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Endocrine And Metabolic Disordersm Flashcards

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1
Q

What causes type 1 diabetes

A

Deficient insulin due to T-cell mediated autoimmune destruction of B-cells in pancreatic islets of langerhans

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2
Q

How much destruction of B cells for T1DM to become clinically significant ?

A

90%

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3
Q

What happens when blood glucose levels exceed renal threshold?

A

Osmotic diuresis - increased urination due to increased substances that can’t be reabsorbed eg. Glucose

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4
Q

What are the 3 key clinical features of T1DM ?

A

Polyuria
Polydipsia
Weight loss

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5
Q

Diagnosis of type 1 DM

A

Symptomatic child with random blood glucose >11mmol/L (+/-glycosuria/ketouria)

If doubt - glucose tolerance test -> fasting glucose >7mmol/L

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6
Q

4 parts of management for type 1 diabetes

A

Insulin replacement
Diet and exercise
Monitoring
Education & psychological support

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7
Q

Why do you need less insulin initially after diagnosis of T1DM ? What is the average requirement

A

Honeymoon period while remaining Bcells are destroyed

0.5-1 unit/Kg/day

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8
Q

Eg of insulin regimes

A

Twice daily
Basal bolus
Continuous pump infusion

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9
Q

How does a twice daily regime work with insulin

A

Total daily dose split 1:2 between short acting and Medium acting insulin.
2/3 in breakfast injection
1/3 in evening injection

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10
Q

What happens in a basal bolus injection

A

Multiple daily injections of short acting insulin and once daily long acting (glargine / detemir) to provide a background

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11
Q

What is continuous pump infusion insulin

A

Subcutaneous insulin infusion SII

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12
Q

Where is insulin injected and why

A

*Subcutaneously into upper arms, outer thighs or abdomen

Sites should be related to decreased risk of lypohypertrophy & atrophy *

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13
Q

What foods should be eaten in diabetes ? What pattern of eating ? When should food intake increase and why?

A

High fibre, complex carbohydrates as these give sustained release of glucose (avoid refined carbs eg. Sweets)
3 even main meals with snacks
After exercise to avoid hypoglycaemia

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14
Q

When should blood glucose be tested ? What is the aim level?

A

Morning and evening and before meals

4-6mmol/L

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15
Q

What other than blood glucose should be monitored? What level do you want it at

A

HBA1C

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16
Q

What are two risks with adolescents who have diabetes ?

A

Increase demand in monitoring

Risk of non compliance

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17
Q

What needs to be taught to diabetics ? Eg of voluntary group to support ?

A

Injection of insulin - technique and sites, monitoring

Diabetes UK

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18
Q

Clinical features of DKA (9 things)

A

Vomiting, dehydration, abdo pain, hyperventilation due to acidosis, kussmaul breathing, drowsiness, acetone smell on breath, coma, hypovolaemic shock

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19
Q

What investigations should be done in DKA ? What results ?

A

Blood glucose - >11mmol
U&E, creatinine - dehydration
ABG - metabolic acidosis (ph

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20
Q

What are the ECG changes in hypokalaemia

A

t wave inverted / flattened

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21
Q

Management of severe DKA

A

*Fluid - 10mls/kg normal saline, then replace
Insulin - 0.05-0.1 units /kg/ hour
Potassium - initiate as soon as urine passed *
Reestablish oral fluids, SC insulin & diet
Identify and treat underlying cause (eg. Infection, steroids, puberty)

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22
Q

Why is HCO3 not indicated to treat acidosis

A

Self corrects with insulin and fluid

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23
Q

What 3 things can kill a child in DKA

A

Cerebral oedema
Hypokalaemia
Aspiration pneumonia

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24
Q

When do you get symptoms with hypoglycaemia ? What are the symptoms? How do you treat ?

A

seizures / coma)

