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2a Medicine > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is gigantism?

A

Excess growth hormone during teenage years, before the epiphysis of the long bone have fused.

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2
Q

What are physical signs of acromegaly?

A

Thickened lips, squared off jaw, prognathism (protrusion of lower jaw) due to excess bony growth, increase in supra orbital ridges, large hands.

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3
Q

What causes acromegaly.

A

Excess growth hormone.

Pituitary tumour secrete excess growth hormone (usually macro adenomas so bigger than 1cm).

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4
Q

What does growth hormone cause?

A

The release of IGF-1 (insulin-like growth factor 1). The main site of production is the liver so growth hormone binds to cell surface receptors on the liver.

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5
Q

What are the effects of IGF-1?

A
  • Excess growth in hands (often described as changing ring size)
  • Sweating of hands
  • Increase in shoe size (increase in soft tissue in feet)
  • Gigantism
  • Increased size of almost all organs e.g. macroglossia (enlarged tongue), increased oropharynx (sleep apnea), cardiomegaly and cardiomyopathy (increases in blood pressure)
  • Insulin resistance as it offsets the action of insulin so diabetes or glucose intolerance (completely reversed by surgery).
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6
Q

What is the mean age at diagnosis of acromegaly?

A

44 years old. The mean duration of symptoms prior to diagnosis is 8 years.

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7
Q

What are acromegaly co-morbidities?

A

Cerebrovascular events and headache (IGF-1 changes the way nerves sense pain so prone to headaches).
Arthritis: swelling of synovium and increased fluid in the joint spaces so pain and arthritis.
Insulin-resistant diabetes.
Sleep apnea.
Hypertension and heart disease.

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8
Q

How do you measure growth hormone and IGF-1 hormone levels?

A

IGF-1 is a single one off blood test whereas growth hormone requires multiple and is harder to measure.

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9
Q

In what way is growth hormone secreted?

A

In a pulsatile way. So it has low levels and then spikes in between.
Hormone levels therefore need to be taken throughout the day to determine acromegaly.

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10
Q

What are the growth hormone levels of somebody with acromegaly like?

A

Growth hormone levels are up and down but they never return to baseline.

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11
Q

What is the test for acromegaly?

A

75mg oral glucose tolerance test.
In a normal patient, glucose suppresses growth hormone fairly quickly. In patients with acromegaly, there is a paradoxal increase or the growth hormone is not suppressed.

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12
Q

What is the criteria for the diagnosis of acromegaly?

A

Acromegaly excluded if:
• Random growth hormone level < 0.4 ng/ml and normal IGF-1/.

If either are abnormal proceed to:
• 75 gm Glucose tolerance test (GTT).

Acromegaly excluded if:
• IGF-1 normal and
• GTT nadir GH <1 ng/ml (now more like <0.2ng/ml).

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13
Q

What is the treatment for acromegaly?

A
  • Pituitary surgery (most likely to cure)
  • Medical therapy
  • Radiotherapy (takes many years for response, can cause hypopituitarism).
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14
Q

What is the medical therapy in acromegaly?

A
  • Dopamine agonists e.g. cabergoline (binds to the D2 receptors on the growth hormone secreting cells in the pituitary to switch off the secretion of growth hormone)
  • Somatostatin analogues (bind to somatostatin type 2 receptors in the pituitary cells to switch off the production of the growth hormone) e.g. ocreotide/lanreotide
  • Growth hormone receptor antagonist (growth hormone binds to its receptor at site 1 but there is a mutation at site 2 which blocks the dimerisation of the receptor, also blocks the production of IGF-1). e.g. pegvisomant.
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15
Q

How is IGF-1 produced?

A

Hypothalamus -> Growth hormone releasing factor-> anterior pituitary -> GH -> liver -> Insulin-like GF-1 -> protein synthesis and cell division.

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16
Q

What inhibits growth factor?

A

Somatostatin and high glucose.

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17
Q

What increases growth hormone secretion?

A

Ghrelin, which is synthesised in the stomach.

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18
Q

Is measuring serum IGF-1 levels for acromegaly useful?

A

It is a genetically modified growth hormone so levels would still be high.

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19
Q

What is the first line treatment in acromegaly?

A

Transsphenoidal surgical resection to remove the adenoma and correct compression of surrounding structures e.g. optic chiasm. Complications include: hypopituitary, infection, diabetes insipidus.

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20
Q

Who is prolactinoma more common in?

A

Much more common in women than men (due to presence of oestrogen).

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21
Q

What causes prolactinoma?

A

Lactotroph cell tumour (adenoma) of the pituitary most commonly.
Also hyperthyroidism as TSH stimulates prolactin.
Oestrogen containing drugs.

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22
Q

What controls prolactin secretion?

A

It is under tonic inhibition by dopamine.

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23
Q

What type of feedback loop is prolactin involved in?

A

Positive feedback loops to switch on the production of milk it the breast when there is stimulation.

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24
Q

What happens when there is interruption in the prolactin pathway?

A

Interruption can be an interruption in the pituitary stalk which disrupts the flow of dopamine (non-functioning tumour) or a tumour which is secreting prolactin (functioning tumour).

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25
Q

What are the clinical features of prolactinoma?

A

Local effect of tumour (macroadenoma):
• Headache
• Visual field defect (bitemporal hemianopia)
• CSF leak (rare).

Effect of prolactin:
•	Menstrual irregularity/amenorrhoea (due to interference with release of gonadotrophins)
•	Hypogonadism in men
•	Infertility
•	Galactorrhoea
•	Low libido 
•	Low testosterone in men.
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26
Q

What is the management for prolactinoma?

A

Dopamine agonists e.g. cabergoline, bromocriptine, quinagolide.

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27
Q

What are the consequences of prolactinoma?

A

Infertility, hypogonadism and galactorrhea.

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28
Q

Why does prolactinoma cause infertility?

A

Prolactin inhibits GnRH.

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29
Q

What is the function of PTH?

A

In the kidney:
Increases vitamin D activation, decreases phosphate reabsorption and increases calcium reabsorption.
In bone: increased bone remodelling so more bone resorption than bone formation. Osteoclast function is driven.
In the gut: increased calcium reabsorption due to increased activated vitamin D.

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30
Q

When is PTH secreted?

