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Phase 2a > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the definition of diabetes mellitus?

A

A disease in which the body’s ability to produce or respond to the insulin is impaired, resulting in abnormal metabolism of carbohydrates and elevated levels of glucose in the blood

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2
Q

Briefly outline the pathology of type 1 diabetes

A

An insulin deficiency disease characterised by loss of beta cells due to autoimmune destruction

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3
Q

Briefly outline the pathology of type 2 diabetes

A

Inappropriately low insulin secretion and peripheral insulin resistance

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4
Q

Name 3 examples of endocrine causes of secondary diabetes.

A

Acromegaly
Cushing’s syndrome
Drug-induced diabetes

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5
Q

Give 3 subacute presentations of diabetes

A

Thirst, polyuria, weight loss and fatigue, hunger, blurred vision

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6
Q

Give 3 acute presentations of diabetes

A

Diabetic ketoacidosis - polyuria and polydipsia, abdominal pain, hyperventilation, hypotension, coma

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7
Q

What investigations are carried out for the diagnosis of diabetes?

A

Fasting plasma glucose >7mmol/L
HbA1c 48mmol/mol
C peptide decreases in type 1

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8
Q

How do we screen for neuropathy?

A

Sensation - 10mg monofilament
Vibration perception (tuning fork)
Ankle reflexes

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9
Q

What is a serious consequence of missing a type 1 diabetes diagnosis?

A

Formation of ketone bodies:
Reduced insulin leads to fat breakdown and formation of glycerol and free fatty acids.
These impair glucose uptake and are transported to the liver, providing energy for gluconeogenesis.
Oxidised to form ketone bodies which dissolve in the blood and release H+, causing acidosis

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10
Q

What are the complications of diabetes?

A

Diabetic retinopathy, nephropathy, peripheral vascular disease, stroke, CVD, diabetic peripheral neuropathy

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11
Q

What is a hyperglycaemic hyperosmolar state and how does it present?

A

Hyperglycaemic hyperosmolar state - a diabetic emergency glucose >30mmol/L
Dehydration, severe hyperglycaemia, weakness, leg cramps, vision problems, altered level of consciousness
LMWH prophylaxis, then rehydrate with IV saline

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12
Q

What is hypoglycaemia and how does it present?

A

Endocrine emergency - plasma glucose <3mmol/L
Sweating, anxiety, hunger, tremor, palpitations, dizziness, confusion, drowsiness, visual trouble, seizures, coma
Treat with quick-acting carb snack

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13
Q

How is type 1 diabetes managed?

A

BD Biphasic regimen - twice daily premixed insulins by pen
QDS regimen - before meals ultra-fast insulin + bedtime long-acting analogue
Once-daily before bed long-acting insulin
Awareness of blood glucose lowering effect of exercise
DAFNE - dose adjustment for normal eating

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14
Q

How is type 2 diabetes managed?

A

Lifestyle Modification - weight loss and exercise
Ramipril - control BP, statins control cholesterol
1st line - metformin - increases cell sensitivity to insulin (SE: diarrhoea, nausea, weight loss)
HbA1c > 53 add a sulfonylurea
HbA1c > 57 add isoprene insulin
DDP4 inhibitors - prevent breakdown of incretins

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15
Q

What are the 3 mechanisms for increased levels of thyroid hormone?

A
  1. Overproduction of thyroid hormone
  2. Leakage of preformed hormone from thyroid
  3. Ingestion of excess thyroid hormone
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16
Q

What are some causes of hyperthyroidism?

A

Grave’s disease, congenital, thyroiditis, toxic adenoma

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17
Q

Name 4 symptoms of hyperthyroidism

A

Weight loss, tachycardia, anxiety, heat intolerance, sweating, diarrhoea, menstrual disturbance

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18
Q

How is hyperthyroidism diagnosed?

A

Thyroid function tests
Diagnosis of underlying cause
Clinical history, physical signs
Thyroid antibodies

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19
Q

How is hyperthyroidism treated?

