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Phase 3a > Paeds - Endocrine > Flashcards

Paeds - Endocrine Flashcards

1
Q

Early onset Type 2 diabetes

A

< 40 y/o

Has more complications

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2
Q

MODY

A

Typically affects every generation (single gene autosomal dominant)

Doesn’t necessarily need insulin

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3
Q

Diagnosis of T1DM

A

Point of care FINGER PRICK test if suspect
- if indicative -> SAME DAY REFERAL

Don’t wait for OGTT or HbA1c - kids can decompensate very fast and typically tend to present acutely

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4
Q

T2DM RFx in kids

A
  • FEMALE
  • Non-white ethnicity
  • Obesity
  • Deprivation
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5
Q

T2DM presentation in kids

A

More insidious

Many have acanthosis nigricans (outward sign of insulin resistance)

can present with DKA

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6
Q

T2DM Dx

A

Usually OGTT
- HbA1c

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7
Q

T2DM common comorb

A

HTN
Kidney disease
OBESITY

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8
Q

Insulin management in T1DM

A
  • Commence on 0.5-0.8 Units/kg/day
  • 50% long acting; 50% rapid acting for meals (10% breakfast, 20% lunch, 20% tea)
  • Pen therapy usually initial
  • pump therapy if indicated /appropriate
  • Fixed doses to start with and then carb counted meals with a set insulin:carbohydrate ratio (ICR)
  • Insulin sensitivity factor for correction doses (ISF), based on total daily dose of insulin and 100 rule
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9
Q

How much should blood glucose be tested + which other times

A

At least 5 times a day

pre-meals, pre bedtime, exercise, feeling unwell and post-prandial

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10
Q

Diff ways to test blood glucose

A
  • Finger prick test
  • Continuous Glucose Monitoring System
  • Flash Glucose Monitoring System
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11
Q

Advantages of finger prick test

A

accurate + no time lag

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12
Q

Advantages of Flash Glucose Monitoring System

A

Glucose trends, alarms for highs and lows, ‘follow’ facility for carers and teachers, can communicate with pump delivery systems, less trauma to fingers

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13
Q

DKA severity

A
  • MILD – pH < 7.3 or plasma bicarbonate <15 mmol/l
  • MODERATE – pH <7.2 or plasma bicarbonate < 10 mmol/l
  • SEVERE – pH < 7.1 or plasma bicarbonate < 5 mmol/l

One to one nursing or HDU if under 2 years or severe DKA

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14
Q

DKA Mx

A
  • FLuids
  • Insluin
  • Hourly glucose monitoring
  • 2-4 hourly Electrolytes (K+ and ketones)
  • Hourly strict fluid balance
  • Hourly neuro obs
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15
Q

Complications of DKA

A

Cerebral oedema
shock
hypokaelaemia
aspiration
thrombus (viscous)

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16
Q

Calculating total fluid requirement

A
  • If clinically dehydrated but not in shock: give IV 10ml/kg saline over 30 mins
    • SUBTRACT this bolus from total fluid deficit
  • If shocked give 20 ml/kg
    - DON’T SUBTRACT from fluid deficit
17
Q

T2DM Tx

A

DIET + LIFESTYLE (10% weight loss in pre-pubertal child can reverse diabetes)

Metformin +/- insulin

Consider GLP-1 agonists:
- Liraglutide >10 years
- Semaglutide >18 years

18
Q

Glucose targets for T2DM

A

Pre-meal: 4-7 mmol/l
Pre-bedtime: 5-8
Post-prandial: <10
Average: <7

HbA1c <48 mmol/mol

19
Q

Calculating how much insulin to give

A
  • 1 unit per 15g of carbs
  • 1 unit brings blood glucose down by 8 (correction factor)
20
Q

Options for insulin therapy

A
  • MDI
  • Simple insulin pump
  • Hybrid closed loop (pump + continuous glucose monitor)
    • automatically suspends if going hypo
  • Closed loop (artificial pancreas)
21
Q

Complications of DM (further than the usual)

A
  • Lipohypertrophy
  • Diabetes burnout
  • Biabulimia
  • Self harm with insulin
  • High carb loads + insulin therapy -> insulin resitance + high BMI
  • increase prevelance of overweight + obesity
22
Q

Hypo management

A

Mild/management:

  • glucose tablets, gells, or very fast acting food/drink e.g. lucozade
  • only take prescribed dose
  • Check glucose in 15 mins
  • Follow up with long acting carbs

