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Endocrine Flashcards

1
Q

What are the types of thyroid cancer?

A

Papillary
Follicular
Medullary
Anaplastic
Lymphoma

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2
Q

Which the most common thyroid cancer?

A

Papillary -70% often young females

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3
Q

What type of medication causes proximal myopathy?

A

Corticosteroids may cause proximal myopathy

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4
Q

Which two conditions account for 90% of cases of hypercalcaemia:

A
  1. Primary hyperparathyroidism: commonest cause in non-hospitalised patients
  2. Malignancy: the commonest cause in hospitalised patients. This may be due to a number of processes, including;
    PTHrP from the tumour e.g. squamous cell lung cancer
    bone metastases
    myeloma,: due primarily to increased osteoclastic bone resorption caused by local cytokines (e.g. IL-1, tumour necrosis factor) released by the myeloma cells
    for this reason, measuring parathyroid hormone levels is the key investigation for patients with hypercalcaemia
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5
Q

Which drug causes hypercalicaemia?

A

Thiazides, calcium-containing antacids

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6
Q

What are other causes of hypercalcaemia?

A

sarcoidosis
other causes of granulomas may lead to hypercalcaemia e.g. tuberculosis and histoplasmosis
vitamin D intoxication
acromegaly
thyrotoxicosis
Milk-alkali syndrome
drugs:
thiazides
calcium-containing antacids
dehydration
Addison’s disease
Paget’s disease of the bone
usually normal in this condition but hypercalcaemia may occur with prolonged immobilisation

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7
Q

what acid-base imbalance would you expect in cushings syndrome?

A

hypokalaemic metabolic alkalosis. This patient is presenting with the classical features of Cushing’s syndrome: central adiposity, stretch marks, bruising, hirsutism and acne. The condition is caused by an excess of corticosteroids and has been probably exacerbated by the corticosteroid therapy for her adhesive capsulitis.

Cushing’s syndrome causes hypokalaemic metabolic alkalosis because when the levels of cortisol are high, the cortisol that is not inactivated by 11β-hydroxysteroid dehydrogenase is free to bind to mineralocorticoid receptors. This causes an increase in water and sodium retention, increased potassium excretion, and increased hydrogen ions excretion. Lower levels of hydrogen ions cause alkalosis and less potassium causes hypokalemia.

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8
Q

What are beginin causes of thyroid nodule?

A

Multinodular goitre
Thyroid adenoma
Hashimoto’s thyroiditis
Cysts (colloid, simple, or hemorrhagic)

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9
Q

Which drugs can induce neutrophilia?

A

Glucocorticoids

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10
Q

What is the best test to diagnose Addison’s disease?

A

ACTH stimulation test (short Synacthen test)

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11
Q

What is the first-line management in patients with hypercalcaemia?

A

IV fluids, saline

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11
Q

What is the management of hypercalcaemia?

A

The initial management of hypercalcaemia is rehydration with normal saline, typically 3-4 litres/day. Following rehydration bisphosphonates may be used. They typically take 2-3 days to work with maximal effect being seen at 7 days

Other options include:
calcitonin - quicker effect than bisphosphonates
steroids in sarcoidosis

Loop diuretics such as furosemide are sometimes used in hypercalcaemia, particularly in patients who cannot tolerate aggressive fluid rehydration. However, they should be used with caution as they may worsen electrolyte derangement and volume depletion.

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11
Q

What is the mechanism of action of empagliflozin?

A

SGLT-2 inhibitors reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule

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12
Q

What is mechanism of action of SGLT-2 inhibitors?

A

SGLT-2 inhibitors reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.

Examples include canagliflozin, dapagliflozin and empagliflozin.

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12
Q

What is the dietary advice for diabetes?

A

encourage high fibre, low glycaemic index sources of carbohydrates
include low-fat dairy products and oily fish
control the intake of foods containing saturated fats and trans fatty acids
limited substitution of sucrose-containing foods for other carbohydrates is allowable, but care should be taken to avoid excess energy intake
discourage the use of foods marketed specifically at people with diabetes
initial target weight loss in an overweight person is 5-10%

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12
Q

What are the adverse effects of SGLT-2 inhibitors?

A

Important adverse effects include
urinary and genital infection (secondary to glycosuria). Fournier’s gangrene has also been reported
normoglycaemic ketoacidosis
increased risk of lower-limb amputation: feet should be closely monitored

Patients taking SGLT-2 drugs often lose weight, which can be beneficial in type 2 diabetes mellitus.

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12
Q

What are the HbAc1 targets?

