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Phase 2a Sheffield Medicine > Endocrinology and Dermatology > Flashcards

Endocrinology and Dermatology Flashcards

1
Q

Define Endocrine

A

Pour secretions into blood stream

e.g. thyroid, adrenal and beta cells of pancreas

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2
Q

Define Exocrine

A

Glands pour secretions into a duct to the site of action

e.g. pancreas - amylase+lipase

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3
Q

Define Endocrine

A

Acts on distant cells

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4
Q

Define Paracrine

A

Acting on adjacent cells

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5
Q

Define Autocrine

A

Feedback on same cell that secreted the hormone

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6
Q

What are 5 ways to control hormone action?

A
  1. Metabolism
  2. Receptor induction
  3. Receptor down regulation
  4. Synergism e.g. Glucagon + adrenaline
  5. Antagonism e.g. Glucagon + insulin
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7
Q

What is the function of Oxytocin?

A

Milk secretion and uterine contraction

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8
Q

What is the function of Theca Cells?

A

Stimulated by LH to produce androgens that diffuse into granulosa cells to be converted into oestrogen.

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9
Q

What is the function of Sertoli cells?

A

Sertoli cells produce MIF and inhibin and activin which acts on the pit gland to regulate FSH

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10
Q

What is the function of granulosa cells?

A

Granulosa cells are stimulated by FSH to convert androgen’s into oestrogen using aromatase

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11
Q

What is the function of Leydig Cells?

A

Stimulated by LH to produce testosterone

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12
Q

What does LH act on?

A

In ovaries - Theca cells

In testes - Leydig Cells

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13
Q

What does FSH act on?

A

In ovaries - Granulosa cells

In Testes - Sertoli cells

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14
Q

What is the LH/FSH axis?

A

Hypothalamus –> GnRH –> AP –> FSH/LH –> Ovaries/testes

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15
Q

What does FSH do to granulosa cells?

A

Produces Oestrogen

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16
Q

What does FSH do to Sertoli cells?

A

Induces spermatogenesis

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17
Q

What does LH do to Theca cells?

A

Produces androgens to diffuse to the granulosa cells to be converted to oestrogen.

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18
Q

What does LH do to Leydig Cells?

A

Produce testosterone.

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19
Q

What are some characteristics of Water soluble hormones?

A

Unbound and binds to surface receptor, short half-life and fast clearance e.g. peptide (receptors in cell membrane)

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20
Q

What are the characteristics of fat soluble hormones?

A

Protein bound and diffuses into cell, long half life and slow clearance e.g. Thyroid hormone + cortisol (receptors in cytoplasm)

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21
Q

What is a prolactinoma?

A

A condition where an adenoma causes excess production + release of prolactin.

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22
Q

What are 2 causes of prolactinoma?

A

Pituitary adenoma

Anti-dopaminergic drugs

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23
Q

What are 5 signs of prolactinoma?

A 
Infertility
Amenorrhoea
Libido loss
Visual field effects (bitemporal hemianopia) 
Headaches.
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24
Q

What is the treatment for prolactinoma?

A

Dopamine agonist e.g. Cabergoline

This causes a negative feedback –> promoting dopamine and preventing the release of prolactin.

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25
Q

What does prolactin act on?

A

The mammary glands to produce milk –> + feedback mechanism, breast sucking = less dopamine.

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26
Q

What is the mechanism of prolactin release?

A

Hypothalamus –> dopamine (-) –> AP –> Prolactin

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27
Q

What would happen if you block the AP’s ability to produce dopamine?

A

Levels of prolactin would increase.

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28
Q

What are the consequences of too much prolactin?

A

Galactorrhoea
Low libido and testosterone
Infertility
Menstrual irregularity

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29
Q

What is acromegaly?

A

Hormonal disorder resulting from too much GH

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30
Q

What is the cause of acromegaly?

A

Benign adenoma on the pit gland.

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31
Q

What comorbidities are seen in Acromegaly?

A

T2 Diabetes, arthritis, Cerebrovascular events, hypertension + HD, sleep apnoea

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32
Q

What are the symptoms of Acromegaly?

A
  • Bigger hands and feet
  • Excessive sweating
  • Headache
  • Tiredness
  • Weight gain
  • Deep voice
  • Amenorrhoea
  • Change in appearance
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33
Q

What signs might someone with acromegaly present with?

A

Bi-temporal hemianopia, spade like hands and feet, large tongue, jaw protrusion, interdental separation .

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34
Q

What investigations might you do on a patient with suspected acromegaly?

A

Plasma GH levels can exclude acromegaly

Serum IGF-1 level raised

Oral glucose tolerance test  failure of glucose to suppress serum GH and thus IGF-1

MRI of pituitary

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35
Q

What is the treatment for acromegaly?

A

Trans-sphenoidal surgical resection

Radiotherapy

Medical therapy –> dopamine agonists, somatostatin analogues

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36
Q

Give an advantage and disadvantage of Trans-sphenoidal surgical resection.

A

Advantage - Complete removal of the tumour

Disadvantage - many complications are possible e.g. Haemorrhage, CNS injury and hypopituitarism

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37
Q

Give an advantage and disadvantage of dopamine agonists in the treatment of acromegaly.

A

Advantage - no risk of hypopituitarism

Disadvantage - maybe ineffective.

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38
Q

How do dopamine agonists and somatostatin analogues work in the treatment of acromegaly?

A

They look to control IGF and GH levels.

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39
Q

What two drugs can be used to treat acromegaly?

A

Cabergoline - dopamine agonist

Octreotide - somatostatin analogue - v effective.

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40
Q

What is the main reason for diabetic complications?

A

Poor glycaemic control

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41
Q

What can acute hyperglycaemia cause?

A

DKA and Hyperosmolar coma

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42
Q

What can chronic hyperglycaemia cause?

A

Micro/macrovascular complications

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43
Q

What are 3 microvascular complications of diabetes?

A
  1. Diabetic retinopathy
  2. Diabetic nephropathy
  3. Diabetic peripheral neuropathy
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44
Q

What are 2 macrovascular complications of diabetes?

