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Phase 2a > Endocrine Conditions > Flashcards

Endocrine Conditions Flashcards

1
Q

Define Diabetes Mellitus

A

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

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2
Q

What is the principle organ of glucose homeostasis?

What is its role?

A

Liver

  1. Stores and absorbs glucose as glycogen
  2. Performs gluconeogenesis
  3. HIGH blood glucose - makes glycogen
  4. LOW blood glucose - splits glycogen, makes glucose
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3
Q

What are the normal levels of blood glucose?

A

3.5-8.0mmol/L under all conditions

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4
Q

How does the brain use glucose?

A

Major consumer.

Cannot use free fatty acids as cannot cross the blood brain barrier.

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5
Q

How does muscle utilise glucose?

A

Stored as glycogen
OR
metabolised to lactate
OR
to CO2 and H2O

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6
Q

How does adipose tissue utilise glucose?

A

Uses it as a substrate for triglyceride synthesis

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7
Q

What are the two m ain regulators of blood glucose levels?

A

Insulin

Glucagon

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8
Q

Describe the role of insulin as a regulator of blood glucose levels (2)

A
  1. Supresses hepatic glucose output
  2. Increases glucose uptake into insulin sensitive tissues
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9
Q

Describe the role of glucagon as a regulator of blood glucose levels (5)

A
  1. Increases hepatic glucose output
  2. Reduces peripheral glucose uptake
  3. Stimulates peripheral release of gluconeogenesis precursors
  4. Simulates glycogenolysis and breakdown
  5. Stimulates lipolysis
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10
Q

Describe biphasic release of insulin

A

B-cells sense rising glucose levels and aim to metabolise it by releasing insulin.

1st phase - rapid release of stored insulin

2nd phase (if levels still high) - more insulin synthesised (takes longer)

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11
Q

Name 3 other counter regulatory hormones in blood glucose levels

What are their roles?

A

Adrenaline, cortisol and growth hormones

Increase glucose production in the liver and reduce its utilisation in fat and muscle

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12
Q

How is insulin determined as natural or synthetic?

A

Presence of C peptide

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13
Q

What is insulin coded on?

Where is it produced?

A

Chromosome 11

Beta cells of islets of Langerhans of the pancreas

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14
Q

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

A

Regulate glucose release by the liver

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15
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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16
Q

What transporter allows glucose into cells

A

Glucose-transporter (GLUT) proteins

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17
Q

What is the role of GLUT-1

A

Enables basal non-insulin stimulated glucose uptake into many cells

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18
Q

What is the role of GLUT-2

A

Transport glucose into the beta cells.

Can detect high levels of glucose and release insulin as a response

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19
Q

What is the role of GLUT-3

A

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

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20
Q

What is the role of GLUT-4

A

Mediates much of the peripheral action of insulin

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21
Q

Diabetes - name 3 microvascular complications

A
  1. Retinopathy
  2. Nephropathy
  3. Neuropathy
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22
Q

Describe the microvascular complication of diabetes on the eye

A

High blood glucose and high BP can damage the eye blood vessels, causing retinopathy, cataracts and glaucoma

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23
Q

Describe the microvascular complication of diabetes on the kidney

A

High blood pressure damages small vessels and excess blood glucose overworks the kidneys resulting in nephropathy

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24
Q

Describe the microvascular complication of diabetes on the neuropathy

A

Hyperglycaemia damages nerves in the peripheral nervous system

This may result in pain and/or numbness

Feet wounds may go undetected and get infected and lead to gangrene

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25
Q

Describe the macrovascular complications of diabetes on the brain

A

Increases risk of stroke and cerebrovascular disease, including transient ischaemia attack, cognitive impairment etc.

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26
Q

Describe the macrovascular complications of diabetes on the heart

A

High blood pressure and insulin resistance increases risk of coronary heart disease

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27
Q

Describe the macrovascular effects of diabetes on extremities

A

Peripheral vascular disease results from narrowing of blood vessels increasing the risk for reduced or lack of blood flow to the legs

Feet wounds are likely to heel slowly contributing to gangrene and other complications

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28
Q

Diabetes - Name 4 macrovascular complications

A
  1. Strokes
  2. Renovascular disease
  3. Limb ischaemia
  4. Heart disease
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29
Q

Define type 1 diabetes

A

Metabolic autoimmune disorder characterised by hyperglycaemia due to an absolute deficiency of insulin.

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30
Q

What is type 1 diabetes caused by

A

Caused by autoimmune destruction of beta cells of the pancreas.

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31
Q

Define type 2 diabetes

A

Characterised by insulin resistance and less severe insulin deficiency

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32
Q

Define diabetic ketoacidosis

A

Acute metabolic complication of diabetes that is potentially fatal and requires prompt medical attention for successful treatment

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33
Q

Name the causes of DKA

A

Untreated type 1 diabetes (occasionally type 2 diabetes)
Undiagnosed diabetes
Exacerbations of type 1 diabetes

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34
Q

What are the possible causes for type 1 dm

A

Autoimmune
Idiopathic
Genetics
Enterovirus

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35
Q

Describe the pathophysiology of type 1 dm

A

Autoimmune destruction by autoantibodies of Beta-cells.

Causes insulin deficiency.

