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Phase2a > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is endocrinology?

A

The study of hormones (and their glands of origin), their receptors, their intracellular signalling pathways, and their associated diseases.

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2
Q

What can the two chains of a peptide hormone be joined by?

A

Carbohydrates

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3
Q

Are peptide hormones released continuously or at intervals?

A

They are released in pulses/bursts.

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4
Q

How are peptide hormones cleared from the bloodstream?

A

By tissues or circulating enzymes.

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5
Q

What are the three ‘forms’ of a peptide hormone?

A
  • Preprohormone
  • Prohormone
  • Hormone
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6
Q

What is the stage of hormone production called when a preprohormone is cleaved to form a prohormone?

A

Synthesis

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7
Q

What is the stage of hormone production called when a prohormone is cleaved to form a hormone?

A

Packaging

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8
Q

Which amino acid are amine hormones produced from?

A

Tyrosine

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9
Q

Give the stages in adrenaline production from an amino acid.

A
  1. Phenylalanine
  2. Tyrosine
  3. L-DOPA
  4. Dopamine
  5. Noradrenaline
  6. Adrenaline
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10
Q

How do thyroid hormones travel in the bloodstream?

A

99% protein bound

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11
Q

Which amino acid are thyroid hormones produced from?

A

Tyrosine

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12
Q

Is T3 or T4 more active?

A

T3 (T4 is cleaved to T3 in the peripheries)

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13
Q

Give five factors that influence hormone action.

A
  • Metabolism
  • Receptor induction
  • Receptor downregulation
  • Synergism
  • Antagonism
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14
Q

Give an example of hormone receptor induction.

A

FSH induces LH receptors.

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15
Q

When does hormone receptor downregulation occur?

A

When the hormone is in high concentrations.

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16
Q

Give an example of hormone synergism.

A

Glucagon and epinephrine

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17
Q

Which hormones bind to receptors on the cell membrane?

A

Peptide hormones

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18
Q

Which hormones bind to receptors in the cytoplasm?

A

Adrenocorticosteroids
Androgens
Progesterone

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19
Q

Which hormones bind to receptors in the nucleus?

A

Oestrogen
Thyroid hormones
Vitamin D

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20
Q

How is a positive feedback loop stopped?

A

An outside factor is required to shut off the cycle.

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21
Q

Give four patterns of hormone secretion.

A
  • Basal secretion
  • Superadded rhythm
  • Releasing factors
  • Release inhibiting factors
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22
Q

Is basal hormone secretion continuous or pulsatile?

A

It can be either.

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23
Q

Give an example of a superadded hormone secretion.

A

Diurnal rhythm

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24
Q

Give three factors that can be releasing factors for hormones.

A

Humoural
Neural
Hormonal

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25
Q

What is appetite?

A

A psychological desire to eat food.

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26
Q

What is hunger?

A

A physiological need of eating.

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27
Q

What is satiety?

A

Feeling of fullness (disappearance of appetite after a meal)

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28
Q

What is the formula for BMI?

A

Weight (KG)/Height2 (M2)

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29
Q

What range of BMI is classed as underweight?

A

<18.5

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30
Q

What range of BMI is classed as normal?

A

18.5-24.9

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31
Q

What range of BMI is classed as overweight?

A

25.0-29.9

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32
Q

What range of BMI is classed as obese?

A

30.0-39.9

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33
Q

What range of BMI is classed as morbidly obese?

A

> 40

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34
Q

Is subcutaneous fat or visceral fat more dangerous in obesity?

A

Visceral fat

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35
Q

What two factors influence weight regulation?

Which factor has the bigger influence?

A

Genes and Environment

Environment has the bigger influence.

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36
Q

What are the three structures/parts of the body which contribute hormones to weight regulation?

A
  • Brain
  • GI tract
  • Adipose tissue
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37
Q

How is weight influenced by genes?

A

It is polygenic.

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38
Q

Where is the hunger centre located?

A

Lateral hypothalamus

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39
Q

Where is the satiety centre located?

A

Ventromedial hypothalamic nucleus

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40
Q

Where is leptin expressed?

A

White fat

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41
Q

Where are leptin receptors located and what family are they part of?

A

Cytokine receptor family in hypothalamus

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42
Q

What is the ultimate role of leptin?

A

Switches off appetite

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43
Q

How does leptin affect the immune system?

A

It is immunostimmulatory

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44
Q

What is the result of a leptin deficiency or an improperly functioning leptin receptor?

A

Obesity

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45
Q

Name another hormone which works in a similar way to leptin.

A

Insulin

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46
Q

What is the role of peptide YY?

A

Binds to NPY receptors to inhibit them.

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47
Q

Where is peptide YY secreted, and by what cells?

A

Ileum
Pancreas
Colon
By neuroendocrine cells

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48
Q

How does peptide YY affect gastric motility?

A

Inhibits it

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49
Q

How does peptide YY affect appetite?

A

Inhibits it

NPY increases appetite

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50
Q

Where is cholecystokinin released?

A

Duodenum

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51
Q

Where are the receptors for cholecystokinin located?

A

Pyloric sphincter

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52
Q

Give four functions of cholecystokinin.

A
  • Delays gastric emptying
  • Gall bladder contraction
  • Insulin release
  • Stimulates vagus nerve to signal satiety
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53
Q

How does cholecystokinin affect appetite?

A

Reduces it

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54
Q

Where is ghrelin expressed?

A

Stomach

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55
Q

What hormone is released in response to ghrelin release?

A

Growth hormone

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56
Q

How does ghrelin affect appetite?

A

Increases it

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57
Q

What is proopiomelanocortin (POMC)?

A

A hormone precursor which is cleaved to form multiple hormones.

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58
Q

Which hormone is cleaved from POMC which affect appetite?

A

A-MSH (melanocyte stimulating hormone)

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59
Q

Which melanocortin receptors does a-MSH act on to affect appetite?

A

MCR3 and MCR4 in the brain

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60
Q

How does POMC/a-MSH affect appetite?

A

Signals satiety

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61
Q

What condition results from POMC deficiency?

