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Phase 2A medicine > 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 3 causes of generalised pruritus with rash.

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

What are emollients used for?

A

They hydrate the skin and reduce itching.

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7
Q

In what diseases would the use of emollients be indicated?

A

Dry skin, eczema.

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8
Q

What receptors do glucocorticoids target?

A

Cytoplasmic receptors.

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9
Q

In what diseases would the use of hydrocortisone be indicated?

A

Eczema and contact dermatitis.

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10
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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11
Q

What receptors do vitamin A analogues target?

A

Nuclear retinoic acid receptors.

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12
Q

Name a Vitamin D analogue.

A

Calcipotriol.

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13
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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14
Q

In what diseases would the use of calcipotriol be indicated?

A

Psoriasis.

Calcipotriol is a vitamin D analogue.

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15
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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16
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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17
Q

In what diseases would the use of tazarotene be indicated?

A

Psoriasis and acne.

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18
Q

Would you prescribe tazarotene to a pregnant lady?

A

NO! Tazarotene is highly teratogenic.

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19
Q

What class of drug is tacrolimus?

A

Calcineurin inhibitor.

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20
Q

When might you prescribe someone tacrolimus?

A

2nd line for eczema

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

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21
Q

Name 3 drug induced dermatological reactions.

A
  1. Exanthematous reactions.
  2. Urticaria.
  3. Stephen Johnson syndrome.
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22
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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23
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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24
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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25
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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26
Q

What is psoriasis?

A

A chronic hyper-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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27
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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28
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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29
Q

What is necrotising fasciitis?

A

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

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30
Q

Give 3 risk factors for necrotising fasciitis.

A
  1. IVDU.
  2. Diabetes mellitus.
  3. Homeless.
  4. Recent surgery.
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31
Q

What bacteria can cause necrotising fasciitis?

A
  1. Type 1: aerobic and anaerobic (e.g. S.aureus)

2. Type 2: group A strep e.g. s.pyogenes.

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32
Q

What is the treatment for necrotising fasciitis?

A
  1. Surgical debridement.

2. Aggressive IV benzylpenicillin and clindamycin.

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33
Q

What is cellulitis?

A

Inflammation of the SC layer of the skin.

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34
Q

What bacteria is the commonest causal organism of cellulitis?

A

S.pyogenes.

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35
Q

Give 5 signs of cellulitis.

A
  1. Inflammation.
  2. Swelling.
  3. Redness.
  4. Warmth.
  5. Pain.
  6. Unilateral.
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36
Q

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

A

DVT!

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37
Q

What is the treatment for cellulitis?

A

Penicillin and flucloxacillin.

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38
Q

Give an example of a water soluble hormone.

A

Peptides e.g. TRH, LH, FSH.

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39
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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40
Q

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

A

They bind to cell surface receptors.

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41
Q

Give an example of a fat soluble hormone.

A

Steroids e.g. cortisol.

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42
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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43
Q

Give an example of an amine hormone.

A

Noradrenaline and adrenaline.

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44
Q

Describe the pathway for noradrenaline synthesis.

A

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

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45
Q

Name 2 enzymes that break down catecholamines.

A

MAO and COMT.

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46
Q

What are noradrenaline and adrenaline broken down into?

A

Normetadrenaline and metadrenaline.

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47
Q

Where in a cell are peptide cell receptors located?

A

Peptide cell receptors are located on the cell membrane.

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48
Q

Where in a cell are steroid cell receptors located?

A

Steroid cell receptors are located in the cytoplasm.

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49
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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50
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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51
Q

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

A

Ectoderm (Rathke’s pouch).

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52
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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53
Q

What is the posterior pituitary derived form?

A

The floor of the ventricles.

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54
Q

Where are posterior pituitary hormones synthesised?

A

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

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55
Q

Name 2 hormones secreted from the posterior pituitary.

A

Oxytocin and ADH.

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56
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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57
Q

Give 2 functions of oxytocin.

A
  1. Milk secretion.

2. Uterine contraction.

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58
Q

Which has a longer half life, triiodothyronine or thyroxine?

A

Thyroxine (T4) has a half life of 5-7 days whereas triiodothyronine (T3) has a half life of only 1 day.

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59
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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60
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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61
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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62
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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63
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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64
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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65
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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66
Q

What cells does FSH act on?

A
  • In the ovaries: granulosa cells.

- In the testes: sertoli cells.

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67
Q

What cells does LH act on?

A
  • In the ovaries: theca cells.

- In the testes: leydig cells.

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68
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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69
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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70
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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71
Q

What is the function of leydig cells?

A

Leydig cells are stimulated by LH to produce testosterone.

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72
Q

Describe the GH/IGF-1 axis.

A

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

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73
Q

What is the function of IGF-1?

A

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

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74
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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75
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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76
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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77
Q

Give 2 causes of prolactinoma.

A
  1. Pituitary adenoma.

2. Anti-dopaminergic drugs.

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78
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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79
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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80
Q

Describe the treatment for prolactinoma.

A

Dopamine agonist e.g. cabergoline.

