Diabetes and Endocrine Flashcards

1
Q

Classification of diabetes

A

Type 1: autoimmune beta cell destruction
Type 2: insulin resistance followed by beta cell failure
Maturity onset diabetes of the young
Medications .e.g. corticosteroids
Pancreatic insufficiency .e.g. cystic fibrosis, thalassaemia
Endocrine disorder .e.g. Cushing
Genetic/chromosomal syndromes .e.g. Downs, Turners
Neonatal: transient and permanent
Gestational diabetes

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2
Q

Presentation diabetes

A
Excessive drinking (polydipsia)
Polyuria
Weight loss
Enuresis
Skin sepsis
Candida and other infections
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3
Q

Presentation DKA

A
Smell of acetone on breath
Vomiting
Dehydration
Abdominal pain
Hyperventilation (Kussmaul breathing)
Hypovolaemic shock
Drowsiness
Coma and death
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4
Q

Aetiology T1DM

A

Molecular mimicary between environmental trigger and antigen on beta-cell surface of pancreas
Possible triggers: enteroviral infections, cow’s milk protein, overnutrition
Autoimmune destruction of the pnacreatic B cells causing insulin deficiency

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5
Q

T1DM associated diseases

A

Hypothyroidism
Addisons disease
Coeliac disease
Rheumatoid arthritis

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6
Q

Markers of beta-cell destruction

A

Antibodies to glutamic acid decaroxylase, islet cells, insulin

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7
Q

Diagnosis T1DM

A
Raised random blood glucose >11.1mmol/L
Glycosuria
Ketosis
Fasting blood glucose >7mmol/L
Raised HbA1c
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8
Q

Features T2DM

A
Severely obese children
Family history
PCOS in females
Acanthosis nigrican: velvety dark skin in armpits or neck
Skin tags
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9
Q

Patient education T1DM

A
Basic pathophysiology
Insulin injection tech and sites
blood glucose monitoring to allow insulin adjustment
Blood ketones when unwell
healthy diet: carb counting
Regular exercise
Insulin sick day and exercise adjustment
Recognition of hypoglycaemia
How to get advice 24/7
psychological impact of life long condition
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10
Q

Insulin

A

All insulin used in children is human
Concentration 100units/ml (U-100)
Types:
-rapid acting insulin analogues .e.g. insulin lispro
-long acting insulin analogues .e.g. levemir, lantus
-short acting soluble human regular insulin
-Intermediate acting
- predermined mixed preparations with 25-30% short acting component

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11
Q

Short acting insulin properties

A
Effect within 30-60m
Peak effect 2-4h
Duration 8h
Given 15-30m before food
E.g. Actrapid, Humulin S
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12
Q

Intermediate acting insulin properties

A

Onset 1-2h
Peak 4-12h
Isophane insulin: insulin and protamine .e.g. insulatard, Humulin I

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13
Q

Insulin injection technique

A

Subcutaneous injection
Anterior and lateral aspect of the thigh, buttocks and abdomen
Rotation of sites
Cx of repeated site use: lipohypertropy, lipoatrophy
Skin gentley pinched and insulin injected at 45’
Long needles/high angle causes painful bruised IM injection
Shallow dermal injections cause scarring

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14
Q

Factors increase blood glucose

A
Insufficient insulin
Food especially carbohydrates
Illness
Menstruation (shortly before onset)
Growth hormone
Corticosteroids
Sex hormones at puberty
Stress
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15
Q

Factors decreasing blood glucose

A
Insulin
Exercise
Alcohol
Some medications
Marked anxiety/excitement
Hot weather
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16
Q

Diet with T1DM

A

Match insulin dose to carbohydrate intake
High complex carbohydrate
Modest fat content <30% calories
High in fibre: sustained release of glucose

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17
Q

Monitoring blood glucose

A

Pre-meal 4-7mmol/L target
Diary of insulin doses and blood glucose
Typically BM taken before breakfast, lunch, dinner, bed
During illness, change in routine >5 tests per day
Blood ketone testing during illness or with poor control
HbA1c shows control over previous 6-12w
-misguiding in reduced rbc lifespan e.g. sickle cell, thalassaemia

