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Finals HH > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Px of Cushing’s disease?

A
  • Moon face
  • Central obesity
  • Abdominal striae
  • Buffalo hump
  • Proximal muscle wasting
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2
Q

Px of Acromegaly?

A

Bitemporal hemianopia +

  • Large nose & tongue
  • Thick, soft tissue
  • Prominent forehead
  • Profuse sweat
  • Skin-tags
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3
Q

Px of Prolactinoma?

A
  • Galactorrhoea
  • Menstrual irregularity
  • Infertility
  • Impotence
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4
Q

Causes of cushing’s syndrome pneomnonic?

A

CAPE

C - Cushing’s disease (pituitary adenoma)
A - Adrenal adenoma
P - Paraneoplastic syndrome
E - Exogenous steroids

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5
Q

Most common cause of paraneoplastic syndrome causing cushing’s?

A

Small cell lung cancer -> ectopic ACTH

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6
Q

Ix for cushing’s syndrome?

A

Dexamethasone suppression test
- Low dose overnight
- Low dose 48hr
- High dose 48hr

24hr urinary free cortisol

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7
Q

What do the results of a high dose 48hr dexamethasone suppression test indicate in sus[ected Cushing’s syndrome?

A

Cortisol will be suppressed in a pituitary adenoma (cushing’s disease)

Cortisol will not be suppressed in an adrenal adenoma or ectopic ACTH

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8
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

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9
Q

What drug can be used to reduce the production of cortisol?

A

Metyrapone

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10
Q

Ix for acromegaly?

A

Serum IGF1 elevated
Glucose tolerance test - normally would suppress GH
MRI pituitary

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11
Q

Drugs used in acromegaly when surgery not suitable?

A
  • GH antagonist (Pegvisomant)
  • Somatostatin analogue (Sandostatin LAR)
  • Dopamine agonist (cabergoline)
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12
Q

What are prolactinomas associated with?

A

Multiple endocrine neoplasia (MEN) type 1 (AD)

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13
Q

Drug Mx of prolactinomas?

A

Dopamine agonists - bromocriptine, cabergoline

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14
Q

The surgical management of pituitary adenoma?

A

Trans-sphenoidal removal of pituitary adenoma

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15
Q

Causes of nephrogenic diabetes inspidus?

A

Medications - lithium
Genetic
Kidney disease
Hypercalcaemia
Hypokalaemia

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16
Q

Urine and serum osmolality in diabetes insipidus?

A

Low urine osmolality (lots of water diluting the urine)

High/normal serum osmolality (water loss may be balanced by increased intake)

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17
Q

Urine osmolality after water deprivation and after desmopressin in diabetes insipidus types?

A

After : Water deprivation Desmopressin

Cranial Low High

Nephrogenic Low Low

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18
Q

Drug Mx of cranial diabetes inspidus?

A

Desmopressin

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19
Q

What is SIADH?

A

Excessive ADH -> Excessive water reabsorption in collecting ducts -> hyponatraemia + more concentrated urine

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20
Q

What is Cushing’s disease and Addison’s?

A

Cushing’s disease is due to a pituitary adenoma -> excess cortisol

Addison’s is autoimmune destruction of adrenal glands -> reduced cortisol + reduced aldosterone

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21
Q

What is Sheehan syndrome?

A

Major post-partum haemorrhage causes avascular necrosis of the pituitary gland -> adrenal insufficiency

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22
Q

What is and causes tertiary adrenal insufficiency?

A

Hypothalamus decreases CRH output, often due to long-term exogenous steroid use

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23
Q

Causes of SIADH?

A

Increased secretion by posterior pituitary
Ectopic ADH (from small cell lung cancer)
Trauma - head injury or post-op surgery
Pulmonary - atypical pneumonia, abscess, TB

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24
Q

Urine and serum osmolality in SIADH?

A

Serum has no sodium and lots of water – low serum osmolality, low serum Na+

Urine has lots of sodium and no water – high urine osmolality, high urine Na+

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25
Q

Px of SIADH?

A

Headache
Fatigue
Muscle aches and cramps
Confusion

Severe hyponatraemia -> seizures + reduced conciousness

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26
Q

Causes of SIADH?

