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Endocrinology Flashcards

1
Q

Prevalence of diabetes in children

A

1/500 children have diabetes. 96% type 1, 2% type 2.

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2
Q

Long term effects of DM

A
  • leading cause of renal failure & blindness in people <60yrs & 2nd commonest cause of limb amputation
  • increased risk miscarriages, still births (5 x increase) & congenital malformations in mums with DM
  • estimated that 50% men with long standing diabetes are impotent
  • Life expectancy -10 years
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3
Q

1st presentation of diabetes

A
  • Polyuria (previously dry, now wetting bed)
  • Polydipsia
  • Weight loss
  • Tiredness
  • Blurred vision
  • Abdominal pain
  • Constipation
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4
Q

Diagnosis of diabetes

A
  • Screening – Urine with glucose
  • Blood sugar – Fasting >7.0mmol/L – Random >11.1mmol/
  • High blood sugar could be due to stress response or infection
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5
Q

Symptoms of DKA

A
  • Polyuria (previously dry at night, now wetting?)
  • Polydipsia (excessive thirst)
  • Breathless
  • Tiredness, drowsy
  • Weight loss
  • Nausea & Vomiting
  • Headache
  • Abdominal pain
  • Constipation
  • Ketotic breath
  • Dehydration
  • Shock
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6
Q

Immediate management of DKA

A

Put in recovery position, call ambulance

Manage with ABC, fluids (with KCL added)
Insulin and glucose IV after 1 hr
Monitor (K+, Na+, Gluc, ECG, renal bloods). Aim to bring down blood glucose level by max 5mmol/hr

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7
Q

5 causes of hyperglycaemic crisis in T1DM patients

A 
5 I's
Infection
Infarction
Infant (pregnancy)
Indiscretion (including cocaine use) 
Insulin lack (non adherence or inappropriate dosing).
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8
Q

What is the main risk of treatment in DKA

A

Cerebral oedema

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9
Q

Cerebral oedema symptoms

A
  • Headache
  • Drowsiness
  • Incontinence
  • Vomiting recurrence
  • Decreased level of consciousness
  • Bradycardia
  • Rising BP
  • Decreasing O2 sats
  • Neurological signs
  • Abnormal pupil responses
  • Abnormal posturing
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10
Q

What do you do if you suspect DKA cerebral oedema?

A

⇒ Get help!
⇒ Reduce fluids by 1/3
⇒ IV Mannitol 0.25-1g / kg given over 20 min
⇒ Repeat again after 2 hours

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11
Q

How do you differentiate between the 1st presentation of T1 and T2 DM?

A

⇒ Islet cell antibodies will be found in the blood of a T1DM patient

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12
Q

What is part of the yearly screening for T1DM patients? When does this commence?

A 
From age 12:
•	Coeliac
•	Thyroid function
•	Urine (microalbuminuria)
•	Cholesterol and lipid levels (fasting test)
•	HbA1c (35-45 is aim)
•	Fundoscopy
•	Feet filament test
•	Height and weight
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13
Q

Name 2 useful apps for management of DM

A
  • Carbs & Cals

* MyFitnessPal

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14
Q

Describe how T1DM affects pregnancy

A
  • High glucose acts as a teratogen
  • Badly controlled diabetes can lead to deformities in the fetus
  • Macrosomic babies-> shoulder dystocia
  • Hypoglycaemia after birth is common (baby is used to a sugary environment so has high production of insulin as base level)
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15
Q

What is Maturity Onset Diabetes of the Young?

A
  • 1-2% of diabetes cases
  • Autosomal dominant mutation, strong family history of diabetes
  • Not type 1 or type 2
  • Insulin independence, absence of pancreatic autoantibodies (not type 1DM)
  • Detectable endogenous insulin production (C-peptide measurable in hyperglycaemia) (not type 1DM)
  • Lack of obesity, normal TG levels, high HDL levels (not type 2DM)
  • Diabetes develops before the age of 25
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16
Q

What mutations might cause maturity onset diabetes of the young

A

HNF1A, Glucokinase, HNF1B (including Renal Cysts and Diabetes (RCAD)), HNF4A, IPF1, NEUROD1

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17
Q

Treatment of maturity onset diabetes of the young?

A

Usually insulin not used, instead sulphonylureas are used (eg gliclazide)

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18
Q

How can you kill a diabetic?

A

• Not recognising DKA
Hypoglycaemia
• Hypokalamia (when treating DKA)
• Cerebral oedema (when treating DKA)

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19
Q

How is the hypothalamus involved in thyroid hormone?

