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Phase 2a Medicine > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Name 5 diseases of the pituitary.

A
  • Benign pituitary adenoma
  • Craniopharyngioma
  • Trauma
  • Sheehans
  • Sarcoid / TB
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2
Q

What are the three vital presentation points of pituitary tumour?

A
  1. Pressure on local structures
  2. Pressure on normal pituitary function - HYPOPITUITARISM
  3. Functioning tumour - HYPERPITUITARISM
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3
Q

What local structure is at risk with a pituitary tumour? What is the outcome?

A

Optic chiasm, causing bitemporal hemianopia

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4
Q

What does hypopituitarism (as a result of a pituitary tumour) look like in males?

A
  • Pale
  • No body hair (9 months to occur)
  • Central obesity
  • Effeminate skin
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5
Q

What does hypopituitarism (as a result of a pituitary tumour) look like in females?

A
  • Loose body hair

- Sallow complexion

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6
Q

What is the main danger with hypopituitarism?

A

Cortisol deficiency can be fatal

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7
Q

What three outcomes can hyperpituitarism cause?

A
  • Prolactinoma
  • Acromegaly
  • Cushing’s
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8
Q

What is a prolactinoma?

A

Benign pituitary adenoma results in an increase in prolactin production

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9
Q

What is the clinical presentation for prolactinoma?

A
  • Usually young women
  • Increased milk production
  • Galactorrhoea
  • Reduced fertility
  • Amenorrhoea
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10
Q

How do you treat prolactinoma?

A

Dopamine agonist which inhibits prolactin release

e.g. CABERGOLINE

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11
Q

What is acromegaly?

A

Excessive production of growth hormone by the pituitary

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12
Q

What is the clinical presentation of acromegaly?

A
  • Thick, greasy, sweaty skin

- Enlarged organs (e.g. cardiomegaly increasing risk of heart disease)

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13
Q

What is Cushing’s disease?

A

Increased production of ACTH by pituitary (causing increased CTH)

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14
Q

What is the clinical presentation for Cushing’s?

A
  • Too much cortisol
  • Central obesity
  • Bruising
  • Thin skin
  • Osteoporosis
  • Ulcers
  • Purple stretch marks
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15
Q

Define diabetes mellitus.

A

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

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16
Q

What does hyperglycaemia cause?

A

Serious microvascular or macrovascular problems

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17
Q

What are some microvascular problems caused by hyperglycaemia?

A
  • Retinopathy
  • Nephropathy
  • Neuropathy
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18
Q

What are some macrovascular problems caused by hyperglycaemia?

A
  • Strokes
  • Renovascular disease
  • Limb ischaemia
  • Heart disease
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19
Q

What are the normal blood glucose levels?

A

3.5-8.0mmol/L

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20
Q

Where does glucose homeostasis take place?

A

Liver

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21
Q

How is glucose stored in the liver?

A

As glycogen

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22
Q

If blood glucose is high, how does the liver react?

short term and long term hyperglycaemia

A

Short term - glycogenosis

Long term - Lipogenesis

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23
Q

If blood glucose is low, how does the liver react?

short term and long term hypoglycaemia

A

Short term - glycogenolysis

Long term - gluconeogenesis

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24
Q

How much glucose is produced and utilised each day?

A

~200g

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25
Q

Where is the majority of glucose derived from?

A

Hepatic gluconeogenesis

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26
Q

What fuel does the brain use?

A

Glucose, metabolised to CO2 + H₂O

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27
Q

Why can’t the brain use free fatty acids for fuel?

A

They cannot cross the blood brain barrier

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28
Q

Does insulin affect the brain’s uptake of glucose?

A

No, glucose uptake is obligatory and is independent of insulin

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29
Q

What do muscles and fat respond to with regards to insulin absorption?

A

They have insulin-responsive glucose transports, and absorb glucose in response to postprandial peaks in glucose and insulin

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30
Q

How does muscle tissue store and use glucose?

A

Stored as glycogen

Metabolised to lactate or CO2 + H₂O

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31
Q

How does fat use glucose?

A

As a substrate for triglyceride synthesis

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32
Q

What is the product of lipolysis of triglycerides?

A

Lipolysis of triglycerides releases FAs + glycerol, and the glycerol is used as a substrate for hepatic gluconeogenesis

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33
Q

What does insulin do?

A
  • Suppresses hepatic glucose output

- Increases glucose uptake into insulin sensitive tissues

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34
Q

How does insulin suppress hepatic glucose output?

A

Decreases glycogenolysis and gluconeogenesis

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35
Q

How does insulin increase glucose uptake into insulin sensitive tissues?

A
  • Causes glycogen and protein synthesis in muscles
  • Causes fatty acid synthesis in fats
  • Suppresses lipolysis and ketogenesis
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36
Q

Describe biphasic insulin release

A
  • Pancreatic B-cells sense the rising glucose levels and aim to metabolise it by releasing insulin
  • First phase response is RAPID release of stored insulin
  • If glucose levels remain high, second phase is initiated (new insulin is synthesised and released)
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37
Q

What does glucagon do?

A
  • Increases hepatic glucose output
  • Reduces peripheral glucose uptake
  • Stimulates peripheral release of gluconeogenic precursors
  • Stimulates lipolysis and ketogenesis
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38
Q

How does glucagon increase hepatic glucose output?

A

Increases glycogenolysis and gluconeogenesis

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39
Q

What other hormones are involved in glucose regulation?

A
  • Adrenaline
  • Cortisol
  • Growth hormone

These increase glucose production in liver and reduce its utilisation in fat and muscle

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40
Q

Where is insulin coded for on the genome?

A

Chromosome 11

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41
Q

Which cells produce insulin?

A

Beta cells of the Islets of Langerhans of the pancreas

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42
Q

What is the precursor for insulin?

A

Proinsulin

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43
Q

What is the structure of proinsulin? What happens when proinsulin becomes insulin?

A
  • Alpha and beta chains of insulin joined together by a C peptide
  • Proinsulin is cleaved from C peptide and then is used to make insulin
  • Insulin is packaged into insulin secretory granules
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44
Q

What is the difference between naturally produced insulin and synthetic insulin?

A

Synthetic insulin does not have a C peptide

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45
Q

What happens to insulin immediately after it is secreted into the blood?

A

It enters the portal circulation and is carried to the liver

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46
Q

How much insulin is extracted and degraded in the liver?

A

~50%

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47
Q

What is the main action of insulin in the fasting state?

A

Regulate glucose release by the liver

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48
Q

What is the main action of insulin in the post-prandial state?

A

Promote glucose uptake by fat and muscle

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49
Q

Are cell membranes inherently permeable to glucose?

A

No, GLUT proteins are required

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50
Q

How does insulin cross the cell membrane?

A

Specialised glucose-transporter (GLUT) proteins carry it across the membrane

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51
Q

What does GLUT-1 do?

A

Enables basal non-insulin-stimulated glucose uptake into many cells

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52
Q

What does GLUT-2 do?

A

Transports glucose into beta-cells and enables them to sense blood glucose levels

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53
Q

Where are GLUT-2 proteins found?

A

In beta-cell in the Islets of Langerhans mainly

also found in renal tubules and hepatocytes

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54
Q

How do GLUT-2 proteins work?

A

They are low affinity transports that only allows glucose into the beta-cells when there is a high glucose concentration

Thus, they are able to detect high glucose levels and trigger the release of insulin in response

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55
Q

What does GLUT-3 do?

A

Enables non-insulin-mediated glucose uptake into brain neurones and placenta

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56
Q

What does GLUT-4 do?

A

Mediates peripheral action of insulin

It is the channel through which glucose is taken up into muscle and fat tissue cells following stimulation of the insulin receptor by insulin binding to it

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57
Q

Describe insulin receptors

A

Glycoprotein, coded for on the short arm of chromosome 19, which straddles cell membranes

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58
Q

What happens when insulin binds to an insulin receptor?

A

It activates tyrosine kinase, and initiates a cascade response

One consequence of the cascade response is the migration of GLUT-4 transporters to the cell surface, thus increasing transportation of glucose into the cell

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59
Q

What does hypoglycaemia stimulate?

A

Release of glucagon, which stimulates;

  • Glycogenolysis (glycogen -> glucose)
  • Gluconeogenesis (lactic acid / amino acids -> glucose)
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60
Q

Diabetes may occur secondary to other conditions, including…

A
  • Pancreatic pathology (e.g. pancreatectomy, chronic pancreatitis, haemochromatosis)
  • Endocrine diseases (e.g. acromegaly and Cushing’s disease)
  • Drug induced (commonly by thiazide diuretics and corticosteroids)
  • Maturity onset of diabetes of youth (MODY)
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61
Q

Are type 1 diabetics usually older or younger?

A

Younger (<30yrs)

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62
Q

Are type 2 diabetics usually older or younger?

A

Older (>30yrs)

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63
Q

Are type 1 diabetics usually lean or overweight?

A

Lean

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64
Q

Are type 2 diabetics usually overweight or lean?

A

Overweight

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65
Q

Which ethnic groups are at higher risk of developing type 1 diabetes?

A

Northern European (particularly Finland)

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66
Q

Which ethnic groups are at higher risk of developing type 2 diabetes?

A

Asian, African, Polynesian, and Native American

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67
Q

Which type of diabetes is hereditary 90% of the time?

A

Type 1

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68
Q

Which type of diabetes is an autoimmune disease?

A

Type 1

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69
Q

Which type of diabetes causes ketonuria?

A

Type 1

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70
Q

What are the clinical features of type 1 diabetes?

A
  • Insulin deficient
  • Higher risk of ketoacidosis
  • Insulin dependent
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71
Q

What are the clinical features of type 2 diabetes?

A
  • Partial insulin deficiency initially
  • Potentially in a hyperosmolar state
  • Will eventually need insulin when B-cells fail
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72
Q

Define diabetes mellitus type 1 (DMT1).

A

Disease of insulin deficiency, usually caused by autoimmune destruction of beta-cells of the pancreas

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73
Q

When is DMT1 typically manifested?

A

In childhood, reaching peak incidence at puberty

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74
Q

What is LADA?

A

Latent autoimmune diabetes in adults

  • ‘Slow burning’ variant of DMT1 with slower progression to insulin deficiency
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75
Q

Describe the aetiology of DMT1

A
  • Autoimmune (auto-antibodies forming against insulin and islet beta cells)
  • Idiopathic
  • Genetic susceptibility
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76
Q

What other autoimmune diseases is DMT1 associated with?

A
  • Autoimmune thyroid
  • Coeliac disease
  • Addison’s disease
  • Pernicious anaemia
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77
Q

What environmental factors can contribute to DMT1?

A
  • Dietary constituents
  • Enteroviruses (e.g. Coxsackie B4)
  • Vitamin D deficiency
  • Clean environments
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78
Q

How does DMT1 affect the liver?

A

Continued breakdown of liver glycogen (producing more glucose and ketones), leading to glycosuria and ketonuria, as there is more glucose in the blood

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79
Q

How does DMT1 affect skeletal muscles and fats?

A
  • Blood glucose increases
  • When blood glucose >10mmol/L, the body can no longer absorb glucose
  • Therefore, you become thirsty and get polyuria as the body attempts to remove excess glucose
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80
Q

What happens if DMT1 patients don’t take their insulin?

A

DIABETIC KETOACIDOSIS

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81
Q

Describe diabetic ketoacidosis

A
  • Results from a reduced supply of glucose (since there will be a significant decline in circulating insulin) and an increase in FA oxidation (due to increase in circulating glucagon)
  • Increased production of acetyl-CoA leads to ketone body production that exceeds the ability of peripheral tissues to oxidise them
  • Ketone bodies (pH 3.5) lowers pH of blood, causing ketoacidosis
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82
Q

What is the major consequence of acidification of the blood?

A

Impaired ability of haemoglobin to bind to oxygen

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83
Q

What does the presence of ketones in the blood do to a patients breath?

A

Causes it to smell of peardrops (ketones)

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84
Q

What are the consequences of excess fat breakdown in ketoacidosis?

A
  • Acidotic
  • Anorexic
  • Dehydration, leading to AKI
  • Hyperglycaemia
  • Death
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85
Q

What results from the eventual complete beta-cell destruction DMT1?

A

Absence of serum C-peptide

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86
Q

What is diabetes mellitus type 2 (DMT2)?

A

Combination of insulin resistance and less severe insulin deficiency

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87
Q

Who tends to get DMT2?

A
  • Populations enjoying an affluent lifestyle
  • > 30yrs
  • Overweight (lack of exercise, calorie / alcohol excess)
  • South Asian, African, Caribbean, middle eastern and Hispanic ancestry
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88
Q

What is the link between DMT2 and low birth weight?