A

Antithyroid drugs e.g. thionamides
Radioiodine
Surgery (partial/ subtotal thyroidectomy)

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20
Q

Describe the pathology of Graves’ disease

A

Increased levels of TSH receptor stimulating antibody which causes excess thyroid hormone secretion

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21
Q

What is Graves’ disease?

A

An autoimmune disease affecting the thyroid that causes hyperthyroidism and results in an enlarged thyroid

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22
Q

Give 4 symptoms of Graves’ disease.

A 
Bulging eyes - Graves' ophthalmopathy 
Thick, red skin on shins/top of feet - Graves' dermopathy
Heat sensitivity
Weight loss
Fine tremor of hands
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23
Q

How is Graves’ disease diagnosed?

A

Physical exam - eye exam or enlarged thyroid gland
Blood sample - low TSH and high thyroid hormones
Ultrasound - to identify enlarged thyroid gland

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24
Q

How is Graves’ disease managed?

A

Radioactive iodine therapy to destroy the overactive thyroid cells over time
Beta blockers - provide rapid relief of irregular heartbeats, tremors, heat tolerance and muscle weakness
Thyroidectomy

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25
Q

What is primary hypothyroidism?

A

Absence/dysfunction of the thyroid gland - most cases due to Hashimoto’s thyroiditis

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26
Q

What is secondary hypothyroidism?

A

Pituitary/ hypothalamic dysfunction with isolated TSH deficiency

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27
Q

What are the causes for hypothyroidism in children?

A

Neonatal hypothyroidism
Resistance to thyroid hormone
Isolated TSH deficiency

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28
Q

Describe the pathophysiology of primary hypothyroidism

A

Disease associated with the thyroid - Antibodies bind and block TSH receptors leading to inadequate thyroid hormone production and secretion

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29
Q

Describe the pathophysiology of secondary hypothyroidism

A

Disease associated with the pituitary or hypothalamus - reduced release or production of TSH leading to reduced T3/T4 release

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30
Q

Describe the pathophysiology of tertiary hypothyroidism

A

Disease associated with treatment withdrawal - thyroid overcompensates until it can re-establish correct concentrations of thyroid hormone

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31
Q

Name 3 symptoms of hypothyroidism

A 
Fatigue, lethargy
Weight gain
Cold intolerance
Menstrual disturbances
Decreased perspiration
Dry skin
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32
Q

Name 3 signs of hypothyroidism

A

Weight gain, jaundice, slowed speech, pallor, loss of scalp, axillary or pubic hair, bradycardia, pericardial effusion

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33
Q

What is a differential diagnosis for hypothyroidism?

A

Chronic fatigue syndrome

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34
Q

How is hypothyroidism diagnosed?

A

Bloods - increased TSH, usually decreased T3/T4 (secondary/tertiary - TSH low)
Low pulse pressure and sinus bradycardia

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35
Q

How is hypothyroidism managed?

A

Replacement of thyroid hormone - levothyroxine

Requirements vary according to cause, dose is tired until TSH normalises

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36
Q

What is Hashimoto’s thyroiditis?

A

Hypothyroidism due to aggressive autoimmune destruction of thyroid cells

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37
Q

What are the risk factors for Hashimoto’s?

A 
Sex - women
Age - middle age
Hereditary - family history
Other autoimmune disease
Radiation exposure
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38
Q

What can trigger Hashimoto’s?

A

Iodine, infection, smoking

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39
Q

Describe the pathophysiology of Hashimoto’s?

A

Antibodies bind and block TSH receptors leading to inadequate thyroid hormone production and secretion

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40
Q

How does Hashimoto’s present?

A

Fatigue, increased sensitivity to cold, constipation, dry skin, brittle nails, hair loss, muscle weakness, unexplained weight gain

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41
Q

How is Hashimoto’s diagnosed?

