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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is the difference between a endocrine and an exocrine gland?

A
  • Endocrine = glands ‘pour’ secretions into the bloodstream
  • Exocrine = glands ‘pour’ secretions through a duct to site of action
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2
Q

What are the endocrine glands?

A
  • Hypothalamus
  • Pineal Gland
  • Pituitary Gland
  • Thyroid
  • Parathyroid
  • Thymus
  • Adrenal
  • Pancreas
  • Ovaries
  • Testes
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3
Q

What are the three types of hormone action?

A
  • Endocrine: the hormone is distributed in blood and binds to distant target cells
  • Paracrine: the hormone acts locally on adjacent cells
  • Autocrine: the hormone acts on the same cell that secreted it
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4
Q

Give an example of a water soluble hormone.

A

Peptides e.g. TRH, LH, FSH

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5
Q

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

A

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

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6
Q

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

A

They bind to cell surface receptors

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7
Q

Give an example of a fat soluble hormone.

A

Steroids, e.g. cortisol

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8
Q

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

A

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

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9
Q

Where are the receptors found for:

a) peptide hormones
b) steroid hormones
c) thyroid hormone

A

a) cell membrane
b) cytoplasm
c) nuclear receptors

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10
Q

Give 5 ways in which hormone action is controlled.

A
  1. Hormone metabolism - increased metabolism to reduce function
  2. Hormone receptor induction
  3. Hormone receptor down-regulation
  4. Synergism - combined effects of two hormones amplified, e.g. glucagon and adrenaline
  5. Antagonism - one hormone opposes other hormone, e.g. glucagon antagonises insulin
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11
Q

Name two hormones that reduce appetite.

A

Leptin and PPY

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12
Q

Name a hormone that increases appetite.

A

Ghrelin (GREEDY)

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13
Q

Where is parathyroid hormone released from? What is it released in response to? What is its role?

A
  • Parathyroid hormone (PTH) is released from the four parathyroid glands
  • It is released in response to low calcium serum. It is also released in response to low magnesium and high phosphate serum
  • Its role is to increase the serum calcium concentration
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14
Q

What does a high serum calcium concentration cause the release of and from where?

A

A high serum calcium concentration causes the release of calcitonin from the c-cells of the thyroid gland

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15
Q

What are the functions of PTH?

A
  • Increases calcium reabsorption at the kidney (so less excreted in urine) and decreases phosphate reabsorption
  • Stimulates the kidneys to convert vitamin D3 into calcitriol, which is the active form of vitamin D that promotes calcium absorption from food in the small intestine
  • Increases bone resorption (increases number of osteoclasts in bone, causing reabsorption of calcium from the bone into the blood)
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16
Q

What is calcium used in?

A

Calcium is used in neurotransmission and muscle contraction

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17
Q

What are the causes of hypocalcaemia?

A
  • Vitamin D deficiency (secondary hyperparathyroidism)
  • Hypoparathyroidism
  • Pseudohypoparathyroidism (PTH resistance)
  • Hyperventilation
  • Drugs
  • Malignancy
  • Toxic shock
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18
Q

What will the PTH, calcium and phosphate levels be like in vitamin D deficiency (secondary hyperparathyroidism)? Is this an appropriate or innapropriate response?

A
  • PTH high
  • Calcium low (Vitamin D causes calcium and phosphate reabsorption)
  • Phosphate low
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19
Q

What will the PTH, calcium and phosphate levels be like in hypoparathyroidism? Is this an appropriate or innapropriate response?

A
  • PTH low
  • Calcium low (as less PTH to reabsorb it)
  • Phosphate high (as less PTH to lower it)
  • Innapropriate response as low PTH is the problem
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20
Q

What will the PTH, calcium and phosphate levels be like in pseudohypoparathyroidism (PTH resistance)?

A
  • PTH high
  • Calcium low
  • Phosphate high
  • Appropriate response because the PTH resistance is the problem
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21
Q

What are the symptoms and signs of hypocalcaemia?

A
  • Symptoms: CATS go numb - convulsions, arrhythmias, tetany, spasm and numbness

  • Signs: Chevostek’s (tapping facial nerve induces spasm) + Trousseau’s (BP cuff 20 mm Hg above systolic for 5 minutes causes wrist to flex and fingers to draw together)
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22
Q

What are the investigations for hypocalcaemia?

A
  • Corrected calcium levels - done using serum calcium and serum albumin
  • ECG (long QT interval)
  • Parathyroid function
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23
Q

What is the management for hypocalcaemia?

A
  • 10ml calcium gluconate/chloride 10% slow IV
  • Oral calcium
  • Vit D
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24
Q

What are the complications of hypocalcaemia?

A

Seizure, cardiac arrest (decreases heart rate and contractility) - a medical emergency!

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25
Q

What are the causes of hypercalcaemia?

A
  • Malignancy (hypercalcaemia of malignancy)
  • Primary hyperparathyroidism
  • Sarcoidosis
  • Thyrotoxicosis
  • Drugs
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26
Q

What will the PTH and calcium levels be like in hypercalcaemia of malignancy? Is this an appropriate or inappropriate response?

A
  • PTH low
  • Calcium high (because this problem starts with a high Ca2+)
  • Appropriate response
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27
Q

What will the PTH, calcium and phosphate levels be like in primary hyperparathyroidism? Is this an appropriate or innapropriate response?

A
  • PTH high
  • Calcium high
  • Phosphate low
  • Innapropriate response
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28
Q

What are the symptoms and signs of hypercalcaemia?

A
  • Bones - bone pain
  • Stones - kidney stones/renal calculi
  • Groans - abdominal groans, e.g. abdominal pain, N+V, constipation
  • Moans - psychic moans, e.g. depression/cognitive impairment
  • Short QT interval
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29
Q

What are the investigations for hypercalcaemia?

A
  • Corrected calcium levels
  • ECG (short QT interval)
  • Look for cause
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30
Q

What is the management for hypercalcaemia?

A
  • Treat underlying cause
  • Increase circulation volume, increase excretion
  • Bisphosphonates, glucocorticoids, gallium, dialysis
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31
Q

What are the complications of hypercalcaemia?

A

Pancreatitis, confusion, coma, death

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32
Q

What is primary, secondary and tertiary hyperparathyroidism?

A
  • Primary: 1 parathyroid gland produces excess PTH
  • Secondary: increased secretion of PTH to compensate hypocalcaemia
  • Tertiary: autonomous secretion of PTH even after correction of calcium deficiency, due to Chronic Kidney Disease (CKD)
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33
Q

What are the primary, secondary and tertiary causes of hyperparathyroidism?

A
  • Primary: adenomas (80%), hyperplasia of all glands (20%)
  • Secondary: low vit D/CKD (PTH increases Calcium through bone resorption, gut absorption, renal reabsorption and activating Vit D)
  • Tertiary: develops from a prolonged secondary hyperparathyroidism
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34
Q

What is the epidemiology of hyperparathyroidism?

A
  • Women
  • 50-60 y/o
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35
Q

What are the symptoms and signs of hyperparathyroidism?

A
  • Symptoms: bones, stones, groans and psychic moans:
  • Osteoporosis
  • Kidney stones (renal calculi)
  • Constipation + acute pancreatitis
  • Confusion
  • Signs: hypercalcaemia, kidney stones
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36
Q

What are the investigations for hyperparathyroidism?

A
  • PTH/bone profile - high PTH, high calcium, low phosphates:
  • Primary: high calcium
  • Secondary: high PTH, low calcium
  • Tertiary: raised PTH, raised calcium
  • DEXA, X ray (salt and pepper degradation of bone), ultrasound for stones
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37
Q

What is the management for hyperparathyroidism?

A
  • Watchful waiting
  • Primary = surgical removal of adenoma, give bisphosphonates
  • Secondary = calcium correction, treat underlying cause
  • Tertiary = Cinacalcet (calcium mimetic), total/partial parathyroidectomy
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38
Q

What are the complications of hyperparathyroidism?

A
  • Hungry bone - rapid decrease in calcium/phosphate
  • Pancreatitis, kidney stones causing damage, fractures
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39
Q

What are the causes of hypoparathyroidism?

A

Autoimmune, congential - acquired damage leads to low calcium

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40
Q

What is hypoparathyroidism? Describe primary and secondary hypoparathyroidism.

A
  • Hypoparathyroidism = reduced PTH production
  • Primary - gland failure. Autoimmune destruction, congenital - DiGeorge syndrome (22q11 del)
  • Secondary - SURGICAL REMOVAL, decreased Mg (required for PTH secretion)
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41
Q

What are the risk factors for hypoparathyroidism?

A

Other autoimmune diseases

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42
Q

What are the symptoms and signs of hypoparathyroidism?

A
  • Symptoms: Convulsions, arrythmias, tetany and numbness (CATs go numb)
  • Signs: hypocalcaemia, Chevostek’s (facial nerve tap induces spasm), Trousseau’s (BP cuff causes wrist flexion and fingers to pull together)
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43
Q

What are the investigations for hypoparathyroidism?

A
  • Bone profile - low PTH, low calcium, high phosphate
  • ECG = prolonged QT + ST segments
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44
Q

What is the management for hypoparathyroidism?

A
  • IV calcium
  • AdCal-D3
  • Synthetic PTH if required
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45
Q

What are the complications of hypoparathyroidism?

A

Cardiac arrest

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46
Q

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

A

Diabetes mellitus

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47
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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48
Q

What do these cells produce:

a) alpha cells
b) beta cells
c) delta cells
d) polypeptide secreting cells

A

a) glucagon
b) INSULIN
c) somatostatin
d) pancreatic polypeptide

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49
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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50
Q

Describe the mechanism of insulin secretion from beta cells.

A
  • LEARN:
  • Blood glucose levels rise. Glucose enters beta cells via GLUT-2 transporter
  • Glycolysis begins to occur. This means that ATP is produced
  • The rise in ATP causes the ATP-sensitive potassium channels to close, so K+ ions can no longer diffuse out of the cell, causing the membrane to depolarise
  • The change in potential difference causes voltage-gated calcium channels to open, so Ca2+ ions diffuse into the beta cells down their concentration gradient
  • Calcium ions cause vesicles containing insulin to move + fuse with the cell membrane, releasing insulin by exocytosis
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51
Q

What does a low blood glucose mean for glucagon and insulin levels? 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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52
Q

How many carbon precursors are needed for gluconeogenesis?