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81
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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82
Q

What can cause acromegaly?

A

A benign pituitary adenoma producing excess GH.

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83
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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84
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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85
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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86
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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87
Q

What test is diagnostic for acromegaly?

A

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

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88
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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89
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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90
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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91
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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92
Q

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

A

Cabergoline.

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93
Q

Give 5 causes of hypothyroidism.

A
  1. Autoimmune thyroiditis e.g. Hashimoto’s and atrophic thyroiditis.
  2. Post-partum thyroiditis.
  3. Iatrogenic - thyroidectomy.
  4. Drug induced e.g. carbimazole, amiodarone, lithium.
  5. Iodine deficiency.
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94
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.
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95
Q

Give an example of a transient cause of hypothyroidism.

A

Post-partum thyroiditis.

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96
Q

Give 2 examples of iatrogenic causes of hypothyroidism.

A
  1. Thyroidectomy.

2. Radioiodine therapy.

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97
Q

Name 3 drugs that can cause hypothyroidism.

A
  1. Carbimazole (used to treat hyperthyroidism).
  2. Amiodarone.
  3. Lithium.
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98
Q

Why can amiodarone cause hypo/hyperthyroidism?

A

Because it is iodine rich.

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99
Q

Give 5 symptoms of hypothyroidism.

A
  1. Menorrhagia – heavy bleeding.
  2. Obesity/weight gain.
  3. Malar flush.
  4. Tiredness.
  5. Intolerance to cold.
  6. Energy levels fall/eyebrow loss.
  7. Depression/dry skin and hair.
  8. GOITRE!
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100
Q

Give 5 signs of hypothyroidism.

A
  1. Mental slowness.
  2. Dry thin hair.
  3. Bradycardia.
  4. Anaemia.
  5. Hypertension.
  6. Loss of eyebrows.
  7. Cold peripheries.
  8. Carpal tunnel syndrome.
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101
Q

What investigations might you do in someone who you suspect has hypothyroidism?

A
  • TFT’s - serum TSH will be raised and T3/T4 will be low.

- Thyroid antibodies.

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102
Q

Describe the management for hypothyroidism.

A

Levothyroxine.

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103
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.
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104
Q

Give 2 causes of hyperthyroidism.

A
  1. Grave’s disease.

2. Toxic adenoma.

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105
Q

Briefly describe the pathophysiology of Grave’s disease.

A

Autoimmune disease. TSH receptor antibodies stimulate thyroid hormone production -> hyperthyroidism.

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106
Q

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

A
  1. Weight loss.
  2. Increased appetite.
  3. Irritable.
  4. Tremor.
  5. Palpitations.
  6. Goitre.
  7. Diarrhoea.
  8. Heat intolerance.
  9. Malaise.
  10. Vomiting.
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107
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).
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108
Q

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

A

Grave’s disease.

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109
Q

Give 5 Grave’s opthlmopathy signs.

A
  1. Exophthalmos (bulging eyes).
  2. Lid lag stare.
  3. Redness.
  4. Conjuctivitis.
  5. Pre-orbital oedema.
  6. Bilateral.
  7. Extra-ocular muscle swelling.
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110
Q

What investigations might you do in someone who you suspect has hypothyroidism?

A

TFT’s - serum TSH is suppressed and T3/4 are elevated.

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111
Q

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

A

Lymphocyte infiltration and thyroid follicle destruction.

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112
Q

Describe the treatment for Grave’s disease.

A
  1. Anti-thyroid drugs e.g. carbimazole.
  2. Radioiodine drugs.
  3. Surgery - partial thyroidectomy.
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113
Q

How does carbimazole work in treating Grave’s disease?

A

It targets thyroid peroxidase and so prevents the formation of T3/4.

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114
Q

Give a potential serious side effect of taking carbimazole to treat Grave’s disease.

A

Agranulocytosis.

Patient’s are advised to seek medical attention if they develop an unexplained sore throat or fever.

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115
Q

How do radioiodine drugs work in treating Grave’s disease?

A

Radioiodine drugs emit beta particles that destroy thyroid follicles and so thyroid hormone production is decreased.

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116
Q

Give 3 potential complications of a partial thyroidectomy.

A
  1. Bleeding.
  2. Hypocalcaemia.
  3. Hypothyroidism.
  4. Recurrent laryngeal nerve palsy.
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117
Q

What disease would you treat with Carbimazole?

A

Grave’s disease.

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118
Q

What disease would you treat with levothyroxine?

A

Hypothyroidism.

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119
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.
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120
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.
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121
Q

At what week are foetal thyroid follicles and T4 synthesised?

A

Week 10.

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122
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.

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123
Q

Is hypothyroidism or thyrotoxicosis more common in pregnancy?

A

Hypothyroidism is more common in pregnancy.

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124
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.
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125
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.
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126
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.
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127
Q

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

A

Diabetes mellitus.

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128
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.
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129
Q

What do beta cells produce?

A

Insulin.

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130
Q

What do alpha cells produce?

A

Glucagon.

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131
Q

What do delta cells produce?

