Paediatrics Passmed Flashcards
(120 cards)
1
Q
Key points to consider in sexual abuse
A
Adults do not often believe child’s allegations
Higher incidence in children with special needs
30% father
15% unrelated man
10% brother
2
Q
Features of sexual abuse
A
Pregnancy STIs, recurrent UTIs Sexually precocious behaviour Anal fissures, bruising Reflex anal dilatation enuresis and encopresis Behavioural problems e.g. self-harm Recurrent symptoms e.g. headache, abdo pain
3
Q
Complications of Kawasaki disease
A
Coronary artery aneurysm
4
Q
Features of Kawasaki disease
A
High-grade fever which lasts for >5 days. Fever is characteristically resistant to antipyretics
Conjunctival injection
Bright red, cracked lips
Strawberry tongue
Cervical lymphadenopathy
Red palms of the hands and soles of the feet which later peel
5
Q
Diagnosis of Kawasaki disease
A
Clinical diagnosis as there is no specific diagnostic test
6
Q
Management of Kawasaki disease
A
High-dose aspirin (Kawasaki disease is one of the few indications for the use of aspirin in children because of Reyes syndrome)
IVIG
Echo to screen for coronary artery aneurysms
7
Q
Acute scrotal disorders in children, and when they are most common?
A
Torsion- most common around puberty
Irreducible inguina hernia- <2 years old
Epididymitis - rare in prepubescent children
8
Q
Is pyloric stenosis more common in M or F?
A
Incidence of 4/1000 live births
4 times more common in males
10-15% of infants have a positive family history
First-borns are more commonly affected
9
Q
Features of pyloric stenosis
A
Projectile vomiting, typically 30 minutes after a feed
Constipation and dehydration may also be present
A palpable mass may be present in the upper abdomen
Hypochloremic, hypokalaemic alkalosis due to persistent vomiting
10
Q
Diagnosis and management of pyloric stenosis?
A
Ultrasound
Management with Ramstedt pyloromyotomy
11
Q
Fraser guidelines are used to assess if a patient <16 is competent to consent to treatment: what are these guidelines?
A
the young person understands the professional’s advice
the young person cannot be persuaded to inform their parents or allow the professional to contact them on their behalf the young person is likely to begin, or continue having, sexual intercourse with or without contraceptive treatment unless the young person receives contraceptive treatment, their physical or mental health, or both, is likely to suffer the young person's best interests require them to receive contraceptive advice or treatment with or without parental consent
12
Q
Risk factors for Surfactant deficient lung disease
A
Prematurity (risk decreases with gestation) Male Diabetic mother C-section Second born of premature twins
13
Q
Clinical features of surfactant deficient lung disease
A
tachypnoea
Intercostal recession
Expiratory grunting
Cyanosis
CXR characteristically shows ground-glass appearance with an indistinct heart border
14
Q
Management of surfactant deficient lung disease
A
Prevention during pregnancy: maternal corticosteroids to induce fetal lung maturation
Oxygen
Assisted ventilation
Exogenous surfactant given via endotracheal tube
15
Q
Risk factors for developmental dysplasia of the hip
A
Female sex (6 times greater risk) Breech presentation Positive family history Firstborn children Oligohydramnios Birth weight >5kg Congenital calcaneovalgus foot deformity
DDH is slightly more common in left hip; 20% bilateral
16
Q
Who is offered screening for developmental dysplasia of the hip?
A
All infants are screened at both the newborn check and also the six-week baby check using the Barlow and Ortolani tests
Require a routine ultrasound examination if:
First-degree family history of hip problems in early life
Breech presentation at or after 36 weeks gestation, irrespective of presentation at birth or mode of delivery
Multiple pregnancy
17
Q
Clinical examination of developmental dysplasia of the hip
A
Barlow test: attempts to dislocate an articulated femoral head
Ortolani tests: attempts to relocate a dislocated femoral head
Symmetry of leg length
Level of knees when hips and knees are bilaterally felxed
Restricted abduction of the hip in flexion
US used to confirm diagnosis if clinically suspected
18
Q
Management of DDH
A
most unstable hips will spontaneously stabilise by 3-6 weeks of age
Pavlik harness (dynamic flexion-abduction orthosis) in children younger than 4-5 months older children may require surgery
19
Q
What percentage of childhood leukaemias are accounted for by ALL?
