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Phase 2a > Endocrinology 2 > Flashcards

Endocrinology 2 Flashcards

1
Q

Where does ingested glucose go?

A

40% to liver
60% to periphery (mostly muscle)

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2
Q

What is glucagon?

A

A peptide hormone that raises the concentration of glucose and fatty acids in the bloodstream

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3
Q

Which cells secrete glucagon?

A

Alpha cells of the Islets of Langerhans (in pancreas)

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4
Q

Which cells secrete insulin?

A

Beta cells of the Islets of Langerhans (in pancreas)

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5
Q

What is paracrine ‘crosstalk’ between alpha and beta cells?

A

When beta cells secrete insulin, there is tonic inhibition on alpha cells so that they cannot release glucagon

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6
Q

What are examples of counterregulatory hormones?

A

Glucagon, adrenaline, cortisol and growth hormone

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7
Q

What is type 1 diabetes?

A

Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency

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8
Q

Describe the epidemiology of type 1 diabetes

A
  • Usually presents between ages 5-15
  • 10% of diabetes diagnoses
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9
Q

Name the 3 risk factors for type 1 diabetes

A
  1. Family history (HLA DR3-DQ2 or HLA DR4-DQ8)
  2. Northern European
  3. Other autoimmune disease
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10
Q

Describe the pathophysiology of type 1 diabetes

A
  • Autoantibodies attach to beta cells
  • This causes an insulin deficiency and leads to hyperglycaemia
  • Insulin absence results in an increased breakdown of glycogen (hepatic gluconeogenesis)
  • This decreases peripheral glucose causing glycosuria
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11
Q

Name 5 symptoms of type 1 diabetes

A
  1. Polydipsia
  2. Polyuria
  3. Weight loss (BMI<25)
  4. Fatigue
  5. Ketosis
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12
Q

What is type 2 diabetes?

A

Patient gradually becomes insulin resistant or pancreatic beta cells fail to secrete enough insulin. Progresses from impaired glucose tolerance

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13
Q

Name 6 causes of type 2 diabetes

A
  1. Reduced insulin secretion
  2. Increased insulin resistance
  3. Gestational diabetes
  4. Steroids
  5. Cushing’s
  6. Chronic pancreatitis
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14
Q

Name the 4 risk factors for type 2 diabetes

A
  1. Lifestyle (e.g. obesity, lack of exercise, excess of alcohol, diet)
  2. Asian men
  3. Age 40 and above
  4. Hypertension
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15
Q

Name 6 symptoms of type 2 diabetes

A
  1. Polydipsia
  2. Polyuria
  3. Glycosuria
  4. Central obesity
  5. Blurred vision
  6. Fatigue
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16
Q

What are the normal and diabetes levels of fasting plasma glucose?

A

Normal = <6mmol/L
Diabetes = >7mmol/L
* pre diabetes = between

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17
Q

What are the normal and diabetes levels of random plasma glucose?

A

Normal = <11mmol/L
Diabetes = >11mmol/L

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18
Q

What are the normal and diabetes levels of HbA1c?

A

Normal = <42mmol/L
Diabetes = >48mmol/L
* pre diabetes = between

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19
Q

What does HbA1c measure?

A

Measures the amount of glucose latched onto circulating RBCs. As RBCs live for about 3 months, it tells you about glucose levels throughout the last 3 months

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20
Q

What is the 1st line management for type 2 diabetes?

A

Lifestyle changes:
- Dietary advice
- Weight control
- Smoking cessation
- Decreased alcohol intake
- Encourage exercise
- Regular blood glucose and HbA1c monitoring

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21
Q

What is the 2nd line management for type 2 diabetes?

A

Medications:
- Biguanides
- Dual therapy (biguanides + sulfonylureas)
- Triple therapy
- Insulin

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22
Q

What are biguanides? Give an example and side effects

A
  • E.g. metformin
  • Cause decreased gluconeogenesis in the liver
  • Increase cell sensitivity to insulin
  • Side effects include GI disturbances
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23
Q

What are sulfonylureas? Give an example and side effects

A
  • E.g. gliclazide
  • Promote insulin secretion by binding to beta cells
  • Side effects include hypoglycaemia and weight gain
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24
Q

What is diabetic ketoacidosis (DKA)?

A

Complete lack of insulin resulting in high ketone production (serious complication of type 1 diabetes)

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25
Q

Describe the pathophysiology of diabetic ketoacidosis

A
  • Absence of insulin causes unrestrained gluconeogenesis –> hyperglycaemia
  • Hyperglycaemia causes osmotic diuresis and dehydration
  • Increase in circulating free fatty acids which are oxidised to Acetyl CoA which form ketone bodies (which are acidic –> acidosis)
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26
Q

Name 5 signs of diabetic ketoacidosis

A
  1. Kussmaul’s breathing (deep and laboured breathing)
  2. Pear drop breath
  3. Hypotension
  4. Tachycardia
  5. Reduced tissue turgor
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27
Q

Name 5 symptoms of diabetic ketoacidosis

A
  1. Extreme diabetes symptoms
  2. Nausea and vomiting
  3. Confusion and reduced mental state
  4. Lethargy
  5. Abdominal pain
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28
Q

What are 6 investigations for patients with diabetic ketoacidosis?

A
  1. Random plasma glucose >11mmol/L
  2. Plasma ketones >3mmol/L
  3. Blood pH <7.35 or bicarb <15mmol/L
  4. Urine dipstick = glucosuria and ketonuria
  5. Serum U+E = raised urea and creatine
  6. Serum U=E = decreased total K+ and increased serum K+
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29
Q

What is the treatment for diabetic ketoacidosis?

