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5. Endocrinology > Dermatology and Endocrine > Flashcards

Dermatology and Endocrine Flashcards

1
Q

Describe the progression from melanocytic naevi (mole) to nodular melanoma.

A

Melanocytic naevi -> dysplastic melanocytic naevi -> in situ melanoma -> superficial spreading melanoma -> nodular melanoma.

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2
Q

What is the main cause of all skin cancer?

A

SUN EXPOSURE - UV light.

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3
Q

What is the treatment for malignant melanoma?

A

Surgical excision.

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4
Q

Give 5 causes of generalised pruritus but no rash.

A
  1. AGEING.
  2. Chronic renal failure.
  3. Cholestasis e.g. PBC.
  4. Iron deficiency.
  5. Lymphoma.
  6. Polycythaemia.
  7. Hypothyroid.
  8. Drugs.
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5
Q

Give 3 causes of generalised pruritus with rash.

A
  1. Urticaria.
  2. Atopic eczema.
  3. Psoriasis.
  4. Scabies.
  5. Lichen planus.
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6
Q

What investigations might you do in someone with pruritus?

A
  1. FBC.
  2. Ferritin levels.
  3. U+E.
  4. LFT’s.
  5. TFT’s.
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7
Q

What cytokines are commonly targeted in the treatment of pruritus?

A

IL-4 and IL-13.

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8
Q

Why do transdermal drugs need to be lipophilic?

A

They need to be lipophilic in order to get through the lipid rich stratum corneum.

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9
Q

Give 2 essential properties of transdermal drugs.

A
  1. Lipophilic.
  2. High affinity for their targets.
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10
Q

Give 3 advantages of transdermal drug delivery.

A
  1. Avoids first pass effect, hardly metabolised.
  2. No pain.
  3. Controlled dosing.
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11
Q

What are emollients used for?

A

They hydrate the skin and reduce itching.

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12
Q

In what diseases would the use of emollients be indicated?

A

Dry skin, eczema.

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13
Q

What receptors do glucocorticoids target?

A

Cytoplasmic receptors.

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14
Q

How does hydrocortisone work?

A

Hydrocortisone targets cytoplasmic receptors. It leads to a reduction in pro-inflammatory cytokines and an increase in anti-inflammatories.

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15
Q

In what diseases would the use of hydrocortisone be indicated?

A

Eczema and contact dermatitis.

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16
Q

Give 3 potential side effects of glucocorticoids.

A
  1. Skin thinning.
  2. Oral candidiasis.
  3. Acne.
  4. Striae.
  5. Bruising.
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17
Q

What receptors do vitamin A analogues target?

A

Nuclear retinoic acid receptors.

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18
Q

Name a Vitamin D analogue.

A

Calcipotriol.

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19
Q

How does calcipotriol work in the treatment of psoriasis?

A

Calcipotriol is a vitamin D analogue. It has anti-proliferative and anti-inflammatory effects.

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20
Q

In what diseases would the use of calcipotriol be indicated?

A

Psoriasis.

Calcipotriol is a vitamin D analogue.

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21
Q

What receptors does tazarotene bind to?

A

Tazarotene is a Vitamin A analogue. It binds to nuclear retinoic acid receptors.

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22
Q

How does tazarotene work in the treatment of acne and psoriasis?

A

Tazarotene is a Vitamin A analogue. It binds to nuclear retinoic acid receptors and modifies gene expression and inhibits cell proliferation.

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23
Q

In what diseases would the use of tazarotene be indicated?

A

Psoriasis and acne.

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24
Q

Would you prescribe tazarotene to a pregnant lady?

A

NO! Tazarotene is highly teratogenic.

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25
Q

What class of drug is tacrolimus?

A

Calcineurin inhibitor.

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26
Q

When might you prescribe someone tacrolimus?

A

Tacrolimus is often used as a second line treatment for eczema.

(1st line = glucocorticoids e.g. hydrocortisone).

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27
Q

Name 3 drug induced dermatological reactions.

A
  1. Exanthematous reactions.
  2. Urticaria.
  3. Stephen Johnson syndrome.
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28
Q

Give 5 signs of eczema.

A
  1. Superficial skin redness/inflammation.
  2. Oozing.
  3. Scaling.
  4. Pruritus.
  5. Flexors typically affected e.g. at elbows.
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29
Q

Describe the aetiology of eczema.

