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Phase 2A revision > ENDOCRINE > Flashcards

ENDOCRINE Flashcards

1
Q

Give 5 parathyroid hormone actions

A
  1. Increase Ca2+ reabsorption
  2. Decrease phosphate reabsorption
  3. Increase 1 alpha-hydroxylation of 25-OH vit D
  4. Increase bone remodelling (bone resorption >bone formation)
  5. Increase Ca2+ absorption because of increase 1,25(OH)2D (no direct effect)
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2
Q

When serum calcium levels are low, what are PTH levels?

A

PTH levels are high

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3
Q

When serum calcium levels are high, what are PTH levels?

A

PTH levels are low

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4
Q

What is the effect of hyperparathyroidism on serum calcium levels?

A

Hyperparathyroidism –> hypercalcaemia

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5
Q

what are the clinical features of hyperparathyroidism?

A

SYMPTOMS

 - BONES – excess bone resorption caused by PTH Pain, fractures, osteopenia, osteomalacia, osteoporosis
  - STONES – due to excess Ca. Renal colic from renal calculi and biliary stones
  - GROANS – abdominal pain, malaise, nausea, constipation, polydipsia, polyuria, dehydration, confusion, risk of cardiac arrest
  - MOANS – depression, anxiety, cognitive dysfunction, insomnia, coma

SIGNS
hypercalcaemia

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6
Q

Give 2 causes of primary hyperparathyroidism

A
  • Parathyroid adenoma
  • Hyperplasia
  • Parathyroid cancer
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7
Q

what is the the pathophysiology of secondary hyperparathyroidism

A

Physiological compensatory hypertrophy of all parathyroid resulting in excess PTH due to hypocalcaemia
Often due to CKD and vitamin D deficiency

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8
Q

what is the pathophysiology of tertiary hyperparathyroidism?

A

Prolonged uncorrected hypertrophy - glands become autonomous producing excess PTH

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9
Q

What blood results would you see in the 3 types of hyperparathyroidism?

A

PRIMARY =

  • PTH = high
  • calcium = high
  • phosphate = low
  • alk phos = high

SECONDARY =

  • PTH = high
  • calcium = low
  • phosphate = high
  • alk phos = high

TERTIARY -

  • PTH = high
  • calcium = high
  • phosphate = high
  • alk phos = high
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10
Q

Describe the treatment for hyperparathyroidism

A
  • adenoma = surgical removal
  • hyperplasia = all 4 glands surgically removed
  • calcimimetric = ORAL CINACALET
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11
Q

How does a calcium mimetic work?

A

Increases sensitivity of parathyroid cells to calcium so less PTH secretion occurs

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12
Q

What is the affect of hypoparathyroidism on serum calcium levels?

A

Hypoparathyroidism –> hypocalcaemia

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13
Q

what are the clinical features of hypoparathyroidism?

A

SYMPTOMS:CATs go numb

  1. convulsions / seizures
  2. arrhythmias / anxious
  3. tetany / muscle spasms
  4. numbness

SIGNS:

  • CHVOSTEK’S SIGN - tap over facial nerve and look for spasm of facial nerves
  • TROUSSEAU’S SIGN - inflate BP cuff 20 mmHg above systolic for 5 mins = hand spasm - hypocalcaemia
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14
Q

what are the causes of hypoparathyroidism?

A
  • secondary to increased serum phosphate
  • severe vitamin D deficiency
  • reduced PTH function
  • drugs - calcitonin, bisphosphonates
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15
Q

What are blood results for someone with hypoparathyroidism?

A 
Calcium = Low 
PTH = Low
Phosphate = High
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16
Q

What is the treatment for hypoparathyroidism?

A 
Acute = IV calcium 
Persistant = Vitamin D analogue - ORAL ADCAL
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17
Q

what are the causes of Hypercalcaemia?

A 
Hyperparathyroidism
Malignancy
Sarcoidosis
Thyrotoxicosis
Drugs
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18
Q

What is the treatment for hypercalcaemia?

A
  • Treat underlying cause
  • increase circulation volume, increase excretion
    .- Bisphosphonates, glucocorticoids, gallium, dialysis
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19
Q

Give 2 ECG changes that you might see in someone with hypercalcaemia

A
  1. Tall T waves

2. Shortened QT interval

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20
Q

Name 3 causes of hypocalcaemia

A 
Hypoparathyroidism
Vitamin D deficiency
Hyperventilation
Drugs
Malignancy
Toxic shock
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21
Q

what are the investigations for hypocalcaemia?

A

Corrected Calcium levels,
ECG (prolonged QT)
Parathyroid function - PTH

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22
Q

what is the treatment for hypocalcaemia?

A

10ml calcium gluconate/chloride 10% slow IV,

oral calcium and Vit D

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23
Q

Give 2 ECG changes that you might see in hypocalcaemia?

A
  1. Small T waves

2. Long QT interval

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24
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

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25
Q

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

A

PTH - secreted in response to low serum calcium

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26
Q

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

A

Calcitonin

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27
Q

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

A

PTH measurement

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28
Q

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

A

Diabetes mellitus

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29
Q

what is T1DM?

A

Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency.

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30
Q

what is the pathophysiology of T1DM

A
  • autoimmune destruction of beta cells in the Islets of Langerhans by autoantibodies cause insulin deficiency and continued breakdown of liver glycogen
  • this causes hyperglycaemia and glycosuria
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31
Q

Is T1DM characterised by a problem with insulin secretion, insulin resistance or both?

A

Characterised by impaired insulin secretion - severe insulin deficiency

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32
Q

what are the risk factors for developing T1DM?

A
  • Northern European
  • Family History:
    - HLA DR3-DQ2 or
    - HLA-DR4-DQ8
  • Other autoimmune diseases:
    - Autoimmune thyroid
    - Coeliac disease
    - Addison’s disease
    - Pernicious anaemia
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33
Q

what are the clinical features of T1DM?

A

Polydipsia - Thirst (fluid and electrolyte losses)
Polyuria (due to osmotic diuresis)
Weight loss

  • usually short history of severe symptoms
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34
Q

Describe the epidemiology of T1DM

A 
Onset younger (<30 years) 
Usually lean 
More Northern European ancestry
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35
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 >7 mmol/L

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36
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 >11 mmol/L

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37
Q

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

A

> 48 mmol/L>6.5%

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38
Q

What happens to C-peptide in T1DM?

A

C-peptide reduces

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39
Q

How do you treat T1DM?

A

Education

Glycaemic control through diet (low sugar, low fat, high starch)

Insulin SC

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40
Q

Give 6 complications of Diabetes Mellitus

A
  1. Diabetic ketoacidosis
  2. Diabetic nephropathy
  3. Diabetic retinopathy
  4. Diabetic neuropathy
  5. Hyperosmolar hyperglycaemic coma
  6. Stroke, ischaemic heart disease, peripheral vascular disease
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41
Q

Give 2 potential consequences of T1DM

A
  1. Hyperglycaemia

2. Raised plasma ketones –> ketoacidosis

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42
Q

How is insulin administered in someone with T1DM?

A

Subcutaneous injections

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43
Q

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

A

Insulin pump

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44
Q

what are the different types of insulin used to treat T1DM?

A
  • short acting - 4-6hrs
  • short acting analogues -
  • long acting - 12-24hrs
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45
Q

Give 4 potential complications of insulin therapy

A
  1. Hyperglycaemia
  2. Lipohypertrophy at injection site
  3. Insulin resistance
  4. Weight gain
  5. Interference with life style
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46
Q

What is the affect of cortisol on insulin and glucagon?

A

Inhibits insulin

Activates glucagon

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47
Q

Describe the pathophysiology of diabetic ketoacidosis

A

Results from a reduced supply of glucose and an increase in fatty acid oxidation.