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18
Q

Presentation hypoglycaemia

A
Hunger
Tummy ache
Pallor
Irritability/ Unreasonable behaviour
Sweatiness
Feeling faint/dizzy/wobbly
Seizure/coma
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19
Q

Mx Hypoglycaemia

A

Administration of easily absorbed gluycose .e.g. glucose tablets, sugary drink
Oral glucose gels on buccal mucosa
Glucagon injection kit for severe hypo with reduced GCS- IM glucagon

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20
Q

Ix DKA

A

Blood glucose <11.1mmol/L
Blood ketones >3mmol/L
Urea, electrolytes, creatinine (dehydration)
Blood gas analysis (severe metabolic acidosis)
Blood and urine cultures (indicated if infection underlying cause)
Cardiac monitoring: T wave changes in hypokalaemia
Weight (assessing dehydration)
DKA can cause a neutrophilia

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21
Q

Mx DKA

A
Fluids 0.9% saline 10ml/Kg in shock
Gradual correction of dehydration over 24hrs
Insulin infusion
Potassium
Identify underlying cause
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22
Q

Long term Cx T1DM

A
hypertension
coronary heart disease
cerebrovascular disease
retinopathy
nephropathy
neuropathy
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23
Q

Problems with diabetes control

A
Eating too many sugary foods
Infrequent or unreliable blood glucose testing
Illness
Exercise
Eating disorders
Family disruption
Inadequate family motivation
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24
Q

Annual assessment diabetes

A
Normal growth and pubertal development
Blood pressure check for hypertension
Renal disease: screening for microalbuminuria
Circulation: pulse and sensation
Eyes: retinopathy and cataracts
Feet: good foot care
Screening for caeliac (only on presentation), thyroid
Annual flu vaccination
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25
Q

Diabetic changes in puberty

A

Growth hormone, oestrogen and testosterone antagonise insulin action
Increase in insulin requirement during puberty to 2U/Kg/day
Increase marked during morning due to peak growth hormone secretion overnight

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26
Q

Ix Hypoglycaemia

A

Lab blood glucose
Growth hormone, IGF-1, cortisol, insulin, C-peptide, fatty acids, ketones, glycerol, branched-chain amino acids, acylcarnitine profile, lactate, pyruvate
Urine organic acids

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27
Q

Clinical features hypoglycaemia

A

Sweating
Pallor
CNS signs of irritability, headache, seizure, coma

28
Q

Causes hypoglycaemia

A
Excess exogenous insulin
beta cell tumours/disorders
Drug induced .e.g. suphonylurea
Autoimmune
Beckwith syndreom
Galactosaemia
Liver disease
Ketotic hypoglycaemia of childhood
Inborn errors of metabolism
Hormonal deficiency
Leucine sensitivity
Fructose intolerance
Maternal diabetes
Hormonal deficiency
Aspirin/alcohol poisoning
29
Q

Features ketotic hypoglycaemia

A
Young children readily become hypoglycaemic following short periods of starvation
Often thin
Low insulin levels
resolves spontaneously in later life
Prevented by regular glucose intake
30
Q

Features transient neonatal hypoglycaemia

A

Exposure high levels of insulin in utero

31
Q

Features hypoglycaemic hyperinsulinism of infancy

A
Recurrent severe neonatal hypoglycaemia
Rare disorder of infancy
dysregulation of insulin release by islet cells 
Profound nonketotic hypoglycaemia
Localised lesions in the pancreas
32
Q

Mx hypoglycaemic hyperinsulinism

A

High concentration glucose solutions
Diazoxide maintains safe blood glucose
Partial resection/total pancreatectotmy

33
Q

Mx Hypoglycaemia

A

IV infusion of glucose (Max 5ml/Kg 10% glucose bolus)
-Excess volume can cause cerebral oedema
Oral glucose
IM glucagon
Corticosteroids in pituitary or adrenal dysfunction