A

3

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53
Q

What does a high blood glucose mean for insulin and glucagon levels? 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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54
Q

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

A

Fasting plasma glucose >7mmol/l

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55
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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56
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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57
Q

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

A

>48mmol/l

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58
Q

What is the effect of cortisol on insulin and glucagon?

A

Cortisol inhibits insulin and activates glucagon

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59
Q

What is the definition of type 1 diabetes mellitus? What is the epidemiology of the disease?

A
  • Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency
  • Epidemiology: 5-15 years (but can present at ANY age), 10% of DM
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60
Q

What are the risk factors for T1DM?

A
  • Northern European
  • Family history: HLA DR3-DQ2 or HLA-DR4-DQ8
  • Other autoimmune diseases (90%), e.g. autoimmune thyroid, Coeliac disease, Addison’s disease, pernicious anaemia
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61
Q

What is the pathophysiology of T1DM?

A
  • Autoantibodies attack beta cells in the Islets of Langerhans = insulin deficiency = hyperglycaemia
  • Continued breakdown of liver glycogen (gluconeogenesis) = glycosuria
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62
Q

What are the symptoms and signs of T1DM?

A
  • CLASSIC TRIAD: POLYDIPSIA, POLYURIA, WEIGHT LOSS (BMI < 25)
  • Usually a short history of severe symptoms
  • Typical patient with T1DM: polydipsia, polyuria, ketosis, rapid weight loss, young, BMI < 25, personal or family history of autoimmune disease
  • Symptoms:
  • Polydipsia
  • Polyuria
  • Unexplained weight loss (more common in T1)
  • Hunger
  • Nausea (more common in T1)
  • Pruritis vulvae and balantis
  • Signs:
  • Breath smells of acetone
  • Kussmaul breathing
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63
Q

Fill in the blanks: T_DM patients usually present with a ____ history of _____ symptoms.

A

T1DM patients usually present with a SHORT history of SEVERE symptoms (important)

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64
Q

When are we likely to make a diagnosis of T1DM?

A
  • RANDOM PLASMA GLUCOSE of >11mmol/l
  • Fits clinical picture: signs and symptoms, e.g. polydispsia, polyuria, weight loss, young, BMI < 25, personal and/or FHx of autoimmune disease
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65
Q

Why is polyuria a symptom of diabetes?

A
  • Usually, when your kidneys create urine, they reabsorb all of the glucose and direct it back to the bloodstream
  • In diabetes, excess glucose ends up in the urine, where it pulls more water, resulting in more urine
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66
Q

What is the treatment for T1DM?

A
  • INSULIN (specifically basal-bolus insulin therapy, which involves taking slow-acting insulin to moderate blood glucose when fasting, and short-acting insulin around mealtimes to quickly reduce the impact of dietary glucose)
  • Short-acting insulins and insulin analogues = 4-6 hours
  • Longer-acting insulin = 12-24 hours
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67
Q

What are the different types of insulin?

A
  • Rapid acting: insulin lispro, aspart or glulisine
  • Short acting: regular insulin
  • Intermediate acting: NPH
  • Long acting: insulin glargine
  • Insulin determir
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68
Q

Give 2 potential consequences of T1DM.

A
  1. Hyperglycaemia
  2. Diabetic ketoacidosis
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69
Q

What is diabetic ketoacidosis?

A

Complete lack of insulin results in high ketone production (cells can’t use glucose for energy, so they use fat for fuel instead. Burning fat makes acids called ketones). MEDICAL EMERGENCY

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70
Q

What is the aetiology of diabetic ketoacidosis?

A
  • Untreated or undiagnosed T1DM
  • Infection/illness
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71
Q

What is the pathophysiology of diabetic ketoacidosis?

A
  • Complete absence of insulin = UNRESTRAINED increased hepatic gluconeogenesis and decreased peripheral glucose uptake = hyperglycaemia
  • Peripheral lipolysis = increase FFA = oxidised to Acetyl CoA = ketones (acidic, cause anorexia and vomiting) = ACIDOSIS
  • Hyperglycaemia (+ increased ketones) = more in urine = osmotic diuresis = dehydration
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72
Q

What are the symptoms and signs of diabetic ketoacidosis?

A
  • Symptoms:
  • Diabetes symptoms ++
  • Polyuria and polydipsia
  • Nausea and vomiting
  • Weight loss
  • Drowsy/confused
  • Abdominal pain
  • Signs:
  • Kussmaul’s breathing
  • Breath smells of ketones - ‘pear drop’
  • Hypotension
  • Tachycardia
  • Dehydration
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73
Q

Which investigations would we perform for diabetic ketoacidosis? What would positive results look like?

A
  • Hyperglycaemia: random plasma glucose >11mmol/l
  • Ketonaemia: plasma ketones > 3mmol/l
  • Acidosis: blood pH < 7.35 or bicarbonate <15mmol/l
  • Urine dipstick: glycosuria/ketonuria
  • Serum U+E: raised urea and creatinine, decreased total K+, increased serum K+
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74
Q

What are the complications of diabetic ketoacidosis?

A
  • Coma
  • Cerebral oedema
  • Thromboembolism
  • Aspiration Pneumonia
  • DEATH
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75
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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76
Q

How do we manage diabetic ketoacidosis?

A
  1. ABC
  2. Replace fluid loss with 0.9% saline IV (ALWAYS COMES UP, THIS IS BEFORE INSULIN)
  3. IV insulin
  4. Restore electrolytes e.g. K+

FIG-PICK:

F - fluids; IV fluid resuscitation with normal saline

I - insulin; actrapid at 0.1 unit/kg/hr

G - glucose monitoring

P - potassium monitoring (should not be infused at >10mmol/hr)

I - infection; treat underlying triggers

C - chart fluid balance

K - ketone monitoring

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77
Q

What is the definition of type 2 diabetes mellitus?

A

A combination of peripheral insulin resistance and less severe insulin deficiency - patients gradually become insulin resistant/pancreatic beta cells fail to secrete enough insulin or BOTH

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78
Q

What are the risk factors for T2DM?

A
  • Lifestyle factors: obesity, lack of exercise, calorie and alcohol excess
  • Increase w/ age
  • M > F
  • Ethnicity: African-Caribbean, Black African and South Asian
  • Obesity
  • Hypertension
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79
Q

What would the clinical presentation of someone with T2DM be?

A
  • Polydipsia and polyuria (more T2DM than T1DM)
  • Glycosuria
  • Central obesity
  • Blurred vision
  • SLOWER ONSET but similar symptoms to T1DM - but may present with complications
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80
Q

What are the normal levels for:

a) random glucose
b) fasting glucose
c) 2h post prandial glucose
d) HbA1c (mmol/mol)
e) HbA1c (%)

A

a) <11.1
b) <6.1
c) <7.8
d) <42
e) <6.0

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81
Q

What are the pre-diabetes levels for:

a) random glucose
b) fasting glucose
c) 2h post prandial glucose
d) HbA1c (mmol/mol)
e) HbA1c (%)

A

a) N/A
b) 6.1-6.9
c) 7.8-11.0
d) 42-47
e) 6.0-6.4

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82
Q

What are the diabetic levels for:

a) random glucose
b) fasting glucose
c) 2h post prandial glucose
d) HbA1c (mmol/mol)
e) HbA1c (%)

A

a) 11.1
b) 7.0
c) 11.1
d) >47
e) >6.4

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83
Q

What are the investigations for T2DM?

A
  • Fasting plasma glucose: >7mmol/L
  • Random plasma glucose: >11mmol/L
  • HbA1c: >48mmol/L
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84
Q

What are the 5 steps for treating type 2 diabetes mellitus?

A
  1. FIRST LINE = lifestyle modification (diet, weight control, exercise, decrease alcohol intake, smoking cessation)
  2. 1st line therapy - METFORMIN (biguanide) = increases insulin sensitivity
  3. If HbA1c is still high, then DUAL THERAPY with metformin:
    - DPP4 inhibitor
    - Sulfonylureas - increase insulin secretion
    - Pioglitazone
    - SGLT-2i
  4. If HbA1c is still high, try triple therapy
  5. Insulin
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85
Q

What is the mechanism of action and side effects for biguanides, e.g. metformin?

A
  • Mechanism of action: decreased gluconeogenesis in liver and increase cell sensitivity to insulin
  • Side effects: NOT hypoglycaemia, GI disturbances (anorexia, diarrhoea, vomiting)
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86
Q

What is the mechanism of action for sulfonylureas, e.g. glicazide?

A
  • Mechanism of action: promote insulin secretion
  • Side effects: hypoglycaemia, weight gain
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87
Q

What is a hyperosmolar hyperglycaemic state (HHS)? What is it a complication of?

A
  • Marked hyperglycaemia
  • Hyperosmolality
  • MILD/NO KETOSIS
  • Serious complication of T2DM
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88
Q

What is the pathophysiology of a hyperosmolar hyperglycaemic state?

A
  • LOW INSULIN = increased gluconeogenesis = hyperglycaemia, but enough insulin to inhibit ketogenesis
  • Hyperglycaemia -> osmotic diuresis -> dehydration
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89
Q

What are the characteristics of a hyperosmolar hyperglycaemic state?

A
  • Caused by uncontrolled T2DM:
  • Marked hyperglycaemia
  • Hyperosmolality
  • Mild/no ketosis
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90
Q

What is the clinical presentation of a hyperosmolar hyperglycaemic state?

A
  • Extreme diabetes symptoms PLUS:
  • Confusion and reduced mental state
  • Lethargy
  • Severe dehydration
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91
Q

How can we diagnose a hyperglycaemic hyperosmolar state?

A
  • Random plasma glucose >11mmol/l
  • Urine dipstick: heavy glycosuria
  • Plasma osmolality: high
  • U+E - decreased total body K+, increased serum K+
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92
Q

What is the treatment for a hyperglycaemic hyperosmolar state?

A
  • Fluid replacement w/ 0.9% saline IV
  • Insulin - at low rate of infusion!
  • Restore electrolyte loss (K+)
  • LMWH, e.g. SC enoxaparin to decrease risk of thromboembolism
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93
Q

Give 3 microvascular complications of diabetes mellitus.

A
  1. Diabetic retinopathy.
  2. Diabetic nephropathy.
  3. Diabetic peripheral neuropathy.
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94
Q

Give two macrovascular complications of diabetes mellitus.

A

CV disease and stroke

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95
Q

What is the commonest form of diabetic neuropathy?