A

the average patient who is taking metformin for T2DM, you can titrate up metformin and encourage lifestyle changes to aim for a HbA1c of 48 mmol/mol (6.5%), but should only add a second drug if the HbA1c rises to 58 mmol/mol (7.5%)

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13
Q

Why is Raised total T3 and T4 but normal fT3 and fT4 normal in pregnancy?

A

suggest high concentrations of thyroid binding globulin, which can be seen during pregnancy

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13
Q

What is a side affect of Metoclopramide and why?

A

galactorrhoea.

Metoclopramide is a dopamine receptor antagonist, hence blocking its action. Dopamine normally acts as a natural inhibitor of prolactin release from the pituitary gland. By blocking dopamine receptors, metoclopramide interferes with this inhibitory effect. As a result, prolactin secretion is disinhibited, leading to an increase in circulating prolactin levels, causing galactorrhoea, and the release of breast milk.

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13
Q

What is an important side effect of sulfonylureas?

A

hypoglycaemia

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13
Q

What is the BMI classification?

A
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13
Q

What are the Important adverse effects of SGLT-2 inhibitors?

A

urinary and genital infection (secondary to glycosuria). Fournier’s gangrene has also been reported
normoglycaemic ketoacidosis
increased risk of lower-limb amputation: feet should be closely monitored

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14
Q

What is the treatment of MODY?

A

The treatment for MODY depends on the specific genetic subtype. For example, MODY2 often does not require specific treatment, as the hyperglycemia is mild and usually does not lead to complications. In contrast, MODY associated with HNF1A often respond well to treatment with low-dose sulfonylureas. Insulin therapy may be necessary in some cases, especially during pregnancy or if sulfonylureas are contraindicated or ineffective.

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15
Q

What is the typical presentation of subacute thyroiditis (de Quervain’s thyroiditis)?

A

hyperthyroidism associated with a tender goitre after an upper respiratory tract infection which is the typical presentation

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16
Q

What are the phases of subacute (De Quervain’s) thyroiditis?

A

There are typically 4 phases;
phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR
phase 2 (1-3 weeks): euthyroid
phase 3 (weeks - months): hypothyroidism
phase 4: thyroid structure and function goes back to normal

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17
Q

What are the investigations for subacute (De Quervain’s) thyroiditis?

A

thyroid scintigraphy: globally reduced uptake of iodine-131

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18
Q

What is the management of subacute (De Quervain’s) thyroiditis?

A

usually self-limiting - most patients do not require treatment
thyroid pain may respond to aspirin or other NSAIDs
in more severe cases steroids are used, particularly if hypothyroidism develops

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19
Q

What is Hyperosmolar Hyperglycaemic State ?

A

Hyperosmolar Hyperglycaemic State (HHS) is a life-threatening medical emergency that occurs primarily in individuals with type 2 diabetes mellitus. It is characterized by severe hyperglycemia, extreme dehydration, and a significant increase in plasma osmolality, without substantial ketosis or acidosis, which differentiates it from diabetic ketoacidosis (DKA).

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20
Q

What is the pathophysiology of Hyperosmolar Hyperglycaemic State ?

A

Insulin Deficiency: Relative insulin deficiency leads to hyperglycemia but is sufficient to suppress lipolysis and ketogenesis.

Osmotic Diuresis: Excess glucose is excreted in urine, pulling water and electrolytes along with it, leading to dehydration and electrolyte imbalances.

Increased Plasma Osmolality: The concentration of solutes in the blood rises, causing cellular dehydration and contributing to neurological symptoms.

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21
Q

What are the Precipitating factors of Hyperosmolar Hyperglycaemic State ?

A

intercurrent illness
dementia
sedative drugs

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22
Q

What are the clinical features of Hyperosmolar Hyperglycaemic State ?

A

whilst DKA presents within hours of onset, HHS comes on over many days, and consequently, the dehydration and metabolic disturbances may be more extreme
consequences of volume loss
clinical signs of dehydration
polyuria
polydipsia
systemic
lethargy
nausea and vomiting
neurological
altered level of consciousness
focal neurological deficits
haematological
hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)

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23
Q

What is the management of Hyperosmolar Hyperglycaemic State ?

A

fluid replacement
fluid losses in HHS are estimated to be between 100 - 220 ml/kg
IV 0.9% sodium chloride solution
typically given at 0.5 - 1 L/hour depending on clinical assessment
potassium levels should be monitored and added to fluids depending on the level
insulin
should not be given unless blood glucose stops falling while giving IV fluids
venous thromboembolism prophylaxis
patients are at risk of thrombosis due to hyperviscosity

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24
Q

What are the complications of Hyperosmolar Hyperglycaemic State ?