34
Q

Thyroid Physiology Neonatal Period

A

Small amount of thyroxine transfered from mother
Fetal thyroid produces reverse T3 (inactive T3 derivative)
After burth: surge in TSH, T3 and T4
TSH decline to normal adult levels within weeks
Preterm infants have low T4 for first few weeks, with normal TSH

35
Q

Causes of congenital hypothyroidism

A

Maldescent of thyroid and athyrosis: remains as lingual mass or uniglobular small gland
Dyshormonogenesis: poor synthesis
Iodine deficiency
TSH deficiency: RARE, associated with pituitary dysfunction

36
Q

Clinical features congenital hypothyroidism

A
Usually asymptomatic and identified on screening
Falterning growth
Feeding problems
Prolonged Jaundice
Constipation
Pale, cold, mottled, dry skin
Coarse facies
Large tongue
Hoarse cry
Goitre
Umbilical hernia
Delayed development
37
Q

Clinical features acquired hypothyroid

A
Females
Short stature/poor growth
Cold intolerance
Dry skin
Cool peripheries
Bradycardia
Thin, dry hair
Pale, puffy eyes with loss of eyebrows
Goitre
Slow releasing reflexes
Constipation
Delayed puberty/amenorrhea
Obesity
SUFE
Poor concentration
Deterioration in school work/ learning difficulty
38
Q

Mx congenital hypothyroid

A

Thyroxine started before 2-3w
Lifelong oral replacement of thyroxine
Titration to maintain normal growth

39
Q

Features Autoimmune thyroiditis

A

Associated with Downs and Turners, Addisons, autoimmune diseases (vitiligo, rhuematoid arthritis, diabetes mellitus)
Common in females
Delayed bone age
Goitre present (may be physiological in pubertal girls)

40
Q

Clinical features hyperthyroid

A
Anxiety, restlessness
Increased appetite
Sweating
Diarrhoea
Weight loss
Rapid growth in height
Advanced bone maturity
Tremor
Tachycardia, wide pulse pressure
Warm, vasodilated peripheries
Goitre (bruit)
Learning difficulty and behavioural problems
Eyes: exopthalmos, oipthalmoplegia, lid retraction, lid lag
41
Q

Mx hyperthyroid

A

Carbimazole/propythiouracil: interefer with thyroid hormone synthesis
-risk neutropenia
Beta blockers: symptomatic for anxiety, tremor and tachycardia
Medicine continues for 2y to control thyrotioxicosis
-40-75% relapse
Permanent remission: radioiodine treatment or subtotal thyroidectomy

42
Q

Causes of congenital pituitary disorders

A

Structural .e.g. midline defects

Pituitary hypoplasia or aplasia

43
Q

Causes of acquired pituitary disorders

A
Brain tumour affecting hypothalamus or pituitary
Cranial irradiation
Trauma 
Infection
Infiltration .e.g. histiocytosis
Structural
44
Q

Associated disorders hypoparathyroid

A

DiGeorge
Autoimmune disorders
Addisons Disease

45
Q

Features of DiGeorge

A

Thymic aplasia
Defective immunity
Cardiac defects
Facial abnormality

46
Q

Features pseudohypoparathyroidism

A

End-organ resistance to parathyroid hormone

PTH normal, serum Ca and PO4 abnormal

47
Q

Associated abnormality pseudohypoparathyroidism

A
Short stature
Obesity
Subcutaneous nodules
short 4th metacarpals
learning difficulty
teeth enamel hypoplasia
calcification of basal ganglia
48
Q

Features pseudopseudohypoparathyroidism

A

Abnormality associated with pseudohypoparathyroidism

Normal calcium, phosphate and PTH

49
Q

Mx hypocalcaemia

A

IV calcium gluconate 10% diluted
Oral calcium and vitamin D anaolgues
Monitoring urine calcium excretion

