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PHASE 2A (Mine) > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Give an example of a water-soluble hormone

A

Peptides, Monoamines

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2
Q

Give an example of a fat-soluble hormone

A

Thyroid hormones, Steroids (e.g. cortisol)

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3
Q

What are the different types of hormone?

A

Peptides, Amines, Iodothyronines, Cholesterol derivatives and Steroids

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4
Q

How are fat-soluble hormones transported?

A

Bound to proteins

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5
Q

How do water-soluble hormones interact with cells?

A

Bind to surface receptors.

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6
Q

How do fat- soluble hormones interact with cells?

A

Diffuse into the cell and bind to target receptor

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7
Q

Which type of hormone has a longer half life? (water or fat soluble)

A

Fat-soluble

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8
Q

Which type of hormones has faster clearance?

A

Water-soluble.

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9
Q

How are peptide hormones synthesised?

A

Preprohormones–> Prohormones. Then packaged as prohormones requiring further processing to acitvate

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10
Q

How are steroid hormones synthesised?

A

From a series of reactions from cholesterol

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11
Q

How are amino acid derivative hormones synthesised?

A

From Tyrosine

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12
Q

How are peptides stored and secreted?

A

In vesicles/secretory granules with regulatory secretion (in pulses/bursts)

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13
Q

How are steroid hormones stored and secreted?

A

Released immediately

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14
Q

How do steroid hormones induce changes?

A

Enter cells directly to nucleus to alter gene expression

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15
Q

What is the structure of peptide hormones?

A

Can vary in length and be linear or ring structures.

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16
Q

What are some examples of peptide hormones?

A

Insulin, LH, FSH

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17
Q

What are the main cholesterol derivative hormones?

A

Vitamin D, Adrenocrotical and gonadal steroids.

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18
Q

Are thyroid hormones water soluble?

A

No- 99% is protein bound.

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19
Q

Where are peptide hormone receptors?

A

Cell membrane

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20
Q

Where are steroid hormone receptors?

A

Cytoplasm

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21
Q

Where are thyroid hormone receptors

A

Nucleus

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22
Q

Give an example of an amine hormone

A

Dopamine, Noradrenaline and adrenaline

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23
Q

what hormones does the hypothalamus release?

A

TRH, CRH, GnRH, Somatostatin, GHRH, Dopamine

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24
Q

Does the anterior or posterior pituitary produce hormones?

A

Anterior (posterior just stores and secretes)

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25
Q

What hormones does the anterior pituitary gland release? (FLATP(I)G)

A

TSH, ACTH, FSH, LH, GH, Prolactin

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26
Q

What hormones does the posterior pituitary release?

A

Oxytocin, ADH (both produced in the hypothalamus)

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27
Q

What are the main causes of pituitary dysfunction?

A

Tumour mass defects, hormone excess and hormone deficiency

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28
Q

What is the anterior pituitaries blood supply?

A

Through a portal venous circulation from the hypothalamus.

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29
Q

What are the 3 main signs of a pituitary tumour?

A

1= Pressure on local structures (e.g. optic nerves causing bitemporal hemianopia) 2= Pressure on normal pituitary causing hypopituitarism. 3= Functioning tumour (produces own hormones) causing prolactinoma, acromegaly or Cushing’s disease.

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30
Q

How would you investigate pituitary function?

A

Hormonal tests- if target organ working then pituitary is working. If abnormal, perform MRI.

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31
Q

What is the function of the thyroid?

A

Regulate metabolic rate, control heart rate, muscle and digestive function, Brain development and growth rate.

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32
Q

Draw out the H-P-Thyroid axis

A

Hypothalamus–> TRH (Thyrotropin-releasing hormone)–> Anterior pituitary –> TSH (Thyroid stimulating hormone)–> Thyroid –> T3 and T4

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33
Q

What is T3’s full name and half life?

A

Tri-iodothronine

1 day

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34
Q

What is T4’s full name and half life?

A

Thyroxine

7 days

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35
Q

What is the effect of T3?

A

Acts on all peripheral tissues to increase metabolic rate.

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36
Q

What is the action of thyroid stimulating hormone?

A

Increases uptake and usage of Iodine, stimulates production of thyroid hormones and stimulates calcitonin production.

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37
Q

Outline the synthesis of T3 and T4

A

Iodide is actively transported into the thyroid from the blood stream. It reacts with a Tyrosine molecule from thyroglobulin to form thyroid hormones.

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38
Q

Which is the more active/ main thryoid hormone?

A

T3. T4 is a store which is converted as required in tissues.

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39
Q

What happens to T4 at peripheral tissues?

A

It is converted to T3

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40
Q

What hormones does the adrenal cortex produce?

A

Mineralocorticoids (ALDOSTERONE), Glucocorticoids (CORTISOL), Androgens (TESTOSTERONE)

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41
Q

What hormones does the adrenal medulla produce?

A

Catecholamines (Adrenaline, noradrenaline, dopamine)

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42
Q

Draw out the HPA axis

A

Hypothalamus –> CRH (Corticotrophin releasing hormone)–> Anterior pituitary–> ACTH (Adrenocorticotrophic hormone)–> Adrenal gland–> Cortisol (+Androgens + Adrenaline)

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43
Q

What are the actions of cortisol?

A

Stress hormone: increases alertness, Inhibits immune system, inhibits bone formation, raises blood glucose, increases metabolism.

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44
Q

What is the rhythm of cortisol release?

A

natural circadian rhythm- rises just before we wake up and falls before we go to sleep

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45
Q

Where are the adrenal glands located?

A

Above the kidneys

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46
Q

Draw out the growth hormones axis

A

Hypothalamus–> GHRH (Growth hormone releasing hormone) (-ve Somatostatin)–> Anterior pituitary–> GH (Growth hormone)–> Liver–> IGF-1.

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47
Q

What is IGF-1 and what is its function?

A

Insulin like growth factor. Stimulates muscle growth, increases bone density and strength, stimulates cell regeneration and reproduction and growth of internal organs.

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48
Q

Draw out the male gonadal axis

A

Hypothalamus–> GnRH–> Pituitary gland–> LH and FSH–> Testicles–> Testosterone, ABG and inhibin

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49
Q

What does LH stimulate in males?

A

Leydig cells to produce testosterone which causes spermatogenesis.

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50
Q

What does FSH stimulate in males?

A

Sertoli cells to produce Androgen binding globulin and inhibin.

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51
Q

What is the action of ABG (Androgen binding globulin)?

A

A protein which binds to testosterone and prevents is from leaving the semineferous tubules.

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52
Q

What is the action of Inhibin in males?

A

Supports spermatogenesis and inhibits the production of FSH, LH and GnRH

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53
Q

Draw out the female gonadal axis

A

Hypothalamus–> GnRH–> anterior pituitary–> LH, FSH–> Ovaries–> Oestrogen, progesterone and Inhibin

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54
Q

What is the function of Oestrogen?