A
Around 80%
Peak incidence arat 2-5 years of age and boys are slightly more commonly affected than girls
20
Q
Clinical features of ALL
A
Features may be divided into those predictable by bone marrow failure:
(Anaemia: lethargy and pallor
Neutropenia: Frequent or severe infections
Thrombocytopenia: easy bruising, petechiae)
And other features:
(Bone pain secondary to bone marrow infiltration
Hepatosplenomegaly
Fever in up to 50% cases (representing infection or constitutional symptoms)
Testicular swelling)
21
Q
Types of ALL
A
Common ALL, CD10 present, pre-B phenotype (75%)
T-cell ALL (20%)
B-cell ALL (5%)
22
Q
Poor prognostic factors for ALL
A
Age <2 years or >10 years WBC> 20x10^9/1 at diagnosis T or B cell surface markers Non-Caucasian Male sex
23
Q
What mutation is responsible for achondroplasia?
A
Autosomal dominant disroder associated with short stature, caused by a mutation in the fibroblast growth factor receptor 3 (FGFR-3) gene. This results in abnormal cartilage, which gives rise to clinical features
24
Q
Clinical features of achondroplasia
A
Short limbs (rhizomelia) with shortened fingers (brachydactyly)
Large head with frontal bossing and narrow foramen magnum
Midface hypoplasia with a flattened nasal bridge
Trident hands
Lumbar lordosis
25
Risk factors for achondroplasia
Mostly sporadic mutations
| Main risk factor is advancing parental age at the time of conception
26
Treatment for achondroplasia
No specific therapy, though some individuals benefit from limb lengthening procedures (usually involve application of Ilizarov frames and targeted bone fractures)
27
Who are most commonly affected by intussusception?
Usually affects infants between 6-18 months old
| Boys are affected twice as often as girls
28
Features of intussusception
Paroxysmal abdominal colic pain- during paroxysm the infant wil characteristically draw their knees up and turn pale
Vomiting
Bloodstained (redcurrant jelly) stool is a late sign
Sausage-shaped mass in the RUQ
29
Investigation and management of intussususception
US is now investigation of choice and may show a target-like mass
Majority of children can be treated with reduction by air insufflation under radiological control, which is now widely used first-line compared to traditional barium enema
If this fails, or the child has signs of peritonitis, surgery is performed
30
Criteria for severe asthma attack in children
SpO2 <92%
PEF 33-50% best or predicted
Too breathless to talk or feed
Heart rate >125 (>5years) or >140 (1-5 years)
Respiratory rate >30/minute (>5 years) or >40 (1-5 years)
use of accessory neck muscles
31
Criteria for life-threatening asthma attack in children
```
SpO2 <92%
PEF <33% best or predicted
Silent chest
Poor respiratory effort
Agitation
Altered consciousness
Cyanosis
```
32
What are the commonest causes of epistaxis in children?
Nose picking (most common cause)
Foreign body
URTI
Allergic rhinitis
33
What are the constituent elements of the Apgar score?
```
Pulse
Respiratory rate
Muscle tone
Colour
Reflex irritability
```
34
What is the main feature of choanal atresia?
Posterior nasal airway occluded by soft tissue or bone
Associated with other congenital malformations e.g. coloboma
35
How do babies with choanal atresia present?
Babies with unilateral disease may go unnoticed
Babies with bilateral disease will present early in life as they are obligate nose breathers
36
How to treat choanal atresia?
Feenstration procedures designed to restore patency
37
NICE recommendations for diagnosing obesity in children?
NICE recommend considering tailored clinical intervention if BMI at 91st centile or above, and consider assessing for comorbidities if BMI at 98th centile or above
38
Risk factors for obesity in children
Asian children are four times more likely to be obese than white children
Female
Taller children
39
Causes of obesity in children
```
Growth hormone deficiency
Hypothyroidism
Down's
Cushing's
Prader-Willi
```
40
Consequences of obesity in children
Orthopaedic problems: slipped upper femoral epiphyses, Blount's disease (a development abnormality of the tibia resulting in bowing of the legs), musculoskeletal pains
Psychological consequences: poor self-esteem, bullying
Sleep apnoea
Benign intracranial hypertension
Long-term consequences: increased incidence of type 2 diabetes mellitus, hypertension and IHD
41
Which organisms cause meningitis in neonates-3 months?
