My endocrine Flashcards
1
Q
What is diabetes mellitus?
A
Diabetes mellitus is a disorder of carbohydrate metabolism characterised by hyperglycaemia
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
3
Q
What is the HbA1c concentration needed to diagnose diabetes?
A
HbA1c of 48 mmol/mol (6.5%)
4
Q
What is pancreatic diabetes?
A
Part of the pancreas is damaged or removed due to pancreatitis
5
Q
What is endocrine diabetes?
A
Diabetes caused by acromegaly or cushing’s
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
7
Q
What is diabetic ketoacidosis?
A
A triad of hyperglycaemia with metabolic acidosis and ketonaemia. Causes hyperventilation, nausea, vomiting, abdominal pain.
8
Q
How can chronic hyperglycaemia cause morbidity?
A
- Microvascular and macrovascular tissue complications.
- Diabetic retinopathy
- Stroke
- Cardiovascular disease
- Diabetic neuropathy
- Diabetic nephropathy
9
Q
How else can diabetes cause morbidity?
A
Side effects of treatment, such as hypoglycaemia
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.
11
Q
What does hypoglycaemia in the brain lead to?
A
- Cognitive dysfunction
- Confusion
- Drowsiness
- Vision changes
- Difficulty speaking
- Blackouts
- Seizures
- Comas
12
Q
How does hypoglycaemia affect the heart?
A
- Arrhythmias
- Risk of myocardial ischaemia
13
Q
How does hypoglycaemia affect the circulation?
A
- Inflammation
- Blood coagulation abnormalities
- Haemodynamic changes
- Endothelial dysfunction
14
Q
How does hypoglycaemia affect the skeleton?
A
Falls and accidents due to cognitive dysfunction
Leads to fractures and dislocations
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)
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)
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
18
Q
What is lipodystrophy?
A
Unusual distribution of adipose tissue
Very high insulin resistance
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
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
21
Q
What is pancreatic neoplasia?
A
Common cause of cancer death
Require subcutaneous insulin
Prone to hypoglycaemia due to loss of glucagon function
22
Q
What is cystic fibrosis and how does it lead to diabetes?
A
Makes all secretions viscous, obstructs pancreatic ducts
Insulin treatment required
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
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
25
How can drugs induce diabetes?
Glucocorticoids increase insulin resistance - iatrogenic due to steroids
26
Describe type I diabetes
Insulin deficiency disease characterised by a loss of beta cells due to autoimmune destruction.
27
How is type I initiated?
Genetic susceptibility coupled with environmental triggers
28
What is the visceral and peripheral response to lack of insulin in type I diabetes?
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
29
When does glucose begin to appear in urine?
When the renal threshold of 10mM is exceeded
30
What does this lack of insulin response lead to?
Percieved stress leads to increased cortisol and adrenaline Progressive catabolic state and increasing levels of ketones
31
How does type I diabetes present in young patients?
2-6 week history
* Thirst
* Polyuria
* Weight loss
* Hunger
32
What testing would be done in a young patient with symptoms pointing to type I - and what would the results show?
Urine dipstick: detect glucose and ketones
Blood antibody test: detect high levels of islet antibodies
33
Why do type I diabetics experience thirst?
High blood glucose causes osmotic activation of the hypothalamus
34
Why do type I diabetics experience polyuria?
Blood glucose exceeds renal tubular eabsorptive capacity (renal threshold) This leads to osmotic diuresis of water
35
Why do type I diabetics experience weight loss?
Fluid depletion and insulin deficiency leads to muscle and fat breakdown
36
Why do type I diabetics experience hunger?
Lack of useable energy source
37
How do older patients with type I present?
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
38
What is basal and prandial insulin?
Basal insulin: maintains constant, low concentration of insulin Prandial insulin: rapid acting, taken just before meal time
39
Describe type II diabetes
Impaired insulin secretion and insulin resistance due to a combination of genetic predisposition and environmental factors
40
What does impaired insulin action in type II diabetes lead to?
* 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
41
Are blood ketone levels high in type II?
No, because even low levels of insulin restrict muscle catabolism and ketogenesis
42
Presentation of type II
* Gradual onset
* Lack of energy
* Likely to have a family history
43
How is type II diabetes tested?
* Fasting plasma glucose of above 7mmol/L
* Random plasma glucose of above 11mmol/L
44
Ideal treatment for type II
Weight loss and exercise, which if substantial will reverse hyperglycaemia
45
Why is type II treated with drugs instead of lifestyle typically?
