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Phase 2 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the main components of the end crime system

A 
Pituitary 
Thyroid 
Parathyroid 
Adrenal glands 
Pancreas 
Ovary 
Testes
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2
Q

What is endocrinology

A

Study of hormones (And gland of origin), their receptors, their intracellular signalling pathways and their associated disease

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3
Q

What is an endocrine gland

A

A gland that pours hormones into the bloodstream

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4
Q

What is an exocrine gland

A

A gland that pours secretions through a duct to a site of action

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5
Q

Define paracrine

A

Acting on adjacent cells

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6
Q

Define Autocrine

A

Feedback on same cell that secreted that hormone

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7
Q

How are water soluble hormones transported

A

Unbound

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8
Q

How are fat soluble hormones transported

A

Protein bound

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9
Q

Where do water soluble hormones interact with target cell

A

Bind to a surface receptor

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10
Q

Where do fat soluble hormones interact with target cell

A

Diffuse into cell and bind to receptors in the cytoplasm

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11
Q

What is the half life of water soluble and fat soluble hormones

A

Water soluble = short

Fat soluble = long

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12
Q

What is the clearance rate of water soluble hormones and fat soluble hormones

A

Water soluble = Fast

Fat soluble = Slow

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13
Q

What is an example of a water soluble hormone

A

Peptides (TRH, LH and FSH) and monoamines

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14
Q

What is an example of a fat soluble hormone

A

Thyroid hormones and steroids (Cortisol)

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15
Q

Where are water soluble hormones stored

A

In vesicles

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16
Q

Where are fat soluble hormones stored

A

Synthesised on demand not stored

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17
Q

What are the different hormone classes

A 
Peptides
Amines 
Iodothryonines 
Cholesterol derivatives 
Steroids
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18
Q

Give an example of a peptide hormone and name some of its properties

A

INSULIN
Stored in granules
Water soluble
Released in pulses

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19
Q

Describe the synthesis, packaging, storage and secretion of a peptide hormone

A 
Synthesis = preprohormone to pro hormone 
Packaging = pro hormone to hormone 
Storage= hormone 
Secretion = hormone
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20
Q

Give an example of an amine hormone

A

Adrenaline, noradrenaline, dopamine

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21
Q

What is the precursor molecule for Amine hormones and describe the pathway for noradrenaline synthesis

A

Phenylalanine –> L-tyrosine –> L-DOPA –> Dopamine –> Nad –> AD

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22
Q

What enzyme is required to convert noradrenaline into adrenaline

A

Catechol-O-methyl-transferase

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23
Q

Why do iodothyronines need to be bound to proteins and what protein are they bound to

A

Because they are not water soluble

Thyroid binding globulin

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24
Q

Where are the hormone receptors located

A

Cell wall for peptides
Cytoplasm for steroids
Nucleus for thyroid hormones

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25
Q

What controls the action of a hormone

A
  1. Hormone metabolism - increased metabolism reduces function
  2. Hormone receptor induction
  3. Hormone receptor down regulation
  4. Syngergism
  5. Antagonism
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26
Q

what are the hypophysiotropic hormones that move down the hypothalmaic-axis to the anterior pituitary

A

Corticotropin releasing hormone

Growth hormone releasing hormone

Thyrotropin releasing hormone

Gonadotropin releasing hormone

Dopamine

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27
Q

What are the 6 Peptide hormones secreted by the anterior pituitary (FLATPIG)

A 
FSH
LH
ACTH
TSH
Prolactin 
GH
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28
Q

What are the 5 different cell types in the anterior pituitary

A 
Gonadotrophs 
Corticotrophs 
Thyrotrophs 
Lactotrophs 
Somatotrophs
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29
Q

Prolactin secretion is inhibited by what

A

Dopamine

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30
Q

Which two peptide hormones are stored in the posterior pituitary

A

Oxytocin and ADH

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31
Q

Which hypothalamic cell type synthesises ADH

A

Supra-optic nucleus

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32
Q

Which hypothalamic cell type synthesises oxytocin

A

Paraventricular nucleus

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33
Q

What are the two main functions of oxytocin

A
  1. Ejection of milk during breast feeding

2. Stimulates the contraction of the uterine smooth muscle during labour

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34
Q

On what sort of receptor do all pituitary and hypothalamic hormones act on

A

GPCRs

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35
Q

Which stimuli causes the release of ADH

A 
Drop in blood pressure 
Increase in blood osmolality 
Nausea 
Vomiting 
Exercise 
Stress
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36
Q

What stimuli inhibit the release of ADH

A

Caffeine

Alcohol

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37
Q

What are the functions of thyroid hormone

A 
Accelerate food metabolism 
Increase protein synthesis 
Stimulation of CHO metabolism 
Enhance fat metabolism 
Increase ventilation rate 
increase Cardiac output 
Brain development during foetal life 
Acceleration of growth rate
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38
Q

What is the effect of leptin and insulin on appetite

A

Have a net effect of increasing satiety and reducing appetite

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39
Q

What is the effect of gherkin on appetite

A

Increases appetite and stimulates food intake

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40
Q

When is parathyroid hormone released?

A

In response to a decrease in serum calcium

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41
Q

What are the effects of an increase in parathyroid hormone secretion

A
  1. Increase Ca2+ absorption in kidney
  2. Increase bone resorption
  3. Increase Ca2+ reabsorption from the gut
  4. Increase alpha hydroxylation of 25-OH bit D (Calcitriol) in the kidney
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42
Q

What is the set point for serum calcium

A

1.1mmol/l

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43
Q

Why is It important that calcium levels are regulated

A

Important for function of nerves and muscles as dysregulatedcalcium leads to ECG chnages with depolarisation and depolarisation moving closer or further apart

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44
Q

Describe what happens to vitamin D when it is absorbed from sunlight

A

Hydroxlated in the liver to 25-hydroxy vitamin D where it is taken to the kidney and hydroxylated again to form 1,25-(OH) D = calcitriol

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45
Q

What stimulates the release of calcitriol

A

Low plasma Ca2+
Low plasma phosphate
PTH

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46
Q

What is the effect of calcitriol

A

INCREASE Ca2+ levels
increase Ca2+ and phosphate absorption in the gut
Inhibit PTH release
Enhanced bone turnover
increased Ca2+ and phosphate reabsorption by the kidneys

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47
Q

How do correct for calcium

A

Serum calcium + 0.02 * (40-serum albumin)

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48
Q

What are the consequences of hypocalcaemia

A 
Parathesia (Numbness and tingling)
Muscle spasm (Hands, feet, larynx)
Seizures 
Basal ganglia calcification 
Cataracts 
Long QT interval on ECG 
Chvostek's sign 
Trosseau's sign
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49
Q

What is Chvosteks sign

A

Sign of neuromuscular irritability - tap over the facial nerve and look for spasms of the ipsilateral facial muscle

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50
Q

What is Trosseau’s Sign

A

Inflate the blood pressure cuff to 20mmHg above systolic for 5 minutes which causes carpopedal spasm

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51
Q

What are the causes of hypocalcaemia

A

Vitamin D deficiency

Hypoparathyroidism

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52
Q

What are the causes of hypoparathyroidism

A
  1. Syndromes ie. Di George
    Genetic
  2. Surgical ie. surgery to the neck such as thyroid or cancer
  3. Radiation - cancer treatment
  4. Autoimmune - isolated against parathyroid gland or polyglandular
  5. Infiltration - haemochromatosis (iron) or Wilsons Disease (Copper)
  6. Magesium deficiency
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53
Q

What happens in hypoparathyroidism

A
  1. Decreased PTH
  2. Decreased renal Ca2+ absorption
  3. Increased renal phosphate reabsorption
  4. Decreased bone resorption
  5. Decreased formation of 1,25-OH 2D leading to decreased intestinal calcium absorption
    6 = decreased serum calcium
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54
Q

What happens in pseudohypoparathyroidism

A

Resistance to PTH so get no calcium metabolism response ie

  • No increases in bone resorption
  • no increased Ca2+ absorption in the gut
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55
Q

What are the symptoms of pseudohypoparathyroidism

A 
Short stature 
Obesity 
Round facies 
Mild learning difficulties
Subcutaneous ossification 
SHORT 4th METACARPAL
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56
Q

What are the symptoms of hypercalcaemia

A 
Thirst 
Polyuria 
Nausea 
Constipation 
Confusion leading to coma 
Renal stones 
ECG abnormalities = short QT
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57
Q

What are the most common causes of hypercalcaemia

A
  1. Malignancy including bone mets which destroy bone and release calcium, myeloma, PTH releasing protein secreting tumours, lymphoma full of macrophages that convert Via D to 1,25 via D
  2. Primary Hyperparathyroidism
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58
Q

What are the other causes of hypercalcaemia

A 
Thiazides 
Thyrotoxicosis 
Sarcoidosis 
Familial hypocalciuric 
Immobilisation
Milk-alkali 
Adrenal insufficiency 
Phaechromocytoma
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59
Q

What are the consequences of primary hyperparathyroidism

A

BONES = osteitis fibres cystic and osteoporosis
Kidney/biliary STONES
Psychic GROANS = confusion
Abdominal MOANS = constipation and acute pancreatitis
polyuria

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60
Q

What is the main cause of primary hyperparathyroidism

A

Single benign adenoma on one of the parathyroid glands

More rarely caused by 4 gland hyperplasia disease

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61
Q

What are the mechanism of hyperparathyroidism

A
  1. Increased PTH
  2. Increase bone resorption
  3. Increase renal reabsorption of calcium
  4. Increased calcium absorption
    5 = hypercalcaemia
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62
Q

Where might you see patients with tertiary hyperparathyroidism

A

In patients with renal disease because renal failure means they cant activate Via D so cant absorb calcium leading to hypocalcaemia, this leads to increased PTH secretion and PT glands become hyperplasic and autonomous leading to hypercalcaemia

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63
Q

Where does the pituitary lie in terms of the BBB

A

Pituitary lies outside the BBB

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64
Q

How does the anterior pituitary receive a blood supply?

