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Thick Stuff > Level 1 - Endocrine, Neuro > Flashcards

Level 1 - Endocrine, Neuro Flashcards

1
Q

Define T1DM?

A
  • Autoimmune disorder caused by T-cell-mediated destruction of pancreatic beta-cells, leading to insulin deficiency and hyperglycaemia
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2
Q

Define MODY?

A
  • Maturity-onset diabetes of the young (MODY)
    • Autosomal dominant kind of non-ketotic diabetes
    • Impaired insulin secretion
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3
Q

How common is T1DM and when is most common?

A
  • 3rd most common chronic disease in UK children
  • 90% type 1 in children
  • Peak onset 5-7 years with second peak at or just before puberty
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4
Q

RF for T1DM?

A
  • Family history of type 1 diabetes

* IDDM1 gene represents the HLA-greatest susceptibility

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5
Q

Aetiology of T1DM?

A

• Destruction of pancreatic Beta-cells in Islet of Langerhans by an autoimmune process (anti-islet cell, anti-insulin, anti-GAD antibodies)

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6
Q

Pathophysiology of T1DM?

A

• T-Cell activation leads to B-Cell inflammation (insulitis) and cell loss via apoptosis

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7
Q

What can cause DKA in T1DM?

A

• Can be caused by infection or non-compliance

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8
Q

Symptoms and Signs of T1DM?

A
  • Onset over quick
  • Polyuria, polydipsia, weight loss
  • Young children may get secondary enuresis
  • Skin infections (Candida)
  • DKA
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9
Q

Symptoms and Signs of DKA?

A
  • Confusion
  • Vomiting
  • Abdominal pain
  • Dehydration
  • Deep and Rapid breathing (Kussmaul)
  • Ketotic breaths
  • Shock
  • Cerebral oedema in 1%
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10
Q

Diagnosis of T1DM?

A
  • Symptoms of hyperglycaemia plus:
    • Random blood glucose ≥11.1mmol/L
    • Fasting blood glucose ≥7mmol/L
  • Raised venous blood glucose on 2 or more occasions with no symptoms
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11
Q

What other tests can be done in T1DM?

A
  • Autoantibody to islet-cells, insulin, GluAD, IA2

- Screen for other autoimmune diseases (coeliac, TFTs)

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12
Q

Definition of DKA?

A
  • Hyperglycaemia (≥11.1mmol/L and present in urine)
  • Ketone (blood >3mmol/L and present in urine)
  • Acidosis (venous pH <7.3 and bicarbonate <15mmol/L)
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13
Q

Where is T1DM managed and what education is given?

A
  • Managed by MDT paediatric diabetes care team
  • Intensive Education on disease
    • Understanding of disease and insulin devices
    • Adjustments in insulin doses for diet, illness
    • Finger prick monitoring and recognising hypoglycaemia
    • Local voluntary groups ‘Diabetes UK’
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14
Q

Diet and blood glucose monitoring needed in T1DM?

A
  • Diet
    • Referral to paediatric dietician
    • High complex carbohydrates and relatively low fat content (<30% of total calories)
    • High fibre diet
  • Blood glucose monitoring
    • Aim 4-6mmol/L but anywhere from 4-10mmol/L
    • Regular glucose monitoring and blood ketone testing when ill
    • HbA1c every 4 months, maintain <58mmol/mol
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15
Q

Drug treatment of T1DM?

A
  • Insulin therapy
    • 1/3 rapid acting and 2/3 long acting
    • May benefit from continuous SC insulin infusion
    • Rotation of injection site prevents lipohypertrophy
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16
Q

Screening needed in T1DM?

A
  • Microalbuminuria screening every appointment

- Retinopathy screening annually

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17
Q

Management of DKA in T1DM?

A

• Get senior help
• Do GCS
• Resuscitate
 0.9% saline to correct dehydration (correct gradually over 48 hours)
 Consider admission to ITU if BP dropping
• Confirm DKA
 History
 Finger-prick glucose and ketones
 VBG
 Urine dip for ketones/glucose
• Investigations
 Weight, FBC, U&Es, glucose, Ca, blood gas, ECG (for hyper/hypokalaemia)
 Assess dehydration to calculate fluid deficit and maintenance
• IV fluids
 0.9% saline with 20mmol KCl/500mL
 Add 5% glucose when blood glucose <14mmol/L
 After 12 hours, change to 0.45% saline
• IV insulin (after 1 hour of fluids)
 Fast acting insulin (0.1 unit/kg/hour), can reduce once pH, normalises

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18
Q

Complications of T1DM?

