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Focused 2 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are 6 causes of SIADH?

A
  1. Idiopathic (most common)
  2. Drugs
  3. CNS disease - tumour, trauma, infection, CVA, MS
  4. Pulmonary disease - tumour, pneumonia, COPD, abscess, TB
  5. Carcinoma - lung, pancreas, thymoma
  6. Surgery - postop
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2
Q

What are 12 drug causes of SIADH?

A
  1. carbamazepine
  2. NSAIDs
  3. vasopressin
  4. chlorpropramide
  5. nicotine
  6. diuretics
  7. tricyclic antidepressants
  8. SSRIs
  9. vincristine
  10. cyclophosphamide
  11. thioridazine
  12. clofibrate
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3
Q

What is the management of a patient with Addison’s who is vomiting and unable to take oral hydrocortisone/fludrocortisone?

but systemically well

A

Take IM hydrocortisone (if unwell with systemic symptoms - admit for IVF/IV hydrocort)

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4
Q

What is the commonest cause of thyrotoxicosis?

A

Graves’ disease

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5
Q

What conditions are associated with anti-TPO (thyroid peroxidase) antibodies?

A
  • Hashimoto’s thyroid it is (90%)
  • Graves’ disease (75%)
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6
Q

Which 2 types of autoantibodies are seen in Graves’ disease?

A
  • TSH-stimulating receptor antibodies (90%)
  • anti TPO (75%)
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7
Q

What is seen in thyroid scintigraphy in Graves’ disease?

A

Diffuse homogenous increased uptake of radioactive iodine

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8
Q

What is seen in thyroid scintigraphy in Graves’ disease?

A

Diffuse homogenous increased uptake of radioactive iodine

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9
Q

What is the definition of precocious puberty?

A

development of secondary sexual characteristics before 8 years in females and 9 in males

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10
Q

What is thelarche?

A

first stage of breast developemtn

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11
Q

What is adrenarche?

A

the first stage in pubic hair development

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12
Q

What are 2 groups that all causes of precocious puberty may be classified into?

A
  1. Gonadotrophin dependent (central/ true) - premature activiation of HPGA, FSH and LH raised
  2. Gonadotrophin independent (pseudo/false) - due to excess sex hormones, FSH and LH low
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13
Q

What key feature can help distinguish the cause of precocious puberty in males?

A

testicular size
* bilateral enlargement - gonadotrophin release from intracranial lesion e.g. astrocytoma
* unilateral enlargement - gonadal tumour e.g. sex cord-gonadal stromal tumour
* small testes - adrenal cause (tumour or adrenal hyperplasia)

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14
Q

What is most commonly the cause of precocious puberty in females?

A

idiopathic / familial

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15
Q

What features are associated with female precocious puberty and what is an example?

A

rapid onset, neurological symptoms/signs
e.g. McCune Albright syndrome

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16
Q

What are 4 things that can cause a lower-than-expected HbA1c?

A
  1. sickle cell anaemia
  2. G6PD deficiency
  3. hereditary spherocytosis
  4. haemodialysis

(reduce red blood cell lifespan, most glycosylation in days 90-120)

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17
Q

What are 3 conditions that can lead to a higher-than-expected HbA1c?

A
  1. vitamin B12 / folic acid deficiency
  2. iron deficiency anaemia
  3. splenectomy

(increase red blood cell lifespan)

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18
Q

What is the new internationally standardised method for reporting HbA1c that has been developed?

A

IFCC-HbA1c (mmol/mol)

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19
Q

What may be a suitable alternative to HbA1c in conditions that increase/shorten the lifespan of RBCs?

A

fructosamine - reflects glycaemic control over 2-3 weeks

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20
Q

What is the management of subclinical hypothyroidism (raised TSH 5.5-10, normal T4)?

A

offer patients <65 years a 6 month trial of thyroxine IF thyroxine remains that level on 2 separate occasions, 3 months apart, AND symptomatic

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21
Q

What are 8 situations when HbA1c shouldn’t be used to diagnose diabetes mellitus?

