Endocrinology Flashcards

1
Q

Describe the thyroid axis.

A

Hypothalamus releases TRH
Pituitary releases TSH
Thyroid releases T4 mostly and some T3 (T4 is converted to T3 peripherally)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name 4 functions of thyroid hormone.

A

Increase heart rate and cardiac output
Increases gut motility
Increase hepatic glucose output
Increase lipolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the epidemiology of hyperthyroidism?

A

Much more common in femaes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List the causes of hyperthyroidism

A

Graves’ Disease - 2/3 of cases
Toxic multinodular goitre
Solitary toxic adenoma
Drug induced - ie. amiodarone or lithium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the pathophysiology of Graves’ Disease

A

Autoimmune condition. Increase in TSH stimulating antibody which mimics TSH to stimulate thyroid hormone release from the thyroid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

List the symptoms of hyperthyroidism.

A
Diarrhoea
Weight loss 
Increased appetite
Sweats 
Heat intolerance 
Palpitations 
Tremor
Anxiety 
Menstrual disturbance - slow or no periods.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

List the signs of hyperthyroidism

A
Tachycardia 
Thin hair 
Goitre 
Fine tremor 
Lid lag
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the specific sign of Graves’ Disease?

A

Graves’ ophthalmology - swelling of the extra-ocular muscles causes pain and lid retraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the investigations for suspected hyperthyroidism?

A

Thyroid function tests - T3, T4 and TSH
Thyroid autoantibodies - TSH receptor stimulating antibodies in Graves’
Iodine uptake scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the results of thyroid function tests in primary hyperthyroidism (problem with the thyroid itself ie. toxic multinodular goitre)

A

Low TSH, raised T3/T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the results of thyroid function tests in secondary hyperthyroidism (problem with the pituitary ie. pitutary adenoma)

A

High TSH, raised T3/T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the treatment options for hyperthyroidism?

A

Block and replace - Carbimazole (anti-thyroid drug), thyroxine (to replace the thyroid hormone)
Radioiodine
Thyroidectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the treatment for a thyroid storm?

A

Beta blockers ie. propanolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the complications of hyperthyroidism?

A
Heart failure
Angina 
Atrial Fibrillation 
Ophthalmology 
Thyroid storm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the epidemiology of hypothyroidism?

A

Much more common in women.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the causes of hypothyroidism?

A

Primary atrophic hypothyroidism (autoimmune)
Hashimoto’s thyroiditis (autoimmune - causes goitre)
Iodine deficiency - biggest worldwide cause
Drug induced - amiodarone, lithium
Treatment of hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the symptoms of hypothyroidism?

A
Constipation  
Intolerance to cold 
Weight gain 
Tired 
Menstrual disturbance - heavy periods
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the signs of hypothyroidism?

A
Bradycardia 
Cold hands 
Ascites 
Goitre 
Round puffy face
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the mainstay of investigation for hypothyroidism?

A

Thyroid function tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the results of thyroid function tests for primary hypothyroidism (problem with the thyroid - ie. Hashimoto’s)

A

High TSH, Low T3/T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the results of thyroid function tests for secondary hypothyroidism (problem with the pituitary)

A

Low TSH, low T3/T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the treatment of hypothyroidism?

A

Give levothyroxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is a drug that can interfere with thyroid function?

A

Amiodarone - iodine rich drug.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What stimulates parathyroid hormone release?