A
  1. Genetic predisposition - loss of function mutations in filaggrin.
  2. Environmental triggers and irritants.
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30
Q

Describe the treatment for eczema.

A
  1. Avoid irritants and allergens.
  2. Use emollients liberally and frequently.
  3. First line - hydrocortisone.
  4. Second line - tacrolimus.
  5. Third line - sedative anti-histamines.
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31
Q

Briefly describe the pathophysiology of acne.

A

Seborrhea (increased sebum production) -> narrowed follicle blocks sebum, comedo formation -> sebum stagnates and p.acne colonises -> inflammation of pilosebaceous unit.

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32
Q

Describe the treatment for acne.

A

Treatment is important to avoid scarring and psychological distress:
- Regular washing with acne soaps to remove grease.
- Benzoyl peroxide and topical clindamycin.
- 2nd line - topical retinoids e.g. tazarotene.
- 3rd line - low dose oral antibiotics e.g. doxycycline.
- Hormone treatment can also be used.

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33
Q

What is psoriasis?

A

A chronic hypo-proliferative disorder characterised by well demarcated silvery grey, scaly plaques over extensor surfaces such as elbows and knees and in the scalp.

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34
Q

What environmental factors can cause psoriasis in a genetically susceptible individual?

A
  1. Group A streptococcal infection.
  2. Lithium.
  3. UV light.
  4. Alcohol.
  5. Stress.
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35
Q

Describe the treatment for psoriasis.

A
  1. Emollients and reassurance.
  2. Vitamin D and A analogues e.g. calcipotriol and tazarotene.
  3. Phototherapy.
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36
Q

What is necrotising fasciitis?

A

Deep spreading infection of all layers of the skin -> necrosis.

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37
Q

Give 3 risk factors for necrotising fasciitis.

A
  1. IVDU.
  2. Diabetes mellitus.
  3. Homeless.
  4. Recent surgery.
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38
Q

What bacteria can cause necrotising fasciitis?

A
  1. Type 1: aerobic and anaerobic.
  2. Type 2: group A strep e.g. s.pyogenes.
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39
Q

What is the treatment for necrotising fasciitis?

A
  1. Surgical debridement.
  2. Aggressive IV benzylpenicillin and clindamycin.
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40
Q

What is cellulitis?

A

Inflammation of the SC layer of the skin.

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41
Q

What bacteria is the commonest causal organism of cellulitis?

A

S.pyogenes.

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42
Q

Give 5 signs of cellulitis.

A
  1. Inflammation.
  2. Swelling.
  3. Redness.
  4. Warmth.
  5. Pain.
  6. Unilateral.
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43
Q

What is the differential diagnosis in someone with the signs and symptoms of cellulitis?

A

DVT!

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44
Q

What is the treatment for cellulitis?

A

Penicillin and flucloxacillin.

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45
Q

Give an example of a water soluble hormone.

A

Peptides e.g. TRH, LH, FSH.

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46
Q

Are water soluble hormones stored in vesicles or synthesised on demand?

A

Water soluble hormones e.g. peptides are stored in vesicles.

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47
Q

How do water soluble hormones e.g. peptides get into a cell?

A

They bind to cell surface receptors.

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48
Q

Give an example of a fat soluble hormone.

A

Steroids e.g. cortisol.

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49
Q

Are fat soluble hormones stored in vesicles or synthesised on demand?

A

Fat soluble hormones e.g. steroids are synthesised on demand.

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50
Q

Give an example of an amine hormone.

A

Noradrenaline and adrenaline.

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51
Q

Describe the pathway for noradrenaline synthesis.

A

Phenylalanine -> L-tyrosine -> L-dopa -> dopamine -> NAd and Ad.

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52
Q

Name 2 enzymes that break down catecholamines.

A

MAO and COMT.

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53
Q

What are noradrenaline and adrenaline broken down into?

A

Normetadrenaline and metadrenaline.

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54
Q

Where in a cell are peptide cell receptors located?

A

Peptide cell receptors are located on the cell membrane.

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55
Q

Where in a cell are steroid cell receptors located?

A

Steroid cell receptors are located in the cytoplasm.

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56
Q

Where in a cell are thyroid/vitamin A and D cell receptors located?

A

Thyroid, vitamin A and D and oestrogen act on nuclear receptors.

