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PHASE 2A > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the difference between endocrine and exocrine secretion?

A 
Endocrine = secrete directly into the bloodstream, without ducts 
Exocrine = secrete through ducts to a site of action
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2
Q

What are the 3 types of hormone action?

A
  1. Endocrine - blood-borne, acting at distant sites
  2. Paracrine - acting on nearby adjacent cells
  3. Autocrine - feedback on same cells that secreted that hormone
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3
Q

What 7 organs comprise the major endocrine system?

A
  1. Pituitary
  2. Thyroid
  3. Parathyroid
  4. Adrenal
  5. Pancreas
  6. Ovary
  7. Testes
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4
Q

Are water-soluble hormones stored in vesicles or synthesised on demand?

A

Water soluble hormones are stored in vesicles

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5
Q

How do water soluble hormones get into cells?

A

They bind to cell surface receptors

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6
Q

Give an example of a water soluble hormone

A

Peptides - TRH, LH, FSH

Monoamines

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7
Q

Are fat soluble hormones stored in vesicles or synthesised on demand?

A

Fat soluble hormones are synthesised on demand

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8
Q

How do fat soluble hormones get into cells?

A

They diffuse into the cell

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9
Q

Give an example of a fat soluble hormone

A

Steroids - cortisol, thyroid hormone

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10
Q

What are the differences between the half-life and clearance of water soluble and fat soluble hormones?

A

Water soluble = short half life and fast clearance

Fat soluble = long half life and slow clearance

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11
Q

Name 4 hormone classes

A
  1. Peptides
  2. Amines
  3. Iodothyrosines
  4. Cholesterol derivatives and steroids
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12
Q

Give 5 examples of a peptide hormones

A
  1. Insulin
  2. Growth hormone
  3. ADH
  4. CRH
  5. Somatostatin
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13
Q

Give an example of an amine hormone

A

Noradrenaline and adrenaline

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14
Q

Describe the pathway of adrenaline synthesis

A

Phenylalanine –> L-tyrosine –> L-dopa –> Noradrenaline –> Adrenaline

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15
Q

Name the enzyme that breaks down noradrenaline and adrenaline

A

Catechol-O-methyl transferase (COMT)

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16
Q

What are noradrenaline and adrenaline broken down into?

A

Normetadrenaline and metadrenaline

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17
Q

Name 3 sites of hormone receptor location

A
  1. Cell membrane
  2. Cytoplasm
  3. Nucleus
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18
Q

Where in the cell are peptide cell receptors located?

A

On the cell membrane

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19
Q

Where in the cell are steroid hormone receptors located?

A

In the cytoplasm

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20
Q

Where in the cell are thyroid/vitamin A and D cell receptors located?

A

In the nucleus

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21
Q

Give 5 ways in which hormone action is controlled

A
  1. Hormone metabolism
  2. Hormone receptor induction
  3. Hormone receptor down-regulation
  4. Synergism - combined effects of 2 hormones amplified (e.g. glucagon and adrenaline)
  5. Antagonism - one hormone opposes other hormone (e.g. glucagon and insulin)
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22
Q

What are the 2 types of feedback control?

A
  1. Negative feedback - response causes response loop to shut off
  2. Positive feedback - response causes more response to occur
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23
Q

What layer of the trilaminar disc is the anterior pituitary derived from?

A

Ectoderm (Rathke’s pouch)

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24
Q

What is the posterior pituitary derived from?

A

The floor of the ventricles

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25
Q

Name the 6 hormones that the anterior pituitary produces

A
  1. TSH - thyroid stimulating hormone
  2. FSH - follicle stimulating hormone
  3. LH - luteinising hormone
  4. ACTH - adrenocorticotrophic hormone
  5. Prolactin
  6. GH - growth hormone
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26
Q

Name the 2 hormones secreted form the posterior pituitary

A
  1. Oxytocin

2. ADH - antidiuretic hormone

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27
Q

Where are the posterior hormones synthesised?

A

In the hypothalamus
oxytocin = paraventricular nucleus
ADH = supraoptic nucleus

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28
Q

How are oxytocin and ADH transported form the hypothalamus to the posterior pituitary?

A

Transported down the icons of the hypothalamic hypophyseal tract

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29
Q

Give 2 functions of oxytocin

A
  1. Milk secretion

2. Uterine contraction

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30
Q

What is the function of ADH?

A

It acts on the collecting ducts of the nephron and increased insertion of aquaporin 2 channels –> water retention
Causes vasoconstriction

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31
Q

Give the 6 hypophysiotropic hormones released by the hypothalamus

A
  1. Thyrotropin-releasing hormone (TRH)
  2. Corticotrophin-releasing hormone (CRH)
  3. Gonadotrophin-releasing hormone (GRH)
  4. Growth hormone releasing hormone (GHRH)
  5. Somatostatin
  6. Dopamine
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32
Q

Describe the thyroid axis

A

Hypothalamus –> TRH –> Anterior pituitary –> TSH –> thyroid –> T3 and T4
T3 and T4 have a negative effect on the hypothalamus and the anterior pituitary

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33
Q

Which has a longer half life, triiodothyronine or thyroxine?

A

T3 has a half life of 1 day and T4 has a half life of 5-7 days

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34
Q

What would be the effect on TSH if you had an under active thyroid?

A

TSH would be raised as you have less T3/4 being produced so no negative feedback

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35
Q

What would a low TSH tell you about the action of the thyroid?

A

Indicates an over active thyroid

Lots of T3/4 being produced so more negative feedback on the pituitary and therefore less TSH

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36
Q

Give 4 functions of thyroid hormones (T3 and T4)

A
  1. Accelerates food metabolism
  2. Increases protein synthesis
  3. Stimulation of carbohydrate metabolism
  4. Enhances fat metabolism
  5. Increase in ventilation rate
  6. Increase in cardiac output and heart rate
  7. Brain development during foetal life and postnatal development
  8. Growth rate accelerated
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37
Q

Describe the mechanism of ACTH

A

Hypothalamus –> CRH –> Anterior pituitary –> ACTH –> adrenal cortex (zona fasciculata) –> glucocorticoid synthesis (cortisol)
Cortisol has a negative feedback on the hypothalamus and the anterior pituitary

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38
Q

Give 3 functions of cortisol in response to stress

A
  1. Mobilises energy sources - lipolysis, gluconeogenesis, protein break down
  2. Vasoconstriction
  3. Suppresses inflammatory and immune responses
  4. Inhibits non-essential functions - growth and reproduction
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39
Q

Describe the mechanism of LH and FSH

A

Hypothalamus –> GnRH –> anterior pituitary –> FSH/LH –> ovaries/testes

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40
Q

What cells does FSH act on?

A 
Ovaries = Granulosa cells 
Testes = Sertoli cells
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41
Q

What cells LH act on?

A 
Ovaries = theca cells 
Testes = Leydig cells
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42
Q

What is the function of granulosa cells?

A

Stimulated by FSH to convert androgens into oestrogen using aromatase

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43
Q

What is the function of theca cells?

A

Stimulated by LH to produce androgens that diffuse into granulosa cells to be converted into oestrogen

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44
Q

What is the function of Sertoli cells?

A

Produce Mullerian inhabiting factor (MIF) and inhibin and activins which acts on the pituitary gland to regulate FSH
Stimulates spermatogenesis

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45
Q

What is the function of leydig cells?

A

Stimulated by LH to produce testosterone

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46
Q

Describe the GH axis

A

Hypothalamus –> GHRH (+) or Somatostatin (-) –> anterior pituitary –> GH –> Liver –> IGF-1

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47
Q

What is the function of GH?

A

Stimulates growth and protein synthesis

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48
Q

What is the function of IGF-1

A

It induces cell division, cartilage and skeletal growth and protein synthesis

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49
Q

Briefly describe the mechanism of prolactin

A

Hypothalamus –> dopamine (-) –> anterior pituitary –> prolactin

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50
Q

What would happen to serum prolactin levels if something was to impact on the pituitary stalk and block dopamine release?

A

Prolactin levels would increase

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51
Q

Give 3 reasons that result in pituitary dysfunction

A
  1. Tumour mass effects
  2. Hormone excess
  3. Hormone deficiency
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52
Q

Define appetite

A

Desire to eat food

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53
Q

Define satiety

A

Feeling of fullness - disappearance of appetite after a meal

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54
Q

Define overweight/obesity

A

Abnormal or excessive fat accumulation that may impair health

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55
Q

Give 5 risks of obesity

A
  1. Life expectancy decreases by 10 years
  2. Type 2 diabetes
  3. Hypertension
  4. Coronary artery disease
  5. Stroke
  6. Osteoarthritis
  7. Obstructive sleep apnea
  8. Carcinoma
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56
Q

Where is leptin expressed and what is its effect on appetite?

A 
Expressed in white fat 
Suppresses appetite (Anorexigenic)
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57
Q

Where is ghrelin expressed and what is its effect on appetite?

A 
Expressed in the stomach
Stimulates appetite (orexigenic)
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58
Q

Name 2 other hormones that decrease appetite

A
  1. Insulin
  2. PYY 3-36
  3. CKK
  4. Glucagon-like peptide (GLP)
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59
Q

Give 5 parathyroid hormone actions

A
  1. Increase Ca2+ reabsorption
  2. Decrease phosphate reabsorption
  3. Increase 1 alpha-hydroxylation of 25-OH vit D
  4. Increase bone remodelling (bone resorption >bone formation)
  5. Increase Ca2+ absorption because of increase 1,25(OH)2D (no direct effect)
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60
Q

When serum calcium levels are low, what are PTH levels?

A

PTH levels are high

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61
Q

When serum calcium levels are high, what are PTH levels?

A

PTH levels are low

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62
Q

What is the effect of hyperparathyroidism on serum calcium levels?

A

Hyperparathyroidism –> hypercalcaemia

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63
Q

Name 4 symptoms of hyperparathyroidism

A 
Hyperparathyroidism = hypercalcaemia 
1. Renal/biliary stones 
2. Bone pain
3. Abdominal pain
4. Depression, anxiety, malaise 
Stones, Bones, Groans and Moans
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64
Q

Give 2 causes of primary hyperparathyroidism

A

Parathyroid adenoma
Hyperplasia
Increase PTH –> increase calcium –> decrease phosphate

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65
Q

Describe the pathophysiology of secondary hyperparathyroidism

A

Becomes hyperplastic to increase secretion of pTH to compensate chronic hypocalcaemia
Often due to CKD

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66
Q

How does tertiary hyperparathyroidism occur?

A

Prolonged uncorrected hypertrophy - glands become autonomous producing excess PTH

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67
Q

What blood results would you see in the 3 types of hyperparathyroidism?

A 
Primary = hypercalcaemia 
Secondary = low serum calcium 
Tertiary = Raised calcium and PTH
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68
Q

Describe the treatment for hyperparathyroidism

A 
Primary = surgical removal of adenoma 
Secondary = calcium correction and treatment of the underlying cause 
Tertiary = Calcium mimetic (cinacalcet) and possibly a total or subtotal parathyroidectomy
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69
Q

How does a calcium mimetic work?

A

Increases sensitivity of parathyroid cells to calcium so less PTH secretion occurs

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70
Q

What is the affect of hypoparathyroidism on serum calcium levels?

A

Hypoparathyroidism –> hypocalcaemia

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71
Q

Give 5 symptoms of hypoparathyroidism

A

Hypoparathyroidism = hypocalcaemia

  1. Spasm
  2. Paraesthesia around mouth and lips
  3. Convulsions
  4. Tetany
  5. Cramps
  6. Confusion
  7. Chvosteks sign - tap over facial nerve and look for spasm of facial nerves
  8. Trousseaus sign - inflate BP cuff 20 mmHg above systolic for 5 mins = hand spasm
  9. QT prolongation
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72
Q

Name 4 causes of hypoparathyroidism

A
  1. Transient
  2. Can follow anterior neck surgery
  3. Genetic - defects in PTH gene
  4. Autoimmune - DiGeorge syndrome
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73
Q

What are blood results for someone with hypoparathyroidism?

A 
Calcium = Low 
PTH = Low
Phosphate = High
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74
Q

What is the treatment for hypoparathyroidism?