A

Decrease circulating calcium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is the action of parathyroid hormone?
Increase bone resorption of calcium Increase gut absorption of calcium Increase kidney reabsorption of calcium
26
What is the cause of primary hyperparathyroidism?
Solitary adenoma | Diffuse hyperplasia
27
What is the presentation of hyperparathyroidism?
THINK INCREASED CALCIUM Weak, tired, depressed, thirsty, renal stones. Osteoporosis and fracture susceptibility Increased blood pressure
28
What investigations should be carried out in hyperparathyroidism?
Serum calcium, PTH and phosphate
29
What are the serum investigation results in primary hyperparathyroidism?
Raised calcium, raised PTH and low phosphate
30
What are the causes of secondary hyperparathyroidism?
This is an appropriate response to hypocalcaemia - caused by vit D deficiency or CKD.
31
What are the causes of tertiary hyperparathyroidism?
Often occurs as a result of longstanding secondary hyperparathyroidism and parathyroid hyperplasia.
32
What are the serum investigation results in secondary hyperparathyroidism?
Low calcium, high PTH, high phosphate
33
What are the serum investigation results in tertiary hyperparathyroidism?
High calcium, high PTH, high phosphate
34
What is the management of hyperparathyroidism?
Increase fluid intake to prevent stones Give bisphosphonates to support bones Excision of causative adenoma Parathyroidectomy
35
What are the three groups of hormones the adrenal cortex produces and give an example of each.
Glucocorticoids ie. cortisol Mineralocorticoid ie. aldosterone Androgens ie. DHEA
36
What is the axis that stimulates cortisol release from the adrenal gland?
Hypothalamus secreted CRH Anterior pituitary secretes ACTH Adrenal glands secrete cortisol
37
What is the function of cortisol
Many functions - think metabolism regulation.
38
What is Cushing's syndrome?
Clinical state of increased free circulating glucocorticoid (cortisol)
39
What is Cushing's Disease?
Clinical state of increased free circulating glucocorticoid (cortisol) caused by a pituitary adenoma.
40
What are the ACTH dependant causes of Cushing's syndrome?
``` Pituitary adenoma (ACTH secreting) - Cushing's disease Ectopic ACTH production - ie. small cell lung cancer. ```
41
What are the ACTH independent causes of Cushing's?
Adrenal adenoma Adrenal hyperplasia Exogenous steroids!!
42
What are the symptoms of Cushing's disease?
Increased weight Mood change - depression, psychosis Acne Muscular weakness
43
What are the signs of Cushing's disease?
``` central obesity Striae Moon face Glycosuria Skin and muscle atrophy ```
44
What investigations do you carry out in suspected Cushing's?
24-hour dexamethasone test - is dexamethasone does not suppress cortisol levels then Cushing's likely/ 24-hour urinary free cortisol - if normal Cushing's is unlikely.
45
Why do you not carry out a random plasma cortisol test in Cushing's?
Cortisol varies according to a circadian rhythm, stress and illness can influence levels also.
46
What is the treatment of iatrogenic Cushing's?
Stop steroids if possible
47
What is the treatment of Cushing's disease?
Surgical removal of pituitary adenoma.
48
What is the treatment of adrenal adenoma Cushing's?
Surgical removal or radiotherapy.
49
What is Nelson's syndrome?
A syndrome often caused by adrenalectomy, where there is no cortisol produced and so a build up of ACTH. causes bronze pigmentation, visual disturbances and headaches.
50
What is Addison's disease?
This is a form of autoimmune primary adrenal insufficiency
51
What are the causes of primary adrenal insufficiency?
Autoimmune - Addison's TB Adrenal metastases
52
What is the the most common worldwide cause of adrenal insufficiency?
TB
53
What are the symptoms of Addison's disease?
``` Weight loss Tiredness Low mood Nausea and vomiting 'tanned, tired, toned, tearful' ```
54
What are the signs of Addison's disease?