A

Regulates menstrual cycle and many other processes

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55
Q

What is the function of inhibin in females?

A

Causes inhibition of activin which is responsible for GnRH production

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56
Q

Under what circumstances is Parathyroid hormone released?

A

Low serum calcium
Low magnesium
Low serum Phosphate

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57
Q

What is the function of the parathyroid glands?

A

Increase serum calcium concentration

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58
Q

What are the 3 main actions of PTH?

A
  1. Increases activity and number of osteoclasts in BONE, causing reabsorption of calcium into blood.
  2. Stimulates increase in calcium reabsorption in KIDNEYS so less calcium is excreted.
  3. Stimulates kidneys to convert vitamin D3 into calcitriol (active form of vitamin D) which promotes calcium absorption in small INTESTINE.
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59
Q

Draw RAAS Sysem

A

Liver–> Angiotensinogen–> RENIN from kidneys–> Angiotensin I–> ACE from lungs–> Angiotensin II

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60
Q

What are the actions of angiotensin II?

A

Causes vasoconstriction, and stimulates aldosterone release, increasing blood pressure.

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61
Q

What are the 4 types of hormone secretion pattern?

A

Continuous (e.g. prolactin), pulsatile (insulin), Circadian (ACTH, cortisol),.

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62
Q

What action does Somatostatin have?

A

Inhibits growth hormone.

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63
Q

Where does the pituitary gland lie?

A

In the pituitary fossa of the sphenoid bone, just below the hypothalamus

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64
Q

What structures are around the pituitary gland?

A

Optic chiasm, two cavernous sinuses

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65
Q

What is the Infundibulum?

A

Also known as the pituitary stalk- connects hypothalamus and pituitary- contains acons from neurons and small blood vessels.

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66
Q

What is the action of Dopamine

A

Inhibits the release of prolactin, type of neurotransmitter

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67
Q

What is the function of LH in females?

A

Stimulates the release of the egg, which stimulates progesterone release which thickens uterine wall.

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68
Q

What is the action of prolactin and where is it released from?

A

Stimulates the breast to produce milk and helps with breast development. Produced in the anterior pituitary.

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69
Q

what are hypophysiotropic hormones?

A

Hormones produced in the hypothalamus

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70
Q

Which hormone has a short loop mechanism and describe it?

A

Prolactin: Released from the anterior pituitary but this stimulates the secretion of dopamine from the hypothalamus which in turn inhibits the secretion of prolactin.

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71
Q

What is the action of Vasopressin?

A

Acts to retain fluid and maintain blood volume. Causes vasoconstriction and increased water reabsorption. Also stimulates ACTH release to increase aldosterone release to further increase fluid retention.

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72
Q

What triggers ADH release?

A

Decreased blood volume, trauma, stress, Increase blood CO2, Decrease blood O2, increased osmotic pressure.

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73
Q

What are the two main functions of Oxytocin?

A

Ejection of milk during breast feeding, contractions and onset of labour.

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74
Q

What are the most common diseases of the pituitary?

A

Bening pituitary adenoma, craniopharyngioma, trauma, Sheehans, Sarcoid/TB

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75
Q

What are the 3 main diseases caused by a functioning pituitary tumour? (Hyperpituitarism)

A 
Prolactinoma= Increased prolactin
Acromegaly= Increased GH 
Cushings= Increased CTH
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76
Q

What is the definition of diabetes mellitus?

A

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

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77
Q

What are the main micro and macrovascular complications with DM?

A

Micro: Retinopathy, nephropathy, neuropathy.
Macro: Heart disease, strokes, renovascular disease, limb ischeamia

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78
Q

What range should blood glucose levels be between under all conditions?

A

3.5-8.0 mmol/L

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79
Q

What organ is principally in charge of glucose homeostasis?

A

Liver

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80
Q

What does the liver do if blood glucose is high?

A

Glyogenesis (gluocose-> glycogen)

Lipogenesis (Makes triglycerides if there are sustained high sugar levels)

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81
Q

What does the liver do if blood glucose is low?

A

Glyogenolysis ( glycogen-> glucose)

Gluconeogenesis (from amino acids/ fat/ lactate) .

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82
Q

How much glucose is produced/used each day and how much of this is from liver glycogen?

A

200g
90% derived from liver glycogen and hepatic gluconeogenesis
(rest from renal gluconeogenesis)

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83
Q

Which organ is the major consumer of glucose and doesn’t depend on insulin?

A

Brain- its function depends on uninterrupted supply.

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84
Q

Why can the brain not use ketones as an energy source?

A

Free fatty acids can’t cross the blood brain barrier.

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85
Q

What happens to glucose taken up by muscle?

A

It is stored as glycogen or metabolised to CO2 and H2O or Lactate.

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86
Q

What is the action of insulin?

A

Lowers blood glucose:

  • Suppresses hepatic glucose output by decreasing glyocogenolysis and gluconeogenesis.
  • Increases glucose uptake into insulin sensitive tissues
  • Suppresses lipolysis and breakdown of muscles
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87
Q

Which tissues take up glucose under instruction from insulin?

A

Muscle: Glycogen and protein synthesis
Fat: Fatty acid synthesis

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88
Q

What type of hormone is insulin and where is it secreted from?

A

Peptide hormone secreted from the Beta cells in the Islets of Langerhans in the pancreas

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89
Q

What pattern is insulin released and what is the trigger?

A

Released in response to B-cells sensing rising glucose levels.
Biphasic- Rapid release of stored insulin followed by insulin synthesis and release is glucose levels remain high.

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90
Q

Outline insulin synthesis.

A

Coded for on chromosome 11.
Proinsulin–> insulin
Insulin packaged into secretory granules.

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91
Q

What is C- peptide and what does it indicate?

A

It is what joins the alpha and beta chains together. It is cleaved off when insulin is packaged so with insulin release there are high levels of C peptide in the blood.
Synthetic insulin does not contain C-peptide so blood tests can tell if insulin in natural or synthetic.

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92
Q

Where does insulin go after secretion?

A

Enters the portal circulation and is carried to the liver.

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93
Q

What is insulins main action in the fasting state?

A

Regulate glucose release by the liver

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94
Q

What is insulins main actin on the post-prandial state (after eating)?

A

Promote glucose uptake by fat and muscle.

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95
Q

What allows glucose to bypass the cell membrane and enter cells?

A

GLUT proteins: Specialised glucose- transporter proteins.

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96
Q

Function of the GLUT-1 transporter?

A

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

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97
Q

Function of GLUT-2 transporter?

A

Found in pancreatic B-cells.
Transports glucose into Beta cell, enabling them to sense glucose levels.
(only allows glucose in when there is a high concentration of glucose.)

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98
Q

Function of GLUT-3 transporters?

A

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

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99
Q

Function of GLUT-4 transporters?

A

Channel through which glucose is taken up into muscle and adipose tissue following stimulation of insulin receptor.