A
  • Delayed sexual maturity
  • Frequent injections and blood tests
  • Impaired body image
  • Parental overprotection
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19
Q

Define hypoglycaemia? What are the 3 criteria?

A
  • Can be defined as glucose <3mmol/L
  • The diagnosis of hypoglycaemia rests on three criteria (Whipple’s triad):
    • Plasma hypoglycaemia.
    • Symptoms attributable to a low blood sugar level.
    • Resolution of symptoms with correction of the hypoglycaemia
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20
Q

Causes of hypoglycaemia?

A
  • Due to excess of insulin or oral hypoglycaemic agents combined with reduced sugar intake and increased activity
  • Causes:
    • Excess exogenous insulin
    • Persistent hypoglycaemic hyperinsulinism of infancy
    • Insulinoma
    • Drug (sulphonylureas, aspirin, alcohol)
    • Hormonal deficiencies (GH, ACTH, Addisons)
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21
Q

Symptoms and signs of hypoglycaemia?

A
  • Sweating
  • Pallor
  • Pins and needles in lips and tongue
  • Slurring of speech, confusion, change of behaviour
  • Irritability, headache, seizures and coma
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22
Q

Investigations in hypoglycaemia?

A
  • Bedside blood glucose test
  • Laboratory blood glucose
  • Blood and urine for toxicology
  • GH, IGF-1, cortisol, insulin, C-peptide, fatty acids, ketones , glycerol
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23
Q

Management of mild/moderate hypoglycaemia?

A

• Oral glucose (tablets or sugary drink)

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24
Q

Management of severe hypoglycaemia?

A
  • Get IV access
  • Intra-oral Gluco-Gel (if no IV access)
  • Glucose 5mL/kg of 10% dextrose by IVI (or by rectal tube if no IV access)
  • Glucagon 0.5-1mg IM/IV
  • If glucose not responding, give IV dexamethasone
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25
Q

Define FTT?

A
  • Poor weight gain in infancy (falling across centile lines)

- Mild FTT being fall across 2 centiles, severe FTT across 3 centiles

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26
Q

How common is FTT?

A
  • 95% due to not enough food offered or taken
  • 5% of children will cross two line
  • Big cause worldwide is poverty
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27
Q

Causes of FTT - most common?

A

• Normal child of small stature

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28
Q

Causes of FTT - inadequate intake?

A

 Non-Organic
- Inadequate availability of food
- Psychosocial deprivation
- Neglect/Child Abuse
 Organic
- Impaired suck/swallow (CP, cleft palate)
 Chronic illness (Crohn’s, chronic renal failure, CF, lung disease)

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29
Q

Causes of FTT - inadequate retention?

A

 Vomiting, GORD

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30
Q

Causes of FTT - malabsorption?

A

 Coeliac, CF, cow’s milk protein intolerance, NEC

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31
Q

Causes of FTT - syndrome that fail to utilise nutrients?

A

 Increased requirements in HIV, malignancy, CF, thyrotoxicosis, CHD

32
Q

Normal but short infants present as what?

A
  • Normal but short infants usually happy, no symptoms, responsive and development is satisfactory
33
Q

Difference in acute of chronic FTT?

A
  • Recent onset FTT may retain height but chronic FTT will compromise growth in height too
34
Q

History for FTT?

A

 Food diary, exact details of feeding patterns
 Is the child well with lots of energy, tired, diarrhoea, vomiting, cough?
 Was the child premature, IUGR or significant medial problems?
 Growth in other family members or illnesses in family?
 Child development normal?
 Psychosocial problems at home?

35
Q

Examination findings in FTT?

A

 Signs of dysmorphism
 Malabsorption (thin buttocks, distended abdomen)
 Respiratory disease (chest wall deformity, clubbing)

36
Q

Investigations to find cause of FTT?