A

Obesity

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62
Q

Give seven risks that come with obesity.

A
  • Type II diabetes
  • Hypertension
  • Coronary artery disease
  • Stroke
  • Osteoarthritis
  • Obstructive sleep apnoea
  • Carcinoma (breast, endometrium, prostate, colon)
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63
Q

Why do people who do shift work have a higher risk of becoming obese?

A

Their metabolic circadian rhythms are altered.

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64
Q

Give three reasons why people eat?

A
  • Internal physiological drive to eat
  • Feeling that prompts thought of food and motivates food consumption
  • External psychological drive to eat
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65
Q

How does highly refined sugar affect satiety?

A

Quick and short satiety

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66
Q

How do foods high in protein affect satiety?

A

They result in a prolonged satiety

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67
Q

How are water-soluble hormones stored?

A

In vesicles

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68
Q

How are water-soluble hormones transported?

A

Unbound

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69
Q

How do water-soluble hormones interact with cells?

A

Bind to surface receptor

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70
Q

Describe the half-life of water-soluble hormones.

A

Short

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71
Q

Describe the rate of clearance of water-soluble hormones.

A

Fast

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72
Q

Give two examples of hormone classes that are water-soluble.

A

Peptides

Monoamines

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73
Q

Describe the storage of fat-soluble hormones.

A

They are not stored - they are synthesised on demand

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74
Q

How are fat-soluble hormones transported?

A

Protein-bound

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75
Q

How do fat-soluble hormones interact with cells?

A

Diffuse into cell

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76
Q

Describe the half-life of fat-soluble hormones.

A

Long

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77
Q

Describe the rate of clearance of fat-soluble hormones.

A

Slow

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78
Q

Give two classes of hormones which are fat-soluble.

A

Thyroid hormones

Steroids

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79
Q

What is the effect of leptin/insulin on anabolic processes (food intake)?

A

Inhibition

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80
Q

What is the effect of leptin/insulin on catabolic processes (energy expenditure)?

A

Activation

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81
Q

Name two central controllers which increase appetite.

A

NPY (neuropeptide Y)

AgRP (agouti-related peptide)

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82
Q

Name four central controllers which decrease appetite.

A

A-MSH
CART
GLP-1
Serotonin

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83
Q

What does CART stand for?

A

Cocaine and amphetamine regulated transcript

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84
Q

How do leptin/insulin affect POMC and CART neurons?

A

Stimulate them

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85
Q

How does leptin/insulin affect NPY and AgRP neurons?

A

Inhibit them

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86
Q

What affect do GABA and NPY have on POMC and CART neurons?

A

Inhibition

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87
Q

What affect does ghrelin have on NPY and AgRP neurons?

A

Stimulation

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88
Q

Where are POMC/CART/NPY/AgRP neurons found?

A

Arcuate nucleus

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89
Q

How does AgRP increase appetite?

A

Blocks MCR receptors to stop aMSH from working.

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90
Q

Where do a-MSH and NPY have their effects?

A

Paraventricular nucleus

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91
Q

What happens to AMPK in cells in the fasted state?

A

It is activated

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92
Q

What is the role of AMPK?

A

Inhibits acetyl CoA carboxylase so reduces Malonyl CoA production

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93
Q

How does malonyl CoA affect appetite?

A

Increased malonyl CoA decreases appetite.

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94
Q

What happens to AMPK in cells in the fed state?

A

It is deactivated

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95
Q

What is an orexigenic drug?

A

An appetite stimulant

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96
Q

What is obesity?

A

Abnormal or excessive fat accumulation that may impair health.

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97
Q

Give four consequences of poor nutrition in childhood.

A
  • Emotional and behavioural effects (stigma, bullying, self-esteem)
  • School absence
  • Poor physical health
  • Long-term effects into adulthood
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98
Q

What are the four As which determine someone’s chances of becoming obese?

A
  • Accessibility
  • Availability
  • Acceptability/awareness
  • Affordability
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99
Q

What does tier 1 of the obesity care pathway involve?

A

Universal prevention

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100
Q

What does tier 2 of the obesity care pathway involve?

A

Lifestyle intervention

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101
Q

What does tier 3 of the obesity care pathway involve?

A

Specialist services

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102
Q

What does tier 4 of the obesity care pathway involve?

A

Surgery

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103
Q

What are the four stages of the satiety cascade?

A

Sensory
Cognitive
Postingestive
Postabsorptive

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104
Q

Name two hormones which are released from the posterior pituitary gland.

A

Oxytocin

Vasopressin

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105
Q

What type of hormone is oxytocin?

A

Peptide

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106
Q

What type of hormone is vasopressin?

A

Peptide

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107
Q

Where is oxytocin synthesised?

A

Paraventricular nucleus in hypothalamus

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108
Q

Where is vasopressin synthesised?

A

Supraoptic nucleus in hypothalamus

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109
Q

Give six factors that stimulate vasopressin release.

Which factor is vasopressin most responsive to?

A
  • Increased osmolality (most responsive)
  • Low blood volume
  • Exercise
  • Stress
  • Nausea
  • Vomiting
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110
Q

Which receptors does vasopressin act on in smooth muscle and what is the effect.

A

Acts on V1a receptors to cause vasoconstriction.

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111
Q

What receptors does vasopressin act on in the kidney and what is the effect?

A

Acts on V2 receptors to increase aquaporins and water retention.

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112
Q

What two sites does oxytocin act on?

A
  • Myoepithelial cells of mammary glands

- Uterus/cervix

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113
Q

What is the effect of oxytocin acting on myoepithelial cells?

A

Milk ejection

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114
Q

What is the effect of oxytocin acting on the uterus?

A

Labour

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115
Q

Give two factors which stimulate oxytocin release.

A
  • Suckling

- Uterine contractions

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116
Q

What are three features that pituitary dysfunction can cause?

A
  • Tumour mass effects (pressure on local structures)
  • Hormone excess (functioning tumour)
  • Hormone deficiency (tumour pressing on normal pituitary)
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117
Q

What investigations should be carried out if a pituitary dysfunction is suspected?

