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Finals > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the pathophysiology of T1DM?

A

Condition where the pancreas stops being able to produce insulin due to destruction of the beta cells in the pancreas

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2
Q

What is the classical symptoms associated with hyperglycaemia?

A

Polyuria, polydipsia, weight loss

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3
Q

How does insulin work to decrease blood sugar?

A
  1. It causes cells to absorb glucose from the blood and use it as fuel
  2. It causes muscle and liver cells to absorb glucose from the blood and store it as glycogen (glycogenesis)
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4
Q

Why are ketones raised in a patient in DKA?

A

Ketones are made from fatty acids in the liver when there is insufficient glucose supply and glycogen stores are exhausted - occurs when all the glucose is stuck in the blood and unable to be used by the cells

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5
Q

What are the 3 features of DKA?

A

Ketoacidosis, dehydration and potassium imbalance

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6
Q

Why does potassium imbalance occur in DKA?

A

Normally insulin drives potassium into the cells, without insulin potassium is not added to and stored in cells

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7
Q

What can cause DKA to occur?

A

Infection, infarction, inflammation

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8
Q

What are the 3 diagnostic features of DKA?

A

Hyperglycaemia >11mol/L
Ketosis >3mmol/l or ++ on urine dipstick
Acidosis - pH <7.3

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9
Q

What is the initial step done in managing DKA?

A

Fluid resuscitation to correct dehydration and electrolyte disturbances - 0.9% saline 1L in first hour followed by 1 litre every 2 hours

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10
Q

Apart from fluid resuscitation what other steps are required in managing DKA?

A

Insulin - fixed rate insulin infusion + long acting SC insulin

Glucose - required when glucose <14mmol/L needs regular monitoring

Potassium - add potassium to IV fluids and monitor closely

Treat any underlying triggers such as infection

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11
Q

What are the complications of treating DKA?

A

Cerebral oedema (in children), hypoglycaemia, hypokalaemia, pulmonary oedema, VTE

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12
Q

What is the long term management of T1DM?

A

Insulin regimes - pumps, basal/bolus

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13
Q

What is a variable rate IV insulin infusion?

A

IV insulin of variable rate according to regular capillary glucose measurements (need finger pricks every hour)

Accompanied by infusion fluid usually 5% glucose with KCl

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14
Q

When is a variable rate insulin infusion used?

A

Patients with known diabetes unable to take oral food/medication, vomiting, T1DM and having surgery, severe illness and need to achieve good glycaemic control

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15
Q

When a patient is on a variable rate insulin infusion should you continue short acting and long acting insulin?

A

Stop short acting
Continue long acting

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16
Q

What is considered as hypoglycaemia?

A

Blood glucose <4mmol/L

At less than 2 they cannot maintain their airway

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17
Q

What symptoms are associated with hypo’s?

A

Hunger, tremor, sweating, irritability, dizziness, pallor, reduced GCS

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18
Q

What is the management for hypoglycaemia?

A

Rapid acting glucose

Oral if able to eat

IM glucagon if no access

IV dextrose 200ml of 10% over 10 minutes

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19
Q

What are the long term complications associated with hyperglycaemia?

A

Infections due to immune system dysfunction

CHD/stroke/hypertension

Peripheral ischaemia causing poor skin healing and diabetic foot ulcers

Peripheral neuropathy

Retinopathy

Diabetic nephropathy

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20
Q

What is the pathophysiology of T2DM?

A

Combination of insulin resistance and reduced insulin production caused by persistently high blood sugar levels

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21
Q

What is the presentation of someone with T2DM?

A

Tiredness, polyuria, polydipsia, opportunistic infections, visual blurring, slow wound healing, acanthosis nigricans

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22
Q

What is the HbA1c for someone with pre-diabetes?

A

42-47mmol/L

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23
Q

What are the glucose levels required for diagnosing diabetes?

A

HbA1c >48 mmol/L - need 2 samples to confirm or 1 sample with symptoms

Fasting glucose >7mmol/l

Random glucose >11mmol/l

OGTT >11mmol/L

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24
Q

What is the HbA1c target for someone with T2DM?

A

48mmol/l for new patients

53mmol/l for patients requiring more than one antidiabetic drug

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25
Q

What is the stepwise approach to managing T2DM?