The increased production of Acetyl-CoA leads to ketone body production that exceeds the ability of peripheral tissues to oxidise them.

Ketone bodies are relatively strong acids (pH 3.5), and their increase lowers the pH of blood

it IMPAIRS THE ABILITY OF HAEMOGLOBIN TO BIND TO OXYGEN

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48
Q

Name 3 ketone bodies

A
  1. Acetoacetate
  2. Acetone
  3. Beta hydroxybutyrate
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49
Q

Where does ketogenesis occur?

A

Liver

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50
Q

what are the clinical features of diabetic ketoacidosis?

A

SIGNS

  • Breath smells of pear drops (ketones)
  • Kussmaul’s breathing - deep, rapid breathing
  • Tachycardia
  • Hypotension
  • Reduced tissue turgor

SYMPTOMS

  • Nausea and vomiting
  • Dehydration
  • exacerbated by vomiting
  • Weight loss
  • Drowsy/confused
  • Abdominal pain
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51
Q

Give 3 microvascular compilation of DM

A
  1. Diabetic retinopathy
  2. Diabetic nephropathy
  3. Diabetic peripheral neuropathy
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52
Q

Give 2 macrovascular complications fo DM

A

CV disease

Stroke

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53
Q

What is the main risk factor for diabetic complications?

A

Poor glycemic control

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54
Q

What is the treatment for diabetic ketoacidosis?

A
  • ABC
  • Replace fluid loss with 0.9% saline IV
  • IV insulin
  • Restore electrolytes e.g. K+
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55
Q

Give 3 endocrine diseases that can cause diabetes

A
  1. Cushing’s
  2. Acromegaly
  3. Phaeochromocytoma
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56
Q

What class of drugs can cause diabetes?

A

Steroids
Thiazides
Anti-psychotics

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57
Q

Is T2DM characterised by problem with insulin secretion, insulin resistance or both?

A

Characterised by impaired insulin secretion and insulin resistance

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58
Q

what is the aetiology of T2DM?

A
  • Decreased insulin secretion and increased insulin resistance
  • No immune disturbance
  • No HLA disturbance but strong genetic link
  • Polygenic
  • Associated with obesity, lack of exercise, calorie and alcohol excess
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59
Q

Describe the pathophysiology of T2DM

A

Insulin binds normally to its receptor – insulin resistance develops post-receptor
Circulating insulin levels are higher than in healthy patients but inadequate to restore glucose homeostasis
Increased glucose production in liver- inadequate suppression of gluconeogenesis and there’s reduced glucose uptake in peripheral tissues
Hyperglycaemia and lipid excess are toxic to beta cells - reduced beta cell mass
Don’t tend to develop ketoacidosis but do get glycosuria

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60
Q

Why is insulin secretion impaired in T2DM

A

Due to lipid deposition in the pancreatic islets

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61
Q

what are the risk factors for T2DM?

A 
Increase w/ age
M > F
Ethnicity: African-Carribean, Black African and South Asian
Obesity
Hypertension
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62
Q

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

A

Insulin resistance increase Insulin secretion decreases Fasting and post-prandial glucose increase

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63
Q

Why do you rarely see diabetic ketoacidosis in T2DM?

A

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

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64
Q

By how much has the beta cell mass reduced in T2DM when diagnosis usually occurs?

A

50% of normal beta cell mass

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65
Q

Describe the epidemiology of T2DM

A

Onset older (>30)
Usually overweight
More common in African/Asian populations
Males > Females

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66
Q

Describe the treatment pathway for T2DM

A
  1. Lifestyle changes - lose weight, exercise, healthy diet and control of contributing conditions
  2. Monotherapy - Metformin
  3. dual therapy
  4. triple therapy

i) metformin
ii) DPP4 inhibitor
iii) SU, gliclazide
iv) SGLT-2 inhibitor
v) pioglitazone
vi) insulin

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67
Q

How does metformin work in treating T2DM?

A

Increase insulin sensitivity and inhibits glucose production

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68
Q

How does sulfonylurea work in treating T2DM?

A

Stimulates insulin release

block ATP dependent K+ channels in beta cells -> causes depolarisations and opening of voltage gated Ca2+ channels -> stimulates insulin secretion

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69
Q

what are the side effects of Sulfonylurea?

A

Hypoglycaemia
weight gain
hyponatraemia

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70
Q

What is hypoglycaemia classified as?

A

Plasma glucose <3.9 mmol/L and if <3.0 mmol/L it is severe hypoglycaemia

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71
Q

Give 5 symptoms of hypoglycaemia

A
  1. Hunger
  2. Sweating
  3. Tachycardia
  4. Anxious
  5. Shaking
  6. Confusion
  7. Weakness
  8. Vision changes
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72
Q

Why does hypoglycaemia continuously get worse?

A

Glucagon is not produced so rely only on adrenaline and the threshold for adrenaline release gradually lowers after time

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73
Q

Give 6 consequences of hypoglycaemia

A
  1. Seizures
  2. Comas
  3. Cognitive dysfunction
  4. Fear
  5. Decrease in qualitative life
  6. Accidents
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74
Q

Briefly describe the treatment of hypoglycaemia

A

Oral sugar and long acting starch
50% GLUCOSE IV or IM GLUCAGON
If episodes persist, suggest many small high starch meals
Re-educate diabetics on insulin use

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75
Q

Why are patient with diabetes at a particular risk of hypoglycaemia?

A

In Diabetes there are defects in the physiological defences to hypoglycaemia and there is reduced awareness

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76
Q

What does prevention of hypoglycaemia include?

A

Eduction
Correct choice of therapy
Adjusting glucose targets in those at high risk
Specialist support from a MDT

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77
Q

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

A

Hepatic insulin resistance is the driving force

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78
Q

Give a potential consequence of acute hyperglycaemia

A

Diabetic ketoacidosis and hyperosmolar coma

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79
Q

Give a potential consequence of chronic hyperglycaemia

A

Mirco/macrovascular tissue complications

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80
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

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81
Q

Name 5 possible diseases of the pituitary

A
  1. Benign pituitary adenoma
  2. Craniopharygioma
  3. Trauma
  4. Apoplexy/Sheehans
  5. Sarcoid/TB
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82
Q

Give 3 potential consequences of a pituitary tumour

A
  1. Pressure on local structures - e.g. optic chasm = bilateral hemianopia
  2. Pressure on normal pituitary (lack of function) - Hypopituitarism
  3. Functioning tumours - e.g. Cushing’s, acromegaly, prolactinoma
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83
Q

Describe the growth hormone secretion from the anterior pituitary

A

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

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84
Q

What is acromegaly?

A

Overgrowth of all organ systems due to excess growth hormone in adults

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85
Q

What is gigantism?

A

Excess GH production in children before fusion of the epiphyses of the long bones

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86
Q

what are the clinical features of acromegaly?

A 
SYMPTOMS: 
large hands, 
box jaw, 
thick skin, 
arthritis, 
sight problems
weight gain
SIGNS: 
hypertension, 
insulin resistance, 
bitemporal hemiopia
large tongue
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87
Q

what is the pathophysiology of acromegaly?

A

GH exerts activity indirectly through IGF-1 or directly on tissue
Excessive IGF- levels mediate most of the skeletal and soft tissue growth like features of acromegaly

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88
Q

What can cause acromegaly?

A
  • A benign pituitary adenoma producing excess GH

- rarely due to hyperplasia

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89
Q

Describe the epidemiology of acromegaly

A

Average age is 40 years
male = female
Reduces life expectancy by 10 years

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90
Q

What complications are associated with acromegaly?

A

type 2 diabetes
sleep aponea
heart disease
arthritis

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91
Q

What are the investigations for acromegaly?