A
  • Hormonal tests

- If hormonal tests abnormal or tumour mass effects perform MRI pituitary

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118
Q

What types of hormones are released by the hypothalamus?

A

Mostly peptide.

Dopamine is an amine hormone

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119
Q

Give the six hormones that are released from the hypothalamus.

A
  • Growth hormone releasing hormone
  • Somatostatin
  • Corticotropin releasing hormone
  • Thyrotropin releasing hormone
  • Gonadotropin releasing hormone
  • Dopamine
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120
Q

Give the six hormones released from the anterior pituitary.

A
  • Growth hormone
  • Adrenocorticotropic hormone
  • Thyroid stimulating hormone
  • FSH
  • LH
  • Prolactin
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121
Q

Describe the indirect actions of growth hormone.

A

Stimulates the liver to release insulin-like growth factors which stimulate growth.

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122
Q

Describe the direct actions of growth hormone.

A

Metabolic and anti-insulin, so increased fat breakdown and increased blood glucose.

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123
Q

Give three main consequences of cortisol release.

A
  • Gluconeogenesis
  • Fat breakdown
  • Immune suppression
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124
Q

Give eight functions of thyroid hormones.

A
  • Increased food metabolism
  • Increased protein synthesis
  • Increased carbohydrate metabolism
  • Increased fat metabolism
  • Increased ventilation rate
  • Increased heart rate and cardiac output
  • Brain development in foetal life
  • Increased growth rate
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125
Q

What is the function of prolactin?

A

Milk production

Inhibition of FSH/LH

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126
Q

Which cells does FSH act on?

A

Sertoli cells

Granulosa cells

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127
Q

Which cells does LH act on?

A
  • Granulosa cells
  • Theca cells
  • Leydig cells
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128
Q

How many people are living with diabetes in England?

A

3.8 million

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129
Q

What is meant by primary prevention of diabetes?

A

Preventing diabetes

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130
Q

What is meant by secondary prevention of diabetes?

A

Diagnosing diabetes earlier

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131
Q

What is meant by tertiary prevention of diabetes?

A

Effective management and supporting self-management of diabetes

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132
Q

Give three environmental factors that increase risk of diabetes.

A
  • Sedentary job / leisure activities
  • Diet high in calorie-dense foods / low in fruit and vegetables, pulses, and wholegrain
  • Obesogenic environment
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133
Q

Give three aspects of the obesogenic environment, with examples.

A
  • Physical Environment (TV remote, lifts, cars)
  • Economic environment (cheap TV, expensive fruit)
  • Sociocultural environment (family eating patterns)
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134
Q

Give three types of mechanisms that maintain obesity.

A
  • Physical/physiological
  • Psychological
  • Socioeconomic
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135
Q

How do physical/physiological mechanisms maintain obesity?

A

More weight results in difficulty exercising and dieting.

There is also a metabolic response.

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136
Q

How do psychological mechanisms maintain obesity?

A

Low self-esteem
Guilt
Comfort eating

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137
Q

How do socioeconomic mechanisms maintain obesity?

A
  • Reduced employment opportunities
  • Relationships
  • Social mobility
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138
Q

Give some risk factors for diabetes that may be recorded in a patient record.

A
  • Age
  • Sex
  • Ethnicity
  • Family history
  • Weight
  • BMI
  • Waist circumference
  • History of gestational diabetes
  • Hypertension / vascular disease
  • Impaired glucose tolerance (IGT)
  • Impaired fasting glucose (IFG)
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139
Q

Give five screening tests available for impaired glucose tolerance and impaired fasting glucose.

A
  • HbA1c
  • Random capillary blood glucose
  • Random venous blood glucose
  • Fasting venous blood glucose
  • Oral glucose tolerance test (venous blood glucose 2 hours after oral glucose load)
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140
Q

What is the diagnostic threshold for diabetes for a fasting blood glucose?

A

7.0mmol/L or higher

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141
Q

What is the diagnostic threshold for diabetes in a 2 hour glucose tolerance test?

A

11.1mmol/L or higher

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142
Q

Give four approaches used to diagnose diabetes earlier.

A
  • Raising awareness of diabetes and symptoms in community
  • Raising awareness of diabetes and symptoms in health professionals
  • Using clinical records to identify those at risk
  • Blood tests to screen
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143
Q

Give four steps for preventing a wide spread public health issue like diabetes.

A
  1. Identify people at risk
  2. Early prevention in those at risk
  3. Diagnose earlier
  4. Effective management and support self management
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144
Q

Name the sinuses which are located close to the pituitary gland.

A

Sphenoid sinus

Cavernous sinus

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145
Q

What is the bony structure in which the pituitary gland sits?

A

Sella turcica

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146
Q

Why is the optic chiasm important when looking at pituitary disorders?

A

It is located just above the pituitary gland so can be compressed by pituitary tumours.

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147
Q

Describe the blood supply of the anterior pituitary gland.

A

Receives blood through a portal venous circulation from the hypothalamus.

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148
Q

Give four things that the pituitary gland is responsible for.

A
  • Growth
  • Thyroid function
  • Puberty
  • Steroids
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149
Q

What is the difference between primary and secondary thyroid dysfunction?

A 
Primary = problem with thyroid gland
Secondary = problem with pituitary gland
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150
Q

Do can anabolic steroids affect LH and FSH levels?

A

They will decrease due to negative feedback.

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151
Q

What will be the effect on prolactin if a patient is on dopamine antagonists?

A

More prolactin

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152
Q

Give five diseases of the pituitary.

A
  • Benign pituitary adenoma
  • Craniopharyngioma
  • Trauma
  • Apoplexy/Sheehans
  • Sarcoid/TB
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153
Q

Which is the most common disease of the pituitary?

A

Benign pituitary adenoma

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154
Q

What is a craniopharyngioma?

A

A benign cystic lesion

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155
Q

What can be a consequence of pituitary trauma?

A

Severed pituitary stalk

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156
Q

What is Sheehans?

A

Bleeding after childbirth results in no perfusion and pituitary necrosis.

157
Q

What is an ‘incidentaloma’?