A
  • ABC management
  • Replace fluid (0.9% saline IV)
  • IV insulin
  • Restore electrolytes
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30
Q

What is hyperosmolar hyperglycaemia state (HHS)?

A

Marked hyperglycaemia, hyperosmolality and mild/no ketosis (serious complication of type 2 diabetes)

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31
Q

Describe the pathophysiology of hyperosmolar hyperglycaemia state

A
  • Low insulin causes increased gluconeogenesis –> hyperglycaemia (however there are sufficient enough levels of insulin to inhibit ketogenesis)
  • Hyperglycaemia causes osmotic diuresis and dehydration
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32
Q

Name 5 symptoms of hyperosmolar hyperglycaemic state

A
  1. Extreme diabetes symptoms
  2. Confusion and reduced mental state
  3. Lethargy
  4. Hyperosmolality
  5. No ketones in blood or urine
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33
Q

What are the investigations for patients with hyperosmolar hyperglycaemic state?

A
  1. Random plasma glucose >11mmol/L
  2. Urine dipstick = glycosuria
  3. High plasma osmolality
  4. U+E = decreased total K+ and increased serum K+
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34
Q

What is the treatment for hyperosmolar hyperglycaemia state?

A
  • Replace fluid (0.9% saline IV)
  • Insulin
  • Restore electrolytes
  • Low molecular weight heparin (to decrease risk of thromboembolism)
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35
Q

What is hypoglycaemia?

A

Low glucose levels

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36
Q

How is hypoglycaemia classified?

A
  • Level 1 = plasma glucose <3.9mmol/L and no symptoms
  • Level 2 = plasma glucose <3mmol/L
  • Non-severe = patient has symptoms but can self treat and cognitive function is mildly impaired
  • Severe = patient has impaired cognitive function sufficient to require external help tor recover
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37
Q

Name 5 autonomic symptoms of hypoglycaemia

A
  1. Trembling
  2. Palpitations
  3. Sweating
  4. Anxiety
  5. Hunger
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38
Q

Name 6 neuroglycopenic symptoms of hypoglycaemia

A
  1. Difficulty concentrating
  2. Confusion
  3. Weakness
  4. Drowsiness/dizziness
  5. Vision changes
  6. Difficulty speaking
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39
Q

Name 2 non specific symptoms of hypoglycaemia

A
  1. Nausea
  2. Headache
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40
Q

What is the treatment for hypoglycaemia?

A
  • Treat with 15g fast-acting carbohydrate
  • Retest in 15 mins to ensure blood glucose >4mmol/L
  • Eat long-acting carbohydrate
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41
Q

What is hyperthyroidism and what are the two types?

A

Excess thyroid hormone
Primary = abnormal increased thyroid function
Secondary = abnormal increased TSH production

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42
Q

Name 5 primary causes of hyperthyroidism

A
  1. Grave’s disease2. Nodules (multinodular goitre, toxic adenomas)3. Iodine excess4. Amiodarone5. Metastatic follicular thyroid cancer
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43
Q

Name a secondary cause of hyperthyroidism

A

TSH pituitary tumour

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44
Q

What is Grave’s disease?

A

An autoimmune condition in which there is increased production of T3 and T4 due to antibodies binding to TSH receptors

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45
Q

Describe how Grave’s disease works

A
  • IgG autoantibodies (anti-TSHR-Ab) are produced which bind to and activate thyrotropin receptors
  • This results in the increased production of thyroid hormones (T3 and T4)
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46
Q

What does Grave’s disease cause?

A
  • Symptoms of hyperthyroidism
  • Thyroid eye disease = eyelid retraction, periorbital swelling, proptosis/exophthalmos
  • Pretibial myxoedema
  • Thyroid acropachy
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47
Q

What is pretibial myxoedema?

A

Accumulation of excess glycosaminoglycans in the dermis and subcutis of the skin

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48
Q

What does thyroid acropachy cause?

A
  • Nail clubbing
  • Painful swelling of digits/toes
  • Periosteal reaction (bone growth)
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49
Q

What are the 5 risk factors for hyperthyroidism?

A
  1. Being female (F:M = 9:1)2. Smoking3. Stress4. Genetic (HLA-DR3)5. Other autoimmune diseases
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50
Q

Describe the pathophysiology of hyperthyroidism

A
  • Increased T3 causes an increase in metabolic rate
  • This activates the sympathetic nervous system and so increases cardiac output, bone resorption etc.
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51
Q

What are the 3 signs of hyperthyroidism?

A
  1. Periorbital swelling2. Goitre3. Tachycardia
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52
Q

What are 8 symptoms of hyperthyroidism?

A
  1. Hot and sweaty
  2. Diarrhoea
  3. Weight loss
  4. Anxiety/restlessness
  5. Hyperphagia (increased desire to eat)
  6. Oligomenorrhoea (irregular menstrual bleeding)
  7. Palpitations
  8. Tremor
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53
Q

What are the investigations for patients with hyperthyroidism?

A
  • Thyroid function tests (TFTs) = high T3/T4 but low TSH (primary), high T3/T4 and high TSH (secondary)
  • Thyroid autoantibodies (anti-TSHR)
  • US and CT head
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54
Q

What is the treatment for hyperthyroidism?

