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Finals Revision > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Where does the thyroid attach to?

A

Thyroid cartilage
Cricoid cartilage
Trachea

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2
Q

What does the hypothalamus secrete with regard to the thyroid?

A

Thryotropin releasing hormone (TRH)

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3
Q

What does the pituitary secrete with regard to thyroid?

A

TSH

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4
Q

What hormones does the thyroid produce?

A

T3 and T4

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5
Q

Which thyroid hormone is more abundant?

A

T4 (90%)

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6
Q

Which thyroid hormone is more potent?

A

T3 (4x)

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7
Q

What is thyroid hormone needed for?

A

BMR, thermogenesis, metabolism, growth, normal CNS function

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8
Q

When are thyroid hormones at their highest?

A

At night

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9
Q

What is hypothyroidism?

A

Clinical effects of having a lack of thyroid hormone

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10
Q

What are symptoms of hypothyroidism?

A

Tiredness, lower mood, cold intolerance, weight gain, constipation, hoarseness, dry skin, decreased memory, myalgia, cramps

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11
Q

What are some signs of hypothyroidism?

A

Bradycardia, ataxia, cold hands, yawning, oedema, round puffy face

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12
Q

What is the difference between primary and secondary hypothyroidism?

A

Primary is a problem with the thyroid gland

Secondary is due to a problem in pituitary or hypothalamus

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13
Q

What are causes of primary hypothyroidism?

A

Hashimotos thyroiditis, iodine deficiency, past thyroidectomy, drug induced (amiodarone, lithium)

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14
Q

What are causes of secondary hypothyroidism?

A

Congenital, craniopharyngioma, panhypopituitarism,

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15
Q

What do TFTs show in primary hypothyroidism?

A

High TSH, Low T4

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16
Q

What is the management of hypothyroidism?

A

Thyroxine replacement - start at 50mcg and adjust every 4 weeks until optimised

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17
Q

When should you check TFTs after a dose change?

A

8-12 weeks

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18
Q

How many thyroxine need adjusted in pregnancy?

A

Dose increase by 25-50mcg

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19
Q

What are side effects of thyroxine?

A

Hyperthyroidism, worsening of angina, AF

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20
Q

What is hyperthyroidism?

A

Clinical effects of excess thyroid hormone

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21
Q

What are symptoms of hyperthyroidism?

A

Diarrhoea, weight loss, appetite increase, sweating, heat intolerance, palpitations, tremor, irritability, labile emotions

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22
Q

What are the signs of hyperthyroidism?

A

Fast/irregular pulse, warm moist skin, fine tremor, palmar erythema, lid lag, goitre, nodules, bruit

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23
Q

What are the specific signs of Graves disease?

A

Exophthalmos, pretibial myxoedema, thyroid acropachy

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24
Q

What are the main causes of hyperthyroidism?

A

Graves disease, toxic multinodular goitre, toxic adenoma, ectopic thyroid tissue, subacute thyroiditis, post partum thyroiditis, drugs (amiodarone/lithium)

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25
Q

What do TFTs show in hyperthyroidism?

A

Low TSH and high free T4

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26
Q

What is the management of hyperthyroidism?

A

Carbimazole

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27
Q

What is the major risk of carbimazole?

A

Agranulocytosis

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28
Q

What drug is given for hyperthyroidism during pregnancy?

A

Propythiouracil

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29
Q

What do TFTs show in sick euthyroid syndrome?

A

Low TSH and low T4

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30
Q

What do TFTs show in subclinical hypothyroidism?

A

High TSH normal T4

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31
Q

What do TFTs show in poor thyroid medication compliance?

A

High TSH normal T4

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32
Q

What surgical options are there for hyperthyroidism?

A

Thyroidectomy or radioiodine ablation

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33
Q

What is thyroid cancer strongly associated with?

A

Radiation

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34
Q

How does thyroid cancer present?

A

Palpable nodules. Often no signs of hypo/hyperthyroidism as does not secrete hormones

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35
Q

What is the commonest type of thyroid cancer?