A
  1. Lifestyle modifications
  2. Metformin
  3. SGLT-2 inhibitors if existing heart disease or high QRISK or
    Sulfonylurea, pioglitazone, DPP4-inhibitor
  4. Triple therapy or insulin
  5. Can also add GLP-1 agonist if BMI>35
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26
Q

What is the mechanism of action for metformin and what are the common side effects?

A

Increases insulin sensitivity and decreases glucose production by the liver

Side effects = GI symptoms (improved on modified release)

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27
Q

What is the mechanism of action for SGLT-2 inhibitors, some examples and the common side effects?

A

Blocks the action of protein that reabsorbs glucose from urine into blood –> excess glucose excreted in urine

Empagliflozin, dapagliflozin

Side effects = genital and urinary infections, increased urine output and frequency

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28
Q

What is the mechanism of action for pioglitazone and what are the common side effects?

A

Increases peripheral insulin sensitivity and decreases liver production of glucose

Side effects = increased risk of bladder cancer, weight gain, fluid retention

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29
Q

What is the mechanism of action for sulfonylureas, some examples and the common side effects?

A

Stimulate insulin release from the pancreas

Gliclazide

Side effects = hypoglycaemia, weight gain

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30
Q

What is the mechanism of action for DPP4-inhibitors, some examples and the common side effects?

A

Prevents the blocking of incretins which act to lower blood glucose

Sitagliptin and alogliptan

Side effects = headaches, low risk of acute pancreatitis, nausea

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31
Q

What is the mechanism of action for GLP-1 mimetics, some examples and the common side effects?

A

Imitate the action of incretins which act to lower blood glucose

Exenatide, liraglutide

Side effects = reduced appetitie, weight loss, GI symptoms, AKI, pancreatitis

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32
Q

How is peripheral neuropathy managed in diabetes?

A

Amitriptyline or duloxetine

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33
Q

What medications can be used to help CKD in those with diabetes?

A

ACE inhibitors if ACR above 3
SGLT-2 inhibitors if ACR above 30

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34
Q

How is diabetic gastroparesis managed?

A

Metoclopramide or domperidone

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35
Q

What is the management for hyperosmolar hyperglycaemic state?

A

0.9% saline 3-6L over 12 hours (the glucose will follow the water into the cells)

Only give insulin if refractory hyperglycaemia following adequate rehydration

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36
Q

How is hyperosmolar hyperglycaemic state diagnosed?

A

Hypovolaemia, hyperosmolality (concentrated blood), high sugar levels, absence of ketones

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37
Q

What is the first line antihypertensive for patients with T2DM (irrespective of age)?

A

ACE inhibitors/ARB

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38
Q

What is the difference between primary and secondary hyperthyroidism?

A

Primary = thyroid pathology
Secondary = pathology in the hypothalamus or pituitary gland

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39
Q

What is subclinical hyperthyroidsim?

A

When thyroid hormone levels are normal but TSH is supressed

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40
Q

What are the causes of hyperthyroidism?

A

Graves disease, thyroiditis (hyper followed by hypo), solitary toxic thyroid nodule, toxic multi nodular goitre

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41
Q

What are the antibodies associated with Graves disease?

A

TSH receptor antibodies

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42
Q

What are the risk factors for hyperthyroidism?

A

Female, 20-40, smoking, high iodine intake, stress, other autoimmune conditions

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43
Q

What symptoms are associated with hyperthyroidism?

A

Anxiety, sweating, heat intolerance, tachycardia, palpitations, weight loss, fatigue, weakness, diarrhoea, sexual dysfunction, oligomenorrhoea, fine tremor

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44
Q

What is a complication of hyperthyroidism?

A

Thyroid storm - may require fluid resuscitation, anti-arrhythmic medication and beta blockers

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45
Q

What features are specific to Grave’s disease?

A

Diffuse goitre
Pretibial myxoedema
Finger clubbing and hand swelling
Eye disease - exophthalmos, eyelid retraction and periorbital oedema

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46
Q

What are the TFTs of someone with hyperthyroidism?

A

Serum TSH will be low, T3/T4 levels will be high

47
Q

What medications can be used to treat hyperthyroidism?

