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Paediatrics (Y4) > 9- Paediatric Endocrinology 1/2) > Flashcards

9- Paediatric Endocrinology 1/2) Flashcards

1
Q

normal blood glucose

A

Ideal blood glucose : 4.4 and 6.1 mmol/l

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2
Q

T1DM background

A
  • Pancreas doesn’t produce enough insulin
  • Lack of insulin causes high blood glucose
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3
Q

Pathophysiology T1DM

A
  • Insulin is produced by beta cells in the islets of Langerhans in the pancreas
  • Insulin reduces blood sugar in two ways
    1) Allows cells to absorb glucose to use as fuel
    2) Causes muscle and liver cells to absorb glucose and convert it glycogen for storage
  • Ketogenesis occurs when there is insufficient glucose and glycogen stores are exhausted e.g. prolonged fasting
    1) Involves converting fatty acids into ketones
    2) Ketones can be used as fuel (characteristic acetone breath)
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4
Q

Risk factors T1DM

A
  • Genetic
  • Viral triggers e.g. coxsackie and enterovirus
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5
Q

presentation of T1DM

A
  • In Diabetic ketoacidosis
  • Triad of symptoms of hyperglycaemia
    o Polyuria
    o Polydipsia
    o Weight loss
  • Recurrent infections
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6
Q

investigations for T1DM

A
  • Baseline bloods including FBC, renal profile (U&E) and a formal laboratory glucose
  • Blood cultures should be performed in patients with suspected infection (i.e. with fever)
  • HbA1c can be used to get a picture of the blood sugar over the previous 3 months. This gives an idea of how long they have been diabetic prior to presenting.
  • Thyroid function tests and thyroid peroxidase antibodies (TPO) to test for associated autoimmune thyroid disease
  • Tissue transglutaminase (anti-TTG) antibodies for associated coeliac disease
  • Insulin antibodies, anti-GAD antibodies and islet cell antibodies to test for antibodies associated with destruction of the pancreas and the development of type 1 diabetes
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7
Q

diagnostic criteria for T1DM

A

Normal range- 3.3- 7 mmol/l

  • Symptoms (polyuria, polydipsia, fatigue) retinopathy, neuropathy etc) plus one abnormal result or
  • Two abnormal results at different times (at least week)
  • Glucose levels
    o Fasting >7.0 mmol/l and/or
    o 2 hours after 75g glucose >11.1 mmol/l
    o Hba1c >6.5%
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8
Q

fasting blood glucose above

A

> 7.0 mmol/l suggests diabetes mellitus

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9
Q

oral glucose tolerance test

A

2h after 75g of glucose >11.1 mmol

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10
Q

Hba1C above

A

> 6.5% or 48mmol

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11
Q

management of T1DM

A
  • Education
    o Exercise
    o Diet
    o Carbohydrate and Glucose monitoring with BM
  • Subcutaneous insulin regimes
  • Monitoring and management of both short and long term complications
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12
Q

short term complications

A
  • hypoglycaemia
  • nocturnal hypoglycaemia
  • hyperglycaemia and DKA
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13
Q

hypoglycaemia

A

Presentation: hunger, tremor, sweating, irritability, dizziness and pallor
- Severe: unconsciousness, coma and death

Management
- Rapid acting glucose e.g. Lucozade and slower acting carbs e.g. biscuits
- If severe: IV dextrose and IM glucagon

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14
Q

nocturnal hypoglycaemia

A
  • Presentation: sweaty at night
  • Management: altering bolus insulin regimes
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15
Q

Hyperglycaemia and DKA

A
  • Management of hyperglycaemia: will need insulin dose increased
  • Management of DKA: inpatient management (see later)
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16
Q

long term complications of T1DM

A

Damage to endothelial cells of blood vessels and suppression of the immune system.
- macrovascular
- microvascular
- ingection related complications

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17
Q

macrovascular complications

A

o CAD
o Peripheral ischaemia e.g. diabetic foot
o Stroke
o Hypertension

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18
Q

microvascular complications

A

o Peripheral neuropathy
o Retinopathy
o Nephropathy e.g. glomerulosclerosis

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19
Q

Infection related complications

A

UTI, pneumonia, skin and soft tissue infections, candidiasis

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20
Q

normal insulin prescription in children invovles

A
  • Long acting given once a day
  • Short acting given 30 mins before meals
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21
Q

Basal bolus regimes

A

1) Basal: long acting insulin e.g. Lantus
- Typically given in evening

2) Bolus: short acting e.g. Actrapid
- 3 times a day before meals or when carbohydrates consumed

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22
Q

what are replacing basal bolus regimes in children

A

insulin pumps

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23
Q

insulin pumps

A

Devices which continuously infuse insulin at different rates to control blood sugar