A

Somatostatin.

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132
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.

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133
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.

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134
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.
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135
Q

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

A

Fasting state = low blood glucose.

Raised glucagon and low insulin.

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136
Q

How many carbon precursors are needed for gluconeogenesis?

A

3.

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137
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.
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138
Q

Describe the effect on insulin and glucagon secretion after feeding.

A

Insulin is high and glucagon is low.

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139
Q

A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons fasting plasma glucose be if they were diabetic?

A

Fasting plasma glucose >7mmol/L.

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140
Q

A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons random plasma glucose be if they were diabetic?

A

Random plasma glucose >11mmol/L.

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141
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.

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142
Q

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

A

> 48mmol/mol.

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143
Q

What is the affect of cortisol on insulin and glucagon?

A

Cortisol inhibits insulin and activates glucagon.

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144
Q

Describe the aetiology of type 1 diabetes mellitus.

A

Beta cells express HLA antigens. Autoimmune destruction -> beta cell loss -> impaired insulin secretion.

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145
Q

Is type 1 diabetes characterised by a problem with insulin secretion, insulin resistance or both?

A

Type 1 diabetes is characterised by impaired insulin secretion - there is severe insulin deficiency.

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146
Q

At what age do people with T1DM present?

A

Often people with Type 1 diabetes will present in childhood.

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147
Q

Give 2 potential consequences of T1DM.

A
  1. Hyperglycaemia.

2. Raised plasma ketones -> ketoacidosis.

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148
Q

Describe the natural history of T1DM.

A

Genetic predisposition + trigger -> insulitis, beta cell injury -> pre-diabetes -> diabetes.

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149
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.

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150
Q

Give 3 symptoms of T1DM.

A
  1. Weight loss.
  2. Thirst (fluid and electrolyte losses).
  3. Polyuria (due to osmotic diuresis).
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151
Q

Would you associate ketoacidosis with T1 or T2 DM?

A

TYPE 1.

Occurs due to the absence of insulin.

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152
Q

Describe the pathophysiology of diabetic ketoacidosis.

A

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

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153
Q

Name 3 ketone bodies.

A
  • acetoacetate.
  • acetone.
  • beta hydroxybutyrate.
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154
Q

Where does ketogenesis occur?

A

In the liver.

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155
Q

Give 4 signs of diabetic ketoacidosis.

A
  1. Hypotension.
  2. Tachycardia.
  3. Kussmaul’s respiration.
  4. Breath smells of ketones.
  5. Dehydration.
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156
Q

Describe the treatment for T1DM.

A
  1. EDUCATION - make sure the patient understands the benefits of good glycaemic control.
  2. Healthy diet - low in sugar, high in carbohydrates.
  3. Regular activity, healthy BMI.
  4. BP and hyperlipidaemia control.
  5. Insulin.
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157
Q

How is insulin administered in someone with T1DM?

A

Injected into SC fat.

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158
Q

Other than SC injections, how else can insulin be administered?

A

Insulin pump.

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159
Q

Give 4 potential complications of insulin therapy.

A
  1. Hypoglycaemia.
  2. Lipohypertrophy at ejection site.
  3. Insulin resistance.
  4. Weight gain.
  5. Interference with life style.
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160
Q

Is type 2 diabetes characterised by a problem with insulin secretion, insulin resistance or both?

A

Type 2 DM is characterised by impaired insulin secretion AND insulin resistance.

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161
Q

Describe the aetiology of T2DM.

A

Genetic predisposition and environmental factors e.g. obesity and lack of exercise.

162
Q

Why is insulin secretion impaired in T2DM?

A

Impaired insulin secretion is thought to be due to lipid deposition in the pancreatic islets.

163
Q

Describe the pathophysiology of T2DM.

A

Impaired insulin secretion and resistance -> IGT -> T2DM -> hyperglycaemia and high FFA’s.

164
Q

Is insulin secretion or insulin resistance the driving force of hyperglycaemia in T2DM?

A

Hepatic insulin resistance is the driving force of hyperglycaemia.

165
Q

Give 3 risk factors for insulin resistance in T2DM.

A
  1. Obesity.
  2. Physical inactivity.
  3. Family history.
166
Q

What happens to insulin resistance, insulin secretion and glucose levels in T2DM?

A
  • Insulin resistance increases.
  • Insulin secretion decreases.
  • Fasting and post-prandial glucose increase.
167
Q

Why do you rarely see diabetic ketoacidosis in T2DM?

A

Insulin secretion is impaired but there are still low levels of plasma insulin. Even low levels of insulin can prevent muscle catabolism and ketogenesis.

168
Q

Describe the treatment pathway for T2DM.

A
  1. Lifestyle changes: lose weight, exercise, healthy diet.
  2. Metformin.
  3. Metformin + sulfonylurea.
  4. Metformin + sulfonylurea + insulin.
  5. Increase insulin dose as required.
169
Q

How does metformin work in treating T2DM?

A

Metformin increases insulin sensitivity and inhibits glucose production.