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100
Q

What happens when insulin bings to a cell surface receptor?

A

It triggers a cascade response that results in translocation of the GLUT-4 transporter to the cell surface, increasing transport of glucose into the cell.

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101
Q

What is the action of glucagon?

A

Increases blood glucose levels:

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102
Q

By what mechanisms to glucagon increase blood glucose?

A

Increases hepatic glucose output (glycogenolysis and gluconeogenesis.)
Reduces peripheral glucose uptake.
Stimulates peripheral release of gluconeogenic precursors (e.g. glycerol and amino acids)
Stimulates lipolysis and ketogenesis.

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103
Q

Where is glucagon produced?

A

Alpha cells in the islets of Langerhans of the pancreas.

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104
Q

In what conditions is diabetes secondary?

A

Pancreatic disease (e.g. pancreatectomy, pancreatitis e.t.c.) Endocrine disease (e.g. acromegaly, Cushing’s) Drug induced (by thiazide diuretics or corticosteroids) MODY (Maturity onset diabetes of youth- genetic condition)

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105
Q

What kind of patient usually presents with Type 1 diabetes?

A

Young (<30), lean (Northern European more common)

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106
Q

What kind of patient usually presents with Type 2 diabetes?

A

Older (Usually >30), overweight.

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107
Q

What is the cause of Type 1 diabetes?

A

Insulin deficiency caused by autoimmune destruction of pancreatic beta-cells

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108
Q

What is LADA?

A

Latent autoimmune diabetes in adults: Slower progression so insulin deficiency occurs late in life. Can be hard to differentiate from type 2.

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109
Q

What is the aetiology of Type 1 diabetes?

A

Autoimmune, idiopathic, genetic susceptibility.

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110
Q

What are the risk factors of type 1 diabetes?

A

Northern european, Family history (HLA-DR-DQ gene), other autoimmune disease, environmental factors (viruses/diet)

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111
Q

What is insulitis?

A

Inflammation of the islets of Langerhans.

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112
Q

What does type 1 diabetes cause?

A

Insulin deficiency which leads to hyperglycaemia, glycosuria and ketonuria.

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113
Q

What are the key presentations of type 1 diabetes?

A

Polydipsia, polyuria, weight loss and ketosis (more severe).

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114
Q

Why do patients get polyuria (and polydipsia) in type 1 diabetes?

A

The excess glucose draws water into the urine by osmosis.

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115
Q

How long is the typical history of symptoms in type 1 diabetes?

A

2-6 weeks

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116
Q

Why is weight loss a main symptom in type 1 diabetes ?

A

Due to fluid depletion and the accelerated breakdown of fat and muscle.

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117
Q

What glucose levels are needed for a diabetes diagnosis?

A

Random plasma glucose> 11.1mmol/L

Fasting plasma glucose > 7mmol/L

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118
Q

What is the HbA1c test and ideal level?

A

Measures amount of glucose attached to haemoglobin. HbA1c>6.5% (48mmol/mol)= diabetes

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119
Q

What is the main treatment for Type 1 diabetes (especially in those who have been in ketoacidosis or under 40)?

A

Synthetic (recombinant) human insulin.

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120
Q

What are the three main types on insulin treatment?

A
  1. Short acting (soluble) insulins
  2. Short-acting insulin analogues
  3. Longer-acting insulins
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121
Q

When would short acting insulin be used and how long does it last?

A

Given 15-30 minutes before meals for patients on multiple dose regimens/ during medical emergencies/ in surgery/labour. Lasts for 4-6 hours.

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122
Q

What are short-acting insulin analogues and when are they used?

A

e.g. (Lispro, Aspart, Glulisine) Have fast onset and shorter duration than normal insulin. Used with the evening meal in patients prone to nocturnal hypoglycaemia.

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123
Q

How long do long-acting insulins work?

A

Intermediate: 12-24 hours

long acting: >24 hours.

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124
Q

What is the most common treatment regimen for those with type 1 diabetes?

A

Basal-bolus: Involves longer acting form of insulin to keep blood glucose levels stable through periods of fasting and separate injections of shorter acting insulin to prevent rises in blood glucose levels resulting from meals.

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125
Q

How is insulin usually given?

A

Subcutaneous injection

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126
Q

What are the complications of insulin treatment?

A

Hypoglycaemia, lipohypertrophy at injection site, insulin resistance, weight gain.

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127
Q

What happens if insulin is not given in type 1 diabetes (and severe type 2)?

A

Diabetic ketoacidosis (DKA)

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128
Q

When is diabetic ketoacidosis usually seen?

A

In undiagnosed diabetes, if insulin therapy is interupted or due to stress from illness (e.g. surgery or infection).

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129
Q

Summarise the pathophysiology of ketoacidosis?

A

In the complete absence of insulin, the body tries to find other sources of energy: ↑gluconeogenesis
↑glycolysis
↑fat and muscle lysis.
Free fatty acids are converted to ketones in the liver and their accumulation causes metabolic acidosis, excarcebated by dehydration from hyperglycaemia.

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130
Q

What are the clinical presentations of ketoacidosis?

A

Pear drop- smelling breath
Dehydration- frequent urination and extreme thirst
Gradual drowsiness and vomiting
Kussmaul’s respiration (deep rapid breathing)

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131
Q

How is ketoacidosis diagnosed?

A

Hyperglycaemia (Blood glucose >11mmol/L)
Raised plasma ketones (>3mmol/L)
Metabolic acidosis (plasma bicarbonate<15mmol/L)

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132
Q

How is ketoacidosis treated?

A 
Immediate ABC
Replacement of fluid loss with saline
Replacement of electrolytes
Acid- base balance restores
Replacement of deficient insulin (usually given with glucose to prevent hypoglycaemia)
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133
Q

Which of the bodies reactions to ketoacidosis actually make it worse?

A

Release of stress hormones (adrenaline, noradrenaline, glucagon and cortisol).
Vomiting (leads to futher loss of fluid and electrolytes)
Respiratory compensation (leads to hyperventilation)

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134
Q

What are the complications of DKA?

A 
Death
cerebral oedema
Adult respiratory distress syndrome
coma
pneumonia
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135
Q

What are the risk factors for Type 2 Diabetes?

A

(central) obesity, lack of exercise, age, family history, ethnicity

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136
Q

What is the pathophysiology of type 2 diabetes?

A

Combination of deficient insulin secretion and resistance to action of insulin resulting in hyperglycaemia and high FFA’s.

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137
Q

At the usual time of type 2 diabetes diagnosis what is the usual reduction in Beta cell mass?

A

50% reduction

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138
Q

What is the Starling curve of the pancreas?

A

When circulating insulin levels are higher then in non-diabetics following diagnosis and rise further, only to decline again after months/years due to eventual secretory failure.

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139
Q

Why is DKA much less likely in type 2 diabetes?

A

Even a small amount of insulin can halt the breakdown of fat and muscle into ketones.

