Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2a Conditions > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is the definition of type I diabetes mellitus?

A

Autoimmune destruction of pancreatic β cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the aetiology of type I diabetes mellitus?

A

HLA-DR3 + HLA-DR4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the clinical presentation of type I diabetes mellitus?

A

Polyuria, polydipsia, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the investigations of type I diabetes mellitus?

A

o Random plasma glucose: >11.1 mmol/L
o Fasting plasma glucose: >7 mmol/L
o Plasma or urine ketones: medium or high quantity
o HbA1c: >48 mmol/mol (6.5%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the treatment of type I diabetes mellitus?

A

Insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the complications of type I diabetes mellitus?

A

Diabetic ketoacidosis, hypoglycaemia, diabetic retinopathy, nephropathy and neuropathy, stroke, CVD, PVD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the definition of diabetic ketoacidosis?

A

Acute metabolic complication of diabetes characterised by hyperglycaemia, ketosis, and metabolic acidosis due to absolute insulin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the aetiology of diabetic ketoacidosis?

A

Idiopathic, infection, myocardial infarction, treatment errors, undiagnosed diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the pathophysiology of diabetic ketoacidosis?

A

Insulin deficiency leads to fat breakdown and the formation of glycerol and free fatty acids. Free fatty acids are transported to the liver, where they are oxidised to ketone bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the clinical presentation of diabetic ketoacidosis?

A

Polyuria, polydipsia, nausea and vomiting, weight loss, hyperventilation, acetone scented breath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the investigations of diabetic ketoacidosis?

A

o Random plasma glucose: >11.0 mmol/L
o Venous/arterial blood gas: pH <7.3 or bicarbonate < 15 mmol/L
o Ketone testing: capillary blood ketone ≥ 3 mmol/L or urinary ketones +++ or above

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the treatment of diabetic ketoacidosis?

A

IV fluids, insulin, potassium replacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the definition of type II diabetes mellitus?

A

Impaired insulin secretion and insulin resistance leads to impaired glucose tolerance, hyperglycaemia, and increased free fatty acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the clinical presentation of type II diabetes mellitus?

A

Polyuria, polydipsia, polyphagia, infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the investigations of type II diabetes mellitus?

A

o Random plasma glucose: >11.1 mmol/L
o Fasting plasma glucose: >7 mmol/L
o HbA1c: >48 mmol/mol (6.5%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the treatment of type II diabetes mellitus?

A

Lifestyle and risk factor modifications, glycaemic management with metformin (increase insulin sensitivity and decrease hepatic gluconeogenesis), sulfonylureas (stimulate insulin secretion), insulin therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the definition of hyperosmolar hyperglycaemic state?

A

Acute metabolic complication of diabetes characterised by hyperglycaemia, hyperosmolality, and hypovolaemia in the absence of ketoacidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the aetiology of hyperosmolar hyperglycaemic state?

A

Infection (UTI, pneumonia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the pathophysiology of hyperosmolar hyperglycaemic state?

A

Decreased insulin and increased counterregulatory hormones results in increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilisation by peripheral tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the clinical presentation of hyperosmolar hyperglycaemic state?

A

Altered mental status, polyuria, polydipsia, nausea and vomiting, dehydration, tachycardia, hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the investigations of hyperosmolar hyperglycaemic state?

A

o Random plasma glucose: >30 mmol/L
o Serum osmolality: ≥320 mOsm/kg
o Ketone testing: capillary blood ketone < 3 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the treatment of hyperosmolar hyperglycaemic state?

A

IV fluids, electrolyte replacement, treatment of precipitating events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the definition of hypoglycaemia?

A

Blood glucose concentration < 3.0 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the aetiology of hypoglycaemia?

A

Excess insulin, growth hormone deficiency, adrenal insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the clinical presentation of hypoglycaemia?

A
  • Autonomic Symptoms: Tremor, palpitations, anxiety, sweating, hunger, nausea, headache
  • Neuroglycopenic Symptoms: Paraesthesia, dizziness, weakness, drowsiness, confusion, altered mental status, seizure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the investigations of hypoglycaemia?

A

Serum glucose: < 4.0 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the treatment of hypoglycaemia?

A
  • Alert treatment: oral glucose load (Lucozade) and complex carbohydrate meal
  • Coma treatment: IV glucose, glucagon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the definition of Graves’ disease?

A

Autoimmune hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the aetiology of Graves’ disease?

A

HLA-DR3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the pathophysiology of Graves’ disease?