A

Decreased serum calcium levels.

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31
Q

What type of feedback is calcium homeostasis?

A

Negative.

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32
Q

What is a normal level of serum calcium?

A

1.1mmol/l.

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33
Q

Why are calcium levels important?

A

In the heart, serum calcium affects conductivity. Affects ST duration, distance from depolarisation to repolarisation.
Can cause dysrhythmias which can be fatal.

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34
Q

What do you look for in hypocalcaemia?

A

Check for low serum albumin because calcium travels bound to albumin and may cause calcium to look low when it is not. So there could be a low total serum calcium but ionised calcium is not low.

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35
Q

How do you calculate corrected calcium?

A

Corrected calcium = total serum calcium + 0.02*(40- serum albumin).

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36
Q

What are the symptoms of hypocalcaemia?

A

· Parasthesia (pins and needles)
· Muscle spasm in hands and feet and larynx
· Premature labour
· Seizures
· Basal ganglia calcification (chronic)
· Cataracts (if left untreated for a long time)
· ECG abnormalities (long QT interval).

Chvostek’s Sign: tap over the facial nerve and look for spasm of facial muscles.

Trousseau’s Sign: inflate the blood pressure cuff to 20mm Hg above systolic for 5 minutes and hand reflex.

Remember SPASMODIC:
S pasms (carpopedal spasms = trousseau’s sign)
P erioral paraesthesia (around mouth)
A nxious, irritable, irrational
S eizures
M uscle tone weakness
O rientation impaired and confusion
D ermatitis
I mpetigo herpetiformis: psoriatic pustules
Chvostek’s sign, cataracts, cardiomyopathy.

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37
Q

Which cells secrete PTH?

A

Chief cells.

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38
Q

What causes hypocalcaemia?

A

Vitamin D deficiency which leads to osteomalacia (presents with low phosphate).
Secondary hypoparathyroidism due to post parathyroidectomy (presets with high phosphate).
Osteomalacia (presents with low phosphate) and so calcium can’t be absorbed from bone.
CKD (presents with high phosphate) causes poor uptake of calcium in the kidneys.
Psuedohypoparathyroidism, resistant to PTH.
Drugs: calcitonin decreases Ca2+ and phosphate. Bisphosphonates reduce osteoclast activity resulting in reduced calcium.

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39
Q

What ECG change is shown in hypocalcaemia?

A

Long QT interval.

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40
Q

What is the management for hypocalcaemia?

A

Mild: Adcal supplement (calcium carbonate) or cholecalciferol.
Severe: calcium gluconate.

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41
Q

What is haemochormatosis?

A

Excess iron.

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42
Q

What is Wilson’s disease?

A

Excess copper.

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43
Q

What causes hypoparathyroidism?

A

• Autoimmune destruction of parathyroid glands: Di-George syndrome
• Vitamin D deficiency: results in less Ca2+. Can cause mild and occasionally severe hypocalcaemia and osteomalacia
• Congenital
• Parathyroidectomy (secondary)
• Magnesium deficiency.
Alson infiltration by haemochromatosis and Wilson’s disease.

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44
Q

What are the symptoms of hypoparathyroidism?

A

Symptoms of hypocalcaemia.
Remember SPASMODIC:
S pasms (carpopedal spasms = trousseau’s sign)
P erioral paraesthesia (around mouth)
A nxious, irritable, irrational
S eizures
M uscle tone weakness
O rientation impaired and confusion
D ermatitis
I mpetigo herpetiformis: psoriatic pustules
Chvostek’s sign, cataracts, cardiomyopathy..

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45
Q

What is the management for hypoparathyroidism?

A
  • Calcium supplement
  • Calcitriol (active vitamin D)
  • Synthetic PTH.
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46
Q

What is pseudohypoparathyroidism?

A

Resistance to PTH hormone due to mutation with Galpha subunit on parathyroid.
So PTH is still working but it has no effect when it gets to bones etc.

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47
Q

What are the signs of pseudohypoparathyroidism?

A

Associated with short stature, short metacarpals (especially 4th and 5th), obesity, subcutaneous calcification and sometimes intellectual impairment.

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48
Q

What would the bloods show in pseudohypoparathyroidism?

A

Low calcium and high PTH.

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49
Q

Is hypercalcaemia or hypocalcaemia more common?

A

Hypercalcaemia.

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50
Q

What might falsely suggest hypercalaemia?

A

May be a false result if tourniquet was on for too long or sample was old and had haemolysed.

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51
Q

What are the symptoms of hypercalcaemia?

A

Painful bones: typically osteitis fibrosa cystica.
Renal stones: calcium deposition in renal tubules causes polyuria and nocturia. Can lead to kidney stones and kidney failure.
Psychiatric moans: lethargy, fatigue, memory loss, psychosis and depression.
Abdominal groans: Gi upset.

Also: 
•	Nausea
•	Vomiting
•	Constipation
•	Indigestion
•	Cardiac arrest.
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52
Q

What is the ECG change in hypercalcaemia?

A

Short QT which can lead to dysrhythmias.

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53
Q

What can hypercalcaemia cause when chronic?

A

Renal stones.

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54
Q

What causes hypercalcaemia?

A

Excessive PTH secretion usually caused by single parathyroid adenoma. Bone metastases so cancer cells damaging bone and releasing calcium.
Cancers (most commonly lung and kidney) cause secretion of parathyroid related peptide (PTHrP) which acts like PTH in receptors, raising serum cancer.
Primary hyperparathyroidism.
Physiological compensatory hypertrophy of all the glands in response to hypocalcaemia e.g. in CKD, Crohn’s or vitamin D deficiency.
Development of apparently autonomous parathyroid hyperplasia after long-standing secondary hyperparathyroidism (most commonly in renal disease). Plasma calcium and PTH are both raised. Treated by parathyroidectomy.
Thiazide diuretics cause calcium retention in the kidney.
Immobilisation as increased bone turnover.
Adrenal insufficiency.

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55
Q

What accounts for 90% of causes of hypercalcaemia?

A

Malignancy and primary hyperparathyroidism.

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56
Q

How do you tell the difference between hypercalcaemia of malignancy or or hypercalcaemia due to primary hyperparathyroidism?

A

Look at PTH.

PTH is low in malignancy.