140
Q

What are IGF and IGT?

A

pre-diabetes:
IGT= Impaired glucose tolerance
IGF= Impaired fasting glucose.

141
Q

What are the key presentations of Type 2 diabetes?

A

Asymptomatic: diagnosed incidentally
Obese
Polydipsia + polyuria

142
Q

What are the symptoms of type 2 diabetes?

A

Polydipsia, polyuria, blurred vision, unexplained weight loss, recurrent infections, tiredness

143
Q

What are signs of type 2 diabetes?

A

Acanthosis nigricans, retinopathy, tingling/numbness in feet, erectile dysfunction, arterial disease

144
Q

How do you diagnose Type 2 diabetes?

A
  • HbA1c > 48mmol/mol (6.5%)
  • Fasting plasma glucose > 7.0 mmol/L
  • Random plasma glucose > 11.1 mmol/L in the presence of signs or symptoms.
  • If symptomatic: single abnormal HbA1c or fasting plasma glucose level can be used.
  • If asymptomatic, repeat testing needed.
145
Q

What is the first line type 2 diabetes treatment?

A 
Lifestyle changes: 
Dietary changes
Blood pressure and hyperlipidaemia control
Exercise
Reduction of alcohol/ smoking/ drugs
Weight loss
146
Q

What is the second line treatment of type 2 diabetes?

A

Oral metformin

147
Q

What is the action of metformin?

A

Reduces rate of gluconeogenesis
Increases cells sensitivity to insulin
Weight loss

148
Q

What is the second line treatment of type 2 diabetes?

A

Dual therapy: Metformin + Sulfonylurea

149
Q

What is the action of Sulfonylureas?

A

Promote insulin secretion

150
Q

What is the third line treatment of type 2 diabetes?

A

Triple therapy: metformin + sulfonylurea + insulin/ glitazone e.t.c.

151
Q

What are the main life threatening complication of type 2 diabetes?

A

Hyperosmolar hyperglycaemic state

152
Q

What is hyperosmolar hyperglycaemia?

A

A metaboilc emergency where high blood sugar results in high osmolarity without significant ketoacidosis.

153
Q

What are the risk factors for hyperosmolar hyperglycaemia?

A

Infection: usually pneumonia
Consumption of high glucose fluids
Concurrent medication

154
Q

What are the clinical presentations of hyperosmolar hyperglycaemia?

A

Severe dehydration
Decreased level of consciousness
Hyperglycaemia
Hyperosmolality

155
Q

What is the treatment of hyperosmolar hyperglycaemia?

A

Low rate infusion of insulin
Fluid replacement with saline
Low molecular weight heparin to reduce risk of vascular disease
Restore electrolyte loss.

156
Q

What are the main macrovascular complications of diabetes?

A

Atherosclerosis resulting in stroke, Ischeamic heart disease, MI, peripheral vascular disease, lower limb amputation

157
Q

Why does diabetes cause vascular disease?

A

High glucose levels damage blood vessels.

158
Q

What are signs of peripheral vascular disease?

A

Intermittent claudication and rest pain.

Diminished or absent peal pulses, coolness of feet and toes, poor skin and nails and absence of hair.

159
Q

What are the main microvascular complications of diabetes?

A

Retinopathy, nephropathy and neuropathy.

160
Q

What are the signs/ symptoms of diabetic retinopathy?

A

Blindness
Microaneuryssms: tiny red dots
Heamorrhages: blots
Blurred vision, vision loss, impaired colour vision.

161
Q

What are the different types of diabetic retinopathy?

A

Non-proliferative
Pre-proliferative: micro-infarcts due to occluded vessels.
Proliferative: Retinal ischeamia resylts in release of vascular growth factors.
Maculopathy: Fluid from leaking vessels cleared poorly in the macular area causing oedema.

162
Q

When does clinical nephropathy usually manifest?

A

15-25 years after diabetes diagnosis

163
Q

Why does nephropathy occur?

A

Thickening of basement membrane due to poor glyceamic control causes glomerular damage and leads to microalbuminuria.

164
Q

How do you diagnose nephropathy?

A

Undetectable by dipstick

Albumin:creatinine ratio>3

165
Q

How do you treat diabetic nephropathy?

A

Aggressive blood pressure treatment.

166
Q

Why does diabetic neuropathy occur?

A

Results from occlusion of the vasa nervorum in addition to accumulation of fructose and sorbitol disrupting the structure and functions of nerves.

167
Q

What are the vasa nervorum?

A

Small arteries that supply peripheral nerves

168
Q

What are the symptoms of diabetic neuropathy?

A 
Numbness/ reduced ability to feel pain or temperature
Tingling/ burning sensations
Sharp pain
Hypersensitivity
muscle weakness
loss of balance/ coordination
Ulcers/ infection/ amputation
169
Q

What is DFU?

A

Diabetic foot ulceration: Common consequence of diabetes. Neuropathy results in increased risk of repeated ‘silent traume’

170
Q

What is hypoglycaemia?

A

Plasma glucose< 3 mmol/L.

Usually due to insulin or sulphonylurea treatment.

171
Q

What are the causes of hypoglycaemia in non-diabetics? EXPLAIN

A 
EX: Exogenous drugs 
P: Pituitary insufficiency
L: Liver failure
A: Addison's disease
I: Islets cell tumour/ Immune hypoglycaemia
N: Non-pancreatic neoplasm
172
Q

What are the presentations of hypoglycaemia?

A

Autonomic: Sweating, anxiety, hunger, tremor, palpitations, dizziness

Neuroglycopenic (lack of glucose in the brain): confusion, drowsiness, visual problems, seizures, comas.

173
Q

How do you diagnose hypoglycaemia?

A

Fingerprick
Bloods: glucose, inslin, C-peptide, plasma ketones.
Take drug history and exclude liver failure.

174
Q

How do you treat hypoglycaemia?

A

Oral sugar and long-acting starch

If cannot swallow: 50% glucose.

175
Q

What is DAFNE?

A

Dose adjusted for normal eating: training for insulin administration in those with type 1 diabetes.

176
Q

What is MODY?

A

MATURITY ONSET DIABETES OF YOUNG: Rare autosomal dominant form of T2DM affecting young people

177
Q

What is gestational diabetes?

A

Diabetes during pregnancy: usually in the third trimester.

178
Q

What important structures need to be considered when operating on the thyroid gland?

A 
Superior and recurrent larygneal nerves
Trachea 
Parathyroid glands
Common carotid artery
Internal jugular vein
179
Q

What is primary hyperthyroidism?

A

An over production of thyroid hormone by the thyroid itself.

180
Q

What is secondary hyperthyroidism?

A

Condition where the thyroid is producing excessive thyroid hormone as a result of overstimulation by TSH (due to hypothalamus or pituitary dysfunction).

181
Q

What is Theyrotoxicosis?

A

An abnormal and excessive quantity of thyroid hormone in the body.

