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MY PHASE 2A MEDICINE > ENDOCRINOLOGY > Flashcards

ENDOCRINOLOGY Flashcards

1
Q

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

A
  1. Beta cells (70%).
  2. Alpha cells (20%).
  3. Delta cells (8%).
  4. Polypeptide secreting cells.
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2
Q 
What do
a) beta cells
b) alpha cells
c) delta cells 
 produce?
A

a) insulin
b) glucagon
c) somatostatin

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3
Q

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

A

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

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4
Q

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

A

Low blood glucose = high glucagon and low insulin.

  • Glycogenolysis and gluconeogenesis.
  • Reduced peripheral glucose uptake.
  • Stimulates the release of gluconeogenic precursors.
  • Lipolysis and muscle breakdown.
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5
Q

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

A

Fasting state = low blood glucose.

Raised glucagon and low insulin.

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6
Q

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

A

High blood glucose = high insulin and low glucagon.

  • Glycogenolysis and gluconeogenesis are suppressed.
  • Glucose is taken up by peripheral muscle and fat cells.
  • Lipolysis and muscle breakdown suppressed.
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7
Q

Describe the effect on insulin and glucagon secretion after feeding.

A

Insulin is high and glucagon is low.

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8
Q

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

A

Fasting plasma glucose >7mmol/L.

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9
Q

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

A

Random plasma glucose >11mmol/L.

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10
Q

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

A

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

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11
Q

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

A

> 48mmol/mol.

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12
Q

What is the affect of cortisol on insulin and glucagon?

A

Cortisol inhibits insulin and activates glucagon.

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13
Q

Describe the aetiology of type 1 diabetes mellitus.

A

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

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14
Q

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

A

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

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15
Q

At what age do people with T1DM present?

A

Often people with Type 1 diabetes will present in childhood.

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16
Q

Give 2 potential consequences of T1DM.

A
  1. Hyperglycaemia.

2. Raised plasma ketones -> ketoacidosis.

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17
Q

Describe the natural history of T1DM.

A

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

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18
Q

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

A
  1. Severe insulin deficiency -> glycogenolysis /gluconeogensis /lipolysis all not suppressed
  2. Addition of reduced peripheral glucose uptake -> hyperglycaemia and glycosuria.
  3. Perceived stress -> cortisol and Ad secretion -> catabolic state -> increased plasma ketones.
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19
Q

Give 3 symptoms of T1DM.

A
  1. Weight loss.
  2. Thirst (fluid and electrolyte losses).
  3. Polyuria (due to osmotic diuresis).
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20
Q

Would you associate ketoacidosis with T1 or T2 DM?

A

TYPE 1.

Occurs due to the absence of insulin.

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21
Q

Describe the pathophysiology of diabetic ketoacidosis.

A
  1. INSUFFICIENT insulin -> less glucose available
  2. Increased KETOGENESIS
  3. Ketoacidosis
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22
Q

Name 3 ketone bodies.

A
  • acetoacetate.
  • acetone.
  • beta hydroxybutyrate.
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23
Q

Where does ketogenesis occur?

A

In the liver.

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24
Q

Give 4 signs of diabetic ketoacidosis.

A
  1. Vomiting/ Abdo pain
  2. KUSSMAUL breathing
  3. Breath smells of ketones. (fruity)
  4. Dehydration. (tachycardia/hypotension)
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25
Q

Describe the treatment for T1DM.

A
  1. EDUCATION - make sure the patient understands the benefits of good glycaemic control.
  2. Healthy diet - low in sugar, high in carbohydrates.
  3. Regular activity, healthy BMI.
  4. BP and hyperlipidaemia control.
  5. Insulin.
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26
Q

How is insulin administered in someone with T1DM?

A

Injected into SC fat/insulin pump

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27
Q

Give 4 potential complications of insulin therapy.

A
  1. Hypoglycaemia.
  2. Lipohypertrophy at ejection site.
  3. Insulin resistance.
  4. Weight gain.
  5. Interference with life style.
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28
Q

What is T2DM?

A

Chronic hyperglycemia due to inappropriately low insulin secretion AND peripheral insulin resistance

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29
Q

Describe the aetiology for T2DM

A

Genetics (polygenic) and environment (Associated with obesity, lack of exercise, calorie and alcohol excess)

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30
Q

Why is insulin secretion impaired in T2DM?

A

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

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31
Q

Describe the pathophysiology of T2DM.