A

A tumour which is identified on a scan which was originally carried out for a different reason.

158
Q

What are the symptoms of a pituitary tumour which is pressing upwards?

A
  • Headaches

- Bitemporal hemianopia

159
Q

Give two reasons why pituitary tumours can cause headaches.

A
  • Stretching of dura

- Ventricle obstruction

160
Q

Give two consequences of a pituitary tumour pressing sideways.

A
  • Cranial nerve palsies

- Temporal lobe epilepsy

161
Q

What does a pituitary tumour cause if it presses downwards?

A

CSF rhinorrhoea

162
Q

Give three symptoms of a tumour pressing on the normal pituitary.

A
  • Pale
  • Lack of body hair
  • Central obesity
163
Q

What mechanism controls circadian rhythms in humans?

A

The body clock

164
Q

How long is the body clock cycle in humans?

A

24.2 hours

165
Q

How do central body clocks and peripheral body clocks in individual organs communicate?

A

Glucocorticoids act as a secondary messenger

166
Q

Which area of the brain controls the circadian rhythm in humans?

A

Suprachiasmatic nucleus in the hypothalamus

167
Q

What is a zeitgeber?

A

Any external or environmental cue that synchronises the circadian rhythm to the Earth’s 24 hour/12 month cycle.

168
Q

What is the primary zeitgeber?

A

Light

169
Q

Name another factor, apart from light, which affects circadian rhythms.

A

Food

170
Q

What is meant by nadir in a circadian rhythm?

A

The lowest level of a hormone

171
Q

What is meant by acrophase in a circadian rhythm?

A

The peak of a hormone level

172
Q

What is meant by MESOR in a circadian rhythm?

A

The overall average level of a hormone.

173
Q

Give eight functions of cortisol.

A
  • Permissive effects on glucagon
  • Carbohydrate metabolism (increased glucose)
  • Lipolysis and ketogenesis
  • Gluconeogenesis
  • Increased myocardial contraction
  • Increased vascular tone
  • Conserves glucose for brain
  • Suppresses immune system
174
Q

What time of day is the peak in cortisol levels?

A

Morning, between 08:00 and 09:00.

175
Q

What is the threshold for a diabetes diagnosis in a random blood glucose sample?

A

11.1 mmol/L or higher

176
Q

Give the four effects of parathyroid hormone.

A
  • Increased bone resorption
  • Increased intestinal calcium absorption (via Vitamin D activation)
  • Increased renal calcium reabsorption
  • Increased renal phosphate excretion
177
Q

Give the three effects that parathyroid hormone has on the kidneys.

A
  • Increased calcium reabsorption
  • Decreased phosphate reabsorption
  • 1a-hydroxylation of vitamin D
178
Q

Give the effect of parathyroid hormone on bone.

A
  • Increased bone remodelling (bone resorption outweighs bone formation)
179
Q

Give the effect of parathyroid hormone on the intestines.

A

No direct effect (but increased calcium absorption due to increased vitamin D activation)

180
Q

Why is calcium important?

A

For the functioning of nerves and muscles

181
Q

What is the prevalence of hyperthyroidism?

A

2.5%

182
Q

What is the prevalence of hypothyroidism?

A

5%

183
Q

What is the prevalence of goitres?

A

5-15%

184
Q

Define hyperthyroidism.

A

An excess of thyroid hormone in the blood.

185
Q

Which gender is more likely to get thyroid autoimmunity?

A

Females

186
Q

When does thyroid autoimmunity commonly present in females?

A

Post partum

187
Q

What causes neonatal thyrotoxicosis?

A

Maternal antibodies for thyroid stimulating hormone receptor cross the placenta.

188
Q

Which genes play a part in a person’s predisposition to thyroid autoimmunity?

A

HLA genes

189
Q

Give three environmental factors which increase risk of predisposition to thyroid autoimmunity.

A
  • Stress
  • High iodine intake
  • Smoking
190
Q

What is a goitre?

A

A palpable and visible thyroid enlargement.

191
Q

Where in the world do goitres commonly occur?

A

Iodine deficient areas

192
Q

What are the three mechanisms for increased thyroid hormone in the blood?

A
  • Overproduction of thyroid hormone
  • Leakage of preformed hormone from thyroid
  • Ingestion of excess thyroid hormone
193
Q

Name four drugs or types of drugs which commonly cause thyroid dysfunction.

A
  • Amiodarone
  • Lithium
  • Interferon
  • Immune therapies
194
Q

Give two drugs used in immune therapies which affect the thyroid.

A

Ipilimumab

Nivolumab

195
Q

What is amiodarone used for?

A

Anti-arrhythmic drug used in atrial fibrillation.

196
Q

Why does amiodarone commonly affect the thyroid?

A

37% iodine by weight

197
Q

Give two thyroid conditions that amiodarone can cause.

A
  • Amiodarone induced hypothyroidism (AIH)

- Amiodarone induced thyrotoxicosis (AIT)

198
Q

What is the Wolf-Chaikoff effect?

A

Presumed reduction in thyroid hormone in response to excess iodine ingestion.

199
Q

What is the Jode-Basedow effect?

A

Increased thyroid hormone in response to increased iodine intake.

200
Q

Give an alternative drug to amiodarone which does not contain iodine.

A

Dronedarone

201
Q

Give three predominantly intracellular ions.

A
  • Potassium
  • Magnesium
  • Phosphate
202
Q

Give three predominantly extracellular ions.

A
  • Sodium
  • Chloride
  • Bicrobonate
203
Q

Define osmolality.

A

Concentration of solute per kilo.

204
Q

Define osmolarity.

A

Concentration of solute per litre.

205
Q

Give six solutes which affect osmolality.

A
  • Sodium
  • Potassium
  • Chloride
  • Bicarbonate
  • Urea
  • Glucose
206
Q

Give four exogenous solutes which may affect osmolality.

A
  • Alcohol
  • Methanol
  • Polyethylene glycol
  • Manitol
207
Q

Give an equation used to estimate osmolality at the bedside.

A

2Na + urea + glucose

208
Q

What is the day to day release of ADH controlled by?

