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CC2 - exam preparation > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is first line treatment for a phaeochromocytoma?

A

Alpha blockade using phenoxybenzamine is used in treatment of secondary hypertension in pheochromocytoma.

Patients should always be well alpha blocked before commencing any beta blockade.

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2
Q

What are two tumours of the adrenal glands that could cause secondary hypertension?

A

Conns tumour and phaeochromacytoma

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3
Q

What are some investigations for endocrine hypertension?

A

Investigations to assess the kidneys, arteries, heart and the endocrine organs are required to derive the correct diagnosis. It is essential that an endocrine disorder is diagnosed biochemically prior to performing imaging to avoid the detection of incidentalomas. 5-HIAA is a test for carcinoid which can present with a hypertensive crisis but this is rare and not well described in the literature so not part of standard screens.

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4
Q

How should patients on hydrocortisone with hypoadrenalism deal with their infections?

A

Patients with primary or secondary hypoadrenalism (i.e. due to an adrenal or a pituitary problem) are advised to double their doses of hydrocortisone in the event of intercurrent illnesses such as ‘flu’ or if they have fever for the duration of the illness.

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5
Q

What can cause bitemporal hemiopia?

A

Craniopharyngioma (a tumour above the pituitary)

Pituitary adenoma

Suprasellar meningioma

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6
Q

In which endocrine condition is carpal tunnel syndrome likely to cause parasthesia?

A

Acromegaly

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7
Q

What are some of the main changes that occur in patients with acromegaly?

A

Cardiomyopathy

Colonic polyps

Enlarged liver and spleen

Enlarged hands carpal tunnel

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8
Q

What are two features of Grave’s disease?

A

thyroid eye disease and a goitre with a bruit are diagnostic.

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9
Q

What is a side effect of carbamazole?

A

Agranulocytosis/ neutropenia

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10
Q

What happens to patients after radioiodine therapy?

A

any patients become hypothyroid after radioiodine therapy and this reveals itself over weeks to months. They are treated with levothyroxine

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11
Q

What are some features of Addisons?

A

Weight loss, weakness, bruises, hypotension and pigmentation

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12
Q

What are some causes of adrenal failure in the Western world?

A

Mostly autoimmune.

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13
Q

What type of lung cancer causes ACTH release?

A

Small cell lung carcinoma secreting ACTH can cause Cushing’s syndrome

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14
Q

What is Lantus and Humolog?

A

Insulin types

Lantus is slow/ long acting

Humolog/ novarapid is fast acting

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15
Q

Name four types of insulin that can be taken?

A

Lantus (lomg haul)

NPH (6-14 H peak)

Regular

Lispro / fast

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16
Q

What are DDP4 inihibitors?

A

Dipeptidyl peptidase-4 (DPP-4) inhibitors (e.g. Vildagliptin, sitagliptin)

Key points

dipeptidyl peptidase-4, DPP-4 inhibitors increase levels of incretins (GLP-1 and GIP) by decreasing their peripheral breakdown

oral preparation

trials to date show that the drugs are relatively well tolerated with no increased incidence of hypoglycaemia

do not cause weight gain

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17
Q

What are GLP-1 mimetics and what is an advantage of them?

A

Exenatide is an example of a glucagon-like peptide-1 (GLP-1) mimetic. These drugs increase insulin secretion and inhibit glucagon secretion. One of the major advances of GLP-1 mimetics is that they typically result in weight loss, in contrast to many medications such as insulin, sulfonylureas and thiazolidinediones. They are sometimes used in combination with insulin in T2DM to minimise weight gain.

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18
Q

When are GLP 1 mimetics used in diabetes?

A
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19
Q

What is type 2 diabetes?

A

In adults with type 2 diabetes, if HbA1c levels are not adequately controlled by a single drug and rise to 58 mmol/mol (7.5%) or higher

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20
Q

What is carcinoid syndrome?

A

usually occurs when metastases are present in the liver and release serotonin into the systemic circulation

may also occur with lung carcinoid as mediators are not ‘cleared’ by the liver

Features

flushing (often earliest symptom)

diarrhoea

bronchospasm

hypotension

right heart valvular stenosis (left heart can be affected in bronchial carcinoid)

other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing’s syndrome

pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour

Investigation

urinary 5-HIAA

plasma chromogranin A y

Management

somatostatin analogues e.g. octreotide

diarrhoea: cyproheptadine may help

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21
Q

What should blood glucose be regulated to in someone with diabetes for it tio be controlled?