A
  1. Drug management2. Radioiodine3. Thyroidectomy
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55
Q

Describe drug management for hyperthyroidism

A

1st line = carbimazole (blocks synthesis of T4)2nd line = propylthiouracil (prevents conversion of T4 into T3)Beta blockers = provide rapid symptom relief

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56
Q

What is hypothyroidism and what are the two types?

A

Lack of thyroid hormone
Primary = abnormal decreased thyroid function
Secondary = abnormal decreased TSH production

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57
Q

Name 5 primary causes of hypothyroidism

A
  1. Hashimoto’s2. Primary atrophic hypothyroidism3. Iodine deficiency4. Drugs5. Post thyroidectomy/radioiodine
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58
Q

Name a secondary cause of hypothyroidism

A

Hypopituitarism

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59
Q

What is Hashimoto’s?

A

An autoimmune condition in which antibodies attack the thyroid causing inflammation and dysfunction, lowering T3/T4 levels

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60
Q

What are the 3 risk factors for hypothyroidism?

A
  1. Being female (F:M = 6:1)2. Post partum3. Other autoimmune diseases
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61
Q

Describe the pathophysiology of hypothyroidism

A
  • Decreased T3 levels mean that there is an insufficient amount for normal body functions
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62
Q

What are the 3 signs of hypothyroidism?

A
  1. Delayed reflexes2. Goitre3. Bradycardia
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63
Q

What are the 8 symptoms of hypothyroidism?

A
  1. Cold intolerance2. Constipation3. Weight gain4. Fatigue and lethargy5. Loss of appetite6. Menorrhagia (heavy menstrual bleeding)7. Brain fog8. Depression
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64
Q

What are the investigations for patients with hypothyroidism?

A
  • Thyroid function tests (TFTs) = low T3/T4 but high TSH (primary), low T3/T4 and low TSH (secondary)- Autoantibodies (anti-TPO)
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65
Q

What is the treatment for hypothyroidism?

A

Levothyroxine (T4)

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66
Q

What are 4 other causes of thyroid disorders?

A
  1. De Quervain’s Thyroiditis2. Post-partum thyroiditis3. Amiodarone4. Lithium toxicity
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67
Q

What is De Quervain’s Thyroiditis?

A
  • Mild hyperthyroidism following a viral infection of the thyroid- Lasts for a few weeks- Pain and tenderness over thyroid gland- Flu-like symptoms- Beta blockers given to relief symptoms, no other treatment given
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68
Q

What is post-partum thyroiditis?

A
  • Mild hyperthyroidism which develops in the first year after childbrith- Lasts for a few weeks- Often very few symptoms- Beta blockers given to relief symptoms, no other treatment given
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69
Q

What is amiodarone and how does it affect the thyroid?

A
  • An iodine-containing drug used for the treatment of certain irregularities of heart rhythm- Can cause hyperthyroidism or hypothyroidism- Blood thyroid levels should be checked before and throughout taking the drug
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70
Q

What is lithium toxicity and how does it affect the thyroid?

A
  • Lithium carbonate is used for depression and mania- It can cause goitres and hypothyroidism- Thyroxine is given alongside treatment
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71
Q

What are the two main types of thyroid cancer?

A
  1. Papillary cancer - tumour contains papillae or fronds2. Follicular cancer - distinctly abnormal appearance with some structures that resemble the normal follicles of the thyroid
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72
Q

How is thyroid cancer diagnosed?

A

Fine needle aspiration (type of biopsy) or following surgery

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73
Q

How is papillary cancer treated?

A

Total thyroidectomy as there is a tendency for the cancer to occur in various places throughout the gland

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74
Q

How is follicular cancer treated?

A

Hemithyroidectomy as it tends to only occur in one part of the thyroid

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75
Q

What additional treatment is given following thyroidectomys?

A
  • Radioactive iodine given to remove any remaining cancer cells- Thyroxine (T4) given to reduce TSH levels in the blood
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76
Q

Where is the pituitary gland?

A

Embedded in the sella turcica just below the optic chiasma

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77
Q

Describe the blood supply of the anterior pituitary gland (adenohypophysis)

A
  • No arterial blood supply- Receives blood through a portal venous system from the hypothalamus
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78
Q

What 4 things does the pituitary gland control?

A
  • Growth (GH)- Thyroid (TSH)- Puberty/fertility (LH, FSH)- Cortisol
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79
Q

Describe the thyroid axis

A
  • Hypothalamus releases TRH (thyrotropin releasing hormone)- This stimulates the release of TSH (thyroid stimulating hormone) from the anterior pituitary- This stimulates the thyroid follicular cells to release T3 ad T4- T3 and T4 feedback to the hypothalamus and pituitary (negative feedback)
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80
Q

If the thyroid gland is removed, will TSH levels increase or decrease?

A

Increase

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81
Q

If the thyroid is overactive (thyrotoxicosis), will TSH levels increase or decrease?

A

Decrease

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82
Q

Describe the gonadal axis

A
  • The hypothalamus releases GnRH (gonadotrophin-releasing hormone)- This triggers the release of LH and FSH from the anterior pituitary- LH stimulates the release of testosterone from the testis (men) and oestrogen/estradiol (women) from the ovaries to trigger ovulation- FSH triggers the production of sperm (men) and eggs (women)- Oestrogen and testosterone feedback at the pituitary and hypothalamus (negative feedback)
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83
Q

Describe what happens to LH, FSH and oestrogen levels at menopause

A

Ovaries fail and stop secreting oestrogen which causes LH and FSH levels to increase

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84
Q

Describe what happens to gonadotropin levels if people are taking testosterone/anabolic steroids

A

Gonadotropin levels will decrease

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85
Q

Describe the hypothalamus-pituitary-adrenal (HPA) axis

A
  • Hypothalamus produced CRH (corticotrophin releasing hormone)- This stimulates the anterior pituitary to release ACTH (adrenocorticotrophic hormone)- This stimulates the release of cortisol from the adrenal glands- Cortisol feeds back to the hypothalamus and pituitary (negative feedback)
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86
Q

Describe what happens to the adrenal glands if pateints are taking steroids?