A

Based on signs and symptoms
Blood tests - low thyroid hormone but raised TSH
Antibody test - antibodies against thyroid peroxidase (TPO antibodies)

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42
Q

How is Hashimoto’s managed?

A

Synthetic hormones - synthetic thyroid hormone levothyroxine

Resection of obstructive goitre

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43
Q

What are the 4 types of thyroid cancer?

A

Papillary, follicular, medullary, anaplastic

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44
Q

How do thyroid cancers present?

A

Painless, palpable, solitary thyroid nodule

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45
Q

How is thyroid cancer diagnosed?

A

Fine-needle aspiration biopsy (FNAB)
Indirect laryngoscopy
Elevated serum calcitonin suggests medullary thyroid carcinoma

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46
Q

How is thyroid cancer managed?

A

Malignancies require surgical intervention

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47
Q

How is papillary thyroid cancer treated?

A

Total thyroidectomy to remove non-obvious tumour

Give levothyroxine to suppress TSH

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48
Q

How is follicular thyroid cancer treated?

A

Total thyroidectomy, T4 suppression, radioiodine ablation

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49
Q

How is medullary thyroid cancer treated?

A

Thyroidectomy and node clearance

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50
Q

How is anaplastic thyroid cancer treated?

A

Excision and radiotherapy - poor response to any treatment

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51
Q

How is lymphoma treated?

A

Chemotherapy

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52
Q

What is Cushing’s syndrome?

A

An abnormal condition caused by chronic excess levels of corticosteroids in the body due to hyper function of the adrenal gland

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53
Q

What is Cushing’s disease?

A

A TUMOUR on the pituitary gland that CAUSES the gland to produce too much ACTH, leading to high levels of cortisol production

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54
Q

What are the symptoms of Cushing’s?

A

Weight gain, mood change, proximal weakness, gonadal dysfunction, acne

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55
Q

What are the signs of Cushing’s?

A

Central obesity, skin and muscle atrophy, purple abdominal striae, osteoporosis

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56
Q

How is Cushing’s diagnosed?

A

Overnight dexamethasone suppression test - 1mg dexamethasone at midnight, take serum cortisol at 8am. Normally should suppress to 50nmol/L, no suppression indicates Cushing’s syndrome
Test for plasma ACTH - if undetectable, a tumour is likely

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57
Q

How is Cushing’s managed?

A

Iatrogenic - stop causative medications

Cushing’s disease - selective removal of pituitary adenoma

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58
Q

What is the main cause of Cushing’s syndrome?

A

Corticosteroid medication

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59
Q

What is acromegaly?

A

The abnormal growth of hands, feet and face due to overproduction of growth hormone

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60
Q

Describe the pathophysiology of acromegaly?

A

Growth hormone stimulates growth of bone and soft tissue, through secretion of insulin-like growth factor-1

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61
Q

Name 3 symptoms of acromegaly

A

Acral enlargement, arthralgias, maxillofacial changes, excessive sweating, headache, backache, hypogonadal symptoms, acroparaesthesia, amenorrhoea

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62
Q

Name 3 signs of acromegaly

A

Coarsening face - wide nose, macroglossia, puffy lips, eyelids and skin, obstructive sleep apnoea

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63
Q

Name a differential diagnosis of acromegaly

A

Gigantism

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64
Q

How is acromegaly diagnosed?

A

GH >0.4ng/ml, 75mg glucose tolerance test, abnormal IGF-I

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65
Q

How is acromegaly managed?

A

Trans-sphenoidal surgery 1st line

Radiotherapy/ somatostatin analogues

66
Q

What is Conn’s syndrome?

A

Excess aldosterone production (primary hyperaldosteronism) due to a solitary aldosterone-producing adenoma

67
Q

What is primary hyperaldosteronism?

A

A disease of the adrenal glands involving excess production of aldosterone. (It can cause high BP)

68
Q

What are the symptoms of Conn’s syndrome?

