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Endocrinology Flashcards

1
Q

What hormones are released by the anterior pituitary gland?

A

TSH
FSH/LH
Prolactin
GH
ACTH

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2
Q

What hormones are released by the posterior pituitary?

A

Oxytocin
ADH

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3
Q

Describe the thyroid axis

A

Hypothalamus releases thyrotropin releasing hormone (TRH) -> Anterior pituitary releases TSH -> Thyroid gland releases T3 and T4
T3 and T4 have negative feedback on both anterior pituitary and hypothalamus

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4
Q

Describe the adrenal axis

A

Hypothalamus releases corticotrophin-releasing hormone (CRH) -> anterior pituitary releases ACTH -> Adrenal glands release cortisol (negative feedback)

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5
Q

What is the role of cortisol?

A

Increase alertness
Inhibit immune system
Inhibit bone formation
Raise blood glucose
Increase metabolism

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6
Q

Describe the parathyroid axis

A

Parathyroid hormone (PTH) released from parathyroid glands in response to low calcium
PTH increases activity and number of osteoclasts in bone, increases calcium reabsorption in the kidney and stimulated kidney to convert D3 to calcitriol to increase intestinal absorption

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7
Q

Describe the growth hormone axis

A

Hypothalamus releases GHRH -> anterior pituitary releases GH which stimulates release of IGF-1 from liver

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8
Q

Describe the Renin-Angiotensin-Aldosterone system

A

Renin secreted by Juxtaglomerular cells in afferent arterioles -> sense blood pressure and secrete more renin if BP low
Renin converts angiotensinogen-> angiotensin I -> angiotensin II in lungs with the help of ACE
Angiotensin II causes vasoconstriction and stimulates aldosterone
aldosterone causes cardiac remodelling, increases Na reabsorption, increase K secretion and hydrogen secretion

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9
Q

What are 4 causes of primary hyperthyroidism

A

Graves disease
Inflammation (thyroiditis)
Solitary toxic thyroid nodule
Toxic multinodular goitre

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10
Q

What are 3 causes of primary hypothyroidism

A

Hashimoto’s thyroiditis
Iodine deficiency
Treatment for hyperthyroidism

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11
Q

What can radioisotope scans be used for and what would they show

A
  • Diffuse high uptake in Grave’s disease
  • Focal high uptake in toxic multinodular goitre and adenomas
  • Cold areas in thyroid cancer
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12
Q

What are the TSH, T3 and T4 levels in primary hyperthyroidism

A

TSH = low
T3 + T4 = high

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13
Q

What are the TSH, T3 and T4 levels in secondary hyperthyroidism

A

TSH = high
T3 and T4 = high

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14
Q

What are the TSH, T3 and T4 levels in primary hypothyroidism

A

TSH = high
T3 + 4 = low

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15
Q

What are the TSH, T3 and T4 levels in secondary hypothyroidism

A

TSH = low
T3 + 4 = low

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16
Q

what causes secondary hyperthyroidism

A

pathology in hypothalamus or pituitary

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17
Q

What is subclinical hyperthyroidism

A

Thyroid hormones (T3 and T4) are normal and thyroid-stimulating hormone (TSH) is suppressed (low). There may be absent or mild symptoms.

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18
Q

What is the pathophysiology of Grave’s disease

A

autoimmune, TSH receptor antibodies stimulate TSH receptors on the thyroid causing primary hyperthyroidism

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19
Q

What is a toxic multinodular goitre? (Plummer’s disease)

A

nodules develop on the thyroid gland, which are unregulated by the thyroid axis and continuously produce excessive thyroid hormones. It is most common in patients over 50 years.

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20
Q

What are 4 types of thyroiditis

A

De Quervain’s thyroiditis
Hashimoto’s thyroiditis
Postpartum thyroiditis
Drug-induced thyroiditis

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21
Q

How can hyperthyroidism present

A
  • anxiety and irritability
  • sweating and heat intolerance
  • tachycardia
  • weight loss
  • fatigue
  • insomnia
  • frequent loose stools
  • sexual dysfunction
  • brisk reflexes
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22
Q

What are some specific features of Graves relating to presence of TSH receptor antibodies

A
  • Diffuse goitre
  • Graves’ eye disease (incl. exophthalmos)
  • Pretibial myxoedema
  • thyroid acropachy (hand swelling and finger clubbing)
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23
Q

What are the 3 phases of De Quervain’s thyroiditis?

