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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the 4 types of diabetes mellitus?

A

T1DM, T2DM, MODY, LADA

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2
Q

What is T1DM?

A

Absolute insulin deficiency, autoimmune destruction of pancreatic beta cells.

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3
Q

When does T1DM normally present?

A

Presents ages 5-15.

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4
Q

What percentage of diabetes is T1DM?

A

10%

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5
Q

What are the four risk factors for T1DM?

A

HLA DR2-DQ3, HLA DR4-DQ8, other autoimmune disease, environmental infection.

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6
Q

What is the pathophysiology of T1DM?

A

Autoimmune destruction of pancreatic beta islets, resulting in hyperglycaemia and low cellular glucose.

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7
Q

What are the 6 main symptoms/signs of T1DM?

A

Weight loss, nocturia, glycosuria, polyuria, polyphagia, polydipsia.

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8
Q

What is the typical patient that presents with T1DM?

A

Lean and young, with rapid weight loss, polydipsia, polyuria, nocturia, ketosis, FHx of autoimmune disease.

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9
Q

How is T1DM diagnosed?

A

By RPG (random), FPG (fasting for 8+h) and HbA1c (48+).

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10
Q

What are the values of RPG and FPG in T1DM?

A

RPG - >11mmol/LFPG - > 7mmol/L

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11
Q

What is the value of HbA1c in T1DM?

A

> 48mmol/L

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12
Q

Compare RPG/FPG and HbA1c.

A

RPG/FPG = Instant results.HbA1c = Slower but more accurate.

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13
Q

What is the treatment for T1DM?

A

Insulin - Fast acting (4-6h) and slow acting (12-24h).

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14
Q

What is the main complication of T1DM?

A

Diabetic ketoacidosis (DKA)

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15
Q

How does diabetic ketoacidosis occur in T1DM?

A

Often from undiagnosed/poorly managed T1DM. Maybe from infection/illness.

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16
Q

What is the pathophysiology of diabetic ketoacidosis?

A

Absolute insulin deficiency from T1DM, so there is lots of lipolysis and gluconeogenesis. Not all is used so it is converted to ketones (acidic).

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17
Q

What are the signs and symptoms of DKA?

A

Sx of T1DM and:
-Kussmaul breathing - Blow off CO2 (acidic blood)
-Pear drop breath - Fruity ketone smell
-Hypotension, N+V, tachycardia, weight loss, pain.

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18
Q

How is diabetic ketoacidosis diagnosed?

A

Same symptoms and RPG/FPG as T1DM and:
-High ketones, >3mmol/L.
-Acidosis, <7.35pH.
-Ketonuria.

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19
Q

What is the first line treatment for diabetic ketoacidosis?

A

After ABCDE - IV fluids (prevent dehydration).

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20
Q

What is the second line treatment for diabetic ketoacidosis?

A

Insulin and restore electrolytes.

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21
Q

What is T2DM?

A

When patients gradually become insulin resistant or pancreatic beta cells fail to secrete enough insulin, or both.

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22
Q

When does T2DM normally present?

A

Later in life (40+) and is more common in males.

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23
Q

What are the seven risk factors for T2DM?

A

Genetic link, smoking, obesity, hypertension, sedentary lifestyle, alcohol, Asian men.

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24
Q

What are the two main causes of T2DM?

A

Reduced insulin secretion /+ increased insulin resistance.
Others = Steroids, gestational, Cushing’s.

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25
Q

What four conditions is T2DM a risk factor for?

A

Hypertension, silent MI, nephrotic syndrome, CKD.

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26
Q

What are the seven main symptoms of T2DM?

A

Obese, hypertensive, nocturia, polydipsia, polyuria, glycosuria, blurred vision.

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27
Q

How is T2DM diagnosed?

A

Same as T1DM - RPG (>11mmol/L), FPG (>7mmol/L) and HbA1c (>48mmol/L).

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28
Q

What states are there in T2DM that there isn’t in T1DM?

A

Prediabetic states - impaired glucose tolerance (IGT) and impaired fasting glucose (6.1-6.9).