A

Receives blood through a portal venous circulation from the hypothalamus called the hypathalmo-hypophyseal portal veins

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65
Q

What are the 5 hormone producing cell types in the anterior pituitary

A 
Somatotrophs 
Lactotrophs 
Gonadotrophs 
Thyrotrophs 
Corticotrophs
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66
Q

Describe the thyroid axis of the anterior pituitary

A

Thyrotropin releasing hormone passes down the hypothalamic axis to the anterior pituitary where it acts on thyrotroph cells to released TSH. TSH causes the release of T4 and T3 from the thyroid

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67
Q

Which thyroid hormone is the active form

A

T3 is the active form so T4 needs to be deiodinated to become active

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68
Q

Describe the gonadal axis of the anterior pituitary

A

Hypothalamus releases gonadotrophin releasing hormone that acts on the anterior pituitary gonadotroph cells to release LH and FSH

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69
Q

Which two hormones potentiate the release of LH and FSH from the anterior pituitary

A

Inhibin and testosterone

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70
Q

Describe the HPA axis of the anterior pituitary

A

Corticotrophin releasing hormone released from the hypothalamus act on the anterior pituitary to cause the release of ACTH which acts on the adrenal glands to cause the release of cortisol

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71
Q

Describe the GH/IGF-I axis of the anterior pituitary

A

GHRH (Promotes) and somatostatin (Inhibits) are released from the hypothalamus and either cause or inhibit the release of GH from the anterior pituitary which causes the release of IGF-I from the liver

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72
Q

Describe the dopamine axis of the hypothalamus

A

Dopamine released from the hypothalamus inhibits the release of prolactin from the lactotrophs of the anterior pituitary

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73
Q

What are the 6 different presentations of pituitary disease

A
  1. Benign pituitary adenoma
  2. Craniopharyngioma (Common in children and affects appetite)
  3. Trauma
  4. Apoplexy (Bleed into pituitary causing pituitary expansion reducing the function of nearby structures
  5. /Sheehans (During pregnancy the pituitary expands and drop in blood pressure causes the pituitary to infarct
  6. Sarcoid/TB
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74
Q

What can pituitary tumours cause

A
  1. Pressure on local structures (Optic chiasm (Bitemporal hemianopia) or oculomotor nerves - large tumour can compress brainstem or cause CSF leak)
  2. Pressure on normal pituitary = HYPOpituitarism (Lack of pituitary function)
  3. High functioning tumour (HYPERpituitarism)
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75
Q

What does hypopituitarism cause in males

A

Paleness due to loss of testosterone and ACTH

No body hair

Central obesity

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76
Q

What does hypopituitarism cause in females

A

Loose body hair

Sallow complexion

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77
Q

What does hyperpituitarism cause

A
  1. Prolactinoma = increased prolactin = increased milk production and reduced fertility
  2. Acromegaly and gigantism
  3. Cushing’s Disease
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78
Q

What are the three layers of the adrenal cortex

GFR = Makes Good Sex

A

Zona glomerulosa = Mineralocorticoids (Aldosterone)

Zona Fasciculata = glucocorticoids (Cortisol)

Zona Reticularis = Androgens

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79
Q

What is Cushing’s disease?

A

Chronic, elevated and inappropriate elevated levels of circulating plasma glucocorticoids (Cortisol) due to innapropriate ACTH secretion from pituitary tumour

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80
Q

What are the functions of cortisol

A 
Increased carbo and protein breakdown 
Increased deposition of fat and glycogen 
Na+ Retention 
Increased renal K+ loss 
Diminished host response to infection
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81
Q

What is the most common cause of Cushing’s disease

A

Excess endogenous glucocorticoids

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82
Q

What are the clinical features of Cushing’s Disease

A
  1. Child puts on weight but loses height
  2. Obesity - fat redistributed to central trunk (Buffalo hump)
  3. Repeated skin brushing
  4. Thinned scalp hair
  5. Hirsutism
  6. Acne
  7. Facial plethora (Ruddy and swollen)
  8. Moon face
  9. Gonadal dysfunction (Irregular periods and erectile dysfunction)
  10. Purple striae on abdomen, breasts and thighs
  11. Impaired glucose tolerance
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83
Q

What are the causes of Cushing’s Disease

A
  1. Exogenous steroids
  2. Tumour of pituitary producing too much ACTH = too much cortisol
  3. Ectopic tumour in the lung producing too much ACTH
  4. Adrenal tumour making too much cortisol
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84
Q

What are the ACTH dependent causes of Cushing’s disease

A
  1. ACTH secreting pituitary adenomA

2. ECTOPIC ACTH syndrome ie. Small cell lung cancer and carcinoid tumours

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85
Q

What are the ACTH independent causes of Cushing’s disease

A

Adrenal adenoma which is a cancer of the adrenal gland that releases cortisol

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86
Q

What are the three main tests used in the diagnosis of Cushing’s Disease?

A
  1. urinary free cortisol = Cortisol usually bound to albumin so when binding capacity is exceeded the cortisol will spill into the urine
  2. Low dose dexamethosone suppression test = give synthetic sterioids that suppresses pituitary and adrenal and measure the cortisol levels - in healthy patient the dexamethasone causes negative feedback causing decreased ACTH and cortisol, in Cushing’s disease there will be no suppression
  3. Late night/midnight serum or salivary cortisol
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87
Q

What is the surgical treatment for Cushing’s disease

A

Transphenoidal surgery to remove the pituitary tumour

Bilateral adrenalectomy

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88
Q

What is the surgical treatment for an ectopic tumour causing Cushing’s

A

Remove the source - bilateral adrenalectomy

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89
Q

What is the surgical treatment for Adrenal adenoma

A

Adrenalectomy

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90
Q

What is the radiotherapy treatment option for Cushing’s disease

A

Adjuvant (primary) therapy

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91
Q

Which hormone inhibits the release of GH

A

Somatostatin

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92
Q

Which hormone increases the release of GH

A

Growth hormone release hormone

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93
Q

How does a growth hormone secreting tumour lead to the clinical features of acromegaly

A

GH causes the release of IGF-I from the liver which leads to the enlargement of parts of the body including large extremities and increased height before fusion of the epiphyses

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94
Q

What is gigantism

A

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

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95
Q

What is acromegaly

A

Excess GH in adults

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96
Q

What is the cause of acromegaly and gigantism

A

benign pituitary GH producing adenoma which causes increased GH secretion which causes increased IGF-I release from the liver which further stimulates skeletal and soft tissue growth

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97
Q

What are the co-morbidities associated with acromegaly

A 
Hypertension and heart disease 
Sleep apnoea 
Cerebrovascular events 
Arthritis 
Insulin resistant diabetes
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98
Q

How do we diagnose acromegaly

A

clinical features
GH
IGF-I

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99
Q

What are the clinical features of acromegaly

A
  1. Acral enlargement (increased size of hands and feet)
  2. Arthralgias
  3. Maxofacial change
  4. Excessive sweating
  5. Headache
  6. Hypogonadal symptoms
  7. Acroparathesia (Numbness and tingling of extremities
  8. Tiredness
  9. Weight gain
  10. Amenorrhoea
  11. Deep voice
  12. Goitre
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100
Q

What are the signs of acromegaly

A 
Skin darkening 
Coarsening of face and wide nose 
Prognathism 
Big supraorbital ridge
Large tongue 
Tight rings
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101
Q

How Is acromegaly diagnosed using the oral glucose tolerance test?

A

Use the glucose tolerance test - giving glucose suppresses GH release in a normal person but in acromegaly the GH secretion increases following glucose

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102
Q

What are the objectives of acromegaly treatment

A
  1. Restoration of basal GH and IGF-1 levels
  2. Relief of symptoms
  3. Reversal of visual and soft tissue changes
  4. Prevention of further skeletal deformity
  5. Normalisation of pituitary function
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103
Q

What are the treatment options for acromegaly

A

Pituitary surgery
Medical therapy
Radiotherapy

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104
Q

What are the surgical options for acromegaly

A

Removal of the tumour (transphenoidaly) leads to rapid fall in GH

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105
Q

What does the success of pituitary surgery depend on

A
  1. Size of the tumour

2. Surgeon skill level

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106
Q

What are the radiotherapy options for acromegaly

A

Stereotactic single fraction radiotherapy which uses highly specific proton beam to minimise radiation to surrounding tissues
Gamma knife
LINAC
Proton beam

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107
Q

When is conventional radiotherapy effective in acromegaly

A

When the tumour is extended and GH levels are high

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108
Q

What are the disadvantages of radiotherapy in the treatment of acromegaly

A

Delayed response
Hypopituitarism
Rare secondary tumours
Rare visual defects

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109
Q

What is the medical therapy options for acromegaly

A
  1. Dopamine agonists ie. Cabergoline which weakly controls IGF-I
  2. Somatostatin analogues ie. octreotide and lanreotide which inhibit GH release
  3. Growth hormone receptor antagonist
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110
Q

When are dopamine agonists useful?

A

In GH and prolactin co-secreting tumours as they dramatically shrink the tumour and control the secretion of GH

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111
Q

What are the advantages of dopamine agonists for acromegaly

A

No hypopituitarism
Oral administration
Rapid onset

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112
Q

What are the disadvantages of dopamine agonists for acromegaly

A

Ineffective

Side effects

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113
Q

What is prolactinoma

A

Tumour of the pituitary resulting in the excessive prolactin release - can be micro or macro adenoma

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114
Q

What are the clinical features of prolactinoma

A 
Menstrual irregularity/amenorrhoea 
Infertility 
Galactorrhea 
Low libido 
Low testosterone in men 
Erectile dysfunction 
Reduced facial hair
Visual field defects and headaches due to the local effect of the tumour
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115
Q

How do you manage prolactinoma

A

Medical rather than surgical

Dopamine agonists such as cabergolide usually shrink the macroadenoma

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116
Q

Where is the bodies clock?

A

Suprachiasmatic nuclei

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117
Q

What is Addinson’s Disease

A

Primary hypoadrenalism - destruction of the entire adrenal cortex resulting in mineralocorticoid (Aldosterone), glucocorticoid (Cortisol) and sex steroid deficiency

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118
Q

What are the causes of primary hypoadrenalism

A
  1. Autoimmune adrenalitis (Destruction of the adrenal cortex by specific antibodies)
  2. Congential adrenal hyperplasia
  3. Adrenoleukodystrophy
  4. Mets, haemorrhage and infection
  5. Infection (TB) and infiltration (Amyloid)
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119
Q

What is secondary hypoadrenalism

A

Lack of ACTH = hypopituitarism

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120
Q

What are the causes of secondary hypoadrenalism

A 
Pituitary macroadenoma 
Apoplexy 
Hypophysitis 
Met, infiltration, infection 
Radiotherapy 
Congenital
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121
Q

What are the causes of tertiary hypoadrenalism

A

Suppression of the HPA due to presence of exogenous glucocorticoids such as steroids, inhalers and creams

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122
Q

What are the symptoms Addinson’s

A 
Fatigue
Tearful
Weight loss 
Poor recovery from illness
Adrenal crisis 
Headache 
Lethargy 
Vitiligo 
Tanned skin 
Pigmentation
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123
Q

How do we diagnose Addinson’s

A

Measure cortisol and ACTH levels at 0900
If cortisol <100nmol/l then adrenal insufficiency likely
if ACTH<5ng/l = secondary
If ACTH >22ng/l = primary

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124
Q

What is the treatment for Addison’s disease

A

Hydrocortisone twice or three times daily at a dose to replace the lost cortisol levels (15-25mg)

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125
Q

What is a normal blood glucose range

A

3.5-8.0mmol/l

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126
Q

What happens in the fasting state?