A
  1. Thyrotoxicosis
  2. Hypothyroidism
  3. return to normal
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24
Q

What are some features of thyrotoxicosis

A

Excessive thyroid hormones
Thyroid swelling and tenderness
Flu-like illness
Raised inflammatory markers

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25
Q

What is the treatment for De Quervain’s thyroiditis

A

supportive
- NSAIDS (pain and inflammation)
- Beta blockers (symptoms of hyperthyroidism)
- Levothyroxine (symptoms of hypothyroidism)

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26
Q

Features of a thyroid storm (thyrotoxic crisis)

A

Fever, tachycardia, delirium

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27
Q

Management of thyroid storm

A

admission and monitoring
may need fluid resuscitation, anti-arrhythmic medications, beta blockers

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28
Q

What is the 1st line drug for hyperthyroidism

A

Carbimazole

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29
Q

What is the 2nd line drug for hyperthyroidism

A

Propylthiouracil

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30
Q

What are some cautions for radioactive iodine therapy

A
  • pregnant or breast feeding women, women must not get pregnant within 6m of treatment
  • men must not father children within 4m of treatment
  • limit contact with people after dose (esp children and pregnant women)
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31
Q

What is the first choice medication for the adrenalin-related symptoms of hyperthyroidism

A

Propranolol

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32
Q

What are 4 causes of primary hypothyroidism

A

Hashimoto’s thyroiditis
Iodine deficiency
Treatments for hyperthyroidism e.g. Carbimazole
Medications e.g. lithium, amiodarone

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33
Q

What is the most common cause of hypothyroidism in the developed world

A

Hashimoto’s thyroiditis

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34
Q

What is the most common cause of hypothyroidism in the developing world?

A

Iodine deficiency

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35
Q

Name 2 antibodies associated with Hashimoto’s thyroiditis

A

anti-thyroid peroxidase (anti-TPO)
anti-thyroglobulin (anti-Tg)

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36
Q

What are some causes of secondary hypothyroidism

A

Tumours (pituitary adenomas)
Surgery to the pituitary
Radiotherapy
Sheehan’s syndrome
Trauma

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37
Q

what are some features of hypothyroidism

A

Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (incl. oedema, pleural effusions and ascites)
Heavy or irregular periods
Constipation

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38
Q

What types of hypothyroidism cause a goitre

A

Iodine deficiency
Hashimoto’s can initially cause a goitre after which there is atrophy of the thyroid gland

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39
Q

What is the management of hypothyroidism

A

Oral Levothyroxine

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40
Q

What is Cushing’s syndrome

A

prolonged high levels of glucocorticoids e.g. cortisol

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41
Q

What causes Cushing’s disease

A

pituitary adenoma secreting excessive adrenocorticotrophic hormone (ACTH) stimulating excess cortisol release from the adrenal glands

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42
Q

What are some features of Cushing’s syndrome

A

round face
central obesity
abdominal striae
enlarged fat pad on upper back (buffalo hump)
proximal limb muscle wasting
hirsutism
easy bruising and poor skin healing
hyperpigmentation (in Cushing’s disease due to high ACTH)

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43
Q

What are some metabolic effects of Cushing’s syndrome

A

Hypertension
Cardiac hypertrophy
Type 2 diabetes
Dyslipidaemia
Osteoporosis

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44
Q

What are some mental health effects of Cushing’s syndrome

A

Anxiety
Depression
Insomnia
Psychosis

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45
Q

What are the causes of Cushing’s syndrome

A

Cushing’s disease - pituitary adenoma releases excessive ACTH
Adrenal adenoma - adrenal tumour secreting excess cortisol
Paraneoplastic syndrome
Exogenous steroids