Most with type II have been making the opposite lifestyle choices their whole lives
46
What are the aims of drugs for type II?
* Control blood pressure
* Control blood glucose
* Control lipids
47
Describe metformin
Insulin sensitiser
48
Effects of sulphonylureas
Stimulate insulin release by binding to beta cell receptors
Improve glycaemic control
49
Negatives of sulphonylureas
* Cause weight gain
* Do not prevent gradual failure of insulin secretion
* Can cause hypoglycaemia
50
Describe thiazoldinediones
* Bind to nuclear receptors to activate genes associated with glucose uptake and utilisation, and lipid metabolism
* Improve insulin sensitivity
* Used alongside insulin
51
Describe SGLT2 inhibitors
Sodium-glucose cotransporters reabsorb glucose into blood from the kidney
Inhibitors block the reabsorption of glucose, increase excretion, and lower blood glucose levels
52
Are thyroid disorders more common in men or women?
Women
53
What causes hyperthyroidism?
* Overproduction of thyroid hormone
* Leakage of pre-formed hormone from the thyroid
* Ingestion of excess thyroid hormone
* Drugs eg iodine, lithium
54
Symptoms of hyperthyroidism
* Thin hair
* Lid retraction
* Anxiety
* Irritability
* Hyperphagia
* Goitre
* Tachycardia (>100bpm)
* Palpitations
* Menstrual disturbance - oligomenorrhoea
* Heat intolerance and sweating
* Tremor
* Diarrhoea
* Weight loss
55
Investigations for hyperthyroidism
Thyroid function tests - test for low thyroid stimulating hormone, and high free T4 and T3.
Can also perform visual field test electronically
56
What would symptoms of hyperthyroidism as well as high blood TSH show?
A pituitary function issue
57
What do isotope scans do?
Use radoiactive iodine to show the thyroid's shape and size
58
Drug treatments for hyperthyroidism
* Beta blockers ameliorate tachycardia, palpitations, anxiety, and heat intolerance
* Antithyroid drugs (carbimazole) decrease synthesis of new thyroid hormone
59
Non-drug treatments for hyperthyroidism
* Radioiodine delivers radiation to the thyroid gland to cause local distruction
* Total thyroidectomy (rare)
60
What are the negatives of radioiodine and thyroidectomy?
Both can lead to hypothyroidism
Radioiodine: cannot be given during pregnancy or breastfeeding
Thyroidectomy: can damage the laryngeal nerve
61
Describe Grave's disease
Autoimmune process driven by TSH receptor antibodies. These stimulate the thyroid to produce thyroid hormone.
62
What can trigger Grave's disease?
Childbirth
63
Additional hyperthyroid symptoms caused by Grave's disease
* 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
How is Grave's disease tested?
Test for thyroid stimulating antibodies. Will also have high T3 and T4, and lower TSH
65
Treatment for Grave's disease
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
Types of hypothyroidism
Primary: absent or dysfunctional thyroid gland
Secondary: due to pituitary or hypothalamic dysfunction
Transient: after withdrawal of drugs, pregnancy, congenital
67
Causes of primary hypothyroidism
* Hashimoto's thyroiditis
* Atrophic thyroiditis
* Iodine deficiency
* Congenital defects
68
Symptoms of hypothyroidism
* 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
How is hypothyroidism investigated?
Blood tests: high TSH, low free T4 and T3
70
What would symptoms of hypothyroidism as well as low blood TSH show?
A pituitary function issue
71
How does atrophic thyroiditis show in a blood test?
High TSH, low free T3 and T4
anti-TPO and anti-TSH antibodies
72
How is hypothyroidism treated?
Levothyroxine (T4)
Some patients may also need T3
73
Describe Hashimoto's thyroiditis
Hypothyroidism due to aggressive destruction of thyroid cells.
Antibodies bind and block TSH receptors, leading to inadequate thyroid hormone production and secretion.
74
How can Hashimoto's cause dyspnoea or dysphagia?
The thyroid gland may enlarge rapidly, leading to pressure on the neck.
75
How is Hashimoto's tested?
High TSH levels, and thyroid antibodies in the plasma.
76
How is Hashimoto's treated
Thyroid replacement - levothyroxine
77
Why can pregnancy affect thyroid function?