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57
Q

What is the acronym to remember causes of hypercalcaemia?

A 
Chimpanzees:
C alcium supplementation
H yperparathyroidism
I atrogenic drugs e.g. thiazides
M ilk alkali syndrome
P aget’s disease of bone
A cromegaly and Addison’s
Z olinger-Ellison Syndrome, MEN type 1
E xcess vitamin D
E xcess vitamin A
S arcoidosis.
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58
Q

What is the management for hypercalcaemia?

A
  • Lowering calcium levels and treatment of underlying cause. In primary hyperparathyroidism this is surgical removal of symptomatic parathyroid adenoma
  • IV saline: helps to dilute levels of calcium in blood
  • Bisphosphonates: encourage osteoclasts to undergo apoptosis so there is less bone breakdown.
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59
Q

What are the symptoms of hyperparathyroidism?

A

Same as hypercalcaemia:
Bones: osteitis fibrosa cystica (big loosened areas in bone which are clumps of osteoclasts because there is too much), osteoporosis.
Kidney stones because of increased renal filtration of calcium.
Psychic organs: confusion.
Abdominal moans: constipation and acute pancreatitis.

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60
Q

What is the main cause of hyperparathyroidism?

A

80% of primary hyperparathyroidism is due to a single benign adenoma (on one of the four glands which has become overgrown and secretes too much PTH and this gland can be removed).
15-20% due to four gland hyperplasia (may be part of multiple endocrinal neoplasia syndrome (MEN) I or II).
<0.5% due to malignant (if calcium and PTH levels are extremely high).

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61
Q

What is the consequence of vitamin D deficiency?

A

Impairs gut absorption of calcium which causes hypocalcaemia so PTH rises.

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62
Q

Why does phosphate increase with PTH resistance?

A

Calcium not reabsorbed and phosphate not pushed out.

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63
Q

When is the action of PTH appropriate?

A

Vitamin D deficiency (secondary hyperparathyroidism), psuedohypoparathyroidism and hyperglycaemia of malignancy.

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64
Q

When is the action of PTH inapparopriate?

A

Hypoparathyroidism and primary hyperparathyroidism.

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65
Q

What would the bloods show in Vitamin D deficiency?

A

High PTH, low calcium and low potassium.

Calcium and potassium are both low because Vitamin D is needed to absorb both phosphate and calcium from the gut.

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66
Q

What would the bloods show in hypoparathyroidism?

A

Decreased PTH and calcium. Increased phosphate.

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67
Q

What would the bloods show in psuedohypoparathyroidism?

A

High PTH, low calcium and high phosphate.

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68
Q

What would the bloods show in hypercalcaemia of malignancy?

A

High PTH and calcium. Phosphate levels difficult to predict due to varying causes (if caused by PTHrP, phosphate will be low but if caused by lots of bone resorption by malignancy, there is phosphate release from bone which increases it).

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69
Q

What would bloods show in primary hyperparathyroidism?

A

High PTH and calcium. Low phosphate.

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70
Q

What is under the control of the pituitary gland?

A

Thyroid, adrenal cortex, testis, ovary.

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71
Q

Where does the pituitary gland lie?

A

In the sella turcica.

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72
Q

How much does the pituitary gland weight?

A

Around 0.5g.

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73
Q

When is ACTH secreted from the pituitary gland?

A

During stress.

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74
Q

Where is vasopressin produced?

A

Hyopthalamus.

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75
Q

Where is vasopressin secreted from?

A

Posterior pituitary.

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76
Q

Which hormones have a circadian rhythm?

A

Cortisol, testosterone, DHEA, 17-OH progesterone.

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77
Q

What is diabetic ketoacidosis?

A

A state of uncontrolled catabolism associated with insulin deficiency.

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78
Q

What are the 3 things that categorise diabetic ketoacidosis?

A
  • Hyperglycaemia
  • Raised plasma ketones
  • Metabolic acidosis.
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79
Q

What is the pathophysiology of diabetic ketoacidosis?

A

In the absence if insulin, there is an unrestrained increase in hepatic gluconeogenesis. High circulating glucose levels result in an osmotic diuresis by the kidneys and consequent dehydration. Peripheral lipolysis leads to an increase in circulating free fatty acids which are converted to acidic ketones in the liver. This causes metabolic acidosis (ketones increases acidicity of blood). The entire process is accelerated by “stress hormones” (catecholamines, glucagon and cortisol) which are secreted in response to dehydration and intercurrent illness.

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80
Q

What are the symptoms of diabetic ketoacidosis?

A
  • Dehydration: result of water and electrolyte loss from kidney, exacerbated by vomiting. Reduced tissue turgor so time for skin to snap back in place is longer
  • Vomiting and abdominal pain: caused by electrolyte disturbances
  • Sunken eyes and dry tongue
  • Low BP
  • Kussmaul’s respiration: deep and rapid breathing, sign of respiratory compensation for metabolic acidosis
  • Fruity breath: smells of ketones (acetone)
  • Low body temperature.
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81
Q

What blood glucose is hyperglycaemia?

A

> 11mmol/L.

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82
Q

What are the investigations for diabetic ketoacidosis?

A
  • Blood tests for hyperglycaemia (blood glucose >11mmol/L)
  • Ketonaemia: blood ketones. Best measured using a finger-prick sample and near-patient meter which measures B-hydroxybutyrate (major ketone in DKA)
  • Acidaemia: blood pH <7.3 and/or bicarbonate <15mmol/L
  • Urine dipstick: heavy glycosuria and ketonuria
  • Serum U+E: urea and creatinine often raised as a result of dehydration. Total body potassium is low as a result of osmotic diuresis but serum potassium concentration is raised because of absence of insulin allowing K+ shift out of cells.
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83
Q

What is the management for diabetic ketoacidosis?

A
  • Fluid replacement 0.9% saline: 1L in 30mins then 1L in 1hour then 1L in 2hours then 1L in 4 hours then 1L in 6 hours
  • IV insulin: typical starting dose is 6units/hour
  • Electrolytes (K+).
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84
Q

What is hyperglycaemia hyperosmolar state characterised by?

A

Marked hyperglycaemia, hyperosmolality and mild/no ketosis.

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85
Q

What is the common cause of hyperglycaemia hyperosmolar state?

A

Infection, particularly pneumonia.