A

Hypothalamus production of TRH is influenced by negative feedback from circulating levels of TSH and T3 & T4

TRH (thyroid releasing hormone) from hypothalamus causes anterior pituitary gland (thyrotrophs) to produce TSH.

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20
Q

Where is TSH made?

A

Anterior pituitary gland, from thyrotrophs

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21
Q

What is the active form of thyroid hormone?

A

T3

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22
Q

Action of T3 & T4?

A

T3 +T4 ↑ basal metabolic rate, ↑O2 consumption
↑ cardiac output ↑ventilation ↑thermogenesis
↑number of ß-receptors in tissues-> ↑sympathetic function

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23
Q

Describe thyroid hormone physiology in fetus

A

In fetus it is responsible for brain, bone and lung maturation
The fetal hypothalamic-pituitary-thyroid system develops independently of the mother’s pituitary-thyroid axis.

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24
Q

How is the thyroid gland formed?

When does it begin to function?

A

During embryogenesis, primordial thyroid cells arise from epithelial cells on the pharyngeal floor; they then migrate caudally to fuse with the ventral aspect of the fourth pharyngeal pouch by 4 weeks gestation. The thyroid continues to develop anteriorly to the third tracheal cartilage.
Thyroglobulin is produced by 8 weeks gestation.
Trapping of iodine occurs by 10-12 weeks’ gestation, followed by the synthesis of iodothyronines.
Colloid formation and pituitary secretion of TSH occur by 12 weeks gestation.

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25
Q

What is congenital hypothyroidism?

What’s seen on blood tests?

A

Usually due to agenesis, dysplasia, or ectopy of the thyroid (75%).
Also caused by autosomal recessive defects in the organification of iodine (thyroid hormone synthesis) and defects in other enzymatic steps in T4 synthesis and release
Less/no T3&T4 produced by newborn.
Decreased negative feedback on TSH so really high TSH but low T3/T4.

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26
Q

Signs of congenital hypothyroidism

A
  • Prolonged gestation
  • Elevated birth weight
  • Delayed stooling after birth, constipation
  • Prolonged indirect jaundice
  • Poor feeding, poor management of secretions, noisy respirations
  • Large fontanels
  • Myxoedema of the eyelids, hands, and/or scrotum
  • Large protruding tongue (secondary to accumulation of myxoedema in the tongue)
  • Goitre
  • Hypothermia
  • Decreased activity level
  • Hoarse cry
  • Umbilical hernia
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27
Q

When is congenital hypothyroidism usually diagnosed?

A

From the Guthrie heel-prick test day 5-8

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28
Q

Management of congenital hypothyroidism

A
  • Levothyroxine 10 to 15 μg/kg/day within 2 weeks of life
  • If untreated and severe-> cretinism and mental retardation
  • Once treatment is initiated for congenital hypothyroidism, serum total T4 and TSH concentrations should be assessed monthly until the total or free T4 levels normalise, then every 3 months until the patient is aged 3 years. Thereafter, total T4 and TSH should be measured every 6 months.
29
Q

What is the most common cause of acquired hypothyroidism in children?

A

Autoimmune Hashimoto’s thyroiditis

30
Q

Signs and symptoms of acquired hyopthyroidism (10)

A
  • Asymptomatic goitre
  • Slow growth, delayed puberty
  • Delayed osseous maturation
  • Increased weight (obesity) despite decreased appetite
  • Lethargy
  • Dry skin, and puffiness
  • Sleep disturbance, typically obstructive sleep apnea
  • Cold intolerance, constipation
  • Pseudoprecocious puberty (testicular enlargement in boys or early breast development or onset of vaginal bleeding in girls) & galactorrhoea
31
Q

Differential diagnoses to hypothyroidism

A
  • Constipation
  • Short Stature
  • Constitutional Growth Delay
  • Hyposomatotropism
  • Malnutrition
  • Paediatric Depression
  • Paediatric Growth Hormone Deficiency
  • Paediatric Malabsorption Syndromes
32
Q

What is hyperthyroidism? Usual cause in children

A

Overactive thyroid gland leading to ↑basal metabolic rate

Rare in children, usually caused by Grave’s disease.

33
Q

Causes of hyperthyroidism

A 
Graves disease
Toxic adenoma, toxic nodular goitre
Pituitary causes of thyrotoxicosis in childhood: 
Pituitary adenoma
Pituitary resistance to T4
34
Q

What is Grave’s disease? Signs? What is seen on blood tests?

