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Phase 2a > My endocrine > Flashcards

My endocrine Flashcards

1
Q

What is diabetes mellitus?

A

Diabetes mellitus is a disorder of carbohydrate metabolism characterised by hyperglycaemia

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2
Q

What are the plasma glucose concentrations needed to diagnose diabetes?

A
  • Symptoms and random plasma glucose >11 mmol/l
  • Fasting plasma glucose >7 mmol/l
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3
Q

What is the HbA1c concentration needed to diagnose diabetes?

A

HbA1c of 48 mmol/mol (6.5%)

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4
Q

What is pancreatic diabetes?

A

Part of the pancreas is damaged or removed due to pancreatitis

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5
Q

What is endocrine diabetes?

A

Diabetes caused by acromegaly or cushing’s

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6
Q

How can acute hyperglycaemia cause morbidity or mortality?

A

If untreated, acute hyperglycaemia leads to metabolic emergencies, such as
- diabetic ketoacidosis
- hyperosmolar coma

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7
Q

What is diabetic ketoacidosis?

A

A triad of hyperglycaemia with metabolic acidosis and ketonaemia. Causes hyperventilation, nausea, vomiting, abdominal pain.

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8
Q

How can chronic hyperglycaemia cause morbidity?

A
  • Microvascular and macrovascular tissue complications.
  • Diabetic retinopathy
  • Stroke
  • Cardiovascular disease
  • Diabetic neuropathy
  • Diabetic nephropathy
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9
Q

How else can diabetes cause morbidity?

A

Side effects of treatment, such as hypoglycaemia

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10
Q

Why is hypoglycaemia common in diabetes patients?

A

The inability of insulin therapy to mimic the physiology of the beta cell. Patients with diabetes are at particular risk of hypoglycaemia due to defects in the physiological defences to hypoglycaemia, and reduced awareness.

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11
Q

What does hypoglycaemia in the brain lead to?

A
  • Cognitive dysfunction
  • Confusion
  • Drowsiness
  • Vision changes
  • Difficulty speaking
  • Blackouts
  • Seizures
  • Comas
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12
Q

How does hypoglycaemia affect the heart?

A
  • Arrhythmias
  • Risk of myocardial ischaemia
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13
Q

How does hypoglycaemia affect the circulation?

A
  • Inflammation
  • Blood coagulation abnormalities
  • Haemodynamic changes
  • Endothelial dysfunction
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14
Q

How does hypoglycaemia affect the skeleton?

A

Falls and accidents due to cognitive dysfunction
Leads to fractures and dislocations

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15
Q

What is MODY?

A

Maturity-onset diabetes of the young (MODY)

  • Autosomal dominant - most of the family has diabetes
  • Some forms don’t need insulin treatment - some still produce insulin
  • Treated with sulphonylureas (stimulate insulin production)
  • Single gene affecting beta cell function, eg mutation in glucose-sensor of beta cells which control insulin release
  • Type I signs, but no islet antibodies, and c peptide in blood (shows insulin production)
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16
Q

What is permanent neonatal diabetes?

A
  • Present from birth
  • Causes beta cells to release inslin less often
  • Treated with sulphonylureas (stimulate insulin production)
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17
Q

What is MIDD?

A

Maternally inherited diabetes and deafness (MIDD)

  • Mutation in mitochondrial DNA
  • Loss of beta cell mass
  • Similar presentation to Type II
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18
Q

What is lipodystrophy?

A

Unusual distribution of adipose tissue
Very high insulin resistance

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19
Q

How can inflammatory processes lead to diabetes?

A

Acute pancreatitis, leading to hyperglycaemia due to increased glucagon secretion
Chronic pancreatitis, due to alcohol consumption which alters pancreas secretions

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20
Q

What is hereditary haemochromatosis?

A

Chromatosis: unusual deposit of pigment

  • Autosomal recessive
  • Excess iron deposited in the liver, pancreas, heart etc
  • Most patients need insulin
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21
Q

What is pancreatic neoplasia?