A 
Acute = IV calcium 
Persistant = Vitamin D analogue (alfacalcidol)
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75
Q

Give 3 causes of Hypercalcaemia

A
  1. Primary hyperparathyroidism
  2. Malignancy
  3. Vitamin D toxicity
  4. Myeloma
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76
Q

What is the treatment for hypercalcaemia?

A

Loop diuretic to return calcium to normal (furosemide)
Calcitonin
If Primary hyperparathyroidism = surgical removal

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77
Q

Give 2 ECG changes that you might see in someone with hypercalcaemia

A
  1. Tall T waves

2. Shortened QT interval

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78
Q

Name 3 causes of hypocalcaemia

A
  1. Increase serum phosphate due to CKD (most common) or phosphate therapy
  2. Reduced PTH function due to primary hypoparathyroidism, post thyroidectomy and parathyroidectomy
  3. Vitamin D deficiency due to reduced exposure of light
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79
Q

How would you diagnose hypocalcaemia?

A

Detailed history
eGFR to search for CKD
PTH levels
Vitamin D levels

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80
Q

How would you treat hypocalcaemia?

A

Acute = IV calcium
Persistent in vitamin D deficiency = vitamin D supplement
Persistent in hypoprarythroidism = alfacalcidol

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81
Q

Give 2 ECG changes that you might see in someone with hypocalcaemia

A
  1. Small T waves

2. Long QT interval

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82
Q

What does the parathyroid control?

A

Serum calcium levels

A low serum calcium triggers the release of PTH and a high serum calcium triggers c-cells to release calcitonin

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83
Q

What hormone does the parathyroid secrete and what is its function?

A

PTH - secreted in response to low serum calcium

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84
Q

What is released by c-cells in the parathyroid in response to high serum calcium?

A

Calcitonin

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85
Q

What biochemical test might you want to do to establish the cause of hypercalcaemia?

A

PTH measurement

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86
Q

What disease is described as being a ‘disorder of carbohydrate metabolism characterised by hyperglycaemia’?

A

Diabetes mellitus

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87
Q

What are the 4 cells that make up the islets of langerhans?

A
  1. Beta cells (70%)
  2. Alpha cells (20%)
  3. Delta cells (8%)
  4. Polypeptide secreting cells
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88
Q

What do beta cells produce?

A

Insulin

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89
Q

What to alpha cells produce?

A

Glucagon

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90
Q

What do delta cells produce?

A

Somatostatin

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91
Q

What is the importance of alpha and beta cells being located next to each other in the islets of langerhans?

A

Enables them to ‘crosstalk’

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92
Q

Describe the mechanism of insulin secreting from beta cells

A
  1. Glucose binds to beta cells
  2. Glucose metabolism occurs
  3. ADP –> ATP
  4. Causes K+ channels to close
  5. Membrane depolarisation occurs
  6. Calcium channels open allowing influx
  7. Insulin is released
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93
Q

Describe the insulin action at muscle and fat cells

A
  1. Insulin binds to membrane receptors
  2. Intracellular signalling cascade is stimulated
  3. GLUT-4 mobilisation to plasma membrane
  4. GLUT-4 integrates into plasma membrane
  5. Glucose enters cells via GLUT-4
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94
Q

Describe the physiological process that occur in the fasting state in response to low blood glucose

A

Low blood glucose = high glucagon and low insulin

  • Glucogenolysis and gluconeogenesis
  • Reduced peripheral glucose uptake
  • Stimulates the release of gluconeogenic precursors
  • Lipolysis and muscle breakdown
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95
Q

Describe the effect on insulin and glucagon secretion int he fasting state

A

Fasting state = low blood glucose

Raised glucagon and low insulin

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96
Q

How many precursors are needed for gluconeogensis?

A

3

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97
Q

Describe the physiological processes that occur after feeding in response to high blood glucose

A

High blood glucose = high insulin and low glucagon

  • Glycogenolysis and gluconeogenesis are suppressed
  • Glucose is taken up by peripheral muscle and fat cells
  • Lipolysis and muscle breakdown suppressed
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98
Q

Describe the effect on insulin and glucagon secretion after feeding

A

Insulin is high, glucagon is low

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99
Q

Give 3 effects of insulin

A
  1. Suppresses hepatic glucose output - decrease glycogenolysis and gluconeogenesis
  2. Increases glucose uptake into insulin sensitive tissues
  3. Suppresses lipolysis and breakdown of muscle
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100
Q

Give 3 effects of glucagon

A
  1. Stimulates hepatic glucose output - increases glycogenolysis and gluconeogenesis
  2. Reduces peripheral glucose uptake
  3. Stimulates lipolysis and breakdown of muscle
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101
Q

Give 3 ways in which diabetes Mellitus can cause morbidity and mortality

A
  1. Acute hyperglycaemia which if untreated leads to acute metabolic emergencies, diabetic ketoacidosis (DKA) and hyperosmolar coma
  2. Chronic hyperglycaemia leading tissue complications - macrovasculaa and microvascular
  3. Side effects of treatment - hyperglycaemia
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102
Q

What type are gestational and medication induced diabetes refereed to?

A

Type 2 diabetes mellitus

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103
Q

Describe the natural history of T1DM

A

Genetic predisposition + trigger –> insulitis, beta cell injury –> pre-diabetes –> diabetes

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104
Q

T1DM is characterised by impaired insulin secretion. Describe the pathophysiological consequence of this

A

Severe inducing deficiency –> glycogenolysis/gluconeogensis/lipolysis all not suppressed and reduced peripheral glucose uptake –> hyperglycaemia and glycosuria
Perceived stress –> cortisol and adrenaline secretion –> catabolic state –> increased plasma ketones

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105
Q

Is T1DM characterised by a problem with insulin secretion, insulin resistance or both?

A

Characterised by impaired insulin secretion - severe insulin deficiency

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106
Q

Describe the pathophysiology of T1DM

A

Beta cells express HLA antigens

Autoimmune destruction –> beta cell loss –> impaired insulin secretion

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107
Q

At what are do people with T1DM present?

A

Usually present in childhood

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108
Q

Name 3 symptoms of DM

A

Thirst (fluid and electrolyte losses)
Polyuria (due to osmotic diuresis)
Weight loss

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109
Q

Describe the epidemiology of T1DM

A 
Onset younger (<30 years) 
Usually lean 
More Northern European ancestry
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110
Q

A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons fasting plasma glucose be if they were diabetic?

A

Fasting plasma glucose >7 mmol/L

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111
Q

A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons random plasma glucose be if they were diabetic?

A

Random plasma glucose >11 mmol/L

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112
Q

What might someone’s HbA1c be if they have diabetes?

A

> 48 mmol/L

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113
Q

What happens to C-peptide in T1DM?

A

C-peptide reduces

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114
Q

How do you treat T1DM?

A 
Education 
Glycaemic control through diet (low sugar, low fat, high starch) 
Insulin – twice daily and with meals
Regular activity and healthy BMI 
BP and hyperlipidaemia control
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115
Q

Give 6 complications to Diabetes Mellitus

A
  1. Diabetic ketoacdiosis
  2. Diabetic nephropathy
  3. Diabetic retinopathy
  4. Diabetic neuropathy
  5. Hyperosmolar hyperglycaemic nonteotic coma
  6. Stroke, ischaemic heart disease, peripheral vascular disease
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116
Q

Give 2 potential consequences of T1DM

A
  1. Hyperglycaemia

2. Raised plasma ketones –> ketoacidosis

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117
Q

How is insulin administered in someone with T1DM?

A

Subcutaneous injections

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118
Q

Other than SC injections, how else can insulin be administered?

A

Insulin pump

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119
Q

Describe the different types of subcutaneous insulins that can be given to people with T1DM

A
  1. Ultra fast acting - Humalog - taken before eating in conjunction with a long acting insulin at night
  2. Long-acting insulin - insulin Glargine - taken before going to bed
  3. Pre-mixed insulin - NovoMix - taken twice daily
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120
Q

Give 4 potential complications of insulin therapy

A
  1. Hyperglycaemia
  2. Lipohypertrophy at injection site
  3. Insulin resistance
  4. Wight gain
  5. Interference with life style
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121
Q

What is the affect of cortisol on insulin and glucagon?

A

Inhibits insulin

Activates glucagon

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122
Q

Describe the pathophysiology of diabetic ketoacidosis

A

No insulin –> lipolysis –> FFA’s –> oxidised in the liver –> ketone bodies –> ketoacidosis

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123
Q

Name 3 ketone bodies

A
  1. Acetoacetate
  2. Acetone
  3. Beta hydroxybutyrate
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124
Q

Where does ketogenesis occur?

A

Liver

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125
Q

Give 5 signs of diabetic ketoacidosis

A
  1. Hypotension
  2. tachycardia
  3. Kassmaul’s respiration
  4. Breath smells of ketones
  5. Dehydration
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126
Q

Would you associate ketoacidosis with T1 or T2 DM?

A

Type 1

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127
Q

Give 3 microvascular compilation of DM

A
  1. Diabetic retinopathy
  2. Diabetic nephropathy
  3. Diabetic peripheral neuropathy
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128
Q

Give 2 macrovascular complications fo DM

A

CV disease

Stroke

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129
Q

What is the main risk factor for diabetic complications?

A

Poor glycemic control

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130
Q

What is the treatment for someone presenting with ketoacidosis?

A
  1. ABCDE
  2. IV normal saline
  3. IV soluble insulin via syringe driving and sliding scale
  4. Restore potassium levels
  5. Look for underlying cause
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131
Q

Give 3 endocrine diseases that can cause diabetes

A
  1. Cushing’s
  2. Acromegaly
  3. Phaeochromocytoma
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132
Q

What class of drugs can cause diabetes?

A

Steroids
Thiazies
Anti-psychotics

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133
Q

Is T2DM characterised by problem with insulin secretion, insulin resistance or both?

A

Characterised by impaired insulin secretion and insulin resistance

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134
Q

Describe the aetiology of T2DM

A

Genetic predisposition and environmental factors

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135
Q

Describe the pathophysiology of T2DM

A

Impaired insulin secretion and resistance –> impaired glucose tolerance –> T2DM –> hyperglycaemia and high FFAs

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136
Q

Why is insulin secretion impaired in T2DM

A

Due to lipid deposition in the pancreatic islets

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137
Q

Give 3 risk factors for insulin resistance in T2DM

A
  1. Obesity
  2. Physical inactivity
  3. Family history
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138
Q

What happens to insulin resistance, insulin secretion and glucose levels in T2DM?

A

Insulin resistance increase
Insulin secretion decreases
Fasting and post-prandial glucose increase

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139
Q

Why do you rarely see diabetic ketoacidosis in T2DM?

A

Insulin secretion is impaired but there are still low levels of plasma insulin
Low levels of insulin prevent muscle catabolism and ketogenesis

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140
Q

By how much has the beta cell mass reduced in T2DM when diagnosis usually occurs?

A

50% of normal beta cell mass

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141
Q

Describe the epidemiology of T2DM

A

Onset older (>30)
Usually overweight
More common in African/Asian populations
More common in general

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142
Q

Describe the treatment pathway for T2DM

A
  1. Lifestyle changes - lose weight, exercise, healthy diet and control of contributing conditions
  2. Metformin
  3. Metformin and sulfonylurea
  4. Metformin + sulfonylurea + insulin
  5. Increase insulin dose as required
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143
Q

How does metformin work in treating T2DM?

A

Increase insulin sensitivity and inhibits glucose production

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144
Q

How does sulfonylurea work in treating T2DM?

A

Stimulates insulin release

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145
Q

Give a potential consequence of taking Sulfonylurea for the treatment of T2DM

A

Hypoglycaemia

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146
Q

What is hypoglycaemia classified as?

A

Plasma glucose <3.9 mmol/L and if <3.0 mmol/L it is severe hypoglycaemia

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147
Q

Give 5 symptoms of hypoglycaemia

A
  1. Hunger
  2. Sweating
  3. Tachycardia
  4. Anxious
  5. Shaking
  6. Confusion
  7. Weakness
  8. Vision changes
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148
Q

Why does hypoglycaemia continuously get worse?

A

Glucagon is not produced so rely only on adrenaline and the threshold for adrenaline release gradually lowers after time

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149
Q

What are 5 risk factors of hypoglycaemia for those with T1DM?

A
  1. History of severe episodes
  2. HbA1c < 48 mmol/L
  3. long duration of diabetes
  4. Renal impairment
  5. Impaired awareness of hypoglycaemia
  6. Extremes of age
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150
Q

What are 5 risk factors of hypoglycaemia for those with T2DM?