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29
Q

What is the treatment for prediabetes?

A

Lifestyle changes - healthier diet, exercise, modify RFs.

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30
Q

What is the first line treatment for T2DM?

A

Lifestyle changes - Healthier diet, more exercise, less alcohol, stop smoking, regular monitoring.

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31
Q

What is the second line treatment for T2DM?

A

Medications.

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32
Q

What is the first medication for T2DM and how does it work?

A

Metformin - increases sensitivity to insulin.

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33
Q

When is the 2nd line medication given for T2DM and what is it?

A

If HbA1c - 58+mmol/L.
Add another drug to metformin such as sulfonylureas (gliclazide) which increases insulin secretion.

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34
Q

When is a 3rd line medication given for T2DM and what is it?

A

If HbA1c levels remain persistently high - Add a 3rd drug to metformin and sulfonylureas:
-DPP4 inhibitor.
-SGLT-2 inhibitors

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35
Q

What is the last resort medication for T2DM?

A

Insulin.

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36
Q

What are some complications to T2DM?

A

Macrovascular - MI, ischaemic stroke, PVD.
Microvascular - Retinopathy, neuropathy (Charcot foot), nephropathy (CKD).

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37
Q

What is a serious complication to T2DM?

A

Hyperosmolar hyperglycaemic state (HHS).

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38
Q

What is HHS and how does it present?

A

Excessive hepatic gluconeogenesis - glucose is osmotically active, so an excess means hyperosmolar blood.
Often precipitated with undiagnosed/uncontrolled T2DM and infection/illness.

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39
Q

What are the five main symptoms of HHS?

A

Severe T2DM, lethargy, decreased consciousness, severe dehydration, confusion.

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40
Q

How is HHS diagnosed?

A

Heavy glycosuria, increased plasma osmolality with hyperglycaemia. NO ketosis/ketonuria.

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41
Q

How is HHS treated?

A

Insulin, IV fluids, LMWH.

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42
Q

Why is an anticoagulant given as a treatment for HHS?

A

Hyperosmolar blood is thicker so to prevent clots.

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43
Q

What is diabetes insipidus?

A

Decreased ADH secretion or action with more than 3L of urine daily.

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44
Q

What are the two types of diabetes insipidus?

A

Cranial - decreased ADH secretion.
Nephrogenic - decreased kidney response to ADH.

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45
Q

What is the pathophysiology of diabetes insipidus?

A

Decreased ADH means increased losses of H2O in urine, producing urine with dilute high volumes.

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46
Q

What are the main three symptoms of diabetes insipidus? What are four severe symptoms?

A

Polyuria, polydipsia, hypernatraemia.
Severe = Lethargy, confusion, coma and severe dehydration.

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47
Q

When would diabetes insipidus be suspected?

A

When there is more than 3L of urine daily.

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48
Q

What is the gold standard test to diagnose diabetes insipidus and what are the results?

A

Water deprivation test (no fluid for 8h).
Normally, serum osmolality test remains the same as urine osmolality increases but it’s the opposite in diabetes insipidus:
-Serum osmolality rises while urine osmolality is unchanged.

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49
Q

How is cranial and nephrogenic diabetes insipidus differentiated?

A

By injecting IM desmopressin (synthetic ADH).
-Cranial: urine osmolality rises (ADH works on kidney).
-Nephrogenic: urine osmolality is unchanged (ADH has no effect).

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50
Q

What are the five main causes of cranial diabetes insipidus?

A

Idiopathic, congenital, tumour, trauma, infection.

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51
Q

What are the four main causes of nephrogenic diabetes insipidus?

A

Inherited, drugs (lithium), metabolic, CKD.

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52
Q

How is mild diabetes insipidus treated?

A

Conservatively - stay hydrated.

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53
Q

How is cranial diabetes insipidus treated?

A

Desmopressin (synthetic ADH).

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54
Q

How is nephrogenic diabetes insipidus treated?

A

-Thiazide diuretics and NSAIDs to stop kidneys producing as much urine.