A

Below 53mmol/mol

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22
Q

If metformin is contraindicated, what drugs should be given to diabetics?

A

drug treatment with: －

a dipeptidyl peptidase-4 (DPP-4) inhibitor or －

pioglitazone or －

a sulfonylurea.

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23
Q

What is a problem with Pioglitazone?

A

Pioglitazone: exercise particular caution if the person is at high risk of the adverse effects of the drug. Pioglitazone is associated with an increased risk of heart failure, bladder cancer and bone fracture. Known risk factors for these conditions, including increased age, should be carefully evaluated before treatment: see the manufacturers’ summaries of product characteristics for details. Follow the MHRA guidance on the risk of bladder cancer with pioglitazone

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24
Q

SGLT2 inhibitors increase risk of lower limb amputation. T or F?

A

Partly true. Canagliflozin may increase the risk of lower-limb amputation (mainly toes) in patients with type 2 diabetes. Evidence does not show an increased risk for dapagliflozin and empagliflozin, but the risk may be a class effect. Preventive foot care is important for all patients with diabetes.

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25
Q

What are some key facts about T2DM?

A

if HbA1c levels are not adequately controlled by a single drug and rise to 58 mmol/mol (7.5%) or higher

－ support the person to aim for an HbA1c level of 53 mmol/mol (7.0%)

Metformin, diet

In adults with type 2 diabetes, if metformin is contraindicated or not tolerated, consider initial drug treatment with: － a dipeptidyl peptidase-4 (DPP-4) inhibitor or － pioglitazone or － a sulfonylurea.

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26
Q

What should you do if an asymptomatic patient has a high HbA1c but no symptoms?

A

‘In an asymptomatic person, the diagnosis of diabetes should never be based on a single abnormal HbA1c or fasting plasma glucose level; at least one additional abnormal HbA1c or plasma glucose level is essential.’

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27
Q

What is subclinical hypothyroidism?

A

High TSH, normal T3 and normal T4

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28
Q

What is sick euthyroid syndrome?

A

TSH normal

Everything else low

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29
Q
A
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30
Q

What is type 3 hyperaparathyroidism?

A

Even though calcium is back gto normal PTH secretion is still high

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31
Q

What causes primary adrenocortical insufficiency?

A

Autoimmune disease e.g. Addisons

TB

Haemorrhage

Malignancy

Drugs: mitotane, metyrapone (inhibitors 11b hydroxylase), etomidate, and ketoconzaole all reduce adrenal function.

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32
Q

Name some drugs that cause adrenocortical insufficiency?

A

Drugs: mitotane, metyrapone (inhibitors 11b hydroxylase), etomidate, and ketoconzaole all reduce adrenal function.

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33
Q

What is metyrapone?

A

A drug that targets 11b hydroxylation and reduces cortisol.

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34
Q

What is etomidate?

A

Induction agent for anaesthesia

35
Q

What are some effects of adrenocortical insufficiency?

A

Weakness and fatigue–Nausea and vomiting–Abdominal pain–Hypotension may lead to shock–Pigmentation of mucous membrane and skin creases

36
Q

Why do you get hyperpigmentation in Addisons disease?

A

It is caused by the stimulant effect of excess adrenocorticotrophic hormone (ACTH) on the melanocytes to produce melanin. The hyperpigmentation is caused by high levels of circulating ACTH that bind to the melanocortin 1 receptor on the surface of dermal melanocytes.

37
Q

What are the biochemical features of adrenocortical insufficiency?

A

Biochemical features–Low sodium–High potassium –High urea–Low blood glucose (recurrent hypoglycaemia in a Type 1 diabetic patient)

38
Q

How could you diagnose adrenocortical insufficiency?

A

–Symptoms and signs–Plasma ACTH increased–Impaired response to short Synacthen test–Adrenal autoantibodies

39
Q

What is the short synthacten test?

