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Phase 2a Medicine > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Give 2 examples of water-soluble hormones

A
  1. Peptides

2. Monoamines

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2
Q

Give 2 examples of fat-soluble hormones

A
  1. Thyroid hormone

2. Steroids

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3
Q

How are peptide hormones released?

A

In pulses or bursts

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4
Q

How are peptide hormones synthesised?

A

Preprohormone > prohormone > hormone

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5
Q

How is adrenaline synthesised?

A

Phenylalanine > tyrosine > L-DOPA > DA > NA > Adr

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6
Q

What is NA converted to?

A

Normetanephrine

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7
Q

What is Adrenaline converted to?

A

Metanephrine

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8
Q

How does adrenaline cause vasoconstriction?

A

Binds alpha adrenoceptor to stimulate secondary messenger system and Ca is released to exert tissue function

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9
Q

How does adrenaline cause bronchodilation?

A

Binds beta adrenoceptor > cAMP converts inactive protein kinase to active protein kinase

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10
Q

What thyroid hormone is most abundant?

A

T4

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11
Q

What thyroid hormone is more active?

A

T3

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12
Q

What gives rise to T3 and T4?

A

Iodine incorporates tyrosine molecules to form iodothyrosines which conjugate to form T3/T4

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13
Q

What stimulates T3/T4 synthesis?

A

TSH

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14
Q

What can control hormone secretion?

A
  1. Basal secretion
  2. Superadded rhythms
  3. Release inhibiting factors
  4. Releasing factors
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15
Q

What can control hormone action?

A
  1. Hormone metabolism
  2. Hormone receptor induction
  3. Hormone receptor downregulation
  4. Synergism
  5. Antagonism
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16
Q

What is synergism?

A

Combined effects of 2 hormones amplified

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17
Q

Pituitary gland growth can press on which cranial nerves?

A

CN III, IV, VI, V

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18
Q

What controls vasopressin?

A
  1. Blood volume

2. Osmolality

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19
Q

How can the pituitary dysfunction?

A
  1. Tumour mass effects
  2. Hormone excess
  3. Hormone deficiency
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20
Q

Give 5 functions of thyroid hormone

A
  1. Accelerates food metabolism
  2. Increases protein synthesis
  3. Increases ventilation rate
  4. Increases HR and CO
  5. Accelerates growth rate
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21
Q

What % of the UK population are obese?

A

22%

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22
Q

Why are shift workers more at risk of obesity?

A

Their cortisol rhythms shift to being highest when sleeping instead of when waking

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23
Q

What does weight regulation depend on?

A

Environment and genes

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24
Q

What influences the satiety cascade?

A
  1. Meal quality
  2. Meal quantity
  3. Nutrient status
  4. Energy balance
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25
Q

Where is the hunger centre?

A

Lateral hypothalamus

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26
Q

Where is the satiety centre?

A

Ventromedial hypothalamic nucleus

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27
Q

Name 3 hormones heavily involved in appetite regulation

A
  1. Leptin
  2. Insulin
  3. Ghrelin
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28
Q

Where is leptin expressed?

A

White fat

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29
Q

What is the function of leptin?

A

Switches off appetite and is immunostimulatory

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30
Q

When do leptin levels increase?

A

After a meal

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31
Q

What happens in an individual with increased fat regarding leptin?

A

Leptin expression increases > more leptin in hypothalamus > POMC activation > no appetite suppression

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32
Q

Where is peptide YY secreted?

A

Neuroendocrine cells in ileum, pancreas and colon

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33
Q

What is the function of peptide YY?

A

Inhibits gastric motility and reduces appetite

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34
Q

What is the function of cholecystokinin?

A
  1. Delays gastric emptying
  2. Gall bladder contraction
  3. Insulin release
  4. Satiety
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35
Q

What is the function of ghrelin?

A
  1. Growth hormone release

2. Appetite

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36
Q

When are ghrelin levels high?

A

When fasting

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37
Q

What is POMC?

A

Proopiomelanocortin

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38
Q

What do POMC produce when bound?

A

Cortisol

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39
Q

What happens in POMC deficiency?

A
  1. ACTH deficiency
  2. Pale skin
  3. Adrenal insufficiency
  4. Hyperphagia
  5. Obesity
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40
Q

What are the effects of increased PTH?

A
  1. Increase bone resorption
  2. Increase Ca absorption in gut
  3. Increase Ca reabsorption in kidney
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41
Q

Why might changes in PTH be appropriate?

A

To maintain Ca balance

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42
Q

Give 4 symptoms of hypocalcaemia

A
  1. Paraesthesia
  2. Muscle spasm
  3. Seizure
  4. Cataracts
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43
Q

Give 3 signs of hypocalcaemia

A
  1. Long QT interval
  2. Chvostek’s sign
  3. Trousseau’s sign
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44
Q

What can cause hypocalcaemia?

A

Undermineralised bones and pseudofractures

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45
Q

Give 3 syndromes relates to hypoparathyroidism

A
  1. Di George
  2. Kenney-Caffey
  3. Sanjad-Sakati
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46
Q

Give 3 symptoms of Di George syndrome

A
  1. Hypoparathyroidism
  2. Cleft palate
  3. Thymic aplasia
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47
Q

What causes Di George syndrome?

A

Developmental abnormality of 3rd and 4th branchial pouches

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48
Q

What causes functional hypoparathyroidism?

A

Magnesium deficiency

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49
Q

Give 4 symptoms of pseudohypoparathyroidism

A
  1. Short stature
  2. Obesity
  3. Round facies
  4. Short 4th metacarpals
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50
Q

What causes pseudohypoparathyroidism?

A

PTH resistance

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51
Q

Give 4 symptoms of pseudopseudohypoparathyroidism

A
  1. Short stature
  2. Normal Ca metabolism
  3. Round facies
  4. Obesity
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52
Q

Give 4 symptoms of hypercalcaemia

A
  1. Thirst
  2. Nausea
  3. Constipation
  4. Confusion
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53
Q

Give 3 causes of hypercalcaemia

A
  1. Malignancy
  2. Primary hyperparathyroidism
  3. Thiazides
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54
Q

Why is hypercalcaemia seen in malignancy?