A

Low blood glucose = high glucagon and low insulin

Glucose released mainly from the liver
- glycogen breakdown (Glycogenolysis)
- Gluconeogenesis
- Reduced peripheral glucose uptake
- Stimulates release of gluconeogenic precursors
- Lipolysis and muscle breakdown
Glucose is delivered to insulin independent tissues

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127
Q

What happens in the post prandial state

A

High blood glucose = high insulin and low glucagon

Glycogenolysis and gluconeogenesis are suppressed

Glucose taken up by peripheral muscle and fat cells

Lipolysis and muscle breakdown is suppressed

  • 40% glucose to liver and 60% to muscle
  • Ingested glucose helps to replenish glycogen stores in liver and muscle
  • High insulin and glucose levels suppress lipolysis and FFA levels fall
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128
Q

How is insulin secreted by B cells

A
  1. Glucose enters B cell via GLUT2 transporter and glucokinase
  2. Glucose undergoes metabolism to glucose-6-phosphate which generates ADP
  3. ADP closes the potassium channel causing depolarisation of the cell membrane
  4. Depolarisation causes calcium channels to open enabling a Ca2+ influx
  5. Insulin released from insulin secretory granules
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129
Q

How does insulin act at fat and muscle cells

A
  1. Insulin acts on the receptor
  2. Causes an intracellular cascade
  3. cascade causes GLUT4 vesicles to be moved to the plasma membrane which stimulates entry of glucose in the tissue
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130
Q

What are the effects of insulin

A
  1. Suppress hepatic glucose output (Decreased glycogenolysis and gluconeogenesis)
  2. increase glucose uptake into fat and muscle (Muscle = glycogen synth) (Fat = FFA synthesis)
  3. Suppresses lipolysis and the breakdown of muscle
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131
Q

Why does insulin have a biphasic release

A

First phase is rapid release of pre-stored insulin

if glucose levels remain high then a second phase Is initiated which takes longer as more insulin has to be synthesised

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132
Q

What are the effects of glucagon

A
  1. Increases hepatic glucose output (Increases glycogenolysis and gluconeogenesis)
  2. reduced peripheral glucose uptake
  3. Stimulate peripheral release of gluconeogeneic precursors (glycerol and AAs)
    - lipolysis
    - Muscle glycogenolysis and breakdown
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133
Q

What is diabetes mellitus

A

A disorder of carbohydrate metabolism characterised by hyperglycaemia

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134
Q

What is the defining criteria of diabetes

A

Symptoms and random plasma glucose >11mmol/l
Fasting plasma glucose >7mmol/l
No symptoms - glucose tolerance test fasting >7 or 2hr value >11

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135
Q

What is the pathogenesis of T1 diabetes

A

An insulin deficiency disease characterised by the loss of beta cells due to autoimmune destruction. Insulin deficiency leads to continued breakdown of liver glycogen producing ketones and glucose leading to glycosuria and ketonuria

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136
Q

When does the clinical onset of diabetes begin?

A

10% of beta cells remain

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137
Q

What does a failure of insulin secretion result in

A
  1. Continued liver glycogen breakdown
  2. Lipolysis and skeletal muscle breakdown producing gluconeogenic precursors
  3. Inappropriate increase in hepatic glucose output and suppression of peripheral glucose uptake
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138
Q

Describe the process of ketoacidosis

A
  1. Absence of insulin leads to hyperglycaemia and rising ketones
    This is because increased production of acetyl-CoA leads to ketone body production that exceeds the ability of the peripheral tissues to oxidise them
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139
Q

What are the causes of type 2 diabetes

A

Impaired insulin secretion and insulin resistance

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140
Q

What are the effects of impaired insulin action?

A

Reduced muscle and fat uptake of glucose after eating

Failure to suppress lipolysis and high circulating FFA’s

Abnormally high glucose output after a meal

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141
Q

What are some of the risk factors for T2 diabetes

A 
Family history 
Increasing age 
Obesity 
Lack of exercise 
Ethnicity (Middle East and SE Asia)
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142
Q

What are the two types of insulin

A

Basal insulin

Prandial/meal type insulin (Rapid Acting)

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143
Q

Individuals with T1 diabetes need what sort of insulin

A

Long acting

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144
Q

Individuals with T2 diabetes need what sort of insulin

A

Short acting

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145
Q

When is basal insulin used

A

To control blood glucose between meals and during the night to ensure that the blood glucose concentration remains between 5-7mmol/l

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146
Q

What are the advantages of basal insulin for T2 diabetics

A

Simple - adjust insulin themselves based on fasting glucose

Less risk with hypoglycaemia at night

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147
Q

What are the disadvantages of basal insulin for T2 diabetics

A

Doesn’t cover meals and are best used with long acting insulin analogues which are expensive

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148
Q

What are the advantages of pre-mixed insulin for T2 diabetics?

A

Both basal and prandial components are covered in single preparation which covers insulin requirements for most of the day

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149
Q

What are the disadvantages of pre-mixed insulin for T2 diabetics

A

Not physiological so requires a consistent meal and exercise pattern
Risk of nocturnal hypoglycaemia
Cannot separately titrate individual components

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150
Q

Define hypoglycaemia

A

Low plasma glucose causing impaired brain function <3.9mmol/l

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151
Q

What are the autonomic symptoms of hypoglycaemia

A 
Trembling 
Palpitations 
Sweating 
Anxiety 
Hunger
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152
Q

What are the neuroglycopenic symptoms of hypoglycaemia

A 
Difficulty concentrating 
Confusion 
Weakness 
Drowsiness, dizziness 
Vision changes 
Difficulty speaking
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153
Q

When blood glucose falls below 3.8mmol/l, what hormone is produced

A

Glucagon

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154
Q

When blood glucose falls below 3.5mmol/l, what hormone is produced

A

Adrenaline

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155
Q

When blood glucose falls below 3.2mmol/l what happens

A

Neuroglycopenic symptoms are observed

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156
Q

What are the risk factors for severe hypoglycaemia in T1DM

A 
History of severe episodes 
HbA1c <6.5%
Long duration of diabetes 
Renal impairment 
Extremes of age 
Impaired awareness of hypoglycaemia
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157
Q

What are the risk factors for severe hypoglycaemia in T2 diabetes

A 
Advancing age 
Cognitive impairment 
Depression 
Aggressive glycaemia treatment 
Duration of insulin therapy
Renal impairment 
Impaired awareness of hypoglycaemia
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158
Q

Describe the patient education approaches for someone with hypoglycaemia

A
  1. Discuss hypo risk factors and treatments with patient on insulin
  2. Educate patients on how to recognise and treat hypo
  3. Instruct patients to report hypo episodes to doctor
  4. consider enrolling patients with frequent hypo episodes in blood glucose awareness training programme
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159
Q

How can we treat hypoglycaemia

A

15g fast-acting carbohydrate to relieve the symptoms

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160
Q

Name the 5 types of hormone producing cell in the anterior pituitary

A 
Sommatotrophs 
Lactotrophs 
Corticotrophs 
Thyrotrophs 
Gonadotrophs
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161
Q

What are the 6 peptide hormones released from the anterior pituitary

A 
FSH
LH
TSH
GH
Prolactin 
ACTH
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162
Q

Describe the thyroid acxis

A
  1. Thyrotropin releasing hormone passes down hypothalamic axis to anterior pit where it acts on thyrotroph cells to release TSH
  2. TSH acts on the thyroid causing release of T3 and T4
  3. T3 and T4 negatively feedback to reduce the secretion of TSH and TRH
  4. T3 is the active form so T4 must be converted by de-iodinases to T3
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163
Q

Describe the HPA axis

A
  1. Corticotrophin releasing hormone released from the hypothalamus acts on the corticotrophin cells of the anterior pituitary release ACTH
  2. ACTH causes the release of cortisol from the adrenal glands
  3. ACTH switches off secretion of the pituitary and hypothalamic hormones
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164
Q

Describe the GH/IGF-I Axis

A
  1. GHRH and somatostatin are released from the hypothalamus
  2. If more GHRH is released then GH is released
  3. If more somatostatin is released there is decreased GH release
  4. GH causes the release of IGHF-I which feeds back
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165
Q

What inhibits the release of prolactin

A

Dopamine

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166
Q

What are the 5 different presentations of pituitary disease?

A
  1. Benign pituitary adenoma
  2. Craniopharyngioma
  3. Trauma
  4. Apoplexy (Bleed into pituitary causing pituitary expansion thus reducing function of nearby structures) /Sheehans (During pregnancy the pituitary expands and drop in blood pressure causes pituitary to infarct
  5. Sarcoid/TB
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167
Q

What are the 3 presentation points of a pituitary tumour

A
  1. Pressure on local structures
    - ie. optic chiasm causing bitemporal hemianopia
    - Oculomotor nerve causing eye movement difficulties
    - CSF leak/brainstem compression
  2. Pressure on normal pituitary
    - Leads to hypopituitarism
  3. High functioning tumour (Hyperpituitarism)
    - Prolactinoma
    - Acromegaly and gigantism
    - Cushings
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168
Q

What are the signs seen in a male with hypopituitarism

A

Pale due to loss of testosterone and lack of ACTH causes loss of pigment
No body hair
Central obesity

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169
Q

What are the signs seen in a female with hypopituitarism

A

Loose body hair

Sallow complexion

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170
Q

What are the three layers of the adrenal cortex

A
  1. Zona glomerulosa
  2. Zona fasciculata
  3. Zona reticularis
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171
Q

What does the zona glomerulosa produce

A

Mineralocorticoids (Aldosterone)

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172
Q

What does the Zona fasciculate produce

A

Glucocorticoids (Cortisol)

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173
Q

What does the zona reticularis produce

A

Androgens

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174
Q

What does the adrenal medulla produce

A

Catecholamines (Adrenaline and noradrenaline)

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175
Q

Define Cushing’s syndrome

A

Chronic, excessive and inappropriate elevated levels of circulation plasma cortisol (Glucocorticoid)

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176
Q

What is the normal cause of the elevated glucocorticoids seen in Cushing’s disease

A

Inappropriate ACTH secretion from the pituitary gland due to a tumour

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177
Q

What are the functions of cortisol

A 
Increased carbo and protein breakdown 
Increased deposition of fat and glycogen 
Na+ retention 
Increased renal K+ loss 
Diminished response to infection
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178
Q

Describe the clinical presentation of Cushing’s Disease

A

Obesity - fat distribution to central trunk (Buffalo hump)
Plethoric complexion (Ruddy and swollen)
Moon face
Hirsutism
Hypertension
Muscle thinning
Thinned scalp hair
Mood changes (Depression, lethargy, irritable)
Proximal weakness
Gonadal dysfunction(Irregular period and erectile dysfunction)
Failure of children to grow tall despite excess weight
Osteoporosis
Impaired glucose tolerance
Skin that bruises easily
Purple striae on abdomen, breasts and thighs

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179
Q

What can cause Cushing’s disease

A
  1. Adrenal tumour (Adenoma or carcinoma)
  2. Pituitary tumour (Cushing’s Disease)
  3. Exogenous Steroids
  4. Ectopic ACTH syndrome
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180
Q

What are the ACTH dependent causes of Cushing’s

A
  1. Cushing’s disease where there is bilateral adrenal hyperplasia from an ACTH secreting pituitary adenoma
  2. Ectopic ACTH syndrome where there is an ACTH secreting tumour elsewhere in the body normally small cell lung cancer or carcinoid tumours
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181
Q

What are the ACTH independent causes of Cushing’s Disease

A
  1. Adrenal Adenoma which is a tumour of the adrenal gland which raises cortisol production
  2. Iatrogenic causes such as administration of glucocorticoids such as prednisolone
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182
Q

Why is taking a careful drug history important in Cushing’s disease

A

Because Cushing’s can be caused by oral steroids

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183
Q

What are the diagnostic tests for Cushing’s Disease

A
  1. Urinary free cortisol
  2. Overnight Dexamethasone suppression test
  3. Late night serum/salivary cortisol
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184
Q

Describe the urinary free cortisol diagnostic test for Cushing’s

A

Cortisol is bound to albumin normally so when the binding capacity is exceeded the cortisol will spill into the urine as is the case in Cushing’s patients

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185
Q

Describe low dose dexamethasone suppression test for Cushing’s patients

A

Give patient a synthetic steroid that suppresses the pituitary and adrenal gland and then measure the cortisol levels
In healthy patient the dexamethasone causes decreased ACTH and reduced cortisol
In healthy patient there will be no suppression

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186
Q

Once a diagnosis of Cushing’s disease has been confirmed, what is the next test?