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57
Q

Give 5 ways in which hormone action is controlled.

A
  1. Hormone metabolism.
  2. Hormone receptor induction.
  3. Hormone receptor down-regulation.
  4. Synergism e.g. glucagon and adrenaline.
  5. Antagonism e.g. glucagon and insulin.
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58
Q

What layer of the trilaminar disc is the anterior pituitary derived from?

A

Ectoderm (Rathke’s pouch).

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59
Q

Name 6 hormones that the anterior pituitary produces.

A
  1. TSH.
  2. FSH.
  3. LH.
  4. ACTH.
  5. Prolactin.
  6. GH.
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60
Q

What is the posterior pituitary derived form?

A

The floor of the ventricles.

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61
Q

Where are posterior pituitary hormones synthesised?

A

They are synthesised in the para-ventricular and supra-optic nuclei.

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62
Q

Name 2 hormones secreted from the posterior pituitary.

A

Oxytocin and ADH.

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63
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.

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64
Q

Give 2 functions of oxytocin.

A
  1. Milk secretion.
  2. Uterine contraction.
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65
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.

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66
Q

Describe the thyroid axis.

A

Hypothalamus -> TRH -> AP -> TSH -> thyroid -> T3 and T4.

T3/4 have a negative feedback effect on the hypothalamus and the anterior pituitary.

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67
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.

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68
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.

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69
Q

Describe the mechanism of ACTH.

A

Hypothalamus -> CRH -> AP -> ACTH -> adrenal cortex (zona fasciculata) -> glucocorticoid synthesis e.g. cortisol.

Cortisol has a negative feedback effect on the hypothalamus and the anterior pituitary.

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70
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.
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71
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.
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72
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.

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73
Q

What cells does FSH act on?

A
  • In the ovaries: granulosa cells.
  • In the testes: sertoli cells.
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74
Q

What cells does LH act on?

A
  • In the ovaries: theca cells.
  • In the testes: leydig cells.
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75
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.

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76
Q

What is the function of granulosa cells?

A

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

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77
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.

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78
Q

What is the function of leydig cells?

A

Leydig cells are stimulated by LH to produce testosterone.

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79
Q

Describe the GH/IGF-1 axis.

A

Hypothalamus -> GHRH (+) or SMS (-) -> AP -> GH -> Liver -> IGF-1.

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80
Q

What is the function of IGF-1?

A

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

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81
Q

Briefly describe the mechanism of prolactin.

A

Hypothalamus -> dopamine (-) -> AP -> prolactin.

Prolactin acts on the mammary glands to produce milk.

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82
Q

What would happen to serum prolactin levels if something was to impact on the pituitary stalk and block dopamine release?

A

Prolactin levels would increase.

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83
Q

Give 3 potential consequences of a pituitary tumour.

A
  1. Pressure on local structures e.g. optic chiasm.
  2. Hypo-pituitary.
  3. Functioning tumour e.g. Cushing’s, gigantism, prolactinoma.
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84
Q

Give 2 causes of prolactinoma.

A
  1. Pituitary adenoma.
  2. Anti-dopaminergic drugs.
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85
Q

Give 5 signs of prolactinoma.

A
  1. Infertility.
  2. Golactorrhoea.
  3. Amenorrhoea.
  4. Loss of libido.
  5. Visual field defects and headaches due to local effect of tumour.
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86
Q

What investigation would you do on someone presenting with difficulty getting pregnant, golactorrhoea, amenorrhoea, loss of libido and headaches?

A

You would measure serum prolactin.

These are symptoms of prolactinoma.

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87
Q

Describe the treatment for prolactinoma.

A

Dopamine agonist e.g. cabergoline.

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88
Q

Describe growth hormone secretion from the anterior pituitary.

A

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

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89
Q

What can cause acromegaly?

A

A benign pituitary adenoma producing excess GH.

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90
Q

Give 5 symptoms of acromegaly.

A
  1. Change in appearance.
  2. Increase in size of hands and feet.
  3. Excessive sweating.
  4. Headache.
  5. Tiredness.
  6. Weight gain.
  7. Amenorrhoea.
  8. Deep voice.
  9. Goitre.
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91
Q

Give 5 signs of acromegaly.