A

Papillary

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36
Q

What is the 2nd commonest type of thyroid cancer?

A

Follicular

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37
Q

What is medullary thyroid cancer associated with?

A

MEN2

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38
Q

What does medullary thyroid cancer secrete?

A

Calcitonin

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39
Q

What thyroid cancer carries the worst prognosis?

A

Anaplastic

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40
Q

How is thyroid cancer treated?

A

Mainly surgical

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41
Q

What hormone regulates calcium homeostasis?

A

PTH

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42
Q

How does PTH work?

A

Stimulates osteoclast activity to get calcium released from the bones and increase calcium levels in the blood

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43
Q

What hormone does the opposite of PTH?

A

Calcitonin

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44
Q

What are symptoms of hypercalcaemia?

A

Hypertension, ulcers, fractures, abdominal pain, myopathy, polyuria, thirst/dehydration, confusion, renal stones

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45
Q

What are causes of hypercalcaemia?

A 
Primary hyperparathyroidism
Malignancy
Drugs (vitamin D, thiazides)
Granulomatous disease - sarcoid, TB
Pagets disease
Being bedridden
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46
Q

Who does primary hyperparathyroidism commonly affect?

A

Elderly females

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47
Q

What is primary hyperparathyroidism associated with?

A

MEN1

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48
Q

What do bloods show in primary hyperparathyroidism?

A

Increased calcium, decreased phosphate, increased PTH

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49
Q

What are the main causes of primary hyperparathyroidism?

A

Adenoma, hyperplasia, cancer

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50
Q

What is the treatment of primary hyperparathyroidism?

A

Total parathyroidectomy, conservative management if unsuitable for surgery (Cinacalet)

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51
Q

Why does secondary hyperparathyroidism occur?

A

Because of a low calcium

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52
Q

What are causes of secondary hyperparathyroidism?

A

Low dietary calcium, low vitamin D, chronic renal failure

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53
Q

What do bloods show in secondary hyperparathyroidism?

A

Low calcium, high phosphate, high PTH

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54
Q

What treatment do you use for secondary hyperparathyroidism?

A

Correct the causes

Phosphate binders, calcium & vitamin D

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55
Q

When does tertiary hyperparathyroidism occur?

A

After prolonged secondary hyperparathyroidism

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56
Q

What do bloods show in tertiary hyperparathyroidism show?

A

Increased calcium, increased phosphate, increased PTH

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57
Q

What are symptoms of hypocalcaemia?

A

Weakness, seizures, bronchospasm, QT prolongation, muscle cramps, paraesthesia, Trousseau sign, fatigue

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58
Q

What are causes of hypocalcaemia?

A

Hypoparathyroidism, vitamin D deficiency, chronic renal failure, pancreatitis, hyperventilation, bone mets

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59
Q

What do bloods show in primary hypoparathyroidism?

A

Low calcium, high phosphate, low PTH

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60
Q

What are causes of hypoparathyroidism?

A

Removal of parathyroids, DiGeorge syndrome, autoimmune, haemochromatosis

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61
Q

What is pseudohypoparathyroidism?

A

Failure of target cells to respond to PTH

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62
Q

What features do people with pseudohypoparathyroidism have?

A

Round faces, obesity, bracydactyly, low IQ

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63
Q

What do bloods show in people with pseudohypoparathyroidism?

A

Low calcium, high phosphate, normal/high PTH

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64
Q

What is pseudopseudohypoparathyrodism?

A

Same as pseudohypoparathyroidism but with normal biochemistry

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65
Q

How is hypoparathyroidism treated?

A

Calcium supplements and calcitriol

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66
Q

What is Pagets disease?

A

Abnormality of bone remodelling resulting in thick but weak bone

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67
Q

What do bloods show in Pagets?

A

An isolated rise in ALP

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68
Q

How is Pagets treated?

A

Bisphosphonates

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69
Q

Where are the adrenal glands found?