A

Measure plasma ACTH to determine whether it is ACTH independent or dependent Cushing’s disease
If ACTH is undetectable = adrenal tumour is likely
If ACTH Is detectable then distinguish between ectopic and pituitary with high dose dexamethasone or corticotrophin releasing hormone test

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187
Q

Describe the corticotrophin hormone releasing test used to determine if ACTH depend t Cushing’s has a pituitary or ectopic cause

A

Give CRH

If cortisol rises then pituitary disease, if it doesn’t then ectopic ACTH likely

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188
Q

What is the treatment for ACTH dependent Cushing’s disease

A

Surgical removal of pituitary adenoma by trans-sphenoidal surgery or bilateral adrenalectomy

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189
Q

What is the treatment for Ectopic ACTH secreting tumour

A

Remove the tumour or bilateral adrenalectomy

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190
Q

What is the treatment for an adrenal carcinoma

A

Adrenalectomy

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191
Q

Define gigantism

A

Excessive growth hormone in children before the fusion of the epiphyses of the long bones

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192
Q

Define acromegaly

A

Excess growth hormone in adults

193
Q

What are the causes of Acromegaly

A

Benign pituitary GH producing adenoma or ectopic carcinoid tumour

Increased GH from these tumours travels to the liver where it binds to receptors and increases insulin like growth factor which stimulates the skeletal and soft tissue growth giving rise to giant like appearance

194
Q

What are the co-morbidities associated with acromegaly

A 
Hypertension 
Heart disease 
Sleep apnoea 
Cerebrovascular events 
Arthritis 
Insulin resistant diabetes
195
Q

What are the symptoms of Acromegaly

A
  1. Acral enlargement (increase feet and hand size)
  2. Headaches
  3. Excessive sweating
  4. Maxillofacial changes
  5. Acroparathesia (Tingling and numbness of extremities)
  6. Arthralgias
  7. Hypogonadal symptoms
196
Q

What are the signs of acromegaly

A
  1. Skin darkening
  2. Coarsening of face and wide nose
  3. Prognathism
  4. Big supraorbital ridge
  5. Fatigue
  6. Deep voice
197
Q

What diagnostic criteria can be used to exclude acromegaly diagnosis

A

Random GH <0.4ng/ml and normal IGF-I

198
Q

Why is a high plasma value of GH non diagnostic in acromegaly

A

Because GH secretion is pulsatile and GH often increases in stress, puberty, sleep and pregnancy

199
Q

What test is used to determine acromegaly

A

Glucose tolerance test can be diagnostic if there is no suppression of glucose as glucose should normally inhibit GH release

200
Q

What are the objectives of treatment in acromegaly

A
  1. restore basal GH and IGF-I to normal
  2. Relieve symptoms
  3. Reverse visual and soft tissue changes
  4. Prevent further skeletal deformity
  5. Normalise pituitary function
201
Q

What are the surgical treatment options for acromegaly

A

Trans-sphenoidal surgery to remove tumour or correct tumour compression on surrounding structure (Optic chiasm)

202
Q

Describe the radiological approaches for treatment of acromegaly

A

Stereotactic radiotherapy provides better tumour localisation and irradiation whilst reducing damage to normal brain tissue
(Gamma knife, proton beam, LINAC)

203
Q

Describe the medical approaches to management of acromegaly

A
  1. Somatostatin Analogues (IM Octreotide and IM Lanreotide) - inhibit GH release
  2. GH receptor antagonist (Pegvisomant)
  3. Dopamine Agonist (Oral Cabergoline or oral bromocriptine) - weakly control IGF-I
204
Q

What are the effects of prolactin secretion

A

Lactation

Inhibition of GnRH which reduces LH/FSH and thus reduced oestrogen and testosterone

205
Q

What are the causes of prolactinoma

A
  1. pituitary tumour resulting in excess prolactin secretion
  2. Pituitary stalk damage causing less dopamine and less inhibition of prolactin
  3. Antidopaminergic drugs
206
Q

What is the clinical presentation of prolactinoma

A
  1. Galactorrhoea/Amenorrhoea
  2. Infertility
  3. Low libido
  4. Low testosterone
  5. Erectile dysfunction and reduced facial hair
207
Q

How do you diagnose prolactinoma

A

Measure basal prolactin levels and they will be very high

208
Q

What are the treatment options for prolactinoma

A

medical better than surgical
1. Dopamine agonists ie. Oral cabergoline or oral bromocriptine

  • Shrink the tumour
  • Shrink macro adenoma
209
Q

Where in the body is the main body clock

A

Suprachiasmatic nuclei

210
Q

What is Addison’s disease?

A

Destruction of the entire adrenal cortex resulting in mineralocorticoid, glucocorticoid and sex steroid deficiency

211
Q

What are the causes of primary adrenal insufficiency (Where the adrenal gland doesn’t work)

A 
Addisons Disease 
Autoimmune adrenalitis 
TB
Congenital adrenal hyperplasia 
Adrenoleukodystrophy
Mets (From lung, kidney and breast), haemorrhage and infection
212
Q

What are the causes of secondary adrenal insufficiency (Lack of ACTH)

A 
Hypopituitarism 
Pituitary macroadenoma 
Apoplexy 
Hypophysitis 
Mets, Haemorrhage and infection 
Congenital
213
Q

What are the causes of tertiary adrenal insufficiency (Suppression of HPA due to presence of exogenous glucocorticoids)

A

Steroids, inhalers, creams

214
Q

Describe the pathophysiology of Addisons

A

Destruction of the entire adrenal cortex resulting in reduced glucocorticoid, mineralocorticoid and sex androgen production
Reduced cortisol levels feedback to increased CRH and ACTH production causing hyperpigmentation

215
Q

Describe the clinical presentation of Addison’s disease

A 
Fatigue
Weight loss 
Poor recovery from illness 
Adrenal crisis 
Headache 
Lethargy 
Vitiligo 
Tanned skin 
Pigmentation of skin 
Diarrhoea 
Postural hypotension
216
Q

What are the diagnostic biochemical signs of Addison’s

A

Hyponatraemia and hyperkalaemia due to decreased aldosterone

Hypoglycaemia due to low cortisol

Hypoaldosteronism

Eosinophilia

217
Q

Describe the synACTHen test for diagnosing Addison’s

A

Measure cortisol before and 30 mins after IM Tetracosactide

Addison’s excluded if 30 min cortisol >550nmol/L

218
Q

Other than synACTHen, name another test for diagnosing Addison’s

A 
Adrenal antibodies 
(21 hydroxyls antibody detected in autoimmune adrenalitis)
219
Q

What is the treatment for Addison’s

A

IV hydrocortisone

Steroids 3x daily to mimic circadian rhythm

220
Q

What are the common symptoms of an adrenal crisis

A 
Hypotension and cardiovascular collapse 
Fatigue 
Fever 
Hypoglycaemia 
Hyponatraemia and hyperkalaemia
221
Q

What are the treatment options for adrenal crisis

A

Immediate hydrocortisone (100mg)
Fluid resuscitation
Fludrocortisone

222
Q

T3 is known as

A

Triiodothyronine

223
Q

T4 is known as

A

Thryoxine

224
Q

Describe the physiology of thyroid hormone production

A
  1. Circulating iodide actively transported with Na+ across basolateral membrane into follicular cells
  2. Iodide ion transported to apical membrane of follicular cell and moved into colloid
  3. In colloid, iodide oxidised to iodine which binds to tyrosine found on thyroglobulin molecules under the influence of thyroid peroxidase
  4. Tyrosine can either bind one iodine (monoiodotyrosine) or two iodine (Diiodotyrosine)
  5. When thyroid is stimulated, T1 and T2 molecules are cleaved from tyrosine backbone and join to create T3 to T4
  6. For thyroid hormones to be secreted into the blood, extensions of the colloid facing portion of follicular cells engulf portions of colloid by endocytosis
  7. TSH from pituitary stimulates movement of T3 and T4 containing colloid into secretory cells
  8. Iodated thyroglobulin is brought into contact with lysosomes and proteolysis of the thyroglobulin results in release of T3 and T4 which are able to diffuse out of the follicular cells into the blood
225
Q

Which is more prevalent, hyper or hypothyroidism

A

Hypothyroidism

226
Q

What is a goitre

A

Swelling of the thyroid gland that causes a palpable lump in front of the neck that moves up and down during swallowing

227
Q

Why does a goitre develop?

A

TSH stimulation which causes the thyroid to grow in size

228
Q

What is the most common presentation of thyroid disease

A

Goitre

229
Q

What are the 2 main causes of goitre

A
  1. Hyperthyroidism - Graves disease where there is excessive TSH receptor stimulation causing thyroid to produce more hormones and grow larger
  2. Hypothyroidism -
    Pituitary detects low thyroid levels so produces more TSH which stimulates TSH receptors on the thyroid resulting in thyroid enlargement
230
Q

Define thyrotoxicosis

A

Excess thyroid hormone in the blood

231
Q

What are the 3 mechanisms for increased production of thyroid hormone

A
  1. Overproduction of thyroid hormones (Hyperthyroidism)
  2. Leakage of pre-formed thyroid hormone (Can occur if follicular cells are destroyed by infection or autoimmune)
  3. Ingestion of excess hormone
232
Q

What are the 7 causes of hyperthyroidism?

A
  1. Grave’s disease
  2. Toxic multi nodular goitre
  3. Toxic Adenoma (Benign)
  4. Ectopic thyroid tissue
  5. Exogenous Iodine (T4 excess)
  6. De Quervain’s thyroiditis (Transient hyperthryoidism resultingg from acute inflammation of thyroid following viral infection)
  7. Drug induced (Amiodarone iodine, lithium)
233
Q

What are the causes of primary hypothyroidism

A
  1. Primary atrophic hypothyroidism (Autoimmune)
  2. Hashimoto’s thyroiditis (Autoimmune)
  3. Post-partum thyroiditis
  4. Iodine deficiency
  5. Post-thyroidectomy
  6. Drug induced (Lithium, carbimazole, amiodarone)
234
Q

What is the cause of secondary hypothyroidism

A

Hypopituitarism - reduced TSH from anterior pituitary

235
Q

What is Grave’s disease?