A
  1. Serum Ca rises
  2. PTH decreases
  3. Reduced bone resorption, Ca absorption and Ca reabsorption
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55
Q

Give 4 consequences of primary hyperparathyroidism

A
  1. Bones - osteoporosis
  2. Kidney Stones
  3. Psychic Groans - confusion
  4. Abdominal Moans - constipation
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56
Q

What causes most primary hyperparathyroidism?

A

Single benign adenoma of one of 4 thyroid glands

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57
Q

What are the consequences of tertiary hyperparathyroidism?

A
  1. Nodular hyperplasia
  2. Autonomy
  3. Hypercalcaemia
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58
Q

What causes tertiary hyperparathyroidism?

A

Renal failure so can’t activate vitamin D

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59
Q

What is seen in secondary hyperparathyroidism?

A

Excessive secretion of PTH in response to hypocalcaemia

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60
Q

Give 3 symptoms of secondary hyperparathyroidism

A
  1. Osteoporosis
  2. Kidney stones
  3. Polyuria
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61
Q

How are primary and secondary hyperparathyroidism treated?

A

Diet based

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62
Q

How is tertiary hyperparathyroidism treated?

A

Cinacalcet and surgery

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63
Q

Where does glucose come from?

A

Liver

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64
Q

How is glucose made?

A
  1. Breakdown of glycogen

2. Gluconeogenesis

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65
Q

Where does ingested glucose go?

A

40% to liver, 60% to periphery

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66
Q

Where are insulin and glucagon secreted?

A
  1. Endocrine pancreas

2. Islet of Langerhans

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67
Q

What cells secrete insulin?

A

Beta cells

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68
Q

What cells secrete glucagon?

A

Alpha cells

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69
Q

How is insulin secreted?

A
  1. Glucose enters and is metabolised
  2. ADP and ATP made
  3. K channels close
  4. Depolarisation of membrane
  5. Ca inwardly enters cell
  6. Insulin secretory granules stimulated
  7. Insulin released
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70
Q

What is mobilised to the cell surface to allow glucose entry to cells?

A

GLUT4

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71
Q

What is the function of insulin?

A
  1. Reduces glycogenolysis
  2. Reduces gluconeogenesis
  3. Increases glucose uptake into cells
  4. Suppresses lipolysis
  5. Suppresses muscle breakdown
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72
Q

What are the functions of glucagon?

A
  1. Increases glycogenolysis
  2. Increases gluconeogenesis
  3. Reduce glucose uptake
  4. Stimulate lipolysis
  5. Stimulate muscle breakdown
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73
Q

What is diabetes mellitus?

A

A disorder of carbohydrate metabolism characterised by hyperglycaemia

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74
Q

How does diabetes cause morbidity?

A
  1. Acute hyperglycaemia
  2. Diabetic ketoacidosis
  3. Chronic hyperglycaemia
  4. Hypoglycaemia
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75
Q

Give 3 serious complications of diabetes

A
  1. Diabetic retinopathy
  2. Renal disease
  3. Stroke
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76
Q

What FBG is seen in diabetes?

A

> 7 mmol/L

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77
Q

What HbA1c is seen in diabetes?

A

48 mmol/mol (6.5%)

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78
Q

What is the pathogenesis of diabetes?

A

Loss of beta cells due to autoimmune destruction called insulitis

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79
Q

What are the stages of diabetes?

A
  1. Genetic predisposition
  2. Insulitis beta cell injury
  3. Pre-diabetes
  4. Diabetes
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80
Q

What proportion of beta cells remain when a DM diagnosis is made?

A

10%

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81
Q

What is the result of insulin secretion failure?

A
  1. Continued glycogenolysis
  2. Unrestrained lipolysis and muscle breakdown
  3. Increase in hepatic glucose output
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82
Q

What are the results of untreated DM?

A
  1. Increase circulating glucagon
  2. Increased cortisol and Adrenaline
  3. Weight loss
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83
Q

What is the result of reduced insulin?

A
  1. Lipolysis

2. Formation of glycerol and FFA

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84
Q

What is the function of FFA?

A

They are oxidised to form ketone bodies

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85
Q

What causes ketoacidosis?

A

Absence of insulin and rising counterregulatory hormones leads to increasing hyperglycaemia and rising ketones

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86
Q

What are the signs and symptoms of ketoacidosis?

A
  1. Anorexia
  2. Vomiting
  3. Dehydration
  4. Hyperglycaemia
  5. Circulatory collapse
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87
Q

What causes T2DM?

A

Impaired insulin secretion and insulin resistance resulting in impaired glucose tolerance

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88
Q

What is the pathogenesis of T1DM?

A

Severe insulin deficiency due to autoimmune destruction of the beta cell

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89
Q

What is the pathogenesis of T2DM?

A

Insulin resistance and impaired insulin secretion due to a combination of genetic predisposition and environmental factors

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90
Q

Why would T2DM patients end up on insulin?

A

Lipotoxicity

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91
Q

Which insulin mimics normal physiology?

A

Basal bolus insulin

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92
Q

What is the problem with basal analogue insulin?

A

There is a lag before it reaches hepatic portal system – takes a while for insulin to kick in so sugars rise from a meal when this is happening

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93
Q

What insulin approaches are there for T2DM?

A
  1. Once daily basal insulin
  2. Twice daily basal insulin
  3. Basal bolus therapy
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94
Q

Give 2 advantages of basal insulin in T2DM

A
  1. Simple for patient, self-administered

2. Less risk of hypoglycaemia at night

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95
Q

Give 1 disadvantage of basal insulin in T2DM

A

Doesn’t cover meals

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96
Q

What is the best T1DM treatment?

A

Basal bolus insulin therapy

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97
Q

What is the BGL for hypoglycaemia?