Group B strep: usually acquired from the mother at birth; more common in low birth weight babies and following prolonged rupture of the membranes
E.coli and other Gram -ve organisms
Listeria monocytogenes
42
Which organisms cause meningitis in 1 month-6 year olds?
Neisseria meningitidis
Strep pneumonia
Haemophilus infleunzae
43
Which organisms cause meningitis in children greater than 6 years?
Neisseria meningitidis
| Strep pneumoniae
44
What type of organism is the measles virus?
RNA paramyxovirus
45
How is measles spread?
Droplets
Infective from prodrome until 4 days after rash starts
Incudbation period = 10-14 days
46
Clinical features of measles infection
Prodrome: irritable, conjunctivitis, fever
Koplik spots (before rash): white spots ('grain of salt') on buccal mucosa
Rash: starts behind the ears and then to whole body, discrete maculopapular rash becoming blotchy and confluent
47
Investigations for measles infection
IgM antibodies can be detected within a few days of rash onset
48
Management of measles infection
Mainly supportive
Admission may be considered in immunosuppressed or pregnant patients
Notifiable disease --> inform public health
If a child not immunised against measles comes into contact with measles then MMR should be offered (vaccine-induced measles antibody develops more rapidly following natural infection)- this should be given within 72 hours
49
Complications of measles infection
```
Otitis media: most common
Pneumonia: most common COD
Encephalitis: typically ocurs 1-2 weeks following the onset of illness
Subacute sclerosing panencephalitis: v. rare, may present 5-10 years following the illness
Febrile convulsions
Keratoconjunctivitis, corneal ulceration
Diarrhoea
Increased incidence of appendicitis
Myocarditis
```
50
Which organism causes erythema infectiosum, and how does it present?
Parvovirus B19
Lethargy, fever, headache
Slapped-cheek rash spreading to proximal arms and extensor surfaces
51
What testicular volume indicates onset of puberty in males?
>4ml
52
At what level of reduced haemoglobin can central cyanosis be recognised clinically in the neonate?
Central cyanosis can be recognised when the concentration of reduced haemoglobin in the blood exceeds 5g/dl
53
How to distinguish between cardiac and non-cardiac causes of cyanosis in the newborn?
Nitrogen washout test: infant given 100% oxygen for ten minutes after which ABGs are taken. A pO2 of less than 15kPa indicates cyanotic congenital heart disease
54
Causes of cyanotic congenital heart disease
Tetralogy of Fallot
Transposition of the great arteries
Tricuspid atresia
55
Initial management of susepcted cyanotic congenital heart disease
```
Supportive care
Prostaglandin E2 (used to maintain patent ductus arteriosus in ductal-dependent congenital heart defect)
```
56
What causes Acrocyanosis?
Acracyanosis is the peripheral cyanosis seen around the mouth and extremities in healthy newborns
It is caused by benign vasomotor changes that result in peripheral vasoconstriction and increased tissue oxygen extraction.
It occurs immediately after birth in healthy infants, distinguishing it from other causes of peripheral cyanosis with significant pathology.
57
Management of ADHD
Following presentation, a ten-week 'watch and wait' period should follow. If symptoms persist, referral to secondary care is required (either to paediatrician with SI or CAMHS)
Drug therapy as last-resort and only available for those >5 years
58
Drug therapy for ADHD
Methylphenidate 1st line
If there is inadequate response, switch to lisdexamfetamine
Dexamfetamine should be started in those who have benefited from lisdexamfetamine, but who cannot tolerate its side effects
ALl of these drugs are potentially cardiotoxic --> perform a baseline ECG before starting treatment, and refer to a cardiologist if there is any significant past medical history or family history, or any doubt or ambiguity
59
Mechanism of action of methylphenidate
CNS stimulant which primarily acts as a dopamine/norepinephrine reuptake inhibitor
60
Side-effects of methylphenidate
Abdo pain
Nausea
Dyspepsia
In children:
Weight and height should be monitored every 6 months
61
Clinical features of febrile convulsions
Usually occur early in a viral infection as the temperature rises rapidly
Seizures are usually brief, lasting less than 5 minutes
Are mostly tonic-clonic
62
Simple febrile convulsions
<15 minutes
Generalised seizure
Typically no recurrence within 24 hours
Should be a complete recovery within an hour
63
Complex febrile convulsions
15-30 minutes
Focal seizure
May have a repeat seizure within 24 hours
64
Febrile status epilepticus duration?