A
  1. Prognathism - jaw protrusion.
  2. Interdental separation.
  3. Large tongue.
  4. Spade like hands and feet.
  5. Tight rings.
  6. Bi-temporal hemianopia.
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92
Q

What co-morbidities are associated with acromegaly?

A
  1. Arthritis.
  2. Cerebrovascular events.
  3. Hypertension and heart disease.
  4. Sleep apnea.
  5. T2 DM.
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93
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.
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94
Q

What test is diagnostic for acromegaly?

A

Oral glucose tolerance test - failure of glucose to suppress serum GH.

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95
Q

Describe the treatment for acromegaly.

A
  1. Trans-sphenoidal surgical resection.
  2. Radiotherapy.
  3. Medical therapy: somatostatin analogues, dopamine agonists e.g. cabergoline.
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96
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.
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97
Q

Give 3 advantages of using dopamine agonists in the treatment of acromegaly.

A
  1. No hypopituitarism.
  2. Oral administration.
  3. Rapid onset.
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98
Q

Give 2 disadvantages of using dopamine agonists in the treatment of acromegaly.

A
  1. Can be ineffective.
  2. Risk of side effects.
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99
Q

Name a dopamine agonist that can be used in the treatment of acromegaly.

A

Cabergoline.

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100
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.
101
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.
102
Q

What disease is described as being a ‘disorder of carbohydrate metabolism characterised by hyperglycaemia’?

A

Diabetes mellitus.

103
Q

What are the 4 cells to make up the islets of langerhans?

A
  1. Beta cells (70%).
  2. Alpha cells (20%).
  3. Delta cells (8%).
  4. Polypeptide secreting cells.
104
Q

What do beta cells produce?

A

Insulin.

105
Q

What do alpha cells produce?

A

Glucagon.

106
Q

What do delta cells produce?

A

Somatostatin.

107
Q

What is the importance of the alpha and beta cells being located next to each other in the islets of langerhans?

A

This enables them to ‘cross talk’ - insulin and glucagon show reciprocal action.

108
Q

Describe the mechanism of insulin secretion from beta cells.

A

Glucose binds to beta cells -> glucose-6-phosphate -> ADP -> ATP -> K+ channels close -> membrane depolarisation -> Ca2+ channels open, influx -> insulin release.

109
Q

Describe the physiological processes that occur in the fasting state in response to low blood glucose.

A

Low blood glucose = high glucagon and low insulin.

  • Glycogenolysis and gluconeogenesis.
  • Reduced peripheral glucose uptake.
  • Stimulates the release of gluconeogenic precursors.
  • Lipolysis and muscle breakdown.
110
Q

Describe the effect on insulin and glucagon secretion in the fasting state.

A

Fasting state = low blood glucose.
Raised glucagon and low insulin.

111
Q

How many carbon precursors are needed for gluconeogenesis?

A

3.

112
Q

Describe the physiological processes that occur after feeding in response to high blood glucose.

A

High blood glucose = high insulin and low glucagon.

  • Glycogenolysis and gluconeogenesis are suppressed.
  • Glucose is taken up by peripheral muscle and fat cells.
  • Lipolysis and muscle breakdown suppressed.
113
Q

Describe the effect on insulin and glucagon secretion after feeding.

A

Insulin is high and glucagon is low.

114
Q

What is the affect of cortisol on insulin and glucagon?

A

Cortisol inhibits insulin and activates glucagon.

115
Q

Would you associate ketoacidosis with T1 or T2 DM?

A

TYPE 1.

Occurs due to the absence of insulin.

116
Q

Describe the pathophysiology of diabetic ketoacidosis.

A

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

117
Q

Name 3 types of skin cancer.

A
  1. BCC (75%) - in situ, grows slowly.
  2. SCC (20%) - can metastasise, grows rapidly.
  3. Melanoma (5%).
118
Q

What is Keratoacanthoma?

A

A benign variant of SCC. It is unlikely to metastasise.

119
Q

What is Bowen’s disease?

A

Bowen’s disease is also known as SCC in situ. It is characterised by red and scaly patches.

120
Q

Give 5 early signs of melanoma.

A

MAJOR
1. Enlargement.
2. Colour change (almost always darkening).
MINOR
3. Irregular shape.
4. Bleeding.
5. Itching.

121
Q

What is Hutchinson’s sign?

A

Pigmentation of the nail and proximal nail fold. It is an important sign of subungual melanoma.