A

CV Disease

Stroke

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45
Q

What is the most common type of diabetic neuropathy?

A

Distal symmetrical polyneuropathy

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46
Q

What are 5 signs of autonomic neuropathy?

A
  1. Hypotension
  2. HR affected
  3. Diarrhoea/constipation
  4. Erectile dysfunction
  5. Dry skin
  6. Incontinence
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47
Q

What is a consequence of insensitivity?

A

Foot ulceration –> failure to heal –> infection and amputation.

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48
Q

How is neuropathy distributed?

A

Glove and stocking - starts at the toes and moves proximally.

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49
Q

What are the risk factors for diabetic neuropathy?

A
  1. Poor glycaemic control
  2. Hypertension
  3. Smoking
  4. HbA1c
  5. Overweight
  6. Long duration of DM
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50
Q

What is the treatment for diabetic neuropathy?

A
  • Improve glycaemic control
  • Pain relief
  • Antidepressants
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51
Q

What are the consequences of diabetic neuropathy?

A
  1. Pain - burning and triggered nocturnally
  2. Autonomic neuropathy – damage to nerves that supply structures that reg HR, BP, emptying
  3. Insensitivity
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52
Q

Would you have a decreased or increased pulse in a diabetic neuropathic foot?

A

Increased.

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53
Q

What is diabetic retinopathy?

A

Complication of diabetes caused by damage to light sensitive tissue in the retina.

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54
Q

What is the pathophysiology of diabetic retinopathy?

A

Micro-aneurysm –> pericyte loss + protein leakage –> occlusion = ischaemia.

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55
Q

What are the risk factors for diabetic retinopathy?

A
  1. Long term DM
  2. Poor glycaemic control
  3. Pregnancy
  4. Hypertension
  5. High HbA1c
  6. Insulin treatment
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56
Q

What can diabetic retinopathy be subdivided into?

A

Proliferation - evidence of neovascularisation

Nonproliferation

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57
Q

What are the 3 stages of diabetic retinopathy?

A

R1 Retinopathy grade – non-proliferative – interretinal hemorrhages, exudate and micro-aneurysms

R2 Retinopathy grade – Pre proliferative – venous beading, growth of new vessels

R3 Retinopathy grade – Proliferative – new blood vessel on disk

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58
Q

What is the treatment of diabetic retinopathy?

A

People with diabetes are offered regular screening

Laser therapy treats neovascularisation

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59
Q

Give 3 signs of acute ischaemia in someone with PVD

A
  1. Pulseless
  2. Pale
  3. Cold
  4. Pain
  5. Paralysis
  6. Paraesthesia
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60
Q

How can you avoid amputation in patients with diabetes?

A
  • Screening for insensitivity
  • Education
  • MDT Food clinics
  • Podiatry
  • Revascularisation
  • Pressure relieving footwear
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61
Q

What is diabetic nephropathy?

A

Chronic loss of kidney function in those with DM.

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62
Q

What is the hallmark of diabetic nephropathy?

A

Development of proteinuria and progressive decline in renal function.

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63
Q

What happens to the glomerular basement membrane in Diabetic nephropathy?

A

It thickens.

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64
Q

How does microalbuminuria present in Type 1 and Type 2 DM?

A

Type 1 - 5-10 years post diagnosis

Type 2 - Immediately

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65
Q

How can you treat diabetic nephropathy?

A 
Glycaemic control 
BP Control 
ACEi
Cholesterol control
Proteinuria
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66
Q

What controls serum calcium levels?

A

The parathyroid.

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67
Q

What two hormones does the Parathyroid release to modify calcium levels.

A

PTH

Calcitonin

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68
Q

When is PTH triggered and what is its action?

A

Low serum Ca2+ triggers release of PTH –> increases

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69
Q

When is Calcitonin triggered and what is its action?

A

High serum Ca2+ triggers c-cells to release calcitonin

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70
Q

What is the action of PTH?

A

Increases bone resorption

Increases calcium reabsorption at the kidney

Activates vit D –> acts on the intestine to increase calcium absorption

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71
Q

What does hyperparathyroidism cause?

A

Hypercalcaemia

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72
Q

What does hypoparathyroidism cause?

A

Hypocalcaemia

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73
Q

What are the causes of hyperparathyroidism?

A
  1. Primary – Parathyroid adenoma  PTH and Ca up, phosphate down (Most common)
  2. Secondary – Physiological hypertrophy to correct low Ca
  3. Tertiary – Renal failure, can’t activate Vit D
  4. Prolonged uncorrected hypertrophy
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74
Q

What are the symptoms of hyperparathyroidism?

A 
Renal/biliary stones 
Bone pain 
Abdo Pain 
Polyuria 
Depression, anxiety and malaise

Stones, bones, groans, thrones, moans.

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75
Q

What is the treatment for hyperparathyroidism?

A
  1. High fluid intake, low calcium diet.
  2. Excision of adenoma
  3. Correct underlying cause
  4. Parathyroidectomy
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76
Q

What investigations would you do for hyperparathyroidism?

A

ECG

Thyroid function tests

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77
Q

What ECG changes would you see in hyperparathyroidism?

A

Tall T waves

Short QT waves

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78
Q

What is hypercalcaemia?

A

High serum Ca2+ levels.

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79
Q

What are 3 causes of hypercalcaemia?

A
  1. Hyperparathyroidism
  2. Hypercalcaemia of malignancy
  3. Vit D toxicity
  4. Myeloma
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80
Q

How could you establish the cause of hypercalcaemia?

A

PTH test for hyperparathyroidism

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81
Q

What are the symptoms of hypercalcaemia?

A
  1. Constipation
  2. Vomiting
  3. Depression
  4. Confusion
  5. Increased thirst and frequent urination
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82
Q

What is the treatment of hypercalcaemia?

A
  1. IV normal saline
  2. Iv Furosemide
  3. IV calcitonin
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83
Q

What are the symptoms of hypoparathyroidism?

A
  1. Spasm
  2. Anxious/irritable
  3. Seizures
  4. Increased muscle tone
  5. Confusion
  6. QT prolongation
  7. Paraesthesia around lips
  8. Tetany and increased reflexes
  9. QT elongation
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84
Q

What are the causes of hypoparathyroidism?

