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Phase 2a - conditions > Endocrinology > Flashcards

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)

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2
Q

Name 4 functions of thyroid hormone.

A

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

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3
Q

What is the epidemiology of hyperthyroidism?

A

Much more common in femaes

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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

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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.

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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.
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7
Q

List the signs of hyperthyroidism

A 
Tachycardia 
Thin hair 
Goitre 
Fine tremor 
Lid lag
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8
Q

What is the specific sign of Graves’ Disease?

A

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

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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

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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

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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

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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

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13
Q

What is the treatment for a thyroid storm?

A

Beta blockers ie. propanolol

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14
Q

What are the complications of hyperthyroidism?

A 
Heart failure
Angina 
Atrial Fibrillation 
Ophthalmology 
Thyroid storm
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15
Q

What is the epidemiology of hypothyroidism?

A

Much more common in women.

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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

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17
Q

What are the symptoms of hypothyroidism?

A 
Constipation  
Intolerance to cold 
Weight gain 
Tired 
Menstrual disturbance - heavy periods
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18
Q

What are the signs of hypothyroidism?

A 
Bradycardia 
Cold hands 
Ascites 
Goitre 
Round puffy face
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19
Q

What is the mainstay of investigation for hypothyroidism?

A

Thyroid function tests

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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

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21
Q

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

A

Low TSH, low T3/T4

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22
Q

What is the treatment of hypothyroidism?

A

Give levothyroxine

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23
Q

What is a drug that can interfere with thyroid function?

A

Amiodarone - iodine rich drug.

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24
Q

What stimulates parathyroid hormone release?

A

Decrease circulating calcium.

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25
Q

What is the action of parathyroid hormone?

A

Increase bone resorption of calcium
Increase gut absorption of calcium
Increase kidney reabsorption of calcium

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26
Q

What is the cause of primary hyperparathyroidism?

A

Solitary adenoma

Diffuse hyperplasia

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27
Q

What is the presentation of hyperparathyroidism?

A

THINK INCREASED CALCIUM
Weak, tired, depressed, thirsty, renal stones.
Osteoporosis and fracture susceptibility
Increased blood pressure

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28
Q

What investigations should be carried out in hyperparathyroidism?

A

Serum calcium, PTH and phosphate

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29
Q

What are the serum investigation results in primary hyperparathyroidism?

A

Raised calcium, raised PTH and low phosphate

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30
Q

What are the causes of secondary hyperparathyroidism?

A

This is an appropriate response to hypocalcaemia - caused by vit D deficiency or CKD.

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31
Q

What are the causes of tertiary hyperparathyroidism?

A

Often occurs as a result of longstanding secondary hyperparathyroidism and parathyroid hyperplasia.

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32
Q

What are the serum investigation results in secondary hyperparathyroidism?

A

Low calcium, high PTH, high phosphate

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33
Q

What are the serum investigation results in tertiary hyperparathyroidism?

A

High calcium, high PTH, high phosphate

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34
Q

What is the management of hyperparathyroidism?

A

Increase fluid intake to prevent stones
Give bisphosphonates to support bones
Excision of causative adenoma
Parathyroidectomy

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35
Q

What are the three groups of hormones the adrenal cortex produces and give an example of each.

A

Glucocorticoids ie. cortisol
Mineralocorticoid ie. aldosterone
Androgens ie. DHEA

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36
Q

What is the axis that stimulates cortisol release from the adrenal gland?

A

Hypothalamus secreted CRH
Anterior pituitary secretes ACTH
Adrenal glands secrete cortisol

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37
Q

What is the function of cortisol

A

Many functions - think metabolism regulation.

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38
Q

What is Cushing’s syndrome?

A

Clinical state of increased free circulating glucocorticoid (cortisol)

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39
Q

What is Cushing’s Disease?

A

Clinical state of increased free circulating glucocorticoid (cortisol) caused by a pituitary adenoma.