A

 Bloods
- FBC (anaemia, neutropenia, lymphopenia)
- Creatinine, U&Es, electrolytes and bone profile (Renal failure, metabolic disorders, William syndrome)
- LFTs (Liver disease, malabsorption, metabolic disease), TFTs (hypo/hyperthyroidism)
- CRP
- Ferritin (iron def anaemia)
- IgA TTG (coeliac disease)
 Urine and stool M,C, & S
 Karyotyping
 CXR and sweat test (CF)

37
Q

Non-Organic management of FTT?

A
  • Home visits by health visitor to assess eating behaviour and provide support
  • Dietician may be helpful
  • Clinical psychologists, SALT, nursery teachers all useful
38
Q

Organic management of FTT?

A

• Treat underlying cause

39
Q

Prognosis of FTT?

A

• Non-organic tend to continue to under-eat and there is a lasting deficit but impairment of development is usually only short-term

40
Q

What is CP?

A

Cerebral palsy

41
Q

Define CP?

A
  • Chronic disorders of posture and movement caused by non-progressive CNS lesions sustained before 2 years old
  • Results in motor delay, evolving CNS signs, learning disability and epilepsy
42
Q

Classification of CP?

A

1) spastic (90%),
2) dyskinetic (6%)
3) ataxic (4%)

43
Q

Distribution of affected limbs and functional limitation in CP?

A

Distribution pattern of affected limbs: hemiplegic, quadriplegic, diplegic
- Functional limitations: motor function and manual ability affected

44
Q

How common is CP?

A
  • Risk increases with more premature infants

- Occurs in 1 in 500 births

45
Q

Risk factors for CP - antenatally?

A

 Preterm, congenital malformations, multiple births, intrauterine infection, alcohol, smoking

46
Q

Risk factors for CP - perinatally?

A

 Low birth weight, neonatal encephalopathy, sepsis

47
Q

Risk factors for CP - postnatally?

A

 Meningitis, intracranial haemorrhage, trauma, hyperbilirubinemia, hypoxia

48
Q

Aetiology of CP?

A 
•	Antenatal (80%)
	Vascular occlusion, cortical migration disorders, teratogenic, toxins
•	HIE (10%)
•	Postnatal (10%)
	Meningitis, infections, head injury
49
Q

Early features in CP?

A
  • Abnormal limb tone or posture with delayed motor milestones
  • Persistent primitive reflexes
  • Feeding difficulties – oromotor incoordination, slow feeding, gagging
  • Abnormal gait
  • Asymmetrical hand function <12 months
50
Q

Symptoms of spastic CP?

A
  • Damage to upper motor neurone (pyramidal or corticospinal tract) pathway
  • Limb tome increased (spasticity) – dynamic catch hallmark
  • Brisk deep tendon reflexes and extensor plantar responses
  • Leg valgus/varus, hip flexion, often internal rotation, wrist and elbow flexed
51
Q

Types of spastic CP?

A

 Hemiplegia
- Unilateral involvement of arm and leg (arm>leg)
- Often fisting of affected hand, flexed arm, pronated forearm, asymmetric hand preference
- Tiptoe walk
 Quadriplegia
- Most severe form, all four limbs, extensor posturing and poor head control, low central tone
- Associated with microcephaly, intellectual impairment
 Diplegia
- Both legs affected worse than arms, child looks normal until picked up
- Walking/gait is abnormal

52
Q

Symptoms of dyskinetic CP?

A
  • Due to damage to basal ganglia and extrapyramidal
  • Associated with kernicterus, HIE
  • Involuntary, uncontrolled movements often more evident with active movement or stress
  • Muscle tone may be spasticity/hypotonia
53
Q

Describe features of dyskinetic CP?

A

 Chorea- irregular, sudden and brief non-reparative movements
 Athetosis- slow withering movements occurring more distally such as fanning of the fingers
 Dystonia- simultaneous contraction of agonist and antagonist muscles of the trunk and proximal muscles twisted appearance

54
Q

Symptoms of ataxic CP?

A
  • Signs occur on same side of lesion but usually symmetrical
  • Early trunk, limb hypotonia
  • Poor balance, delayed motor development
  • Incoordinate movements, ataxic gait
55
Q

Diagnosis of CP?