A
  • Antibody to infection mimics TSH & stimulates thyroid hormone production & antibodies against IGFs
  • Large smooth thyroid
  • Pretibial myxoedema (rare in children)
  • Exophthalmus (eye popping)
  • Ophthalmopathy (hyaluronan, GAGs, collagen and T&B cell infiltrates in periorbital space-> proptosis, chemosis, lid retraction, oedema)
  • Low TRH and TSH, really high T3 & T4
35
Q

Explain how toxic nodules work in hyperthyroidism

A
  • Rare in children and masses are usually non functional
  • Growth of nodules of thyroid tissue constantly producing T3 & T4 without TSH input
  • T3 & T4 constantly produced at higher than normal levels
  • Normal thyroid tissue no longer stimulated by TSH as it is above the set point
  • Bumpy nodular thyroid
  • Hot points on radioactive scan
36
Q

Treatment of hyperthyroidism

A
  • Surgery + replacement thyroxine
  • Radioactive iodine + replacement thyroxine
  • CARBIMAZOLE (anti-thyroid)
  • PROPRANOLOL (treats symptoms)
  • WARFARIN (in case of AF)
  • PREDNISOLONE (for exophthalmos)
37
Q

Function of aldosterone

A
  • Sodium down, potassium up or hypotension-> juxtaglomerular cells -> RAAS
  • Aldosterone works at distal convoluted tubule, sodium and water reabsorption (in exchange for either K+ or H+)
38
Q

What is Conn’s syndrome?

A

Overproduction of aldosterone due to hyperactivity of the zona glomerulosa cells of the adrenal glands

39
Q

Physiology of Conn’s syndrome?

A

Hyperactivity of the zona glomerulosa cells of the adrenal glands
• Retention of sodium
• Loss of potassium (hypokalaemia, weakness, lethargy)
• Alkalosis
• Hypertension

40
Q

What mimics Conn’s?

A

Secondary hyperaldosteronism
Due to excessive RAAS activation
Renal artery stenosis, chronic heart failure and nephrotic syndrome can affect juxtaglomerular cell function and cause increased renin and increased aldosterone

41
Q

How can you differentiate between Conn’s and 2º hyperaldosteronism?

A

• Aldosterone:renin blood test ↑aldosterone: ↡renin shows Conn’s
↑renin ↑aldosterone shows 2º hyperaldosteronism
• Saline suppression test
Expanded volume ↡aldosterone and renin levels in 2º hyperaldosteronism
In Conn’s, aldosterone not suppressed

42
Q

Treatment of Conn’s

A
  • Spironolactone (K+ sparing diuretic, anti-aldosterone)

* Adrenalectomy if unilateral

43
Q

Name the layers of the adrenal gland

A 
GFR
Capsule (outside)
Zona Glomerulosa (aldosterone)
Zona fasciculata (cortisol)
Zona Reticularis (androgens)
Medulla (adrenaline)
44
Q

What is hypoadrenalism?

A

= Deficiency of adrenal cortical hormones (cortisol + aldosterone)

45
Q

Causes of hypoadrenalism?

A
  • TB, HIV
  • Metastatic tumour/lymphoma
  • Addison’s disease
  • Haemorrhage of adrenals (meningococcal septicaemia) or infarction
46
Q

Signs and symptoms of hypoadrenalism

A
  • Tiredness and weakness
  • GI disturbance (abdo pain)
  • Weight loss
  • Postural hypotension + dizziness (due to low aldosterone) + fainting
  • Hypoglycaemia (low cortisol) -> confusion-> convulsions -> death
  • Hyperkalaemia (low aldosterone)
  • Pigmentation (loss of negative feedback for melanocyte stimulating hormone)
  • Other autoimmune disorders?
  • Calcification of pinna of the ear (rare)
47
Q

How is hypoadrenalism diagnosed?

A
  • Hypercalcaemia, eosinophilia, hypoglycaemia, hyperkalaemia, hyponatraemia, metabolic acidosis
  • Antibodies (adrenal cortex Ab, 21-hydroxylase antibodies)
  • ACTH stimulation test (serum cortisol should risk, no rise = addison’s)
  • Will rise in 2º adrenal failure (as bypasses the failing pituitary)
48
Q

Treatment of hypoadrenalism

A
  • Cortisol replacement (HYDROCORTISONE) 3xdaily
  • Aldosterone replacement (FLUDROCORTISONE) 1xdaily
  • DHEA replacement?
49
Q

Signs and symptoms of Cushing’s

A 
Moon face
Buffalo hump
Thin skin
Easy bruising
Central obesity
Muscle weakenss
Osteoporosis
Ulcers
Purple striae
Enlarged heart
Hypertension
50
Q

What does cortisol do? (4)

A
  • ↑lipolysis + mobilisation of fatty acids
  • ↑Protein breakdown + mobilisation of amino acids
  • ↑gluconeogenesis, glycogenesis and glycogen storage (prepare for starvation)
  • Immunosuppression and anti-inflammatory actions
51
Q

What is the difference between Cushing’s syndrome and Cushing’s disease?