Eventual complete beta cell destruction

No transport of insulin into cells = hyperglycaemia = increased gluconeogenesis

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36
Q

What can be used to see how well beta cells are working

A

Serum-C peptide

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37
Q

In type 1 diabetes what will serum-C peptide be

A

Absent

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38
Q

When does type 1 diabetes tend to present

A

When only 10% beta cells remaining

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39
Q

Name 6 clinical manifestations of type 1 dm

A

Thirst
Polyuria
Weight loss and fatigue
Hunger
Pruritis vulvae and balitis
Blurred vision

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40
Q

Why is polyuria a manifestation of diabetes

A

Blood glucose > 10 mmol/L blood can no longer be absorbed

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41
Q

Describe the investigations of diabetes mellitus

A

Fasting plasma glucose > 7mmol/L (symptoms) or equal to

Random plasma glucose > 11.1 mmol/L (no symptoms x2) equal to

HbA1c > 48 mmol/mol (6.5%)

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42
Q

What is the management of type 1 diabetes

A

Insulin treatment

2x daily treatment short/medium acting insulin basal bolus and long acting insulin

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43
Q

What does monitoring of diabetes involve

A

HbA1c
Self-monitoring 4x a day
Annual checks

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44
Q

Name the risk factors of type 1 DM

A

Younger patients
Northern Europeans
Other autoimmune diseases

HLA-DR3-DQ2
HLA-DR4-DQ8

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45
Q

What are the serotypes for type 1 dm

A

HLA-DR3-DQ2
HLA-DR4-DQ8

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46
Q

Describe the causes of type 2 diabetes

A

Obesity
Lack of exercise
Calorie
Alcohol excess
Genetic link

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47
Q

Describe the pathophysiology of type 2 dm

A

Insulin levels tend to be higher than in non-diabetics, fall again months/years after - starling curve of the pancreas

Exhaustion of pancreas leads to hypoplasia and hypotrophy.

Hyperglycaemia and lipid excess are toxic to beta cells (glucotoxicity) = further beta cell loss

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48
Q

Name 7 symptoms of type 2 dm

A

Polydipsia
Polyuria
Blurred vision
Unexplained weight loss
Recurrent infections
Tiredness
Slow wound healing

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49
Q

Name a sign of type 2 diabetes

A

Acanthosis nigricans

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50
Q

Approx what % of beta cells are left at diagnosis of type 2 dm

A

50%

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51
Q

Describe the 1st line management for type 2 dm

A
  1. Weight loss and exercise

150 mins moderate exercise over 3 days

DESMOND/xpert

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52
Q

Describe the pathophysiology of DKA

A

Complete lack of insulin = uncontrolled lipolysis = increased fatty acids = converted into ketones = metabolic acidosis

Increased FFA = increased acetyl-coA which synthesises ketone bodies.

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53
Q

What are the symptoms of DKA

A

Develop over days

Polyuria and polydipsia
Vomiting and nausea
Weight loss
Weakness
Abdominal pain
Drowsiness and confusion

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54
Q

What are the signs of DKA

A

Hyperventilation - Kussmaul breathing. Acetone smelling breath

Dehydration
Hypotension
Tachycardia
Coma

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55
Q

What are the risk factors for DKA

A

Incurrent illness
Treatment errors
Physiological stress
Previously undiagnosed diabetes
Unknown

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56
Q

What are the investigations for a DKA

A

Plasma glucose > 11 mol

Blood (serum) ketones > 3 mmol

Urine ketones > 2

Bicarbonate < 15 mmol

U&E

K+

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57
Q

What is the management for DKA

A

FIG PICK

Fluids 3L in 1st 3 hours
Insulin - sliding scale
Glucose (dextrose) + insulin
Potassium
Infection
Chart fluid balance
Ketone monitoring

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58
Q

Define hypoglycaemia

A

Lower than normal blood glucose concentration

< 3.9 mmol/L

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59
Q

Describe the pathophysiology of hypoglycaemia

A

Results from an imbalance between glucose supply and glucose utilisation and existing insulin

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60
Q

Name the 3 clinical features of hypoglycaemia

A
  1. Autonomic
  2. Neuroglycopenic
  3. Non-specific
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61
Q

What is the value of hypoglycaemia

A

Blood glucose level < 3.9 mmol/L

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62
Q

Name the 5 steps of management in hypoglycaemia

A
  1. Recognise symptoms
  2. Confirm
  3. Treat 15g fast acting carbohydrates to relieve symptoms
  4. Re-rest in 15 minutes to ensure blood glucose > 4.0 mmol/L and re-treat if needed
  5. Eat long acting carbohydrates to prevent recurrence
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63
Q

Define hyperosmolar hyperglycaemia state

A

Non-ketotic hyperglycaemic hyperosmolar syndrome, characterise by profound hyperglycaemia, hyperosmolality and volume depletion in the absence of significant ketoacidosis

Decreased insulin but not enough to cause ketogenesis

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64
Q

Describe the causes of hyperosmolar hyperglycaemic state

A

Most common reaction - infection

Cardiovascular insult
Chronic uncontrolled T2DM
Sedative drugs
Dementia

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65
Q

What are the clinical features of hyperosmolar hyperglycaemic state

A

Happens over days

Polyuria
Polydipsia
Weight loss
Dehydration
Tachycardia
Hypotension
Confusion
N&V
Severe case - shock

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66
Q

What are the investigations of hyperosmolar hyperglycaemic state

A

Hyperglycaemia > 30 mmol

Serum osmolality > 320 osmole/kg

No ketonuria

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67
Q

What is the management of hyperosmolar hyperglycaemic state

A

ABC approach

IV fluids - saline

LMWH

Restore electrolytes

Careful monitoring

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68
Q

Why is LMWH given in the management of hyperosmolar hyperglycaemic state

A

Due to increased risk of thrombolytic events (blood viscosity)