A

Common cause of cancer death
Require subcutaneous insulin
Prone to hypoglycaemia due to loss of glucagon function

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22
Q

What is cystic fibrosis and how does it lead to diabetes?

A

Makes all secretions viscous, obstructs pancreatic ducts
Insulin treatment required

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23
Q

What is acromegaly and how does it lead to diabetes?

A

Excessive secretion of growth hormone
This makes people very insulin resistant - similar to type II diabetes

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24
Q

What is cushing’s and how does it lead to diabetes?

A
  • Excess of glucocorticoids
  • This leads to increased insulin resistance and reduced glucose uptake into peripheral tissues
  • Hepatic glucose production increased through stimulation of gluconeogenesis
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25
Q

How can drugs induce diabetes?

A

Glucocorticoids increase insulin resistance - iatrogenic due to steroids

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26
Q

Describe type I diabetes

A

Insulin deficiency disease characterised by a loss of beta cells due to autoimmune destruction.

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27
Q

How is type I initiated?

A

Genetic susceptibility coupled with environmental triggers

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28
Q

What is the visceral and peripheral response to lack of insulin in type I diabetes?

A

Continuous breakdown of liver glycogen
Unrestrained lipolysis and skeletal muscle breakdown, providing glucogeogenic precursors
Inappropriate increase in hepatic glucose output and suppression of peripheral glucose uptake

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29
Q

When does glucose begin to appear in urine?

A

When the renal threshold of 10mM is exceeded

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30
Q

What does this lack of insulin response lead to?

A

Percieved stress leads to increased cortisol and adrenaline Progressive catabolic state and increasing levels of ketones

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31
Q

How does type I diabetes present in young patients?

A

2-6 week history

  • Thirst
  • Polyuria
  • Weight loss
  • Hunger
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32
Q

What testing would be done in a young patient with symptoms pointing to type I - and what would the results show?

A

Urine dipstick: detect glucose and ketones
Blood antibody test: detect high levels of islet antibodies

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33
Q

Why do type I diabetics experience thirst?

A

High blood glucose causes osmotic activation of the hypothalamus

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34
Q

Why do type I diabetics experience polyuria?

A

Blood glucose exceeds renal tubular eabsorptive capacity (renal threshold) This leads to osmotic diuresis of water

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35
Q

Why do type I diabetics experience weight loss?

A

Fluid depletion and insulin deficiency leads to muscle and fat breakdown

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36
Q

Why do type I diabetics experience hunger?

A

Lack of useable energy source

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37
Q

How do older patients with type I present?

A

Same as young patients, but over a longer period

  • Lack of energy
  • Eye problems - blurred vision
  • Neuropathy if not picked up earlier or if untreated
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38
Q

What is basal and prandial insulin?

A

Basal insulin: maintains constant, low concentration of insulin Prandial insulin: rapid acting, taken just before meal time

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39
Q

Describe type II diabetes

A

Impaired insulin secretion and insulin resistance due to a combination of genetic predisposition and environmental factors

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40
Q

What does impaired insulin action in type II diabetes lead to?

A
  • Reduced uptake of glucose by muscle and fat tissue after eating
  • Failure to suppress lipolysis and gluconeogenesis
  • High circulating free fatty acids
  • Abnormally high glucose output after a meal
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41
Q

Are blood ketone levels high in type II?

A

No, because even low levels of insulin restrict muscle catabolism and ketogenesis

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42
Q

Presentation of type II

A
  • Gradual onset
  • Lack of energy
  • Likely to have a family history
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43
Q

How is type II diabetes tested?

A
  • Fasting plasma glucose of above 7mmol/L
  • Random plasma glucose of above 11mmol/L
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44
Q

Ideal treatment for type II

A

Weight loss and exercise, which if substantial will reverse hyperglycaemia

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45
Q

Why is type II treated with drugs instead of lifestyle typically?

A

Most with type II have been making the opposite lifestyle choices their whole lives

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46
Q

What are the aims of drugs for type II?