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55
Q

What is hyperthyroidism?

A

The clinical effects of excess thyroid hormone.

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56
Q

What is the difference between primary and secondary hyperthyroidism?

A

Primary - Abnormally increased thyroid function.
Secondary - Abnormally increased TSH production.

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57
Q

Who is hyperthyroidism most common in?

A

Young women aged 20-40.
More common in women to men 9:1.

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58
Q

What is the main cause of primary hyperthyroidism?

A

Graves’ disease - 70%

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59
Q

What are some other primary causes of hyperthyroidism?

A

Toxic adenoma, toxic goitre, drugs, cancer.

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60
Q

Which drugs can cause primary hyperthyroidism?

A

Amiodarone, lithium, iodine.

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61
Q

What is a secondary cause of hyperthyroidism?

A

TSH secreting pituitary tumour.

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62
Q

What is the pathophysiology of hyperthyroidism?

A

Increased T3 increases metabolic rate, which increases CO, bone resorption and activates the SNS.

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63
Q

What are the four risk factors for hyperthyroidism?

A

Smoking, stress, HLA-DR3 and other autoimmune diseases (T1DM, Addison’s).

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64
Q

What are the five main symptoms of hyperthyroidism?

A

Heat intolerance/sweaty, diarrhoea, weight loss, hyperphagia, anxiety.

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65
Q

What are four signs of hyperthyroidism?

A

Goitre, tachycardia, fine tremor, muscle wasting.

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66
Q

What is first used to diagnose hyperthyroidism?

A

Thyroid function tests (TFTs).

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67
Q

How is primary and secondary hyperthyroidism differentiated?

A

TFTs:
-Primary: Decreased TSH, increased T4/T3.
-Secondary: Increased TSH, increased T4/T3.

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68
Q

What other tests are used to diagnose hyperthyroidism?

A

Thyroid USS, CT of head and anti-TPO antibodies.

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69
Q

Which drugs used are used for symptom relief in hyperthyroidism?

A

Beta blockers (block adrenaline of SNS).

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70
Q

What is the first line treatment for hyperthyroidism and how does it work?

A

Carbimazole - blocks T4 synthesis.

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71
Q

What is the second line treatment for hyperthyroidism?

A

Propylthiouracil (prevents T4-T3 conversion).

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72
Q

What is a less common treatment for hyperthyroidism?

A

Radioiodine.

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73
Q

What is the last resort treatment for hyperthyroidism?

A

Thyroidectomy.

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74
Q

What is the pathophysiology of Grave’s disease?

A

IgG autoantibodies bind to TSH receptors to increase T4/T3 production. (70% of hyperthyroidism).

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75
Q

What are signs and symptoms of Grave’s disease?

A

Sx of hyperthyroidism and:
-Thyroid eye disease (eyelid retraction, periorbital swelling and proptosis - eye bulging).
-Pretibial myxedema: waxy, skin discolouration.
-Thyroid acropachy: nail clubbing, finger/toe swelling.

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76
Q

What is hypothyroidism?

A

Clinical effect of lack of thyroid hormone.

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77
Q

What is the difference between primary and secondary hypothyroidism?

A

Primary - Abnormally low thyroid function.
Secondary - Abnormally low TSH production.

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78
Q

What is the most common cause of primary hypothyroidism worldwide?

A

Iodine deficiency.

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79
Q

What is the most common primary cause of hypothyroidism in the developed world?

A

Hashimoto’s thyroiditis - autoimmune thyroid destruction, inflammation leads to goitre.

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80
Q

What is a cause of primary hypothyroidism that doesn’t cause a goitre?

A

Primary atrophic hypothyroidism.

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81
Q

What four other things cause primary hypothyroidism?

A

Postpartum thyroiditis, drugs, post-thyroidectomy and radioiodine.

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82
Q

What causes secondary hypothyroidism?

A

Hypopituitarism - less TSH released.
Pituatry adenomas.

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83
Q

What is the pathophysiology of hypothyroidism?

A

Not enough T3 to increase metabolic rate for normal bodily functions.