A

ACTH production is switched off so the release of cortisol is decreased and the adrenal glands are suppressed

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87
Q

Describe the growth hormone (GH)/insulin-like growth factors (IGF-1) axis

A
  • The hypothalamus releases GHRH (growth hormone releasing hormone) and SMS (somatostatin)- These stimulate the anterior pituitary to release GH (growth hormone)- This stimulates the release of ILGF-1 (insulin-like growth factor-1) from the liver- IGF-1 feeds back
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88
Q

Describe the release of prolactin

A
  • Dopamine is secreted from the hypothalamus- This inhibits prolactin release (inhibitory hormone)- Prolactin is released from the anterior pituitary gland when dopamine levels are low
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89
Q

Describe what happens to prolactin levels when a patient has a damaged hypothalamus or is taking anti-dopaminergic drugs

A

Prolactin levels will increase as there is a lack of dopamine to inhibit it

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90
Q

Name 5 diseases of the pituitary

A
  1. Benign pituitary adenoma2. Craniopharyngioma3. Trauma4. Sheehan syndrome –> apoplexy5. Sarcoidosis/TB
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91
Q

Describe the effect of benign pituitary adenomas on the pituitary

A

Can grow bigger and cause damage e.g. by pressing on optic nerves

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92
Q

Describe the effect of craniopharygiomas on the pituitary

A

Benign tumours that are epithelial in origin. Despite being benign, they can grow large and have cysts

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93
Q

Describe the effect of trauma on the pituitary

A

Shaking/rupture of the pituitary stalk from trauma can cause hypopituitarism

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94
Q

Describe the effect of Sheehan syndrome on the pituitary (apoplexy)

A

The pituitary gland may grow (particularly in pregnancy). Extreme blood loss (e.g. during childbirth/post partum bleeds) can cause injury/infarction of the pituitary causing apoplexy

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95
Q

What is apoplexy?

A

Unconsciousness/incapacity resulting from cerebral haemorrhage or stroke

96
Q

Describe the effect of sarcoidosis/TB on the pituitary

A

Inflammatory conditions can cause inflammation of the hypothalamus and pituitary which can cause hypopituitarism

97
Q

What 3 questions should be asked regarding pituitary tumours?

A
  1. Is there pressure on local structures?2. Is there pressure on the normal pituitary?3. Is it a functioning tumour?
98
Q

Why should you ask if there is pressure on local structures regarding pituitary tumours?

A
  • Pressure on optic chiasm can cause bitemporal hemianopia (visual field defects)
  • Pressure on the 4th ventricle can cause hydrocephalus/stretching of dura which can lead to headaches
  • Lateral extension of tumour can cause other cranial nerve palsies
  • Downward extension of tumour can cause CSF to leak through the sella turcica into the sphenoid sinus and out through the nose
99
Q

Why should you ask if there is pressure on the normal pituitary regarding pituitary tumours?

A
  • Can cause hypopituitarism (may need to replace hormones)
  • Commonly presents in males as pale, hairless and central obesity (fat, pale, hairless male)
100
Q

Why should you ask if it is a functioning tumour regarding pituitary tumours?

A
  • Prolactinoma- Acromegaly/gigantism- Cushing’s disease
101
Q

What is a prolactinoma?

A

A non cancerous tumour of the pituitary gland causing it to produce too much prolactin

102
Q

What does prolactin do?

A
  • Initiates lactation and breast development- Controls osmolality and carbs/fat metabolism
103
Q

What is a sign of a prolactinoma?

A

Low testosterone

104
Q

What are 4 symptoms of a prolactinoma?

A
  1. Amenorrhoea (absence of menstruation)2. Galactorrhoea (nipple discharge)3. Gynaecomastia (swelling of breasts in males)4. Low libido
105
Q

What is the treatment for patients with prolactinomas?

A
  • Surgery- Bromocriptine/cabergoline (dopamine agonists)
106
Q

What is acromegaly?

A

Rapid growth of body tissues and bones due to excess production of growth hormone by pituitary tumours (gigantism in children)

107
Q

What does growth hormone do?

A
  • Stimulates bone and muscle growth- Increases protein synthesis and fat/glycogen breakdown- ILGF-1 also drives growth
108
Q

What are the 3 signs of acromegaly?

A
  1. Hypertension2. Insulin resistance3. Bitemporal hemianopia
109
Q

What are the 5 symptoms of acromegaly?

A
  1. Large hands2. Box jaw3. Thick skin4. Arthritis5. Sight problems
110
Q

How is acromegaly diagnosed?

A
  • ILGF-1 blood test- Ask about changes in ring/shoe size over time
111
Q

How is acromegaly treated?

A
  • Tumour surgery- Dopamine agonist (cabergoline)- Somatostatin analogue (octreotide)- GH receptor antagonist (pegvisomant)
112
Q

What is Cushing’s syndrome?