A

Autoimmune induced excess production of thyroid hormone

236
Q

Describe the pathophysiology of Grave’s disease

A
  1. Serum antibodies (TSHR-Ab) bind to TSH receptors in the thyroid
  2. Stimulates thyroid hormone production
  3. Results in excess secretion of thyroid hormones and hyperplasia of thyroid follicular cells
237
Q

What are the risk factors for thyroid autoimmunity

A
  1. Female
  2. Genetic - association with HLA-B8, DR3 and DR2
  3. Smoking
  4. Stress
  5. High iodine intake
238
Q

What autoimmune diseases are associated with thyroid autoimmunity

A 
T1DM 
Addison's Disease
Pernicious Anaemia 
Vitiligo 
Myasthenia Gravis
239
Q

What is the clinical presentation of Grave’s Disease

A

Swelling in neck
Red, puffy protruding eyes
Graves Opthalmopathy

240
Q

What is Grave’s Opthomalopathy

A

Retro-orbital inflammation and swelling of extra ocular muscles

  • eye discomfort
  • increased tear production
  • Photophobia
  • Exophthalmos
  • Redness
  • lid lag stare
241
Q

What is the clinical presentation of hyperthyroidism

Everything goes up

A 
Weight loss 
increased appetite
irritable
goitre
Tachycardia 
Hyperphagia 
Anxiety 
Tremor 
Heat intolerance 
sweating 
Diarrhoea 
Lid lag and stare 
menstrual disturbance 
palpitations 
Irritability 
Hyperkinesis
242
Q

What are the diagnostic tests for hyperthyroidism

A

Thyroid function tests
Thyroid antibodies
Isotope uptake scan

243
Q

What would a thyroid function test result be for someone with primary hyperthyroidism

A

increased free T3
Increased free T4
Suppressed TSH because high T3 and T4 negatively feedback to the anterior pituitary to turn of TSH production

244
Q

What would the thyroid function test result be for someone with secondary hyperthyroidism

A

Increased free T3
increased free T4
Innapropriately high TSH because the issue is with the pituitary

245
Q

What is the treatment for hyperthyroidism

A
  1. Beta blockers (propranolol) for symptoms
  2. Anti-thyroids - thionamides
    (Propylthiouracil - stops T4 to T3 conversion)
    (Carbimazole - blocks thyroid hormone biosynthesis by blocking TPO)
  3. Radioactive iodine
  4. Surgery - total thyroidectomy
246
Q

What are the 2 strategies for thionamide administration?

A

(i) Titration - give carbimazole for 4 weeks then reduce dose according to thyroid function tests
(ii) Block-replace therapy - carbimazole + thyroxine

247
Q

What are the side effects of thionamides

A

AGRANULOCTOSIS (Low WBC) (sore throat, mouth ulcers, fevers)

Rash
Arthralgia
Hepatitis 
Neuritis 
Vasculitis
248
Q

What are the effects of 131 Iodine radiotherapy

A

Emits B particles that result in ionisation of thyroid cells causing direct damage so thyroid hormone production is decreased

249
Q

What is primary hypothyroidism

A

Underactivity of the thyroid due to disease of the thyroid gland

250
Q

What is secondary hypothyroidism

A

Underactivity of the thyroid gland due to hypothalamus or pituitary disease

251
Q

What are the 5 main causes of primary hypothyroidism

A 
Primary atrophic hypothyroidism 
Hashimoto's thyroiditis 
Iodine deficiency 
Post-thyroidectomy 
Lithium
252
Q

What are the clinical symptoms of hypothyroidism

A 
Fatigue 
Weight gain 
Cold intolerance 
Constipation 
Goitre 
Hoarse voice 
Menstrual disturbance (Menorrhagia- heavy bleeding)
Muscle cramps
Tired
253
Q

What are the clinical signs of hypothyroidism (BRADYCARDIC)

A 
Bradycardia 
Ataxia 
Dry thinned hair/skin
Yawning 
Cold hands 
Ascites 
Round puffy face 
Defeated demeanour 
Immobile 
Congestive cardiac failure
254
Q

Would would the thyroid function test result be for someone with primary hypothyroidism

A

Increased TSH but low T3 and T4

255
Q

What would the thyroid function test result be for someone with secondary hypothyroidism

A

TSH inappropriately low for reduced T4/T3

256
Q

What is the treatment for hypothyroidism

A

Life long hormone replacement therapy - Oral levothyroxine

Dose needs to be titrated until TSH normalises in primary hypothyroidism - check T4 levels 6-8 weeks later

Secondary hypothyroidism then monitor T4 because TSH will always be low

257
Q

Where is vasopressin produced

A

paraventricular nucleus

258
Q

Where is oxytocin produced

A

Supra-optic nucleus

259
Q

Describe osmotic regulation

A

Osmoreceptor sends afferent projections to the PVN and SON sensing the osmolality of the blood - this determines whether they fire and release vasopressin or not

260
Q

What receptor does vasopressin bind to

A 
GPCR V1a (Vasculature)
GPCR V2 ( Renal collecting tubes)
GPCR V1b (Pituitary)
261
Q

The release of vasopressin is controlled by what 2 factors

A

(i) Osmoreceptors in the hypothalamus (Day to day)

ii) Baroreceptors in the brainstem and great vessels (Emergency

262
Q

Describe distribution of fluid in the body

A

Extracellular (14L)
- Intravascular (3.5L)
- INterstitial (10.5L)
Intracellular (28L)

263
Q

What ions are mostly prevalent In the extracellular fluid

A

Sodium
Chloride
Bicarbonate

264
Q

What ions are most prevalent in the intracellular fluid

A

Potassium
Magnesium
Phosphate

265
Q

Describes what happens in terms of fluid regulation when there is excess water

A
  1. Fall in plasma osmolality and influx of water into cells increasing intracellular water content
  2. This reduces thirst and suppresses the release of vasopressin tush’s decreasing water intake and increasing water excretion
  3. Overall effect is decrease in amount of water in the body
266
Q

What are the insensible water losses from the body each day

A

(i) 0.1L from stool
(ii) 0.1L from sweat
(iii) 0.3L from respiration
= 500ml total

267
Q

Describe the mechanism of action of vasopressin

A
  1. Vasopressin binds V2 receptors stimulating intracellular cascade
  2. Binding V2 receptors leads to activation of Gs which activates adenylate cyclase
  3. Leads to increased formation of cAMP
  4. cAMP activates pKA which phosphorylates micro tubular subunits that aggregate to form AQP2
  5. AQp2 inserted into apical membrane
  6. AQP2 enables water to be reabsorbed and returned to bloodstream
  7. When the stimulus is removed, AQP2 is removed from apical membrane by endocytosis
268
Q

Define Osmolality

A

Concentration in the plasma mOsmol/Kg)

269
Q

What is a normal plasma osmolality?

A

282-295mOsmol/kg

270
Q

How do you calculate plasma osmolality

A

2x Na+ conc + glucose conc + urea conc

271
Q

A lack of vasopressin is associated with what condition

A

Cranial diabetes insipidus

272
Q

Resistance to the action of vasopressin is associated with what condition

A

Nephrogenic diabetes insipidus

273
Q

Too much vasopressin release when it shouldn’t be released is associated with what condition

A

Syndrome of inappropriate anti-diuretic hormone secretion (SIADH)

274
Q

What are the three most common symptom seen in diabetes insipidus

A

Polyuria
Polydipsia
No glycosuria

275
Q

How do we diagnose diabetes insipidus

A

Measure 24 hour urine volume =
DI unlikely if dilute urine volume <3L/day

Water deprivation test - urine will not concentrate when asked not to drink

Serum Oslo >300 and urine Oslo <200 is consistent with DI

Normonatraemia or hypernatraemia

276
Q

What are the 6 acquired causes of cranial diabetes insipidus

A
  1. Idiopathic
  2. Tumours
  3. Trauma
  4. Infections
  5. Vascular
  6. Inflammatory
277
Q

What tumours can cause acquired diabetes inspidus

A

Craniopharyngioma
Germinoma
Metastases
Never an anterior pituitary tumour

278
Q

What infections can cause acquired diabetes inspidus

A

TB
Encephalitis
Meningitis

279
Q

What vascular conditions can cause acquired diabetes insipidus

A

Aneurysm
Infarction
Sheenan’s
Sickle Cells

280
Q

What inflammatory conditions can cause acquired diabetes insipidus

A

Neurosarcoidosis
Langerhans Histiocytosis
Guillain Barre
Granuloma

281
Q

What are the primary causes of diabetes insipidus

A

Genetic
- Wolfram syndrome
Developmental
- Septo-optic dysplasia

282
Q

What is the pathophysiology of nephrogenic diabetes insipidus

A

In X-linked there is a V2 receptor defect

In autosomal there is an aquaporin 2 defect

283
Q

What are the causes of nephrogenic diabetes insipdus

A 
Osmotic diuresis (Diabetes)
Drugs (Lithium, tetracycline)
Chronic renal impairment 
Post obstructive nephropathy 
Metabolic - hypercalcaemia/hypokalaemia 
Renal infiltration (Amyloid)
284
Q

How does the water deprivation test work

A

Don’t give the patient water - if they have DI they will still pass out dilute urine and their urine osmolality will increase

Give 2ug of desmopressin that acts at V2 receptor - kidney can respond in cranial but not in nephrogenic

285
Q

How do we manage cranial diabetes insipidus?

A

Treat underlying condition

Desmopressin - high activity at the V2 receptor analogue (Tablets, nasal spray or injection)

286
Q

How do we manage nephrogenic diabetes insipidus?

A

Avoid precipitating drugs

Free access to water alongside high dose of desmopressin

287
Q

What is normal serum sodium level

A

Between 135 and 144mmol

288
Q

What is the definition of hyponatraemia

A

Serum sodium <135mmol

Biochemically severe = serum sodium <125mmol

289
Q

Name 7 moderate symptoms of hyponatraemia

A
  1. Headache
  2. irritability
  3. Nausea and vomiting
  4. Mental slowness
  5. Unstable gait
  6. Confusion and delirium
  7. Disorientation
290
Q

Name 3 severe symptoms of hyponatraemia

A
  1. Stupor/coma
  2. Convulsions
  3. Respiratory arrest
291
Q

What are the causes of hyponatraemia

A

Hypovolaemia

Hypervolaemia

292
Q

What is syndrome of innappropriate secretion of ADH (SIADH)

A

Continued ADH secretion despite plasma being dilute leading to water retention, excess blood volume and hyponatraemia, concentrated urine

293
Q

What are the 4 different causes of SIADH (Name a few for each)

A
  1. CNS Disorders (Guillain barre, meningitis, encephalitis)
  2. Respiratory Causes (Pneumonia, TB, Severe asthma)
  3. Tumours (Lung carcinoma, prostate, thymus)
  4. Drugs (Chlorpropamide, Carbamazepine, SSRIs)
294
Q

What diagnostic signs are needed to diagnose SIADH?