A
  • Control blood pressure
  • Control blood glucose
  • Control lipids
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47
Q

Describe metformin

A

Insulin sensitiser

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48
Q

Effects of sulphonylureas

A

Stimulate insulin release by binding to beta cell receptors
Improve glycaemic control

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49
Q

Negatives of sulphonylureas

A
  • Cause weight gain
  • Do not prevent gradual failure of insulin secretion
  • Can cause hypoglycaemia
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50
Q

Describe thiazoldinediones

A
  • Bind to nuclear receptors to activate genes associated with glucose uptake and utilisation, and lipid metabolism
  • Improve insulin sensitivity
  • Used alongside insulin
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51
Q

Describe SGLT2 inhibitors

A

Sodium-glucose cotransporters reabsorb glucose into blood from the kidney
Inhibitors block the reabsorption of glucose, increase excretion, and lower blood glucose levels

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52
Q

Are thyroid disorders more common in men or women?

A

Women

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53
Q

What causes hyperthyroidism?

A
  • Overproduction of thyroid hormone
  • Leakage of pre-formed hormone from the thyroid
  • Ingestion of excess thyroid hormone
  • Drugs eg iodine, lithium
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54
Q

Symptoms of hyperthyroidism

A
  • Thin hair
  • Lid retraction
  • Anxiety
  • Irritability
  • Hyperphagia
  • Goitre
  • Tachycardia (>100bpm)
  • Palpitations
  • Menstrual disturbance - oligomenorrhoea
  • Heat intolerance and sweating
  • Tremor
  • Diarrhoea
  • Weight loss
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55
Q

Investigations for hyperthyroidism

A

Thyroid function tests - test for low thyroid stimulating hormone, and high free T4 and T3.
Can also perform visual field test electronically

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56
Q

What would symptoms of hyperthyroidism as well as high blood TSH show?

A

A pituitary function issue

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57
Q

What do isotope scans do?

A

Use radoiactive iodine to show the thyroid’s shape and size

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58
Q

Drug treatments for hyperthyroidism

A
  • Beta blockers ameliorate tachycardia, palpitations, anxiety, and heat intolerance
  • Antithyroid drugs (carbimazole) decrease synthesis of new thyroid hormone
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59
Q

Non-drug treatments for hyperthyroidism

A
  • Radioiodine delivers radiation to the thyroid gland to cause local distruction
  • Total thyroidectomy (rare)
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60
Q

What are the negatives of radioiodine and thyroidectomy?

A

Both can lead to hypothyroidism
Radioiodine: cannot be given during pregnancy or breastfeeding
Thyroidectomy: can damage the laryngeal nerve

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61
Q

Describe Grave’s disease

A

Autoimmune process driven by TSH receptor antibodies. These stimulate the thyroid to produce thyroid hormone.

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62
Q

What can trigger Grave’s disease?

A

Childbirth

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63
Q

Additional hyperthyroid symptoms caused by Grave’s disease

A
  • Thyroid associated opthalmopathy - swelling in extraocular muscles and photophobia
  • nail clubbing
  • swelling of digits and toes
  • thick scaly skin and swelling on lower legs
  • diffuse goitre
64
Q

How is Grave’s disease tested?

A

Test for thyroid stimulating antibodies. Will also have high T3 and T4, and lower TSH

65
Q

Treatment for Grave’s disease

A

Carbimazole for 12-18 months (antithyroid - reduces synthesis of thyroid hormone)
Around 50% of patients relapse, so go on to have surgery or radioiodine

66
Q

Types of hypothyroidism

A

Primary: absent or dysfunctional thyroid gland
Secondary: due to pituitary or hypothalamic dysfunction
Transient: after withdrawal of drugs, pregnancy, congenital

67
Q

Causes of primary hypothyroidism

A
  • Hashimoto’s thyroiditis
  • Atrophic thyroiditis
  • Iodine deficiency
  • Congenital defects
68
Q

Symptoms of hypothyroidism

A
  • Rough, dry hair
  • Slowing of intellectual activity
  • Tiredness, lethargy
  • Periorbital oedema
  • Decreased appetite
  • Goitre
  • Deep, hoarse voice
  • Weight gain
  • Bradycardia ( 60bpm)
  • Cold intolerance
  • Menorrhagia - heavy or prolonged menstrual bleeding
  • Muscle cramps
  • Delayed muscle reflexes
  • Constipation
    Oedema, ascites - puffy face, hands, feet
    Dry, rough skin
    Carotenaemia
69
Q

How is hypothyroidism investigated?