A

Osmoreceptors in the hypothalamus

209
Q

What stimulates ADH release in an emergency?

A

Baroreceptors in brainstem and great vessels.

210
Q

Where is the V1a receptor found?

A

Vasculature

211
Q

Where is the V1b receptor found?

A

Pituitary

212
Q

Where is the V2 receptor found?

A

Renal collecting tubules

213
Q

How does the cell absorb more water when ADH binds to the receptor?

A

ADH binding increases levels of cAMP.

Vesicles with aquaporin 2 are inserted into membrane.

214
Q

What is hyponatraemia defined as?

A

Serum sodium <135mmol/L

215
Q

What level does sodium have to drop to to be classed as severe hyponatraemia?

A

<125mmol/L

216
Q

What are 10 signs/symptoms of hyponatraemia?

A
  • Asymptomatic
  • Headache
  • Lethargy
  • Anorexia/abdominal pain
  • Weakness
  • Confusion/hallucinations
  • Agitation
  • Decreased consciousness
  • Fitting
  • Coma
217
Q

What nine investigations should be done if hyponatraemia is suspected?

A
  • Plasma osmolality
  • Urine osmolality
  • Plasma glucose
  • Urine sodium
  • Urine diptest for protein
  • TSH
  • Cortisol
  • Short synacthen if low cortisol
  • Consider alcohol
218
Q

Describe how the CNS adapts to hyponatraemia.

A

Water gain causes loss of sodium/potassium/chloride and in the long term, organic osmolytes.
Water follows out of brain and the brain adapts.

219
Q

How should hyponatraemia be corrected in an acute situation?

A

Rapid correction is safer and may be necessary.

220
Q

How should hyponatraemia be corrected in a chronic case?

A

Correction must be slow because brain has adapted.

<8mmol/24hr

221
Q

Does onset of puberty correspond better with bone age or chronological age?

A

Bone age

222
Q

What is puberty?

A

Puberty describes the physiological, morphological, and behavioural changes as the gonads switch from infantile to adult forms.

223
Q

What are the definitive signs of puberty for boys and girls?

A

Boys - First ejaculation

Girls - Menarche

224
Q

What are the true signs of the start of puberty for girls and boys?

A

Boys - Testes >3ml

Girls - breast bud noted/palpable

225
Q

What is thelarche?

A

Breast development

226
Q

What is thelarche induced by?

A

Oestrogen

227
Q

What changes does oestrogen induce in the breast at puberty?

A
  • Ductal proliferation
  • Adipose deposition
  • Nipple/areola enlargement
228
Q

Other than oestrogen, give three other hormones involved in thelarche.

A
  • Prolactin
  • Glucocorticoids
  • Insulin
229
Q

What is adrenarche?

A

Maturation of the adrenal gland.

230
Q

Which zone of the adrenal cortex develops during adrenarche?

A

Zona reticularis

231
Q

Which steroid is produced in adrenarche?

A

DHEA

232
Q

What physical changes occur at adrenarche?

A
  • Growth of pubic/axillary hair
  • Oily skin
  • Mild acne
  • Body odour
233
Q

What is pubarche?

A

First appearance of pubic hair at puberty.

234
Q

What may occur as a consequence of menarche before 9 years?

A

Short stature

235
Q

Define precocious puberty.

A

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

236
Q

What causes true precocious puberty?

A

Increased GnRH secretion.

237
Q

What other condition has to be ruled out in precocious puberty?

A

Brain tumour

238
Q

Is precocious puberty more common in boys or girls?

A

Girls

239
Q

Describe the relative stimulated LH/FSH levels in true precocious puberty.

A

LH:FSH ratio >1, levels are high.

240
Q

What causes precocious pseudopuberty?

A

Secreting tumours or production of adrenal sex hormones.

241
Q

Describe the relative stimulated levels of LH/FSH in precocious pseudopuberty.

A

LH/FSH ratio <1. Levels in normal range.

242
Q

What treatment is given for precocious puberty?

A

GnRH superagonist (suppresses pulsatile secretion)

243
Q

Will congenital adrenal hyperplasia cause true precocious puberty or precocious pseudopuberty?

A

Precocious pseudopuberty

244
Q

Give two consequences of delayed puberty.

A
  • Osteoporosis

- Reduced peak bone mass

245
Q

Is delayed puberty more common in boys or girls?

A

Boys

246
Q

Define delayed puberty.

A

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

247
Q

Give three types of delayed puberty.

A
  • Constitutional delay of growth and puberty (CDGP)
  • Hypogonadotrophic hypogonadism
  • Hypergonadotrophic hypogonadism
248
Q

What causes constitutional delay of growth and puberty?

A

Delayed activation of hypothalamic pulse generator.

249
Q

What will the family history often reveal in constitutional delay of growth and puberty?

A

Frequent family history of late menarche (mother/sister) or delayed growth spurt (father).

250
Q

What can hypogonadotrophic hypogonadism also be known as?

A

Secondary hypogonadism

251
Q

Name a syndrome which can cause hypogonadotrophic hypogonadism.

A

Kallmann’s syndrome

252
Q

What is a common feature of Kallmann’s syndrome?

A

Anosmia (no smell)

253
Q

Why is GnRH not released properly in Kallmann’s syndrome?

A

Failure of migration of GnRH neurones.

254
Q

What are four mechanisms which can cause hypogonadotrophic hypogonadism?

A
  • Failure of GnRH neurone migration
  • Failure of GnRH synthesis/release
  • Failure of GnRH action
  • Failure of gonadotropin synthesis
255
Q

What is the most common cause of delayed puberty in both sexes?

A

Constitutional delay in growth and puberty

256
Q

What is another name for hypergonadotrophic hypogonadism?

A

Primary hypogonadism

257
Q

Give two syndromes which can cause hypergonadotrophic hypogonadism.

A
  • Klinefelter’s Syndrome (47XXY)

- Turner’s Syndrome (45XO)

258
Q

Give six features of Klinefelter’s syndrome.