170
Q

How does sulfonylurea work in treating T2DM?

A

Sulfonylurea stimulates insulin release.

171
Q

Give a potential consequence of taking Sulfonylurea for the treatment of T2DM.

A

Hypoglycaemia.

(Sulfonylurea stimulates insulin release).

172
Q

Give 3 microvascular complications of diabetes mellitus.

A
  1. Diabetic retinopathy.
  2. Diabetic nephropathy.
  3. Diabetic peripheral neuropathy.
173
Q

Give a macrovascular complication of diabetes mellitus.

A

CV disease and stroke.

174
Q

What is the main risk factor for diabetic complications?

A

Poor glycaemic control!

175
Q

Give a potential consequence of acute hyperglycaemia?

A

Diabetic ketoacidosis and hyperosmolar coma.

176
Q

Give a potential consequence of chronic hyperglycaemia?

A

Micro/macrovascular tissue complications e.g. diabetic reinopathy, nephropathy, neuropathy, CV disease etc.

177
Q

What is the commonest form of diabetic neuropathy?

A

Distal symmetrical polyneuropathy.

178
Q

Give 3 major clinical consequences of diabetic neuropathy.

A
  1. Pain.
  2. Autonomic neuropathy.
  3. Insensitivity.
179
Q

Describe the pain associated with diabetic neuropathy.

A
  • Burning.
  • Paraesthesia.
  • Nocturnal exacerbation.
180
Q

Diabetic neuropathy clinical consequences: what is autonomic neuropathy?

A

Autonomic neuropathy - damage to the nerves that supply body structures that regulate functions such as BP, HR, bowel/bladder emptying.

181
Q

Diabetic neuropathy: give 5 signs of autonomic neuropathy.

A
  1. Hypotension.
  2. HR affected.
  3. Diarrhoea/constipation.
  4. Incontinence.
  5. Erectile dysfunction.
  6. Dry skin.
182
Q

What are the consequences of insensitivity as a result of diabetic neuropathy?

A

Insensitivity -> foot ulceration -> infection -> amputation.

183
Q

Describe the distribution of insensitivity as a result of diabetic neuropathy?

A

Insensitivity starts in the toes and moves proximally. Glove and stocking distribution.

184
Q

Give 5 risk factors for diabetic neuropathy.

A
  1. POOR GLYCAEMIC CONTROL.
  2. Hypertension.
  3. Smoking.
  4. HbA1c.
  5. Overweight.
  6. Long duration of DM.
185
Q

Describe the treatments for diabetic neuropathy.

A
  1. Improve glycaemic control.
  2. Antidepressants.
  3. Pain relief.
186
Q

PVD is a potential complication of Diabetes. Give 6 signs of acute ischaemia.

A
  1. Pulseless.
  2. Pale.
  3. Perishing cold.
  4. Pain.
  5. Paralysis.
  6. Paraesthesia.
187
Q

Give 5 ways in which amputation can be prevented in someone with diabetic neuropathy.

A
  1. Screening for insensitivity.
  2. Education.
  3. MDT foot clinics.
  4. Pressure relieving footwear.
  5. Podiatry.
  6. Revascularisation and abx.
188
Q

Would there be increased or decreased pulses in a diabetic neuropathic foot?

A

There would be increased foot pulses.

189
Q

Give 5 risk factors for diabetic retinopathy.

A
  1. Long duration DM.
  2. Poor glycaemic control.
  3. Hypertension.
  4. Insulin treatment.
  5. Pregnancy.
  6. High HbA1c.
190
Q

Describe the pathophysiology of diabetic retinopathy.

A

Micro-aneurysms -> pericyte loss and protein leakage -> occlusion -> ischaemia.

191
Q

How can diabetic retinopathy be sub-divided?

A

Diabetic retinopathy is divided into:

  • Proliferative - evidence of neovascularisation in retina.
  • Non-proliferative.
192
Q

What would you see in someone with an R1 retinopathy grade?

A

R1 - non-proliferative/background.

  • Micro-aneurysms.
  • Intraretinal haemorrhages.
  • Exudates.
193
Q

What would you see in someone with an R2 retinopathy grade?

A

R2 - pre-proliferative.

  • Venous beading.
  • Growth of new vessels.
194
Q

What would you see in someone with an R3 retinopathy grade?

A

R3 - proliferative.

  • New blood vessel on disc.
195
Q

What is the treatment for diabetic retinopathy?

A

People with diabetes are offered regular screening to assess visual acuity.

  • Laser therapy treats neovascularisation.
196
Q

What is the hallmark of diabetic nephropathy?

A

Development of proteinuria and progressive decline in renal function.

197
Q

What happens to the glomerular basement membrane in someone with diabetic nephropathy?

A

On microscopy there is thickening of the glomerular basement membrane.

198
Q

Give one way in which the presentation of diabetic nephropathy differs between T1 and T2DM.

A

T1 DM: microalbuminuria develops 5-10 years after diagnosis.

T2 DM: microalbuminuria is often present at diagnosis.

199
Q

Describe the treatment for diabetic nephropathy.