A

Chronic excess of cortisol hormone released by the adrenal glands due to an ACTH secreting pituitary adenoma (leads to bilateral hyperplasia)

113
Q

What can cause excess cortisol levels (besides Cushing’s syndrome)?

A
  • ACTH dependent causes (ectopic ACTH production or ACTH treatment)- ACTH independent causes (adrenal adenomas/iatrogenic)
114
Q

How does Cushing’s syndrome present clinically?

A
  1. Central obesity2. Plethoric complexion (red)3. Moon face4. Mood change5. Proximal muscle weakness6. Purple abdominal striae7. Gastric ulcers8. Osteoporosis9. Hirsutism (excess hair growth)10. Buffalo hump
115
Q

How is Cushing’s syndrome diagnosed?

A
  • Drug history (can be caused by oral steroids)- Screening = random plasma cortisol- High random plasma cortisol –> overnight dexamethasone suspension test- ^ positive = test plasma ACTH
116
Q

What is the treatment for Cushing’s syndrome?

A
  • If caused by pituitary adenoma = trans sphenoidal surgical resection- If caused by adrenal adenoma = adrenalectomy
117
Q

What is a carcinoid tumour?

A

Rare tumour of the neuroendocrine system that secretes serotonin

118
Q

What is a carcinoid crisis?

A
  • When a carcinoid tumour outgrows its blood supply or is handled too much during surgery, mediators flood out- Results in life threatening vasodilation, hypotension, tachycardia, bronchoconstriction and hyperglycaemia
119
Q

How is a carcinoid crisis treated?

A

High dose octreotide and supportive measures/careful management of fluid balance

120
Q

What is carcinoid syndrome?

A

Groups of symptoms due to the release of serotonin and their vasoactive peptides into the systemic circulation from a carcinoid tumour

121
Q

What are the characteristics of carcinoid syndrome?

A
  • Tend to express somatostatin receptors- Affects the lung, stomach and bowel- Metastasises to the liver
122
Q

What are the 4 symptoms of carcinoid syndrome?

A
  1. Palpitations2. Abdominal cramps3. Diarrhoea4. Flushing
123
Q

What are the 2 signs of carcinoid syndrome?

A
  1. Signs of right heart failure2. Bronchospasm
124
Q

What are the investigations for patients with carcinoid syndrome?

A
  • 24 hours 5 hydroxyindoleacetic acid increase (product of serotonin breakdown)- Metabolic panel and LFTs- Liver ultrasound to confirm metastases
125
Q

How is carcinoid syndrome treated?

A
  • Local = surgical resection and peri-operative octreotide infusion- Metastases = above and additional radiofrequency and ablation
126
Q

What is octreotide?

A
  • A somatostain analogue- Blocks the release of tumour mediators and counters peripheral effects
127
Q

What is Conn’s syndrome?

A

Autonomous aldosterone production that exceeds the body’s requirements and is independent of the renin-angiotensin II system (primary hyperaldosteronism)

128
Q

What are the 2 causes of Conn’s syndrome?

A
  1. Aldosterone-producing unilateral adenoma in adrenal gland (one gland)2. Bilateral adrenal hyperplasia (both glands)
129
Q

Describe the consequences of excess aldosterone

A
  • Causes increased K+ excretion and increased Na/water retention- = hypokalaemia –> muscle dysfunction –> heart problems
  • Low renin release
130
Q

What are the 2 signs of Conn’s syndrome?

A
  1. Hypertension (resistant)2. Hypokalemia
131
Q

What are the 6 symptoms of Conn’s syndrome?

A
  1. Polyuria/polydipsia2. Nocturia3. Mood disturbance4. Difficulty concentrating5. Muscle weakness6. Parasthesia
132
Q

What are the investigations for patients with Conn’s syndrome?

A
  • Aldosterone:renin ratio blood test = increased- Plasma potassium = reduced- U+E
133
Q

What are the aims of treatment for Conn’s syndrome?

A
  • Lower blood pressure- Decrease aldosterone levels- Resolve electrolyte imbalance
134
Q

What are the treatments for Conn’s syndrome?

A
  • If single benign adrenal tumour = laparoscopic unilateral adrenalectomy- If bilateral adrenal hyperplasia = spironolactone (aldosterone antagonist)
135
Q

What is Addison’s disease?

A
  • Primary adrenal insufficiency- Disorder that affects the adrenal glands, causing decreased production of adrenocortical hormones (cortisol/aldosterone)
136
Q

What are the 3 causes of Addison’s disease?

A
  • Autoimmune destruction (21-hydroxylase antibodies)- TB- Adrenal metastases
137
Q

Describe the pathophysiology of Addison’s disease

A
  • Destruction of adrenal cortex- Decreased production of glucocorticoid (cortisol) and mineralocorticoid (aldosterone)
138
Q

What are the 3 risk factors for Addison’s disease?

A
  1. Being female2. Adrenocortical antibodies3. Other autoimmune diseases
139
Q

What are the 3 signs of Addison’s disease?

A
  1. Hyperpigmentation2. Postural hypotension3. Hypoglycaemia
140
Q

What are the 3 symptoms of Addison’s disease?

A
  1. Fatigue2. Weakness3. Weight loss
141
Q

What are the investigations for patients with Addison’s disease?

A
  • Serum electrolytes = decreased Na+ and increased K+
  • U+E = hyponatraemia, hyperkalaemia and hypoglycaemia
  • Short SynACTHen test (ACTH stimulation test) = low cortisol and high ACTH
  • FBC = anaemia and eosinophilia
  • Reduced morning serum cortisol
  • Adrenal CT/MRI
  • 21-hydroxylase adrenal autoantibodies
142
Q

What is the management for Addison’s disease?