A

3.9 mmol/L

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98
Q

What is hypoglycaemia?

A

Low plasma glucose causing impaired brain function neuroglycopenia

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99
Q

Give 5 symptoms of hypoglycaemia

A
  1. Trembling
  2. Palpitations
  3. Confusion
  4. Weakness
  5. Nausea
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100
Q

What are the symptoms of severe hypoglycaemia?

A
  1. Reduced conscious levels
  2. Convulsions
  3. Coma
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101
Q

What are 3 risk factors for severe hypoglycaemia in T1DM?

A
  1. Hx of severe episodes
  2. Renal impairment
  3. Extremes of age
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102
Q

What are 3 risk factors for severe hypoglycaemia in T2DM?

A
  1. Age
  2. Cognitive impairment
  3. Depression
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103
Q

What is the aim for HbA1c in T2DM?

A

<7.0%

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104
Q

What is the treatment for hypoglycaemia?

A
  1. 15g fast-acting carbohydrate

2. Eat a long-acting carbohydrate to prevent recurrence of symptoms

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105
Q

What are the effects of the pituitary gonadal axis not working properly?

A

Men > low testosterone

Women > no periods

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106
Q

What is the consequence of HPA axis malfunction?

A

CV collapse

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107
Q

What inhibits prolactin secretion?

A

Dopamine

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108
Q

What is craniopharyngioma?

A

Condition causing a lack of pituitary function and issues with satiety and appetite regulation

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109
Q

What is Sheehans?

A

During pregnancy pituitary doubles in size and can outstrip its blood supply and infarct

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110
Q

What is the result of pituitary tumours?

A
  1. Pressure on local structures
  2. Pressure on normal pituitary
  3. Functioning tumour
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111
Q

What conditions can arise from functioning pituitary tumours?

A
  1. Prolactinoma
  2. Acromegaly
  3. Cushing’s
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112
Q

What can be the result of pressure on local structures from pituitary tumours?

A
  1. Bitemporal hemianopia
  2. Headaches
  3. Ptosis
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113
Q

What are 3 symptoms of tumours causing pressure on the pituitary?

A
  1. No body hair
  2. Menstrual dysfunction
  3. Central obesity
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114
Q

What is the pathogenesis of Cushing’s disease?

A

Chronic, excessive and inappropriate elevated levels of circulating plasma glucocorticoids

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115
Q

What is the presentation of Cushing’s disease?

A
  1. Central obesity
  2. Decreased linear growth
  3. Thin skin
  4. Muscle wasting
  5. Easy bruising
  6. Hirsutism
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116
Q

What are the causes of Cushing’s disease?

A
  1. Excess glucocorticoid
  2. Tumour producing too much ACTH
  3. Adrenal tumour making too much cortisol
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117
Q

What happens to the adrenal axis in Cushing’s disease?

A

Feedback isn’t working as tumour is resistant to it so continues to make ACTH

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118
Q

What are the symptoms in Cushing’s syndrome?

A
  1. Moon face
  2. Hirsutism
  3. Facial plethora
  4. Acne
  5. Thinned scalp hair
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119
Q

Give 5 clinical features of Cushing’s

A
  1. Diabetes
  2. Hypertension
  3. Immune suppression
  4. Depression
  5. Loss of libido
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120
Q

How is Cushing’s syndrome screened?

A
  1. High urinary free cortisol
  2. High serum cortisol
  3. High plasma night cortisol
  4. High late-night salivary cortisol
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121
Q

What imaging is used in Cushing’s disease?

A

Pituitary MRI

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122
Q

What is the treatment for Cushing’s?

A
  1. Adrenal blockade
  2. Surgery
  3. Radiotherapy
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123
Q

What is the pathogenesis of acromegaly?

A

GH hormone secreting tumour causing IGF1 production to increase in liver which gives rise to clinical features

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124
Q

What is the mean age of diagnosis in acromegaly?

A

44

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125
Q

Give 3 co-morbidities of acromegaly

A
  1. Arthritis
  2. Diabetes
  3. Sleep apnoea
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126
Q

How is acromegaly diagnosed?

A
  1. Clinical features
  2. GH
  3. IGF-1
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127
Q

What are 5 clinical features in acromegaly?

A
  1. Acral enlargement
  2. Wide jaw
  3. Large lips
  4. Excessive sweating
  5. Arthralgias
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128
Q

What is the test for acromegaly?

A

75mg glucose tolerance test

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129
Q

What is the Tx for acromegaly?

A
  1. Pituitary surgery
  2. Medical therapy
  3. Radiotherapy
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130
Q

What is the cure rate for micro adenoma surgery?

A

90%

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131
Q

What is the cure rate for macroadenoma surgery?

A

<50%

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132
Q

What are the disadvantages of radiotherapy in acromegaly?

A
  1. Delayed response
  2. Hypopituitarism
  3. Secondary tumours
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133
Q

What drugs can be used for acromegaly?

A
  1. Cabergoline (DA agonist)
  2. Samatostatin analogues e.g. octreotide
  3. GH receptor antagonist e.g. pegvisomant
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134
Q

What is the incidence of prolactinoma?

A

1 in 10,000

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135
Q

What causes prolactinoma?

A

Lactotroph cell tumour of the pituitary causing too much prolactin

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136
Q

What are the clinical features of prolactinoma?

A
  1. Headache
  2. Bitemporal hemianopia
  3. Menstrual irregularity
  4. Infertility
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137
Q

What can be used to treat prolactinoma?

A
  1. Cabergoline

2. Bromocriptine

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138
Q

When do cortisol levels peak?

A

Around an hour after waking

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139
Q

What is the cause for 60% of Addison’s disease cases?

A

Autoimmune adrenalitis

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140
Q

What is seen in congenital adrenal hyperplasia (CAH)?

A

Can’t produce cortisol so ACTH levels rise; high androgens but low cortisol so ambiguous genitalia and salt losing crises

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141
Q

How common is CAH?

