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AKT > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Diagnosis of thyroid pathology from radioactive iodine scans.

A

Diffuse high uptake is found in Grave’s Disease
Focal high uptake is found in toxic multinodular goitre and adenomas
“Cold” areas (abnormally low uptake) can indicate thyroid cancer

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2
Q

Pretibial myxoedema

A

A skin condition caused by deposits of glycosaminoglycans under the skin on the anterior aspect of the leg (the pre-tibial area). It gives the skin a discoloured, waxy, oedematous appearance over this area. It is specific to Grave’s disease and is a reaction to TSH receptor antibodies.

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3
Q

Exophthalmos (also known as proptosis)

A

Describes the bulging of the eyes caused by Graves’ disease. Inflammation, swelling and hypertrophy of the tissue behind the eyeballs force them forward, causing them to bulge out of the sockets.

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4
Q

Thyroiditis causes

A

Initial period of hyperthyroidism, followed by under-activity of the thyroid gland (hypothyroidism). The causes of thyroiditis include:

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5
Q

Treatment for hyperthyroidism

A

Carbimazole is the first-line anti-thyroid drug, usually taken for 12 to 18 months. Once the patient has normal thyroid hormone levels (usually within 4-8 weeks), they continue on maintenance carbimazole and either:

The carbimazole dose is titrated to maintain normal levels (known as titration-block)

A higher dose blocks all production, and levothyroxine is added and titrated to effect (known as block and replace)

Beta blockers

Surgery

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6
Q

Risk of carbimazole

A

Acute pancreatitis

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7
Q

Most common cause of hypothyroidism

A

Iodine deficiency

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8
Q

Which drugs have side effects which can cause hypothyroidism?

A

Lithium inhibits the production of thyroid hormones in the thyroid gland and can cause a goitre and hypothyroidism.

Amiodarone interferes with thyroid hormone production and metabolism, usually causing hypothyroidism but can also cause thyrotoxicosis.

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9
Q

Does iodine deficiency cause a goitre?

A

Yes

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10
Q

Does Hashimoto’s cause a goitre?

A

Yes initially, then atrophy

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11
Q

Layers of the adrenal cortex and what they produce

A

Inner Zona reticularis - androgens
Middle Zona fasciculata - glucocorticoids (cortisol)
Outer Zona glomerulosa - mineralocorticoids (aldosterone)

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12
Q

Causes of Cushing’s syndrome

A

C - Cushing’s disease (a pituitary adenoma releasing excessive ACTH)
A – Adrenal adenoma (an adrenal tumour secreting excess cortisol)
P – Paraneoplastic syndrome (ACTH is released from a tumour somewhere other than the pituitary gland - small cell lung cancer most common)
E – Exogenous steroids (patients taking long-term corticosteroids)

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13
Q

Sign of Cushing’s disease which suggests excess production of ACTH

A

A high level of ACTH causes skin pigmentation by stimulating melanocytes in the skin to produce melanin

This sign is absent in an adrenal adenoma or exogenous steroids.

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14
Q

A normal response to dexamethasone vs in Cushing’s syndrome

A

Suppressed cortisol due to negative feedback.

Dexamethasone causes negative feedback on the hypothalamus, reducing the corticotropin-releasing hormone (CRH) output. It causes negative feedback on the pituitary, reducing the ACTH output. The lower CRH and ACTH levels result in a low cortisol output by the adrenal glands.

A lack of cortisol suppression in response to dexamethasone suggests Cushing’s syndrome.

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15
Q

Three types of dexamethasone suppression test

A

Low-dose overnight test (used as a screening test to exclude Cushing’s syndrome)

Low-dose 48-hour test (used in suspected Cushing’s syndrome)

High-dose 48-hour test (used to determine the cause in patients with confirmed Cushing’s syndrome)

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16
Q

Normal result for low-dose overnight dexamethasone suppression test

A

Suppressed cortisol

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16
Q

Normal result for low-dose overnight dexamethasone suppression test

A

Suppressed cortisol

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17
Q

When is ACTH low and high in different causes of Cushing’s

A

ACTH is suppressed due to negative feedback on the pituitary when excess cortisol comes from an adrenal tumour (or endogenous steroids).

It is high when produced by a pituitary tumour or ectopic ACTH (e.g., small cell lung cancer).

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18
Q

Nelson’s syndrome

A

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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19
Q

Conn’s syndrome

A

Adrenal adenoma producing too much aldosterone

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20
Q

What stimulates aldosterone release?

A

Angiotensin II

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21
Q

Serum renin in primary hyperaldosteronism

A

Adrenal produces too much aldosterone, renin will be low because blood pressure rises and suppresses it

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22
Q

Causes of primary hyperaldosteronism (3)

A

Bilateral adrenal hyperplasia (most common)

An adrenal adenoma secreting aldosterone (known as Conn’s syndrome)

Familial hyperaldosteronism (rare)

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23
Q

Causes and pathology of secondary hyperaldosteronism

A

Secondary hyperaldosteronism is caused by excessive renin stimulating the release of excessive aldosterone.