>30 minutes
65
Management following a first seizure?
Children who have had a first seizure OR any features of a complex seizure should be admitted to paediatrics
66
How to manage a child with recurrent febrile convulsions?
Try teaching parents how to use rectal diazepam or buccal midazolam. Parents should be advised to phone for an ambulance if the seizure lasts >5 minutes
67
Risk factors for recurrent febrile convulsions
Overall risk = 1 in 3
Age of onset <18 months
Fever <39 degrees
Shorter duration of fever before seizure
Family history of febrile convulsions
68
Risk factors for progression of febrile convulsions to epilpesy
Family history of epilepsy
Complex febrile seizures
Background of neurodevelopmental disorder
Children with no risk factors have 2.5% risk of developing epilepsy (50% with all three risk factors)
69
What is the main risk factor for necrotising enterocolitis?
Prematurity
Increased risk when empirical antibiotics are given to infants beyond five days
70
Clinical features of necrotising enterocolitis
Early features include abdominal distension and passage of bloody stools
X-ray may show pneumatosis intestinalis and evidence of free air
71
Treatment of necrotising enterocolitis
Total gut rest and TPN
| Babies with perforations require laparotomy
72
Diagnostic criteria for Kawasaki disease?
Fever > 5 days + 4 of the following:
Conjunctival injection
Mucous membrane changes (dry cracked lips, strawberry tongue)
Cervical lymphadenopathy
Polymorphous rash
Red and oedematous palms/soles, peeling of fingers and toes
73
What organism causes Scarlet fever?
Scarlet fever is a reaction to erythrogenic toxins produced by Group A haemolytic streptococci (usually Strep pyogenes)
74
What is the commonest age for presentation of Scarlet fever?
2-6 years (peak incidence at 4 years)
75
How is Scarlet fever transmitted?
Respiratory route, either via inhalation or ingesting respiratory droplets
Direct contact with throat and nose discharges
76
Clinical features of Scarlet fever
```
Fever (typically lasts 24 to 48 hours)
Malaise, headache, nausea/vomiting
sore throat
Strawberry tongue
Rash - fine punctate erythema which generally appears first on the torso and spares the palms and soles (sandpaper rash)
```
77
Diagnosis and management of Scarlet fever
A throat swab is normally taken but antibiotic treatment should be commenced immediately, rather than waiting for the results
Oral penicillin V for 10 days (azithromycin if penicillin allergy)
Children can return to school 24 hours after commencing antibiotics
Notifiable disease
78
Complications of Scarlet fever
Otitis media
Rheumatic fever
Acute glomerulonephritis
Invasive complications (e.g. bacteraemia, meningitis, necrotising fasciitis)
79
Clinical features of malrotation
High caecum at the midline
Exomphalos
Congenital diaphragmatic hernia
Intrinsic duodenal atresia
May be complicated by volvulus development (resulting in bile-stained vomiting)
80
How is malrotation diagnosed?
Upper GI contrast study and USS
81
How is malrotation treated?
Laparotomy
| Ladds procedure is volvulus or high risk fo volvulus
82
What is Hirschsprungs disease?
Absence of ganglion cells from myenteric and submucosal plexuses
83
How is Hirschsprungs diagnosed?
Full-thickness rectal biopsy
84
Features of Hirschsprungs disease
Delayed passage of meconium and abdominal distension
85
Treatment of Hirschsprungs disease
Rectal washouts
| Anorectal pull through prcoedure
86
What is the hydrogen breath test used for?
Diagnose IBS or some food intolerances
87
What gene is coeliac associated with?
HLA-DQ2 and HLA-DQ8
88
Clinical features of coeliac disease
```
Failure to thrive
Diarrhoea
Abdominal distension
Older children may present with anaemia
Many cases not diagnosed until adulthood
```
89
How is coeliac disease diagnosed?
Jejunal biopsy showing subtotal villous atrophy
| Anti-endomysial and anti-gliadin antibodies are useful screening tests
90
What kind of disorder is Fragile X syndrome?