A

Bilaterally superior and medial to the upper poles of the kidneys

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70
Q

What are the adrenal glands composed of?

A

Outer cortex and inner medulla

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71
Q

What does the zona granulosa of the adrenal cortex secrete?

A

Mineralocorticoids

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72
Q

What does the zona fasciculata of the adrenal cortex secrete?

A

Glucocorticoids

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73
Q

What does the zona reticularis of the adrenal cortex secrete?

A

Sex steroids

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74
Q

What does the medulla of the adrenal gland secrete?

A

Catecholamines

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75
Q

What are the main causes of primary adrenal insufficiency?

A

Addisons disease, congenital adrenal hyperplasia, adrenal TB, adrenal malignancy, meningococcal septicaemia

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76
Q

What are the main causes of secondary adrenal insufficiency?

A

Lack of ACTH stimulation, iatrogenic (steroid use). pituitary/hypothalamic disorders

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77
Q

What is Addison’s disease?

A

Autoimmune destruction of adrenal glands

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78
Q

What are symptoms of Addison’s disease?

A

Lethargy, weakness, N&V, weight loss, salt craving, bronzed skin, hypotension

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79
Q

What does the biochemistry show in Addison’s?

A

Low sodium, High potassium
Hypoglycaemia
Metabolic acidosis

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80
Q

How is Addison’s investigated?

A

Short synacthen test (cortisol remains low)

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81
Q

How is Addison’s treated?

A

Hydrocortisone and fludricortisone

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82
Q

What are sick day rules for Addison’s?

A

Double dose of hydrocortisone

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83
Q

How is an Addisonian crisis treated?

A

Hydrocortisone 100mg IV/IM

1 litre IV saline/saline with dextrose over 1 hour

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84
Q

What is congential adrenal hyperplasia?

A

Group of autosomal recessive disorders

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85
Q

How does CAH present?

A

Virilisation in females, precocious puberty in males, salt wasting crisis

86
Q

How is CAH treated?

A

Glucocorticoid and mineralocorticoid replacement

Timely recognition important to allow growth

87
Q

What is Cushing’s syndrome?

A

Chronic glucocorticoid excess, loss of HPA negative feedback and loss of cortisol circadian rhythm

88
Q

When is cortisol highest?

A

In the morning

89
Q

What are ACTH depdendent causes of Cushings syndrome?

A 
Cushings disease (Pituitary adenoma)
Ectopic ACTH (SCLC)
90
Q

What are ACTH independent causes of Cushing’s?

A

Adrenal adenomas, iatrogenic (steroids), Carney complex, McCune-Albright Syndrome

91
Q

What are symptoms of Cushing’s?

A

Weight gain, mood change, gonadal dysfunction, proximal myopathy

92
Q

What are signs of Cushing’s?

A

Striae, central obesity, moon face, easy bruising

93
Q

What is the investigation for Cushings?

A

Overnight dexamethasone suppression test

94
Q

How is Cushings treated?

A

Depends on cause
Iatrogenic - stop steroids
Cushings disease - transphenoidal adrenalectomy

95
Q

What is primary aldosteronism?

A

Autonomous production of aldosterone independent of its regulators

96
Q

What are the main causes of primary aldosteronism?

A

Bilateral adrenal hyperplasia

Conn’s syndrome (adrenal adenoma)

97
Q

How does primary aldeosteronism present?

A

Asymptomatic or signs of hypokalaemia, increased BP, LVH, atheroma

98
Q

What does the biochemistry show in primary aldosteronism?

A

High sodium

Low potassium

99
Q

What investigation should be done in primary aldosteronism?

A

Aldosterone:renin ratio

Saline suppression test

100
Q

How is Conn’s treated?

A

Laparoscopic adrenalectomy

101
Q

How is bilateral adrenal hyperplasia treated?

A

Spironolactone

102
Q

What is phaeochromocytoma?

A

Rare catecholamine producing tumour in the adrenals

103
Q

What is phaeochromocytoma associated with?