A

Association between low weight (as a result of poor nutrition) and birth and 12months with glucose intolerance in later life

This is thought to be caused by poor nutrition impairing beta-cell development and function

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89
Q

What is the difference in insulin uptake between healthy people and DMT2 patients?

A

Insulin stills binds to its receptor normally, but insulin resistance develops post-receptor

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90
Q

How much is the mass of beta cells reduced by at the time of diagnosis of DMT2?

A

~50%

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91
Q

At autopsy, what does the pancreas of a DMT2 patient look like?

A

Amyloid deposition in the islets of the pancreas, derived from a peptide (amyloid) co-secreted with insulin

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92
Q

What is an early sign of DMT2?

A

Loss of first phase of normal biphasic insulin release

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93
Q

What is established DMT2 associated with?

A

Hypersecretion of insulin from depleted beta-cell populations

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94
Q

What are circulating insulin levels like in DMT2 patients?

A

Higher than in healthy individuals, but inadequate to restore normal glucose homeostasis

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95
Q

Why are insulin levels higher in DMT2 patients?

A

Increased glucose production from liver (due to inadequate suppression of gluconeogenesis)

  • Reduced glucose uptake by peripheral tissues (insulin resistant)
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96
Q

How does hyperglycaemia and lipid excess affect beta cells?

A

Toxic to beta cells (glucotoxicity), which causes further beta cell loss and deterioration of glucose homeostasis

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97
Q

What is the Starling curve of the pancreas?

A

Circulating insulin levels are typically higher than in non-diabetics following diagnosis and tend to rise further, only to decline again after months or years due to eventual secretory failure

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98
Q

Do DMT2 patients become ketoacidotic?

A

No, even a small amount of insulin can halt the breakdown of fat and muscle into ketones

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99
Q

Do DMT2 patients get glycosuria?

A

Yes

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100
Q

What is prediabetes?

A

Preliminary phase of impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)

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101
Q

What is prediabetes useful for?

A

It is a unique window for lifestyle intervention to prevent full DMT2 progression

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102
Q

Which is more likely to progress to DMT2; IFG or IGT?

A

IGT

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103
Q

If a patient has IGT, what are the…

a) fasting plasma glucose levels
b) oral glucose tolerance of 2hrs glucose levels

A

Fasting plasma glucose <7mmol/L

Oral glucose tolerance of 2hrs glucose > 7.8-11mmol/L

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104
Q

If a patient has IFG, what are the fasting plasma glucose levels?

A

Fasting plasma glucose 6.1-7mmol/L

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105
Q

What is the typical clinical presentation for DMT1?

A
  • Leaner
  • Marked polydipsia
  • Marked polyuria
  • Weight loss
  • Ketosis
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106
Q

What is the typical clinical presentation for DMT2?

A
  • Overweight in abdominal area
  • Polydipsia
  • Polyuria
  • Weight loss
  • Ketosis (only when very advanced with total insulin deficiency)

LESS MARKED THAN DMT1

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107
Q

How long is the history for a patient presenting with DMT1?

A

Usually 2-6 week history

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108
Q

What is the classic triad of symptoms for a patient presenting with DMT1?

A
  • Polyuria and nocturia
  • Polydipsia
  • Weight loss
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109
Q

Why does DMT1 cause polyuria and nocturia?

A
  • Glucose draws water into urine by osmosis

- Not enough glucose can be reabsorbed as kidneys have reached renal maximum reabsorptive capacity

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110
Q

Why does DMT1 cause polydipsia?

A

Due to loss of fluid and electrolytes from excess glucose and thus water being lost in urine

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111
Q

Why does DMT1 cause weight loss?

A
  • Fluid depletion and accelerated breakdown of fat and muscle secondary to insulin deficiency
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112
Q

What is the subacute presentation of diabetes?

A
  • Less marked acute presentation symptoms (e.g. polyuria, polydipsia, etc.)
  • Lethargy
  • Visual blurring (due to glucose-induced changes in refraction)
  • Pruritus vulvae or balantis (due to Candida infection)
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113
Q

What are the complications of diabetes that patients might present to their GP with?

A
  • Staphylococcal skin infections
  • Retinopathy found by optician
  • Polyneuropathy causing tingling and numbness in feet
  • Erectile dysfunction
  • Arterial disease resulting in MI or peripheral gangrene
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114
Q

Who is asymptomatic diabetes more common in?

A

Older people, who have raised renal threshold for glucose

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115
Q

What can you not use as a diagnostic criteria in asymptomatic diabetes?

A

Glycosuria is NOT diagnostic for diabetes, but indicates the need for further investigations

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116
Q

What might you observe on the skin in a physical examination that suggests severe insulin resistance?

A

Acanthosis nigerians - blackish pigmentation at nape of neck and in axillae

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117
Q

At what value is the random plasma glucose concentration diagnostic for diabetes?

A

Random plasma glucose >11.1mmol/L = DIABETES DIAGNOSIS

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118
Q

At what value is the fasting plasma glucose concentration diagnostic for diabetes?

A

Fasting plasma glucose > 7mmol/L = DIABETES DIAGNOSIS

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119
Q

What is the difference in diagnosing diabetes between symptomatic and asymptomatic patients?

A

In symptomatic patients, you only need ONE abnormal blood glucose conc. value

In asymptomatic patients, you need TWO abnormal blood glucose conc. values

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120
Q

If you do an oral glucose tolerance test on a patient who is FASTING, what result is diagnostic for diabetes?

A

OGTT: Fasting > 7mmol/L = DIABETES DIAGNOSIS

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121
Q

If you do an oral glucose tolerance test on a patient who 2 hours after glucose, what result is diagnostic for diabetes?

A

OGTT: 2 hours after glucose > 11.1mmol/L = DIABETES DIAGNOSIS

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122
Q

What test can detect IGT?

A

Oral glucose tolerance tests (OGTT)

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123
Q

If you do an oral glucose tolerance test on a patient who is FASTING, what result is diagnostic for IGT?

A

OGTT: Fasting < 7mmol/L = IGT DIAGNOSIS

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124
Q

If you do an oral glucose tolerance test on a patient who 2 hours after glucose, what result is diagnostic for IGT?

A

OGTT: 2 hours after glucose > 7.8-11.0mmol/L = IGT DIAGNOSIS

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125
Q

What does HbA1c measure?

A

Measures amount of glycated haemoglobin, thus tells you glucose concentration

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126
Q

At what level is HbA1c diagnostic for diabetes?

A

HbA1c > 6.5% normal = DIABETES DIAGNOSIS

HbA1c > 48mmol/mol = DIABETES DIAGNOSIS

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127
Q

How do you assess kidney disease in diabetic patients?

A

Screen urine for microalbuminuria

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128
Q

Why do you look at blood pH in diabetics?

A

To look for metabolic acidosis (high H+ and low HCO3-, due to ketoacidosis)

Seen in DMT1 and advanced DMT2

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129
Q

What approach is vital to treating DMT1 and DMT2?

A

MDT approach

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130
Q

What must you do to a patient with newly diagnosed diabetes?

A

Educate them on the disease and risks

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131
Q

What lifestyle factors can you amend to help control diabetes?

A
  • Maintain lean weight
  • Stop smoking
  • Take care of feet
  • Regular physical activity
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132
Q

What should the diet of a diabetic look like to aid in good glycemic control?

A
  • Low in sugar
  • High in starchy carbohydrates with low glycemic index (e.g. pasta)
  • High in fibre
  • Low in fat
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133
Q

How do you treat hypertension in diabetics?

A

ACE-inhibitors

e.g. RAMIPRIL

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134
Q

How do you treat hyperlipidaemia in diabetics?

A

Statins

e.g. SIMVASTATIN

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135
Q

What is the treatment for DMT1 patients who have been in ketoacidosis?

A

Insulin

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136
Q

What is the standard treatment for DMT1 patients who are lean and under 40?

A

Insulin

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137
Q

How do you ensure good control of DMT1?

A

Educate patients on self-adjusting insulin doses

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138
Q

How can DMT1 patients get help with their treatment?

A
  • Phone support (24/7 nurse)
  • Aware of how to modify diet and avoid binge drinking
  • Ensure their partner knows how to avoid hypoglycaemia (e.g. sugary drinks)
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139
Q

How do DMT1 patients administer insulin?

A

Via subcutaneous injection into abdomen, thighs, or upper arm

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140
Q

What must an insulin-dependent diabetic do with regards to the DVLA?

A

Legal obligation to inform the DVLA

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141
Q

What happens if DMT1 patients don’t change injection sites frequently?

A

Lipohypertrophy (fatty lumps)

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142
Q

What does the finger pricking glucose test tell a DMT1 patient?

A
  • Before meal test informs about long-acting insulin doses

- After a meal test informs about short-acting insulin doses

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143
Q

What are short-acting insulins?

A
  • Start working within 30-60 minutes and last 4-6 hours
  • Given 15-30 minutes before meals in patients on multiple dose regimens, and by continuous IV infusion during labour, medical emergencies, surgery, and patients using insulin pumps
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144
Q

What are short-acting insulin analogues?

A
  • Fast onset and short duration but DO NOT IMPROVE DIABETIC CONTROL
  • Reduced carry-over effect compared to soluble insulin
  • Used with evening meal in patients who are prone to nocturnal hypoglycaemia
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145
Q

What are longer-acting insulins?

A
  • Insulin premixed with retarding agents (either protamine or zinc)
  • Can be intermediate (12-24 hours) or long-acting (more than 24hrs)
  • Protamine insulins are known as isophane or NPH insulins
  • Zinc insulins are known as lente insulins
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146
Q

Why does the insulin dose in newly diagnosed DMT1 patients have to be closely monitored in the beginning of treatment?

A

In many patients who present acutely with diabetes, there is some recovery of endogenous insulin secretion soon after diagnosis, and the insulin dose may need to be reduced

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147
Q

What is the most appropriate treatment for younger DMT1 patients?

A

Multiple injection regimen which improves control and allows greater meal flexibility

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148
Q

What are the complications of insulin treatment?

A
  • Hypoglycaemia
  • Injection site lipohypertrophy
  • Insulin resistance
  • Weight gain (insulin increases appetite)
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149
Q

What is the first line treatment for DMT2?

A
  • Lifestyle and dietary changes
  • Spread nutrient load
  • Blood pressure control
  • Hyperlipidaemia control
  • Exercise
  • Weight loss
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150
Q

How does a spread nutrient load help control DMT2?

A

Nutrient load should be spread throughout the day to reduce swings in blood glucose

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151
Q

How does orlistat help with obesity?

A

It is an intestinal lipase inhibitor, which reduces the absorption of fat from diet

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152
Q

When should you integrate second line treatments for DMT2?

A

When first line treatments have failed to control hyperglycaemia

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153
Q

What is the first thing you try in second line treatment of DMT2?

A

A biguanide, e.g. ORAL METFORMIN

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154
Q

What does oral metformin do?

A
  • Reduces rate of gluconeogenesis in liver
  • Increases cells insulin sensitivity
  • Helps with weight issues
  • Reduces CVS risk in diabetes
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155
Q

What are the side effects of oral metformin?

A
  • Anorexia
  • Diarrhoea
  • Nausea
  • Abdo. pain
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156
Q

What are the contraindications for biguanides (e.g. oral metformin)?

A
  • Heart failure
  • Liver disease
  • Renal disease

Induce lactic acidosis

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157
Q

If HbA1c >53mmol/L 16 weeks after starting a biguanide, what should you do?

A

Prescribe a sulfonylurea (e.g. ORAL GLICLAZIDE)

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158
Q

What does oral gliclazide do?

A

Promotes insulin secretion

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159
Q

Who can you not use sulfonlyureas on?

A
  • Pregnant women

- Patients without functional beta-cell mass

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160
Q

What are the side effects of sulfonylureas?

A
  • Hypoglycaemia

- Weight gain

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161
Q

What must you remember when prescribing sulfonylureas to patients with renal impairment?

A

You can only use sulfonylureas which are primarily excreted by the liver

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162
Q

Which sulfonylurea should you use in the very elderly?

A

Oral tolbutamide, since it has a very short duration of action

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163
Q

What course of action should you take if at 6 months the HbA1c > 57mmol/L?

A
  • Consider adding insulin (e.g. ISOPHANE INSULIN or a long-acting analogue)
  • Consider a glitazone (e.g. ORAL PIOGLITAZONE) which replaces metformin and sulfonylureas
  • Consider sulfonylurea receptor binders (e.g. ORAL NATEGLINIDE)
  • Consider glucagon-like peptide analogues (GLPs)
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164
Q

What do glitazones do?

A

Increase insulin sensitivity

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165
Q

What are the side effects of glitazones (e.g. oral pioglitazone)?

A
  • Hypoglycaemia
  • Fractures
  • Fluid retention
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166
Q

What contraindicates the use of glitazones?