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86
Q

What are the symptoms of hyperglycaemia hyperosmolar state?

A
  • Dehydration: result of osmotic diuresis
  • Decreased levels of consciousness: result of elevated plasma osmolality
  • Polyuria.
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87
Q

What is the management for hyperglycaemia hyperosmolar state?

A

Same as DKA.

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88
Q

What is thyrotoxicosis?

A

Hyperthyroidism.

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89
Q

Who is hyperthyroidism more common in?

A

Women.

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90
Q

What is the main cause of hyperthyroidism?

A

Graves disease.

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91
Q

What is Graves disease?

A

Autoimmune induced excess production of thyroid hormone due to pathological stimulation of TSH receptor.
Associated with other autoimmune conditions e.g. T1DM.

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92
Q

What are risk factors for hyperthyroidism?

A
  • Female
  • Family history/genetic association with HLA-B8, DR3 and Dr4
  • Stress
  • Smoking
  • Amiodarone.
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93
Q

What antibodies are involved in Graves disease?

A

Serum IgG antibodies called TSH receptor stimulating antibodies.

94
Q

What is the pathophysiology of Graves disease?

A

Serum IgG antibodies called TSH receptor stimulating antibodies (TRAb) bind to TSH receptors on the thyroid and stimulate T3/4 production. Thyroxine (T4) receptors in the pituitary gland are activated by excess hormone. This results in excess secretion, hyperplasia of the thyroid follicular cells, hyperthyroidism and goitre. Reduced release of TSH in negative feedback loop so very high levels of circulating thyroid hormones with a low TSH.

95
Q

What are the levels of TSH like in hyperthyroidism?

A

Low due to negative feedback.

96
Q

What are the levels of T3 and T4 like in hyperthyroidism?

A

High.

97
Q

What are the symptoms of hyperthyroidism?

A

Graves’ specific:
• Graves ophthalmology: extraocular muscle swelling (protruding eyes), eye discomfort, lacrimation, diplopia
• Pretibial myxoedema: raised purple-red symmetrical skin lesions over anterolateral aspects of the shins
• Thyroid acropachy: clubbing (swelling of fingers and toes)
• Goitre.

Other:
•	Weight loss
•	Irritability
•	Heat intolerance
•	Insomnia
•	Diarrhoea
•	Sweats
•	Palpitations
•	Anxiety
•	Menstrual disturbance (oligomenorrhea and amenorrhoea).
98
Q

What are the TSH levels like in secondary hyperthyroidism?

A

High.

99
Q

What are the T3 and T4 levels like in secondary hyperthyroidism?

A

High.

100
Q

What is the management for hyperthyroidism?

A

• Beta blockers for rapid system control in attacks

  1. Carbimazole or propylthiouracil): anti-thyroid drug.
  2. Radioiodine therapy
  3. Thyroidectomy: removal of the thyroid gland leaving a small remnant in order to maintain thyroid function.
101
Q

What is a major complication of hyperthyroidism?

A

Thyroid crisis (thyroid storm): rare life-threatening condition in which there is a rapid deterioration of thyrotoxicosis with:
• Hyperpyrexia
• Tachycardia
• Extreme restlessness
• Even delirium, coma and death.
Usually precipitated by:
• Infection
• Stress
• Surgery
• Radioactive iodine therapy.
Treatment:
• Large doses of carbimazole or propylthiouracil
• Propranolol
• Potassium iodide (to actually block release of thyroid hormone from gland)
• Hydrocortisone (to inhibit peripheral conversion of T4 to T3.

102
Q

What are the 3 types of hypothyroidism?

A
  1. Primary (from disease of the thyroid gland): aggressive destruction of thyroid cells by various cell and antibody mediated immune processes
  2. Secondary (pituitary/hypothalamic disease): reduced release or production of TSH so reduced T3 and T4 release.
  3. Transient: withdrawal of thyroid suppressive therapy.
103
Q

What is postpartum thyroiditis?

A

Usually transient phenomenon following pregnancy. If conventional antibodies are present, there is a high chance of proceeding to permanent hypothyroidism

104
Q

What are the causes of hypothyroidism?

A 
Autoimmune.
Iodine deficiency.
Drug-induced: carbimazole, lithium, amiodarone, interferon.
Iatrogenic e.g. thyroidectomy.
Congenital.

Secondary:
Hypopituitarism.
Hypothalamic disorders.

105
Q

What are the symptoms of hypothyroidism?

A
  • Hoarse voice
  • Goitre
  • Weight gain
  • Constipation
  • Cold intolerance
  • Menorrhagia (heavy periods)
  • Tiredness
  • Lethargy
  • Poor memory
  • Puffy eyes
  • Arthralgia/myalgia.
106
Q

What are the signs of hypothyroidism?

A 
Think of BRADYCARDIC:
B radycardia
R eflexes relax slowly
A taxia
D ry thin hair/skin
Y awning
C old hands
A scites
R ound puffy face
D efeated demeanour
I mmobile (ileus, temporary arrest of intestinal peristalsis)
C ongestive heart failure.
107
Q

What are the TSH levels like in primary hypothyroidism?

A

High.

108
Q

What are the T4 levels like in primary hypothyroidism?

A

Low free T4.

109
Q

Where is T4 converted to T3?

A

Liver.

110
Q

What are the TSH levels like in secondary hypothyroidism?

A

Inappropriately low.

111
Q

What are the T3/4 levels like in primary hypothyroidism?

A

Low since the issue is pituitary.

112
Q

What is the management for hypothyroidism?

A

Lifelong oral Levothyroxine (T4). Aim is to get TSH >0.5 in primary.

113
Q

What is a major complication of hypothyroidism?

A

Myxoedema coma: 20-50% mortality. Reduced level of consciousness, seizures, hypothermia and hypothyroidism.

114
Q

What is the most common cause of goitre hypothyroidism?

A

Hashimoto’s thyroiditis.

115
Q

What are the triggers for Hashimoto’s thyroiditis?

A
  • Iodine
  • Infection
  • Smoking
  • Stress.
116
Q

What is the pathophysiology of Hashimoto’s thyroiditis?

A

Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes. Antibodies bind and block TSH receptors causing inadequate thyroid hormone production and secretion.

117
Q

What are the symptoms of hypothyroidism?