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46
Q

What investigations are used to diagnose Cushing’s syndrome

A

dexamethasone suppression tests

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47
Q

What would dexamethasone suppression tests show for a patient with an adrenal adenoma

A

low dose test cortisol = not suppressed
high dose = not suppressed
ACTH = low

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48
Q

What would dexamethasone suppression tests show for a patient with a pituitary adenoma

A

low dose test cortisol = not suppressed
high dose = low
ACTH = high

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49
Q

What would dexamethasone suppression tests show for a patient with an ectopic ACTH e.g. small cell lung cancer

A

Low dose test cortisol = not suppressed
high dose = not suppressed
ACTH = high

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50
Q

What is an alternative test to dexamethasone suppression test for Cushing’s syndrome

A

24-hour urinary free cortisol

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51
Q

What is the treatment of Cushing’s disease

A

Trans-sphenoidal removal of pituitary adenoma

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52
Q

What is Nelson’s syndrome

A

the development of an ACTH-producing pituitary tumour after the surgical removal of both adrenal glands due to a lack of cortisol and negative feedback. It causes skin pigmentation (high ACTH), bitemporal hemianopia and a lack of other pituitary hormones.

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53
Q

What is Conn’s syndrome

A

an adrenal adenoma producing too much aldosterone

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54
Q

what is primary hyperaldosteronism

A

adrenal glands are directly responsible for producing too much aldosterone

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55
Q

What are some causes of primary hyperaldosteronism

A

bilateral adrenal hyperplasia (most common)
adrenal adenoma (Conn’s)
familial hyperaldosteronism

56
Q

What is secondary hyperaldosteronism

A

caused by excessive renin stimulating the release of excessive aldosterone. Excessive renin is released due to disproportionately lower blood pressure in the kidneys

57
Q

What are 3 causes of secondary hyperaldosteronism

A

renal artery stenosis
heart failure
liver cirrhosis and ascites

58
Q

What are some symptoms of hyperaldosteronism

A

HYPERTENSION
headaches, muscle weakness, fatigue

59
Q

what investigation is used to screen for hyperaldosteronism

A

aldosterone-to-renin ratio

60
Q

What would the aldosterone-to-renin ratio be in primary hyperaldosteronism

A

high aldosterone
low renin

61
Q

What would the aldosterone-to-renin ration be in secondary hyperaldosteronism

A

high aldosterone
high renin

62
Q

What electrolyte would be low in hyperaldosteronism

A

low potassium

63
Q

What is the medical management of hyperaldosteronism

A

aldosterone antagonists e.g. Eplerenone, spironolactone

64
Q

What investigations can be done to find the underlying cause of hyperaldosteronism

A

CT/MRI for adrenal tumour or adrenal hyperplasia
Renal artery imaging e.g. doppler for renal artery stenosis
Adrenal vein sampling

65
Q

What is the most common cause of secondary hypertension

A

hyperaldosteronism

66
Q

What is Addison’s disease

A

damage to adrenal glands resulting in reduced cortisol and aldosterone secretion

67
Q

What is secondary adrenal insufficiency + causes

A

inadequate ACTH leading to low cortisol as a result of damage to pituitary gland
causes: tumours, surgery, radiotherapy, Sheehan’s, trauma

68
Q

What is tertiary adrenal insufficiency

A

inadequate CRH released by hypothalamus - suddenly stopping exogenous steroids

69
Q

What are some symptoms of adrenal insufficiency

A

fatigue
muscle weakness + cramps
dizziness and fainting
thirst and salt craving
weight loss
abdominal pain
depression
reduced libido

70
Q

what are some signs of adrenal insufficiency

A

bronze hyperpigmentation (particularly in skin creases)
hypotension

71
Q

what is a key biochemical finding in adrenal insufficiency

A

hyponatraemia

72
Q

What tests is used to diagnose adrenal insufficiency

A

short Synacthen test

73
Q

What are the ACTH levels in primary vs secondary adrenal insufficiency

A

primary = high
secondary = low

74
Q

What is the management of adrenal insufficiency

A

hydrocortisone (to replace cortisol)
Fludrocortisone (to replace aldosterone)

75
Q

How would an adrenal crisis present

A

reduced consciousness
hypotension
hypoglycaemia
hyponatraemia and hyperkalaemia

76
Q

What is the management of an adrenal crisis

A

ABCD
IM or IV hydrocortisone(100mg followed by an infusion or 6hrly doses)
IV fluids
Correct hypoglycaemia e.g. IV dextrose
monitor electrolytes and fluid balance

77
Q

What is the classic triad of symptoms of hyperglycaemia seen in type 1 diabetes ?