A 
Low serum sodium (<135mmol/L)
High urine sodium 
Low plasma osmolality 
High urine osmolality >100mOsm/Kg
Normal circulating blood volume
295
Q

How do you manage SIADH

A
  1. treat the underlying cause
  2. Restrict fluid intake <1L/24 hour
  3. Give oral demeclocycline which induces nephrogenic diabetes (Inhibits ADH action on kidneys)
  4. If sodium <115mmol an patient is fitting then saline
  5. Selective V2 receptor oral antagonist (Tolvaptan) which promotes water excretion
296
Q

What are the different types of pituitary mass lesion

A
  1. Non functioning adenoma (Prolactinoma)
  2. Malignant pituitary tumours
  3. Metastasis in pituitary
  4. Pituitary cysts (Rathke’s cleft cyst)
  5. Developmental abnormalities (Craniopharygioma)
  6. Primary CNS tumours (Optic glioma)
  7. Vascular tumours (Hemangioblastoma)
  8. Malignant systemic disease (Hodgkins and non Hodgkins lymphoma)
  9. Granulomatous Disease (Neurosarcoidosis and tuberculosis)
297
Q

What is a craniopharyngioma

A

Arises from the squamous epithelial remnants of Rathke’s pouch

Benign tumour that does not infiltrate surrounding tissues

298
Q

What are the symptoms of craniopharyngioma

A 
Raised ICP
Visual disturbance 
Growth failure 
Pituitary hormone deficiency 
Weight increase
299
Q

What is Rathke’s Cyst

A

Derived remnants of Rathke’s pouch

300
Q

What are the symptoms of Rathke’s cyst

A

Headache
Amenorrhoea
Hypopituitarism
Hydrocephalus

301
Q

What is a meningioma?

A

Commonest tumour of region after pituitary adenoma

302
Q

What are the symptoms associated with meningioma

A

Visual disturbance, endocrine dysfunction

303
Q

What is lymphocytic adenohypophysitis

A

Inflammation of the pituitary gland due to an autoimmune reaction

304
Q

What are the local mass effect of a pituitary tumour

A
  1. Visual defects (Bitemporal hemianopia)
  2. CSF rhinorrhoea
  3. Headaches
  4. Cranial nerve palsy
305
Q

Raised TSH and low T4 would be suggestive of what condition

A

Primary hypothyroidism

306
Q

Low T4 with normal or low TSH is suggestive of what condition

A

Hypopituitarism

307
Q

Suppressed TSH with High T4 is suggestive of what condition

A

Grave’s disease

308
Q

High T4 with normal or high TSH is suggestive of what condition

A

TSHoma

309
Q

What is the definition of diabetes?

A

Symptoms and random plasma glucose >11mmol/L

Fasting plasma glucose >7mmol

No symptoms need oral glucose tolerance test fasting >7 or 2h value >11mmol/l

HbA1c 48mmol/mol

310
Q

What are the 6 common presenting features of diabetes?

A
  1. Thirst
  2. Polyuria
  3. Weight loss and fatigue
  4. Hunger
  5. Puritis vulvae and balanitis
  6. Blurred vision
311
Q

What features would be suggestive of someone with type 1 diabetes

A
  1. Onset in childhood (5-15yr)
  2. Lean body hiatus
  3. Acute onset of osmotic symptoms
  4. Prone to ketoacidosis
  5. higher levels of islet autoantibodies
312
Q

What are the clinical features of newly diagnosed T1 diabetes

A
  1. Weight loss
  2. Short history of severe symptoms
  3. urinary ketones
313
Q

What features would be suggestive of someone with type 2 diabetes

A
  1. Present in over 30’s
  2. Onset is gradual
  3. Family history
314
Q

Type 1 diabetes is associated with what autoimmune conditions

A

Hypothyroidism
Addison’s
Coeliac Disease

315
Q

What happens if T1 diabetes is missed?

A

Insulin deficiency causes continued fat breakdown leading to formation of glycerol and free fatty acids

FFA’s impair glucose uptake and are transported to the liver to provide energy for gluconeogenesis

FFA are oxidised to form ketone bodies (Beta hydroxybutyrate, acetone, acetoacetate)

Rising glucose and ketones escape into the urine and lead to osmotic diuresis and falling circulating volume

Ketones are weak organic acids and cause anorexia and vomiting and eventually lead to circulatory collapse and death

316
Q

What is the definition of diabetic ketoacidosis

A
  1. Hyperglycaemia (Plasma glucose <50mmol/l)
  2. Raised plasma ketones (Urine ketones >2+)
  3. Metabolic Acidosis (Plasma bicarbonate <15mmol/l
317
Q

What are the 4 causes of diabetic ketoacidosis

A
  1. Unknown
  2. Intercurrent illness (infection, MI)
  3. Treatment errors (Stop/reduce insulin)
  4. Previously undiagnosed diabetes
318
Q

What are the symptoms of DKA

A
  1. Develops over days
  2. Polyuria and polydipsia
  3. Nausea and vomiting
  4. Weight loss
  5. weakness
  6. Abdominal pain
  7. Drowsiness/confusion
319
Q

What are the signs of DKA

A
  1. Hyperventilation
  2. Dehydration (Loss of 5-6L)
  3. Hypotension
  4. Tachycardia
  5. Coma
320
Q

What is the biochemical diagnosis of DKA

A
  1. Hyperglycaemia (<50mmol/l)
  2. K+ high on presentation followed by drop due to acute K+ shift out the cell with acidosis then driven back into cells with drop in insulin
  3. HCO3- <15mmol/l
  4. Urea and creatine raised due to pre-renal failure
  5. Urinary ketones >2+
  6. Blood ketones >3.0
321
Q

What is the management for diabetic ketoacidosis

A
  1. Rehydration (3L in first 3hrs)
  2. Insulin
  3. Replace electrolytes
  4. Treat underlying cause
  5. Treatment must be started without delay
  6. Follow DKA hospital protocol
322
Q

What are the potential complications of DKA

A

(i) Cerebral oedema in children
(ii) Adult respiratory distress syndrome
(iii) Thromboembolism
(iv) Aspiration Pneumonia

323
Q

What are the three microvascular complications of diabetes

A
  1. Nephropathy
  2. Neuropathy
  3. Retinopathy
324
Q

What symptoms might you see if you give someone too much insulin

A
  1. Shaking
  2. Fast heartbeat
  3. Sweating
  4. Dizziness
  5. Anxious
  6. Hunger
  7. Impaired vision
  8. weakness fatigue
  9. Headache
  10. Irritable
325
Q

What is maturity onset diabetes of the young (MODY)

A

Autosomal dominant non insulin dependent diagnosed in <25yr

Single gene defect alters beta cell function

326
Q

What is transcription factor MODY

A

Where hepatic nuclear factor mutations alter insulin secretion and reduce beta cell proliferation

327
Q

Which patients are likely to be MODY

A

Pateitns with parents with diabetes

Absence of islet autoantibodies

Evidence of non insulin dependence

328
Q

What is permanent neonatal diabetes

A

Diagnosed <6 months
Mutations in the Kir6.2 and SUR1 subunits of beta ATP sensitive K+ channel - mutations prevent the closure of the channel so beta cells unable to secrete insulin

329
Q

What is maternal inherited diabetes and deafness

A

Result of mutations in mitochondrial DNA resulting in loss of beta cell mass

Similar presentation to T2 diabetes

330
Q

Name 5 diseases of the exocrine pancreas

A
  1. Inflammation
  2. Hereditay hemochromatosis (Excess iron deposition)
  3. Deposition (Amyloidosis and cystinosis)
  4. Pancreatic Neoplasia
  5. Cystic fibrosis (Viscous secretions lead to duct obstruction)
331
Q

What are the endocrine causes of diabetes

A
  1. Acromegaly
  2. Cushing’s syndrome
  3. Phaechromocytoma
332
Q

What drugs can induce diabetes

A

Glucocorticoids
Thiazides
Protease inhibitors
Antipsychotics

333
Q

Define puberty

A

Physical, morphological and behavioural changes as gonads switch from infantile to adult forms

334
Q

What are the definitive signs of puberty in the male and female

A

Male = first ejaculation

Female = menarche

335
Q

What are secondary sexual characteristics in girls

A

Ovarian oestrogen regulate the growth of breast and genitalia

Ovarian and adrenal androgens control pubic hair and axillary hair

336
Q

What are the secondary sexual characteristics in boys

A

Testicular androgens lead to external genitalia and pubic hair growth growth and enlargement of laryngeal muscles

337
Q

What is thelarche

A

Breast development induced by oestrogen

338
Q

How does the uterus change during puberty

A

Tubular to pear shape
Increase in length and volume
Endometrium thickness increases

339
Q

How do the ovaries change during puberty

A

Increase in volume

Become multi cystic

340
Q

How does the vagina change during puberty

A 
Red colour Dullens 
Epithelium thickens 
Becomes acidic 
Produces secretions 
Increases in length
341
Q

What are the effects of oestrogen on the female external genitalia

A 
Labia minora and major increase in size and thickness 
Rugation 
Hymen thickens 
Clitoris enlarges 
Vestibular glands begin secretion
342
Q

Define precocious puberty

A

Onset of secondary sexual characteristics before 8yrs (Girl) 9yrs (boy)

343
Q

Defined delayed puberty

A

Absence of secondary sexual characteristics by 14 yrs (girl) 16yrs (boy)

344
Q

In precocious puberty, brain tumours are most commonly seen in boys or girls

A

Boys

345
Q

How would you determine if an individual has precocious puberty or precocious pseudo puberty

A

GnRH test - inject GnRH and measure after the 30-60 minutes

HPG axis should become activated causing a rise in LH and FSH - in pseudo puberty, there will be no rise in Lh or FSH

346
Q

what are the causes of true precocious puberty

A

Idiopathic
CNS tumours (Optic glioma)
CNS disorders (Encephalitis)
Psychosocial

347
Q

What are the causes of precocious pseudo puberty

A

Increased androgen secretion
Gonadotrophin secreting tumours
Oestrogen secreting neoplasm

348
Q

What are the indications in girls for investigation of delayed puberty

A

(i) Lack of breast development by 13 years
(ii) More than 5 years between breast development and menarche
(iii) Lack of pubic hair by 14
(iv) Absent menarche by 15-16

349
Q

What are the indications in boys for the investigation of delayed puberty

A

(i) Lack of testicular enlargement by age 14
(ii) Lack of pubic hair by 15
(iii) More than 5 years to complete genital enlargement

350
Q

Describe primary hypogonadism in the female

A

Ovary fails so oestrogen drops - lack of feedback leads to LH and FSh increase

351
Q

Describe secondary hypogonadism in the female

A

Hypothalamus and pituitary fail so LH and FSH are low meaning there is no response to feedback leading to oestrogen decrease

352
Q

Describe primary hypogonadism in the male

A

testis fail leading testosterone to drop and the lack of feedback causes Lh and FSH to rise

353
Q

Describe secondary hypogonadism in the female

A

Hypothalamus and pituitary fail leading to low FSH and LH and no response to feedback so testosterone decreases

354
Q

Give a cause of primary hypogonadism.

A

Klinefelter’s syndrome - extra X chromosome

355
Q

What is the affect of primary hypogonadism on testosterone and FSH/LH levels?

A

Testosterone will be low.