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40
Q

What are the ACTH dependant causes of Cushing’s syndrome?

A 
Pituitary adenoma (ACTH secreting) - Cushing's disease 
Ectopic ACTH production - ie. small cell lung cancer.
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41
Q

What are the ACTH independent causes of Cushing’s?

A

Adrenal adenoma
Adrenal hyperplasia
Exogenous steroids!!

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42
Q

What are the symptoms of Cushing’s disease?

A

Increased weight
Mood change - depression, psychosis
Acne
Muscular weakness

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43
Q

What are the signs of Cushing’s disease?

A 
central obesity 
Striae 
Moon face 
Glycosuria 
Skin and muscle atrophy
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44
Q

What investigations do you carry out in suspected Cushing’s?

A

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.

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45
Q

Why do you not carry out a random plasma cortisol test in Cushing’s?

A

Cortisol varies according to a circadian rhythm, stress and illness can influence levels also.

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46
Q

What is the treatment of iatrogenic Cushing’s?

A

Stop steroids if possible

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47
Q

What is the treatment of Cushing’s disease?

A

Surgical removal of pituitary adenoma.

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48
Q

What is the treatment of adrenal adenoma Cushing’s?

A

Surgical removal or radiotherapy.

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49
Q

What is Nelson’s syndrome?

A

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.

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50
Q

What is Addison’s disease?

A

This is a form of autoimmune primary adrenal insufficiency

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51
Q

What are the causes of primary adrenal insufficiency?

A

Autoimmune - Addison’s
TB
Adrenal metastases

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52
Q

What is the the most common worldwide cause of adrenal insufficiency?

A

TB

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53
Q

What are the symptoms of Addison’s disease?

A 
Weight loss 
Tiredness 
Low mood 
Nausea and vomiting 
'tanned, tired, toned, tearful'
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54
Q

What are the signs of Addison’s disease?

A

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

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55
Q

Investigation sin Addison’s disease?

A

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.

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56
Q

What is the management of Addison’s disease?

A

Replace steroids - hydrocortisone

Replace aldosterone - fludrocortisone

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57
Q

How does someone in an Addison’s crisis present?

A

Shock, fluid loss, severe hypotension, loss of consciousness

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58
Q

How do you treat an Addison’s crisis?

A

Steroids and fluids ASAP.

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59
Q

What is the cause of secondary adrenal insufficiency?

A

Long term steroids can suppress the pituitary-adrenal axis - so on withdrawal of steroids the adrenals no longer produce cortisol (aldosterone still produced).

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60
Q

What is Conn’s syndrome?

A

Excess production of aldosterone caused by an aldosterone producing adenoma.

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61
Q

What is primary hyperaldosteronism?

A

Excess production of aldosterone independent of RAAS, causing sodium and water retention and decreased renin release.

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62
Q

What is the function of aldosterone?

A

Increase sodium (and water) retention and increase potassium excretion in the kidneys –> maintenance of blood pressure.

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63
Q

What are the causes of hyperaldosteronism?

A

Conn’s syndrome - aldosterone producing adenoma

Bilateral adrenal hyperplasia

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64
Q

What are the symptoms of hyperaldosteronism?

A 
Either asymptomatic or liked to hypokalaemia: 
Weakness 
Cramps
Constipation
Paraesthesia 
Polyuria 
Polydypsia
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65
Q

What are the signs of hyperaldosteronism?

A

Hypertension (sometimes)

Hypokalaemia (sometimes)

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66
Q

What are the investigations for suspected hyperaldorsteronism?

A

Plasma aldosterone - raised
Plasma renin - low
U+E - hypokalaemia

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67
Q

What is the treatment of Conn’s syndrome?

A

laparoscopic adrenalectomy

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68
Q

What are the medical treatments of hyperaldorseronism?

A

Spinonolactone - this is a direct aldosterone antagonist

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69
Q

What is acromegaly?

A

Increased production of growth hormone in adults after fusion of the epiphyseal growth plates.

