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Phase 2a Conditions > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Definition of Diabetes Mellitus Type I

A

Metabolic autoimmune disorder from destruction of insulin producing beta cells in the pancreas, results in absolute insulin deficiency

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2
Q

Is DM Type I more common in Women or Men?

A

Women

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3
Q

At what age is DM Type I most commonly diagnosed?

A

Commonly diagnosed in youth

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4
Q

What causes DM Type I? (Aetiology)

A
  1. Environmental factors / viruses may trigger the destruction of beta cells
  2. HLA-DR and HLA-DQ provide protection from / increase susceptibility to it
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5
Q

Name all risk factors for DM Type I.

A
  1. Geographic region (European >Asian)
  2. genetic predisposition
  3. infectious agents
  4. Dietary factors
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6
Q

What are the key presentations of DM Type I?

A

Polyuria, polydipsia, blurred vision, fatigue / tiredness

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7
Q

Explain the pathophysiology of DM Type I.

A
  • usually develops as a result of autoimmune pancreatic beta-cell destruction
  • ~90 % will have autoantibodies
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8
Q

How many beta cells have to be destroyed for hyperglycaemia to develop (DM Type I) ?

A

80 - 90 %

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9
Q

What does long term hyperglycaemia lead to?

A
  1. induces oxidative stress and inflammation

2. Oxidative stress caused endothelial dysfunction via NO

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10
Q

Name the signs of DM Type I.

A
  1. Young age (<50)
  2. Weight loss
  3. low BMI
  4. FHx of autoimmune disease
  5. Ketoacidosis
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11
Q

Name the symptoms of DM Type I.

A
  1. Thirst
  2. Dry mouth
  3. Lack of energy
  4. Blurred vision
  5. Hunger
  6. Weight loss
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12
Q

Name the first-line investigations of DM Type I.

A
  1. Random glucose tolerance test
  2. Fasting plasma glucose
  3. 2-hour plasma glucose
  4. plasma/urine ketones
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13
Q

Name the gold standard investigation of DM Type I and expected result.

A
  1. Glycated Haemoglobin A1c (HbA1c) test

2. 42 - 47 mmol/L (prediabetes), >48 mmol/L (diabetes)

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14
Q

Name other investigations that can be useful in investigating DM Type I.

A

C peptide levels

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15
Q

Differential diagnoses of DM Type I include…

A

DM Type II, other diabetes subtypes

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16
Q

Name the first-line treatment of DM Type I.

A
  1. Basal - bolus insulin (glargine s/c)
  2. Pre-meal insulin correction dose
  3. Amylin analogue (pramlintide)
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17
Q

Name the second-line treatment of DM Type I.

A

fixed insulin dose

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18
Q

List the side effects of insulin prescribed in DM Type I.

A
  1. Hypoglycaemia
  2. Weight gain
  3. Lipodystrophy
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19
Q

How do you monitor a patient with DM Type I?

A
  1. Check BP at each visit, should be <140 / 90 mmHg

2. Check lipid profile in adults with diabetes at the time of first diagnosis/initial medical evaluation / 5-yearly

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20
Q

Name any microvascular complications of DM Type I.

A
  1. Retinopathy
  2. Nephropathy
  3. Neuropathy
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21
Q

Name any macrovascular complications of DM Type I.

A
  1. CAD
  2. Cerebrovascular disease
  3. PAD
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22
Q

What is the prognosis for a patient with DM Type I?

A

Untreated - fatal due to diabetic ketoacidosis

Poorly controlled - RF for blindness, renal failure, foot amputations and MIs

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23
Q

Define DM Type II.

A

Lifelong chronic disease characterised by insulin resistance and relative insulin deficiency

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24
Q

Is DM Type I or II more common in general?

A

DM Type II

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25
Q

Is DM Type II more common in younger or older people?

A

Older people (onset is usually >30 years)

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26
Q

Is DM Type II more common in people with a specific ethnicity?

A

Yes, African / Asian

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27
Q

What causes DM Type II? (Aetiology)

A
  1. Genetic susceptibility but no HLA link

2. Insulin resistance aggravated by ageing, physical inactivity and being overweight

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28
Q

Name all risk factors for DM Type II.

A
  1. older age (increasing at younger age recently)
  2. Being overweight / obese
  3. gestational diabetes
  4. pre-diabetes
  5. FHx of Type II
  6. non-white ethnicity
  7. physical inactivity
  8. Hypertension
  9. CVD
  10. stress
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29
Q

What is the pathophysiology of DM Type II?

A
  1. polygenic
  2. Environmental factors trigger onset in genetically susceptible
  3. Beta cell mass reduction
  4. Low insulin secretion
  5. Peripheral insulin resistance
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30
Q

How many beta cells have to be destroyed to cause DM Type II?

A

~ 50 %

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31
Q

What are the key presentations of patients with DM Type II?

A

Polyuria, polydipsia, fatigue, blurred vision, polyphagia, candida and skin infections, UTIs

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32
Q

What are the signs of DM Type II?

A

Presence of risk factors

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33
Q

What are the symptoms of DM Type II?

A

Thirst, Dry mouth, lack of energy, Blurred vision, neuropathy

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34
Q

Name the first-line investigations of DM Type II.

A
  1. HbA1c test
  2. fasting plasma glucose
  3. random plasma glucose
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35
Q

Name the gold standard investigation of DM Type II.

A

Oral glucose tolerance test (OGTT)

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36
Q

Name any other investigations that can be done in patients with suspected DM Type II.

A
  1. urine ketones
  2. fasting lipid profile
  3. random c peptide
  4. serum creatinine and eGFR
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37
Q

Differential diagnoses of DM Type II include…

A

Prediabetes, DM Type I, any other subtypes of diabetes

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38
Q

What is the first-line management of DM Type II?

A
  1. Diet and exercise changes
  2. if these do not have an effect then Biguanide (Metformin)
  3. +sulfonylurea (glicazide) OR DPP4 inhibitor (Sitagliptin)
  4. +sulfonylurea (glicazide) AND DPP4 inhibitor (Sitagliptin)
  5. +insulin
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39
Q

How do you monitor a patient with DM Type II?

A
  1. regular monitoring and control of BP, HbA1c, tobacco use, and statin/aspirin use
  2. diabetes assessment every 3-4 months
  3. eye examination ever 1 - 2 years
  4. Renal function assessment annually
  5. Foot examinations
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40
Q

Name any complications of DM Type II.

A 
Diabetic ketoacidosis, DIabetic nephropathy,
Diabetic neuropathy
Diabetic retinopathy, 
Hyperosmolar hyperglycaemia,
CVD,
Stroke
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41
Q

What is the prognosis for someone with DM Type II?

A

Men lose an average of 5.8 years of life, Women an average of 6.8 years of life, excess mortality ~15% higher

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42
Q

What is the definition of Grave’s disease?

A

It is an autoimmune thyroid condition associated with hyperthyroidism.

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43
Q

Is Grave’s disease more common in women or men?

A

Women

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44
Q

Is Grave’s disease more common at what age?

A

Older age (>40)

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45
Q

What ethnicity/ies is Grave’s disease most commonly associated with?

A

White and Asian

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46
Q

In which countries is grave’s disease the most common cause of hyperthyroidism?

A

In countries with sufficient iodine intake.

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47
Q

What causes Grave’s disease? (Aetiology)

A
  1. autoimmune condition

2. combination of genetic (80%) and environmental factors (20%)

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48
Q

Name all risk factors for Grave’s disease.

A
  1. FHx of autoimmune conditions
  2. Female sex
  3. smoking
  4. High iodine intake
  5. Lithium therapy
  6. Stress
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49
Q

What is the pathophysiology of Grave’s disease?

A
  1. Thyroid stimulating immunoglobulins recognise and bind to the TSH receptor which stimulates T4 and T3
  2. thyroxine (T4) receptors in the pituitary gland are activated by excess hormone
  3. reduced release of TSH in a negative feedback look 4. Very high levels of circulating thyroid hormones, with a low TSH
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50
Q

What are the key presentations of Grave’s disease?

A

Tachycardia, tremors, eye problems (buldging outwards and lid retraction), weight loss, onycholysis (detachment of nail from nail bed)

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51
Q

What are the signs of Grave’s disease?

A

diffuse palpable goitre with audible bruit, high T3 and T4, lower TSH than normal, presence of risk factors

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52
Q

What are the symptoms of Grave’s disease?

A

Rapid heartbeat, tremors, Heat intolerance (High body temp), sweating, muscle weakness

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53
Q

What are the first-line investigations for Grave’s disease and expected results?

A
  • TSH (low)
  • serum free / total T4 (elevated)
  • serum free or total T3 (elevated)
  • total T3/T4 or FT3/FT4 ratio (high)
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54
Q

What are the gold standard investigations for Grave’s disease and the expected result?

A
  • TSH receptor antibody test (TRAb)

- positive

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55
Q

Name any other test that can be used to investigate Grave’s disease.

A
  • Thyroid ultrasound
  • CT / MRI of orbit
  • Thyroid isotope scan
  • Radioactive Iodine uptake
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56
Q

Differential diagnoses for Grave’s disease include…

A
  • Toxic nodular goitre
  • gestational hyperthyroidism
  • iodine-induced hyperthyroidism
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57
Q

What is the first-line treatment of Grave’s disease?

A
  1. Antithyroid drugs (carbimazole/thiamayzole) with dose titration or ‘block and replace’.
  2. Radioactive iodine +/- corticosteroid Thyroidectomy
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58
Q

What are adjunct treatments for Grave’s disease?

A
  1. Treatment for orbitopathy (methylprednisolone) and dermopathy (triamcinolone acetonide topical)
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59
Q

How do you monitor a patient with Grave’s disease?

A

serum TSH at 6-week intervals until stable, then with serum TSH at least annually, orbitopathy follow-up

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60
Q

Name complications associated with Grave’s disease and its treatment.

A
  • Thyroid storm – high heart rate, BP and Body temp (treat with propylthiouracil)
  • bone mineral loss
  • atrial fibrillation
  • congestive heart failure
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61
Q

What is the prognosis for a patient with Grave’s disease?

A
  • Increased mortality (CV)
  • high degree of relapse
  • excellent prognosis following antithyroid medication therapy
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62
Q

Define Hashimoto’s thyroiditis (long)

A

Autoimmune mediated inflammation of thyroid gland with release of TH resulting in transient hyperthyroidism (very rare usually straight hypo), frequently followed by hypothyroid phase before recovery of normal thyroid function

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63
Q

Give a simple definition of Hashimoto’s thyroiditis

A

Hypothyroidism due to aggressive destruction of thyroid cells

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64
Q

Is Hashimoto’s thyroiditis more common in men or women?