Trinucleotide repeat disorder
91
Clinical features of Fragile X syndrome
```
In males:
Learning difficulties
Large low set ears, long thin face, high arched palate
Macroorchidism
Hypotonia
Autism is more common
Mitral valve prolapse
```
IN females: range from normal to mild
92
Diagnosis of Fragile X syndrome
Can be made antenatally by chorionic villus sampling or amniocentesis
Analysis of the number of CGG repeats using restriction endonuclease digestion and Southern blot analysis
93
Classification of precocious puberty
Gonadotrophin dependent: central, true (due to premature activation of the htpothalamic-pituitary-gonadal axis; FSH and LH raised)
Gonadotrophin independent: pseudo, false (due to excess sex hormones, FSH and LH low)
Uncommon in males and usually has an organic cause:
Bilateral enlargement of testes= gonadotrophin release from intracranial lesion
Unilateral enlargement= gonadal tumour
Small testes = adrenal cause
Females - usually idiopathic or familial and follows normal sequence of puberty
Organic causes are rare, associated with rapid onset, neurological symptoms and signs and dissonance (e.g. McCune Albright syndrome)
94
Management of children with mild to moderate asthma
Give a beta-2 agonist via a spacer (for a child<3 years use a close-fitting mask)
Give 1 puff every 30-60 seconds up to maximum of 10 puffs
If symptoms are not controlled repeat beta-2 agonist and refer to hospital
Steroid therapy should be given to all children with an asthma exacerbation and treatment should be given for 3-5 days
95
Clinical features of eczema in children
In infants the face and trunk are often affected
In younger children eczema often occurs on the extensor surfaces
In older children a more typical distribution is seen, with flexor surfaces affected and the creases of the face and neck
96
Management of eczema in children
Avoid irritants
Simple emollients
Topical steroids
In severe cases wet wraps and oral ciclosporin may be used
97
What are the features of constipation?
```
Poor appetite
Reduced frequency of stools
Soiling
Abdominal pain
Passing hard large poos or small pellets
Painful passing of faeces
```
98
What are the four different classes of laxatives?
Osmotic (movicol (a macrogol) or lactulose)
Stimulant (Bisacodyl, Senna glycoside)
Bulk forming (unprocessed wheat bran)
Stool softening (arachis oil, docusate sodium)
99
What are the indications for a rectal biopsy?
DO NOT PERFORM RECTAL BIOPSY UNLESS ANY OF THE FOLLOWING CLINICAL FEATURES OF HIRSCHSPRUNG'S DISEASE OR HAVE BEEN PRESENT:
Delayed passage of meconium (more than 48 hours after birth in term babies)
Constipation since first few weeks of life
Chronic abdominal distension plus vomiting
Family history of Hirschsprung's disease
Faltering growth in addition to any of the previous features
100
Red flag symptoms for constipation
Failure to pass meconium within 24 hours of life (Hirschsprung)
Failure to thrive/grow (hypothyroid, coeliac)
Gross abdominal distension (Hirschsprung or GI dysmotility)
Abnormal lower limb neurology/deformity (lumbosacral pathology)
Sacral dimple above natal cleft over the spine (Spina bifida occulta)
Abnormal appearance/position/patency of anus (abnormal anatomy)
Perianal bruising or multiple fissures (sexual abuse)
Perianal fistulae, abscesses (perianal Crohns disease)
101
Management of idiopathic constipation
Reassure there is treatment but warn it may take some months
Give some information on idiopathic information
Assess for faecal impaction (large faecal mass unlikely to be passed on demand)
102
When is disimpaction indicated?
If faecal impaction is present
103
Outline maintenance therapy for idiopathic constipation
Reassess child frequently to ensure they do not become reimpacted and assess issues in maintaining treatment such as taking medicine and toileting
104
What must be noted about dietary and lifestyle changes to treat idiopathic constipation?
Do not use dietary interventions alone as first-line treatment
105
What are the indications for DRE?
Refer urgently to a healthcare professional competent to perform a DRE and interpret features of anatomical abnormalities or Hirschsprungs disease, children younger than 1 year with idiopathic constipation that does not respond to optimum treatment within 4 weeks.