A

Distal symmetrical polyneuropathy

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96
Q

Give 3 major clinical consequences of diabetic neuropathy.

A
  1. Pain
  2. Autonomic neuropathy
  3. Insensitivity
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97
Q

Describe the pain associated with diabetic neuropathy.

A
  • Burning
  • Paraesthesia
  • Nocturnal exacerbation
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98
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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99
Q

Diabetic neuropathy: give 6 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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100
Q

Give 6 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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101
Q

What are the symptoms of hypoglycaemia?

A
  • Trembling
  • Palpitations
  • Sweating
  • Difficulty concentrating and speaking
  • Confusion
  • Drowsiness
  • Vision changes
  • Nausea
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102
Q

What are some causes of hypoglycaemia?

A
  • Long duration of diabetes
  • Tight glycaemic control with repeated episodes of non-severe hypoglycaemia
  • Increasing age
  • Use of drugs (prescribed, alcohol)
  • Sleeping
  • Increased physical activity
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103
Q

What is the alert value for hypoglycaemia? How do we treat hypoglycaemia?

A
  • Alert value for hypoglycaemia: blood glucose = <3.9mmol/l
  • Treat with 15g fast-acting carbohydrates
  • Re-test in 15 minutes to ensure blood glucose >4.0mmol/l and re-treat if needed
  • Eat a long-acting carbohydrate to prevent recurrence of symptoms
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104
Q

What sits above the pituitary gland? What does it do?

A

The hypothalamus sits above the pituitary gland and stimulates it with various hormones

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105
Q

What are the two parts of the pituitary gland? For either part, do they store or produce their hormones?

A
  • Anterior pituitary - produces and releases its own hormones (under the regulation of hormones made by the hypothalamus)
  • Posterior pituitary - stores and releases hormones produced by the hypothalamus
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106
Q

Which hormones are released by the anterior and posterior pituitary?

A
  • Anterior pituitary = FLAGTOP:
  • F: Follicle Stimulating Hormone (FSH)
  • L: Luteinizing Hormone (LH)
  • A: ACTH
  • G: Growth Hormone (GH)
  • T: Thyroid Stimulating Hormone (TSH)
  • O: MSH – melanOcyte stimulating hormone
  • P: Prolactin
  • Posterior pituitary:
  • ADH
  • Oxytocin
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107
Q

Does the anterior pituitary have an arterial blood supply?

A

The anterior pituitary has no arterial blood supply but receives blood through a portal venous circulation from the hypothalamus

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108
Q

What 3 things can pituitary adenomas cause?

A
  1. Pressure on local structure e.g. optic nerves – Bitemporal hemianopia
  2. Pressure on normal pituitary – hypopituitarism
  3. Functioning tumour, e.g. prolactinoma, acromegaly, Cushing’s disease/syndrome
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109
Q

Describe the different groups of hormones secreted from the adrenal glands. State which part of the adrenal glands they are secreted from and give an example for each.

A
  • MG’s got a GF called ARiana - Completely Caught Me!
  • Mineralocorticoids - Zona Glomerulosa in cortex, e.g. aldosterone
  • Glucocorticoids - Zona fasciculata of cortex, e.g. cortisol
  • Androgens - Zona reticularis of cortex, e.g. sex hormones
  • Catecholamines - Chromaffin cells in the adrenal medulla, e.g. adrenaline
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110
Q

Under normal circumstances, how is cortisol released?

A
  • HPA axis
  • Hypothalamus releases CRH (Corticotropin Releasing Hormone)
  • This stimulates the anterior pituitary to release ACTH (Adrenocorticotropic hormone)
  • Adrenal cortex releases cortisol
  • Cortisol acts on liver, muscle, pancreas etc.
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111
Q

What is the aetiology of Cushing’s syndrome?

A

Chronic excess of cortisol released by the adrenal glands

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112
Q

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

A

Cushing’s syndrome refers to the state of elevated cortisol levels. Cushing’s disease is specifically caused by an ACTH secreting pituitary tumour (pituitary adenoma)

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113
Q

What are the two types of causes of excess cortisol?

A
  • ACTH dependent causes
  • ACTH independent causes
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114
Q

What are the ACTH dependent causes of excess cortisol?

A
  • Cushing’s disease: most common, caused by an ACTH secreting pituitary adenoma, leads to bilateral adrenal hyperplasia
  • Ectopic ACTH production
  • ACTH treatment
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115
Q

What are the ACTH independent causes of excess cortisol?

A
  • Iatrogenic - steroid use (most common)
  • Adrenal adenoma
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116
Q

What would the clinical presentation be of someone with Cushing’s syndrome?

A
  • Central obesity
  • Plethoric complexion
  • Hirsutism
  • Moon face
  • Buffalo hump
  • Mood change
  • Proximal muscle weakness
  • Purple abdominal striae
  • Hypertension
  • Acne
  • Gastric ulcers
  • Osteoporosis
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117
Q

What is the process of diagnosing Cushing’s syndrome?

A
  1. Drug history - Cushing’s can be caused by oral steroids, so exclude this first
  2. Random plasma cortisol (screening). IF HIGH…
  3. Overnight dexamethasone suppression test - cortisol will not be suppressed in Cushing’s disease (but normally they should decrease because dexamethasone should suppress ACTH levels)
  4. Urinary free cortisol (24 hr)
  5. Test plasma ACTH
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118
Q

Which investigation can be used to differentiate between the 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 hour

  • Cushing’s syndrome (not including disease) = no suppression
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119
Q

Is Cushing’s syndrome progressive? How do we treat Cushing’s syndrome?

A
  • Cushing’s syndrome is progressive
  • The treatment is dependent on the cause:
  • Iatrogenic: stop medications if possible
  • Pituitary adenoma = transsphenoidal surgical resection (1st line)
  • Adrenal adenoma = adrenalectomy (1st line)

ALSO drugs to inhibit cortisol synthesis, e.g. metyrapone, ketoconazole

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120
Q

What are the complications of Cushing’s syndrome?

A
  • Cardiovascular disease
  • Hypertension
  • Diabetes mellitus
  • Osteoporosis
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121
Q

Describe the growth hormone axis.

A
  • Growth hormone releasing hormone (GHRH) is released from the hypothalamus
  • This stimulates growth hormone (GH) release from the anterior pituitary
  • Growth hormone stimulates the release of insulin-like growth factor 1 (IGF-1) from the liver
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122
Q

What are the roles of growth hormone and IGF-1?

A
  • Growth hormone stimulates bone and muscle growth, increases protein synthesis, stimulates the growth of internal organs
  • IGF-1 drives growth too
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123
Q

What is acromegaly? What are the primary and secondary causes?

A
  • Acromegaly = release of excess growth hormone causing overgrowth of all systems
  • Causes:
  • Primary: pituitary adenoma = most common (99%)
  • Secondary to a malignancy that secretes ectopic GH, e.g. lung cancer
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124
Q

What are the symptoms and signs of acromegaly?

A
  • Symptoms: large hands, box jaw, thick skin, arthritis, increased sweating, obstructive sleep apnoea, lower pitch of voice
  • Signs: hypertension, insulin resistance, bitemporal hemianopia
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125
Q

What are the investigations required for acromegaly?

A
  • 1st line = IGF-1 BLOOD TEST = raised
  • Gold standard = ORAL GLUCOSE TOLERANCE TEST
  • Other tests: random serum GH raised, MRI scan of pituitary fossa
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126
Q

How can we manage acromegaly?

A
  • 1st line = Transsphenoidal pituitary surgery (if cause is adenoma)
  • 2nd line = Somatostatin analogue, e.g. ocreotide - inhibits GH secretion
  • 3rd line = GH receptor antagonist, e.g. pegvisomant
  • 4th line = Dopamine agonist, e.g. cabergoline - bind to D2 receptor and suppress GH hypersecretion
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127
Q

What are the complications of acromegaly?

A
  • Erectile dysfunction
  • Diabetes
  • Sleep apnoea
  • Heart disease
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128
Q

What is the difference between acromegaly and gigantism?

A

Gigantism occurs if acquired before epiphyseal fusion. Often get people around 2.7m or 8ft11. Puberty often delayed

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129
Q

What is the epidemiology of prolactinoma?

A
  • 2/10,000
  • F > M
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130
Q

What is prolactinoma? What is a cause of hyperprolactinoma? What happens after?

A
  • Prolactinoma = benign adenoma of pituitary gland producing excess prolactin
  • Cause of hyperprolactinoma: non-functioning pituitary tumour - compresses pituitary stalk -> no inhibition of prolactin release
  • This initiates lactation, breast development, controls osmolality + carbohydrate/fat metabolism
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131
Q

What is the pathophysiology of prolactinoma?

A

2 types:

  • Micro (tumour less than 10mm diameter on MRI; most common (90%))
  • Macro (tumour more than 10mm diameter on MRI)
  • Increased release of prolactin can cause galactorrhoea by stimulating milk production from mammary gland, as well as inhibiting FSH and LH
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132
Q

What are the symptoms and signs of prolactinoma?

A
  • Symptoms: amenorrhea, galactorrhoea, gynaecomastia, headache, visual field defect
  • Signs: low testosterone/oestrogen, infertility
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133
Q

What are the investigations for prolactinoma?

A
  • Prolactin levels
  • CT head scan
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134
Q

What is the management for a prolactinoma?

A
  • 1st line = DOPAMINE AGONISTS: bromocritipine/cabergoline (dopamine has an inhibitory effect on prolactin)
  • Gold standard = TRANSSPHENOIDAL RESECTION SURGERY OF PITUITARY GLAND
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135
Q

What are the complications of prolactinoma?

A
  • Infertility
  • Sight loss
  • Raised intercranial pressure
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136
Q

Define puberty.

A

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

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137
Q

What is the first sign of puberty in girls?

A

Menarche (first occurence of menstruation)

138
Q

What hormone is responsible for regulating the growth of the breasts and female genitalia? What are the three major types of this hormone?

A
  • Oestrogen
  • Estradiol, estriol and estrone
139
Q

What is the first sign of puberty in boys?

A

First ejaculation, often nocturnal

140
Q

What are the roles of testicular androgens in male puberty?

A
  1. Development of external genitalia
  2. Growth of pubic and axillary hair
  3. Deepening of voice
141
Q

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

A

Tanner scale

142
Q

What is thelarche?

A

Breast development

143
Q

Describe the 3 stages of breast development.

A
  1. Ductal proliferation
  2. Adipose deposition
  3. Enlargement of areola and nipple
144
Q

What is adrenarche?