A
  • Congestive heart failure

- Osteoporosis

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167
Q

How do you take sulfonylurea receptor binders?

A

30mins before a meal

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168
Q

When do you usually see diabetic ketoacidosis?

A
  • Previously undiagnosed diabetes
  • Interruption of insulin therapy
  • Stress of intercurrent illness (e.g. surgery, infection)
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169
Q

Why do you never see DKA in non-advanced DMT2?

A

There is some residual insulin left which is enough to prevent hepatic ketogenesis

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170
Q

What is the most common error of DMT1 management which leads to DKA?

A

Patients reducing or omitting insulin because they feel unable to eat, owing to nausea or vomiting

INSULIN MAY NEED ADJUSTING BUT MUST NEVER EVER BE STOPPED

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171
Q

Briefly summarise DKA

A

Ketoacidosis is a state of uncontrolled catabolism (break down) associated with insulin deficiency

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172
Q

What happens in the total absence of insulin?

A
  • Unrestrained increase in hepatic gluconeogenesis

- Peripheral uptake of glucose by tissues is reduced

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173
Q

How do high circulating glucose levels affect urination?

A

It causes osmotic diuresis, leading to dehydration and loss of electrolytes

Glycosuria (high glucose in urine) draws water into the urine via osmosis

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174
Q

Why does glycosuria lead to dehydration?

A

Glucose in urine draws water out of circulation and into the urine, causing dehydration

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175
Q

How do high circulating glucose levels affect plasma osmolality and renal perfusion?

A 
> High circulating glucose levels 
> Glycosuria
> Osmotic diuresis 
> Increased plasma osmolality 
> Decreased renal perfusion
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176
Q

How does peripheral lipolysis lead to metabolic acidosis?

A

> Increase in circulating free fatty acids (FFAs)

> FFAs broken down into acetyl-CoA in hepatocytes

> Acetyl-CoA converted into ketone bodies in mitochondria

> Ketone bodies accumulate and cause metabolic acidosis

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177
Q

What bodily function contributes to dehydration and loss of electrolytes?

A

Vomiting

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178
Q

How does the respiratory system try to counteract acidosis?

A

Respiratory compensation of acidosis leads to hyperventilation

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179
Q

How does dehydration affect acidosis?

A

Progressive dehydration impairs renal excretion of H+ ions and ketones, aggravating acidosis

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180
Q

What happens when the body’s pH falls below 7?

A

pH dependent enzyme systems in many cells function less effectively

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181
Q

What are ‘stress hormones’ and how do they affect the progression of ketoacidosis?

A
  • Adrenaline, noradrenaline, glucagon, and cortisol

- Released in response to dehydration

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182
Q

What is the clinical presentation of a patient with DKA?

A
  • Ketone breath
  • Ketonuria
  • Dehydration
  • Drowsiness
  • Vomiting
  • Sunken eyes
  • Reduced tissue turgor
  • Dry tongue (SEVERE cases)
  • Kussmaul’s respiration (respiratory compensation)
  • Disturbance of consciousness
  • Abdominal pain
  • Low fever
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183
Q

What is Kussmaul’s respiration?

A

Deep, rapid breathing

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184
Q

What is the blood glucose for DKA diagnosis?

A

> 11mmol/L - HYPERGLYCAEMIA

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185
Q

What is the plasma ketone value for DKA diagnosis?

A

> 3mmol/L - RAISED PLASMA KETONES

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186
Q

How do you measure plasma ketones in a suspected DKA patient?

A

Finger prick sample and near-patient meter that measures beta-hydroxybutyrate (major ketone)

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187
Q

What is the blood pH for DKA diagnosis?

A

pH < 7.3 - ACIDAEMIA

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188
Q

What is the bicarbonate value for DKA diagnosis?

A

bicarbonate < 15mmol/L - METABOLIC ACIDOSIS

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189
Q

How do you test for glycosuria and ketonuria in a suspected DKA patient?

A

Urine stick test

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190
Q

What would urea and creatinine values be like for a DKA patient?

A

Raised as a result of dehydration

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191
Q

What would the total body K+ values be like for a DKA patient?

A

Low / hypokalaemic, as a result of osmotic diuresis

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192
Q

What causes the difference between total body K+ values and serum K+ values?

A

Serum K+ is often raised due to absence of insulin, which allows K+ to shift out of cells

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193
Q

What would the FBC look like for a DKA patient?

A

May show raised white cell count even in absence of infection

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194
Q

What tests would you run on a suspected DKA patient to look for infection?

A
  • Blood cultures
  • CXR
  • Urine microscopy
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195
Q

Why would you look for infection in a DKA patient?

A

Infection can trigger DKA

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196
Q

What tests would you run on a suspected DKA patient to look for MI?

A
  • ECG

- Cardiac enzymes

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197
Q

Why would you look for an MI in a DKA patient?

A

MI can trigger DKA

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198
Q

What is the immediate treatment for DKA patient?

A
  • Immediate ABC management
  • Replace fluid loss with 0.9% saline - 3L in 3hrs
  • Restore electrolyte loss (K+)
  • Restore acid-base balance over 24hrs
  • Replace deficient insulin - give insulin AND glucose
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199
Q

How is acid-base balance restored in DKA patients?

A

The kidneys usually restore it themselves once circulating volume has been restored

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200
Q

Why do you give insulin and glucose to a patient with DKA?

A
  • Give glucose to prevent hypoglycaemia

- Give both to inhibit gluconeogenesis and thus ketone production

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201
Q

What are the complications of DKA management?

A
  • Hypotension
  • Coma
  • Cerebral oedema
  • Hypothermia
  • Pneumonia (late complication)
  • DVT (late complication)
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202
Q

If a DKA patient develops hypotension as a complication of treatment, how do you address this?

A

Increase circulating volume with saline

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203
Q

If a DKA patient falls into a coma, what do you do?

A

Insert a nano-gastric tube to prevent aspiration

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204
Q

Why would a DKA patient develop cerebral oedema as a complication of their treatment?

A

Rapid lowering of blood glucose, thus osmolality of blood

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205
Q

How long do the symptoms of DKA take to develop?

A

A few days

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206
Q

What is hyperosmolar hyperglycaemic state?

A

A life-threatening emergency, characterised by marked hyperglycaemia, hyperosmolality, and mild/no ketosis, and is usually the result of uncontrolled DMT2

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207
Q

Who tends to get hyperosmolar hyperglycaemic state?

A

Patients in middle / later life with undiagnosed diabetes

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208
Q

What are some of the risk factors associated with a hyperosmolar hyperglycaemic state?

A
  • Infection (most common)
  • Consumption of glucose rich fluids
  • Concurrent medication (e.g. thiazide diuretics or steroids)
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209
Q

Describe the pathophysiology of a hyperosmolar hyperglycaemic state?

A

Endogenous insulin levels are reduced but are still sufficient to inhibit hepatic ketogenesis but insufficient to inhibit hepatic glucose production

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210
Q

What is the clinical presentation of a hyperosmolar hyperglycaemic state?

A
  • Severe dehydration (secondary to osmotic diuresis)
  • Decreased level of consciousness (secondary to elevation of plasma osmolality)
  • Hyperglycaemia
  • Hyperosmolality
  • No ketones in blood or urine
  • Stupor / coma
  • Bicarbonate is NOT LOWERED
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211
Q

What are the blood glucose values for hyperosmolar hyperglycaemic state?

A

> 11mmol/L - HYPERGLYCAEMIA

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212
Q

What does a urine stick test show for a suspected hyperosmolar hyperglycaemic state patient?

A

Heavy glycosuria

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213
Q

What is the plasma osmolality like for a HHS patient?

A

Extremely high

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214
Q

What is the total body K+ value like for HHS patients?

A

Low as a result of osmotic diuresis, but serum is high due to absence of insulin which allows K+ to shift out of cells

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215
Q

What is the complication of treating HHS patients with insulin?

A

They are more sensitive, so you give a lower rate of infusion

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216
Q

What is the treatment for a HHS patient?

A
  • Slow rate of insulin infusion
  • Fluid replacement with 0.9% saline
  • Low molecular weight heparin (e.g. SC ENOXAPARIN)
  • Restore electrolyte loss
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217
Q

Why do you give a low molecular weight heparin to HHS patients?

A

Reduce the risk of thromboembolism, MI, stroke, and arterial thrombosis which patients are at a greater risk of due to hyperosmolality

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218
Q

What is a potential complication of treating HHS patients?

A

Risk of cerebral oedema - rapid lowering of blood glucose, and thus osmolality of blood

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219
Q

How does diabetes affect life expectancy?

A

Even well managed diabetes reduces life expectancy

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220
Q

What percentage of premature deaths in diabetics is caused by cardiovascular problems?

A

70%

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221
Q

What percentage of premature deaths in diabetics is caused by chronic kidney disease?

A

10%

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222
Q

What causes the associated complications of diabetes (er.g. CVD, CKD, etc)

A

Degree and duration of hyperglycaemia

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223
Q

Diabetes is a risk factor for atherosclerosis, TRUE OR FALSE?

A

True, and is worsened when combined with smoking, hypertension, and hyperlipidaemia

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224
Q

How much more likely are diabetics to have a stroke than healthy people?

A

Twice as likely

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225
Q

How much more likely are diabetics to have an MI than healthy people?

A

4x as likely, and MIs are more likely to be silent

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226
Q

What causes peripheral vascular disease?

A

Decreased perfusion to peripheries due to atherosclerosis

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227
Q

How much more likely are peripheral vascular disease patients to have lower limb amputation than healthy people?

A

15-40x

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228
Q

What are the symptoms of peripheral vascular disease?

A

Intermittent claudication and rest pain

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229
Q

What are the signs of peripheral vascular disease?

A
  • Diminished / absent pedal pulses
  • Coolness of feet & toes
  • Poor skin and nails
  • Absence of hair on feet and legs
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230
Q

How can you detect peripheral vascular disease?

A

Doppler ultrasound

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231
Q

How do you treat peripheral vascular disease?

A
  • Walking through claudication pain (encourages formation of new collaterals)
  • Surgical intervention
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232
Q

Which gender is at higher risk of macrovascular complications of DM?

A

Females, as DM removes the vascular advantage conferred by the female sex

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233
Q

How can you modify risk factors to prevent macrovascular complications of DM?

A
  • Aggressive BP control
  • Smoking cessation
  • Statin treatment
  • ACE inhibitor treatment (or angiotensin receptor blocker if intolerant)
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234
Q

Which branch of complications is specific to diabetes?

A

Microvascular complications

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235
Q

Which three sites are in particular danger of vessel damage with DM?

A
  • Retina
  • Glomerulus
  • Nerve sheath
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236
Q

How long does it take for microvascular damage to manifest after diabetes diagnosis?

A

~ 10-20 years in young patients

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237
Q

What is the most common cause of blindness in the working population?

A

Diabetic retinopathy

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238
Q

What are the greatest risk factors for diabetic retinopathy (DR)?

A
  • Long duration DM
  • Poor glycemic control
  • Hypertensive
  • Insulin treatment
  • Pregnancy
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239
Q

How do you reduce the risk of getting DR?

A

Keeping HbA1c below 7%, since each % increase increases DR progression exponentially

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240
Q

At diagnosis, what percentage of diabetics have early stage retinal damage?

A

~ 30%

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241
Q

What are microaneurysms of the retina of diabetics with background retinopathy?

A

Metabolic consequence of poorly controlled diabetes, causing intramural pericyte death and thickening of basement membrane of small blood vessels

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242
Q

What causes haemorrhages on the retina of diabetics with background retinopathy?

A

Breach of microaneurysms resulting in leakage of fluid into the retina

The fluid is cleared into the retinal veins, leaving behind protein and lipid deposits, resulting in hard exudates which are bright yellowish and white in colour

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243
Q

Describe pre-proliferative DR.

A
  • Micro-infarcts within retina due to occluded vessels cause “cotton wool spots” - sign of retinal ischaemia
  • Haemorrhage and venous bleeding
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244
Q

Describe proliferative DR.

A
  • Consequence of damage to retinal blood vessels and resultant retinal ischaemia
  • Ischaemia results in release of vascular growth factors (VEGF)
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245
Q

What do vascular growth factors do?

A
  • Cause new blood vessels to grow in retina
  • Some are inside retina (GOOD)
  • Some emerge through retina and lie on surface (BAD)
  • Causes stress within the eye and can result in poorly supported vessels bleeding
  • Small haemorrhages give rise to pre-retinal haemorrhages
  • Further bleeding causes vitreous haemorrhages which lead to sudden loss of vision
  • Collagen tissue grows along margins of new vessels and form fibrotic bands, which can contract and pull on retina, causing further haemorrhage and tractional retinal detachment
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246
Q

Describe maculopathy.

A

Fluid from leaking vessels is cleared poorly in the macular area (since its anatomy differs from the rest of the retina)

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247
Q

What happens to the retina in maculopathy in DR?

A

It is distorted and thickened at the macula

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248
Q

How do you treat DR?

A

Laser therapy - it doesn’t improve sight but it stabilises deterioration and prevents progression

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249
Q

What are the risks of laser therapy to treat DR?

A
  • Loss of night vision

- Loss of peripheral vision

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250
Q

How long after diagnosis of glomerular disease (as a complication of diabetes) does it take for clinical nephropathy to manifest?

A

15-25 years after diagnosis

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251
Q

How many diabetics suffer from clinical nephropathy secondary to glomerular disease?

A

25-35% of patients diagnosed under 30yo

252
Q

Describe diabetic nephropathy

A

Thickening of basement membranes of glomerulus due to poor glycemic control, leading to microalbuminuria

253
Q

What chemical present in the blood is an early warning sign of impending renal problems?

A

Albumin - MICROALBUMINURIA

254
Q

What happens if you test for microalbuminuria using a conventional dipstick?

A

It shows up negative for proteins

255
Q

How do you diagnose microalbuminuria?

A

Urine albumin:creatinine ratio > 3

256
Q

How does microalbuminuria progress?

A

> Intermittent albuminuria
Persistent proteinuria
Induces transient nephrotic syndrome

257
Q

What will a blood test of a patient with diabetic nephropathy show?

A
  • Normochromic normocytic anaemia

- Raised ESR

258
Q

How do you treat diabetic nephropathy?

A

Aggressive treatment of blood pressure with ACE inhibitors (e.g. RAMIPRIL) or angiotensin receptor blockers (e.g. CANDESARTAN)

259
Q

What should you NOT give someone with diabetic nephropathy?

A

Oral hypoglycaemic agents which are partially excreted via the kidneys

260
Q

What action needs to be taken with a diabetic nephropathic’s insulin?

A

Their insulin sensitivity increases so you need to lower insulin doses

261
Q

What is the prognosis for diabetic nephropathy?

A

Many patients will develop end stage kidney disease and require dialysis and kidney transplants (eventually)

262
Q

How many diabetics have diabetic neuropathy?

A

30-35%

263
Q

What is the most common form of diabetic neuropathy?

A

Distal symmetrical neuropathy

264
Q

How do isolated mononeuropathies form?

A

Occlusion of vasa nervorum

265
Q

What are vasa nervorum?

A

Small arteries that provide blood supply to peripheral nerves

266
Q

How do more diffuse neuropathies form?

A

The accumulation of fructose and sorbitol which disrupts the structure and function of the nerve

267
Q

What are the risk factors for diabetic neuropathy?

A
  • Hypertension
  • Smoking
  • HbA1c
  • Diabetes duration
  • BMI
268
Q

What are the ‘pain’ clinical features of diabetic neuropathy?

A
  • Allodynia (triggering of pain from stimuli that do not normally cause pain)
  • Paraesthesia (abnormal dermal sensation with no apparent cause, e.g. tingling)
  • Burning and pain (as though walking on broken glass) - WORSE AT NIGHT
269
Q

What are the ‘autonomic’ clinical features of diabetic neuropathy?

A
  • Postural hypotension
  • Gastroparesis
  • Diarrhoea
  • Constipation
  • Incontinence
  • Erectile dysfunction
270
Q

What are the ‘insensitivity’ clinical features of diabetic neuropathy?

A

“Glove and stocking” sensory loss

271
Q

What can sensory loss of the feet lead to in diabetics?

A

Foot ulceration, infection, and amputation

272
Q

Describe the ‘mononeuritis multiplex’ clinical feature of diabetic neuropathy

A
  • Abrupt onset and sometimes painful
  • Isolated palsies to nerves of external eye muscles (III & VI) are most common
  • Characteristic feature of diabetic CN3 lesion is that pupillary reflexes are retained owing to sparing of the pupillomotor fibres
273
Q

Describe the ‘diabetic amyotrophy’ clinical feature of diabetic neuropathy

A
  • Typically seen in older men
  • Painful asymmetrical wasting of quadriceps and other pelviformal muscles
  • Knee reflexes diminished / absent
  • Associated with poor glycaemic control but resolves with control
274
Q

How do you treat diabetic neuropathy?

A
  • Good glycaemic control
  • Paracetamol
  • Tricyclic antidepressants (e.g. AMITRIPTYLINE)
  • Anticonvulsants (e.g. GABAPENTIN or PREGABLIN)
  • Opiates (e.g. TRAMADOL)
  • Transcutaneous nerve stimulation
  • Avoidance of weight bearing
275
Q

What is a serious consequence of insensitivity associated with diabetic neuropathy?

A

Diabetic foot ulceration

276
Q

What percentage of diabetics experience a diabetic foot ulcer (DFU) in their lifetime?

A

15%

277
Q

Describe the pathology of DFU

A

> Neuropathy increases risk of ‘silent trauma’ - patient injures foot but doesn’t realise

  • Neuropathy results in dry skin on feet, which means they are susceptible to cracking

> Causes ulcer formation

> Ischaemia means ulcer cannot heal

> Causes infection and eventually amputation

278
Q

What is the clinical presentation of a DFU?

A

Painless, punched-out ulcer of foot in an area of a thick callus

279
Q

How can you manage DFUs?

A
  • FEET SCREENINGS
  • Education
  • Check feet daily (to detect ulcers early)
  • Check shoes for sharps before putting them on
  • Tie laces loosely
  • Keep feet away from heat and check bath temperatures before stepping in
280
Q

What are the four main threats to skin and subcutaneous tissue in diabetics with diabetic neuropathy?

A
  • Infection - can take hold RAPIDLY
  • Ischaemia
  • Abnormal blood pressure - must not put pressure on a DFU
  • Wound environment - use dressings that absorb & remove exudes
281
Q

Why can poorly controlled diabetes lead to increased susceptibility to infections?

A

It impairs the function of polymorphonuclear leucocytes and confers

282
Q

Which infections does poorly controlled diabetes confer an increased susceptibility to?

A
  • UTIs
  • Boils and abscesses
  • Staphylococcal skin infections
  • Mucocutaneous candidiasis
  • Rectal abscesses
  • Pyelonephritis
  • Staphylococcal and pneumococcal pneumonia
  • TB
  • G-ve bacterial pneumonia
283
Q

What can infections lead to in diabetics?

A
  • Loss of glycaemic control

- Ketoacidosis

284
Q

What causes lipohypertrophies in diabetics?

A

Using the same injection site frequently

285
Q

How can childhood diabetes affect the skin in later life?

A

Skin contractures are a common consequence of childhood diabetes

286
Q

How can you demonstrate skin contractures in a patient?

A

> Ask them to join their hands as if in prayer

> Metacarpopalangeal and interphalangeal joints cannot be opposed

287
Q

What is the most common endocrine emergency?

A

Hypoglycaemia

288
Q

What is the definition of hypoglycaemia?

A

Plasma glucose < 3mmol/L

289
Q

What is the aetiology of hypoglycaemia in diabetics?

A

Insulin or sulphonylurea treatment

  • Increased activity
  • Missed meals
  • Overdose (accidental or non-accidental)
290
Q

What is the aetiology of hypoglycaemia in non-diabetics?

A
  • EXogenous drugs (e.g. insulin, alcohol binge with no food)
  • Pituitary insufficiency
  • Liver failure
  • Addison’s disease
  • Islets cell tumour (insulinoma) & Immune hypoglycaemia
  • Non-pancreatic neoplasm (e.g. fibrosarcomas and haemangiopericytomas)

Remember: EXPLAIN

291
Q

What are the autonomic clinical presentation features of hypoglycaemia?

A
  • Sweating
  • Anxiety
  • Hunger
  • Tremor
  • Palpitations
  • Dizziness
292
Q

What are the neuroglycopenic clinical presentation features in hypoglycaemia?

A
  • Confusion
  • Drowsiness
  • Visual trouble
  • Seizures
  • Coma
293
Q

How do you diagnose hypoglycaemia?

A

Fingerpick blood during attack (on filter paper if at home) then send for analysis

294
Q

What do you look for in the blood if you have a suspected hypoglycaemic patient?

A
  • Glucose
  • Insulin
  • C-peptide
  • Plasma ketones
295
Q

Why would a patient be hypoglycaemic hyperinsulinaemic?

A
  • Insulinoma
  • Sulfonylurea or insulin injection (only if no C-peptide in serum)
  • Congenital
296
Q

Why would a patient have low insulin and high ketones?

A
  • Alcohol
  • Pituitary insufficiency
  • Addison’s disease
297
Q

How do you treat hypoglycaemia if a patient can eat?

A

Oral sugar and long-acting starch (e.g. toast)

298
Q

How do you treat hypoglycaemia if a patient cannot swallow?

A

50% glucose IV or IM glucagon (if no IV access)

299
Q

If a diabetic is hypoglycaemic what is it important you do?

A

Re-educate them on insulin use and safety

300
Q

What is the most common endocrine disorder?

A

Thyroid disease

301
Q

Which sex is more likely to get thyroid disease?

A

Females

302
Q

What is the prevalence of hyperthyroidism?

A

2.5%

303
Q

What is the prevalence of hypothyroidism?

A

5%

304
Q

What is the most common clinical presentation of thyroid disease?

A

Goitre (5-15%)

305
Q

What is a goitre?

A

A swelling of the thyroid gland that causes a palpable lump to form in the front of the neck which will move when you swallow

306
Q

Why do goitres form in hyperthyroidism?

A

(e.g. in Grave’s) there is excess stimulation of the TSH receptor, which stimulates the thyroid to produce more hormone and grow larger

307
Q

Why do goitres form in hypothyroidism?

A

When the pituitary detects low thyroid levels, it produces more TSH which in turn stimulates TSH receptors on the thyroid, resulting in thyroid enlargement (aka. a goitre)

308
Q

Where are goitres endemic?

A

In iodine deficient areas

309
Q

What are the three physical descriptions of goitres?

A
  • Diffuse
  • Nodular
  • Solitary
310
Q

What causes a diffuse goitre?

A
  • Graves’ disease
  • Hashimoto’s thyroiditis
  • De Quervain’s
311
Q

What causes a nodular goitre?

A
  • Adenoma / cyst

- Carcinoma

312
Q

Define ‘thyrotoxicosis’

A

Excess of thyroid hormones in blood

313
Q

What are the mechanisms for thyrotoxicosis?

A
  • Overproduction of thyroid hormones (hyperthyroidism)
  • Leakage of preformed hormone from thyroid
  • Ingestion of excess hormone
314
Q

What causes leakage of preformed hormones from thyroid?

A

Follicular cells being destroyed by either infection or autoimmunity, thereby releasing 2-3 months supply of hormone

315
Q

What causes hyperthyroidism?

A
  • Graves’ disease (MOST COMMON)
  • Toxic multi-nodular goitre
  • Toxic adenoma (benign)
  • Ectopic thyroid tissue (metastases)
  • Exogenous (iodine/T4 excess)
  • De Quervain’s thyroiditis (post-viral)
316
Q

What is myxoedema?

A

Swelling of the skin and underlying tissues, giving a waxy appearance

317
Q

What are the two categories of hypothyroidism?

A

Primary and secondary hypothyroidism

318
Q

What are the causes of primary hypothyroidism?

A
  • Primary atrophic hypothyroidism (PAH)
  • Hashimoto’s thyroiditis
  • Iodine deficiency
  • Post-thyroidectomy / radio iodine / anti-thyroid drugs
  • Lithium / amiodarone
319
Q

What is the definition of primary hypothyroidism?

A

Reduced T4, and thus reduced T3

320
Q

What causes secondary hypothyroidism?

A

Hypopituitarism

321
Q

What is the definition of secondary hypothyroidism?

A

Reduced TSH from anterior pituitary

322
Q

What is Graves’ disease?

A

Autoimmune induced excess production of thyroid hormone

323
Q

Describe the epidemiology of Graves’ disease?

A
  • Most common cause of hypothyroidism (2/3rds of cases)
  • More common in females
  • Typical onset at 40-60yrs
324
Q

What is a common trigger for hypothyroidism in women?

A

Post-partum

325
Q

What are the risk factors for Graves’ disease?

A
  • Post-partum
  • Genetics
  • E.coli and other G-ve organisms
  • Smoking
  • Stress
  • High iodine intake
  • Vitiligo (AID)
  • Addison’s disease (AID)
  • Pernicious anaemia (AID)
  • Myasthenia gratis (AID)
  • DMT1 (AID)
326
Q

Why do E.coli and other G-ve organisms cause Graves’ disease?

A

They contain TSH-binding sites so may initiate pathogenesis via ‘molecular mimicry’

327
Q

Describe the pathophysiology of Graves’ disease

A

> Serum IgG antibodies specific for Graves’ disease (TSH receptor stimulating antibodies, TSHR-Ab) bind to TSH receptors in thyroid

> Stimulates thyroid hormone production (T3 & T4) - antibodies behave like TSH

> Results in excess secretion of thyroid hormones and hyperplasia of thyroid follicular cells

> Hyperthyroidism and diffuse goitre

328
Q

What is the ophthalmological clinical presentation SPECIFIC to Graves’ disease?

A
  • Retro-orbital inflammation and extraocular muscle swelling
  • Eye discomfort, grittiness, increased tear production, photophobia, diplopia, reduce acuity
  • Exophthalmos (protruding eye appearance)
  • Proptosis (eye protrudes beyond orbit)
  • Conjunctival oedema
  • Corneal ulceration
  • Ophthalmoplegia (paralysis of eye muscles)
329
Q

How do you examine opthalmopathy?

A

CT scan or MRI of orbit

330
Q

How can you conservatively treat eye deformities in Graves’ disease?

A
  • Smoking cessation

- Sunglasses

331
Q

How can you pharmacologically / surgically treat eye deformities in Graves’ disease?

A
  • IV methylprednisolone
  • Surgical decompression
  • Eyelid surgery
332
Q

What is the dermopathy clinical presentation SPECIFIC to Graves’ disease?

A
  • Pretibial myxoedema (raised, purple-red symmetrical skin lesions over the anterolateral aspect of the shin)
  • Thyroid acropachy (clubbing, swollen fingers and periosteal bone formation)
333
Q

What are toxic multi-modulate goitres?

A

Nodular goitres that secrete thyroid hormones

334
Q

What is the epidemiology for toxic multi-nodular goitres?

A
  • Elderly people
  • Common in older women
  • Iodine deficient areas
335
Q

What is the prognosis of drug therapy on toxic multi-nodular goitres?

A

Rarely produces prolonged remission

336
Q

How many hyperthyroidism cases can be attributed to solitary toxic adenomas / nodules?

A

~ 5%

337
Q

What is De Quervain’s thyroiditis?

A

Transient hyperthyroidism, resulting from acute inflammation of the thyroid, probably due to viral infection

338
Q

What usually accompanies De Quervain’s thyroiditis?

A
  • Fever
  • Malaise
  • Neck pain
339
Q

How do you treat De Quervain’s thyroiditis?

A

Treat with asipirin

Only give prednisolone for severely symptomatic cases

340
Q

Which drugs can cause drug-induced hyperthyroidism?

A
  • Amiodarone
  • Iodine
  • Lithium
341
Q

What is amiodarone?

A

Anti-arrhythmic drug

342
Q

Why can amiodarone cause both hyperthyroidism and hypothyroidism?

A

Hyperthyroidism - due to high iodine content of amiodarone

Hypothyroidism - since it inhibits the conversion of T4 to T3

343
Q

What is the general clinical presentation for hyperthyroidism?

(i.e. all types, not specific to Graves’)

HINT: There are 19

A
  • Palpitations
  • Diarrhoea
  • Weight loss & appetite increase
  • Oligomenorrhoea (infrequent periods)
  • (potential) Infertility
  • Heat intolerance (i.e. sweating a lot)
  • Irritability / behaviour change
  • Tremor
  • Hyperkinesis
  • Warm (peripheral vasodilation)
  • Proximal myopathy and myoatrophy
  • Lymphadenopathy and splenomegaly
  • Anxiety
  • Palmar erythema, warm moist palms, & fine hand tremor
  • Lid lag and ‘stare’
  • AF (in elderly)
  • Tachycardia (in elderly)
  • Excessive height or growth rate (in children)
  • Behaviour problems (e.g. hyperactivity) (in children)
344
Q

What is the differential diagnosis for hyperthyroidism, and what should you look for to differentiate?

A

Anxiety

Look for;

  • eye signs
  • diffuse goitre
  • proximal myopathy and atrophy
345
Q

What test do you do to diagnose hyperthyroidism?

A

Thyroid function test (TST)

346
Q

What are the results of a thyroid function test (TST) which would diagnose hyperthyroidism?

A
  • Suppressed TSH

- Raised T4 & T3 - DIAGNOSTIC

347
Q

Why is TSH suppressed in someone with hyperthyroidism?

A

Due to negative feedback produced by hyperthyroidism

348
Q

How would the TST results differ between primary and secondary hyperthyroidism?

A

TSH will be very elevated in secondary hyperthyroidism, as the problem is with the pituitary

Thus, negative feedback does not work to suppress pituitary TSH output

349
Q

What antibodies will you find in the blood of someone with hyperthyroidism?

A
  • Thyroid peroxidase (TPO)
  • Thyroglobulin antibodies

(Only found in 80% of Graves’ patients)

350
Q

How do you differentiate between Graves’ and a toxic adenoma of the thyroid?

A

Ultrasound

351
Q

How do you diagnose someone with Graves’, as opposed to another type of hyperthyroidism?

A
  • Raised TSH receptor stimulating antibodies (TSHR-Ab) - DIAGNOSTIC OF GRAVES’
  • Mild neutropenia
352
Q

How do you rapidly control the symptoms of hyperthyroidism?

A

Beta-blockers, e.g. PROPANOLOL

353
Q

Name 2 anti-thyroid drugs

A
  • Propylthiouracil (PTU)

- Carbimazole

354
Q

What does propylthiouracil do?

A

Stops the conversion of T4 to T3

355
Q

What does oral carbimazole do?

A
  • Blocks thyroid hormone biosynthesis

- Immunosuppressive effects (which will affect Graves’ progression)

356
Q

What strategies can you use when treating hyperthyroidism with carbimazole?

Describe them

A
  • Titration therapy
    > oral carbimazole for 4 weeks, then reduce doses according to thyroid function test
    > TST: TSH, T4, T3
  • Block-replace therapy
    > oral carbimazole + thyroxine (T4)
    > less of a risk of developing hypothyroidism
357
Q

What is the risk of discontinuing drug treatment with Graves’ disease?

A

Half of those with Graves’ disease relapse with treatment discontinuation after 2 years

358
Q

What are the side effects of anti-thyroid drugs?

A
  • Agranulocytosis (main SE) - results in severe leukopenia
  • Rash (common)
  • Arthralgia
  • Hepatitis
  • Vasculitis
359
Q

What is the risk of agranulocytosis with anti-thyroid drug treatment?

A

If they get a sore throat, mouth ulcers, and fevers you must STOP DRUG TREATMENT IMMEDIATELY

360
Q

How can you treat hyperthyroidism?

A
  • Beta-blockers (treats symptoms, not hyperthyroidism)
  • Anti-thyroid drugs
  • Radioactive iodine
  • Surgery
361
Q

What drug do you give in radioactive iodine treatment of hyperthyroidism?

A

Radioactive I(131)

362
Q

What contraindicates radioactive iodine treatment of hyperthyroidism?

A

Pregnancy and breast feeding

363
Q

Can you take antithyroid drugs and radioactive iodine at the same time?

A

No - you must stop antithyroid drugs 4 days before giving iodine

364
Q

Why is radioactive iodine useful for treating hyperthyroidism?

A

Iodine is essential for thyroid hormone production, so it is readily taken up by the thyroid gland

365
Q

Why is radioactive iodine an effective treatment for hyperthyroidism?

A

The radioactive iodine accumulates and results in local irradiation and tissue damage, with return to normal function over 4-12 weeks

366
Q

What are the side effects of radioactive iodine treatment of hyperthyroidism?

A
  • Discomfort in the neck

- Initial hyperthyroidism (as you stop all anti-thyroid treatment)

367
Q

When would you recommend surgery for hyperthyroidism?

A
  • Patients with large goitres
  • Poor response to drugs
  • Severe side effects to drugs
368
Q

Who gets subtotal thyroidectomies?

A

Patients who have been rendered euthyroid (normal functioning gland)

369
Q

Who gets total thyroidectomies?

A

Patients with;

  • large goitres
  • suspicion of malignancy in a nodule
  • Graves’
370
Q

What do you need to do to prepare for thyroid surgery to treat hyperthyroidism?

A
  • Stop anti-thyroid drugs 10-14 days before

- Give potassium iodide to reduce vascularity of gland

371
Q

What is the consequence of surgery to treat hyperthyroidism?

A

Patients become hypothyroid

372
Q

What are the complications of thyroid surgery?

A
  • Tracheal compression from post-operative bleeding
  • Laryngeal nerve palsy resulting in hoarse voice
  • Transient hypocalcaemia (due to removal of parathyroid gland too)
373
Q

What are the complications of hyperthyroidism?

A

Thyroid crisis / thyroid storm - MEDICAL EMERGENCY

374
Q

What is a thyroid storm / crisis?

A

Rare, life-threatening condition in which there is a rapid deterioration of thyrotoxicosis - RAPID T4 INCREASE

375
Q

What are the features of thyroid storm?

A
  • Hyperpyrexia
  • Tachycardia
  • Extreme restlessness
  • Eventual delirium, coma, and death
376
Q

What usually precipitates a thyroid crisis?

A
  • Stress
  • Infection
  • Surgery
  • Radioactive thyroid therapy in an unprepared patient
377
Q

How do you treat thyroid storm?

A
  • Oral carbimazole
  • Oral propanolol
  • Oral potassium iodide (to acutely block the release of thyroid hormone from gland)
  • IV hydrocortisone (to inhibit peripheral conversion of T4 to T3)
378
Q

Define hypothyroidism

A

Underactivity of the thyroid gland; may be primary (from disease of the thyroid) or much less commonly secondary to hypothalamic or pituitary disease

379
Q

What is the chief cause of hypothyroidism?

A

Iodine deficiency

380
Q

What is the most common cause of hypothyroidism in areas with no iodine deficiency?

A

Autoimmune / atrophic hypothyroidism

381
Q

What is the prevalence of hypothyroidism?

A

0.1-2%

382
Q

Which sex is more likely to get hypothyroidism?

A

Females

383
Q

What is autoimmune hypothyroidism associated with?

A

Other autoimmune diseases (e.g. DMT1, pernicious anaemia, etc.)

384
Q

Which conditions is hypothyroidism associated with?

A
  • Turner’s syndrome
  • Down’s syndrome
  • Cystic fibrosis
  • Primary biliary cirrhosis
  • Ovarian hyper-stimulation
385
Q

What causes autoimmune / atrophic hypothyroidism?

A

Antithyroid antibodies leading to lymphoid infiltration of the gland and eventual atrophy and fibrosis

386
Q

Do you get goitres with autoimmune / atrophic hypothyroidism?

A

No - the thyroid / goitre atrophies

387
Q

Describe the epidemiology of autoimmune / atrophic hypothyroidism

A
  • More common in females
  • Incidence increases with age
  • Associated with other autoimmune conditions
388
Q

Describe the epidemiology of Hashimoto’s thyroiditis

A
  • More common in females (60-70yrs)

- Most common in middle age

389
Q

Do you get goitres with Hashimoto’s thyroiditis?

A

Yes - Hashimoto’s thyroiditis produces atrophic changes with regeneration that result in goitre formation, due to lymphocytic and plasma cell infiltration

390
Q

What does the thyroid feel like with Hashimoto’s thyroiditis?

A

Firm and rubbery

391
Q

What is thyroid peroxidase?

A

Essential enzyme for the production and storage of thyroid hormone

392
Q

What do you blood results show in Hashimoto’s thyroiditis?

A

Thyroid peroxidase antibodies (TPO-Ab) are present in high titres

393
Q

How do you treat Hashimoto’s thyroiditis?

A

Levothyroxine therapy to shrink the goitre

394
Q

What is postpartum thyroiditis?

A

Transient phenomenon following pregnancy, which may cause hyperthyroidism, hypothyroidism, or the two sequentially

395
Q

What is thought to be the cause of postpartum thyroiditis?

A

Modifications to the immune system necessary in pregnancy

396
Q

How can postpartum thyroiditis progress?

A

It is usually self-limiting, but when conventional antibodies are found there is a high chance of it progressing to permanent hypothyroidism

397
Q

What is postpartum thyroiditis often diagnosed as?

A

Postpartum depression

398
Q

What does ‘iatrogenic’ mean?

A

Caused by treatment or examination

399
Q

What are the iatrogenic causes of hypothyroidism?

A
  • Thyroidectomy

- Radioactive iodine treatment

400
Q

Which drugs can induce hypothyroidism?

A
  • Carbimazole
  • Lithium
  • Amiodarone
  • Interferon
401
Q

Do goitres form with iodine deficiency?

A

Yes

402
Q

What is the difference between hypothyroid and euthyroid?

A

Hypothyroidism - underractive thyroid

Euthyroid - normal functioning thyroid

403
Q

What are the symptoms of hypothyroidism?

A
  • Hoarse voice
  • Goitre
  • Constipation
  • Cold intolerant
  • Weight gain
  • Menorrhagia
  • Myalgia
  • Tired, low mood, dementia
  • Myxoedema - accumulation of mucopolysaccharide in SC tissue
404
Q

What are the clinical signs of hypothyroidism?

A
  • Bradycardia
  • Reflexes relax slowly
  • Ataxia (cerebellar)
  • Dry, thin hair/skin
  • Yawning/drowsy/coma
  • Cold hands +/- temperature drop
  • Ascites
  • Round puffy face
  • Defeated demeanour
  • Immobile +/- Ileus (temporary arrest of intestinal peristalsis)
  • Congestive cardiac failure

Remember: BRADYCARDIA

405
Q

What is the clinical presentation of a child with hypothyroidism?

A
  • Slow growth velocity
  • Poor school performance
  • Arrest in puberty (sometimes)
406
Q

If a young woman comes in with query hypothyroidism, when can you exclude this from your differential diagnoses?

A

If she has oligomenorrhoea, amenorrhoea, menorrhagia, infertility, or hyperprolactinaemia

407
Q

If an elderly person comes in with query hypothyroidism, when can you exclude this from your differential diagnoses?

A

If they have cognitive impairment

408
Q

What are the results of a TFT if someone has hypothyroidism?

A
  • Raised serum TSH (confirms PRIMARY hypothyroidism)

- Low serum free T4 - DIAGNOSTIC

409
Q

What would you find in the blood of someone with Hashimoto’s thyroiditis?

A
  • Thyroid antibodies
  • Organ specific-antibodies

e.g. TPO-Ab

410
Q

What would the blood results be for someone with hypothyroidism?

A
  • Anaemic
  • Raised serum aspartate transferase from muscle / liver
  • Increased serum creatinine kinase levels (myopathy)
  • Hypercholesterolaemia
  • Hyponatraemia (increase in ADH and impaired free water clearance)
411
Q

What is the treatment for hypothyroidism?

A

Lifelong thyroid hormone replacement e.g. LEVOTHYROXINE (T4)

412
Q

What do you have to do if you diagnose a patient with ischaemic heart disease with hypothyroidism?

A

Start levothyroxine on a lower dose and use with caution

413
Q

What is the aim with hypothyroidism treatment?

A

Aim is normal TSH conc. which can be achieved with levothyroxine, but too much can completely suppress TSH and risks AF and osteoporosis

414
Q

How do you monitor primary hypothyroidism?

A
  • Titrate dose until TSH normalises

- Check T4 levels 6-8 weeks after dose adjustment

415
Q

How do you monitor secondary hypothyroidism?

A
  • TSH will always be low

- Monitor T4

416
Q

What are the complications of hypothyroidism treatment with levothyroxine?

A

Myxoedema coma

417
Q

What is myxoedema coma?

A

Severe hypothyroidism (reduced T4) which may result in confusion and coma (especially in the elderly)

418
Q

What is the clinical presentation of myxoedema coma?

A
  • Hypothermia
  • Cardiac failure
  • Hypoventilation
  • Hypoglycaemia
  • Hyponatraemia
419
Q

How do you treat someone with myxoedema coma?

A
  • IV / Oral T3
  • Glucose infusion
  • Gradual rewarming
420
Q

Describe the epidemiology of thyroid carcinoma

A
  • Not common
  • 400 deaths pa in the UK
  • More common in females
421
Q

What is the risk factor for thyroid carcinoma?

A

Radiation

422
Q

What are the five types of thyroid carcinoma? How common are they?

A
  • Papillary (70%)
  • Follicular (20%)
  • Anaplastic (<5%)
  • Lymphoma (2%)
  • Medullary cell (5%)
423
Q

Describe papillary thyroid carcinomas

A
  • Well differentiated
  • More common in young people
  • Local spread
  • Good prognosis
  • Arise from thyroid epithelium
424
Q

Describe follicular thyroid carcinomas

A
  • Middle age
  • Spread to lung / bone
  • Good prognosis (usually)
  • Well differentiated
  • Arise from thyroid epithelium
425
Q

Describe anaplastic thyroid carcinomas

A
  • Very undifferentiated
  • Arise from thyroid epithelium
  • Aggressive
  • Local spread
  • Poor prognosis
426
Q

Where do medullary cell thyroid carcinomas arise from?

A

Calcitonin C cells of thyroid gland

427
Q

Over 90% of thyroid carcinomas secrete what?

A

Thyroglobulin

428
Q

Do thyroid glands still function hormonally even if they are cancerous (thyroid carcinomas)?

A

No - thyroid carcinomas are minimally active hormonally

429
Q

What can you use as a tumour marker for thyroid carcinomas?

A

Thyroglobulin

430
Q

What do 90% of thyroid carcinomas present as clinically?

A

Thyroid nodules

431
Q

In 5% of thyroid carcinoma cases, what else do they present with?

A
  • Cervical lymphadenopathy

- Lung, cerebral, hepatic, or bone metastases

432
Q

What appearance of the thyroid gland should make you think ‘thyroid carcinoma’?

A
  • Increases in size
  • Hardens
  • Irregular shape
433
Q

Why might patient with thyroid carcinomas go to the doctor?

A
  • Dysphagia (difficulty swallowing)

- Hoarseness of voice

434
Q

How do you distinguish between benign and malignant nodules?

A

Fine need aspiration cytology biopsy

435
Q

Before you operate on a thyroid carcinoma, what do you need to do?

A

A blood test to check if patient is hypothyroid or hyperthyroid, as this needs to be treated before surgery

436
Q

How can you differentiate between benign and malignant thyroid tumours?

A

Ultrasound of thyroid

437
Q

How can you treat thyroid carcinomas?

A
  • Radioactive iodine therapy
  • Levothyroxine
  • Chemotherapy
  • Thyroidectomies
438
Q

Why should you give levothyroxine to patients with thyroid carcinomas?

A

To keep TSH reduced as it is a growth factor for the cancer

439
Q

What is the specific treatment for papillary / follicular thyroid carcinomas?

A
  • Total thyroidectomy

- Ablative radioactive iodine

440
Q

What is the specific treatment for anaplastic thyroid carcinomas and lymphomas?

A
  • External radiotherapy (for brief respite)

- Mainly palliative

441
Q

What is the specific treatment for medullary thyroid carcinomas?

A
  • Thyroidectomy

- Lymph node removal

442
Q

Define Cushing’s syndrome

A

General term which refers to chronic, excessive, and inappropriately elevated of circulating cortisol, whatever the cause

443
Q

What mimics Cushing’s syndrome?

A

Alcohol excess

444
Q

Define Cushing’s disease

A

Specifically refers to excess glucocorticoids, resulting from inappropriate ACTH secretion from the pituitary due to tumour

445
Q

Where is cortisol released from?

A

Zona glomerulosa of the adrenal cortex

446
Q

What are the functions of cortisol?

A
  • Increases carbohydrate and protein catabolism
  • Increases deposition of fat and glycogen
  • Na+ retention
  • Increased renal K+ loss
  • Diminished host response to infection
447
Q

What determines CRH and cortisol release?

A

Circadian rhythms and stress

448
Q

When are CRH / cortisol levels the highest?

A

7/9am

449
Q

When are CRH / cortisol levels the lowest?

A

Midnight

450
Q

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

A

Oral steroids, i.e. glucocorticoid therapy

451
Q

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

A

Raised ACTH

452
Q

What is the main cause of raised ACTH?

A

Pituitary adenoma (Cushing’s disease)

453
Q

When might people normally have high cortisol levels?

A
  • Alcohol pseudo-Cushing’s syndrome
  • Depression
  • Obesity
  • Pregnancy
454
Q

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

A
  • ACTH-dependent causes (RAISED ACTH)

- ACTH-independent causes (LOW ACTH due to negative feedback from raised cortisol)

455
Q

How does Cushing’s disease result in Cushing’s syndrome?

A

Benign ACTH-secreting pituitary adenoma causes bilateral adrenal hyperplasia

456
Q

Describe the epidemiology of Cushing’s disease

A
  • Equal prevalence in men and women

- Peak age is 30-50yrs

457
Q

What is ectopic ACTH production?

A

An ACTH-producing tumour elsewhere the body (particularly small cell lung cancers and carcinoid tumours)

458
Q

What are the three main causes of ACTH-dependent Cushing’s syndrome?

A
  • Cushing’s disease (MOST COMMON)
  • Ectopic ACTH production
  • ACTH treatment (e.g. for asthma)
459
Q

What are the two ACTH-independent causes for Cushing’s syndrome?

A
  • Adrenal adenoma (benign tumour of adrenal gland that releases cortisol)
  • Iatrogenic (e.g. administration of glucocorticoid, e.g. PREDNISOLONE)
460
Q

What is the clinical presentation of Cushing’s syndrome?

A
  • Obesity
  • Plethoric complexion with moon face
  • Mood change
  • Proximal weakness
  • Gonadal dysfunction
  • Muscle atrophy
  • Thin skin that bruises easily
  • Purple striae (breasts, abdomen, thighs)
  • Acne
  • Increased BP
  • Failure for children to grow tall despite excess weight
  • Infections
  • Osteoporosis
  • Hyperglycaemia
461
Q

What is the fat distribution like in patients with Cushing’s syndrome?

A

Typically central, affecting trunk, abdomen, and neck

462
Q

Why are patients with Cushing’s syndrome more susceptible to infections?

A

Cortisol has anti-inflammatory and poor healing properties

463
Q

What is the differential diagnosis for Cushing’s syndrome?

A

Pseudo-Cushing’s syndrome

464
Q

What causes pseudo-Cushing’s syndrome and how do you treat it?

A
  • Alcohol excess

- 1-3 weeks of alcohol abstinence

465
Q

When diagnosing Cushing’s syndrome, what is it important you do?

A

Take a careful drug history, as it can be caused by oral steroids

466
Q

If the random plasma cortisol results show increased levels in a suspected Cushing’s syndrome patient, what should you do?

A

Proceed to 1st line test

467
Q

What external factors may make random plasma cortisol blood results come up high?

A
  • Illness
  • Time of day
  • Stress
468
Q

What is the basis for the first line test in Cushing’s syndrome?

A

Dexamethasone should, in a healthy patient, send negative feedback to the pituitary and hypothalamus resulting in decrease ACTH and thus reduced cortisol

The first line test is to give oral dexamethasone

469
Q

Describe the first line test for Cushing’s syndrome

A

> 1mg oral dexamethasone 00:00

> Measure serum cortisol at 8am

> Normally there will be cortisol suppression < 50nmol/L

> In Cushing’s syndrome there will be no suppression

470
Q

What is a positive test for Cushing’s with the overnight dexamethasone suppression test?

A

No suppression of cortisol

471
Q

What is the alternative to the overnight dexamethasone suppression test?

A

Urine free cortisol over 24 hours

472
Q

Describe the urine free cortisol test

A
  • Take >2 measurements in 24 hours

- Cortisol is bound to albumin, when capacity is reached, cortisol will spill out into the urine

473
Q

What do you do if you have a suspected Cushing’s syndrome patient, dexamethasone is not suppressed in the first line test?

A

Perform a 48 hour dexamethasone suppression test

474
Q

Describe the 48 hour dexamethasone test

A

> Oral dexamethasone 4x a day for 2 days

> Measure cortisol at 0hrs and 48hrs

> In Cushing’s, there will be no suppression

475
Q

What do you do both overnight and 48 hour dexamethasone suppression tests are positive (i.e. there is suppression)?

A

Check plasma ACTH

476
Q

What do you do if 1st and 2nd line tests for Cushing’s syndrome are positive, and plasma ACTH is undetectable?

A
  • Perform CT/MRI of adrenal glands to detect adenomas or carcinomas
  • If there is no mass, do adrenal vein sampling
477
Q

What do you do if 1st and 2nd line tests for Cushing’s syndrome are positive, and plasma ACTH is detectable?

A
  • Distinguish if the cause is from the pituitary or an ectopic ACTH production
  • Perform HIGH dose dexamethasone suppression test

OR

  • Perform corticotropin releasing hormone (CRH) test
478
Q

How do you perform a CRH test?

A

> Human IV CRH given

> Measure cortisol at 120 minutes

> Cortisol will rise with pituitary disease, but NOT with ectopic ACTH production

479
Q

What do you do if CRH test shows that cortisol responds to CRH?

A
  • Cushing’s disease is likely

- Pituitary MRI to locate neoplasm

480
Q

What do you do if CRH test shows that cortisol does not respond to CRH?

A
  • Hunt for ectopic source of ACTH
  • IV contrast CT of chest, abdomen, and pelvis
  • MRI of neck, thorax, and abdomen
  • CXR to look at lungs for small cell lung cancer
481
Q

What is the treatment for iatrogenic Cushing’s syndrome?

A

Stop steroids!

482
Q

What is the treatment for Cushing’s disease?

A
  • Surgical selective removal of pituitary adenoma (trans-sphenoidal approach)
  • Bilateral adrenalectomy (remove both adrenal glands)
483
Q

Why might you do a bilateral adrenalectomy to treat Cushing’s disease?

A
  • Source is unlocatable

- Cushing’s syndrome recurs post-operatively

484
Q

What is Nelson’s syndrome?

A

Increased skin pigmentation due to significantly increased ACTH from an enlarging pituitary tumour, as the adrenalectomy will remove negative feedback

485
Q

What is the complication of a bilateral adrenalectomy?

A

Nelson’s syndrome

486
Q

How do you treat Nelson’s syndrome?

A

Pituitary radiotherapy

487
Q

How do you treat an adrenal adenoma?

A

Adrenalectomy

488
Q

How do you treat an adrenal carcinoma?

A
  • Adrenalectomy
  • Radiotherapy
  • Adrenolytic drugs (e.g. MITOTANE)
489
Q

How do you treat ectopic ACTH?

A
  • Surgery if tumour is located and hasn’t spread
  • Drugs that inhibit cortisone synthesis (e.g. METYRAPONE, KETOCONAZOLE, FLUCONAZOLE are used pre-op or if awaiting effects of radiation)
490
Q

How is growth hormone secreted?

A

In a pulsatile fashion under the control of two hypothalamic hormones;

  • Growth hormone releasing hormone (GHRH) - STIMULATES GH secretion
  • Somatostatin (SST) - INHIBITS GH secretion
491
Q

What molecule in high concentration inhibits GH secretion?

A

Glucose

492
Q

What molecule inhibits GH secretion?

A

Ghrelin, which is synthesised in the stomach

493
Q

How does GH exert its action?

A
  • Indirectly through induction of insulin-like growth factor (IGF-1)
  • Directly on tissues, such as liver, muscle, bone, or fat to induce metabolic changes
494
Q

Where is insulin-like growth factor synthesised?

A

Liver and other tissues

495
Q

Define gigantism

A

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

496
Q

Define acromegaly

A

Excess GH in adults

497
Q

Describe the epidemiology of acromegaly

A
  • Rare
  • Equal prevalence in males and females
  • Incidence is highest in middle age
498
Q

What is the most common cause of acromegaly?

A

Benign GH-producing pituitary adenoma

499
Q

Aside from a pituitary adenoma, what else can cause acromegaly?

A

Hyperplasia, e.g. ectopic GH-releasing hormone from a carcinoid tumour

500
Q

What is a risk factor for acromegaly?

A

5% are associated with MEN-1 (multiple endocrine neoplasia-1)

501
Q

Describe the pathophysiology of acromegaly?

A

> Increased GH (either secreted due to pituitary tumour or due to ectopic carcinoid tumour) travels to tissues (e.g. liver) where it binds to reporters

> Increase in IGF-1

> Stimulates skeletal and soft tissue growth

> Causing ‘giant-like’ appearance and symptoms

502
Q

What can happen if a benign GH-producing pituitary tumour expands>

A

It can suppress surrounding structures and cause headaches and visual field loss

503
Q

What are the symptoms of acromegaly?

A
  • Headaches - very common
  • Increased size of hands & feet (acral enlargement)
  • Excessive sweating
  • Visual deterioration
  • Snoring
  • Wonky bite - malocclusion
  • Increase weight
  • Decreased libido
  • Amenorrhea
  • Arthralgia and backache
  • Acroparaesthesia (tingling and numbness of the extremities)
504
Q

What are the signs of acromegaly?

A
  • Skin darkening
  • Coarsening face with wide nose
  • Prognathism (relationship between mandible/maxilla with base of skull)
  • Big supraorbital ridge
  • Interdental seperation
  • Rings become tight
  • Fatigue
  • Deep voice
  • Carpal tunnel syndrome in 50%
    Large tongue - macroglossia
505
Q

What are the co-morbidities / complications associated with acromegaly?

A
  • Impaired glucose tolerance (40%)
  • Diabetes mellitus (15%)
  • Sleep apnea (due to excess soft tissue in larynx)
  • Hypertension
  • Left ventricular hypertrophy
  • Cardiomyopathy
  • Arrhythmias
  • Ischaemic heart disease
  • Stroke
  • Colon cancer
  • Arthritis
506
Q

What substances are raised in the blood of a patient with acromegaly?

A
  • Glucose
  • Ca2+
  • Phosphate
507
Q

When doing a blood test, what results mean you can exclude acromegaly from your suspicions?

A
  • Random GH is undetectable
  • GH < 0.4ng/ml
  • Normal IGF-1
508
Q

Is a detectable value of GH diagnostic for acromegaly? Why?

A

Not necessarily, since;

  • GH secretion is pulsatile
  • GH increases in stress, sleep, puberty, and pregnancy
509
Q

If GH is detected in the blood of someone with suspected acromegaly, what do you do?

A

Proceed to glucose tolerance test (GTT)

510
Q

Describe the GTT use for diagnosis of acromegaly

A

Can be diagnostic for acromegaly if there is no suppression of glucose, as glucose should inhibit GH release

511
Q

How can you use IGF-1 values in diagnosis of acromegaly?

A
  • Almost always raised in acromegaly

- Fluctuates less than GH - DIAGNOSTIC

512
Q

If someone has a benign pituitary adenoma pressing on their optic chiasm, how will this affect their vision?

A

Bilateral hemianopia

513
Q

If you suspect a patient’s acromegaly is due to benign GH-producing pituitary adenoma, what do you do to confirm this?

A
  • MRI scan of pituitary fossa

- Pituitary function test to look for partial / complete hypopituitarism

514
Q

What non-clinical thing can you use to help you with your diagnosis of acromegaly?

A

Old photos for comparison

515
Q

What is the first line treatment for a benign pituitary adenoma?

A

Trans-sphenoidal surgery to remove tumour and correct any compression caused by it

516
Q

If surgery fails to correct GH/IGF-1 hypersecretion, what can you do?

A
  • Treat with somatostatin analogues (SSAs) (e.g. IM OCTREOTIDE or IM LANREOTIDE)
  • GH receptor antagonists (e.g. SC PEGVISOMANT)
  • Dopamine agonists (e.g. ORAL CABERGOLINE or ORAL BROMOCRIPTINE)
517
Q

How do somatostatin analogues help treat acromegaly?

A

They inhibit GH release, like GH secretion

518
Q

What are the side effects of using somatostatin analogues?

A
  • GI and abdominal cramps
  • Flatulence
  • Loose stools
519
Q

Why would you give someone GH receptor antagonists to treat acromegaly?

A

They are intolerant to somatostatin analogues

520
Q

What do GH receptor antagonists do?

A

Suppress IGF-1

521
Q

What are the pros and cons of using dopamine agonists to treat acromegaly?

A

Cons;
- not as effective as GH receptor antagonists and SSAs

Pros;

  • rapid onset
  • oral administeration
  • no hypopituitarism
522
Q

What are the benefits of using stereotactic radiotherapy to treat acromegaly?

A
  • More accurate than conventional radiotherapy

- Better tumour localisation and irradiation whilst reducing radiation to normal brain tissue

523
Q

What affects prolactin release?

A

Negative feedback by dopamine from hypothalamus

524
Q

What does raised prolactin lead to?

A
  • Lactation

- Inhibition of gonadotropin releasing hormone resulting in reduced LH/FSH, and thus reduced testosterone / oestrogen

525
Q

What is the most common hormonal disturbance of the pituitary?

A

Prolactin

526
Q

What is the difference between the onset of hyperprolactinaemia in men and women?

A
  • Presents earlier in women (with menstrual disturbance)

- Presents later in men (with erectile dysfunction)

527
Q

What are the four causes / risk factors for hyperprolactinaemia?

A
  • Prolactinoma
  • Pituitary stalk damage
  • Drugs
  • Physiological
528
Q

What is a prolactinoma?

A

Tumour of pituitary which results in prolactin release

529
Q

How does pituitary stalk damage lead to hyperprolactinaemia?

A

Less dopamine to the anterior pituitary, so disinhibition of prolactin

530
Q

What can cause damage to pituitary stalk?

A
  • Pituitary adenomas
  • Surgery
  • Trauma
531
Q

What is the most common cause of hyperprolactinaemia?

A

Drug usage

532
Q

Which drugs are most likely to cause hyperprolactinaemia?

A
  • Metoclopramide

- Ecstasy

533
Q

What is the clinical presentation for someone with hyperprolactinaemia?

A
  • Amenorrhoea / oligomenorrhoea
  • Infertility
  • Galactorrhea
  • Low libido
  • Low testosterone in men
  • Erectile dysfunction and reduced facial hair in men
  • Local effect of tumour:
  • Headache
  • Visual defect e.g. bitemporal hemianopia as affecting optic chiasm
534
Q

How do you diagnose hyperprolactinaemia?

A

Measure basal prolactin level - it will be VERY high

535
Q

What is difference between treating prolactinomas and treating other benign pituitary adenomas?

A

It is more effective to treat prolactinomas medically rather than surgically

536
Q

How do you treat prolactinoma?

A

Dopamine agonists (e.g. ORAL CABERGOLINE or ORAL BROMOCRIPTINE)

537
Q

How do dopamine agonists affect prolactinomas?

In particular, how do they affect macroadenomas?

How do they affect microadenomas?

A

Massive shrinkage of the tumour

Remarkable sight-saving shrinkage of macroadenoma

Microadenomas respond to small doses of dopamine agonists once / twice a week

538
Q

What is Conn’s syndrome also known as?

A

Primary hyperaldosternism

539
Q

Describe Conn’s syndrome

A

Excess production of aldosterone, independent of the renin-angiotensin system

> resulting in increased sodium, and thus water retention (increasing BP) and decreased renin- release

540
Q

Describe the epidemiology of Conn’s syndrome

A

Rare condition accounting for <1% of all hypertension

541
Q

Describe the aetiology of hyperaldosteronism

A
  • 2/3rds - adrenal adenoma that secretes aldosterone - CONN’S SYNDROME
  • 1/3rd - bilateral ardenocortical hyperplasia
542
Q

What are the risk factors for hyperaldosteronism?

A

Hypertension in patients;

  • under 35 with no FHx
  • with accelerated hypertension
  • with hypokalaemia before diuretic surgery
  • resistant to conventional antihypertensive therapy (i.e. more than 3 drugs)
  • with unusual symptoms
543
Q

Describe the pathophysiology of hyperaldosteronism

A

> Disorder of adrenal cortex characterised by excess aldosterone production

> leading to Na+ and water retention, and K+ loss (balance charge)

> thus, hypokalaemia and hypertension

> due to aldosterone producing carcinoma (Conn’s) or adrenocortical hyperplasia

544
Q

What is the clinical presentation of hyperaldosteronism?

A
  • Often asymptomatic
  • Hypertension
  • Hypokalaemia
545
Q

What is the clinical presentation of hypokalaemia?

A
  • Weakness / cramps
  • Paraesthesia
  • Polyuria
  • Polydipsia
546
Q

What is secondary hyperaldosteronism?

A

Excess renin (and hence angiotensin II) which stimulates aldosterone release

547
Q

What causes secondary hyperaldosteronism?

A
  • Renal artery stenosis
  • Accelerated hypertension
  • Diuretics
  • Congestive heart failure
  • Hepatic failure
548
Q

What does the ECG look like for someone with Conn’s syndrome?

A

Hypokalaemia ECG;

  • Flat T waves
  • ST depression
  • Long QT
549
Q

What is the first test you run when trying to diagnose Conn’s syndrome? What is a positive result for Conn’s?

A

Plasma aldosterone:renin ratio (ARR)

Aldosterone is MUCH higher - NOT DIAGNOSTIC but used for screening

550
Q

What do you need to do 6 weeks before running an ARR test?

A

Stop spirolactone and eplerenone

551
Q

What test result is diagnostic for Conn’s syndrome?

A

Increased plasma aldosterone levels that are not suppressed with 0.9% saline infusion or fludrocortisone administration (a mineralocorticoid) - DIAGNOSTIC

552
Q

How do you differentiate between adrenal adenomas and adrenal hyperplasia?

A

CT or MRI scan or adrenal glands

553
Q

How do you treat Conn’s syndrome?

A
  • Laparoscopic adrenalectomy

- Aldosterone antagonist (e.g. ORAL SPIRONOLACTONE for 4 weeks pre-op to control BP and K+)

554
Q

What is Addison’s disease?

A

Primary hypoadrenalism

555
Q

Describe Addison’s disease

A

Destruction of the entire adrenal cortex resulting in mineralocorticoid (aldosterone), glucocorticoid (cortisol) and sex steroid (androgens) deficiency

556
Q

Describe the epidemiology of Addison’s disease

A
  • Very rare - 0.8 per 100,000
  • Can be fatal
  • Marked female preponderance
557
Q

What are the causes of Addison’s disease?

