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Focused Xtra > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What do we use on top of metformin in T2DM pts with cardiac disease?

A

SGLT-2 inhibitors should be used in addition to metformin as initial therapy for T2DM if CVD, high-risk of CVD or chronic heart failure, like empagliflozin

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2
Q

Some Hormones Create Funny Knockers

A

Spironolactone, Hormones, Cimetidine, Finasteride, Ketoconazole:

“Some Hormones Create Funny Knockers (gynaecomastia)

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3
Q

What is HONK, and how is it characterised?

A

This patient has hyperglycaemic hyperosmolar non-ketotic coma (HONK). HONK is characterised by:
1.) Severe hyperglycemia
2.) Dehydration and renal failure
3.) Mild/absent ketonuria

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4
Q

How do we manage HONK?

A

The central management of HONK is supportive care and slow metabolic resolution. Patients with HONK often have a deficit of over 8 litres. Caution to avoid rapid fluid replacement as rapid osmolar shifts can cause cerebral oedema.

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5
Q

How do we treat DKA?

A

This patient is presenting in diabetic ketoacidosis (DKA) as evidenced by her known diabetes diagnosis, glucose > 11 mmol/L, pH < 7.3, bicarbonate < 15 mmol/L and ketones > 3 mmol/L. She needs treatment with fixed-rate insulin and fluids. While this takes place, her normal long-acting insulin should be continued, but her short-acting insulin should be stopped.

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6
Q

How do we alter the glucocorticoids and the fludrocortisone in a pt with recurring illness in Addison’s?

A

Double the glucocorticoids, maintain the fludro

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7
Q

How does bendroflumethiazide cause hypercalcaemia?

A

Bendroflumethiazide is a thiazide diuretic which can cause hypercalcaemia by increasing renal tubular reabsorption of calcium.

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8
Q

How does hypercalcaemia present?

A

Stones: Kidney stones, nephrocalcinosis, and diabetes insipidus (polyuria and polydipsia)
Bones: Osteoporosis (weak bones)
Groans: Abdominal pain, such as pancreatitis or reflux disease
Psychic moans: Mental issues, such as depression, irritability, worsening concentration, and worsening short-term memoryloss of appetite, nausea, fatigue

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9
Q

How do we manage hypercalcaemia?

A

Rehydration with 3-4L IVI, followed by ? bisphosphonates

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10
Q

How does Subacute (De Quervain’s) thyroiditis present?

A

Subacute thyroiditis (also known as De Quervain’s thyroiditis) is thought to occur following viral infection and typically presents with hyperthyroidism

Features
hyperthyroidism
painful goitre
raised ESR
globally reduced uptake on iodine-131 scan

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11
Q

How do we manage De Quervain’s thyroiditis?

A

Management
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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12
Q

What is the difference in presentation between DKA and alcoholic ketoacidosis?

A

Normal glucose in AKA

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13
Q

How do we use PTH to determine the cause of hypercalcaemia?

A

A parathyroid hormone that is normal or raised suggests primary hyperparathyroidism.

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14
Q

What is gliclazide? Common SE?

A

Sulfonylurea, weight gain

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15
Q

Which diabetes med is linked to Fournier’s Gangrene?

A

SGLT-2 inhibitors, like dapagliflozin, have been linked to necrotising fasciitis of the genitalia or perineum (Fournier’s Gangrene)

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16
Q

What is goserelin?

A

GnRH agonists (e.g. goserelin) used in the management of prostate cancer

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17
Q

What is pioglitazone?

A

Pioglitazone is a thiazolidinedione that acts as an insulin sensitiser by activating peroxisome proliferator-activated receptor gamma (PPARγ). However, it has been found to cause fluid retention and exacerbate heart failure, hence it is contraindicated in patients with heart failure.

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18
Q

How does primary hyperaldosteronism present?

A

Primary hyperaldosteronism can present with hypertension, hypernatraemia, and hypokalemia

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19
Q

How do we treat prolactinomas?