A
  • Give glucocorticoid (cortisol - hydrocortisone) and mineralocorticoid (aldosterone - fludrocortisone)- Treat underlying cause
143
Q

What is secondary adrenal insufficiency?

A
  • Decreased ACTH levels which leads to adrenal failure- Occurs in patients with pituitary or hypothalamic involvement
144
Q

What is the most common cause of secondary adrenal insufficiency?

A

Iatrogenic due to long term steroid therapy (can cause suppression of the pituitary adrenal axis). Only becomes apparent upon withdrawal of steroids

145
Q

Describe the pathophysiology of secondary adrenal insufficiency

A
  • Pituitary gland does not produce enough ACTH (adrenocorticotropic hormone)- ACTH therefore cannot act on the adrenal cortex to release cortisol, aldosterone and androgens
146
Q

What is SIADH?

A
  • Syndrome of inappropriate ADH- Inappropriately large amounts of ADH (antidiuretic hormone) secretion causing water to be reabsorbed in the collecting duct
147
Q

Name 6 causes of SIADH

A
  1. Lung Disease (Small cell lung cancer)2. Infection3. Abscess or cancer4. Drugs 5. Head/brain injury6. Hypothyroidism
148
Q

What are the 4 signs of SIADH?

A
  1. Severe hyponatraemia2. Raised jugular venous pressure (JVP)3. Oedema4. Ascites (fluid in abdomen)
149
Q

What are the 5 symptoms of SIADH?

A
  1. Headache2. Nausea/vomiting3. Fatigue/lethargy4. Muscle cramps/weakness5. Confusion
150
Q

What are the investigations for patients with SIADH?

A
  • Diagnosis of exclusion- U+E = hyponatraemia (low Na+, normal K+ - need to exclude causes of hyponatraemia)- High urine Na+- High urine osmolality
151
Q

How is SIADH treated?

A
  • Treat underlying cause- Stop causative medicine- Fluid restriction - Tolvaptan (ADH receptor blocker to increase osmolarity)
152
Q

What is diabetes insipidus?

A

The passage of large volumes (>3L/day) of dilute urine due to impaired water resorption by the kidney due to lack of ADH

153
Q

What are the 5 cranial causes of diabetes insipidus?

A
  1. Idiopathic2. Congenital3. Tumour4. Trauma5. Infection
154
Q

What are the 4 nephrogenic causes of diabetes insipidus?

A
  1. Inherited2. Metabolism (low K+, high Ca2+)3. Drugs (lithium)4. Chronic renal disease
155
Q

Describe the pathophysiology of diabetes insipidus (cranial)

A
  • Reduced ADH secretion from the posterior pituitary so large volumes of dilute urine
  • Impaired water retention from the kidneys
156
Q

Describe the pathophysiology of diabetes insipidus (nephrogenic)

A
  • Impaired response of kidneys to ADH so large volumes of dilute urine
  • Impaired water retention from the kidneys
157
Q

Diabetes insipidus is an important cause of…?

A

Hyponatraemia

158
Q

What are the 3 signs of diabetes insipidus?

A
  1. Dry mucosa2. Sunken eyes3. Changes to skin turgidity
159
Q

What are the 2 symptoms of diabetes insipidus?

A
  1. Polyuria2. Polydipsia
160
Q

What are the treatments for patients with diabetes insipidus?

A
  • Treat underlying cause - Rehydration- Cranial = desmopressin (synthetic ADH)- Nephrogenic = bendroflumethiazide (thiazide diuretics)
161
Q

What is hyperparathyroidism?

A

Excessive secretion of parathyroid hormone (PTH)

162
Q

Describe the types of hyperparathyroidism

A

Primary - 1 parathyroid gland produces excess PTH
Secondary - increased secretion of PTH to compensate hypocalcaemia
Tertiary - autonomous secretion of PTH even after correction of calcium deficiency due to chronic kidney disease (CKD)

163
Q

What are the 2 causes of primary hyperparathyroidism?

A
  1. Adenomas (80%)2. Hyperplasia of all glands (20%)
164
Q

What are the 2 causes of secondary hyperparathyroidism?

A
  1. CKD2. Low vitamin D
165
Q

What is the cause of tertiary hyperparathyroidism?

A

Develops from prolonger secondary hyperparathyroidism

166
Q

Describe the pathophysiology of hyperparathyroidism

A

PTH increases Ca2+ levels through increased bone resorption, gut absorption, renal re absorption and activating vitamin D

167
Q

What is the main sign of hyperparathyroidism?

A

Hypercalcaemia

168
Q

What are the 4 symptoms of hyperparathyroidism?

A
  1. Bones (bone pain)2. Stones (renal calculi)3. Moans (psychic moans/depression)4. Groans (abdominal problems - constipation, indigestion, nausea, vomiting)
169
Q

What are the investigations for patients with hyperparathyroidism?

A
  • PTH/bone profile = high PTH, high Ca2+, low phosphates (low serum Ca2+ in secondary)- DEXA scan- X ray = salt and pepper degradation of bone- Ultrasound for stones
170
Q

How is primary hyperparathyroidism treated?

A
  • Surgical removal of adenoma- Give bisphosphonates
171
Q

How is secondary hyperparathyroidism treated?

A
  • Calcium correction- Treat underlying cause
172
Q

How is tertiary hyperparathyroidism treated?