A
  1. children and young people <18y
  2. pregnant / 2 months postpartum
  3. symptoms of diabetes <2 months
  4. acutely ill
  5. medication causing hyperglycaemia e.g. steroids
  6. acute pancreatic damage / surgery
  7. ESRD
  8. HIV
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22
Q

What is the risk of subclinical hypothyroidism progressing to overt hypothyroidism and what increases the risk?

A

2-5% per year; increased by presence of thyroid autoantibodies

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23
Q

What is the guidance for subclinical hypothyroidism if TSH is >10 and T4 is normal?

A

consider offering levothyroxine if TSH >10 on 2 separate occasions, 3 months apart

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24
Q

In patients >80 years with subclinical hypothyroidism what is the recommended management?

A

watch and wait

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25
Q

Which 2 alleles are risk factors for T1DM?

A

HLA-DR3 or DR4

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26
Q

What is the starting dose for levothyroxine?

A

In healthy young patients start at 50-100mcg; >50y start at 25mcg

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27
Q

When should TFTs be tested after starting levothyroxine?

A

8-12weeks

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28
Q

What’s the target for levothyroxine therapy in hypothyroidism?

A

Aiming for low end of normal TSH as most people in the low end - 0.5-2.5 (whole range of normal 0.5-5.5)

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29
Q

What are 4 adverse effects of levothyroxine?

A
  1. Hyperthyroidism
  2. Worsening angina
  3. Reduced bone mineral density
  4. AF
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30
Q

What is first line line treatment for T2DM if metformin (inc MR) is not tolerated in
a) normal QRISK
b) QRISK >10

A

a) sulphonylurea or glitazone or DPP4 inhibitor (gliptin)
b) SGLT2i

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31
Q

What are the 3 NICE criteria, 1 of which must be met for SGLT2i to be added to metformin?

A
  1. High risk of CVD E.g. QRISK >10%
  2. Established CVD
  3. Chronic heart failure
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32
Q

What should be done before SGLT2i is added to metformin?

A

metformin should be established and titrated up

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33
Q

What should HbA1c rise to before adjusting T2DM medication?

A

58

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34
Q

When should a GLP1 mimetic be considered for T2DM?

A

If triple therapy not effective AND:
- BMI > 35 and specific psych or other medical problems associated with obesity OR
- BMI <35 and insulin CI (E.g. occupation) or weight loss would benefit other comorbidities

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35
Q

What criteria must be met to continue on a GLP1 inhibitor?

A

Reduction of HbA1c by 11 and Wright loss 3% body weight in 6 months

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36
Q

What is the first line antihypertensive in T2DM?

A

ACEi (ARB if Afro-Caribbean)

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37
Q

When is IV treatment with calcium gluconate indicated in hypocalcaemia?

A

Severe hypocalcaemia:
- QT prolongation
- carpopedal spasms
- tetany
- seizures

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38
Q

What is the definition of DKA?

A

positive serum ketones, arterial blood pH <7.30 +- serum bicarb <15

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39
Q

What are 4 hormones that are increased in DKA? What is the ultimate effect?

A

Counter-regulatory hormones
1. glucagon
2. cortisol
3. growth hormone
4. adrenaline

Effect: enhances hepatic gluconeogenesis, glycogenolysis, lipolysis

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40
Q

If not using HbA1c, is a patient is symptomatic what are 2 possible diagnostic criteria for type 2 diabetes mellitus?

A
  • fasting glucose greater than or equal to 7.0
  • random glucose greater than or equal to 11.1
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41
Q

What is the criteria for diagnosing T2DM (not using HbA1c) if the patient is asymptomatic?

A
  • fasting glucose greater than or equal to 7.0
  • random glucose greater than or equal to 11.1

demonstrated on 2 separate occasions

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42
Q

How is HbA1c used to diagnose diabetes?