A
  1. Advancing age
  2. Cognitive impairment
  3. Depression
  4. Aggressive treatment of glycaemia
  5. Impaired awareness of hypoglycaemia
  6. Duration of MDI insulin therapy
  7. Renal impairment and other co-morbidities
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151
Q

Give 3 impacts of non-severe hypoglycaemia

A
  1. Reduced quality of life
  2. Cause fear of hypoglycaemia
  3. Causes psychological morbidity
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152
Q

Give 6 consequences of hypoglycaemia

A
  1. Seizures
  2. Comas
  3. Cognitive dysfunction
  4. Fear
  5. Decrease in qualitative life
  6. Accidents
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153
Q

Briefly describe the treatment of hypoglycaemia

A

Recognise symptoms
Confirm the need for treatment (blood glucose <3.9 mmol/L)
Treat with 15g of fast-acting carbohydrate
Retest in 15 mins to ensure blood glucose >4.0 mmol/L and retreat if necessary
Eat a long acting carbohydrates to prevent recurrence

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154
Q

Why are patient with diabetes at a particular risk of hypoglycaemia?

A

In Diabetes there are defects in the physiological defences to hypoglycaemia and there is reduced awareness

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155
Q

What does prevention of hypoglycaemia include?

A

Eduction
Correct choice of therapy
Adjusting glucose targets in those at high risk
Specialist support from a MDT

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156
Q

Is insulin secretion or insulin resistance the driving force of hyperglycaemia in T2DM?

A

Hepatic insulin resistance is the driving force

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157
Q

Give a potential consequence of acute hyperglycaemia

A

Diabetic ketoacidosis and hyperosmolar coma

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158
Q

Give a potential consequence of chronic hyperglycaemia

A

Mirco/macrovascular tissue complications

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159
Q

A man presents with a history of weight loss, polyuria and nocturia. He is very unwell. The GP performs a capillary blood glucose which is found to be 17.2mmol/l. What is the most likely diagnosis of this mans symptoms?

A

Type 1 Diabetes Mellitus

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160
Q

Name 5 possible diseases of the pituitary

A
  1. Benign pituitary adenoma
  2. Craniopharygioma
  3. Trauma
  4. Apoplexy/Sheehans
  5. Sarcoid/TB
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161
Q

Give 3 potential consequences of a pituitary tumour

A
  1. Pressure on local structures - e.g. optic chasm = bilateral hemianopia
  2. Pressure on normal pituitary (lack of function) - Hypopituitarism
  3. Functioning tumours - e.g. Cushing’s, acromegaly, prolactinoma
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162
Q

Describe the growth hormone secretion from the anterior pituitary

A

It is secreted in a pulsatile fashion and increases during deep sleep

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163
Q

What is acromegaly?

A

Overgrowth of all organ systems due to excess growth hormone in adults

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164
Q

What is gigantism?

A

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

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165
Q

Give 5 symptoms of acromegaly

A
  1. Change in appearance
  2. Increase in size of hands and feet
  3. Excessive sweating
  4. Headache
  5. Tiredness
  6. Weight gain
  7. Amenorrhoea
  8. Deep voice
  9. Arthralgia
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166
Q

Give 5 signs of acromegaly

A
  1. Prognathism - jaw protrusion
  2. Interdental separation
  3. Large tongue
  4. Spade like hands and feet
  5. Tight rings
  6. Bitemporal hemianopia
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167
Q

What can cause acromegaly?

A

A benign pituitary adenoma producing excess GH

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168
Q

Describe the epidemiology of acromegaly

A

1/200,000
Average age is 40 years
Mean duration of symptoms is 8 years
Reduces life expectancy by 10 years

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169
Q

What complications are associated with acromegaly?

A
  1. Arthritis
  2. Cerebrovascular events
  3. Hypertension and heart disease
  4. Sleep apnea
  5. T2DM
  6. Colorectal cancer
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170
Q

What investigation might you do on someone who you suspect has acromegaly?

A
  1. Plasma GH levels can exclude acromegaly
  2. Serum IGF-1 and GH = raised
  3. Oral glucose tolerance test
  4. MRI pituitary
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171
Q

What does the plasma GH level need to be to exclude acromegaly?

A

<0.4 ng/ml

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172
Q

What is the diagnostic test for acromegaly?

A

Oral glucose tolerance test - failure of glucose to suppress serum GH

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173
Q

What are the treatment options for acromegaly?

A
  1. Transsphenoidal surgical resection
  2. Radiotherapy
  3. Medical therapy
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174
Q

Give 3 potential complications of transsphenoidal surgical resection for the treatment of acromegaly

A
  1. Hypopituitarism
  2. Diabetes insidious
  3. Haemorrhage
  4. CNS injury
  5. Meningitis
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175
Q

What does the success of pituitary surgery depend on?

A

Size of the tumour and surgeon

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176
Q

What type of radiotherapy is usually used to treat acromegaly?

A

Stereotactic radiotherapy - highly specific so less radiation to surrounding tissues

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177
Q

What types of medical therapy can be used to treat acromegaly?

A

Dopamine agonists - Cabergoline
Somatosatin analogues - octreotide/ianreotide
GH receptor antagonists - pegvisomant

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178
Q

Give 3 advantages of using dopamine agonists in the treatment of acromegaly

A
  1. No hypopituitarism
  2. Oral administration
  3. Rapid onset
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179
Q

Give 2 disadvantages of dopamine agonists in the treatment of acromegaly using

A
  1. Can be ineffective

2. Risk of side effects

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180
Q

Name a dopamine agonist that can be used as a treatment for acromegaly

A

Cabergoline

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181
Q

Why can somatostatin analogues be used in the treatment of acromegaly?

A

They inhibit GH release

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182
Q

Why can GH receptor antagonists be used in the treatment of acromegaly?

A

They suppresses IGF-1

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183
Q

What is prolactinoma?

A

Lactotroph cell tumour of the pituitary

Prolactin secreting tumour

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184
Q

Name the 2 types of prolactinoma

A
  1. Microprolactinoma = most common, >90%

2. Macroprolactinoma = >10mm

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185
Q

Describe the epidemiology of prolactinoma

A

Incidence is 10/100,000
Prevalence is 90/100,000
Women > men

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186
Q

Give 3 causes of prolactinoma

A
  1. Pituitary adenoma
  2. Anti-dopaminergic drugs
  3. Head injury
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187
Q

Give 6 signs of prolactinoma

A
  1. Infertility
  2. Galactorrhoea
  3. Amenorrhoea
  4. Loss of libido
  5. Hypogonadism
  6. Visual field defects and headaches due to local effect of tumour
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188
Q

Briefly describe the pathophysiology of Prolactinoma

A

Increased release of prolactin can cause galactorrhoea and can inhibit FSH and LH

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189
Q

What test do you do to diagnose prolactinoma?

A

Measure serum prolactin

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190
Q

What is the treatment for prolactinoma?

A

Dopamine agonists - cabergoline, bromocriptine
- remarkable shirked with macro adenoma
Occasionally transsphenoidal pituitary resection

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191
Q

What is Cushing’s Syndrome?

A

Chronic, excessive and inappropriate elevated levels of circulating plasma glucocorticoids (cortisol)

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192
Q

What is Cushing’s Disease?

A

When Cushing’s syndrome is caused by a pituitary tumour so excess glucocorticoids due to inappropriate ACTY secretion

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193
Q

Give 8 signs/symptoms go Cushing’s disease

A
  1. Central obesity
  2. Moon face
  3. Hypertension
  4. Skin thinning and bruising
  5. Abdominal striae
  6. Mood changes - depression, lethargy, irritability
  7. Osteoporosis
  8. Muscle wasting
  9. Weight gain
  10. Gonadal dysfunction
  11. Immune dysfunction
  12. Acne
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194
Q

What can cause Cushing’s syndrome?

And are they ACTH dependent or independent?

A
  1. Adrenal tumour (adenoma or carcinoma) = ACTH independent
  2. Exogenous steroid (excess glucocorticoid administration) = ACTH independent
  3. Pituitary tumour (causes excess ACTH production) = ACTH dependent
  4. Ectopic ACTH syndrome (too much ACTH stimulating too much Cortisol) = ACTH dependent
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195
Q

What is a differential diagnosis of Cushing’s syndrome?

A

Pseudo-Cushing’s = excessive alcohol consumption can mimic the clinical and biochemical signs but resolved on alcohol recession

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196
Q

Describe the epidemiology of Cushing’s syndrome

A

10/1,000,000
Higher incidence in Diabetes
2/3 cases are Cushing’s disease

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197
Q

How can you diagnose Cushing’s syndrome?

A
  1. Overnight dexamethasone suppression test - failure to suppress cortisol
  2. Late night salivary cortisol - loss of circadian rhythm so cortisol is raised
  3. Urinary free cortisol = raised
  4. Loss of circadian rhythm
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198
Q

How does a dexamethasone suppression test work?

A

Give synthetic steroids that suppress pituitary and adrenals and then measure the cortisol
In Cushing’s there is no suppression of cortisol

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199
Q

What happens after a official diagnosis of Cushing’s syndrome has been made?

A

Figure out if it is ACTH dependent or independent

CT and MRI of adrenals and pituitary

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200
Q

What is the treatment for Cushing’s syndrome?

A

Tumours = surgical removal

Drugs to inhibit cortisol synthesis - metyrapone, ketoconazole

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201
Q

What are some complications associated with Cushing’s Syndrome?

A

Hypertension
Obesity
Death

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202
Q

What is the circadian system?

A

Body clock that regulates your body

Clear rhythm of cortisol production follows circadian rhythm

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203
Q

When do cortisol levels peak?

A

At around 8:30 am

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204
Q

What’s the primary cue that synchronises an organism’s biological rhythms?

A

Light

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205
Q

What is adrenal insufficiency?

A

Adrenocortical insufficiency resulting in a reduction of mineralocorticoids, glucocorticoids and androgens

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206
Q

Name the 3 types of adrenal insufficiency

A
  1. Primary - Addison’s disease (adrenal glands not working)
  2. Secondary - Hypopituitarism (lack of ACTH)
  3. Tertiary - Suppression of HPA due to presence of exogenous glucocorticoids
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207
Q

Give 5 primary causes of adrenal insufficiency

A
  1. Addison’s disease (autoimmune destruction of the adrenal cortex)
  2. Congenital adrenal hyperplasia (CAH)
  3. TB
  4. Adrenal metastases
  5. Drugs
  6. Haemorrhage
  7. Infection
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208
Q

Give 6 symptoms of adrenal insufficiency

A
  1. Tanned - pigmentations
  2. Fatigue
  3. Tearful
  4. Weight loss
  5. Headaches
  6. Abdominal cramps
  7. Myalgia
  8. Poor recovery from illness
  9. Adrenal crisis
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209
Q

What is the treatment for adrenal insufficiency?

A

Hormone replacement - any steroids - hydrocortisone

In Primary adrenal insufficiency (Addison’s disease) replace aldosterone with fludrocortisone

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210
Q

Give 3 secondary causes of adrenal insufficiency

A
  1. Hypopituitarism
  2. Withdrawal from long term steroids
  3. Infiltration
  4. Infection
  5. Radiotherapy
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211
Q

What biochemical investigations might you do in someone who you suspect has adrenal insufficiency?

A

0900 Cortisol and ACTH
Renin = elevated in primary
U+E (decrease sodium, increase potassium due to decrease aldosterone - increase in calcium and urea)
Synacthen test - > 450 nmol/L = AI unlikely

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212
Q

What results of cortisol and ACTH tests suggest adrenal insufficiency is likely?

A

Cortisol >500 nmol/L = AI unlikely
Cortisol <100 nmol/L = AI likely
ACTH > 22 ng/L = primary
ACTH < 5 ng/L = secondary

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213
Q

What investigations would you do to determine whether Adrenal insufficiency is primary or secondary?

A 
Primary = adrenal antibodies, very long chain fatty acids, imaging and genetics 
Secondary = any steroids?, imaging and genetics
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214
Q

Adrenal crisis is a common presentation of adrenal insufficiency. Give 6 features of an adrenal crisis

A
  1. Hypotension
  2. Fatigue
  3. Fever
  4. Hypoglycaemia
  5. Hyponatreamia
  6. Hyperkalameia
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215
Q

What is the management of adrenal crisis?