A

1:15,000

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142
Q

What is secondary adrenal insufficiency?

A

Hypopituitarism

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143
Q

What is seen in secondary adrenal insufficiency?

A
  1. Apoplexy
  2. Hypophysitis
  3. Pituitary macroadenoma
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144
Q

What are the symptoms of adrenal insufficiency?

A
  1. Fatigue
  2. Weight loss
  3. Poor recovery from illness
  4. Adrenal crisis
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145
Q

What are the signs of adrenal insufficiency?

A
  1. Pigmentation
  2. Pallor
  3. Hypotension
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146
Q

What is the biochemistry in adrenal insufficiency (AI)?

A
  1. Low Na
  2. High K
  3. Eosinophilia
  4. High TSH
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147
Q

What ACTH levels of seen in Addison’s?

A

> 22ng/L

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148
Q

What ACTH levels are seen in secondary AI?

A

<5ng/l

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149
Q

What is the investigations for Addison’s disease?

A
  1. Adrenal antibodies
  2. Long chain FA
  3. Imaging
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150
Q

What is the treatment for Addison’s disease?

A

Hydrocortisone + fludrocortisone

151
Q

What is the treatment for secondary AI?

A

Hydrocortisone

152
Q

Give 5 symptoms seen in an adrenal crisis?

A
  1. Hyponatraemia
  2. Hyperkalaemia
  3. Hypotension
  4. Fatigue
  5. Fever
153
Q

What is the treatment for an adrenal crisis?

A
  1. Hydrocortisone
  2. Fluids
  3. Fludrocortisone (in Addison’s)
154
Q

How much more likely are females to get thyroid diseases?

155
Q

What is the prevalence of hyperthyroidism?

156
Q

What is the prevalence of hypothyroidism?

157
Q

Name 2 autoimmune hypothyroidisms

A
  1. Hashimoto’s thyroiditis

2. Atrophic thyroiditis

158
Q

What is Graves’ disease?

A

Thyroid associated ophthalmopathy

159
Q

What antibodies are found in most patients with autoimmune hypothyroidism?

A

Thyroglobulin and thyroid peroxidase (TPO)

160
Q

What happens in autoimmune hyperthyroidism?

A

Thyroid fails to synthesises T3/4

161
Q

What mediated thyroid cell destruction?

162
Q

What is the clinical presentation of Graves’ disease?

A
  1. Swollen, protruding, red eyes
  2. Periorbital oedema
  3. Haemosis
  4. Graves; opthalmopathy
163
Q

What antibodies cause Graves’ disease?

A

Thyroid stimulating antibodies

164
Q

What causes neonatal Graves?

A

TSH-receptor antibodies cross placenta

165
Q

Give 4 risk factors for thyroid autoimmunity

A
  1. Female
  2. Stress
  3. High iodine intake
  4. HLA-DR3
166
Q

Why is it important to monitor postpartum thyroid autoimmunity patients?

A

In pregnancy the condition gets bettie due to down regulation in TSH-R antibody action but it comes back with a vengeance postpartum

167
Q

Give 3 conditions associated with thyroid autoimmunity

A
  1. T1DM
  2. Addison’s disease
  3. Pernicious anaemia
168
Q

What is the most common pathological feature of hypothyroid autoimmunity conditions?

A

Swelling in extra ocular muscles

169
Q

What is goitre?

A

Palpable and visible thyroid enlargement

170
Q

What is the commonest endocrine disorder?

A

Sporadic non-toxic goitre

171
Q

What is hyperthyroidism?

A

Excess of thyroid hormones in the blood

172
Q

What are the mechanisms for increased levels of thyroid hormone?

A
  1. Overproduction of thyroid hormone
  2. Leakage of preformed hormone from thyroid
  3. Ingestion of excess thyroid hormone
173
Q

What are the common causes of hyperthyroidism?

A
  1. Graves’ disease
  2. Toxic multinodular goitre
  3. Toxic adenoma
174
Q

What % of hyperthyroidism cases are caused by Graves?

175
Q

What drugs can induce hyperthyroidism?

A
  1. Iodine
  2. Amiodarone
  3. Lithium
  4. Radiocontrast agents
176
Q

What are 5 clinical features of hyperthyroidism?

A
  1. Weight loss
  2. Tachycardia
  3. Hyperphagia
  4. Heat intolerance
  5. Diarrhoea
177
Q

What are 4 signs specific to Graves?

A
  1. Diffuse goitre
  2. Thyroid eye disease
  3. Pretibial myxoedema
  4. Acropachy
178
Q

What sign is specific to thyroid adenoma?

A

Solitary nodule

179
Q

What thyroid function tests can be used?

A
  1. Free T4
  2. Free T3
  3. TSH
  4. Thyroid antibodies e.g. TPO
180
Q

What is seen in primary hyperthyroidism TFTs?

A
  1. High free T4
  2. High free T3
  3. Low TSH
181
Q

What is seen in secondary hyperthyroidism TFTs?

A
  1. High free T4
  2. High free T3
  3. High TSH
182
Q

What treatments can be used for hyperthyroidism?

A
  1. Antithyroid drugs (thionamides)
  2. Radioiodine 131I
  3. Surgery
183
Q

Name 3 thionamides

A
  1. Carbimazole
  2. Propylthiouracil
  3. Methimazole
184
Q

Give 3 factors which give a poor prognosis for treatment from thionamides

A
  1. Male
  2. Smoking
  3. Large goitre
185
Q

Give 3 side effects of thionamides

A
  1. Rash
  2. Agranulocytosis
  3. Sore throat
186
Q

What symptoms are seen in agranulocytosis?

A
  1. Sore throat
  2. Fever
  3. Mouth ulcers
187
Q

What is the half life of 131I?

188
Q

How does 131I work?

A

Emission of beta particles results in ionisation of thyroid cells

189
Q

Give 3 side effects of 131I

A
  1. Necrosis of follicular cells
  2. Vascular occlusion
  3. Atrophy and fibrosis
190
Q

What is hypothyroidism?