A

Blood tests: high TSH, low free T4 and T3

70
Q

What would symptoms of hypothyroidism as well as low blood TSH show?

A

A pituitary function issue

71
Q

How does atrophic thyroiditis show in a blood test?

A

High TSH, low free T3 and T4
anti-TPO and anti-TSH antibodies

72
Q

How is hypothyroidism treated?

A

Levothyroxine (T4)
Some patients may also need T3

73
Q

Describe Hashimoto’s thyroiditis

A

Hypothyroidism due to aggressive destruction of thyroid cells.
Antibodies bind and block TSH receptors, leading to inadequate thyroid hormone production and secretion.

74
Q

How can Hashimoto’s cause dyspnoea or dysphagia?

A

The thyroid gland may enlarge rapidly, leading to pressure on the neck.

75
Q

How is Hashimoto’s tested?

A

High TSH levels, and thyroid antibodies in the plasma.

76
Q

How is Hashimoto’s treated

A

Thyroid replacement - levothyroxine

77
Q

Why can pregnancy affect thyroid function?

A

HCG has a similar structure to thyroid stimulating hormone, and can act like a weak form of TSH to stimulate the thyroid

78
Q

Name the 5 types of thyroid cancer

A
  • Papillary
  • Follicular
  • Anaplastic
  • Lymphoma
  • Medullary
79
Q

Describe papillary thyroid cancer

A
  • Most common thyroid cancer
  • Asymptomatic thyroid nodule usually in one lobe
  • Tends to spread locally in the neck, compressing the trachea
80
Q

Describe follicular thyroid cancer

A
  • Asymptomatic thyroid nodule
  • May infiltrate the neck
  • Develops from follicular cells
  • Next most common after papillary
81
Q

How are thyroid cancers typically removed?

A

Total thyroidectomy, followed by radioactive iodine

82
Q

How is pituitary disregulation identified?

A

If a given hormone is low, and the pituitary hormone which stimulates its production is also low.
If a given hormone is high, and the pituitary hormone which stimulates its production is also high

83
Q

Name the 6 hormones released by the anterior pituitary gland

A
  • Growth hormone
  • Thyroid-stimulating hormone
  • Follicle-stimulating hormone
  • Lutenising hormone
  • Prolactin
  • Adrenocorticotropic hormone
84
Q

What causes diabetes insipidus?

A

Either due to:

  • Cranial: Lack of vasopressin release by the hypothalamus
  • Nephrogenic: Resistance to action of vasopressin
85
Q

What does diabetes insipidus lead to?

A
  • Polyuria, polydipsia
  • Urine volume 3L a day
  • High plasma osmolality
  • Seen with low copeptin (released with normal ADH production)
86
Q

What occurs if the posterior pituitary releases too much vasopressin?

A
  • Urine is inappropriately concentrated
  • Causes hyponatremia
  • Can have no/ mild symptoms if chronic, more severe if acute
  • Causes brain swelling: headache, irritability, nausea, mental slowing, unstable gait, confusion
87
Q

What causes cranial diabetes insipidus?

A
  • Neurosurgery
  • Trauma
  • Tumour
  • Infiltrative disease
  • Idiopathic
  • Genetic: mutation in the ADH gene
88
Q

How is cranial diabetes insipidus treated?

A

Typically: Thiazide to increase urine, drugs to sensitise the renal tubules to endogenous vasopressin (carbamazepine, chlorpropamide)
If more treatment needed: desmopressin to replace ADH

89
Q

What causes nephrogenic diabetes insipidus?

A
  • Disruption to the channels, or damage to the kidney
  • Hypokalaemia
  • Hypercalcaemia
  • Drugs
  • Renal tubular acidosis
  • Prolonged polyuria
  • Chronic kidney disease
  • Genetic: mutation in ADH receptor
90
Q

How is nephrogenic diabetes insipidus treated?