A

Immediate Hydrocortisone 100mg
Fluid resuscitation - saline (IV)
Hydrocortisone 50-100 mg 6 hourly
In primary start fludocortisone

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216
Q

What would sodium and potassium levels be in someone with adrenal insufficiency?

A

Hyponatraemia = low sodium
Hyperkalaemia = high potassium
Lack of aldosterone and so less sodium reabsorbed and less potassium excreted

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217
Q

Give a sign of Cushing’s syndrome that is due to impairments in carbohydrate metabolism

A

Diabetes Mellitus

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218
Q

Give a sign of Cushing’s syndrome that is due to electrolyte disturbances

A
  1. Sodium retention

2. Hypertension

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219
Q

People with Cushing’s syndrome may have immune dysfunction. Give a consequence of this

A

Increased susceptibility to infection

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220
Q

Why is it important to take a drug history when speaking to someone with potential Cushing’s?

A

To exclude exogenous glucocorticoid exposure as a potential cause

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221
Q

When might you see signs of hypercortisolism without Cushing’s Disease?

A
  1. Pregnancy
  2. Depression
  3. Alcohol dependence
  4. Obesity
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222
Q

Briefly describe the mechanism of thyroid destruction

A

Cytotoxic (CD8+) T cell mediated
thyroglobulin and Thyroid peroxidase (TPO) antibodies may cause secondary damage (alone have no effect)
Antibodies against the TSH receptor may block the effect of TSH (uncommon)

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223
Q

What are the main 3 types of cells that cause thyroid destruction?

A
  1. Cytotoxic T cells
  2. Thyroglobulin
  3. TPO antibodies
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224
Q

Briefly describe the pathophysiology of Grave’s disease

A

Autoimmune disease
TSH receptor antibodies stimulate thyroid hormone production
Leads to hyperthyroidism
High circulating levels of thyroid hormone, with a low TSH

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225
Q

Give 5 Gravers opthlmopathy signs

A
  1. Exophthalmos eyes (bulging)
  2. Lid lag stare
  3. Redness
  4. Conjunctivitis
  5. Pre-orbital oedema
  6. Bilateral
  7. Extra ocular muscle swelling
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226
Q

Give 5 symptoms of Grave’s disease that don’t include opthalmopathy signs

A
  1. Weight loss
  2. Increased appetite
  3. Irritable
  4. Tremor
  5. Palpitations
  6. Goitre
  7. Diarrhoea
  8. Heat intolerance
  9. Malaise
  10. Vomiting
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227
Q

Give 5 signs of Grave’s disease that don’t include opthalmopathy signs

A
  1. Tachycardia
  2. Arrhythmias (e.g. AF)
  3. Warm peripheries
  4. Muscle spasm
  5. Pre-tibial myxoedema (raised purple lesions over the shins)
  6. Thyroid acropachy (clubbing and swollen fingers)
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228
Q

Name 5 risk factors for Graves disease

A
  1. Female
  2. Genetic association
  3. E.coli
  4. Smoking
  5. Stress
  6. High iodine intake
  7. Autoimmune diseases
229
Q

Name 5 autoimmune diseases associated with thyroid autoimmunity

A
  1. T1DM
  2. Addison’s disease
  3. Pernicious anaemia
  4. Vitiligo
  5. Alopecia areata
  6. Rheumatoid arthritis
230
Q

What would you see histological in someone with Graves disease?

A

Lymphocyte infiltration and thyroid follicle destruction

231
Q

What is goitre?

A

Palpabel and visible thyroid enlargement

232
Q

Why does goitre occur and when is is most commonly found?

A

Due to TSH receptor stimulation resulting in thyroid growth

Seen in hypo and hyperthyroidism

233
Q

Name 4 types of sporadic non toxic goitre

A
  1. Diffuse –> physiological –> Graves
  2. Multi nodular
  3. Solitary nodule
  4. Dominant nodule
234
Q

Define hyperthyroidism

A

Overactivity of the thyroid gland

235
Q

Define thyrotoxicosis

A

Excess of thyroid hormone in the blood (can be used interchangeably with hyperthyroidism)

236
Q

Name the 3 mechanisms of how hyperthyroidism may come about

A
  1. Overproduction of thyroid hormone
  2. Leakier of preformed hormone from the thyroid
  3. Ingestion fo excess thyroid hormone
237
Q

Give 5 causes of hyperthyroidism

A
  1. Grave’s disease
  2. Toxic adenoma
  3. Toxic multi nodular goitre
  4. Ectopic thyroid tissues (metastases)
  5. Drugs
  6. De quervain’s thyroiditis
238
Q

Name 4 drugs which can induce hyperthyroidism

A
  1. Iodine
  2. Amiodarone
  3. Lithium
  4. Radioconstrast agents
239
Q

Give 6 clinical signs feature of hyperthyroidism

A
  1. Weight loss
  2. Tachycardia
  3. Hyperphagia
  4. Anxiety
  5. Exophthalmos
  6. Tremor
  7. Heat intolerance
240
Q

What investigations are done to diagnose hyperthyroidism?

A 
Thyroid function tests 
Diagnosis of underlying cause 
Clinical history, physical signs 
Thyroid antibodies 
Isotope uptake scan
241
Q

What are the realist so thyroid function rests in primary hyperthyroidism?

A

Increase in T4 and T3 with low levels of TSH (due to negative feedback)

242
Q

What are the realist so thyroid function rests in secondary hyperthyroidism?

A

Increase in T4 and T3 but inappropriately high TSH

243
Q

What are the 4 main treatments for hyperthyroidism?

A
  1. Beta blockers
  2. Anti-thyroid drugs
  3. Radioiodine
  4. Surgery - partial/total thyroidectomy
244
Q

Why are beta blockers used?

A

For rapid control of symptoms

245
Q

Give examples of anti-thyroid drugs and why are they used?

A

Carbimazole, methimazole, proplythiouracil (PTU) - (thionamides)
Decreases synthesis of new thyroid hormone by targeting thyroid peroxidase
PTU also inhibits conversion of T4 to T3

246
Q

What are the 2 strategies of treatment using anti-thyroid drugs?

A
  1. Thionamides titration regime

2. Block and replace regime with T4 for Graves

247
Q

Give 4 poor prognostic factors of those on anti-thyroid drugs

A
  1. Severe biochemical hyperthyroidism
  2. Large goitre
  3. Male
  4. Young age of disease onset
248
Q

Give 5 side effects of anti-thyroid drugs

A
  1. Rash
  2. Arthralgia
  3. Hepatitis
  4. Neuritis
  5. Vasculitis
  6. Agranulocytosis - very serious
249
Q

Why can radioiodine be used as a treatment for hyperthyroidism?

A

Emit beta particle that destroy thyroid follicle and therefore reducing the production fo thyroid hormones

250
Q

What are 4 long term dose effects fo radioiodine treatment?

A
  1. Shorter cell survival
  2. Impaired replication of cells
  3. Atrophy and fibrosis
  4. Chronic inflammation resembling Hashimoto’s
  5. Late hypothyroidism
251
Q

Give 4 potential consequences of a partial thyroidectomy

A
  1. Bleeding
  2. Hypoglycaemia
  3. Hypothyroidism
  4. Recurrent laryngeal nerve palsy
252
Q

What is a complication of hyperthyroidism?

A

Thyroid crisis/storm

253
Q

Briefly explain thyroid crisis/storm

A

Rapid deterioration of thyrotoxicosis
Hyperpyrexia, tachycardia and extreme restlessness
Delirium –> coma –> death

254
Q

What is the treatment for a thyroid crisis?

A

Large doses of oral carbimazole, oral propranolol, oral potassium iodide and IV hydrocortisone

255
Q

Define hypothyroidism

A

Under-activity of the thyroid gland

256
Q

Name the 3 types of hypothyroidism

A
  1. Primary - absence/dysfunction of thyroid gland
  2. Secondary - reduced TSH from anterior pituitary
  3. Tertiary - associated with treatment withdrawal
257
Q

Briefly describe the pathophysiology of primary hypothyroidism

A

Aggressive destruction of thyroid cells by various cell and antibody mediated immune processed
Antibodies bind and block TSH receptors
Inadequate thyroid hormone production and secretion

258
Q

Briefly describe the pathophysiology of secondary hypothyroidism

A

Reduced release or production of TSH so reduced thyroid hormone release

259
Q

Briefly describe the pathophysiology of tertiary hypothyroidism

A

Thyroid gland overcompensates until it can reestablish correct concentration fo thyroid hormone

260
Q

Name 4 causes of primary hypothyroidism

A
  1. Autoimmune thyroiditis - Hashimoto’s
  2. Post partum thyroiditis
  3. Post thyroidectomy
  4. Drug induced
  5. Iodine deficiency
  6. Primary atrophic hypothyroidism
261
Q

Give 2 examples of iatrogenic causes of hypothyroidism

A
  1. Thyroidectomy

2. Radioiodine therapy

262
Q

Give an example of a transient cause of primary hypothyroidism

A

Post-partum thyroiditis

263
Q

Name 4 drugs that can cause hypothyroidism

A
  1. Carbimazole (used to treat hyperthyroidism)
  2. Amiodarone
  3. Lithium
  4. Iodine
264
Q

Name 3 casques of secondary hypothyroidism

A
  1. Hypopituitarism
  2. Hypothalamic disease
  3. Isolated TSH deficiency
265
Q

Why can amiodarone cause both hypo and hyperthyroidism?

A

Because it is iodine rich

266
Q

Give 5 symptoms of hypothyroidism

A
  1. Goitre
  2. Weight gain
  3. Menorrhagia
  4. Malar flush
  5. Cold intolerance
  6. Energy level fall
  7. Depression
267
Q

Give 5 signs of hypothyroidism

A

BRADYCARDIC

  1. Bradycardia
  2. Reflexes relax slowly
  3. Ataxia (cerebellar)
  4. Dry, thin hair/skin
  5. Yawning/drowsy/coma
  6. Cold hands
  7. Ascites
  8. Round puffy face
  9. Defeated demeanor
  10. Immobile
  11. Congestive cardiac failure
268
Q

What investigations are conducted to diagnose hypothyroidism?

A

Thyroid function tests

Thyroid antibodies

269
Q

What are the TFT results for primary hypothyroidism?

A

High TSH

Low T4 and T3

270
Q

What are the TFT results for secondary hypothyroidism?

A

Inappropriately low TSH for low T4 and T3

271
Q

Name 3 antibodies that may be present in the serum in someone with autoimmune thyroiditis

A
  1. TPO (thyroid peroxidase)
  2. Thyroglobulin
  3. TSH receptor
272
Q

What is the treatment for primary hypothyroidism?

A

Thyroid hormone replacement - levothyroxine

Resection of obstructive goitre

273
Q

Name a complication of hypothyroidism

A

Myxoedema coma

274
Q

Briefly explain a myxoedema coma

A

Severe hypothyroidism
Reduced level of consciousness, seizures, hypothermia
IV/oral T3 and glucose infusion needed

275
Q

What is Hashimoto’s thyroiditis?

A

Hypothyroidism due to aggressive destruction of thyroid cells

276
Q

Give 3 symptoms of Hashimoto’s thyroiditis

A
  1. Rapid formation of Goitre
  2. Dyspnoea or dysphagia
  3. General hypothyroidism symptoms
277
Q

Name 3 triggers of Hashimoto’s thyroiditis

A
  1. Iodine
  2. Infections
  3. Smoking
  4. Stress
278
Q

What diagnostic test are conducted for Hashimoto’s thyroiditis?

A

TFTs - high TSH

Thyroid antibodies - high TPO antibodies

279
Q

What is the treatment for Hashimoto’s thyroiditis?

A

Levothyroxine

Resection fo obstructive goitre

280
Q

Name a complication fo Hashimoto’s thyroiditis

A

Hyperlipidaemia

281
Q

What is a sequelae to Hashimoto’s thyroiditis?

A

Hashimoto’s encephalopathy

282
Q

What disease would you treat with Carbimazole?

A

Hyperthyroidism/Graves disease

283
Q

What disease would you treat with Levothyroxine?