A
  • Cinacalcet (calcium mimetic)- Total/partial parathyroidectomy
173
Q

What is a phaeochromocytoma?

A

Adrenal medullary tumour that secretes catecholamines (VERY RARE)

174
Q

Phaeochromocytomas occur in certain familial syndromes including…?

A
  1. Multiple endocrine neoplasia (MEN syndrome)2. Neurofibromatosis3. Von-Hippel Lindau Disease
175
Q

What are the 5 signs of phaeochromocytoma?

A
  1. Hypertension2. Postural hypotension3. Tremor4. Hypertensive retinopathy5. Pallor
176
Q

What are the 4 symptoms of phaeochromocytoma?

A
  1. Headache2. Profuse sweating3. Palpitations4. Tremor
177
Q

What are the investigations for patients with phaeochromocytoma?

A
  • Plasma metanephrines and normetanephrines- 24 hour urinary total catecholamines- CT for tumour
178
Q

What are the treatments for phaeochromocytoma?

A
  • Without HTN crisis (hypertensive crisis) = alpha blockers (phenoxybenzamine) and removal of tumour- With HTN crisis = antihypertensive agents (phentolamine)
179
Q

What is the action of PTH on the kidneys?

A
  • Increased Ca2+ reabsorption- Decreased phosphate reabsorption- Increased 1 alpha-hydroxylation (activation) of 25-OH vitamin D
180
Q

What is the action of PTH on bone?

A
  • Increased bone remodelling- Bone resorption > bone formation
181
Q

What is the action of PTH on the GI tract?

A
  • No direct effect- Increased Ca2+ absorption due to increased 1,25(OH)2 vitamin D
182
Q

What is the set point of serum ionised calcium?

A

1.1mmol/L

183
Q

Explain the parathyroid response to low serum calcium

A
  • PTH increases- Increased Ca2+ reabsorption at the kidneys- Increased bone resorption- Urinary phosphate excretion increases so serum phosphate decreases- 1,25-(OH)2 vitamin D increases therefore increased Ca2+ absorption in the GI tract
184
Q

What is hypocalcaemia?

A

Low calcium

185
Q

What can cause patients to appear as if they have hypocalcaemia but don’t?

A

Low serum albumin can cause low total serum calcium but not a low ionised calcium

186
Q

What are the 4 symptoms of hypocalcaemia?

A

CATs go numb1. Convulsions2. Arrhythmias3. Tetany4. Numbness/parasthesia in hands, feet, around mouth/lips

187
Q

What are the 2 signs of hypocalcaemia?

A
  1. Chevosteks (contraction of facial muscle when light tapping of facial nerve in front of ear)2. Trousseaus (spasm of hand/wrist when BP cuff inflated)
188
Q

How do you calculate corrected calcium?

A

Total serum calcium + (0.02 x (40 - serum albumin))

189
Q

How does hypocalcaemia affect an ECG?

A

Long QT interval

190
Q

Describe what happens to calcium, phosphate and PTH levels in patients with a vitamin D deficiency

A
  • Calcium levels decrease as there is reduced absorption in the GI tract- PTH levels increase in order to increase calcium levels- Phosphate levels decrease due to increased PTH
191
Q

Describe what happens to calcium, phosphate and PTH levels in patients with hypoparathyroidism

A
  • PTH levels decrease due to underactive parathyroid glands- Calcium levels therefore decrease as there is decreased renal reabsorption and increased excretion- Phosphate levels increase due to increased renal reabsorption
192
Q

What is pseudohypoparathyroidism?

A

Resistance to PTH (parathyroid hormone)

193
Q

Describe what happens to calcium, phosphate and PTH levels in patients with pseudohypoparathyroidism

A
  • Calcium levels decrease as PTH is ineffective- PTH levels increase as there are continuously low calcium levels- Phosphate levels increase
194
Q

What is hypercalcaemia?

A

High calcium

195
Q

What can cause patients to appear as if they have hypercalcaemia but don’t?

A
  • Tourniquet being on for too long- Old/haemolysed sampled being used
196
Q

Name 3 causes of hypercalcaemia

A
  1. Malignancy (bone mets, myeloma, lymphoma)2. Primary hyperparathyroidism3. Thiazides
197
Q

What are the 4 symptoms of hypercalcaemia?

A
  1. Bones (bone pain)2. Stones (renal calculi)3. Moans (psychic moans/depression)4. Groans (abdominal problems - constipation, indigestion, nausea, vomiting)
198
Q

What are the 2 signs of hypercalcaemia?

A
  1. Kidney stones2. Short QT interval
199
Q

Describe what happens to calcium and PTH levels in patients with hypercalcaemia of malignancy

A
  • Calcium levels will be high- Therefore PTH levels will decrease as there is less Ca2+ reabsorption required
200
Q

Describe what happens to calcium, phosphate and PTH levels in patients with primary hyperparathyroidism

A
  • PTH levels increase due to overactive parathyroid glands- Calcium levels therefore increase as there is increased renal reabsorption- Phosphate levels decrease due to decreased renal reabsorption
201
Q

What is hyperkalaemia?

A

Higher than normal potassium levels in the blood (>5.5mmol/L)

202
Q

What are the 3 general causes of hyperkalaemia?

A
  1. Impaired excretion2. Increased intake3. Shift to extracellular
203
Q

What are the 4 impaired excretion causes of hyperkalaemia?

A
  1. AKI (acute kidney injury) or CKD (chronic kidney disease)2. Drug affect (ACE inhibitors, NSAIDs, beta blockers)3. Renal tubular acidosis4. Addison’s disease
204
Q

What are the 2 increased intake causes of hyperkalaemia?

A
  1. IV K+ therapy2. Increased dietary intake
205
Q

What are the 4 shift to extracellular causes of hyperkalaemia?

A
  1. Metabolic acidosis2. Rhabdomyolysis3. Decreased insulin4. Tumour lysis syndrome
206
Q

What are the 3 signs of hyperkalaemia?

A
  1. Arrhythmia
  2. Reduced power and reflexes
  3. Flaccid paralysis
207
Q

What are the 4 symptoms of hyperkalaemia?

A
  1. Fatigue and light headedness2. Weakness3. Chest pain4. Palpitations
208
Q

What are the investigations for patients with hyperkalaemia?

A
  • ECG
  • FBC and U+E
  • Urine osmolality and electrolytes
209
Q

How does hyperkalaemia affect an ECG?

A
  • Small/absent P waves
  • Prolonged PR interval (>200ms)
  • Wide QRS interval (>120ms)
  • Tall tented T waves
210
Q

What is the treatment for hyperkalaemia?

A
  • ABC- Cardiac monitoring- Calcium gluconate (to protect myocardium)- Insulin + Dextrose or nebulised salbutamol (to drive K+ intracellularly)- Treat underlying cause
211
Q

What is hypokalaemia?

A

Lower than normal potassium levels in the blood (<3.5mmol/L)

212
Q

What are the 3 general causes of hypokalaemia?

A
  1. Increased excretion2. Decreased intake3. Shift to intracellular
213
Q

What are the 4 increased excretion causes of hypokalaemia?

A
  1. Renal disease2. Drug effect (thiazide, loop diuretics, laxatives)3. GI loss (diarrhoea and vomiting)4. Conn’s syndrome
214
Q

What are the 2 decreased intake causes of hypokalaemia?

A
  1. Dietary deficiency or fasting2. Liquorice abuse
215
Q

What are the 2 shift to intracellular causes of hypokalaemia?

A
  1. Metabolic alkalosis2. Drug effects (insulin, B2 agonists (SABAs e.g. salbutamol and LABAs)
216
Q

What are the 3 signs of hypokalaemia?

A
  1. Arrhythmia2. Muscle paralysis3. Rhabdomyolysis
217
Q

What are 4 symptoms of hypokalaemia?

A

Asymptomatic
1. Fatigue
2. Generalised weakness
3. Muscle cramps and pain
4. Palpitations

218
Q

What are the investigations for patients with hypokalaemia?

A
  • ECG- FBC and U+E- Urine osmolality and electrolytes
219
Q

How does hypokalaemia affect an ECG?

A
  • Prolonged PR interval
  • ST depression
  • Flat T waves
  • Prominent U waves
220
Q

What is the treatment for hypokalaemia?

A
  • Potassium (PO/IV)- Other electrolytes- Treat underlying cause
221
Q

What is hyponatraemia?

A

Lower than average sodium levels in the blood

222
Q

What is hypernatraemia?

A

Higher than average sodium levels in the blood

223
Q

What is hypoparathyroidism?

A

Insufficient secretion of parathyroid hormone (PTH)

224
Q

What are the 2 causes of primary hypoparathyroidism?

A
  1. Autoimmune2. Congenital
225
Q

Describe the pathophysiology of hypoparathyroidism

A

Lack of PTH decreases Ca2+ levels through decreased bone resorption, gut absorption, renal re absorption and no activation of vitamin D

226
Q

What are the 3 signs of hypoparathyroidism?

A
  1. Hypocalcaemia
  2. Chevosteks (contraction of facial muscle when light tapping of facial nerve in front of ear)
  3. Trousseaus (spasm of hand/wrist when BP cuff inflated)
227
Q

What are the 4 symptoms of hypoparathyroidism?

A

CATs go numb1. Convulsions2. Arrhythmias3. Tetany4. Numbess/parasthesia in hands, feet, around the mouth/lips

228
Q

What are the investigations for patients with hypoparathyroidism?

A
  • PTH/bone profile = low PTH, low Ca2+, normal/high phosphates
229
Q

How is hypoparathyroidism treated?

A
  • IV calcium
  • adcalD3
230
Q

What is a complication of hypoparathyroidism?

A

Cardiac arrest

231
Q

What is adrenal hyperplasia?

A

Defective enzymes mediating the production of adrenal cortex products

232
Q

How does adrenal hyperplasia present in females?

A
  1. Salt loss2. Ambiguous genitalia with common urogenital sinus
233
Q

How does adrenal hyperplasia present in males?

A
  1. Salt loss2. No/very few signs at birth3. Subtle hyperpigmentation 4. Possible penile enlargement
234
Q

Describe the pathophysiology of adrenal hyperplasia

A
  • Defective 21-hydroxylase disrupts cortisol biosynthesis- Causes cortisol deficiency with or without aldosterone deficiency and androgen excess
235
Q

Describe the aetiology of adrenal hyperplasia

A

Genetic 21-hydroxylase deficiency causes about 95% of cases

236
Q

What are the investigations in patients with adrenal hyperplasia?

A

Serum 17-hydroxyprogesterone (precursor to cortisol) levels - high

237
Q

What is the treatment for adrenal hyperplasia?

A
  • Glucocorticoids (cortisol) - hydrocortisone- Mineralocorticoid (aldosterone) - to control electrolytes- Sodium chloride supplement if salt loss

Phase 2a (29 decks)

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