A

HbA1c >48 diagnostic; <48 doesn’t exclude DM
if asymptomatic, must be repeated

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43
Q

What is the definition of impaired fasting glucose?

A

fasting glucose 6.1-7.0

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44
Q

What is the definition of impaired glucose tolerance?

A

fasting plasma glucose <7.0 and OGTT 2-hour value 7.8 to 11.1

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45
Q

What does Diabetes UK suggest for the management of impaired fasting glucose?

A

oral glucose tolerance test to rule out diagnosis of diabetes; result <11.1 but >7.9 indicates IGT but not diabetes

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46
Q

What is the best test for response to levothyroxine therapy?

A

TSH

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47
Q

What is Addison’s disease?

A

commonest cause of primary hypoadrenalism in UK - autoimmune destruction of the adrenal glands, results in less cortisol and aldosterone production

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48
Q

What are 5 key features of Addison’s disease?

A
  1. hyperpigmentation
  2. hypotension
  3. hypoglycaemia
  4. hyponatraemia
  5. hyperkalaemia
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49
Q

In addition to Addison’s disease what are 5 other causes of primary hypoadrenalism?

A
  1. TB
  2. mets e.g. bronchial carcinoma
  3. meningococcal sepsis (Waterhouse-Friderichsen syndrome)
  4. HIV
  5. antiphospholipid syndrome
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50
Q

What are 2 things that can cause secondary hypoadrenalism?

A
  1. pituitary disorders e.g. tumours, irradiation, infiltration
  2. exogenous glucocorticoid therapy
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51
Q

What can distinguish primary Addison’s and secondary adrenal insufficiency?

A

primary Addison’s is associated with hyperpigmentation whereas secondary is not

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52
Q

What is often a trigger for de Quervain’s tenosynovitis (subacute thyroiditis)?

A

Viral infection

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53
Q

What are the 4 typical phases of de Quervain’s tenosynovitis?

A
  1. Phase I (3-6 weeks): hyperthyroid, painful goitre, raised ESR
  2. Phase II (1-3 weeks): euthyroid
  3. Phase III (weeks-months): hypothyroidism
  4. Phase IV: thyroid structure and function back to normal
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54
Q

What is the key investigation for de Quervain’s thyroiditis and what does it show?

A

Thyroid scintigraphy - globally reduced uptake of iodine 131

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55
Q

What is the management of de Quervain’s tenosynovitis?

A
  • Usually self limiting and doesn’t require treatment
  • thyroid pain may respond to aspirin / NSAIDS
  • steroids if severe
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56
Q

What is the presentation of a branchial cyst?

A

Oval, mobile cystic mass between SCM and pharynx, present early adulthood. Due to failure of obliteration of 2nd branchial cleft in embryonic development

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57
Q

What is a cystic hygroma?

A

Fluctuant lump L side of neck, presents at birth or <2 years due to congenital lymphatic lesion (lymphangioma)

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58
Q

What are the key features of a thyroglossal cyst?

A

< 20 years old, midline, between isthmus of thyroid and hyoid bone, moves up with protrusion of tongue

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59
Q

What are 3 types of amiodarone-induced thyroid disease?

A
  1. Hypothyroidism - high iodine content causing Wolff Chaikoff effect (thyroxine level inhibited due to high circulating iodide)
  2. Amiodarone-induced thyrotoxicosis type 1 - excess iodine induced thyroid synthesis
  3. AIT type 2 - Amiodarone-related destructive thyroiditis
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60
Q

Which type of amiodarone induced thyrotoxicosis is associated with goitre?

A

AIT type 1 - excess iodine induced thyroid hormone synthesis

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61
Q

What is the treatment of AIT type 1?

A

Carbimazole or potassium perchlorate

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62
Q

What is the treatment of AIT type 2?

A

Corticosteroids

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63
Q

What are 4 key features of primary hyperaldosteronism?