182
Q

What is Grave’s disease?

A

An autoimmune condition where TSH receptor antibodies (abnormal antibodies produced by the immune system that mimic TSH and stimulate TSH receptors on the thyroid) cause a primary hyperthyroidism.

183
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease

184
Q

What are the main causes of hyperthyroidism?

A

Grave’s disease, toxic multinodular goitre, solitary toxic thyroid nodule, thyroiditis (e.g. De Quervain’s, Hashimoto’s e.t.c)

185
Q

What is toxic multinodular goitre (Plummer’s disease)?

A

A condition where nodules develop on the thyroid gland that act independently off the normal system and continuously produce excessive thyroid hormone

186
Q

What is exopthalmos and what causes it?

A

Bulging of the eyeballs out of their socket (typical of Grave’s disease) due to inflammation, swelling and hypertrophy of the tissue behind the eyeball.

187
Q

What is pretibial myxoedema?

A

A dermatological condition where there are deposits of mucin under the skin on the anterior aspect of the skin., giving is a discoloured waxy appearance.

188
Q

What cause pretibial myxoedema?

A

A reaction to the TSH receptor antibodies in Grave’s disease

189
Q

What are the universal features of hyperthyroidism?

A 
Anxiety and irritability
Sweating/ heat intolerance
Tachycardia
Weight loss
Fatigue
Frequent loose stools
Sexual dysfunction
190
Q

What are the unique features of Grave’s disease?

A

Diffuse goitre (swelling of neck without nodules)
Graves eye disease
Bilateral exopthalmos
Pretibial Myxoedema

191
Q

What are the unique features of toxic multinodular goitre?

A

Goitre with firm nodules

Patients over 50

192
Q

What are solitary toxic thyroid nodules and how are they treated?

A

A single abnormal thyroid nodule releasing thyroid hormone (usually a benign adenoma)
Treated with surgical removal

193
Q

What is De Quervain’s Thyroiditis?

A

Viral infection that begins with hyperthyroidism.

194
Q

What is thyroid storm/ thyrotoxic crisis?

A

Rare presentation of hyperthyroidism with pyrexia, tachycardia and delirium.

195
Q

How is hyperthyroidism treated?

A 
Carbimazole 
Propylthioracil
Radioactive iodine
Beta blockers
Surgery
196
Q

What is the first line anti-thyroid drug and how long does it take to work?

A

CARBIMAZOLE: 4-8 weeks

197
Q

What happens when levels return to normal after treatment with Carbimazole?

A
  1. Maintenance levels continued
  2. Titration-block: the dose is carefully titrated to maintain normal levels
  3. Block and replace: The dose is sufficient to block all production and the patient takes levothyroxine titrated to effect.
198
Q

How does radioactive iodine work to treat hyperthyroidism?

A

A single dose of radioactive iodine is drunk. It is taken up by the thyroid gland and the emitted radiation destroys a proportion of the thyroid cells. This results in a reduction of thyroid hormone production.

199
Q

What are the main causes of hypothyroidsm?

A 
Hashimoto's thyroiditis
Iodine deficiency
Secondary to treatment of hyperthyroidism
Medications
Secondary hypothyroidism
200
Q

What is Hashimoto’s thyroitis?

A

Autoimmune inflamation of the thyroid gland causing hypothyroidism (most common cause in the developed world).

201
Q

Which medications can cause hypothyroidism?

A

Lithium –> inhibits the production of thyroid hormones in the thyroid gland.
Amiodarone–> interferes with thyroid hormone production and metabolism.

202
Q

What are secondary (central) causes of hypothyroidism?

A

Where the pituitary gland is failing to produce enough TSH. Can be due to tumours, infection, vascular or radiation.

203
Q

What are the main presentations of hypothyroidism?

A

Weight gain, fatigue, dry skin, Coarse hair and hair loss, fluid retention, heavy/ irregular periods, constipation.

204
Q

How do you manage hypothyroidism?

A

Replace thyroid hormone with titrated oral levothyroxine (synthetic T4) .

205
Q

How do you test for thyroid disease? And if positive, how do you get more information?

A

TSH screening test.

Then test T3 and T4 levels.

206
Q

What are the TSH and T3/T4 levels like in Hyperthyroidism? What is the exception?

A 
TSH= Low
T3/T4= High

Pituitary adenoma secretes TSH so levels are high.

207
Q

What are the TSH and T3/T4 levels like in primary hypothyroidism?

A 
TSH= High
T3/T4= Low
208
Q

What are the TSH and T3/T4 levels like in secondary hypothyroidism?

A 
TSH= Low
T3/T4= Low.
209
Q

What other tests can be done to test thyroid disease?

A

Antibodies
Thyroid ultrasound
Radioisotope scan

210
Q

What antibodies can be tested for to confirm thyroid disease?

A

Anti-TPO antibodies are (antibodies against the thyroid itself.)
Antithyroglobulin antibodies. (antibodies against thyroglobulin)
TSH receptor antibodies (mimic TH)

211
Q

What is the most common clinical presentation of thyroid disease?

A

Goitre ( swelling of the thyroid gland causing a visible lump in the neck)

212
Q

What does the ZONA GLOMERULOSA of the adrenal cortex produce?

A

Mineralocorticoids (e.g. Aldosterone)

213
Q

What does the ZONA FASCICULATA produce?

A

Glucocorticoids e.g. Cortisol

214
Q

What does the ZONE RETICULARIS produce?

A

Androgens (sex hormones such as testosterone)

215
Q

What does the adrenal medulla secrete?

A

Catecholamines (adrenaline and noradrenaline)

216
Q

What stimulates cortisol and androgen production by the adrenal cortex?

A

ACTH secretion from the pituitary.

217
Q

What is Cushing’s syndrome?

A

The signs and symptoms that develop after prolonged abnormal elevation of cortisol.

218
Q

What is Cushing’s disease?

A

Specific form of Cushing’s syndrome caused by a pituitary adenoma secreting excessive ACTH.

219
Q

What are the main features of Cushing’s syndrome?

A

Round in the middle with thin limbs (round face, central obesity, abdominal striae e.t.c)
High levels of stress hormone ( Hypertension, cardiac hypertrophy, hyperglyceamia, depression, insomnia)
Osteoperosis, easy bruising.

220
Q

What are the causes of Cushing’s syndrome?

A

Exogenous steroids
Cushing’s disease (pituitary adenoma)
Adrenal adenoma
Paraneoplastic Cushing’s

221
Q

What is paraneoplastic cushing’s?

A

When excess ACTH is released from a cancer (somewhere other than the pituitary) and stimulates excessive cortisol release.

222
Q

What test is used to diagnose Cushing’s disease?

A

DST test (dexamethasone suppression test)

223
Q

How does the DST test work?

