?

A

All four limbs

As for the others, but in all four limbs. Increased tone throughout, decreased spontaneous movements - worse on running

Swallowing difficulties (bulbar palsy). Weak suck. Tongue thrust. 
High incidence of seizure disorders, significant intellectual impairment, associated developmental abnormalities (speech, vision)
54
Q

How does dyskinetic CP present?

A
  • Movements are involuntary and uncontrolled. Become more evident with active movement or stress.
  • Infants = initially hypotonic with poor head control. But show increased tone and dyskinetic movements as they develop.
  • Oropharyngeal muscles are affected  speech and feeding problems.
  • Seizures uncommon, intellect usually preserved.
55
Q

Three main features of dyskinetic CP?

A

DAC

DYSTONIA
Involuntary, sustained contractions of opposing muscle groups. Leads to abnormal posture, twisting movements and repetitive movements.

ATHEOSIS
Slow, involuntary writhing movements – distal (fingers)

CHOREA
Brief, irregular, non-repetitive/rhythmic movements. Appear to flow smoothly, giving the appearance of dance-like movements.

56
Q

How does ataxic CP present?

A

Rare and poorly understood

Lack of voluntary co-ordinated movements of muscle. 
o	Usually symmetrical
o	Hypotonia
o	Poor balance
o	Delayed motor development

Later signs
o Intention tremor
o Ataxic gait (staggering and broad-based)
o Poor co-ordination (dysdiadochokinesia, past-pointing)

57
Q

Early features of CP?

A

Abnormal limb and/or trunk posture

Delayed motor milestones
o May be accompanied by delayed head growth
o Primitive reflexes may persist

Feeding difficulties
o Slow feeding, gagging, vomiting

Abnormal gait
o Once walking is achieved (usually 12-18 months)

Asymmetric hand function
o Before 12 years of age

58
Q

Non-pharmacological management of CP?

A

Nutrition
At risk of malnutrition and faltering growth. May need NG or PEG feeding.

SALT
Promote use of language and improve swallowing.

Occupational Therapy/Physio
Promote mobility and physical activity for normal daily living.

Adaptive and Communicative Equipment Walkers, poles, frames, braces, splints, wheelchairs/special seats are useful aids.

Education
May need special needs education. Vocational training can help prepare adults for jobs.

Psychologist/Counsellor
Address emotional needs of child/family.

59
Q

Pharmacological management of CP?

A

Anti-Muscarinics
Prevent drooling. Glycopyrronium bromide, hyoscine patches, botulinum injection into salivary gland.

Anti-Reflux Medication Reflux a common feature – domperidone, ranitidine.

Bisphosphonates
Prevent osteoporosis – pamidronate.

Anti-spasmodics
Help relieve spasticity – benzos, baclofen (intrathecal), dantrolene, botulinum toxin.

Reserpine
Vesicular monoamine transporter (VMAT) blocker – good for hyperkinetic movements.

60
Q

Causes of Down’s syndrome?

A

Majority = trisomy 21 due to non-disjunction during maternal oogenesis.

2% are Robertsonian translocation

2% are mosaic with normal cell line and trisomy 21 line.

61
Q

How common is Down’s syndrome?

A

Most common autosomal trisomy. Most common genetic cause of severe learning disabilities.

1 in 1000 live births. 1 in 110 at maternal age 45.

62
Q

Facial features in Down’s syndrome?

A 
ROSEOLA
•	Round face
•	Occiput flattening
•	Speckled iris (brushfield spots) Epicanthic folds
•	Open mouth with protruding tongue
•	Low set ears
•	Almond (oval) upward slanting eyes
63
Q

Hand/feet features in Down’s syndrome?

A

Hands
• Single palmar crease
• Short fingers
• Clinodactyly (Curved little finger)

Feet
• Sandal gap between big toe and other digit

64
Q

Conditions associated with Down’s syndrome?

A

CARDIAC
• ASD/VSD/Complete AVSD
• Mitral/tricuspid regurgitation
Leads to Eisenmenger’s syndrome

GI
• Duodenal atresia
• Anal atresia
• Hirchsprung’s disease

OTHERS
•	Hypothyroidism
•	Eczema
•	Leukaemia (1%) 
•	Developmental hip dysplasia 
•	Deafness (sensorineural and conductive)
•	Alzheimer’s by 5th decade 
•	Infection
•	Psychological – anxiety etc
65
Q

Management of Down’s syndrome?

A 
SCREENING
Cardiac - Echo
Hip US – Developmental hip dysplasia
Audiology – deafness
TFTs – acquired hypothyroidism 
In adulthood, annual health screening in primary care. “Personal health action plan” to address any health needs identified.

GENETIC COUNSELLING
Parents - only needed if Robertsonian translocation is the cause and are thinking of another baby.

MDT
Developmental paediatrician, child development centre, physiotherapy, dieticians, occupational therapists, SALT.
Almost all educated in mainstream schools with appropriate educational support.

66
Q

Prognosis in Down’s syndrome?

A

Huge variability. Some lead active, semi-independent lives (education, employment).
Life expectancy better now – most live to be over 60. Many will develop Alzheimer’s by 40.

67
Q

Types of squint?

A

Concomitant (Non-paralytic)
• Common
• Usually due to refractive error in one or both eyes.
• Can be treated with glasses but may require surgery.
• Squinting eye most often turns inwards (convergent) but there can be outwards (divergent), or rarely vertical deviation.

Non-Concomitant (Paralytic)
• Rare
• Usually due to paralysis of cranial nerves (III, IV, VI)
• Squint varies with gaze direction due to muscle paralysis
• Can be sinister as possibility of underlying brain tumour

68
Q

Presentation of squint?

A

Convergent (esotropia) = bad eye turns inwards (COMMON)

Divergent (exotropia) = bad eye turns outwards

Latent = squint controlled by subconscious effort and is not always apparent. In situations such as fatigue, the control is lost and the squint will manifest. Only appears when fixation interrupted (cover test.

Pseudosquint = arises when epicanthic folds give the appearance of a squint which is excluded on testing.

69
Q

Corneal light reflex test for squint?

A

Pen torch held at distance to produce reflections on both corneas simultaneously. Light reflection should appear in same position on both pupils – if not, they are misaligned.

70
Q

Cover test for squint?

A

Ask child to fix on object 1 metre away. Cover each eye and look for movement of uncovered eye.

If manifest…

May correct and fix on object being focused on (NON-PARALYTIC)
May stay in same position (paralytic)

If latent…

Can only identify by looking through a semi-transparent ‘cover’ or by quickly removing the cover and looking for correction of the eye.

71
Q

Management of squint?

A 
Aim to get weaker eye ‘trained up’
•	Correct refractive error – glasses
o	Hypermetropia = long-sighted – most common refractive error
o	Myopia = short sighted, common
•	Eye patch on good eye
•	Eye muscle exercises
•	Eye (muscle) surgery if large squint.
72
Q

What can happen if you don’t correct a squint?

A

AMBLYOPIA

Signal from bad eye depressed to avoid double vision. Constant depression –> failure of visual development

4th Year Paeds (7 decks)

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