A

B lymphocytes produce stimulating IgG antibodies against the TSH receptors on the thyroid gland. The antibodies bind to the receptor and stimulate the release of T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the clinical presentation of Graves’ disease?

A

Heat intolerance, sweating, weight loss, palpitations, tremor, hyperphagia, proximal muscle weakness, diarrhoea, anxiety, tachycardia, Graves ophthalmopathy, pretibial myxoedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the investigations of Graves’ disease?

A

o TFTs: low TSH, high T3/4
o TSH receptor antibodies: positive
o Isotope uptake scan: diffuse uptake (irregular uptake with hot and cold areas in toxic multinodular goitre)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the treatment of Graves’ disease?

A

symptomatic treatment (propranolol), antithyroid medication (carbimazole and propylthiouracil (PTU), risk of agranulosis), radioactive iodine therapy, surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the definition of thyroid storm?

A

Potentially fatal result of untreated or undertreated hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the aetiology of thyroid storm?

A

Thyroid surgery, exogenous iodine from contrast, discontinuation of medication, illness, infection, and other stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the clinical presentation of thyroid storm?

A

Hyperpyrexia, tachycardia, hypotension, arrhythmia, volume depletion, sweating, diarrhoea, vomiting, severe agitation, anxiety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the investigations of thyroid storm?

A

TFTs: low TSH, high T3/4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the treatment of thyroid storm?

A

Symptomatic treatment (propranolol), external cooling, IV fluids, antithyroid medication and steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the definition of hypothyroidism?

A

Underproduction of the thyroid hormones T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the aetiology of hypothyroidism?

A

Hashimoto’s disease (associated with HLA-DR3/4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the pathophysiology of hypothyroidism?

A

B lymphocytes produce antibodies against TPO and thyroglobulin. There is lymphoid infiltration, autoimmune destruction, and inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the clinical presentation of hypothyroidism?

A

Non-tender, painless rubbery goitre with symmetrical enlargement, dry or coarse skin, bradycardia, cold intolerance, constipation, weight gain, depression, menstrual irregularity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the investigations of hypothyroidism?

A

o TFTs: high TSH, low T3/4
o Anti-TPO antibodies: elevated in Hashimoto’s disease
o Isotope uptake scan: low uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the treatment of hypothyroidism?

A

moderate and severe hypothyroidism is treated with levothyroxine (synthetic T4, risk of atrial fibrillation with overtreatment)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the definition of myxoedema coma?

A

Life threatening complication of untreated or undertreated hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the aetiology of myxoedema coma?

A

Infection, surgery, trauma, illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the clinical presentation of myxoedema coma?

A

Impaired mental status, hypothermia, hypoglycaemia, hypotension, myxoedema, elevated creatine kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the investigations of myxoedema coma?

A

TFTs: high TSH, low T3/4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the treatment of myxoedema coma?

A

IV levothyroxine and hydrocortisone, oxygen, gradual rewarming, glucose infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the definition of subacute granulomatous thyroiditis (De Quervain’s)?

A

Inflammation of the thyroid gland characterised by a triphasic course of transient thyrotoxicosis, followed by hypothyroidism and then a return to euthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the aetiology of subacute granulomatous thyroiditis (De Quervain’s)?

A

Usually follows an upper respiratory tract infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the pathophysiology of subacute granulomatous thyroiditis (De Quervain’s)?

A

Cytotoxic T cell recognition of viral and cell antigens presentation leads to thyroid follicular cell damage and the formation of granulomas and fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the clinical presentation of subacute granulomatous thyroiditis (De Quervain’s)?

A

Neck pain, tender, firm, enlarged thyroid, fever, palpitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the investigations of subacute granulomatous thyroiditis (De Quervain’s)?

A

o TFTs: TSH is low in thyrotoxic phase and variable in hypothyroid and recovery phases, T3/4 is usually elevated due to the initial thyrotoxic phase
o CRP: elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the treatment of subacute granulomatous thyroiditis (De Quervain’s)?

A

o Hyperthyroid phase: analgesia for pain, beta blockers for symptom control, corticosteroids for thyrotoxicosis
o Hypothyroid phase: levothyroxine

56
Q

What is the definition of Cushing’s syndrome?

A

Pathological hypercortisolism

57
Q

What is the aetiology of Cushing’s syndrome?

A

Exogenous corticosteroid use, Cushing’s disease (ACTH-secreting pituitary adenoma), adrenal adenoma, ectopic tumours producing ACTH

58
Q

What is the clinical presentation of Cushing’s syndrome?