A

vascular complications may occur due to hyperviscosity:
such as myocardial infarction
stroke

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25
Q

What is the diagnostic criteria Hyperosmolar Hyperglycaemic State ?

A

There are no precise diagnostic criteria but the following are typically seen

hypovolaemia
marked hyperglycaemia (>30 mmol/L)
significantly raised serum osmolarity (> 320 mosmol/kg)
can be calculated by: 2 * Na+ + glucose + urea
no significant hyperketonaemia (<3 mmol/L)
no significant acidosis (bicarbonate > 15 mmol/l or pH > 7.3 - acidosis can occur due to lactic acidosis or renal impairment)

26
Q

Which patients should be followed up regularly by the local diabetic foot centre.

A

Low risk
* no risk factors except callus alone

Moderate risk
* deformity or
* neuropathy or
* non-critical limb ischaemia.

High risk
* previous ulceration or
* previous amputation or
* on renal replacement therapy or
* neuropathy and non-critical limb ischaemia together or
* neuropathy in combination with callus and/or deformity or
* non-critical limb ischaemia in combination with callus and/or deformity.

27
Q

When should Refer to the local vascular team - to be seen within 2 weeks be considered?

A

Referral to a vascular team should be considered if there are signs of peripheral arterial disease or critical limb ischemia.

patient’s foot pulses are not palpable, suggesting inadequate blood flow

28
Q

What is the key parameter to monitor in patients with hyperosmolar hyperglycaemic state?

A

Serum osmolality

29
Q

What is the firstline investigation in suspected primary hyperaldosteronism?

A

aldosterone/renin ratio

30
Q

What are the different layers of the adrenal gland?

A

The adrenal gland has two main parts: the adrenal cortex and the adrenal medulla. The adrenal cortex is made up of three layers, each producing different hormones.

31
Q

What are the layers of the adrenal cortex and what hormones do they produce?

A

Zona glomerulosa
The outermost layer that produces aldosterone, which regulates sodium and potassium levels

Zona fasciculata
The middle layer that produces cortisol, which helps the body respond to stress

Zona reticularis
The innermost layer that produces androgens, such as DHEA, which can be converted to estrogen or testosterone

32
Q

Does digoxin causes gynaecomastia?

A

Yes

33
Q

What drug should you give in the case of PHaeochromocytoma?

A

PHaeochromocytoma - give PHenoxybenzamine before beta-blockers

The first-line treatment for a phaeochromocytoma is a non-selective alpha blocker, in this case, phenoxybenzamine.

34
Q

headache, sweating and palpitations.blood pressure is found to be 180/90 mmHg and a fine tremor is noted in both hands. His urine is sampled and shows raised levels of urinary metanephrines What is the diagnosis?

A

young man presenting with palpitations, tremor and a headache. Given his presentation, his most likely underlying diagnosis is a phaeochromocytoma. This is confirmed by the raised blood pressure on examination and the raised levels of urinary metanephrines.

35
Q

What is Phaeochromocytoma ?

A

Phaeochromocytoma is a rare catecholamine secreting tumour. About 10% are familial and may be associated with MEN type II, neurofibromatosis and von Hippel-Lindau syndrome

Basics
bilateral in 10%
malignant in 10%
extra-adrenal in 10% (most common site = organ of Zuckerkandl, adjacent to the bifurcation of the aorta)

36
Q

What are the features of Phaeochromocytoma ?

A

Features are typically episodic
hypertension (around 90% of cases, may be sustained)
headaches
palpitations
sweating
anxiety

37
Q

What is the test for Phaeochromocytoma ?

A

24 hr urinary collection of metanephrines (sensitivity 97%*)

38
Q

What is the management for Phaeochromocytoma ?

A

Surgery is the definitive management. The patient must first however be stabilized with medical management:
alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)

39
Q

What is the management of prolactinoma?

A

Prolactin release is persistently inhibited by dopamine

therefore cabergoline

39
Q

What increases prolactin secretion?

A

thyrotropin releasing hormone
pregnancy
oestrogen
breastfeeding
sleep
stress
drugs e.g. metoclopramide, antipsychotics

40
Q

What decreases prolactin secretion?

A

dopamine
dopaminergic agonists

41
Q

Where is prolactin secreted from and what are its functions?

A

Anterior pituitary

Stimulates breast development (both initially and further hyperplasia during pregnancy)
Stimulates milk production

It decreases GnRH pulsatility at the hypothalamic level and to a lesser extent, blocks the action of LH on the ovary or testis.

