Someone recently bought our

students are currently browsing our notes.

X

Endocrine And Growth Notes

Medicine Notes > Paediatrics Notes

This is an extract of our Endocrine And Growth document, which we sell as part of our Paediatrics Notes collection written by the top tier of University Of Nottingham students.

The following is a more accessble plain text extract of the PDF sample above, taken from our Paediatrics Notes. Due to the challenges of extracting text from PDFs, it will have odd formatting:

Endocrine / Growth

Diabetes Mellitus

*

2 per 1000 by age 16

*

More common in Northern countries

*

Almost all children have type 1 requiring insulin from the onset

*

Type 2 is starting to occur due to obesity

Type 1 Diabetes Aetiology

*

Genetic predisposition and environmental precipitants

*

Inherited susceptibility demonstrated by:

*

o

Identical twin of a diabetic has a 3040% chance of developing disease

o

If a parent has IDDM the risk is increased from 1 in 4001 in 2040 if the father1 in 4080 if the mother is affected

o

HLADR3 or DR4 result in increased risk

o

DR2 and DR5 reduce risk

Molecular mimicry probably occurs between an environmental trigger and an antigen on the surface of the B cells of the pancreas autoimmune damage of the pancreas

*

Triggers include enteroviral infection (presents commonly in spring and autumn), diet including Cow's milk proteins

*

Markers of B cell destruction include:

o

Islet cell antibodies (ICA)

o

Antibodies Vs. Glutamic acid decarboxylase (GAD), the islet cells and insulin (IAA)

Clinical Features

*

*

Classic Triad occurs over weeks

o

Polydipsia

o

Polyuria

o

Weight loss

Less commonly

o

Enuresis (secondary)

o

Skin sepsis

o

Candida and other infections

*

Late Presentation - DKA

o

Hyperventilation due to acidosis (Kussmaul breathing)

o

Smell of acetone on breath

o

Vomiting

o

Dehydration

o

Abdominal pain

o

Hypovolaemic shock

o

Drowsiness, coma, death

Diagnosis

*

Usually confirmed in a symptomatic child by:

o

A raised random blood glucose (>11.1 mmol/L)

o

Glycosuria

o

Ketonuria

*

If any doubt fasting blood glucose (>7 mmol/L)

*

OR a raised glycosylated haemoglobin (HbA1c) is useful

*

ICA, GAD, IAA

*

TFT, Coeliac screen

Initial Management of Type 1 Diabetes

*

*

Diet

o

High complex carbohydrate (5060% of intake)

o

Reduce refined carbohydrate

o

Fat should be <30% of total calories

Insulin

o

All types have a 100 U/ml concentration

o

Types include:Human insulin analogues long or short actingShort acting soluble human regular insulin give 1530 minutes before meals, onset within 1 hour, peak 24 hours, duration up to 8 hoursIntermediate acting insuling onset 12 h, peak 412 hCan mix intermediate and short

o

Most children are started on an insulin pump or a 34 time daily injection regimen (basal bolus) with short acting insulin being given before each meal and snack. Plus long acting before breakfast and/or in the late evening

o

Shortly after presentation, when some pancreatic function is preserved, insulin requirements often become minimal - 'honeymoon period'

o

Normal requirements are 0.51 U/kg*

Increase during puberty due to hormones which antagonise insulin (2 U/kg/day)

Blood Glucose Monitoring

o

Aim is to maintain 46 mmo/L

o

In practice, in order to avoid hypoglycaemic episodes this means;

o410 in children48 in adolescents

Bloopd ketone testing is mandatory during infections (when insulin requirement increases) or when control is poor to avoid severe ketoacidosis

o

Glycosylated Hb is used as a guide to overall control over a period of 612 weeksCheck 3 times per yearMay be misleading if RBC lifespan is reduced (sickle cell) or if the HbA molecule is abnormal (thalassaemia)Level of <7.5% (58 mmol/mol)

Complications Hypoglycaemia

*

When blood glucose falls below about 4 mmol/L symptoms may develop

*

Symptoms include:

o

Hunger

o

Tummy ache

o

Sweatiness

o

Feeling faint or dizzy

o

Pallor

o

Irritability

*

May progress to seizures and coma if untreated or in hypoglycaemia unawareness

*

Treatment

o

Administration of easily absorbed glucose n the form of tablets or a non diet sugary drink

o

Glucagon injection kit for severe hypo

Diabetic Ketoacidosis

*

Decrease in insulin associated with an increase in counterregulatory hormones (glucagon, catecholamines, cortisol, GH)