50
Q

Hyperparathyroidism features

A
High calcium
Constipation
Anorexia
Lethargy
Behavioural effects
Polyuria
Polydipsia
Bony erosions of phalanges
51
Q

Associated conditions hyperparathyroidism

A

Williams syndrome
Adenomas
Multiple endocrine neoplasia syndrome

52
Q

Mx hypercalcaemia

A

Rehydration
Diuretics
Bisphosphonates

53
Q

Features congenital adrenal hyperplasia

A
Virilisation of external genitalia in females
-clitoral hypertrophy
-fusion of labia
In males:
-penis enlargment
-pigmentation of scrotum
Salt losing adrenal crisis
Tall stature and precocious puberty
54
Q

Features salt-losing adrenal crisis

A
80% of males
1-3w old
Vomiting
Weight loss
Hypotonia
Circulatory collapse
55
Q

Pathology congenital adrenal hyperplasia

A

Insufficient cortisol and mineralcorticoid secretion
21-hydroxylase deficiency
All products make excessive quantities of testosterone in absence of other pathways
Psotive feedback increases cholesterol synthesis

56
Q

Dx congenital adrenal hyperplasia

A
Raised levels of metabolic precursor 17a-hydroxy-progesterone in blood
In salt losers:
-Low plasma sodium
-High plasma potassium
-Metabolic acidosis
-Hypoglycaemia
57
Q

Mx congenital adrenal hyperplasia

A

Corrective surgery to external genitalia within 1y
-possibly delay until after puberty for cliteral hypertrophy
Salt losing crisis: NaCl, glucose, hydrocortisone IV
Lifelong glucocorticoids to suppress ACTH
Monitoring of growth, skeletal maturity, plasma androgens
Mineralcorticoids in salt loss with slow weaning
Additional hormone replacement in illness or surgery

58
Q

Cx hormone replacement congenital adrenal hyperplasia

A

insufficient: rapid initial growth, skeletal maturation, detrimental to final height
Excessive: skeletal delay, slow growth

59
Q

Causes Addisons

A
Autoimmune process
Haemorrhage/infection
X linked adrenoleucodystrophy (rare)
TB
secondry to pituitary dysfunction/corticosteroid therapy
60
Q

Features of adrenal insufficiency

A
Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Dehydration
Hypotension
Growth failure
Circulatory collapse
Vomiting
Lethargy
Brown pigmentation: gums, scars, skin creases
61
Q

Dx Adrenal insufficiency

A

Hyponatreamia with hyperkalaemia with metabolic acidosis and hypoglycaemia
Low plasma cortisol and high ACTH
Synacthen test: cortisol remains low

62
Q

Mx Adrenal insuffiency

A

Adrenal crisis: IV saline, glucose, hydrocortisone
Glucocorticoid and mineralcorticoid replacement
Increase (x3) dose of glucocorticoid during illness/surgery
Parental education IM hydrocortison injection

63
Q

Features Cushing Syndrome

A
Growth failure/short stature
Face and trunk obesity
Red cheeks
Hirsutism
Striae
Hypertension
Bruising
Carbohydrate intolerance
Muscle wasting and weakness
Osteopenia
Psychological problems
64
Q

Causes of cushings

A

Usually S/E long term glucocorticoids
-reduced by morning meds on alternate days
Pituitary adenoma
Ectopic ACTH producing tumours
Adrenocorticoid tumours (occurs with virilisation)

65
Q

Ix Cushing Syndrome

A

Loss of normal cortisol diurnal variation
High midnight conc
High 24hr urine free cortisol
Failure to suppress 9am cortisol after night time dexamethaone
MRI brain and abdomen (tumour)

66
Q

Causes Disorders of sex development

A

Congenital adrenal hyperplasia: excessive androgens causing virilisation of female
Androgen insensitivity syndrome
5a-reducatase deficieny: poor conversion to testosterone
Prada-will: gonadotrophin insufficiency
Ovotesticular DSD: XX ad XY cells present allows development of both tissues