A

Maturation of the adrenal gland - the development of the zona reticularis cells

145
Q

Give 2 signs of adrenarche.

A
  1. Body odour
  2. Mild acne
146
Q

What is pubarche?

A

Growth of pubic hair

147
Q

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

A

Precocious puberty

148
Q

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

A

Brain tumour

149
Q

What is the treatment for precocious puberty?

A

GnRH super agonist to suppress pulsatility of GnRH secretion (stimulates LH and FSH secretion from the anterior pituitary)

150
Q

What is delayed puberty?

A

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

151
Q

What is the most likely cause of delayed puberty in boys?

A

Constitutional delay - runs in the family; late menarche in mum or delayed growth spurt in father

152
Q

Give 3 consequences of delayed puberty.

A
  1. Psychological problems
  2. Reproduction defects
  3. Reduced bone mass
153
Q

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

A

Turner syndrome (45X). They might also have recurrent ear infections

154
Q

Give 7 functional causes of delayed puberty.

A
  1. Anorexia
  2. Bulimia
  3. Over exercising
  4. CKD
  5. Drugs
  6. Stress
  7. Sickle cell disease
155
Q

What investigations might you do in someone with delayed puberty?

A
  1. FBC - red cell count especially
  2. U+E
  3. LH/FSH measurements
  4. Thyroid function tests (TFTs)
  5. Karyotyping for Turner’s
156
Q

What is hypergonadotropic hypogonadism?

A

Primary gonadal failure - testes or ovarian failure

157
Q

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

A

High FSH/LH, low oestrogen/testosterone

158
Q

Give 2 examples of hypergonadotropic hypogonadism.

A
  1. Turner Syndrome (45X)
  2. Klinefelter’s syndrome (47XXY)
159
Q

What is hypogonadotropic hypogonadism?

A

Secondary gonadal failure - hypopituitary or problems with the hypothalamus

160
Q

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

A

Low FSH/LH and low testosterone/oestrogen

161
Q

Give an example of hypogonadotropic hypogonadism.

A

Kallman syndrome

162
Q

What is Turner syndrome?

A

In Turner syndrome the patient is missing an X chromosome - 45X. It is an example of primary gonadal failure (hypergonadotropic hypogonadism).

163
Q

Give 3 signs of Turner syndrome.

A
  1. Short stature
  2. Delayed puberty
  3. Recurrent otitis media
164
Q

What is Klinefelter’s syndrome?

A

In Klinefelter’s syndrome the patient has an extra X chromosome - 47XXY. It is an example of primary gonadal failure (hypergonadotropic hypogonadism)

165
Q

Give 4 signs of Klinefelter’s syndrome.

A
  1. Azoospermia
  2. Gynaecomastia (enlargement of male breast tissue)
  3. Increased risk of breast cancer
  4. Testicular size <5ml
166
Q

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

A

Azoospermia - semen contains no sperm

167
Q

Give 4 symptoms of Klinefelter’s syndrome.

A
  1. Reduced pubic hair
  2. Tall stature
  3. Reduced IQ
  4. Small testicles (<5ml)
168
Q

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

A

Breast cancer

169
Q

What is Kallman syndrome?

A

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

170
Q

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

A

Smell - 75% have anosmia

171
Q

How is Kallman syndrome inherited?

A

X linked recessive or dominant

172
Q

Explain the thyroid axis.

A
  • The hypothalamus releases thyrotropin-releasing hormone (TRH)
  • This stimulates the anterior pituitary to release thyroid stimulating hormone (TSH)
  • This in turn stimulates the thyroid gland to release triiodothyronine (T3) and thyroxine (T4). T3 is the active form of thyroxine - approximately 20% is secreted into the bloodstream by the thyroid gland, the rest is produced by the conversion of thyroxine by organs such as the liver and kidneys
173
Q

What is hyperthyroidism? What is primary and secondary hyperthyroidism? What are the risk factors?

A
  • When your body makes excess thyroid hormones: T3 (triiodothyronine) and T4 (thyroxine)
  • Primary - abnormal increased thyroid function
  • Secondary - abnormal increased TSH production
  • Risk factors: young/middle-aged women, stress, smoking, family history of thyroid disease/autoimmune disease, existing autoimmune disease, HLA-DR3
174
Q

What are the causes of hyperthyroidism? How about a secondary cause?

A
  • Graves’ disease - about 3/4 of hyperthyroidism is caused by this. IgG autoantibodies (anti-TSHR-antibodies or TRAb) bind to TSH receptor - this causes more T3/T4 to be made
  • Toxic multicellular goitre, iodine overdose (e.g. IV contrast), toxic adenoma, metastatic follicular thyroid cancer
  • Secondary cause: TSH SECRETING PITUITARY TUMOUR
175
Q

What are the symptoms and signs of hyperthyroidism?

A

Everything goes fast:

  • Hot and sweaty
  • Diarrhoea
  • Increased appetite
  • Weight loss
  • Palpitations
  • Tremor
  • Irritability
  • Anxiety/restlessness
  • Oligomenorrhoea (infrequent menstrual periods)
  • Goitre
  • Fine hair and hair loss
  • Thyroid acropachy (clubbing)
  • Oncholysis
176
Q

If someone’s hyperthyroidism is caused by Graves’ disease, what additional signs and symptoms may they have?

A
  • Hyperthyroidism symptoms plus:
  • THYROID EYE DISEASE (25-50%):
  • Eyelid retraction
  • Periorbital swelling
  • Proptosis/exophthalmos
  • Pretibial myxoedema
  • Thyroid acropachy
177
Q

What are the investigations for hyperthyroidism?

A
  • Thyroid function tests - high T3/4, low TSH in primary, high TSH in secondary
  • Thyroid autoantibodies (anti-TSHR)
  • US and CT head
178
Q

How do we manage hyperthyroidism?

A
  • Drug management:
    a. Beta-blockers - rapid symptom relief
    b. 1ST LINE CARBIMAZOLE - blocks synthesis of T4
    c. 2nd line Propylthiouracil - prevents T4 -> T3 conversion
  • Under specialist care, 1st line treatment is radioactive iodine. Thyroidectomy is also recommended
179
Q

What are the complications of hyperthyroidism?

A
  • Grave’s ophthalmopathy (thyroid eye disease)
  • Hypothyroidism (due to carbimazole)
  • Thyroid storm - medical emergency!
180
Q

What is hypothyroidism? What is primary and secondary hypothyroidism? What are the risk factors?

A
  • Hypothyroidism is where the thyroid gland does not produce enough thyroid hormones: T3 and T4
  • Primary = abnormal decreased thyroid function
  • Secondary = abnormal decreased TSH production
  • Risk factors: other autoimmune diseases, postpartum
181
Q

What are the causes of hypothyroidism? How about the secondary cause?

A
  • Hashimoto’s (inflammation -> goitre) = most common cause of hypothyroidism. Anti-TPO antibodies attack the thyroid gland causing inflammation and dysfunction, lowering T3/T4 levels
  • Primary atrophic hypothyroidism (atrophy -> no goitre)
  • Other primary - iodine deficiency, drugs (antithyroid drugs, iodine, lithium), post thyroidectomy/radioiodine
  • Secondary - HYPOPITUITARISM
182
Q

What are the symptoms and signs for hypothyroidism?

A
  • Everything goes slow:
  • Fatigue
  • Weight gain
  • Loss of appetite
  • Cold
  • Lethargy
  • Constipation
  • Low mood/depression
  • Menorrhagia (heavy periods)
  • Goitre
  • Dry flaky skin
  • Coarse thinning hair
  • Brittle nails
183
Q

What is the mnemonic for the signs of hypothyroidism?

A

BRADYCARDIC:

  • Bradycardia
  • Reflexes
  • Ataxia
  • Dry hair/skin
  • Yawning
  • Cold hands
  • Ascites
  • Round face (puffy)
  • Defeated demeanour
  • Immobile
  • Congestive cardiac failure
184
Q

What are the investigations for hypothyroidism?

A
  • Thyroid function tests - low T3/4, high TSH (primary), low TSH (secondary)
  • Autoantibodies - anti-TPO
185
Q

How do we manage hypothyroidism?

A

Levothyroxine (T4)

186
Q

What are the complications of hypothyroidism?

A
  • Heart disease
  • Pregnancy problems
  • Myxoedema coma - medical emergency!
187
Q

What is Graves’ disease?

A

Graves’ disease - IgG autoantibodies (anti-TSHR-antibodies or TRAb) bind to TSH receptor - this causes more T3/T4 to be made

188
Q

What is Hashimoto’s disease?

A

Hashimoto’s = most common cause of hypothyroidism. Anti-TPO antibodies attack the thyroid gland causing inflammation and dysfunction, lowering T3/T4 levels

189
Q

What is De Quervain’s thyroiditis? In whom is it most common? What are the symptoms?

A
  • De Quervain’s (subacute) thyroiditis is a painful swelling of the thyroid gland thought to be triggered by a viral infection, such as mumps or flu
  • It’s most commonly seen in women aged 20 to 50
  • It usually causes high temperature and pain in the neck, jaw or ear
190
Q

What is thyroid storm?

A

Thyroid storm, also referred to as thyrotoxic crisis, is an acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones in individuals with thyrotoxicosis (hyperthyroidism is a subset of thyrotoxicosis)

191
Q

What are the two types of diabetes insipidus? Explain both conditions.

A
  • Cranial diabetes insipidus is a condition in which the hypothalamus does not produce enough ADH (vasopressin)
  • Nephrogenic diabetes insipidus is a condition in which the kidneys fail to respond to ADH
192
Q

What does a reduced ADH cause?

A

A reduced ADH causes excessive water loss - this is because ADH works to control the amount of water that is reabsorbed at the kidneys. We get LARGE VOLUMES of DILUTE URINE

193
Q

What are the causes of cranial and nephrogenic diabetes insipidus?

A
  • Cranial:
  • Idiopathic
  • Congenital
  • Tumour
  • Trauma
  • Infection
  • Nephrogenic:
  • Inherited
  • Metabolic (low potassium, high calcium)
  • Drugs (lithium)
  • Chronic renal disease
194
Q

What are the symptoms and signs of diabetes insipidus?

A

Polyuria, polydipsia, and dehydration

195
Q

What are the investigations for cranial and nephrogenic diabetes insipidus?