A

Patient takes a dose of dexamethasone (synthetic glucocorticoid steroid) at night and their cortisol and ACTH are measured in the morning. This is used to see if dexamethasone suppresses their normal morning spike of cortisol . Patient is initially given a low dose test. If this is abnormal, a high dose test is used to differentiate between underlying causes.

224
Q

What is the low dose dexamethasone suppression test and what do the results tell you?

A

When 1mg dexamethasone is given and ACTH and cortisol levels are checked in the morning. A normal response is for dexamethasone to suppress the release of cortisol by effecting negative feedback on the hypothalamus and pituitary. If the cortisol level is not suppressed this abnormal and a high dose test needs to be used to diagnose Cushing’s

225
Q

What is the high dose dexamethasone suppression test and what do the results tell you? (Pituitary adenoma, adrenal adenoma, ectopic ACTH?)

A

8mg used after an abnormal low dose test.
In Cushing’s disease, the pituitary will still show some response and suppress cortisol and ACTH.
With an adrenal adenoma, cortisol production is independent from the pituitary so cortisol is not suppressed but ACTH is due to negative feedback.
With ectopic ACTH, neither cortisol or ACTH will be suppressed.

226
Q

What other investigations can be used to test for Cushing’s disease?

A 
24 hour urinary free cortisol 
FBC + electrolytes
MRI brain (pituitary adenoma) 
Chest CT (small cell lung cancer)
Abdominal CT (adrenal tumours)
227
Q

What is the main treatment for Cushing’s disease?

A

Remove underlying cause: surgically remove tumour.

228
Q

What is adrenal insufficiency?

A

Where the adrenal glands don’t produce enough steroid hormones (cortisol and aldosterone)

229
Q

What is the action of cortisol?

A

Main stress hormone. Stimulates gluconeogenesis (breakdown of protein and fat).
Activates antistress and anti-inflammatory pathways
Supresses immune response.

230
Q

What is the action of aldosterone?

A

Causes an increase in salt and water reabsorption in the kidney- restoring salt levels and blood pressure.

231
Q

What is Addison’s disease?

A

Condition where the adrenal glands have been damaged, causing a reduction in the cortisol and aldosterone secretion. (Primary adrenal insufficiency)

232
Q

What is the most common cause of primary adrenal insufficiency?

A

Autoimmune

233
Q

What is secondary adrenal insufficiency?

A

Low cortisol release due to inadequate ACTH levels as a result of pituitary gland damage or loss.

234
Q

What is Sheehan’s syndrome?

A

A condition where massive blood loss during childhood leads to pituitary gland necrosis.

235
Q

What is tertiary adrenal insufficiency?

A

The result of inadequate CRH release by the hypothalamus.

236
Q

What is the usual cause of tertiary adrenal insufficiency?

A

When a patient has been on long term oral steroids and then they are suddenly withdrawn, the hypothalamus does not wake up fast enough.

237
Q

What are the main symptoms of adrenal insufficiency?

A 
Fatigue
Nausea
Cramps
Abdominal pain
Reduced libido
Bronze hyperpigmentation of skin
hypotension
238
Q

What investigations can be done to test for adrenal insufficiency?

A 
Short synacthen test
Blood tests: Hyponatraemia*, hypokalamiea, early morning cortisol, ACTH
Adrenal autoantibodies (present in 80%)
CT/ MRI of adrenals
MRI of pituitary
239
Q

What is the short synacthen test?

A

Synacthen (synthetic ACTH) is given in the morning and cortisol levels are tested straight after, 30 and 60 minutes after. A failure of cortisol to rise to at least double the baseline indicates Addison’s disease.

240
Q

How do you treat adrenal insufficiency?

A

Replace steroids titrated.
HYDROCORTISONE: Replaces cortisol
FLUDROCORTISONE: Replaces aldosterone

241
Q

What is an Addisonian crisis?

A

An acute presentation of severe Addisons where an absence of steroid hormones causes a life threatening presentation.

242
Q

What are the presentation of Addisonian crisis?

A

Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkalaemia

243
Q

How is Addisonian Crisis managed?

A

Intensive monitoring
Steroids
IV fluids
Correct electrolytes.

244
Q

Where is aldosterone released from?

A

Adrenal glands

245
Q

What stimulated the release of aldosterone?

A

Angiotensin II from the RAAS system.

246
Q

What type of hormone is aldosterone?

A

A mineralocorticoid steroid hormone

247
Q

What is the actions of aldosterone?

A

Electrolyte balance:

  • Increases SODUM REABSORPTION from the distal tubule.
  • Increase POTASSIUM SECRETION from the distal tubule.
  • Increase HYDROGEN SECRETION from the collecting ducts.
248
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism- when the adrenal glands produce too much aldosterone

249
Q

What happens to serum renin in primary hyperaldosteronism?

A

It is low as it is suppressed by high blood pressure.

250
Q

What are the main causes of Conn’s syndrome?

A

Adrenal adenoma secreting aldosterone
Bilateral adrenal hyperplasia
Familial hyperaldosteronism
Adrenal carcinoma

251
Q

What is secondary hyperaldosteronism? What is the serum renin like?

A

When excessive renin stimulates the adrenal glands to produce more aldosterone- high serum high

252
Q

What are the main causes of unnecessarily high renin levels?

A

When the blood pressure is disproportionately lower than the blood pressure in the rest of the body due to:

  • Renal artery stenosis
  • Renal artery obstruction
  • Heart failure.
253
Q

What causes renal artery stenosis and how can this be diagnosed?

A

Atherosclerotic plaque causes narrowing of the vessel.

Can be confirmed with doppler ultrasound, CT angiogram or MRA

254
Q

What is the best screening tool for hyperaldosteronism?

A

Check renin and aldosterone levels and calculate renin/aldosterone ratio:
High aldosterone/low renin= primary
High aldosterone/ high renin= secondary

255
Q

What other investigations can be used to confirm Hyperaldosteronism?

A

Blood pressure
Serum electrolytes
Blood gas analysis (check for alkalosis)
CT/ MRI of adrenals

256
Q

How is hyperaldosteronism treated?

A
  • Aldosterone antagonists (Eplerenon, Spironolactine)

- Treat underlying cause (e.g. surgical removal of adenoma, precutaneous renal artery angioplasty)

257
Q

What is the most common cause of secondary hypertension?

A

Hyperaldosteronism

258
Q

What is acromegaly?

A

Clinical manifestation of excessive growth hormone (GH)

259
Q

What is the most common cuase of acromegaly?

A

Unregulated growth hormone secretion by a pituitary adenoma

260
Q

What are other potential causes of acromegaly?

A

Secondary to a cancer that secretes ectopic GHRH or GH.

261
Q

What is the main symptom of a substantial pituitary tumour?

A

Bitemporal hemianopia due to pressure on the optic chiasm.

262
Q

What are the main symptoms of acromegaly?

A
  • Headaches/ visual field defects
  • overgrowth of tissues–> Prominent forehead/brow, large nose, tongue, jaw, hands and feet
  • arthritis from imbalanced joint growth
  • Development of new skin tags
  • profuse sweating
263
Q

What other signs can GH cause?

