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Phase 2a Annabel > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Define endocrinology

A

Study of hormones and their glands or origin, receptors, intracellular signalling pathways and associated diseases

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2
Q

Define endocrine

A

Glands pouring secretions directly into bloodstream without ducts

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3
Q

Define exocrine

A

Glands pour secretions through a duct to the site of action

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4
Q

Where do endocrine secretions act?

A

Blood borne- act at distant sites

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5
Q

Where do paracrine secretions act?

A

Nearby adjacent cells

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6
Q

Where do autocrine secretions act?

A

Feedback excerted on same cell that secretes the hormone

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7
Q

What are the features of water soluble hormones?

A

Unbound
Bind to surface receptors
Short half life
Fast clearance

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8
Q

What are the features of fat soluble hormones?

A

Protein bound
Diffuse into cell
Long half life
Slow clearance

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9
Q

What is an example of a peptide hormone?

A

Insulin

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10
Q

Outline peptide hormone synthesis, packaging and storage+secretions

A

Synthesis: prehormone -> prohormone
Packaging: prohormone -> hormone stored in vesicle
Storage and secretion: hormone released

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11
Q

What are 3 amine hormones?

A

Dopamine
Adrenaline
Noradrenaline

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12
Q

How are peptide hormones released?

A

Pulses/ bursts

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13
Q

What are adrenaline and noradrenaline broken down by?

A

COMT

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14
Q

What is adrenaline broken down into?

A

Metanephrine

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15
Q

What is noradrenaline broken down into?

A

Normetanephrine

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16
Q

What occurs when adrenaline binds to alpha receptors?

A

Vasoconstriction
Bowel contraction
Sweating and anxiety

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17
Q

What occurs when adrenaline binds to beta receptors?

A

Vasodilation
Increased heart rate and contractility
Relaxation of bronchi

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18
Q

What are 2 examples of iodothyronines?

A

T3: triiodothyronine
T4: thyroxine

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19
Q

What are T3 and T4 bound to?

A

TBG: thyroid binding globulin

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20
Q

Is T3 or T4 more active?

A

T3 more active but T4 more numerous

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21
Q

Where is most T3 derived from?

A

Breakdown of T4

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22
Q

What are 4 cholesterol derived hormones?

A

Cortisol
Aldosterone
Testosterone
Oestrogen

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23
Q

How do steroids activate mRNA production?

A

Fat soluble so diffuses into cell
Receptor hormone complex enters nucleus
Binds to GRE
Binding initiates mRNA transcription

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24
Q

What are 4 hormone receptor locations?

A
  1. Cell membrane
  2. Cytoplasm
  3. Nucleus
  4. Cytoplasm/nucleus
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25
Q

Where are peptide hormone receptors located?

A

Cell membrane

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26
Q

Where are steroid hormone receptors located?

A

Cytoplasm

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27
Q

Where are thyroid hormone receptors located?

A

Nucleus

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28
Q

What are 4 hormone secretion patterns?

A
  1. Continuous release
  2. Pulsatile
  3. Circadian rhythm
  4. Release inhibiting patterns
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29
Q

What is a hormone that is continuously released?

A

Prolactin

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30
Q

What is a hormone that is released in a Pulsatile pattern?

A

Insulin

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31
Q

What is a hormone that is released in a circadian rhythm?

A

Cortisol
GH
ACTH

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32
Q

What is a hormone that is controlled by release inhibiting factors?

A

Somatostatin and GH

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33
Q

Define synergism

A

Combined effects of 2 hormones amplified

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34
Q

Define antagonism (in term of hormones)

A

One hormone opposes the other hormone

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35
Q

Define diabetes mellitus

A

syndrome of chronic hyperglycaemia due to relative insulin deficiency, resistance, or both

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36
Q

Describe DMT1

A

When the pancreas doesn’t make any/insufficient insulin

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37
Q

What are normal blood glucose levels?

A

3.5-8 mmol/L

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38
Q

What are the functions of insulin?

A

Decreases glycogenolysis and gluconeogenesis
Increases glucose uptake in tissues
Suppresses lipolysis and ketogenesis

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39
Q

What are the 2 phases of insulin release?

A
  1. B cells detect rising glucose and rapidly release insulin
  2. If levels remain high, more is synthesised and released
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40
Q

What are the functions of glucagon?

A

Increases glycogenolysis and gluconeogenesis
Reduces peripheral glucose uptake
Stimulates peripheral release of gluconeogenic precursors
Stimulates lipolysis and ketogenesis

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41
Q

What is the precursor of insulin?

A

Proinsulin`

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42
Q

How is synthetic insulin detected?

A

Lack of C peptide
-C peptide is present when natural glucose is cleaved

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43
Q

What is the function of insulin in the fasting state?

A

Regulate glucose release by liver

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44
Q

What is the function of insulin in the post-prandial state?

A

Promote glucose uptake by fat and muscle

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45
Q

How is glucose transported into cells?

A

GLUT proteins

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46
Q

What is the function of GLUT-1 receptors?

A

Enables basal non-insulin stimulated glucose uptake

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47
Q

What is the function of GLUT-2 receptors?

A

In beta cells- transport in glucose enabling sensing of glucose levels and release insulin in response to high glucose

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48
Q

Where are GLUT-2 receptors found?

A

Beta cells mainly
-Renal tubules
-hepatocytes

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49
Q

What is the function of GLUT-3 receptors?

A

Enables non-insulin mediated glucose uptake in neurones and placenta

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50
Q

What is the function of GLUT-4 receptors?

A

Mediates peripheral insulin action- how glucose is taken into muscle and adipose tissue

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51
Q

What happens when glucose binds to a glucose receptor?

A
  1. Activation of tyrosine kinase
  2. Initiates cascade response
  3. Migration of GLUT-4 to cell surface
  4. Glucose uptake
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52
Q

What are some conditions that diabetes may be secondary to?

A

Pancreas issues eg. Pancreatitis
Endocrine disease eg. Acromegaly or Cushings
Drugs
MODY

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53
Q

Who is DMT1 most common in?

A

Children and young people
- Northern Europeans and especially Finnish people

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54
Q

What is LADA?

A

Latent autoimmune diabetes in adults
- DMT1 with slower progression to insulin deficiency

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55
Q

Outline the aetiology of DMT1

A

Autoimmune response destroys the beta cells of the pancreas

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56
Q

What are the risk factors of DMT1?

A

Northern European
Family history
Autoimmune disease- Addisons, pernicious anaemia, thyroid issues, coeliac
Dietary factors
Enteroviruses
Vitamin D deficiency

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57
Q

Outline the pathophysiology of DMT1

A
  1. Destruction of beta cells via autoantibodies
  2. Decreased insulin secretion
  3. Breakdown of glycogen
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58
Q

Is C peptide found in patients with DMT1?

A

No- complete beta cell destruction

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59
Q

What is the main antibody in the circulation of patients with DMT1?

A

Glutamic acid decarboxylase (GAD)

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60
Q

What are the 3 main symptoms of DMT1?

A

Polyuria and nocturia
Polydipsia
Weight loss

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61
Q

Why does polyuria occur in DMT1?

A

Glucose dries water into urine and it can not be re absorbed as the maximum capacit has been reached

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62
Q

Why does polydipsia occur in DMT1?

A

Loss of fluid and electrolytes from excess water and glucose in urine

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63
Q

Why does weight loss occur in DMT1?

A

Fluid depletion
Breakdown of fat and muscle

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64
Q

What signs of DMT1 can be seen on physical examination?

A

Fruity breath
Lean patient
Cuts and bruises taking a while to heal
Signs of dehydration

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65
Q

What 4 investigations are carried out to diagnose DMT1 and 2?

A

HbA1c test
Fasting plasma glucose
Random plasma glucose
Oral glucose tolerance tests

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66
Q

What random plasma glucose value indicates diabetes?

A

> 11.1 mmol/L

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67
Q

What fasting plasma glucose value indicates diabetes?

A

> 7mmol/L

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68
Q

When are 2 abnormal values needed to diagnose diabetes?

A

Asymptomatic individuals

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69
Q

What test is used for borderline diabetes diagnosis?

A

OGTT

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70
Q

What values of an OGTT indicate diabetes?

A

Fasting = > 7mmol/L
2 hours post glucose = > 11.1mmol/L

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71
Q

What value on a HbA1c test indicates diabetes?

A

48mmol/mol (> 6.5% normal)

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72
Q

What does a HbA1c test measure?

A

Glycated haemoglobin shows average blood glucose over the past 3 months

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73
Q

What is the first line treatment for DMT1?

A

Basal bolus insulin

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74
Q

Why may some DMT1 patients be unable to drive?

A

Hypoglycaemia
Retinopathy

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75
Q

What are the 3 types of insulin doses?

A

Short acting soluble insulin
Short acting insulin analogues
Longer acting insulin

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76
Q

When are short acting soluble insulins given?

A

15-30 mins before meals
Insulin pumps
IV infusion in labour

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77
Q

When are short acting insulin analogues given?

A

Evening meal in patients prone to nocturnal hypoglycaemia

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78
Q

How long to short acting soluble insulins take to start working and last?

A

Work in 30-60 mins
Last for 4-6 hours

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79
Q

How are longer acting insulins made?

A

Retarding agents precipitate crystals

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80
Q

What are the complications of DMT1?

A

Heart disease
Stroke
Feet problems
Circulatory issues
Neuropathy
Nephropathy, sight problems

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81
Q

What are the complications of insulin treatment?