122
Q

What is the ABCDE of melanoma?

A

Asymmetrical.
Border irregularity.
Colour variability.
Diameter >5mm.
Elevation irregularity.

123
Q

Give 4 risk factors for melanoma.

A
  1. High density freckles.
  2. Red hair.
  3. > 100 moles.
  4. > 5 atypical moles.
  5. Family history.
124
Q

Give 3 factors that can be used to determine the prognosis of melanoma?

A
  1. Breslow’s thickness - the thinner (<1mm) the better.
  2. Younger = better prognosis.
  3. Female = better prognosis.
125
Q

Give 4 differential diagnoses for melanoma.

A
  1. Melanocytic neavi.
  2. Seborrhoeic wart.
  3. Freckle.
  4. BCC.
  5. Pyogenic granuloma.
126
Q

Describe the distribution and characteristics of infantile eczema.

A

Infantile eczema is generalised. The cheeks and foreheads are commonly affected.

Scaly, dry and red patches.

127
Q

Describe the distribution and characteristics of childhood eczema.

A

There is a shift from extensor surfaces being affected to flexural surfaces.

Lichenification.

128
Q

Describe the distribution and characteristics of adult eczema.

A

There is increasing dryness and lichenification.

S.aureus infections may be common.

129
Q

Describe the diagnostic criteria of eczema.

A

The patient must have had an itchy skin condition in the past 6 months and >3 or more of:
- History of involvement of skin creases.
- Personal history of asthma or hay-fever.
- History of generally dry skin.
- Visible flexural dermatitis.

130
Q

Briefly describe the natural history of eczema.

A

Sub-clinical skin barrier defect -> sub-clinical inflammation -> AD phase 1 (non-atopic) -> AD phase 2 (true atopic, extrinsic), high IgE.

131
Q

Where does Seborrhoeic dermatitis usually affect?

A

The scalp and face, there is thickened and scaly skin.

132
Q

What can trigger Seborrhoeic dermatitis?

A

Yeast infection.

133
Q

What is cradle cap an example of?

A

Seborrhoeic dermatitis.

134
Q

Describe the treatment for Seborrhoeic dermatitis?

A
  1. Anti-fungal treatment.
  2. Keratolytic agents to reduce thickening.
135
Q

Describe the signs of acne.

A
  1. Open comedones (black heads).
  2. Closed comedones (white heads).
  3. Papules and pustules.
136
Q

When might biological agents be indicated in the treatment of psoriasis?

A

In someone with a PASI score > 10 - severe psoriasis.

137
Q

What type of psoriasis might you associate with streptococcal infections?

A

Guttate psoriasis.

138
Q

Give 3 signs of Rosacea?

A
  1. Flushing.
  2. Erythema.
  3. Papules and pustules.

NO comedones!

139
Q

How does Rosacea differ from Acne?

A

Rosacea tends to affect older people and isn’t associated with comedone formation.

Acne affects adolescents and often the presenting feature is open and closed comedones.

140
Q

Describe the treatment for rosacea.

A

Metronidazole.

141
Q

Briefly describe the pathophysiology of urticaria.

A

Mast cell and basophil activation, with resultant histamine release.

142
Q

Give 2 clinical features of urticaria.

A
  1. Wheals (hives) - superficial redness and swelling. Itching/burning.
  2. Angio-oedema - more severe swelling. Painful.
143
Q

Describe the sub-types of chronic urticaria.

A

Chronic - recurrent or continous signs:

  1. Chronic spontaneous: idiopathic or associated with infection.
  2. Chronic inducible: physical (triggered by temperature or pressure) OR contact (triggered by allergens).
144
Q

What is the treatment for urticaria?

A

Anti-histamines and manage triggers.

145
Q

Name the suprasellar neoplasm that can result from benign cysts and calcification of Rathke’s pouch?

A

Craniopharyngioma.

146
Q

Give 4 signs of Craniopharyngioma.

A
  1. Raised ICP.
  2. Vision affected.
  3. Growth failure.
  4. Puberty affected.
147
Q

Give 4 local effects of pituitary adenoma.

A
  1. Headaches.
  2. Visual field defects - bitemporal hemianopia.
  3. Cn palsy and temporal lobe epilepsy.
  4. CSF rhinorrhoea.
148
Q

Give a cause of primary hypogonadism.