A

MEN, neurofibromatosis, Von-Hippel-Lindau

104
Q

How does phaeochromocytoma present?

A

Headache, sweating, tachycardia, flushing, weight loss,, hypertension, hyperglycaemia, lactic acidosis

105
Q

What investigations are important in phaeochromocytoma?

A

24hr urinary collection of metanephrines/catecholamines

106
Q

What is the definitive treatment of a phaeochromocytoma?

A

Surgical excision

107
Q

What treatment is given before surgery for a phaeochromocytoma?

A

Alpha and beta blockade (alpha blockade given first)

108
Q

What is diabetes?

A

A chronic condition characterised by elevated glucose levels

109
Q

What is type 1 diabetes?

A

Autoimmune destruction of type 1 pancreatic beta cells which produce insulin
Results in an absolute deficiency of insulin and raised glucose levels

110
Q

What are symptoms of type 1 diabetes?

A

Classic triad of polyuria, polydipsia and weight loss. Fatigue, blurred vission, candida. May present as DKA in younger patients

111
Q

What is type 2 diabetes?

A

Relative insulin deficiency due to an excess of adipose tissue

112
Q

What are the symptoms of type 2 diabetes?

A

Asymptomatic or may present with complications e.g. MI, vision issues, kidney failure

113
Q

What is pre-diabetes?

A

Term used to describe patients who do not yet reach the criteria for T2DM

114
Q

How should pre-diabetes be managed?

A

Require monitoring and lifestyle interventions

115
Q

What is maturity onset diabetes of the young (MODY)?

A

Autosomal dominant inherited disorder affecting insulin production

116
Q

What does MODY result in?

A

Younger patients with a T2DM picture

117
Q

How is MODY treated?

A

Sulphonylureas

118
Q

What is latent autoimmune diabetes of adults (LADA)?

A

Autoimmune destruction of B islet cells occuring in young adults aged 25-40

119
Q

What may be a clue that the patient has LADA not T2DM?

A

Inadequate control on T2DM drugs

120
Q

If a patient has symptoms of diabetes, what criteria is needed for a diagnosis of diabetes?

A

Fasting glucose more than 7 OR

Random glucose/2 hr post OGTT of over 11.1

121
Q

If a patient has no symptoms, what criteria is needed for a diagnosis of diabetes?

A

Fasting glucose more than 7 OR
random glucose/2hr post OGTT over 11.1
TWICE ON 2 SEPARATE OCCASIONS

122
Q

What is impaired fasting glucose defined as?

A

Fasting glucose between 6.1 and 7

123
Q

What should patients with an impaired fasting glucose be offered?

A

OGTT to rule out diabetes

124
Q

What is an impaired glucose tolerance?

A

Between 7.8 and 11.1 on OGTT

125
Q

What sort of insulin regime is best for mimicking the bodys natural secretions of insulin?

A

Basal bolus

126
Q

How are basal bolus doses of insulin divided up?

A

50% basal and 50% prandial

127
Q

How many units of insulin per Kg are started to begin with?

A

0.3 per kg

128
Q

How often should self glucose monitoring be done?

A

4 times/day - before each meal and before bed

129
Q

What should be the glucose targets for T1DM before meals?

A

4-7mmol/L

130
Q

What should be the glucose targets for T1DM 1-2hrs after meals?

A

<10mmol/L

131
Q

What does HbA1C measure?

A

Glycosylated haemoglobin

132
Q

What should be the aim for HbA1C?

A

48mmol/mol

133
Q

What are side effects of insulin therapy?

A

Hypoglycaemia

Lipodystrophy

134
Q

What is the first line treatment for T2DM?

A

Metformin

135
Q

How does metformin work?

A

Increases insulin sensitivity, decreases gluconeogenesis and carbohydrate absorption

136
Q

How does metformin affect weight?

A

Causes weight loss

137
Q

Does metformin cause hypos?

A

No

138
Q

What are side effects of metformin?

