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Phase 2a > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Features of water soluble hormones?

A
  • transported unbound
  • bind to cell surface receptors
  • short half-life
  • cleared fast
  • stored in vesicles before secretion
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2
Q

Example of water-soluble hormones?

A
  • peptides

- monoamines

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3
Q

Features of fat soluble hormones?

A
  • transported bound to protein
  • diffuse into cells
  • long half-life
  • cleared slowly
  • synthesised on demand
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4
Q

Examples of fat-soluble hormones?

A
  • thyroid hormone

- steroids

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5
Q

What is the main example of a peptide hormone?

A

Insulin

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6
Q

How are peptide hormones stored?

A

Stored in secretory granules.

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7
Q

How are peptide hormones released? (Timing)

A

Pulses / bursts

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8
Q

How are peptide hormones cleared?

A

Tissue enzymes / circulating enzymes.

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9
Q

How does insulin cause glucose uptake?

A
  • binds to insulin receptors
  • results in phosphorylation of the receptor
  • this activates tyrosine kinase (secondary messenger)
  • causing phosphorylation of signal cascade molecules
  • results in glucose uptake (via GLUT4 channels)
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10
Q

Examples of amine hormones?

A
  • dopamine
  • adrenaline
  • noradrenaline
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11
Q

What is the adrenaline (amine) synthesis pathway?

A

Phenylalanine > L-tyrosine > L-dopa > dopamine > noradrenaline > adrenaline

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12
Q

Which enzyme breaks down noradrenaline / adrenaline?

A

COMT (Catechol-O-methyl transferase)

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13
Q

What are the breakdown products of noradrenaline/ adrenaline?

A

Noradrenaline > normetanephrine

Adrenaline > metanephrine

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14
Q

What does binding of nor(adrenaline) to alpha receptors cause?

A
  • vasoconstriction
  • bowel muscle contraction
  • sweating
  • anxiety
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15
Q

What does binding of nor(adrenaline) to beta receptors cause?

A
  • vasodilation
  • increased HR
  • increased force of contractility
  • relaxation of bronchial smooth muscles
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16
Q

What are iodothyronines (T3/T4) bound to?

A

Thyroid-binding globulin (TBG)

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17
Q

Which is more active, T3 or T4?

A

T3

T4 is a reservoir for additional T3.

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18
Q

Which hormone is produced more, T3 or T4?

A

T4

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19
Q

How are T3/T4 synthesised?

A
  • iodine binds to tyrosine on thyroglobulin
  • this forms iodothyrosines (MIT / DIT)
  • conjugation of MIT / DIT forms T3 / T4
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20
Q

How are T3 / T4 stored?

A

Stored in colloid of thyroid follicular cells (bound to thyroglobulin).

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21
Q

Thyroglobulin vs TBG?

A

Thyroglobulin binds T3/T4 in colloid of thyroid follicular cells.
TBG binds T3/T4 in the bloodstream.

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22
Q

What does TSH stimulate?

A

Movement of colloid into secretory cell, where T4 and T3 are cleaved from thyroglobulin.

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23
Q

Where does breakdown of T4 > T3 occur?

A

Outside the thyroid gland.

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24
Q

How does vitamin D act on a cell?

A
  • enters cell directly (lipid soluble)

- binds to nucleus to stimulate mRNA production

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25
Q

How is vitamin D transported?

A

Vitamin D binding protein

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26
Q

Adrenal cortex vs adrenal medulla?

A

Adrenal cortex - GFR makes good sex.

Adrenal medulla - fight/flight (catecholamines, adrenaline)

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27
Q

How does oestrogen act on a cell?

A

Enters cell and acts directly on the nucleus.

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28
Q

How do cortisol, aldosterone, progesterone & testosterone act on a cell?

A
  • enters cell and binds to cytoplasmic receptor
  • receptor-hormone complex enters nucleus
  • complex binds to glucocorticoid response element (GRE)
  • binding initiates transcription
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29
Q

Which hormone receptors are located on the cell surface membrane?

A

Insulin

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30
Q

Which hormone receptors are located in the cytoplasm?

A

Steroids:

  • glucocorticoids (cortisol)
  • mineralocorticoids (aldosterone)
  • androgens (testosterone)
  • progesterone
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31
Q

Which hormone receptors are nuclear?

A
  • thyroid hormones
  • oestrogen
  • vitamin D
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32
Q

Which hormones follow circadian rhythm?

A
  • ACTH
  • prolactin
  • GH
  • TSH
  • cortisol
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33
Q

Which hormone inhibits prolactin?

A

Dopamine

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34
Q

Example of hormone receptor induction?

A

Induction of LH receptors by FSH.

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35
Q

What type of hormone are LH and FSH?

A

Peptide hormones.

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36
Q

Example of hormone synergism?

A

Glucagon + adrenaline.

Released when hypoglycaemic.

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37
Q

How are the hypothalamus and pituitary connected?

A

By the infundibulum (pituitary stalk).

Contains axons from hypothalamic neurones and small blood vessels.

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38
Q

Examples of hypophysiotropic hormones?

A
  • CRH
  • GHRH
  • TRH
  • GnRH
  • dopamine
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39
Q

How does hypothalamus-anterior pituitary regulation work?

A
  • hypothalamus is stimulated to release hypophysiotropic hormones by other areas of the CNS
  • hormones reach the anterior pituitary via the hypothalamo-hypophyseal portal vessels
  • hormones stimulate the release of hormones from the anterior pituitary
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40
Q

What is the blood supply to the anterior pituitary gland?