- FSH/LH will be high.

356
Q

What is the affect of hypopituitarism on testosterone and FSH/LH levels?

A
  • Testosterone will be low.

- FSH/LH will be low.

357
Q

When should serum testosterone be measured?

A

At 9am due to circadian rhythm.

358
Q

Give 5 consequences of androgen deficiency in a male.

A
  1. Loss of libido.
  2. High pitched voice.
  3. Loss of facial, axillary, limb and pubic hair.
  4. Loss of erections.
  5. Poorly developed scrotum and penis.
359
Q

What is the treatment for hypogonadism?

A

Testosterone gel/injection.

360
Q

What syndrome is characterised by a congenital deficiency of GnRH?

A

Kallmann’s syndrome.

361
Q

Are the levels of oestradiol and FSH/LH low or high before puberty?

A

Before puberty there are very low levels of these hormones in the serum.

362
Q

What is the affect of primary ovarian failure on oestradiol and FSH/LH levels?

A
  • FSH/LH is high.

- Oestradiol is low.

363
Q

What is the function of ADH?

A

It acts on the collecting ducts of the nephron and increases insertion of aquaporin 2 channels -> there is H2O retention.

364
Q

Which has a longer half life, triiodothyronine or thyroxine?

A

Thyroxine has a half life of 5-7 days whereas triiodothyronine has a half life of only 1 day.

365
Q

What would be the effect on TSH if you had an under-active thyroid?

A

TSH would be raised as you have less T3/4 being produced and so no negative feedback.

366
Q

What would a low TSH tell you about the action of the thyroid?

A

A low TSH indicates an over-active thyroid. Lots of T4 and T3 is being produced and so there is more negative feedback on the pituitary and less TSH.

367
Q

Give 3 functions of thyroid hormones (T3/4).

A
  1. Food metabolism.
  2. Protein synthesis.
  3. Increased sympathetic action e.g. CO and HR.
  4. Heat production.
  5. Needed for growth and development.
368
Q

Give 3 functions of cortisol in response to stress.

A
  1. Mobilises energy sources -> lipolysis, gluconeogenesis and protein break down.
  2. Vasoconstriction.
  3. Suppresses inflammatory and immune repsonses.
  4. Inhibits non-essential functions e.g. growth and reproduction.
369
Q

Briefly describe the mechanism of LH and FSH.

A

Hypothalamus -> GnRH -> AP -> FSH/LH -> ovaries/testes.
FSH acts on granulosa cells to produce oestrogen and sertoli cells to stimulate spermatogenesis. LH acts on theca cells to produce androgens or leydig cells to produce testosterone

370
Q

What cells does FSH act on?

A

In the ovaries: granulosa cells.

- In the testes: sertoli cells

371
Q

What cells does LH act on?

A

In the ovaries: theca cells.

- In the testes: leydig cells.

372
Q

What is the function of theca cells?

A

Theca cells are stimulated by LH to produce androgens that diffuse into granulosa cells to be converted into oestrogen.

373
Q

What is the function of granulosa cells?

A

Granulosa cells are stimulated by FSH to convert androgens into oestrogen using aromatase.

374
Q

What is the function of sertoli cells?

A

Sertoli cells produce MIF (mullerian inhibiting factor) and inhibin and activin which acts on the pituitary gland to regulate FSH.

375
Q

What is the function of leydig cells?

A

Leydig cells are stimulated by LH to produce testosterone.

376
Q

What is the function of IGF-1?

A

It induces cell division, cartilage and skeletal growth and protein synthesis

377
Q

Describe growth hormone secretion from the anterior pituitary.

A

It is secreted in a pulsatile fashion and increases during deep sleep

378
Q

What investigations might you do on someone who you suspect has acromegaly?

A
  1. Plasma GH levels can exclude acromegaly - not diagnostic!
  2. Serum IGF-1 levels raised.
  3. Oral glucose tolerance test - diagnostic!
  4. MRI of pituitary.
379
Q

Give 3 potential complications of trans-sphenoidal surgical resection for the treatment of acromegaly.

A
  1. Hypopituitarism.
  2. Diabetes insipidus.
  3. Haemorrhage.
  4. CNS injury.
  5. Meningitis.
380
Q

Hypothyroidism: name 3 anti-bodies that may be present in the serum in someone with autoimmune thyroiditis.

A
  1. TPO (thyroid peroxidase).
  2. Thyroglobulin.
  3. TSH receptor.
381
Q

Give 2 examples of iatrogenic causes of hypothyroidism.

A
  1. Thyroidectomy.

2. Radioiodine therapy.

382
Q

Name 3 drugs that can cause hypothyroidism.

A
  1. Carbimazole (used to treat hyperthyroidism).
  2. Amiodarone.
  3. Lithium.
383
Q

Why can amiodarone cause hypo/hyperthyroidism?

A

Because it is iodine rich.

384
Q

Give 5 causes of thyrotoxicosis.

A

Thyrotoxicosis - excess thyroid hormone due to any cause:

  1. Increased production e.g. Grave’s, toxic adenoma.
  2. Leakage of T3/4 due to follicular damage.
  3. Ingestion.
  4. Thyroiditis.
  5. Drug induced
385
Q

Give 5 signs of Grave’s disease that don’t include opthalmopathy signs.

A
  1. Tachycardia.
  2. Arrhythmias e.g. AF.
  3. Warm peripheries.
  4. Muscle spasm.
  5. Pre-tibial myxoedema (raised purple lesions over the shins).
  6. Thyroid acropachy (clubbing and swollen fingers).
386
Q

With what disease would you associated pre-tibial myxoedema and thyroid acropachy?

A

Grave’s disease.

387
Q

What would you see histologically in someone with Grave’s disease?

A

Lymphocyte infiltration and thyroid follicle destruction.

388
Q

Give 3 potential complications of a partial thyroidectomy.

A
  1. Bleeding.
  2. Hypocalcaemia.
  3. Hypothyroidism.
  4. Recurrent laryngeal nerve palsy
389
Q

Give 5 metabolic changes that occur in pregnancy.

A
  1. Increased EPO, cortisol and NAd.
  2. High CO.
  3. High cholesterol and triglycerides.
  4. Pro thrombotic and inflammatory state.
  5. Insulin resistance.
390
Q

Give 5 gestational syndromes.

A
  1. Pre-eclampsia.
  2. Gestational diabetes.
  3. Obstetric cholestasis.
  4. Gestational thyrotoxicosis.
  5. Postnatal depression.
  6. Post partum thyroiditis
391
Q

At what week are foetal thyroid follicles and T4 synthesised?

A

Week 10.

392
Q

Why can hCG activate TSH receptors and cause hyperthyroidism?

A

HCG and TSH are glycoprotein hormones with very similar structures. HCG can therefore activate TSH receptors

393
Q

Is hypothyroidism or thyrotoxicosis more common in pregnancy?

A

Hypothyroidism is more common in pregnancy.

394
Q

How can you differentiate between Grave’s disease and gestational thyrotoxicosis?

A
  • Grave’s: symptoms predate pregnancy; symptoms are severe during pregnancy; goitre and TSH-R antibodies present.
  • Gestational thyrotoxicosis: symptoms do not predate pregnancy; lots of N/V - hyperemesis gravidarum associated. No goitre or TSH-R antibodies.
395
Q

Give 3 potential consequences of untreated hypothyroidism in pregnancy.

A
  1. Gestational hypertension.
  2. Placental abruption.
  3. Post partum haemorrhage,
  4. Low birth weight.
  5. Neonatal goitre.
396
Q

Give 3 potential consequences of untreated hyperthyroidism in pregnancy.

A
  1. Intra-uterine growth restriction.
  2. Low birth weight.
  3. Pre-eclampsia.
  4. Risk of still birth/miscarriage
397
Q

How many carbon precursors are needed for gluconeogenesis?

A

3.

398
Q

A diagnosis of diabetes can be made by measuring plasma glucose levels. What would the results of the oral glucose tolerance test be if someone was diabetic?

A

Fasting plasma glucose >7mmol/L and 2-hour value >11mmol/L.

399
Q

What might someone’s HbA1c be if they have diabetes?

A

> 48mmol/mol.

400
Q

What is the affect of cortisol on insulin and glucagon?

A

Cortisol inhibits insulin and activates glucagon.

401
Q

T1DM is characterised by impaired insulin secretion. Describe the pathophysiological consequence of this.

A

Severe insulin deficiency -> glycogenolysis/gluconeogensis/lipolysis all not suppressed AND reduced peripheral glucose uptake -> hyperglycaemia and glycosuria.
Perceived stress -> cortisol and Ad secretion -> catabolic state -> increased plasma ketones.

402
Q

Describe the pathophysiology of diabetic ketoacidosis.

A

No insulin -> lipolysis -> FFA’s -> oxidised in liver -> ketone bodies -> ketoacidosis.

403
Q

Name 3 ketone bodies.

A
  • acetoacetate.
  • acetone.
  • beta hydroxybutyrate.
404
Q

What is the affect of primary adrenal insufficiency on cortisol and ACTH levels?

A
  • Cortisol is low.

- ACTH is high.

405
Q

What is the affect of hypopituitarism on cortisol and ACTH levels?

A
  • Cortisol is low.

- ACTH is low.

406
Q

What can lead to elevated levels of prolactin?

A
  1. Stress.
  2. Drugs.
  3. Pressure on the pituitary stalk.
407
Q

Give 5 signs of diabetes insipidus.

A
  1. Excessive urine production (>3L/24h).
  2. Very dilute urine - <300 mOsmol/Kg.
  3. Severe thirst.
  4. Hypernatraemia.
  5. Dehydration.
408
Q

What is the treatment for neurological diabetes insipidus?

A

Desmopression.

409
Q

Give 4 causes of polyuria.

A
  1. Hypokalaemia.
  2. Hypercalcaemia.
  3. Hyperglycaemia.
  4. Diabetes insipidus.
410
Q

What is Cushing’s disease?

A

A set of signs/symptoms resulting from inappropriate ACTH secretion from the pituitary.
ACTH dependent.

411
Q

What is the treatment for Cushing’s syndrome?

A
  1. Surgical removal of pituitary tumours.

2. Drugs to inhibit cortisol synthesis e.g. metyrapone, ketoconazole.

412
Q

Give 3 symptoms of SIADH.

A
  1. Anorexia.
  2. Nausea.
  3. Malaise.
  4. Headache.
  5. Confusion.
413
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism - high aldosterone levels independent of RAAS activation -> H2O and sodium retention and potassium excretion.

414
Q

What are the 2 main signs of Conn’s syndrome?

A
  1. Hypertension.
  2. Hypokalaemia.
    Sodium will be normal or slightly raised.
415
Q

Give 3 symptoms of Conn’s syndrome. A deficiency in which electrolyte causes these symptoms?

A
  1. Muscle weakness.
  2. Tiredness.
  3. Polyuria.
    Due to potassium deficiency - hypokalaemia.
416
Q

What can cause Conn’s syndrome?

A

Adrenal adenoma.

417
Q

What hormone is raised in Conn’s syndrome and what hormone is reduced? Where are these hormones synthesised?