A

GI upset, reduced B12 absorption, lactic acidosis

139
Q

When is metformin contraindicated?

A

End stage CKD

140
Q

How do sulphonylureas work?

A

Increase insulin secretion

141
Q

How do sulphonylureas affect weight?

A

Cause weight gain

142
Q

Do sulphonylureas cause hypos?

A

Yes

143
Q

What are examples of sulphonylureas?

A

Gliclazide, gliblenclamide, glipizide

144
Q

How do SGLT-2 inhibitors work?

A

Block glucose reabsorption in the proximal kidney tubule

145
Q

How do SGLT-2 inhibitors affect weight?

A

Cause weight loss

146
Q

Do SGLT-2 inhibitors cause hypos?

A

No

147
Q

What are side effects of SGLT-2 inhibitors?

A

UTIs, genital thrush

148
Q

What are examples of SGLT-2 inhibitors?

A

Dapagliflozin - ‘gliflozins’

149
Q

How do DPP-4 inhibitors work?

A

Propagate the effects of the incretin system

150
Q

How do DPP-4 inhibitors affect weight?

A

Neutral

151
Q

Do DPP-4 inhibitors cause hypos?

A

No

152
Q

What are side effects of DPP-4 inhibitors?

A

Nausea, pancreatitis

153
Q

What are examples of DPP-4 inhibitors?

A

Sitagliptin

154
Q

How do thiazolidinedones work?

A

Enhance effects of insulin at target sites

155
Q

How do thiazolidinedones affect weight?

A

Gain

156
Q

Do thiazolidinedones cause hypos?

A

Yes

157
Q

What are side effects of thiazolidinedones?

A

Fluid retention, hepatotoxicity, bone fractures

158
Q

When are thiazolidinedones contraindicated?

A

CCF, osteoporosis, over 65s

159
Q

What are examples of thiazolidinedones?

A

Pioglitazones

160
Q

How do GLP-1 agonists work?

A

Propagate natural insulin response

161
Q

How do GLP-1 agonists affect weight?

A

Cause weight loss

162
Q

Do GLP-1 agonists cause hypos?

A

No

163
Q

What is an example of a GLP-1 agonist?

A

Exenatide

164
Q

What is gliclazide?

A

Sulphonylurea

165
Q

What is dapagloflozin?

A

SGLT-2 inhibitor

166
Q

What is sitagliptin?

A

DPP-4 inhibitor

167
Q

What is pioglitozone?

A

Thiazolidinedone

168
Q

What is exentaide?

A

GLP-1 agonist

169
Q

What is the HbA1C target in T2DM?

A

53mmol/mol or less

170
Q

How long should a diabetic drug be trialled for before discontinuing/introducing a new drug?

A

3-6 months

171
Q

How does peripheral diabetic neuropathy present?

A

Symmetrical sensory neuropathy, glove and stocking numbness, tingling, worse at night

172
Q

How is peripheral neuropathy in diabetics treated?

A

Simple analgesia then neuropathic pain agents

173
Q

How does autonomic neuropathy present in diabetics?

A

Erectile dysfunction, gastroparesis, sweating, increased HR

174
Q

What focal neuropathies can be a complication of diabetes?

A

Carpal tunnel, Bells palsy

175
Q

What changes can be found in diabetic feet?

A

Neuropathic and ischameic changes

176
Q

What sort of ulcers are common in diabetic foot disease?

A

Typically painless, punched out ulcer, overlying a callus

177
Q

What treatment is important in diabetic foot disease?

A

Regular chiropady to remove calluses, check for infections, relieve any high pressure areas
All help to prevent amputation

178
Q

What is diabetic nephropathy also known as?

A

Kimmelsteil Wilson syndrome

Nodular glomerulosclerosis

179
Q

Why doe diabetic nephropathy occur?

A

Poor glycaemic control first leads to renal hypertrophy and increased eGFR
> increased pressure causes capillary damage and sclerosis
> results in hypertension and further decline in function

180
Q

What screening test is done in diabetic neprhopathy?