A

1 x ampoule of Synacthen (250 ug) from the pharmacy

Given as IV

Measure serum cortisol at 0, 30 and 60 min

Serum cortisol of > 450nmol/ L = normal result

40
Q

How is adrenocortical insufficiency treated?

A
  1. Hydrocortisone 10mg morning, 5mg at lunch and 5mg afternoon, no later than 6pm
  2. Double hydrocotrisone in times of stress
  3. Fludrocortisone for primary adrenal failure.
  4. Hydrocortisone should precede thyroxine treatments
41
Q

What are some signs of hyperaldosteronism/ Conn’s?

A

Hypertension (1-2% of hypertensives)

HTN with low K+ and metabolic alkalosis

Renin is suppressed

Use a fludrocortisone suppression test or adrenal vein sampling

42
Q

How do you treat Conn’s syndrome?

A

Excision or spirnolactone

43
Q

What is the difference between the short synacthen test and the dexamethasone suppression test?

A

The SST is for adrenal insufficiency to test adrenal output and low cortisol, whereas the dexamethasone suppression test is for high ACTH.

44
Q

How is Cushing’s disease tested?

A

24 hour free cortisol,

plasma ACTH,

perimetry,

inferior petrosal sampling

45
Q

What is a microadenoma?

A

Pituitary tumour less than 1 cm

46
Q

What is a macroadenoma?

A

A pituitary tumour greater than 1cm

47
Q

What are the causes of hypercalcemia?

A

–Common:•Primary hyperparathyroidism•Malignancy: humoral or metastatic–Less common:•Multiple myeloma•Lymphoma•Sarcoidosis•Hyperthyroidism•Drugs: lithium, thiazide diuretics

48
Q

What are the features of hypercalcemia?

A

–Polyuria/polydipsia–Constipation–Muscle weakness–Psychological symptoms–Bone pain–Renal stones if there is hypercalciuria

49
Q

What investigations are there for hypercalcemia?

A

FBC, ESR–Serum calcium, phosphate, alkaline phosphatase, albumin, urea, creatinine–Vitamin D, PTH–Plasma electrophoresis if myeloma is suspected–24-hr urinary calcium and creatinine

50
Q

How is hypercalcemia treated?

A

Severe hypercalcaemia is often caused by malignancy –

Immediate measures•IV fluids: normal saline•

Additional frusemide IV•Salmon calcitonin s/c–Intravenous bisphosphonates•Pamidronate•Zolendronate–

Subcutaneous denosumab

51
Q

How should hypoglycaemia be treated?

A

Severe hypocalcaemia is uncommon–Immediate measures•IV calcium gluconate•May need to replace magnesium to normalise calcium levels–Long-term•Treat underlying cause•Calcium and Vitamin D replacement

52
Q

Who is at risk of lower vitamin D availability?

A

Asian Indians need 3 times as much sun exposure for vitamin D

Dark skin needs 10 times as much.

Reduced absorption - IBD.

53
Q

What other risk factors are there for low vitamin D?

A

Liver failure 25(OH) D3

Kidney failure 1,25 (OH) D3

54
Q

What is the pathway for obtaining vitamin D?

A

7 dehydrocholesterol –> uvb –> ergocalciferol {D2), cholcalciferol (D3) –> calcidiol 25 hydroxyD3, –> calcitriol (1,25 hydroxyD3)

55
Q

What are some investigations for hypocalcemia?

A

FBC, ESR–Serum calcium, phosphate, alkaline phosphatase, albumin, urea, creatinine–Vitamin D, PTH–24-hr urinary calcium and creatinine–Tests for malabsorption syndrome and pancreatitis

56
Q

What are some clinical feaures of calcium deficiency?

A

Clinical features–In children•Classical triad: carpopedal spasm, stridor and convulsions–In adults•Paraesthesia in the hands, feet and around the mouth•Less commonly painful carpopedal spasm and seizures

57
Q
A
58
Q

What might be seen on an ABG for Conn’s syndrome?

A

a metabolic alkalosis that is also shows hypokalaemia. This would be contributing to the patients weakness and fatigue

59
Q
A
60
Q

What are some tests for acromegaly?