A
  • AI disease e.g. Addison’s disease
  • Injury to Parathyroid gland
  • Low blood magnesium levels
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85
Q

What ECG changes would you see in hypoparathyroidism?

A
  • Small T waves

- Long QT interval

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86
Q

What is the treatment of hypoparathyroidism?

A

Calcium supplements

Resolve underlying cause

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87
Q

What is the cause of hypocalcaemia?

A
  1. Dietary insufficiency
  2. Anticonvulsant therapy
  3. CKD
  4. Vit D deficiency
  5. Osteomalacia
  6. Hypoparathyroidism
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88
Q

What are the symptoms of hypocalcaemia?

A
  1. Muscle cramps and spasms
  2. Bradycardia
  3. Muscle weakness
  4. Seizures
  5. Facial twitching
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89
Q

What is the treatment for hypocalcaemia?

A
  • Calcium supplements

- Treat underlying cause

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90
Q

What metabolic changes are associated with pregnancy?

A
  1. Increased EPO, Cortisol, Nad
  2. High CO
  3. High Cholesterol + TG
  4. Pro thrombotic and inflammatory state
  5. Insulin resistance
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91
Q

When does the thyroid gland start to develop?

A

Foetal thyroid follicles and thyroxine synthesis starts at week 10

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92
Q

What condition is common in pregnancy?

A

Hypothyroidism

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93
Q

What is the treatment for hypothyroidism?

A

Levothyroxine

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94
Q

Give 5 gestational syndromes

A
  • Pre-eclampsia
  • Gestational diabetes
  • Obstetric Cholestasis
  • Gestational thyrotoxicosis
  • Transient Diabetes insipidus
  • Postnatal depression
  • Postpartum thyroiditis
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95
Q

What are some of the complications post pregnancy from untreated hypothyroidism?

A
  1. Gestational hypertension
  2. Placental abruption
  3. Post-partum haemorrhage
  4. Low birth weight
  5. Neonatal goitre
  6. Pre-eclampsia
  7. Risk of miscarriage
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96
Q

Why can hCG activate TSH receptors and cause hyperthyroidism?

A

HCG and TSH are glycoprotein hormones –> very similar structures so hCG can activate TSH receptors

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97
Q

Is hypothyroidism or thyrotoxicosis more commin pregnancy?

A

Hypothyroidism

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98
Q

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

A

Graves - symptoms predate pregnancy and get more severe during it –> Goitre + TSH-R antibodies present

Gestational thyrotoxicosis - symtpoms do not predate pregnancy –> No goitre or TSH-R antibodies

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99
Q

Consequences of untreated hypothyroidism in pregnancy?

A
  1. Gestational hypertension
  2. Placental abruption
  3. Post-partum haemorrhage
  4. Low birth weight
  5. Neonatal goitre
  6. Pre-eclampsia
  7. Risk of miscarriage
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100
Q

Consequences of untreated hyperthyroidism in pregnancy?

A

Intra-uterine growth restriction
Low birth weight
pre-eclampsia
risk of still birth/miscarriage.

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101
Q

What disease is described as a disorder of carb metabolism characteristed by Hyperglycaemia

A

DM

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102
Q

What is the most common cause of hyperthyroidism in Pregnancy?

A

Graves

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103
Q

What is the management for hyperthyroidism?

A

Carbimazole - can harm foetus so given later

Propylthiouracil

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104
Q

What are the different types of hypothyroidism?

A
  • Primary - Thyroid gland dysfunction
  • Secondary – Pituitary (TSH not being made)
  • Tertiary – Hypothalamic dysfunction - not making TRH
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105
Q

What are 5 causes of hypothyroidism?

A

AI Thyroiditis e.g. Hashimoto’s
Post-partum thyroiditis
Iatrogenic – thyroidectomy + radioiodine therapy
Drug induced – carbimazole, amiodarone and lithium
Iodine deficiency

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106
Q

What are the signs of hypothyroidism?

A
  • Mental slowness
  • Bradycardia
  • Anaemia
  • Loss of eyebrows
  • Dry thin hair
  • Cold peripheries
  • Hypertension
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107
Q

What is the management of hypothyroidism?

A

Levothyroxine

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108
Q

What would be the investigations you would order in suspected hypothyroidism?

A
  • TFT – serum TSH high, T4 low

- Thyroid antibodies –> TPO, TG, TRAb

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109
Q

What is thyrotoxicosis?

A

Excess thyroid hormone production due to any cause

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110
Q

What are 5 causes of thyrotoxicosis?

A
  • Increase production e.g. Graves, toxic adenoma
  • Leakage of t3/4 due to follicular damage
  • Ingestion
  • Thyroiditis
  • Drug induced
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111
Q

What is the pathophysiology of graves disease?

A

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

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112
Q

Give 5 symptoms of Grave’s disease that doesn/t include opthalmopathy signs

A 
weight loss, 
increased appetite,
irritable, tremor,
 palpitations,
 goitre
 diarrhoea
malaise
vomiting
muscle spasm
tachycardia, Tachycardia, arrhythmias, heat intolerance
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113
Q

Give 5 signs of Graves that dont include opthalmopathy signs.

A
  1. Tachycardia
  2. Arrythmia e.g. AF
  3. Warm peripheries
  4. Muscle spasm
  5. Pre-tibial myxoedema
  6. Thyroid acropach (clubbing and swollen fingers)
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114
Q

Give 5 opthalmology signs of Grave’s

A

exophthalmos (bulging eyes), redness, conjunctivitis, pre-orbital oedema, extra-ocular swelling

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115
Q

What histology would you see in someone with grave’s disease?

A

lymphocyte infiltration and thyroid follicle destruction

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116
Q

What is the treatment for Grave’s disease?

A

Surgery –> partial thyroidectomy

Radioiodine drugs – emit beta particles that destroy thyroid follicles, so TH production goes down.

Ant-thyroid drugs e.g. carbimazole.

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117
Q

How does carbimazole work in treating Grave’s disease?

A

Targets TPO so prevents T3/T4 formation.