A
  1. Glycaemic and BP control.
  2. ARB/ACEi.
  3. Proteinuria and cholesterol control.
200
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%).
201
Q

What is Keratoacanthoma?

A

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

202
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.

203
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.
204
Q

What is Hutchinson’s sign?

A

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

205
Q

What is the ABCDE of melanoma?

A 
Asymmetrical.
Border irregularity.
Colour variability.
Diameter >5mm.
Elevation irregularity.
206
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.
207
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.
208
Q

Give 4 differential diagnoses for melanoma.

A
  1. Melanocytic neavi.
  2. Seborrhoeic wart.
  3. Freckle.
  4. BCC.
  5. Pyogenic granuloma.
209
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.

210
Q

Describe the distribution and characteristics of childhood eczema.

A

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

Lichenification.

211
Q

Describe the distribution and characteristics of adult eczema.

A

There is increasing dryness and lichenification.

S.aureus infections may be common.

212
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.
213
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.

214
Q

Where does Seborrhoeic dermatitis usually affect?

A

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

215
Q

What can trigger Seborrhoeic dermatitis?

A

Yeast infection.

216
Q

What is cradle cap an example of?

A

Seborrhoeic dermatitis.

217
Q

Describe the treatment for Seborrhoeic dermatitis?

A
  1. Anti-fungal treatment.

2. Keratolytic agents to reduce thickening.

218
Q

Describe the signs of acne.

A
  1. Open comedones (black heads).
  2. Closed comedones (white heads).
  3. Papules and pustules.
219
Q

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

A

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

220
Q

What type of psoriasis might you associate with streptococcal infections?

A

Guttate psoriasis.

221
Q

Give 3 signs of Rosacea?

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

NO comedones!

222
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.

223
Q

Describe the treatment for rosacea.

A

Metronidazole.

224
Q

Briefly describe the pathophysiology of urticaria.

A

Mast cell and basophil activation, with resultant histamine release.

225
Q

Give 2 clinical features of urticaria.

A
  1. Wheals (hives) - superficial redness and swelling. Itching/burning.
  2. Angio-oedema - more severe swelling. Painful.
226
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).
227
Q

What is the treatment for urticaria?

A

Anti-histamines and manage triggers.

228
Q

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

A

Craniopharyngioma.

229
Q

Give 4 signs of Craniopharyngioma.

A
  1. Raised ICP.
  2. Vision affected.
  3. Growth failure.
  4. Puberty affected.
230
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.
231
Q

What is the affect of hypothyroidism on TSH and T4 levels?

A
  • TSH will be high.

- T4 will be low.

232
Q

What is the affect of hyperthyroidism on TSH and T4 levels?

A
  • TSH will be low.

- T4 will be high.

233
Q

What is the affect of hypopituitarism on TSH and T4 levels?

A
  • TSH will be low.

- T4 will be low.

234
Q

What is the treatment for thyroid hypopituitarism?

A

Levothyroxine.

235
Q

Give a cause of primary hypogonadism.

A

Klinefelter’s syndrome - extra X chromosome.

236
Q

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

A
  • Testosterone will be low.

- FSH/LH will be high.

237
Q

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

A
  • Testosterone will be low.

- FSH/LH will be low.

238
Q

When should serum testosterone be measured?

A

At 9am due to circadian rhythm.

239
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.
240
Q

What is the treatment for hypogonadism?

A

Testosterone gel/injection.

  • Can improve BMD, QOL and libido etc.
241
Q

What syndrome is characterised by a congenital deficiency of GnRH?

A

Kallmann’s syndrome.

242
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.

243
Q

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

A
  • FSH/LH is high.

- Oestradiol is low.

244
Q

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

A
  • FSH/LH are low.

- Oestradiol is low.

245
Q

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

A
  • Cortisol is low.

- ACTH is high.

246
Q

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

A
  • Cortisol is low.

- ACTH is low.

247
Q

What can lead to elevated levels of prolactin?

A
  1. Stress.
  2. Drugs.
  3. Pressure on the pituitary stalk.
248
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.

249
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.
250
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.
251
Q

What is the treatment for neurological diabetes insipidus?

A

Desmopression.

252
Q

Give 4 causes of polyuria.

A
  1. Hypokalaemia.
  2. Hypercalcaemia.
  3. Hyperglycaemia.
  4. Diabetes insipidus.
253
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).

254
Q

What is Cushing’s syndrome?

A

A set of signs/symptoms resulting from chronic glucocorticoid excess with a loss of normal feedback mechanisms.

255
Q

What can cause Cushing’s syndrome?

A
  1. Adrenal Tumour (adenoma or carcinoma).
  2. Pituitary tumour (Cushing’s disease).
  3. Exogenous steroids.
  4. Ectopic ACTH syndrome.
256
Q

What is Cushing’s disease?

A

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

ACTH dependent.

257
Q

Give 7 signs/symptoms of Cushing’s disease.