A

Cushing’s syndrome
=Excessive cortisol release
Cushing’s disease = pituitary tumour that raises ACTH levels

52
Q

What are the 5 causes of Cushing’s syndrome?

A

1) Tumour of adrenal gland
2) Pituitary tumour (↑ACTH) = Cushing’s disease
3) Hypersecretion of CRH from hypothalamus
4) Overadministration of glucocorticoid drugs (asthma, Crohn’s, organ transplantation)
5) Cancer-> ectopic ACTH production (eg small cell lung cancer)

53
Q

How do you diagnose the cause of Cushing’s syndrome?

A

3 tests:
Dexamethasone suppression test (adrenal tumour/pituitary tumour/ectopic ACTH or not)
Baseline cortisol (cushing’s syndrome or not)
Petrosal sinus sampling (pituitary/ectopic ACTH)

54
Q

Explain different results of Dexamethasone suppression test

A
  • Give cortisol analogue at midnight, next day lots of steroid around but no ACTH and no cortisol (-ve feedback)
  • If cortisol <40 normal
  • If cortisol >40 and ACTH low = abnormal as cortisol has been produced without ACTH stimulation due to adrenal tumour
  • In pituitary tumours the dexamethasone doesn’t reach the higher set point of the abnormal pituitary cells so ACTH and cortisol still produced. Would respond to higher dexamethasone levels
  • In ectopic ACTH production, ACTH is really high + doesn’t suppress even with higher dexamethasone
55
Q

Explain the different results from baseline cortisol tests

A
  • From 24hr urine sample (high-> cushing’s)

* Salivary cortisol. Loss of diurnal variation-> cushing’s

56
Q

Explain the different results from pertrosal sinus sampling

A
  • ACTH concentration in arm and sinus = same = ectopic ACTH cancer
  • ACTH concentration very high in sinus and low in arm = pituitary tumour
57
Q

Treatment of Cushing’s

A
  • Block cortisol production (METYRAPONE, KETOCONAZOLE, MITOTANE)
  • Pituitary tumour excision (trans-sphenoidal hypophysectomy) +/- radiotherapy
  • Ectopic ACTH usually palliative (surgery, chemo)
  • Adrenal tumour excision
58
Q

What is a phaeochromocytoma?

A
  • Adrenaline and noradrenaline (NA) secreting tumour of the chromaffin cells of the adrenal medulla
  • Produces massive spikes of adrenaline with non-physiological causes & no external stimuli
59
Q

What is a tumour of the chromaffin cells called?

A

Phaechromocytoma

60
Q

Signs and symptoms of phaemochromocytoma

A
  • Overwhelming sense of doom
  • Startled, anxiety
  • Turns and headaches
  • Sweating
  • Tachyarrhythmias
  • Hypertension (due to α receptors)
  • Tremor
  • Weakness
  • Epigastric pain
  • Constipation (Ileus)
  • Cardiomyopathy
  • Neurofibromatosis?
61
Q

Diagnosis of phaeochromocytoma

A

CLONIDINE suppression test (α-2 agonist)

62
Q

Treatment of phaeochromocytoma

A
  • α blockade (PHENOXYBENZAMINE)
  • Then ß-blockers for relaxation of smooth muscle and decrease HR (PROPRANOLOL)
  • Surgical excision of tumour
63
Q

Prognosis of phaeochromocytoma

A

Death due to coronary artery dissection due to spiked BP is common

64
Q

What is CAH?

A

Congenital adrenal hyperplasia

65
Q

What causes CAH? What does it cause?

A

= Deficiency in adrenal enzyme 21hydroxylase
↡ mineralocorticoids, ↡glucocorticoids
Excess androgens (don’t need 21-hydroxylase for androgens)
Ambiguous genitalia at birth, virilisation

66
Q

What enzyme is involved in CAH?

A

21-hydroxylase

67
Q

When mother is an insulin dependent diabetic, what is the baby more at risk of?

A 
Macrosomia (shoulder dystocia)
Hypoglycaemia
RDS
Polycythaemia
Congenital malformations
Hypertrophic cardiomyopathy
68
Q

3 pathological causes of obesity

A

Prader-Willi syndrome
Cushing’s
Hypothyroidism

69
Q

Signs of CAH

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia

Paeds (14 decks)

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