A
  • GOLD STANDARD - 8 hour water deprivation test to diagnose
  • Then desmopressin test = establish cranial or nephrogenic
  • Other investigations = cranial MRI
196
Q

Describe the treatment for cranial and nephrogenic diabetes insipidus.

A
  • Treat the UNDERLYING CAUSE
  • Cranial = desmopressin (synthetic ADH) to replace ADH
  • Nephrogenic = if cause persists, give Bendroflumethiazide
197
Q

What is the aetiology of hyponatraemia?

A
  • Hypervolaemic, i.e. drinking too much fluid
  • Kidney failure
  • Heart failure
  • Cirrhosis
  • Use of diuretics
  • Chronic vomiting or diarrhoea
  • Syndrome of inappropriate anti-diuretic hormone (SIADH)
198
Q

What are the three classifications for hyponatraemia and their values?

A
  • Mild - serum sodium concentration 130-135 mmol/L
  • Moderate - serum sodium concentration 125-129 mmol/L
  • Severe - serum sodium concentration <125 mmol/L
199
Q

What are the symptoms and signs of hyponatraemia?

A
  • Nausea and vomiting
  • Headache
  • Confusion
  • Irritability
  • Mental slowing
  • Coma
200
Q

What are the investigations for hyponatraemia?

A
  • Check serum osmolality. If low…
  • Check urine Na and osmolality
201
Q

How do we treat hyponatraemia?

A
  • Treat underlying cause
  • Stop offending drugs and fluids (if hypervolaemic or euvolaemic hyponatraemia)
  • Give 0.9% saline if it is hypovolaemic hyponatraemia
202
Q

What is the aetiology of hypernatraemia?

A
  • Insufficient fluid intake
  • Too much water loss
203
Q

What are the three classifications of hypernatraemia and their values?

A
  • Mild (146-149 mmol/L)
  • Moderate (150-169 mmol/L)
  • Severe (≥170 mmol/L)
204
Q

What are the signs and symptoms of hypernatraemia?

A
  • Muscle weakness
  • Restlessness
  • Extreme thirst
  • Confusion
  • Lethargy
  • Irritability
  • Seizures
  • Unconsciousness
205
Q

What are the investigations for hypernatraemia?

A
  • Serum electrolyte panel with glucose, urea, and creatinine
  • Urine osmolality
  • Serum osmolality
  • Urine electrolytes
206
Q

How do we treat hypernatraemia?

A
  • Treat shock as a priority - severe hypernatraemia is a medical emergency
  • Mild hypernatraemia - treat underlying cause and repeat UEC in 4-6 hours
  • Moderate hypernatraemia - treatment dependent on underlying cause: water deficit or sodium excess. Water deficit = replace water deficit over 48 hours with IV 0.9% sodium chloride and 5% glucose. Replace ongoing losses mL for mL with 0.9% sodium chloride. Sodium excess = aim to reduce excess sodium intake. May need hypotonic fluid (0.45% sodium chloride) or dialysis if overloaded
207
Q

What is SIADH?

A
  • Syndrome of inappropriate anti-diuretic hormone
  • It is where too much ADH is released from the posterior pituitary causing more water to be reabsorbed in the collecting duct
208
Q

What are the causes of SIADH?

A
  • Medications (thiazide diuretics) is most common cause
  • Post-operative from major surgery
  • Brain injury
  • Infection, e.g. meningitis, encephalitis, pneumonia
  • Tumours, e.g. carcinoma, mesothelioma
209
Q

What are the symptoms and signs of SIADH?

A
  • Very non-specific:
  • Headache
  • Nausea
  • Fatigue
  • Muscle cramps
  • Confusion
  • Severe hyponatraemia
210
Q

What are the investigations for SIADH?

A
  • A diagnosis of exclusion:
  • U+E = HYPONATRAEMIA
  • Urine sodium = high
  • Urine osmolality = high
  • Causes of hyponatraemia need to be excluded:
  • -ve short SynACTHen test - exclude adrenal insufficiency
  • No diarrhoea, vomiting
  • No history of diuretic use
  • No AKI/CKD
211
Q

How do we treat SIADH?

A
  • Treat underlying cause:
  • Stop causative medication
  • Fluid restriction - 1L/24hr
  • Tolvaptan (ADH receptor blocker)
  • Increase osmolarity - <8mmol/l increase in Na+ per 24 hours if chronic
212
Q

What are the complications of SIADH?

A
  • Cerebral oedema
  • Seizure
  • Coma
  • Death
213
Q

What is the aetiology of hypokalaemia?

A
  • Increased excretion: drugs, e.g. thiazide, loop diuretics, renal disease, GI loss (N+V), increased aldosterone (lose K+ and retain Na+)
  • Reduced intake: dietary deficiency
  • Shift to intracellular: metabolic alkalosis, drug effect, e.g. insulin, B2 agonists - SABAs and LABAs
214
Q

What levels of potassium define hypokalaemia?

A

Hypokalaemia - <3.5mmol/l

215
Q

What are the symptoms and signs of hypokalaemia?

A

Symptoms:

  • Asymptomatic
  • Fatigue
  • Generalised weakness
  • Muscle cramps and pain
  • Palpitations
  • Constipation

Signs:

  • Arrhythmias
  • Hypotonia
  • Hyporeflexia
  • Muscle paralysis and rhabdomyolysis
216
Q

What are the investigations for hypokalaemia? What would the ECG show?

A
  • ECG
  • Urine osmolality, electrolytes
  • Bloods: U+E and FBC
217
Q

What is the appearance of an ECG in hypokalaemia?

A
  • Prolonged PR interval
  • ST depression
  • Flat T waves
  • Prominent U waves
218
Q

How do we manage hypokalaemia?

A
  • Potassium PO or IV
  • Other electrolyte replacements
  • Treat underlying cause
219
Q

What is the aetiology of hyperkalaemia?

A
  • Impaired excretion: AKI and CKD, drug effect, renal tubular acidosis (T4)
  • Increased intake: IV K+ therapy, increased dietary intake
  • Shift to extracellular: metabolic acidosis, decreased insulin, rhabdomyolysis
220
Q

What levels of potassium define hyperkalaemia?

A
  • Hyperkalaemia = >5.5mmol/l
221
Q

What are the symptoms and signs of hyperkalaemia?

A

Symptoms:

  • Fatigue
  • Generalised weakness
  • Chest pain
  • Palpitations
  • Diarrhoea
  • Anxiety

Signs:

  • Arrhythmias
  • Hyperreflexia
  • Flaccid paralysis
  • Signs of underlying cause
222
Q

What are the investigations for hyperkalaemia? What would the ECG show?

A
  • ECG
  • Bloods: U+E, FBC
  • Urine osmolality and electrolytes
223
Q

What is the appearance of an ECG in hyperkalaemia?

A
  • TALL TENTED T WAVES
  • Small/absent P waves
  • Prolonged PR interval (>200ms)
  • Wide QRS interval (>120ms)
224
Q

How do we manage hyperkalaemia?

A
  • ABC
  • Cardiac monitoring
  • CALCIUM GLUCONATE - to protect myocardium
  • INSULIN + DEXTROSE OR NEBULISED SALBUTAMOL - drive K+ intracellularly
  • Treat underlying cause
225
Q

How do hypo- and hyperkalaemia affect smooth, skeletal and cardiac muscle?

A
  • Hypo = slows everything down:
  • Smooth: constipation
  • Skeletal: weakness/cramps
  • Cardiac: arrhythmias and palpitations
  • Hyper = speeds everything up:
  • Smooth: cramping
  • Skeletal: weakness/flaccid paralysis. Due to over contraction, muscles become totally drained of energy
  • Cardiac: arrhythmias and arrest
226
Q

In hypo- and hyperkalaemia, what happens with insulin, pH and beta-2 receptors?

A
  • Hypokalaemia:
  • Insulin: excess - too much K+ follows insulin into cell
  • pH: alkalosis (high pH) - H+ out and K+ in
  • Beta-2 receptor: beta-2 agonists (SABA/LABA) - increase B2 pumping of K+ into cell
  • Hyperkalaemia:
  • Insulin: deficiency - not enough K+ follows into the cell
  • pH: acidosis (low pH) - H+ in and K+ out
  • Beta-2 receptor: beta blocker - inhibits pumping of K+ into cell
227
Q

What are the 5 main actions of cortisol within the body?

A
  • Inhibits the immune system
  • Inhibits bone formation
  • Raises blood glucose
  • Increases metabolism
  • Increases alertness
228
Q

What are the two types of adrenal insufficiency? Describe both.

A
  • Primary adrenal insufficiency = ADDISON’S DISEASE, or primary adrenal insufficiency, is a disorder that affects the adrenal glands, causing decreased production of adrenocortical hormones (specifically CORTISOL and ALDOSTERONE). Others = surgical removal, trauma
  • Secondary adrenal insufficiency = secondary adrenal insufficiency occurs in patients with pituitary or hypothalamic involvement. This results in decreased ACTH secretion, which ultimately results in adrenal failure. Steroids, congenital
229
Q

What are the most common causes for adrenal insuffiency in both developed and developing countries?

A
  • In developed countries - autoimmune destruction (21-hydroxylase present in 60-90% of people)
  • In developed countries - TB is one of the commonest causes
230
Q

What is the pathophysiology of Addison’s disease?

A

Destruction of adrenal cortex leads to decreased production of glucocorticoid (cortisol) and mineralocorticoid (aldosterone)

231
Q

What is the cumulative risk, for patients with a positive adrenocortical autoantibody test, of developing Addison’s disease?

A

Approximately 50%

232
Q

What are the risk factors for adrenal insuffiency?

A
  • Female sex
  • Adrenocortical autoantibodies
  • Other autoimmune diseases
233
Q

What are the signs and symptoms of adrenal insufficiency?

A
  • Tanned
  • Lean
  • Fatigue
  • HYPERPIGMENTATION - only in Addison’s disease
  • Postural hypotension
  • Weakness
  • Hypoglycaemia
  • Other signs of autoimmunity may be present (vitiligo, Hashimoto’s etc.)
234
Q

What are the investigations for adrenal insufficiency?

A
  • 1st line: U+E = hyponatraemia, hyperkalaemia, blood glucose (hypoglycaemia)
  • Gold standard = SHORT SYN(ACTH)EN TEST (ACTH stimulation test). Presents with: low cortisol, high ACTH
  • Plasma renin and aldosterone - high renin and low aldosterone
  • Can also do:
  • Adrenal CT or MRI
  • 21-hydroxylase adrenal autoantibodies - is positive in autoimmune diseases in more than 80%
235
Q

How do we manage adrenal insufficiency?