A

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

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32
Q

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

A

Hepatic insulin resistance is the driving force of hyperglycaemia.

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33
Q

Give 3 risk factors for insulin resistance in T2DM.

A
  1. Obesity (mostly central).
  2. Physical inactivity.
  3. Family history.
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34
Q

Why do you rarely see diabetic ketoacidosis in T2DM?

A

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

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35
Q

Describe the treatment pathway for T2DM.

A
  1. Lifestyle changes: lose weight, exercise, healthy diet.
  2. Metformin. (gradual to avoid GI SE)
    • LINAGLIPTIN (DPP-4 inhibitor)
    • GLICAZIDE (sulfonylurea)
  5. Try insulin
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36
Q

How does metformin work in treating T2DM?

A

Metformin increases insulin sensitivity and inhibits glucose production.

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37
Q

How does sulfonylurea work in treating T2DM?

A

Sulfonylurea stimulates insulin release.

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38
Q

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

A

Hypoglycaemia.

(Sulfonylurea stimulates insulin release).

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39
Q

Give 3 microvascular complications of diabetes mellitus.

A
  1. Diabetic retinopathy.
  2. Diabetic nephropathy.
  3. Diabetic peripheral neuropathy.
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40
Q

Give a macrovascular complication of diabetes mellitus.

A

CV disease and stroke.

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41
Q

What is the main risk factor for diabetic complications?

A

Poor glycaemic control!

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42
Q

Give a potential consequence of acute hyperglycaemia?

A

Diabetic ketoacidosis and hyperosmolar coma.

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43
Q

Give a potential consequence of chronic hyperglycaemia?

A

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

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44
Q

What is the commonest form of diabetic neuropathy?

A

Distal symmetrical polyneuropathy. (gloves and socks)

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45
Q

Give 3 major clinical consequences of diabetic neuropathy.

A
  1. Pain.
  2. Autonomic neuropathy.
  3. Insensitivity.
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46
Q

What is the effect of insulin on peripheral cells?

A

Insulin binds to receptor which results in activation of tyrosine kinase and initiation of cascade response.

One consequence of this is the migration of GLUT-4 transporters to the cell surface and increased transport of glucose into cell.

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47
Q

Name 4 causes of secondary diabetes.

A

Diabetes is usually primary but may be secondary to:

  1. total pancreatectomy
  2. acromegaly
  3. cushing’s
  4. maturity onset diabetes of youth (single gene is affected which alters B-cells function).
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48
Q

Give 3 causes of DKA.

A
  1. Unknown.
  2. Infections.
  3. Treatment errors - not administering enough insulin.
  4. Having undiagnosed T1DM.
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49
Q

Describe the triad of DKA.

A
  1. Acidaemia – blood pH < 7.3
  2. Hyperglycaemia – blood glucose > 11mmol/L.
  3. Ketonaemia.
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50
Q

Give 4 potential complications of untreated DKA.

A
  1. Oedema.
  2. Adult respiratory distress syndrome.
  3. Aspiration pneumonia.
  4. Thromboembolism.
  5. Death.
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51
Q

Give 5 symptoms of hypoglycaemia.

A
  1. Seizures
  2. Sweating (fight/flight response)
  3. Tachycardia (fight/flight response)
  4. Anxious/ aggressive
  5. Shaking.
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52
Q

What class of drugs can cause diabetes?

A
  1. Steroids.
  2. Thiazides.
  3. Anti-psychotics.
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53
Q

In what class of drugs does metformin belong?

A

Biguanide.

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54
Q

Give an example of a sulfonylurea.

A

Tolazamide and gliclazide.

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55
Q

Describe the pain associated with diabetic neuropathy.

A
  • Burning.
  • Paraesthesia.
  • Nocturnal exacerbation.
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56
Q

Diabetic neuropathy clinical consequences: what is autonomic neuropathy?

A

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

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57
Q

Diabetic neuropathy: give 5 signs of autonomic neuropathy.

A
  1. Hypotension.
  2. HR affected.
  3. Diarrhoea/constipation.
  4. Incontinence.
  5. Erectile dysfunction.
  6. Dry skin.
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58
Q

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

A

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

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59
Q

Give 5 risk factors for diabetic neuropathy.