A
  • Azoospermia
  • Gynaecomastia
  • Reduced secondary sexual hair
  • Osteoporosis
  • Tall stature
  • Reduced IQ in 40%
259
Q

Give six features of Turner’s syndrome.

A
  • Short stature
  • Oedema of hands/feet at birth
  • CV malformations
  • Renal malformations
  • Recurrent otitis media
  • Distinct physical features
260
Q

Give four indications for investigation in girls with delayed puberty.

A
  • Lack of breast development (13yrs)
  • > 5yrs between breast development and menarche
  • Lack of pubic hair (14yrs)
  • Absent menarche (15-16yrs)
261
Q

Give three indications for investigation in delayed puberty in boys.

A
  • Lack of testicular enlargement (14yrs)
  • Lack of pubic hair (15yrs)
  • > 5yrs to complete genital enlargement
262
Q

What four laboratory tests should be carried out to test for delayed puberty?

A
  • Complete RBC count, U&E, renal, LFT, Coeliac Ab
  • LF, FSH, Testosterone, Oestradiol
  • Thyroid, prolactin, DHEA-S, ACTH, cortisol
  • Karyotyping & GnRH stimulation test
263
Q

What replacement therapy are females with delayed puberty usually given?

A

Gradual oestrogen, with the eventual addition of progesterone.

264
Q

What replacement therapy are males with delayed puberty usually given?

A

Gradual testosterone

265
Q

Which cells do craniopharyngiomas arise from?

A

Squamous epithelial remnants of Rathke’s pouch

266
Q

Is a craniophryngioma benign or malignant?

A

Benign, although it can infiltrate surrounding tissues.

267
Q

Give five consequences of a craniopharyngioma.

A
  • Raised ICP
  • Visual disturbances
  • Growth failure
  • Pituitary hormone deficiency
  • Weight increase
268
Q

What is Rathke’s cyst derived from?

A

Remnants of Rathke’s pouch

269
Q

Describe the histology of a Rathke’s cyst.

A

Single layer of epithelial cells with mucoid, cellular, or serous fluid.

270
Q

What are the typical presentations of a Rathke’s cyst?

A
  • Headache/hydrocephalus

- Amenorrhoea/hypopituitarism

271
Q

What is the most common tumour of the pituitary region after a pituitary adenoma?

A

Meningioma

272
Q

How do patients typically present with a meningioma?

A
  • Loss of visual acuity
  • Endocrine dysfunction
  • Visual field defects
273
Q

Briefly describe lymphocytic hypophysitis.

A

Inflammation of the pituitary gland due to an autoimmune reaction.

274
Q

Give three types of lymphocytic hypophysitis.

A
  • Lymphocytic adenohypophysitis
  • Lymphocytic infundibuloneurohypophysitis
  • Lymphocytic panhypophysitis
275
Q

What is the preferred imaging method for the pituitary gland?

A

MRI

276
Q

What is measured when testing thyroid function?

A

Free T4 and TSH

277
Q

How is the gonadal axis tested in men?

A

Measure 0900h fasted testosterone and LH/FSH

278
Q

How is the HPA axis tested?

A

Measure 0900h cortisol and ACTH, and do a synacthen test

279
Q

How is the GH/IGF-1 axis tested?

A

Stimulation tests (insulin stress test / glucagon test)

280
Q

How is prolactin tested?

A

Via a cannula (prolactin is released in stress (potentially of venipuncture))

281
Q

How is ADH release tested?

A

Water deprivation test

282
Q

Give four consequences of growth hormone deficiency.

A
  • Short stature
  • Abnormal body composition
  • Decreased muscle mass
  • Poor quality of life
283
Q

What is the treatment for growth hormone deficiency?

A

Growth hormone

284
Q

Give four consequences of LH/FSH deficiency.

A
  • Hypogonadism
  • Decreased sperm count
  • Infertility
  • Menstruation problems
285
Q

How is LH/FSH deficiency treated in males and females?

A 
Males = testosterone
Females = oestradiol with or without progesterone
286
Q

How is hypothyroidism treated?

A

Levothyroxine

287
Q

Give two consequences of ACTH deficiency.

A
  • Adrenal failure

- Decreased pigmentation

288
Q

What will the blood results be for a patient with primary hypothyroidism?

A

Low T4

Raised TSH

289
Q

What will the blood results be for a patient with hypopituitary thyroid dysfunction?

A

Low T4

Normal/Low TSH

290
Q

What will the blood results be for a patient with Graves’ disease?

A

High T4

Suppressed TSH

291
Q

What will the blood results be for a patient with a TSHoma?

A

High T4

Normal/high TSH

292
Q

What will the blood results be for a patient with thyroid hormone resistance?

A

High T4

Normal/high TSH

293
Q

What will the blood results be for a patient with primary hypogonadism (male)?

A

Low testosterone

High LH/FSH

294
Q

What will the blood results be for a patient with hypopituitary gonadal dysfunction (male)?

A

Low testosterone

Normal/low LH/FSH

295
Q

What will the blood results be for a patient with anabolic use (male)?

A

Low testosterone

Suppressed LH

296
Q

What will the blood results be for a patient before puberty (female)?

A

Low/undetectable oestradiol

Low LH/FSH (FSH>LH)

297
Q

What will the blood results be for a patient during puberty (female)?

A

Oestradiol increased

Pulsatile LH increased

298
Q

What will the blood results be for a patient post menarche (female)?

A

Oestradiol increase throughout cycle.

Mid-cycle surge of LH/FSH.

299
Q

What will the blood results be for a patient with primary ovarian failure / menopause (female)?

A

Low oestradiol

High LH/FSH (FSH>LH)

300
Q

What will the blood results be for a patient with hypopituitary gonadal dysfunction (female)?

A

Low oestradiol

Normal/low LH/FSH

301
Q

What will the blood results be for a patient with primary adrenal insufficiency?

A

Low cortisol
High ACTH
Poor response to synacthen

302
Q

What will the blood results be for a patient with hypopituitary adrenal insufficiency?

A

Low cortisol
Low/normal ACTH
Poor response to synacthen

303
Q

What will the water deprivation test results be for a patient with cranial diabetes insipidus?