A
  • no arterial supply

- portal venous circulation (hypothalamo-hypophyseal vessels)

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41
Q

What are the 6 hormones secreted by the pituitary?

A
  • FSH
  • LH
  • ACTH
  • TSH
  • prolactin
  • GH
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42
Q

Name of cells where FSH is produced?

A

Gonadotrophs

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43
Q

Name of cells where LH is produced?

A

Gonadotrophs

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44
Q

Name of cell where ACTH is produced?

A

Corticotrophs

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45
Q

Name of cell where TSH is produced?

A

Thyrotrophs

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46
Q

Name of cell where prolactin is produced?

A

Lactotrophs

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47
Q

Name of cell where GH is produced?

A

Somatotrophs

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48
Q

What is the function of FSH?

A
  • stimulates germ cell development (ovum / sperm)

- stimulates oestrogen release (in females)

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49
Q

What does the release of oestrogen stimulate in the menstrual cycle?

A

Release of LH.

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50
Q

What is the function of LH?

A
  • in females: stimulates the release of the egg, which stimulates progesterone release and causes thickening of the uterine wall
  • in males: acts on leydig cells, stimulating testosterone release
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51
Q

What is the function of GH?

A
  • stimulates gluconeogenesis and inhibits insulin (causing increased glucose)
  • breaks down fat in adipose tissue
  • acts on liver to increase protein synthesis
  • stimulates IGF-1 which acts to increase cartilage proliferation
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52
Q

What is the function of ACTH?

A
  • stimulates adrenal cortex to secrete cortisol (from zona fasiculata)
  • stimulates androgen release (from zona reticularis)
  • stimulates adrenaline release (from the adrenal medulla)
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53
Q

What is the function of cortisol?

A
  • regulating & breaking down proteins, fats and carbohydrates
  • anti-inflammatory effect (resulting in a lowered immune response)
  • helps the body overcome stress (avoiding adrenal crisis)
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54
Q

What is the function of TSH?

A
  • stimulates the release of thyroid hormone
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55
Q

What is the function of thyroid hormone?

A
  • controls rate of metabolic reactions
  • accelerates food metabolism
  • increases protein synthesis
  • stimulates carbohydrate metabolism
  • enhances fat metabolism
  • increases ventilation rate
  • increases CO and HR
  • brain development (foetal & post-natal)
  • accelerates growth rate
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56
Q

What are the half lives of T3 and T4?

A

T3 - 1 day

T4 - 5-7 days

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57
Q

What is the function of prolactin?

A
  • stimulates breasts to produce milk

- helps breast development

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58
Q

How does negative feedback work with prolactin?

A

Short-loop mechanism.

Prolactin acts on the hypothalamus to stimulate dopamine. Dopamine inhibits the secretion of prolactin.

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59
Q

What tissue type is the posterior pituitary?

A
  • many glial-type cells present

- originates from neuronal tissue (extension of the hypothalamus)

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60
Q

What are glial cells?

A

Non-neuronal cells in the CNS that provide physical and metabolic support to neurons. (Like a Schwann cell but for the CNS).

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61
Q

Does the posterior pituitary synthesise hormones?

A

No, the hormones are synthesised in the hypothalamus and stored in the posterior pituitary.

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62
Q

Where is vasopressin synthesised?

A

Supraoptic nucleus.

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63
Q

Where is oxytocin synthesised?

A

Paraventricular nucleus.

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64
Q

How do vasopressin / oxytocin reach the posterior pituitary from the hypothalamus?

A
  • axons of the supraoptic / paraventricular nuclei pass down the pituitary stalk and terminate in the posterior pituitary
  • hormones move down the axons enclosed in vesicles and accumulate at the axon terminal in the posterior pituitary
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65
Q

What is the function of vasopressin?

A
  • decreases water secretion in urine (helps maintain blood volume)
  • acts on smooth muscle cells of blood vessels to cause vasoconstriction and increase BP (e.g. in response to low BP due to blood loss)
  • stimulates ACTH release to increase aldosterone release
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66
Q

What stimulates vasopressin release?

A
  • decreased blood volume
  • trauma
  • stress
  • increased blood CO2 / decreased blood O2
  • increased osmotic pressure of blood
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67
Q

What is the function of oxytocin?

A
  • ejection of milk in response to mammary gland stimulation during breast feeding
  • promotes the onset of labour and stimulates uterine smooth muscle contraction
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68
Q

What is the half life of vasopressin / oxytocin?

A

Very short, they are released on a minute to minute basis.

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69
Q

What receptors do all pituitary and hypothalamic hormones act on?

A

G-protein coupled receptors. (Cell-surface membrane receptors).
All are peptide hormones.

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70
Q

What are 6 main diseases of the pituitary?

A
  • benign pituitary adenoma
  • craniopharyngioma
  • trauma
  • Sheehan’s syndrome (pituitary infarction after labour)
  • sarcoidosis (development of granulomas)
  • TB
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71
Q

What are three main effects of pituitary tumours?

A
  • pressure on local structures
  • pressure on normal pituitary (hypopituitarism)
  • functioning tumour (hyperpituitarism)
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72
Q

What might result from a tumour causing pressure on local structures?

A
  • bitemporal hemianopia (pressure on optic chiasm)
  • hydrocephalus (pressure on ventricles)
  • CSF leak
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73
Q

What can result from a tumour causing pressure on the pituitary?

A
  • cortisol deficiency - can be fatal
  • presentation in males: pale, no body hair, central obesity, effeminate skin
  • presentation in females: loose body hair, sallow complexion
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74
Q

What are the features of a prolactinoma?