A

Dopamine agonists (e.g. cabergoline, bromocriptine) are first-line treatment for prolactinomas, even if there are significant neurological complications.
If doesn’t work, for surgery

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20
Q

Corticosteroids can induce neutrophilia

A

Corticosteroids can induce neutrophilia

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21
Q

What is steroid psychosis?

A

A rare but recognised complication of corticosteroid therapy is steroid psychosis

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22
Q

What is the difference between Cushing’s Syndrome and Cushing’s Disease?

A

I remember a Neurosurgeon telling me ‘Cushing’s DISEASE is for the Neurosurgeon (from tumour); the medics can keep the syndromes’.

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23
Q

How do we manage subclinical hypothroidism?

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

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24
Q

Give a side effect of pioglitazone

A

Fluid retention

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25
Q

How does sick euthyroid present?

A

Sick euthyroid syndrome = low T3/T4 and normal TSH with acute illness

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26
Q

How might we distinguish Graves disease from other causes of hyperthyroidism?

A

Exopthalmos

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27
Q

Where might you see hyperpigmentation of the palmar creases?

A

Addison’s disease

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28
Q

How does Cushing’s syndrome present?

A

weight gain, impotence, hypertension, purple striae, and decreased muscle strength

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29
Q

What causes Cushing’s syndrome?

A

Cushing’s syndrome can be caused by an excess of cortisol production from the adrenal glands or exogenous glucocorticoid use. The excess cortisol can lead to sodium and water retention, causing hypertension and hypokalaemic metabolic alkalosis.

30
Q

What is the most common SE of SGLT-2 inhibitors?

A

Recurrent UTIs

31
Q

How do we manage hypoglycaemia?

A

a hospital setting:
If the patient is alert, a quick-acting carbohydrate may be given (as above)
If the patient is unconscious or unable to swallow, subcutaneous or intramuscular injection glucagon may be given.
Alternatively, intravenous 20% glucose solution may be given through a large vein

32
Q

Why do we avoid amitriptyline in BPH?

A

it is better to avoid amitriptyline due to the risk of urinary retention.

33
Q

How do we monitor treatment response in hyperthyroidism?

A

TSH

34
Q

How does Graves disease present on radioactive iodine uptake test?

A

Increased, homogenous uptake on a radioactive iodine uptake test suggests Grave’s disease

35
Q

Where would you see faint diffuse uptake on radioactive iodine uptake test?

A

Faint diffuse uptake would be found in subacute thyroiditis (De Quervain’s thyroiditis). The low uptake of iodine in this condition is due to the tissue, not over-producing thyroid hormone (as in Grave’s disease).

36
Q

Which tablets reduce absorption of levothyroxine?

A

Iron / calcium carbonate tablets

37
Q

Which electrolyte disturbances would you expect in Addison’s?

A

Adrenal insufficiency - hypona and hyperk

38
Q

How do we diagnose DM on BGC?

A

fasting > 7.0, random > 11.1

39
Q

What is acromegaly?

A

It refers to the clinical syndrome caused by excessive secretion of growth hormone (GH), typically from a pituitary adenoma.

40
Q

How does acromegaly present?

A

Features
coarse facial appearance, spade-like hands, increase in shoe size
large tongue, prognathism, interdental spaces
excessive sweating and oily skin: caused by sweat gland hypertrophy
features of pituitary tumour: hypopituitarism, headaches, bitemporal hemianopia
raised prolactin in 1/3 of cases → galactorrhoea
6% of patients have MEN-1

41
Q

What is myxoedema coma?

A

Myxoedema coma is a potentially fatal complication of longstanding undertreated hypothyroidism. It may be precipitated by illness, stress, and certain drugs. Apart from confusion and hypothermia, patients may have non-pitting periorbital and leg oedema, reduced respiratory drive, pericardial effusions, anaemia, seizures, and other symptoms of hypothyroidism.

42
Q

How does duloxetine work in peripheral diabetic neuropathy?

A

It works by inhibiting the reuptake of serotonin and norepinephrine in the central nervous system, thereby increasing their concentration and enhancing pain suppression.

43
Q

Where do you see anti-TPO antibodies/

A

Whilst anti-thyroid peroxidase antibodies are seen in 90% of Hashimoto’s disease they are also seen in 75% of patients with Graves’ disease.