A
  • Glucocorticoid (HYDROCORTISONE - replaces cortisol) and mineralocorticoid (FLUDROCORTISONE - replaces aldosterone) (these are the two main hormones produced by the adrenal cortex)
  • Treat underlying cause and warn against abruptly stopping steroids
236
Q

Addison’s disease is to do with the adrenal cortex. What is a pheochromocytoma? How common is it? Where is adrenaline produced?

A
  • A pheochromocytoma is an adrenal medullary tumour that secretes catecholamines (adrenaline, noradrenaline, dopamine). It is very rare
  • Adrenaline is produced in the ‘chromaffin cells’ of the adrenal medulla
237
Q

What are the main catecholamines?

A

The main catecholamines are epinephrine (adrenaline), norepinephrine (noradrenaline), and dopamine

238
Q

What is the aetiology of pheochromocytoma?

A

Phaeochromocytomas occur in certain familial syndromes:

– Multiple endocrine neoplasia (MEN) syndrome

– Neurofibromatosis

– Von-Hippel Lindau Disease

239
Q

What are the symptoms and signs of pheochromocytomas?

A
  • Symptoms: headache, profuse sweating, palpitations, tremor etc.
  • Signs: hypertension, postural hypotension, tremor, hypertensive retinopathy, pallor
240
Q

What are the investigations for pheochromocytomas?

A
  • Plasma METANEPHRINES (made when your body breaks down catecholamines) and NORMETANEPHRINES
  • 24 hour urinary total CATECHOLAMINES
  • CT - look for tumour
241
Q

How do we manage pheochromocytomas?

A
  • WITHOUT HTN CRISIS:
  • 1st line: alpha blockers - PHENOXYBENZAMINE
  • Most patients will eventually get the tumour removed (ADRENALECTOMY = definitive treatment) and then managed medically
  • WITH HTN CRISIS:
  • 1st line: antihypertensive agents - PHENTOLAMINE
  • 2nd line = SODIUM NITROPRUSSIDE
242
Q

Describe the RAAS system.

A
  • Renin is secreted by the juxtaglomerular cells that sit in the afferent (and some in the efferent) arterioles in the kidney. They sense the blood pressure in these vessels. They secrete more renin in response to low blood pressure
  • Renin acts to convert angiotensinogen (released by the liver) into angiotensin I. Angiotensin I converts to angiotensin II in the lungs with the help of angiotensin-converting enzyme (ACE).
  • Angiotensin II acts on blood vessels to cause vasoconstriction = higher blood pressure. Angiotensin II also stimulates the release of aldosterone from the adrenal glands.
  • Aldosterone is a mineralocorticoid steroid hormone. It acts on the nephrons in the kidneys to:
  • Increase sodium reabsorption from the distal tubule. When sodium is reabsorbed in the kidneys water follows it by osmosis. This leads to an increase in intravascular volume and subsequently blood pressure
  • Increase potassium secretion from the distal tubule
  • Increase hydrogen secretion from the collecting ducts
243
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism due to an aldosterone producing adenoma

244
Q

What is the pathophysiology of Conn’s syndrome?

A

Excess aldosterone production independent of RAAS = increased sodium + water reabsorption and potassium excretion in the kidneys, low renin release = hypertension (because of fluid retention) and potential hypokalaemia

245
Q

What is the clinical presentation of Conn’s syndrome?

A
  • Hypertension
  • Hypokalaemia
  • Nocturia and polyuria
  • Mood disturbance
  • Difficulty concentrating
246
Q

What are the investigations for Conn’s syndrome? What would they show?

A
  • High aldosterone:renin ratio
  • Low plasma potassium
  • U+E
247
Q

What is the treatment for Conn’s syndrome?

A
  • 1ST LINE = aldosterone antagonists (SPIRONOLACTONE) - if the cause is due to bilateral adrenal hyperplasia
  • GOLD STANDARD = unilateral adrenalectomy - if the cause is a single benign adrenal tumour
  • Aim is to lower BP, decrease aldosterone levels and resolve electrolyte imbalance
248
Q

What is Carcinoid syndrome?

A

Groups of symptoms due to release of serotonin and other vasoactive peptides into the systemic circulation from a carcinoid tumour (rare cancerous tumour)

249
Q

What are the symptoms and signs of Carcinoid syndrome?

A

Symptoms:

  • Diarrhoea
  • Flushing

Signs:

  • Palpitations
  • Abdominal cramps
  • Signs of right heart failure
  • Bronchospasm
250
Q

What are the investigations for Carcinoid syndrome?

A
  • Serum chromogranin A/B
  • Urinary 5-hydroxyindoleacetic acid (breakdown product of serotonin)
  • Metabolic panel and LFTs
  • Liver ultrasound: confirm metastases
251
Q

How can we treat Carcinoid syndrome?

A
  1. Local disease: surgical resection + peri-operative octreotide infusion
  2. Metastases: above + additional radiofrequency ablation
252
Q

What is Serotonin syndrome? What is its main cause?

A
  • Serotonin syndrome is a medical condition that can happen when there is too much serotonin in your brain or other parts of your nervous system. It can be mild, but in rare situations, it can kill you
  • Main cause is drugs, e.g. overdose of antidepressants, antidepressants + migraine medication, antidepressant + opioid
253
Q

What are the symptoms and signs of Serotonin syndrome?

A
  • Agitation or restlessness
  • Confusion
  • Rapid heart rate and high blood pressure
  • Dilated pupils
  • Loss of muscle coordination or twitching muscles
  • Muscle rigidity
  • Heavy sweating
  • Diarrhoea
254
Q

What are the investigations for Serotonin syndrome?

A

There is no specific investigation to confirm Serotonin syndrome, but can eliminate others:

  • Blood and urine tests
  • Chest X-ray
  • CT scan
  • Lumbar puncture
255
Q

How do we treat Serotonin syndrome?

A
  • Treatment depends on symptoms and their severity:
  • Muscle relaxants can help control agitation, seizures and muscle stiffness
  • Serotonin-production blocking agents, e.g. cyproheptadine
  • Oxygen and IV fluids
256
Q

Which of the following is not under the control of the pituitary gland?

A. Thyroid

B. Adrenal cortex

C. Adrenal medulla

D. Testis

E. Ovary

A

C. Adrenal medulla

257
Q

Which of the following statements is false?

A. The pituitary gland lies in the sella turcica

B. The weight of the pituitary gland is around 0.5g

C. ACTH is secreted from the pituitary during stress

D. The pituitary regulates calcium metabolism

E. The anterior and posterior pituitary are distinct on an MRI scan

A

D. The pituitary regulates calcium metabolism

258
Q

In men all the following are mainly produced in the adrenal cortex except?

A. DHEAS

B. Testosterone

C. Aldosterone

D. 17-OH progesterone

E. Androstenedione

A

B. Testosterone

259
Q

Which of the following regarding AVP is false?

A. AVP levels have a linear relationship with serum osmolality

B. Is produced in the pituitary gland

C. Stimulates reabsorption of water in the collecting duct of the nephron

D. In hypotension baroreceptors predominantly activate ADH production and secretion

E. Further AVP production is no longer effective once urine osmolality has reached a plateau

A

B. Is produced in the pituitary gland

260
Q

Where is growth hormone’s main site of action to stimulate IGF1 release?

A. Bone

B. Liver

C. Adrenal cortex

D. Muscle

E. Pancreas

A

B. Liver

261
Q

The following are typical features of excess growth hormone secretion except?

A. Polyuria

B. Joint pains

C. Sweating

D. Hypotension

E. Headaches

A

D. Hypotension

262
Q

The following hormones all have a circadian rhythm except?

A. Cortisol

B. Testosterone

C. DHEA

D. 17OH progesterone

E. Thyroxine (T4)

A

E. Thyroxine (T4)

263
Q

Typical features of cortisol deficiency include the following except?

A. Hypotension

B. Muscle aches

C. Weight loss

D. Hyperglycaemia

E. Lethargy

A

D. Hyperglycaemia

264
Q

A 38 year old lady presented with weight gain, menorrhagia and constipation. She is most likely to be suffering from?

A. Cushing’s syndrome

B. Addison’s disease

C. Primary hypothyroidism

D. Graves disease

E. Acromegaly

A

C. Primary hypothyroidism

265
Q

Which test would you likely want to perform in a patient with proximal muscle weakness, purple striae and thin skin?

A. Synacthen test

B. Overnight dexamethasone suppression test

C. Insulin tolerance test

D. Glucagon test

E. Skin allergy tests

A

B. Overnight dexamethasone suppression test

266
Q

A 24 year old girl presented with hirsutism, oligomenorrhoea and acne. What test would you likely carry out from the ones below?

A. Ultra sound adrenals

B. Ultra sound ovaries

C. MRI ovaries

D. CT scan adrenals

E. Prolactin

A

B. Ultra sound ovaries

267
Q

A 54 year old gentleman presented with hyponatraemia. All the following conditions need excluding before confirming SIADH except?

A. Hypothyroidism

B. Hypervolaemia

C. Euvolaemia

D. Adrenal insufficiency

E. Diuretic use

A

C. Euvolaemia

268
Q

A 66 year old gentleman had a serum sodium of 124 mmol/l, serum osmolality 265 mmol/l and a urine sodium of 52 mmol/l. What would you like to perform first?

A. Chest X-ray

B. CT brain

C. Skin turgor and jugular venous pressure test

D. Thyroid function tests

E. Synacthen test

A

C. Skin turgor and jugular venous pressure test

269
Q

The following are most likely causes of SIADH except?

A. Multiple sclerosis

B. Lung abscess

C. Subdural haemorrhage

D. Lymphoma

E. Cerebrovascular accident

A

A. Multiple sclerosis

270
Q

A 28 year old presented with a microprolactinoma. What is the most unlikely symptom?

A. Galactorrhoea

B. Oligomenorrhoea

C. Decreased sexual appetite

D. Headaches

E. Visual field defects

A

E. Visual field defects

271
Q

The following suppress appetite except:

A. Peptide YY

B. Ghrelin

C. CCK

D. GLP1

E. Glucose

A

B. Ghrelin

272
Q

The main adipose signal to the brain is:

A. CCK

B. Neuropeptide y

C. Leptin

D. Agouti-related peptide

E. Adiponectin

A

C. Leptin

273
Q

A 65 year old lady is diagnosed with SIADH. Her sodium is 123mmol/l. What is your first line of management?

