Endocrinology Flashcards

1
Q

underlying pathology of Cushing’s syndrome

A

excessive cortisol

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2
Q

causes of Cushing’s syndrome (4)

A

1- Exogenous steroids
2- Pituitary Adenoma
3- Adrenal Adenoma
4- Paraneoplastic (e.g. Small Cell Lung Cancer)

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3
Q

Conditions that can be caused by Cushing’s syndrome (4)

A

1- Hypertension
2- T2DM
3- Depression
4- Osteoporosis

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4
Q

Diagnostic test for Cushing’s syndrome

A

Dexamethasone Suppression Test

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5
Q

Primary Adrenal Insufficiency- pathology

A

damaged adrenal glands cause decreased secretion of Cortisol and Aldosterone

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6
Q

Secondary adrenal insufficiency- pathology

A

decreased ACTH from the pituitary causes decreased steroid secretion

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7
Q

tertiary adrenal insufficiency

A

decreased CRH from the Hypothalamus causes decreased ACTH secretion from the pituitary which causes decreased steroid secretion from the adrenal glands

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8
Q

clinical features specific to Grave’s disease (3)

A

1- Exopthalmos (pictured)
2- diffuse goitre (no nodules)
3- Pretibial Myxoedema

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9
Q

Symptomatic treatment of Grave’s disease

A

Propranolol

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10
Q
  1. First line treatment option for Grave’s disease
  2. Other treatment options
A
  1. Carbimazole
  2. Propylthiouracil
  3. Radioactive Iodine
  4. Surgery
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11
Q

antibodies associated with Hashimoto’s Thyroiditis

A

Anti-TPO Antibodies (antithyroid peroxidase)
Antithyroglobulin antibodies

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12
Q

medications that can cause hypothyroidism

A

Lithium
Amiodarone
Bromocriptine / Ocreotide

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13
Q

treatment of hypothyroidism

A

Levothyroxine

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14
Q

criteria for acute diagnosis of ketoacidosis

A

1- Ketones (<3)
2- hyperglycaemia (<11)
3- Acidosis (pH<7.3)

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15
Q

Initial management of ketoacidosis

A

FIG PICK

Fluids
Insulin (fixed rate 0.1 units/kg/hr)
Glucose (monitor blood glucose and add dextrose if below certain level e.g. 14mmol/l)
Potassium (monitor 4hrly and correct as required)
Infection (treat underlying causes like infection)
Chart fluid balance
Ketone monitoring (monitor ketones or blood bicarbonate if ketones are unavailable)

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16
Q

initial blood test for Acromegaly

A

Insulin-like growth factor (IGF-1)

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17
Q

options for blocking growth hormone (in Acromegaly)

A
  • GH antagonist (i.e. Pegvisomant)
  • Somatostatin analogs (e.g. Ocreotide)
  • Dopamine agonists (e.g. Bromocriptine)
18
Q

how does PTH increase serum calcium? (4)

A

1- increased osteoclast activity in bones
2- increased calcium absorption in Kidneys
3- increased vit D activity
4- increased gut absorption of calcium

19
Q

Primary Hyperparathyroidism:
1- PTH level
2 - Ca2+ level
3- Phosphate

A

1- PTH elevated
2- Ca2+ elevated
3- Phosphate low

20
Q

Secondary hyperparathyroidism:
1- PTH level
2- Ca2+ level
3- Phosphate level
4- Vit D level

A

1- PTH elevated
2- Ca2+ low or normal
3- Phosphate elevated
4- Vit D low

21
Q

tertiary hyperparathyroidism:
1- PTH level
2- Ca2+ level
3- Phosphate level
4- Vit D level
5- ALP level

A

1- PTH elevated
2- Ca2+ normal or high
3- phosphate decreased or normal
4- vit D normal or decreased
5- ALP elevated

22
Q

primary causes of Conn’s (primary hyperaldosteronism)

A

1- adrenal adenoma
2- bilateral adrenal hyperplasia

23
Q

secondary causes of hyperaldosteronism (3)

A
  • renal artery stenosis
    2- renal artery obstruction
    3- heart failure
24
Q

test to distinguish primary and secondary hyperaldosteronism

A

Renin:
- Primary (Conn’s): decreased Renin
- Secondary hyperaldoseronism: increased Renin

25
Q

Findings in Conn’s syndrome (3)

A
  • Hypertension
  • Hypokalaemia
  • Alkalosis on ABG
26
Q

Treatment options for Conns if caused by:
1- adrenal adenoma
2- bilateral adrenocortical hyperplasia

A

1- Surgery

2- aldosterone antagonist e.g. Spironolactone or Eplerenone

27
Q

cancer associated with ectopic ADH

A

small cell lung cancer

28
Q

sodium level in SIADH

A

Hyponatraemia

29
Q

Treatment- SIADH

A
  • Fluid restriction
  • ADH Receptor blockers (e.g. Tolvaptan)
30
Q

concern with rapid changes in blood sodium when correcting SIADH

A

Central Pontine Myelinolysis- In CPM, a rapid increase of sodium to correct low sodium levels (hyponatremia) damages nerve cells.

31
Q

Endocrine causes of hyponatraemia

A
  • SIADH
  • Adrenal Insufficiency
32
Q

common medications that cause hyponatraemia (4)

A

1- Diuretics
2- SSRIs
3- NSAIDs
4- Carbemazepine

33
Q

Diabetes insipidus:
1- Serum osmolality
2- urine osmolality

A

1- serum osmolality high
2- urine osmolality low

34
Q

diabetes insipidus- diagnostic test

A

water deprivation test (no water for 8 hours + measure urine osmolality –> give desmopressin –> 8hrs later measure urine osmolality again)

35
Q

how to differentiate between cranial and nephrogenic diabetes insipidus?

A

water deprivation test:

-Cranial:
after deprivation: urine osmolality low
after synthetic ADH (Desmopressin): urine osmolality high

  • Nephrogenic:
    after deprivation: urine osmolality low
    after synthetic ADH (Desmopressin): urine osmolality low
36
Q

medical treatment of diabetes insipidus

A

Desmopressin

37
Q

cells affected in phaechromocytoma

A

chromaffin cells in the adrenal medulla (which release adrenaline and noradrenaline)

38
Q

genetic condition associated with Phaechromocytoma

A

Multiple Endocrine Neoplasia Type 2 (MEN2)

39
Q

initial test options for Phaechromocytoma

A
  1. Plasma free metanephrines
  2. 24 hour urinary metanephrines
40
Q

management of phaechromocytoma

A
  • Alpha blockers e.g. phenoxybenzamine
  • beta blockers (after alpha blockers)
  • adrenalectomy to remove the tumour