A

Hypertrophic heart
Hypertension
Type 2 diabetes
Colorectal cancer

264
Q

Why is a random growth hormone test not helpful in investigating acromegaly?

A

GH fluctuates so may give false positives and negatives

265
Q

What investigation can be done for acromegaly?

A

IGF-1 levels
Oral glucose tolerance test whilst measuring GH
MRI brain for pituitary tumour
Visual field testing

266
Q

How is acromegaly treated?

A

Primary: trans-sphenoidal surgical removal of pituitary tumour
Secondary: surgical removal of cancer
Medication to block growth hormone–> Pegvisomant, Somatostatin analogues, Dopamine agonists.

267
Q

Why is a somatostatin analogue given?

A

Somatostatin is a growth hormone inhibiting hormone secreted by the brain, GI tract and pancreas. It blocks GH release from the pituitary gland. (Dopamine also does this on a smaller scale.)

268
Q

What things have an effect on GH secretion?

A

GHRH and Ghrelin stimulate secretion

Somatostatin and high glucose levels inhibit secretion

269
Q

How does GH exert its action?

A

Indirectly through IGF-1.

Directly on tissues such as the liver, muscle, bone or fat to induce metabolic changes.

270
Q

What is gigantism?

A

Excessive GH production in children before fusion of the epiphyses of the long bones.

271
Q

What is a prolactinoma?

A

Pituitary adenoma secreting excess prolactin

272
Q

What are the symtpoms of prolactinoma?

A

Irregular/ absent periods,
milk production
sexual dysfunction.

273
Q

Where is ADH produced and secreted from?

A

Produced in the hypothalamus and secreted from the posterior pituitary

274
Q

What is SIADH?

A

Syndrome of inappropriate Anti-Diuretic Hormone–> Excessive amounts of ADH

275
Q

What causes SIADH?

A

Posterior pituitary secreting too much ADH or a cancer (e.g. small cell lung cancer) secreting ectopic ADH.

276
Q

What does the excess ADH result in?

A

Excessive water reabsorption in the collecting ducts. This dilutes the sodium in the blood, causing hyponatreamia and high urine osmolality.

277
Q

What are the symptoms of SIADH?

A 
Non-specific:
Headache
Fatigue
Muscle aches/ cramps
Confusion
Sever hyponatraemia can cause seizures/ loss of consciousness.
278
Q

What are some of the causes of SIADH?

A 
Post operative
Infection (e.g. pneumonia, lung abscesses)
Head injury
Medications
Malignancy
Meningitis
279
Q

How is SIADH diagnosed?

A

Tests will show:

  • Euvolemia (normal volume)
  • U+E’s show hyponataemia
  • High urine sodium + osmolality.

**Diagnosis of exclusion–> exclude other causes of hyponatraemia (e.g. adrenal insufficiency)

280
Q

How is SIADH managed?

A 
Establish and treat cause:
e.g. stop causative medication. 
Correct sodium slowly.
Fluid restriction 
ADH receptor blockers--> Vaptans e.g. Tolvaptan
281
Q

What is central pontine mylinolysis?

A

Osmotic demyelination syndrome–> Complication of long term severe hyponatraemia being treated too quickly.

282
Q

Why should you correct sodium levels slowly after long term hyponatraemia?

A

As blood sodium levels fall, water moves across the blood-brain barrier, causing the brain to swell. The brain adapts to this by reducing the solutes in the brain cells so the brain does not become oedematous. THis adaptation takes a few days so if hyponatreamia has been present for a long time, the brain cells will have low osmolality. If the blood sodium levels rapidly rise, then water will rapidly shift out of brain cells and into the blood.

283
Q

What happens in the first phase of central pontine mylinolysis?

A

Patient presents as encephalopathic and confused with headache or nausea/ vomiting caused by electrolyte imbalance

284
Q

What happens in the second phase of central pontine mylinolysis?

A

Occurs after a few days–> Demyelination of neurones (especially in the pons) causes spastic quadriparesis, pseudobulbar palsy and cognitive/behavioural changed. Significant risk of death.

285
Q

What is the action of ADH on the collecting duct?

A

Binds to V2R (vasopressin receptor) where kinase actions results in the insertion of aquaporin 2 channels into the apical membrane.

286
Q

What is diabetes insipidus?

A

A lack of ADH or a lack of response to ADH, preventing the kidneys from being able to concentrate the urine.

287
Q

What are the two types of diabetes insipidus?

A

Nephrogenic and Cranial

288
Q

What happens in nephrogenic diabetes insipidus?

A

When the collecting ducts of the kidneys do not respond to ADH.

289
Q

What causes nephrogenic diabetes?

A

Drugs (lithium)
Genetic mutation
Intrinsic kidney disease
Electrolyte disturbance

290
Q

What happens in cranial diabetes insipidus?

A

When the hypothalamus does not produce ADH for the pituitary gland to secrete

291
Q

What are the main causes of cranial diabetes insipidus?

A
  • Idiopathic
  • Brain tumours
  • Head injury
  • Brain malformations
  • Brain infections
  • Brain surgery or radiotherapy
292
Q

What are the key presentations of diabetes insipidus?

A 
Polyuria
Polydipsia
Dehydration
Postural hypotension
Hypernatraemia
293
Q

How is diabetes insipidus investigated?

A

Low urine osmolality
High serum osmolality
Water deprivation test

294
Q

What is the water deprivation test?

A

Patient must avoid fluid for 8 hours. Urine osmolality measured, then Desmopressin (synthetic ADH) given. 8 hours later urine osmolality is measured again.

295
Q

What are the results of the water deprivation test in cranial diabetes insipidus?

A

After fluid deprivation–> Low urine osmolality

After desmopressin–> High urine osmolality

296
Q

What are the results of the water deprivation test in nephrogenic diabetes insipidus?

A

After deprivation–> Low

After desmopressin–> Low

297
Q

What is primary polydipsia?

A

When a patient has normally functioning ADH but are drinking excessive quantities of water leading to excessive urine production

298
Q

What are the results of the water deprivation test in primary polydipsia?

A

After deprivation–> High

After ADH–> High

299
Q

How is diabetes insipidus treated?

A

Treat underlying cause.

Desmopressin (synthetic ADH)

300
Q

What do the parathyroid glands do?

A

Produce parathyroid hormone in response to hypocalcaemia.

301
Q

Where is parathyroid hormone produced?

A

In chief cells

302
Q

What are the actions of parathyroid hormones?

A

Increase osteoclast activity in bones (reabsorb calcium)
Increase calcium absorption from the gut
Increase calcium absorption from kidneys
Increase vitamin D activity by converting it to its active forms.

303
Q

What is the action of Vitamin D?

A

Increases calcium absorption from the intestines

304
Q

What are symptoms of hypercalcaemia?