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84
Q

What are four symptoms of hypothyroidism?

A

Cold intolerance, constipation, weight gain, lethargy.

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85
Q

What are four signs of hypothyroidism?

A

Bradycardia, slow reflexes, cold hands, goitre.

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86
Q

What is first used to diagnose hypothyroidism?

A

Thyroid function tests (TFTs).

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87
Q

How is primary and secondary hypothyroidism differentiated?

A

TFTs:
-Primary: Increased TSH, decreased T4/T3.
-Secondary: Decreased TSH, decreased T4/T3.

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88
Q

What other tests can be used to diagnose hypothyroidism?

A

Anti-TPO autoantibodies are increased and maybe anaemic.

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89
Q

How is hypothyroidism treated?

A

Levothyroxine (T4) - same for primary and secondary.

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90
Q

What can hypothyroidism treatment cause?

A

Iatrogenic hyperthyroidism.

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91
Q

What is a complication of hypothyroidism?

A

Myxedema coma - rapidly decreased T4 and severe hypothyroidism.
Sx - hypothermia, LOC, heart failure.
Tx - Levothyroxine, hydrocortisone.

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92
Q

What are the three main types of thyroid cancer?

A

Popullary (70%), follicular (25%) and anaplastic (worst prognosis).

93
Q

How does thyroid cancer present?

A

Hard and irregular thyroid lump, compression may cause hoarse voice.

94
Q

How is thyroid cancer diagnosed?

A

TFTs, USS of thyroid and aspiration biopsy.

95
Q

How is thyroid cancer treated?

A

Popullary/follicular - thyroidectomy, radioiodine.
Anaplastic - palliative.

96
Q

What is Cushing’s syndrome?

A

Long term exposure to excessive cortisol homorne which is released by the adrenal glands - hypercortisolemia.

97
Q

What is Cushing’s disease?

A

Cushing’s syndrome (hypercortisolemia) that is caused by an ACTH secreting adenoma.

98
Q

What are the two types of causes of Cushing’s syndrome?

A

ACTH dependent (pituitary adenoma, SCLC) and ACTH independent (adrenal adenoma/iatrogenesis).

99
Q

What are some ACTH dependent causes of Cushing’s syndrome?

A

Cushing’s disease and ectopic CTH (SCLC).

100
Q

What are some ACTH independent causes of Cushing’s syndrome?

A

Iatrogenesis and adrenal adenoma.

101
Q

What is the most common cause of Cushing’s syndrome overall?

A

Iatrogenesis (steroids).

102
Q

What are the main eight signs and symptoms of Cushing’s syndrome?

A

Moon face, buffalo hump, obesity, striae, acne, muscle atrophy, weight gain, hypertension, hirituism.

103
Q

What is the first step of diagnosing Cushing’s syndrome?

A

Rule out if on steroids - if so, stop.

104
Q

What is the first line at diagnosing Cushing’s syndrome and what are the results?

A

Overnight dexamethasone suppression test:
-Low dose = Synthetic cortisol should be suppressed via negative feedback but in Cushing’s syndrome there is little/no suppression.
-High dose = If suppressed it is Cushing’s disease.

If not suppressed measure plasma ACTH.

105
Q

What has to be measured before first line test in Cushing’s syndrome?

A

Random serum cortisol test at 12am, if this is high then it is very abnormal (cortisol is lowest at 12am).

106
Q

What else is measured in Cushing’s syndrome if the first line test is positive?

A

Measure plasma ACTH and urinary free cortisol.

107
Q

What can be interpreted if plasma ACTH is high in Cushing’s syndrome?

A

ACTH dependent - potential Cushing’s disease or SCLC.

108
Q

What can be interpreted if plasma ACTH is low/normal in Cushing’s syndrome?

A

ACTH independent - consider adrenal adenoma.

109
Q

How is Cushing’s syndrome treated if iatrogenic cause?

A

Stop medications.

110
Q

How is Cushing’s disease treated?

A

Transsphenoidal resection of pituitary adenoma.

111
Q

How is Cushing’s syndrome treated if caused by adrenal adenoma?