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70
Q

What is gigantism?

A

Increased production of growth hormone occurring in children.

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71
Q

What is the cause of acromegaly?

A

GH secreting pituitary tumour (99%)

pituitary hyperplasia

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72
Q

What is the growth hormone axis?

A

GHRH is secreted from the hypothalamus
GH is secreted from the anterior pituitary
GH acts on its target tissues

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73
Q

What are the symptoms of acromegaly?

A

Excessive sweating
Decreased libido
Headaches
Muscular weakness

74
Q

What are the signs of acromegaly?

A

Massive growth of hands, feet and jaw.
Big tongue with widely spaced teeth
Thick, greasy skin
Deep voice

75
Q

What are the complications of acromegaly?

A

Hypertension
Obstructive sleep apnoea
Heart disease
Impaired glucose tolerance

76
Q

Why do you not carry out a random GH test to diagnose?

A

This is pulsatile, increases with stress etc.

77
Q

What is the typical diagnostic test for acromegaly?

A

Glucose tolerance test. Normally blood sugar rise will suppress GH, if they remain raised acromegaly is confirmed.

78
Q

What other tests are carried out in acromegaly?

A

IGF-1 levels

MRI of pituitary fossa

79
Q

What is the interventional treatment for acromegaly?

A

Surgery to remove the pituitary adenoma or radiotheraot

80
Q

What are the pharmacological options available in acromegaly?

A

GH antagonist - pegvisomant
Somatostatin analogues
Dopamine agonists

81
Q

What is diabetes insipidus?

A

A dysfunction of ADH - either reduced secretion from posterior pituitary or impaired response from the kidneys.

82
Q

What is the action of ADH?

A

V1a receptor - vasoconstriction

V2 receptor - increased water resporption in the DCT and collecting duct of kidneys.

83
Q

What are the causes of cranial diabetes insipidus?

A 
Idiopathic 
Infection 
Head trauma 
Hypothalamic pituitary surgery 
Genetic
84
Q

What are the causes of nephrogenic diabetes insipidus?

A

Chronic kidney disease
Drugs - ie. lithium
Genetic

85
Q

What is the clinical presentation of diabetes insipidus?

A

Polyuria
Polydypsia
Dehydration

86
Q

What are the investigations for diabetes insipidus?

A

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
Q

What is the treatment of cranial diabetes insipidus?

A

Give desmopressin - ADH analogue

88
Q

What is the treatment of nephrogenic diabetes insipidus?

A

Give diuretic bendroflumethizide and NSAIDsq

89
Q

What does SIADH stand for?

A

Syndrome of inappropriate ADH secretion

90
Q

What is SIADH?

A

Excess ADH secretion

91
Q

What is the pathophysiological consequence of SIADH?

A

Water retention and hyponatraemia

92
Q

What are the causes of SIADH?

A

Endocrine tumour ie. lung small cell
Drugs ie. opiates
CNS dysfunction

93
Q

What is the clinical presentation of SIADH?

A 
confusion 
Anorexia 
Nausea 
High urine osmolarity 
Hyponatraemia
94
Q

What are the diagnostic features of SIADH?

A

Low plasma osmolarity with inappropriately high urine osmolarity. Absence of hypovolaemia, oedema and diuretics.

95
Q

What is the treatment of SIADH?

A

Fluid intake restriction - if asymptomatic
Give saline - if symptomatic
Treat the cause
Vasopressin receptor antagonists ‘vaptans’

96
Q

What are the causes of hypercalcaemia?

A

Malignancy

Primary hyperparathyroidism

97
Q

What are the signs and symptoms of hypercalcaemia?

A 
'Bones, stones, groans and moans'
Painful bones 
Kidney stones 
GI - nausea, vomiting and constipation 
CNS - lethargy, weakness and confusion.
98
Q

How to differentiate between hypercalcaemia of malignancy or hyperparathyroidism?