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69
Q

Describe the pathophysiology of hyperosmolar hyperglycaemic state

A

Medical emergency - due to chronic T2DM

Decreased insulin - but not enough that ketogenesis happens

Overtime causes
- osmotic diuresis
- dehydration
- electrolyte deficiency - hyperglycaemia, diuresis causing hyperosmolality
- mild/no ketones

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70
Q

Name 5 features of an ECG seen in a DKA

A

Tall peaking T waves
Prolonged QT interval
Widening QRS complex
Prolongation of the ST interval
ST segment elevation

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71
Q

Define hyperthyroidism (Grave’s)

A

Thyroid stimulating hormone receptor antibodies stimulate the thyroid gland

Overproduction of T3/T4

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72
Q

Describe the presentation of hyperthyroidism (Grave’s)

A

Weight decrease
HR increase
Painless goitre
Exothalamous (protrusion of eyes out of the orbit)
Pretibial myxedema
Thyroid acropachy

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73
Q

What is the GS investigation of hyperthyroidism (Grave’s)

A

Measurement of TSH receptor antibody

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74
Q

What condition would this be seen in

TSH - low
T3 - high
T4 - high

A

Hyperthyroidism (Grave’s)

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75
Q

What would be the thyroid function tests of hyperthyroidism (Grave’s)

A

TSH - low
T3 - high
T4 - high

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76
Q

What is the 1st line management in hyperthyroidism (Grave’s)

A

Block - carbimazole

Treat - levothyroxine

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77
Q

What is 2nd line management in hyperthyroidism (Grave’s)

A

Propylthiouracil

Reduction of thyroid gland

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78
Q

Name the conditions which can cause hyperthyroidism

A

GIST

Graves disease
Inflammatory (thyroiditis)
Solidary toxic thyroid nodule
Toxic multinodular goitre

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79
Q

Define hypothyroidism (Hashimoto’s thyroiditis)

A

Autoimmune causing antithyroid antibodies to damage the thyroid = decreased production of T4/T3

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80
Q

Describe the presentation of hypothyroidism (Hashimoto’s thyroiditis)

A

Dry skin, hair and brittle nails
Fatigue
Weight gain
Cold sensitivity
Constipation
Heavy or irregular periods

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81
Q

What is the GS investigation for hypothyroidism (Hashimoto’s thyroiditis)

A

Thyroid function tests

Anti-thyroid peroxide antibodies

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82
Q

What condition would this be seen in

TSH high
T4 normal/low
T3 normal/low

A

hypothyroidism (Hashimoto’s thyroiditis)

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83
Q

What would be the thyroid function test in hypothyroidism (Hashimoto’s thyroiditis)

A

TSH high
T4 normal/low
T3 normal/low

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84
Q

What is the 1st line management in hypothyroidism (Hashimoto’s thyroiditis)

A

Levothyroxine

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85
Q

Describe thyroid cancer

A

Genetic alterations + mutations

4 types
- papillary
- follicular
- anaplastic
- medullary

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86
Q

Name a key presentation of thyroid cancer

A

Palpable thyroid nodule

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87
Q

What is the GS investigation in thyroid cancer

A

Ultrasound neck + fine needle biopsy

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88
Q

What is the 1st line management of thyroid cancer

A

Thyroidectomy + radioactive iodine

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89
Q

What is the 2nd line management of thyroid cancer

A

Ablation + suppression of TSH

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90
Q

What are the risk factors of thyroid cancer

A

Head and neck irradiation
Female

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91
Q

Name 2 complications of thyroid cancer

A

Increased risk of laryngeal nerve damage

Increased risk of hypoparathyroidism

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92
Q

Define cushing’s syndrome

A

Excess cortisol

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93
Q

Define cushing’s disease

A

Caused by endogenous cortisol - ACTH-producing pituitary adenoma

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94
Q

Describe the presentation of cushing’s syndrome

A

Central obesity
Hirsutism
Purple abdominal striae
Buffalo hump
Moon face
Hyperpigmentation

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95
Q

What is GS investigation of cushing’s syndrome

A

Dexamethasone suppression test (low dose)

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96
Q

What is a 2nd line investigation in cushing’s syndrome

A

High dose dexamethasone test - diagnose pituitary adenoma

24-hour urinary free cortisol

MRI pituitary

CT chest and abdomen

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97
Q

What test is used to diagnose cushings disease (caused by a pituitary adenoma)

A

High dose dexamethasone suppression test

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98
Q

What is GS management for cushing’s syndrome

A

Trans-sphenoidal surgery for pituitary adenoma

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99
Q

What is 2nd line management for cushing’s syndrome

A

Cessation of steroids

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100
Q

What is the most common cause of cushing’s syndrome (disease)

A

Pituitary adenoma

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101
Q

What are the causes of cushing’s syndrome

A

Pituitary adenoma

Small cell lung cancer

Exogenous steriods

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102
Q

Define acromegaly

A

Exocrine disorder

Excessive secretion of growth hormone

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103
Q

Describe the clinical features of acromegaly

A

Bitemporal hemianopia
Large spade hands and feet
Acroparathesia
Back pain
Arthralgia
Oily skin
Amenorrhoea

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104
Q

What is the GS investigation for Acromegaly

A

Oral glucose tolerance test

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105
Q

What is the 1st line investigation for acromegaly

A

Insulin-like growth factor-1

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106
Q

What is a possible extra investigation for acromegaly

A

MRI brain

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107
Q

What is the GS management for acromegaly

A

Trans-sphenoidal surgery for pituitary tumour

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108
Q

What type of condition is acromegaly

A

Benign

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109
Q

What is the 2nd line management of acromegaly

A

Somatostatin analogues e.g. octreotide

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110
Q

What is the 3rd line management of acromegaly

A

Growth hormone receptor antagonists e.g. Pegvisomant

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111
Q

Name the cause of acromegaly

A

Anterior pituitary adenoma

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112
Q

Describe the pathophysiology of acromegaly

A

Excessive production of GH = excessive production of insulin like growth factor (IGF-1) = stimulates bone and soft tissue growth