A
  • Fatigue
  • Cold
  • Intolerance
  • Slowed movement
  • Decreased sweating.
118
Q

What are the signs of Hashimoto’s thyroiditis?

A

TSH levels usually raised and thyroid antibodies.

119
Q

What is the management for Hashimoto’s thyroiditis?

A

Thyroid hormone replacement (Levothyroxine) and restriction of obstructive goitre).

120
Q

What are the types of thyroid cancer?

A

Papillary, follicular, medullary cell, lymphoma and anaplastic.

121
Q

What are the symptoms of thyroid cancer?

A

• Thyroid nodules: increased size, hardness and irregularity
• Dysphagia
• Hoarseness of voice: tumour pressing on recurrent laryngeal nerve.
Papillary, follicular, anaplastic:
• Usually asymptomatic thyroid nodule (usually hard and fixed)
• Possibly enlarged lymph nodes on examination.
Lymphoma:
• Rapidly growing mass in the neck.
Medullary:
• Diarrhoea
• Flushing episodes
• Itching.

122
Q

What are the signs of thyroid cancer?

A
  • Lymph node metastases
  • Lung or bone metastases (rare)
  • Thyroid nodule with history of progressive increase in size
  • Hard and irregular nodule
  • Enlarged lymph nodes.
123
Q

What lymphoma is often associated with Hashimoto’s hypothyroiditis?

A

Non-Hodgkin’s lymphoma.

124
Q

What are the investigations of thyroid cancer?

A
  • Fine needle aspiration cytology biopsy best for distinguishing between benign and malignant thyroid nodules (medullary shows elevated serum calcitonin)
  • Thyroid ultrasound
  • TFTs: hyper/hypothyroidism needs to be treated before surgery.
125
Q

What is the management for thyroid cancer?

A

Follicular and papillary cancers:
• Total thyroidectomy with neck dissection for local nodal spread
• Ablative radioiodine subsequently given: taken up by remaining thyroid tissue or metastatic lesions.
Anaplastic and lymphoma:
• External radiotherapy may produce brief respite
• Otherwise treatment is largely palliative.
Medullary:
• Total thyroidectomy
• Prophylactic central lymph node dissection.

126
Q

What is Cushing’s?

A

Hypercortisolism. Persistently and inappropriately elevated circulating glucocorticoid (cortisol).

127
Q

What axis feedback is there loss of in Cushing’s?

A

Loss of hypothalamic pituitary axis feedback.

128
Q

Is there a loss of circadian rhythm in Cushing’s?

A

Yes.

129
Q

What is the most common cause of hypercortisolism?

A

Oral steroids e.g. glucocorticoid therapy.

130
Q

What are the causes of hypercortisolism?

A

ACTH independent causes:
• Oral steroid use (iatrogenic) is most common
• Adrenal adenomas/carcinomas: tumour of the adrenal gland that releases cortisol.
ACTH dependent causes:
• Cushing’s disease: bilateral adrenal hyperplasia due to ACTH hypersecretion by pituitary adenoma
• Ectopic Cushing’s syndrome: coming from elsewhere. Due to paraneoplastic syndrome e.g. small cell lung cancer producing ACTH.

131
Q

What are the symptoms of Cushing’s?

A 
Remember CUSHING:
C ataracts
U lcers
S triae (purple strokes on skin)
H ypertension and hyperglycaemia due to impaired glucose intolerance
I ncreased risk of infection due to dampening of inflammatory response
N ecrosis
G lucosuria.

Also amenorrhoea.

132
Q

What are the signs of Cushing’s?

A
  • Truncal/central obesity
  • Moon face
  • Buffalo humpy (fatty bump on upper back)
  • Acne
  • Hirsutism: unwanted male pattern hair growth in women
  • Thin skin/bruising
  • Osteoporosis.
133
Q

What is the first line investigation in Cushing’s?

A

First lone if random cortisol is high: overnight dexamethasone suppression test. Dexamethasone usually suppresses cortisol level and failure to suppress over 24-hour period if diagnostic of Cushing’s syndrome. If low dose dexamethasone is given, normal individuals suppress cortisol to <50nmol 2 hours after last dose and this is the most reliable screening tests. If high dose dexamethasone is given, most patients with pituitary-dependant Cushing’s disease suppress plasma cortisol by 48 hours and failure to do so suggests an ectopic source of ACTH or an adrenal tumour.

134
Q

What causes pseudo-Cushing’s?

A

Alcohol excess, resolves after 1-3 weeks of alcohol abstinence.

135
Q

What is the management for Cushing’s?

A

Transsphenoidal removal of pituitary adenoma.

136
Q

What drugs are used for cortisol synthesis inhibition?

A

Metyrapone, ketoconazole.

137
Q

What is Conn’s syndrome?

A

Hyperaldosteronism. A solitary aldosterone producing adrenal adenoma.

138
Q

What are the causes of Conn’s syndrome?

A

2/3 of cases: Conn’s syndrome.

1/3 of cases: bilateral adrenocortical hyperplasia (technically not Conn’s).

139
Q

What is the pathophysiology of hyperaldosteronism?

A

Excess production of aldosterone, independent of RAAS causes:
• Exchange of sodium and potassium in the distal renal tubule so increases K+ loss and Na+ and water retention which raises BP
• Decreased renin release
• Hypokalaemia.

140
Q

What are the symptoms of hyperaldosteronism?

A 
Usually asymptomatic.
Symptoms of hypokalaemia:
•	Constipation
•	Muscle weakness and cramps
•	Polyuria and polydipsia
•	Paraesthesia.
141
Q

What would the U&Es show in hyperaldosteronism?

A

Decreased renin and increased aldosterone.

142
Q

What does the ECG show for hyperaldosteronism?

A

Remember rhyme U have no Pot (K+) and no T but a long PR and a long QT.

  • Flat T waves
  • ST depression
  • Long QT intervals
  • Long PR intervals
  • Pathological U waves.
143
Q

What investigation confirms the presence of an aldosterone producing adenoma?

A

CT/MRI.

144
Q

What is the management for Conn’s?

A

Laparoscopic adrenalectomy if adenoma.

Oral spironolactone: aldosterone antagonist (K+ sparing diuretic) if hyperplasia.

145
Q

What is Addison’s disease?