Excessive renin is released due to disproportionately lower blood pressure in the kidneys, usually due to:

Renal artery stenosis
Heart failure
Liver cirrhosis and ascites

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24
Q

Screening test for hyperaldosteronism

A

Aldosterone to renin ration

High aldosterone and low renin indicate primary hyperaldosteronism

High aldosterone and high renin indicate secondary hyperaldosteronism

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25
Q

Three investigations of hyperaldosteronism

A

CT or MRI to look for an adrenal tumour or adrenal hyperplasia

Renal artery imaging for renal artery stenosis (Doppler, CT angiogram or MR angiography)

Adrenal vein sampling of blood from both adrenal veins to locate which gland is producing more aldosterone

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26
Q

Treatment of hyperaldosteronism

A

Eplerenone
Spironolactone

Surgical removal of tumour

27
Q

Primary adrenal insufficiency

A

Do not produce enough aldosterone or cortisol, Addison’s disease, usually autoimmune

28
Q

Causes of secondary adrenal insufficiency

A

Reduced release of ACTH

Tumours (e.g., pituitary adenomas)
Surgery to the pituitary
Radiotherapy
Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland)
Trauma

29
Q

Tertiary adrenal insufficiency

A

Tertiary adrenal insufficiency results from inadequate corticotropin-releasing hormone (CRH) release by the hypothalamus.

This is usually the result of patients taking long-term oral steroids (for more than 3 weeks), causing suppression of the hypothalamus (via negative feedback).

Therefore, long-term steroids must be tapered slowly to allow the adrenal axis to regain normal function.

30
Q

Signs of adrenal insufficiency

A

Bronze hyperpigmentation of the skin, particularly in creases (ACTH stimulates melanocytes to produce melanin)

Hypotension (particularly postural hypotension – with a drop of more than 20 mmHg on standing)

31
Q

Biochemical findings in a patient with adrenal insufficiency

A

Hyperkalaemia (high potassium)
Hypoglycaemia (low glucose)
Raised creatinine and urea due to dehydration
Hypercalcaemia (high calcium)

32
Q

Short synacthen test

A

Synacthen is synthetic ACTH. The blood cortisol is checked before and 30 and 60 minutes after the dose. The synthetic ACTH will stimulate healthy adrenal glands to produce cortisol. The cortisol level should at least double. A failure of cortisol to double indicates either:

Primary adrenal insufficiency (Addison’s disease)

Very significant adrenal atrophy after a prolonged absence of ACTH in secondary adrenal insufficiency

33
Q

Treatment for patients with adrenal insufficiency

A

Hydrocortisone (a glucocorticoid) is used to replace cortisol. Fludrocortisone (a mineralocorticoid) is used to replace aldosterone, if aldosterone is also insufficient.

34
Q

Signs and symptoms of adrenal insufficiency

A

Reduced consciousness
Hypotension
Hypoglycaemia
Hyponatraemia and hyperkalaemia

35
Q

DKA three key features

A

Ketoacidosis
Dehydration
Potassium imbalance

36
Q

Reason for K+ imbalance in DKA and when treated with insulin

A

Insulin normally drives potassium into cells.

Without insulin, potassium is not added to and stored in cells.

The serum potassium can be high or normal as the kidneys balance blood potassium with the potassium excreted in the urine. However, total body potassium is low because no potassium is stored in the cells.

When treatment with insulin starts, patients can develop severe hypokalaemia (low serum potassium) very quickly, leading to fatal arrhythmias.

37
Q

Diagnosis of DKA requires

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)

38
Q

Treatment of DKA

A

F – Fluids – IV fluid resuscitation with normal saline (e.g., 1 litre in the first hour, followed by 1 litre every 2 hours)

I – Insulin – fixed rate insulin infusion (e.g., Actrapid at 0.1 units/kg/hour)

G – Glucose – closely monitor blood glucose and add a glucose infusion when it is less than 14 mmol/L

P – Potassium – add potassium to IV fluids and monitor closely (e.g., every hour initially)

I – Infection – treat underlying triggers such as infection

C – Chart fluid balance

K – Ketones – monitor blood ketones, pH and bicarbonate

39
Q

Hypoglycaemia causes in diabetic patients

A

This may be caused by too much insulin, not consuming enough carbohydrates or not processing the carbohydrates correctly, for example, in malabsorption, diarrhoea or vomiting

40
Q

Hypoglycaemia treatment

A

Hypoglycaemia needs to be treated initially with rapid-acting glucose (e.g., high sugar content drink).

Once the blood glucose improves, they consume slower-acting carbohydrates (e.g., biscuits or toast) to prevent it from dropping again. Options for treating severe hypoglycaemia are IV dextrose and intramuscular glucagon.

41
Q

Acanthosis nigricans

A

Thickening and darkening of the skin (giving a “velvety” appearance), often at the neck, axilla and groin. It is often associated with insulin resistance.

42
Q

HbA1c and diabetes diagnosis

A

A HbA1c of 42 – 47 mmol/mol indicates pre-diabetes.

A HbA1c of >48mmol/mol diagnoses T2D

43
Q

First, second and third line diabetes medications

A

First-line is metformin.

Once settled on metformin, add an SGLT-2 inhibitor (e.g., dapagliflozin) if the patient has existing cardiovascular disease or heart failure. NICE suggest considering an SGLT-2 inhibitor in patients with a QRISK score above 10%.

Second-line is to add a sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor.

Third-line options are:

Triple therapy with metformin and two of the second-line drugs
Insulin therapy (initiated by the specialist diabetic nurses)

44
Q

Metformin MOA

A

Metformin increases insulin sensitivity and decreases glucose production by the liver. It is a biguanide (the class of medication). It does not cause weight gain (and may cause some weight loss). It does not cause hypoglycaemia.

45
Q

Metformin side effects

A

Notable side effects of metformin:

Gastrointestinal symptoms, including pain, nausea and diarrhoea (depending on the dose)
Lactic acidosis (e.g., secondary to acute kidney injury)

46
Q

SGLT-2 inhibitors MOA

A

The sodium-glucose co-transporter 2 protein is found in the proximal tubules of the kidneys. It acts to reabsorb glucose from the urine back into the blood. SGLT-2 inhibitors block the action of this protein, causing more glucose to be excreted in the urine.

Loss of glucose in the urine lowers the HbA1c, reduces the blood pressure, leads to weight loss and improves heart failure.

47
Q

SGLT-2 inhibitors side effects

A

Glycosuria (glucose in the urine)

Increased urine output and frequency

Genital and urinary tract infections (e.g., thrush)

Weight loss

Diabetic ketoacidosis, notably with only moderately raised glucose

Lower-limb amputation may be more common in patients on canagliflozin (unclear if this applies to the others)

Fournier’s gangrene (rare but severe infection of the genitals or perineum)

48
Q

Name of most common sulfonylurea and method of action

A

Gliclazide

Sulfonylureas stimulate insulin release from the pancreas.

49
Q

Hyperosmolar hyperglycaemic state

A

Characterised by hyperosmolality (water loss leads to very concentrated blood), high sugar levels (hyperglycaemia) and the absence of ketones, distinguishing it from ketoacidosis.

It presents with polyuria, polydipsia, weight loss, dehydration, tachycardia, hypotension and confusion.

It is a medical emergency with high mortality. Involve experienced seniors early. Treatment is with IV fluids and careful monitoring.

50
Q

Carpal tunnel syndrome is commonly associated with

A

Acromegaly

51
Q

Primary hyperparathyroid

A

Primary hyperparathyroidism is 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.

52
Q

Secondary hyperparathyroid

A

Secondary hyperparathyroidism is where 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. The serum calcium level will be low or normal, but the parathyroid hormone will be high. Treatment is to correct the underlying vitamin D deficiency or chronic kidney disease (e.g., renal transplant).

53
Q

Tertiary hyperparathyroid

A

Tertiary hyperparathyroidism happens when 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. Then, when the underlying cause of the secondary hyperparathyroidism is treated, the baseline parathyroid hormone production remains inappropriately high. 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.

54
Q

Hashimoto’s is associated with which type of cancer

A

MALT lymphoma

55
Q

Insulin in treatment of DKA

A

In the acute management of DKA, insulin should be fixed rate whilst continuing regular injected long-acting insulin but stopping short actin injected insulin

56
Q

What type of drug is Dapaglifozin?

A

SGLT-2 inhibitor

57
Q

Current NICE guidance recommends referral for consideration of parathyroid surgery if a patient has one or more of the following…

A

Symptoms of hypercalcaemia (e.g. thirst, polyuria, constipation)
End-organ disease (renal calculi, fragility fractures or osteoporosis)
Corrected serum calcium of 2.85 mmol/L or above

58
Q

Important side effect of sulphonyureas like gliclazide

A

Hypoglycaemia

59
Q

What is Pioglitazone

A

Thiazolidinedione. It increases insulin sensitivity and decreases liver production of glucose. It does not typically cause hypoglycaemia.

60
Q

Notable side effects of pioglitazone include

A

Weight gain
Heart failure
Increased risk of bone fractures
A small increase in the risk of bladder cancer

61
Q

Treatment for toxic multinodular goitre

A

Radioiodine therapy is the appropriate treatment. Radioiodine is taken up by and ablates any autonomous nodules, leaving healthy tissue intact.

62
Q

PTH in hyperparathyroidism

A

PTH may be raised or (inappropriately, given the raised calcium) normal

63
Q

What is a drug used to treat hyperthyroidism?

A

Carbimazole

64
Q

Side effect of carbimazole

A

Myelosuppression

65
Q

High calcitonin is associated with which thyroid cancer.

A

Medullary thyroid cancer.

66
Q

Headaches, amenorrhoea, visual field defects →

A

Prolactinoma

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