A

Albumin:creatinine ratio (ACR)

181
Q

How often should patients ACR be screened in diabetes?

A

Annually

From aged 12 in T1DM and from diagnosis in T2DM

182
Q

How is diabetic nephropathy treated?

A

All patients with microalbuminuria are placed on ACEi/ARB regardless of BP

183
Q

What changes are seen in diabetic retinopathy?

A

Blot haemorrhages, cotton wool spots, hard exudates

184
Q

How often should a diabetic patient without diabetic retinopathy be screened?

A

Every 2 years

185
Q

How often should a diabetic patient with diabetic retinopathy be screened?

A

Every year

186
Q

How are macrovascular complications of diabetes prevented?

A

All diabetics over 40 should be on a statin

187
Q

What causes diabetic ketoacidosis?

A

Insulin deficiency resulting in an osmotic diuresis and rapid lipolysis

188
Q

What blood gas is seen in DKA?

A

Metabolic acidosis

189
Q

What may precipitate DKA?

A

Infection, missed insulin doses, MI

190
Q

What are symptoms of DKA?

A

Abdominal pain, polyuria, polydipsia, dehydration, kussmaul breathing, acetotic breath

191
Q

What biochemical perameters are needed for diagnosis?

A

Blood glucose >11 (or known diabetes)
Ketones >3/++ on urine dip
Bicard <15 or pH <7.3

192
Q

How is DKA managed?

A

Fluids - 0.9% NaCl bolus
Insulin IV infusion - 0.1 unit/kg/hr
When BG <15, add dextrose to the bag
Add potassium to the bag to correct hypokalaemia

193
Q

What are complications of DKA?

A

Gastric stasis, VTE, arrythmias, AKI

194
Q

What is hypoglycaemia?

A

Plasma glucose below 3mmol/L

195
Q

What are symptoms of hypoglycaemia?

A

Sweating, anxiety, hunger, tremor, palpitations, dizziness, confusion, drowsiness

196
Q

What is the cause of hypoglycaemia?

A

Fasting (commonly due to insulin, sulphonylureas etc), Post-prandial (T2DM, after gastric surgery)

197
Q

How is hypoglycaemia treated if the patient is concious?

A

10-20g of oral sugar if able to taken then long acting carb (e.g. toast)

198
Q

How is hypoglycaemia treated if the patient is unconcious?

A 
IV glucose (150ml of 10%) or
IM glucagon
199
Q

What is the main cause of acromegaly?

A

Excress growth hormone due to a pituitary adenoma

200
Q

What are features of acromegaly?

A

Coarse facial appearance, spade like hands, large tongue, interdental spaces, excessive sweating, headache, bitemporal hemaniopia

201
Q

How is acromegaly investigated?

A

OGTT and measure GH levels (GH levels will not be suppressed in acromegaly)

202
Q

How is acromegaly treated?

A

Transphenoidal surgery

Somatostain analogue - octreotide

203
Q

Which hormones are reduced in stress responses?

A

Insulin, testosterone, oestrogen

204
Q

What biochemistry is seen in an addisonian crisis?

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia

205
Q

What are features of Kleinfelters?

A

Small testes, tall, gynaecomastia, infertility (47XXY)

206
Q

What are features of Kallmans?

A

Anosmia, infertility - due to failure of GnRH secretion

207
Q

What can cause HbA1C to be underestimated?

A

Sickle cell anaemia
G6PD deficiency
Hereditary spherocytosis

208
Q

What can cause HbA1C to be overestimated?

A

Vitmain B12/Folate deficiency
Iron deficient anaemia
Splenectomy

209
Q

Which patients on insulin do NOT have to inform the DVLA?

A

People on temporary treatment for 3 months or less and gestational diabetes

210
Q

What HBA1C is indicative of pre-diabetes?

A

42-47mmol/mol

211
Q

What blood gas does Cushings cause?

A

Hypokalaemia Metabolic Alkalosis

Finals Revision (22 decks)

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