A

Primary adrenal insufficiency.
An autoimmune condition in which there is destruction of the adrenal cortex. Results in mineralocorticoid (aldosterone), glucocorticoid (cortisol) and androgen (sex hormones) deficiency.
The opposite of Cushing’s.

146
Q

What is the pathophysiology of Addison’s?

A
  • Destruction of the entire adrenal cortex resulting in reduced glucocorticoid (cortisol), mineralocorticoid (aldosterone) and androgen production
  • All steroids are reduced which differs from hypothalamic-pituitary disease in which mineralocorticoid and androgen secretion remains largely intact due to their relative independence from the pituitary
  • In Addison’s, the reduced cortisol levels lead (through feedback), to increased CRH and ACTH production (ACTH responsible for hyperpigmentation).
147
Q

What does reduced cortisol levels lead to in Addison’s?

A

Increased CRH and ACTH production (ACTH responsible for hyperpigmentation).

148
Q

What is the secondary cause of adrenal insufficiency?

A

Steroids.

149
Q

What is the most common primary cause of adrenal insufficiency in the UK?

A

Addison’s (90%).

150
Q

What is the most common primary cause of adrenal insufficiency worldwide?

A

TB.

151
Q

What are the symptoms of Addison’s?

A

Remember tanned, tired, toned and tearful.
• Postural hypotension caused by salt and water loss
• Hyperpigmentation caused by stimulation of melanocytes by excess ACTH in primary hypoadrenalism
• Vitiligo and loss of body hair in females due to dependence on adrenal androgens
• Hypoglycaemia
• Nausea and vomiting
• Abdominal pain
• Weight loss
• Lethargy
• Depression (and tearfulness)
• Anorexia.

152
Q

What is the investigation for Addison’s?

A

Short ACTH stimulation test: take baselines cortisol. Give ACTH (synACTHen) then measure cortisol level (shows failure of exogenous ACTH to increase plasma cortisol). In Addison’s, cortisol remains low after giving ACTH. Doesn’t distinguish between primary and secondary.

153
Q

What plasma ACTH levels confirms primary hypoaldrenalism?

A

High ACTH with low or normal cortisol.

154
Q

What plasma ACTH levels confirms secondary hypoaldrenalism?

A

Low ACTH and cortisol indicate secondary or tertiary hypoadrenalism.

155
Q

What does U&E show in hypoaldosteronism?

A
  • Shows high plasma renin (low sodium, high potassium) due to low aldosterone
  • Eosinophilia
  • Raised Urea.
156
Q

What is the role of aldosterone?

A

Aldosterone causes an increase in salt and water reabsorption into the bloodstream from the kidney thereby increasing the blood volume, restoring salt levels and blood pressure.

157
Q

What is the RAAS system?

A
  1. The liver produces angiotensinogen.
  2. A decrease in renal perfusion (juxtaglomerular apparatus) causes the kidneys to release renin
  3. Renin converts angiotensinogen to angiotensin I
  4. ACE is secreted from pulmonary and renal endothelium
  5. ACE converts angiotensin I to angiotensin II
  6. Angiotensin II: increases sympathetic activity, tubular reabsorption of Na+ and Cl- (and subsequent H20 retention) and K+ excretion, causes the production of aldosterone, causes arteriole constriction so increases blood pressure and stimulates the posterior pituitary to secrete ADH which causes H2O reabsorption in the collecting duct
  7. Aldosterone causes further tubular reabsorption of Na+ and Cl- (and subsequent H20 retention) and K+ excretion.
158
Q

What is the management for Addison’s?

A
  • Glucocorticoids: oral Hydrocortisone/prednisolone to replace cortisol
  • Mineralocorticoids: fludrocortisone to replace aldosterone.
159
Q

What is diabetes insipidus?

A

Not enough ADH is produced.

160
Q

What are the 2 types of diabetes insipidus?

A 
Cranial diabetes insipidus:
•	Neurosurgery
•	Head trauma
•	Pituitary tumour
•	Infiltrative disease (sarcoidosis, histiocytosis)
•	Idiopathic
•	Congenital defect in ADH gene.
Nephrogenic diabetes insipidus:
•	Drugs e.g. lithium chloride, demeclocycline
•	Hypokalaemia
•	Hypercalcaemia
•	Renal tubular acidosis
•	Sickle cell disease
•	Familial: mutation in ADH receptor.
161
Q

What are the symptoms of diabetes insipidus?

A
  • Polyuria/nocturia
  • Polydipsia
  • Dehydration.
162
Q

What is the test for diabetes insipidus?

A

Water deprivation test.
Aims to determine whether kidneys continue to produce dilute urine despite dehydration. Normal responses is for urine osmolality to remain within normal range and urine will be concentrated as a normal response. Positive for DI if uric osmolarity is low.

163
Q

How do you determine between cranial and nephrogenic diabetes?

A

Water deprivation test with desmopressin (ADH analogues). If urine osmolarity remains the same then nephrogenic DI and if urine osmolarity increased then cranial DI.

164
Q

Where is ADH produced?

A

Hypothalamus.

165
Q

What are the plasma sodium levels in diabetes insipidus?

A

High or normal.

166
Q

What is the treatment for cranial diabetes insipidus?

A

Desmopressin.

167
Q

What is the treatment for nephrogenic diabetes insipidus?

A

Bendroflumethiazide (diuretic) which causes more Na+ secretion in DCT and so increased water lost makes body respond by reducing GFR. Also give NSAIDs to reduce GFR by inhibiting prostaglandin synthase (prostaglandins locally inhibit ADH action).

168
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion. Continued ADH secretion despite plasma being very dilute and so causes water retention, excess blood volume and hyponatraemia.

169
Q

What are the causes of SIADH?

A

Malignancy: small cell lung carcinoma most common.
Drugs: opiates.
Brain issues: meningitis, cerebral abscess, tumour.
Lung: pneumonia, TB.
Metabolic: alcohol withdrawal.

170
Q

What is the pathophysiology of SIADH?

A

Excess ADH so insertion of aquaporin 2 increases and increases water retention so dilution of blood plasma which causes hyponatraemia.

Also this water retention causes decreased RAAS (aldosterone). This causes secretion of Na+ and so excess water being excreted with Na+ (body is removing sodium from blood that already has a low concentration of sodium) which means normovolaemia but hyponatraemia.