A

Post-operative
Drugs - SSRIs, Carbamazepine
Small cell lung cancer

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27
Q

Ix / Mx of SIADH?

A

Exclude malignancy + pulmonary cause
Fluid restriction
Vasopressin receptor antagonists (tolvaptan)

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28
Q

What are the two phases of central pontine myelinolysis?

A

o Phase 1 – confusion, headache, N&V

o Phase 2 – spastic quadriparesis, pseudobulbar palsy, cognitive changes due to pontine demyelination

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29
Q

Antibodies associated with Graves?

A

TSH receptor antibodies (TRAB)

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30
Q

Antibodies associated with Hashimoto’s?

A

Anti-thyroid peroxidase (anti-TPO) antibodies

Anti-thyroglobulin (anti-Tg) antibodies

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31
Q

Specific px of Grave’s?

A

Diffuse goitre
Bilateral exophthalmos (bulging eyes)
Peripheral myxoedema (shin becomes discoloured and waxy)
Thyroid acropachy (hand swelling and finger clubbing)

32
Q

Specific Px of toxic multi-nodular goitre?

A

Goitre with firm nodules
Age >50

33
Q

Hyper-thyroidism drug mx?

A
  1. Carbimazole
  2. Propylthiouracil
  3. Radioactive iodine

Symptomatic -> b-blockers

Definitive -> surgery

34
Q

TSH levels in thyroidism?

A
  • TSH T3&T4
    1 hyper L H
    2 hyper H/N H
    1 hypo H L
    2 hypo L/N L
35
Q

Cause of hypothyroidism?

A

Iodine deficiency
Hashimoto’s thyroiditis
Drugs - Lithium, amiodarone

Secondary causes - tumours, surgery, trauma, radiotherapy

36
Q

Mx of hypothyroidism?

A

Levothyroxine

37
Q

What is Conn’s syndrome?

A

Adrenal adenoma -> too much aldosterone

38
Q

What does aldosterone do?

A

Increase sodium reabsorption from the distal tubule
Increase potassium secretion from the distal tubule
Increase hydrogen secretion from the collecting ducts

39
Q

Causes of primary and secondary hyperaldosteronism?

A

Primary:
- Bilateral adrenal hyperplasia (most common)
- An adrenal adenoma secreting aldosterone (known as Conn’s syndrome)
- Familial hyperaldosteronism (rare)

Secondary (due to low BP in kidneys):
- Renal artery stenosis
- Heart failure
- Liver cirrhosis and ascites

40
Q

Hyperaldosteronism px?

A

Hypertension (resistant)
Non-specific - headaches, muscle weakness, fatigue
Low potassium (can be normal)

41
Q

Ix for hyperaldosteronism?

A

Aldosterone-to-renin ratio (ARR)
- High aldosterone and low renin indicate primary hyperaldosteronism

  • High aldosterone and high renin indicate secondary hyperaldosteronism
42
Q

Mx of high aldosterone?

A

Aldosterone antagonists - Eplerenone, spironolactone

Underlying cause - remove adenoma or angioplasty renal artery stenosis

43
Q

Px of adrenal insufficiency?

A

Bronze hyperpigmentation (excessive ACTH)
Hypotension

Fatigue, muscle weakness, weight loss, abdo pain, depression

44
Q

Biochemicals of adrenal insufficiency?

A

Low sodium
High potassium
High calcium

45
Q

Ix for adrenal insuficciency?

A

Short synacthen test (synthetic ACTH)

  • This causes cortisol to increase, failure of this indicates Addison’s disease or secondary adrenal atrophy
46
Q

Antibodies px in autoimmune adrenal insufficiency?

A

Adrenal cortex antibodies
21-hydroxylase antibodies

47
Q

Mx of adrenal insufficiency?

A

Hydrocortisone (replace cortisol)
Fludrocortisone (replace aldosterone)

48
Q

Px of adrenal crisis?

A

Reduced consciousness
Hypotension
Hypoglycaemia
Hyponatraemia and hyperkalaemia

49
Q

Mx of adrenal crisis?

A

ABCDE
IM / IV hydrocortisone
IV fluids
Correct hypoglycaemia (IV dextrose)
Monitor electrolytes and fluid balance

50
Q

What is a pheochromocytoma?