A

Often asymptomatic

Symptoms of hypokalaemia - weakness, cramps, paraesthesia, polyuria, polydipsia

69
Q

What are the signs of Conn’s syndrome?

A

High blood pressure - causes headaches, blurred vision, dizziness
Low potassium - causes fatigue, increased urination and thirst

70
Q

How is Conn’s syndrome diagnosed?

A

Investigate for suppressed renin and increased aldosterone, adrenal vein sampling, U&E - potassium may be low or normal

71
Q

How is Conn’s syndrome managed?

A

Laparoscopic adrenalectomy

72
Q

What is adrenal insufficiency?

A

A condition in which the adrenal glands do not produce adequate amounts of steroid hormone (cortisol)

73
Q

Describe the pathophysiology of adrenal insufficiency

A

Autoimmune destruction of the entire adrenal cortex. Loss of cortex leads to reduction in ability to produce cortisol and/or aldosterone.

74
Q

What is primary adrenal insufficiency and what are the causes?

A

Addison’s disease - destruction of the adrenal cortex leads to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency
Caused by adrenal antibodies, very long chain fatty acids, genetics

75
Q

What is secondary adrenal insufficiency and what are the causes?

A

Hypopituitarism/ long-term steroid therapy leading to suppression of the pituitary-adrenal axis
Caused by any steroids, imaging, genetic

76
Q

What are the symptoms of Adrenal insufficiency?

A

Fatigue, weight loss, dizzy, faints, poor recovery from illness, headache, abdominal pain, diarrhoea, constipation

77
Q

What is as an adrenal crisis?

A

Hypotension and cardiovascular collapse, fatigue, fever, hypoglycaemia, hyponatraemia and hyperkalaemia

78
Q

What are the signs of adrenal insufficiency?

A

Pigmentation (primary) and pallor (secondary), hypotension

79
Q

How is adrenal insufficiency diagnosed?

A

Family history of autoimmunity, any previous use of steroids

Low Na, high K, anaemia, borderline elevated TSH

80
Q

How is adrenal insufficiency managed?

A

Replace aldosterone with fludrocortisone
Hydrocortisone 2/3 times daily
Mineralocorticoids to correct postural hypertension

81
Q

What is diabetes insipidus?

A

A rare metabolic disorder in which the patient produces large quantities of dilute urine and is constantly thirsty

82
Q

Describe the pathology of diabetes insipidus

A

it is due to a deficiency of the pituitary hormone vasopressin (ADH), which regulates reabsorption of water in the kidneys. This means that the body can’t make enough concentrated urine and too much water is passed

83
Q

What is cranial diabetes insipidus?

A

Not enough AVP in the body to regulate urine production. Caused by damage to the hypothalamus/ pituitary gland e.g. after infection, operation, tumour, injury

84
Q

What is nephrogenic diabetes insipidus?

A

When there is enough AVP in the body, but the kidneys fail to respond to it. Caused by kidney damage or inherited as a problem

85
Q

What are the symptoms of diabetes inspidus?

A

Polydipsia, polyuria, tiredness, irritability, difficulty concentrating

86
Q

How is diabetes insipidus diagnosed?

A

Water deprivation test - no liquid for 8 hours - in DI the body will still pass large amounts of dilute urine instead of small amount of concentrated urine.
Vasopressin test - inject small dose AVP and if it stops urine production it’s cranial DI, if urine production continues it’s nephrogenic

87
Q

How is cranial diabetes insipidus managed?

A

Desmopressin can be used to replicate the functions of AVP

88
Q

How is nephrogenic diabetes insipidus managed?

A

Thiazide diuretics, which reduce the amount of urine the kidneys produce

89
Q

What is syndrome of inappropriate secretion of ADH?

A

The hyponatraemia and hypo-osmolality resulting from inappropriate, continued secretion or action of the ADH arginine vasopressin (AVP) despite normal or increased plasma volume, which results in impaired water excretion

90
Q

What are the causes of syndrome of inappropriate secretion of ADH?