A
  • common in young women
  • increased milk production in breast and galactorrhea)
  • reduced fertility
  • amenorrhoea
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75
Q

Treatment for prolactinoma?

A

Dopamine agonist to inhibit prolactin release. E.g. cabergoline.

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76
Q

What are some features of acromegaly?

A
  • thick, greasy, sweaty skin
  • large hands and feet
  • enlarged organs (increased risk of heart disease)
  • large brow and nose
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77
Q

What are some features of Cushing’s disease?

A
  • central obesity
  • bruising
  • thin skin
  • osteoporosis
  • ulcers
  • purple stretch marks
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78
Q

How does glucose uptake by the brain work?

A
  • uptake independent of insulin

- brain cannot use FFAs as an energy source as they cannot cross the BBB

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79
Q

What happens during biphasic insulin release?

A
  • initially there is a rapid release of stored insulin

- more insulin is synthesised and release if glucose levels remain high

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80
Q

What are some other counter-regulatory hormones of glucose (opposing insulin)?

A
  • adrenaline, cortisol, GH
  • increase glucose production in the liver
  • reduce glucose utilisation in fat and muscle
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81
Q

Proinsulin vs insulin?

A

Proinsulin - contains alpha and beta insulin chains joined by C peptide.
Insulin - C peptide has been cleaved from alpha and beta chains.

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82
Q

Function of GLUT-1?

A

Enables basal, non-insulin stimulated glucose uptake into cells.

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83
Q

Function of GLUT-2?

A
  • found in beta cells of pancreas (also renal tubules and hepatocytes)
  • enables cells to sense glucose levels, by transporting glucose into the beta cell
  • low affinity transporter: only allows glucose in when glucose concentration is high
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84
Q

Function of GLUT-3?

A

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

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85
Q

Function of GLUT-4?

A

Channel in muscle and adipose

cell surface membranes for glucose uptake stimulated by insulin.

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86
Q

Examples of when diabetes is secondary to another condition?

A
  • pancreatic pathology (total pancreatectomy, chronic pancreatitis, haemochromatosis)
  • endocrine disease (acromegaly, Cushing’s disease)
  • drug-induced (thiazide diuretics, corticosteroids)
  • MODY
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87
Q

Where is the most common place for carcinoid tumours to metastasise to?

A

Liver

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88
Q

What are some side effects of metformin?

A
  • GI disturbances
  • peripheral neuropathy due to decreased absorption of B12
  • lactic acidosis
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89
Q

What is the mechanism of action of metformin?

A

Decreases gluconeogenesis and encourages insulin sensitivity.

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90
Q

What is the risk of metformin in patients with renal impairment?

A

Lactic acidosis.

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91
Q

What is the mechanism of action of sulphonylureas?

A

Act on beta cells to promote insulin secretion.

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92
Q

Side effects of sulphonylureas?

A
  • GI disturbances
  • frequent hypoglycaemia
  • weight gain
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93
Q

Mechanism of action of pioglitazone?

A

Reduces peripheral insulin resistance.

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94
Q

Side effects of pioglitazone?

A
  • bone fractures
  • weight gain
  • bladder cancer
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95
Q

Mechanism of action of DPP-4 inhibitors?

A

Inhibition of DPP-4 increases insulin secretion and lowers glucagon secretion.

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96
Q

Side effects of DPP-4 inhibitors?

A
  • headache

- acute pancreatitis

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97
Q

Mechanism of action of SGLT-2 inhibitors?

A

Inhibition of sodium-glucose co-transporter 2 results in reduced glucose reabsorption and increased urinary glucose excretion.

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98
Q

Side effects of SGLT-2 inhibitors?

A
  • UTI
  • genital pruritus
  • DKA
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99
Q

What nerve roots are associated with carpal tunnel syndrome?

A

Median nerve (C5/6 - T1).

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100
Q

Diagnostic criteria for DKA?

A
  • ketones >= 3.0 mmol/L
  • glucose > 11.0 mmol/L
  • pH < 7.3
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101
Q

What is the management of acromegaly?

A
  1. Transphenoidal surgery.
  2. Somatostatin analogue (ocreotide) +/- dopamine agonist.
  3. GH-receptor antagonist (pegvisomant).
  4. Radiotherapy
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102
Q

Non-diabetic HbA1c?

A

Less than 42 mmol/mol

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103
Q

Pre-diabetic HbA1c?

A

42 mmol/mol < HbA1c < 48 mmol/mol

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104
Q

Diabetic HbA1c?

A

> 48 mmol/mol

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105
Q

What is the cause of Cushing’s disease?

A

ACTH-secreting pituitary adenoma.

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106
Q

First line treatments for DKA?

A 
IV fluids (0.9% sodium chloride).
IV insulin +/- potassium.
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107
Q

Which arrhythmia is a consequence of untreated hyperkalaemia?

A

Ventricular tachycardia

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108
Q

Gold standard test for acromegaly?

A

Oral glucose tolerance test.

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109
Q

Treatment of hypercalcaemia?

A
  • fluids

- bisphosphonates with calcitonin

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110
Q

Potassium in DKA?

A

Hyperkalaemia

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111
Q

Immediate management for carcinoid syndrome?

A

Somatostatin analogue (octreotide).

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112
Q

What is the definition of type 1 diabetes?

A

Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency.

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113
Q

What proportion of diabetes is type 1?

A

10%

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114
Q

Pathophysiology of T1D?