A
  • Clinical Diagnosis determined upon symptoms

- MRI imaging

56
Q

General management of CP?

A
  • Complex MDT input with carers

• Live a high QoL and ty for full integration into society

57
Q

Specialist management of CP?

A 
-	Physiotherapy
•	Posture and movement
•	Improve symmetry, joint movement, muscle power
-	Communication
•	 SALT and language therapy
-	Learning support
•	Tailored education programmes
-	Orthopaedic Surgeons
•	Callipers may prevent deformity
58
Q

Medical management of CP?

A

• Botulinum toxin benefits many children with spasticity

59
Q

Complications of CP?

A
  • muscle spasms and contractures
  • Feeding difficulties and nutritional problems
  • Scoliosis, hip dislocation and other orthopaedic problems
  • Epilepsy
60
Q

Define febrile fit?

A
  • Seizure associated with fever in a young child who is otherwise neurologically normal
  • Can occur in infants or small children
61
Q

Typical fit in febrile fit?

A
  • Most last 1/2mins or few secs. Others last >10mins. No previous indications of neuro disease.
62
Q

Which children have higher risk of subsequent epilepsy in febrile fits?

A

lengthy febrile seizures affect only part of the body; recur within 24hrs, or who have neurological abnormalities

63
Q

Categories of febrile fits?

A

o Simple febrile seizures (typical): generalised tonic-clonic, lasting <10mins with associated fever.
o Complex febrile seizures (atypical): occur in up to 15% of cases and characterised by focal seizure activity or prolonged seizure longer than 10 min, or multiple seizures in a day. 4-12% of subsequent epilepsy

64
Q

How common are febrile fits?

A
  • 4% of children between 6 months – 6 years

- Little risk of epilepsy <3%

65
Q

Risk factors for febrile fits?

A
  • ½ have no risk factors
    o A first-degree relative who has had a febrile seizure
    o A relative with epilepsy
66
Q

Cause of febrile fits?

A

o The mechanisms causing febrile seizures are not known
o Infections
 Viral infections, otitis media, and tonsillitis are the most common causes
 Other causes include urinary tract infection, gastroenteritis, lower respiratory tract infection, and post-immunization reactions

67
Q

Symptoms and signs of febrile fits?

A
  • Single generalised tonic-clonic, symmetrical seizure
  • <15 minutes
  • Fever
68
Q

DDx of febrile fits?

A
  • Meningo-encephalitis
  • Epilepsy
  • CNS Lesion
  • Trauma
  • Low glucose, calcium, magnesium
69
Q

Diagnosis of febrile fits?

A
  • Can be clinical diagnosis but think about differentials if atypical
70
Q

Immediate management of febrile fits?

A

o ABCDE
 Protect child from injury, note the time
 When seizure stops, put child in recovery position

71
Q

Management of febrile fits if >5 mins?

A

• Rectal diazepam repeated once after 5 minutes if the seizure has not stopped or one dose of buccal midazolam

72
Q

Management if seizure lasts >10 mins?

A

o If seizure lasts for >10 minutes, treat as status epilepticus
o Measure blood glucose if child cannot be roused

73
Q

When to arrange immediate paediatric hospital assessment in febrile fits?

A

o This is the child’s 1st febrile seizure or if it is a subsequent febrile seizure and the child has not previously been assessed by a paediatrician.
o Uncertainty about the cause of the seizure, atypical symptoms
o The child is less than 18 months of age

74
Q

Education about of febrile fits?

A

o Inform parents that febrile seizures are not the same as epilepsy. The risk of epilepsy developing later is low but slightly higher than the general population. Not harmful to the child. About 1 in 3 children will have another febrile seizure

75
Q

Management of febrile fit - next time at home?

A

 Protect and not restrain them or put anything in their mouth.
 Place them in the recovery position when the seizure stops.
 Seek medical advice if a seizure lasts for less than 5 minutes, or call an ambulance if the seizure continues for more than 5 minutes

76
Q

How to manage fever in future in febrile fits?

A

o Advise parents about managing fever, but explain that reducing fever does not prevent recurrence. Paracetamol/ibuprofen and hydration key

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