A

Polyuria
Polydipsia
Weight loss

78
Q

What are some presenting features of diabetic ketoacidosis

A

Hyperglycaemia
Dehydration
Ketosis
Metabolic acidosis (with low bicarbonate)
Potassium imbalance
Polyuria
Polydipsia
N+V
Hypotension
Altered consciousness

79
Q

What are the 3 diagnostic features of DKA

A

Hyperglycaemia (e.g., blood glucose above 11 mmol/L)
Ketosis (e.g., blood ketones above 3 mmol/L)
Acidosis (e.g., pH below 7.3)

80
Q

How do you manage a patient in diabetic ketoacidosis?

A

‘FIG-PICK’
Fluids (IV saline)
Insulin (fixed rate insulin infusion e.g. Actrapid)
Glucose (closely monitor blood glucose and add glucose infusion when less than 14mmol/L)
Potassium (add K to IV fluids and monitor closely)
Infection (treat any underlying infection)
Ketones (monitor blood ketones, pH and bicarbonate)

81
Q

What are some key complications in the treatment of DKA

A

hypoglycaemia
hypokalaemia
cerebral oedema (particularly in children)
pulmonary oedema

82
Q

What autoantibodies are present in type 1 diabetes?

A

Anti-islet cell antibodies
Anti-GAD antibodies
Anti-insulin antibodies

83
Q

What does the Basal-Bolus Regime consist of?

A

combination of:

Background, long-acting insulin injected once a day
Short-acting insulin injected 30 minutes before consuming carbohydrates (e.g., at meals)

84
Q

Why should patients rotate their injection sites?

A

risk of lipodystrophy

85
Q

What are some macrovascular complications of diabetes

A

Coronary artery disease
Peripheral ischaemia
Stroke
Hypertension

86
Q

What are some microvascular complications of diabetes

A

Peripheral neuropathy
Retinopathy
Kidney disease

87
Q

What are some non-modifiable risk factors for type 2 diabetes

A

Older age
Ethnicity (black African or Caribbean and South Asian
Family history

88
Q

What are some modifiable risk factors of type 2 diabetes

A

Obesity
Sedentary lifestyle
High carbohydrate diet

89
Q

What are some presenting features of type 2 diabetes

A

Tiredness
Polyuria + polydipsia
unintentional weight loss
opportunistic infections
slow wound healing
glucose in urine

90
Q

What HbA1c indicates pre-diabetes

A

42-47 mmol/mol

91
Q

What HbA1c is diagnostic for type 2 diabetes

A

> 48 mmol/mol, sample is repeated after 1 month to confirm diagnosis

92
Q

how should type 2 diabetes be managed?

A

A structured education program
Low-glycaemic-index, high-fibre diet
Exercise
Weight loss (if overweight)
Antidiabetic drugs
Monitoring and managing complications

93
Q

what are the treatment targets for type 2 diabetes

A

48 mmol/mol for new type 2 diabetics
53 mmol/mol for patients requiring more than one antidiabetic medication

94
Q

What are the medical management options for type 2 diabetes

A

1st: Metformin
+ SGLT-2 inhibitor e,g, dapagliflozin if CVD
2nd: + sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor
3rd: Triple therapy, insulin therapy

95
Q

What are some side effects of metformin

A

GI symptoms
Lactic acidosis

96
Q

What are some side effects of SGLT-2 inhibitors?

A

Glycosuria
Increased urine output + frequency
Genital and urinary tract infections
Weight loss
DKA
lower limb amputations
Fournier’s gangrene

97
Q

What are some side effects of pioglitazone?