171
Q

What are the symptoms of SIADH?

A
  • Reduction in GCS and confusion with drowsiness
  • Irritability
  • Headaches
  • Anorexia
  • Nausea
  • Concentrated urine
  • Mild dilutional hyponatraemia (could lead to fits and coma).
172
Q

What are the diagnostic criteria for SIADH?

A
  • Low serum sodium
  • Low plasma osmolality with “inappropriate” urine osmolarity
  • Continued urinary sodium excretion
  • Absence of hypokalaemia, hypotension and hypovolaemia
  • Normal renal, adrenal and thyroid function.
173
Q

How do you distinguish between hyponatraemia and SIADH?

A

Test with 1-2L of 0.9% saline: sodium depletion will respond, and SIADH will not.

174
Q

What is the management for SIADH?

A

• Treat underlying cause
• Restrict fluid: to increase Na+ concentration
• Demeclocycline: inhibits action of vasopressin on kidney i.e. causes nephrogenic DI
• Vasopressin receptor antagonists (vaptans): V2 blocker
• Tolvaptan: used for treatment of hyponatraemia secondary to SIADH as promotes water excretion with no loss of electrolytes
Oral furosemide: salt and loop diuretics if severe and to prevent circulatory overload.

175
Q

What are the causes of hyperkalaemia?

A

Excess consumption at a fast rate e.g. IV fluids.
Low levels of aldosterone in the kidneys due to adrenal insufficiency.
Drugs e.g. ACE inhibitors (block the binding of aldosterone to receptor), spironolactone (potassium-sparing diuretic), NSAIDs, cyclosporin, heparin.
Acute kidney injury so decreased filtration so more K+ maintained in the blood.

176
Q

What are the effects of hyperkalaemia?

A

When K+ levels in blood rise, this reduces the difference in electrical potential between cardiac myocytes and outside of the cells and so the threshold for action potential is significantly decreased. This abnormal action potential can cause arrhythmias and then cardiac arrest.

177
Q

What are the symptoms of hyperkalaemia?

A 
Typically asymptomatic until high enough to cause cardiac arrest.
•	Muscle weakness
•	Impaired neuromuscular transmission
•	Flaccid paralysis
•	Chest pain
•	Light headedness.
178
Q

What are the signs of hyperkalaemia?

A

Metabolic acidosis causing Kussmaul’s respiration (low, deep, sighing inspiration and expiration).
Tachycardia.

179
Q

What potassium level is hyperkalaemia?

A
  • Over 5.5mmol/L = hyperkalaemic

* Over 6.5mmol/l = medical emergency.

180
Q

How does hyperkalaemia show on an ECG?

A

• Tall tented T waves
• Small P waves
• Wide QRS complex.
Also prolonged PR interval and bradycardia.

181
Q

What is the management for hyperkalaemia?

A

Mild:
• Treat underlying cause
• Dietary potassium restriction
• Restriction of drugs causing hyperkalaemia
• Loop diuretics e.g. furosemide: increase urinary K+ excretion.

Severe:
• Calcium gluconate: decreases VF risk in the heart and protects myocardium by reducing excitability of cardiac myocytes
• Insulin and dextrose: drives K+ into the cells
• Polystyrene sulphonate resin: binds K+ in the gut decreasing uptake.

182
Q

What are the causes of hypokalaemia?

A
  • Fasting
  • Anorexia
  • High levels of aldosterone in kidneys: majority of K+ excretion is through the kidneys and aldosterone stimulates secretion of K+ . Cushing’s and Conn’s
  • Increased renal excretion: thiazides diuretics e.g. Bendroflumethiazide and loop diuretics e.g. furosemide
  • GI losses: vomiting, severe diarrhoea and laxative abuse.
183
Q

What is the pathophysiology of hypokalaemia?

A

Low K+ in the serum (ECF) causes a water concentration gradient out of the cell (ICF). Increased leakage from ICF causing hyperpolarisation of the myocyte membrane decreasing myocyte excitability.

184
Q

What are the symptoms of hypokalaemia?

A
  • Usually asymptomatic
  • Muscle weakness
  • Cramps
  • Tetany (intermittent muscle spasms)
  • Palpitations
  • Constipation.
185
Q

What potassium level is hypokalaemia?

A
  • Serum K+ < 3.5mmol/L = hypokalaemia

* Serum K+ < 2.5mmol/L = medical emergency.

186
Q

How does hypokalaemia show on an ECG?

A 
•	U waves
•	Small or inverted T waves
•	Depressed ST segments
•	Long PR
•	Long QT
Rhyme : U have no Pot (K+) and no Tea but a Long PR and a Long QT.
187
Q

What is the management for hypokalaemia?

A

Mild: oral K+ e.g. oral Sando-K and spironolactone (K+ sparing).
Severe: IV K+.

188
Q

What are the symptoms of carcinoid syndrome?

A
  • Flushing
  • Diarrhoea
  • Heart failure
  • Vomiting
  • Bronchoconstriction.
189
Q

What is carcinoid syndrome?

A

The collection of symptoms some people get when a neuroendocrine tumour, usually one that has spread to the liver, releases hormones such as serotonin and kallikrein into the bloodstream.

190
Q

What is the pathway of T3/4 release?

A

Hypothalamus produces TRH (thyrotropin releasing hormone) -> stimulates thyroid stimulating hormone (TSH) release from pituitary -> stimulates the thyroid to release thyroxin to control metabolism.
Inhibited by somatostatin.

191
Q

What is the pathway of cortisol production?

A

Hypothalamus produces corticotropin releasing hormone (CRH) -> stimulates adrenocorticotropic hormone (ACTH) release from pituitary -> stimulates glucocorticoids (cortisol) in zone fasciculata of adrenal cortex and androgen production.

192
Q

What is the pathway of oestrogen and testosterone production?

A

Gonadotrophin Releasing Hormone (GnRH) produced in the hypothalamus -> stimulates LH and FSH release from pituitary -> stimulates release of oestrogen and testosterone from gonads.
In women, LH stimulates ovulation and androgen production. FSH stimulates ovarian follicle growth by stimulating oestrogen and progesterone and converts androgens to oestrogen by aromatase.
In men, LH stimulates testosterone production from Leydig cells and FSH stimulates testicular growth and sperm maturation in sertoli cells.