Severe:

Glucose injection (IM)

23
Q

Neonatal diabetes

A

Rare. If transient, oft reoccurs later in life

Very sensitive to insulin
Frequent small milk feeds

Practical problems of testing and injections
Risks of hypoglycaemia vs risk of longstanding diabetes

24
Q

Difficulties of DM in toddlers

A
  • Food – tend to graze, small meals little and often
  • Behavioural issues – eating, injections, tests
  • Hypos – may be difficut to recognise
  • Hypos may affect neurodevelopment
25
Q

Challenges of DM Tx in kids

A
  • Food – making own choices, school dinners
  • Effect of exercise – PE, playground, after school activity, clubs, and team sport
  • Behaviour and compliance
  • Sleepovers
  • School residentials and trips
26
Q

Challenges of glycaemic control in adolescence

A

Poorest glycaemic control due to non-compliacne + risk-taking behaviour

weight manipulation
sex / drugs / alcohol

Insulin resistance

27
Q

Diabetes care package

A
  • Admit + therapy + education
  • Home + school visits
  • Remote reviews via cloud
  • 3 monthly outpatient appointment
  • Annual review; more frequent if needed
    • coeliac and thyroid screening, injection sites for all. From 12 years, bp, ACR, lipids, retinopathy, psychological screening, dietetic review, foot examination
  • age appropriate education
  • admit to stabalise as required
28
Q

Congenital adrenal hyperplasia

A

Congenital deficiency of 21-hydroxylase enzyme -> underproduction of cortisol + aldosterone and OVERPRODUCTION OF ANDROGENS from birth

  • AUTOSOMAL RECESSIVE INHERITANCE

(sometimes caused by 11-beta-hydroxylase def)

29
Q

Congenital adrenal hyperplasia pathophys

A
  • 21-hydroxylase converts Progesterone into Aldosterone + Cortisol
    - Progesterone can convert to testosterone WITHOUT 21-hydroylase
  • When 21-hydroxylase is defective -> Progesterone can’t be converted so:
    - LOW aldoseterone + cortisol
    - High excess progesterone which converts to EXCESS TESTOSTERONE
30
Q

Congenital adrenal hyperplasia Px

A

Severe - present from birth:

  • Virilised ‘ambigous’ genetalia + enlarged clitoris
  • Hyponatraemic hypokalaemia
    + Hypoglycaemia     (because of low aldosterone + cortisol)
    - Poor feeding
    - Vomiting
    - Dehydration
    - Arrhythmias

Mild - present in childhood/puberty:

  • Female:
    • Tall for age
    • Facial hair
    • Absent periods
    • Deep voice
    • Early puberty
  • Male:
    • Tall for age; Deep voice
    • Early puberty
    • Large penis; small testicles

Can also get skin hyperpigmentation due to increased melanocyte stimulating hormone due to increased ACTH production to compensate for low cortisol

31
Q

Congenital adrenal hyperplasia Mx

A

Specialist endocrinologists + monitor growth/development

  • Cortisol replacement
    • HYDROCORTISONE
  • Aldosterone replacement
    • FLUDROCORTISONE
  • female patients with virilised genitalia may require corrective surgery
32
Q

Androgen insenitivity

A

46 XY - X-LINKED RECESSIVE with normal chromosomal number

33
Q

Androgen insenitivity pathophys

A
  • Defect in ANDROGEN RECEPTOR
  • END-ORGAN RESISTANCE to testosterone
  • Male genotype but female phenotype
34
Q

Androgen insensitivity Px

A

Range from complete to mild (female genetalia - normal male genitalia)

  • Undermasculinization of external genitalia at birth
  • Presence of rudimentary vagina / testes
  • Elevated testosterone, oestrogen + LH on testing

Impaired virilization at puberty

  • may have some FHx
    Can also get some reduced virilization during puberty in genotypical females (carriers?)
35
Q

Androgen insensitivity Mx

A
  • Sex correction as newborn
  • Oft gonadectomy after puberty if complete / mostly female phenotype
  • Survaillence for complications (osteoporosis, gynacomastia)
    • sometimes genetalia may develop differently post-nataly
  • Genetic counselling / genetic testing
  • Consider gender counselling / INFORM child at some point in a controlled environment
36
Q
A

Phase 3a (26 decks)

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