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118
Q

What is a serious side effect of Carbimazole?

A

Agranulocytosis

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119
Q

How do radioiodine drugs treat Grave’s disease?

A

Radioiodine drugs emit B particles that destroy Thyroid follicles so TH production goes down.

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120
Q

What are 3 potential complications of a partial thyroidectomy?

A

hypothyroidism, hypocalcaemia, recurrent laryngeal palsy, bleed

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121
Q

How does PTU work in hyperthyroidism?

A

Preventing the synthesis of new thyroid hormone by stopping T4–>T3

122
Q

What is hyperthyroidism?

A

An excess of TH

123
Q

What is the mechanisms causing hyperthyroidism?

A
  1. Overproduced thyroid hormone
  2. Leakage of preformed hormone from thyroid e.g. Thyroiditis
  3. Ingestion of excess TH.
124
Q

What is the cause of hyperthyroidism?

A
  1. Graves’ disease
  2. Toxic multinodular goitre
  3. Toxic adenoma
  4. Thyroiditis
  5. Drug induced – Iodine, amiodarone, lithium
125
Q

What can amiodarone cause?

A

Thyroiditis and leakage

126
Q

What can radiocontrast agents cause?

A

Temporary hyperthyroidism

127
Q

What are the clinical features of hyperthyroidism?

A
  • Sweating + Heat intolerance
  • Anxiety
  • Tremor
  • Tachycardia
  • Weight loss
  • Hyperphagia
  • Lid Lag + stare
128
Q

What investigations would you order in someone with suspected hyperthyroidism?

A

Thyroid function test to confirm biochemical hyperthyroidism

Diagnosis of underlying cause is important to treat it

129
Q

What would be the effect on Free T4+3 and TSH in primary hyperthyroidism?

A

Free t4 + t3 up, suppressed TSH in primary hyperthyroidism

130
Q

What would be the effect on Free T4+3 and TSH in secondary hyperthyroidism?

A

Free t4 + t3 up, but high TSH due to adenoma in secondary hyperthyroidism

131
Q

What are the 3 thyroid antibodies?

A

TPO, TG, TRAb

132
Q

What 3 thyroid antibodies would you find in a person with AI thyroid disease?

A

TPO, TG, TRAb

133
Q

What is the treatment of hyperthyroidism?

A
  • Antithyroid drugs – Carbimazole, propylthiouracil (PTU), methimazole
  • Radioiodine
  • Surgery (partial or total thyroidectomy)
134
Q

Who is predisposed to thyroid autoimmunity?

A

Genetic and environmental factors
Women and postpartum is the biggest risk (HLADR3)
Environmental – stress, high iodine intake, smoking

135
Q

What AI diseases are associated with Thyroid autoimmunity?

A
  1. T1DM
  2. Addison’s disease
  3. Vitiligo
  4. Alopecia areata
  5. MG
136
Q

What is a goitre?

A

Palpable and visible thyroid enlargement

137
Q

What are the symptoms of hypothyroidism?

A
  1. Meorrhagia – heavy bleeding
  2. Obesity/weight gain
  3. Malar flush
  4. Tiredness
  5. Cold inteolerance
  6. Goitre
  7. Depression/ poor energy levels/ eyebrow loss
138
Q

What is Conns syndrome?

A

Primary hyperaldosteronism – high aldosterone independent of RAAS causing increased H20 and sodium retention and potassium excretion.

139
Q

What are the main signs of Conn’s syndrome?

A
  1. Hypertension
  2. Hypokalaemia
    Sodium will be normal or raised
140
Q

What are the main symptoms of Conn’s syndrome?

A
  1. Muscle weakness
  2. Tiredness
  3. Polyuria
  4. Hypokalaemia
141
Q

What is the cause of Conn’s syndrome?

A

Adrenal Adenoma

142
Q

What are the hormones involved in Conn’s syndrome?

A

Aldosterone raised – synthesised in zona glomerulosa

Renin is reduced – synthesised by juxta-glomerular cells

143
Q

What investigations would you use to diagnose Conn’s syndrome?

A
  1. Bloods – U+E (for renin and aldosterone)

2. Plasma aldosterone renin ratio can be used as an initial screening test.

144
Q

What ECG changes would you see in Conn’s syndrome?

A
  • Increased amplitude and width of P waves
  • Flat T waves
  • ST depression
  • Prolonged QT interval
  • U waves
145
Q

What is the management of Conn’s syndrome?

A
  1. Laparoscopic adrenalectomy

2. Spironolactone (aldosterone antagonist)

146
Q

What are the constituents of the islets of langerhans?

A
  • Beta cells (70%) – Secrete Insulin
  • Alpha Cells (20%) – Secrete Glucagon
  • Delta Cells (8%) – secrete somatostatin
  • Polypeptide secreting cells (2%)
147
Q

Why are A and B cells close together in the IOL?

A

To allow them to crosslink

148
Q

What does cortisol inhibit and activate?

A

Inhibits insulin

Activates glucagon

149
Q

What is the mechanism of insulin secretion?

A

Glucose binds to Beta cells –> Glucose-6-phosphate –> ADP –> ATP –> K channels close –> membrane depolarisation –> Ca2+ channels open and influx  insulin release

150
Q

What is the physiological response to low blood glucose in a fasting state?

A
  • Glycogenolysis and gluconeogenesis
  • Reduced peripheral glucose intake
  • Lipolysis and muscle breakdown
  • Stimulates release of gluconeogenic precursors
151
Q

What is the physiological response to high blood glucose after feeding?

A

High blood glucose = high insulin and low glucagon

  • Glycogenolysis and gluconeogenesis supressed
  • Glucose is taken up by peripheral muscle and fat cells
  • Lipolysis and muscle breakdown supressed

3 carbon precursors are needed for gluconeogenesis

152
Q

What are the tests you would order in a patient suspected with diabetes?

A

Oral glucose tolerance
Random glucose
Fasting glucose
HbA1c

153
Q

What test results would you consider an indicator of DM?