A

Plasma osmolality increases and then decreases after administration of desmopressin.
Urine osmolality stays the same but rises after administration of desmopressin.

304
Q

What will the water deprivation test results be for a patient with nephrogenic diabetes insipidus?

A

Plasma osmolality continues to increase even after desmopressin administration.
Urine osmolality does not rise even after administration of desmopressin.

305
Q

Why doesn’t ketoacidosis occur in people with type 2 diabetes?

A

Even low levels of insulin can suppress unrestrained lipolysis.

306
Q

Describe the paracrine signalling in the islets of the pancreas.

A

Local insulin suppresses glucagon and local glucagon suppresses insulin.

307
Q

How do blood glucose levels rise in the fasting state?

A

Glucose is released from the liver via glycogenolysis and gluconeogenesis.

308
Q

Which tissues receive glucose in the fasting state?

A
  • Insulin-independent tissues
  • Brain
  • Red blood cells
309
Q

What do muscles use as fuel in the fasting state?

A

Free fatty acids

310
Q

Name four hormones that act in opposite ways to insulin.

A
  • Glucagon
  • Adrenaline
  • Cortisol
  • Growth hormone
311
Q

Give three roles of glucagon.

A
  • Increase hepatic glucose output
  • Reduce peripheral glucose uptake
  • Stimulate release of gluconeogenic precursors
312
Q

What is the overall name for monogenic causes of diabetes?

A

Maturity onset diabetes of the young (MODY)

313
Q

Give five mutations or types of MODY.

A
  • HNF1A
  • HNF4A
  • Glucokinase mutation
  • Permanent neonatal diabetes
  • Maternally inherited diabetes and deafness
314
Q

What treatment usually works best for HNF1A diabetes?

A

Sulfonylurea treatment

315
Q

What treatment is usually given in glucokinase mutation diabetes?

A

No treatment is usually required.

316
Q

Which mutations occur in permanent neonatal diabetes?

A

Mutations occur to the Kir6.2 and SUR1 subunits of the beta cell metabolic potassium channel.

317
Q

Give three signs associated with permanent neonatal diabetes.

A
  • Small baby
  • Epilepsy
  • Muscle weakness
318
Q

Describe the pathogenesis of maternally inherited diabetes and deafness.

A

Mutation in mitochondrial DNA results in loss of beta cell mass.

319
Q

Give four clinical features of MODY.

A
  • Parent affected
  • Absence of autoantibodies
  • Sensitive to sulfonylurea
  • Evidence of non-insulin dependence
320
Q

Describe lipodystrophy diabetes.

A

Selective loss of adipose tissue associated with insulin resistance, dyslipidaemia, hepatic steatosis, hyperandrogenism, and PCOS.

321
Q

Describe diabetes causes by an acute disease of the exocrine pancreas.

A

Usually transient hyperglycaemia due to increased glucagon secretion.

322
Q

What is chronic pancreatitis commonly caused by?

A

Alcohol

323
Q

How does chronic pancreatitis cause diabetes?

A
  • Altered secretions

- Formation of proteinaceous plugs that block ducts and act as foci for calculi formation

324
Q

What are three disorders of depositions that can cause diabetes?

A
  • Hereditary haemochromatosis
  • Amyloidosis
  • Cystinosis
325
Q

How does pancreatic neoplasia cause diabetes?

A

Pancreatic resection removes insulin and glucagon function.

326
Q

How does cystic fibrosis lead to diabetes?

A

Viscous secretions lead to duct obstruction and fibrosis.

327
Q

Give three ways that insulin can improve cystic fibrosis.

A
  • Improves body weight
  • Reduces infection
  • Improves lung function
328
Q

Give three endocrine causes of diabetes.

A
  • Acromegaly
  • Cushing’s syndrome
  • Pheochromocytoma
329
Q

Give four drugs that can induce diabetes.

A
  • Glucocorticoids
  • Thiazides
  • Protease inhibitors (HIV)
  • Antipsychotics
330
Q

Define diabetes.

A

A disorder of carbohydrate metabolism characterised by hyperglycaemia.

331
Q

What are the two general categories of diabetes complications?

A

Microvascular and macrovascular

332
Q

Give three macrovascular complications of diabetes.

A
  • Stroke
  • Cardiovascular disease
  • Peripheral vascular disease
333
Q

Give three microvascular complications of diabetes.

A
  • Diabetic retinopathy
  • Diabetic nephropathy
  • Diabetic peripheral neuropathy
334
Q

What is the commonest form of diabetic neuropathy?

A

Distal symmetrical polyneuropathy

335
Q

What percentage of patients with diabetes are affected by diabetic neuropathy?

A

30-50%

336
Q

What is the typical pattern of sensory loss in diabetic neuropathy?

A

Glove and stocking

337
Q

What are the two common symptoms of diabetic neuropathy?

A

Pain

Insensitivity

338
Q

Give six consequences of autonomic diabetic neuropathy.

A
  • Orthostatic hypotension
  • Gastroparesis
  • Diarrhoea
  • Constipation
  • Incontinence
  • Erectile dysfunction
339
Q

Give the six steps leading to diabetic amputation.

A
  1. Neuropathy/vascular
  2. Trauma
  3. Ulceration
  4. Failure to heal
  5. Infection
  6. Amputation
340
Q

Why do people with diabetes often get dry skin on their feet?

A

Autonomic neuropathy results in decreased sweating, leading to dry skin.

341
Q

What are the two symptoms of peripheral vascular disease?

A
  • Intermittent claudication

- Rest pain

342
Q

Give four signs of peripheral vascular disease in a diabetic patient.

A
  • Diminished/absent pedal pulses
  • Coolness of feet and toes
  • Poor skin and nails
  • Absence of hair on feet and legs
343
Q

What three treatments are used for peripheral vascular disease in diabetes?

A
  • Quit smoking
  • Walk through the pain
  • Surgical intervention
344
Q

Give five factors that increase a patients’ risk of diabetic retinopathy.

A
  • Long duration diabetes
  • Poor glycaemic control
  • Hypertensive
  • On insulin treatment
  • Pregnancy
345
Q

What three mechanisms cause damage in diabetic retinopathy?