A
  1. POOR GLYCAEMIC CONTROL.
  2. Hypertension.
  3. Smoking.
  4. HbA1c.
  5. Overweight.
  6. Long duration of DM.
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60
Q

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

A
  1. Pulseless.
  2. Pale.
  3. Perishing cold.
  4. Pain.
  5. Paralysis.
  6. Paraesthesia.
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61
Q

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

A
  1. Screening for insensitivity.
  2. Education.
  3. MDT foot clinics.
  4. Pressure relieving footwear.
  5. Podiatry.
  6. Revascularisation and abx.
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62
Q

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

A

There would be increased foot pulses.

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63
Q

What is the hallmark of diabetic nephropathy?

A

Development of proteinuria and progressive decline in renal function.

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64
Q

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

A

On microscopy there is thickening of the glomerular basement membrane.

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65
Q

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

A

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

T2 DM: microalbuminuria is often present at diagnosis.

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66
Q

Describe the treatment for diabetic nephropathy.

A
  1. Glycaemic and BP control.
  2. ARB/ACEi.
  3. Proteinuria and cholesterol control.
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67
Q

What is the metabolic emergency characteristic of T2DM?

A

hyperosmolar hyperglycaemic state

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68
Q

What are the risk factors for hyperosmolar hyperglycaemic state?

A
  1. Insufficient oral hypoglycaemic agents!
  2. Infection (most common) e.g. pneumonia
  3. Consumption of glucose rich foods
  4. Concurrent meds e.g. thiazide diuretics or steroids
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69
Q

Describe 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.

(no ketogenesis just hyperglycaemia)

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70
Q

What would be the clinical presentation of someone with hyperosmolar hyperglycaemic state?

A

Severe DEHYDRATION (2ndary to osmotic diuresis)

Decreased level of consciousness
Hyperosmolality
Stupor
Bicarbonate is not lowered

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71
Q

How do you diagnose hyperosmolar hyperglycaemic state?

A
  • Hyperglycaemia > 11 mmol/L
  • Urine stick test shows heavy glycosuria
  • Plasma osmolality is v. high
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72
Q

What is the treatment for hyperosmolar hyperglycaemic state?

A
  1. Lower rate infusion of insulin
  2. Fluid replacement with 0.9% saline
  3. LMWH!!! (SC Enoxaparin)
  4. Restore electrolyte loss (K+)
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73
Q

How often are diabetics reviewed?

A

Every 12 months

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74
Q

What is checked for in a review of a diabetic patient?

A
  1. HbA1C
  2. BP
  3. cholesterol
  4. eye screening
  5. foot and leg check
  6. kidney function test
  7. diet advice/ BMI
  8. sexual advice/support
  9. injection sites review
  10. emotional/psychological help
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75
Q

What is the grading system for diagnosing with HbA1C result?

A
  1. 6% (below 42 mmol/mol) is considered non-diabetic
  2. 6-6.4% (42 to 47 mmol/mol) indicates impaired fasting glucose regulation and is considered prediabetes
  3. 6.5% or more (48 mmol/mol and above) indicates the presence of type 2 diabetes
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76
Q

How is diabetes diagnosed?

A
  1. Symptoms + 1 abnormal blood result
  2. No symptoms + 2 separate abnormal blood results
  3. HbA1c of 48mmol/mol (6.5%)
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77
Q

What blood glucose would someone with Impaired Fasting Glucose (prediabetes) have?

A

6.1 - 6.9 mmol/l

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78
Q

What blood glucose results would you expect 2hr post prandial?

A

7.8 - 11 = Impaired Glucose Tolerance

>11 = Diabetes

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79
Q

What do results of IGT/ IFG suggest?

A

Insulin resistance but NOT diabetes (prediabetes)

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80
Q

How would you manage a patient who is prediabetic?

A
  1. Lifestyle advice

2. Annual review

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81
Q

What is the criteria for diagnosing a patient with DM2?

A
  1. Symptomatic + 1 abnormal blood result
  2. Asymptomatic + 2 separate abnormal glucose result
  3. Abnormal HbA1C
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82
Q

Give 4 potential symptoms of DM2

A

MOSTLY ASYMPTOMATIC but can have

  1. Polyuria
  2. Polydipsia
  3. Unexplained weight loss
  4. Visual blurring
  5. Genital thrush
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83
Q

How would you diagnose and manage diabetic ketoacidosis?