A

Malignancy (lung small cell, pancreas, prostate, thymus, lymphoma)
CNS disorders - abscess, stroke
Chest disease - TB, pneumonia

91
Q

Describe the pathophysiology of syndrome of inappropriate secretion of ADH

A

Ectopic production increases the amount of ADH produced, beyond mechanisms of control. This secretion results in enhanced water reabsorption, leading to hyponatreamia

92
Q

What are the clinical presentations of syndrome of inappropriate secretion of ADH?

A

Nausea, irritability and headache with mild dilution hyponatraemia, fits and coma with severe hyponatraemia

93
Q

Name a differential diagnosis of syndrome of inappropriate secretion of ADH

A

Cerebral salt-wasting syndrome (CSW) - excessive ADH secretion caused by stimulation of the hypothalamus after trauma or ischaemia

94
Q

How is syndrome of inappropriate secretion of ADH diagnosed?

A

Diagnose by serum concentrations of sodium, potassium, chloride and bicarbonate
Hyponatraemia (>20mmol/L) with corresponding hypo-osmolality (>100mOsmol/kg)

95
Q

How is syndrome of inappropriate secretion of ADH managed?

A

Treat the cause and restrict the fluid
Consider salt +/- loop diuretic if severe
Vasopressin receptor antagonists

96
Q

Describe the clinical chemistry of syndrome of inappropriate secretion of ADH

A

Decreased sodium and plasma osmolality

Increased urine osmolality and urine sodium

97
Q

What is hyperparathyroidism?

A

Excessive secretion of parathyroid hormone, usually due to a small tumour in one of the parathyroid glands.

98
Q

What causes primary hyperparathyroidism?

A

A solitary adenoma, or occasionally hyperplasia of all glands

99
Q

What causes secondary hyperparathyroidism?

A

Decreased vitamin D intake or chronic renal failure

100
Q

What causes tertiary hyperparathyroidism?

A

Occurs after prolonged secondary hyperparathyroidism, causing glands to act autonomously after undergoing hyper plastic or adenomatous change

101
Q

Briefly outline the pathophysiology of PTH.

A

Parathyroid hormone is normally secreted in response to low ionised Ca2+ levels, by 4 parathyroid glands situated posterior to the thyroid. The glands are controlled by negative feedback via Ca2+ levels

102
Q

What are the symptoms of primary hyperparathyroidism?

A

Often asymptomatic, bones (osteoporosis), stones (kidney), groans (confusion), moans (abdominal - constipation)

103
Q

What are the symptoms of secondary hyperparathyroidism?

A

Kidney disease, with skeletal or cardiovascular complications

104
Q

What are the symptoms of tertiary hyperparathyroidism?

A

Bones (osteoporosis), stones (kidney), groans (confusion), moans (abdominal - constipation)

105
Q

Name a differential diagnosis of hyperparathyroidism

A

Cancers producing parathyroid hormone

106
Q

How is hyperparathyroidism diagnosed?

A

Primary - raised Ca2+, PTH and ALP (bone resorption
Secondary - low Ca2+, raised PTH
Tertiary - raised Ca2+ and PTH

107
Q

How is hyperparathyroidism managed?

A

Primary - surgical removal of adenoma

Secondary - calcium correction (underlying cause)

108
Q

What is hypoparathyroidism?

A

Subnormal activity of the parathyroid glands, causing a fall in the blood concentration of calcium and muscular spasms

109
Q

What are the causes of hypoparathyroidism?

A

Genetics, autoimmune, infiltration of the parathyroid glands by iron overload, surgery

110
Q

Describe the pathology of hypoparathyroidism

A

PTH stimulates the activation of vitamin D, which facilitates intestinal calcium absorption, renal reabsorption of calcium as well as calcium release from bone

111
Q

What are the symptoms of hypoparathyroidism?