44
Q

How does subacute (De Quervain’s) thyroiditis present?

A

Thyrotoxicosis with tender goitre

45
Q

How do gliptins work?

A

sitagliptin reduces the peripheral break down of incretins. Sitagliptin is one of the Gliptins (DPP-4 inhibitors) which reduce the peripheral breakdown of incretins such as GLP-1.

46
Q

What is impaired glucose tolerance?

A

On OGTT, if the fasting glucose is <7 and the OGTT 2-hour value is =/>7.8 but <11, we call them to have Impaired glucose tolerance and offer lifestyle advice and call them prediabetic.

47
Q

Why should we not abruptly stop long term steroid treatment?

A

Secondary adrenal insufficiency. Prolonged use of exogenous corticosteroids suppresses the hypothalamic-pituitary-adrenal (HPA) axis, leading to reduced endogenous cortisol production. When corticosteroids are suddenly withdrawn, the adrenal glands cannot produce enough cortisol to meet the body’s needs, resulting in an Addisonian crisis.

48
Q

Where do you see reduced c-peptide levels?

A

T1DM
This peptide is the result of the cleavage of proinsulin into insulin. Very low levels indicate the absolute absence of insulin, indicating type 1 diabetes mellitus.

49
Q

What are the HbA1c targets in T2DM?

A

First and second line therapy are recommended when HbA1c > 6.5%, and third line therapy and or insulin are recommended only when HbA1c >7.5%

50
Q

Why does splenectomy increase HbA1c?

A

Splenectomy can give a falsely high HbA1c level due to the increased lifespan of RBCs

51
Q

Why do you see hypoglycaemia in Addison’s disease?

A

Hypoglycaemia is the most likely investigation finding. Glucocorticoids such as cortisol act by various mechanisms to increase blood glucose levels, one of these mechanisms being through an increase in hepatic gluconeogenesis. This means that a reduction in cortisol could lead to hypoglycaemia.

52
Q

What is bromocriptine?

A

Bromocriptine is a dopamine agonist and it works by inhibiting prolactin secretion. Galactorrhoea, the spontaneous flow of milk from the breast unrelated to childbirth or nursing, is often caused by hyperprolactinaemia. Therefore, bromocriptine, which reduces prolactin levels, would not cause galactorrhoea but rather could be used in its treatment.

53
Q

Which hormones are abnormal in Kallman’s syndrome?

A

Low FSH/LH and low testosterone is correct. In normal physiology, the hypothalamus produces GnRH, GnRH then stimulates LH and FSH production from the anterior pituitary, and FSH/LH go on to stimulate testosterone from the testes. The absence of GnRH producing cells in Kallman’s syndrome means there is no downstream stimulation of LH/FSH production and therefore no stimulation of testosterone production. Further, failure of olfactory nerve development causes a reduced or absent sense of smell, which is characteristic for Kallman’s syndrome.

54
Q

Why do we add dapagliflozin regardless of HbA1c in HF?

A

To clarify, dapagliflozin’s role here extends beyond its glycaemic effects; it is primarily being introduced to manage cardiovascular risk. Therefore, initiation of dapagliflozin should proceed regardless of the patient’s HbA1c levels.

Start it after metformin tolerance can be evaluated

55
Q

A 52-year-old woman who was diagnosed as having primary atrophic hypothyroidism 12 months ago is reviewed following recent thyroid function tests (TFTs):

TSH 12.5 mU/l
Free T4 14 pmol/l

She is currently taking 75mcg of levothyroxine once a day. How should these results be interpreted?

A

The TSH level is high. This implies that over recent days/weeks her body is thyroxine deficient. However, her free T4 is within normal range. The most likely explanation is that she started taking the thyroxine properly just before the blood test. This would correct the thyroxine level but the TSH takes longer to normalise.

56
Q

How do sulfonylureas work?

A

They work by increasing pancreatic insulin secretion and hence are only effective if functional B-cells are present. On a molecular level they bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells.