A

Autoantibodies attack beta cells in the islets of Langerhans, leading to insulin deficiency and hyperglycaemia. There is continuous breakdown of glycogen from the liver.

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115
Q

Risk factors for T1D?

A
  • other autoimmune diseases
  • HLA DR3-DQ2 or HLA DR4-DQ8
  • northern european ancestry
116
Q

Classic presentation of T1D?

A
  • polydipsia
  • polyuria
  • weight loss
  • ketosis
    Usually short history of severe symptoms.
117
Q

Diagnosis of T1D?

A
  • random plasma glucose > 11 mmol/L
  • fasting plasma glucose > 7 mmol/L
  • HbA1c > 48 mmol/mol
118
Q

Treatment of T1D?

A

Insulin therapy:

  • quick-acting insulin given at mealtimes
  • long-acting insulin given once or twice daily
119
Q

Definition of type 2 diabetes?

A

Progressive disorder defined by deficits in insulin secretion and increased insulin resistance, leading to abnormal glucose metabolism and hyperglycaemia.

120
Q

Secondary causes of type 2 diabetes?

A
  • corticosteroid therapy (long term)
  • Cushing’s disease
  • chronic pancreatitis
121
Q

Risk factors for T2D?

A
  • obesity
  • physical inactivity
  • aged > 40
122
Q

Signs and symptoms of T2D?

A
  • polydipsia
  • polyuria
  • central obesity
  • blurred vision
123
Q

Investigations for T2D?

A
  • fasting plasma glucose > 7 mmol/L
  • random plasma glucose > 11 mmol/L
  • HbA1c > 48 mmol/mol
124
Q

T2D management summary?

A
  1. Lifestyle changes.
  2. Metformin
  3. Dual therapy with metformin + DPP4 inhibitor / sulphonylurea / pioglitiazone
  4. Triple therapy.
  5. Insulin therapy.
125
Q

What is diabetic ketoacidosis?

A

Acute complication of T1D characterised by hyperglycaemia, ketonaemia and metabolic acidosis.

126
Q

Causes of DKA?

A
  • untreated T1D
  • inadequate insulin therapy
  • infection
  • acute illness (MI, pancreatitis)
127
Q

Pathophysiology of DKA?

A
  • reduced insulin and increased insulin counter-regulatory hormones
  • increased gluconeogenesis and glycogenolysis, with impaired glucose uptake in peripheral tissues
  • this results in hyperglycaemia and hyperosmolality
  • insulin deficiency leads to lipolysis and ketogenesis, resulting in metabolic acidosis
  • osmotic diuresis results in severe dehydration and hypovolaemia
128
Q

Why does hyperkalaemia occur in DKA?

A
  • insulin normally drives potassium uptake into cells
  • insulin deficiency increases serum potassium
  • eventually total body potassium becomes low due to increased urinary excretion
129
Q

What is the risk when correcting dehydration and hyperglycaemia in DKA?

A

Cerebral oedema - due to rapid shift in water from the extracellular space to the intracellular space in brain tissues.

130
Q

Signs and symptoms of DKA?

A
  • polydipsia and polyuria
  • nausea & vomiting
  • weight loss
  • acetone smell on breath
  • dehydration
  • confusion / lethargy
  • Kussmaul breathing (acidosis)
  • tachycardia and hypotension
131
Q

Investigations for DKA?

A
  • random plasma glucose > 11 mmol/L
  • plasma ketones > 3 mmol/L
  • venous / arterial blood gas - pH < 7.35
  • urine dipstick - glycosuria, ketouria
  • raised urea and creatinine
  • low total K+, elevated serum K+
132
Q

Management of DKA?

A

ABCDE approach:

  • IV fluids (0.9% saline) for rehydration
  • IV insulin
  • correct hypokalaemia
133
Q

What is hyperosmolar hyperglycaemic state?

A

Serious complication of T2D - characterised by hyperglycaemia, hyperosmolality, and volume depletion in the absence of ketoacidosis.

134
Q

Causes of HHS?

A
  • infection (UTI, pneumonia)
  • untreated T2D
  • acute illness (MI, stroke)
135
Q

Pathophysiology of HHS?

A
  • relative insulin deficiency results in hyperglycaemia and hyperosmolality
  • there may also be increased insulin counter regulatory hormones due to infection
  • insulin concentration is sufficient to suppress lipolysis and ketogenesis, but insufficient to promoto glucose uptake and regulate gluconeogenesis and glycogenolysis
  • osmotic diuresis results in hypovolaemia
136
Q

What are insulin counter regulatory hormones?

A
  • catecholamines (adrenaline)
  • glucagon
  • cortisol
  • growth hormone
137
Q

Signs and symptoms of HHS?

A
  • nausea & vomiting
  • weight loss
  • polydipsia and polyuria
  • dehydration
  • confusion and lethargy
138
Q

Investigations for HHS?

A
  • random plasma glucose > 11 mmol/L
  • urine dipstick - glycosuria
  • plasma osmolality elevated
  • raised creatinine
  • raised serum K+, low total K+
139
Q

Management of HHS?

A
  • IV fluids (0.9% saline)
  • IV insulin
  • correct potassium
140
Q

Causes of primary hyperthyroidism?

A
  • Grave’s disease

- toxic multinodular goitre

141
Q

Cause of secondary hyperthyroidism?

A

TSH-secreting pituitary adenoma

142
Q

Most common cause of hyperthyroidism?

A

Grave’s disease

143
Q

Pathophysiology of hyperthyroidism?

A

Increased thyroid hormone increases metabolic rate, cardiac output, bone resorption, and activates the sympathetic nervous system.

