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Diabetes and Endocrine Flashcards

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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
Diabetic changes in puberty
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
26
Ix Hypoglycaemia
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
27
Clinical features hypoglycaemia
Sweating Pallor CNS signs of irritability, headache, seizure, coma
28
Causes hypoglycaemia
``` 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
Features ketotic hypoglycaemia
``` 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
Features transient neonatal hypoglycaemia
Exposure high levels of insulin in utero
31
Features hypoglycaemic hyperinsulinism of infancy
``` Recurrent severe neonatal hypoglycaemia Rare disorder of infancy dysregulation of insulin release by islet cells Profound nonketotic hypoglycaemia Localised lesions in the pancreas ```
32
Mx hypoglycaemic hyperinsulinism
High concentration glucose solutions Diazoxide maintains safe blood glucose Partial resection/total pancreatectotmy
33
Mx Hypoglycaemia
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
Thyroid Physiology Neonatal Period
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
Causes of congenital hypothyroidism
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
Clinical features congenital hypothyroidism
``` 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
Clinical features acquired hypothyroid
``` 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
Mx congenital hypothyroid
Thyroxine started before 2-3w Lifelong oral replacement of thyroxine Titration to maintain normal growth
39
Features Autoimmune thyroiditis
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
Clinical features hyperthyroid
``` 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
Mx hyperthyroid
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
Causes of congenital pituitary disorders
Structural .e.g. midline defects | Pituitary hypoplasia or aplasia
43
Causes of acquired pituitary disorders
``` Brain tumour affecting hypothalamus or pituitary Cranial irradiation Trauma Infection Infiltration .e.g. histiocytosis Structural ```
44
Associated disorders hypoparathyroid
DiGeorge Autoimmune disorders Addisons Disease
45
Features of DiGeorge
Thymic aplasia Defective immunity Cardiac defects Facial abnormality
46
Features pseudohypoparathyroidism
End-organ resistance to parathyroid hormone | PTH normal, serum Ca and PO4 abnormal
47
Associated abnormality pseudohypoparathyroidism
``` Short stature Obesity Subcutaneous nodules short 4th metacarpals learning difficulty teeth enamel hypoplasia calcification of basal ganglia ```
48
Features pseudopseudohypoparathyroidism
Abnormality associated with pseudohypoparathyroidism | Normal calcium, phosphate and PTH
49
Mx hypocalcaemia
IV calcium gluconate 10% diluted Oral calcium and vitamin D anaolgues Monitoring urine calcium excretion
50
Hyperparathyroidism features
``` High calcium Constipation Anorexia Lethargy Behavioural effects Polyuria Polydipsia Bony erosions of phalanges ```
51
Associated conditions hyperparathyroidism
Williams syndrome Adenomas Multiple endocrine neoplasia syndrome
52
Mx hypercalcaemia
Rehydration Diuretics Bisphosphonates
53
Features congenital adrenal hyperplasia
``` 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
Features salt-losing adrenal crisis
``` 80% of males 1-3w old Vomiting Weight loss Hypotonia Circulatory collapse ```
55
Pathology congenital adrenal hyperplasia
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
Dx congenital adrenal hyperplasia
``` Raised levels of metabolic precursor 17a-hydroxy-progesterone in blood In salt losers: -Low plasma sodium -High plasma potassium -Metabolic acidosis -Hypoglycaemia ```
57
Mx congenital adrenal hyperplasia
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
Cx hormone replacement congenital adrenal hyperplasia
insufficient: rapid initial growth, skeletal maturation, detrimental to final height Excessive: skeletal delay, slow growth
59
Causes Addisons
``` Autoimmune process Haemorrhage/infection X linked adrenoleucodystrophy (rare) TB secondry to pituitary dysfunction/corticosteroid therapy ```
60
Features of adrenal insufficiency
``` Hyponatraemia Hyperkalaemia Hypoglycaemia Dehydration Hypotension Growth failure Circulatory collapse Vomiting Lethargy Brown pigmentation: gums, scars, skin creases ```
61
Dx Adrenal insufficiency
Hyponatreamia with hyperkalaemia with metabolic acidosis and hypoglycaemia Low plasma cortisol and high ACTH Synacthen test: cortisol remains low
62
Mx Adrenal insuffiency
Adrenal crisis: IV saline, glucose, hydrocortisone Glucocorticoid and mineralcorticoid replacement Increase (x3) dose of glucocorticoid during illness/surgery Parental education IM hydrocortison injection
63
Features Cushing Syndrome
``` Growth failure/short stature Face and trunk obesity Red cheeks Hirsutism Striae Hypertension Bruising Carbohydrate intolerance Muscle wasting and weakness Osteopenia Psychological problems ```
64
Causes of cushings
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
Ix Cushing Syndrome
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
Causes Disorders of sex development
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

Paediatrics (22 decks)

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