A

Hypothyroidism

284
Q

Give 5 metabolic changed that occur in pregnancy

A
  1. Increase erythropoietin, cortisol and noradrenaline
  2. High cardiac output
  3. High cholesterol and triglycerides
  4. Pro thrombotic and inflammatory state
  5. Insulin resistance
  6. Plasma volume expansion
285
Q

Give 5 gestational syndromes

A
  1. Pre-eclamsia
  2. Gestational diabetes
  3. Obstetric cholestasis
  4. Gestational thyrotoxicosis
  5. Postnatal depression
  6. Post partum thyroiditis
286
Q

At what week are foetal thyroid follicles and T4 synthesised?

287
Q

Why can hCG activate TSH receptors and cause hyperthyroidism?

A

hCG and TSH are glycoprotein hormones with very similar structure
hCG can therefore activate TSH receptors

288
Q

Is hypothyroidism or thyrotoxicosis more common in pregnancy?

A

Hypothyroidism is more common in pregnancy

289
Q

How can you differentiate between Grave’s disease and gestational thyrotoxicosis?

A

Graves - symptoms predate pregnancy, symptoms are severe during pregnancy, goitre and TSH-R antibodies present
Gestational thyrotoxicosis - symptoms do not predate pregnancy, lots of N/V - hyperemesis gravid arum associated. No goitre or TSH-R antibodies

290
Q

Give 4 potential consequences of untreated hypothyroidism in pregnancy

A
  1. Gestational hypertension
  2. Placental abruption
  3. Post partum haemorrhage
  4. Low birth weight
291
Q

Give 4 potential consequences of untreated hyperthyroidism in pregnancy

A
  1. Intrauterine growth restriction
  2. Low birth weight
  3. Pre-eclampsia
  4. Preterm delivery
292
Q

What pregnant women do you screen for risk of hypothyroidism in their pregnancy?

A 
Age >30 
BMI >40 
Miscarriage 
Personal or FH
Goitre 
Anti TPO
T1DM
Amiodarone, lithium or contrast use
293
Q

What type of receptor does vasopressin bind to?

A

G-protein couples transmembrane domain receptors
V1a - vasculature
V1b - pituitary
V2 - renal collecting ducts

294
Q

What is the release of vasopressin controlled by?

A

Osmoreceptors in hypothalamus - day to day

baroreceptors in brainstem and great vessels - emergency

295
Q

How much of the human body is fluid?

296
Q

How much water makes up the:

a) ECF
b) ICF

A

a) 14 L - 10.5L interstitial, 3.5L intravascular

b) 28L

297
Q

What is the primary cation in ICF?

298
Q

What is the primary cation in the ECF?

299
Q

What are the primary anions in the ECF?

A

Cl- and HCO3-

300
Q

What are the units for osmolality?

301
Q

Define osmolality

A

Concentration of all solutes per kilogram of water in plasma

302
Q

What is the effect of water excess on thirst and ADH secretion?

A

Decreased thirst and decreased ADH

Reduced intake and increased excretion

303
Q

What is the effect of water deficit on thirst and ADH secretion?

A

Increased thirst and increased ADH

Increase water intake and reduced secretion

304
Q

What GPCR does ADH bind to on renal tubules?

305
Q

What is the volume of insensible losses?

A

500 ml/day

306
Q

Briefly describe the thirst axis

A

Water deficit causes secretion of ADH which acts on principal cells of CDs
ADH binds to adenyl cyclase couple V2R
Kinase action results in insertion of aquaporin 2 channels in apical membrane of CD
Increased water permeability so increase water absorption

307
Q

Give an equation for plasma osmolality

A

Plasma osmolality = 2[Na+] + [glucose] + [urea]

308
Q

What is the range for normal osmolality?

A

282-295 mOsmol/kg

309
Q

Name 3 disease associated with the posterior pituitary

A
  1. Cranial diabetes insipidus - lack of ADH
  2. Nephrogenic diabetes insipidus - resistance to action of ADH
  3. Syndrome of antidiuretic hormone secretion - too much ADH release inappropriately
310
Q

Define diabetes insipidus

A

Passage of large volumes (>3L/day) of dilute urine due to impaired water reabsorption in the kidney due to hypo secretion or insensitivity to ADH

311
Q

Name the 2 types of DI

A
  1. Cranial DI = hyposecretion

2. Nephrogenic DI = insensitivity

312
Q

Give 5 signs of DI

A
  1. Excessive urine production - >3L/day (polyuria)
  2. Severe thirst (polydipsia)
  3. Very dilute urine - <300 mOsmol/Kg
  4. Hypernatraemia
  5. Dehydration
313
Q

Give 4 causes of cranial DI

A
  1. Tumours
  2. trauma
  3. Infections
  4. Idiopathic
  5. Genetic - mutations in ADH gene
314
Q

Give 4 causes of nephrogenic DI

A
  1. Osmotic diuresis (DM)
  2. Drugs
  3. CKD
  4. Metabolic - hypercalcaemia, hypokalaemia
  5. Genetic - mutation in ADH receptor
315
Q

Give 3 possible differential diagnosis’s of DI

A
  1. DM
  2. Hypokalaemia
  3. Hypercalcaemia
316
Q

What investigations might you do to determine whether someone has diabetes insipidus?

A
  1. Measure 24hr urine volume - >3L/day = suggests DI
  2. Plasma biochemistry - hypernatraemia
  3. Water deprivation test - urine will not concentrate when asked nor to drink
  4. U+Es - confirm it isn’t a more common causes of polyuria
  5. MRI of hypothalamus - confirm cranial DI
317
Q

What is the treatment for cranial DI?

A

Treat underlying condition
Thiazide diuretics, carbamazepine, chlorpropamide - sensitise renal tubules to endogenous vasopressin
Desmopressin - high activity at V2 receptor

318
Q

What is the treatment for nephrogenic DI?

A

Free access to water
Very high dose desmopressin
Treatment of causes
Thiazide diuretics - offset water losses
NSADs - inhibits prostaglandin synthesis which locally inhibit ADH action

319
Q

Do you have hyponatraemia or hypernatraemia in diabetes insipidus?

A

Hypernatraemia

320
Q

Give 4 causes of polyuria

A
  1. Hypokalaemia
  2. Hypercalcaemia
  3. Hyperglycaemia
  4. Diabetes insipidus
321
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion
Continuous ADH secretion inspire of plasma hypotonicity, leading to retention of water and excess blood volume and thus hyponatraemia

322
Q

Give 4 symptoms of SIADH

A
  1. Anorexia
  2. Nausea
  3. Malaise
  4. Headache
  5. Confusion
  6. Fits and coma with severe hyponatraemia
323
Q

Give 4 causes of SIADH

A
  1. Disordered hypothalamic pituitary secretion or ectopic production of ADH
  2. Malignancy
  3. CNS disorders - meningitis, brain tumour, cerebral haemorrhage
  4. TB
  5. Pneumonia
  6. Drugs
324
Q

Describe 5 features of the essential criteria for SIADH

A
  1. Hyponatraemia - <135 mol/L)
  2. Plasma hypo-osmolality - <275 mOsmol/Kg
  3. High urine osmolality
  4. Clinical euvolaemia
  5. Increased urinary sodium excretion with normal salt and water intake
325
Q

Name 3 diseases you must exclude in someone you suspect could have SIADH

A
  1. Renal disease
  2. Hypothyroidism
  3. Hypocortism
  4. Recent diuretic use
326
Q

Describe the treatment for SIADH

A
  1. Restrict fluid - <1L/day
  2. Give salt
  3. Loop diuretics - furosemide
  4. ADH-R antagonists - vaptans - primate water excretion with no loss of electrolytes
  5. Demeoclocycline - inhibitor of ADH
327
Q

How do you treat asymptomatic SIADH?

A

Fluid restriction

328
Q

How do you treat very symptomatic SIADH?

A

Give 3% saline (hypertonic)

329
Q

Would you expect a patient with SIADH to be hypovolaemic, euvolaemic or hypervolaemic?

A

Euvolaemic

330
Q

Would you associate SIADH with hyponatraemia or hypernatraemia?

A

Hyponatraemia - <135 mmol/L

331
Q

Would you associate SIADH with plasma hypo-osmolality or hyper-osmolality?

A

Plasma hypo-osmolality - <275 mOsmol/Kg

332
Q

Would you associate SIADH with a high to low urine osmolality?

A

High urine osmolality

333
Q

Define hyponatraemia

A

<135 mmol/L

Biochemically severe = serum sodium <125 mmol/L

334
Q

Give 4 signs of hyponatraemia

A
  1. Anorexia
  2. Confusion
  3. Headache
  4. Lethargy
  5. Weakness
335
Q

Give 4 causes of hyponatraemia

A
  1. SIADH
  2. Sodium deficiency
  3. Renal failure
  4. Malignancy
336
Q

Give 4 ways in which you can classify hyponatraemia

A
  1. Biochemical - mild, moderate, severe
  2. Symptoms - mild, moderate, severe
  3. Aetiology - hypovolaemic, euvolaemic, hypervolaemic
  4. Acuity of onset - Acute (<48hrs), Chronic
337
Q

What is the treatment for acute hyponatraemia?

A

Give a bolus dose of saline

338
Q

What stimulates the posterior pituitary to release ADH?

A

Osmoreceptors in the hypothalamus detect raised plasma osmolality
Posterior pituitary is signalled to release ADH

339
Q

Name the suprasellar neoplasm that can result from benign cysts and calcification of Rathke’s pouch

A

Craniopharyngioma

340
Q

Give 4 signs of Craniopharyngioma

A
  1. Raised ICP
  2. Visual disturbances
  3. Growth failure
  4. Puberty affected - pituitary hormone deficiency
  5. Weight gain
341
Q

Give 4 signs of Rathke’s Cyst

A
  1. Headache
  2. Amenorrhoea
  3. Hypopituitarism
  4. Hydrocephalus
342
Q

Give 4 local effects a pituitary adenoma

A
  1. Headaches
  2. Visual field defects - bitemporal hemianopia
  3. Cranial nerve palsy and temporal lobe epilepsy
  4. CSF rhinorrhoea
343
Q

What investigations are done when pituitary dysfunction is suspected?

A

Hormonal tests

If hormonal tests are abnormal or tumour mass effect perform MRI pituitary

344
Q

What do you test the thyroid axis for in pituitary disease?

A

Measure Free T4 and TSH

345
Q

What is the affect of hypothyroidism on TSH and T4 levels?

A

TSH high

T4 low

346
Q

What is the effect of hypopituitarism on TSH and T4 levels?

A

TSH low

T4 low

347
Q

What is the affect of hyperthyroidism on TSH and T4 levels?

A

TSH low

T4 high

348
Q

What do you test the gonadal axis for in pituitary disease?

A

Measure 0900h fasted testosterone and LH/FSH

349
Q

What is the effect of primary hypogonadism on testosterone and FSH/LH levels?

A

Testosterone low

FSH/LH high

350
Q

What is the effect of hypopituitarism on testosterone and FSH/LH levels?

A

Testosterone low

FHS/LH low

351
Q

When should serum testosterone be measure?

A

At 9am due to circadian rhythm

352
Q

Are the levels of oestradiol and FSH/LH low or high before puberty?

A

Very low levels in serum

353
Q

What is the effect of primary ovarian failure on oestradiol and FSH/LH levels?

A

FSH/LH high

Oestradiol low

354
Q

What is the effect of hypopituitarism on oestradiol and FSH/LH levels?

A

FSH/LH low

Oestradiol low

355
Q

What do you test the HPA axis for in pituitary disease?

A

Measure 9am cortisol and synacthen

356
Q

What is the effect of primary adrenal insufficiency on cortisol and ACTH levels and response to synacthen test?

A

Cortisol low
ACTH high
Synacthen - poor response

357
Q

What is the effect of hypopituitarism on cortisol and ACTH levels and response to synacthen test?

A

Cortisol low
ACTH low
Synacthen - poor response

358
Q

What do you test the GH/IGF1 axis for in pituitary disease?

A

Perform IGF-1 and GH stimulation test

Insulin stress test and glucagon test

359
Q

What can lead to elevated levels of prolactin?

A
  1. Stress
  2. Drugs
  3. Pressure on pituitary stalk
  4. Prolactinoma
360
Q

Why is dynamic hormone testing used?

A

Dynamic stimulation or suppression test may be useful in select cases to further evaluate pituitary reserve and/or for pituitary hyper function

361
Q

What is the best radiological evaluation for the pituitary?