A
  1. High IGF
  2. High GH
  3. After 75mg of glucose given the GH still remains high
  4. Visual field defect
61
Q

What is the Synthacten test for?

A

Addisons - no response - no cortisol

62
Q
A
63
Q

What does 21 hydroxylase deficiency do?

A

Pregnenolone –> progesterone uses 3b HSD. Progesterone then uses 21 hydroxylase to becomes precursors of cortisol and aldosterone.

Instead 21 hydroxylase defiiency causes progesterone to become 17OH progesterone via 17a HSD, then becomes DHEA or androstenedione via 17.20n lyase and then 17 beta hydroxylase makes testosterone. Testosterone can become poestrogen via aromatase or DHT by 5AR.

64
Q

What are the tests for primary hyperaldosternism?

A

Aldosterone: renin ratio tests

High IV saline loading and oral loading

Fludrocortisone suppression test

65
Q

What are the symptoms of Addisons disease?

A

Pigmentation, hypotension, dizziness and nausea

66
Q

What are some symptoms of prolactinoma in males? (GIGI)

A

Galactorrhea/ gynecomastia

Infertility

Gonads smaller

inhibited libido

67
Q

What are the treatments for prolactinoma?

A

Pharmacology: bromocriptine short acting, cabergoline, quinagoline longer acting

68
Q

What is lagopthalmos?

A

Inability to close eyes fully

69
Q

How would a patient with Graves disease be diagnosed?

A

Radioisotope of iodine taken up homeogenously in the gland. A single hot nodule with the rest of the gland suppressed would be consistent with a toxic adenoma (a single hyperfunctioning area of thyroid tissue).De Quervains is diffuse uptake.

70
Q

What is the effect of gastroparesis in T1DM?

A

Erratic blood glucose control, bloating and vomiting think gastroparesis

71
Q
A
72
Q

How is pain dealt with for diabetic neuropathy?

A

NICE updated it’s guidance on the management of neuropathic pain in 2013. Diabetic neuropathy is now managed in the same way as other forms of neuropathic pain:

first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin

if the first-line drug treatment does not work try one of the other 3 drugs

tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain

topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)

pain management clinics may be useful in patients with resistant problems

73
Q

What is characteristic of a myxoedema coma?

A

Confusion. cerebral anxoia, tiredness

74
Q

What are the treatments for type 2 diabetes?

A

My Sister Does Play The Game

75
Q

What is the Wolf Chaikoff effect?

A

The Wolff-Chaikoff effect is an effective means of rejecting the large quantities of iodide and therefore preventing the thyroid from synthesizing large quantities of thyroid hormones.

76
Q

What is the Jod-Basedow effecr

A

The opposite of Wolf Chaikoff where excess iodine leads to hyperthyrodism

77
Q

What is the difference between type 1 and type 2 amiadarone induced disease?

A

Type 1 already has a background of thyroid disease

78
Q

What is the difference between MEN1, MEN 2A and MEN2B?

A
  1. PPP (pituitary, parathyroid, pancreas)
  2. PMP (parathyoid, medullary thyroid, pheocromocytosma)
  3. MMP (marfanoid/ mucosal nodules, medullary thyroid and,phaeochromocytoa
79
Q

What is pituitary apoplexy?

A
80
Q

What is the phenomena in which increase iodine reduces thyroid hormone production?

A

Wolf Chaikoff

81
Q

What are the phases of subacute thyroiditis?

A

Thyrotoxic phase (4 to 6 weeks in length)

Acute viral-like illness with thyroid (neck) pain, fever, myalgias, malaise, and pharyngitis, which precedes severe neck pain that may start on one side and migrate to the contralateral side.

Thyroid destructive phase with high T4 and T3 levels.

Thyroid uptake with I-123 or Tc-99m is very low (<1% at 24 hours).

ESR is usually elevated at >40-60 mm/hour.

Hypothyroid phase (2 to 6 months in length)

Thyroid hormone levels are usually mildly or moderately low.

Thyroid uptake is variable.

Thyroid autoantibody levels are variably elevated.

Euthyroid phase

Thyroid function returns to normal in ≥90% of patients.

Thyroid histology returns to normal.

82
Q

What is the algorithm for hypoglycaemia?

A
83
Q
A

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