57
Q

What is the first-line tx for phaeochromocytoma

A

PHaeochromocytoma - give PHenoxybenzamine before beta-blockers

58
Q

What is the most common endogenous cause of Cushing’s syndrome?

A

The most common endogenous cause of Cushing’s syndrome is a pituitary adenoma (also known as Cushing’s disease)

59
Q

How do we diagnose Addison’s disease?

A

After stabilisation, his condition could be diagnosed with a short synacthen test which measures cortisol after a stimulating hormone (synacthen) is given.

60
Q

What is the overnight dexamethasone suppresion test used for?

A

An overnight dexamethasone suppression test is also not useful in this scenario. It is used to detect excess cortisol rather than deficiency. The test can help rule out Cushing’s syndrome.

61
Q

Give a bone complication of prolonged steroid use

A

Avascular necrosis. This condition refers to the death of bone tissue due to a lack of blood supply, which can lead to tiny breaks in the bone and the bone’s eventual collapse. Avascular necrosis is a well-documented complication of long-term corticosteroid use, such as prednisolone. Steroids are thought to interfere with the ability of blood to flow to the bones.

62
Q

Give the limits for fasting glucose and OGTT

A

If the patient is symptomatic:
fasting glucose greater than or equal to 7.0 mmol/l
random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

63
Q

A 51-year-old woman who is known to have poorly controlled type 1 diabetes mellitus is reviewed. Her main presenting complaint is bloating and vomiting after eating. She also notes that her blood glucose readings have become more erratic recently. Which one of the following medications is most likely to be beneficial?

A

Metoclopramide - prokinetic

64
Q

How can we manage acromegaly medically?

A

octreotide, a somatostatin analogue that directly inhibits GH release, is used as medical therapy.

65
Q

What is prochloperazine, and how does it cause amenorrhoea?

A

Prochlorperazine is a dopamine antagonist and so reduces dopaminergic inhibition of prolactin release

66
Q

How do we manage primary hyperaldosteronism?

A

This patient is presenting with primary hyperaldosteronism which is due to bilateral hyperplasia of his adrenal glands. The aldosterone levels are elevated due to hyperplasia and this leads to increased sodium retention which then gives negative feedback to renin release. This is the most common cause of this condition accounting for around 2/3 of cases, and unilateral adrenal adenoma for around 1/3 cases. When the underlying cause is due to bilateral adrenal hyperplasia the preferred treatment is 4 weeks of spironolactone which is an antagonist of aldosterone receptors.

67
Q

Why does Cushing’s syndrome - hypokalaemic metabolic alkalosis

A

Most commonly, it is related to exogenous glucocorticoid therapy but may also stem from autonomous overproduction by the adrenal glands or increased production of adrenocorticotrophic hormone. Cortisol at high levels can simulate the effects of aldosterone. There is increased sodium and subsequently water retention and increased potassium excretion, resulting in hypokalaemia. Bicarbonate resorption is increased in the tubules with potassium depletion causing metabolic alkalosis. Due to the potassium excretion, there is a hypokalaemic metabolic alkalosis

68
Q

What do we do in T2DM if triple therapy hasn’t worked?

A

Stop pioglitazone and start a GLP-1 mimetic is the correct answer as the patient has not been managed adequately on triple therapy - his HbA1c is greater than 58 mmol/mol. He meets the criteria of a GLP-1 mimetic addition due to his BMI (calculated as 40.75 kg/m²). Furthermore, insulin may be contraindicated in his line of work as a heavy goods vehicle operator due to the risk of hypoglycaemic episodes.

If the patient were amenable to insulin, this would likely have been started in secondary therapy when 2 drugs were inadequate. When starting insulin, it is important to continue metformin in type 2 diabetic patients - as such, stop triple therapy and start subcutaneous insulin only is an incorrect answer.

69
Q

How do we manage thyroid storm?

A

IV beta blockers

70
Q

What is thyroid storm?

A

To do

71
Q

Nuclear scintigraphy scan which reveals patchy uptake. Dx?

A

In toxic multinodular goitre, nuclear scintigraphy reveals patchy uptake

72
Q
A

Focused Xtra (21 decks)

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