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113
Q

Define prolactinoma

A

Benign lactotroph adenoma expressing and secreting prolactin

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114
Q

What type of condition is the hypersecretion of prolactin

A

Secondary hypogonadism

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115
Q

What are the clinical features of prolactinoma in females

A

Amenorrhea
Oligomenorrhea
Infertility
Galactorrhoea
Low libido

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116
Q

What are the clinical features of prolactinoma in males

A

Low testosterone
Erectile dysfunction
Reduced facial hair
Low libido

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117
Q

What is the GS investigation in prolactinoma

A

Serum prolactin levels = elevated

Followed by a pituitary MRI

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118
Q

What is the GS management in prolactinoma

A

Dopamine agonist e.g. oral cabergoline/bromocriptine

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119
Q

What is prolactinoma caused by

A

Pituitary adenoma

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120
Q

Describe the pathophysiology of prolactinoma

A

Hormone made by lactotrophs in the anterior pituitary gland - milk in the breast

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121
Q

Define carcinoid syndromes

A

Release of serotonin and other vasoactive particles into the systemic circulation from a carcinoid tumour

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122
Q

Define a carcinoid tumour

A

Neuroendocrine tumour growing from neuroendocrine cells

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123
Q

Describe the clinical features of carcinoid tumours and syndromes

A

Flushing
Diarrhoea
Wheeze
Palpitations
Telangiectasia (vessels visible on the skin)
Abdominal pain

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124
Q

What is the GS investigation for carcinoid tumours and syndromes

A

Urinary 5-hydrozyincholeacetic acid = elevated levels

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125
Q

What is the GS (cure) of carcinoid tumours and syndromes

A

Surgery

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126
Q

What is the 2nd line management of carcinoid tumours and syndromes

A

Somatostatin analogues e.g. octreotide

= blocks the release of tumour mediators and counter peripheral effects

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127
Q

Where do the most common carcinoid tumours arise from

A

GI tract

then
lungs
liver (common site of metastases)
ovaries thymus

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128
Q

Describe GI carcinoid tumours

A

Hormone is secreted - enters enterohepatic circulation - live activated hormone = no symptoms

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129
Q

Describe liver metastases carcinoid tumours

A

Hormone is secreted - released into the circulation due to liver dysfunction = symptoms

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130
Q

Name the risk factors of Graves (hyperthyroidism)

A

Strong association with other autoimmune conditions - DM1, Addison’s disease, vitiligo

Females

40-60

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131
Q

Describe post-partum thyroiditis

A

Presents transient acute phase of thyrotoxocosis followed by a period of hypothyroidism

2-6 months after birth or miscarriage

132
Q

What is Grave’s disease (hyperthyroidism) mediated by

A

Autoimmune condition via TSH-receptor antibodies (anti-TSHR)

133
Q

Describe the pathophysiology of Grave’s disease

A

Bind to TSH-receptors on the thyroid gland + stimulate increased T3 + T4 from the thyroid gland = results in thyrotoxicosis

134
Q

Describe iatrogenic causes of thyrotoxicosis

A

Amiodarone + levothyroxine

135
Q

Describe the pathophysiology of iatrogenic causes of thyrotoxicosis

A

Contains iodine - increases iodine levels = increases follicular thyroid hormone production

136
Q

What is causes De Quervain’s thyroiditis

A

Viral infections

137
Q

Describe the pathophysiology of De Quervain’s thyroiditis

A

Cause transient rise in thyroid hormone production due to inflammation of the thyroid gland

Subsequent excessive excretion of thyroid hormones into the circulation

138
Q

How does subacute De Quervain’s thyroiditis present

A

Painful lump in neck

139
Q

What are the risk factors of Hashimoto’s disease (hypothyroidism)

A

Women
30-50
Other autoimmune conditions

140
Q

What is Hashimoto’s disease (hypothyroidism) mediated by

A

Anti-TPO (anti-thyroid peroxidase) attack the thyroid gland

141
Q

Describe the pathophysiology of De Quervain’s thyroiditis

A

Transient inflammation of the thyroid gland causing 3 stages - thyrotoxicosis, hypothyroidism, euthyroidism

142
Q

What is the treatment of De Quervain’s

A

Self-limiting

143
Q

Describe lithium as a cause of hypo (more common) or hyperthyroidism

A

Inhibits uptake, iodination and release of thyroid hormones

144
Q

Name 4 risk factors of cushing’s syndrome

A

Long term use of corticosteroids

Tumour

Familial

Increased stress

145
Q

Name the risk factors for Acromegaly

A

Sporadic (most common)
Middle aged

Familial - younger.
- MEN-1, McCune-Albright syndrome, Carney complex.