Bronze pigmentation - Nelson's syndrome due to ACTH build up. High potassium and low sodium (due to low aldosterone) Low glucose (due to low cortisol) Postural hypotension (low aldosterone) Muscle wasting
55
Investigation sin Addison's disease?
Blood tests show - High potassium and low sodium (due to low aldosterone) Low glucose (due to low cortisol) Adrenal autoantibody tests ACTH stimulation test - cortisol will be low.
56
What is the management of Addison's disease?
Replace steroids - hydrocortisone | Replace aldosterone - fludrocortisone
57
How does someone in an Addison's crisis present?
Shock, fluid loss, severe hypotension, loss of consciousness
58
How do you treat an Addison's crisis?
Steroids and fluids ASAP.
59
What is the cause of secondary adrenal insufficiency?
Long term steroids can suppress the pituitary-adrenal axis - so on withdrawal of steroids the adrenals no longer produce cortisol (aldosterone still produced).
60
What is Conn's syndrome?
Excess production of aldosterone caused by an aldosterone producing adenoma.
61
What is primary hyperaldosteronism?
Excess production of aldosterone independent of RAAS, causing sodium and water retention and decreased renin release.
62
What is the function of aldosterone?
Increase sodium (and water) retention and increase potassium excretion in the kidneys --> maintenance of blood pressure.
63
What are the causes of hyperaldosteronism?
Conn's syndrome - aldosterone producing adenoma | Bilateral adrenal hyperplasia
64
What are the symptoms of hyperaldosteronism?
``` Either asymptomatic or liked to hypokalaemia: Weakness Cramps Constipation Paraesthesia Polyuria Polydypsia ```
65
What are the signs of hyperaldosteronism?
Hypertension (sometimes) | Hypokalaemia (sometimes)
66
What are the investigations for suspected hyperaldorsteronism?
Plasma aldosterone - raised Plasma renin - low U+E - hypokalaemia
67
What is the treatment of Conn's syndrome?
laparoscopic adrenalectomy
68
What are the medical treatments of hyperaldorseronism?
Spinonolactone - this is a direct aldosterone antagonist
69
What is acromegaly?
Increased production of growth hormone in adults after fusion of the epiphyseal growth plates.
70
What is gigantism?
Increased production of growth hormone occurring in children.
71
What is the cause of acromegaly?
GH secreting pituitary tumour (99%) | pituitary hyperplasia
72
What is the growth hormone axis?
GHRH is secreted from the hypothalamus GH is secreted from the anterior pituitary GH acts on its target tissues
73
What are the symptoms of acromegaly?
Excessive sweating Decreased libido Headaches Muscular weakness
74
What are the signs of acromegaly?
Massive growth of hands, feet and jaw. Big tongue with widely spaced teeth Thick, greasy skin Deep voice
75
What are the complications of acromegaly?
Hypertension Obstructive sleep apnoea Heart disease Impaired glucose tolerance
76
Why do you not carry out a random GH test to diagnose?
This is pulsatile, increases with stress etc.
77
What is the typical diagnostic test for acromegaly?
Glucose tolerance test. Normally blood sugar rise will suppress GH, if they remain raised acromegaly is confirmed.
78
What other tests are carried out in acromegaly?
IGF-1 levels | MRI of pituitary fossa
79
What is the interventional treatment for acromegaly?
Surgery to remove the pituitary adenoma or radiotheraot
80
What are the pharmacological options available in acromegaly?
GH antagonist - pegvisomant Somatostatin analogues Dopamine agonists
81
What is diabetes insipidus?
A dysfunction of ADH - either reduced secretion from posterior pituitary or impaired response from the kidneys.
82
What is the action of ADH?
V1a receptor - vasoconstriction | V2 receptor - increased water resporption in the DCT and collecting duct of kidneys.
83
What are the causes of cranial diabetes insipidus?
``` Idiopathic Infection Head trauma Hypothalamic pituitary surgery Genetic ```
84
What are the causes of nephrogenic diabetes insipidus?