A

In primary hyperparathyroidism - PTH will be high. In malignancy it will be low.

99
Q

What is the treatment of hypercalcaemia?

A

Give saline to correct dehydration
Give bisphosphonates to prevent bone resorption
Treat the cause.

100
Q

What are the causes of hypocalcaemia?

A 
Hypoparathyroidism
Psuedohypoparathyroidism (high PTH low response as there is a diminished response) 
Acute pancreatitis 
Vitamin D deficiency
Osteomalacia 
Chronic kidney disease 
HAVOC.
101
Q

What are the symptoms of hypocalcaemia?

A 
Spasms 
Peripheral paraesthesia 
Anxious 
Seizures 
Muscle tone increase 
SPASM
102
Q

What are the signs of hypocalcaemia?

A

ECG - long QT interval
Chovsteck’s sign - facial nerve spasm
Trousseau’s sign - hand spasm with BP cuff use.

103
Q

Investigations for hypocalcaemia?

A

Serum corrected calcium = total serum calcium + 0.02 x (40-albumin).
ECG
To identify cause - PTH, creatinine, calcitriol.

104
Q

How do you calculate corrected serum calcium?

A

Total serum calcium + 0.02 x (40-albumin).

105
Q

Why is it necessary to calculate corrected calcium levels?

A

Serum calcium bind to albumin, so a low albumin may present as low serum calcium.

106
Q

How do you treat mild hypocalcaemia?

A

Calcium supplements

107
Q

How do you treat severe hypocalcaemia?

A

IV calcium gluconate

108
Q

What are the causes of hypokalaemia?

A 
Diuretics 
Hyperaldorsteronism 
Vomiting and diarrhoea 
GI absorption problems 
Alkalosis 
Renal tubular failure
109
Q

What is the effect of hypokalaemia on the body?

A

Low potassium in ECF - water moves out of cells - the cells are hyperpolarised - there is a decrease in monocyte excitability.

110
Q

What is the clinical presentation of hypokalaemia?

A 
Muscle weakness 
Hypotonia
Hyporeflexia
Cramps
Palpitations 
Constipatiom
111
Q

What are suitable investigations of hypokalaemia?

A

Blood tests - U+E

ECG

112
Q

What is the sign of hypokalaemia on ECG

A 
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
Q

What is the treatment of mild hypokalaemia?

A

Oral potassium supplementation

114
Q

What is the treatment of severe hypokalaemia?

A

IV potassium cautiously

115
Q

What are the causes of hyperkalaemia?

A 
K+ sparing diuretics 
Acidosis
Excess K+ therapy 
Drugs - ACEi 
Addison's disease 
Mass cell lysis - ie. burns
116
Q

What is the effect of hyperkalaemia on the body?

A

Partial depolarisation of the membranes moves the resting potential closer the the threshold potential and so there is hyper-excitability of the muscles.

117
Q

What is the clinical presentation of hyperkalaemia?

A

Fast irregular pulse
Chest pain
Weakness
Palpitations –> arrhythmias –> arrest

118
Q

How may hyperkalaemia present as an artefact?

A

Haemolysis - band on venepuncture too tight or old sample.

Contamination with potassium anticoagulant in FBC bottle (always do FBC after U+E)

119
Q

What are the ECG changes in hyperkalaemia?

A

Tall tented
Small P waves
Wide QRS >0.12s
Ventricular fibrillation likely

120
Q

What is the treatment in mild hyperkalaemia?

A

Polystyrene sulphonate resin - biks K+ in the gut preventing absoprtion

121
Q

What is the treatment in severe hyperkalaemia?

A

Calcium gluconate - cardiac protective

Insulin - drives K+ into cells

122
Q

What is the function of insulin?

A

Decreases hepatic glucose output

Increases glucose uptake by tissues

123
Q

What cells secret insulin?

A

B-cells in the islets of Langerhans

124
Q

What is the pathophysiology of type 1 diabetes?

A

A deficiency of insulin.