Procedure: pump with cannula inserted in skin which pushes insulin under the skin. Cannula replaced every 2-3 days and insertion site rotates
- Child >12

Advantages
- Better glucose control

Disadvantages
- Difficulties learning to use
- Having it attached at all times
- Infection

2 types
o Tethered
o Patch

24
Q

complications of insulin

A

Lipodystrophy
- Patients should rotate site of injection
- Tissues can harden and prevents normal absorption of insulin

Hypoglycaemia

25
Q

monitoring blood glucose in T1DM involves

A

HbA1C
capillary blood glcuose
flash glucose monitoring e.g. FreeStyle libre

26
Q

HbA1c

A
  • Measures glycated haemoglobin
  • Reflects average BG over past 3 months since they have a lifespan of 120 (3 months) days
  • Measured every 3-6 months to track
27
Q

Capillary blood glucose

A

o Measured using glucose meter
o Immediate result
o Used to self-test before insulin admin

28
Q

Flash glucose monitoring e.g. FreeStyle Libre

A
  • Sensor on the skin which measures glucose in interstitial fluid and subcut tissue
  • 5 min lag behind blood glucose (still require FGM), but measures at intervals to give a good impression of what glucose is doing over time
  • Reader and sensor system (sensor replaced every 2) weeks
  • Expensive
29
Q

Diabetic ketoacidosis

A

Background
A life threatening, medical emergency. It is the most common way that children with a new diagnosis of type 1 diabetes present.

30
Q

Pathophysiology

A
  • T1DM- not enough insulin and therefore cant use glucose
  • Ketoacidosis, dehydration and potassium imbalance is what kills patients
31
Q

Ketoacidosis

A
  • Due to starvation picture, ketones produced by the liver to use as fuel
  • Overtime glucose and ketones rise
  • Ketones are acidic, therefore the kidneys produce bicarbonate to buffer the ketone acids in the blood and maintain normal pH
  • Overtime ketone acids use up bicarbonate and blood becomes acidic
32
Q

Dehydration

A
  • Hyperglycaemia overwhelms kidneys and glucose starts being filtered into the urine
  • Glucose in urine draw water out due to osmotic diuresis – polyuria – severe hydration - polydipsia
33
Q

potassium imbalance

A
  • Insulin drives potassium into cells
  • Without insulin potassium is not stored in cells
  • Causes high potassium, however this is then excreted in the urine – meaning total body potassium is low due to no storage
  • When insulin is started- > hypokalaemia -> arrhythmia
34
Q

Presentation of DKA

A
  • Polyuria
  • Polydipsia
  • Nausea and vomiting
  • Weight loss
  • Acetone smell to their breath
  • Dehydration and subsequent hypotension
  • Altered consciousness
  • Symptoms of an underlying trigger (i.e. sepsis)
35
Q

Investigations for DKA

A
  • Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
  • Ketosis (i.e. blood ketones > 3 mmol/l)
  • Acidosis (i.e. pH < 7.3)
36
Q

ketogenesis

A

normally occurs when there is an insufficient supply of glucose and glycogens stores are exhausted.
- This may happen during prolonged fasting or very low carbohydrate diets

37
Q

process of ketogenesis

A

The liver takes fatty acids and converts them to ketones.

  • Ketones are water soluble fatty acids that can be used as fuel.
  • They can cross the blood brain barrier and be used by the brain.
  • Producing ketones is normal and not harmful in healthy patients when under fasting conditions or on a very low carbohydrate, high fat diet.
  • Ketone levels can be measured in the urine using a urine dipstick and in the blood using a ketone meter.
  • People in ketosis have a characteristic acetone smell to their breath.
38
Q

why does ketogenesis cause metabolic acidosis in DKA

A
  • Ketone acids (ketones) are buffered in normal patients so the blood does not become acidotic. When underlying pathology (i.e. type 1 diabetes) causes extreme hyperglycaemic ketosis, this results in a metabolic acidosis that is life threatening. This is called diabetic ketoacidosis.
39
Q

Management of DKA

A
  1. Correct dehydration evenly over 48 hours. This will correct the dehydration and dilute the hyperglycaemia and the ketones. Correcting it faster increases the risk of cerebral oedema.
  2. Give a fixed rate insulin infusion This allows cells to start using glucose again. This in turn switches off the production of ketones.