A

MRI - better visualisation fo soft tissue and vascular structures

362
Q

T1DM can be associated with autoimmunity. What 4 antibody tests are conducted to try and diagnose this?

A
  1. ANti GAD
  2. Pancreatic islet cell antibodies
  3. Islet antigen-2 antibodies
  4. ZnT8
363
Q

What do free fatty acids do?

A

Impair glucose uptake
Transported to liver –> gluconeogenesis
Oxidised to form ketone bodies

364
Q

Name 3 ketone bodies

A
  1. Beta hydroxybutyrate
  2. Acetoacetate
  3. Acetone
365
Q

Does diabetic ketoacidosis occur in T1 or T2 DM?

366
Q

Describe the triad of DKA

A
  1. Hyperglycaemia - blood glucose >11 mmol/L
  2. Acidaemia - blood pH <7.3 or plasma bicarbonate <15 mmol/L
  3. Raised plasma ketones - urine ketones >2+
367
Q

Give 4 causes of DKA

A
  1. Unknown
  2. Infection
  3. Treatment error - not administering enough insulin
  4. Having undiagnosed T1DM
368
Q

Give 5 symptoms of DKA

A
  1. Polyuria
  2. Polydipsia
  3. Weight loss
  4. Nausea and vomiting
  5. Confusion
  6. Weakness
369
Q

Give 3 signs of DKA

A
  1. Hyperventilation
  2. Dehydration
  3. Hypotension
  4. Tachycardia
  5. Coma
370
Q

What is the treatment for DKA

A

Rehydration (3L in first 3 hours)
Insulin
Replacement of electrolytes - K+
Treat underlying cause

371
Q

Give 4 potential complications of untreated DKA

A
  1. Cerebral oedema
  2. Adult respiratory distress syndrome
  3. Aspiration pneumonia
  4. Thromboembolism
  5. Death
372
Q

In what class of drugs does metformin belong?

373
Q

Give an example of a sulfonylurea

A

Tolazamide

Gliclazide

374
Q

What are the physiological defences to hypoglycaemia?

A

Release of glucagon and adrenaline

375
Q

What are the symptoms of hypoglycaemia?

A

Autonomic - sweating, tremor, palpitations
Neuroglycopenic - confusion, drowsiness, incoordination
Severe neuroglycopenic - convulsions, coma

376
Q

Name 3 other types of diabetes other than T1DM, T2DM and DI

A
  1. Maturity onset diabetes of the young (MODY)
  2. Permanent neonatal diabetes
  3. Maternal inherited diabetes and deafness
377
Q

Name 3 exocrine causes of Diabetes

A
  1. Inflammatory - actue/chronic pancreatitis
  2. Hereditary haemochromatosis
  3. Pancreatic neoplasia
  4. Cystic fibrosis
378
Q

Name 3 endocrine causes of Diabetes

A
  1. Acromegaly
  2. Cushing’s syndrome
  3. Peochromocytoma
379
Q

What is Pheochromocytoma?

A

A rare catecholamine secreting tumour in the adrenal medulla (chromatin cells)

380
Q

Name the 2 types of pheochromocytoma

A
  1. Familial type - more NAd

2. Sporadic - more Ad

381
Q

Give 6 symptoms of pheochromocytoma

A
  1. Headache
  2. Sweating
  3. Tachycardia
  4. Hypertension
  5. Palpitations
  6. Tremor
  7. Anxiety
  8. Nausea/vomiting
  9. Confusion
382
Q

What investigations might you do in order to diagnose someone with pheochromocytoma?

A

Bloods - raised WCC, increased plasma metadrenaline and normetadrenaline
24hr urine collecting for urinary catecholamine and metabolites (metanephrines)

383
Q

What is the treatment for pheochromocytoma?

A
  1. Alpha blocker - phenoxybenzamine
  2. Beta blockers
  3. Surgery resection of tumour
384
Q

What is the major complication of surgery on a patient with a pheochromocytoma?

A

Can stoke out during surgery due to rapid effect of adrenaline on the BP

385
Q

What is the major concern in someone with pheochromocytoma?

A

Dangerous cause of hypertension

386
Q

17 year old man presents with intermittent headaches and anxiety. He is sweating and vomiting. His BP is 223/159 and his pulse is 115. What is the likely cause?

A

Phaeochromocytoma crisis

Hypertension and tachycardia = phaeochromocytoma until proved otherwise (especially in younger patients)

387
Q

What is the management of a phaeochromocytoma crisis?

A

Non-competitive alpha-blocker e.g. phenoxybenzamine
Excision of paraganglioma
Biochemistry: measure plasma and serum metanephrines

388
Q

What are the 3 main sites where microvascular complications of Diabetes cause particular damage?

A
  1. Retina = retinopathy
  2. Glomerulus = nephropathy
  3. Nerve sheath = neuropathy
389
Q

How long after a young patient has been diagnosed do microvascular complications start to manifest?

A

10-20 years after diagnosis

390
Q

Give 5 risk factors for diabetic retinopathy

A
  1. Long duration DM
  2. Poor glycaemic control
  3. Hypertensive
  4. On insulin treatment
  5. Pregnancy
  6. High HbA1c
391
Q

Describe the pathophysiology of diabetic retinopathy

A

Micro-aneurysms –> pericyte loss and protein leakage –> occlusion –> ischaemia

392
Q

How can diabetic retinopathy be sub-divided?

A 
R1 = non-proliferative/background
R2 = pre-proliferative 
R3 = Proliferative
393
Q

What would you see in someone with an R1 retinopathy grade?

A

Non-proliferative/background
Micro-aneurysms
Intraretinal haemorrhages
Exudates

394
Q

What would you see in someone with an R2 retinopathy grade?

A

Pre-proliferative
Venous bleeding
Growth of new vessels

395
Q

What would you see in someone with an R3 retinopathy grade?

A

Proliferative

New blood vessel on disc

396
Q

What is the treatment for diabetic retinopathy?

A

Regular screening to assess visual acuity

Laser therapy treats neovascaularisation - doesn’t improve sight but stabilises

397
Q

What are the main risks of laser treatment of diabetic retinopathy?

A

Loss of night vision and peripheral vision

398
Q

What is diabetic maculopathy?

A

Fluid form leaking vessel is cleared poorly in macular area causing macula oedema which distorts and thickens the retina at the macula
Leads to loss of central vision

399
Q

What is the hallmark of diabetic nephropathy?

A

Development of proteinuria and progressive decline in renal function

400
Q

What happens to the glomerular basement membrane in someone with diabetic nephropathy?

A

On microscopy there is thickening of the glomerular basement membrane

401
Q

Give one way in which the presentation of diabetic nephropathy differs between T1 and T2DM

A

T1DM - microalbuminuria develops 5-10 years after diagnosis

T2DM - microalbuminuria is often present at diagnosis

402
Q

Give 2 risk factors for diabetic nephropathy

A
  1. Poor blood pressure

2. Poor blood glucose control

403
Q

Describe the treatment for diabetic nephropathy

A
  1. Glycaemic and BP control
  2. Angiotensin receptor blockers/ACE inhibitors
  3. Proteinuria and cholesterol control
404
Q

What is the commonest form of diabetic neuropathy?

A

Distal symmetrical neuropathy

405
Q

Give 5 risk factors for diabetic neuropathy

A
  1. Poor glycaemic control
  2. Hypertension
  3. Smoking
  4. High HbA1c
  5. Overweight
  6. Long duration DM
406
Q

What do isolated mononeuropathies result from in diabetic neuropathy?

A

Occlusion of vasa nervorum - small arteries that provide blood supply to peripheral nerves

407
Q

Why do more diffuse neuropathies arise in diabetic neuropathy?

A

Accumulation of fructose and sorbitol which disrupts the structure and formation of the nerve

408
Q

Give 3 major clinical consequences of diabetic neuropathy

A
  1. Pain
  2. Autonomic neuropathy
  3. Insensitivity
409
Q

Describe the pain associated with diabetic neuropathy

A

Burning
Paraethesia
Allodynia - triggering of pain from stimuli that doesn’t usually cause pain

410
Q

What is autonomic neuropathy in relation to diabetic neuropathy?

A

Damage to the nerves that supply body structures that regulate function such as BP, HR, bowel/bladder emptying

411
Q

Give 5 signs of autonomic neuropathy in diabetic neuropathy

A
  1. Hypotension
  2. HR affected
  3. Diarrhoea/constipation
  4. Incontinence
  5. Erectile dysfunction
  6. Dry skin
412
Q

What are the consequences of insensitivity as a result of diabetic neuropathy?

A

Insensitivity –> foot ulceration –> infection –> amputation

413
Q

Describe the distribution of insensitivity as a result of diabetic neuropathy

A

Glove and sticking distribution - starts in the toes and moves proximally

414
Q

Describe the treatments for diabetic neuropathy

A
  1. Improve glycaemic control
  2. Antidepressants
  3. Pain relief
415
Q

Give 5 ways in which amputation can be prevented in someone with diabetic neuropathy

A
  1. Screening for insensitivity
  2. Education
  3. MDT foot clinics
  4. Pressure relieving footwear
  5. Podiatry
  6. Revascularisation and antibiotics
416
Q

What are the 4 main threats to skin and subcutaneous tissues in someone with diabetic neuropathy

A
  1. Infections
  2. Ischaemia
  3. Abnormal pressure
  4. Wound environments
417
Q

Would there be increased or decreased pulses in diabetic neuropathic foot?

A

Decreased foot pulses

418
Q

Peripheral vascular disease is a complication of Diabetes. Give 6 signs of acute ischaemia

A
  1. Pulseless
  2. Pale
  3. Perishing cold
  4. Pain
  5. Paralysis
  6. Paraesthesia
419
Q

Name 4 infections poorly controlled diabetes can lead to

A
  1. UTIs
  2. Staphylococcal infection of skin
  3. Mucocutaneous candidiasis
  4. Pyelonephritis
  5. TB
  6. Pneumonia
420
Q

Why does the site of insulin injection need to be varied day to day?

A

Can cause lipohypertrophy if the same site is used everyday

421
Q

Name 4 non insulin treatments for diabetes

A
  1. Metformin
  2. Sulphonylurea
  3. Incretin based agents
  4. Thiazolidinediones (TZDs)
  5. SGLT-2 inhibitors
422
Q

Why is metformin the first line therapy for diabetes?

A

Associated with less weight gain and less hypoglycaemia than insulin and sulfonylurea

423
Q

When is sulfonylurea considered as treatment for diabetes?

A

In individuals:

  • Who are not overweight (as causes weight gain)
  • Require rapid response due to hyperglycaemia symptoms
  • Are unable to tolerate metformin or where metformin is contraindicated
424
Q

How do incretin based agents treat diabetes?

A

Influence glucose homeostasis via:

  • glucose dependent insulin secretion
  • postprandial glucagon suppression
  • slowing gastric emptying
425
Q

Give examples of Thiazolidinediones (TZDs)

A

Rosiglitazone and Pioglitazone

426
Q

How do Thiazolidinediones treat diabetes?

A

Effective glucose lowering agents

427
Q

Define puberty

A

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

428
Q

What is the first sign of puberty in girls?

429
Q

What is the first sign of puberty in boys?

A

First ejaculation, often nocturnal

430
Q

What hormone is responsible for regulating the growth of the breast and female genitalia?

A

Ovarian oestrogen

431
Q

Which hormones are responsible for controlling the growth of pubic and axillary hair in females?

A

Ovarian and adrenal androgens

432
Q

What are the roles of testicular androgen in Male puberty?

A
  1. development of external genitalia
  2. Growth of pubic and axillary hair
  3. Deepening of voice
433
Q

What scale is used to describe the physical development based on external sex characteristics?

A

Tanner scale

434
Q

Give 5 consequences of androgen deficiency in a male

A
  1. Loss of libido
  2. High pitched voice
  3. Loss of facial, axillary, limb and pubic hair
  4. Loss of erections
  5. Poorly developed scrotum and penis
435
Q

What is thelarche?

A

Breast development

436
Q

What hormone is thelarche controlled by and how long is thelarche?

A

Controlled by oestrogen and is completed in about 3 years

437
Q

Describe the 3 stages of thelarche

A
  1. Ductal proliferation
  2. Site specific adipose deposition
  3. Enlargement of areola and nipple
438
Q

What are the main differences between a prepubertal and adult uterus?