125
Q

What is the pathogenesis of type 1 diabetes?

A

Autoimmune destruction of B-cells in the pancreas.

126
Q

What is the effect of insulin deficiency?

A

Continued glycogen breakdown
Uncontrolled gluconeogenesis
Inappropriate hepatic glucose output
–> uncontrolled hyperglycaemia.

127
Q

What is the most common age of onset of type 1 diabetes?

A

Childhood - 5-15years.

128
Q

What are the symptoms of type 1 diabetes?

A 
Short, relatively sudden history
Weight loss 
Nausea and vomiting 
Thirst
Polyuria 
Hyperventilation - Kussmaul breathing (ketoacidosis)
Blurred vision
129
Q

What are the signs of type 1 diabetes?

A 
Polyuria 
Polydipsia 
Underweight 
Ketouria 
Fruity smelling breath (due to ketones)
130
Q

What are the genetic associations for type 1 diabetes?

A

HLA D3 and D4 association

131
Q

What are the diagnostic criteria for type 1 diabetes?

A 
Random plasma glucose test >11mmol/l
OR 
Fasting plasma glucose >7mmol/l
AND 
Symptoms of hyperglycaemia (weight loss, polyuria etc.)
132
Q

What investigations to carry out in suspected diabetes?

A

Random plasma glucose test and/or fasting plasma glucose test.

133
Q

What is the treatment of type 1 diabetes?

A

Insulin

134
Q

What types of insulin therapies are there?

A

Short acting - typically given pre meal
Long acting - typically given overnight
Specific insulin regimes are constructed for individuals.

135
Q

What are the difficulties of insulin therapy?

A

Complicated for patient to manage
Injection site injury
Weight gain
Risk of hypoglycaemia

136
Q

What are the possible complications of type 1 diabetes?

A

Hypoglycaemia

Diabetic ketoacidosis

137
Q

What causes hypoglycaemia in type 1 diabetes?

A

Too much insulin leaves a glucose level of <3mmol/l

138
Q

What are the symptoms of hypoglycaemia?

A 
Trembling 
Sweating 
Confusion 
Seizure 
Weakness
139
Q

How do you diagnose hypoglycaemia?

A

Blood glucose test <3mmol/l

140
Q

How do you treat hypoglycaemia?

A

Give 15g glucose

Repeat test after 15 minutes and give more glucose if necessary.

141
Q

What is diabetic ketoacidosis?

A

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
Q

What are the symptoms of diabetic ketoacidosis?

A

Vomiting and nausea
Confusion –> coma
Weakness

143
Q

What are the signs of diabetic ketoacidosis?

A

Fruity breath
Hypotension
Tachycardia
Kussmaul breathing - deep and rapid breaths.

144
Q

How do you diagnose ketoacidosis?

A

Acidaemia pH<7.3
Hyperglycaemia
Ketonaemia

145
Q

How do you treat diabetic ketoacidosis?

A

Fluid replacement and electrolytes as needed

Give insulin

146
Q

What is the pathophysiology of type 2 diabetes?

A

A combination of insulin deficiency and resistance.

147
Q

What is the pathogenesis of type 2 diabetes?

A

Progressive insulin resistance and B-cell decline results in reduced glucose uptake and failure to suppress elements of gluconeogenesis.

148
Q

Why are is there not muscle wasting and ketogenesis in type 2 diabetes?

A

The low level of insulin produced is enough to suppress excessive gluconeogenesis.

149
Q

What is the epidemiology of type 2 diabetes?

A 
Older 
Obese
Asian 
Male 
'western lifestyle'
150
Q

What are the risk factors for type 2 diabetes?

A 
Male 
Asian 
Elderly 
Sedentary lifestyle 
High calorie intake 
Family history 
Obesity
151
Q

What are the causes of type 2 diabetes?

A

Lifestyle choices - risk factors

Genetic inheritance

152
Q

What are the symptoms of type 2 diabetes?

A

It is asymptomatic usually.