A

Dx =

  • Acideamia (blood pH)
  • Hyperglycaemia
  • Ketonaemia/ketoniuria

Mx = Fluid/Insulin

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84
Q

Give 4 hypoglycaemic agents and their mechanism of action

A
  1. Metformin - reduces gluconeogensis in liver + increases insulin sensitivity)
  2. Gliclazide (sulfonylurea) - stimulates beta cells to secrete insulin
  3. Sitagliptin (DPP4 inhibitor) - stimulates insulin secretion
  4. Pioglitazone (enhance uptake of FFA and glucose)
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85
Q

Which hypoglycaemic agents may cause weight gain?

A

Gain = Gliclazide + PioGlitazone

86
Q

Describe the thyroid axis.

A

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

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

87
Q

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

A

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

88
Q

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

A

A low TSH indicates an over-active thyroid.

Lots of T4 and T3 is being produced and so there is more negative feedback on the pituitary and less TSH.

89
Q

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

A
  1. Food metabolism.
  2. Protein synthesis.
  3. Increased sympathetic action e.g. CO and HR.
  4. Heat production.
  5. Needed for growth and development.
90
Q

Give 4 causes of thyrotoxicosis.

A

Thyrotoxicosis - excess thyroid hormone due to any cause:

  1. Increased production e.g. Grave’s, toxic adenoma.
  2. Leakage of preformed T3/4 due to follicular damage.
  3. Ingestion of excess thyroid hormone
  4. Drug induced e.g. iodine/lithium
91
Q

Give 2 causes of hyperthyroidism.

A
  1. Grave’s disease

2. Toxic adenoma

92
Q

What is the epidemiology of hyperthyroidism?

A
  1. Female

2. 20-40 y/o

93
Q

What are the symptoms of hyperthyroidism?

A
  1. Diarrhoea
  2. Weight loss
  3. Sweats
  4. Heat intolerance
  5. Palpitations
  6. Tremor/ anxiety
  7. Hyperphagia
  8. Menstrual disturbance
94
Q

Give 8 signs of hyperthyroidism

A
  1. Tachycardia.
  2. Arrhythmias e.g. AF.
  3. Warm peripheries.
  4. Muscle spasm.
  5. Eye lid lag = Onycholysis
  6. Eye lid retraction = Exophthalmos
95
Q

How would you diagnose hyperthyroidism?

A
  1. Thyroid function tests:
    - Primary = low TSH, high T3/T4
    - Secondary = high TSH, high T3/T4
  2. Thyroid autoantibodies (Thyroid peroxidase, thyroglobulin, TSH receptor antibody)
  3. Radioactive iodine isotope uptake scan
96
Q

What is the treatment for hyperthyroidism?

A
  1. Beta blockers - rapid symptom control in attacks
  2. CARBIMAZOLE = anti-thyroid drug
  3. Radioiodine therapy
  4. Thyroidectomy
97
Q

Briefly describe the pathophysiology of Grave’s disease.

A
  1. Autoimmune disease.
  2. TSH receptor antibodies stimulate thyroid hormone production (TRAb)
  3. Excess TH secretion from thyroid
98
Q

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

A

Grave’s disease (+ diffuse goitre)

99
Q

Give 4 signs of Grave’s ophthalmology

A
  1. EXTRAOCULAR MUSCLE SWELLING
  2. Eye discomfort
  3. Lacrimation
  4. Diplopia
  5. EXOPTHALMOS
100
Q

What antibody would you find high levels of in Grave’s disease?

A
  1. TSH Receptor STIMULATING Antibody (TRAb)
  2. Thyroglobulin/ Thyroperoxidase (TPO) antibodies
    - also found in autoimmune hypothyroidism
101
Q

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

A
  1. Lymphocyte infiltration

2. Thyroid follicle destruction.

102
Q

What antibody is responsible for the pathology of autoimmune hypothyroidism?

A
  1. TSH Receptor BLOCKING Antibody

2. Thyroglobulin/ Thyroperoxidase (TPO) antibodies

103
Q

What are risk factors for thyroid autoimmunity?

A
  1. Genes - HLA-D3
  2. Environment - stress/ smoking
  3. Endogenous - pregnancy/ birthweight
104
Q

What autoimmune diseases are associated with thyroid autoimmunity?

A
  1. DM1
  2. Addisons
  3. Pernicious anaemia
  4. Vitiligo
105
Q

What is a goitre?

A
  1. Palpable and visible thyroid enlargement

2. Endemic in iodine deficient areas

106
Q

How does carbimazole work in treating Grave’s disease?

A

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

107
Q

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

A
  1. Emit beta particles
  2. Destroy follicular cells
  3. Inhibit production of T4/T3
108
Q

Is hypothyroidism or thyrotoxicosis more common in pregnancy?