A 
Prepubertal = tubular shape 
Adult = Pear shape with a thicker endometrium
439
Q

What is adrenarche?

A

Maturation of the adrenal gland - the development of the zone reticular cells
Peri-pubertal adrenal androgen production

440
Q

Give 2 signs of adrenarche

A
  1. Body odour

2. Mild acne

441
Q

What is pubarche?

A

Growth of pubic hair

442
Q

What is precocious puberty?

A

Onset of secondary sexual characteristics before 8 (girl) or 9 (boy) years old

443
Q

What must you rule out as a cause of precocious puberty in boys?

A

Brain tumour

444
Q

What is the treatment for precocious puberty?

A

GnRh super agonist to suppress pulsatility of GnRH secretion

445
Q

What is Precocious pseudopuberty?

A

Secreting tumours leading to hormone excess

446
Q

Name 3 causes of Precocious puberty

A
  1. Idiopathic
  2. CNS tumours
  3. CNS disorders
447
Q

Name 3 causes of Precocious pseudopuberty

A
  1. Increased androgen secretion
  2. Gonadotrophin secreting tumours
  3. Ovarian cyst
  4. Oestrogen secreting neoplasm
448
Q

What is delayed puberty?

A

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

449
Q

Which is the most likely causes of delayed puberty in boys?

A

Constitutional delay - runs in the family, late menarche in mum or delayed growth spurt in father

450
Q

Give 3 consequences of delayed puberty

A
  1. Psychological problems
  2. Reproduction defects
  3. Reduced bone mass
451
Q

Give 5 functional causes of delayed puberty

A
  1. Anorexia
  2. Bulimia
  3. Over exercising
  4. CKD
  5. Drugs
  6. Stress
  7. Sickle cell
452
Q

What investigations might you do in someone with delayed puberty?

A
  1. FBC - red cell count especially
  2. U+Es
  3. LH/FSH measurements
  4. TFTs
  5. Karyotyping for Turners
453
Q

What must you rule our in girls with delayed puberty and short stature?

A 
Turner syndrome (45X)
They might also have recurrent ear infections
454
Q

Name the 3 types of Hypogonadism

A
  1. Primary = Hypergonadotropic hypogonadism
  2. Secondary = Hypogonadotropic hypogonadism
  3. Tertiary = Hypogonadotropic hypogonadism
455
Q

What is Hypergonadotropic hypogonadism?

A

Primary gonadal failure - Testes or ovarian failure

456
Q

Briefly describe the mechanism of Hypergonadotropic hypogonadism

A
  • Gonads not working properly so less oestrogen/testosterone
  • Increase in GnRH as less negative feedback
  • Increase in LH and FSH
  • Hypogonadism occurs
457
Q

Give 2 causes of primary hypogonadism

A

Hypergonadotropic hypogonadism

  1. Klinefelter’s Syndrome (47XXY)
  2. Tuner’s Syndrome (45X)
458
Q

What is the effect of Hypergonadotropic hypogonadism on FSH/LH and oestrogen/testosterone levels?

A 
FSH/LH = high 
Oestrogen/testosterone = low
459
Q

What is Hypogonadotropic hypogonadism?

A

Secondary gonadal failure = problem with pituitary
OR
Tertiary gonadal failure = Problem with hypothalamus

460
Q

Briefly describe the mechanism of secondary hypogonadism

A
  • Less FSH and LH
  • So less activation at gonads
  • Girls = no response to feedback so oestrogen decreases
  • Boys = no response to feedback so testosterone decreases
461
Q

Briefly describe the mechanism of tertiary hypogonadism

A
  • Less GnRH produced
  • So less FSH and LH
  • So less activation at gonads
  • Girls = no response to feedback so oestrogen decreases
  • Boys = no response to feedback so testosterone decreases
462
Q

Give 2 causes of Hypogonadotropic hypogonadism

A
  1. Kallmann’s Syndrome

2. Tumours - craniopharyngiomas, germinomas

463
Q

What is the effect of hypogonadotropic hypogonadism on FSH/LH and oestrogen/testosterone levels?

A 
FSH/LH = low 
Oestrogen/testosterone = low
464
Q

What is the treatment for hypogonadism?

A

Hormone replacement therapy

  • Males = testosterone gel/injections
  • Females = Ethinyl oestradiol or oestrogen (tablet or transdermal), progesterone added once full oestrogen dose reached
465
Q

What is Turner syndrome?

A

Patient is missing an X chromosome - 45X

Primary gonadal failure (hypergonadotropic hypogonadism)

466
Q

Give 3 signs of Turner syndrome

A
  1. Short stature
  2. Delayed puberty
  3. CV and renal malformations
  4. Recurrent otitis media
467
Q

What is Klinefelter’s Syndrome?

A

Male patient has an extra X chromosome - 47XXY

Primary gonadal failure (hypergonadotropic hypogonadism)

468
Q

Give 2 signs of Klinefelter’s Syndrome

A
  1. Azoospermia
  2. Gynaecomastia (enlargement of male breast tissue)
  3. Increased risk of breast cancer
  4. Testicular size <5ml
469
Q

Why might someone with Klinefelter’s Syndrome have fertility problems?

A

Azoospermia - semen contain no sperm

470
Q

Give 4 symptoms of Klinefelter’s Syndrome

A
  1. Reduced pubic hair
  2. Tall stature
  3. reduced IQ
  4. Small testicles <5ml
471
Q

What cancer is someone with Klinefelter’s Syndrome at an increased risk of developing?

A

Breast cancer

472
Q

What syndrome is characterised by a congenital deficiency of GnRH?

A

Kallmann’s Syndrome

473
Q

What is Kallmann’s Syndrome?

A

Congenital deficiency of GnRH

Secondary gonadal figure - hypogonadotropic hypogonadism

474
Q

What must you test in a person who you suspect has Kallmann syndrome?

A

Smell - 75% are anosmia

475
Q

How is Kallmann syndrome inherited?

A

X linked recessive or dominant

476
Q

What is hirsutism?

A

Excess hair growth in women in a male pattern

477
Q

What is the cause of hirsutism?

A

Increased androgen production by the ovaries or adrenal glands
Most commonly polycystic ovary syndrome

478
Q

What diseases are associated with polycystic ovary syndrome?

A
  1. Insulin resistance - T2DM
  2. Hypertension
  3. Hyperlipidaemia
  4. CV disease
479
Q

Give 5 symptoms of polycystic ovary syndrome

A
  1. Amenorrhoea
  2. Oligomenorrhoea
  3. Hirsutism
  4. Acne
  5. Overweight
  6. Infertility
480
Q

What criteria can be used to make a diagnosis of polycystic ovary syndrome?

A

Rotterdam diagnostic criteria

  1. Menstrual irregularity
  2. Clinical or biochemical evidence of hyperandrogenism
  3. Polycystic ovaries on USS
481
Q

Describe the treatment for polycystic ovary syndrome

A
  1. Hirsutism therapy - shaving/waxing excess hair OR oestrogen (e.g. OCP)
  2. Menstrual disturbance therapy - cyclic oestrogen/progesterone
  3. Metformin can improve hyperinsulinaemia and regulates menstrual cycle
482
Q

A 27-year- old woman comes to see you because she is having infrequent periods (oligomenorrhoea). You note, on examination, that she has facial acne and is overweight. What is the most likely diagnosis? Give 3 other signs you might see in this patient

A 
Polycystic ovary syndrome
Other signs: 
1. Hirsutism
2. Amenorrhoea
3. Infertility
483
Q

Give 2 clinical signs of hypervolaemia

A
  1. Ascites

2. Oedema

484
Q

Give 3 clinical signs of hypovolaemia

A
  1. Hypotension
  2. Tachycardia
  3. Decreased skin turgor
  4. Dry mucus membranes
485
Q

pH 7.1; pCO2 1.2 kPa; pO2 11.1 kPa; Bicarbonate 4mmol/l.

Interpret this blood gas result

A

Severe metabolic acidosis

486
Q

Give 3 causes of severe metabolic acidosis

A
  1. Diabetic ketoacidosis
  2. Severe sepsis
  3. Uraemia
  4. Lactic acidosis
487
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism

High aldosterone levels independent of RAAS activation - H20 and sodium retention and potassium excretion

488
Q

What are the 2 main signs of Conn’s syndrome?

A
  1. Hypertension
  2. Hypokalaemia
    Sodium will be normal or slightly raised
489
Q

Give 3 symptoms of Conn’s syndrome

A deficiency in which electrolyte causes these?

A
  1. Muscle weakness
  2. Tiredness
  3. Polyuria
    Due to potassium deficiency
490
Q

What can causes Conn’s syndrome?

A 
Adrenal adenoma (2/3) 
Bilateral adrenal hyperplasia (1/3)
491
Q

What hormone is raised in Conn’s syndrome and what hormone is reduced?
Where are these hormones synthesised?

A
  1. Aldosterone is raised - synthesised in the zone glomerulosa
  2. Renin is reduced - synthesised in the juxta-glomerular cells
492
Q

What investigations might you do in someone to confirm a diagnosis of Conn’s syndrome?

A
  1. Bloods - U+E, renin (low), aldosterone (high)

2. Plasma aldosterone renin ratio - initial screening - raised = further tests

493
Q

Give 4 ECG changes you might see in someone with Conn’s syndrome

A
  1. Increased amplitude and width of P waves
  2. Flat T waves
  3. ST depression
  4. Prolonged QT interval
  5. U waves
494
Q

What is the treatment for Conn’s syndrome?

A
  1. Laparoscopic adrenalectomy (adenoma)

2. Aldosterone antagonist - Spironolactone (hyperplasia)

495
Q

What is adrenal hyperplasia?

A

Defective enzymes mediating the production of adrenal cortex products - low levels of cortisol and high levels of male hormones

496
Q

How does adrenal hyperplasia present?

A

Salt loss
Females - ambiguous genitalia with common urogenital sinus
Males - no signs at brith, subtle hyperpigmentation and possible penile enlargement

497
Q

Briefly describe the pathophysiology of adrenal hyperplasia

A

Defective 21-hydroxylase –> disruption of cortisol biosynthesis
With or without aldosterone deficiency and androgen excess

498
Q

What diagnostic test would be done to confirm adrenal hyperplasia?

A

Serum 17-hydorxyprogesterone (precursor to cortisol) = high

499
Q

What is the treatment for adrenal hyperplasia?

A

Glucocorticoids - hydrocortisone
Mineralocorticoids - control elecytrolytes
If salt loss - sodium chloride supplement

500
Q

What is hyperkalaemia?

A

Excess of potassium
Serum K+ >5.5 mmol/L
Serum K+ >6.5 mmol/L = medical emergency

501
Q

Give 3 symptoms of hyperkalaemia

A
  1. Weakness
  2. Palpitations
  3. Tachycardia
  4. Chest pain
502
Q

Give 3 causes of hyperkalaemia

A
  1. AKI
  2. Drug interferences - NSAIDs, K+ sparing diuretics, ACEi
  3. Metabolic acidosis
  4. DKA
  5. Excess K+
503
Q

What ECG changes might you see in someone with hyperkalaemia?

A
  1. Tall tented T waves
  2. Widened QRS
  3. Small P wave
  4. Prolonged PR
504
Q

What is the treatment for hyperkalaemia?

A

Dietary potassium restriction

Loop diuretic

505
Q

What is a complication for someone with hyperkalaemia?

A

Myocardial infarction –> death

506
Q

What is hypokalaemia?

A

Deficiency in potassium
Serum K+ <3.5 mmol/L
Serum K+ <2.5 mmol/L = medical emergency

507
Q

Give 5 symptoms of hypokalaemia

A
  1. Muscle weakness
  2. Hypotonia
  3. Hyperflexia
  4. Tetany
  5. Palpitations
  6. Arrhythmia
  7. Nausea and vomiting
  8. Cramps
508
Q

Give 3 causes of hypokalaemia

A
  1. Diuretics
  2. Hyperaldosteronism (Conn’s syndrome)
  3. Insulin
  4. D+V
  5. Renal disease
509
Q

What ECG changes might you see in someone with hypokalaemia?

A
  1. Increased amplitude and width of P waves
  2. ST depression
  3. Flat T waves
  4. U waves
  5. QT prolongation
510
Q

What is the treatment for hypokalaemia?