A

1st line = IGF-1
2nd line = oral glucose tolerance test
3rd line = pituitary function tests
4th line = MRI

also investigate for complications

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92
Q

What is the gold standard diagnostic test for acromegaly?

A

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

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93
Q

what is the management for acromegaly?

A

1st line = trans sphenoidal surgery

2nd line = OCTREOTIDE (somatostatin analogue) +/- CABERGOLINE (dopamine agonist) if GH secretions persist

3rd line = PEGVISOMANT (GH receptor antagonist)

4th line = radiotherapy

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94
Q

Give 3 potential complications of transsphenoidal surgical resection for the treatment of acromegaly

A
  1. Hypopituitarism
  2. Diabetes insidious
  3. Haemorrhage
  4. CNS injury
  5. Meningitis
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95
Q

What types of medical therapy can be used to treat acromegaly?

A

somatostatin analogue = octreotide

dopamine agonist = cabergoline

GH receptor antagonist = pegvisomant

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96
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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97
Q

Give 2 disadvantages of dopamine agonists in the treatment of acromegaly

A
  1. Can be ineffective

2. Risk of side effects

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98
Q

Name a dopamine agonist that can be used as a treatment for acromegaly

A

Cabergoline

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99
Q

Why can somatostatin analogues be used in the treatment of acromegaly?

A

They inhibit GH release

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100
Q

Why can GH receptor antagonists be used in the treatment of acromegaly?

A

They suppresses IGF-1

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101
Q

What is prolactinoma?

A

Lactotroph cell tumour of the pituitary

Prolactin secreting tumour

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102
Q

Name the 2 types of prolactinoma

A
  1. Microprolactinoma = most common, >90%

2. Macroprolactinoma = >10mm

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103
Q

what are the causes of prolactinoma?

A
  1. Pituitary adenoma
  2. Anti-dopaminergic drugs
  3. Head injury - compression of the pituitary stalk
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104
Q

what are the clinical features of prolactinoma

A 
SYMPTOMS: 
amenorrhea, 
galactorrhoea, 
gynaecomastia, 
low libido, 
possible cerebral symptoms

SIGNS:
low testosterone,
infertility

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105
Q

Briefly describe the pathophysiology of Prolactinoma

A

Increased release of prolactin can cause galactorrhoea and can inhibit FSH and LH

Compression of the pituitary stalk
Prevents secretion of dopamine from hypothalamus - stops inhibition of prolactin

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106
Q

what are the investigations for prolactinoma?

A

Serum prolactin levels - HIGH

CT head

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107
Q

What is the treatment for prolactinoma?

A

Dopamine agonists - cabergoline - inhibits prolactin release

Occasionally transsphenoidal pituitary resection

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108
Q

What is Cushing’s Syndrome?

A

Chronic, excessive and inappropriate elevated levels of circulating plasma glucocorticoids (cortisol)

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109
Q

What is Cushing’s Disease?

A

When Cushing’s syndrome is caused by a pituitary tumour so excess glucocorticoids due to inappropriate ACTH secretion

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110
Q

what is the clinical presentation of Cushing’s disease?

A 
Central obesity
Plethoric complexion
Moon face
Mood change
Proximal muscle weakness
Purple abdominal striae
Gastric ulcers
Osteoporosis
Hirsutism
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111
Q

what are the causes of excess cortisol?And are they ACTH dependent or independent?

A

ACTH dependent:

  • Cushing’s disease
  • Ectopic ACTH production
  • ACTH treatment

ACTH independent

  • adrenal adenoma
  • iatrogenic
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112
Q

What is a differential diagnosis of Cushing’s syndrome?

A

Pseudo-Cushing’s = excessive alcohol consumption can mimic the clinical and biochemical signs but resolved on alcohol recession

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113
Q

Describe the epidemiology of Cushing’s syndrome

A

women > men
majority diagnosed 20-50y/o
most common cause is oral steroids

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114
Q

what are the investigations for Cushing’s syndrome?

A
  1. drug history - oral steroids
  2. random plasma cortisol - high
  3. overnight dexamethasone suppression test and urinary free cortisol (24hr) - positive (no suppression = cushings)
  4. test plasma ACTH
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115
Q

How does a dexamethasone suppression test work?

A

Give synthetic steroids that suppress pituitary and adrenals and then measure the cortisol
In Cushing’s there is no suppression of cortisol

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116
Q

What is the treatment for Cushing’s syndrome?

A

Tumours = surgical removal
- pituitary adenoma = transsphenoidal surgical resection
- adrenal adenoma = adrenalectomy
Drugs to inhibit cortisol synthesis - metyrapone, ketoconazole

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117
Q

What are some complications associated with Cushing’s Syndrome?

A

cardiovascular disease
hypertension
diabetes mellitus
osteoporosis

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118
Q

What is the circadian system?

A

Body clock that regulates your body

Clear rhythm of cortisol production follows circadian rhythm

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119
Q

When do cortisol levels peak?

A

At around 8:30 am

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120
Q

What’s the primary cue that synchronises an organism’s biological rhythms?

A

Light

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121
Q

What is adrenal insufficiency?

A

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

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122
Q

what is Addison’s disease?

A

Destruction of entire adrenal cortex resulting in mineralocorticoid (aldosterone), glucocorticoid and androgen deficiency

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123
Q

what are the causes of Addison’s disease?

A
  • autoimmune destruction (21-hydroxylase present in 60-90%) - most common in developed countries
  • TB - most common in developing countries
  • adrenal metastases- long term steroid use
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124
Q

what are the clinical features of Addison’s disease?

A

SYMPTOMS
Fatigue
Weakness
Weight loss

SIGNS
Hyperpigmentation 
Postural hypotension
Hypoglycaemia
Other signs of autoimmunity
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125
Q

What is the treatment for adrenal insufficiency?

A

Hormone replacement - any steroids
ORAL HHYDROCORTISONE
ORAL FLUDROCORTISONE

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126
Q

What is the pathophysiology of Addison’s disease?

A

Destruction of the adrenal cortex results in decreased production of the hormones
All steroids reduced
Reduced cortisol levels = increased CRH and ACTH production through feedback

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127
Q

What are the investigations for Addison’s disease?

A
  • SynACTHen test = giving synthetic ACTH does not increase cortisol levels
  • Serum electrolytes = low Sodium, high Potassium
  • FBC: Anaemia and eosinophilia
  • Morning serum cortisol = Reduced
  • Adrenal CT or MRI
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128
Q

What investigations would you do to determine whether Adrenal insufficiency is primary or secondary?

A 
Primary = adrenal antibodies, very long chain fatty acids, imaging and genetics 
Secondary = any steroids?, imaging and genetics
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129
Q

what are the features of addisonian crisis?

A 
Vomiting
abdominal pain
profound weakness
hypoglycaemia 
hypovolemic shock
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130
Q

What is the management of adrenal crisis?

A

Immediate IV Hydrocortisone

Fluid resuscitation - saline (IV)

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131
Q

What would sodium and potassium levels be in someone with adrenal insufficiency?

A

Hyponatraemia = low sodium
Hyperkalaemia = high potassium
Lack of aldosterone and so less sodium reabsorbed and less potassium excreted

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132
Q

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

A

To exclude steroid use as a potential cause

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133
Q

Briefly describe the mechanism of thyroid destruction

A

Cytotoxic (CD8+) T cell mediated thyroglobulin and Thyroid peroxidase (TPO) antibodies may cause secondary damage (alone have no effect)
Antibodies against the TSH receptor may block the effect of TSH (uncommon)

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134
Q

What are the main 3 types of cells that cause thyroid destruction?

A
  1. Cytotoxic T cells
  2. Thyroglobulin
  3. TPO antibodies
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135
Q

Briefly describe the pathophysiology of Grave’s disease

A

Specific serum IgG (TSH receptor stimulating antibodies) bind to TSH receptors in thyroid

Behave like TSH – stimulate T3 and T4 production

This results in excess secretion and hyperplasia of thyroid follicular cells – causing hyperthyroidism and graves ophthalmopathy

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136
Q

what is the clinical presentation of Grave’s opthlmopathy?

A 
SYMPTOMS
Eye discomfort
Grittiness
increased tear production
Photophobia
Diplopia
reduced acuity 
SIGNS
Exophthalmos – protruding eye 
Proptosis – eye protrudes beyond orbit 
Conjunctival oedema
Corneal ulceration 
Ophthalmoplegia – paralysis of eye muscles
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137
Q

what is the clinical presentation of grave’s dermopathy?

A

Pretibial myxoedema – raised, purple red symmetrical skin lesions over anterolateral aspects of shin

Thyroid acropachy – clubbing, swollen fingers and periosteal bone formation

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138
Q

what is the treatment for Grave’s ophthalmology?

A

Conservative treatment – smoking cessation and sunglasses

IV METHYLPREDNISOLONE and surgical decompression/eyelid surgery

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139
Q

Name 5 risk factors for Graves disease

A
  1. Female
  2. Genetic association
  3. E.coli
  4. Smoking
  5. Stress
  6. High iodine intake
  7. Autoimmune diseases
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140
Q

Name 5 autoimmune diseases associated with thyroid autoimmunity

A
  1. T1DM
  2. Addison’s disease
  3. Pernicious anaemia
  4. Vitiligo
  5. Alopecia areata
  6. Rheumatoid arthritis
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141
Q

What would you see histological in someone with Graves disease?

A

Lymphocyte infiltration and thyroid follicle destruction

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142
Q

What is goitre?

A

Palpabel and visible thyroid enlargement

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143
Q

Why does goitre occur and when is is most commonly found?

A

Due to TSH receptor stimulation resulting in thyroid growth

Seen in hypo and hyperthyroidism

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144
Q

Name 4 types of sporadic non toxic goitre

A
  1. Diffuse –> physiological –> Graves
  2. Multi nodular
  3. Solitary nodule
  4. Dominant nodule
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145
Q

Define hyperthyroidism

A

Overactivity of the thyroid gland

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146
Q

Define thyrotoxicosis

A

Excess of thyroid hormone in the blood (can be used interchangeably with hyperthyroidism)

147
Q

Name the 3 mechanisms of how hyperthyroidism may come about

A
  1. Overproduction of thyroid hormone
  2. Leakage of preformed hormone from the thyroid
  3. Ingestion of excess thyroid hormone
148
Q

what are the causes of hyperthyroidism?

A
  • Grave’s disease
  • Toxic multinodular goitre
  • Solitary toxic nodule/adenoma - benign
  • De Quervarians thyroiditis
  • Postpartum thyroiditis
  • Drug induced
149
Q

Name 4 drugs which can induce hyperthyroidism

A
  1. Iodine
  2. Amiodarone
  3. Lithium
  4. Radioconstrast agents
150
Q

what are the clinical features of hyperthyroidism?

A 
SYMPTOMS: 
hot and sweaty, 
diarrhoea, 
wt. loss, 
anxiety/restlessness, 
hyperphagia

SIGNS:
periorbital swelling,
goitre,
tachycardia

151
Q

What investigations are done to diagnose hyperthyroidism?

A

TFTs:
primary = high T3 and T4, low TSH
secondary = high T3 and T4, high TSH

152
Q

What are the thyroid function test results in primary hyperthyroidism?

A

high T4
high T3
low TSH

153
Q

What are the thyroid function rests in secondary hyperthyroidism?

A

high T4
high T3
high TSH

154
Q

What are the 4 main treatments for hyperthyroidism?

A
  1. Beta blockers - PROPRANOLOL
  2. Anti-thyroid drugs - CARBIMAZOLE
  3. Radioiodine
  4. Surgery - partial/total thyroidectomy
155
Q

Why are beta blockers used to treat hyperthyroidism?

A

For rapid control of symptoms

156
Q

Give examples of anti-thyroid drugs and why are they used?

A
  • Carbimazole, methimazole, proplythiouracil (PTU) - (thionamides)
  • Decreases synthesis of new thyroid hormone by targeting thyroid peroxidase
  • PTU also inhibits conversion of T4 to T3
157
Q

Give 4 poor prognostic factors of those on anti-thyroid drugs

A
  1. Severe biochemical hyperthyroidism
  2. Large goitre
  3. Male
  4. Young age of disease onset
158
Q

Give 5 side effects of anti-thyroid drugs

A
  1. Rash
  2. Arthralgia
  3. Hepatitis
  4. Neuritis
  5. Vasculitis
  6. Agranulocytosis - very serious
159
Q

Why can radioiodine be used as a treatment for hyperthyroidism?

A

Emit beta particle that destroy thyroid follicle and therefore reducing the production of thyroid hormones

160
Q

Give 4 potential consequences of a partial thyroidectomy

A
  1. Bleeding
  2. Hypoglycaemia
  3. Hypothyroidism
  4. Recurrent laryngeal nerve palsy
161
Q

What is a complication of hyperthyroidism?

A

Thyroid crisis/storm
graves ophthalmopathy
hypothyroidism

162
Q

Briefly explain thyroid crisis/storm

A

Rapid deterioration of thyrotoxicosis

Hyperpyrexia, tachycardia and extreme restlessness Delirium –> coma –> death

163
Q

What is the treatment for a thyroid crisis?

A

Large doses of oral carbimazole, oral propranolol, oral potassium iodide and IV hydrocortisone

164
Q

Define hypothyroidism

A

Under-activity of the thyroid gland

165
Q

Name the 3 types of hypothyroidism

A
  1. Primary - absence/dysfunction of thyroid gland
  2. Secondary - reduced TSH from anterior pituitary
  3. Tertiary - associated with treatment withdrawal
166
Q

Briefly describe the pathophysiology of primary hypothyroidism

A

Underactivity usually primary from disease of the thyroid but may be secondary due to hypothalamic-pituitary disease resulting in reduced TSH

167
Q

Briefly describe the pathophysiology of secondary hypothyroidism

A

Reduced release or production of TSH so reduced thyroid hormone release

168
Q

Briefly describe the pathophysiology of tertiary hypothyroidism

A

Thyroid gland overcompensates until it can reestablish correct concentration fo thyroid hormone

169
Q

Name 4 causes of primary hypothyroidism

A
  1. autoimmune thyroiditis
  2. postpartum thyroiditis
  3. iatrogenic
  4. drug induced
  5. iodine deficiency
  6. congenital
170
Q

Give 2 examples of iatrogenic causes of hypothyroidism

A
  1. Thyroidectomy

2. Radioiodine therapy

171
Q

Give an example of a transient cause of primary hypothyroidism

A

Post-partum thyroiditis

172
Q

Name 4 drugs that can cause hypothyroidism

A
  1. Carbimazole (used to treat hyperthyroidism)
  2. Amiodarone
  3. Lithium
  4. Iodine
173
Q

Name 3 causes of secondary hypothyroidism

A
  1. Hypopituitarism
  2. Hypothalamic disease
  3. Isolated TSH deficiency
174
Q

Why can amiodarone cause both hypo and hyperthyroidism?

A

Because it is iodine rich

175
Q

what are the clinical features of hypothyroidism?

A

SYMPTOMS: wt. gain, depression, constipation, cold intolerance, “brain fog”

SIGNS: bradycardia, delayed reflexes

176
Q

What investigations are conducted to diagnose hypothyroidism?

A

Thyroid function tests

Thyroid antibodies

177
Q

What are the TFT results for primary hypothyroidism?

A

High TSH

Low T4 and T3

178
Q

What are the TFT results for secondary hypothyroidism?

A

Inappropriately low TSH for low T4 and T3

179
Q

Name 3 antibodies that may be present in the serum in someone with autoimmune thyroiditis

A
  1. TPO (thyroid peroxidase)
  2. Thyroglobulin
  3. TSH receptor
180
Q

What is the treatment for primary hypothyroidism?

A

Thyroid hormone replacement - levothyroxine Resection of obstructive goitre

181
Q

what are the complications of hypothyroidism?

A

Myxoedema coma - medical emergency
heart disease
pregnancy problems

182
Q

Briefly explain a myxoedema coma

A

Severe hypothyroidism

Reduced level of consciousness, seizures, hypothermia IV/oral T3 and glucose infusion needed

183
Q

What is Hashimoto’s thyroiditis?

A

Hypothyroidism due to aggressive destruction of thyroid cells

184
Q

Give 3 symptoms of Hashimoto’s thyroiditis

A
  1. Rapid formation of Goitre
  2. Dyspnoea or dysphagia
  3. General hypothyroidism symptoms
185
Q

Name 3 triggers of Hashimoto’s thyroiditis

A
  1. Iodine
  2. Infections
  3. Smoking
  4. Stress
186
Q

What are the investigations for Hashimoto’s thyroiditis?

A

TFTs - high TSH, low T3 and T4

high TPO antibodies

187
Q

What is the treatment for Hashimoto’s thyroiditis?

A

Levothyroxine

188
Q

Name a complication fo Hashimoto’s thyroiditis

A

Hyperlipidaemia

189
Q

what are the complications of Hashimoto’s thyroiditis?

A

Hashimoto’s encephalopathy

190
Q

What disease would you treat with Carbimazole?

A

Hyperthyroidism/Graves disease

191
Q

What disease would you treat with Levothyroxine?

A

Hypothyroidism

192
Q

Name 3 disease associated with the posterior pituitary

A
  1. Cranial diabetes insipidus - lack of ADH
  2. Nephrogenic diabetes insipidus - resistance to action of ADH
  3. Syndrome of antidiuretic hormone secretion - too much ADH release inappropriately
193
Q

Define diabetes insipidus

A

Passage of large volumes (>3L/day) of dilute urine due to impaired water reabsorption in the kidney due to hypo secretion or insensitivity to ADH

194
Q

Name the 2 types of DI

A
  1. Cranial DI = reduced vasopressin (ADH) produced by hypothalamus and secreted by the posterior pituitary
  2. Nephrogenic DI = impaired response of the kidney to ADH
195
Q

what are the clinical features of DI?

A

SYMPTOM

  • Polyuria
  • Polydipsia
  • No glycosuria

SIGNS

  • Dry mucosa
  • Sunken eyes
  • Changes in skin turgidity
  • Can lead to dehydration
  • Hypernatremia
196
Q

what are the causes of cranial DI?

A 
Idiopathic 
Congenital defects in ADH gene 
Disease of hypothalamus 
Tumour – metastases, posterior pituitary 
Trauma – neurosurgery
Infiltrative disease
197
Q

what are the causes of nephrogenic DI?

A
  • Hypokalaemia
  • Hypercalcaemia
  • Drugs
    - lithium chloride
    - Demeclocycline
    - glibenclamide
  • Renal tubular acidosis
  • Sickle cell disease
  • Prolonged polyuria of any cause
  • Familial (mutation in ADH receptor)
198
Q

Give 3 possible differential diagnosis’s of DI

A
  1. DM
  2. Hypokalaemia
  3. Hypercalcaemia
199
Q

what are the investigations for diabetes insipidus?

A
  • Water deprivation test
  • Desmopressin given and urine osmolality measured for 2-4 hrs with free fluids allowed
    - NDI diagnosed if urine osmolality stays the same
    - CDI diagnosed if urine osmolality increases by >50%ADH suppression test- shows neurogenic
  • Urine dip, glucose, U&E, fluid status
200
Q

What is the treatment for cranial DI?

A
  • Treat underlying condition
  • Thiazide diuretics (BENDROFLUMETHIAZIDE) - sensitise renal tubules to endogenous vasopressin
  • DESMOPRESSIN - high activity at V2 receptor
201
Q

What is the treatment for nephrogenic DI?

A
  • treat cause
  • thiazide diuretics - (BENDROFLUMETHIAZIDE) - Produces hypovolaemia which will encourage the kidneys to take up more Na+ and water in proximal tubule
  • NSAIDs - IBUPROFEN - Lower urine volume and plasma Na+ by inhibiting prostaglandin synthase. Prostaglandins locally inhibit the action of ADH
202
Q

Do you have hyponatraemia or hypernatraemia in diabetes insipidus?

A

Hypernatraemia

203
Q

Give 4 causes of polyuria

A
  1. Hypokalaemia
  2. Hypercalcaemia
  3. Hyperglycaemia
  4. Diabetes insipidus
204
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion
Continuous ADH secretion inspire of plasma hypotonicity, leading to retention of water and excess blood volume and thus hyponatraemia

205
Q

what are the clinical features of SIADH?

A 
SYMPTOMS:
Nausea and vomiting
Headache
Lethargy
Cramps
Weakness
Confusion / irritability

SIGNS
raised JVP
oedema
ascites

206
Q

what are the causes of SIADH?

A 
brain injury
infection
hypothyroidism
cancers
lung diseases
207
Q

what are the investigations for SIADH?

A
  • ADH levels
  • U and Es (low sodium normal potassium),
  • fluid status

distinguish SIADH from salt & water depletion - test with 1-2L of
0.9% saline:
• Sodium depletion will respond
• SIADH will NOT RESPOND

208
Q

what is the pathophysiology of SIADH?

A
  • Excess release of ADH will result in increased insertion of aquaporin 2 channels in apical membrane of collecting duct
  • Excess water retention which dilutes blood plasma
  • Result in hyponatremia as Na+ conc decreases
209
Q

Describe the treatment for SIADH

A
  1. Restrict fluid - <1L/day
  2. Give salt
  3. Loop diuretics - furosemide
  4. Demeoclocycline - inhibitor of ADH
  5. ADH-R antagonists - vaptans - primate water excretion with no loss of electrolytes
210
Q

How do you treat asymptomatic SIADH?

A

Fluid restriction

211
Q

How do you treat very symptomatic SIADH?

A

Give 3% saline (hypertonic)

212
Q

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

A

Euvolaemic

213
Q

Would you associate SIADH with hyponatraemia or hypernatraemia?

A

Hyponatraemia - <135 mmol/L

214
Q

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

A

Plasma hypo-osmolality - <275 mOsmol/Kg

215
Q

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

A

High urine osmolality

216
Q

Define hyponatraemia

A

<135 mmol/L

Biochemically severe = serum sodium <125 mmol/L

217
Q

What stimulates the posterior pituitary to release ADH?

A

Osmoreceptors in the hypothalamus detect raised plasma osmolality Posterior pituitary is signalled to release ADH

218
Q

Give 4 local effects a pituitary adenoma

A
  1. Headaches
  2. Visual field defects - bitemporal hemianopia
  3. Cranial nerve palsy and temporal lobe epilepsy
  4. CSF rhinorrhoea
219
Q

What investigations are done when pituitary dysfunction is suspected?

A

Hormonal tests If hormonal tests are abnormal or tumour mass effect perform MRI pituitary

220
Q

What do you test the thyroid axis for in pituitary disease?

A

Measure Free T4 and TSH

221
Q

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

A

TSH highT4 low

222
Q

What is the effect of secondary hypopituitarism on TSH and T4 levels?

A

TSH low

T4 low

223
Q

What can lead to elevated levels of prolactin?

A
  1. Stress
  2. Drugs
  3. Pressure on pituitary stalk
  4. Prolactinoma
224
Q

What is the best radiological evaluation for the pituitary?

A

MRI - better visualisation of soft tissue and vascular structures

225
Q

Name 3 ketone bodies

A
  1. Beta hydroxybutyrate
  2. Acetoacetate
  3. Acetone
226
Q

Does diabetic ketoacidosis occur in T1 or T2 DM?

227
Q

Describe the triad of DKA

A
  1. Hyperglycaemia - blood glucose >11 mmol/L
  2. Acidaemia - blood pH <7.3 or plasma bicarbonate <15 mmol/L
  3. Raised plasma ketones - urine ketones >2+
228
Q

Give 4 causes of DKA

A
  1. Unknown
  2. Infection
  3. Treatment error - not administering enough insulin
  4. Having undiagnosed T1DM
229
Q

Give 5 symptoms of DKA

A
  1. Polyuria
  2. Polydipsia
  3. Weight loss
  4. Nausea and vomiting
  5. Confusion
  6. Weakness
230
Q

Give 3 signs of DKA

A
  1. Hyperventilation
  2. Dehydration
  3. Hypotension
  4. Tachycardia
  5. Coma
231
Q

What is the treatment for DKA

A

Rehydration (3L in first 3 hours)
Insulin
Replacement of electrolytes - K+Treat underlying cause

232
Q

Give 4 potential complications of untreated DKA

A
  1. Cerebral oedema
  2. Adult respiratory distress syndrome
  3. Aspiration pneumonia
  4. Thromboembolism
  5. Death
233
Q

In what class of drugs does metformin belong?

234
Q

Give an example of a sulfonylurea

A

Tolazamide

Gliclazide

235
Q

What are the physiological defences to hypoglycaemia?

A

Release of glucagon and adrenaline

236
Q

What are the symptoms of hypoglycaemia?

A

Autonomic - sweating, tremor, palpitations
Neuroglycopenic - confusion, drowsiness, incoordination
Severe neuroglycopenic - convulsions, coma

237
Q

Name 3 other types of diabetes other than T1DM, T2DM and DI

A
  1. Maturity onset diabetes of the young (MODY)
  2. Permanent neonatal diabetes
  3. Maternal inherited diabetes and deafness
238
Q

Name 3 exocrine causes of Diabetes

A
  1. Inflammatory - actue/chronic pancreatitis
  2. Hereditary haemochromatosis
  3. Pancreatic neoplasia
  4. Cystic fibrosis
239
Q

Name 3 endocrine causes of Diabetes

A
  1. Acromegaly
  2. Cushing’s syndrome
  3. Peochromocytoma
240
Q

What is Pheochromocytoma?

A

A rare catecholamine secreting tumour in the adrenal medulla (chromatin cells)

241
Q

what are the different types of pheochromocytoma?

A
  1. Familial type - more NAd

2. Sporadic - more Ad

242
Q

what are the clinical features of pheochromocytoma?

A 
SYMPTOMS
Headache
Profuse Sweating
Palpitations
Tremor 
SIGNS
Hypertension
Postural hypotension
Tremor
hypertensive retinopathy
Pallor
243
Q

What are the investigations for pheochromocytoma?

A
  • Plasma metanephrines and normetanephrines
  • 24 hour urinary total catecholamines
  • CT – look for tumour
244
Q

What is the treatment for pheochromocytoma?

A

Without HTN crisis:
1st Line: Alpha blockers: PHENOXYBENZAMINE
Most patients will eventually get the tumour removed and then managed medically.

With HTN crisis:
1st Line: Antihypertensive agents: PHENTOLAMINE

245
Q

What is the major complication of surgery on a patient with a pheochromocytoma?

A

Can stoke out during surgery due to rapid effect of adrenaline on the BP

246
Q

What is the major concern in someone with pheochromocytoma?

A

Dangerous cause of hypertension

247
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)

248
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

249
Q

What are the 3 main sites where microvascular complications of Diabetes cause particular damage?

A
  1. Retina = retinopathy
  2. Glomerulus = nephropathy
  3. Nerve sheath = neuropathy
250
Q

How long after a young patient has been diagnosed do microvascular complications start to manifest?

A

10-20 years after diagnosis

251
Q

Give 5 risk factors for diabetic retinopathy

A
  1. Long duration DM
  2. Poor glycaemic control
  3. Hypertensive
  4. On insulin treatment
  5. Pregnancy
  6. High HbA1c
252
Q

Describe the pathophysiology of diabetic retinopathy

A

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

253
Q

How can diabetic retinopathy be sub-divided?

A 
R1 = non-proliferative/background
R2 = pre-proliferative 
R3 = Proliferative
254
Q

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

A

Non-proliferative/background
Micro-aneurysms
Intraretinal haemorrhages
Exudates

255
Q

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

A

Pre-proliferative
Venous bleeding
Growth of new vessels

256
Q

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

A

Proliferative

New blood vessel on disc

257
Q

What is the treatment for diabetic retinopathy?

A

Regular screening to assess visual acuity

Laser therapy treats neovascularisation - doesn’t improve sight but stabilises

258
Q

What are the main risks of laser treatment of diabetic retinopathy?

A

Loss of night vision and peripheral vision

259
Q

What is diabetic maculopathy?

A

Fluid form leaking vessel is cleared poorly in macular area causing macula oedema which distorts and thickens the retina at the macula
Leads to loss of central vision

260
Q

What is the hallmark of diabetic nephropathy?

A

Development of proteinuria and progressive decline in renal function

261
Q

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

A

On microscopy there is thickening of the glomerular basement membrane

262
Q

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

A

T1DM - microalbuminuria develops 5-10 years after diagnosis

T2DM - microalbuminuria is often present at diagnosis

263
Q

Give 2 risk factors for diabetic nephropathy

A
  1. Poor blood pressure

2. Poor blood glucose control

264
Q

Describe the treatment for diabetic nephropathy

A
  1. Glycaemic and BP control
  2. Angiotensin receptor blockers/ACE inhibitors - RAMIPRIL or CANDESARTAN
  3. Proteinuria and cholesterol control
265
Q

What is the commonest form of diabetic neuropathy?

A

Distal symmetrical neuropathy

266
Q

Give 5 risk factors for diabetic neuropathy

A
  1. Poor glycaemic control
  2. Hypertension
  3. Smoking
  4. High HbA1c
  5. Overweight
  6. Long duration DM
267
Q

Why do isolated mononeuropathies result from in diabetic neuropathy?

A

Occlusion of vasa nervorum - small arteries that provide blood supply to peripheral nerves

268
Q

Why do more diffuse neuropathies arise in diabetic neuropathy?

A

Accumulation of fructose and sorbitol which disrupts the structure and formation of the nerve

269
Q

Give 3 major clinical consequences of diabetic neuropathy

A
  1. Pain
  2. Autonomic neuropathy
  3. Insensitivity
270
Q

Describe the pain associated with diabetic neuropathy

A

Burning
Paraethesia
Allodynia - triggering of pain from stimuli that doesn’t usually cause pain

271
Q

What is autonomic neuropathy in relation to diabetic neuropathy?

A

Damage to the nerves that supply body structures that regulate function such as BP, HR, bowel/bladder emptying

272
Q

Give 5 signs of autonomic neuropathy in diabetic neuropathy

A
  1. Hypotension
  2. HR affected
  3. Diarrhoea/constipation
  4. Incontinence
  5. Erectile dysfunction
  6. Dry skin
273
Q

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

A

Insensitivity –> foot ulceration –> infection –> amputation

274
Q

Describe the distribution of insensitivity as a result of diabetic neuropathy

A

Glove and sticking distribution - starts in the toes and moves proximally

275
Q

Describe the treatments for diabetic neuropathy

A
  1. Improve glycaemic control
  2. tricyclic antidepressants - AMITRIPTYLINE
  3. Pain relief - PARACETAMOL and TRAMADOL
276
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 antibiotics
277
Q

What are the 4 main threats to skin and subcutaneous tissues in someone with diabetic neuropathy

A
  1. Infections
  2. Ischaemia
  3. Abnormal pressure
  4. Wound environments
278
Q

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

A

Decreased foot pulses

279
Q

Peripheral vascular disease is a complication of Diabetes. Give 6 signs of acute ischaemia

A
  1. Pulseless
  2. Pale
  3. Perishing cold
  4. Pain
  5. Paralysis
  6. Paraesthesia
280
Q

what infections can poorly controlled diabetes lead to?

A
  1. UTIs
  2. Staphylococcal infection of skin
  3. Mucocutaneous candidiasis
  4. Pyelonephritis
  5. TB
  6. Pneumonia
  7. rectal abscess
281
Q

Why does the site of insulin injection need to be varied day to day?

A

Can cause lipohypertrophy if the same site is used everyday

282
Q

Name 4 non insulin treatments for diabetes

A
  1. Metformin
  2. Sulphonylurea
  3. Incretin based agents
  4. Thiazolidinediones (TZDs)
  5. SGLT-2 inhibitors
283
Q

Why is metformin the first line therapy for diabetes?

A

Associated with less weight gain and less hypoglycaemia than insulin and sulfonylurea

284
Q

When is sulfonylurea considered as treatment for diabetes?

A

In individuals:

  • Who are not overweight (as causes weight gain)
  • Require rapid response due to hyperglycaemia symptoms
  • Are unable to tolerate metformin or where metformin is contraindicated
285
Q

How do incretin based agents treat diabetes?

A

Influence glucose homeostasis via:

  • glucose dependent insulin secretion
  • postprandial glucagon suppression
  • slowing gastric emptying
286
Q

Give examples of Thiazolidinediones (TZDs)

A

Rosiglitazone and Pioglitazone

287
Q

How do Thiazolidinediones treat diabetes?

A

Effective glucose lowering agents

288
Q

What diseases are associated with polycystic ovary syndrome?

A
  1. Insulin resistance - T2DM
  2. Hypertension
  3. Hyperlipidaemia
  4. CV disease
289
Q

Give 5 symptoms of polycystic ovary syndrome

A
  1. Amenorrhoea
  2. Oligomenorrhoea
  3. Hirsutism
  4. Acne
  5. Overweight
  6. Infertility
290
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
291
Q

Describe the treatment for polycystic ovary syndrome

A
  1. Hirsutism therapy - shaving/waxing excess hair OR oestrogen (e.g. OCP)
  2. Menstrual disturbance therapy - cyclic oestrogen/progesterone
  3. Metformin can improve hyperinsulinaemia and regulates menstrual cycle
292
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
293
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism

High aldosterone levels independent of RAAS activation - H20 and sodium retention and potassium excretion

294
Q

What are the clinical features of Conn’s syndrome?

A
  • hypertension
  • nocturia and polyuria
  • mood disturbance
  • difficulty concentrating
  • hypokalaemia
295
Q

A deficiency in which electrolyte causes the symptoms of Conn’s syndrome?

A
  1. Muscle weakness
  2. Tiredness
  3. Polyuria
    Due to potassium deficiency
296
Q

What are the causes of Conn’s syndrome?

A 
Adrenal adenoma (2/3) 
Bilateral adrenal hyperplasia (1/3)
297
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 zone glomerulosa
  2. Renin is reduced - synthesised in the juxta-glomerular cells
298
Q

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

A
  • first line = aldosterone renin ratio - high
  • increased plasma aldosterone levels that aren’t suppressed with 0.9% saline infusion or fludrocortisone administration - DIAGNOSTIC
  • Bloods - plasma potassium = low
    4. ECG - flat T waves, ST depression and long QT
299
Q

Give 4 ECG changes 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
300
Q

What is the treatment for Conn’s syndrome?

A
  • If the cause is a single benign adrenal tumour - Unilateral adrenalectomy
  • If the cause is due to bilateral adrenal hyperplasia - Aldosterone antagonists (spironolactone)
301
Q

What is adrenal hyperplasia?

A

Defective enzymes mediating the production of adrenal cortex products - low levels of cortisol and high levels of male hormones

302
Q

How does adrenal hyperplasia present?

A

Salt loss
Females - ambiguous genitalia with common urogenital sinus
Males - no signs at brith, subtle hyperpigmentation and possible penile enlargement

303
Q

Briefly describe the pathophysiology of adrenal hyperplasia

A

Defective 21-hydroxylase –> disruption of cortisol biosynthesis
With or without aldosterone deficiency and androgen excess

304
Q

What diagnostic test would be done to confirm adrenal hyperplasia?

A

Serum 17-hydorxyprogesterone (precursor to cortisol) = high

305
Q

What is the treatment for adrenal hyperplasia?

A

Glucocorticoids - hydrocortisone
Mineralocorticoids - control electrolytes
If salt loss - sodium chloride supplement

306
Q

What is hyperkalaemia?

A

Excess of potassium Serum K+ >5.5 mmol/L

Serum K+ >6.5 mmol/L = medical emergency

307
Q

what are the clinical features of hyperkalaemia?

A 
SYMPTOMS
Fatigue
Generalised weakness
Chest pain
Palpitations
SIGNS
Arrhythmias
Reduced power
Reduced reflexes
Signs of underlying cause
308
Q

what are the causes of hyperkalaemia

A

IMPAIRED EXCRETION

  • AKI and CKD
  • drug effect
  • renal tubular acidosis (T4)

INCREASED INTAKE

  • IV therapy
  • increased dietary intake

SHIFT TO EXTRACELLULAR

  • metabolic acidosis
  • rhabdomyolysis
309
Q

What ECG changes might you see in someone with hyperkalaemia?

A

GO - absent P waves
GO LONG - prolonged PR
GO TALL - Tall T waves
GO WIDE - Wide QRS

310
Q

What is the treatment for hyperkalaemia?

A
  • ABC assessment
  • Consider cardiac monitoring
  1. Protect myocardium: 10ml, 10% calcium gluconate
  2. Drive K+ intracellularly: Insulin/Dextrose, Nebulised Salbutamol
311
Q

What is a complication for someone with hyperkalaemia?

A

Myocardial infarction –> death

312
Q

What is hypokalaemia?

A

Deficiency in potassium
Serum K+ <3.5 mmol/L
Serum K+ <2.5 mmol/L = medical emergency

313
Q

what are the clinical features of hypokalaemia?

A 
SYMPTOMS:
Asymptomatic
Fatigue
Generalised weakness
Muscle cramps and pain
Palpitations

SIGNS:
Arrhythmias
Muscle paralysis and rhabdomyolysis

314
Q

Give 3 causes of hypokalaemia

A
  • INCREASED EXCRETION
    • drugs e.g. thiazide, loop
    • renal disease
    • GI loss
    • increased aldosterone

REDUCED INTAKE
- dietary deficiency

SHIFT TO INTRACELLULAR
- drugs e.g. insulin, salbutamol

315
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
316
Q

What is the treatment for hypokalaemia?

A
  • Potassium PO/IV
  • Other electrolyte replacements
  • Treat underlying cause
317
Q

What are 2 possible complications of hypokalaemia?

A
  1. Cardiac arrhythmias

2. Sudden death

318
Q

Name 5 types of thyroid cancer

A
  1. Papillary - thyroid epithelium
  2. Follicular - thyroid epithelium
  3. Anaplastic - thyroid epithelium
  4. Lymphoma
  5. Medullary - calcitonin C cells
319
Q

What types of thyroid cancers are usually asymptomatic thyroid nodule (usually hard and fixed)?

A

Papillary
Follicular
Anaplastic

320
Q

what is the clinical presentation of thyroid cancer?

A
  • In 90% present as thyroid nodules
  • Occasionally they present with cervical lymphadenopathy or with lung, cerebral, hepatic or bone mets.
  • If thyroid gland increases in size, becomes hard and irregular in shape think cancer
  • May experience dysphagia or hoarseness of voice if tumour presses on surrounding structures
321
Q

How does a medullary cancer of the thyroid present?

A

Diarrhoea
Flushing episodes
Itching

322
Q

Why is an anaplastic cancer of the thyroid one of the most aggressive cancers?

A

Cancer of the follicular cells of the thyroid but doesn’t retain original cell features like iodine uptake or synthesis of thyroglobulin

323
Q

What hormone does a medullary cancer of the thyroid produce?

A

Calcitonin from C cells

324
Q

What is the most common form of thyroid cancer?

A

Papillary - 70%, young people, 3x more common in women

Follicular - 20%

325
Q

What investigations can you do to confirm a thyroid cancer?

A

Fine needle aspiration
For a Medullary cancer - elevated serum calcitonin
Blood tests – check TFTs (TSH, T4, T3) – check if hyper or hypo thyroid
Ultrasound - benign/malignant

326
Q

What is the treatment for thyroid cancer?

A
  • LEVOTHYROXINE T4 to keep TSH reduced as this is a growth factor for cancer Papillary and follicular
  • total thyroidectomy
  • ablative radioactive iodine Anaplastic and lymphoma
  • external radiotherapy to provide relief
  • largely palliative Medullary
  • total thyroidectomy and prophylactic central lymph node dissection
327
Q

what is de quervain’s thyroiditis?

A

Transient hyperthyroidism sometimes results from acute inflammation of
the thyroid gland, probably due to viral infection

328
Q

what is the clinical presentation of de quervain’s thyroiditis?

A

Usually accompanied by fever, malaise and pain in the neck

329
Q

what is the treatment for de quervain’s thyroiditis?

A

Treat with aspirin and only give prednisolone for severely symptomatic
cases

330
Q

what are the side effects of metformin?

A

GI upset

lactic acidosis

331
Q

what is the mechanism of action for SGLT-2 inhibitors?

A

inhibits resorption of glucose in the kidney

332
Q

what are the side effects of SGLT-2 inhibitors?

333
Q

what is the mechanism of action for glitazones?

A

Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake

334
Q

what are the side effects of glitazones?

A

Weight gain

Fluid retention

335
Q

what is the mechanism of action for levothyroxine?

A

synthetic T4

336
Q

what is the diagnostic criteria for diabetic ketoacidosis?

A

glucose >11mmol/L
pH <7.3
bicarbonate <15mmol/L
ketones >3mmol/l or ketones in urine

337
Q

what is hyperosmolar hyperglycaemic state?

A

This is a life-threatening emergency characterised by marked hyperglycaemia,
hyperosmolality and mild or no ketosis
characteristic of uncontrolled type 2 diabetes

338
Q

what are the risk factors for hyperosmolar hyperglycaemic state?

A
  • infection
  • consumption of glucose rich fluids
  • concurrent medication (thiazides or steroids)
339
Q

what is the pathophysiology of hyperosmolar hyperglycaemic state?

A
  • Endogenous insulin levels are reduced but are still sufficient to inhibit hepatic ketogenesis but insufficient to inhibit hepatic glucose production
340
Q

what is the clinical presentation of hyperosmolar hyperglycaemic state?

A
  • severe dehydration
  • decreased level of consciousness
  • hyperglycaemia
  • hyperosmolality
  • not ketones in blood or urine
  • stupor or coma
  • bicarbonate NOT LOWERED
341
Q

what are the investigations for hyperosmolar hyperglycaemic state?

A

Random plasma glucose >11mmol/L
Urine dipstick: glucosuria
Plasma osmolality - high
U+E - ↓ total body K+, ↑serum K+

342
Q

what is the treatment for hyperosmolar hyperglycaemic state?

A
  • Replace fluid - 0.9% saline IV
  • Insulin - At low rate of infusion!
  • Restore electrolytes - e.g. K+
  • LMWH
343
Q

what conditions is hashimotos thyroiditis associated with?

A
  • other autoimmune conditions - coeliac disease, T1DM, vitiligo
  • MALT lymphoma
344
Q

what are the side effects of levothyroxine?

A
  • usually due to excessive doses

- GI disturbance, cardiac arrhythmias and neurological tremors

345
Q

what is the mechanism of action for carbimazole?

A

prevents thyroid peroxidase from producing T3 and T4

346
Q

what is the mechanism of action for GH receptor antagonist’s e.g. pegvisomant?

A

blocks action of GH at GH receptor -> reduces production of IGF-1

347
Q

what are the side effects of GH receptor antagonists e.g. pegvisomant?

A
  • reactions at injection site
  • GI disturbance
  • hypoglycaemia
  • chest pain
  • hepatitis
348
Q

what is the mechanism of action for vasopressin antagonists e.g. tolvaptan?

A
  • inhibits vasopressin-2 receptor -> increases fluid excretion
  • causes aquaresis (excretion of H2O with no electrolyte loss) -> increased Na+
349
Q

what are the side effect of vasopressin antagonists e.g. tolvaptan?

A
  • GI disturbance
  • headache
  • increased thirst
  • insomnia
350
Q

what is the mechanism of action for vasopressin analogues e.g. desmopressin?

A

binds to V2 receptors -> aquaporin 2 inserted in collecting duct which increases water reabsorption

351
Q

what are the side effects of vasopressin analogies e.g. desmopressin?

A
  • headache
  • facial flushing
  • nausea
  • seizures
352
Q

what is the mechanism of action for metyrapone?

A
  • blocks cortisol synthesis by irreversibly inhibiting steroid 11 beta-hydroxide enzyme
353
Q

what are the side effects of metyrapone?

A
  • GI disturbance
  • headache
  • dizziness
  • drowsiness
  • hirsutism
354
Q

how would cortisol levels react to the synacthen test if there was secondary adrenal insufficiency?

A

short ACTH = no change

long ACTH = increase

355
Q

where is the most common site for carcinoid tumours to metastasise?

356
Q

what is the most common cause of hypothyroidism in the developing world and the developed world?

A

developing = iodine deficiency

developed = Hashimoto’s thyroiditis

357
Q

what is the levels of HbA1c in normal, pre-diabetes and diabetes?

A 
normal = < 42
pre-diabetes = 42-47
diabetes = >48
358
Q

what is the difference between cushing’s syndrome and cushing’s disease?

A 
syndrome = elevated cortisol levels
disease = caused by ACTH secreting pituitary adenoma
359
Q

what investigation can be used to differentiate between cushing’s syndrome and cushing’s disease?

A

dexamethasone suppression test
- overnight = cushing’s syndrome (including disease) is confirmed when there is no suppression

  • 48 hours = cushing’s syndrome (not disease) = no suppression
360
Q

which condition would cause TSH = low and T4 = high?

A

hyperthyroidism
thyrotoxicosis
graves

361
Q

which condition would cause TSH = high T4 = normal?

A

subclinical hypothyroidism

poor compliance with thyroxine

362
Q

which condition would cause TSH = high T4 = low?

A

primary hypothyroidism

hashimotos

363
Q

which condition would cause TSH = low T4 = low?

A

secondary hypothyroidism

364
Q

what arrhythmia is a consequence of untreated hyperkalaemia?

A

ventricular tachycardia

  • due to cell membranes becoming partially depolarised -> lower threshold potential so ventricles contract faster

Phase 2A revision (38 decks)

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