193
Q

What is the pathway of growth hormone production?

A

Hypothalamus produces growth hormone releasing hormone (GHRH) -> stimulates pituitary to release growth factor -> acts on the liver to produce IGF-1.
Inhibited by somatostatin.

194
Q

What is the pathway of dopamine production?

A

Inhibits prolactin. Prolactin stimulates lactation when dopamine inhibition is removed).

195
Q

What produce the posterior pituitary hormones?

A

Supraoptic nuclei and paraventricular nuclei.

196
Q

Where is ADH produced?

A

Supraoptic nucleus.

197
Q

Where does ADH act on?

A

DCT and collecting duct.

198
Q

What does ADH do?

A

Increases water reabsorption by increasing sodium reabsorption.
Causes vasoconstriction of blood vessels.

199
Q

Where is oxytocin produced?

A

Produced by paraventricular nuclei.

Causes uterine contractions and the production of breast milk upon suckling.

200
Q

What is essential for thyroid protection?

A

Iodine.

201
Q

What are the effects on smooth muscle in hyperkalaemia and hypokalaemia?

A

Hypo: constipation.
Hyper: cramping.

202
Q

What are the effects on skeletal muscle in hyperkalaemia and hypokalaemia?

A

Hypo: weakness/cramps.
Hyper: overcontraction of muscles leads to them being totally drained of energy.

203
Q

What are the effects on cardiac in hyperkalaemia and hypokalaemia?

A

Hypo: arrhythmias and palpitations.
Hyper: arrhythmias and arrest.

204
Q

What stimulates calcitriol release?

A

Low plasma calcium, low plasma phosphate and PTH.

205
Q

What are the roles of calcitriol?

A
  • Increased Ca2+ and phosphate absorption in the gut
  • Inhibits PTH release by negative feedback
  • Enhanced bone turnover by increasing osteoclasts
  • Increased Ca2+ and phosphate reabsorption in the kidney.
206
Q

What is calcitonin?

A
  • Made in C-cells of thyroid

* Causes a decrease in plasma Ca2+ and phosphate. Increases osteoblast activity.

207
Q

What are the three vital points when assessing a tumour?

A
  1. Pressure on local structures: e.g. optic nerves: can cause headaches, visual field defects
  2. Pressure on the normal pituitary (then hypopituitary): can cause hypopituitarism
  3. Functioning tumour (Prolactinoma, acromegaly or cushings).
208
Q

What does craniopharyngioma arise from?

A

Squamous epithelial remnants of Rathke’s pouch.

209
Q

What is the commonest pituitary tumour?

A

Pituitary adenoma.

Then meningioma.

210
Q

What drug is commonly associated with hypokalaemia?

A

Salbutamol inhaler.

211
Q

What drug is commonly associated with hyperkalaemia?

A

ACE-I.

212
Q

What is the difference between the two types of diabetes insipidus?

A

A decrease in production of ADH is a cranial cause. An impaired response to ADH is a nephrogenic cause.

213
Q

What are suggestive features of hyperaldosteronism?

A

Hypertension (resistant to 3+ antihypertensives). Hypokalaemia e.g. muscle weakness.
Alkalosis.

214
Q

What is the first line investigation in hyperaldosteronism?

A

First line = ARR (aldosterone renin ratio): high aldosterone levels + low renin levels (negative feedback due to sodium retention from aldosterone).
• Adrenal Venous Sampling (AVS): identify the gland secreting excess hormone in primary hyperaldosteronism
• HRCT abdomen + AVS is used to differentiate between unilateral (Conn’s) and bilateral adrenal hyperplasia

215
Q

What is a pheochromocytoma?

A

A tumour that secretes catecholamines derived from the chromaffin cells within the adrenal medulla. Management of a pheochromocytoma is commonly a surgical resection of the tumour with alpha-blockers e/g phenoxybenzamine typically given before surgery.

216
Q

What does the zona glomerulosa of the adrenal cortex secrete?

A

Produces and secretes mineralocorticoids e/g aldosterone.

217
Q

What does the zona fasciculata of the adrenal cortex secrete?

A

Produces and secretes corticosteroids e/g cortisol.

218
Q

What does the zona reticularis of the adrenal cortex secrete?

A

Produces and secretes androgens.

219
Q

What does the adrenal medulla secrete?

A

Contains chromaffin cells which secretes catecholamines such as adrenaline/

220
Q

Does Graves disease lead to weight loss or weight gain?

A

Weight loss.

221
Q

What is the gold standard diagnosis for phaeochromocytoma?

A

Elevated plasma free Metanephrine.

222
Q

What causes secondary adrenal insufficiency?

A

Corticosteroid withdrawal. Long-term corticosteroid (e.g. prednisone) for Crohn’s disease leads to the suppression of the adrenal glands. With prolonged suppression, the adrenal glands atrophy, which means that they can’t produce enough corticosteroids if exogenous corticosteroids are stopped abruptly, leading to symptoms of adrenal insufficiency.

223
Q

What cancers can cause SIADH?

A

Small cell carcinoma Prostate cancer
Pancreatic cancer
Lymphomas
Cancer of the thymus.

224
Q

How does acromegaly cause loss of peripheral vision?

A

Bitemporal hemianopia – pressure on the optic chiasm from a pituitary adenoma.

225
Q

What is the most common cause of Cushing’s syndrome?

A

Exogenous causes e.g. glucocorticoid use (corticosteroids).

226
Q

How do you distinguish between primary and secondary hyperaldosteronism?

A

High ratio = primary and low ratio = secondary.

227
Q

What are the three key aspects of Conn’s?

A
  1. Hypertension associated with hypokalaemia
  2. Hypertension despite being on 3 or more antihypertensives
  3. Hypertension before 40 years of age.
228
Q

What is secondary hyperladosteronism?

A

Hyperaldosteronism due to high renin levels.

229
Q

What HbA1c level is diagnostic of diabetes mellitus?

A

≥48mmol/mol.

230
Q

What is the triad for carcinoid syndrome?

A

Cardiac involvement, diarrhoea and flushing.

231
Q

What causes carcinoid syndrome?

A

The tumour cells producing 5-HT.

2a Medicine (11 decks)

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