A

Treatment of the underlying cause

91
Q

How is diabetes insipidus diagnosed?

A
  • Urine volume
  • Water deprivation test
  • Urea and electrolyte test to check for a more common cause of polyurea
  • MRI of hypothalamus to diagnose cranial DI
92
Q

What is secondary hypothyroidism?

A

Hypothyroidism caused by low thyroid-stimulating hormone release by the pituitary

93
Q

Name tumours that can affect the pituitary

A
  • Pituitary adenoma - benign, can be functional or non-functional
  • Pituitary carcinoma - malignant
  • Metastases from eg breast, lung, kidney
  • Craniopharyngioma (from above pituitary)
  • Meningioma (from meninges)
  • Rathke’s cyst
94
Q

Other than tumours, what else can affect pituitary function?

A
  • Trauma to the head
  • Haemorrhage and stroke
  • Sarcoidosis
95
Q

What are the effects of pituitary tumours?

A

Pressure on local structures Pressure on normal pituitary causing hypopituitarism Functional tumours producing hormones

96
Q

How would a patient with a non-functional pituitary tumour present?

A

Headaches due to stretching of dura Bitemporal hemianopia due to pressure on the optic chiasm Seizures due to pressure on temporal lobe Leakage of CSF through the nose (in downward growth) Compression of pituitary stalk affects vasopressin and oxytocin Pressure on pituitary causes pallor, lack of body hair, obesity around the midline

97
Q

Main three functional pituitary tumours

A

Prolactinoma Growth hormone-producing ACTH-producing

98
Q

Affects of prolactinoma

A

Galactorrhea (milk production) Amenorrhoea (menstrual irregularity) Men have low testosterone, so low libido If large, can cause headaches and visual field defects

99
Q

How is prolactinoma treated?

A

Dopamine agonists, causing shrinkage of the tumour (dopamine inactivates prolactin)

100
Q

Affects of growth hormone-producing tumour

A

Acromegaly: Simulates muscle, bone, and fat Stimulates the liver to produce IGF-I In childhood, causes gigantism

101
Q

Acromegaly presentation in adults

A

Headache Pronounced jaw and orbital ridge Sleep apnoea Excessive sweating Hypertension, heart disease, cardiovascular events Arthiritis Large feet and hands Insulin-resistant diabetes

102
Q

How is acromegaly tested?

A

First test growth hormone and IGF If abnormal, glucose tolerance test where glucose is given and IGF-I levels will increase instead of decrease

103
Q

How is acromegaly treated?

A

Transsphenoidal pituitary surgery: cure Medical therapy: dopamine agonists (suppress secretion), somatostatin analogues (slow production of GF), growth hormone receptor agonists Radiotherapy, but can lose pituitary function in long-term

104
Q

Describe Cushing’s disease

A

Due to persistently elevated glucocorticoid (cortisol) due to innapropriate ACTH secretion from the pituitary or from taking glucocorticoid medicines

105
Q

Symptoms of Cushing’s

A

Obesity with central fat distribution Rounded moon face Striae (stretch marks) Bruising Hypertension Pathological fractures Plethoric complexion

106
Q

What causes pseudo-cushings?

A

Excessive alcohol consumption - resolves on alcohol recession

107
Q

How is Cushing’s diagnosed?

A

Cortisol and ACTH measured in urine and blood tests Imaging of pituitary and adrenals to show tumours Late night salivary cortisol (usually low, in cushings will be high)

108
Q

Describe syndrome of innapropriate ADH secretion

A

Continued ADH secretion in spite of plasma hypotonicity and normal plasma volume.

109
Q

What does syndrome of innapropriate ADH secretion lead to?

A

urine is inappropriately concentrated causes hyponatremia (serum sodium 135) causes brain swelling, structures pushed against skull the brain can adapt with loss of osmolytes over 48 hours however

110
Q

Symptoms of syndrome of inappropriate secretion of ADH

A

can be no or mild symptoms if chronic - more severe if acute headache, irritability, nausea, mental slowing, unstable gait, confusion

111
Q

Causes of syndrome of inappropriate secretion of ADH

A

can be caused by drugs eg PPIs ectopic production of ADH eg brain tumour, trauma, infection eg lung small cell cancer, mesothelioma, cystic fibrosis

112
Q

What can cause hypoparathyroidism?

A

Typically iatrogenic - during surgery Radiation in cancer treatment - can damage parathyroid Certain rare syndromes eg DiGeorge Genetics Autoimmune conditions Infiltration of metals into the parathyroids Magnesium deficiency - prevents vesicles of parathyroid being released

113
Q

What are the effects of hypoparathyroidism?

A

Decreased renal calcium reabsorption Increased renal phosphate reabsorption Decreased bone resorption Decreased activation of vitamin D - decreased intestinal calcium absorption

114
Q

What are the effects of hypocalcaemia?

A

parasthesia (numbness) muscle spasm in hands, feet, larynx (also premature labour) seizures anxious, irritable basal ganglia calcification cataracts ECG abnormalities sections of unmineralised bone seen in X-ray

115
Q

How is hypoparathyroidism investigated?

A

Bloods will show decreased calcium, increased phosphate, decreased parathyroid hormone Calcium is largely albumin bound, serum calcium is calculates with this in mind total serum calcium + 0.02 * (40 ‚Äìserum albumin) Chvostek ‘s Sign: Tap over the facial nerve, look for spasm of facial muscles Trousseau ‘s Sign: Inflate the blood pressure cuff to 20 mmHg above systolic for 5 minutes, hand forms Italian hand

116
Q

Treatment of hypoparathyroidism

A

Calcium supplements Calcitriol - mimics calcium

117
Q

What causes pseudohypoparathyroidism?

A

Resistance to parathyroid hormone, typically due to rare inherited disorders

118
Q

What are the effects of pseudohypoparathyroidism?

A

Low serum calcium increased parathyroid hormone low bone resorption kidney calcium reabsorption gut absorption

119
Q

What are the symptoms of pseudohypoparathyroidism?

A

Symptoms of hypocalcaemia Short stature Obesity Round face Mild learning difficulties Subcutaneous ossification Short fourth metacarpals

120
Q

What are the causes of primary hyperparathyroidism?

A

An adenoma or hyperplasia provides additional secretive tissue, which provides excess parathyroid hormone. 80% due to single benign adenoma, which is removed, issues resolve 20% are due to four gland hyperplasia, due to syndromes 0.5% are due to malignancy, where calcium will be extremely high

121
Q

Effects of primary hyperparathyroidism

A

Bones: osteitis fibrosa cystica (rare), osteoporosis Kidney stones (renal calculi) Psychic groans: confusion Abdominal moans: constipation, acute pancreatitis

122
Q

Symptoms of primary hyperparathyroidism

A

70-80% of patients are asymptomatic bone pain nausea neuropsychiatric effects

123
Q

Investigation of primary hyperparathyroidism

A

Bloods will show hypercalcaemia (and raised parathyroid)

124
Q

Treatment of primary hyperparathyroidism

A

Adenoma will need surgical removal Biphosphonates (strengthen bones)

125
Q

What causes secondary hyperparathyroidism?

A

Due to increased secretion of parathyroid hormone to compensate hypocalcaemia. Chronic hypocalcaemia causes hyperplasia of the parathyroid. Can be due to chronic kidney disease, vitamin D deficiency, or any condition which causes hypocalcaemia.

126
Q

Effects of secondary hyperparathyroidism

A

Kidney disease Skeletal complications Cardiovascular complications

127
Q

Investigation of secondary hyperparathyroidism

A

Bloods will show hypocalcaemia (and raised parathyroid)

128
Q

Treatment of secondary hyperparathyroidism

A

Calcium correction Treat underlying condition

129
Q

Cause of tertiary hyperparathyroidism

A

Autonomous secretion of parathyroid hormone due to chronic kidney disease. Glands become autonomous following secondary hyperparathyroidism, producing an excess of parathyroid hormone even after the correction of calcium deficiency.

130
Q

Symptoms of tertiary hyperparathyroidism

A

Same as primary: Bone pain Renal stones Nausea Neuropsychiatric

131
Q

Investigations of tertiary hyperparathyroidism

A

Bloods will show hypercalcaemia (and raised parathyroid).

132
Q

Treatment of tertiary hyperparathyroidism

A

Calcium mimetic - cinacalcet Total or subtotal parathyroidectomy - this may lead to hypocalcaemia

133
Q

Conn’s syndrome

A

An adrenal adenoma causing primary hyperaldosteronism - high aldosterone levels independent of the renin-angiotensin-aldosterone system.

134
Q

What is the other cause of primary hyperaldosteronism?

A

Adrenocortical hyperplasia

135
Q

Effects of primary hyperaldosteronism

A

Hypertension Hypokalaemia

136
Q

Treatment of primary hyperaldosteronism

A

Conn’s: Surgical removal of adenoma Aldosterone agonist (spironolactone) for hyperplasia

137
Q

What causes secondary hyperaldosteronism?

A

Hyperaldosteronism due to high renin levels

138
Q

Addison’s disease

A

Primary adrenal insufficiency due to autoimmune destruction of the adrenal cortex. This leads to a reduction in cortisol and aldosterone.

139
Q

Symptoms of adrenal insufficiency

A
  • Lethargy - Depression - Anorexia - Weight loss - Weakness - Fatigue - Hyperpigmentation - 4 Ts: thin, tanned, tired, tearful
140
Q

Investigation of adrenal insufficiency

A

Sodium reduction, potassium elevation - Cortisol taken across multiple time points

141
Q

Treatment of adrenal insufficiency

A

Hormone replacement: glucocorticoid and mineralocorticoid

142
Q

Causes of secondary adrenal insufficiency

A

Due to reduction in adrenal cortex stimulation, low ACTH from inadequate pituitary or hypothalamic stimulation. Hypothalamic-pituitary disease Long term steroid therapy leading to hypothalamic-pituitary-adrenal axis suppression.

143
Q

Symptoms of secondary adrenal insufficiency

A

Same as primary, but without hyperpigmentation.

144
Q

Investigations of secondary adrenal insufficiency

A

Long ACTH test to distinguish from primary insufficiency - will be lowered in secondary, raised in primary

145
Q

Treatment of secondary adrenal insufficiency

A

Hormone replacement of hydrocortisone

146
Q

What occurs in the hypothalamus before onset of puberty?

A

GnRH neurons become functional before birth From birth to puberty these neurons are supressed

147
Q

What occurs in the hypothalamus at onset of puberty?

A

GnRH neurons become activated Hypothalamus begins a pulsatile secretion of GnRH

148
Q

What is adrenarche?

A

Maturation process of the adrenal gland at puberty

149
Q

What does adrenarche lead to?

A

Pubic hair Acne Body odour Oily skin and hair

150
Q

Describe precocious puberty

A

The hypothalamus begins to secrete GnRH early. 90% of these patients are female. Can be idiopathic, or due to CNS tumours or disorders

151
Q

How is precocious puberty investigated and treated?

A

A GnRH test is done where GnRH is injected, in true precocious puberty the body responds and LH and FSH are produced. Treatment with GnRH super-agonist, which suppresses the pulsatility of GnRH release.

152
Q

What causes precocious pseudo-puberty?

A

Due to too much androgen production, or secreting tumours.

153
Q

How are precocious puberty and precocious pseudo-puberty differentiated?

A

GnRH is injected In precocious the body responds and LH and FSH are produced. In precocious pseudo there is no response from the body.

154
Q

What defines delayed puberty in women?

A
  • lack of breast development by 13 - absent menarche by age 15-16
155
Q

What defines late puberty in men?

A
  • lack of pubic hair by 15 years - lack of testicular enlargement by 14
156
Q

What are the ‘syndrome’ causes of delayed puberty in men and women?

A

Men: Klinefelter syndrome Women: Turner syndrome

157
Q

Describe thelarche

A

Breast development Induced by oestrogen Ductal proliferation, adipose deposition, enlargement of areola and nipple

Phase 2a (7 decks)

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