A
  1. Central obesity.
  2. Moon face.
  3. Hypertension.
  4. Skin thinning.
  5. Abdominal striae.
  6. Mood change.
  7. Osteoporosis.
  8. Muscle thinning.
  9. Weight gain.
258
Q

What investigations might you do in someone with Cushing’s syndrome?

A
  1. Overnight dexamethasone suppression test - failure to suppress cortisol.
  2. Late night salivary cortisol - loss of circadian rhythm.
  3. Urinary free cortisol is raised.
  4. Loss of circadian rhythm.
259
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.

260
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion.

Too much ADH = very concentrated urine and hyponatreamia.

261
Q

Give 3 symptoms of SIADH.

A
  1. Anorexia.
  2. Nausea.
  3. Malaise.
  4. Headache.
  5. Confusion.
262
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.
263
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.
264
Q

What is Conn’s syndrome?

A

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

265
Q

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

A
  1. Hypertension.
  2. Hypokalaemia.

Sodium will be normal or slightly raised.

266
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.

267
Q

What can cause Conn’s syndrome?

A

Adrenal adenoma.

268
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.
269
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.
270
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.
271
Q

What is the treatment for Conn’s syndrome?

A
  1. Laparoscopic adrenalectomy.

2. Spironolactone (aldosterone antagonist).

272
Q

What does the parathyroid control?

A

Serum calcium levels.

A low serum calcium triggers the release of PTH and a high serum calcium triggers c-cells to release calcitonin.

273
Q

What hormone does the parathyroid secrete and what is its function?

A

PTH - secreted in response to low serum calcium.

PTH increases bone resorption; increases calcium reabsorption at the kidney and activates vitamin D which then acts on the intestine to increase calcium absorption.

274
Q

What is released by c-cells in the parathyroid in response ot high serum calcium?

A

Calcitonin.

275
Q

What is the affect of hyperparathyroidism on serum calcium levels?

A

Hyperparathyroidism -> hypercalcaemia.

276
Q

Give 5 symptoms of hyperparathryoidism.

A

Hyperparathyroidism -> hypercalcaemia:

  1. Renal/biliary stones.
  2. Bone pain.
  3. Abdominal pain.
  4. Polyuria.
  5. Depression, anxiety, malaise.

Stones,bones, groans, thrones, moans.

277
Q

Give 3 causes of hyperparathyroidism.

A
  1. Primary: parathyroid adenoma - ↑PTH ↑Calcium ↓Phosphate.
  2. Secondary: physiological hypertrophy in an attempt to correct low calcium.
  3. Prolonged uncorrected hypertrophy.
278
Q

Describe the treatment for hyperparathyroidism.

A
  1. High fluid intake, low calcium diet.
  2. Excision of adenoma.
  3. Correct underlying cause.
  4. Parathyroidectomy.
279
Q

What is the affect of hypoparathyroidism on serum calcium levels?

A

Hypoparathyroidism -> hypocalcaemia.

280
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.
281
Q

What is the treatment for hypoparathyroidism?

A

Calcium supplements.

282
Q

Give 5 causes of hypocalcaemia.

A
  1. Dietary insufficiency.
  2. Anticonvulsant therapy.
  3. CKD.
  4. Vitamin D deficiency.
  5. Osteomalacia.
  6. Hypoparathyroidism.
283
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.
284
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.
285
Q

What is phaeochromocytoma?

A

A rare catecholamine secreting tumour in the adrenal medulla.

286
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.
287
Q

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

A

Bloods - raised WCC, increased plasma metadrenaline and normetadrenaline.

288
Q

What is the treatment for phaeochromocytoma?

A
  1. Alpha blocker e.g. phenoxybenzamine.
  2. Beta blockers.
  3. Surgical resection of tumour.
289
Q

What is the major concern in someone with phaeochromocytoma?

A

Phaeochromocytomare are a dangerous but treatable cause of hypertension.

290
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.
291
Q

What is adrenal insufficiency?

A

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

292
Q

Give 6 symptoms of adrenal insufficiency.

A
  1. Tanned - pigmentation.
  2. Tired.
  3. Tearful.
  4. Thin - weight loss.
  5. Headaches.
  6. Abdominal cramps.
  7. Myalgia.
  8. Throwing up.
  9. Weakness.
293
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.
294
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.
295
Q

What is the treatment for adrenal insufficiency?

A

Hormone replacement - any steroids e.g. hydrocortisone.

In addison’s disease replace aldosterone with fludrocortisone.

296
Q

Give 3 causes of hypokalaemia.

A
  1. Diuretics.
  2. D+V.
  3. Conn’s syndrome.
  4. Insulin.
297
Q

Give 5 symptoms of hypokalaemia.

A
  1. Muscle weakness.
  2. Hypotonia.
  3. Hyporeflexia.
  4. Palpitations.
  5. Arrhythmia.
  6. Nausea and vomiting.
  7. Cramps.
298
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.
299
Q

Give 3 causes of hyperkalaemia.

A
  1. AKI.
  2. NSAIDs.
  3. Metabolic acidosis.
  4. K+ sparing diuretics.
300
Q

Give 3 symptoms of hyperkalaemia.