Chronic kidney disease Drugs - ie. lithium Genetic
85
What is the clinical presentation of diabetes insipidus?
Polyuria Polydypsia Dehydration
86
What are the investigations for diabetes insipidus?
Water deprivation test - restrict fluid, if urine osmolarity is low with a high plasma osmolarity then DI is indicated. Blood test shows high sodium levels.
87
What is the treatment of cranial diabetes insipidus?
Give desmopressin - ADH analogue
88
What is the treatment of nephrogenic diabetes insipidus?
Give diuretic bendroflumethizide and NSAIDsq
89
What does SIADH stand for?
Syndrome of inappropriate ADH secretion
90
What is SIADH?
Excess ADH secretion
91
What is the pathophysiological consequence of SIADH?
Water retention and hyponatraemia
92
What are the causes of SIADH?
Endocrine tumour ie. lung small cell Drugs ie. opiates CNS dysfunction
93
What is the clinical presentation of SIADH?
``` confusion Anorexia Nausea High urine osmolarity Hyponatraemia ```
94
What are the diagnostic features of SIADH?
Low plasma osmolarity with inappropriately high urine osmolarity. Absence of hypovolaemia, oedema and diuretics.
95
What is the treatment of SIADH?
Fluid intake restriction - if asymptomatic Give saline - if symptomatic Treat the cause Vasopressin receptor antagonists 'vaptans'
96
What are the causes of hypercalcaemia?
Malignancy | Primary hyperparathyroidism
97
What are the signs and symptoms of hypercalcaemia?
``` 'Bones, stones, groans and moans' Painful bones Kidney stones GI - nausea, vomiting and constipation CNS - lethargy, weakness and confusion. ```
98
How to differentiate between hypercalcaemia of malignancy or hyperparathyroidism?
In primary hyperparathyroidism - PTH will be high. In malignancy it will be low.
99
What is the treatment of hypercalcaemia?
Give saline to correct dehydration Give bisphosphonates to prevent bone resorption Treat the cause.
100
What are the causes of hypocalcaemia?
``` Hypoparathyroidism Psuedohypoparathyroidism (high PTH low response as there is a diminished response) Acute pancreatitis Vitamin D deficiency Osteomalacia Chronic kidney disease HAVOC. ```
101
What are the symptoms of hypocalcaemia?
``` Spasms Peripheral paraesthesia Anxious Seizures Muscle tone increase SPASM ```
102
What are the signs of hypocalcaemia?
ECG - long QT interval Chovsteck's sign - facial nerve spasm Trousseau's sign - hand spasm with BP cuff use.
103
Investigations for hypocalcaemia?
Serum corrected calcium = total serum calcium + 0.02 x (40-albumin). ECG To identify cause - PTH, creatinine, calcitriol.
104
How do you calculate corrected serum calcium?
Total serum calcium + 0.02 x (40-albumin).
105
Why is it necessary to calculate corrected calcium levels?
Serum calcium bind to albumin, so a low albumin may present as low serum calcium.
106
How do you treat mild hypocalcaemia?
Calcium supplements
107
How do you treat severe hypocalcaemia?
IV calcium gluconate
108
What are the causes of hypokalaemia?
``` Diuretics Hyperaldorsteronism Vomiting and diarrhoea GI absorption problems Alkalosis Renal tubular failure ```
109
What is the effect of hypokalaemia on the body?
Low potassium in ECF - water moves out of cells - the cells are hyperpolarised - there is a decrease in monocyte excitability.
110
What is the clinical presentation of hypokalaemia?
``` Muscle weakness Hypotonia Hyporeflexia Cramps Palpitations Constipatiom ```
111
What are suitable investigations of hypokalaemia?
Blood tests - U+E | ECG
112
What is the sign of hypokalaemia on ECG
``` U waves No P waves No T waves Long PR Long QT U have no P, no T, but a long PR and a long QT. ```
113
What is the treatment of mild hypokalaemia?
Oral potassium supplementation
114
What is the treatment of severe hypokalaemia?
IV potassium cautiously
115
What are the causes of hyperkalaemia?
``` K+ sparing diuretics Acidosis Excess K+ therapy Drugs - ACEi Addison's disease Mass cell lysis - ie. burns ```
116