A

Treat underlying causes
Withdraw harmful medication (diuretics or laxatives)
Normalise magnesium as well as potassium

511
Q

What are 2 possible complications of hypokalaemia?

A
  1. Cardiac arrhythmias

2. Sudden death

512
Q

Name 5 types of thyroid cancer

A
  1. Papillary
  2. Follicular
  3. Anaplastic
  4. Lymphoma
  5. Medullary
513
Q

What types of thyroid cancers are usually asymptomatic thyroid nodule (usually hard and fixed)?

A

Papillary
Follicular
Anaplastic

514
Q

How does a lymphoma of the thyroid present?

A

Rapidly growing mass in the neck

515
Q

How does a medullary cancer of the thyroid present?

A

Diarrhoea
Flushing episodes
Itching

516
Q

Why is an anaplastic cancer of the thyroid one of the most aggressive cancers?

A

Cancer of the follicular cells of the thyroid but doesn’t retain original cell features like iodine uptake or synthesis of thyroglobulin

517
Q

What hormone does a medullary cancer of the thyroid produce?

A

Calcitonin from C cells

518
Q

What is the most common form of thyroid cancer?

A

Papillary - 70%, young people, 3x more common in women

Follicular - 20%

519
Q

What investigations can you do to confirm a thyroid cancer?

A

Fine needle aspiration

For a Medullary cancer - elevated serum calcitonin

520
Q

What is the treatment for thyroid cancer?

A 
Papillary and follicular 
 - total thyroidectomy 
 - ablatie radioactive iodine 
Anaplastic and lymphoma 
 - external radiotherapy to provide relief 
 - largely palliative 
Medullary 
 - total thyroidectomy and prophylactic central lymph node dissection
521
Q

What is a carcinoid tumour?

A

Serotonin secreting tumour which tend to express somatostatin receptors

522
Q

What are the types of carcinoid tumour?

A
  1. Foregut
  2. Midgut
  3. Hind gut
523
Q

Name 5 effects of serotonin

A
  1. Bowel function
  2. Mood
  3. Clotting
  4. Nausea
  5. Bone density
  6. Vasoconstriction
  7. Increase force of contraction and HR
524
Q

Name 3 symptoms of a carcinoid tumour

A
  1. Pain
  2. Weight loss
  3. Palpable mass
525
Q

What is carcinoid syndrome?

A

Carcinoid tumour where there is hepatic involvement

526
Q

What are 4 more symptoms of carcinoid syndrome?

A
  1. Bronchospasm
  2. Diarrhoea
  3. Skin flushing
  4. Right sided heart lesion
527
Q

What is a carcinoid crisis?

A

When a carcinoid tumour outgrows its blood supply or is handled too much during surgery - mediators flow out

528
Q

Name 3 events that occur due to a carcinoid crisis

A
  1. Vasodilation - due to bradykinin
  2. Hypotension - due to ACTH which increases cortisol
  3. Tachycardia - due to serotonin
  4. Bronchoconstriction - due to bradykinin
  5. hyperglycaemia - due to glucagon and ACTH
529
Q

How do you treat a carcinoid crisis?

A

High dose somatostatin analogue - octreotide

530
Q

Briefly describe the pathophysiology that begins a carcinoid tumour

A

Derived from enterchromaffin cells

Tend to secrete bioactive compounds –> serotonin, bradykinin precursors –> carcinoid syndrome

531
Q

What investigations can be done to diagnose a carcinoid tumour?

A

Urine - high volume of 5-hydroxyindoleacetic acid (breakdown product of serotonin)
Liver ultrasound
Octreoscan - radio labelled ocreotide hits the somatostatin receptors

532
Q

What is the treatment for a carcinoid tumour?

A

Somatostatin analogue - octreotide/lanreotide

Surgical resection - reduce tumour mass

533
Q

Which of the following is not under the control of the pituitary gland?

a. Thyroid
b. Adrenal cortex
c. Adrenal medulla
d. Testis
e. Ovary

A

c) Adrenal medulla

534
Q

Which of the following statements is false?

a. The pituitary gland lies in the sella turcica
b. The pituitary gland weight around 0.5g
c. ACTH is secreted from the pituitary during stress
d. The pituitary regulates calcium metabolism
e. The anterior and posterior pituitary are distinct on an MRI scan

A

d) The pituitary regulates calcium metabolism

535
Q

In men all the following are mainly produced in the adrenal cortex except

a. DHEAS
b. Testosterone
c. Aldosterone
d. 17-PH progesterone
e. Androstenedione

A

b) Testosterone

536
Q

Which of the following regarding ADP (vasopressin) is false?

a. ADP levels have a linear relationship with serum osmolality
b. Is produced in the pituitary gland
c. Stimulates reabsorption of water in the collecting duct of the nephron
d. In hypotension baroreceptors predominantly activate ADH production and secretion
e. Further ADP production is no longer effective once urine osmolality has reaches a plateau

A

b) Is produced in the pituitary gland

537
Q

Hypothalamic hormones act to mainly stimulate the release of all these hormones except?

a. ACTH
b. GH
c. TSH
d. Prolactin
e. LH

A

d) Prolactin

538
Q

Where is growth hormone’s main site of action to stimulate IGF1 release?

a. Bone
b. Liver
c. Adrenal cortex
d. Muscle
e. Pancreas

539
Q

The following are typical features of excess growth hormone secretion except?

a. Polyuria
b. Joint pains
c. Sweating
d. Hypotension
e. Headaches

A

d) Hypotension

540
Q

The following hormones all have a circadian rhythm except?

a. Cortisol
b. Testosterone
c. DHEA
d. 17OH progesterone
e. Thyroxine (T4)

A

e) Thyroxine (T4)

541
Q

Typical features of cortisol deficiency include the following except?

a. Hypotension
b. Muscle aches
c. Weight loss
d. Hyperglycaemia
e. Lethargy

A

d) Hyperglycaemia

542
Q

A 38-year-old lady presented with weight gain, menorrhagia and constipation. She is most likely to be suffering from?

a. Cushing’s syndrome
b. Addison’s disease
c. Primary hypothyroidism
d. Graves disease
e. Acromegaly

A

c) Primary hypothyroidism

543
Q

Which test would you likely want to perform in a patient with proximal muscle weakness, purple striae and thin skin?

a. Synacthen test
b. Overnight dexamethasone suppression test
c. Insulin tolerance test
d. Glucagon test
e. Skin allergy test

A

b) Overnight dexamethasone suppression test

544
Q

A 24-year-old girl presented with hirsutism, oligomenorrhoea and acne. What test wold you likely carry out?

a. Ultrasound adrenal
b. Ultrasound ovaries
c. MRI ovaries
d. CT scan adrenals
e. Prolactin

A

b) Ultrasound ovaries

545
Q

The following may cause nephrogenic diabetes insipidus except?

a. Lithium
b. Myeloma
c. Amyloidosis
d. Hyperkalaemia
e. Hypercalcaemia

A

b) Myeloma

546
Q

A 54-year-old gentleman presented with hyponatraemia. All the following conditions need excluding before confirming SIADH except?

a. Hypothyroidism
b. Hypovolaemia
c. Euvolaemia
d. Adrenal insufficiency
e. Diuretic use

A

c) Euvolaemia

547
Q

A 66-year-old gentleman had a serum sodium of 124 mmol/l, serum osmolality 265 mmol/l and a urine sodium of 52 mmol/l. What would you like to perform first?

a. Chest X-ray
b. CT brain
c. Skin turgor and jugular venous pressure test
d. Thyroid function tests
e. Synacthen test

A

c) Skin turgor and jugular venous pressure test

548
Q

The following are most likely causes of SIADH except?

a. Multiple sclerosis
b. Lung abscess
c. Subdural haemorrhage
d. Lymphoma
e. Cerebrovascular accident

A

a) Multiple sclerosis

549
Q

A 28-year-old presented with a microprolactinoma? What is the most unlikely symptom?

a. Galactorrhoea
b. Oligomenorrhoea
c. Decreased sexual appetite
d. Headaches
e. Visual field defects

A

e) Visual filed defects

550
Q
  1. The following suppress appetite except?
    a. Peptide YY
    b. Ghrelin
    c. CCK
    d. GLP1
    e. Glucose
A

b) Ghrelin

551
Q

The main adipose signal to the brain is?

a. CCK
b. Neuropeptide y
c. Leptin
d. Agouti-related peptide
e. Adiponectin

552
Q

A 65-year-old lady is diagnosed with SIADH. Her sodium is 123mmol/l. What is your first line of management?

a. If she is symptomatic, I will treat with fluid restriction
b. If she is asymptomatic, I will treat with hypertonic saline
c. If she is asymptomatic, I will treat with fluid restriction
d. If she is asymptomatic, I will repeat the sodium level the next day
e. If she is asymptomatic, I will give normal saline

A

c) If she is asymptomatic, I will treat with fluid restriction

553
Q

A patient with Addison’s disease presents with a chest infection. What do you do?

a. Omit his steroids to avoid immunosuppression
b. Stop his steroids as they have precipitated a chest infection
c. Double his steroid dose whilst unwell
d. Keep him on his usual steroid dose
e. None of the above

A

c) Doublers this steroid dose whilst unwell

554
Q
  1. The following tests are typical of secondary hypogonadism
    a. Low LH; High testosterone
    b. Low LH; Low testosterone
    c. High prolactin; high testosterone
    d. Low FSH; Low prolactin
    e. None of the above
A

b) Low LH; Low testosterone

555
Q

Typical features of hypogonadism in a male include the following except?

a. Decreased sweating
b. Joint and muscular aches
c. Decreased sexual appetite
d. Decreased hair growth

A

a) Decreased sweating

556
Q

A patient has a noon testosterone level below the normal range. What will you do?

a. Treat with testosterone gel
b. Repeat the test at 0900h and check for symptoms
c. Repeat the test at noon to keep things equal
d. Refer to endocrinology
e. Ignore it

A

b) Repeat the test at 0900h and check for symptoms

557
Q

Osmoreceptors are found in the:

a. Subfornical organ
b. Organum vasculosum of the lamina terminalis
c. Hypothalamus
d. All of the above
e. None of these

A

d) All of the above

558
Q

The first line treatment for a patient with a symptomatic prolactinoma is usually?

a. Radiotherapy
b. Transphenoidal surgery
c. Dopamine agonists
d. Transfrontal surgery
e. Somatostatin analogues

A

c) Dopamine agonists

559
Q

Typical visual field defect of a patient with a large pituitary mass is?

a. Unilateral quadrantanopia
b. Bitemporal hemianopia
c. Complete unilateral visual field loss
d. Complete bilateral visual field loss
e. None of the above

A

b) Bitemporal hemianopia

560
Q

Satiety is?

a. The physiological feeling of no hunger
b. Inhibited by activation of POMC neurons
c. The physiological feeling of hunger
d. Induced by ghrelin release
e. Enhanced by Agouti-related peptide

A

a) The physiological feeling of no hunger

561
Q

The centres of appetite regulation in the brain are mainly found in the?

a. Pituitary
b. Cerebellum
c. Hypothalamus
d. Basal ganglia
e. Brain cortex

A

c) Hypothalamus

562
Q

What is peripheral vascular disease?

A

Decreased perfusion to the peripheries due to macrovascular disease

563
Q

What is the treatment for peripheral vascular disease?

A

Stop smoking
Walk through the pain
Surgical intervention

564
Q

What investigations can be done on someone you think has PVD?

A

Doppler pressure studies
Duplex arterial imaging
Doppler ultrasound

565
Q

What are the main objective of T2DM treatment?

A

Reducing risk - CVD, CKD and microvascular complications

Reducing weight - Increase exercise, decrease dietary fat

566
Q

What lifestyle interventions can be put in place for someone with T2DM?

A 
Compliance
Lifestyle and patient eduction
30 minutes of exercise a day
Dietitian
Local educational programmes
567
Q

How do DPP4 inhibitors work as a treatment for T2DM?

A

Competitive antagonist of DPP4 enzyme (enhance effects of GIP and GLP1)
So they inactivate incretin hormones GIP and GLP1

568
Q

What are thiazolidinediones contraindicated by?

A

CCF, high risk fractures and macula oedema

569
Q

How do SGLT-2 inhibitors work as a treatment for T2DM?

A

Increases renal excretion of glucose

Risk of hypotension

PHASE 2A (16 decks)

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