A 
Increased excitability of muscles and nerves.
Numbness around the mouth/ extremities
Cramps
Tetany
Convulsions
112
Q

What is Chvostek’s sign (hyperparathyroidism)?

A

The twitching of the facial muscles in response to tapping over the area of the facial nerve

113
Q

What is Trousseau’s sign (hyperparathyroidism)?

A

Carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure for 3 minutes

114
Q

What is pseudohypoparathyroidism?

A

A genetic defect that causes lack of response to parathyroid hormone.

115
Q

What are the symptoms of pseudohypoparathyroidism?

A

Short stature, obesity, round faces, mild learning difficulties, short fourth metacarpals

116
Q

What is hypercalcaemia of malignancy?

A

A higher-than-normal level of calcium in the blood due to a malignancy secreting parathyroid hormone-related protein

117
Q

Which malignancies can cause hypercalcaemia and how?

A

Lung, oesophagus, skin, cervix, breast and kidney

The tumour secretes parathyroid hormone-related protein which results in increased calcium levels

118
Q

How does hypercalcaemia of malignancy present?

A

Bones (osteoporosis), stones (kidney), groans (confusion), moans (abdominal - constipation)
Weight loss, anorexia, nausea, polydipsia, polyuria, constipation, abdo pain

119
Q

What effect can a hypercalcaemia of malignancy seizure have on an ECG?

A

Short QT interval

120
Q

How is hypercalcaemia of malignancy diagnosed?

A

Raised calcium and phosphate, decreased albumin, chloride and potassium
Alkalosis

121
Q

How is hypercalcaemia of malignancy managed?

A

Aggressive rehydration, bisphosphonates, control of underlying malignancy

122
Q

Whats is hypocalcaemia?

A

An abnormally low calcium concentration in the blood

123
Q

What are the causes of hypocalcaemia?

A 
HAVOC
Hypoparathyroidism
Acute pancreatitis
Vit D deficiency
Osteomalacia
CKD
124
Q

How does hypocalcaemia present?

A

SPASMODIC
Spasms, paraesthesiae, anxious, seizures, muscle tone increase, orientation impaired, dermatitis, impetigo herpetiformis, Chvostek’s sign

125
Q

What effect can a hypocalcaemia seizure have on an ECG?

A

QT prolongation

126
Q

Name 2 differential diagnoses of hypocalcaemia

A

Hypoparathyroidism, acute kidney injury

127
Q

What are the complications of hypocalcaemia?

A

Dysphagia, wheezing, syncope, congestive heart failure, angina

128
Q

How is hypocalcaemia diagnosed?

A

Measure serum albumin levels (rule out hypoalbuminaemia)
Chvostek’s/Trousseau’s sign
eGFR to look for CKD
PTH and vit D levels

129
Q

How is hypocalcaemia managed?

A

Treat with calcium (oral/IV)
CKD - alfacalcidol
Respiratory alkalosis - correct alkalosis

130
Q

What is hyperkalaemia?

A

An abnormally high concentration of potassium in the blood, usually due to a failure of the kidneys to secrete it

131
Q

What are the causes of hyperkalaemia?

A

Renal impairment, metabolic acidosis, Addison’s disease, burns

132
Q

How does hyperkalaemia present?

A

Dyspnoea, paraethesia, a fast, irregular pulse, chest pain, weakness, palpitations

133
Q

What is a differential diagnosis for hyperkalaemia?

A

Rhabdomyolysis (muscle injury- death of muscle fibres that release their contents into the bloodstream)

134
Q

How is hyperkalaemia diagnosed?

A

Plasma potassium >6.5mmol/L

ECG: tall tented T waves, small P waves, wide QRS complex and ventricular fibrillation

135
Q

How is hyperkalaemia managed?

A

Treat underlying cause, polystyrene sulfonate resin - binds K+ in the gut preventing absorption and bringing K+ levels down over a few days
Dietary potassium and loop diuretic

136
Q

What is hypokalaemia?