146
Q

Describe the difference between acromegaly + gigantism

A

Acromegaly - post-epiphyseal fusion

Gigantism - condition of childhood due to excessive growth hormone secretion prior to epiphyseal growth plate fusion

147
Q

What are the risk factors for prolactinoma

A

More common in women

Genetic - MEN-1, FIPA

Male 30-60

Female 20-50

Oestrogen therapy

148
Q

What is the full name for MEN-1

A

Multiple endocrine neoplasia-1

149
Q

What is the full name for FIPA

A

Familial isolated pituitary adenoma

150
Q

What are the normal levels of prolactin

A

< 400 mU/L in males

< 500mU/L in females

151
Q

Define Conn’s

A

Adrenal glands produce too much aldosterone

152
Q

Define Conn’s syndrome

A

Adrenal adenoma secreting aldosterone

153
Q

Describe the clinical features of Conn’s

A

Often asymptomatic

Hypertension
Headache
Hyperkalaemia
Muscle cramps
Paraesthesia
Polyuria
Nocturia
Polydipsia

154
Q

Name the risk factors of Conn’s

A

30-40

Obesity

Family history

Female

Increased BP

155
Q

What is the GS investigation of Conn’s

A

Selective adrenal venous sampling

156
Q

Name the 1st investigation of Conn’s

A

Serum renin low = supressed

157
Q

What is the GS management of Conn’s

A

Aldosterone antagonist

158
Q

What are possible management of Conn’s

A

Treat underlying cause

Adrenalectomy

Percutaneous renal artery angioplasty

159
Q

What type of hyperaldosteronism is Conn’s

A

Primary hyperaldosteronism caused by adrenal adenoma

160
Q

Define Adrenal insufficiency

A

Adrenal glands do not produce enough steroid hormones - particularly cortisol and aldosterone

161
Q

What is the key symptom of adrenal insufficiency

A

Hyperpigmentation

162
Q

Name the risk factors of adrenal insufficiency

A

Female

Other autoimmune disorders

Presence of adrenocortical antibodies

Sepsis - cause adrenal haemorrhage

163
Q

Name the GS investigation for adrenal insufficiency

A

Short Synacthen - failure to double

164
Q

Describe the Short Synacthen test

A

Measures response to cortisol levels to a synthetic ACTH

165
Q

Describe blood test results in adrenal insufficiency

A

Decreased Na+
Increased K+
Low cortisol

166
Q

In adrenal insufficiency caused by primary what would ACTH be

A

High

167
Q

In adrenal insufficiency caused by secondary what would ACTH be

A

Low

168
Q

What test can be used to differentiate adrenal insufficiency with primary or secondary causes

A

ACTH

Primary - high
Secondary - low

169
Q

Name the GS management of adrenal insufficiency

A

Hydrocortisone (cortisol)

Fludrocortisone (aldosterone)

170
Q

What hormone can hydrocortisone replace

A

Cortisol

171
Q

What hormone can fludrocortisone replace

A

Aldosterone

172
Q

Describe primary adrenal insufficiency

A

Addison’s disease

Adrenal glands are damaged

173
Q

What is the most common cause of primary adrenal insufficiency

A

Autoimmune adrenalitis

174
Q

What is the most common cause of adrenal insufficency

A

Autoimmunity

175
Q

Describe secondary adrenal insufficiency

A

Inadequate ACTH stimulating the adrenal glands

176
Q

What is the cause of secondary adrenal insufficiency

A

Loss or damage to the pituitary gland

177
Q

What is a complication of adrenal insufficiency

A

Addison’s crisis - acute adrenal insufficiency

178
Q

What is the full name of SIADH

A

Syndrome of inappropriate antidiuretic hormone secretion

179
Q

Define SIADH

A

Inappropriate secretion of ADH

180
Q

Describe the clinical features of SIADH

A

Largely due to hyponatraemia

Seizures
Reduced consciousness

181
Q

What is diagnosis of SIADH

A

Usually diagnosis of exclusion

182
Q

Name 4 clinical signs of SIADH

A

Euvolemic hyponatraemia
Increased urine osmolality
Increased urine sodium

183
Q

Describe the treatment of acute SIADH

A

Treat cause

Fluid restriction - 500mL/1L

184
Q

Describe the treatment of chronic SIADH

A

Vasopressin receptor antagonist e.g. tolvaptan

185
Q

Describe the pathophysiology of SIADH

A

ADH produced by hypothalamus - secreted by posterior pituitary gland

Stimulates water reabsorption from collecting ducts in kidneys

186
Q

Name a complication of SIADH

A

Central pontine myelinolysis

187
Q

Describe central pontine myelinolysis

A

Osmotic demyelination

188
Q

Name the risk factors of SIADH

A

CNS disorders
Small-cell lung cancer
Medication - SSRIs + amitriptyline
Surgery - postoperative

189
Q

Define arginine vasopressin deficiency

A

Lack of ADH - hypothalamus does not produce

190
Q

Define arginine vasopressin resistance

A

Lack of response - collecting ducts do not respond

191
Q

Name the clinical features of arginine vasopressin deficiency/resistance

A

Polyuria - > 3L urine
Polydipsia
Dehydration
Postural hypotension
No glycosuria

192
Q

What is the GS investigation for arginine vasopressin deficiency/resistance

A

Water deprivation test - desmopressin stimulation test

193
Q

What would be the results of water deprivation test then desmopressin test for arginine vasopressin deficiency

A

Water deprivation test - urine osmolality low

Desmopressin test = urine osmolality high

194
Q

What would be the results of water deprivation test then desmopressin test for arginine vasopressin resistance

A

Water deprivation test - urine osmolality low

Desmopressin test = urine osmolality low

195
Q

Name the risk factors of arginine vasopressin deficiency

A

Genetic problem in chromosome 20

Damage/dysfunction of hypothalamus/pituitary gland

196
Q

Name the risk factors of arginine vasopressin resistance

A

Genetic predisposition

Medication use e.g. lithium

Kidney condition e.g. PKD, sickle cell anaemia, Sjogren’s syndrome

197
Q

Name the GS management in arginine vasopressin deficiency

A

Desmopressin - replace ADH

198
Q

Name the GS management in arginine vasopressin resistance

A

High dose desmopressin

199
Q

Name 2nd line management in arginine vasopressin deficiency

A

Sort underlying cause

Serum sodium monitored

200
Q

Name multiple 2nd line management in arginine vasopressin resistance

A

Thiazide diuretics
NSAIDS

Avoid precipitating drugs

201
Q

Define the clinical diagnosis using biochemistry of arginine vasopressin deficiency/resistance

A

Inappropriate dilute urine for plasma osmolality.