If extreme - polyuria/polydypsia

153
Q

What investigations can be used to diagnose type 2 diabetes?

A

Random blood glucose test
Fasting blood glucose test
Oral glucose tolerance test
HbA1c test

154
Q

What results do you need to diagnose type 2 diabetes?

A

1 abnormal result and symptoms
2 abnormal results and asymptomatic
Abnormal HbA1c

155
Q

What are the results of a random blood glucose test?

A

> 11mmoll = diabetes

156
Q

What are the results of a fasting blood glucose test?

A

> 7mmol/l = diabetes

6 - 6.9mmol/l = pre-diabetes

157
Q

What are the results of oral glucose tolerance test?

A

> 11mmol/l = diabetes

7.8 - 11mmol/l = pre diabetes

158
Q

What are the results of HbAc1 test?

A

> 48mmol/l = diabetes

159
Q

What is impaired glucose tolerance?

A

Abnormality of glucose tolerance (OGTT 7.8-11mmol/l) that predispose a person to diabetes later on.

160
Q

What is impaired fasting glucose?

A

Abnormality of fasting glucose (Fasting glucose 6.1-6.9mmol/l) that predispose a person to diabetes later on.

161
Q

What is the treatment for pre diabetes?

A

Lifestyle advice only - healthy diet, exercise, weight control.

162
Q

What is the first line pharmacological therapy for type 2 diabetes?

A

Metformin (act to increase sensitivity to insulin).

163
Q

What are other hypoglycaemic agents that can be used in type 2 diabetes?

A 
Sulphonylureas 
PPP4 inhibitor 
Pioglitazone 
SGLT-2i
INSULIN
164
Q

What are the possible complications of type 2 diabetes?

A

Hypoglycaemia

Hyperglycaemic hyperosmolar state

165
Q

What is hyperglycaemic hyperosmolar state?

A

When sever hyperglycaemia develops without significant ketoacidosis.

166
Q

What are the symptoms of hyperglycaemic hyperosmolar state?

A

Extreme dehydration

Confusion –> coma

167
Q

How do you treat hyperglycaemic hyperosmolar state?

A

Insulin delivered cautiously.

168
Q

What are the macrovascular complications of diabetes?

A

Diabetes is a risk factor for atherosclerosis which in turn is a risk for -
Stroke
Myocardial infarction
Peripheral vascular risk

169
Q

What are the three main microvascular complications of diabetes?

A

Diabetic retinopathy
Diabetic neuropathy
Diabetic nephropathy

170
Q

What are the risk factors for microvascular complications?

A

Poo glycaemic control
Hypertension
Long duration of diabetes

171
Q

What is the screening programme for diabetic retinopathy?

A

Once yearly after the age of 11

172
Q

How to treat diabetic retinopathy?

A

Laser eye treatment

173
Q

What causes diabetic retinopathy?

A

Microaneurysms, haemorrhages, lipid deposits, ischaemic damage.

174
Q

What causes diabetic nephropathy?

A

Raised GFR causes damage and eventually microalbuminuria.

175
Q

How do you diagnose diabetic nephropathy?

A

Presence of microalbuminuria.

176
Q

How do you manage diabetic nephropathy?

A

Blood pressure control, glycaemic control, cholesterol control

177
Q

What is diabetic neuropathy?

A

Decreased sensation in the peripheries - typically symmetrical sensory.

178
Q

What are the consequences of diabetic neuropathy?

A

Foot ulceration - injury goes unnoticed
Infection
Motor nerve damage

179
Q

How to manage diabetic neuropathy?

A 
Patient eduction - foot inspection 
Regular chiropody 
Improve glycaemic control
Vascular surgery 
Eventually --> amputation
180
Q

What are rarer causes of diabetes?

A

Maturity onset diabetes of the young
Permanent neonatal diabetes
Lipodystrophy
Endocrine causes - acromegaly

Phase 2a - conditions (11 decks)

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