A. If she is symptomatic I will treat with fluid restriction

B. If she is asymptomatic I will treat with hypertonic saline

C. If she is asymptomatic I will treat with fluid restriction

D. If she is asymptomatic I will repeat the sodium level the next day

E. If she is asymptomatic I will give normal saline

A

C. If she is asymptomatic I will treat with fluid restriction

274
Q

A patient with Addison’s disease presents with a chest infection. What do you do?

A. Omit his steroids to avoid immunosuppression

B. Stop his steroids as they have precipitated a chest infection

C. Double his steroid dose whilst unwell

D. Keep him on his usual steroid dose

E. Not of the above

A

C. Double his steroid dose whilst unwell

275
Q

The following tests are typical of secondary hypogonadism:

A. Low LH; High testosterone

B. Low LH; Low testosterone

C. High prolactin; high testosterone

D. Low FSH; Low prolactin

E. None of the above

A

B. Low LH; Low testosterone

276
Q

Typical features of hypogonadism in a male include the following except:

A. Decreased sweating

B. Joint and muscular aches

C. Decreased sexual appetite

D. Decreased hair growth

E. Asymptomatic

A

A. Decreased sweating

277
Q

A patient has a noon testosterone level below the normal range. What will you do?

A. Treat with testosterone gel

B. Repeat the test at 0900h and check for symptoms

C. Repeat the test at noon to keep things equal

D. Refer to endocrinology

E. Ignore it

A

B. Repeat the test at 0900h and check for symptoms

278
Q

The first line treatment for a patient with a symptomatic prolactinoma is usually:

A. Radiotherapy

B. Transphenoidal surgery

C. Dopamine agonists

D. Transfrontal surgery

E. Somatostatin analogues

A

C. Dopamine agonists

279
Q

Typical visual field defect of a patient with a large pituitary mass is:

A. Unilateral quadrantanopia

B. Bitemporal hemianopia

C. Complete unilateral visual field loss

D. Complete bilateral visual field loss

E. None of the above

A

B. Bitemporal hemianopia

280
Q

Satiety is:

A. The physiological feeling of no hunger

B. Inhibited by activation of POMC neurons

C. The physiological feeling of hunger

D. Induced by ghrelin release

E. Enhanced by Agoutirelated peptide

A

A. The physiological feeling of no hunger

281
Q

The centres of appetite regulation in the brain are mainly found in the:

A. Pituitary

B. Cerebellum

C. Hypothalamus

D. Basal ganglia

E. Brain cortex

A

C. Hypothalamus

282
Q

A 48-year-old man has a 4-month history of increasing fatigue and anorexia. He has lost 5.5 kg and noticed increased skin pigmentation. He has been otherwise healthy. His mother has Hashimoto’s thyroiditis and one of his sisters has type 1 diabetes. His blood pressure is 110/85 mmHg (supine) and 92/60 mmHg (sitting). His face shows signs of wasting and his skin has diffuse hyperpigmentation, which is more pronounced in the oral mucosa, palmar creases, and knuckles.

What condition does this man likely have?

A) Conn’s syndrome

B) Type 1 diabetes

C) Addison’s disease

A

C) Addison’s disease

283
Q

A 12-year-old girl is brought to the emergency department by her parents due to 12 hours of rapidly worsening nausea, vomiting, abdominal pain, and lethargy. Over the last week she has felt excessively thirsty and has been urinating a lot. Physical examination reveals a lean, dehydrated girl with deep rapid respirations, tachycardia, and no response to verbal commands.

What is the most likely condition she is suffering from?

A) Hyperosmolar-hyperglycaemic state

B) Diabetic Ketoacidosis

C) Adrenal crisis

D) Anaphylactic shock

A

B) Diabetic ketoacidosis

284
Q

A 34-year-old woman presents with complaints of weight gain and irregular menses for the last several years. She has gained 20 kg over the past 3 years and feels that most of the weight gain is in her abdomen and face. She notes bruising without significant trauma, difficulty rising from a chair, and proximal muscle wasting. She was diagnosed with type 2 diabetes and hypertension 1 year ago.

What is the most likely condition she is suffering from?

A) Addison’s disease

B) Cushing syndrome

C) Pheochromocytoma

D) Polycystic Ovary Syndrome

A

B) Cushing’s syndrome

285
Q

What is the action of metformin?

A

Metformin decreases gluconeogenesis and increases peripheral utilisation of glucose; since it acts only in the presence of endogenous insulin it is effective only if there are some residual functioning pancreatic islet cells

286
Q

What are the side effects, indications, contra-indications and interactions of metformin?

A
  • Side effects: abdominal pain, decreased appetite, diarrhoea, GI disorder, nausea, altered taste, vomiting
  • Indications: T2DM, PCOS
  • Contra-indications: acute metabolic acidosis
  • Interactions: dolutegravir, gliclazide
287
Q
  1. What will the % of the HbA1c be over in a patient with diabetes?(1)
  2. How would you carry out an oral glucose tolerance test?(2 - method of the test + timings)
  3. What are the rules for driving when you are an insulin dependant diabetic? (2)
  4. Give 3 long term complications of diabetes (1)
  5. Sally is a 15 year old diabetic who suffers from a long standing eating disorder. She comes to A+E reporting abdominal pain and vomiting. Her mother states that she appears to be drowsier than usual and confused. She is breathing rapidly on examination and her cap refill time is 4. How would you treat her? (2mrks)
  6. What ion level in her bloods would you want to watch out for closely during this treatment? (1)
  7. A lady who is previously known to suffer from graves presents with palpitations, tremor, confusion, vomiting, abdo pain and extreme anxiety. Her temperature is high and HR is 150 bpm. What condition would you suspect? (1)
  8. Give an eye sign that is seen in graves disease. (1)
  9. How would you test a patient with suspected Addison’s disease? (1)
  10. Give 2 causes of raised calcium? (2)
A
  1. Over 6.5% (1mrk)
  2. Starve for 8hrs before the test. Measure fasting blood glucose then give 100gs of sweet liquid. Take blood test after 1-2 hrs of this. An abnormal result is over 11.1 mmol/L (2mrks- one for glucose challenge, one for timings)
  3. Notify DVLA. Take blood glucose levels within 2 hours before driving and then take again every 2 hours while driving. If glucose level is below 4, you cannot drive. (2 marks for any of above points)
  4. Vascular disease, nephropathy, retinopathy, maculopathy, peripheral neuropathy, ulcers, autonomic neuropathy, erectile dysfunction, charcot foot. (1mark)
  5. Firstly fluids, 0.9% sodium chloride for 1hr. Start to introduce insulin 0.05-0.1 U (aim to reduce glucose by 2mmol/hr) hourly neuro obs, repeat bloods every 2 hrs. (2 marks, one for fluids, one for insulin)
  6. Potassium levels may fall as consequence of insulin treatment. This can cause life threatening arrythmias . watch out for ECG changes! A low level is under 3.5. (1 mark)
  7. Thyrotoxic crisis/thyroid storm. (1 mark)
  8. Exopthalmus, opthalmoplegia. (1 mark)
  9. A synacthen test / Short ACTH test. This tests the cortisol level after stimulation with adrenocorticotropic hormone or a corticotropic agent such as tetracosactide. If there is response (cortisol over 550 after test) addisons can be excluded. (1 mark)
  10. Primary hyperparathyroidism, malignancy, sarcoidosis, TB, thyrotoxicosis, phaeochromocytoma, addisons, drugs.
288
Q
  1. What hormone is secreted in excess in Conn’s syndrome, and where from?
  2. How is this hormone usually suppressed and where from?
  3. Give 4 ECG features of hypokalaemia.
  4. What diagnostic imaging would you do?
  5. Sprinolactone, how does it work?
A
  1. Aldosterone from the adrenal cortex
  2. Renin from juxtaglomerular apparatus of the kidney
  3. Small T waves, prominent U waves, long PR interval, ST depression
  4. Adrenal CT
  5. Aldosterone antagonist, inhibits sodium resorption in collecting duct affecting epithelial sodium channels
289
Q
A

A. Alpha cell

290
Q
A

D. Follicular cells

291
Q
A

D. Renal artery

292
Q
A

C. Insulin release

293
Q
A

D. Splenic artery

294
Q
A

E. Hypocalcaemia

295
Q
A

C. Inhibition of aldosterone

296
Q
A

B. The zona fasciculata mainly secretes glucocorticoids

297
Q
A

B. Secretin

298
Q
A

A. Antidiuretic hormone

299
Q
A

B. Dopamine agonist

300
Q
A

B. Colloid

301
Q
A

B. Recurrent laryngeal nerve

302
Q
A

B. Hypothyroidism

303
Q
A

B. Weight gain

304
Q
A

B. 51 year old male with lethargy, polyuria and polydipsia

305
Q
A

B. Increase insulin sensitivity

306
Q
A

C. Cortisol

307
Q
A

D. Menorrhagia

308
Q

Match the drug to the drug class:

A. Metformin

A. Gliclazide

A. Dapagliflozin

A. Pioglitazone

A. Sitagliptin

  1. Sulphonylurea
  2. Biguanide
  3. DPP4 inhibitor
  4. Thiazolidinediones
  5. SGLUT2 inhibitor
A
  • Metformin = biguanide
  • Gliclazide = sulphonylurea
  • Dapagliflozin = SGLUT2 inhibitor
  • Pioglitazone = thiazolidinediones
  • Sitagliptin = DPP4 inhibitor
309
Q

Which of these is the priority in the treatment of a DKA?

A. Potassium monitoring

B. Insulin administration

C. Ketone monitoring

D. Fluid resuscitation

E. Glucose monitoring

A

D) Fluid resuscitation

310
Q

A 41-year-old lady has recently been started on carbimazole for Grave’s disease. She attends her GP as she believes she is having side effects from the medication.

Which of these would not be a potential side effect of taking carbimazole?

a) Palpitations
b) Constipation
c) Hair loss
d) Fatigue

A

A) Palpitations

311
Q
A

B

312
Q

Increase instead of deficit

A

D

313
Q
A

A

314
Q
A

C

315
Q
A

B

316
Q
A

A

317
Q
A

C. Median nerve due to carpal tunnel syndrome from acromegaly

318
Q
A

C. Anti TPO is Hashimoto’s

319
Q
A

D

320
Q
A

B

321
Q
A

C

322
Q
A

A

323
Q

a. What is the difference in symptoms between the two? List 5 for Hyper and 5 for hypothyroidism.
b. How does first line management differ in Hyperthyroidism + Hypothyroidism?
c. What is the most common cause of hypothyroidism in the developing world?