A

Thyroid hormone levels abnormally low in blood

191
Q

What causes most causes of primary hypothyroidism?

A

Hashimoto’s thyroiditis

192
Q

What is the pathophysiology of primary hypothyroidism?

A

Absence/dysfunction of thyroid gland

193
Q

What is the pathophysiology of secondary hypothyroidism?

A

TSH is not being made

194
Q

What is the pathophysiology of tertiary hypothyroidism?

A

TSH is not being made

195
Q

What can cause secondary or tertiary hypothyroidism?

A
  1. Pituitary disease

2. Hypothalamic disease

196
Q

Give 4 drug types that can cause hypothyroidism

A
  1. Iodine
  2. Lithium
  3. Thionamides
  4. Interferon-alpha
197
Q

Give 3 causes of hypothyroidism in children

A
  1. Resistance to thyroid hormone
  2. Neonatal hypothyroidism
  3. Isolated TSH deficiency
198
Q

Give 5 symptoms of hypothyroidism

A
  1. Fatigue
  2. Weight gain
  3. Cold intolerance
  4. Oedema
  5. Dry, rough skin
199
Q

What is seen in TFTs in primary hypothyroidism?

A
  1. High TSH
  2. Low free T4
  3. Low free T3
200
Q

What distinguishes Hashimoto’s from other causes of hypothyroidism?

A

Positive titre of TPO antibodies

201
Q

What is seen in TFTs in secondary hypothyroidism?

A
  1. Low TSH
  2. Low free T4
  3. Low free T3
202
Q

What is the treatment of choice for hypothyroidism?

A

Synthetic L-thyroxine (T4)

203
Q

What metabolic changes are seen in pregnancy?

A
  1. Increased erythropoietin, cortisol and NA
  2. High CO
  3. Insulin resistance
204
Q

Give 2 gestational syndromes

A
  1. Pre-eclampsia

2. Gestational diabetes

205
Q

What is the prevalence of hypothyroidism during pregnancy?

206
Q

What can be the results of inadequate hypothyroidism treatment in pregnancy?

A
  1. Gestational hypertension
  2. Preeclampsia
  3. Placental abruption
207
Q

What can be done to treat hypothyroidism in pregnancy?

A

Increase dose by 30%

208
Q

Give 3 groups screened for hypothyroidism

A
  1. Age >30
  2. BMI >40
  3. Miscarriage preterm labour
209
Q

What is the definitive treatment for thyrotoxicosis?

A

Thyroidectomy

210
Q

Why does agranulocytosis cause a risk of sepsis?

A

Stop making white cells

211
Q

What causes foetal thyrotoxicosis?

A

Transplacental crossover of TSH-R antibodies

212
Q

Give 3 things associated with foetal thyrotoxicosis

A
  1. Foetal goitre
  2. Foetal tachycardia
  3. Foetal hydrops
213
Q

What 3 groups are at risk of postpartum thyroiditis?

A
  1. T1DM
  2. Graves’ disease in remission
  3. Chronic viral hepatitis
214
Q

What is the main treatment for postpartum thyroiditis?

A

Amiodarone

215
Q

What abnormalities are associated with amiodarone?

A
  1. Amiodarone induced hypothyroidism

2. Amiodarone induced thyrotoxicosis

216
Q

What treatments are recommended for advanced melanoma?

A

Ipilimumab and nivolumab

217
Q

What is the mode of action for Ipilimumab and nivolumab?

A

Monoclonal antibody, activates immune system by inhibiting CTLA-4 which normally downregulates immune system

218
Q

How much ECF is in a 70kg person?

219
Q

How much ICF is in a 70kg person?

220
Q

How much interstitial fluid is in a 70kg person?

221
Q

How much intravascular fluid is in a 70kg person?

222
Q

What are the major ions in ECF?

A

Cation: Na, anion: Cl

223
Q

What are the major ions in ICF?

A

Cation: K, anion: PO3

224
Q

What happens in water excess?

A
  1. Reduce plasma osmolality
  2. Increase cellular hydration
  3. Reduce vasopressin secretion
  4. Increase urine water excretion
225
Q

What happens in water deficit?

A
  1. Increase plasma osmolality
  2. Decrease cellular hydration
  3. Increase vasopressin secretion
  4. Decrease urine water excretion
226
Q

How does vasopressin act on the collecting duct?

A

Binds its receptor to insert aquaporin 2 into membrane so water can pass across cell and be reabsorbed into circulation

227
Q

What happens as urine concentration increases?

A

There is an increase in thirst which pushes osmolality back down

228
Q

What is the result of a lack of vasopressin?

A

Cranial diabetes insipidus

229
Q

What is the result of resistance to the action of vasopressin?

A

Nephrogenic diabetes insipidus

230
Q

What is the result of too much vasopressin release when it shouldn’t be released?

A

Syndrome of anti-diuretic hormone secretion (SIADH)

231
Q

Give 3 clinical features of diabetes insipidus

A
  1. Polyuria
  2. Polydipsia
  3. No glycosuria
232
Q

What very rarely causes cranial diabetes insipidus (CDI)?

A

Anterior pituitary tumour

233
Q

Give 3 acquired causes of CDI

A

(1. Idiopathic)
2. Germinoma
3. TB
4. Aneurysm

234
Q

Which syndrome is associated with primary CDI?

A

Wolfram syndrome

235
Q

Give 3 causes of acquired nephrogenic diabetes insipidus (NDI)

A
  1. Diabetes mellitus
  2. Chronic renal failure
  3. Lithium
236
Q

What test is done to investigate DI?

A

Water deprivation test

237
Q

What is seen in CDI using the water deprivation test?

A

Patient responds to desmopressin and urine conc. increases

238
Q

What is seen in NDI using the water deprivation test?

A

Desmopressin will make no difference, urine is still diluted so osmolality worsens

239
Q

What alternative DI investigations are there?