42
Q

Features of hypokalaemia coupled with hypertension are suggestive of….

A

primary hyperaldosteronism

43
Q
A
44
Q

What is Addisonian crisis?

A

a life-threatening medical emergency that occurs when the body has low levels of cortisol. Cortisol is a hormone that helps regulate blood sugar and the body’s response to stress.

45
Q

What should pregnant women with hypothyroidism do with medication?

A

Women with hypothyroidism may need to increase their thyroid hormone replacement dose by up to 50% as early as 4-6 weeks of pregnancy

46
Q

What are the features of Addisonian crisis?

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia

47
Q

What are the causes of Addisonian crisis?

A

sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism)

adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)

steroid withdrawal

48
Q

What is the management of adrenal crisis?

A

hydrocortisone 100 mg im or iv
1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action
oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days

49
Q

What is the management for Addison’s disease and when are the doses given?

A

Patients who have Addison’s disease are usually given both glucocorticoid and mineralocorticoid replacement therapy.

This usually means that patients take a combination of:
hydrocortisone: usually given in 2 or 3 divided doses. Patients typically require 20-30 mg per day, with the majority given in the first half of the day
fludrocortisone

50
Q

What should patients using glucocorticoids be educated about?

A

emphasise the importance of not missing glucocorticoid doses
consider MedicAlert bracelets and steroid cards
patients should be provided with hydrocortisone for injection with needles and syringes to treat an adrenal crisis
discuss how to adjust the glucocorticoid dose during an intercurrent illness (see below)

Management of intercurrent illness
in simple terms the glucocorticoid dose should be doubled, with the fludrocortisone dose staying the same
the Addison’s Clinical Advisory Panel have produced guidelines detailing particular scenarios - please see the CKS link for more details

51
Q

What is the treatment for subclinical hypothyroidism?

A

Subclinical hypothyroidism with TSH level of level is 5.5 - 10mU/L: offer patients < 65 years a 6-month trial of thyroxine if TSH remains at that level on 2 separate occasions 3 months apart and they have hypothyroidism symptoms

52
Q

What treatment worsens thyroid eye disease?

A

If there is active Grave’s eye disease then radioiodine therapy is not recommended as it can worsen the eye disease

53
Q

Asymptomatic patients with an abnormal HbA1c or fasting glucose must be confirmed with….

A

a second abnormal reading before a diagnosis of type 2 diabetes is confirmed

54
Q

During Ramadan how should the metformin doses be split?

A

one-third of the normal metformin dose should be taken before sunrise and two-thirds should be taken after sunset

55
Q

Glucocorticoid treatment can induce

A

neutrophilia

56
Q

proximal myopathy is a side effect of which type of medication?

A

Corticosteroids

57
Q

What treatment in Subclinical hypothyroidism in the elderly?

A

watch and wait

58
Q

Over-replacement with thyroxine increases the risk

A

osteoporosis

59
Q

what is the T2DM initial therapy: if metformin is contraindicated (and no risk of CVD, established CVD or chronic heart failure)

A

choice of DPP-4 inhibitor or Pioglitazone or Sulfonylurea or even SGLT-2 (if NICE criteria met)

60
Q

Causes of Primary Hypothyroidism?

A

Hashimoto’s thyroiditis is the most common cause of hypothyroidism in the developed world. It is an autoimmune condition causing inflammation of the thyroid gland. It is associated with anti-thyroid peroxidase (anti-TPO) antibodies and anti-thyroglobulin (anti-Tg) antibodies.

Iodine deficiency is the most common cause of hypothyroidism in the developing world. In the UK, iodine is particularly found in dairy products and may be added to non-dairy milk alternatives (e.g., soya milk).

Treatments for hyperthyroidism have the potential to cause hypothyroidism:

Carbimazole
Propylthiouracil
Radioactive iodine
Thyroid surgery

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.

61
Q

Causes of Secondary Hypothyroidism?

A

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

62
Q

What is the presentation of hypothyroidism?

A

Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (including oedema, pleural effusions and ascites)
Heavy or irregular periods
Constipation

63
Q

What is the management of hypothyroidism?

A

Oral levothyroxine is the mainstay of treatment of hypothyroidism. Levothyroxine is a synthetic version of T4 and metabolises to T3 in the body.

The dose is titrated based on the TSH level, initially every 4 weeks.

Liothyronine sodium is a synthetic version of T3 and is very rarely used under specialist care where levothyroxine is not tolerated.