A

Fasting plasma glucose in diabetes = >7mmol/L

Random plasma glucose in diabetes = >11mmol/L

Oral glucose tolerance test in diabetes = 7mmol/L fasting and >11mmol/L over 2 hours

HbA1c in diabetes = >48mmol/L

154
Q

What is type 1 diabetes mellitus?

A

A disorder of carb metabolism characterised by hyperglycaemia

155
Q

What is T1DM characteristed by?

A

Presentation in childhood

Severe impaired insulin secretion

156
Q

What is the aetiology of type 1 diabetes?

A

Beta cells express HLA antigens –> AI destruction –> Beta cell loss –> impaired insulin secretion

157
Q

What are the symptoms of T1DM?

A
  • Weight loss
  • Thirst (fluid + electrolyte loss)
  • Polyuria (osmotic diuresis)
158
Q

What are the two main consequences of T1DM?

A

Hyperglycaemia and Diabetic ketoacidosis

159
Q

What are the investigations and results for diagnosis in DM?

A

Fasting plasma glucose in diabetes = >7mmol/L

Random plasma glucose in diabetes = >11mmol/L

Oral glucose tolerance test in diabetes = 7mmol/L fasting and >11mmol/L over 2 hours

HbA1c in diabetes = >48mmol/L

160
Q

What is the treatment/management of T1DM?

A
  • Education
  • Healthy diet – low in sugar, high in carbs
  • Regular activity and healthy BMI
  • BP and Hyperlipidaemia control
  • Insulin – injected into SC fat.
161
Q

What is Type 2 diabetes mellitus?

A

Characterised by both Impaired insulin secretion and insulin resistance

162
Q

What are characteristics of T2DM?

A

Insulin secretion is impaired due to lipid deposition in pancreatic islets

Hepatic insulin resistance is the driving force of hyperglycaemia in T2DM

DKA rarely seen as insulin levels are still low to prevent muscle catabolism

163
Q

What is the aetiology of T2DM?

A

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

164
Q

What is the pathophysiology of T2DM?

A

Impaired insulin secretion and resistance -> IGT –> T2DM –> Hyperglycaemia and high FFA’s

165
Q

What are the risk factors of T2DM?

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

What are the symptoms of T2DM?

A
  1. Increased thirst
  2. Urination
  3. Hunger
  4. Unexplained weight loss
  5. Ketones in urine
  6. Fatigue and irritability
167
Q

What are the investigations and expected results in T2DM?

A

Fasting plasma glucose in diabetes = >7mmol/L

Random plasma glucose in diabetes = >11mmol/L

Oral glucose tolerance test in diabetes = 7mmol/L fasting and >11mmol/L over 2 hours

HbA1c in diabetes = >48mmol/L

168
Q

What is the management of T2DM?

A
  1. Lifestyle changes –> lose weight, increase exercise, healthy diet
  2. Metformin
  3. Metformin and sulfonylurea
  4. Metformin and sulfonylurea and urea
  5. Increased insulin if needed
169
Q

How does metformin work?

A

By increasing insulin sensitivity and inhibiting glucose production

170
Q

How does Sulfonylurea work?

A

Stimulates insulin release (can cause hypoglycaemia)

171
Q

Which hormone is insulin antagonistic too?

172
Q

What is the pathophysiological consequence of impaired insulin function?

A
  • Severe glucose deficiency –> glycogenolysis + gluconeogenesis not suppressed, and glucose uptake reduced
  • This causes hyperglycaemia and glycosuria
  • Perceived stress –> Cortisol and Ad secretion –> catabolic state –> increased plasma ketone
173
Q

What is the pathophysiology of DKA?

A

No insulin –> lipolysis –> FFA –> oxidised in liver –> Ketone bodies –> ketoacidosis

174
Q

What are 3 examples of Ketones?

A

Acetoacetate, acetone, beta hydroxybutyrate.

175
Q

Why is DKA only associated with type 1 DM?

A

Due to severe insulin impairment.

176
Q

Where are FFA oxidised into Ketone bodies?

177
Q

What are 5 signs of DKA?

A
  1. Hypotension
  2. Tachycardia
  3. Kussmaul’s respiration
  4. Breath smells of ketones
  5. Dehydration
178
Q

Give 3 microvascular complications of DM

A

Diabetic retinopathy
Diabetic nephropathy
Diabetic peripheral neuropathy

179
Q

Macrovascular complications of DM

A

CV disease

Stroke

180
Q

What is the main risk factor of complications in DM?

A

Poor glycaemic control

181
Q

What is a hallmark of Diabetic nephropathy?

A

Development of proteinuria and progressive decline in renal function

182
Q

What can acute hyperglycaemia induce?

A

DKA

Hyperosmolar coma

183
Q

What happens to the GBM in diabetic nephropathy?

184
Q

What can Chronic hyperglycaemia induce?

A

Micro/macrovasc complications

e.g. CV disease, Diabetic nephropathy, DIabetic retinopathy

185
Q

What is the commonest form of diabetic neuropathy?

A

Distal symmetrical polyneuropathy

186
Q

What is autonomic neuropathy?

A

Damage to nerves that supply body structures that regulate functions such as BP, HR, Bowel/bladder emptying.

187
Q

In peripheral vascular disease, what are the signs of acute ischaemia?

A
  1. Pulseless
  2. Pale
  3. Cold
  4. Pain
  5. Paralysis
  6. Paraesthesia
188
Q

What are the major consequences of diabetic neuropathy?

A
  1. Pain
  2. Autonomic neuropathy
  3. Insensitivity
189
Q

What is the pain associated with diabetic neuropathy like?

A
  1. Burning
  2. Paraesthesia
  3. Nocturnal exacerbation
190
Q

What are the risks of diabetic complications?

A

Poor glycaemic control, hypertension, smoking, HbA1c, overweight, long duration of DM

191
Q

What is the treatment for diabetic neuropathy?

A
  • Improve glycaemic control
  • Antidepressants
  • Pain relief
192
Q

What are the signs of autonomic neuropathy?

A
  1. Hypotension
  2. HR affected
  3. Diarrhoea/constipation
  4. Incontinence
  5. Erectile dysfunction
  6. Dry skin
193
Q

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

A

insensitivity –> foot ulceration –> infection then amputation

194
Q

Describe where insensitivity as a result of diabetic neuropathy starts and how it spreads.