144
Q

Signs and symptoms of hyperthyroidism?

A
  • hot and sweaty
  • diarrhoea
  • weight loss
  • palpitations
  • tremor
  • irritability
  • anxiety
  • oligomenorrhoea
  • goitre
145
Q

Pathophysiology of Grave’s disease?

A

TSH receptor autoantibodies cause thyroid hormone hyper-production, thyroid hypertrophy, and hyperplasia of thyroid follicular cells.

146
Q

What causes extra-thyroidal manifestations of Grave’s disease?

A

TSH receptors are also found in retro-orbital and dermal tissue. Autoantibodies stimulate fibroblasts, resulting in retro-orbital tissue expansion.

147
Q

Signs and symptoms of Grave’s disease?

A
  • signs and symptoms of hyperthyroidism
  • diffuse goitre
  • orbitopathy (upper eyelid retraction, exophthalmos)
  • pretibial myxoedema
  • thyroid acropachy (digital clubbing)
148
Q

Investigations for Grave’s disease?

A
  • serum T3 and T4 - elevated
  • serum TSH - low
  • serum TSH-R autoantibodies
  • ultrasound neck
  • CT head and neck
149
Q

Management of Grave’s disease?

A
  • beta blockers to reduce sympathetic activity
  • carbimazole / propylthiouracil in pregnancy
  • radioiodine therapy
  • thyroidectomy
150
Q

Treatment of Grave’s dermopathy?

A

Topical corticosteroid

151
Q

Treatment of Grave’s orbitopathy?

A
  • eye drops

- high dose corticosteroids if sight-threatening

152
Q

Complications of thyroidectomy?

A
  • laryngeal nerve damage

- parathyroid damage

153
Q

Complications of hyperthyroidism?

A
  • AF
  • congestive heart failure
  • vision loss
154
Q

What is Hashimoto’s thyroiditis?

A

Autoimmune-mediated inflammation of the thyroid, usually resulting in hypothyroidism due to destruction of thyroid cells.

155
Q

Causes of primary hypothyroidism?

A
  • Hashimoto’s thyroiditis
  • primary atrophic hypothyroidism
  • iodine deficiency
  • post-thyroidectomy
156
Q

Cause of secondary hypothyroidism?

A

Hypopituitarism

157
Q

Signs and symptoms of hypothyroidism?

A
  • fatigue & lethargy
  • weight gain
  • cold intolerance
  • constipation
  • depression
  • menorrhagia
  • goitre
158
Q

Investigations for hypothyroidism?

A
  • serum T3 and T4 - decreased
  • TSH elevated if primary, decreased if secondary
  • autoantibodies (thyroid peroxidase)
159
Q

Treatment of hypothyroidism?

A

Thyroid replacement therapy with levothyroxine.

160
Q

What is post-partum thyroiditis?

A

Autoimmune inflammation of the thyroid occurring within 12 months of delivery. May involve hyperthyroidism and / or hypothyroidism followed by a return to euthyroid.

161
Q

What is the most common endocrine malignancy?

A

Thyroid cancer.

162
Q

Risk factors for thyroid cancer?

A
  • head and neck irradiation

- family Hx

163
Q

Clinical presentation of thyroid cancer?

A
  • palpable thyroid nodule
  • hoarseness due to laryngeal nerve involvement
  • dysphagia
  • cervical lymphadenopathy
164
Q

Gold standard investigation for thyroid cancer?

A

Thyroid biopsy

165
Q

Investigations for thyroid cancer?

A
  • biopsy

- ultrasound

166
Q

Management of thyroid cancer?

A
  • thyroidectomy
  • radioactive iodine ablation
  • chemotherapy / radiotherapy
167
Q

What is Cushing’s syndrome?

A

The clinical manifestation of pathological hypercortisolism from any cause.

168
Q

What is Cushing’s disease?

A

Pituitary adenoma secretes excessive ACTH, causing Cushing’s syndrome.

169
Q

Causes of Cushing’s syndrome?

A
  • exogenous corticosteroid exposure
  • ACTH-secreting pituitary adenoma
  • adrenal adenoma / carcinoma
  • small cell lung cancer
170
Q

Most common cause of Cushing’s syndrome?

A

Exogenous corticosteroid exposure.

171
Q

Clinical manifestations of Cushing’s syndrome?

A
  • facial rounding
  • violaceous abdominal striae
  • weight gain and central obesity
  • acne
  • depression
  • proximal muscle wasting and weakness
  • dorsal hump
  • hypertension
  • easy bruising
172
Q

Which causes of Cushing’s syndrome are ACTH dependent?

A
  • pituitary adenoma

- small cell lung cancer

173
Q

Which causes of Cushing’s syndrome are not ACTH dependent?

A
  • adrenal adenoma

- exogenous corticosteroid exposure

174
Q

Gold standard investigation for Cushing’s syndrome?

A

Dexamethasone suppression test.

175
Q

Initial investigation for Cushing’s syndrome?

A

Random plasma cortisol.

176
Q

What do the results of the high-dose dexamethasone suppression test indicate?

A

Pituitary adenoma - high dose is sufficient to suppress cortisol.
Adrenal adenoma - high dose suppresses ACTH but not cortisol.
Small cell lung cancer - high dose does not suppress ACTH or cortisol.

177
Q

Management of Cushing’s syndrome?

A
  • stop corticosteroid medication if possible
  • trans-sphenoidal removal of pituitary adenoma
  • adrenalectomy for adrenal adenoma
178
Q

Complications of Cushing’s syndrome?

A
  • hypertension
  • diabetes mellitus
  • osteoporosis
  • thrombosis
179
Q

What is acromegaly?

A

Release of excess growth hormone, causing overgrowth of all systems.

180
Q

Most common cause of acromegaly?

A

Pituitary adenoma.

181
Q

Physiology of growth hormone?

A
  • GH stimulates the release of IGF-1 from the liver
  • IGF-1 causes widespread promotion of growth
  • GH may also directly act on tissues to promote their growth
182
Q

What hormone is a negative regulator of GH?

A

Somatostatin

183
Q

Signs and symptoms of acromegaly?

A
  • prominent forehead (frontal bossing)
  • large protruding jaw (prognathism)
  • large hands, nose, tongue, feet
  • bitemporal hemianopia
  • sweating
  • lower pitch of voice
  • obstructive sleep apnoea
  • polydipsia and polyuria
  • organomegaly
184
Q

First line investigation for acromegaly?

A

Serum IGF-1 - elevated.

185
Q

Gold standard investigation for acromegaly?

A

Oral glucose tolerance test.

186
Q

Management of acromegaly?

A
  1. Trans-sphenoidal resection of pituitary adenoma.
  2. Somatostatin analogue (octreotide).
  3. GH receptor antagonist (pegvisomant).
  4. Dopamine agonist.
187
Q

What is a prolactinoma?

A

Benign pituitary adenoma producing excess prolactin.

188
Q

Signs and symptoms of prolactinoma?

A
  • visual field defect (bitemporal hemianopia)
  • headache
  • menstrual irregularity
  • infertility
  • galactorrhoea
189
Q

Why does a prolactinoma cause infertility?

A

Inhibition of FSH and LH.

190
Q

Investigations for prolactinoma?

A
  • pituitary MRI

- serum prolactin

191
Q

Management of prolactinoma?

A
  1. Trans-sphenoidal resection of prolactinoma.

2. Dopamine agonists.

192
Q

Dopamine agonist example?

A

Cabergoline

193
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism (i.e. due to adrenal adenoma).

194
Q

Pathophysiology of Conn’s syndrome?

A

Excess aldosterone production leads to:

  • increased sodium and water retention
  • increased renal potassium excretion
  • hypertension
  • metabolic acidosis
  • low renin (negative feedback)
195
Q

Signs and symptoms of Conn’s syndrome?

A
  • hypertension
  • hypokalaemia
  • polyuria, polydipsia
  • mood and concentration disturbance
  • muscle cramps
  • arrhythmia (AF)
196
Q

What cells does aldosterone act on?

A 
Principle cells (sodium-potassium transporters) in the DCT.
Intercalated cells in the DCT (acid-base balance).
197
Q

Investigations for Conn’s syndrome?

A
  • aldosterone / renin ratio - increased

- serum potassium - low

198
Q

Management of Conn’s syndrome?

A
  • spironalactone

- laparoscopic adrenalectomy

199
Q

What is Addison’s disease?

A

Primary adrenal insufficiency, resulting in impaired synthesis and secretion of all steroids (glucocorticoids and mineralocorticoids).

200
Q

Causes of Addison’s disease?

A
  • autoimmune
  • infection (TB, pseudomonas, meningococcal)
  • infiltrative disease (amyloidosis, sarcoidosis, haemochromatosis)
  • metastasis
  • bilateral adrenalectomy
  • adrenal infarct
201
Q

What causes skin hyperpigmentation in Addison’s disease?

A

Increased synthesis of ACTH precursor proopiomelanocortin, also a precursor of melanocyte-stimulating hormone.

202
Q

Signs and symptoms of Addison’s disease?

A
  • weight loss
  • abdominal pain
  • bronze hyperpigmentation
  • fatigue
  • postural hypotension
203
Q

First line investigations for Addison’s disease?

A
  • U&Es - hyponatraemia, hyperkalaemia

- blood glucose (hypoglycaemia)

204
Q

Gold standard investigation for Addison’s disease?

A

Short synACTHen test.

205
Q

Serum renin and aldosterone in Addison’s disease?

A

Renin - high

Aldosterone - low

206
Q

Serum cortisol and ACTH in Addison’s disease?

A

Cortisol - low

ACTH - high

207
Q

What autoantibodies may be seen in Addison’s disease?

A

21-hydroxylase antibodies

208
Q

Summary of Addison’s disease investigations?

A 
1. U&Es
Gold standard - short synACTHen test.
- serum renin & aldosterone
- serum cortisol & ACTH
- 21-hydroxylase antibodies
- adrenal CT / MRI
209
Q

Management of Addison’s disease?

A
  • hydrocortisone to replace cortisol
  • fludrocortisone to replace aldosterone
  • treat underlying cause
  • warn against suddenly stopping steroids (emergency ID tag)
210
Q

What is Addisonian (adrenal) crisis?

A

Emergency presenting with hypotension and tachycardia due to lack of cortisol.

211
Q

Management of adrenal crisis?

A
  • IV fluids
  • IV hydrocortisone
  • correct hypoglycaemia
  • correct electrolytes
212
Q

Causes of secondary adrenal insufficiency?

A
  • cessation of long term corticosteroid usage

- hypopituitarism

213
Q

What is SIADH?

A

Syndrome of inappropriate ADH - characterised by hypotonic hyponatraemia, concentrated urine, and a euvolaemic state.

214
Q

Causes of SIADH?

A
  • small cell lung cancer
  • CNS disorders (meningitis, encephalitis, trauma, multiple sclerosis, haemorrhage)
  • anaesthesia and post-operative state
  • nephrogenic (gain of function mutation in the vasopressin 2 receptor)
  • medications (thiazide diuretics)
215
Q

What is the most common cause of SIADH?

A

Medication (thiazide diuretics)

216
Q

Signs and symptoms of SIADH?

A
  • headache
  • nausea
  • fatigue
  • muscle cramps
  • confusion
217
Q

Pathophysiology of SIADH?

A
  • excessive ADH results in excessive water reabsorption in the collecting ducts
  • water dilutes sodium in the blood, causing hyponatraemia
  • increased extracellular volume results in RAA system suppression, and therefore increased naturesis
  • euvolaemia as excessive water reabsorption is not enough to cause fluid overload
  • high urine osmolality
218
Q

Investigations for SIADH?

A
  • hyponatraemia
  • urine osmolality high
  • urine sodium high
  • exclude Addison’s (short synACTHen test)
219
Q

Causes of hyponatraemia?

A
  • SIADH
  • Addison’s disease
  • vomiting / diarrhoea
  • diuretic use
  • AKI / CKD
220
Q

Management of SIADH?

A
  • stop causative medication
  • fluid restriction
  • ADH receptor blocker (tolvaptan)
221
Q

How should tolvaptan be used with caution?

A

ADH receptor blocker - don’t let sodium rise too quickly (aim for increase of less than 10 mmol in 24 hours). Risk of osmotic demyelination syndrome.

222
Q

What potassium level is considered hyperkalaemia?

A

> 5.5 mmol/L

223
Q

Causes of hyperkalaemia?

A
  • AKI / CKD
  • ACE inhibitors
  • Addison’s disease
  • decreased insulin
  • IV K+ therapy
224
Q

Signs and symptoms of hyperkalaemia?

A
  • fatigue
  • light-headedness
  • chest pain
  • palpitations (due to arrhythmia)
  • reduced power and reflexes
  • flaccid paralysis
225
Q

Investigations for hyperkalaemia?

A
  • ECG
  • U&Es
  • urine osmolality and electrolytes
226
Q

Management of hyperkalaemia?

A
  • cardiac monitoring and calcium gluconate to protect the myocardium
  • insulin + dextrose
  • nebulised salbutamol
  • treat underlying cause
227
Q

What potassium level is considered hypokalaemia?

A

< 3.5 mmol/L

228
Q

Causes of hypokalaemia?

A
  • thiazide and loop diuretics
  • Conn’s syndrome
  • diarrhoea and vomiting
  • fasting
  • salbutamol
229
Q

Symptoms of hypokalaemia?

A
  • fatigue
  • light-headedness
  • cramps
  • palpitations (due to arrhythmia)
  • constipation
  • hypotonia and hyporeflexia
  • muscle paralysis
230
Q

Severe complication of hypokalaemia?

A

Rhabdomyolysis

231
Q

ECG signs of hypokalaemia?

A
  • prolonged PR
  • ST depression
  • flat T waves
  • prominent U waves
232
Q

ECG signs of hyperkalaemia?

A
  • tall tented T waves
  • small / absent p waves
  • prolonged PR
  • wide QRS
233
Q

Investigations for hypokalaemia?

A
  • ECG
  • U&Es
  • urine osmolality and electrolytes
234
Q

Management of hypokalaemia?

A
  • potassium replacement (oral or IV)

- treat underlying cause

235
Q

What is diabetes insipidus?

A

Inadequate ADH secretion / inadequate renal response to ADH.

236
Q

Subtypes of diabetes insipidus?

A

Central - abnormal ADH synthesis / secretion.
Nephrogenic - abnormal renal response to ADH.
Gestational - increased ADH metabolism.

237
Q

Causes of central diabetes insipidus?

A
  • brain tumours
  • skull fracture
  • surgical damage to hypothalamus / pituitary stalk
  • CNS infection
  • autoimmune disorders (Hashimoto’s / T1D)
238
Q

Causes of nephrogenic diabetes insipidus?

A

Congenital - X-linked mutation of vasopressin 2 receptors.

Acquired - polycystic kidney disease, lithium.

239
Q

Medication causing diabetes insipidus?

A

Lithium

240
Q

Most common cause of nephrogenic diabetes insipidus?

A

Lithium

241
Q

Where is vasopressin synthesised?

A

Supraoptic and paraventricular nuclei of the hypothalamus.

242
Q

Signs and symptoms of DI?

A
  • polyuria & polydipsia
  • dehydration
  • hypernatraemia (spasticity, hyper-reflexia, irritability)
243
Q

Gold standard investigation for DI?

A

8 hour water deprivation test - no decrease in urine osmolality.

244
Q

How is cranial DI distinguished from nephrogenic DI?

A

Desmopressin test following water deprivation test. If cranial, urine osmolality decreases. No decrease in urine osmolality if nephrogenic.

245
Q

Management of DI?

A
  • conservative management with rehydration in mild cases
  • desmopressin to replace ADH in cranial DI
  • bendroflumethiazide for nephrogenic DI if underlying cause cannot be resolved
246
Q

What is primary hyperparathyroidism?

A

Parathyroid gland produces excess PTH.

247
Q

What is secondary hyperparathyroidism?

A

Increased secretion of PTH to compensate for hypocalcaemia (e.g. due to kidney failure).

248
Q

What is tertiary hyperparathyroidism?

A

Autonomous secretion of PTH even after correction of hypocalcaemia, due to CKD. Develops due to prolonged secondary hyperparathyroidism.