*

Leads to increased glucose production by the liver and impaired peripheral glucose utilisation hyperglycaemia

*

Increased lipolysis results in production of ketones and metabolic acidosis

*

Clinically

*

*

o

Smell of acetone

o

Vomiting

o

Dehydration

o

Abdominal pain

o

Hyperventilation due to acidosis (Kussmaul breathing)

o

Hypovolaemic shock

o

Drowsiness, Coma and death

Early Investigations

o

Blood glucose (>11.1 mmol/L)

o

Blood ketones (>3.0 mmol/L)

o

Urea and electrolytes, creatinine (dehydration)

o

Blood gas analysis (metabolic acidosis)

o

Urinary glucose and ketones (+'ve)

o

Precipitating cause? blood and urine culture

o

Cardiac monitor for T wave changes of hypokalaemia

o

Weight

Management if newly presenting only subcut insulin is reuired. If altered consciousness or child has vomited follow the below regimen

o

o

o

FluidsIf in shock - resusciation with normal salineDehydration corrected over 48 hours, rapid rehydration results in cerebral oedemaMonitor input and output, U&E, creatinine and acid base balance

InsulinInfusion 0.51 U/kg/hrDo NOT give bolusAim for gradual reduction of about 2mmol/h

PotassiumMay be high but will fall with fluids and insulin

oReplace as soon as urine is passedContinuous cardiac monitoring and plasma K measurements

AcidosisShould self correct, avoid bicarbonate unless shocked and not respondingMonitor plasma ketones

o

Reestablish oral fluids, subcut insulin and diet

o

Identify and treat underlying causeDKA causes neutrophilia BUT NOT fever

Long Term

*

Delay in puberty

*

BP - checked once a year

*

Renal disease - microalbuminuria is an early sign of nephropathy (yearly screen from 12 years old)

*

Eyes - retinopathy or cataracts. Monitor after 5 years of diabetes

*

Feet - neuropathy

*

Other associated illness

o

Coeliac screen at diagnosis and screen tissue transglutaminase after 3 years

o

Thyroid disease at diagnosis and yearly

o

Autoimmune - rheumatoid, vitiligo

Hypoglycaemia

*

Common in neonates, thereafter uncommon in nondiabetics

*

Plasma glucose <2.6 mmol/L

*

Clinical Features

*

*

o

Sweating

o

Pallor

o

CNS signs of irritability, headache, seizures and coma

Sequelae, if hypoglycaemia persists include:

o

Epilepsy

o

Learning difficulty

o

Microcephaly

Infants have high energy requirements and relatiely poor reserves of glucose from gluconeogenesis and glycogenesis at risk of hypoglycaemia from fasting, feed every 4 hours

*

Check blood glucose in any child who:

o

Becomes septicaemic of appears seriously ill*

ABC DEFG (don't evenr forget glucose)

o

Prolonged seizure

o

Develops and altered state of consciousness

Investigations

o

If glucose strips show hypoglycaemia confirm wih lab blood glucose

o

Growth hormone, IGF1, cortisol, insulin, C peptite, fatty acids, ketones, glycerol, branched chain amino acids, acylcarnitine profile, lactate pyruvate

o

First urine after hypoglycaemiaOrganic acidsConsider saving blood and urine for toxicology

*

Causes Beyond the Immediate Neonatal Period Include:

*

Fasting

o

Insulin excessExcess exogenous insulin - DM/insulin given surreptitiouslyB cell tumors/disorders - persistent hypoglycaemia hyperinsulinism of infancy (PHHI/nesidioblastosis) or insulinoma

o

oDrug induced (sulphonylurea)Autoimmune (insulin receptor antibodies)Beckwith syndrome

Without hyperinsulinaemiaLiver diseaseKetotic hypoglycaemia of childhood

Inborn errors of metabolism (glycogen storage disorders Specfic enzyme defects, which prevent mobilisation of glucose from glycogen. Abnormal storage of glycogen in lover or muscle)

o

*

Hormone deficiency; GH, ACTH, Addison disease, CAH

Reactive/Non Fasting

o

Galactosaemia Deficieny of the enzyme galactose1phosphate urindyltransferase (essential for galactose metabolism)

o

Leucine sensitivity

o

Fructose intolerance

o

Maternal diabetes

o

Hormonal deficiency

Buy the full version of these notes or essay plans and more in our Paediatrics Notes.