A

Hypothyroidism is more common in pregnancy

109
Q

Give 7 symptoms of hypothyroidism

A
  1. Fatigue / tiredness / lethargy
  2. Cold intolerance
  3. Weight gain
  4. Myalgia
  5. Constipation
  6. Oedema
  7. Menorrhagia
110
Q

What are the signs of hypothyroidism?

A 
B radycardia
R flexes relax slowly
A taxia
D ry/ thin hair/skin 
Y awning
C old hands 
A ascites 
R ound/ puffy face 
D defeated demeanour 
I mmobile 
C ongestive HF
111
Q

Which drugs can be responsible for hyperthyroidism?

A
  1. AMIODARONE
  2. Iodine
  3. Lithium
112
Q

What is amiodarone normally used to treat?

A

Cardiac arrhythmias but has high iodine content so can cause thyrotoxicosis!

113
Q

What are the common causes of hypothyroidism?

A
  1. Hashimoto’s thyroiditis
  2. Iodine deficiency
  3. Previous radioiodine therapy
  4. Over-treatment of hyperthyroidism
114
Q

What is the mechanism of Hashimoto’s thryoiditis?

A

Autoimmune disease causing hypothyroidism!

- associated with presence of anti-TPO antibodies

115
Q

What electrolyte disturbance is often seen in hypothyroidism?

A

Hypo Natraemia!

116
Q

What is Cushing’s syndrome?

A
  1. A set of signs/symptoms resulting from chronic glucocorticoid excess
  2. with a loss of normal feedback mechanisms.
117
Q

What is Cushing’s disease?

A

Bilateral adrenal hyperplasia due to ACTH hypersecretion by pituitary adenoma.

118
Q

What is an ACTH independent cause of Cushing’s syndrome?

A
  1. ORAL STEROIDS (iatrogenic)

2. Adrenal adenomas

119
Q

What are 2 ACTH dependent causes of Cushing’s syndrome?

A
  1. Cushing’s disease

2. Ectopic Cushing’s syndrome

120
Q

What is ectopic Cushing’s syndrome?

A

Due to paraneoplastic syndrome e.g. small cell lung cancer producing ACTH

121
Q

Describe the cortisol axis

A

Hypothalamus -> CRH -> AP -> ACTH -> Adrenal cortex -> Glucocorticoids (cortisol)

122
Q

What is ACTH?

A

Adrenocorticotropic hormone

123
Q

What are the signs and symptoms of Cushing’s?

A 
C Cataracts / Central obesity 
U Ulcers
S Striae
H HTN / Hyperglycaemia / Hirsutism 
I Infections increase
N Necrosis 
G Glucosuria / Growth retardation 
O Osteoporosis
I mmunosuppression 
D iabetes
124
Q

How would you investigate for the presence of Cushing’s disease?

A
  1. Overnight dexamethasone suppression test
    - failure to suppress cortisol.
  2. Late night salivary cortisol
    - loss of circadian rhythm.
  3. Urinary free cortisol is raised.
  4. Loss of circadian rhythm.
125
Q

What is the treatment for Cushing’s?

A
  1. If iatrogenic: Stop steroids
  2. Cushing’s Disease: Transphenoidal removal of pituitary adenoma
  3. Adrenal adenoma: Adrenalectomy*, radiotherapy
  4. Ectopic ACTH: Surgery to remove tumour if location known
126
Q

Why may someone who has had an adrenalectomy develop brown pigmentation of the skin?

A

NELSON’S DISEASE

- no negative feedback on ACTH levels which can cause ACTH to build up in the body tissues

127
Q

Which electrolyte disturbance is Cushing’s associated with?

A

HypoKalaemia

- metabolic alkalosis

128
Q

Give an example of primary adrenal insufficiency

A

Addison’s disease

129
Q

What is the most common cause of primary adrenal insufficiency world wide?

A

TB!

UK = Adisson’s

130
Q

What is adrenal insufficiency?

A

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

131
Q

Give 6 symptoms of adrenal insufficiency.

A
  1. Tall
  2. Tanned
  3. Thin
  4. Tired
  5. Tearful
  6. Toned (lean)
  7. Throwing up (GI symptoms)
132
Q

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

A
  1. Bloods - FBC, U+E (↓Na+ and ↑K+ - due to ↓ aldosterone - ↑Ca2+, ↑Urea).
  2. ↓ Glucose.
  3. ACTH stimulation test - Addison’s will not respond.
  4. Test for 21-hydroxylase adrenal autoabs (+ve in 80% of Addison’s)
133
Q

What is the treatment for adrenal insufficiency?