A

Unilateral adrenalectomy.

112
Q

How is Cushing’s syndrome treated if caused by ectopic ACTH?

A

If tumour causing - remove tumour (SCLC).

113
Q

What are some medications used to treat Cushing’s syndrome?

A

Cortisol synthesis inhibition - metyrapone and ketoconzole.

114
Q

What are two complications of Cushing’s syndrome?

A

Osteoporosis and secondary diabetes.

115
Q

What is acromegaly?

A

Release of excess GH and overgrowth of all systems.

116
Q

What is the difference between acromegaly and gigantism?

A

Acromegaly is in adults after epiphyseal fusion.
Gigantism is in children before epiphyseal fusion.

117
Q

What is the main cause of acromegaly?

A

Functional pituitary adenoma (99%).

118
Q

What is a rare cause of acromegaly?

A

Secondary to lung cancer - ectopic GH (1%).

119
Q

What is the pathophysiology of acromegaly?

A

GH acts directly on some tissues (liver, muscle, bone and fat) and indirectly through IGF-1.

120
Q

What are the five signs of acromegaly?

A

Large hands and feet, large nose and tongue, prominent forehead/brow, box jaw, deep voice.

121
Q

What are the symptoms of acromegaly?

A

Sweating, sleep apnoea, vision defects.

122
Q

What is the 1st line test for acromegaly?

A

Test IGF-1 serum level - increased.

123
Q

What is the gold standard test for acromegaly?

A

Impaired glucose test.

124
Q

What other tests can be used to diagnose acromegaly?

A

Pituitary fossa MRI, serum GH level.

125
Q

What is the 1st line treatment for acromegaly?

A

Transsphenoidal resection of pituitary adenoma.

126
Q

What is the 2nd line treatment for acromegaly?

A

Somatostatin analogue - octreotide.

127
Q

What is the 3rd line treatment for acromegaly?

A

GH antagonist - pegvisomant.

128
Q

What is the 4th line treatment for acromegaly?

A

Dopamine antagonist - cabergoline/bromocriptine.

129
Q

What are the three main complications of acromegaly?

A

T2DM, obstructive sleep apnoea and erectile dysfunction.

130
Q

What is a prolactinoma?

A

A benign pituitary adenoma that causes hyperprolactinemia.

131
Q

What are the two types of prolactinoma and how common are they?

A

Micro (<10mm) - 90%.
Macro (>10mm) - 10%.

132
Q

What is another cause of hyperprolactinemia?

A

Antidopaminergic drugs.

133
Q

What are the main 7 signs and symptoms of prolactinoma?

A

Decreased libido, visual field defect.

Women - Amenorrhoea, galactorrhoea.
Men - Erectile dysfunction, gynecomastia, decreased testosterone.

134
Q

How is a prolactinoma diagnosed?

A

Increased serum prolactin and CT head.

135
Q

What is the first line treatment for prolactinoma and why?

A

Dopamine antagonists (inhibits prolactin).

136
Q

What is the gold standard treatment for prolactinoma?

A

Transsphenoidal resection of tumour.

137
Q

What is Conn’s syndrome?

A

Hyperaldosteronism - excess aldosterone independent of RAAS system. Caused by an adrenal adenoma.

138
Q

How many cases of hyperaldosteronism are caused by Conn’s syndrome?

A

2/3rds

139
Q

What is the other less common cause of hyperaldosteronism?

A

Bilateral adrenal hyperplasia (1/3rd).

140
Q

What condition most commonly causes secondary hypertension?

A

Hyperaldosteronism (Conn’s syndrome).

141
Q

What is the pathophysiology of hyperaldosteronism (Conn’s)?

A

Excess aldosterone - high Na+ and H2O retention with increased K+ excretion (hypokalaemia).

142
Q

What are the main five symptoms of Conn’s syndrome?

A

Resistant hypertension (unfixable with ACE-i/Bb), hypokalaemia, muscle weakness, polydipsia, polyuria.

143
Q

What is the first line test for Conn’s syndrome (hyperaldosteronism)? What are the results?

A

Aldosterone to renin blood test ratio - Increased.
Low renin = Primary hyperaldosteronism.
High renin = Secondary hyperaldosteronism.

144
Q

What does hyperaldosteronism (Conn’s) show on ECG?

A

Hypokalaemia.

145
Q

What is the 1st line treatment for Conn’s/hyperaldosteronism?

A

Spironolactone - aldosterone inhibitor.

146
Q

What is the gold standard treatment for Conn’s syndrome?

A

Laparoscopic adrenalectomy.

147
Q

What is Addison’s disease?

A

Primary adrenal insufficiency. Destruction of adrenal cortex and decreased production of glucocorticoids (cortisol) and mineralocorticoids (aldosterone).

148
Q

Who is Addison’s disease most common in?

A

Females with other autoimmune diseases.

149
Q

What is the most common cause of Addison’s disease in the developed world?

A

Autoimmune destruction.

150
Q

What is the most common cause of adrenal insufficiency worldwide?

A

TB

151
Q

What are other causes of adrenal insufficiency?

A

Adrenal metastases or adrenal haemorrhage.

152
Q

What is a cause of secondary adrenal insufficiency?

A

Main cause is loss or damage of the pituitary gland.

153
Q

What is the difference between primary and secondary adrenal insufficiency?

A

Primary - Destroyed adrenal cortex - Increased ACTH, decreased adrenal hormones.
Secondary - HPA axis suppression - Decreased ACTH, decreased adrenal hormones.

154
Q

What are the five main symptoms and two main signs of adrenal insufficiency?

A

Symptoms - Nausea/abdo pain, fatigue, cramps, reduced libido.
Signs - Hyperpigmentation (primary) and postural hypotension.

155
Q

What is the gold standard test used to diagnose Addison’s?

A

Short synacthen test - synacthen is synthetic ACTH, with Addison’s this results in high ACTH and low cortisol/aldosterone.
-Normally, cortisol/aldosterone should be high and ACTH should decrease.

156
Q

How is primary and secondary adrenal insufficiency differentiated?

A

Primary - ACTH increased
Secondary - ACTH decreased

157
Q

What other tests can be used to diagnose Addison’s?

A

CXR (exclude TB), 21-hydroxylase adrenal autoantibodies.

158
Q

How is Addison’s disease treated?

A

Replace steroids; hydrocortisone (cortisol), fludrocortisone (aldosterone).

159
Q

What is a complication of Addison’s disease?

A

Adrenal crisis.

160
Q

What is SIADH?

A

Syndrome of inappropriate ADH. Inappropriately large amounts of ADH released causing water to be reabsorbed in collecting duct.

161
Q

What are the causes of SIADH?

A

SIADH:
SCLC, infection, abscesses, drugs (SSRI, sulfonylureas, thiazides), head trauma.

162
Q

What are the six symptoms of SIADH?

A

Sx of hyponatraemia:
N+V, headache, muscle weakness/cramps, confusion, brainstem herniation.

163
Q

Which condition causes dilute euvolemia?

A

SIADH - less Na+ (hyponatreaemia)

164
Q

What is the first line test for SIADH and what does it show?

A

U+E - Hyponatraemia and normal K+.
-High urine Na+ and osmolality.

165
Q

What type of diagnosis is SIADH?

A

Diagnosis of exclusion:
-Causes of hyponatraemia need to be excluded.

166
Q

What four things need to excluded before SIADH is diagnosed?

A

Adrenal insufficiency, no D+V, no diuretic use, no AKI/CKD.

167
Q

What is the DDx of SIADH and how is it tested?

A

Na+ depletion - when IV saline is given, serum should normalise (in Na+ depletion) but in SIADH it won’t.

168
Q

What is the 1st line treatment for SIADH?

A

Fluid restriction and hypertonic saline to concentrate the blood. (Also treat underlying cause).

169
Q

What is the treatment for chronic SIADH?

A

Drugs - ADH antagonist (tolvaptan).

170
Q

What is hyperkalaemia?

A

High blood potassium level (>5.5mmol/L).

171
Q

What is the emergency hyperkalaemic serum K+ level?

A

> 6.5mmol/L.

172
Q

What are the three types of causes of hyperkalaemia?

A

Impaired excretion, shift to intracellular and increased intake.

173
Q

What three things can cause impaired excretion and hyperkalaemia?

A

Renal disease, drugs (NSAIDs, spironolactone, ACE-i), Addison’s.

174
Q

What are the three symptoms of hyperkalaemia?

A

Palpitations, muscle weakness and paralysis.

175
Q

What two tests are used to diagnose hyperkalaemia and hypokalaemia?

A

Bloods (FBC, U+E) and ECG.

176
Q

What are the features of a hyperkalaemic ECG?

A

Absent P waves, prolonged PR, wide QRS and tall tented T waves.

177
Q

What is the urgent treatment for hyperkalaemia?

A

Calcium gluconate - protects myocardium.

178
Q

How is non urgent hyperkalaemia treated?

A

Insulin and dextrose, treat underlying cause.

179
Q

What is hypokalaemia?

A

Low blood potassium level (<3.5mmol/L).

180
Q

What is the emergency serum hypokalaemic level?

A

<2.5mmol/L.

181
Q

What are the two main types of hypokalaemia causes?

A

Increased excretion and decreased intake.

182
Q

What five things can increase excretion of K+ in hypokalaemia?

A

Thiazides and diuretics, GI losses (D+V), Conn’s, AKI/CKD.

183
Q

What are the three main symptoms of hypokalaemia?

A

Asymptomatic, maybe muscle weakness and paralysis.

184
Q

What are the features of a hypokalaemic ECG?

A

Prolonged PR, ST depression, flat T waves, prominent U waves.

185
Q

What is the main treatment for hypokalaemia?

A

Treat underlying cause, IV K+ replacement.

186
Q

Which drugs can treat hypokalaemia?

A

Aldosterone antagonist - spironolactone.

187
Q

What is hyperparathyroidism?

A

Excessive secretion of parathyroid hormone (PTH).

188
Q

What are the three types of causes of hyperparathyroidism?

A

Primary, secondary and tertiary.

189
Q

What is primary hyperparathyroidism?

A

Excess PTH secretion from parathyroid glands.

190
Q

What are the two causes of primary hyperparathyroidism?

A

Parathyroid adenoma (80%) and hyperplasia (20%).

191
Q

What is secondary hyperparathyroidism?

A

Increased secretion of PTH to combat hypocalcemia.

192
Q

What are the two causes of secondary hyperparathyroidism?

A

CKD/low vitamin D.

193
Q

What is tertiary hyperparathyroidism and how is it caused?

A

Autonomous secretion of PTH after many years of secondary hyperparathyroidism (CKD).

194
Q

What are the four symptoms of hyperparathyroidism?

A

Sx of hypercalcaemia:
-Bones (bone pain), stones (kidney stones), groans (abdominal pain/constipation) and moans (depression and anxiety).

195
Q

How are primary, secondary and tertiary hyperparathyroidism differentiated and what are the results?

A

By PTH/bone profile:
-Primary - Raised calcium.
-Secondary - Low serum calcium, high PTH.
-Tertiary - Raised calcium and PTH.

196
Q

What other tests can be used to diagnosed hyperparathyroidism?

A

DEXA scan, USS throat, ECG.

197
Q

What does hyperparathyroidism show on ECG?

A

Hypercalcaemia - short QT interval.

198
Q

What is the treatment for primary hyperparathyroidism?

A

Removal of adenoma/parathyroidectomy and bisphosphonates.

199
Q

What is the treatment for secondary and tertiary hyperparathyroidism?

A

Treat cause and correct calcium.

200
Q

What is hypoparathyroidism?

A

Reduced PTH secretion - hypocalcaemia.

201
Q

What are the two main types of causes of hypoparathyroidism?

A

Primary - PTH glands failure.
Secondary - After surgery (parathyroidectomy).

202
Q

What can cause primary hypoparathyroidism?

A

Autoimmune destruction or congenital (DiGeorge syndrome - 22q11 deletion).

203
Q

What are the symptoms of hypoparathyroidism?

A

Sx of hypocalcaemia - CATS go NUMB:
-Convulsions, arrhythmia, tetany, spasm, numbness.

204
Q

What are the two signs of hypoparathyroidism?

A

Chvostek’s sign - Facial nerve trap induces spasm.
Trousseau’s sign - BP cuff/torniquet causes wrist flexion and fingers to pull together.

205
Q

How is hypoparathyroidism diagnosed?

A

PTH/bone profile and ECG.

206
Q

What are the PTH/bone profile results of someone with hypoparathyroidism?

A

Decreased PTH, decreased Ca2+, increased phosphate.

207
Q

What does an ECG look like of hypoparathyroidism?

A

Hypocalcaemia - Long QT and ST segements.

208
Q

How is hypoparathyroidism treated?

A

IV/supplements of calcium, vitamin D3, synthetic PTH if required.

209
Q

What is hypoglycaemia?

A

Abnormally low blood glucose.

210
Q

What can cause hypoglycaemia?

A

Diabetic drugs (insulin, sulfonylureas), liver failure, Addison’s.

211
Q

How is hypoglycaemia treated?

A

IV glucose, if no IV access, then IM glucagon.

212
Q

What is a pheochromocytoma?

A

An adrenal medullary tumour which secretes catecholamines (noradrenaline/adrenaline).

213
Q

What causes pheochromocytoma?

A

Usually inherited.

214
Q

What are the symptoms of pheochromocytoma?

A

Activated SNS - hypertension, pallor, sweaty, tachycardia.

215
Q

How is pheochromocytoma diagnosed?

A

Plasma metanphrines/normetanephrines.

216
Q

How is pheochromocytoma treated?

A

Drugs - alpha/beta blockers.
Surgery to excise tumour.

217
Q

How does a high dose dexamethasone suppression test differentiate the causes of Cushing’s syndrome?

A

Low cortisol (suppression) = Pituitary adenoma (disease).
High cortisol, high ACTH = SCLC.
High cortisol, low ACTH = Adrenal adenoma.

218
Q

What is the difference between primary and secondary hyperaldosteronism?

A

Primary = Adrenal glands release too much aldosterone (hyperplasia/adenoma).
Secondary = Excessive renin stimulate the release of excess aldosterone (renal artery stenosis/obstruction).

219
Q

How is tertiary adrenal insufficiency caused?

A

Abruptly stopping being on long-term steroids that have the suppressed the hypothalamus of releasing CRH.

220
Q

What are carcinoid tumours?

A

Malignant tumours of enterochromaffin cell which produce serotonin (5-HT).

221
Q

Where are carcinoid tumours found?

A

GI tract, liver and lungs.

222
Q

What is the difference between carcinoid tumours and syndrome?

A

Tumours - neoplastic cells without symptoms.
Syndrome - when tumour metastasises to liver and causes symptoms.

223
Q

What are 4 symptoms and one sign of carcinoid syndrome?

A

Flushing, diarrhoea, RUQ pain and respiratory problems.
Sign - tricuspid incompetence.

224
Q

What is the gold standard diagnostic test for carcinoid syndrome?

A

5HIAA in the urine.

225
Q

What other two investigations are done in carcinoid syndrome?

A

Liver USS to confirm mets.
CT/MRI to locate the primary tumour.

226
Q

How is carcinoid syndrome treated?

A

Surgically excise primary tumour.
Octreotide (SST analogue) which blocks serotonin.

227
Q

What is a complication of carcinoid syndrome?

A

Carcinoid crisis.

228
Q

What are the side effects of biguanides and sulphonylureas?

A

Biguanide (metformin) - GI upset.
Sulphonylureas (gliclazide) - hypoglycaemia and weight gain.

229
Q

What electrolyte abnormalities does Addison’s disease result in?

A

Hyperkalaemia and hyponatraemia.

Phase 2a (15 decks)

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