A

Klinefelter’s syndrome - extra X chromosome.

149
Q

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

A
  • Testosterone will be low.
  • FSH/LH will be high.
150
Q

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

A
  • Testosterone will be low.
  • FSH/LH will be low.
151
Q

When should serum testosterone be measured?

A

At 9am due to circadian rhythm.

152
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.
153
Q

What is the treatment for hypogonadism?

A

Testosterone gel/injection.

  • Can improve BMD, QOL and libido etc.
154
Q

What syndrome is characterised by a congenital deficiency of GnRH?

A

Kallmann’s syndrome.

155
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.

156
Q

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

A
  • FSH/LH is high.
  • Oestradiol is low.
157
Q

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

A
  • FSH/LH are low.
  • Oestradiol is low.
158
Q

What can lead to elevated levels of prolactin?

A
  1. Stress.
  2. Drugs.
  3. Pressure on the pituitary stalk.
159
Q

What stimulates the posterior pituitary to release ADH?

A

Osmoreceptors in the hypothalamus detect raised plasma osmolarity -> posterior pituitary is signalled to release ADH.

160
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.
161
Q

What investigations might you do to determine whether someone has diabetes insipidus?

A
  1. Measure 24-hour urine volume - >3L/24h = suggests DI.
  2. Plasma biochemisty - hypernatraemia.
  3. Water deprivation test - urine will not concentrate when asked not to drink.
162
Q

What is the treatment for neurological diabetes insipidus?

A

Desmopression.

163
Q

Give 4 causes of polyuria.

A
  1. Hypokalaemia.
  2. Hypercalcaemia.
  3. Hyperglycaemia.
  4. Diabetes insipidus.
164
Q

Would TSH and T4 be high or low in someone with sub-clinical hypothyroidism?

A

TSH would be high but T4 would be normal. These patients are often asymptomatic and well.

(Hypothyroidism: high TSH and low T4).

165
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion.

Too much ADH = very concentrated urine and hyponatreamia.

166
Q

Give 3 symptoms of SIADH.

A
  1. Anorexia.
  2. Nausea.
  3. Malaise.
  4. Headache.
  5. Confusion.
167
Q

Give 3 causes of SIADH.

A
  1. Malignancy.
  2. CNS disorders e.g. meningitis, brain tumour, cerebral haemorrhage.
  3. TB.
  4. Pneumonia.
  5. Drugs.
168
Q

Describe the treatment for SIADH.

A
  1. Restrict fluid!
  2. Give salt.
  3. Loop diuretics e.g. furosemide.
  4. ADH-R antagonists e.g. vaptans - can be used when people find fluid restriction challenging.
169
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.
170
Q

A man presents with a history of weight loss, polyuria and nocturia. He is very unwell. The GP performs a capillary blood glucose which is found to be 17.2mmol/l. What is the most likely diagnosis of this mans symptoms?

A

Type 1 Diabetes Mellitus.

171
Q

What is the treatment for someone presenting with ketoacidosis?

A
  1. ABCDE.
  2. IV normal saline.
  3. IV soluble insulin via syringe driver and sliding scale.
  4. Restore potassium levels.
  5. Look for underlying cause.
172
Q

pH 7.1; pCO2 1.2 kPa; pO2 11.1 kPa; Bicarbonate 4mmol/l.
Interpret this blood gas result.

A

Severe metabolic acidosis.

173
Q

Give 3 causes of severe metabolic acidosis.

A
  1. Diabetic ketoacidosis.
  2. Severe sepsis.
  3. Uraemia.
  4. Lactic acidosis.
174
Q

What is hirsutism?

A

Excess hair growth in women in a male pattern.

175
Q

What is the cause of hirsutism?

A

Hirsutism indicates increased androgen production by the ovaries or adrenal glands, most commonly polycystic ovary syndrome.

176
Q

What diseases are associated with polycystic ovary syndrome?

A
  1. Insulin resistance and so T2DM.
  2. Hypertension.
  3. Hyperlipidaemia.
  4. CV disease.
177
Q

Give 5 symptoms of polycystic ovary syndrome.

A
  1. Amenorrhoea.
  2. Oligomenorrhoea.
  3. Hirsutism.
  4. Acne.
  5. Overweight.
  6. Infertility.
178
Q

What criteria can be used to make a diagnosis of polycystic ovary syndrome?

A

Rotterdam diagnostic criteria:
1. Menstrual irregularity.
2. Clinical or biochemical evidence of hyperandrogenism.
3. Polycystic ovaries on USS.

179
Q

Describe the treatment for polycystic ovary syndrome?

A
  1. Hirsutism therapy: shaving/waxing excess hair OR oestrogens e.g. OCP.
  2. Menstrual disturbance therapy: cyclic oestrogen/progesterone.
  3. Metformin can improve hyperinsulinaemia and regulates the menstrual cycle.
180
Q

A 27-year- old woman comes to see you because she is having infrequent periods (oligomenorrhoea). You note, on examination, that she has facial acne and is overweight. What is the most likely diagnosis? Give 3 other signs you might see in this patient.

A

Polycystic ovary syndrome.

Other signs:
1. Hirsutism.
2. Amenorrhoea.
3. Infertility.

181
Q

Describe insulin action at muscle and fat cells.

A

Insulin binds to membrane receptors -> intracellular signalling cascade stimulated -> GLUT-4 mobilisation to plasma membrane -> GLUT-4 integrates into plasma membrane -> glucose enters cell via GLUT-4.

182
Q

Which bacteria is responsible for causing impetigo?

A

Staphylococcus aureus.

183
Q

What is the treatment for impetigo?

A

Flucloxacillin.

184
Q

17 year old man presents with intermittent headaches and anxiety. He is sweating and vomiting. His BP is 223/159 and his pulse is 115. What is the likely cause?

A

Phaeochromocytoma crisis!

Hypertension and tachycardia = phaeochromocytoma until proved otherwise; especially in younger patients.

185
Q

What is the management of a phaeochromocytoma crisis?

A

Non-competitive alpha-blocker e.g. phenoxybenzamine.

Excision of paraganglioma.

Biochemistry: measure plasma and serum metanephrines.

186
Q

Give 3 causes of hyponatraemia.

A
  1. SIADH.
  2. Sodium deficiency.
  3. Renal failure.
  4. Malignancy.
187
Q

Define hyponatraemia.

A

Serum sodium <135mmol/L.

188
Q

Give 3 signs of hyponatraemia.

A
  1. Anorexia.
  2. Confusion.
  3. Headache.
  4. Lethargy.
  5. Weakness.
189
Q

What is the treatment for acute hyponatraemia?

A

Give a bolus dose of saline.

190
Q

What are the units for osmolality?

A

mOsmol/Kg.

191
Q

What is the primary cation in ICF?

A

K+.

192
Q

What is the primary cation in the ECF?

A

Na+.

193
Q

what are the primary anions in the ECF?

A

Cl- and HCO3-.

194
Q

What is the effect of water excess on thirst and ADH secretion?

A

Decreased thirst and decreased ADH -> reduced intake and increased excretion.

195
Q

What is the effect of water deficit on thirst and ADH secretion?

A

Increased thirst and increased ADH -> increased water intake and reduced secretion.

196
Q

What GPCR does ADH bind to on renal tubules?

A

V2.

197
Q

Do you have hypernatraemia or hyponatraemia in diabetes insipidus?

A

Hypernatraemia.

198
Q

Give 3 causes of cranial diabetes insipidus.

A
  1. Tumours.
  2. Trauma.
  3. Infections.
  4. Idiopathic.
  5. Genetic - AR.
199
Q

Give 3 causes of nephrogenic diabetes insipidus.

A
  1. Osmotic diuresis - diabetes mellitus.
  2. Drugs.
  3. CKD.
  4. Metabolic e.g. hypercalcaemia and hypokalaemia.
200
Q

Would you expect a patient with SIADH to be hypovolaemic, euvolaemic or hypervolaemic?

A

Euvolaemic.

201
Q

Describe 5 features of the essential criteria for SIADH.

A
  1. Hyponatreamia (<135mmol/L).
  2. Plasma hypo-osmolality.
  3. High urine osmolality.
  4. Clinical euvolaemia.
  5. Increased urinary sodium excretion with normal salt and water intake.
202
Q

Name 3 diseases that you must exclude in someone who you suspect could have SIADH.

A
  1. Renal disease.
  2. Hypothyroidism.
  3. Hypocortism.
  4. Recent diuretic use.
203
Q

Would you associate SIADH with hyponatraemia or hypernatraemia?

A

Hyponatraemia <135mmol/L.

204
Q

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

A

Plasma hypo-osmolality <275mOsm/Kg.

205
Q

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

A

High urine osmolality.

206
Q

Give 2 clinical signs of hypervolaemia.

A
  1. Ascites.
  2. Oedema.
207
Q

Give 3 clinical signs of hypovolaemia.

A
  1. Hypotension.
  2. Tachycardia.
  3. Decreased skin turgor.
  4. Dry mucus membranes.
208
Q

Define puberty.

A

Puberty describes the physiological, morphological and behavioural changes as the gonads switch from infantile to adult forms.

209
Q

What is the first sign of puberty in girls?

A

Menarche.

210
Q

What hormone is responsible for regulating the growth of the breasts and female genitalia?

A

Ovarian oestrogen.

211
Q

Which hormones are responsible for controlling the growth of pubic and axillary hair in females?

A

Ovarian and adrenal androgens.

212
Q

What is the first sign of puberty in boys?

A

First ejaculation, often nocturnal.

213
Q

What are the roles of testicular androgens in male puberty?

A
  1. Development of external genitalia.
  2. Growth of pubic and axillary hair.
  3. Deepening of voice.
214
Q

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

A

Tanner scale.

215
Q

What is thelarche?

A

Breast development.
- Takes about 3 years and is controlled by oestrogen.

216
Q

Describe the 3 stages of thelarche.

A
  1. Ductal proliferation.
  2. Adipose deposition.
  3. Enlargement of areola and nipple.
217
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.

218
Q

Give 2 signs of adrenarche.

A
  1. Body odour.
  2. Mild acne.
219
Q

What is pubarche?

A

Growth of pubic hair.

220
Q

What term is used to describe the onset of secondary sexual characteristics before 8/9 y/o?

A

Precocious puberty.

221
Q

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

A

Brain tumour!

222
Q

What is the treatment for precocious puberty?

A

GnRH super agonist to suppress pulsatility of GnRH secretion.

223
Q

What is delayed puberty?

A

The absence of secondary sexual characteristics by 14y/o or 16y/o.

224
Q

What is precocious puberty?

A

The onset of secondary sexual characteristics before 8/9 y/o.

225
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.

226
Q

Give 3 consequences of delayed puberty.

A
  1. Psychological problems.
  2. Reproduction defects.
  3. Reduced bone mass.
227
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.

228
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.
229
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.
230
Q

What is hypergonadotropic hypogonadism?

A

Primary gonadal failure!
- Testes or ovarian failure.

231
Q

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

A

High FSH/LH low oestrogen/testosterone.

232
Q

Give 2 examples of hypergonadotropic hypogonadism.

A
  1. Turner Syndrome (45X).
  2. Klinefelter’s syndrome (47XXY).
233
Q

What is hypogonadotropic hypogonadism?

A

Secondary gonadal failure!
- Hypopituitary or problems with the hypothalamus.

234
Q

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

A

Low FSH/LH and low testosterone/oestrogen.

235
Q

Give an example of hypogonadotropic hypogonadism.

A

Kallman syndrome.

236
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).

237
Q

Give 3 signs of Turner syndrome.

A
  1. Short stature.
  2. Delayed puberty.
  3. CV and renal malformations.
  4. Recurrent otitis media.
238
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).

239
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.
240
Q

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

A

Azoospermia - semen contains no sperm.

241
Q

Give 4 symptoms of Klinefelter’s syndrome.

A
  1. Reduced pubic hair.
  2. Tall stature.
  3. Reduced IQ.
  4. Small testicles (<5ml).
242
Q

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

A

Breast cancer.

243
Q

What is Kallman syndrome?

A

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

244
Q

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

A

Smell! 75% are ansomia.

245
Q

How is Kallman syndrome inherited?

A

X linked recessive or dominant.

246
Q

How do you treat asymptomatic SIADH?

A

Fluid restriction.

247
Q

How do you treat symptomatic SIADH of acute onset?

A

Give 3% saline.

248
Q

Name 2 drugs that can be used to treat acromegaly. What class of drugs do they belong to?

A
  1. Cabergoline - dopamine agonist.
  2. Octreotide - somatostatin analogue.

5. Endocrinology (20 decks)

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