A

Adrenal gland tumour -> excessive catecholamines (adrenaline)

51
Q

Initial Ix of pheochromocytoma?

A

Plasma free metanephrines
24hr urine catecholamines

52
Q

Mx of pheochromocytoma?

A

Alpha blockers - phenoxybenzamine or doxazosin
Beta blockers (after alpha blockers established)
Surgical removal of tumour

53
Q

Px of pheochromocytoma?

A

Anxiety
Sweating
Hypertension
Tremor
Headache
Palpitation
Tachycardia

(Increased adrenaline)

54
Q

Severity of hypercalcaemia?

A

Mild 2.6 - 3.0
Moderate 3.01 - 3.40
Severe >3.4

55
Q

Px of hypercalcaemia

A

Bone pain
Fatigue, lethargy, muscle weakness
N&V
Rena colic
Constipation, abdo pain
Hypertension

56
Q

Most common 2 causes of hypercalcaemia?

A

Primary hyperparathyroidism
Malignancy

57
Q

What is primary hyperparathyroidism?

A

Due to a parathyroid tumour

58
Q

What is secondary hyperparathyroidism due to?

A

Low Vitamin D or CKD
-> Insufficient calcium absorption
-> High PTH

59
Q

What is tertiary hyperparathyroidism due to?

A

Parathyroid gland hyperplasia due to chronic secondary hyperparathyroidism

60
Q

First line diabetes management?

A

Metformin

61
Q

When should a Sulphonylureas be prescribed in diabetes?

A

Second or third line after metformin

First-line if metformin is not tolerated

62
Q

What is Sulphonylurea therapy is associated with?

A

Hypoglycaemia (caution should be taken in the elderly)
Weight gain

63
Q

How do sulphonylureas act?

A

Sulphonylureas increase endogenous release of insulin from pancreatic β-cells

64
Q

How does metformin act?

A

Complex

There is reduced production of glucose by the liver, weight loss or stabilisation, and improved insulin sensitivity

65
Q

What kind of drugs are gliclazide and glimepiride

A

Sulphonylureas

66
Q

What kind of drug is Pioglitazone?

A

Thiazolidinediones

67
Q

Risks of Pioglitazone? (5)

A

Peripheral oedema
Heart failure
Weight gain
Bladder cancer
Fractures.

68
Q

When can pioglitazone (Thiazolidinediones) be prescribed?

A

Pioglitazone should be considered, usually as dual or triple therapy, for lowering HbA1c

69
Q

When can DDP4 inhibitors be prescribed?

A

DPP-4 inhibitors should be considered, usually as dual or triple therapy, for lowering HbA1c.

70
Q

What are some DDP4 inhibitors?

A

-gliptins

Alogliptin, linagliptin, saxagliptin, sitagliptin and vildagliptin

71
Q

How do DDP4 inhitors work?

A

They inhibit the activity of the enzyme DPP-4 and hence
prolong the actions of endogenous GLP-1

72
Q

How do SGLT2 inhibitors work?

A

They reduce renal glucose re-absorption resulting in increased
glucose excretion equivalent to a net loss of 200–300 kcal/day

73
Q

What drugs can be prescribed as an add-on in T2DM patients with CVD?

A

SGLT2 inhibitors - empagliflozin and canagliflozin
GLP-1 receptor agonist - liraglutide

74
Q

When should GLP-1 agonists be considered?

A

BMI ≥30 in combination with oral glucose-lowering drugs or basal insulin (or both) as third- or fourth-line treatment

Alternative to insulin in people for whom treatment with combinations of oral glucose-lowering drugs has been inadequate.

75
Q

When should GLP-1 agonists be considered?

A

BMI ≥30 in combination with oral glucose-lowering drugs or basal insulin (or both) as third- or fourth-line treatment

Alternative to insulin in people for whom treatment with combinations of oral glucose-lowering drugs has been inadequate.

76
Q

How do GLP-1 agonists work?

A

Augments secretion of insulin from pancreatic
β-cells and inhibit inappropriate glucagon secretion.

Half-life of 2 minutes due to breakdown by DDP4

77
Q

How are GLP-1 receptor agonists administered?

A

Subcutaenous

Finals HH (21 decks)

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