Other important principles:

  • Avoid fluid boluses to minimise the risk of cerebral oedema, unless required for resuscitation.
  • Treat underlying triggers, for example with antibiotics for septic patients.
  • Prevent hypoglycaemia with IV dextrose once blood glucose falls below 14mmol/l.
  • Add potassium to IV fluids and monitor serum potassium closely.
  • Monitor for signs of cerebral oedema.
  • Monitor glucose, ketones and pH to assess their progress and determine when to switch to subcutaneous insulin.
40
Q

why can cerebral oedema occur when treatment DKA

A

o Dehydration and high blood sugar concentration cause water to move from the intracellular space in the brain to the extracellular space.
o This causes the brain cells to shrink and become dehydrated.
o Rapid correction of dehydration and hyperglycaemia (with fluids and insulin) causes a rapid shift in water from the extracellular space to the intracellular space in the brain cells.
o This causes the brain to swell and become oedematous, which can lead to brain cell destruction and death.

41
Q

cerebral oedema management

A

- Neurological observations (i.e. GCS) should be monitored very closely (e.g. hourly) to look for signs of cerebral oedema. Be concerned when patients being treated for diabetic ketoacidosis develop headaches, altered behaviour, bradycardia or changes to consciousness.

Management options for cerebral oedema are
- slowing IV fluids
- IV mannitol
- IV hypertonic saline.

42
Q

Type 2 diabetes mellitus background

A

T2DM is a multifactorial and heterogeneous condition in which the balance between insulin sensitivity and insulin secretion is impaired. The condition is characterized by hyperinsulinemia; however, there is relative insulin insufficiency to overcome underlying concomitant tissue insulin resistance.
- Increasing incidence in developed countries
- Parallels upward trend in childhood obesity
- In US 45% of new diabetes cases in children are T2DM

43
Q

pathophysiology of T2DM

A

Not autoimmune
- No association with HLA-linked genes

RF
- Obesity
- Family history of T2DM
- Ethnic origin
 Asian
 African-American
 Afro-Caribbean
 Pacific islander
- PCOS
- Small for gestational age

44
Q

presentation of T2DM

A
  • Hyperglycaemia
  • Typical manifestation of insulin deficiency e.g.
    o Polydipsia
    o Polyuria
  • Presentations of DKA may occasionally be seen
45
Q

investigations for T2DM

A
  • presence of T2DM risk factors
  • lack of absolute/persistent insulin deficiency;
  • absence of pancreatic autoantibodies.
46
Q

first line management of T2DM

A
  • Educational support
    o diet
    o exercise
  • Manage obesity and comorbiditiesa
  • Screening and management of T2DM comorbidities such as hyperlipidaemia and hypertension
47
Q

second line management of t2DM

A

when lfiestyle interventions have failed
METFORMIN (like adults)

MOA- works by decreasing glucoseneogenesis and increasing sensivity to insulin

48
Q

third line management of T2DM

A

Insulin therapy

49
Q

Diabetes insipidus
Background

A

Posterior pituitary gland secretes two hormones
1) Oxytocin
2) Antidiuretic hormone (ADH)

DI caused by deficiency in ADH (cranial) or resistance to its actions in the kidney (nephrogenic)
- Cranial more common
- Can be acquired or inherited

50
Q

Pathophysiology Cranial DI

A

Damage to hypothalamus or pit gland
- Brain injury e.g. tumour, surgery, infection
- Genetic causes e.g. neurohypophysis diabetes insipidus

51
Q

pathophysiology nephrogenic DI

A
  • Kidney failure
  • Sickle cell
  • Polycystic kidney disease
  • Lithium
  • Genetic causes
52
Q

RF DI

A
  • Brain tumour
  • Head injury
53
Q

presentation of DI

A
  • Large volumes of dilute urine (<300mOsm/L)- polyuria
  • Polydipsia
  • Nocturia
  • Colourless urine
  • Weak muscles
  • Hypernatremia
  • Dehydration
  • Death
  • Infant specific (hereditary)
    o Failure to thrive
    o Fever
    o Constipation
54
Q

Investigations for DI

A
  • 24 hour urinary volume and osmolality
    o >3l
    o High serum osmolality (>300 mOsm) and
    low urine osmolality (<300 mOsm)
  • DM and renal failure should also be excluded
  • Water deprivation test
55
Q

water deprivation test

A

A water deprivation test involves not drinking any liquid for several hours to see how your body responds. If you have diabetes insipidus, you’ll continue to pee large amounts of dilute urine when normally you’d only pee a small amount of concentrated urine
* high plasma osmolality, low urine osmolality
* a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
* water deprivation test
* cranial: urine osmolality will increase after desmopressin
* nephrogenic: urine osmolality will not change

56
Q

management of cranial DI

A
  • Synthetic analogues of ADH- desmopressin (intranasal or oral)
  • Dose titrated to patient
  • Patient education about hazards of excessive water intake
57
Q

managment of nephrogenic DI

A
  • Underlying cause should be reversed, if symptoms persist patient should drink according to thirst and keep with water loss
  • Low salt, low protein diet, thiazide diuretics and NSAIDS

Paediatrics (Y4) (42 decks)

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