A

Central obesity, moon facies, dorsocervical fat pads (buffalo hump), purple striae, diabetes mellitus, osteoporosis, thin skin, easy bruising, hypertension, weakness

59
Q

What are the investigations of Cushing’s syndrome?

A

o 24-hour urinary free cortisol: elevated
o 1mg overnight dexamethasone suppression test: inadequate suppression of cortisol
o High-dose dexamethasone suppression test: adequate suppression shows Cushing disease, while no suppression shows ectopic ACTH secretion

60
Q

What is the treatment of Cushing’s syndrome?

A

o Exogenous steroid use: dose taped down

o Tumour: surgical resection, or drugs to inhibit cortisol synthesis and secretion (metyrapone and ketoconazole)

61
Q

What is the definition of acromegaly?

A

Excessive secretion of growth hormone

62
Q

What is the aetiology of acromegaly?

A

Pituitary adenoma which secretes excess growth hormone

63
Q

What is the clinical presentation of acromegaly?

A

Acral enlargement, arthralgias, maxillofacial changes, excessive sweating, headache, hypogonadal symptoms (excess periods, erectile dysfunction, loss of libido), giantism (in children if before fusion of epiphyseal plates)

64
Q

What are the investigations of acromegaly?

A

o Random serum growth hormone: elevated
o Serum insulin-like growth factor-1: elevated
o Oral glucose tolerance test: growth hormone concentration will rise (usually falls)

65
Q

What is the treatment of acromegaly?

A

Pituitary surgery, somatostatin analogues (octreotide), dopamine agonist (cabergoline), radiotherapy

66
Q

What is the definition of primary aldosteronism?

A

Increased secretion of aldosterone autonomous to the RAAS

67
Q

What is the aetiology of primary aldosteronism?

A

Bilateral adrenal hyperplasia, Conn’s syndrome (aldosterone producing adenoma)

68
Q

What is the clinical presentation of primary aldosteronism?

A

Hypertension, hypokalaemia, nocturia, polyuria, lethargy

69
Q

What are the investigations of primary aldosteronism?

A

o Plasma potassium: normal or low

o Plasma aldosterone: renin ratio: elevated

70
Q

What is the treatment of primary aldosteronism?

A

Aldosterone antagonists (spironolactone) or adrenalectomy

71
Q

What is the definition of adrenal insufficiency?

A

Decreased production of adrenocortical hormones due to destructive process, or interference with hormone synthesis

72
Q

What is the aetiology of adrenal insufficiency?

A

Addison’s disease, tuberculosis (most common cause worldwide)

73
Q

What is the pathophysiology of adrenal insufficiency?

A

Addison’s disease is an autoimmune condition with autoantibodies against 21-hydroxylase, which results in adrenal atrophy and destruction

74
Q

What is the clinical presentation of adrenal insufficiency?

A

Fatigue, anorexia, weight loss, hyperpigmentation, salt craving, hypotension

75
Q

What are the investigations of adrenal insufficiency?

A

o Morning serum cortisol: decreased
o Serum electrolytes: low sodium and high potassium
o Short synacthen test: little or no change in cortisol levels
o Adrenal autoantibody test: positive in Addison’s disease

76
Q

What is the treatment of adrenal insufficiency?

A

Cortisol replacement with hydrocortisone, aldosterone replacement with fludrocortisone

77
Q

What is the definition of adrenal crisis?

A

Sudden acute loss of adrenal function

78
Q

What is the aetiology of adrenal crisis?

A

Stressful events

79
Q

What is the clinical presentation of adrenal crisis?

A

Hypotension, hypovolaemic shock, acute abdominal pain, fatigue, fever, hypoglycaemia, hyponatraemia, hyperkalaemia

80
Q

What is the treatment of adrenal crisis?

A

IV hydrocortisone, IV fluids

81
Q

What is the definition of syndrome of inappropriate anti-diuretic hormone (SIADH)?

A

Impaired free water excretion, usually from excessive ADH release

82
Q

What is the aetiology of syndrome of inappropriate anti-diuretic hormone (SIADH)?

A

Malignancy, CNS disorders, tuberculosis, pneumonia, drugs

83
Q

What is the pathophysiology of syndrome of inappropriate anti-diuretic hormone (SIADH)?

A

ADH binds to V2 receptors on the principal cells of the renal collecting tubules. Aquaporin-2 proteins are inserted into the apical membrane increased the permeability of the collecting duct. Water is reabsorbed from the renal collecting duct, decreasing the plasma osmolality

84
Q

What is the clinical presentation of syndrome of inappropriate anti-diuretic hormone (SIADH)?