A
  • Autoimmune adrenalinitis
  • TB
  • Adrenal metastases
  • Long term steroid use
  • Opportunistic infections in HIV
  • Adrenal haemorrhage / infarction
558
Q

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

A

Autoimmune adrenalinitis (80%)

559
Q

What is autoimmune adrenalinitis?

A

Destruction of the adrenal cortex by organ-specific antibodies, with 21- hydroxylase as the common antigen

560
Q

How does long term steroid use cause Addison’s disease?

A

It will prevent ACTH release via negative feedback mechanisms

561
Q

How does Addison’s disease differ from hypothalamic-pituitary disease?

A

Addison’s = all steroids are reduced

Hypothalamic-pituitary disease = glucocorticoids (e.g. cortisol) are reduced

562
Q

Why do you get hyperpigmentation in Addison’s disease?

A

> Reduced cortisol

> Increased CRH and ACTH production

> Increased ACTH -> hyperpigmentation

563
Q

What is the clinical presentation of Addison’s disease?

A
  • Lethargy, depression, low mood & self esteem
  • Anorexia & weight loss
  • Vitiligo
  • Nausea and vomiting
  • Tanned skin - ‘bronze’
  • Diarrhoea, constipation and abdominal pain
  • Impotence/amenorrhea
  • Postural hypotension
  • Lean build
  • Dizzy
  • Dehydration
564
Q

What are the signs of critical deterioration in someone with Addison’s disease?

A
  • Shock - decreased BP, tachy.
  • Raised temperature
  • Coma
565
Q

Why are patients with Addison’s disease prone to vitiligo?

A

Loss of adrenal androgen

566
Q

Why are patients with Addison’s disease prone to postural hypotension?

A

Loss of aldosterone, resulting in hypovolaemia

567
Q

When should you think of Addison’s disease in patients?

A

If they have unexplained pain or vomiting

568
Q

What do the blood tests of someone with Addison’s show?

A
  • Hyponatraemia
  • Hyperkalaemia
  • Hypoaldosteronism
  • Low cortisol
  • Uraemia
  • Raised Ca2+
  • Eosinophilia
  • Anaemia
569
Q

Why is the blood of an Addison’s patient hyponatraemic and hypokalaemia?

A

Decrease in aldosterone

570
Q

Why does Addison’s disease result in eosinophilia?

A

Cortisol has anti-inflammatory effects, so reduction in cortisol results in raised white cells

571
Q

What test can you use to diagnose Addison’s disease?

A

Short ACTH stimulation test

572
Q

Describe the short ACTH stimulation test

A

Measure plasma cortisol before and 30 mins after IM TETRACOSACTIDE

Addison’s is excluded if after 30 mins, cortisol > 55nmol/L

573
Q

How can you diagnose a patient with autoimmune adrenalitis?

A

21 hydroxyls antibodies are detected in blood

574
Q

If you took a blood sample from a patient with Addison’s disease at 9am, what would you find?

A

High ACTH levels

575
Q

How do you treat an Addison’s patient who is seriously ill or hypotensive on presentation?

A
  • IV hydrocortisone
  • IV 0.9% saline
  • Glucose infusion (if hypoglycaemic)
576
Q

How do you treat Addison’s disease?

A

Replace steroids; take 1-3x a day;

  • Glucocorticoids (e.g. ORAL HYDROCORTISONE / PREDNISOLONE)
  • Mineralocorticoids (e.g. ORAL FLUDROCORTISONE)
577
Q

Under what circumstances should you double the medication for a patient with Addison’s disease?

A
  • Infection
  • Trauma
  • Surgery
  • Nightshifts at work
578
Q

When should you increase the dose of medication for an Addison’s patient?

A
  • During pregnancy

- Before strenuous exercise

579
Q

What is the presentation for adrenal crisis?

A
  • Nausea
  • Vomiting
  • Abdominal pain
  • Muscle cramps
  • Confusion
580
Q

How do you treat adrenal crisis?

A

IV hydrocortisone

581
Q

What is secondary hypoadrenalism?

A

Not an issue with the adrenal glands, but with the pituitary gland

582
Q

What are the causes of secondary hypoadrenalism?

A
  • Iatrogenic

- Hypothalamic-pituitary disease

583
Q

Describe the iatrogenic cause of secondary hypoadrenalism

A

Long term steroid therapy leading to suppression of the pituitary-adrenal axis

584
Q

Describe the pathophysiology of secondary hypoadrenalism

A

> reduction in the release of ACTH

> decreased glucocorticoid (cortisol)

  • Mineralocorticoid production remains unaffected
585
Q

What is the clinical presentation of secondary hypoadrenalism?

A
  • Vague symptoms of feeling unwell

- No skin hyperpigmentation since ACTH is reduced

586
Q

How do you diagnose secondary hypoadrenalism?

A
  • ACTH levels are low

- Mineralocorticoid levels are fine

587
Q

How do you treat secondary hypoadrenalism?

A
  • Oral hydrocortisone
    OR
  • Adrenal glands will recover if you ween patient off long-term steroids, but this is a long and difficult process
588
Q

Describe the Thirst Axis

A
  1. ADH is synthesised in hypothalamus
  2. It migrates in neurosecretory vesicles along axonal pathways to posterior pituitary
  3. Large drop in BP / blood volume is detected by osmoreceptors or baroreceptors which stimulates ADH release
  4. ADP acts on principal cells of collecting duct on kidney
  5. Binds to adenyl-cyclase couple vasopressin receptor (V2R) where kinase actions result in insertion of aquaporin 2 channels into apical membrane of collecting duct
  6. Water permeability of collecting duct increases
  7. Increased water reabsorption causing very concentrated urine
589
Q

What determines secretion of vasopressin?

A

Plasma osmolality (i.e. blood water concentration)

590
Q

What does vasopressin do?

A
  • Increases water reabsorption from collecting duct

- Widespread arteriolar vasoconstriction

591
Q

Describe the relationship between osmolality and vasopressin

A

Linear, as blood gets more concentrated, the amount of vasopressin (and thus water that gets reabsorbed) increases

592
Q

Define diabetes insipid (DI)

A

The passage of large volumes (>3L/day) of dilute urine due to impaired water reabsorption in the kidney

593
Q

What causes the impaired water reabsorption in the kidneys in DI?

A
  • Reduced ADH secretion from posterior pituitary (CRANIAL DI)
  • Impaired response of the kidney to ADH (NEPHROGENIC DI)
594
Q

What are the causes of cranial DI?

A
  • Idiopathic
  • Congenital defects in ADH gene
  • Disease of the hypothalamus
  • Tumour:
    > metastases
    > posterior pituitary tumour
  • Trauma (e.g. neurosurgery)
  • Infiltrative disease (e.g. sarcoidosis)
595
Q

What are the causes of nephrogenic DI?

A
  • Hypokalaemia
  • Hypercalcaemia
  • Drugs (lithium chloride, glibenclamide)
  • Renal tubular acidosis
  • Sickle cell disease
  • Prolonged polyuria of any cause
  • Familial - mutation of ADH receptor
596
Q

What is the clinical presentation for diabetes insipidus?

A
  • Polyuria
  • Compensatory polydipsia
  • NO GLYCOSURIA
  • Hypernatraemia;
  • Lethargy
  • Weakness
  • Irritability
  • Confusion
  • Coma
  • Fits
  • Dehydration
597
Q

What can hypernatraemia cause?

A
  • Lethargy
  • Weakness
  • Irritability
  • Confusion
  • Coma
  • Fits
598
Q

What are the differential diagnoses for diabetes inspidus?

A
  • DM
  • Hypokalaemia
  • Hypercalcaemia

All of which look similar to DI because they cause polyuria and polydipsia

599
Q

How do you confirm polyuria?

A

Measure urine volume

If urine volume < 3L/day it is unlikely to be DI

600
Q

How do you differentiate DI and DM?

A

Check blood glucose

High - DM
Normal - DI

601
Q

What does the water deprivation test aim to do?

A

Aims to determine whether kidneys continue to produce dilute urine despite dehydration

602
Q

Describe the water deprivation test

A

Measure serum and urine osmolality, urine volume, and body weight hourly for up to 8 hours during fasting and without fluids

603
Q

What is a normal response of the body during the water deprivation test?

A

Serum osmolality remains within normal range, but urine concentration rises

604
Q

What are diagnostic results for DI of the water deprivation test?

A

Serum osmolality rises without adequate concentration of urine

605
Q

How do you differentiate between cranial and nephrongenic DI?

A

Give IM desmopressin

Urine will not be concentrated in nephrogenic DI but it will be in cranial DI

606
Q

How do you treat cranial DI?

A
  • MRI of head to find cause

- Give synthetic analogue of ADH (e.g. ORAL DESMOPRESSIN)

607
Q

How do you treat nephrogenic DI?

A
  • Treat the cause (usually renal disease)
  • Thiazide diuretics (e.g. ORAL BENDROFLUMETHIAZIDE)
  • NSAIDS (e.g. IBUPROFEN)
608
Q

Why do you give thiazide diuretics to treat nephrogenic DI?

A

They will produce mild hypovolaemia, which will encourage the kidneys to take up more Na+ and water in the proximal tube, thereby offsetting water loss

609
Q

Why do you use ibuprofen to treat nephrogenic DI?

A

They will lower urine volume and plasma Na+ by inhibiting prostaglandin synthase

*Prostaglandins locally inhibit action of ADH

610
Q

Define syndrome of inappropriate secretion of ADH (SIADH)

A

Continued secretion of ADH despite plasma being very dilute, leading to retention of water and excess blood volume, and thus hyponatraemia

611
Q

What are the four categories of causes of SIADH?

A
  • Tumours
  • Pulmonary lesions
  • Metabolic causes
  • CNS causes
  • Drugs
612
Q

What tumours cause SIADH?

A
  • Small-cell carcinoma of lung
  • Prostate
  • Thymus
  • Pancreas
  • Lymphoma
613
Q

What pulmonary lesions cause SIADH?

A
  • Pneumonia
  • TB
  • Lung abscess
  • Asthma
  • Cystic fibrosis
614
Q

What is the metabolic cause of SIADH?

A

Alcohol withdrawal

615
Q

What are the CNS causes of SIADH?

A
  • Meningitis
  • Tumours
  • Head injury
  • Subdural haematoma
  • SLE
616
Q

What drugs can cause SIADH?

A
  • Chlorpropamide (sulfonylurea for DMT2)
  • Carbamazepine (anti-convulsant)
  • Cyclophosphamide (immunosuppressant)
  • Vincristine (chemotherapy)
  • SSRIs
617
Q

What is the clinical presentation for SIADH?

A
  • Anorexia/nausea and malaise
  • Weakness and aches
  • Reduction in GCS and confusion with drowsiness
  • Fits and coma

SYMPTOMS ARE A RESULT OF HYPONATRAEMIA

618
Q

What do the blood results of someone with SIADH show?

A
  • Low serum Na+
  • Euvolaemia
  • Low plasma osmolality
  • NO hypokalaemia
  • NO hypotension
  • NO hypovolaemia
  • Normal renal, adrenal, and thyroid function
619
Q

What is the urine Na+ concentration in someone with SIADH?

A

High urine Na+ > 30mmol/L

620
Q

How do you differentiate between SIADH and salt&water depletion?

A

Test with 1-2L of 0.9% saline

  • Sodium depletion will respond
  • SIADH will NOT respond
621
Q

How do you treat SIADH?

A
  • Try to treat underlying cause
  • Restrict fluid intake to 500-1000ml daily
  • Hypertonic saline (if really symptomatic) - concentrate with salt
  • Give ORAL DEMECLOCYCLINE daily
  • Give vasopressin antagonist (e.g. ORAL TOLVAPTAN) daily
  • Salt and loop diuretic (e.g. ORAL FUROSEMIDE)
622
Q

Why do you restrict fluid intake in someone with SIADH?

A

To increase Na+ concentration and reduce symptoms

623
Q

Why do you give hypertonic saline to someone with SIAD?

A

Stops the brain from swelling as it keeps water out by attractive forces of Na+

  • In emergencies, give the highest possible dose of Na+ to prevent cerebral oedema
624
Q

Why do you give someone with SIADH oral demeclocycline?

A

It induces nephrogenic DI (inhibits the action of ADH on kidneys)

625
Q

What are the side effects of oral demeclocycline?

A
  • Photosensitive rash

- Nephrotoxicity

626
Q

Why do you give someone with SIADH a vasopressin antagonist?

A

Treats hyponatraemia by promoting water excretion with no loss of electrolytes

Phase 2a Medicine (5 decks)

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