106
Investigations of idiopathic constipation
Physical examination
107
Outline faecal disimpaction regime
Movicol, using an escalating dose regimen as first-line treatment
Add a stimulant laxative if this does not lead to disimpaction after 2 weeks
Substitute a stimulant laxative singly or in combination with an osmotic laxative such as lactulose if movicol is not tolerated
Inform families that disimpaction treatment can initially increase symptoms of soiling and abdominal pain
Continue medication at maintenance dose for several weeks after regular bowel habit is established - this may take several months
Do not stop medication abruptly
108
Symptoms of asthma
Wheeze
breathlessness
Chest tightness
Cough
Variable airflow obstruction
109
Investigations for asthma
```
Respiratory exam
O2 sats
Heart rate
Resp rate
Temperature
```
110
Management of acute asthma
ADMIT, ABC approach
1) High-flow oxygen via tight facemask or nasal cannula - aim for sats >94%
2) Inhaled salbutamol 10 puffs via MDI + spcaer (mild to moderate) or nebulised (severe, life-threatening)
- -> good response: salbutamol 1-4 hourly
- -> poor response: add nebulised ipratropium bromide
- -> still not responding: nebulised magnesium sulphate
3) oral prednisolone for 3 days or until off regular salbutamol
111
Moderate asthma
Sats >92%
PEFR > 50% predicted
No clinical features of severe asthma
112
Severe asthma
```
Sats <92%
PEFR 33-50% predicted
Too breathless to talk or feed
RR > 40 (2-5yo), >30 (5+)
HR>140 (2-5), 125 (5+)
```
113
Life-threatening asthma
```
Sats <92%
PEFR <33% predicted
Silent chest
Cyanosis
Poor respiratory effort
Hypotension
Exhaustion
Confusion/coma
```
114
Management of chronic asthma (5-12yo)
Initially may ask to take PEFR diary; perform spirometry
MDT - asthma specialist nurse, GP, school involvement
1) Inhaled SABA PRN
2) Add inhaled steroid (regular preventer)
3) Add inhaled LABA - assess control
a) Good response --> continue LABA
b) Benefit from LABA but still not sufficient --> continue LABA and increase steroid dose; could consider LTRA also
c) No response --> stop LABA and increase steroid
4) Increase steroid
5) Daily oral steroid
115
What is the worry about use of steroids in children?
inhibit growth
116
Describe initial chest assessment for a child presenting with DIB
```
Obs- HR, RR, SaO2
Observe chest for signs of increased work of breathing:
--> nasal flaring
--> subcostal/intercostal recession
--> paradoxical/see-saw breathing
Cyanosis
CRT
Auscultation
Liver displacement
```
117
What are the diagnostic criteria for DKA in children (NICE guidelines)
Acidosis (pH7.3 or bicarb<18) AND
| Ketonaemia (blood beta-hydroxybutyrate > 3mmol/litre) or Ketonuria (++ or more)
118
Investigations for DKA (NICE guidelines)
1) Basic obs - HR, RR, BP, level of consciousness
2) CBG - look at glucose, ketones, pH, bicarb
3) urine dip - ketones and glucose
4) bloods (FBC, U+E, CRP, glucose > 11.1, ketones > 3), blood gas
5) weight- indicator oif dehydration (plus use CRT, skin tugor, U+E)
119
Management of DKA
1) Stabilise patient--> chest assessment, patent airway? Supplemental oxygen?
2) IV fluid bolus- normal saline, correct hydration over 48 hours (calculate deficit and maintenance but must use reduced maintenance volumes in DKA)- monitor input and output, electrolytes and acid base status regularly, REASSESS ABC (treat with oral fluids and SC insulin only if child is alert, not nauseated/vomiting, and not clinically dehydrated)
3) Insulin infusion (fixed rate, not sliding scale) - aim for gradual glucose reduction of about 2 mmol/hr
4) Potassium - add K to all fluids except initial bolus. K will fall following insulin treatment and rehydration - continuous cardiac monitoring needed
5) Do not give bicarb
Inform senior if suspect DKA
Need to explain to family that condition is serious
ADMIT
Consider NG tube if reduced level of consciousness and vomiting --> reduced risk of aspiration
?anaesthetic r/v if worried about airway patency
120
What dietary and lifestyle measures may aid a parent with a child with constipation?
Negotiated and non-punitive behavioural interventions suited to the child or young person's stage of development: schedule toileting and support to establish regular bowel habit, maintenance and discussion of a bowel diary, information on constipation, and use of encouragement and rewards system
Dietary modifications to ensure a balanced diet and sufficient fluids are consumed (adequate fibre intake, adequate fluid intake)