A
  1. Hydrocortisone (replaces glucocorticoids)

2. Fludrocortisone ( replaces mineralocorticoids)

134
Q

What symptoms are an Addisonian crisis characterised by?

A

SHOCK

- severe hypotension and loss of a lot of fluid through vomiting / reduced reabsorption of Na+

135
Q

How would you treat someone in Adrenal crisis?

A
  • fluids

- hydrocortisone

136
Q

What type of metabolic abnormality does Addison’s disease most commonly cause?

A

Normal anion gap metabolic acidosis

137
Q

What are the causes of secondary adrenal insufficiency?

A
  1. iatrogenic

2. vomiting and abdo pain due to electrolyte imbalance

138
Q

What is the blood supply of the anterior pituitary?

A
  1. The anterior pituitary has no arterial blood supply

2. Receives blood through a portal venous circulation from the hypothalamus

139
Q

Give 4 common diseases of the pituitary

A
  1. Benign pituitary adenoma
  2. Trauma
  3. Sarcoid / TB
  4. Craniopharygioma
140
Q

What hormones does the anterior pituitary secrete?

A
  1. ACTH
  2. LH/ FSH
  3. GRH
  4. Somatostatin
141
Q

What hormones does the posterior pituitary secrete?

A
  1. Oxytocin

2. Anti-Diuretic Hormone

142
Q

What are the 3 clinical outcomes of having a Craniopharygioma?

A
  1. Pressure on local structure e.g. optic nerves – Bitemporal hemianopia
  2. Pressure on normal pituitary – hypopituitarism
  3. Functioning tumour
143
Q

Give 3 examples of functional tumours

A

– Prolactinoma
– Acromegaly
– Cushing’s disease

144
Q

How would you treat a prolactinoma?

A

Dopamine agonist eg Cabergoline/ bromocriptine.

145
Q

Where is the pituitary gland?

A
  1. Lies just inferior to the optic chiasm

2. Connected to the hypothalamus via pituitary stalk (infundibulum)

146
Q

Where are oxytocin/ vasopressin formed?

A

In the hypothalamus!!!

They are only stored in posterior pituitary

147
Q

Describe the GH/IGF-1 axis.

A

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

148
Q

What is the function of IGF-1?

A

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

149
Q

Briefly describe the mechanism of prolactin.

A

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

Prolactin acts on the mammary glands to produce milk.

150
Q

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

A

Prolactin levels would increase.

151
Q

Give 2 causes of prolactinoma.

A
  1. Pituitary adenoma.

2. Anti-dopaminergic drugs.

152
Q

Give 5 signs of prolactinoma.

A
  1. Infertility.
  2. Golactorrhoea. (milky nipple discharge)
  3. Amenorrhoea.
  4. Loss of libido.
  5. Visual field defects and headaches due to local effect of tumour.
153
Q

Describe growth hormone secretion from the anterior pituitary.

A
  1. Pulsatile

2. Increases during deep sleep

154
Q

What is acromegaly?

A
  1. Increased production of growth hormone occurring in adults
  2. After fusion of the epiphyseal plates
155
Q

What can cause acromegaly?

A

A benign pituitary adenoma

156
Q

Give 6 typical presenting features of acromegaly

A
  1. Acral enlargement
  2. Arthralgia
  3. Maxillofacial changes
  4. Excessive sweating
  5. Headache
  6. Hypogonadal symptoms (low libido)
157
Q

What maxillofacial changes would you expect to see in a patient with acromegaly?

A
  1. Prognathism - jaw protrusion.
  2. Interdental separation.
  3. Large tongue.
158
Q

How would you diagnose a patient with acromegaly?

A
  1. Plasma GH levels can exclude acromegaly - not diagnostic!
  2. Serum IGF-1 levels raised.
  3. Oral glucose tolerance test - diagnostic!
  4. MRI of pituitary.
159
Q

Give 2 treatment options for acromegaly

A
  1. Transphenoidal surgery to remove the adenoma
  2. Somatostatin anologues e.g. OCREOTIDE
  3. GH antagonist e.g. PEGVISOMANT
160
Q

What co-morbidities are associated with acromegaly?