A

Renal stones, painful bones, abdominal groans (constipation/ nausea/ vomiting) and psychiatric moans (fatigue/ depression/ psychosis)

305
Q

What is primary hyperparathyroidism?

A

When a tumour of the parathyroid glands releases uncontrolled parathyroid hormone, leading hypercalcaemia.

306
Q

How is primary hyperparathyroidism treated?

A

Surgically removing tumour.

307
Q

What is secondary hyperparathyroidism?

A

When insufficient vitamin D or chronic renal failure leads to low absorption of calcium from the intestines, kidneys and bones, causing hypocalcaemia.

308
Q

How do the parathyroid glands react to secondary hyperparathyroidism and what does this cause over time?

A

Excrete more parathyroid hormone. Over time hyperplasia occurs as the number of cells increases to try and meet demand.

309
Q

How is secondary hyperparathyroidism treated?

A

Correcting vitamin D or treating renal failure (usually with renal transplant)

310
Q

What are the levels of serum calcium and parathyroid hormone like in secondary hyperparathyroidism?

A

Serum calcium = low or normal

Parathyroid hormone= High

311
Q

What is tertiary hyperparathyroidism?

A

Occurs when secondary hyperparathyroidism continues for a long period of time, leading to hyperplasia and the baseline level of PTH to increase dramatically. This means that when secondary hyperparathyroidism is treated, the PTH level remains inappropriately high. , causing hypercalcaemia.

312
Q

How is tertiary hyperparathyroidism treated?

A

By surgically removing part of the parathyroid tissue to return PTH to normal levels.

313
Q

What is the name of vitamin D’s active form in the kidney?

A

Calcitrol

314
Q

How are serum potassium levels controlled in the body?

A
  • Uptake of K+ into cells
  • Renal excretion (mainly controlled by aldosterone)
  • Extrarenal losses (e.g GI)
315
Q

What constitutes as hyperkalaemia?

A

> 5.5mmol/mol

>6.5 mmol/mol =MEDICAL EMERGENCY

316
Q

What are the most common causes of hyperkalaemia?

A

Renal impairment

Drug interference with K+ excretion (e.g. ACE inhibitors with potassium sparing diuretics of NSAIDS)

317
Q

What does the level of K+ in the blood determine and what happens when it rises?

A

Determines the excitability of nerve and muscle cells–> When levels rise, it reduces the electrical potential difference, meaning the threshold for action potential is significantly decreased, causing abnormal action potential and therefore abnormal heart rhythms causing ventricular fibrillation and cardiac arrest.

318
Q

What are the key presentations of hyperkalaemia?

A

Asymptomatic until K+ is high enough to cause cardiac arrest.
Fast irregular pulse, chest pain, weakness, light headedness
Muscle weakness and fatigue

319
Q

How is hyperkalcaemia treated in non-urgent cases?

A

Treat underlying cause

Dietary K+ restriction

320
Q

How is hyperkalcaemia treated in urgent cases?

A

Stabilise cardica membrane—>calcium Gluconate

Drive K+ into cells–> Give soluble insulin with glucose and salbutamol.

321
Q

What constitutes as hypokalaemia?

A

Serum K+ <3.5 mmol/L

<2.5= MEDICAL EMERGENCY

322
Q

What is the most common cause of chronic hypokalaemia?

A

Increased renal excretion due to diuretic treatment (e.g. thiazides or loop diuretics)

323
Q

What are the main clinical presentations of hypokalaemia?

A

Usually asymptomatic

Muscle weakness, craps, constipation, tetany, e.t.c

324
Q

How is hypokalaemia diagnosed?

A

Serum K+

ECG

325
Q

How is hypokalaemia treated?

A

Treat underlying cause

Usually resolves on its own but can give K+ supplements.

326
Q

What are neuroendocrine tumours?

A

Tumours that form from cells that release hormones into the blood in response to a signal from the nervous system.

327
Q

What are the 3 vital presenting signs for diagnosing neuroendocrine tumours?

A
  1. Pressure on local structures (e.g headaches, bitemporal hemianopia)
  2. Pressure on normal pituitary
  3. Functioning tumour
328
Q

What are the 3 main neuroendocrine tumours?

A

Prolactinoma–> Adenoma of pituitary gland producing prolactin
Pheochromocytoma–> Adrenaline secreting tumour
Carcinoid–> Seretonin secreting tumour.

329
Q

What are the risk factors for developing a neuroendocrine tumour?

A

Inherited conditions:
MEN1
Neurofibromatosis type 1
Von-Hippel Linadu syndrome

330
Q

What is a phaeochromocytoma?

A

A Catacholamine (adrenaline) secreting tumour of the adrenal glands

331
Q

Where is adrenaline produced?

A

By Chromaffin cells in the adrenal medulla of the adrenal glands.

332
Q

What happens to adrenaline secretion in patients with phaeochromocytoma?

A

It tends to be secreted in bursts giving periods of worse symptoms followed by settled periods.

333
Q

How is phaeochromocytoma diagnosed?

A

24 hour urine catecholamines

Plasma free metanephrines

334
Q

What are the main presentations of phaeochromocytoma’s?

A

Fluctuating symptoms:

Anxiety, Sweating, headache, hypertension, palpitations, tachycardia, paroxysmal atrial fibirllation

335
Q

How is a phaeochromocytoma treated?

A

Alpha blockers, Beta blockers, Adrenalectomy.

336
Q

What hormones are involved in appetite regulation and what do they do?

A

Ghrelin–> Stimulates appetite
Leptin–> Switches off appetite
Cholecystokinin–> Causes satiety via vagus
Peptide YY–> Reduced appetite and inhibits gastric motility

337
Q

What is precocious puberty?

A

Early on set puberty (before 8 girls, 9 boys)

338
Q

What causes precocious puberty?

A

Idiopathic, CNS tumours/ disorders, psychosocial

339
Q

How is precocious puberty treated?

A

WIth GnRH super-agonist to supress pulsality of GnRH

340
Q

What is precocious ‘pseudo’puberty?

A

When a hCG producing tumour tiggers puberty without pituitary of hypothalamus action.

341
Q

How can you test to see if its true or pseudo precocious puberty?

A

Give GnRH–> If LH/ FSH rise then its true.

342
Q

What is adrenarche?

A

Peri-pubertal activation of adrenal androgen production/ maturation of adrenal glands

343
Q

What is the sign of puberty onset for girls?

A

Menarche- first period

344
Q

What is the first sign of puberty for boys?

A

First ejaculation- often nocturnal

345
Q

What is the scale used to measure pubertal developments?

A

Tanner stages

346
Q

What is therlarche?

A

Breast development- first visible change of puberty

347
Q

When is it classed as delayed puberty and what are the consequences?

A

Absence of secondary sexual characteristics by 14 (girls)/ 16 (boys). Leads to reduced peak bone mass and osteoporosis.

PHASE 2A (Mine) (15 decks)

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