Serum osmolality > 100

AND

Urine osmoality < 200

Normothermia
Hypernatremia

202
Q

Define hyperparathyroidism

A

Excessive secretion of parathyroid by parathyroid glands

203
Q

Name the reasons for hyperparathyroidism clinical features

A

Symptoms of hypercalcaemia

204
Q

What are the key investigation results for primary hyperparathyroidism

A

Increase PTH
Increase calcium
Decrease phosphate

205
Q

What are the key investigation results for secondary hyperparathyroidism

A

Increase PTH
Decrease/normal calcium.
Normal phosphate

206
Q

What are the key investigation results for tertiary hyperparathyroidism

A

Increase PTH
Increase calcium
Increase phosphate

(everything is high)

207
Q

Which hyperparathyroidism would this be

Increase PTH
Increase calcium
Decrease phosphate

A

Primary

208
Q

Which hyperparathyroidism would this be

Increase PTH
Decrease/normal calcium.
Normal phosphate

A

Secondary

209
Q

Which hyperparathyroidism would this be

Increase PTH
Increase calcium
Increase phosphate

A

Tertiary

210
Q

Name the risk factors for hyperparathyroidism

A

Women > 60
Prolonged/severe calcium or vitamin D deficiency
CK Failure
MEN-1

211
Q

What is the GS management for hyperparathyroidism

A

Surgical removal

212
Q

What is 2nd line management for hyperparathyroidism

A

Vitamin D or transplant (depending on cause)

213
Q

What is the 3rd line management for hyperparathyroidism

A

Total/sub parathyroidectomy

Calaminetic

214
Q

What is the role of calaminetic (cinacalcet)

A

Increased sensitivity to parathyroid cells to Ca2+ = causes less PTH secretion.

215
Q

Name the cause of primary hyperparathyroidism

A

Tumour (solitary adenoma)

Hyperplasia of parathyroid glands

216
Q

What is the most common hyperparathyroidism

A

Primary

217
Q

Name the cause of secondary hyperparathyroidism

A

Insufficiency vitamin D or chronic renal failure

218
Q

Name the cause of tertiary hyperparathyroidism

A

Prolonged secondary (CKD)

Does not respond to negative feedback

219
Q

What the level of calcium in primary hyperparathyroidism

A

Hypercalcaemia

220
Q

What is level of calcium is secondary hyperparathyroidism

A

Hypocalcaemia

221
Q

Name the risk factors of hypoparathyroidism

A

Surgery - damage or removal of parathyroid gland

Autoimmune or endocrine conditions e.g. Addison’s

Family history

Radiation therapy

Magnesium deficiency

222
Q

Define hypoparathyroidism

A

Reduced PTH production

223
Q

Name the clinical features of hypoparathyroidism

A

Hypocalcaemia

224
Q

Name 2 signs of hypoparathyroidism

A

Chvostek’s sign
Trousseau’s sign

225
Q

Name 2 signs of low calcium

A

Chvostek’s sign
Trousseau’s sign

226
Q

Describe Chvostek’s sign

A

Low Ca2+

Facial nerve induces spasm

227
Q

Describe Trousseau’s sign

A

Low Ca2+

BP cuff causes wrist flexion and fingers to pull together

228
Q

What is the GS investigations in hypoparathyroidism

A

Bone profile

ECG

229
Q

What is seen in a bone profile of hypoparathyroidism

A

Low calcium
Low/normal phosphate
Low PTH

230
Q

Describe the ECG of hypoparathyroidism

A

Prolonged QT/ST segment

231
Q

Name the GS management in hypoparathyroidism

A

IV calcium

232
Q

Name the 2nd line management in hypoparathyroidism

A

AdCalD3 (calcitriol)

Synthetic PTH if required

233
Q

Describe primary hypoparathyroidism

A

Gland failure

Autoimmune destruction, congenital DiGeorge syndrome (22q11del)

234
Q

Describe secondary hypoparathyroidism (2)

A

Surgical removal or decrease magnesium (required for PTH production)

235
Q

Define hypercalcaemia

A

> (or equal to) 2.6 mmol/L

236
Q

Name the risk factors of hypercalcaemia

A

Disease - TB, sarcoidosis
Immobility
Severe dehydration
Hyperparathyroidism
Cancer

237
Q

Name the cancers which can cause hypercalcaemia

A

Multiple myeloma
Breast cancer
Renal cancer
Ovarian cancer
Endometrial cancer
Squamous cell carcinoma

238
Q

Name the clinical features of hypercalcaemia

A

Renal stones
Painful bones
Abdominal groans
Psychiatric moans

239
Q

Name the GS investigation of hypercalcaemia

A

Fasting serum calcium and phosphate

240
Q

What would be seen on a fasting serum calcium and phosphate in hypercalcaemia

A

Decreased PTH
Decreased calcium

241
Q

Name 2nd line investigations in hypercalcaemia

A

ECG

24-hour urinary calcium - to exclude familial hypocaloric

242
Q

What would be seen on an ECG of hypercalcaemia

A

Short QT

243
Q

Name the management of hypercalcemia

A

1st - rehydration with normal saline

2nd - biphosphates

244
Q

What is the 2 main causes of hypercalcaemia

A

Hyperparathyroidism or malignancy

245
Q

Define hypocalcaemia

A

< 8.5 mg/dl

< 2.2 mmol/L

246
Q

What 2 mnemonics can be used for the clinical features of hypocalcaemia

A

SPASMODIC

CATS GO NUMB

247
Q

Define the mnemonic SPASMODIC

A

Spasm
Perioral, Parathesis
Anxious
Seizure
Muscle contractions (increased)
Orientation impaired and confusion
Dermatitis
Impetigo herpetiformis
Chvostek’s sign/cardiomyopathy