What is the effect of hyperkalaemia on the body?
Partial depolarisation of the membranes moves the resting potential closer the the threshold potential and so there is hyper-excitability of the muscles.
117
What is the clinical presentation of hyperkalaemia?
Fast irregular pulse Chest pain Weakness Palpitations --> arrhythmias --> arrest
118
How may hyperkalaemia present as an artefact?
Haemolysis - band on venepuncture too tight or old sample. | Contamination with potassium anticoagulant in FBC bottle (always do FBC after U+E)
119
What are the ECG changes in hyperkalaemia?
Tall tented Small P waves Wide QRS >0.12s Ventricular fibrillation likely
120
What is the treatment in mild hyperkalaemia?
Polystyrene sulphonate resin - biks K+ in the gut preventing absoprtion
121
What is the treatment in severe hyperkalaemia?
Calcium gluconate - cardiac protective | Insulin - drives K+ into cells
122
What is the function of insulin?
Decreases hepatic glucose output | Increases glucose uptake by tissues
123
What cells secret insulin?
B-cells in the islets of Langerhans
124
What is the pathophysiology of type 1 diabetes?
A deficiency of insulin.
125
What is the pathogenesis of type 1 diabetes?
Autoimmune destruction of B-cells in the pancreas.
126
What is the effect of insulin deficiency?
Continued glycogen breakdown Uncontrolled gluconeogenesis Inappropriate hepatic glucose output --> uncontrolled hyperglycaemia.
127
What is the most common age of onset of type 1 diabetes?
Childhood - 5-15years.
128
What are the symptoms of type 1 diabetes?
``` Short, relatively sudden history Weight loss Nausea and vomiting Thirst Polyuria Hyperventilation - Kussmaul breathing (ketoacidosis) Blurred vision ```
129
What are the signs of type 1 diabetes?
``` Polyuria Polydipsia Underweight Ketouria Fruity smelling breath (due to ketones) ```
130
What are the genetic associations for type 1 diabetes?
HLA D3 and D4 association
131
What are the diagnostic criteria for type 1 diabetes?
``` Random plasma glucose test >11mmol/l OR Fasting plasma glucose >7mmol/l AND Symptoms of hyperglycaemia (weight loss, polyuria etc.) ```
132
What investigations to carry out in suspected diabetes?
Random plasma glucose test and/or fasting plasma glucose test.
133
What is the treatment of type 1 diabetes?
Insulin
134
What types of insulin therapies are there?
Short acting - typically given pre meal Long acting - typically given overnight Specific insulin regimes are constructed for individuals.
135
What are the difficulties of insulin therapy?
Complicated for patient to manage Injection site injury Weight gain Risk of hypoglycaemia
136
What are the possible complications of type 1 diabetes?
Hypoglycaemia | Diabetic ketoacidosis
137
What causes hypoglycaemia in type 1 diabetes?
Too much insulin leaves a glucose level of <3mmol/l
138
What are the symptoms of hypoglycaemia?
``` Trembling Sweating Confusion Seizure Weakness ```
139
How do you diagnose hypoglycaemia?
Blood glucose test <3mmol/l
140
How do you treat hypoglycaemia?
Give 15g glucose | Repeat test after 15 minutes and give more glucose if necessary.
141
What is diabetic ketoacidosis?
If there is an insulin deficiency then gluconeogenesis is uninhibited. Fatty acid - ketone conversion occurs excessively. Build up causes acidosis and dehydration. Eventually leads to circulatory collapse.
142
What are the symptoms of diabetic ketoacidosis?
Vomiting and nausea Confusion --> coma Weakness
143
What are the signs of diabetic ketoacidosis?
Fruity breath Hypotension Tachycardia Kussmaul breathing - deep and rapid breaths.
144
How do you diagnose ketoacidosis?
Acidaemia pH<7.3 Hyperglycaemia Ketonaemia
145
How do you treat diabetic ketoacidosis?
Fluid replacement and electrolytes as needed | Give insulin
146
What is the pathophysiology of type 2 diabetes?
A combination of insulin deficiency and resistance.
147
What is the pathogenesis of type 2 diabetes?