A
  1. Weakness.
  2. Palpitations.
  3. Tachycardia.
  4. Chest pain.
301
Q

What ECG changes might you see in someone with hyperkalaemia?

A
  1. Tall tented T waves.
  2. Wide QRS.
  3. Small P waves.
302
Q

Give 3 causes of hypercalcaemia.

A
  1. Hyperparathyroidism.
  2. Hypercalcaemia of malignancy.
  3. Vitamin D toxicity.
  4. Myeloma.
303
Q

What biochemical test might you want to do to establish the cause of hypercalcaemia?

A

PTH measurement.

304
Q

How can hypercalcaemia be treated?

A
  1. IV normal saline.
  2. IV furosemide.
  3. IV calcitonin.
305
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.

306
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.
307
Q

pH 7.1; pCO2 1.2 kPa; pO2 11.1 kPa; Bicarbonate 4mmol/l.

Interpret this blood gas result.

A

Severe metabolic acidosis.

308
Q

Give 3 causes of severe metabolic acidosis.

A
  1. Diabetic ketoacidosis.
  2. Severe sepsis.
  3. Uraemia.
  4. Lactic acidosis.
309
Q

What is hirsutism?

A

Excess hair growth in women in a male pattern.

310
Q

What is the cause of hirsutism?

A

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

311
Q

What diseases are associated with polycystic ovary syndrome?

A
  1. Insulin resistance and so T2DM.
  2. Hypertension.
  3. Hyperlipidaemia.
  4. CV disease.
312
Q

Give 5 symptoms of polycystic ovary syndrome.

A
  1. Amenorrhoea.
  2. Oligomenorrhoea.
  3. Hirsutism.
  4. Acne.
  5. Overweight.
  6. Infertility.
313
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.
314
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.
315
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.
316
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.

317
Q

Which bacteria is responsible for causing impetigo?

A

Staphylococcus aureus.

318
Q

What is the treatment for impetigo?

A

Flucloxacillin.

319
Q

Give 5 symptoms of DKA.

A
  1. Polyuria.
  2. Polydipsia.
  3. Weight loss.
  4. Nausea/vomiting.
  5. Confusion.
  6. Weakness.
320
Q

Give 3 causes of DKA.

A
  1. Unknown.
  2. Infections.
  3. Treatment errors - not administering enough insulin.
  4. Having undiagnosed T1DM.
321
Q

Describe the triad of DKA.

A
  1. Acidaemia – blood pH < 7.3
  2. Hyperglycaemia – blood glucose > 11mmol/L.
  3. Ketonaemia.
322
Q

Give 4 potential complications of untreated DKA.

A
  1. Oedema.
  2. Adult respiratory distress syndrome.
  3. Aspiration pneumonia.
  4. Thromboembolism.
  5. Death.
323
Q

Give 5 symptoms of hypoglycaemia.

A
  1. Hunger.
  2. Sweating.
  3. Tachycardia.
  4. Anxious.
  5. Shaking.
324
Q

Give 3 endocrine diseases that can cause diabetes.

A
  1. Cushing’s.
  2. Acromegaly.
  3. Phaeochromocytoma.
325
Q

What class of drugs can cause diabetes?

A
  1. Steroids.
  2. Thiazides.
  3. Anti-psychotics.
326
Q

Give 3 secondary causes of adrenal insufficiency.

A
  1. Hypopituitarism.
  2. Withdrawal from long term steroids.
  3. Infiltration.
  4. Infection.
  5. Radiotherapy.
327
Q

An adrenal crisis is a common presentation of adrenal insufficiency. Give 3 features of an adrenal crisis.

A
  1. Hypotension.
  2. Fatigue.
  3. Fever.
  4. Hypoglycaemia.
  5. Hyponatraemia.
  6. Hyperkalaemia.
328
Q

How would you treat an adrenal crisis?

A

Hydrocortisone and IV saline.

329
Q

State whether sodium and potassium levels would be high or low in someone with adrenal insufficiency.

A
  • Hyponatraemia.
  • Hyperkalaemia.

Lack of aldosterone and so less sodium is reabsorbed and less potassium is excreted.

330
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.

331
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.

332
Q

Give 3 causes of hyponatraemia.

A
  1. SIADH.
  2. Sodium deficiency.
  3. Renal failure.
  4. Malignancy.
333
Q

Define hyponatraemia.

A

Serum sodium <135mmol/L.

334
Q

Give 3 signs of hyponatraemia.

A
  1. Anorexia.
  2. Confusion.
  3. Headache.
  4. Lethargy.
  5. Weakness.
335
Q

What is the treatment for acute hyponatraemia?

A

Give a bolus dose of saline.

336
Q

What are the units for osmolality?

A

mOsmol/Kg.

337
Q

What is the primary cation in ICF?

A

K+.

338
Q

What is the primary cation in the ECF?

A

Na+.

339
Q

what are the primary anions in the ECF?

A

Cl- and HCO3-.

340
Q

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

A

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

341
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.

342
Q

What GPCR does ADH bind to on renal tubules?