248
Q

Define mnemonic CATS GO NUMB

A

Convulsions
Arrythmia
Tetany
Spasms/stridor

Numbness in fingers

249
Q

What are the investigations in hypocalcaemia

A

Low calcium

ECG

250
Q

What would be seen on an ECG of hypocalcaemia

A

Prolonged QT interval

251
Q

Name the risk factors of hypocalcaemia

A

Vitamin D deficiency
Thyroidectomy
Hypomagnesemia
Hypoalbuminemia
Hyperphosphatemia
Parathyroid disorder
Family history

252
Q

What is the 1st line management in acute hypocalcaemia

A

IV calcium gluconate (10mL of 10% solution over 10 mins)

253
Q

What is the management of hypocalcaemia if it persists after 1st line management

A

Vitamin D supplements

254
Q

What is the main cause of hypocalcaemia

A

Hypoparathyroidism

255
Q

Name the complications of hypocalcaemia

A

Seizures
Cardiac arrests

Decreased HR and contractility = medical emergency = low QT syndrome

256
Q

Define hyperkalaemia

A

Serum > (or equal to) 5.5 mmol/L

257
Q

When is hyperkalaemia severe

A

serum > (or equal to) 6.5 mmol/L

OR

ECG changes

= emergency

258
Q

Describe the clinical features of hyperkalaemia

A

Muscle weakness
Numbness + tingling
N&V
Irregular heart rhythm
SOB
Palpitations
Chest pain
Fatigue

259
Q

Describe the ECG changes in hyperkalaemia

A

Tall tented T waves
Small p waves
Wide QRS
Complex ventricular fibrillation
Sine wave

260
Q

What does a sine wave on an ECG mean

A

Severe hyperkalaemia

261
Q

Name the risk factors of hyperkalaemia

A

Renal failure
Diabetes
Adrenal disease
Use of - ACEi, ARBs, potassium sparing diuretics

262
Q

What is the 1st line management in hyperkalaemia if there are ECG changes

A

Stabilise cardiac membranes

IV calcium gluconate/chloride

It will not lower K+ levels

263
Q

What is the 1st line management in hyperkalaemia if there are no ECG changes

A

Shift K+ into cells (EC-IC)

Insulin + dextrose + nebulised salbutamol

264
Q

Name the causes of hyperkalaemia

A

Increased uptake (exogenous)
Increased production (endogenous)
Decreased excretion
Redistribution - shift from intracellular to extracellular

265
Q

Define hypokalaemia

A

Serum < 3.5 mmol/L

266
Q

Name the clinical features of hypokalaemia

A

Weakness
Fatigue
Muscle cramps
Constipation
Arrythmias
Leg cramps
Tingling and numbness

267
Q

What is seen on an ECG in hypokalaemia

A

Small or inverted T waves
Prominent U waves
Long PR interval
Deep ST segments

268
Q

What is severe hypokalaemia

A

< 2.5 mmol/L

269
Q

What is the treatment of severe hypokalaemia

A

IV replacement - 40 mmol KCl in IL 0.9 NaCl

270
Q

What is the treatment for mild hypokalaemia

A

3-3.4 mmol/L

Oral replacement - consider IV

271
Q

Describe the causes of hypokalaemia

A

Decreased K+ intake
Increased K+ entry into cells
Increased K+ excretion - sweat, urine, Gi tract
Magnesium depletion
Hyperaldosteronism

272
Q

Name the risk factors of hypokalaemia

A

Bulimia
Hyperhidrosis
Diuretics
Excessive alcohol
Diaorrhea and vomiting

273
Q

Define thyroid storm

A

Severe end spectrum of thyrotoxicosis characterised by compromised organ function

274
Q

Name the clinical features of thyroid storm

A

Fever
Cardiovascular dysfunction
Profuse sweating
Tachycardias
N&V

275
Q

What would be the investigation findings in thyroid storm

A

Free T4 (thyroxine)

TSH completely supressed

276
Q

What is the GS management for thyroid storm

A

Thyroidectomy

277
Q

What is 2nd line management of thyroid storm

A

Antithyroid treatment - carbimzaole + hydrocortisone

278
Q

What are the risk factors of thyroid storm

A

Untreated hyperthyroidism
Damage to thyroid gland
Infections
Surgery
Trauma
Stroke

279
Q

What is the 1st line medical management of T2DM

A

Metformin

+ (if at high risk of CVD) SLGT-2 inhibitor

280
Q

What is the 2nd line management of T2DM

A

Add one of the 4

GLP-1 inhibitors
SGLT2-inhibitors
Sulfonylurea
Pioglitazone

281
Q

What is the 3rd line management of T2DM

A

Add another of the 2nd line drugs

or

start insulin based treatment

282
Q

What is the 4th line management of T2DM

A

If triple therapy not effective

Switch one of the GLP-1 mimetic

283
Q

When would insulin be contradicted in the treatment of T2DM

A

if BMI > (or equal to) 35 kg^2 would have occupational implications

284
Q

What is the mnemonic used to remember the treatment of DKA

A

FIG PICK

285
Q

Describe FIG PICK

A

Treatment of DKA

Fluids first - 3L in 1st 3 hours
Insulin - sliding scale
Glucose (dextrose) + insulin