Progressive insulin resistance and B-cell decline results in reduced glucose uptake and failure to suppress elements of gluconeogenesis.
148
Why are is there not muscle wasting and ketogenesis in type 2 diabetes?
The low level of insulin produced is enough to suppress excessive gluconeogenesis.
149
What is the epidemiology of type 2 diabetes?
``` Older Obese Asian Male 'western lifestyle' ```
150
What are the risk factors for type 2 diabetes?
``` Male Asian Elderly Sedentary lifestyle High calorie intake Family history Obesity ```
151
What are the causes of type 2 diabetes?
Lifestyle choices - risk factors | Genetic inheritance
152
What are the symptoms of type 2 diabetes?
It is asymptomatic usually. | If extreme - polyuria/polydypsia
153
What investigations can be used to diagnose type 2 diabetes?
Random blood glucose test Fasting blood glucose test Oral glucose tolerance test HbA1c test
154
What results do you need to diagnose type 2 diabetes?
1 abnormal result and symptoms 2 abnormal results and asymptomatic Abnormal HbA1c
155
What are the results of a random blood glucose test?
>11mmoll = diabetes
156
What are the results of a fasting blood glucose test?
>7mmol/l = diabetes | 6 - 6.9mmol/l = pre-diabetes
157
What are the results of oral glucose tolerance test?
>11mmol/l = diabetes | 7.8 - 11mmol/l = pre diabetes
158
What are the results of HbAc1 test?
>48mmol/l = diabetes
159
What is impaired glucose tolerance?
Abnormality of glucose tolerance (OGTT 7.8-11mmol/l) that predispose a person to diabetes later on.
160
What is impaired fasting glucose?
Abnormality of fasting glucose (Fasting glucose 6.1-6.9mmol/l) that predispose a person to diabetes later on.
161
What is the treatment for pre diabetes?
Lifestyle advice only - healthy diet, exercise, weight control.
162
What is the first line pharmacological therapy for type 2 diabetes?
Metformin (act to increase sensitivity to insulin).
163
What are other hypoglycaemic agents that can be used in type 2 diabetes?
``` Sulphonylureas PPP4 inhibitor Pioglitazone SGLT-2i INSULIN ```
164
What are the possible complications of type 2 diabetes?
Hypoglycaemia | Hyperglycaemic hyperosmolar state
165
What is hyperglycaemic hyperosmolar state?
When sever hyperglycaemia develops without significant ketoacidosis.
166
What are the symptoms of hyperglycaemic hyperosmolar state?
Extreme dehydration | Confusion --> coma
167
How do you treat hyperglycaemic hyperosmolar state?
Insulin delivered cautiously.
168
What are the macrovascular complications of diabetes?
Diabetes is a risk factor for atherosclerosis which in turn is a risk for - Stroke Myocardial infarction Peripheral vascular risk
169
What are the three main microvascular complications of diabetes?
Diabetic retinopathy Diabetic neuropathy Diabetic nephropathy
170
What are the risk factors for microvascular complications?
Poo glycaemic control Hypertension Long duration of diabetes
171
What is the screening programme for diabetic retinopathy?
Once yearly after the age of 11
172
How to treat diabetic retinopathy?
Laser eye treatment
173
What causes diabetic retinopathy?
Microaneurysms, haemorrhages, lipid deposits, ischaemic damage.
174
What causes diabetic nephropathy?
Raised GFR causes damage and eventually microalbuminuria.
175
How do you diagnose diabetic nephropathy?
Presence of microalbuminuria.
176
How do you manage diabetic nephropathy?
Blood pressure control, glycaemic control, cholesterol control
177
What is diabetic neuropathy?
Decreased sensation in the peripheries - typically symmetrical sensory.
178
What are the consequences of diabetic neuropathy?
Foot ulceration - injury goes unnoticed Infection Motor nerve damage
179
How to manage diabetic neuropathy?
``` Patient eduction - foot inspection Regular chiropody Improve glycaemic control Vascular surgery Eventually --> amputation ```
180
What are rarer causes of diabetes?
Maturity onset diabetes of the young Permanent neonatal diabetes Lipodystrophy Endocrine causes - acromegaly