HCG has a similar structure to thyroid stimulating hormone, and can act like a weak form of TSH to stimulate the thyroid
78
Name the 5 types of thyroid cancer
* Papillary
* Follicular
* Anaplastic
* Lymphoma
* Medullary
79
Describe papillary thyroid cancer
* Most common thyroid cancer
* Asymptomatic thyroid nodule usually in one lobe
* Tends to spread locally in the neck, compressing the trachea
80
Describe follicular thyroid cancer
* Asymptomatic thyroid nodule
* May infiltrate the neck
* Develops from follicular cells
* Next most common after papillary
81
How are thyroid cancers typically removed?
Total thyroidectomy, followed by radioactive iodine
82
How is pituitary disregulation identified?
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
Name the 6 hormones released by the anterior pituitary gland
* Growth hormone
* Thyroid-stimulating hormone
* Follicle-stimulating hormone
* Lutenising hormone
* Prolactin
* Adrenocorticotropic hormone
84
What causes diabetes insipidus?
Either due to:
* Cranial: Lack of vasopressin release by the hypothalamus
* Nephrogenic: Resistance to action of vasopressin
85
What does diabetes insipidus lead to?
* Polyuria, polydipsia
* Urine volume 3L a day
* High plasma osmolality
* Seen with low copeptin (released with normal ADH production)
86
What occurs if the posterior pituitary releases too much vasopressin?
* 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
What causes cranial diabetes insipidus?
* Neurosurgery
* Trauma
* Tumour
* Infiltrative disease
* Idiopathic
* Genetic: mutation in the ADH gene
88
How is cranial diabetes insipidus treated?
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
What causes nephrogenic diabetes insipidus?
* 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
How is nephrogenic diabetes insipidus treated?
Treatment of the underlying cause
91
How is diabetes insipidus diagnosed?
* 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
What is secondary hypothyroidism?
Hypothyroidism caused by low thyroid-stimulating hormone release by the pituitary
93
Name tumours that can affect the pituitary
* 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
Other than tumours, what else can affect pituitary function?
* Trauma to the head
* Haemorrhage and stroke
* Sarcoidosis
95
What are the effects of pituitary tumours?
Pressure on local structures Pressure on normal pituitary causing hypopituitarism Functional tumours producing hormones
96
How would a patient with a non-functional pituitary tumour present?
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
Main three functional pituitary tumours
Prolactinoma Growth hormone-producing ACTH-producing
98
Affects of prolactinoma
Galactorrhea (milk production) Amenorrhoea (menstrual irregularity) Men have low testosterone, so low libido If large, can cause headaches and visual field defects
99
How is prolactinoma treated?
Dopamine agonists, causing shrinkage of the tumour (dopamine inactivates prolactin)
100
Affects of growth hormone-producing tumour
Acromegaly: Simulates muscle, bone, and fat Stimulates the liver to produce IGF-I In childhood, causes gigantism
101
Acromegaly presentation in adults
Headache Pronounced jaw and orbital ridge Sleep apnoea Excessive sweating Hypertension, heart disease, cardiovascular events Arthiritis Large feet and hands Insulin-resistant diabetes
102
How is acromegaly tested?
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
How is acromegaly treated?
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
Describe Cushing's disease
Due to persistently elevated glucocorticoid (cortisol) due to innapropriate ACTH secretion from the pituitary or from taking glucocorticoid medicines
105
Symptoms of Cushing's
Obesity with central fat distribution Rounded moon face Striae (stretch marks) Bruising Hypertension Pathological fractures Plethoric complexion
106
What causes pseudo-cushings?
Excessive alcohol consumption - resolves on alcohol recession
107
How is Cushing's diagnosed?
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
Describe syndrome of innapropriate ADH secretion
Continued ADH secretion in spite of plasma hypotonicity and normal plasma volume.
109
What does syndrome of innapropriate ADH secretion lead to?
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
Symptoms of syndrome of inappropriate secretion of ADH
can be no or mild symptoms if chronic - more severe if acute headache, irritability, nausea, mental slowing, unstable gait, confusion
111
Causes of syndrome of inappropriate secretion of ADH
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
What can cause hypoparathyroidism?
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
What are the effects of hypoparathyroidism?
Decreased renal calcium reabsorption Increased renal phosphate reabsorption Decreased bone resorption Decreased activation of vitamin D - decreased intestinal calcium absorption
114
What are the effects of hypocalcaemia?
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
How is hypoparathyroidism investigated?
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 –serum 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
Treatment of hypoparathyroidism
Calcium supplements Calcitriol - mimics calcium
117
What causes pseudohypoparathyroidism?
Resistance to parathyroid hormone, typically due to rare inherited disorders
118
What are the effects of pseudohypoparathyroidism?