A

Euvolaemic, nausea and vomiting, altered mental status, headache, seizure, coma

85
Q

What are the investigations of syndrome of inappropriate anti-diuretic hormone (SIADH)?

A

o Serum sodium: low
o Serum osmolality: low (<275 mOsmol/kg)
o Urine sodium elevated (>40 mmol/l)
o Urine osmolality: elevated (>100 mOsmol/kg)

86
Q

What is the treatment of syndrome of inappropriate anti-diuretic hormone (SIADH)?

A

Fluid restriction, hypertonic saline, tolvaptan (ADH receptor antagonist), demeclocycline (reduces the responsiveness of the kidney to ADH)

87
Q

What are the complications of syndrome of inappropriate anti-diuretic hormone (SIADH)?

A

Central pontine myelinolysis (demyelination of pontine, basal ganglion, and cerebellar regions)

88
Q

What is the definition of diabetes insipidus?

A

Absolute or relative inability to concentrate urine, resulting in the production of large quantities of dilute urine

89
Q

What is the aetiology of diabetes insipidus?

A 
o	Cranial (absolute or relative deficiency of ADH) – tumours, trauma, infections, idiopathic, genetic
o	Nephrogenic (renal insensitivity or resistance to ADH) – osmotic diuresis, drugs, chronic kidney disease, metabolic (hypercalcaemia, hypokalaemia)
90
Q

What is the clinical presentation of diabetes insipidus?

A

Polyuria, polydipsia, nocturia

91
Q

What are the investigations of diabetes insipidus?

A

o Urine osmolality: low (<300 mOsm/kg)
o Serum osmolality: normal or elevated
o Water deprivation test: plasma osmolality increases while urine osmolality remains constant
o Desmopressin stimulation test:
-Cranial diabetes insipidus: plasma osmolality will decrease, and urine osmolality will increase
-Nephrogenic diabetes insipidus: no response

92
Q

What is the treatment of diabetes insipidus?

A

o Cranial diabetes insipidus: desmopressin

o Nephrogenic diabetes insipidus: maintenance of adequate fluid intake

93
Q

What is the definition of hyperkalaemia?

A

An abnormally high concentration of potassium in the blood, >5.5 mmol/L

94
Q

What is the aetiology of hyperkalaemia?

A

Increased intake of potassium in association with decreased renal excretion and decreased cellular entry of potassium or increased exit of potassium from cells

95
Q

What is the pathophysiology of hyperkalaemia?

A

Increased plasma potassium concentration reduces the difference in electrical potential between the cardiac myocytes and serum

96
Q

What is the clinical presentation of hyperkalaemia?

A

Asymptomatic, arrythmias, bradycardia, fatigue, weakness

97
Q

What are the investigations of hyperkalaemia?

A

o Serum potassium: >5.5 mmol/l

o ECG: tall, tented T waves, wide QRS complex, small P waves

98
Q

What is the treatment of hyperkalaemia?

A

Calcium gluconate (protects the myocardium), IV insulin and dextrose, nebulised salbutamol (activated beta-receptors to promote intracellular potassium shift)

99
Q

What is the definition of hypokalaemia?

A

An abnormally low concentration of potassium in the blood, <3.5 mmol/L

100
Q

What is the aetiology of hypokalaemia?

A

Decreased potassium intake, increased potassium entry into cells, increased potassium excretion, and in special situations such as during dialysis or plasmapheresis

101
Q

What is the pathophysiology of hypokalaemia?

A

Increased leakage from intracellular fluid causing hyperpolarisation of the myocyte membrane decreasing myocyte excitability

102
Q

What is the clinical presentation of hypokalaemia?

A

Asymptomatic, muscle weakness, hypotonia, hyporeflexia, palpitations, arrhythmia, nausea and vomiting, cramps

103
Q

What are the investigations of hypokalaemia?

A

o Serum potassium < 3.5 mmol/L
o ECG: flat T waves, ST depression, prominent U waves, prolonged PR interval (U have no Pot and no T but a long PR and a long QT)

104
Q

What is the treatment of hypokalaemia?

A

Oral or IV replacement

105
Q

What is the definition of hypercalcaemia?

A

An abnormally high serum corrected calcium concentration in the blood, >2.6 mmol/L

106
Q

What is the aetiology of hypercalcaemia?

A

Primary hyperparathyroidism and hypercalcaemia of malignancy

107
Q

What is the pathophysiology of hypercalcaemia?

A

Primary hyperparathyroidism results in increased parathyroid hormone secretion, while hypercalcaemia of malignancy increases serum calcium through osteolytic metastasis, PTH-related protein, and increased 1,25-dihydroxyvitamin D production

108
Q

What is the clinical presentation of hypercalcaemia?