A

Women

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65
Q

At what age is Hashimoto’s thyroiditis most common?

A

older age (~60 - 70)

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66
Q

In which areas is Hashimoto’s thyroiditis the most prevalent?

A

In areas with excess iodine intake.

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67
Q

What causes Hashimoto’s thyroiditis? (Aetiology)

A
  • Unknown cause
  • Autoimmune condition
  • some genetic element
  • Triggers: iodine, infection, smoking
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68
Q

Name all the risk factors for Hashimoto’s thyroiditis.

A
  1. postnatal thyroiditis
  2. thyroid peroxidase antibodies (TPO)
  3. Female sex
  4. FHx
  5. Lithium therapy
  6. immune-modulatory therapy
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69
Q

What is the pathophysiology of Hashimoto’s thyroiditis?

A
  1. Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes
  2. Antibodies bind and block TSH receptors
  3. inadequate thyroid hormone production and secretion
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70
Q

What are the key presentations of Hashimoto’s thyroiditis?

A 
- heat intolerance
weight loss / gain, 
- excessive fatigue
- small non-tender goitre
-  bloating
- muscle cramps,
- Thyroid gland may enlarge rapidly
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71
Q

What are the signs of Hashimoto’s thyroiditis?

A
  • small non-tender goitre
  • palpitations
  • tachycardia
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72
Q

What are the symptoms of Hashimoto’s thyroiditis?

A
  • nervousness
  • excessive fatigue
  • bloating
  • poor concentration
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73
Q

What are the first-line investigations for Hashimoto’s thyroiditis and the expected results?

A
  • serum-free T3 and T4 (elevated = thyrotoxicosis, low = hypothyroid phase)
  • TPO antibodies (positive)
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74
Q

What is the gold standard investigation for Hashimoto’s thyroiditis?

A
  • TSH
  • low = thyrotoxicosis
  • elevated = hypothyroid phase
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75
Q

Name any other tests used to investigate Hashimoto’s thyroiditis.

A

Thyroid biopsy, total T3 / T4 ratio

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76
Q

Differential diagnoses for Hashimoto’s thyroiditis include…

A

Grave’s disease, toxic multinodular goitre

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77
Q

What is the first-line treatment for Hashimoto’s thyroiditis?

A

Thyroid hormone replacement (Levothyroxine) and resection of obstructive goitre

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78
Q

How do you monitor a patient with Hashimoto’s thyroiditis?

A

monitored with period thyroid-stimulating hormone measurements

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79
Q

List any complications of Hashimoto’s thyroiditis.

A

Hyperlipidaemia and consequences

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80
Q

Define primary Hypothyroidism

A

Underproduction of thyroid hormone T3, T4 specifically failure to produce thyroid hormones by the thyroid gland

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81
Q

Is primary hypothyroidism more common in women or men ?

A

Women

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82
Q

At what age is primary hypothyroidism more common?

A

Older age

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83
Q

What causes primary hypothyroidism? (Aetiology)

A

Autoimmune hypothyroidism (Hashimoto’s), iodine deficiency, congenital defects

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84
Q

Name all risk factors for primary Hypothyroidism.

A
  • Iodine deficiency
  • Female sex
  • Age
  • FHx
  • autoimmune disorder
  • Grave’s disease
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85
Q

What is the pathophysiology of primary hypothyroidism?

A
  1. Aggressive destruction of thyroid cells by various cell and antibody-mediated immune processes.
  2. Antibodies bind and block TSH receptors
  3. inadequate thyroid hormone production and secretion
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86
Q

What are the key presentations of primary Hypothyroidism?

A

presence of risk factors, non-specific symptoms

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87
Q

What are the symptoms of primary hypothyroidism?

A

weakness, lethargy, cold sensitivity, constipation, weight gain, depression, myalgia, dry or coarse skin, eyelid oedema, facial oedema, coarse hair

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88
Q

What is the first-line investigation for primary Hypothyroidism and the expected results?

A
  • TSH (low = thyrotoxicosis, elevated = hypothyroid phase)
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89
Q

What is the gold standard investigation for primary Hypothyroidism and the expected results?

A
  • TSH (low = thyrotoxicosis, elevated = hypothyroid phase)
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90
Q

Name any other investigations that can be used to investigate primary Hypothyroidism.

A

Free serum T4, serum cholesterol, antithyroid peroxidase antibodies

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91
Q

Name the differential diagnoses of primary Hypothyroidism.

A

Central/secondary hypothyroidism, depression, Alzheimer’s dementia, Anaemia

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92
Q

What is the first-line treatment of primary Hypothyroidism?

A

Thyroid hormone replacement (Levothyroxine)

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93
Q

How do you monitor a patient with primary hypothyroidism?

A
  • thyroid-stimulating hormone (TSH) should be measured 4-6 weeks after initiation of therapy or dosage change
  • Stable patients with normal serum TSH should have TSH measured every 12 months
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94
Q

List any complications of primary Hypothyroidism.

A

Myxoedema coma:

  • 20-50% mortality
  • Reduced level of consciousness
  • seizures
  • hypothermia
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95
Q

What is the prognosis for a patient with primary hypothyroidism?

A

generally excellent with full recovery upon adequate replacement of thyroid hormones

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96
Q

Define s/c hypothyroidism.

A

Decreased TSH causing low TH synthesis resulting from hypofunction of Anterior pituitary or Hypothalamus

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97
Q

Does s/c hypothyroidism have a sex / age predominance.

A

No.

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98
Q

Is s/c hypothyroidism very common?

A

No, it is rare and accounts for <1% of hypothyroidism.

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99
Q

What causes s/c hypothyroidism? (Aetiology)

A

Hypopituitarism - pituitary adenomas / infection

hypothalamic disorders - neoplasms, trauma

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100
Q

List all risk factors for s/c hypothyroidism

A

Multiple endocrine neoplasia (Type I), head and neck irradiation, traumatic brain injury

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101
Q

What is the pathophysiology of s/c hypothyroidism?

A
  1. Reduced release or production of TSH or decreased stimulation of anterior pituitary by TRH causing deficiency of TSH
  2. reduced T3 and T4 release
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102
Q

What are the key presentations of s/c hypothyroidism?

A

Dry/ coarse skin, reduced body and scalp hair, muscle cramps, Presence of risk factors, fatigue, cold intolerance, weakness

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103
Q

What are the signs of s/c hypothyroidism?

A

Bradycardia

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104
Q

What are the symptoms of s/c hypothyroidism?

A

Weight gain, constipation, dry skin

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105
Q

What are the first-line investigations of s/c hypothyroidism and the expected results?

A

Free serum T4 (low),

TSH (low / normal)

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106
Q

What are the gold standard investigations of s/c hypothyroidism and the expected results?

A

Free serum T4 (low),

TSH (low / normal)

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107
Q

Name any other tests that might be done to investigate s/c hypothyroidism.

A

Brain MRI, head CT

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108
Q

Name the differential diagnoses of s/c hypothyroidism.

A

primary hypothyroidism, non-thyroidal illness, iodine deficiency, chronic fatigue syndrome, depression

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109
Q

What is the first-line management of s/c hypothyroidism?

A

Thyroid hormone replacement (Levothyroxine)

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110
Q

Name adjunct treatments of s/c hypothyroidism.

A

treatment of underlying pituitary tumour, if adrenal insufficiency then corticosteroids

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111
Q

How do you monitor a patient with s/c hypothyroidism?

A

Measurement of serum free thyroxine (T4) should be performed 4 to 8 weeks after new levothyroxine dose, then yearly

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112
Q

List complications of s/c hypothyrodism.

A

Myxoedema coma:

  • 20-50% mortality
  • Reduced level of consciousness
  • seizures
  • hypothermia
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113
Q

What is the prognosis for a patient with s/c hypothyroidism?

A

Prognosis dependent on underlying aetiology, for pituitary adenomas is dependent on the size and functionality

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114
Q

Define papillary thyroid cancer.

A

Cancer that forms in follicular cells in the thyroid and grows in finger-like shapes, Named for the papillae among its cells on microscopy

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115
Q

What % of thyroid cancers are classed as papillary?

A

~70%

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116
Q

Is papillary thyroid cancer more prevalent in women or men?

A

It is 3 x more common in women

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117
Q

Is papillary thyroid cancer more common in younger or older people?

A

Young people

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118
Q

What causes papillary thyroid cancer? (Aetiology)

A
  • Mutation

- usually well differentiated with a tendency towards multi-centricity and lymph node involvement

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119
Q

What are the risk factors for papillary thyroid cancer?

A
  • head and neck irradiation
  • female sex
  • FHx of thyroid cancer
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120
Q

What is the pathophysiology of papillary thyroid cancer?

A
  • tends to spread locally in the neck especially local lymph nodes
  • often compresses the trachea
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121
Q

What are the key presentations of papillary thyroid cancer?

A
  • presence of risk factors
  • asymptomatic palpable thyroid nodule (hard and fixed)
  • (possibly) enlarged lymph nodes on examination
  • young age
    FHx
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122
Q

What are the signs of papillary thyroid cancer?

A

tracheal deviation, palpable thyroid nodule

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123
Q

What are the symptoms of papillary thyroid cancer?

A

Hoarseness, dyspnea, dysphagia

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124
Q

What are the first-line investigations for papillary thyroid cancer and expected results?

A
  • TSH (normal)

- Ultrasound of the neck (nodule-no / characteristic)

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125
Q

What is the gold standard investigation for papillary thyroid cancer and expected results?

A
  • Fine-needle aspiration biopsy (intranuclear holes and grooves)
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126
Q

What other tests can be used to investigate papillary thyroid cancer?

A

Free T4 and T3, CT of neck

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127
Q

Name the differential diagnosis of papillary thyroid cancer.

A

Benign thyroid nodule

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128
Q

What is the first-line management of papillary thyroid cancer?

A
  1. surgery
  2. radioactive iodine ablation
  3. TSH suppression (levothyroxine)
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129
Q

How do you monitor a patient with papillary thyroid cancer?

A
  • radioactive iodine scan post-operatively when the patient becomes hypothyroid (generally in 4 to 6 weeks)
  • The scan detects residual thyroid tissue in the neck and also metastases, followed by ablation of residual cells with radioiodine
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130
Q

Name complications of the treatment of papillary thyroid cancer.

A

TSH suppression related atrial fibrillation

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131
Q

What is the prognosis of a patient with papillary thyroid cancer?

A

Best when young and female

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132
Q

Define anaplastic thyroid cancer.

A

Uncontrolled growth of cells in the thyroid gland, “one of the most aggressive cancers in humans”

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133
Q

What % of thyroid cancers are classed as anaplastic?

A

It is very rare, <5%

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134
Q

Does anaplastic thyroid cancer respond well to treatment?