A

1st line = carbimazole (block and replace regime)

2nd line = propylthiouracil (1st line in 1st trimester of pregnancy)

Radioactive iodine

Beta blockers are used to control symptoms - propranolol is 1st line

Surgery to remove thyroid is also possible

48
Q

What is the difference between primary and secondary hypothyroidism?

A

Primary = thyroid produces inadequate thyroid hormone

Secondary = pituitary behaves abnormally and produces inadequate TSH resulting in under stimulation of the thyroid gland and insufficient thyroid hormone

49
Q

What are the causes of primary hypothyroidism?

A

Hashimotos thyroiditis = most common (associated with anti-TPO antibodies)

Atrophic hypothyroidism

Iodine deficiency

Lithium or amiodarone use

Post-partum thyroiditis

50
Q

What symptoms are associated with hypothyroidism?

A

Weight gain, fatigue, dry skin, coarse hair and hair loss, fluid retention, heavy or irregular periods, constipation, cold intolerance, bradycardia, poor appetite, poor libido, depression

51
Q

What are the TFT results in someone with hypothyroidism?

A

TSH high, T4 low

52
Q

What is subclinical hypothyroidism?

A

When TSH is high but T4 levels remain normal

53
Q

What is the treatment for hypothyroidism?

A

Oral levothyroxine - lifelong

54
Q

What complication can arise due to hypothyroidism?

A

Myxoedema coma - hypothermia, coma and seizures

55
Q

What is the most common type of thyroid cancer?

A

Papillary tumours which are relatively benign

56
Q

Which thyroid cancer types have the worst prognosis?

A

Medullary and anapaestic

57
Q

What is medullary thyroid cancer associated with?

A

Multiple endocrine neoplasia

58
Q

What treatment options are available for thyroid cancer?

A

Thyroidectomy, radioiodine, radiotherapy

59
Q

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

A

Syndrome = high levels of glucocorticoids in the body (cortisol)

Disease = due to pituitary adenoma secreting excessive ACTH –> high cortisol

60
Q

What are the features of Cushing’s?

A

Round face, central obesity, abdominal striae, buffalo hump, proximal limb muscle wasting, easy bruising and poor skin healing, acne, amenorrhoea, hyperpigmentation of skin (disease only), osteoporosis

61
Q

What are the causes of cushing’s?

A

Pituitary adenoma - disease
Adrenal adenoma
Paraneoplastic syndrome (SCLC is most common)
Exogenous steroids
Adrenal carcinoma

62
Q

What test is used to diagnose Cushing’s

A

Dexamethasone suppression test

63
Q

The high dose dexamethasone suppression test differentiates between the causes of Cushing’s disease - what are the results in pituitary adenoma and adrenal adenoma/ectopic ACTH

A

Pituitary adenoma the high dose suppresses high cortisol and ACTH

In adrenal adenoma or ectopic ACTH there is no suppression of cortisol after the high dose of dexamethasone

64
Q

What is the treatment for Cushing’s syndrome?

A

Remove underlying cause

Trans-sphenoidal surgery for removal of pituitary adenoma

Surgical removal of adrenal tumour or tumour producing ectopic ACTH

65
Q

What is Nelson’s syndrome?

A

Occurs after bilateral adrenalectomy for Cushing’s

There is hyperpigmentation due to very high levels of ACTH

66
Q

What are the causes of primary hyperaldosteronism?

A

Bilateral adrenal hyperplasia
Adrenal adenoma (Conn’s)
Familial hyperaldosteronism

67
Q

What is secondary hyperaldosteronism and what are the causes?

A

Excessive renin secretion –> excessive aldosterone

Causes = disproportionately lower BP in kidneys:
Renal artery stenosis
Heart failure
Liver cirrhosis and ascites

68
Q

What is the screening test used for hyperaldosteronism?

A

Aldosterone:renin ratio
High aldosterone and low renin = primary
High aldosterone and high renin = secondary

69
Q

What is the management for hyperaldosteronism?

A

Aldosterone antagonists = eplerenone, spironolactone

If due to renal artery stenosis - percutaenous renal artery angioplasty

Surgical removal of adrenal adenoma

70
Q

What is acromegaly?