A

Starts at the toes and moves proximally.

195
Q

How can you prevent amputation in diabetic neuropathy?

A
  1. Screening for insensitivity
  2. Education
  3. MDT foot clinics
  4. Pressure relieving footwear
  5. Podiatry
  6. Revascularisation and abx
196
Q

What would the pulse be like in a patient with diabetic neuropathy?

197
Q

What is the treatment for Diabetic nephropathy?

A
  • Glycaemic and BP control
  • ARB/ACEi
  • Proteinuria and cholesterol control
198
Q

What are the differences in nephropathy in T1DM and T2DM?

A

T1DM – Microalbuminuria develops 5-10 years after diagnosis

T2DM – Microalbuminuria is present at diagnosis

199
Q

What are the risk factors of diabetic retinopathy?

A

Long duration DM, Poor glycaemic control, Hypertension, pregnancy, insulin treatment

200
Q

What is the pathophysiology of Diabetic retinopathy?

A

Micro-aneurysms –> pericyte loss and protein leakage —> occlusion –> ischaemia

201
Q

What are the subdivisons of diabetic retinopathy?

A
  1. Proliferative – evidence of neovascularisation in retina

2. Non proliferative

202
Q

What are the clinical presentations of Diabetic retinopathies?

A

1R1 – Non proliferative –> microaneurysms and intraretinal haemorrhages

R2 – Pre-proliferative –> venous beading and growth of new vessels

R3 – Proliferative –> New blood vessel on disc

203
Q

What is the treatment of diabetic retinopathy?

A

Laser therapy treats neovascularisation.

204
Q

What is Adrenal insufficiency?

A

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

205
Q

Describe the circadian rhythm

A
  • Eye signals to the SCN to sync your body clock.
  • This rhythm fine tunes physiology to meet demands of the day and metabolic requirements
  • Cortisol should be high when you wake
206
Q

What is the effect of adrenal insufficiency on cortisol and ACTH?

A 
ACTH = HIGH
Cortisol = Low
207
Q

What is the cause of primary adrenal insufficiency?

A
  • Addison’s disease
  • Congenital adrenal hyperplasia
  • TB
  • Adrenal metastases
  • Drugs
  • Haemorrhage
  • Infection
208
Q

What are the symptoms of adrenal insufficiency?

A
  1. Weight loss
  2. Headaches
  3. Abdo cramps
  4. Myalgia
  5. Throwing up
  6. Weakness
  7. Tired
  8. Pigmentation – increased tanning
209
Q

What investigations would you order in adrenal insufficiency?

A
  1. Bloods –> FBC + U, E (Na down K up (due to less aldosterone) CA2+ and urea up
  2. Glucose down
  3. ACTH stimulation test – Addison’s disease won’t respond

Lack of aldosterone causes less sodium to be reabsorbed and less potassium to be excreted

210
Q

What are the secondary causes of adrenal insufficiency?

A
  • Hypopituitarism
  • Withdrawal from steroids
  • Infiltration
  • Infection
  • Radiotherapy
211
Q

What is the treatment for adrenal insufficiency?

A

Hydrocortisone twice or 3 times Daily to replace cortisol levels 15-25mg

  • Primary adrenal insufficiency –> aldosterone treated with fludrocortisone
212
Q

What biochemical investigations could you pursue in adrenal insufficiency?

A

0900 Cortisol and ACTH

If Cortisol is<100 nmol/l Ai is likely AND over 500 Ai is not likely

If ACTH is over >22 ng/l primary is likely and Less than 5 secondary

Renin is elevated in primary

213
Q

What are features of an adrenal crisis?

A
  • Hypotension
  • Fatigue
  • Fever
  • Hypoglycaemia
  • Hyponatremia
  • Hyperkalaemia
214
Q

How can you manage an adrenal crisis?

A
  • Immediate hydrocortisone 100mg IV
  • Fluid resuscitation 1L N/saline for an hr
  • Hydrocortisone 50-100mg IV 6 hourly
  • Start fludrocortisone – 100-200ug
215
Q

What are the sick day rules for adrenal insufficiency?

A
  • When ill double dose
  • Don’t worry to double dose it wont hurt you in short term
  • Carry steroid awareness card
  • If vomiting/increasingly unwell 100mg of HC Sub cut
  • If cant inject, 20mg and repeat if vomit.
216
Q

What is the treatment in Type 1DM?

A
  1. Education
  2. Healthy diet – low in sugar high in carbs
  3. Regular activity – healthy BMI
  4. BP and hyperlipidaemia control
  5. Insulin
217
Q

Where is insulin injected in T1DM and what is a consequence of insulin therapy?

A

Insulin is injected into SC fat, can also be placed into an insulin pump.

Complications of Insulin therapy – Hypoglycaemia, insulin resistance, weight gain, interreference with lifestyle

218
Q

What is the treatment in T2DM?

A
  1. Lifestyle changes – lose wight, exercise, healthy diet
  2. Metformin
  3. Metformin + sulfonylurea
  4. Metformin +sulfonylurea + Insulin
  5. Increase insulin dose as required
219
Q

How does metformin work?

A

increased insulin sensitivity and inhibits glucose production

220
Q

How does sulfonylurea work?

A

Stimulates insulin release –> can cause hypoglycaemia

221
Q

How can T2DM be described as?

A

Impaired insulin secretion and insulin resistance.

222
Q

Describe the portal circulation?

A

Ant pit has no arterial blood supply, receives blood through a portal venous circulation from hypothalamus

223
Q

What does the anterior pituitary produce?

A

TSH, FSH, LH, ACTH, Prolactin and GH

224
Q

Where is the anterior pituitary’s trilaminar disc derived from?

A

ectoderm (rathke’s pouch)

225
Q

What does the hypothalamus secrete?

A

GHRH + SMS, GNRH, CRH, TRH, Dopamine

226
Q

Describe the thyroid axis

A

Hypothalamus –> TRH –> to AP –> TSH –> Thyroid –> T3 and T4

T3/4 have a negative feedback on hypothalamus and ant pituitary

227
Q

What is Low and high TSH associated with?