A

Renal stones, bone pain, polyuria, abdominal pain and psychiatric features (stones, bones, thrones, abdominal groans and psychiatric moans), nausea and vomiting

109
Q

What are the investigations of hypercalcaemia?

A

o Corrected serum calcium: > 2.6 mmol/l
o ECG: short QT interval
o Serum PTH: elevated in primary hyperparathyroidism and decreased in hypercalcaemia of malignancy

110
Q

What is the treatment of hypercalcaemia?

A

Oral or IV fluids, bisphosphonates and calcitonin can be considered in severe cases

111
Q

What is the definition of hypocalcaemia?

A

An abnormally low serum corrected calcium concentration in the blood, <2.2 mmol/L

112
Q

What is the aetiology of hypocalcaemia?

A

Chronic kidney disease, vitamin D deficiency, hypoparathyroidism, pseudohypoparathyroidism (PTH resistance)

113
Q

What is the clinical presentation of hypocalcaemia?

A

Paraesthesia, muscle spasms, arrhythmia, hyperreflexia, Trousseau’s sign, Chvostek’s sign

114
Q

What are the investigations of hypocalcaemia?

A

o Corrected serum calcium: < 2.2 mmol/L

o ECG: prolonged QT interval

115
Q

What is the treatment of hypocalcaemia?

A

o Mild: oral calcium supplements, vitamin D and magnesium replacement if deficient
o Severe: intravenous calcium gluconate

116
Q

What is the definition of prolactinoma?

A

Benign adenoma with secretes excess prolactin

117
Q

What is the pathophysiology of prolactinoma?

A

: Secondary hypogonadism via its inhibitory effects on gonadotropin-releasing hormone and stimulation of milk production by the mammary gland

118
Q

What is the clinical presentation of prolactinoma?

A

Amenorrhea or oligomenorrhea, infertility, galactorrhoea, loss of libido, erectile dysfunction, visual deterioration

119
Q

What are the investigations of prolactinoma?

A

Serum prolactin: elevated

120
Q

What is the treatment of prolactinoma?

A

Dopamine agonists (cabergoline)

121
Q

What is the definition of pheochromocytoma?

A

A tumour of the adrenal medulla which secretes excess catecholamines (adrenaline, noradrenaline, and dopamine)

122
Q

What is the clinical presentation of pheochromocytoma?

A

Headache, palpitations, diaphoresis, hypertension, hypertensive retinopathy, pallor, impaired glucose tolerance and diabetes mellitus

123
Q

What are the investigations of pheochromocytoma?

A

o 24-hour urine collection for catecholamines, metanephrines, normetanephrines, and creatine: elevated
o Serum free metanephrines and normetanephrines: elevated
o CT or MRI of the abdomen and pelvis

124
Q

What is the treatment of pheochromocytoma?

A

α and β blockers, surgical resection

125
Q

What is the definition of carcinoid syndrome?

A

Release of serotonin and other vasoactive peptides from a carcinoid tumour

126
Q

What is the clinical presentation of carcinoid syndrome?

A

Diarrhoea, flushing

127
Q

What are the investigations of carcinoid syndrome?

A

Urinary 5-hydroxyindoleacetic acid: elevated

128
Q

What is the treatment of carcinoid syndrome?

A

Surgical resection (tumour appears yellow), somatostatin analogues (octrotide)

129
Q

What is the aetiology of thyroid cancer?

A

Radiation exposure, iodine deficiency (follicular)

130
Q

What is the clinical presentation of thyroid cancer?

A

Painless, palpable, solitary thyroid nodule

131
Q

What are the investigations of thyroid cancer?

A

o Fine-needle aspiration biopsy
o Indirect laryngoscopy
o Serum calcitonin (elevated suggests medullary)

132
Q

What is the treatment of thyroid cancer?

A

Surgical resection

133
Q

What are the features of papillary thyroid cancer?

A

Younger patients; spreads to lymph nodes and lungs; treatment with total thyroidectomy and levothyroxine to supress TSH

134
Q

What are the features of follicular thyroid cancer?

A

Middle age; spreads early via the blood (bone, lung), treatment with total thyroidectomy, levothyroxine to supress TSH and radioiodine ablation

135
Q

What are the features of medullary thyroid cancer?

A

MEN syndrome; treatment with thyroidectomy and node clearance

136
Q

What are the features of anaplastic thyroid cancer?

A

Three times more common in females, elderly patients; poor response to any treatment

Phase 2a Conditions (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions