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Finals > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is acromegaly and what are the causes?

A

In acromegaly there is excess growth hormone secondary to a pituitary adenoidal in over 95% of cases. A minority of cases are caused by ectopic GHRH or GH production by tumours.

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2
Q

What are the features of acromegaly?

A

Coarse facial appearance, spade like hands, increase in shoe size
Large tongue, prognathism, interdental spaces
Excessive sweating and oily skin
Features of pituitary tumour (hypopituitarism, headaches, bitemporal hemianopia)
Raised prolactin
6% patients have MEN-1

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3
Q

What are the complications of acromegaly?

A 
Hypertension
Diabetes
Cardiomyopathy
Colorectal cancer
Pseudogout
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4
Q

What are the investigations of acromegaly?

A

Insulin-like-growth-factor 1 (IGF-1) is the initial screening test (raised)
Oral glucose tolerance test (glucose normally suppresses growth hormone)
MRI brain for pituitary tumour

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5
Q

What are the treatments for acromegaly?

A

Trans-sphenoidal surgery for pituitary tumour

Medications that block growth hormone:

  1. Pegvisomant
  2. Somatostatin analogues
  3. Dopamine agonists
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6
Q

What is De Quervain’s thyroiditis?

A

Subacute thyroiditis is thought to occur following viral infection and typically presents with hyperthyroidism

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7
Q

What are the four phases of de quervain’s thyroiditis?

A
  1. Hyperthyroidism, painful goitre, raised ESR
  2. Euthyroid
  3. Hypothyroidism
  4. Thyroid structure and function back to normal
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8
Q

What is the investigation for De quervain’s thyroiditis?

A

Thyroid scintigraphy: globally reduced uptake of iodine-131

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9
Q

What is the management of de quervain’s thyroiditis?

A

Usually self-limiting
Aspirin or other NSAIDs for pain
Maybe steroids if severe

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10
Q

What is the difference between the different types of multiple endocrine neoplasia (MEN)?

A

MEN I: Parathyroid, Pituitary, Pancreas (also adrenal and thyroid)

MEN II: Parathyroid, Phaeochromocytoma

MEN III: Phaeochromocytoma

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11
Q

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

A

Cushing’s syndrome is used to refer to the signs and symptoms that develop after prolonged abnormal elevation of cortisol.

Cushing’s disease is used to refer to the specific condition where a pituitary adenoma secretes excessive ACTH.

Cushing’s disease causes a Cushing’s syndrome but not all Cushing’s syndrome is caused by Cushing’s disease.

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12
Q

What are the features of Cushing’s syndrome?

A

Round in the middle with thin limbs:
Round moon face
Central obesity
Proximal limb muscle wasting

High levels of stress hormone:
Hypertension
Cardiac hypertrophy
T2DM
Depression
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13
Q

What causes Cushing’s syndrome?

A

Exogenous steroids
Cushing’s disease
Adrenal adenoma
Paraneoplastic Cushing’s

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14
Q

How is the dexamethasone suppression test used in Cushing’s syndrome?

A 
Low dose (1mg):
Low cortisol = normal
High/normal cortisol = Cushing’s syndrome 
High dose (8mg) to find out the cause:
Low cortisol = Cushing’s disease (pituitary adenoma)
High/normal cortisol + ACTH low = adrenal Cushing’s
High/normal cortisol + ACTH high = ectopic ACTH
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15
Q

What are some other investigations of Cushing’s syndrome other than the dexamethasone suppression test?

A 
24 hour urinary free cortisol 
FBC
MRI brain for pituitary adenoma
Chest CT for small cell lung cancer
Abdominal CT for adrenal tumours
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16
Q

What is the treatment for Cushing’s syndrome?

A

Trans-sphenoid also removal of pituitary adenoma
Surgical removal of adrenal tumour
Surgical removal of tumour producing ectopic ACTH

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17
Q

What is Addison’s disease?

A

Refers to a specific condition where the adrenal glands have been damaged, resulting in reduced secretion of cortisol and aldosterone.

Also called primary adrenal insufficiency

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18
Q

What is the cause of Addison’s disease?

A

Most common cause is autoimmune

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19
Q

What are the features of Addison’s disease?

A

Lethargy, weakness, anorexia, N+V, weight-loss
Bronze Hyperpigmentation (especially palmer creases)
Hyponatraemia and hyperkalaemia

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20
Q

What is the investigation for Addison’s disease?

A

Definitive: ACTH stimulation test (short Synacthen test)

Synthetic ACTH (Synacthen) is given and blood cortisol is measured at baseline, 30 mins and 60 mins.
In healthy people, the adrenal glands should produce at least double cortisol in response to synacthen. 
Failure of cortisol to rise indicates Addison’s
U+E (hyponatraemia and hyperkalaemia)
Blood glucose (Hypoglycaemia) 
Low cortisol
Low aldosterone
High renin
High ACTH
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21
Q

What is the management of Addison’s disease?

A

Hydrocortisone and fludrocortisone hormones are used to replace cortisol and aldosterone respectively.

IV hydrocortisone in addisonian crisis

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22
Q

What are the sick day rules for Addison’s disease?

A

Dose of steroid increased
Blood sugar monitored
IM injection of steroid for D+V

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23
Q

What are the different types of hyperthyroidism?

A

Primary: due to thyroid itself producing excessive thyroid hormones. E.g. Graves is due to an autoimmune condition where TSH receptor antibodies are produced - they mimic TSH.

Secondary: where there is excessive TSH due to pathology in hypothalamus or pituitary

Toxic multinodular goitre: where nodules develop on the thyroid gland that act independently of the normal feedback system and continuously produce excessive thyroid hormone

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24
Q

What are the causes of hyperthyroidism?

A

Grave’s disease
Toxic multinodular goitre
Solitary toxic thyroid nodule
Thyroiditis (e.g. de quervain’s, hashimotos)

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25
Q

What are the unique features of grave’s disease?

A

Diffuse goitre (without nodule)
Grave’s eye disease
Bilateral exopthalmos
Pretibial myxoedema

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26
Q

What are the unique features of toxic multinodular goitre?

A

Goitre with firm nodules
Most patients are over 50
Second most common cause of thyrotoxicosis after graves

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27
Q

What is the management of hyperthyroidism?

A

Carbimazole: First line
Complete remission and the ability to stop taking carbimazole is usually achieved within 18 months of treatment

Propylthiouracil: Second-line

Radioactive iodine

Beta blockers

Surgery: definitive treatment
Will need levothyroxine afterwards

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28
Q

What are the causes of hypothyroidism?

A

Hashimoto’s thyroiditis:

  • associated with anti-TPO antibodies and antithyroglobulin antibodies
  • most common in developed world

Iodine deficiency
- most common in developing world

Secondary to hyperthyroidism treatment

Medications:
Lithium or amiodrone

Secondary hypothyroidism causes:
- tumours, infection, vascular, radiation

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29
Q

What are the presentation and features of hypothyroidism?

A 
Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention
Heavy or irregular periods
Constipation
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30
Q

What are the investigations for hypothyroidism?

A

Primary: High TSH and low T3/4
Secondary: Low TSH and low T3/4

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31
Q

What is the management of hypothyroidism?

A

Oral levothyroxine.

Measure TSH levels monthly until stable.

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32
Q

What is type 1 diabetes mellitus?

A

Where the pancreas stops being able to produce insulin.

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33
Q

What is the triad of of diabetic ketoacidosis?

A

Ketoacidosis, Dehydration and potassium imbalance

34
Q

Describe the presentation of DKA

A 
Polyuria
Polydipsia 
N+V
Acetone smell to breath
Dehydration and subsequent hypotension
Altered consciousness
35
Q

What is the management of DKA?

A

FIG-PICK

Fluids (normal saline 1L stat, then 4L with added potassium over 12hr)
Insulin (Actrapid at 0.1unit/kg/hr)
Glucose (monitor and add dextrose infusion if low)
Potassium (monitor and correct as required)
Infection (treat underlying infection)
Chart (fluid balance)
Ketones (monitor)

36
Q

What is the long term management of type 1 diabetes?

A

Usually prescribed as a combination of background long acting insulin given once a day and a short acting insulin injected 30 mins before intake of carbs at meals

Injecting into the same site can can lipdystrophy so patients should cycle their injection sites

37
Q

What is T2DM?

A

Repeated exposure to glucose and insulin makes the beta cells of the pancreas become fatigued and damaged resulting in chronic hyperglycaemia.

38
Q

What are the risk factors for T2DM?

A

Non-modifiable:

  • older age
  • ethnicity (black, Chinese, south Asian)
  • family history

Modifiable:

  • obesity
  • sedentary lifestyles
  • high carbs
39
Q

What is an oral glucose tolerance test?

A

Performed in the morning prior to having breakfast. It involves taking a baseline fasting plasma glucose result, giving 75g glucose drink and then measuring plasma glucose 2 hours later.

It tests the body’s ability to deal with carbohydrate meal

40
Q

What is the pre-diabetes diagnosis?

A

HbA1c 42-47mmol/mol
Impaired fasting glucose 6.1-6.9mmol/l
Impaired glucose tolerance: at 2 hours 7.8-11.1mmol/l

41
Q

What is the criteria for a diabetic diagnosis?

A

HbA1c >48mmol/mol
Random glucose >11mol/l
Fasting glucose >7mmol/l
OGTT 2 hour result >11mmol/l

42
Q

What is the treatment targets for T2DM?

A

48mmol/mol for new T2DM

53mmol/mol for diabetics that have moved beyond metformin alone

43
Q

What is the medical management of T2DM?

A

Metformin: first-line

Second line add: sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor

Third line: triple therapy with metformin and 2 second line drugs or metformin and insulin

44
Q

Give the mechanism of action and notable side effects of metformin

A

Increases insulin sensitivity and decreases liver production of glucose

SE:
Diarrhoea and abdominal pain
Lactic acidosis

45
Q

Give the mechanism of action and notable side effects of pioglitazone

A

Increases insulin sensitivity and decreases liver production of glucose

SE:
Weight gain
Fluid retention
Anaemia
HF
46
Q

Give the mechanism of action and notable side effects of sulfonylurea

A

Stimulate insulin release from pancreas

SE:
Weight gain
Hypoglycaemia

47
Q

Describe the mechanism of action of the parathyroid hormone

A

Chief cells in the parathyroid glands produce parathyroid hormone in response to hypocalcaemia.

PTH acts to raise blood calcium by:

  1. increasing osteoclast activity
  2. increasing calcium absorption from gut
  3. increasing calcium absorption from kidneys
  4. increasing vit d activity.
48
Q

What are the symptoms of hypercalcaemia

A

Renal stones
Painful bones
Abdominal groans (constipation, N+V)
Psychiatric moans (fatigue, depression and psychosis)

49
Q

Give the cause, presentation and treatment of primary hyperparathyroidism.

A

Caused by uncontrolled parathyroid hormone produced directly by a tumour of the parathyroid gland.

Leads to hypercalcaemia

Treated by surgically removing the tumour.

50
Q

Give the cause, presentation and treatment of secondary hyperparathyroidism.

A

Where insufficient vit D or Chronic renal failure leads to low absorption of calcium leading to hypocalcaemia.

Parathyroid glands reacts to low calcium by making more PTH.

Treated by correcting vit D deficiency or performing a renal transplant

51
Q

Give the cause, presentation and treatment of tertiary hyperparathyroidism.

A

When secondary hyperparathyroidism continues for a long period of time.

Persistent high PTH leads to more absorption of calcium thus hypercalcaemia and high PTJ

Treated by surgically removing part of parathyroid tissue

52
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism - when adrenal glands are directly responsible for producing too much aldosterone.

Renin will be low

53
Q

What are the causes for hyperaldosteronism?

A

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

54
Q

What are the investigations and findings for hyperaldosteronism?

A

Screening tool: renin/aldosterone ratio:

  • High aldosterone and low renin = Conn’s
  • High aldosterone and high renin = secondary hyperaldosteronism

Hypertension
Hypokalaemia
Alkalosis

If high aldosterone then CT/MRI to look for adrenal tumour

55
Q

What is the management for hyperaldosteronism?

A

Aldosterone antagonists:
Eplerenone
Spironolactone

Treat underlying cause:
surgical removal of adenoma
Renal artery angioplasty

56
Q

Define diabetes insipidus

A

A lack of ADH or a lack of response to ADH.

This prevents the kidneys from concentrating urine leading to polyuria and polydipsia.

Can be classified as nephrogenic or cranial.

57
Q

What is nephrogenic diabetes insipidus and the causes

A

When the collecting ducts of the kidneys don’t respond to ADH

Causes:

  • Drugs e.g. lithium
  • Mutations in the AVPR2 gene
  • Intrinsic kidney disease
  • Hypokalaemia and hypercalcaemia
58
Q

What is cranial diabetes insipidus and the causes

A

When the hypothalamus does not produce ADH for the pituitary gland to secrete

Causes:

  • idiopathic
  • brain tumours
  • head injury
  • brain malformations
  • brain infections
  • brain surgery
59
Q

What is the presentation of diabetes insipidus?

A 
Polyuria
Polydipsia
Dehydration
Postural hypotension
Hypernatraemia
60
Q

What are the investigations for diabetes insipidus?

A

Low urine osmolality
High serum osmolality
Water deprivation test (desmopressin stimulation test)

61
Q

What does the water deprivation test (desmopressin) show for diabetes insipidus?

A

Cranial DI:

  • patient lacks ADH but kidneys are still able to respond to ADH
  • initially, urine osmolality will be low
  • after Desmopressin, urine osmolality will be high

Nephrogenic DI:

  • patient is unable to respond to ADH
  • urine osmolality will start low
  • stay low even after desmopressin

Primary polydipsia:
- urine osmolality will be high even before despopressin

62
Q

What is the management of diabetes insipidus?

A

Treat underlying cause.

Cranial: Desmopressin
Nephrogenic: Thiazide diuretics

63
Q

What is the pathophysiology of a pheochromocytoma?

A

It is a tumour of the chromaffin cells which produce adrenaline. Results in bursts of excessive adrenaline production

10% bilateral
10% cancerous
10% outside the adrenal gland

64
Q

What is the diagnosis of pheochromocytoma?

A

24 hour urine catecholamines

Plasma free metanephrines

65
Q

What is the presentation of pheochromocytoma?

A 
Anxiety
Sweating
Headache
Hypertension
Palpitations, tachycardia and paroxysmal AF
66
Q

What is the management of pheochromocytoma?

A
  1. Alpha blockers (i.e. phenoxybenzamine)
  2. Beta blockers
  3. Adrenalectomy
67
Q

How does hyperprolactinaemia cause hypogonadotrophic hypogonadism?

A

High prolactin levels act on the hypothalamus to prevent release of GnRH.

Without GnRH, there is no release of LH and FSH.

This causes hypogonadotropic hypogonadism. 30% women have galactorrhea

68
Q

What is the cause of hyperprolactinaemia?

A

Pituitary adenoma secreting prolactin.

69
Q

What is the diagnosis of hyperprolactinaemia

A

CT or MRI scan of the brain

70
Q

What is the treatment of hyperprolactinaemia?

A

Often no treatment is required.

Dopamine agonists such as bromocriptine or cabergoline can be used to reduce prolactin production

71
Q

What is a complication of addison’s disease?

A

Premature menopause

72
Q

What are the features of metabolic syndrome?

A

3 or more of the following:

Increased waist circumference
BMI >30
Increased triglyceride 
Low HDL
Hypertension
High glucose
High insulin
73
Q

Which hormones are released from the anterior pituitary?

A

FLAT PEG

FSH
LH
ACTH
TSH

Prolactin
Endorphins
Growth hormone

74
Q

Which hormones are released by the posterior pituitary?

A

ADH (vasopressin)

Oxytocin

75
Q

What is the pathophysiology of graves disease?

A

Antibody directed against the thyroid stimulating hormone receptor

76
Q

What is the treatment of a thyrotoxic storm?

A

Propylthiouracil
Beta blockers
Hydrocortisone

77
Q

What does the HbA1c have to be before starting second T2DM drug?

A

> 58mmol

78
Q

Which diabetes drug can be used in CKD for T2DM?

A

DPP4

79
Q

How do you treat a hypo first line?

A

20% glucose by IV infusion

80
Q

What is used to distinguish Types 1 and 2 diabetes?

A

C-peptide and specific diabetic antibodies such as anti-GAD

C-peptide will be low in type 1 as they are produced alongside insulin by the body

Finals (20 decks)

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