A
  1. Aldosterone is raised - synthesised in the zona glomerulosa.
  2. Renin is reduced - synthesised by the juxta-glomerular cells.
418
Q

What investigations might you do in someone to confirm a diagnosis of Conn’s syndrome?

A
  1. Bloods - U+E, renin (low) and aldosterone (high).
  2. Plasma aldosterone renin ratio can be used as an initial screening test - raised ratio indicates the need for further tests.
419
Q

Give 4 ECG changes that you might see in someone with Conn’s syndrome.

A
  1. Increased amplitude and width of P waves.
  2. Flat T waves.
  3. ST depression.
  4. Prolonged QT interval.
  5. U waves.
420
Q

What is the treatment for Conn’s syndrome?

A
  1. Laparoscopic adrenalectomy.

2. Spironolactone (aldosterone antagonist).

421
Q

Describe the treatment for hyperparathyroidism.

A
  1. High fluid intake, low calcium diet.
  2. Excision of adenoma.
  3. Correct underlying cause.
  4. Parathyroidectomy.
422
Q

Give 5 symptoms of hypoparathryoidism.

A

Hypoparathyroidism -> hypocalcaemia:

  1. Spasm.
  2. Paraesthesia around mouth and lips.
  3. Anxious/irritable.
  4. Seizures.
  5. Increased muscle tone.
  6. Confusion.
  7. Dermatitis.
  8. Impetigo herpetiformis.
  9. QT prolongation
423
Q

What is the treatment for hypoparathyroidism?

A

Calcium supplements.

424
Q

Give 5 causes of hypocalcaemia.

A
  1. Dietary insufficiency.
  2. Anticonvulsant therapy.
  3. CKD.
  4. Vitamin D deficiency.
  5. Osteomalacia.
  6. Hypoparathyroidism.
425
Q

Give 2 ECG changes that you might see in someone with hyperparathyroidism.

A

Hyperparathyroidism -> hypercalcaemia and so:

  1. Tall T waves.
  2. Shorted QT interval.
426
Q

Give 2 ECG changes that you might see in someone with hyoparathyroidism.

A

Hyoparathyroidism -> hypocalcaemia and so:

  1. Small T waves.
  2. Long QT interval
427
Q

What is phaeochromocytoma?

A

A rare catecholamine secreting tumour in the adrenal medulla.

428
Q

Give 5 symptoms of phaeochromocytoma.

A

Classic triad of:

  1. Headache.
  2. Sweating.
  3. Tachycardia.

Also:

  1. Hypertension.
  2. Palpitations.
  3. Tremor.
  4. Arrhythmia.
  5. Confusion.
429
Q

What investigations might you do in order to diagnose someone with having a phaeochromocytoma?

A

Bloods - raised WCC, increased plasma metadrenaline and normetadrenaline.

430
Q

What is the treatment for phaeochromocytoma?

A
  1. Alpha blocker e.g. phenoxybenzamine.
  2. Beta blockers.
  3. Surgical resection of tumour.
431
Q

What is the major concern in someone with phaeochromocytoma?

A

Phaeochromocytomare are a dangerous but treatable cause of hypertension.

432
Q

Describe the different types of subcutaneous insulins that can be given to people with T1DM.

A
  1. Ultra-fast acting e.g. Humalog - taken before eating in conjunction with a long-acting insulin at night.
  2. Long-acting insulin e.g. insulin glargine - taken before going to bed.
  3. Pre-mixed insulin e.g. NovoMix - taken twice daily.
433
Q

What is adrenal insufficiency?

A

Adrenocortical insufficiency resulting in a reduction of mineralocorticoids, glucocorticoids and androgens.

434
Q

Give 5 primary causes of adrenal insufficiency?

A
  1. Addison’s disease (autoimmune destruction of the adrenal cortex).
  2. Congenital adrenal hyperplasia (CAH).
  3. TB.
  4. Adrenal metastases.
  5. Drugs.
  6. Haemorrhage.
  7. Infection.
435
Q

What investigations might you do in someone who you suspect has adrenal insufficiency?

A
  1. Bloods - FBC, U+E (↓Na+ and ↑K+ - due to ↓ aldosterone - ↑Ca2+, ↑Urea).
  2. ↓ Glucose.
  3. ACTH stimulation test - Addison’s will not respond.
436
Q

Give 3 causes of hypokalaemia.

A
  1. Diuretics.
  2. D+V.
  3. Conn’s syndrome.
  4. Insulin.
437
Q

Give 5 symptoms of hypokalaemia.

A
  1. Muscle weakness.
  2. Hypotonia.
  3. Hyporeflexia.
  4. Palpitations.
  5. Arrhythmia.
  6. Nausea and vomiting.
  7. Cramps.
438
Q

What ECG changes might you see in someone with hypokalaemia?

A
  1. Increased amplitude and width of P waves.
  2. ST depression.
  3. Flat T waves.
  4. U waves.
  5. QT prolongation.
439
Q

Give 3 causes of hyperkalaemia.

A
  1. AKI.
  2. NSAIDs.
  3. Metabolic acidosis.
  4. K+ sparing diuretics.
440
Q

Give 3 symptoms of hyperkalaemia.

A
  1. Weakness.
  2. Palpitations.
  3. Tachycardia.
  4. Chest pain.
441
Q

What ECG changes might you see in someone with hyperkalaemia?

A
  1. Tall tented T waves.
  2. Wide QRS.
  3. Small P waves.
442
Q

Give 3 causes of hypercalcaemia.

A
  1. Hyperparathyroidism.
  2. Hypercalcaemia of malignancy.
  3. Vitamin D toxicity.
  4. Myeloma.
443
Q

How can hypercalcaemia be treated?

A
  1. IV normal saline.
  2. IV furosemide.
  3. IV calcitonin.
444
Q

Give 4 potential complications of untreated DKA.

A
  1. Oedema.
  2. Adult respiratory distress syndrome.
  3. Aspiration pneumonia.
  4. Thromboembolism.
  5. Death.
445
Q

Give 3 endocrine diseases that can cause diabetes.

A
  1. Cushing’s.
  2. Acromegaly.
  3. Phaeochromocytoma.
446
Q

What class of drugs can cause diabetes?

A
  1. Steroids.
  2. Thiazides.
  3. Anti-psychotics.
447
Q

Give 3 secondary causes of adrenal insufficiency

A

.1. Hypopituitarism.

  1. Withdrawal from long term steroids.
  2. Infiltration.
  3. Infection.
  4. Radiotherapy.
448
Q

Define hyponatraemia.

A

Serum sodium <135mmol/L.

449
Q

Give 3 signs of hyponatraemia.

A
  1. Anorexia.
  2. Confusion.
  3. Headache.
  4. Lethargy.
  5. Weakness.
450
Q

What is the treatment for acute hyponatraemia?

A

Give a bolus dose of saline.

451
Q

Would you associate SIADH with hyponatraemia or hypernatraemia?

A

Hyponatraemia <135mmol/L.

452
Q

Would you associate SIADH with plasma hypo-osmolality or hyper-osmolality?

A

Plasma hypo-osmolality <275mOsm/Kg.

453
Q

Would you associate SIADH with a high or low urine osmolality?

A

High urine osmolality.

454
Q

What scale is used to describe physical development based on external sex characteristics?

A

Tanner scale.

455
Q

Describe the 3 stages of thelarche.

A
  1. Ductal proliferation.
  2. Adipose deposition.
  3. Enlargement of areola and nipple.
456
Q

What is adrenarche?

A

Maturation of the adrenal gland - the development of the zona reticularis cells.

Peri-pubertal adrenal androgen production -> body odour and mild acne.

457
Q

What must you rule out as a cause of precocious puberty in boys?

A

Brain tumour!

458
Q

What is the treatment for precocious puberty?

A

GnRH super agonist to suppress pulsatility of GnRH secretion

459
Q

What is the most likely cause of delayed puberty in boys?

A

Constitutional delay - runs in the family; late menarche in mum or delayed growth spurt in father.

460
Q

Give 3 consequences of delayed puberty.

A
  1. Psychological problems.
  2. Reproduction defects.
  3. Reduced bone mass.
461
Q

What must you rule out in girls with delayed puberty and short stature?

A

Turner Syndrome (45X)!

They might also have recurrent ear infections

462
Q

Give 5 functional causes of delayed puberty.

A
  1. Anorexia.
  2. Bulimia.
  3. Over exercising.
  4. CKD.
  5. Drugs.
  6. Stress.
  7. Sickle cell.
463
Q

What investigations might you do in someone with delayed puberty?

A
  1. FBC - red cell count especially.
  2. U+E.
  3. LH/FSH measurements.
  4. TFT’s.
  5. Karyotyping for Turners.
464
Q

What is hypergonadotropic hypogonadism?

A
  • Testes or ovarian failure
465
Q

What is the affect of hypergonadotropic hypogonadism on FSH/LH and oestrogen/testosterone?

A

High FSH/LH low oestrogen/testosterone.

466
Q

Give 2 examples of hypergonadotropic hypogonadism.

A
  1. Turner Syndrome (45X).

2. Klinefelter’s syndrome (47XXY).

467
Q

What is hypogonadotropic hypogonadism?

A

Secondary gonadal failure!

- Hypopituitary or problems with the hypothalamus.

468
Q

What is the affect of hypogonadotropic hypogonadism on FSH/LH and oestrogen/testosterone?

A

Low FSH/LH and low testosterone/oestrogen

469
Q

Give an example of hypogonadotropic hypogonadism.

A

Kallman syndrome.

470
Q

What is Turner syndrome?

A

In Turner syndrome the patient is missing an X chromosome - 45X. It is an example of primary gonadal failure (hypergonadotropic hypogonadism).

471
Q

Give 3 signs of Turner syndrome.

A
  1. Short stature.
  2. Delayed puberty.
  3. CV and renal malformations.
  4. Recurrent otitis media.
472
Q

What is Klienfelter’s syndrome?

A

In Klinefelter’s syndrome the patient has an extra X chromosome - 47XXY. It is an example of primary gonadal failure (hypergonadotropic hypogonadism).

473
Q

Give 2 signs of Klinefelter’s syndrome.

A
  1. Azoospermia.
  2. Gynaecomastia (enlargement of male breast tissue).
  3. Increased risk of breast cancer.
  4. Testicular size <5ml.
474
Q

Why might someone with Klinefelter’s syndrome have fertility problems?

A

Azoospermia - semen contains no sperm.

475
Q

Give 4 symptoms of Klinefelter’s syndrome.

A
  1. Reduced pubic hair.
  2. Tall stature.
  3. Reduced IQ.
  4. Small testicles (<5ml
476
Q

What cancer is someone with Klinefelter’s at an increased risk of developing?

A

Breast cancer.

477
Q

What is Kallman syndrome?

A

Congenital deficiency of GnRH. It is an example of secondary gonadal failure -
hypogonadotropic hypogonadism.

478
Q

What must you test in a person who you suspect has Kallman syndrome?

A

Smell! 75% are ansomia.

479
Q

How is Kallman syndrome inherited?

A

X linked recessive or dominant.

Phase 2 (16 decks)

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