249
Q

Causes of primary hyperparathyroidism?

A
  • parathyroid adenoma (most common)

- parathyroid hyperplasia

250
Q

Causes of secondary hyperparathyroidism?

A
  • CKD

- low vitamin D

251
Q

Signs and symptoms of hyperparathyroidism?

A

Hypercalcaemia

  • bone pain
  • renal stones
  • psychiatric moans (depression)
  • abdominal groans
252
Q

Investigations for hyperparathyroidism?

A
  • serum PTH

- bone profile (high calcium, low phosphate)

253
Q

Serum PTH and calcium in primary hyperPTH?

A
  • normal / high PTH

- high calcium

254
Q

Serum PTH and calcium in secondary hyperPTH?

A
  • low calcium

- high PTH

255
Q

Serum PTH and calcium in tertiary hyperPTH?

A
  • high calcium

- high PTH

256
Q

Imaging for hyperPTH?

A
  • DEXA scan
  • X ray
  • renal ultrasound for calculi
257
Q

X ray signs in hyperPTH?

A

Salt and pepper degradation of bone.

258
Q

Management of hyperPTH?

A

Mild - watchful waiting.
Primary: bisphosphonates, surgical removal of adenoma.
Secondary: correct calcium, treat underlying cause.
Tertiary: cinacalcet (calcium mimetic), parathyroidectomy.

259
Q

Causes of primary hypoPTH?

A
  • autoimmune destruction

- congenital (DiGeorge syndrome)

260
Q

Causes of secondary hypoPTH?

A
  • surgical removal of parathyroid glands

- damage during thyroidectomy

261
Q

Pathophysiology of hypoPTH?

A
  • hypocalcaemia and hyperphosphataemia

- neurons become more excitable

262
Q

Signs and symptoms of hypoPTH?

A 
Hypocalcaemia (CATS go numb)
- convulsions
- arrhythmias
- tetany
- spasm
- numbness
Chvostek and Trousseau's signs.
263
Q

Investigations for hypoPTH?

A
  • bone profile (low calcium, high phosphate, low PTH)

- ECG

264
Q

ECG findings hypoPTH?

A
  • prolonged QT

- prolonged ST

265
Q

Management of hypoPTH?

A
  • IV calcium
  • AdCal D3
  • synthetic PTH
266
Q

Risk factors for neuroendocrine tumours?

A
  • multiple endocrine neoplasia
  • neurofibromatosis type 1
  • von hippel-lindau
267
Q

Where are neuroendocrine tumours commonly located?

A
  • stomach
  • intestine
  • pancreas
  • lungs
268
Q

Examples of neuroendocrine tumours?

A
  • insulinoma
  • gastrinoma
  • small cell lung cancer
269
Q

What is carcinoid syndrome?

A

Symptoms occurring due to the release of serotonin (5-HT) and other vasoactive peptides into the systemic circulation from a carcinoid (neuroendocrine) tumour.

270
Q

Signs and symptoms of carcinoid syndrome?

A
  • diarrhoea
  • flushing
  • palpitations
  • abdominal cramps
  • telangiectasia
  • wheeze
271
Q

Investigations for carcinoid syndrome?

A
  • urinary 5-hydroxyindoleacetic acid (serotonin metabolite)
  • CT chest, abdomen, pelvis
  • bronchoscopy / endoscopy
272
Q

Management of carcinoid syndrome?

A
  • somatostatin analogue (octreotide)

- surgical resection of tumour

273
Q

What is a pheochromocytoma?

A

Tumour arising from catecholamine-producing chromaffin cells of the adrenal medulla.

274
Q

Hereditary risk factors for pheochromocytoma?

A
  • multiple endocrine neoplasia type 2
  • von hippel-lindau
  • neurofibromatosis type 1
275
Q

Pathophysiology of pheochromocytoma?

A
  • excess secretion of catecholamines
  • activation of alpha and beta adrenergic receptors
  • alpha receptors: increased BP, increased cardiac contractility
  • beta receptors: increased HR and cardiac contractility
276
Q

Pattern of symptoms in pheochromocytoma?

A 
Usually paroxysmal (associated with periods when the tumour is secreting adrenaline).
Can be persistent / asymptomatic.
277
Q

Classic triad of symptoms in pheochromocytoma?

A
  • episodic headache
  • sweating
  • tachycardia
278
Q

Symptoms of hypertensive crisis?

A
  • hypertension
  • hyperthermia
  • confusion
  • end-organ dysfunction
  • hypotension due to circulatory collapse
279
Q

Complication of pheochromocytoma?

A

Hypertensive crisis

280
Q

Investigations for pheochromocytoma?

A
  • plasma free metanephrines (if high probability)
  • urinary fractionated metanephrines (if low probability)
  • CT / MRI
281
Q

Complications of hypertensive crisis?

A
  • stroke
  • cardiac failure
  • seizure
282
Q

Management of pheochromocytoma?

A
  • adrenalectomy

- alpha- and beta-blockers to control hypertension prior to surgery

283
Q

Calcium in Addison’s disease?

A

Raised due to volume depletion and increased release into extracellular space.

284
Q

Addison’s disease and blood volume?

A

Blood volume decreased due to naturesis.

285
Q

Most common cause of Addisonian crisis?

A

Abrupt cessation of long term corticosteroid treatment.

286
Q

Most important treatment for Addisonian crisis?

A

Hydrocortisone

287
Q

What is pseudohypoPTH?

A

Peripheral resistance to PTH.

Phase 2a (10 decks)

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