A

Result of excessive growth hormone after fusion of the growth plates

71
Q

What are the causes of acromegaly?

A

Pituitary adenoma = most common
Ectopic GH being secreted from tumour such as SCLC

72
Q

What are the common presenting features of acromegaly?

A

Headaches, bitemporal hemianopia, prominent forehead and brow, coarse/sweaty skin, large nose/tongue/hands/feet, large protruding jaw, increased interdental spacing, hypertrophic heart, carpal tunnel

73
Q

What is the first line investigation for acromegaly?

A

Insulin-like growth factor 1 blood test
OGTT - done to confirm diagnosis

74
Q

What is the treatment for acromegaly?

A

Trans-sphenoidal surgery to remove the pituitary adenoma = 1st line

Pegvisomant - GH receptor antagonist
Octreotide - somatostatin analogues (1st line medication)
Bromocriptine - dopamine agonists

75
Q

What are the causes of hyperkalaemia?

A

AKI, CKD, rhabdomyolysis, adrenal insufficiency, tumour lysis syndrome, aldosterone antagonists, ACE inhibitors, NSAIDs, beta blockers

76
Q

What ECG signs are associated with hyperkalaemia?

A

Tall tented T waves, flattened or absence of P waves, broad complex QRS

77
Q

When does a patient with hyperkalaemia not require urgent treatment?

A

Potassium <6mmol/l and stable renal function, no ECG changes

78
Q

What treatment is given in acute hyperkalaemia? (in what order?)

A
  1. Calcium gluconate - stabilises the cardiac muscle cells and reduced risk of arrhythmias
  2. Insulin and dextrose - drives glucose into the cells and takes potassium with it (10% IV over 2 minutes)
  3. Nebulised salbutamol - temporarily drives potassium into cells
  4. Calcium resonium - lowers total body potassium

Dialysis may be required in severe or persistent cases

79
Q

What hormones are not produced in adrenal insufficiency?

A

Cortisol and aldosterone

80
Q

What is Addison’s disease?

A

Damage to the adrenal glands causing reduced cortisol and aldosterone (primary)

81
Q

What is secondary adrenal insufficiency and what are the causes?

A

Inadequate ACTH and lack of stimulation of the adrenal glands leading to low cortisol and aldosterone

Caused by damage or loss of the pituitary gland

82
Q

What is the presentation of adrenal insufficiency?

A

Fatigue, muscle weakness, dizziness and fainting, thirst, weight loss, abdominal pain, depression, reduced libido, bronze hyperpigmentation in skin creases (primary only due to raised ACTH)

83
Q

What are the key biochemical findings in adrenal insufficiency?

A

Hyponatraemia, hyperkalaemia, raised creatinine and urea

84
Q

What is the diagnostic test for adrenal insufficiency?

A

Short synacthen test

Cortisol levels should at least double following dose of synthetic ACTH, does not happen in adrenal insufficiency

85
Q

What is the management for adrenal insufficiency?

A

Hydrocortisone (glucocorticoid) and fludrocortisone (mineralocorticoid) lifelong

86
Q

How does adrenal crisis present?

A

Reduced consciousness, hypotension, hypoglycaemia, hyponatraemia and hyperkalaemia

87
Q

What is the management of adrenal crisis?

A

ABCDE
IM/IV hydrocortisone (do not need fludrocortisone)
IV fluids
Correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance

88
Q

What is the pathophysiology of diabetes insipidus?

A

Lack of ADH (cranial) or lack of response to ADH (nephrogenic)

ADH stimulates water reabsorption from the collecting ducts in the kidneys

89
Q

What are the causes of nephrogenic diabetes insipidus?

A

Lithium, genetic, hypercalcaemia, hypokalaemia, kidney diseases

90
Q

What are the causes of cranial diabetes insipidus?

A

Brain tumours, brain injury, brain surgery, brain infection, genetic mutations

91
Q

What are the symptoms of diabetes insipidus?

A

Polyuria, polydipsia, dehydration, postural hypotension

92
Q

What is the diagnostic test for diabetes insipidus and what are the results for each type?