A
  1. Hypertonic saline infusion

2. Measurement of AVP

240
Q

What is the management of CDI?

A
  1. Desmopressin

2. Treat underlying condition

241
Q

What is the management of NDI?

A
  1. Avoid precipitating drugs
  2. High dose desmopressin
  3. Hydrochlorothiazide or indomethacin
242
Q

What usually causes hyponatraemia?

A

Excess water

243
Q

Give 5 symptoms of hyponatraemia

A
  1. Headache
  2. Irritability
  3. Nausea/vomiting
  4. Lethargy
  5. Respiratory arrest
244
Q

What can cause acute hyponatraemia?

A

Subarachnoid haemorrhage

245
Q

Give 5 tests for hyponatraemia

A
  1. Plasma osmolality
  2. Urine osmolality
  3. Urine sodium
  4. TFTs
  5. TSH
246
Q

Give 4 causes for hyponatraemia

A
  1. Cirrhosis of liver
  2. SIADH
  3. Burns
  4. Diuretics
247
Q

Give 5 clinical symptoms of SIADH

A
  1. High AVP
  2. Low osmolality
  3. Low plasma Na
  4. Concentrated urine
  5. Increase GFR
248
Q

Give 4 causes of SIADH

A
  1. Meningitis
  2. Lung carcinoma
  3. Tuberculosis
  4. Carbamazepine
249
Q

What is the management for SIADH?

A
  1. Treat underlying condition
  2. Fluid restriction
  3. Demeclocycline
250
Q

What is the chronic SIADH management?

A

<8 - 10 mmol/l increase in Na+ per 24 hour

251
Q

Give 4 risk factors for osmotic demyelination syndrome (ODS)

A
  1. Severe hyponatraemia
  2. Hypokalaemia
  3. Chronic excess alcohol
  4. Malnutrition
252
Q

What is ODS?

A

Massive demyelination of descending axons

253
Q

What is the management for ODS?

A
  1. Tolvaptan

2. Conivaptan

254
Q

What cancers often metastasise to the pituitary?

A
  1. Breast
  2. Lung
  3. Stomach
  4. Kidney
255
Q

Name 2 primary tumours of the pituitary

A
  1. Perisallar meningioma

2. Optic glioma

256
Q

Give 5 symptoms seen in craniopharyngioma

A
  1. Raised ICP
  2. Visual disturbance
  3. Growth failure
  4. Pituitary hormone deficiency
  5. Weight gain
257
Q

What is meningioma associated with?

A

Visual disturbance and endocrine dysfunction

258
Q

What is the usual age of onset for non-functioning pituitary adenomas (NFPA)?

259
Q

What are the signs of aggressiveness in NFPA?

A
  1. Large size
  2. Cavernous sinus invasion
  3. Lobulated suprasellar margins
260
Q

What are the thyroid function test results for primary hypothyroid?

A

Raised TSH low Ft4

261
Q

What are the thyroid function test results for hypopituitary?

A

Low Ft4 with normal or low TSH

262
Q

What are the thyroid function test results forGraves’ disease?

A

Suppressed TSH high Ft4

263
Q

What are the thyroid function test results for

A

High Ft4 with normal or high TSH

264
Q

What are the thyroid function test results for

A

High Ft4 with normal or high TSH

265
Q

What is measured in pituitary disease?

266
Q

How is the gonadal axis tested in men?

A

Measure 0900h fasted T and LH/FSH in pituitary disease

267
Q

How is the HPA axis tested?

A

Measure 0900h cortisol and synacthen

268
Q

What could cause PRL to be raised?

A
  1. Stress
  2. Antipsychotics
  3. Stalk pressure
  4. Prolactinoma
269
Q

What imaging can be done on the pituitary?

A

MRI and CT

270
Q

What are the presenting features of diabetes?

A
  1. Polydipsia
  2. Polyuria
  3. Weight loss
  4. Fatigue
  5. Hunger
  6. Pruritis vulvae and balanitis
  7. Blurred vision
271
Q

What does the spectrum of T1DM depend o?

A

Rate of beta cell destruction

272
Q

How many functioning beta cells are left by the time someone is diagnosed with T1DM?

273
Q

What are the 3 key features of T1DM?

A
  1. Weight loss
  2. Short Hx of severe symptoms
  3. Moderate or large urinary ketones
274
Q

When is T1DM usually diagnosed?

275
Q

Which autoimmune disease are associated with T1DM?

A
  1. Hypothyroidism
  2. Addison’s
  3. Coeliac disease
276
Q

What is the result of reduced insulin?

A

Fat breakdown, formation of glycerol and free fatty acids

277
Q

What is the triad of ketoacidosis?

A
  1. Hyperglycaemia
  2. Raised plasma ketones
  3. Metabolic acidosis
278
Q

Give 3 causes of ketoacidosis

A
  1. Infection
  2. Treatment errors
  3. Previously undiagnosed diabetes
279
Q

Give 3 symptoms of ketoacidosis

A
  1. Polyuria and polydipsia
  2. Nausea
  3. Weakness
280
Q

Give 3 signs of ketoacidosis

A
  1. Hyperventilation
  2. Dehydration
  3. Hypotension
281
Q

What is the key biochemical diagnosis for ketoacidosis?

A

K - high on presentation despite total body K deficit, subsequently fall with insulin and rehydration

282
Q

Why is there a high K on presentation when there is a total body K deficit in ketoacidosis?

A

Due to acute shift of K out of cell with acidosis

283
Q

Why is it important to anticipate K fall when diagnosing ketoacidosis?

A

It can cause heart arrhythmia

284
Q

What is the ketoacidosis management?

A
  1. Rehydration
  2. Insulin
  3. Replacement of K
285
Q

Give 3 complications of ketoacidosis?

A
  1. Cerebral oedema
  2. Respiratory distress syndrome
  3. Thromboembolism
286
Q

Give 5 symptoms of hypoglycaemia

A
  1. Sweating
  2. Tremor
  3. Palpitations
  4. Loss of concentration
  5. Hunger
287
Q

What causes maturity onset diabetes of young (MODY)?