A
  1. Hypothyroidism: weight gain, lethargy, cold intolerance, dry (anhydrosis), cold, yellowish skin, constipation

Hyperthyroidism: weight loss, restlessness, heat intolerance, palpitations, anxiety

  1. Hyperthyroidism - 1st line: propanolol + carbimazole + iodine

Hypothyroidism - 1st line: levothyroxine

  1. Developing world -> Iodine deficiency

Developed world -> Hashimoto’s Thyroiditis

324
Q

a. What glucose levels are seen in a non diabetic, pre-diabetic and diabetic?
b. Describe the management plan in a patient with newly diagnosed diabetes mellitus type 2 + what would be the follow up management if symptoms progress?
c. What are some complications of DM?

A

a. HbA1c: normal = <42mmol/l, pre-diabetes = 42-47mmol/l, diabetes = 48 mmol/l
b. If 58 mmol/L / 7.5% or higher then step up the treatment
a. Lifestyle modifications - Diet, Exercise, Weight loss
b. Monotherapy - Metformin
c. Dual therapy - if HbA1c rises to 58mmol/mol (7.5%)
d. Triple therapy - if HbA1c rises to 58mmol/mol (7.5%)
i. Metformin
ii. DPP4 inhibitor
iii. SU, Pioglitazone
iv. SGLT-2 inhibitor
v. Thiazolidinedione
vi. Insulin based therapy ONLY WHEN MEDS FAIL
e. Insulin or Glucagon-like peptide (GLP) analogues
i. GLP analogues - incretin mimetics. Incretins - gut peptides that work by increasing insulin release

c.

a. Acute - DKA, HHS, hypoglycaemia
b. Chronic
i. Microvascular - retinopathy, nephropathy, erectile dysfunction, neuropathy (10-20 years after diagnosis in young patients)
ii. Macrovascular - atherosclerosis, ACS, stable angina, PVD, stroke
iii. Diabetic foot and ulcers

325
Q

a. What is the difference between Cushing’s disease and Cushing’s syndrome?
b. Which investigation can be used to differentiate between the two conditions?
c. How does a patient with Cushing’s syndrome present (5 marks)?

A

a. Cushing’s syndrome refers to the state of elevated cortisol levels. Cushing’s disease is specifically caused by an ACTH secreting pituitary tumour (pituitary adenoma)
b. Dexamethasone suppression test:

Overnight

  • Cushing’s syndrome (including disease) is confirmed when there is no suppression

48 hour

  • Cushing’s syndrome (not including disease) = no suppression
    c. Central obesity, moon face, purple abdominal striae, buffalo hump, acne
326
Q

You are an F1 on the endocrine ward and your consultant shows you lots of different ranges of TSH and T3/T4 levels and asks you to interpret the results.

Which conditions would most likely cause the following TSH and T3/T4 results?

A. TSH: Low T4: High

B. TSH: High T4: Normal

C. TSH: High T4: Low

D. TSH: Low T4: Low

A

A.TSH: Low T4: High = hyperthyroidism, thyrotoxicosis, Grave’s

B. TSH: High T4: Normal = subclinical hypothyroidism or poor compliance with thyroxine

C. TSH: High T4: Low = primary hypothyroidism, Hashimoto’s

D. TSH: Low T4: Low = secondary hypothyroidism

327
Q

A patient comes into the Hospital with suspected DKA.

a) What are the first line treatments you would offer?
b) What ECG changes are seen in a patient with hyperkalemia (list 4)?
c) What arrhythmia is a consequence of untreated hyperkalaemia?

A

a) IV Fluids (0.9% Sodium Chloride) and IV insulin +/- Potassium
b) Absent p waves, prolonged PR, tall ‘tented’ T waves, wide QRS
c) Ventricular tachycardia. Occurring due to cell membranes becoming partially depolarised resulting in a lower threshold potential -> ventricles contract quicker

328
Q

Mark has come into the clinic for his regular checkups. He has a 7 year history of chronic hypertension and stage 3 CKD with an eGFR of 44. He has been diagnosed with hyperparathyroidism. A blood test was taken of Mark checking his PTH, Calcium and Phosphate.

What will his findings be? (moderate)

A. PTH: low; Calcium: low; Phosphate: low

B. PTH: high; Calcium: high; Phosphate: high

C. PTH: high; Calcium: low; Phosphate: high

D. PTH: high; Calcium: high; Phosphate: low

E. PTH: low; Calcium: low; Phosphate: high

A

C. PTH: high; Calcium: low; Phosphate: high

329
Q

John comes into the clinic complaining of low mood and energy. He believes that because of his mood, he has been having really bad constipation and abdominal pain that is both on the front and the back side. He says he also has pain when he pees so doesn’t feel like excreting at all which has been making his mood worse. What is the most probable cause of this illness?

A. Hyponatremia

B. Hyperkalemia

C. Carcinoid tumor

D. Hypothyroidism

E. Hyperparathyroidism

A

E. Hyperparathyroidism

330
Q

Patient with stage 3 CKD has forgotten to come in for her dialysis appointments for 2 weeks now. What is the most urgent complication of this that needs to be dealt with?

A. Hypocalcemia

B. Hypertension due to fluid retention

C. Hyperkalemia

D. High Urea retention

E. Hypernatremia

What is the appropriate treatment?

A

C. Hyperkalaemia

Appropriate treatment: insulin with dextrose

331
Q

John is a 43 y.o man who has had increased frequency urination the last few months. He explains he gets up about 4 times at night to pee. He has also explains that he has had some sudden weight loss even though he has not been dieting much. He is really confused and has come to clinic to get it checked. (moderate)

A. What signs of diabetes does this patient show?

B. How do you diagnose a patient with diabetes?

C. What test is done to monitor progression of diabetes?

D. What is the first line management that should be given to John?

E. What is the most dangerous side effect of sulfonylurea?

F. What are two common complications of diabetes?

G. Patient has suddenly gone into ketoacidosis. What is the first step in treating them?

A
332
Q

Patient is given a high dose of insulin as the he is going into diabetic ketoacidosis. An hour after the insulin, he feels fatigued and his muscles have started cramping up whenever he tries to walk. He starts feeling irregular palpitations and so an ECG is done. What is most likely to be seen on the ECG? (easy)

A. Delta waves

B. U waves

C. Shortened PR interval

D. Delta waves

E. Tall tented T waves

A

B. U waves

333
Q

Julia is a 47 y.o lady who has noticed that over the past year she has been having diarrhoea. It is not related to the food that she eats and there is no blood or mucus in her stools. She has went to her GP but no other diagnosis could be made. On further questioning, she reports getting facial flushing quite often but it is usually precipitated by stress, she also gets palpitations that is intermittent.

O/E: Hepatomegaly

Based on the most likely diagnosis, what would be the next best investigation?(++)

A. Urinary 5-hydroxyindoleacetic acid

B. Liver function test

C. Liver biopsy

D. Stool antigen test

E. Serum Chromagranin A/B

A

A. Urinary 5-hydroxyindoleacetic acid

334
Q

Aldridge is a 41 y.o gentleman who presents to the GP with tiredness. He has also been gaining weight recently. Yesterday, while he was reversing his car into a parking lot, he had accidentally crashed his side mirror and he explained that his vision seems to be off lately.

He has a past medical history of Type l Diabetes for which he is on Insulin.

Based on the most likely diagnosis, what would be your 1st line investigation?(+)

A. IGF-1

B. T3, T4 and TSH levels

C. OGTT

D. ACTH

E. Dexamethasone suppression test

A

A. IGF-1

335
Q

Tom presents to the GP with anxiety in the last month. He reports symptoms of tremors and palpitations and he has lost 3 kilos of weight in a month.

An ECG was taken and showed absent P-waves and an irregularly irregular rhythm.

Based on the most likely diagnosis, what is the best investigation? (++)

A. Plasma free metanephrines

B. Echocardiography

C. Thyroid function test

D. Aldosterone-renin ratio

E. Plasma glucose levels

A

C. Thyroid function test

336
Q

Brian comes to the GP with 2 day history of pain in the neck, which radiates to the jaw. He has noticed himself to have palpitations and is sweating more easily lately. He denies weight loss or night sweats. He had recently recovered from a viral infection.

TFTs results return normal. Blood results show raised ESR.

His obs are Temp: 38, RR: 15, PR: 83, BP: 110/85 mmHg, O2: 98%.

What is the most likely diagnosis? (++)

A. Grave’s disease

B. De Quervain’s thyroiditis

C. Drug-induced hyperthyroidism

D. Thyroid carcinoma

E. Hashimoto’s thyroiditis

A

B. De Quervain’s thyroiditis

337
Q

Mrs Lee is a 41 y.o woman with complaints of weight gain and low mood for the last 2 months. She has gained 5kg even though her diet has largely remained the same as before. On examination, you notice that she has difficulty standing from a chair and lifting her hands up, she also has bruising across her lower shins and forearms.

Most common cause for this disease? (1)

Name other causes for this disease? (3)

Name 4 complications of the disease you suspect? (2)

A
338
Q
A

A. Addison’s disease. Autoimmune destruction of the adrenal glands

B. Female sex, autoimmune disease, TB

C. ACTH stimulation test, 9am serum cortisol

D. Hyponatraemia, hyperkalaemia (due to fall in aldosterone)

E. Hydrocortisone, fludrocortisone

339
Q
A

D. Somatotrophs - growth hormone is secreted by somatotrophs in the anterior pituitary

B. Diabetes mellitus 2 - GH mobilises glucose from fat storage thus increase BG -> increased insulin resistance

340
Q
A

C. IV hydrocortisone - 1st line for Addisonian crisis, saline to correct hypertension and dehydration. Once stabilised, normal regime can be resumed

341
Q
A

D. Sertraline - SSRI (SIADH)

342
Q

Also, what is the diagnostic test and what do you expect to see in this case?

A

D. Neurogenic DI - due to lack of ADH production in posterior pituitary. Causes are: tumours, infections (encephalitis), trauma, neurosurgery

Diagnostic test: water deprivation test: after 12 hours, desmopressin is given2mg IM. Neurogenic DI – excessive urination stops, nephrogenic DI – excessive dilute urine continues

Phase 2a (13 decks)

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