A

Hypoglycaemia
Lipohypertrophy
Insulin resistance
Weight gain

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82
Q

Define DMT2

A

Hyperglycaemia due to insulin resistance (mainly) and insulin deficiency

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83
Q

Outline the epidemiology of DMT2

A

More common in black and south Asian people
Usually >30

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84
Q

Describe the aetiology of DMT2

A

Decreased insulin secretion
Increased insulin resistance

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85
Q

List the risk factors of DMT2

A

Family history
Increasing age
Obesity and lack of exercise
Low birth weight

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86
Q

Is DMT2 associated with an insulin binding problem?

A

No- the resistance is post receptor

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87
Q

By how much is beta cell mass reduced in DMT2?

A

50%

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88
Q

What is an early sign of DMT2?

A

Loss of normal biphasic response

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89
Q

Why are circulating insulin levels high in DMT2 patients?

A

-Increased glucose production from lack of gluconeogenesis suppression
- Reduced peripheral glucose uptake

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90
Q

What is shown by starling curve of the pancreas?

A

Insulin levels rise and decline years after diabetes progression due to secretory failure

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91
Q

Why is DKA uncommon in patients with DMT2?

A

Small amounts of glucose can inhibit the breakdown of ketogenesis

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92
Q

What are the symptoms of DMT2?

A

Polyuria
Polydipsia
Weight loss
Retinopathy
Polyneuropathy can cause tingling and numbness in feet
Erectile dysfunction

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93
Q

What signs of DMT2 can be seen on physical examination?

A

Retinopathy
Acanthosis nigricans - insulin resistance causing black pigmentation on base of neck

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94
Q

What is the first line of treatment for DMT2?

A

Lifestyle and dietary changes

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95
Q

What is the first line of oral treatments for DMT2?

A

Biguanide eg. METFORMIN

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96
Q

How does metformin work?

A

Reduces gluconeogeneis
Increases glucose sensitivity
Reduces CVS risk

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97
Q

What has replaced sulfonylureas as the second line oral treatment for DMT2?

A

DPP-4 inhibitors
GLP-1 analogues
SGLT-2 inhibitors

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98
Q

How do sulfonylureas work?

A

Promote insulin secretion by binding to beta cell receptors

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99
Q

What are the risks of sulfonylureas?

A
  • HYPOGLYCAEMIA
  • can be dangerous in people with liver problems
  • Weight gain
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100
Q

How do GLP analogues work?

A

Insulin alternative- mimic 2 peptide hormones and promote insulin release ect

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101
Q

How do SGLT-2 inhibitors work?

A

Block glucose reabsorption in the kidney

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102
Q

What are the side effects of SGLT-2 inhibitors?

A

Thrush
Euglycaemic ketoacidosis

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103
Q

What are the risks of DMT2?

A

CVD
Nephropathy
Strokes
Hearing damage
Sleep apnea

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104
Q

What type of DM is diabetic ketoacidosis (DKA) usually seen in?

A

DMT1

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105
Q

What 3 circumstances are linked with DKA?

A
  1. Undiagnosed diabetes
  2. Interruption of insulin therapy
  3. Stress of intercurrent illness
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106
Q

What are the complications of DMT2?

A

Diabetic retinopathy
Diabetic neuropathy- can lead to amputation
Stroke
CVD (most commmon)
HHS- hyperglycaemic hyperosmolar state

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107
Q

What is the commonest type of monogenic diabetes?

A

MODY

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108
Q

What type of genetic mutation is MODY?

A

Autosomal dominant- single gene affects beta cell function

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109
Q

Outline the epidemiology of MODY

A

<25
Non-obese

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110
Q

What are the risk factors for MODY?

A

Parent with diabetes
Evidence of non-insulin dependence

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111
Q

Describe MODY3

A

HNF1A mutation

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112
Q

How is MODY3 treated?

A

Sensitive to sulphonylurea
Insulin usually not required 80%

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113
Q

Describe MODY2

A

Glucokinase gene mutation

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114
Q

Describe MODY1

A

HNF4A mutation

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115
Q

What are the qualities of MODY1?

A

Macrosomia (4.4kg birthweight)
AND
Neonatal hypoglycaemia

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116
Q

Describe investigations for diagnoses of MODY

A

Absence of islet autoantibodies
Sensitive to sulphonlyurea
No ketones
Measurable C peptide
Good control on low insulin

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117
Q

When can DKA occur in DMT2?

A

Late stage when there is absolute insulin deficiency

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118
Q

What does HHS stand for?

A

Hyperosmolar hyperglycaemic state

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119
Q

What is HHS?

A

Metabolic emergency characteristic of uncontrolled DMT2

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120
Q

What is the gold standard for diagnosing DMT2?

A

HbA1c

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121
Q

What are the micro vascular complications of DMT2?

A

Retinopathy
Neuropathy
Peripheral neuropathy

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122
Q

What are the macrovascular complications of DMT2?

A

Stroke
Hypertension
Peripheral artery disease
Coronary artery disease

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123
Q

Outline the pathophysiology of HHS

A

Insulin levels are reduced but sufficient to inhibit ketogenesis but not glucose production
Hyperglycaemia -> osmotic diuresis -> raised serum osmolarity and hyper viscosity of blood

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124
Q

Outline the epidemiology of HHS

A

Middle or later life of previously undiagnosed diabetes

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125
Q

What are the common presentations of HHS?

A

Severe dehydration
Hyperglycaemia
Decreased consciousness
Hyperosmolarity
No ketones
Stupor or coma

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126
Q

What is used to diagnose HHS?

A

Hyperglycaemia - glucose >11mmol/L
Heavy glycosuria - urine stick test
Hypotension
Hyperosmolarity

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127
Q

How is HHS treated?

A

Fluid replacement 0.9% saline
Low molecular weight heparin (anticoagulant)
Restore K+ loss

Insulin if ketones and lack of glucose decrease after treatment

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128
Q

What are the complications of HHS?

A

Stroke
MI
PE

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129
Q

What are the risk factors for DKA?

A

Stopping insulin
Infection
Surgery
MI
Pancreatitis
Undiagnosed diabetes

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130
Q

What ketone level is required for ketosis?

A

Blood ketones >3mmol/L

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131
Q

Outline the pathophysiology of DKA

A

Absence of insulin -> unrestrained glucose production and decreased uptake -> hyperglycaemia-> dehydration -> lipolysis -> inc. FFA -> ketones -> ACIDOSIS

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132
Q

How does DKA present?

A

Pear drop breath smell
Dehydration and hypotension
Nausea and vomiting
Abdo pain
Hyperventilating
Drowsy/reduced consciousness

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133
Q

How is DKA diagnosed (4 things)?

A

Hyperglycaemia >11mmol/L
Increased ketones >3mmol/L
Acidaemia = >7.3
Metabolic acidosis = bicarbonate <15mmol/L

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134
Q

How is DKA treated?

A

1.ABC
2. 0.9% saline fluid replacement
3. Insulin
4. Restore K+ loss
5. Treat diabetes

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135
Q

What are the complications of DKA?

A

Cerebral oedema (if fluid increased too quickly)
Coma
Hypotension
Thromboembolism

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136
Q

What are some ways to reduce the complications associated with DM?

A

BP control eg. Ramapril
Cessation of smoking
Statin eg simvastatin

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137
Q

When are people most at risk of diabetic retinopathy?

A

Long time DM
Poor glycaemic control
Hypertension
On insulin
Pregnant

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138
Q

What are the signs of diabetic retinopathy?

A

Tiny red dots- micro aneurysms
Blots- haemmorages
Cotton wool spots- micro infarcts of occluded vessels

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139
Q

How is diabetic retinopathy treated?

A

Laser therapy stabilises deterioration and prevents progression

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140
Q

What are the risks of laser surgery for diabetic retinopathy?

A

-Night vision difficulty
- 1/5 lose peripheral vision
- Vitreous haemorrhage
- Temporary drop in acuity with intensive treatment

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141
Q

What is the diagnostic marker for diabetic nephropathy?

A

Proteinuria via albumin: creatine ratio of >3

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142
Q

How does diabetic nephropathy occur?

A

Thickening of basement membrane due to poor glycaemic control

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143
Q

How is diabetic nephropathy treated?

A

Aggressive BP control ie. ACE inhibitor
Avoid metformin
Reduce insulin dose
Late stage = ESKD -> dialysis or transplant

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144
Q

How many diabetics does neuropathy affect?

A

30-35%

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145
Q

What is the most common form of diabetic neuropathy?

A

Distal symmetrical neuropathy

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146
Q

What are the risk factors of diabetic neuropathy?

A

Hypertension
Smoking
High HbA1c
Long duration of diabetes
High BMI

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147
Q

What are the features of diabetic neuropathy?

A

Pain: allodynia, parasthesia, burning
Diarrhoea, constipation
Erectile dysfunction
Loss of sensation in feet

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148
Q

How is diabetic neuropathy treated?

A

Good glycaemic control
Paracetamol
Tricyclic antidepressant eg. Amitriptyline
Anticonvulsant eg. Pregabalin
Opiates eg. Tramadol

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149
Q

Define appetite

A

The desire to eat food

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150
Q

Define anorexia

A

Lack of appetite

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151
Q

Define fullness

A

Feeling of fullness- appetite disappearing after a meal

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152
Q

What is the function of leptin?

A

Switches off appetite and is immunostimulatory

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153
Q

How do leptin levels change before and after a meal?

A

Increase after meal
Decrease after fasting

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154
Q

What are the effects of peptide YY?

A

Inhibits gastric motility
Reduces appetite

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155
Q

When and where is peptide YY secreted?

A

Secreted from ileum, pancreas and colon in response to food

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156
Q

What are the effects of cholecystokinin?

A

Satiety via vagus
-delays gastric emptying
- Gall bladder contraction
- insulin release

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157
Q

Where are cholecystokinin receptors found?