A

Weight gain
Heart failure
Increased risk of bone fractures
Small increase in risk of bladder cancer

98
Q

What are some side effects of sulfonylureas

A

weight gain
hypoglycaemia

99
Q

What are some side effects of DPP-4 inhibitor e.g. sitagliptin

A

headaches
low risk of acute pancreatitis

100
Q

What are some side effects of GLP-1 mimetics?

A

Reduced appetite
Weight loss
GI

101
Q

What are some complications of type 2 diabetes

A

Infections (e.g., periodontitis, thrush and infected ulcers)
Diabetic retinopathy
Peripheral neuropathy
Autonomic neuropathy
Chronic kidney disease
Diabetic foot
Gastroparesis (slow emptying of the stomach)
Hyperosmolar hyperglycemic state

102
Q

how does hyperosmolar hyperglycemic state present

A

polyuria
polydipsia
weight loss
dehydration
tachycardia
hypotension
confusion

103
Q

how is hyperosmolar hyperglycemic state managed

A

IV fluids
careful monitoring

104
Q

What causes Acromegaly?

A

excessive growth hormone most commonly caused by a pituitary adenoma

105
Q

What visual disturbance can be present in acromegaly and why?

A

bitemporal hemianopia due to a pituitary tumour pressing on the optic chiasm

106
Q

What are some features of Acromegaly?

A

Prominent forehead and brow (frontal bossing)
Coarse, sweaty skin
Large nose
Large tongue (macroglossia)
Large hands and feet
Large protruding jaw (prognathism)

107
Q

What are some systematic symptoms of Acromegaly?

A

Hypertrophic heart
Hypertension
Type 2 diabetes
Carpal tunnel syndrome
Arthritis
Colorectal cancer

108
Q

How is Acromegaly investigated?

A

Insulin-like growth factor-1 (IGF-1)
growth hormone suppression test
MRI of pituitary

109
Q

What is the treatment of Acromegaly?

A

1st: Trans-sphenoidal surgery to remove pituitary adenoma
2nd: radiotherapy, medical (Growth hormone receptor antagonist e.g. Pegvisomant, somatostatin analogues, dopamine agonists)

110
Q

What are some symptoms of hypercalcaemia?

A

Kidney stones
Painful bones
Abdominal groans (constipation, nausea and vomiting)
Psychiatric moans (fatigue, depression and psychosis)

111
Q

What causes primary hyperparathyroidism and how is it treated?

A

caused by uncontrolled parathyroid hormone production by a tumour of the parathyroid glands. This leads to a raised blood calcium (hypercalcaemia). Treatment is to remove the tumour surgically.

112
Q

What causes secondary hyperparathyroidism and how is it treated?

A

insufficient vitamin D or chronic kidney disease reduces calcium absorption from the intestines, kidneys and bones. This result in low blood calcium (hypocalcaemia). The parathyroid glands react to the low serum calcium by excreting more parathyroid hormone. Treatment is to correct the underlying vitamin D deficiency or chronic kidney disease (e.g., renal transplant).

113
Q

What causes tertiary hyperparathyroidism and how is it treated?

A

secondary hyperparathyroidism continues for an extended period, after which the underlying cause is treated. Hyperplasia (growth) of the parathyroid glands occurs as they adapt to producing a higher baseline level of parathyroid hormone. In the absence of the previous pathology, this high parathyroid hormone level leads to the inappropriately high absorption of calcium in the intestines, kidneys and bones, causing hypercalcaemia. Treatment is surgically removing part of the parathyroid tissue to return the parathyroid hormone to an appropriate level.

114
Q

What is the PTH and calcium level in primary hyperparathyroidism?

A

PTH = high
Calcium = high

115
Q

What is the PTH and calcium level in secondary hyperparathyroidism?

A

PTH = high
calcium = low/normal

116
Q

What is the PTH and calcium level in tertiary hyperparathyroidism?

A

PTH = high
Calcium = high

117
Q

What is the pathophysiology of inappropriate anti-diuretic hormone?