A

V2.

343
Q

Do you have hypernatraemia or hyponatraemia in diabetes insipidus?

A

Hypernatraemia.

344
Q

Give 3 causes of cranial diabetes insipidus.

A
  1. Tumours.
  2. Trauma.
  3. Infections.
  4. Idiopathic.
  5. Genetic - AR.
345
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.
346
Q

In what class of drugs does metformin belong?

A

Biguanide.

347
Q

Give an example of a sulfonylurea.

A

Tolazamide and gliclazide.

348
Q

Give a sign of Cushing’s syndrome that is due to impairments in carbohydrate metabolism.

A

Diabetes mellitus.

349
Q

Give a sign of Cushing’s syndrome that is due to electrolyte disturbances.

A
  1. Sodium retention.

2. Hypertension.

350
Q

People with Cushing’s syndrome may have immune dysfunction. Give a consequence of this.

A

Increased susceptibility to infection.

351
Q

Why is it important to take a drug history when speaking to someone with potential Cushing’s?

A

To exclude exogenous glucocorticoid exposure as a potential cause.

352
Q

Name 2 drugs that suppress cortisol synthesis and so can be used in the treatment of Cushing’s disease.

A
  1. Metyrapone.

2. Ketoconazole.

353
Q

When might you see signs of hypercortisolism without Cushing’s disease?

A
  1. Pregnancy.
  2. Depression.
  3. Alcohol dependence.
  4. Obesity.
354
Q

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

A

Euvolaemic.

355
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.
356
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.
357
Q

Would you associate SIADH with hyponatraemia or hypernatraemia?

A

Hyponatraemia <135mmol/L.

358
Q

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

A

Plasma hypo-osmolality <275mOsm/Kg.

359
Q

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

A

High urine osmolality.

360
Q

Give 2 clinical signs of hypervolaemia.

A
  1. Ascites.

2. Oedema.

361
Q

Give 3 clinical signs of hypovolaemia.

A
  1. Hypotension.
  2. Tachycardia.
  3. Decreased skin turgor.
  4. Dry mucus membranes.
362
Q

Define puberty.

A

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

363
Q

What is the first sign of puberty in girls?

A

Menarche.

364
Q

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

A

Ovarian oestrogen.

365
Q

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

A

Ovarian and adrenal androgens.

366
Q

What is the first sign of puberty in boys?

A

First ejaculation, often nocturnal.

367
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.
368
Q

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

A

Tanner scale.

369
Q

What is thelarche?

A

Breast development.

- Takes about 3 years and is controlled by oestrogen.

370
Q

Describe the 3 stages of thelarche.

A
  1. Ductal proliferation.
  2. Adipose deposition.
  3. Enlargement of areola and nipple.
371
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.

372
Q

Give 2 signs of adrenarche.

A
  1. Body odour.

2. Mild acne.

373
Q

What is pubarche?

A

Growth of pubic hair.

374
Q

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

A

Precocious puberty.

375
Q

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

A

Brain tumour!

376
Q

What is the treatment for precocious puberty?

A

GnRH super agonist to suppress pulsatility of GnRH secretion.

377
Q

What is delayed puberty?

A

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

378
Q

What is precocious puberty?

A

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

379
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.

380
Q

Give 3 consequences of delayed puberty.

A
  1. Psychological problems.
  2. Reproduction defects.
  3. Reduced bone mass.
381
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.

382
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.
383
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.
384
Q

What is hypergonadotropic hypogonadism?

A

Primary gonadal failure!

- Testes or ovarian failure.

385
Q

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

A

High FSH/LH low oestrogen/testosterone.

386
Q

Give 2 examples of hypergonadotropic hypogonadism.

A
  1. Turner Syndrome (45X).

2. Klinefelter’s syndrome (47XXY).

387
Q

What is hypogonadotropic hypogonadism?

A

Secondary gonadal failure!

- Hypopituitary or problems with the hypothalamus.

388
Q

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

A

Low FSH/LH and low testosterone/oestrogen.

389
Q

Give an example of hypogonadotropic hypogonadism.

A

Kallman syndrome.

390
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).

391
Q

Give 3 signs of Turner syndrome.

A
  1. Short stature.
  2. Delayed puberty.
  3. CV and renal malformations.
  4. Recurrent otitis media.
392
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).

393
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.
394
Q

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

A

Azoospermia - semen contains no sperm.

395
Q

Give 4 symptoms of Klinefelter’s syndrome.

A
  1. Reduced pubic hair.
  2. Tall stature.
  3. Reduced IQ.
  4. Small testicles (<5ml).
396
Q

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

A

Breast cancer.

397
Q

What is Kallman syndrome?

A

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

398
Q

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

A

Smell! 75% are ansomia.

399
Q

How is Kallman syndrome inherited?

A

X linked recessive or dominant.

400
Q

How do you treat asymptomatic SIADH?

A

Fluid restriction.

401
Q

How do you treat symptomatic SIADH of acute onset?

A

Give 3% saline.

402
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.

Phase 2A medicine (11 decks)

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