Sugary drink, glucose tablet or buccal gel

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25
What are the clinical features of congential hypothyroidism
``` Prolonged neonatal jaundice Feeding problems Constipation Large fontanelle, tongue, goitre Hypotonia ```
26
What are the 3 causes of congenital hypothyroidism
Athyrosis / maldescent (?sublingal) Dyshormogenesis - error of TH synthesis Maternal iodine deficiency
27
Where are rates of dyshormogenesis present ? What's usually on baby?
Consanguineous pedigree | Goitre
28
Diagnosis and treatment of hypothyroidism
Increased TSH | Thyroxine
29
When can hyperthyroidism be congential? What's common cause in childhood? Who gets the most?
Mother with graves | Graves - teenage girls most common
30
Diagnosis of hyperthyroidism
Increased t3/ t4 Decreased TSH Antimicrosomal antibodies
31
Treatment of hyperthyroidism ? If there is a relapse ?
Carbimazole is 1st line (+B-blockers for symtomatic relief) | Sub total thyroidectomy or radioiodine can be used if relapse after treatment
32
When should you check for hyperthyroidism
Deteriorating school performance | Delayed / accelerated puberty
33
3 causes of adrenocortical insufficiency
Congenital adrenal hyperplasia 1^ adrenal cortical insufficiency - addisons 2^ adrenal cortical insufficiency - cushings (pit adenoma) / syndrome (usually iatrogenic)
34
Genetics of congential adrenal hyperplasia? What is it?
90% clauses by deficient *21-hydroxylase*, autosomal recessive Group of disorders chased by defect in production of cortisol from cholesterol
35
What causes features of CAH ? What are they? Why?
Androgen excess Female virilization *Salt crises due to mineral corticoid deficiency* (decreased circulating volume, electrolyte imbalance, shock) *cortisol deficiency* (hypoglycaemia, hypotension, shock)
36
Diagnosis of CAH
Elevated serum 17a-hydroxyprogesterone
37
How do you manage a salt losing crisis of CAH
Volume replacement with normal saline and systemic steroids
38
Long term management of CAH
Cortisol replacement with hydrocortisone | Mineral corticoid replacement with fludrocortisone if there is salt wasting
39
What causes addisons ?
*autoimmune disease, haemorrhage & infarction, TB*
40
What is addisons caused by haemorrhage and infarction called
Waterhouse-friderichsen syndrome
41
Features of addisons
Postural hypotension and increased pigmentation
42
What is intercurrent illness ? What can happen with addisons ?
Illness while you have another illness | Adrenal crisis -> *vomiting, dehydration, shock*
43
What is Cushing's syndrome? Causes?
Glucocorticoid excess Primary - adrenal tumours Secondary - ACTH secretion from pituitary adenoma / ectopic source Iatrogenic - long term glucocorticoid use (eg. Nephrotic syndrome)
44
Features of cushings
Short stature , truncal deformity (buffalo hump), rounded moon face, hypertension, signs of virilization
45
2 parts of diagnosis for cushings
Elevated serum cortisol with normal diurnal rhythm (high midnight levels*) *dexamethasone suppression test*
46
What's it for? And What happens in a dexamethasone suppression test ?
Determine cushings disease vs syndrome Disease - bilateral adrenal hyperplasia due to pituitary increased ACTH - SUPPRESSED syndrome - eg. Tumour of adrenal/iatrogenic - NOT SUPPRESSED
47
Is deficiency or excess more common in ant pituitary? Wh of causes?
Deficiency Cranial defects - eg. Agenesis of corpus callosum Tumours - eg. Cranialpharyngioma Idiopathic hormone abnormalities
48
What is a craniopharyngioma
Brain tumour from pituitary embryonic tissue
49
Features of hypopituitarism
Growth retardation common | Adrenal, thyroid, gonadal dysfunction
50
2 disorders due to posterior pituitary
Diabetes insipidus | Syndrome of inappropriate secretion of ADH
51
What causes central diabetes insipidus
ADH deficiency | Can occur in isolation / with anterior pituitary deficiency (eg tumours, infection, trauma)
52
How does diabetes insipidus present ? What are the DDs?
Polydipsia , Polyuria | Hypercalcaemia, CKD, type 1 diabetes, psychogenic water drinking
53
Diagnosis of SIADH
*hypo osmolality with hyponatraemia* Normal renal, thyroid and adrenal function Normal or increased volume status (*HTN*) *Elevated urine sodium osmolality*
54
What causes symptoms in SIADH ? What are they?
Water intoxication | Seizures, behavioural changes, vomiting
55
What causes SIADH ? Why?
Common stress response CNS disease - meningitis, tumours, trauma Lung disease - pneumonia
56
What causes phenylketonuria ?
Autosomal recessive | *defective phenylalanine hydroxylase*
57
What does phenylalanine hydroxylase usually do? What happens when it's defective and this doesn't happen?
Converts phenylalanine to tyrosine. | Phenylalanine builds up and by-products (eg. Phenylacetic acid) build up and are excreted in the urine -> "PKU"
58
Features of phenylketonuria ? Neuro, growth, hypopigmentation
Neuro - Moderate / severe *mental retardation*, hypertonia, tremors, behavioural disorders Growth - *slowed* Hypopigmentation - *fair skinned, light haired*
59
Why do you get hypopigmentation in phemylketouria
Tyrosine is required to form melanin
60
Treatment of phenyketouria
Decreased Phenylalanine in diet until at least 6 years
61
What are the features of glalactosaemia ? When should it be tested for? How is the diagnosis made ?
Neonatal liver dysfunction, coagulopathy & cataracts Severe neonatal jaundice Reducing substances found in urine
62
What happens in glycogen storage diseases ? Features?
Abnormal accumulation of glycogen in tissues | Growth failure, hypoglycaemia, hepatomegally
63
What is mucopolysaccharidoses (MPS) ?
Progressive multiply stem disorders that can affect CNS, heart, eyes, and skeleton
64
What are the features of MPS
Developmental delay in first year | Coarse faces - normal at birth but develop in most cases
65
Treatment of MPS
Bone marrow transplant
66
What are coarse faces seen in? What are features?
Inborn errors of metabolism ( MPS, phenylketonuria) Large head, prominent veins, flat nose, big lips

Peadiatrics (14 decks)

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