A
  1. Arthritis.
  2. Cerebrovascular events.
  3. Hypertension and heart disease.
  4. Sleep apnea.
  5. T2 DM.
161
Q

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

A

Cabergoline

162
Q

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

A
  1. Hypopituitarism.
  2. Diabetes insipidus.
  3. Haemorrhage.
163
Q

Which electrolyte disturbance is characteristically caused by acromegaly?

A

Hypercalcaemia

164
Q

What is hyperaldosteronism?

A

Excess production of aldosterone independent of the renin-angiotensin-aldosterone system

165
Q

What is the most common cause of primary hyperaldosteronism?

A

CONN’S SYNDROME

166
Q

What can cause Conn’s syndrome?

A

Adrenal adenoma

167
Q

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

A
  1. Aldosterone is raised - synthesised in the zona glomerulosa.
  2. Renin is reduced - synthesised by the juxta-glomerular cells.
168
Q

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

A
  1. HYPOKALAEMIA

2. Hypertension

169
Q

What would be the clinical presentation of Conns?

A
  1. HYPOKALAEMIC
    - Constipation
    - Weakness and cramps
    - Paraesthesia
    - Polyuria and polydipsia
  2. HYPERTENSION (inc blood volume)
170
Q

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

A
  1. Bloods - U+E ( renin (low) and aldosterone (high))
  2. Plasma aldosterone/renin ratio can be used as an initial screening test - raised ratio indicates the need for further tests.
171
Q

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

A
  1. Increased amplitude and width of P waves.
  2. Flat T waves.
  3. ST depression.
  4. Prolonged QT interval.
  5. U waves.
172
Q

What is the treatment for Conn’s syndrome?

A
  1. Laparoscopic adrenalectomy.

2. Spironolactone (aldosterone antagonist).

173
Q

What does the parathyroid control?

A

Serum calcium levels.

A low serum calcium triggers the release of PTH.

174
Q

What does a high serum calcium level trigger the release of?

A

Calcitonin from C cells

175
Q

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

A

PTH

  1. Increases bone resorption by osteoclasts
  2. Increases calcium reabsorption at the kidney
  3. Activates vitamin D which then acts on the intestine to increase calcium absorption.
176
Q

What is the affect of hyperparathyroidism on serum calcium levels?

A

Hyperparathyroidism -> hypercalcaemia.

177
Q

Give 5 symptoms of hyperparathryoidism.

A

Hyperparathyroidism -> hypercalcaemia:

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

Stones,bones, groans, thrones, moans.

178
Q

Give 3 causes of hyperparathyroidism.

A
  1. Primary: PARATHYROID ADENOMA
    - ↑PTH ↑Calcium DECREASED Phosphate.
  2. Secondary: Physiological Hypertrophy
    - in an attempt to correct low calcium.
  3. Prolonged uncorrected hypertrophy.
179
Q 
What would the blood results show of patients with 
- primary 
- secondary 
- tertiary 
hyperparathyroidism?
A

Primary: ↑PTH, ↑Ca, ↓Phosph

Secondary: ↑PTH, ↓Ca, ↑Phosph

Tertiary: ↑everything (progression of secondary)

180
Q

Other than bloods, what investigations would you carry out on a patient with hyperparathyroidism?

A
  1. Increased 24hr urinary calcium excretion

2. DEXA bone scan for osteoporosis

181
Q

How do you treat hyperparathyroidism?

A
  1. High fluid intake, low calcium diet.
  2. Excision of adenoma/ correct underlying cause
  3. Parathyroidectomy
182
Q

What would you see on an ECG of a patient with hypokalaemia?

A

U (wave) have No Pot (K+), No T (inverted) but a long PR and QT

183
Q

Give 3 causes of hyperkalaemia.

A
  1. AKI.
  2. NSAIDs.
  3. Metabolic acidosis.
  4. K+ sparing diuretics.
184
Q

Give 3 symptoms of hyperkalaemia.

A
  1. Weakness.
  2. Palpitations.
  3. Tachycardia.
  4. Chest pain.
185
Q

What ECG changes might you see in someone with hyperkalaemia?

A
  1. Tall tented T waves.
  2. Wide QRS.
  3. Small P waves.
186
Q

What can cause excess secretion of potassium?

A

High levels of aldosterone ( Conn’s)

187
Q

What can cause reduced secretion of potassium?

A
  1. Addison’s (low levels of aldosterone)
  2. ACE Inhibitors- block the binding of aldosterone to receptor
  3. AKI- decreased filtration rate so more K+ is maintained in blood
188
Q

How would you treat hyperkalaemia?