A

Abnormally low levels of potassium in the blood (occurs in dehydration)

137
Q

Describe the pathology of hypokalaemia

A

Gi fluid loss -> less chloride -> increase in aldosterone -> decreased potassium reabsorption

138
Q

How does hypokalaemia present?

A

Muscle weakness, hypotonia, hyporeflexia, cramps, tetany, palpitations, light-headedness, constipation

139
Q

Name a differential diagnosis for hypokalaemia

A

Bartter syndrome (inherited defect that causes low potassium levels)

140
Q

How is hypokalaemia diagnosed?

A

ECG: T wave inversion, prominent U wave
Serum potassium levels
Urine potassium, sodium and osmolality

141
Q

How is hypokalaemia managed?

A

Potassium (oral/ IV)

Withdraw harmful medication, normalise magnesium and potassium

142
Q

What are the 3 vital signs of presentation for diagnosing tumours?

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

Which inherited conditions increase your chance of developing a neuroendocrine tumour/

A

Multiple endocrine neoplasia type 1
Neurofibromatosis type 1
Von Hippel-Lindaeu syndrome

144
Q

What is a prolactinoma?

A

Lactotroph cell tumour of the pituitary

145
Q

How do proclactinomas present?

A

Local effect of tumour - headache, visual field defect
Effect of prolactin - amenorrhoea
Loss of libido

146
Q

How are prolactinomas diagnosed?

A

Ultrasound, CT, MRI, PET

147
Q

How are prolactinomas managed?

A

Dopamine agonists e.g. cabergoline

148
Q

What is a pheochromocytoma?

A

A catecholamine (adrenaline) secreting tumour - tumours of the chromaffin cells of the medulla (these produce catecholamine)

149
Q

How do pheochromocytomas present?

A

Episodic, headaches, palpitations, sweating, tremor, anxiety and nausea, hypertension, tachycardia, pallor

150
Q

How are pheochromocytomas diagnosed?

A

24 hour urine collection for urinary catecholamines and metabolites

151
Q

How are pheochromocytomas managed?

A

Surgery preceded by alpha and beta blockers to stagger adrenaline loss

152
Q

What is a carcinoid tumour?

A

Neuroendocrine tumours that particularly affect the small bowel, large bowel or appendix.
Common sites: appendix, ileum, rectum

153
Q

Describe the pathophysiology of carcinoid tumours

A

Carcinoid tumours are a group of tumours of enterochromaffin cell origin, capable of producing 5HT. They secrete bioactive compounds e.g. serotonin and Kallikrein which cause carcinoid syndrome
(only with liver metastasis)

154
Q

How do bowel tumours present?

A

Stomach pain, diarrhoea, constipation, nausea, vomiting, rectal bleeding

155
Q

How do lung tumours present?

A

Cough, wheezing, SOB, chest pain, tiredness

156
Q

How do stomach tumours present?

A

Pain, weight loss, tiredness, weakness

157
Q

What is carcinoid syndrome?

A

The collection of symptoms some people get when a neuroendocrine tumour (usually hepatic involvement) releases hormone such as serotonin into the blood stream

158
Q

How does carcinoid syndrome present?

A

Bronchoconstriction, diarrhoea, skin flushing, carcinoid crisis

159
Q

What is a carcinoid crisis and how is it treated?

A

When a tumour outgrows its blood supply, mediators flow out causing life threatening vasodilation, hypotension, tachycardia and bronchoconstriction.
Treated with octreotide and management of fluid balance

160
Q

How are carcinoid tumours diagnosed?

A

CXR + chest/pelvis MRI/CT to locate primary tumours
Echocardiography - carcinoid heart disease
Liver ultrasound - confirm metastasis

161
Q

How are carcinoid tumours managed?

A

Loperamide for diarrhoea

Tumour resection is only cure for carcinoid tumours - vital to find primary site

Phase 2a (16 decks)

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