Potassium
Infection
Chart fluid balance
Ketone monitoring

286
Q

What is a risk factor in the management of DKA

A

Risk of cerebral oedema - due to rapid fluid replacement

287
Q

Why is dextrose given in the management of DKA

A

Risk of hypo

288
Q

Why is potassium given in the management of DKA

A

insulin caused K+ into cells - cause hypokalaemia (levels must be checked)

289
Q

Define the values of pre-diabetes

A

42-47 mmol/mol

Fasting 6.1-6.9 mmol/L

290
Q

What is the aim of HbA1c in diabetes

A

48%

Measured every 6 months

291
Q

Name the risk factors of hypoglycaemia

A

Long duration diabetes
Increased age
Use of drugs - prescribed/alcohol
Sleeping
Increase in physical activity

292
Q

When may hypoglycaemia be caused when not below 3.9 mmol/L

A

If poor glycaemic control may be experiences at > 3.9 mmol/L

293
Q

When is hypoglycaemia screened for

A

In those at high risk

294
Q

Name the risk factors of hyperosmolar hyperglycaemic state

A

Type 2 diabetes
65+
Infection
Illness
Heart failure
Stroke
Trauma
Medications
Poor diabetes control

295
Q

Define hyponatraemia

A

< 135 mmol/L serum sodium

Severe < 120 mmol/L

Acute < 48 hours or chronic

296
Q

Name the symptoms of hyponatraemia

A

Anorexia
Headache
N&V
Lethargy
Ataxia
Seizures
Cerebral oedema

297
Q

Name the signs of hyponatraemia

A

Cognitive impairment
Drowsiness
Signs of seizures

298
Q

Name the risk factors of hyponatraemia

A

Older age
Medications e.g. diuretics, antidepressants
CKD
Heart disease
SIADH
Extreme physical activity
Warmer climates

299
Q

What is the GS investigation for hyponatraemia

A

U&E

300
Q

Name potential investigations for hyponatraemia

A

Bloods/urine - identify cause

Urine osmolality = confirm diagnosis of SIADH

Urine sodium - renal vs extrarenal causes

301
Q

How is serum osmolality calculated

A

2Na + Glu + Urea (all in mmol/L)

302
Q

What is the management of hyponatraemia

A

IV hypertonic saline bolus with close monitoring of serum sodium

No more than 6 mmol/L in 6 hours
No more than 10 mmol/L in 1st 24 hours

303
Q

What is the most common electrolyte abnormality

A

Hyponatremia

304
Q

How can hyponatraemia be a life threatening condition

A

Due to cerebral fluid shift

305
Q

Name 3 causes of hyponatraemia

A

Hypovolaemic - dehydrated
Hypervolemic - overloaded
Euvolemic

306
Q

Define hypernatremia

A

Serum sodium > 146 mmol/L

Severe > 160 mmol/L

307
Q

Name the symptoms of hypernatremia

A

Excessive thirst
Extreme fatigue
Lack of energy
Confusion

308
Q

Name the signs of hypernatremia

A

Muscle twitching or spasm
Restlessness
Seizures

309
Q

Name the risk factors of hypernatremia

A

Advanced age
Medications
CKD
SIADH
Extreme physical activity

310
Q

What is the GS investigation for hypernatremia

A

U&E

311
Q

Name extra investigations you could do in hypernatremia

A

Blood test

Urine osmolality

Clinical history

Venous blood gas

312
Q

Describe the management of hypernatremia

A

Iv hypotonic fluids without sodium

313
Q

Describe the correction of hypernatremia

A

Should not be corrected

> 0.5 mmol/L per hour

OR

> 10 mmol in 24 hours

Check sodium within 2-4 hours of initiating treatment

314
Q

What is the most common cause of hypernatremia

A

Dehydration

315
Q

What is a side effect of rapid correction of hypernatremia

A

Intracerebral fluid shift

316
Q

Define pheochromocytoma

A

Tumour of the adrenal glands that secrete unregulated and excessive amounts of catecholamine (adrenaline)

317
Q

Describe how signs and symptoms of pheochromocytoma present

A

Fluctuate relating too when tumour is secreting

318
Q

Name the symptoms of pheochromocytoma

A

Anxiety
Headache
Palpitations

319
Q

Name the signs of pheochromocytoma

A

Hypertension
Tachycardia
Tremor
Sweating

320
Q

Name the risk factors of pheochromocytoma

A

MEN 2
Neurofibromatosis type 1
Von Hippel-Lindae disease

321
Q

What is the 1st line investigation of pheochromocytoma

A

Plasma free metanephrilnes

24-hour urine catecholamines

322
Q

Why is serum catecholamine or adrenaline not measured in pheochromocytoma

A

Unreliable

Levels fluctuate

323
Q

Name 2 other investigations other than 1st line which can be used in the investigation of pheochromocytoma

A

CT or MRI - for tumour

Genetic testing

324
Q

What is GS management of pheochromocytoma

A

Surgically remove tumour

Control symptoms medically before surgery to reduce risks

325
Q

What medications can be used in pheochromocytoma

A

Alpha blockers e.g. phenoxybenzamine or doxazosin

Beta blockers - only once established on alpha blockers

326
Q

Describe the pathophysiology of pheochromocytoma

A

Tumour of chromaffin cells (in medulla) secrete unregulated and excessive amounts of adrenaline

Tends to be secreted in bursts

Phase 2a (15 decks)

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