64
Q

Explain TSH and T4 levels with Poor compliance with thyroxine

A

TSH HIGH and T4 is normal

Thyroxine (T4) is used as a replacement hormone in hypothyroidism. When taken regularly, it suppresses thyroid-stimulating hormone (TSH) by providing adequate thyroid hormone levels, maintaining normal thyroid function.
Poor compliance with thyroxine causes fluctuating thyroid hormone levels:
When thyroxine is taken sporadically, serum T4 levels may normalize on the days when it is taken due to its long half-life (~7 days).
However, the pituitary gland, which senses thyroid hormone levels, responds to periods of insufficient T4 (due to missed doses) by increasing TSH secretion to stimulate the thyroid gland.

65
Q

Explain TSH and T4 levels with Steroid therapy?

A

TSH IS LOW and T4 is normal

Glucocorticoids suppress the secretion of thyrotropin-releasing hormone (TRH) from the hypothalamus and TSH from the anterior pituitary.
This suppression occurs because:
Steroids inhibit the hypothalamus and reduce TRH production.
Less TRH means less stimulation of the pituitary, leading to decreased TSH secretion.

Glucocorticoids reduce TSH’s amplitude and frequency of secretion.
This leads to transient low TSH levels, even if thyroid hormone levels (T4 and T3) remain normal.

The suppression of TSH is usually partial and transient with steroid therapy.
The thyroid gland continues to produce adequate T4 under the influence of residual TSH or basal thyroid activity.
T4 has a long half-life (about 7 days), so short-term changes in TSH do not immediately affect circulating T4 levels.

66
Q

Sick euthyroid syndrome is most commonly seen in which type of patients?

A

Sick euthyroid syndrome is most commonly seen in chronically ill patients or those with starvation. The thyroid function tests are often low and the patient clinically euthyroid.

67
Q

What is MEN?

A

Multiple Endocrine Neoplasia (MEN) is a rare, inherited disorder that affects the endocrine glands, causing them to develop tumors or overproduce hormones. These syndromes are caused by genetic mutations and are classified into distinct subtypes based on the affected genes and glands.

68
Q

What is the cause, affected organs and symptoms of MEN1?

A

Cause: Mutation in the MEN1 gene, which encodes the tumor suppressor protein menin.
Affected Organs:
Parathyroid glands (most common): Leads to primary hyperparathyroidism, causing high calcium levels.
Pituitary gland: Can cause tumors like prolactinomas or growth hormone-secreting adenomas.
Pancreas/Enteropancreatic neuroendocrine tumors: Includes insulinomas, gastrinomas (leading to Zollinger-Ellison syndrome), and others. (leading to recurrent peptic ulceration)

Symptoms:
Hypercalcemia (fatigue, kidney stones).
Symptoms related to hormonal excess (e.g., acromegaly, Cushing’s syndrome, or peptic ulcers).

69
Q

What is the cause, affected organs and symptoms of MEN type IIa?

A

Cause: Mutation in the RET proto-oncogene.
Subtypes:
MEN2A:
Medullary thyroid cancer (MTC): Nearly all patients.
Pheochromocytomas (adrenal gland tumors): Cause high blood pressure, palpitations.
Parathyroid hyperplasia: Causes hypercalcemia.

Whilst many develop parathyroid hyperplasia, only a relatively small proportion have hypercalcaemia as a result.

70
Q

What is the cause, affected organs and symptoms of MEN type IIb?

A

Cause: Mutation in the RET proto-oncogene.
MEN2B:
Medullary thyroid cancer: More aggressive than in MEN2A.
Pheochromocytomas.
Distinct physical features: Marfanoid habitus, mucosal neuromas (lips, tongue).
Symptoms:
Neck swelling (thyroid cancer), sweating, and headaches (pheochromocytomas).
Features of hypercalcemia or mucosal neuromas in MEN2B.

71
Q

What would cause Lower-than-expected levels of HbA1c (due to reduced red blood cell lifespan)?

A

Sickle-cell anaemia
GP6D deficiency
Hereditary spherocytosis
Haemodialysis

72
Q

What would cause Higher-than-expected levels of HbA1c (due to increased red blood cell lifespan)?

A

Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy

73
Q

If metformin is contraindicated then what should be given?

A

if the patient has a risk of CVD, established CVD or chronic heart failure:
SGLT-2 monotherapy
if the patient doesn’t have a risk of CVD, established CVD or chronic heart failure:
DPP-4 inhibitor or pioglitazone or a sulfonylurea
SGLT-2 may be used if certain NICE criteria are met

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