A
  • Microaneurysms
  • Leakage
  • Ischaemia
346
Q

How do microaneurysms occur in diabetic retinopathy?

A

Pericyte and smooth muscle loss result in aneurysms adjacent to or upstream of capillary non-perfusion.

347
Q

Give three ways that leakage occurs in diabetic retinopathy.

A
  • Basement membrane thickening
  • Pericyte loss
  • Reduced junctional complexes with endothelial cells
348
Q

Why are microvessels formed in diabetic retinopathy?

A

Ischaemia or occlusion results in proliferation.

349
Q

How does ischaemia occur in diabetic retinopathy?

A

Loss of pericytes, and endothelial cells respond by increasing turnover, resulting in thickening.

350
Q

How does occlusion occur in diabetic retinopathy?

A

Glial cells grow down the capillaries.

351
Q

What is the hallmark of diabetic nephropathy?

A

Development of proteinuria

352
Q

Give two risk factors for developing diabetic nephropathy?

A
  • Poor blood pressure control

- Poor blood glucose control

353
Q

Give the four steps leading to diabetic nephropathy.

A
  1. Glomerulus changes (thicker basement membrane)
  2. Increase of glomerular injury
  3. Filtration of proteins
  4. Diabetic nephropathy
354
Q

How long after diagnosis of type 1 diabetes does microalbuminaemia typically occur?

A

5-10 years

355
Q

How long after the diagnosis of type 2 diabetes does microalbuminaemia typically occur?

A

It can be present at the time of diagnosis.

356
Q

Give five strategies for the treatment of diabetic nephropathy.

A
  • Blood pressure control
  • Glycaemic control
  • ACEi
  • Proteinuria control
  • Cholesterol control
357
Q

Give two decisions that must be made when choosing insulin treatment for someone with diabetes.

A
  • Basal or rapid-acting

- Human or analogues

358
Q

Describe how injected insulin differs from physiological insulin secretion.

A

Levels rise slower and remain below normal physiological levels, and levels do not drop as low as normal baseline.

359
Q

What is the best insulin treatment regime for type 1 diabetes?

A

Intensive basal-bolus

360
Q

When is the insulin bolus given in type 1 diabetes and how much is injected?

A

Bolus is given just before a meal and amount is adjusted according to meal content.

361
Q

What is the purpose of giving basal insulin in diabetes?

A

Controls blood glucose between meals and during the night.

362
Q

How long does it usually take for basal insulin analogues to reach steady state?

A

1-2 days

363
Q

What percentage of people with type 2 diabetes require insulin after 10 years?

A

50%

364
Q

What is the usual schedule for insulin injections for type 2 diabetes?

A

Basal insulin at bedtime and occasionally prandial insulin for biggest meal of the day.

365
Q

Give three possible insulin regimes for type 2 diabetes.

A
  • Once daily basal insulin
  • Twice daily mix insulin
  • Basal-bolus therapy
366
Q

What are the side effects of insulin?

A

Hypoglycaemia and weight gain

367
Q

Give six possible mechanisms for non-insulin treatments for type 2 diabetes.

A
  • Lifestyle intervention
  • Sensitise
  • Replace
  • Secrete
  • Excrete
  • Bariatric surgery
368
Q

What is the purpose of sensitisation treatment in type 2 diabetes?

A

Help the body to respond better to its own insulin.

369
Q

Give two examples of sensitisation treatment in type 2 diabetes.

A
  • Metformin

- Pioglitazone

370
Q

What is the purpose of replacement treatment in type 2 diabetes?

A

Inject insulin to promote uptake/storage of glucose in liver and muscle.

371
Q

What is the purpose of lifestyle interventions to treat type 2 diabetes?

A
  • Prevent or stall development of T2DM

- Prevent or reduce associated complications

372
Q

What is the purpose of secretion treatment for type 2 diabetes?

A

Stimulate the pancreas to secrete more insulin.

373
Q

Give three examples of stimulatory treatments for type 2 diabetes.

A
  • Sulfonylureas
  • DPP-4 inhibitors
  • GLP-1 receptor agonists
374
Q

What is the purpose of excretion treatments for type 2 diabetes?

A

Remove excess glucose load

375
Q

Give an example of an excretion treatment for type 2 diabetes.

A

SGLT2 inhibitors

376
Q

Give three roles of metformin.

A
  • Decreases gluconeogenesis
  • Decreases intestinal absorption of glucose
  • Increases peripheral glucose uptake and utilisation
377
Q

What are incretins?

A

Hormones secreted by intestinal endocrine cells in response to nutrient intake.

378
Q

Give three roles of incretins.

A
  • Stimulate glucose-dependent insulin secretion
  • Post-prandial glucagon suppression
  • Slowing of gastric emptying
379
Q

What is dipeptidyl peptidase 4?

A

Enzyme present in vascular endothelial lining which inactivates the incretin hormones GIP and GLP-1.

380
Q

What is the role of DPP-4 inhibitors?

A

Enhance the effects of GIP and GLP-1.

381
Q

What group of drugs does pioglitazone belong to?

A

Thiazolidinediones (TZD)

382
Q

What are the benefits of TZDs in treating diabetes?

A

Low risk of hypoglycaemia and positive effects on biomarkers.

383
Q

What are the disadvantages of using TZDs to treat diabetes?

A

Increased CV risk, lipid abnormalities, weight gain.

384
Q

What is the role of TZDs?

A

Enhance tissue sensitivity to insulin and reduce gluconeogenesis.

385
Q

What is the role of SGLT2 inhibitors?

A

Prevents glucose reabsorption in proximal convoluted tubule.

386
Q

Explain one side effect of SGLT2 inhibitors.

A

Cause glycosuria, leading to thrush.

387
Q

Name a dopamine agonist which is used as a medical treatment.

A

Cabergoline

388
Q

How should normal urine osmolality relate to serum osmolality.

A

Urine osmolality should be double serum osmolality.

389
Q

Which diabetes medication can cause weight loss?

A

Metformin

Phase2a (12 decks)

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