A

Pyloric sphincter

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158
Q

What are the functions of ghrelin?

A

Stimulates:
Gh release
Appetite

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159
Q

What 2 mechanisms stimulate appetite?

A

Olfactory, gustatory, cognitive and visual stimuli
Ghrelin secretion

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160
Q

What are 4 mechanisms that decrease appetite?

A
  1. Oral receptors alter pleasantness and food intake
  2. Stretch receptors in stomach increase satiety
  3. CCK,GLP, Insulin, PYY increase satiety
  4. Leptin, nutrients and temperature regulates satiety
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161
Q

What is the most common endocrine emergency?

A

Hypoglycaemia

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162
Q

What value indicates serious biochemical hypoglycaemia?

A

Plasma glucose <3 mmol/L

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163
Q

What value indicates alert level hypoglycaemia?

A

Plasma glucose < 3.9 mmol/L

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164
Q

What are the most common causes of hypoglycaemia in diabetics?

A

Insulin
Sulphonylurea
- Ie. Increased activity, missing meals, overdose

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165
Q

What are the non-diabetic causes of hypoglycaemia?

A

EXPLAIN:

EX-Exogenous drugs
P- Pituitary insufficiency
L- Liver failure
A- Addison’s disease
I- islets cell tumour and immune hypoglycaemia
N- Non-pancreatic neoplasm

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166
Q

What are the common symptoms of hypoglycaemia?

A

Autonomic: trembling, palpitations, sweating, anxiety and hunger
Neuroglycopenic: confusion, weakness, dizziness, vision changes
Nausea
Headache

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167
Q

How is hypoglycaemia diagnosed?

A

-Finger prick blood- low glucose < 3.9 mmol/L
-Elevated HbA1c can have symptoms > 3.9mmol/L

Also:
- drug history and exclude liver failure
- bloods: glucose, insulin, C-peptide, ketones

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168
Q

How is hypoglycaemia treated?

A
  1. Oral sugar and long-acting starch
  2. 50% IV glucose if unable to swallow, IM if not possible
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169
Q

What is goitre?

A

Swelling of the thyroid which causes a lump to form in the neck

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170
Q

What causes goitre?

A

TSH receptor stimulation which causes the thyroid to grow in size

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171
Q

How does hyperthyroidism cause goitre?

A

Excessive stimulation of TSH receptor = more hormone = growth

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172
Q

How does hypothyroidism cause goitre?

A

Pituitary detects low thyroid levels = more TSH production = stimulates TSH receptors

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173
Q

Define thyrotoxicosis

A

Excess thyroid hormones in blood

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174
Q

Define hyperthyroidism

A

Overproduction of thyroid hormone
-Increase synthesis of T3 and T4 in the thyroid gland

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175
Q

What is the most common cause of hyperthyroidism?

A

Most common- Graves’ disease
Toxic multinodular goitre
Toxic adenoma
Thyroiditis
Excess iodine

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176
Q

Describe the epidemiology of hyperthyroidism

A

Females
Genetic defects

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177
Q

Describe the risk factors of hyperthyroidism

A

Smoking
Stress
High iodine
Autoimmune disease- vitiligo, Addison’s, MG

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178
Q

Outline the pathophysiology of hyperthyroidism

A
  1. IgG antibodies (in graves) bind to TSH receptors
  2. T3 and T4 production stimulated
  3. Low TSH levels
  4. Effects metabolism, growth, and development
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179
Q

How is hyperthyroidism diagnosed?

A

1st line: thyroid function tests (TFTs)
- Serum TSH low
- High T4 and sometimes T3
TPO and thyroglobulin antibodies present

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180
Q

How is hyperthyroidism treated?

A

Thioamides (carbimazole) and propylthiouracil (PTU)
Propanolol: (ie beta blocker) to control symptoms
Radioactive iodine
Surgery

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181
Q

How does propylthiouracil (PTU) work?

A

Stops conversion of T4 to T3

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182
Q

How does oral carbimazole work?

A

Blocks thyroid hormone biosynthesis and has immunosuppressive effects

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183
Q

What type of drug is carbimazole?

A

Thioamide

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184
Q

What are the 2 strategies of thioadmide administration?

A
  1. Titration: 4 weeks and then reduce doses according to thyroid function test
  2. Block and replace therapy: carbimazole + thyroxine
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185
Q

What are the most common side effects of thiodmides?

A

RASH- most common
Hepatitis
Neuritis
Vasculitis

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186
Q

What side effects of thioamides mean the drug has to be stopped?

A

Sore throat
Mouth ulcers
Fever

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187
Q

What is the most serious side effect of thionamides?

A

Agranulocytosis: decrease in WBCs
- Must warn patients
- Stop if symptoms develop and check FBC

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188
Q

What is given for radioactive iodine treatment?

A

Radioactive I(131)

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189
Q

When is radioactive iodine contraindicated?

A

Pregnancy and breastfeeding

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190
Q

How does radioactive iodine work?

A

Iodine taken up by thyroid
Accumulates and results in local irradiation and tissue damage
Returns to normal thyroid function over 4-12 weeks

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191
Q

What are the side effects of radioactive iodine?

A

Necrosis follicular cells
Vascular occlusion
Atrophy and fibrosis
Chronic inflammation
Late hypothyroidism

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192
Q

When is surgery needed in hyperthyroidism?

A

Large goitre
Poor response to drugs
Side effects of drugs

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193
Q

What are the 2 methods of surgery for hyperthyroidism?

A

Subtotal thyroidectomy
Total thyroidectomy (for large goitre, graves, or malignancy)

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194
Q

What are the complications of thyroid surgery?

A

Thyroidectomy = hypothyroid
Tracheal compression
Laryngeal nerve palsy
Transient hypocalcaemia

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195
Q

What is thyroid crisis/ thyroid storm?

A

Rare, life threatening condition where there is rapid deterioration of thyrotoxicosis (rapid T4 increase)

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196
Q

What are the features of thyroid crisis?

A

Hyperpyrexia
Tachycardia
Delirium
Coma
Death

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197
Q

What are the causes of thyroid crisis?

A

Stress
Infection
Surgery
Radioactive iodine therapy

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198
Q

How is thyroid crisis treated?

A

Large doses of:
- Oral Carbimazole
- Oral propranolol
- Oral potassium iodide
- IV hydrocortisone

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199
Q

What is hypothyroidism?

A

Under activity of thyroid gland due to thyroid disease (primary) or secondary causes

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200
Q

Outline the risk factors of hypothyroidism

A

More common in females
Incidence increases in age
Autoimmune disease

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201
Q

What are the causes of hypothyroidism?

A

Primary:
Iodine deficiency, Hashimoto’s thyroiditis, drugs, thyroidectomy
Secondary: pituitary and hypothalamic disease, genetic disorders

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202
Q

What drugs can cause hypothyroidism?

A

Carbimazole
Lithium
Amiodarone

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203
Q

Outline the pathology of autoimmune/atrophied hypothyroidism

A

Antithyroid antibodies lead to lymphoid infiltration causing atrophy and fibrosis

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204
Q

What are the features of post-partum thyroiditis?

A

Transient condition in pregnancy
Autoimmune modifications causing hypo/hyperthyroidism
Can be misdiagnosed as postpartum depression

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205
Q

What are the symptoms of hypothyroidism?

A

Hoarse voice
Goitre (iodine deficiency)
Weight gain
Cold intolerance
Dry, rough skin
Constipation

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206
Q

What are the symptoms of hyperthyroidism?

A

Weight loss
Tachycardia
Heat intolerance
Anxiety
Tremor
Diarrhoea

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207
Q

What are the signs of hypothyroidism?

A

BRADYCARDIC
B- bradycardia
R- reflexes relax slowly
A- Ataxia
D- dry hair and skin
Y- yawning/ drowsy
C- cold hands
A- ascites
R- round puffy face
D- defeated demeanour
I- immobile
C- congestive heart failure

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208
Q

How is hypothyroidism diagnosed?

A

TFT- thyroid function test
-low T4 and high TSH
-secondary hypothyroidism = low TSH too
-thyroid antibodies eg TPO in Hashimotos

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209
Q

Outline the pathophysiology of primary hypothyroidism

A

T3/T4 not produces
High compensatory TSH

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210
Q

Outline the pathophysiology of secondary hypothyroidism

A

Low TSH levels cause low T3 and T4

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211
Q

How is hypothyroidism treated?

A

Oral levothyroxine (T4)
- dose titrated in primary hypothyroidism
- start lower in IHD patient

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212
Q

What are the complications of hypothyroidism?

A

Myxedema coma (severe deficiency of thyroid hormones)
- hypothermia, heart failure, hypo ventilation ect

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213
Q

How is myxedema treated?

A

IV/oral T3 and glucose infusion

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214
Q

Describe Graves’ disease

A

Autoimmune disease caused by excess production of thyroid hormone (TSH receptor antibodies)

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215
Q

Outline the epidemiology of Graves’ disease

A

Most common cause of hyperthyroidism (2/3)
Females more commonly affected
Typically presents at 40-60 years

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216
Q

What are the risk factors of Graves’ disease?

A

Female
E. coli
Autoimmune disease- Vitiligo, Addisons, pernicious anaemia, MG
Alemtuzmab (MS drug)

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217
Q

Describe the pathophysiology of Graves’ disease

A

Serum IgG antibodies called TSHR-Ab bind to TSH receptors
stimulate thyroid production (behave like TSH)
Cause excess secretion of thyroid hormones -> diffuse goitre

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218
Q

What are the clinical presentations of Graves’ disease?

A

-Graves ophthalmology- exophthalmos (protruding eyes) an ophthalmoplegia (paralysis of eye muscles)
- diffuse goitre
-pretibial myxoedema- raised purple skin lesions over thighs
- thyroid acropachy- clubbing, swollen fingers, periosteal bone formation

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219
Q

How is Graves’ diagnosed?

A

TSHR-Ab raised
TFT- high T4 and low TSH

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220
Q

How is Graves’ disease treated?

A

-Ophthalmology issues treated with IV methylprednisolone (corticosteroid) and surgical decompression
- Anti thyroid drugs

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221
Q

What is Hashimoto’s hypothyroiditis?

A

Autoimmune disease where the thyroid is attacked by antibodies and other cells

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222
Q

Outline the epidemiology of Hashimoto’s hypothyroiditis

A

Females more affected
Middle aged and 60-70 years old

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223
Q

Outline the pathophysiology of Hashimoto’s hyperthyroiditis

A
  1. Formation of antithyroid antibodes
  2. Low T4 and high TSH causes progressive fibrosis
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224
Q

What are the presentations of Hashimoto’s thyroiditis?

A

Goitre formation
Same as hypothyroidism
Loss of hair at lateral 1/3 eyebrows

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225
Q

What investigations are carried out for Hashimoto’s thyroiditis?

A

TFT- low T4 and high TSH
Anti thyroid peroxidase antibodies are positive

226
Q

What is the treatment for Hashimoto’s thyroiditis?

A

Levothyroxine

227
Q

What is de Quervain’s thyroiditis?

A

Subacute granulomatous thyroiditis causing inflammation
-Results in pain and discomfort due to rapid swelling

228
Q

What are the causes/risk factors of De Quervain’s thyroiditis?

A

Viral infection

229
Q

What are thee 4 phases of De Quervain’s thyroiditis?

A

Phase 1: goitre, hyperthyroidism
Phase 2: euthyroid (Normal)
Phase 3: weeks to months hypothyroidism
Phase 4: normal

230
Q

How does De Quervain’s thyroiditis present?

A

Neck pain
Difficulty eating
Tender goitre- PAINFUL
Fever
Palpitations

231
Q

What investigations are carried out for diagnosis of De Quervains thyroiditis?

A

elevated:
T4, T3, CRP, Free thyroxine uptake

232
Q

What are the treatments of De Quervains thyroiditis?

A

Hyperthyroid phase: NSAIDs and corticosteroids
Hypothyroid phase: usually fine to be untreated but can give small amount of levothyroxine

233
Q

What are the complications of De Quervains thyroiditis?

A

Thyroid storm
Long term hypothyroidism

234
Q

What do TSH receptor antibodies help differentiate?

A

Thyroiditis from graves
Positive = Graves

235
Q

What are TPO antibodies useful?

A

Identify autoimmune problems

236
Q

What are the 4 most common types of thyroid cancer (in order)?

A

Papillary (70%)
Follicular (20%)
Anaplastic (<5%)
Lymphoma (2%)

237
Q

Outline the epidemiology of thyroid carcinoma

A

Affects women more
400 deaths a year in UK

238
Q

What are the risk factors for thyroid carcinomas?

A

Radiation

239
Q

What are the features of papillary thyroid cancer?

A

Affects young people
Local spread
Good prognosis

240
Q

What are the features of follicular thyroid cancer?

A

Middle age
Spread to lung/bone
Usually good prognosis

241
Q

What are the features of anaplastic thyroid cancers?

A

Very undifferentiated
Aggressive local spread
Poor prognosis

242
Q

How do thyroid carcinomas present?

A

In 90% present as nodules
- Hard and irregular in shape
Can have dysphagia or hoarseness

243
Q

How is thyroid carcinoma diagnosed?

A

Fine needle aspiration biopsy
TFT blood test
Ultrasound

244
Q

How are thyroid carcinomas treated?

A

Thyroidectomy
Levothyroxine to repress TSH which acts as a growth factor
Radioactive iodine (anaplastic does not respond)

245
Q

where are GLUT1 receptors found?

A

erythrocyte membrane

246
Q

What are the 3 layers of the adrenal cortex?

A

Zona glomerulosa
Zona fasiculata
Zona reticularis

247
Q

What is produced by the zona glomerulosa?

A

Mineralocorticoids
-eg aldosterone

248
Q

What is produced by the zona fasiculata?

A

Glucocorticoids
-eg. Cortisol

249
Q

What is produced by the zona reticularis?

A

Androgens
- Must be converted to testosterone and dihydrotestosterone to be active

250
Q

What is produced by the adrenal medulla?

A

Cathecholamines
-Eg. Adrenaline and noradrenaline
-under sympathetic control

251
Q

Describe how cortisol and androgen production is stimulated

A

CRH from hypothalamus stimulates..
ACTH from pituitary
ACTH stimulates the production of cortisol and androgens

252
Q

What controls the zona glomerulosa secretion?

A

NOT HPA AXIS
Renin release from juxtaglomelular cells of afferent arterioles in kidneys

253
Q

Define Cushing’s syndrome

A

General term referring to excess cortisol whatever the cause

254
Q

Define Cushing’s disease

A

Cortisol excess due to pituitary ACTH secreting tumour

255
Q

Where do thyroid tumours metastasise to?

A

Lung (50%)
Bone (30%)
Liver (10%)
Brain (5%)

256
Q

What can mimic Cushing’s syndrome?

A

Alcohol excess

257
Q

What are the causes of Cushings syndrome?

A

-Oral steroids (glucocorticoids) most common
-80% due to increased ACTH- can be due to Cushings disease

258
Q

What are the ACTH dependent causes of Cushings?

A

-Cushings disease (most common)
-Ectopic ACTH production (ACTH producing tumour elsewhere in the body)
-ACH treatment (eg for asthma)

259
Q

What are the ACTH independent causes of Cushings?

A

Adrenal adenoma (causes cortisol release)
Iatrogenic eg glucocorticoid administration

260
Q

What is the difference in ACTH levels between ACTH dependent and independent causes of Cushings?

A

ACTH dependent: Increased ACTH
ACTH independent: Decreased ACTH due to negative feedback from raised cortisol

261
Q

Outline the pathophysiologies of Cushing’s syndrome

A

1.Excess ACTH stimulates excess cortisol release
2. Neoplasms in adrenals stimulate zona reticularis
3. Ingesting excess glucocorticoids

262
Q

What is an example of a glucocorticoid drug?

A

Prednisolone

263
Q

Describe the signs of Cushing’s syndrome

A

Obese- especially centrally
Plethoric moon face
Proximal weakness
Thin skin, purple striae on stomach
Buffalo hump

264
Q

What are the symptoms of Cushing’s syndrome?

A

Increased BP
Personality changes- irritable, tired, depressed
Gonadal dysfunction- ED, irregular periods
Osteoporosis

265
Q

What investigations are carried out to diagnose Cushing’s syndrome?

A

1st line: raised late night salivary cortisol levels
Gold standard: dexamethasone suppression test (1mg)
-24 hour urinary free cortisol

266
Q

What results from an overnight low dose dexamethasone suppression test indicates Cushings?

A

Serum cortisol at 8am should be suppressed <50nmol/L
- Will NOT be suppressed in Cushings

267
Q

How is adrenal tumour detected?

A

Plasma ACTH is undetectable
-CT and MRI then done

268
Q

What is the next step of diagnosis if cortisol is not suppressed in Cushings?

A

High dose given (8mg)

269
Q

What results of a high dose dexamethasone test indicate a pituitary adenoma (Cushings disease)?

A

Suppressed cortisol and ACTH

270
Q

What results of a high dose dexamethasone test indicate an adrenal adenoma?

A

Cortisol not suppressed
ACTH suppressed

271
Q

What results of a high dose dexamethasone test indicate an ectopic ACTH tumour?

A

Cortisol not suppressed
ACTH not suppressed

272
Q

How is ectopic ACTH treated?

A

Surgery for tumour
Drugs that inhibit cortisone synthesis

273
Q

What is a drug that inhibits cortisone synthesis?

A

Metyrapone

274
Q

What is an adrenolytic drug?

A

Mitotane

275
Q

How is iatrogenic Cushings treated?

A

Stop steroids!

276
Q

How is Cushings disease treated?

A

Surgical removal of pituitary adenoma
If fails….
-Bilateral adrenalectomy
- Radiotherapy

277
Q

How is adrenal adenoma treated?

A

Adrenalectomy- doesn’t cure cancer though
- Radiotherapy
- Adrenolytic drugs eg. Mitotane

278
Q

How is ectopic ACTH treated?

A

Surgery if not spread
Drugs that inhibit cortisone synthesis eg. Metyrapone

279
Q

What are the complications of Cushing’s syndrome?

A

Hypertension
Osteoporosis
CVD
DMT2

280
Q

What stimulates and inhibits growth hormone (GH)?

A

Stimulates: GHRH (also ghrelin)
Inhibits: somatostatin (SST) and high glucose

281
Q

Define gigantism

A

Excessive GH production in children before fusion of the epiphyses of the long bones

282
Q

Define acromegaly

A

Excess GH in adults due to a pituitary secreting tumour (usually)

283
Q

Describe the epidemiology of acromegaly

A

Rare- 3 per million
Equally as common between males and females
Mean diagnosis at 48

284
Q

Describe the aetiology of acromegaly

A

benign GH producing tumour- most common
Rare: ectopic GHRH from carcinoid tumour

285
Q

Outline the pathophysiology of acromegaly

A
  1. Increased GH secreted
  2. Travels to tissue eg. Liver
  3. Binds to receptors causing increased IGF-1
  4. Stimulates skeletal and soft tissue growth leading to giant like appearance
286
Q

What are the symptoms of acromegaly?

A

Headaches
Acral enlargement (hands and feet)
Sweating
Vision problems
Wonky bite
Backache
Acroparaestheisa - tingling and numbness in extremities

287
Q

What are the signs of acromegaly?

A

Skin darkening
Coarsening face with wide nose
Big supraorbital ridge
Deep voice
Rings are tight
Carpal tunnel
Large tongue

288
Q

What are the complications of acromegaly?

A

Impaired glucose tolerance
Sleep apnoea
Hypertension
CVD
Colon cancer
Stroke and cardiovascular events

289
Q

Why is a random growth hormone test not just used for acromegaly diagnosis?

A

Secretion is pulsatile

290
Q

What is the first line test for acromegaly?

A

IGF-1 and plasma GH levels

291
Q

What levels of GH and IGF-1 exclude acromegaly?

A

Random GH undetectable OR GH < 0.4 ng/ml
Normal IGF-1

292
Q

What is the gold standard diagnostic test for acromegaly?

A

Glucose tolerance test (GTT)

293
Q

What results on a OGTT would exclude acromegaly?

A

GH <1ng/ml
-normally GH would be suppressed, but this does not occur in people with acromegaly

294
Q

What other tests can be done to diagnose acromegaly?

A

Visual field examination
MRI of pituitary fossa
Pituitary function test
ECH and ECHO to look for cardiomyopathy

295
Q

What is the first line treatment for acromegaly?

A

Trans-sphenoid also surgery to remove the tumour from the pituitary gland

296
Q

What is the second line treatment for acromegaly?

A

Somatostatin analogues to suppress GH release

297
Q

What are 2 somatostatin analogues?

A

IM octrotide
IM lanreotide

298
Q

What are some 3rd line treatments for acromegaly?

A

GH receptor agonists
Or
Dopamine agonist

299
Q

What is a GH receptor antagonist?

A

Pegvisomant

300
Q

What are 2 dopamine agonists?

A

Oral cabergoline
Oral bromocriptine

301
Q

What does raise prolactin lead to?

A

Lactation
Inhibition of GNRH -> decreased LH/FSH -> decreased testosterone or oestrogen

302
Q

Define prolactinoma

A

Benign prolactin producing tumours of lactotropth cells in anterior pituitary

303
Q

What are the risk factors of prolactinoma?

A

Female sex
Peak incidence in childbearing age

304
Q

Are most prolactinomas microprolactinomas or macroprolactinomas?

A

Micro = 90%
Macro = 10%

305
Q

How big are micro and macroprolactinomas?

A

Micro = <1cm diameter
Macro = _>1cm diameter

306
Q

Outline the pathophysiology of prolactinoma

A
  1. Hyper secretion of prolactin inhibits GNRH
  2. Causes secondary hypergonadism
307
Q

How do females with prolactinoma present?

A

Amenorrhoea
Oliomenorrhoea
Infertility (inhibits ovulation)
Galactorrhoea (spontaneous flow of milk)
Low libido
Visual field defect

308
Q

How does prolactinoma present in males?

A

Low testosterone
Erectile dysfunction
Reduces facial hair
Low libido
Galactorrhoea
Visual field defects

309
Q

What are the investigations for prolactinoma?

A

1st line: basal prolactin level- will be RAISED
2nd line: pituitary MRI to detect adenoma

310
Q

How is prolactinoma treated?

A

1st line: dopamine agonists- inhibit prolactin release causing a decrease in size of tumour
2nd line: HRT

311
Q

What are the 4 effects of aldosterone?

A
  1. Increases Na+ reabsorption from distal tubule
  2. Increases K+ excretion from distal tubule
  3. Increase H+ secretion from collecting ducts
  4. Increase H2O reabsorption
312
Q

Define primary hyperadosteronism

A

Excess production of aldosterone independent from the RAAS system
- By renal glands

313
Q

What are the causes of primary hyperaldosteronism?

A

Bilateral adrenal hypoplasia (70%)
Conn’s syndrome: adrenal adenoma secreting aldosterone

314
Q

Define Conn’s syndrome

A

An adrenal adenoma secreting aldosterone

315
Q

Define secondary hyperaldosteronism

A

Excessive renin stimulates the adrenal glands to produce more aldosterone

316
Q

Describe renin levels in primary and secondary hyperaldosteronism

A

Primary: serum renin low as it is suppressed by high BP
Secondary: serum renin is high

317
Q

What are the causes of secondary hyperaldosteronism?

A

Renal artery stenosis (reduced arterial supply to kidney)
Renal artery obstruction
Heart failure

318
Q

What is the most common secondary cause of hypertension?

A

Conn’s

319
Q

Describe the pathophysiology of hyperaldosteronism

A

High aldosterone -> high Na and H2O
-> low K
Hypertension

320
Q

Describe the pathophysiology of Conn’s syndrome

A

Aldosterone producing carcinoma causes effects of hyperaldosteronism

321
Q

Describe the presentation of Conn’s syndrome

A

Often asymptomatic
Hypertension
Hypokalaemia
Weakness
Polyuria and polydipsia
Headaches

322
Q

What is the differential diagnosis of Conn’s?

A

Secondary hyperaldosteronism
-measure renin levels

323
Q

What investigations are carried out for Conn’s diagnosis?

A

1st line: aldosterone: renin ratio
GS: IV saline- aldosterone would remain high
Hypokalemic ECG
FBC, U&E, LFT
- Low K= primary

324
Q

How is Conn’s and hyperaldosteronism treated?

A

Adrenalectomy
Aldosterone agonist

325
Q

Where is aldosterone secreted from?

A

Adrenal glands

326
Q

What are 2 aldosterone antagonists/potassium sparing diuretics?

A

Spironolactone
Amiloride

327
Q

What are the complications of Conn’s?

A

Heart failure
MI
Stroke
Renal damage

328
Q

What would indicate hypokalaemia on an ECG?

A

Flat T wave
ST suppression
Long QT

329
Q

Define adrenal insufficiency

A

Adrenal glands do not produce enough hormones, particularly aldosterone and cortisol

330
Q

Define Addison’s disease

A

Destruction of entire renal cortex resulting in deficiency of:
Mineralocorticoids- aldosterone
Glucocorticoids- cortisol
Sex steroids- androgens (sex hormone precursors)

331
Q

Describe the epidemiology of Addison’s disease

A

Very rare- 0.8 per 100,000
Marked female preponderance

332
Q

Describe primary adrenal insufficiency

A

AKA Addison’s disease
- Adrenal glands have been damaged

333
Q

What are the causes of Addison’s disease?

A
  1. Autoimmune adrenalitis- most common
    - Adrenal glands destroyed by antibodies eg. 21- hydroxylase
  2. TB- most common cause worldwide
334
Q

Describe secondary adrenal insufficiency

A

Caused by inadequate ACTH, causing low cortisol levels

335
Q

What are the causes of secondary adrenal insufficiency?

A

Loss/damage of pituitary gland
Benign pituitary tumour

336
Q

Describe tertiary adrenal insufficiency

A

Inadequate CRH release by hypothalamus
Pituitary can not be stimulated so no ACTH

337
Q

What is the most common cause of tertiary adrenal insufficiency?

A

Stopping corticosteroids after a long time of taking them

338
Q

What are the symptoms of adrenal insufficiency/Addisons disease?

A

Fatigue and weakness
Anorexia
Nausea
Weight loss
Headaches
Abdominal pain
Poor illness recovery

339
Q

What are the signs of Addison’s disease/ adrenal insufficiency?

A

Bronze pigmentation and pallor
Changes in body hair distribution
Hypotension
Weight loss
Vitiligo

340
Q

What are cortisol levels like in Addisons?

A

Low
<140 mmol/L

341
Q

What are Na and K levels like in Addison’s?

A

Low Na
High K
- due to decrease in aldosterone

342
Q

What will the FBC show in Addison’s disease?

A

Anaemia
Eosinophilia- due to reduced cortisol

343
Q

What are renin and aldosterone levels like in Addison’s disease?

A

High renin
Low aldosterone

344
Q

What 4 tests are used to diagnose Addisons/ adrenal insufficiency?

A

GS: synacthen test (ACTH injection)
2. 9:00 cortisol and ACTH
3. Renin/ aldosterone
4. 21 hydroxylase test in autoimmune adrenal insufficiency

345
Q

What results of a synacthen test indicate adrenal insufficiency?

A

Cortisol low
Primary ACTH = increased
Secondary ACTH = decreased

346
Q

How is Addisons treated?

A

Hydrocortisone 15-25mg 2-3x daily to replace cortisol
Fludrocortisone to replace Mineralocorticoids (Aldosterone)

347
Q

How are hypotensive Addison’s patients treated?

A

IV hydrocortisone
IV 0.9% saline
Glucose infusion in hypoglycaemia

348
Q

What are the symptoms of adrenal crisis?

A

Nausea
Vomiting
Muscle cramps
Abdominal pain
Confusion
Hypotension

349
Q

What are the causes of adrenal crisis?

A

Abrupt steroids withdrawal- MC
Adrenal damage
Pituitary injury

350
Q

What are the treatments for adrenal crisis?

A

Immediate hydrocortisone 100mg
Hydrocortisone 50-100mg IV 6 hourly
Fluid resuscitation 1L/hour

351
Q

How is secondary adrenal insufficiency differentiated from Addisons?

A

Low ACTH
Mineralocorticoid levels intact

352
Q

What is the most common adrenal insufficiency?

A

Tertiary adrenal insufficiency

353
Q

How is vasopressin/ADH secretion stimulated by the body?

A
  1. Large falls in BP or volume detected by osmoreceptors or baroreceptors
  2. Secretion determined by plasma osmolality

Stimulates ADH release from hypothalamus

354
Q

Where does ADH/ vasopressin act?

A

Principal cells on collecting duct of kidney

355
Q

How does ADH/ vasopressin stimulate increased water absorption?

A
  1. Binds to V2R receptors in kidneys
  2. Kinase actions causes insertion of aquaporin channel into apical membrane of collecting duct
  3. Increases water permeability of collecting duct increasing water absorption and concentration of urine
356
Q

What is another affect of vasopressin that causes a restoration in BP?

A

Causes widespread arteriolar vasoconstriction

357
Q

Describe the relationship between blood osmolality and vasopressin

A

Linear- as blood gets more concentrated vasopressin and water reabsorption increases

358
Q

What does SIADH stand for?

A

Syndrome of inappropriate secretion of ADH

359
Q

Define SIADH

A

Excessive secretion of ADH despite plasma being dilute independent of RAAS

360
Q

What are the effects of SIADH?

A

Hyponaetremia
High urine osmolality
Euvolemic state (normal fluid levels)

361
Q

What are the causes of SIADH(tumours)?

A

Small cell lung carcinoma
Prostate tumour
Pancreas tumour
Lymphoma
Thymus tumour

362
Q

What are the respiratory causes of SIADH?

A

SCLC
Pneumonia
TB
Lung abscess
Asthma
CF

363
Q

What are the CNS causes of SIADH?

A

Meningitis
Tumours
Head trauma
Subdural haematoma

364
Q

What drugs can cause SIADH?

A

Chlorpropamide (sulfonylurea)
Carbamazepine (anti convulsant)
Cyclophosphamide (immunosuppressant)
Chemo
SSRIs

365
Q

Describe the pathophysiology of SIADH

A

Excess ADH = insertion of aquaporin 2 channels
= excess water retention = dilute plasma = hyponatraemia

366
Q

What are the signs of SIADH?

A

Absence of hypo/hypervolaemia
Normal thyroid an adrenals
Low osmolaity
High urine Na and low plasma Na
Highly concentrated urine

367
Q

What are the symptoms of SIADH?

A

Headache
Nausea+ vomiting
Fatigue
Cramps and aches
Confusion
Severe hyponatraemia = seizures + coma

368
Q

What would urine tests show in SIADH?

A

High sodium >20mmol/L
High osmolality >100mosmol/L

369
Q

What will plasma tests show in SIADH?

A

Low sodium <125mmol/L
Low osmolality <260mmol/L

370
Q

What factors will be absent in SIADH?

A

Hypo/hypervolaemia
Oedema
Diuretics

371
Q

How are the other causes hyponatraemia excluded in SIADH?

A

Synacthen test (adrenal insufficiency)
No diuretic history
No vomiting burns ect
No excessive water intake
No kidney issues

372
Q

Where is ADH/vasopressin secreted from and produced?

A

Produced: hypothalamus
Secreted: posterior pituitary

373
Q

How is SIADH differentiated from Na and H2o depletion?

A

1-2L 0.9% saline
- SIADH will not respond

374
Q

What are the main methods of managing SIADH?

A

Fluid restriction (500mls-1L a day)
Treat underlying cause

375
Q

What drugs are used to control SIADH?

A

Vasopressin receptor antagonists/ ADH inhibitors
Salt loop diuretics if severe

376
Q

What is an example of a vasopressin receptor antagonist?

A

Tolvaptan

377
Q

What is an example of a loop diuretic?

A

Furosemide

378
Q

What is the main complication of SIADH?

A

Central pontine myelinolysis

379
Q

What causes central pontine myelinolysis?

A

Rapidly corrected low sodium -> osmotic demyelination

  • as Na+ falls, water moves into brain by osmosis causing swelling
380
Q

What are the 2 phases of central pontine myelinolysis?

A

1: encephalopathic: confused and headaches
2. Demyelination of neurons days after rapid sodium correction: spastic quadriparesis and cognitive changes

381
Q

What are the risk factors of central pontine myelinolysis?

A

Alcohol
Malnutrition
K+ depletion
Hepatic failure

382
Q

Where does vasopressin bind to V1a receptors?

A

Vasculature- arteries
- Maintains BP

383
Q

Where does vasopressin bind to V2 receptors?

A

Renal collecting tubule principal cellls

384
Q

Where does vasopressin bind to V1b receptors?

A

Anterior pituitary
-Fire and release of ACTH

385
Q

What 2 things control vasopressin release?

A

Normally: osmoreceptors in hypothalamus
Emergency: baroreceptors in brain stem and great vessels

386
Q

What are the new names for diabetes insipidus?

A

Cranial = AVP DEFICIENCY
Nephrogenic = AVP RESISTANCE

387
Q

Is AVP deficiency or AVP resistance more common?

A

AVP deficiency

388
Q

Define AVP deficiency

A

Decreased secretion of ADH from posterior pituitary

389
Q

Define AVP resistance

A

Insensitivity to ADH

390
Q

What are the effects of AVP deficiency/ resistance?

A

Prevents urine concentration due to impaired water reabsorption leading to polyuria and polydipsia
3L+ urine daily

391
Q

What diseases are also associated with autoimmune adrenalitis?

A

DMT1
Pernicious anaemia
Hypo/hyperthyroidism

392
Q

What are the causes of AVP deficiency?

A

Idiopathic
Trauma
Tumours
Infection
Sarcoidosis
Inflammation
Pituitary surgery

393
Q

What are the causes of AVP resistance?

A

Lithium
Osmotic diuresis
Renal impairment and infiltration
Hypercalcaemia an hypokalaemia
Pregnancy

394
Q

What congenital defects can cause AVP resistance?

A

AVP2 receptor mutation
AQP2 mutation
Wolfram

395
Q

Outline the pathophysiology of AVP resistance/ deficiency

A

Reduced secretion/impairment -> significant water loss -> dilute urine

396
Q

What are the signs and symptoms of AVP deficiency/ resistance?

A

Polyuria and nocturia
Polydipsia
NO glycosuria
Hypernnatraemia
Lithium history

397
Q

What are the differential diagnosis of AVP resistance/ deficiency?

A

Primary polydipsia (drinks too much water)
DM
Cushings
Hypercalcaemia
Hyperkalaemia

398
Q

What is the gold standard for AVP deficiency/resistance diagnosis?

A

Water deprivation test - deprive water for 8 hours
- Diagnosis= high osmolality and inappropriately dilute urine

399
Q

What tests can be used to differentiate AVP deficiency/resistance?

A
  1. AVP stimulation test- 2mcg desmopressin IM
    -AVP resistant: no response
    - AVP deficiency: responds
  2. Hypertonic saline infusion with measurement of copetin
400
Q

What other tests are used to diagnose AVP resistance/ deficiency?

A

Measure polyuria (unlikely if urine is <3L)
Renal function tests
Serum calcium
Urine dipstick to exclude DM

401
Q

How is AVP deficiency treated?

A

Treat underlying condition
Desmopressin V2 analog
Manage hypernatraemia

402
Q

How is AVP resistance treated?

A

Thiazide diuretics (work in DCT)
NSAID- lowers urine and plasma Na+

403
Q

How do thiazide diuretics work?

A

Work on DCT
Induce mild hypovolaemia -> more Na+ and water uptake in DCT -> offsets water loss

404
Q

What is an example of a thiazide diuretic?

A

Oral bendroflumethiazide
indapamide

405
Q

How is serum calcium controlled?

A

PTH (parathyroid hormone)
Vitamin D

406
Q

Is hypercalcaemia or hypocalceamia more common?

A

Hypercalcaemia more common but hypo more common in hospital

407
Q

Where is PTH secreted from?

A

Chief cells in parathyroid glands in response to decreased levels of Ca2+ plasma concentrations

408
Q

How is a decrease of serum Ca2+ detected?

A

G-coupled calcium sensing receptors on the parathyroid glands

409
Q

How does PTH increase plasma Ca2+?

A

Increases osteoclastic resorption of bone
Increases intestinal Ca2+ absorption
Activation of calcitrol in kidney
Increases renal tubular reabsorption of Ca2+
Increases phosphate excretion

410
Q

What stimulates calcitriol release?

A

Low plasma Ca2+
Low plasma phosphate
PTH

411
Q

What are thee 4 roles of calcitrol?

A
  1. Increased Ca2+ and phosphate absorption in gut
  2. Inhibits PTH release
  3. Increases osteoclasts -> enhanced bone turnover
  4. Increased Ca2+ and phosphate reabsorption in kidneys
412
Q

Where is calcitonin made?

A

C-cells of thyroid

413
Q

What are the effects of calcitonin?

A

Causes a decrease in plasma Ca2+ and phosphate

414
Q

Define hyperparathyroidism

A

Excessive secretion of parathyroid hormone (PTH)

415
Q

Describe the epidemiology of hyperparathyroidism

A

Elderly women most affected

416
Q

What is the most common type of hyperparathyroidism?

A

Primary

417
Q

Describe the pathophysiology of primary hyperparathyroidism

A
  1. Tumour/hyperplasia of thyroid glands causes extra secretive tissue
  2. Causes excess PTH production -> hypercalacemia
418
Q

What are the causes of primary hyperparathyroidism?

A

80% due to solitary adenoma
20% due to gland hyperplasia
~ small amount due to parathyroid cancer

419
Q

Outline the pathophysiology of secondary hyperparathyroidism

A
  1. Insufficient vitamin D or chronic renal failure causes low Ca2+ absorption
  2. Causes hypocalcaemia
  3. Hypocalcaemia causes more PTH and hyperplasia = MORE PTH
420
Q

Outline the pathophysiology of tertiary hyperparathyroidim

A

Occurs after prolonged secondary hyperparathyroidism
- Glands continue to secrete PTH after the hypocalcaemia cause has be treated

421
Q

What is the most common cause of tertiary hyperparathyroidism?

A

Long-standing kidney disease

422
Q

What are the risk factors of hyperparathyroidism?

A

Elderly women who have been through menopause
Prolonged severe Ca2+ or vitamin D deficiency

423
Q

What are the lab results in primary hyperparathyroidism?

A

PTH = high
Ca2+ = high
Phosphate = low

424
Q

What are the lab results in secondary hyperparathyroidism?

A

PTH = high
Ca2+ = low/normal
Phosphate = high(ish)

425
Q

What are the lab results in tertiary hyperparathyroidism?

A

PTH = high
Ca2+ = high
Phosphate = high

426
Q

Describe the presentation of hyperparathyroidism

A

Bones, stones, groans and psychiatric moans
——————————————————————
- bone pain, fractures, osteoporosis
- biliary and renal stones
-groans due to malaise, abdo pain, constipation, nausea
- moans = fatigue, depression and psychosis

427
Q

What is alkaline phosphate like in hyperparathyroidism?

A

High

428
Q

How is hyperparathyroidism investigated?

A

Measure PTH, Ca2+ and phosphate levels
- bone scan to differentiate from oestoporosis
- ultrasound for kidney stones
- abdomen X-ray
- detect adenomas

429
Q

How is acute severe hypercalcaemia treated?

A

EMERGENCY

-IV 0.9% saline - prevents stones (1ST LINE)
-Biphosphonates - prevent bone reabsorption
- serum U&E daily and Ca2+ 48 hrs post treatment
-glucocorticoid steroids on myeloma, excess vit D, sarcoidosis

430
Q

What is an example of a biphosponate?

A

Alendronate
IV pamidronate

431
Q

How is primary hyperparathyroidism treated?

A

Surgical removal of tumour

432
Q

How is secondary hyperparathyroidism treated?

A

Treat vitamin D deficiency
Cincalcet
Kidney transplant for CKD

433
Q

How is tertiary hyperparathydroidism treated?

A

Total or partial parathyroidectomy
Calcimimetic

434
Q

What is the function of calcimimetics?

A

Increases sensitivity of parathyroid cells to Ca2+ -> less PTH secretion

435
Q

What is an example of a calcimimetic?

A

Cinacalet

436
Q

Define hypercalcaemia

A

Decreased PTH and increased Ca2+

437
Q

What are the causes of hypercalcaemia?

A

CHIMPANZEES - on drugs

C-calcium supplements
H- hyperparathydroidism
I-iatrogenic
M-multiple myeloma
P-parathyroid hyperplasia
A- alcohol
N- neoplasms
Z- Zollinger-Ellison syndrome
E- Excess vit D
E- excess vit A
S- sarcoidosis

438
Q

What drugs can cause hypercalcaemia?

A

Thiazide diuretics
Vitamin D analogues
Lithium

439
Q

Describe the presentation of hypercalcaemia

A

Bones, stones, groans and psychiatric moans
ECG abnormalities- short QT interval

440
Q

What investigations are carried out for hypercalcaemia diagnosis?

A

Fasting serum Ca2+ and phosphate
Elevated PTH and Ca2+
Ultrasound if indications of hyperparathyroidism
24 hour urinary calcium to exclude hypocalciuric hypercalcaemia

441
Q

How is familial hypocalciuric hypercalcaemia differentiated?

A

24 hour urinary calcium

442
Q

How is hypercalcaemia treated?

A

Rehydration with saline
Biphosphonates
Loop diuretics sometimes

443
Q

What could hypocalcaemia be an artefact of?

A

Hypoalbuminaemia

444
Q

How common is hypocalcaemia?

A

Very common in hospitalised patients- up to 88% of ICU patients

445
Q

Describe the pathophysiology of primary hypoparathyroidism

A

Low PTH due to parathyroid gland failure

446
Q

What are the causes of hypoparathyroidism?

A

Autoimmune DiGeorge syndrome
Idiopathic hypoparathyroidism

447
Q

What is autoimmune DiGeorge syndrome?

A

Congenital familial condition in which the parathyroid glands fail to develop

448
Q

What is idiopathic hypoparathyroidism?

A

Rare autoimmune condition caused by parathyroid antibodies

449
Q

What is the most common hypoparathyroidism?

A

Secondary hypoparathyroidism

450
Q

What causes secondary hypoparathyroidism?

A

After secondary parathyroid/thyroidectomy
Radiation
Hypomagnasaemia

451
Q

What is pseudohypoparathyroidism?

A

Failure of target cell response to PTH

452
Q

What causes pseudohypoparathyroidism?

A

Syndrome of end-organ resistance to PTH causing a mutation in the GNAS1 protein which is coupled with the PTH receptor

453
Q

What are the presentations associated with pseudohypoparathyroidism?

A

Short stature
Short metacarpals (especially pinky and next one)
Subcutaneous calcification
Sometimes intellectual impairment

454
Q

What drugs can cause hypoparathyroidism?

A

Calcitonin
Bisphosphonates

455
Q

What are calcium, PTH and phosphate levels like in primary hypoparathyroidism?

A

Ca2+ is low
Low PTH
Phosphate is high

456
Q

What are phosphate, PTH and Ca2+ levels like in pseudohypoparathyroidism?

A

High phosphate
Low Ca2+
High PTH

457
Q

When may hypoparathyroidism occur when phosphate is normal or reduced?

A

Acute pancreatitis
Osteomalacia

458
Q

What are the presentations of hypoparathyroidism?

A

Symptoms of hypocalcaemia

459
Q

What are the causes of hypocalcaemia?

A

Chronic kidney disease (MC)
Severe vitamin D deficiency
-Reduced UV exposure, malabsorption ect
Sclerosis
Secondary hyperparathydroidism

460
Q

What are the symptoms of hypocalcaemia and hypoparathyroidism?

A

SPASMODIC
S-spasms ie Trousseaus sign
P-perioral parasthesia
A- anxious ect
S- seizures
M- muscle tone increase
O- orientation impaired
D- dermatitis
I- impetigo herpetiformis
C- Chvostek’s sign, cataracts and cardiomyopathy

461
Q

What effect does hypocalcaemia have on an ECG?

A

Prolonged QT

462
Q

What is Chvostek’s sign?

A

Tapping over facial nerve on parotid gland region causes twitching of ipsilateral facial muscles

463
Q

What is Trousseau’s sign?

A

Carpopedal spasm induced by inflating BP cuff above systolic BP

-downturned pinching gesture

464
Q

What investigation results indicate hypocalcaemia?

A

Low PTH (apart from pseudoHP)
High phosphate
Low albumin
Low serum calcium

465
Q

What are the differential diagnoses of hypocalcaemia?

A

CKD
Vitamin D deficiency

466
Q

What are the complications of hypoparathyroidism?

A

CKD
Kidney stones
Cataracts
Basal ganglia calcification
Laryngospasm

467
Q

How is hypoparathyroidism treated?

A

Oral or IV calcium
Calcitrol (activ vitamin D)
Thiazide diuretics (reduce hypercalcureia)

468
Q

How is hypocalcaemia treated?

A

IV calcium gluconate if severe
Vitamin D supplements

469
Q

What level of hyperkalaemia is an emergency?

A

> 6.5mmol/L

470
Q

What are the causes of hyperkalaemia?

A

Self limiting occurs after vigorous exercise
MC: renal impairment and drugs interfering with K+ excretion
Drugs
Addisons
DKA

471
Q

What drugs can cause hyperkalaemia?

A

K+ sparing diuretics
ACE inhibitors
NSAIDs
Ciclosporin
Heparin

472
Q

Outline the pathophysiology of hyperkalaemia

A

K+ level rise causes a reduction in the action potential between inside and outside the cardiac myocyte
= abnormal heart rhythms -> VF and cardiac arrest

473
Q

What would an ECG look like in hyperkalaemia?

A

Tall T wave
Small P wav
Wide QRS
U wave

474
Q

What investigations are carried out for hyperkalaemia diagnosis?

A

Serum K+ test
ECG

475
Q

How do patients with hyperkalaemia present?

A

Irregular pulse
Chest pain
Weakness and fatigue
Lightheadedness

476
Q

How is hyperkalaemia primarily treated?

A

Treat underlying factors

477
Q

How is hyperkalaemia treated if ECG changes after initial treatment?

A

Stabilise cardiac membrane with IV calcium gluconate/chloride
- doesn’t lower serum K+

478
Q

How is hyperkalaemia treated if ECG doesn’t change after initial treatment?

A

Move K+ into cells
Use combined INSULIN/DEXTROSE infusion with nebulised salbutamol

479
Q

How can K+ be removed from the body?

A

Calcium resonium
Loop diuretics
Dialysis

480
Q

How is severe hyperkalaemia treated?

A

IV calcium gluconate
Insulin/dextrose infusion

481
Q

What levels indicate severe hypokalaemia?

A

<2.5 mmol/L serum K+

482
Q

What are the causes of hypokalaemia with alkalosis?

A

Vomiting
Diuretics
Cushings
Conn’s

483
Q

What are the causes of hypokalaemia with acidosis?

A

Diarrhoea
RTA
Partially treated DKA
Acetazolamide

484
Q

What are the presentations of hypokalaemia?

A

Muscle weakness
Hypotonia
Hyporeflexia
Tetany
Palpitations

485
Q

What results on an ECG indicate hypokalaemia?

A

Small or inverted T waves
Long PR interval
Depressed ST segment
Prominent U wave

486
Q

How is mild hypokalaemia treated?

A

Oral replacement
Switch from thiazide to K+ sparing diuretic

487
Q

How is severe hypokalaemia treated?

A

IV replacement 40mmol KCl

488
Q

What are the complications of hypokalaemia?

A

Chronic heart failure
Acute MI
Muscle weakness
Depression of tendon weakness

489
Q

When is TSH high and T4 low?

A

Hypothyroidism- Hashimoto’s

490
Q

When is TSH low and T4 high

A

Hyperthyroidism - Graves

491
Q

When is:
PTH high
Calcium low
Phosphate high

A

Secondary hyperparathydroidism

492
Q

When is:
PTH high
Calcium high
Phosphate high

A

Tertiary hyperparathydroidism

493
Q

Where do carcinoid tumours originate from?

A

Enterochromaffin cells

494
Q

What hormone is produced in carcinoid syndrome?

A

Serotonin 5HT

495
Q

What are the effects of serotonin?

A

Bowel function
Mood
Clotting
Nausea
Bone density
Vasoconstriction
Inotropic and chronotropic

496
Q

Where do carcinoid tumours originate from?

A

GI tract
Lungs
Liver
Ovaries
Thymus

497
Q

Where is the most common site of metastasis of carcinoid tumours?

A

Liver

498
Q

What is carcinoid syndrome?

A

Hepatic involvement ie. Hepatic metastasis

499
Q

What are the symptoms of carcinoid syndrome?

A

Diarrhoea
Upper right quadrant pain
Flushing
Tricuspid incompetence

500
Q

What is the main complication of carcinoid tumours/syndrome?

A

Carcinoid crisis

501
Q

What is carcinoid crisis?

A

A tumour outgrows its blood supply or handled too much in surgery, causing mediators to flow out

502
Q

What are the effects of carcinoid crisis?

A

Vasodilation- bradykinin
Hypotension - ACTH-> cortisol
Tachycardia - bradykinin
Hyperglycaemia- glucagon and ACTH

503
Q

How is carcinoid crisis treated?

A

High dose somatostatin analogue

504
Q

How is carcinoid syndrome/tumour diagnosed?

A

1st line: 5-hydroxyindoeacetic acid (metabolite of serotonin)
Chest and pelvis CXR
Ultrasound of liver

505
Q

What will 5-hydroxyindoeacetic acid levels be like in carcinoid syndrome?

A

High

506
Q

How is carcinoid syndrome/tumour treated?

A

Somatostatin analogues to block the effects of tumour hormones
Surgical resection

507
Q

What is phaeochromocytoma?

A

Adrenal medullary tumour that secretes catecholamines (adrenaline)

508
Q

What are the causes of pheochromocytoma?

A

Usually inherited
Associated with:
Multiple endocrine neoplasia 2a and 2b
Neurofibromatosis

509
Q

What are the symptoms of pheochromocytoma?

A

Hypertension
Pallor
Sweaty
Tachycardia

510
Q

How is pheochromocytoma diagnosed?

A

Increased plasma metanephrines and normetanephrine
CT chest abdo and pelvis

511
Q

How is phaeochromocytoma treated?

A

Alpha beta blocker (phenoxybenzamine)+ beta blocker
Surgery to remove tumour

512
Q

What is the main complication of pheochromocytoma?

A

Hypertension crisis (>180/120)

513
Q

How is hypertension crisis treated?

A

Alpha blocker

514
Q

What are the 5 Tanner stages of female development?

A

Stage 1: no pubic hair and elevated papilla
Stage 2: sparse hair, palpable breast bud
Stage 3: darker coarse hair, breast and areole enlarge
Stage 4: projection of areole and papilla -> secondary mound
Stage 5: hair on medial thighs

515
Q

What are the 5 Tanner stages of male development?

A

Stage 1: no pubic hair, childhood size penis
Stage 2: sparse hair, testes and penis enlarge
Stage 3: dark, curlier hair, penis and testes enlarge
Stage 4: enlargement, darkening of scrotum
Stage 5: hair on medial thighs, adult shape and size

516
Q

Define thelarche

A

Beginning of breast development

517
Q

What is pubarche?

A

First appearance of pubic hair

518
Q

When is adrenarche?

A

Maturation of adrenal gland

519
Q

What is menarche?

A

First menstruation

520
Q

Define precocious puberty

A

Early puberty
GnRH dependent

521
Q

Describe the epidemiology of precocious puberty

A

90% girls
1 in 5-10k

522
Q

Describe the aetiology of precocious puberty

A

Idiopathic
CNS tumours
CNS disorders
Secondary central precocious puberty
Psychosocial

523
Q

What are the risk factors of precocious puberty?

A

Obesity
Genetics
Surgery/radiotherapy on brain

524
Q

Outline the pathology of precocious puberty

A

GnRH secretion activated -> LH and FSH -> sex hormone actions

525
Q

What are the symptoms of precocious puberty?

A

Advanced bone age
Testes >4ml
Thelarche
Pubarche

526
Q

What 3 investigations are carried out for precocious puberty?

A

Bone age assessment
HIGH basal FSH and LH
GnRH test: LH:FSH >1

527
Q

What do high FSH and LH levels indicate?

A

Precocious puberty

528
Q

What does a LH:FSH ratio >1 indicate?

A

Precocious puberty

529
Q

How is precocious puberty treated?

A

GnRH super-agonist
Surgery
Gonsider GH

530
Q

Define precocious pseudopuberty

A

Early puberty
GnRH independent

531
Q

Describe the aetiology of precocious pseudopuberty

A

Increased androgen secretion
Gonadotropin or oestrogen secreting hormones
McCune-Albright syndrome
Ovarian cyst
Hypothyroidism

532
Q

Describe the epidemiology of delayed puberty

A

Mainly boys
Genetics

533
Q

Describe the aetiology of delayed puberty

A

Idiopathic: delayed activation of hypothalamic pulse generator
Hypogonadotrophic hypogonadism
Hypergonadotrophic hypogonadism

534
Q

What is hypogonadotrophic hypogonadism?

A

Sexual infantilism related to gonadotrophin deficiency

535
Q

What are the 2 types of hypogonadotrophic hypogonadism?

A

Secondary: pituitary = low LH/FSH
Tertiary: hypothalamus = low GnRH

536
Q

What is hypergonadotrophic hypogonadism?

A

Primary gonad problems
- high GnRH/FSH/LH but low gonadotrophins

537
Q

What are the effects of delayed puberty?

A

Delay in acquisition of secondary sex characteristics
Psychological defects
Reduced bone mass

538
Q

What are the signs of delayed puberty in girls?

A

Age 13: lack of breast development
Age 14: lack of pubic hair
Age 15-16: absent menarche

539
Q

What are the signs of delayed puberty in boys?

A

Age 14: lack of testicular enlargement
Age 15: lack of pubic hair

540
Q

What are the reversible causes of delayed puberty?

A

Anorexia nervosa
ADHD medication
Extreme exercise
Hypothyroidism
Cushings

541
Q

What investigations are carried out for delayed puberty?

A

RBC count
U&E
LH, FSH, sex hormones
Thyroid function karotyping

542
Q

How is delayed puberty managed?

A

Most don’t need treatment
- short course of sex hormones
-low exogenous sex steroid dose
- girls can have progesterone therapy

543
Q

What is Kallman syndrome?

A

Hypogonadotrophic hypogonadism
- failure of episodic GnRH secretion -> delayed puberty

544
Q

Describe the epidemiology of Kallman syndrome

A

1 in 10k
M:F = 4:1

545
Q

Outline the aetiology of Kallman syndrome

A

X-linked
Mutations in Kal-1, FG receptor 1, prokinectin

546
Q

What are the symptoms of kallman syndrome?

A

Anosmia (no smell/taste)
Cleft palate
Only one kidney
Short digits (4th finger)
Absent/ delayed puberty
Short stature

547
Q

What is unilateral renal agenesis?

A

Only 1 kidney

548
Q

What investigations are carried out for Kallman syndrome?

A

Low testosterone or oestrogen, LH ect
Men with congenital and severe GnRH deficiency have low serum inhibin B

549
Q

How is Kallman syndrome treated?

A

Testosterone enanthate IM
Transdermal testosterone

550
Q

How is Kallman syndrome treated in females?

A

Ethinyloestradiol or Oestrogen
-gradually increase dose until adult dose reached
Progesterone when full dose reached

551
Q

What are the 2 types of hypergonadotrophic hypogonadism?

A

Turner syndrome (females)
Klinefelter syndrome (males)

552
Q

Describe the aetiology of Turner syndrome

A

Part or all of X chromosome missing

553
Q

What are the symptoms of Turner syndrome?

A

Recurrent otitis media
Broad chest
Short 4th finger
Short stature and scoliosis
Prominent ears

554
Q

How is Turner syndrome treated?

A

Oestrogen treatment gradually increased
Progesterone added when full dose reached
GH for short stature

555
Q

What is Klinefelter syndrome?

A

Hypergonadotrophic hypogonadism
47 XXY chromosome defect

556
Q

What are the symptoms of Klinefelter syndrome?

A

Small testicular volume <5ml
Tall stature
Reduced IQ 40%
Reduced pubic hair
Gynaecomastia

557
Q

What is gynaecomastia?

A

Male breasts

558
Q

What are the complications of Klinefelter syndrome?

A

DMT2
Osteoporosis
Malignancies

559
Q

How is Klinefelter syndrome treated in males?

A

Testosterone enanthate IM
Increasing use of transdermal testosterone

560
Q

What is the marker of Rhabdomyolosis?

A

Creatine kinase high

561
Q

Define adrenal crisis

A

Medical emergency caused by lack of cortisol

Phase 2a Annabel (12 decks)

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