A
  • Low TSH = an over-active thyroid
  • High TSH – an Overactive thyroid

Underactive thyroid would raise TSH as you have less T3/T4 so no negative feedback

228
Q

Describe the GH/IGF-1 Axis

A

Hypothalamus –> GNHR (+) or SMS (-)  AP –> GH –> Liver –> IGF-1

IGF1 induces cell division. Cartilage and protein synthesis.

229
Q

Describe the HPA axis

A

Hypothalamus –> CRH –> AP –> ACTH –> Adrenal cortex (zona fasciculata) –> glucocorticoid synthesis (cortisol)

Cortisol has a neg feedback mechanism!

230
Q

What are the functions of cortisol in stress?

A
  1. Mobilises energy sources –> lipolysis, gluconeogenesis
  2. Vasoconstriction
  3. Supresses inflame + immune responses
  4. Inhibits non-essential functions
231
Q

What are some diseases of the pituitary?

A
  • Benign pituitary adenoma
  • Craniopharyngioma – common in children
  • Trauma
  • Apoplexy – bleed causing expansion to local structure
  • Sheehan’s – expands during pregnancy, post-partum haemorrhage
  • Sarcoid/TB
232
Q

What are consequences of pituitary tumours?

A
  • Pressure on local structures – headaches, visual field defects (bitemporal hemianopia)
  • Hypo-pituitary function – pale, obese, no hair.
  • Functioning tumour causing Cushing’s, prolactinoma and gigantism
233
Q

Describe the posterior pituitary and it’s action.

A
  • Derived from the floor of the ventricles
  • Synthesised in the paraventricular and supra-optic nuclei
  • Secretes oxytocin and ADH
234
Q

What is the difference between Cushing’s syndrome and cushing disease?

A

Cushing’s syndrome refers to a disease of excess cortisol abundance no matter what the cause.

Cushings disease is specific to a pituitary tumour!

235
Q

What is a red flag for cushing’s syndrome?

A

Kid is gaining weight but not growing.

236
Q

What are the causes of cushings syndrome?

A
  • Adrenal tumour (adenoma/carcinoma)
  • Pituitary tumour (Cushing’s disease)
  • Exogenous steroids
  • Ectopic ACTH syndrome
237
Q

What are the symptoms of cushings syndrome?

A
  • Fat - Fat increased and redistributed (central obesity and moon face)
  • Protein catabolism – muscle wasting, thin skin and osteoporosis
  • Androgenic effects – Acne, hirsutism
238
Q

What are the clinical features of cushings syndrome?

A
  • Carb metabolism – impaired glucose metabolism and diabetes
  • Immune suppression
  • Central effects – depression, malaise
  • Supressed gonadal function – amenorrhoea, loss of libido
  • Electrolyte imbalance – sodium retention, hypertension, Hypokalaemia
239
Q

What investigations would you order in suspected cushings syndrome?

A
  • Overnight dexamethasone suppression test – failure to supress cortisol
  • Late night salivary cortisol – loss of circadian rhythm
  • Urinary free cortisol is raised
  • Loss of circadian rhythm
240
Q

What is the treatment for cushings syndrome?

A
  1. Removal of pituitary tumour

2. Drugs to inhibit cortisol synthesis –> metyrapone and ketoconazole

241
Q

What investigation could you do to diagnose cushings disease?

A
  • CT scan
  • MRI scan
    Conducted post diagnosis of Cushing’s syndrome.
242
Q

What is the management of cushings disease?

A

surgery + radiotherapy

243
Q

What should you do after you have diagnosed cushing’s disease?

A
  • If plasma ACTH is >15pg/ml = ACTH dependent syndrome

- If less ACTH independent Cushing’s syndrome

244
Q

What is the definition of osmolality?

A

mOsmol/kg –> Measured by an osmometer

Very similar to osmolarity, site of particle isn’t important, but number is

High osmolality = high ADH to reabsorb water.

245
Q

What is the primary cation in ICF?

246
Q

What is the primary cation in ECF?

247
Q

What is the primary anion in ECF?

A

Cl and HCO3

248
Q

What is the function of ADH?

A

Acts on CD of the nephron to insert aquaporin 2 channels –> H2O retention

249
Q

Describe the release of ADH

A
  • Released when osmoreceptors in hypothalamus detect raised plasma osmolarity
  • Post pituitary is signalled to release ADH
  • Binds to V2 GPCR
250
Q

What is meant by water deficit?

A

increased thirst + ADH –> increased water uptake and reduced secretion.

251
Q

What detects the osmolality of a cell?

A

osmoreceptors

252
Q

What are the signs of SIADH?

A
  1. Anorexia
  2. Nausea
  3. Malaise
  4. Headache
  5. Confusion
253
Q

What are the causes of SIADH?

A
  1. Malignancy
  2. CNS disorders –> meningitis, brain tumour, cerebral haemorrhage
  3. TB
  4. Pneumonia
  5. Drugs
254
Q

What is the treatment for SIADH?

A
  1. Restrict fluid (Asymptomatic)
  2. Give salt (3% saline)
  3. Loop diuretics –> furosemide
  4. ADH-R antagonists – Vaptans.
255
Q

What is the essential criteria for diagnosing SIADH?

A
  1. Hyponatremia (<135mmol/L)
  2. Plasma hypo-osmolality
  3. High urine osmolality
  4. Clinical euvolemia
  5. Increased urinary sodium excretion with normal salt and water intake
256
Q

What diseases should you exclude in SIADH?

A
  1. Renal disease
  2. Hypothyroidism
  3. Hypocortism
  4. Recent diuretic use
257
Q

What are the signs of diabetes insipidus?

A
  1. Excessive urine >3L/24hr
  2. Very dilute urine
  3. Severe thirst
  4. Hypernatremia
  5. Dehydration
  6. Polyuria
  7. Polydipsia – overdrinking
258
Q

What are the investigations of diabetes insipidus?

A
  1. Measure 24-hour urine
  2. Test for hyponatremia
  3. Water deprivation test – urine will not concentrate when asked not to drink.
259
Q

What is the treatment of diabetes insipidus?