A
  1. hypertension
  2. hypokalaemia
  3. hypernatraemia
  4. metabolic acidosis
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64
Q

What is the commonest cause of primary hyperaldosteronism?

A

bilateral idiopathic adrenal hyperplasia

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65
Q

In addition to bilateral idiopathic adrenal hyperplasia, what are 4 other causes of primary hyperaldosteronism?

A
  1. Conn’s syndrome - due to adrenal adenoma
  2. Unilateral hyperplasia
  3. Familial hyperaldosteronism
  4. Adrenal carcinoma
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66
Q

What is the first-line investigation in suspected primary hyperaldosteronism and what will it show?

A
  • plasma aldosterone/renin ratio
  • high aldosterone levels, low renin levels (negative feedback due to sodium retention from aldosterone)
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67
Q

What is the next step if serum renin/aldosterone ratio is measured and is suggestive of primary hyperaldosteronsim?

A
  • high-resolution CT abdomen & adrenal vein sampling - to differentiate between unilateral and bilateral sources of aldosterone excess
  • if CT normal, adrenal venous samplling (AVS) can distinguish between unilateral adenoma + bilateral hyperplasia
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68
Q

What are the management options for primary hyperaldosteronism?

A
  • surgery (laproscopic adrenalectomy) - if adrenal adenoma
  • aldosterone antagonist e.g. spironolactone - if bilateral adrenocortical hyperplasia
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69
Q

What is the definitive investigation in Addison’s disease and how is it performed?

A
  • Short synacthen test (ACTH stimulation test) - plasma cortisol measured before and 30 min after giving synacthen 250ug IM.
  • Adrenal autoantibodies such as anti-32-hydroxylase may also be demonstrated
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70
Q

What is an alternative investigation for ?Addison’s if a short synacthen test is not readily available?

A

9am serum cortisol - >500 nmol/L makes Addison’s very unlikely, <100 nmol/L is definitely abnormal, 100-500nmol/L should prompt ACTH stimulation test

71
Q
A
72
Q

Which oral hypoglycaemic drug is associated with pancreatitis?

A

DPP-4 inhibitors (gliptins)

73
Q

What are 4 side effects associated with sulphonylureas?

A
  1. Hypoglycaemia
  2. SIADH
  3. Increased appetite and weight gain
  4. Liver dysfunction (cholestatic)
74
Q

What is thyroid storm?

A

life-threatening complication of thyrotoxicosis; seen in patients with established thyrotoxicosis (rarely seen as presenting features)

75
Q

What are 4 possible precipitants of thyroid storm in someone with thyrotoxicosis?

A
  1. thyroid or non-thyroidal surgery
  2. trauma
  3. infection
  4. acute iodine load e.g. CT contrast media
76
Q

What are 7 clinical features of thyroid storm?

A
  1. fever >38.5 C
  2. tachycardia
  3. confusion and agitation
  4. nausea and vomiting
  5. hypertension
  6. heart failure
  7. abnormal liver function tests + clinical jaundice
77
Q

What are 6 aspects of the treatment of thyroid storm?

A
  1. symptomatic treatment e.g. paracetamol
  2. treat underlying precipitant
  3. beta blockers - IV propranolol
  4. anti-thyroid drugs: methimazole or propylthiouracil
  5. Lugol’s iodine (at least 1h, ideally 4h, after antithyroid drugs)
  6. dexamethasone (blocks conversion of T4 to T3)
78
Q

What is the target HbA1c for Type 1 diabetes mellitus?

A

48 mmol/mol or lower

79
Q

What is recommended for self-monitoring of blood glucose in type 1 diabetes mellitus?

A

at least 4 times a day, including before each meal and before bed

80
Q

What are 6 situations when the frequency of self monitoring of blood glucose should increase in T1DM?

A
  1. if frequency of hypos increases
  2. periods of illness
  3. before, during and after sport
  4. planning pregnancy
  5. during pregnancy
  6. while breastfeeding
81
Q

What are the blood glucose targets for T1DM?