Low serum calcium increased parathyroid hormone low bone resorption kidney calcium reabsorption gut absorption
119
What are the symptoms of pseudohypoparathyroidism?
Symptoms of hypocalcaemia Short stature Obesity Round face Mild learning difficulties Subcutaneous ossification Short fourth metacarpals
120
What are the causes of primary hyperparathyroidism?
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
Effects of primary hyperparathyroidism
Bones: osteitis fibrosa cystica (rare), osteoporosis Kidney stones (renal calculi) Psychic groans: confusion Abdominal moans: constipation, acute pancreatitis
122
Symptoms of primary hyperparathyroidism
70-80% of patients are asymptomatic bone pain nausea neuropsychiatric effects
123
Investigation of primary hyperparathyroidism
Bloods will show hypercalcaemia (and raised parathyroid)
124
Treatment of primary hyperparathyroidism
Adenoma will need surgical removal Biphosphonates (strengthen bones)
125
What causes secondary hyperparathyroidism?
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
Effects of secondary hyperparathyroidism
Kidney disease Skeletal complications Cardiovascular complications
127
Investigation of secondary hyperparathyroidism
Bloods will show hypocalcaemia (and raised parathyroid)
128
Treatment of secondary hyperparathyroidism
Calcium correction Treat underlying condition
129
Cause of tertiary hyperparathyroidism
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
Symptoms of tertiary hyperparathyroidism
Same as primary: Bone pain Renal stones Nausea Neuropsychiatric
131
Investigations of tertiary hyperparathyroidism
Bloods will show hypercalcaemia (and raised parathyroid).
132
Treatment of tertiary hyperparathyroidism
Calcium mimetic - cinacalcet Total or subtotal parathyroidectomy - this may lead to hypocalcaemia
133
Conn's syndrome
An adrenal adenoma causing primary hyperaldosteronism - high aldosterone levels independent of the renin-angiotensin-aldosterone system.
134
What is the other cause of primary hyperaldosteronism?
Adrenocortical hyperplasia
135
Effects of primary hyperaldosteronism
Hypertension Hypokalaemia
136
Treatment of primary hyperaldosteronism
Conn's: Surgical removal of adenoma Aldosterone agonist (spironolactone) for hyperplasia
137
What causes secondary hyperaldosteronism?
Hyperaldosteronism due to high renin levels
138
Addison's disease
Primary adrenal insufficiency due to autoimmune destruction of the adrenal cortex. This leads to a reduction in cortisol and aldosterone.
139
Symptoms of adrenal insufficiency
- Lethargy - Depression - Anorexia - Weight loss - Weakness - Fatigue - Hyperpigmentation - 4 Ts: thin, tanned, tired, tearful
140
Investigation of adrenal insufficiency
Sodium reduction, potassium elevation - Cortisol taken across multiple time points
141
Treatment of adrenal insufficiency
Hormone replacement: glucocorticoid and mineralocorticoid
142
Causes of secondary adrenal insufficiency
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
Symptoms of secondary adrenal insufficiency
Same as primary, but without hyperpigmentation.
144
Investigations of secondary adrenal insufficiency
Long ACTH test to distinguish from primary insufficiency - will be lowered in secondary, raised in primary
145
Treatment of secondary adrenal insufficiency
Hormone replacement of hydrocortisone
146
What occurs in the hypothalamus before onset of puberty?
GnRH neurons become functional before birth From birth to puberty these neurons are supressed
147
What occurs in the hypothalamus at onset of puberty?
GnRH neurons become activated Hypothalamus begins a pulsatile secretion of GnRH
148
What is adrenarche?
Maturation process of the adrenal gland at puberty
149
What does adrenarche lead to?
Pubic hair Acne Body odour Oily skin and hair
150
Describe precocious puberty
The hypothalamus begins to secrete GnRH early. 90% of these patients are female. Can be idiopathic, or due to CNS tumours or disorders
151
How is precocious puberty investigated and treated?
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
What causes precocious pseudo-puberty?
Due to too much androgen production, or secreting tumours.
153
How are precocious puberty and precocious pseudo-puberty differentiated?
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
What defines delayed puberty in women?
- lack of breast development by 13 - absent menarche by age 15-16
155
What defines late puberty in men?
- lack of pubic hair by 15 years - lack of testicular enlargement by 14
156
What are the 'syndrome' causes of delayed puberty in men and women?
Men: Klinefelter syndrome Women: Turner syndrome
157
Describe thelarche
Breast development Induced by oestrogen Ductal proliferation, adipose deposition, enlargement of areola and nipple