A

Single gene defect altering beta cell function

288
Q

What is the glucose sensor of beta cells?

A

Glucokinase gene (GCK)

289
Q

What patients are at risk of MODY?

A
  1. Parent affected with diabetes
  2. Absence of islet autoantibodies
  3. Evidence of non-insulin dependence
  4. Sensitive to sulphonylurea
290
Q

What are the signs of permanent neonatal diabetes?

A
  1. Small babies
  2. Epilepsy
  3. Muscle weakness
291
Q

What is the presentation of lipodystrophy?

A

Make you look muscular and masculine

292
Q

Name 3 conditions associated with lipodystrophy

A
  1. Insulin resistance
  2. Dyslipidaemia
  3. PCOS
293
Q

What triad is associated with hereditary haemochromatosis?

A
  1. Cirrhosis
  2. Diabetes
  3. Bronzed hyperpigmentation
294
Q

Why are pancreatic neoplasia patients prone to hypoglycaemia?

A

Loss of glucagon function

295
Q

What does insulin improve in cystic fibrosis patients?

A
  1. Body weight
  2. Reduces infections
  3. Lung function
296
Q

Name 4 drugs that can cause diabetes

A
  1. Glucocorticoids
  2. Thiazides
  3. Protease inhibitors
  4. Antipsychotics
297
Q

What are the first definitive signs of puberty?

A

Girl - menarche

Boy - first ejaculation

298
Q

What Tanner stage is a good indicator that real puberty has started in boys?

A

Testes >3ml (>2.5cm in longest diameter)

299
Q

What Tanner stage is a good indicator that real puberty has started in girls?

A

Breast bud noted/palpable; enlargement of areola

300
Q

What is thelarche?

A

Breast development

301
Q

What effect does oestrogen have on the breast during thelarche?

A
  1. Ductal proliferation
  2. Site specific adipose deposition
  3. Enlargement of areola and nipple
302
Q

What is the prepubertal to pubertal changes to the uterus?

A

Tubular shape –> pear shape and endometrium increased thickness

303
Q

What is precocious puberty?

A

Onset of secondary sexual characteristics before 8yr (girl), 9yr (boy)

304
Q

What is delayed puberty?

A

Absence of secondary sexual characteristics by 14yr (girl), 16yr (boy)

305
Q

Why is precocious puberty (PCP) a huge concern in boys?

A

High risk of brain tumour

306
Q

What is the test for PCP?

307
Q

What is the GnRH test result for PCP?

A
  1. Stimulation pubertal range

2. Stimulated LH: FSH ratio >1

308
Q

What is the treatment for PCP?

A

GnRH super-agonist

309
Q

Give 4 causes of PCP and pseudopuberty

A
  1. Idiopathic precocious puberty
  2. CNS tumours
  3. Increased androgen secretion
  4. Gonadotropin secreting tumours
310
Q

What causes hypogonadotropic hypogonadism?

A

Sexual infantilism related to gonadotrophin deficiency

311
Q

What causes hypergonadotropic hypogonadism?

A

Primary gonadal problems

312
Q

What are the effects of delay in puberty?

A
  1. Delay in acquisition of secondary sex characteristics
  2. Psychological problems
  3. Defects in reproduction
  4. Reduced peak bone mass
313
Q

What is the most common cause for delayed puberty?

A

Constitutional delay of growth and puberty (CDGP)

314
Q

Give 3 neurologic symptoms of CDGP

A
  1. Headache
  2. Visual disturbances
  3. Seizures
315
Q

Give 5 lab investigations for CDGP

A
  1. FBC
  2. U&E
  3. LH/FSH
  4. TFTs
  5. GnRH stimulation test
316
Q

Give 3 functional causes of CDGP

A
  1. Chronic renal disease
  2. Malnutrition
  3. SCD
317
Q

What fails in primary hypogonadism?

A

Ovary or testis

318
Q

What fails in secondary hypogonadism?

A

Hypothalamus and pituitary

319
Q

What condition can present with hypogonadotropic hypogonadism?

A

Kallmann’s syndrome

320
Q

Give 3 symptoms of Kallmann’s syndrome

A
  1. Wide hips
  2. Small genitalia
  3. Anosmia
321
Q

What conditions can present with hypergonadotropic hypogonadism?

A

Male - Klinefelter’s syndrome

Female - Turner’s syndrome

322
Q

Give 3 symptoms of Klinefelter’s syndrome

A
  1. Reduce secondary sexual hair
  2. Osteoporosis
  3. Tall stature
323
Q

Give 3 symptoms of Turner’s syndrome

A
  1. Webbing of neck
  2. Small mandible
  3. High arched palate
324
Q

What can be used as replacement therapy for females?

A

Ethinyl estradiol or oestrogen

325
Q

What can be used as replacement therapy for males?

A

Testosterone enanthate

326
Q

How is hyperglycaemic hyperosmolar state diagnosed?

A
  1. Hypovolaemia
  2. Marked Hyperglycaemia without significant ketonaemia or acidosis
  3. Significantly raised serum osmolarity
327
Q

What is the treatment for hyperglycaemic hyperosmolar state?

A
  1. Normalise the osmolality slowly
  2. Replace fluid and electrolyte losses
  3. Normalise blood glucose gradually
328
Q

What is Conn’s syndrome?

A

Adrenal aldosterone secreting tumour

329
Q

What is the treatment for Conn’s syndrome?

A

Spironolactone - aldosterone agonist

330
Q

What is the diagnosis for Conn’s syndrome?

A

Aldosterone: renin ratio investigation, CT abdo

331
Q

What is seen in Hashimoto’s thyroiditis?

A
  1. Hypothyroidism
  2. Goitre
  3. Anti-TPO
332
Q

Give 3 symptoms of carcinoid syndrome

A
  1. Flushing
  2. Diarrhoea
  3. Heart failure
333
Q

What is the investigation for carcinoid syndrome?