A

Increased release of antidiuretic hormone (ADH) from the posterior pituitary which increases water reabsorption from the urine, diluting the blood and leading to hyponatraemia

118
Q

How does SIADH present?

A

hyponatraemia
headache
Muscle aches and cramps
confusion
severe = seizures and reduced consciousness

119
Q

What are some causes of SIADH?

A

Post-operative after major surgery
Lung infection, particularly atypical pneumonia and lung abscesses
Brain pathologies, such as a head injury, stroke, intracranial haemorrhage or meningitis
Medications (e.g., SSRIs and carbamazepine)
Malignancy, particularly small cell lung cancer
Human immunodeficiency virus (HIV)

120
Q

What clinical features are useful in the diagnosis of SIADH?

A

Euvolaemia
Hyponatraemia
Low serum osmolality
High urine sodium
High urine osmolality

121
Q

How is primary polydipsia differentiated from SIADH?

A

primary polydipsia has low urine sodium and urine osmolality

122
Q

How is SIADH managed?

A

Admission if symptomatic or severe (e.g., sodium under 125 mmol/L)
Treating the underlying cause (e.g., stopping causative medications or treating the infection)
Fluid restriction
Vasopressin receptor antagonists (e.g., tolvaptan)

123
Q

What is Osmotic Demyelination Syndrome?

A

also known as central pontine myelinolysis (CPM). It is usually a complication of long-term severe hyponatraemia being treated too quickly. Patient presents encephalopathic and confused then demyelination occurs

124
Q

What are the 2 types of diabetes insipidus and what causes them?

A

A lack of antidiuretic hormone (cranial diabetes insipidus)
A lack of response to antidiuretic hormone (nephrogenic diabetes insipidus)

125
Q

What can cause nephrogenic diabetes insipidus?

A

Medications, particularly lithium (used in bipolar affective disorder)
Genetic mutations in the ADH receptor gene (X-linked recessive inheritance)
Hypercalcaemia (high calcium)
Hypokalaemia (low potassium)
Kidney diseases (e.g., polycystic kidney disease)

126
Q

What are some causes of cranial diabetes insipidus?

A

Brain tumours
Brain injury
Brain surgery
Brain infections (e.g., meningitis or encephalitis)
Genetic mutations in the ADH gene (autosomal dominant inheritance)
Wolfram syndrome (a genetic condition also causing optic atrophy, deafness and diabetes mellitus)

127
Q

How does diabetes insipidus present?

A

Polyuria (producing more than 3 litres of urine per day)
Polydipsia (excessive thirst)
Dehydration
Postural hypotension

128
Q

How is diabetes insipidus diagnosed?

A

Water deprivation test (desmopressin stimulation test)

129
Q

What will a water deprivation test show in cranial diabetes insipidus?

A

urine osmolality after water deprivation = low
after desmopressin = high

130
Q

What will a water deprivation test show in nephrogenic diabetes insipidus?

A

urine osmolality after water deprivation = low
after desmopressin = low

131
Q

How is diabetes insipidus managed?

A

Treat underlying cause
Desmopressin in cranial
nephrogenic = water, high-dose desmopressin, thiazide diuretics, NSAIDs

132
Q

What is a phaeochromocytoma?

A

tumour of the adrenal glands that secretes unregulated and excessive amounts of catecholamines (adrenaline).

133
Q

What genetic disorders increase the risk of phaeochromocytoma

A

Multiple endocrine neoplasia type 2 (MEN 2)
Neurofibromatosis type 1
Von Hippel-Lindau disease

134
Q

How does a phaeochromocytoma present?

A

Signs and symptoms tend to fluctuate

Anxiety
Sweating
Headache
Tremor
Palpitations
Hypertension
Tachycardia

135
Q

How are phaeochromocytoma’s diagnosed?

A

Plasma free metanephrines
24-hour urine catecholamines
CT/MRI to look for tumour

136
Q

How are phaeochromocytoma’s managed?

A

Alpha blockers (e.g., phenoxybenzamine or doxazosin)
Beta blockers, only when established on alpha blockers
Surgical removal of the tumour

Finals (21 decks)

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