A

No, usually poor response to treatment

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135
Q

Is anaplastic thyroid cancer more common in younger or older patients?

A

More common in elderly patients

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136
Q

List the risk factors for anaplastic thyroid cancer.

A
  • Head and neck irradiation
  • Female sex
  • FHx of thyroid cancer
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137
Q

What is the pathophysiology of anaplastic thyroid cancer?

A
  • affects the Follicular cells of the thyroid, but does not retain original cell features like iodine uptake or synthesis of thyroglobulin. - undifferentiated carcinoma with a high propensity for local invasion (recurrent laryngeal nerve and trachea, muscle, and/or oesophagus)and metastatic spread.
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138
Q

What are the key presentations of anaplastic thyroid cancer?

A
  • presence of risk factors
  • asymptomatic palpable thyroid nodule (hard and fixed)
  • (possibly) enlarged lymph nodes on examination
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139
Q

What are the signs of anaplastic thyroid cancer?

A

Tracheal deviation, palpable thyroid nodules

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140
Q

What are the symptoms of anaplastic thyroid cancer?

A

Hoarseness, dyspnea, dysphagia

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141
Q

What are the first-line investigations for anaplastic thyroid cancer and expected results?

A
  • TSH (normal)

- Ultrasound of the neck (nodule-no / characteristic)

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142
Q

What is the gold-standard investigation for anaplastic thyroid cancer and expected results?

A
  • Fine-needle aspiration biopsy (wide variations in appearance)
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143
Q

What other tests can be used to investigate anaplastic thyroid cancer?

A

Free T4 and T3, CT of the neck

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144
Q

The differential diagnosis for anaplastic thyroid cancer is?

A

Benign thyroid nodule

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145
Q

What is the first-line management of anaplastic thyroid cancer?

A

total thyroidectomy done when possible otherwise palliative care + chemoradiation

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146
Q

What are adjunct managements of anaplastic thyroid cancer?

A

Thyroid replacement (medication)

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147
Q

Name the complications of the treatment of anaplastic thyroid cancer.

A

TSH suppression related atrial fibrillation

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148
Q

What is the prognosis for a patient with anaplastic thyroid cancer?

A

Average survival a few months, high propensity for local invasion and metastatic spread

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149
Q

Define follicular thyroid cancer.

A

Well-differentiated thyroid cancer like papillary thyroid cancer but more malignant

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150
Q

What percentage of thyroid cancers are classified as follicular?

A

20%

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151
Q

In what areas is follicular thyroid cancer more prevalent?

A

areas of low iodine intake

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152
Q

In patients at what age is follicular thyroid cancer most common?

A

Middle-aged patients

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153
Q

What causes follicular thyroid cancer? (Aetiology)

A

chromosomal translocation

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154
Q

List all risk factors for follicular thyroid cancer.

A
  1. Head and neck irradiation
  2. Female sex
  3. FHx of thyroid cancer
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155
Q

What is the pathophysiology of follicular thyroid cancer?

A
  • early forms indolent but invasive forms aggressive
  • May infiltrate neck, but greater propensity to metastasise to lung and bones
  • spreads haematogenously
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156
Q

What are the key presentations of follicular thyroid cancer?

A
  • presence of risk factors
  • asymptomatic palpable thyroid nodule (hard and fixed)
  • (possibly) enlarged lymph nodes
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157
Q

What are the signs of follicular thyroid cancer?

A
  • tracheal deviation

- palpable thyroid nodule

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158
Q

What are the symptoms of follicular thyroid cancer?

A
  • Hoarseness
  • dyspnea
  • dysphagia
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159
Q

What are the first-line investigations for follicular thyroid cancer and expected results?

A
  • TSH (normal)

- Ultrasound of the neck (nodule-no / characteristic)

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160
Q

What is the gold standard investigation for follicular thyroid cancer and the expected result?

A
  • Fine-needle aspiration biopsy (hypercellularity, micro follicles)
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161
Q

Name any other test used to investigate follicular thyroid cancer.

A

Free T4 and T3, CT of the neck

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162
Q

Name the differential diagnosis for follicular thyroid cancer.

A

Benign thyroid nodule

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163
Q

What is the first-line management of follicular thyroid cancer?

A
  1. surgery
  2. radioactive iodine ablation
  3. TSH suppression (levothyroxine)
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164
Q

How do you monitor a patient with follicular thyroid cancer?

A
  • radioactive iodine scan post-operatively when the patient becomes hypothyroid (generally in 4 to 6 weeks)
  • The scan detects residual thyroid tissue in the neck and also metastases, followed by ablation of residual cells with radioiodine
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165
Q

Name the complications of the treatment of follicular thyroid cancer.

A

TSH suppression related atrial fibrillation

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166
Q

What is the prognosis for a patient with follicular thyroid cancer?

A
  • worse than papillary

- tends to have systemic metastases

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167
Q

Define medullary thyroid cancer.

A

Cancer that develops in the c cells of the thyroid – cells that make calcitonin to maintain healthy level of calcium in the blood

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168
Q

What percentage of thyroid cancers is classified as medullary?

A

5%

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169
Q

What causes medullary thyroid cancer? (Aetiology)

A

Mutations

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170
Q

List the risk factors for medullary thyroid cancer.

A
  1. Head and neck irradiation
  2. Female sex
  3. FHx of thyroid cancer (25% of medullary cancers as part of familial syndrome)
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171
Q

What is the pathophysiology of medullary thyroid cancers?

A
  • Parafollicular calcitonin-producing C cells.
  • Produce large amounts of peptide such as calcitonin, occurs in sporadic and familial forms
  • tendency to multi-centricity and early lymph node spread
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172
Q

What are the key presentations of medullary thyroid cancer?

A
  • Presence of risk factors
  • palpable thyroid nodule
  • young age
  • Diarrhoea
  • flushing epidoses
  • itching
  • FHx
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173
Q

Is medullary thyroid cancer more common in younger or older people?

A

younger people

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174
Q

What are the signs of medullary thyroid cancer?

A

tracheal deviation, palpable thyroid nodule

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175
Q

What are the symptoms of medullary thyroid cancer?

A

Hoarseness, dyspnea, dysphagia

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176
Q

What are the first-line investigations for medullary thyroid cancer and expected results?

A
  • TSH (normal)
  • Ultrasound of the neck (nodule-no / characteristic)
  • serum calcitonin (postive)
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177
Q

What is the gold standard investigation for medullary thyroid cancer and expected result?

A
  • Fine-needle aspiration biopsy (eosinophilic cells arranged in nests or sheets separated by amyloid and vascular stroma, staining +ve for calcitonin)
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178
Q

Name any other tests that can be used to investigate medullary thyroid cancer.

A
  • Free T4 and T3, CT of neck
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179
Q

Name the differential diagnosis for medullary thyroid cancer.

A

Benign thyroid nodule

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180
Q

What is the first-line management for medullary thyroid cancer?

A
  • total thyroidectomy

- ± lymph node dissection / radical neck dissection on site of metastasis

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181
Q

What is an adjunct teatment of medullary thyroid cancer?

A

Thyroid replacement (levothyroxine)

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182
Q

How do you monitor a patient with medullary thyroid cancer?

A
  • monitored with serum calcitonin every 3 months for 2 years, followed by every 6 months for 3 years, - if levels undetectable then annual follow up
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183
Q

Name the complications of the treatment of medullary thyroid cancer.

A

TSh suppression related atrial fibrillation.

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184
Q

What is the prognosis for a patient with medulalry thyroid cancer?

A

5 year survival for medullary cancer is 80%. (with correct treatment)

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185
Q

Define lymphoma thyroid cancer.

A

Lymphoma (cancer of lymphatic system) that arises from lymphocytes that are present within the thyroid gland

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186
Q

What percentage of thyroid cancers is classified as lymphoma?

A

2%

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187
Q

Which thyroid cancer is often associated with Hashimoto’s thyroiditis?

A

Lymphoma

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188
Q

What causes lymphoma? (Aetiology)

A

Rapidly grwing mass in the neck.

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189
Q

List the risk factors for lymphoma thyroid cancer.

A
  • head and neck irradiation
  • female sex
  • FHx of thyroid cancer
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190
Q

What is the pathophysiology of lymphoma thyroid cancer?

A

almost always non-hodkins lymphoma

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191
Q

What are the key presentations of lymphoma thyroid cancer?

A

Presence of risk factors, palpable thyroid nodule

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192
Q

What are the signs of lymphoma thyroid cancer?

A

tracheal deviation, palpable thyroid nodule

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193
Q

What are the symptoms of lymphoma thyroid cancer?

A

Hoarseness, dyspnea, dysphagia

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194
Q

What are the first-line investigations for lymphoma thyroid cancer and expected results?

A
  • TSH (normal)

- Ultrasound of the neck (nodule-no / characteristic)

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195
Q

What is the gold standard investigation for lymphoma thyroid cancer?

A

Fine-needle aspiration biopsy (may be identified by flow cytometry and nuclear atypia)

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196
Q

Name any other test that can be used to investigate lymphoma thyroid cancer.

A

Free T3 and T4, CT of neck

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197
Q

Name the differnetial diagnosis of lymphoma thyroid cancer.

A

Benign thyroid nodule

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198
Q

What is the first line management of lymphoma thyroid cancer?

A

Chemotherapy + external radiation

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199
Q

Name the complications of the treatment of lymphoma thyroid cancer.

A

TSH suppression related atrial fibrillation

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200
Q

What is the prognosis for a patient with lymphoma thyroid cancer?

A

5 year survival <50%

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201
Q

Define Cushing’s syndrome.

A

metabolic disorder caused by overproduction of corticosteroid hormones by the adrenal cortex and often involving obesity and high blood pressure – persistently and inappropriately elevated circulating glucocorticoid (cortisol)

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202
Q

What is the incidence rate of cushing’s syndrome?

A

1/100,000

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203
Q

How many cases of cushing’s syndrome are cushing’s disease?

A

2 / 3 of cases

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204
Q

Are cushing’s syndrome and disease more common in men or women?

A

Women

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205
Q

What are the two types of cushing’s syndrome?

A

ACTH (adrenocorticotropic hormone) dependent disease and Non-ACTH dependent disease

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206
Q

What causes ACTH dependent cushing’s syndrome? (Aetiology)

A
  • excessive ACTH from pituitary
  • ACTH producing tumour (most common)
  • excess ACTH administration
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207
Q

What causes Non-ACTH dependent cushing’s syndrome? (Aetiology)

A
  • adrenal adenomas
  • adrenal carcinomas
  • excess glucocorticoid administration
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208
Q

List the risk factors for Cushing’s syndrome.

A
  • Exogenous corticosteroid use
  • pituitary adenoma
  • adrenal adenoma
  • adrenal carcinoma
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209
Q

What is the pathophysiology of Cushing’ syndrome?

A
  • Many features due to protein-catabolic effects of cortisol; thin skin, easy bruising, striae.
  • Excessive alcohol consumption can mimic the clinical and biochemical signs (Pseudo-Cushings’s), but resolves on alcohol recession
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210
Q

What are the key presentations of Cushing’s syndrome?

A
  • Presence of risk factors
  • Obesity (fat distribution centrally, buffalo hump)
  • plethoric complexion
  • rounded ‘moon’ face
  • thin skin
  • pathological fractures
  • hypertension
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211
Q

What are the signs of Cushing’s syndrome?

A
  • pathological fractures

- hypertension

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212
Q

What are the symptoms of Cushing’s syndrome?

A
  • Acne
  • weight gain
  • easy bruisability
  • weakness
  • unexplained fractures
  • striae
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213
Q

What are the first-line investigations for cushing’s syndrome and expeced results?

A
  • Serum glucose (elevated)
  • late night salivary cortisol (elevated)
  • 48h low dose dexamethasone 2mg test (elevated)
  • Urine preg test (negative)
  • 24h urinary free cortisol (raised)
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214
Q

What is the gold standard test for cushing’s syndrome and expected result?

A
  • Petrosal snus sampling

elevated central / peripheral ACTH ratio indicates pituitary source

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215
Q

Name any other test that can be used to investigate Cushing’s syndrome.

A

Renal / pituitary CT or MRI, morning plasma ACTH

216
Q

DIfferential diagnoses of cushing’s syndrome include…

A

Obesity and metabolic syndrome

217
Q

What is the first line management of Cushing’s syndrome?

A

Tumour: surgical removal

Cortisol synthesis inhibition: metyrapone, ketoconazole

218
Q

How do you monitor a patient with cushing’s syndrome?

A

Periodical screening for recurrence of the disease

219
Q

What are the complications of Cushing’s syndrome?

A
  1. Hypertension
  2. Obesity
  3. CVD
  4. DM
  5. Death
  6. Adrenal insufficiency
220
Q

What is the prognosis for a patient with Cushing’s syndrome?

A
  • Untreated survival rate is 50% at 5 years

- Cushing’s syndrome generally has rare remission

221
Q

Define Cushing’s disease.

A

When elevated glucocorticoid is attributed to inappropriate ACTH secretion from the pituitary

222
Q

Define Acromegaly.

A

Overgrowth of all organ systems due to excess GH being secreted 99% due to pituitary tumour

223
Q

What is the no of cases of Acromegaly in the UK per eyar?

A

~3 million cases / year

224
Q

Is Acromegaly more prevalent in women or men?

A

M = W

225
Q

At what age is Acromegaly usualy diagnosed?

A

Middle age

226
Q

What causes Acromegaly? (Aetiology)

A
  • 99% of cases due to pituitary adenoma

- other: hyperplasia due to neuroendocrine carcinoid tumour that overproduced GH-releasing hormone

227
Q

What are the risk factors for Acromegaly?

A

Multiple endocrine neoplasia Type 1 syndrome, Carney’s complex

228
Q

What is the pathophysiology of Acromegaly?

A
  • Pituitary cells physiologically regulated by hormones, transcription factors, growth factors that stimulate their proliferation and hormone production throughout life.
  • Dysregulation of these signalling pathways can promote tumour development.
  • Pituitary somatotroph adenomas chronically secrete excessive growth hormone, which stimulates insulin-like growth factor 1 production leading to the majority of the clinical manifestations of the disease
229
Q

What are the key presentations of Acromegaly?

A
  • Coarsening of face
  • carpal tunnel syndrome
  • joint pain
230
Q

What are the signs of Acromegaly?

A
  • Increased growth of hand
  • Coarsening face
  • Wide nose
  • Macroglossia
  • Widely spaced teeth
  • puffy lips/eyelids/ skin
231
Q

What are the symptoms of Acromegaly?

A
  • Acroparaesthesia
  • Amenorrhoea
  • Headache
  • increased sweating
  • snoring
  • arthralgia
  • back ache
  • alterations in sexual functioning
232
Q

What are the first-line investigations for Acromegaly and expected results?

A
  • OGTT (GH value >1 microgram/L)
  • IGF-1 (elevated)
  • random serum GH (elevated)
233
Q

What is the Gold standard test for Acromegaly and expected result?

A

OGTT (GH value >1 microgram/L)

234
Q

Name any other tests that can be used to investigate Acromegaly.

A

Pituitary MRI, prolactin, Visual field testing (deficit if pressing on optic chiasm)

235
Q

Differential diagnoses for Acromegaly include…

A

Pseudo-acromegaly

236
Q

What is the first-line management of Acromegaly?

A

Transsphenoidal resection surgery

237
Q

List adjunct treatments for Acromegaly.

A
  1. Dopamine agonist (Cabergoline)
  2. somatostatin analogues (Ocreotide)
  3. GH receptor antagonist (Pegvisomant)
238
Q

How do you monitor a patient with Acromegaly?

A

Lifelong monitoring of growth hormone and IGF-1

239
Q

List the complications of Acromegaly.

A
  • Hypertension
  • DM
  • untreated adenoma can impact optic chiasm (blidness)
240
Q

What is the prognosis for a patient with Acromegaly?

A

May return to normal.

241
Q

What differentiates gigantism from acromegaly?

A

Gigantism happens when the condition happens before the fusion of epiphyseal plates.

242
Q

Define Conn’s syndrome.

A

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

243
Q

What causes Conn’s syndrome? (Aetiology)

A

Solitary aldosterone-producing adenoma – linked to mutations in K+ channels

244
Q

List the risk factors for Conn’s syndrome.

A
  1. FHx of primary aldosteronism

2. FHx of early onset Hypertension and/or stroke

245
Q

What is the Pathophysiology of Conn’s syndrome?

A
  • Aldosterone causes exchange of transport of sodium & potassium in the distal renal tubule.
  • hyperaldosteronism causes increased reabsorption of sodium & excretion of potassium
246
Q

What are the key presentations of Conn’s syndrome?

A
  • presence of risk factors

- Hypertension

247
Q

What are the signs of Conn’s syndrome?

A

Muscle cramps, muscle weakness, palpitations, polyuria, lethargy

248
Q

What are the symptoms of Conn’s syndrome?

A

Nocturia, polyuria, lethargy, mood disturbance, difficulty concentrating

249
Q

What are the first-line investigations of Conn’s syndrome and expected results?

A
  • Plasma K+ (normal / low)

- Aldosterone / renin ratio

250
Q

What is the gold standard investigation for Conn’s syndrome and expected result?

A

Selective adrenal vein sampling

- > unilateral (most common in conn’s)or bilateral production

251
Q

What are the differential diagnoses of Conn’s syndrome?

A
  • Essential hypertension
  • secondary HTN
  • Thiazide induced hypokalaemia
  • Liddle syndrome
252
Q

What is the first line management of Conn’s syndrome?

A

Laparoscopic adrenalectomy

253
Q

Name adjunct treatments of Conn’s syndrome.

A

pre operative aldosterone antagonist (Spironolactone)

254
Q

How do you monitor a patient with Conn’s syndrome?

A

BP, plasma electrolytes, and aldosterone and renin levels should be monitored every 6 to 12 months for clinical and biochemical evidence of recurrence

255
Q

What are the complications of Conn’s syndrome?

A

Heart failure, MI, stroke, atrial fibrillation, impaired renal function

256
Q

What is secondary Hyperaldosteronism (NOT Conn’s)?

A

Hyperaldosteronism due to high renin levels

257
Q

Define Addison’s disease. (Primary Adrenal insufficiency)

A

Decreased secretion of hormones (cortisol, aldosterone, dehydroepiandrosterone) by adrenal glands

258
Q

What is the Incidence of Addison’s disease?

A

1 / 10,000

259
Q

What causes Addison’s disease? (Aetiology)

A

Organ-specific autoantibodies in 90% of cases. Rarely: adrenal gland tuberculosis, surgical removal or haemorrhage

260
Q

List all risk factors for Addison’s disease.

A
  1. Female sex
  2. adrenocortical autoantibodies
  3. adrenal haemorrhage
  4. TB
  5. Autoimmune disease
  6. use of anticoagulants
261
Q

What is the pathophysiology of Addison’s disease?

A
  • Destruction of adrenal cortex (≥ 90%) leads to cortisol and aldosterone deficiency,
  • Excess ACTH stimulates melanocytes
  • hyperpigmentation
262
Q

What are the key presentations of Addison’s disease?

A

Presence of risk factors, fatigue, anorexia, weight loss, hyperpigmentation

263
Q

What are the signs of Addison’s disease?

A

Anorexia, hyperpigmentation

264
Q

What are the symptoms of Addison’s disease?

A

Lean, tired, tanned, tearful, dizzy, faints, unexplained abdominal pain and vomiting

265
Q

What are the first-line investigations of Addison’s disease and expected results?

A
  • serum electrolytes (low Na+, elevated K+)
  • blood urea (may be elevated)
  • FBC (anaemia)
  • morning serum cortisol (v low levels)
266
Q

What is the gold standard investigation of Addison’s disease and expected result?

A
  • ACTH stimulation test (serum cortisol low)
267
Q

What other tests can be used to investigate Addison’s disease?

A

serum ACTH, plasma renin activity, adrenal antibodies

268
Q

Name all differential diagnoses of Addison’s disease.

A
  • 2°/ 3° adrenal insufficiency
  • Hyperthyroidism
  • adrenal suppression due to corticosteroid therapy
269
Q

What is the first-line management of Addison’s disease?

A

Hormone replacement (glucocorticoid (hydrocortisone) and mineralocorticoid (fludrocortisone))

270
Q

How do you monitor a patient with Addison’s disease?

A

Yearly follow up (U&E, BP), regular measurements of bone density

271
Q

List all complications of Addison’s disease.

A

Adrenal crisis can lead to death, secondary Cushing’s syndrome, osteopenia/porosis

272
Q

Define secondary adrenal insufficiency.

A

Condition where pituitary gland does not produce enough ACTH meaning adrenal gland does not produce enough cortisol

273
Q

What is the incidence of secondary adrenal insufficiency.

A

2 / 10,000

274
Q

What causes secondary adrenal insufficiency? (Aetiology)

A

Usually caused by long term steroid therapy (or hypothalamic – pituitary disease) leading to suppression of pituitary – adrenal axis

275
Q

What is the pathophysiology of secondary adrenal insufficiency?

A
  • Reduction of adrenal cortex stimulation by pituitary
  • Less cortical products. Low ACTH
  • less melanocytes stimulation
  • no pigmentation
276
Q

What are the key presentations of secondary adrenal insufficiency?

A
  • Presence of risk factors
  • fatigue
  • anoxeria / weight loss
277
Q

What are the signs of secondary adrenal insufficiency?

A

Anorexia

278
Q

What are the symptoms of secondary adrenal insufficiency?

A

Lean, tired, dizzy, faints

279
Q

What are the first-line investigations of secondary adrenal insufficiency and expected results?

A
  • Long ACTH test = synacthen test (to distinguish from primary - ACTH raised in primary, lowered in secondary)
  • serum electrolytes (low Na+, elevated K+)
  • blood urea (may be elevated)
  • FBC (anaemia)
  • morning serum cortisol (v low levels)
280
Q

What is the gold standard investigation of secondary adrenal insufficiency and expected results?

A

ACTH stimulation test (serum cortisol low)

281
Q

What are the differential diagnoses of secondary adrenal insufficiency?

A

Addison’s disease, adrenal suppression due to corticosteroid therapy

282
Q

What is the first-line management of secondary adrenal insufficiency?

A

Hormone replacement glucocorticoid (hydrocortisone), if from steroid therapy then remove steroids very slow

283
Q

How do you monitor a patient with secondary adrenal insufficiency?

A
  • Yearly follow up (U&E, BP), regular measurements of bone density
284
Q

Define adrenal hyperplasia (congenital).

A

Defective enzymes mediating the production of adrenal cortex products

285
Q

What causes adrenal hyperplasia? (aetiology)

A

Genetic 21-hydroxylase deficiency is the cause of about 95% of cases.

286
Q

What is a risk factor for adrenal hyperplasia?

A

Genetic predisposition

287
Q

What is the pathophysiology of adrenal hyperplasia?

A
  • Defective 21-hydroxylase
  • disruption of cortisol biosynthesis
  • causes cortisol deficiency, with or without aldosterone deficiency and androgen excess
  • severe forms = aldosterone deficiency -> salt loss
288
Q

What are the key presentations of adrenal hyperplasia?

A

Genetic predisposition, weight loss, failure to thrive, vomiting, hypotension, ambiguous genitalia

289
Q

What are the signs of adrenal hyperplasia in a female patient?

A

Ambiguous genitalia with common urogenital sinus

290
Q

What are the signs of adrenal hyperplasia in a male patient?

A

no signs at birth, bar subtle hyperpigmentation and possible penile enlargement

291
Q

What are the symptoms of adrenal hyperplasia?

A

Weight loss, vomiting, hypotension, failure to thrive

292
Q

What are the first-line investigations for adrenal hyperplasia and expected results?

A
  • serum11-deoxycortisol (elevated)
  • serum chem (low Na+, low K+)
  • genetic analysis (mutation)
293
Q

What is the gold standard investigation for adrenal hyperplasia and expected result?

A
  • serum17-hydroxyprogesterone (precursor to cortisol) levels = high
294
Q

Name any other tests that can be used to investigate adrenal hyperplasia.

A

plasma renin activity, pelvic / adrenal ultrasound

295
Q

Name the differential diagnoses of adrenal hyperplasia.

A

Addison’s disease, Gender identity disorder, renal salt-wasting

296
Q

What is the first-line management of adrenal hyperplasia?

A

Glucocorticoids: Hydrocortisone

297
Q

Name any adjunct management of adrenal hyperplasia.

A

Mineralocorticoids: fludrocortisone, If salt loss: NaCl supplement, genital surgery

298
Q

How do you monitor a patient with adrenal hyperplasia?

A

Children – follow up every 3 months, adults – follow up every 6 months

299
Q

List complications of adrenal hyperplasia.

A

Adrenal crisis, testicular adrenal rests, short stature

300
Q

What is the prognosis for a patient with adrenal hyperplasia?

A

Proper treatment – good prognosis and normal life expectancy

301
Q

Define SIADH.

A

Excessive ADH secretion leading to hypotonic hyponatraemia and conc urine

302
Q

What causes SIADH? (Aetiology)

A

Disordered hypothalamic-pituitary secretion, or ectopic production of ADH, - Neurological: Tumour, trauma, infection, , CNS disorders
- Pulmonary: Lung small cell cancer (common), mesothelioma, cystic fibrosis, Drugs

303
Q

List all risk factors for SIADH.

A
  • > 50
  • pulmonary condition
  • nursind home residence
  • malignancy
  • drugs associated with SIADH induction
  • CNS disorders
304
Q

What is the pathophysiology of SIADH?

A

Ectopic production increases the amount of ADH produced, beyond mechanisms of control

305
Q

What are the key presentations of SIADH?

A

presence of risk factors, nausea, irritability and headache with mild dilutional hyponatraemia, Fits and coma with severe hyponatraemia

306
Q

What are the signs of SIADH?

A

Absence of hypo/hypervolaemia, absence of signs of adrenal insufficiency / hypothyroidism

307
Q

What are the symptoms of SIADH?

A

Nausea, vomiting, altered mental status, headache, seizure, coma

308
Q

What is the first-line investigation for SIADH and expected results?

A

Serum sodium (low), Serum osmolality (low), serum urea (low)

309
Q

What is the gold standard investigation for SIADH and expected results?

A

Serum sodium (low)

310
Q

Name any other tests that can be used to investigate SIADH.

A

DIagnostic trial with normal saline, serum TSH

311
Q

Name the differential diagnoses of SIADH.

A
  • Pseudohyponatraemia
  • hypo/hypervolaemia
  • renal failure
  • addison’s disease
  • cerebral salt-wasting
312
Q

What is the first-line management of SIADH.

A

treat underlying cause + restrict fluids , if chronic – ADH suppression

313
Q

How do you monitor a patient with SIADH?

A

Monitor serum sodium daily until stabilised, regular monitoring after (eg every 6 months)

314
Q

What is the prognosis for SIADH?

A

If underlying course found and treated, SIADH typically resolves

315
Q

Define central / cranial diabetes insipidus?

A

Disease that occurs when the body has lower than normal amounts of ADH due to reduced synthesis or release of ADH (= Arginine vasopressin, AVP)

316
Q

Is central / cranial diabetes insipidus more prevalent in men or women?

A

M = W

317
Q

Is central / cranial diabetes insipidus very common?

A

No, generally uncommon (1 in 25,000)

318
Q

What causes central / cranial diabetes insipidus? (Aetiology)

A
  • Acquired – Pituitary surgery, post traumatic head injury, Craniopharygioma, idiopathic (Phenytoin, temozolomide), autoimmune disorder,
  • Genetic – Mutations in the ADH gene
319
Q

What are the risk factors for central / cranial diabetes insipidus?

A
  • Pituitary surgery
  • craniopharyngioma
  • pituitary stalk lesions
  • traumatic brain injury
  • medication
  • autoimmune disease
  • FHx
  • genetic mutations
320
Q

What is the pathophysiology of central /cranial diabetes insipidus?

A
  • Results from any condition that impairs the production, transportation, or release of AVP.
  • Disease of the hypothalamus, where ADH is produced -> Insufficient ADH production. Interestingly, damage to the Posterior Pituitary gland, does not lead to ADH deficiency, as it can still ‘leak’ out.
321
Q

What are the key presentations of central / cranial diabetes insipidus?

A

polyuria, compensatory polydispsia

322
Q

What are the signs of central / cranial diabetes insipidus?

A

FHx, genetic mutations, history of pituitary / hypothalamic disease, history of autoimmune disorders

323
Q

What are the symptoms of central / cranial diabetes insipidus?

A

Nocturia, polydipsia, polyuria

324
Q

What are the first-line investigations for cranial / central diabetes insipidus and expected results?

A
  1. urine osmolality (low)
  2. serum glucose (normal)
  3. 24h urine collection (high)
  4. U&E’s (confirm that there is not a more common cause of polyuria)
325
Q

What is the gold standard investigation for cranial / central diabetes insipidus and expected results?

A

8h water deprivation test (confirm DI)

326
Q

Name any other tests that can be used to investigate cranial / central diabetes insipidus.

A
  • Cranial MRI

- desmopressin stimulation test (distinguish between central / nephrogenic DI)

327
Q

Name the differential diagnoses of central / cranial diabetes insipidus.

A

DM, Diuretics, psychogenic polydipsia, Hypercalcaemia

328
Q

What is the first-line management for central / cranial diabetes insipidus?

A

Desmopressin (synthethic analogue of ADH)

329
Q

Name any adjunct managements for central / cranial diabetes insipidus?

A

Oral / intravenous fluids

330
Q

How do you monitor a patient with central / cranial diabetes insipidus?

A

Follow up imaging to detect pathology if previously undetected, follow up serum electrolytes

331
Q

What is the prognosis for a patient with Central / cranial diabetes insipidus?

A

usually well controlled on desmopressin

332
Q

Define nephrogenic diabetes insipidus.

A

Disease with defect in kidney tubules so that kidneys are unable to properly respond to ADH

333
Q

Is nephrogenic diabetes insipidus more prevalent in men or women?

A

M = W

334
Q

Is nephrogenic diabetes insipidus very common?

A

No, generally uncommon (1 in 25,000)

335
Q

What causes nephrogenic diabetes insipidus? (Aetiology)

A
  • Acquired – Hypokalaemia, hypercalcaemia, drugs: lithium therapy, renal tubular acidosis, sickle cell, prolonged polyuria, chronic kidney disease
  • Genetic – Mutation in ADH receptor (90%)
336
Q

List the risk factors of nephrogenic diabetes insipidus.

A
  1. FHx
  2. genetic mutations
  3. medication (lithium therapy)
337
Q

What is the pathophysiology of nephorgenic diabetes insipidus?

A

depends on the aetiology, Can be due to disruption of the channels, damage to the kidney -> Lack of appropriate response to ADH, results from conditions that impair the renal collecting ducts’ ability to respond to AVP

338
Q

What are the key presentations of nephrogenic diabetes insipidus?

A

Polyuria, compensatory polydipsia

339
Q

What are the signs of nephrogenic diabetes insipidus?

A

Hx of Lithium therapy, FHx, genetic mutations

340
Q

What are the symptoms of nephrogenic diabetes insipidus?

A

Polyuria, compensatory polydipsia

341
Q

What are the first-line investigations for nephrogenic diabetes insipidus and expected results?

A
  1. urine osmolality (low)
  2. serum glucose (normal)
  3. 24h urine collection (high)
  4. U&E’s (confirm that there is not a more common cause of polyuria)
342
Q

What is the gold standard investigation for nephrogenic diabetes insipidus and expected results?

A

8h water deprivation test (confirm DI)

343
Q

Name any other tests that can be used to investigate nephrogenic diabetes insipidus.

A

Desmopressin stimulation test - distinguish between central/cranial and nephrogenic DI

344
Q

What are the differential diagnoses of nephrogenic diabetes insipidus?

A

DM, Diuretics, psychogenic polydipsia, Hypercalcaemia

345
Q

What is the first-line management of nephrogenic diabetes insipidus?

A

maintenance of adequate fluid intake + treatment of underlying cause

346
Q

Name any adjunct treatments for nephrogenic diabetes insipidus.

A

sodium restriction and/or pharmacotherapy

347
Q

How do you monitor a patient with nephorgenic diabetes insipidus?

A

Periodic renal and bladder ultrasonography and regular serum creatinine

348
Q

Define hyperkalaemia.

A

Excess potassium, if >6.5mmol/L then potential EMERGENCY

349
Q

What causes hyperkalaemia? (Aetiology)

A

Renal impairment (most common), Metabolic acidosis, drug interference with potassium excretion, massive blood transfusion, Elevated without any of these may be artefactual (eg venepuncture problems, delayed analysis due to problems in lab)

350
Q

List the risk factors for hyperkalaemia.

A
  1. Renal impairment
  2. DM
  3. Burns
  4. Addison’s disease
351
Q

What is the pathophysiology of hyperkalaemia?

A

Renal impairment can lead to retention of potassium in the nephron. This is possible with potassium sparing diuretic.

352
Q

What are the key presentations of hyperkalaemia?

A

Few symptoms until MI, impaired neuromuscular transmission (muscle weakness and paralysis)

353
Q

What are the signs of hyperkalaemia?

A

Tall tented T waves on ECG

354
Q

What are the symptoms of hyperkalaemia?

A

Irregular fast pulse, chest pain, weakness, palpitations, light-headedness

355
Q

What are the first line investigations for hyperkalaemia?

A

U&E
serum calcium
FBC
ECG (peaked T waves, prolonged PR, widened QRS and reduced P)

356
Q

What is the gold standard investigation for hyperkalaemia?

A

Serum potassium (recheck if unexpected result)

357
Q

What are the differential diagnoses of hyperkalaemia?

A
  • CKD
  • diabetic ketoacidosis
  • potassium supplementation with underlying renal dysfunction
  • drug-related reduced urinary potassium excretion
358
Q

What is the first-line management of hyperkalaemia?

A

dietary potassium restriction and loop diuretic (acts on loop of Henle – furosemide)

359
Q

Name any adjunct treatment for hyperkalaemia.

A

treat underlying condition and review meds

360
Q

What is a serious complication of hyperkalaemia?

A

MI -> Death

361
Q

Define hypokalaemia.

A

Deficiency of potassium (serum potassium <3.5mmol/L), if <2.5 then EMERGENCY

362
Q

What causes hypokalaemia? (Aetiology)

A
  • Diuretic treatment
  • hyperaldosteronism (Conn’s)
  • GI fluid loss by vomiting/diarrhoea
  • pyloric stenosis
  • Cushing’s
  • Alkalosis
  • Renal tubular failure
363
Q

List all risk factors of hypokalaemia.

A
  1. Diuretic treatment
  2. Conn’s syndrome
  3. V / D
364
Q

What is the pathophysiology of hypokalaemia?

A

Excessive loss of potassium through the kidneys in response to aldosterone or diuretic therapy. GI fluid loss -> less chloride -> increase in aldosterone -> Decreased potassium reabsorption

365
Q

What are the key presentations of hypokalaemia?

A

Usually asymptomatic, possibly muscle weakness, increased risk of cardiac arrhythmias, polyuria

366
Q

What are the signs of hypokalaemia?

A

Polyuria, T wave inversion, possible prominent U wave

367
Q

What are the symptoms of hypokalaemia?

A

Possible muscle weakness, polyuria

368
Q

What are the first-line investigations of hypokalaemia?

A

U&E, serum calcium, FBC, ECG (Flat T waves, ST depression, prominent U waves)

369
Q

What is the gold standard investigation of hypokalaemia and expected results?

A

Serum potassium & magnesium (both low)

370
Q

Name the differential diagnoses of hypokalaemia.

A
  • severe V / D
  • Bulimia / anorexia nervosa
  • laxative
  • drug-induced
  • alcoholism
  • diabetic ketoacidosis
371
Q

What is the first-line management of hypokalaemia?

A

K+ and Mg+ supplement

372
Q

Name any adjunct managements of hypokalaemia.

A

treat underlying cause, withdraw harmful medication

373
Q

Name any complications of hypokalaemia.

A

Cardiac arrhythmia and sudden death

374
Q

Define hypercalcaemia.

A

Excess calcium, if serum levels > 3.5mmol/L then potential EMERGENCY

375
Q

What is the incidence of hypercalcaemia?

A

3 / 10,000

376
Q

What causes hypercalcaemia? (Aetiology)

A

> 90% caused by primary hyperparathyroidism or malignancy (eg bone metastases), other (Vit D intoxication, thyrotoxicosis, lithium)

377
Q

List the risk factors of hypercalcaemia.

A
  1. Non-metastatic malignancy
  2. metastatic skeletal involvement
  3. lymphoma
  4. primary hyperparathyroidism
378
Q

What is the pathophysiology of hypercalcaemia?

A

Ectopic secretion of PTH is very rare. Tumour related hypercalcaemia tends to work by a secretion of a peptide with PTH-like activity, direct invasion of bone and production of local factors for calcium mobilisation

379
Q

What are the key presentations of hypercalcaemia?

A

“painful Bones, renal stones, abdominal groans and psychic moans” Occasionally: renal calculi and CKD

380
Q

What are the signs of hypercalcaemia?

A
  • renal failure
  • ectopic calcification
  • Cardiac Arrest
  • shortening of QT interval
381
Q

What are the symptoms of hypercalcaemia?

A
  • Abdominal pain
  • Vomiting
  • constipation
  • polyuria
  • polydipsia
  • depression
  • weight loss
  • hypertension
  • confusion
  • weakness
  • tiredness
382
Q

What are the first-line investigations of hypercalcaemia and expected results?

A
  • serum calcium (elevated)
  • serum albumin (low in malignancy)
  • U&E (high urea and bicarbonate)
  • serum intact PTH (high in 1° hyperparathyroidism)
383
Q

What is the gold standard investigation of hypercalcaemia and expected results?

A
  • serum calcium (elevated)
384
Q

Name any other tests used to investigate hypercalcaemia.

A

Chest Xray, isotope bone scan, FBC

385
Q

Name all differential diagnoses of hypercalcaemia.

A
  • Primary hyperparathyroidism
  • Hyperthyroidism
  • adrenal insufficiency
  • Phaeochromocytoma
  • sarcoidosis
  • med-related hypercalcaemia
  • TB
386
Q

What is the first-line management of hypercalcaemia?

A

IV saline + Biphosphate (palmidronate disodium), If primary hyperparathyroidism – surgery

387
Q

Name any adjunct treatment of hypercalcaemia.

A

calcitonin, loop diuretic (furosemide), treatment of underlying malignancy

388
Q

What is the prognosis for a patient with hypercalcaemia?

A

Eradication of underlying malignancy crucial for permanent reversal of hypercalcaemia

389
Q

What is PTH?

A

PTH = parathyroid hormone that regulates serum calcium conc through its effects on bone, kidney and intestine

390
Q

Define hypocalcaemia.

A

Deficiency of calcium, if serum levels <2mmol/L then potential EMERGENCY

391
Q

What causes hypocalcaemia?

A
  1. increased serum phosphate: Chronic kidney disease (most common), Phosphate therapy
  2. Reduced PTH function: Post thyroidectomy and parathyroidectomy
  3. Vitamin D deficiency: Reduced exposure to sunlight
  4. Other: osteomalacia, acute pancreatitis, over-hydration, hypomagnesaemia
392
Q

List all risk factors for hypocalcaemia.

A

CKD, primary hyperparathyroidism, Vit D deficiency

393
Q

What is the pathophysiology of hypocalcaemia?

A

CKD -> Increased phosphate -> Microprecipitation of calcium phosphate in tissues -> Low serum level of calcium, CKD -> Inadequate production of active vitamin D

394
Q

What are the key presentations of hypocalcaemia?

A

anxious / irritable / irrational, confused, seizures/spasms

Severe / chronic: Trousseau’s sign, Chovtek’s sign, cataract

395
Q

What are the signs of hypocalcaemia?

A

Increased muscle tone in smooth muscle, cardiomyopathy (long QT interval)

396
Q

What are the symptoms of hypocalcaemia?

A

perioral paraesthesiae, spasms, anxious / irritable / irrational, seizures, confusion / impaired orientation, dermatitis, impetigo

397
Q

What are the first-line investigations for hypocalcaemia and expected results?

A
  • History (age of occurance, neck surgery, DHx)
  • eGFR (search for CKD)
  • serum PTH (elevated)
  • Vit D (low)
398
Q

What is the gold standard investigation for hypocalcaemia and expected results?

A

serum calcium (low)

399
Q

List all differential diagnoses of hypocalcaemia.

A
  • Vit D deficiency
  • hypomagnesaemia
  • hyperventilation
  • postsurgical hypoparathyroidism
400
Q

How do you manage acute hypocalcaemia?

A

IV calcium

401
Q

How do you treat persistent hypocalcaemia?

A

if Vit D deficient: supplement, if hypoparathyroidism: alfacalcidol

402
Q

What are the complications of hypocalcaemia?

A

Death

403
Q

Define Primary Hyperparathyroidism.

A

Excessive secretion of PTH as one parathyroid gland produces excess PTH

404
Q

Is primary hyperparathyroidism more common in men or women?

A

W>M

- 1 in 500W and 1 in 2000M

405
Q

At what age is primary hyperparathyroidism more common?

A

Aged >40

406
Q

What causes primary hyperparathyroidism? (Aetiology)

A

Single parathyroid adenoma (~80%) or hyperplasia (~20%)

407
Q

List all risk factors for primary hyperparathyroidism.

A
  • female sex
  • age >50
  • FHx of PHPT
  • endocrine neoplasia
  • lithium treatment
  • hyperparathyroidism -jaw tumour syndrome
408
Q

What is the pathophysiology of primary hyperparathyroidism?

A

Adenoma or hyperplasia provides additional secretive tissue to provide excess PTH

409
Q

What are the key presentations of primary hyperparathyroidism?

A

70 – 80 % asymptomatic presentation, bone pain, poor sleep, fatigue, anxiety, memory loss, myalgias, muscle cramps, constipation

410
Q

What are the signs of primary hyperparathyroidism related to increased calcium?

A
  • weak, tired, depressed, thirsty
411
Q

What are the signs of primary hyperparathyroidism related to bone resorption?

A

bone pain, fractures, osteoporosis

412
Q

What are the symptoms of primary hyperparathyroidism?

A

Fatigue, poor sleep, pain, depression, fractures

413
Q

What is the first-line investigation for primary hyperparathyroidism and expected result?

A

serum calcium (high in normal range or elevated)

414
Q

What is the gold standard investigation for primary hyperparathyroidism and expected result?

A

Serum intact PTH with immunoradiometric / immunochemical assay ( high in normal range or elevated) (inappropriate elevation)

415
Q

Name any other tests that can be used to investigate primary hyperparathyroidism.

A

Vit D, serum phosphorus, 24h urinary calcium, DEXA scan (osteoporosi/penia)

416
Q

What are the differential diagnoses of primary hyperparathyroidism?

A
  • Familial hypocalciuric Hypercalcaemia
  • multiple myeloma
  • milk-alkali syndrome
  • sarcoidosis
  • Thiazides
  • Immobilisation
  • Hypervitaminosis D
  • humoral hypercalcaemia of malignancy
417
Q

What is the first-line management of primary hyperparathyroidism?

A

parathyroidectomy / monitoring (if surgery declined / not candidate for surgery)

418
Q

Name any adjunct treatments of primary hyperparathyroidism.

A

bisphosphonate (alendronic acid) + Vit D supplementation (ergocalciferol)

419
Q

How do you monitor a patient with primary hyperparathyroidism?

A

Monitoring of serum calcium levels for 6 months then annual checks, bone density check every 1-2 years

420
Q

What are the complications of primary hyperparathyroidism?

A

Hypercalcaemia, osteoporosis, bone fractures, recurrent laryngeal nerve damage (hoarse voice)

421
Q

What is the prognosis for a patient with primary hyperparathyroidism?

A

Parathyroidectomy has cure rate of >95%, most common cause of mortality in PHPT patient is stroke/MI

422
Q

Define secondary hyperparathyroidism.

A

Disease outside of glands leads to enlargement of parathyroid glands usually –> Hypocalcaemia leads to increased secretion of PTH to compensate

423
Q

What causes secondary hyperparathyroidism? (Aetiology)

A

CKD, intestinal malabsorption or chronic inadequate sunlight exposure which gives rise to alterations in Vit D, phosphorus and calcium

424
Q

List all risk factors for secondary hyperparathyroidism.

A
  1. Ageing
  2. Chronic renal failure (>60% of patients with CKD at risk of developing secondary HPTH)
  3. low Vit D (malabsorption/inadequate light exposure/nutritional deficiency)
425
Q

What is the pathophysiology of secondary hyperparathyroidism?

A

Parathyroid gland becomes hyperplastic in response to chronic hypocalcaemia as PTH acts to increase ionised calcium in blood

426
Q

What are the key presentations of secondary hyperparathyroidsm?

A

Presence of risk factors, muscle cramps and bone pain, Chovstek’s sign, Trousseau’s sign, fractures

427
Q

What are the signs of secondary hyperparathyroidism?

A

Chovstek’s sign, Trousseau’s sign, fractures, features of chronic renal failure

428
Q

What are the symptoms of secondary hyperparathyroidism?

A

Muscle cramps and bone pain

429
Q

What are the first-line investigations of secondary hyperparathyroidism and expected results?

A
  • serum intact parathyroid hormone (elevated)
  • serum calcium (low)
  • serum creatinine (elevated)
  • serum urea nitrogen (elevated)
430
Q

What is the gold standard investigation for secondary hyperparathyroidism and expected result?

A

Serum intact parathyroid hormone (elevated) (appropriate elevation)

431
Q

Name any other tests that can be used to investigate secondary hyperparathyroidism.

A

Neck Ultrasound / CT / MRI, serum Vit D (low)

432
Q

What is the differential diagnosis of secondary hyperparathyroidism?

A

Primary hyperparathyroidism

433
Q

What is the first-line management of secondary hyperparathyroidism?

A

treat underlying condition (ie if lack of sunlight – UV radiation exposure, malabsorption – different diet / supplements, CKD – dietary phosphate restriction / parathyroidectomy)

434
Q

Name any adjunct treatments of secondary hyperparathyroidism.

A

calcium supplementation (calcium carbonate), Vit D supplementation (ergocalciferol)

435
Q

How do you monitor a patient with secondary hyperparathyroidism?

A

Regular electrolyte examinations , bone densitometry measurements every 2nd year

436
Q

What are the complications of secondary hyperparathyroidism?

A

Development into tertiary hyperparathyroidism, osteodystrophy, osteoporosis

437
Q

What is the prognosis for a patient with secondary or tertiary hyperparathyroidism?

A

prognosis depends on underlying disease

438
Q

Define tertiary hyperparathyroidism.

A

Excess production of Parathyroid hormone that does not follow normal body feedback controls and persists even if initial cause (low Ca2+) has been corrected

439
Q

What causes secondary hyperparathyroidism? (Aetiology)

A

Occurs after prolonged secondary hyperparathyroidism

440
Q

What are the risk factors for tertiary hyperparathyroidism?

A

CKD, secondary hyperparathyroidism

441
Q

What is the pathophysiology of tertiary hyperparathyroidism?

A

Glands become autonomous, producing excess of PTH even after the correction of calcium deficiency

442
Q

What are the key presentations of tertiary hyperparathyroidism?

A

bone pain, poor sleep, fatigue, anxiety, memory loss, myalgias, muscle cramps, constipation, bone pain, fractures, osteoporosis, Hypertension

443
Q

What are the signs of tertiary hyperparathyroidism related to increased calcium?

A

weak, tired, depressed, thirsty

444
Q

What are the signs of tertiary hyperparathyroidism related to bone resorption?

A

bone pain, fractures, osteoporosis

445
Q

What are the symptoms of tertiary hyperparathyroidism?

A

Fatigue, poor sleep, pain, depression, fractures

446
Q

What are the first-line investigations of tertiary hyperparathyroidism and expected results?

A
  • Serum intact parathyroid hormone (elevated)
  • serum calcium (elevated)
  • serum creatinine (elevated)
  • serum urea nitrogen (elevated)
447
Q

What is the gold standard investigation for tertiary hyperparathyroidism and expected results?

A
  • serum intact parathyroid hormone (elevated) (inappropriate elevation)
448
Q

Name any other test that can be used to investigate tertiary hyperparatroidism.

A

Neck Ultrasound / CT / MRI, serum Vit D (low)

449
Q

What is the first-line management of tertiary hyperparathyroidism?

A

Calcium mimetic (Cinacalcet) + total / subtotal parathyroidectomy

450
Q

Name any adjunct treatments of tertiary hyperparathyroidism.

A

treat underlying cause (chronic kidney failure)

451
Q

What are the complications of tertiary hyperparathyroidism?

A

Transient hypocalcaemia follows parathyroidectomy

452
Q

Define hypoparathyroidism.

A

Disease with low synthesis and secretion of parathyroid hormone in blood causing deficiencies of calcium and elevated serum phosphorus

453
Q

What is the epidemiology of hypoparathyroidism?

A

It is rare and usually occurs postoperatively

454
Q

What causes hypoparathyroidism? (Aetiology)

A

Postsurgical hypoparathyroidism, can be genetic: due to defects in PTH gene, can be autoimmune

455
Q

List the risk factors for hypoparathyroidism.

A
  1. Thyroid / parathyroid surgery
  2. hypomagnesaemia
  3. moderate/chronic maternal Hypercalcaemia (leads to neonatal hypocalcaemia)
  4. autosomal dominant conditions (mutations)
456
Q

What is the pathophysiology of hypoparathyroidism?

A
  1. PTH stimulates the activation of vitamin D
  2. Vit D facilitates intestinal calcium absorption, renal reabsorption of calcium as well as calcium release from bone
  3. Phosphate reabsorption is inhibited by PTH
  4. In disease, these processes do not occur.
457
Q

What are the key presentations of hypoparathyroidism?

A
  • History of thyroid/parathyroid/laryngeal surgery
  • muscle twitches/spasms/cramps
  • paraesthesias/numbness/tingling
  • malnutrition/malabsorption
  • chronic alcoholism
458
Q

What are the signs of hypoparathyroidism?

A

Increased excitability of muscles, malnutrition/malabsorption, poor memory

459
Q

What are the symptoms of hypoparathyroidism?

A

Numbness around mouth/extremities, cramps, tetany, convulsions, Chvostek/Trousseauu’s sign

460
Q

What are the first-line investigations of hypoparathyroidism and expected results?

A
  • Serum calcium (low)
  • ECG (prolonged QT interval)
  • plasma intact PTH ( low / normal)
  • serum magnesium (may be low)
  • serum phosphorus (elevated)
461
Q

What is the gold standard investigation for hypoparathyroidism and expected results?

A
  • Serum calcium (low)
462
Q

Name any other investigations used to investigate hypoparathyroidism.

A

Liver function test, 24h urine calcium / creatinine, 24 h magnesium, ABGs, ophthalmological examination, renal imaging, audiology

463
Q

List the differential diagnoses of hypoparathyroidism.

A
  • Hypovitaminosis D
  • Hypomagnesaemia/hypoalbuminaemia
  • Pseudohypoparathyroidism
  • CKD/renal failure
464
Q

What is the first-line management of acute hypoparathyroidism?

A

IV calcium

465
Q

What is the first-line management of persistent hypoparathyroidism?

A

Vit D analogue (calcitriol)

466
Q

How do you monitor a patient with hypoparathyroidism?

A

Serum calcium/albumin and plasma PTH level monitoring every 6 months

467
Q

What are the complications of hypoparathyroidism?

A

Overtreatment with Vit D –> hypercalcaemia, cataract, renal stones

468
Q

What is the prognosis for a patient with hypoparathyroidism?

A

Prognosis dependents on aetiology and severity

469
Q

Define phaeochromocytoma.

A

Rare, usually benign tumour that develops in adrenal gland causing increase in adrenaline production

470
Q

What is the epidemiology of phaechromocytoma?

A
  • Incidence: 0.6/100,000
  • M=W
  • equal incidence across all races
  • usually >40s
471
Q

What is the aetiology of phaeochromocytoma?

A
  • 90% arise in adrenal medullary catecholamine-producing chromaffin cells
  • can be inherited (more noradrenaline) or spontaneous (more adrenaline)
  • can be associated with multiple endocrine neoplasia
472
Q

What are the risk factors for phaeochromocytoma?

A
  • multiple endocrine neoplasias
  • Von hippel-lindau disease
  • succinate dehydrogenase gene mutations
473
Q

What is the pathophysiology of phaeochromocytoma?

A
  1. Catecholamine (adrenaline, noradrenaline) producing tumours of the chromafin cells of the medulla
  2. can be adrenal-origin or extra-adrenal origin as well as benign(90%) or malignant(10%)
474
Q

What are the key presentations of phaeochromocytoma?

A
  1. Presence of risk factors
  2. headache
  3. palpitations
  4. diaphoresis
  5. hypertension
  6. hypertensive retinopathy
  7. pallor
  8. impaired glucose tolerance/DM, EPISODIC
475
Q

What are the signs of phaeochromocytoma?

A
  • tachycardia
  • pallor
  • hypertension
476
Q

What are the symptoms of phaeochromocytoma?

A
  • Headaches
  • palpitations
  • sweating
  • tremors
  • anxiety
  • nausea
  • weight loss
477
Q

Name the first line investigations for phaeochromocytoma and the expected results.

A
  1. 24h urine for metanephrine/normetanephirnes / catecholamines / creatinine (elevated)
  2. abdominal/pelvis CT (localisation)
  3. genetic testing (familial disorders)
  4. Plasma catecholamines (may be elevated)
478
Q

Name the gold standard investigation for phaeochromocytoma and the expected results.

A
  1. Serum free metanephrines/normetanephirnes (elevated)
479
Q

Name any other investigations for phaeochromocytoma.

A
  1. serum calcium (elevated)

2. Serum potassium (may be low)

480
Q

What are the differential diagnoses of phaeochromocytoma?

A
  • Anxiety/panic attack
  • hypertension
  • hyperthyroidism
  • consumption of illicit substance
  • carcinoid syndrome
  • cardiac arrhythmias
  • menopause
  • pre-eclampsia
481
Q

What is the first line management of phaeochromocytoma?

A

Alpha blockers (phenoxybenzamine) + beta blockers (after alpha, tenolol) + surgical excision

482
Q

What are the adjunct treatments for phaeochromocytoma?

A

if malignant tumour then postsurgical chemotherapy / radiotherapy

483
Q

How do yo monitor a patient with phaeochromocytoma?

A

Post-operative 24h urine metanephrine after 2 weeks, monitor BP

484
Q

What are the complications of phaeochromocytoma?

A
  • stroke during surgery due to rapid effect of adrenaline on BP
  • neurological/postoperative complications
485
Q

What si he prognosis of a patient with phaeochromocytoma?

A

Surgery curative method in >85% of cases, 95% 5year survival with benign disease

486
Q

Define carcinoid syndrome.

A

Disease occurring due to release of serotonin and other vasoactive peptides into systemic circulation from carcinoid tumours which are commonly found in GI tract or lungs

487
Q

What is the epidemiology of carcinoid syndrome?

A

M>W, aged >60, incidence: 35 per 100,000,

488
Q

What is the Aetiology of carcinoid syndrome?

A

Caused by Neuroendocrine tumours, Derived from enterochromaffin cells,
seen in 95% of patients with liver metastases,

489
Q

What is the classification of carcinoid tumours?

A

Classified as Foregut, Midgut or Hindgut tumours, carcinoid syndrome occurs in 20-30% of patients with midgut tumours, 1% of foregut and rarely hindgut tumours,

490
Q

What are the risk factors for carcinoid syndrome?

A

Functional (secreting) carcinoid tumour

491
Q

What is the pathophysiology of carcinoid syndrome?

A
  1. GI tumours symptomless unless liver metastases present
  2. tumours tend to secrete bioactive compounds including serotonin and Kallikrein (lead to ↑ bradykinin), which cause carcinoid syndrome.
492
Q

What are the key presentations of carcinoid syndrome?

A
  1. Initially symptomless
  2. diarrhoea
  3. flushing
  4. palpitation
  5. hepatic metastases might cause RUQ pain
  6. bronchoconstriction
  7. Severe: Carcinoid crisis (EMERGENCY)
493
Q

What are the signs of carcinoid syndrome?

A
  1. Palpitation
  2. signs of right heart failure (CCF)
  3. cardiac murmurs
  4. hepatomegaly
494
Q

What are the symptoms of carcinoid syndrome?

A
  1. hepatic metastases might cause RUQ pain
  2. abdominal cramps
  3. bronchoconstriction
495
Q

Name the first line investigations of carcinoid syndrome and expected results.

A
  1. 24h urinary 5-hydroxyindoleacetic acid (elevated)
  2. CXR + pelvis / chest MRI/CT (tumour location)
  3. metabolic panel (elevated creatinine if dehydrated)
496
Q

Name the gold standard investigation of carcinoid syndrome and exected results.

A

Serum chromogranin A/B (CGA): elevated

497
Q

Name any other investigation that can be used to investigate carcinoid syndrome.

A
  1. Bronchoscopy (if lung tumour)
  2. endoscopy
  3. histology
  4. Octreoscan
498
Q

What are the differential diagnoses of carcinoid syndrome?

A
  1. Irritable bowel syndrome
  2. Crohn’s disease
  3. Menopause
  4. Asthma
499
Q

What is the first line management of carcinoid syndrome?

A

Surgical resection (if possible – only cure for carcinoid tumours!) + somatostatin analogue (octreotide)

500
Q

How do you monitor a patient with carcinoid syndrome?

A

Review ever 3 – 4 months including CT scan and CGA test, Octreoscan annually

501
Q

What are the complications of carcinoid syndrome?

A

Carcinoid heart disease, bowel obstruction or intestinal bleeding, carcinoid crisis

502
Q

What is the prognosis for a patient with carcinoid syndrome?

A

Survival rate: 5 – 8 years unless metastases (3 years)

503
Q

Defne prolactinoma.

A

Benign lactotrophs adenoma expressing and secreting prolactin

504
Q

How are prolactinomas classified?

A

classified as Micro (Most common >90%) or Macro (~10%, >10mm in size)

505
Q

What is the epidemiology of prolactinomas?

A

40% of all pituitary adenomas, W>M during child bearing years, then W=M

506
Q

What is the aetiology of prolactinomas?

A

Cause unknown, Some genetic association

507
Q

What are causes of Hyperprolactinaemia excluding prolactinomas?

A

Non-functioning pituitary tumour; compress pituitary stalk -> no inhibition of prolactin release, Antidopaminergic drugs, Head injury -> damage to the pituitary stalk

508
Q

What are the risk factors of prolactinomas?

A
  1. Female gender

2. 20 – 50 years of age

509
Q

What is another name for prolactinoma?

A

anterior pituitary lactotroph tumours

510
Q

What is the pathophysiology of prolactinomas?

A
  1. Increased release of prolactin can cause galactorrhoea by stimulating milk production from mammary gland, as well as inhibit FSH and LH
  2. causes secondary hypogonadism, reduced libido and sexual dysfunction in men
  3. Dopamine has an inhibitory effect on prolactin
  4. Pituitary tumour is located near to the optic chiasm -> visual field disturbances
  5. Very rarely malignant.
511
Q

What are the key presentations of prolactinomas?

A
  • Presence of risk factors
  • Effects of prolactin: amenorrhoea / oligomenorrhoea, infertility, galactorrhoea, loss of libido, erectile dysfunction
  • Local effect of tumour: visual deterioration, headache
512
Q

What are the signs of prolactinomas?

A

Osteoporosis

513
Q

What are the symptoms of prolactinomas?

A

amenorrhoea / oligomenorrhoea, infertility, galactorrhoea, loss of libido, erectile dysfunction, visual deterioration

514
Q

Name the first line investigations for prolactinomas and the expected results.

A
  1. Serum prolactin (elevated)
  2. pituitary MRI (detect small micro adenomas)
  3. computerised visual field examination (visual field defects )
515
Q

Name the gold standard investigation for prolactinomas and the expected result.

A

Serum prolactin (elevated)

516
Q

Name the differential diagnoses of prolactinomas.

A
  1. Non-functioning pituitary macro-adenomas
  2. drug-induced hyperprolactinaemia
  3. primary hypothyroidism
  4. renal insufficiency
  5. pregnancy
  6. polycystic ovarian syndrome
517
Q

What is the first-line management of prolactinomas?

A

Dopamine agonist (cabergoline) or trans-sphenoidal surgery (if intolerant to dopamine agonist)

518
Q

How do you monitor a patient with prolactinoma?

A

Periodic measurement of serum prolactin, regular visual field examination, pituitary MRI annualy

519
Q

What are the complications of prolactinomas?

A
  • Visual field impairment
  • anterior pituitary failure +/- diabetes insipidus
  • hypopituitarism
520
Q

What is the prognosis for a patient with prolactinoma?

A

good prognosis with dopamine agonist treatment

521
Q

What is the classification of pituitary adenomas?

A
  • Clinically functional (eg Cushing’s, Prolactinomas)

- clinically non-functional adenomas

522
Q

How many intra-cranial tumours are non-functional pituitary adenomas?

A

10%

523
Q

What is the epidemiology of non-functional pituitary adenomas?

A
  • no sex / race prevalence
  • Incidence: 28 per 100,000
  • more common in W aged 20 – 45 or M aged 35 – 60
524
Q

What is the aetiology of non-functional pituitary adenomas?

A

Unknown, maybe intrinsic genetic alterations

525
Q

What are the risk factors of non-functional pituitary adenomas?

A
  • Multiple endocrine neoplasisa
  • familial isolated pituitary adenomas
  • carney complex
526
Q

What is the pathophysiology of non-functional pituitary adenomas?

A
  1. Hypermethylation of specific gene locus

2. histopathological subtype knowledge important for clinical course of adenoma

527
Q

What are the signs of non-functional pituitary adenoma?

A

anorexia, gynaecomastia, breast atrophy, visual defect, soft small testicles,

528
Q

What are the symptoms of non-functional pituitary adenoma?

A

headaches, erectile dysfunction, amenorrhoea, infertility, weight gain, fatigue, nausea / vomiting, weakness, diaphoresis, hot flushes, loss of libido,

529
Q

What are the first line investigations of non-functional pituitary adenomas?

A

Different tests to see which specific adenoma eg ACTH, IGF-1, insulin tolerance test

530
Q

What is the gold standard nvestigation of non-functional pituitary adenomas?

A

MRI – location of adenoma

531
Q

Name the differential diagnoses of non-functional pituitary adenomas.

A
  • Prolactinoma
  • Acromegaly
  • Cushing’s syndrome
  • Meningioma
  • Craniopharyngioma
532
Q

What is the management of non-functional pituitary adenomas?

A

Treatment depends on adenoma – could be surgery, hormone replacement, observation etc

533
Q

How do you monitor a patient with non-functional pituitary adenomas?

A

No available evidence based guidance on monitoring!, recommendation of follow up MRI

534
Q

What are the complications of non-functional pituitary adenomas?

A

Diabetes insipidus, Meningitis, hypopituitarism

535
Q

What is the prognosis for a patient with non-functional pituitary adenomas?

A

Generally good prognosis, 10 year progression free survival ~80 – 94%

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