A

Bloods to check for carcinoid tumours

334
Q

What is the treatment for carcinoid syndrome?

A
  1. Sandostatin

2. Ianreotide

335
Q

Give 4 symptoms of hyperkalaemia

A
  1. Muscle weakness
  2. Fatigue
  3. Nausea
  4. Difficulty breathing
336
Q

What is the investigation for hyperkalaemia?

A

ECG - QRS widening, peak T waves, ST depression

337
Q

What is the Tx for hyperkalaemia?

A
  1. IV Ca
  2. Remove K sources
  3. IV glucose and insulin
338
Q

Give 4 symptoms of hypokalaemia

A
  1. Weakness
  2. Muscle cramp
  3. Digestive problems
  4. Heart palpitations
339
Q

What is the investigation for hypokalaemia?

A
  1. Serology

2. U&E

340
Q

What is the Tx for hypokalaemia?

A

Oral or IV K

341
Q

Name 6 complications of diabetes

A
  1. Diabetic retinopathy
  2. Stroke
  3. CVD
  4. Diabetic nephropathy
  5. Diabetic neuropathy
  6. Peripheral vascular disease
342
Q

How many diabetic patients does neuropathy affect?

343
Q

Give 5 symptoms of diabetic neuropathy

A
  1. Burning
  2. Paraesthesia
  3. Foot ulceration
  4. Diarrhoea
  5. Infection
344
Q

How is diabetic neuropathy treated?

A
  1. Glycaemic control
  2. SSRIs
  3. Anticonvulsants (carbamazepine)
  4. Opioids (tramadol)
  5. Capsaicin
345
Q

What is the major consequence of peripheral neuropathy?

A

Diabetic foot ulceration

346
Q

What is the pathway for diabetic amputation?

A
  1. Neuropathy
  2. Trauma
  3. Ulceration
  4. Failure to heal
  5. Infection
  6. Amputation
347
Q

What are other consequences of peripheral neuropathy?

A
  1. Motor nerve damage
  2. Sensory nerve damage
  3. Callus
  4. Autonomic nerve damage
348
Q

What are the screening tests for diabetic peripheral neuropathy?

A
  1. Test sensation
  2. Vibration perception
  3. Ankle reflexes
349
Q

What is the cause for peripheral vascular disease in diabetics?

A

Decreased perfusion due to macrovascular disease

350
Q

What are the signs + symptoms of peripheral vascular disease?

A
  1. Intermittent claudication
  2. Rest pain
  3. Diminished/absent pedal pulses
  4. Coolness of feet and toes
  5. Poor skin and nails
  6. Absence of hair on feet and legs
351
Q

What methods can be used to evaluate peripheral vascular disease?

A
  1. Doppler pressure studies (ABI)

2. Duplex arterial imaging/MRA

352
Q

What is the treatment for peripheral vascular disease?

A
  1. Smoking cessation
  2. Walk through pain
  3. Surgical intervention
353
Q

What preventions are in place for diabetic amputation?

A
  1. Screening to identify risk
  2. Education
  3. Orthotic shoes
  4. MDT foot clinic
  5. Pressure relieving footwear, podiatry, revascularisation, Abx
354
Q

Which groups are at highest risk of diabetic retinopathy?

A
  1. Long duration diabetes
  2. Poor glycaemic control
  3. Hypertensive
  4. On insulin treatment
  5. Pregnancy
355
Q

What is the pathogenesis of diabetic retinopathy?

A
  1. Leakage
  2. Occlusion/ischaemia
  3. Micro-aneurysms
356
Q

What is the treatment for diabetic retinopathy?

A

Laser therapy

357
Q

Give 3 risks of laser therapy

A
  1. Loss of night vision
  2. Loss of peripheral vision
  3. Vitreous haemorrhage
358
Q

What is the hallmark of diabetic nephropathy?

A

Proteinuria

359
Q

What are the risks for diabetic nephropathy?

A
  1. Poor BP

2. Poor BG control

360
Q

What is the pathophysiology of diabetic nephropathy?

A
  1. Glomerulus changes
  2. Increase of glomerular injury
  3. Filtration of proteins
  4. Diabetic nephropathy
361
Q

What is the investigation for diabetic nephropathy?

362
Q

What is the treatment for diabetic nephropathy?

A
  1. BP control
  2. Glycaemic control
  3. ARB/ACEI
  4. Proteinuria control
  5. Cholesterol control
363
Q

What is the Tx for T2DM?

A
  1. Lifestyle changes
  2. Metformin
  3. SU/TZD/glinide
  4. Insulin
364
Q

How can T2DM be prevented?

A
  1. Diet and exercise

2. Metformin/TZDs

365
Q

What are the issues with T2DM prevention?

A
  1. Difficult to maintain long term
  2. Costly
  3. Medication side effects
366
Q

What are incretins?

A

Hormones secreted by intestinal endocrine cells in response to nutrient intake

367
Q

How do incretins influence glucose homeostasis?

A
  1. Glucose-dependent insulin secretion
  2. Postprandial glucagon suppression
  3. Slowing of gastric emptying
368
Q

What is secreted upon ingestion of food by incretins?

369
Q

What is DPP-4?

A

An enzyme present in vascular endothelial lining which inactivates the incretin hormones GIP and GLP-1

370
Q

What is the effect of DPP-4 inhibitors?

A
  1. Small increase endogenous GLP-1

2. No weight effect

371
Q

What is the effect of GLP-1 analogues?

A
  1. Large increase GLP-1
  2. Delay in gastric emptying
  3. Weight loss
372
Q

What groups is TZD contraindicated in?

A
  1. CCF
  2. High risk of fractures
  3. Macula oedema
373
Q

Name 2 SGLT-2 inhibitors

A
  1. Empaglifozin

2. Dapaglifozin

374
Q

What are the side effects of SGLT-2i?

A
  1. Candidiasis
  2. Renal impairment
  3. Hypotension

Phase 2a Medicine (15 decks)

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