A
  • Desmopressin – in cranial diabetes insipidus
  • Hydrochlorothiazide – in nephrogenic DI –> encourages salt + water uptake in Prox tubule.
  • Remove the cause
260
Q

What is the cause of polyuria?

A
  1. Hypokalemia
  2. Hyperglycaemia
  3. Hypercalcemia
  4. Diabetes insipidus
261
Q

How is hyponatremia defined as?

A

Serum sodium 135-144mmol (<135mmol/L is hyponatremia)

- Mortality much higher if it goes below 125

262
Q

What are the signs of hyponatremia?

A
  • Anorexia
  • Confusion
  • Headache
  • Lethargy
  • Weakness
    Rapid fall –> Resp arrest, convulsions/ coma
263
Q

What is the treatment for hyponatremia?

A
  • Bolus dose of saline (if dehydration) fluid restriction if not.
  • Stop hypotonic fluid
264
Q

What is the investigations in hyponatremia?

A
  • Drug chart

- Underlining causes –> Bloods etc.

265
Q

What are the causes of hyponatremia?

A
  1. SIADH
  2. Sodium Deficiency
  3. Renal failure
  4. Malignancy
  5. Drugs
266
Q

What is Diabetic ketoacidosis?

A

Absence of insulin and counter reg hormones = hyperglycaemia and rising ketones

267
Q

How can you diagnose diabetic ketoacidosis?

A
  • Metabolic acidosis – plasma bicarb <15mmol/L
  • Raised plasma ketones (urine bodies >2+)
  • Hyperglycaemia (above <50mmol/L)
268
Q

What is the pathophysiology of ketoacidosis?

A

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

269
Q

What are the symptoms of diabetic ketoacidosis?

A
  • Hypotension
  • Tachycardia
  • Dehydration
  • Breath smells of ketones
  • Kussmaul’s respiration.
270
Q

Which Diabetic condition is Diabetic ketoacidosis seen in?

A

Mainly T1DM.

Rarely seen in T2DM as insulin is still produced which prevents muscle catabolism and ketogenesis.

271
Q

What are 3 endocrine causes of diabetes?

A
  1. Acromegaly – insulin resistance up,, similar to type 2
  2. Cushings -reduced glucose uptake and increased insulin resistance (stimulates new glucose)
  3. Pheochromocytoma – increased gluconeogenesis and decreased glucose uptake
272
Q

What is the definition of Puberty?

A

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

273
Q

What is the first sign of puberty in girls?

274
Q

What is the Hormone responsible for regulating growth of breast and female genitalia?

A

Ovarian oestrogen.

275
Q

What is the hormone responsible for controlling growth of pubic and axillary hair in females?

A

Ovarian and adrenal androgens

276
Q

What is the first sign of puberty in girls?

A

first ejaculation often nocturnal

277
Q

What is the role of testicular androgens in male puberty?

A
  1. Development of external genitalia
  2. Growth of pubic and axillary hair
  3. Deepening of voice
278
Q

What is the tanner scale?

A

used to describe physical development based on external sex characteristics

279
Q

What is thelarche?

A

breast development –> takes 3 years and is controlled by oestrogen

280
Q

What are the 3 stages of thelarche?

A
  1. Ductal proliferation
  2. Adipose deposition
  3. Enlargement of areola and nipple
281
Q

What is adrenarche?

A

Maturation of the adrenal gland –> development of zona reticularis cells

282
Q

What are signs of adrenarche?

A
  • Peri-pubertal adrenal androgen production = mild acne and body odour
283
Q

What is pubarche?

A

growth of pubic hair

284
Q

What is precocious puberty?

A

onset of secondary sexual characteristics before 8/9 years old

MUST RULE OUT A BRAIN TUMOUR IN BOYS

285
Q

What is the treatment for precocious puberty?

A

GnRH super agonist to suppress pulsatility of GnRH secretion

286
Q

What is delayed puberty?

A

Absence of secondary sexual characteristics by 14/16 yo

287
Q

What is the most common cause of delay in boys?

A

constitutional delay –> runs late in the family

288
Q

What are 3 consequences of delayed puberty?

A
  1. Psychological problems
  2. Reproduction defects
  3. Reduced bone mass
289
Q

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

A

Turner’s syndrome.

290
Q

What are the functional causes of delayed puberty?

A

Anorexia, bulimia, over exercising, CKD, Drugs, stress and sickle cell

291
Q

What are the investigations in delayed puberty?

A
  1. FBC – red blood count
  2. U+E
  3. LH/FSH
  4. TFT’s
  5. Karyotyping for turners
292
Q

What is Hypergonadotropic hypogonadism?

A

Primary gonadal failure (Testes or ovarian)

e.g. turners syndrome (45X) Klinefelter’s syndrome (47XXY)

293
Q

What is the effect on hypergonadotropic hypogonadism on FSH/LH and oestrogen and Testosterone.

A
  • High FSH/LH low Oestrogen/Testosterone
294
Q

What is Hypogonadotropic hypogonadism?

A

Secondary gonadal failure – hypopituitary or problems w/ hypothalamus

295
Q

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

A
  • Low FSH/LH and low Testosterone/Oestrogen

- E.g. Kallman syndrome

296
Q

What is turners syndrome?

A

missing an x chromosome – 45x. Primary gonadal failure.

Short stature, delayed puberty, CV and renal malformations, recurrent otitis media.

297
Q

What is Kleinfelters syndrome?

A

patient has an extra X –> 47XXY. Primary gonadal failure.

298
Q

What are 3 symptoms of Kleinfelters syndrome?

A
  • Gynaecomastia, increased risk of breast cancer, testicular size <5ml
  • May have azoospermia – semen with no sperm

Symptoms –> Reduced pubic hair, IQ, small testicles and tall stature
- At risk of developing breast cancer

299
Q

What is Kallmans syndrome?

A

Congenital deficiency of GnRH –> example of secondary gonadal failure

300
Q

What are 2 features of kallmans syndrome?

A
  • 75% cant smell –> ansomia

- X linked recessive or dominant

Phase 2a Sheffield Medicine (10 decks)

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