A

Water deprivation test - water deprivation for 8 hours, then low dose ADH

In primary polydipsia - urine osmolality will be high after water deprivation

In cranial DI - initially urine osmolality is low as it continues to be diluted by excessive water but after ADH is given the urine osmolality is high

In nephrogenic DI - patient is unable to respond to ADH and urine osmolality will be low both times

93
Q

What is the management for diabetes insipidus?

A

Underlying cause should be treated

Desmopressin can be used in cranial diabetes insipidus

For nephrogenic - ensuring plenty of water, high dose desmopressin, thiazide diuretics, NSAIDs

94
Q

What is the pathophysiology of SIADH?

A

Increased release of ADH from the posterior pituitary which increases water reabsorption from the urine diluting the blood and leading to hyponatraemia

95
Q

What are the causes of SIADH?

A

Increased secretion from posterior pituitary or ectopic ADH

Post operative, lung infection, brain pathologies, SSRIs, carbamazepine, HIV, SCLC

96
Q

What symptoms are associated with SIADH?

A

Headache, fatigue, muscle aches and cramps, confusion, severe hyponatraemia

97
Q

How is SIADH treated?

A

Fluid restriction, treat any underlying cause, tolvaptan can be used, sodium is corrected slowly to prevent osmotic demyelination (no more than 10mmol/l in 24 hours)

98
Q

What are the causes of hypokalaemia?

A

Vomiting, diarrhoea, thiazide and loop diuretics, cushing’s, conn’s, magnesium deficiency

99
Q

What ECG changes are associated with hypokalaemia?

A

U waves, small or absent T waves, prolonged PR interval, ST depression

100
Q

What is the management for hypokalameia?

A

Fluids replacement with potassium, may need cardiac monitoring

101
Q

What is primary hypoparathyroidism and how is it managed?

Including whether calcium, phosphate and PTH are high/low/normal

A

Decrease in PTH secretion e.g. secondary to thyroid surgery

Low calcium, high phosphate, low PTH

Manage with alfacalcidol

102
Q

What symptoms are associated with hypocalcaemia?

A

Muscle twitching, cramping and spasm, perioral paraesthesia, Trosseau’s sign, Chvostek’s sign

103
Q

What is pseudohypoparathyroidism?

Including whether calcium, phosphate and PTH are high/normal/low

A

Target cells being insensitive to PTH
Low calcium, high phosphate, high PTH

104
Q

How does PTH increase blood calcium levels?

A

Increasing osteoclast activity in the bones, increasing calcium reabsorption in the kidneys, increasing vitamin D activity resulting in increased calcium absorption in the intestines

105
Q

What are the symptoms associated with hypercalcaemia?

A

Kidney stones, painful bones, abdominal groans (constipation, N+V), psychiatric moans (fatigue, depression)

106
Q

What is primary hyperparathyroidism and how is it managed?

A

Caused by uncontrolled PTH production by a tumour of the parathyroid glands –> hypercalcaemia

Remove tumour surgically

107
Q

What is secondary hyperparathyroidism and how is it managed?

A

Insufficient vitamin or CKD –> reduced calcium absorption from the kidneys/intestines and bones

Hypocalcaemia so more PTH excreted

Low calcium, high PTH

Treatment = correct underlying vitamin D deficiency

108
Q

What is a pheochromocytoma?

A

Tumour of the chromaffin cells that secretes unregulated and excessive amounts of adrenaline

109
Q

What genetic conditions are associated with neuroendocrine tumours?

A

Multiple endocrine neoplasia type 2, neurofibromatosis type 1, Von Hippel-Lindau disease

110
Q

What investigations of done for pheochromocytoma?

A

Plasma free metanephrines and 24 hour urine catecholamines

111
Q

What is the treatment of pheochromocytoma?

A

Alpha blockers, beta blockers and surgical removal of tumour

112
Q

What is the first line treatment for prolactinoma?

A

1st line = dopamine agonists e.g. cabergoline
2nd line = trans-sphenoidal surgery

113
Q

Other than diabetes and diabetes insipidus what can cause polyuria and polydipsia?

A

Hypercalcaemia

114
Q

How does Conn’s syndrome present?

A

Hypertension and hypokalaemia

Finals (21 decks)

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