A
  1. Non-urgent-
    Polystyrene sulphonate resin= Binds K+ in the gut decreasing uptake
  2. Urgent-
    Calcium gluconate= decreases VF risk in the heart
    Insulin= drives K+ into the cells
189
Q

What are the causes of hypocalcaemia?

A 
H - hypoparathyroidism 
A - Acute pancreatits
V - Vit D deficiency 
O - osteoMALACIA
C - CKD
190
Q

What are the signs and symptoms of hypocalcaemia?

A 
S - spasms 
P -  peripheral paraesthesia 
A - anxious
S - seizures
M – muscle tone increase
191
Q

Hypocalcaemia: What investigations and treatment?

A

ECG- Long QT interval

Treatment-
Mild= Adcal – everyone’s on it!
Severe= Calcium gluconate

192
Q

Give 3 causes of hypercalcaemia.

A
  1. Hyperparathyroidism.
  2. Hypercalcaemia of malignancy.
  3. Vitamin D toxicity.
  4. Myeloma.
193
Q

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

A

PTH measurement

194
Q

How can hypercalcaemia be treated?

A
  1. IV normal saline.
  2. IV furosemide.
  3. IV calcitonin.
  4. Bisphosphonates
195
Q

What is hypercalcaemia of malignancy?

A

Malignancy causes unregulated breakdown of bone leading to increased calcium levels in the blood.

196
Q

Which malignancies most commonly cause hypercalcaemia of malignancy?

A
  1. Myeloma!

2. Non- Hodgkins Lymphoma

197
Q

What are the 2 underlying causes of diabetes insipidus?

A
  1. Too little ADH from posterior pituitary gland (cranial)

2. Kidney not responding to ADH (nephrogenic)

198
Q

Give 3 causes of cranial diabetes insipidus.

A
  1. Tumours.
  2. Trauma.
  3. Infections.
199
Q

Give 3 causes of nephrogenic diabetes insipidus.

A
  1. Osmotic diuresis - diabetes mellitus.
  2. Drugs. (lithium)
  3. CKD.
200
Q

Give 3 signs of diabetes insipidus.

A
  1. Polyuria
  2. Polydipsia
  3. Dehydration
201
Q

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

A
  1. Measure 24-hour urine volume - >3L/24h = suggests DI.
  2. Plasma biochemisty - hypernatraemia.
  3. Water deprivation test - urine will not concentrate when asked not to drink.
202
Q

What is the treatment for diabetes insipidus?

A

Cranial DI = Desmopressin

Nephrogenic DI = Bendroflumethizide, NSAIDs

203
Q

How do diuretics work in treating Diabetes insipidus?

A
  1. causes more Na+ excretion

2. the increased water lost makes body responds by reducing GFR, so treat DI

204
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion.

Too much ADH = very concentrated urine and hyponatreamia.

205
Q

Give 3 symptoms of SIADH.

A
  1. Anorexia.
  2. Nausea.
  3. Malaise.
  4. Headache.
  5. Confusion.
206
Q

Give 3 causes of SIADH.

A
  1. Malignancy.
  2. CNS disorders e.g. meningitis, brain tumour, cerebral haemorrhage.
  3. Drugs.
207
Q

Describe the treatment for SIADH.

A
  1. Restrict fluid!
  2. Give salt.
  3. Loop diuretics e.g. furosemide.
  4. ADH-R antagonists e.g. vaptans - can be used when people find fluid restriction challenging.
208
Q

Give 5 diseases that are associated with obesity.

A
  1. T2DM.
  2. Hypertension.
  3. CAD.
  4. Stroke.
  5. Osteoarthritis.
  6. OSA.
  7. Infertility.
209
Q

Describe the association between obesity and shift work.

A

Obesity is more prevalent in people who do shift work.

Sleeping out of phase affects the metabolic circadian rhythm.

210
Q

Which brain structure is responsible for appetite regulation?

A

Hypothalamus.

  • Lateral hypothalamus: hunger centre.
  • Ventromedial: satiety centre.
211
Q

Define obesity.

A

Having a very high amount of body fat in relation to lean body mass. BMI >30kg/m2.

212
Q

Give 3 group’s of people in whom obesity is common.

A
  1. Lower SE groups.
  2. Older people.
  3. People with disabilities.

MY PHASE 2A MEDICINE (14 decks)

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