A
  • 5-7 mmol/l on waking
  • 4-7 mmol/before meals + at other times of day
82
Q

What types of insulin regime can be offered in T1DM?

A
  • basal-bolus - regimen of choice
  • involves twice daily detemir (alternatives = once daily glargine or determir)
  • rapid-acting analogues before meals (not rapid-acting soluble human or animal insulins)
83
Q

When do NICE recommend adding metformin in type 1 diabetes mellitus?

A

if BMI 25 or above

84
Q

What are 3 types of drugs which can cause hypothyroidism?

A
  1. lithium
  2. amiodarone
  3. antithyroid drugs such as carbimazole
85
Q

What are 3 causes of secondary hypothyroidism?

A

pituitary failure:
1. Down’s syndrome
2. Turner’s syndrome
3. coeliac disease

86
Q

What is the commonset cause of hypothyroidism?

A

Hashimoto’s thyroiditis

87
Q

What is the commonst cause of hypercalcaemia in non-hospitalised vs. hospitalised patients?

A
  • non-hospitalised: primary hyperparathyroidism
  • hospitalised: malignancy
88
Q

What are 4 ways in which malignancy can cause hypercalcaemia?

A
  1. PTHrP in squamous cell lung cancer
  2. bony mets
  3. myeloma - due to increased osteoclastic bone resoprtion due to local cytokines (IL-1, TNF) released by myeloma cells
89
Q

What can cause hypercalcaemia in Paget’s disease of the bone?

A

usually normal in this condition but hypercalcaemia may occur with prolonged immobilisation

90
Q

What are 4 groups advised to take vitamin D supplementation?

A
  1. all pregnant + breastfeeding women - 10micrograms / day
  2. all children aged 6 months - 5 years (if >500mls formula milk/day, don’t need)
  3. adults <65y
  4. those not exposed to much sun e.g. housebound
91
Q

Is testing vitamin D levels necessary in osteoporosis?

A

these patients should always be given calcium/vitamin D supplements so testing is not considered neecssary

92
Q

What are 3 patients groups in whom vitamin D levels should be tested?

A
  1. bone diseases that may be improved with vit D treatment - e.g. known osteomalacia or Paget’s
  2. bone diseases prior to specific treatment where correcting deficiency is appropriate e.g. prior to IV zoledronate or denosumab
  3. MSK symptoms that could be attributed to vit D deficiency e.g. bone pain ?osteomalacia
93
Q

What are 8 non-drug causes of gynaecomastia?

A
  1. physiological - normal in puberty
  2. syndomres with androgen insufficiency: Kallmans, Klinefelters
  3. Testicular failure e.g. mumps
  4. Liver disease
  5. Testicular cancer e.g. seminoma secreting hCG
  6. ectopic tumour secretion
  7. hyperthyroidism
  8. haemodialysis
94
Q

What are 8 drug causes of gynaecomastia?

A
  1. spironolactone (most common)
  2. cimetidine
  3. digoxin
  4. cannabis
  5. finasteride
  6. GnRH agonists e.g. goserelin, buserelin
  7. oestrogens
  8. anabolic steroids
95
Q

What are the 2 types of diabetic foot disease?

A
  • neuropathy: loss of protective sensation (e.g. not noticing a stone in the shoe), Charcot’s arthropathy, dry skin
  • peripheral arterial disease: macro + microvascular ischaemia
96
Q

How frequently should diabetic foot screening occur?

A

at least annually

97
Q

What does diabetic foot screening entail?

A
  • palpating for dorsalis pedis pulse + posterior tibial artery pulse
  • 10g monofilament used on various parts of sole of foot
98
Q

What are the 3 groups that patients with diabetic foot disease are classed into?

A
  1. low risk: no risk factors except callus alone
  2. moderate risk: deformity / neuropathy / non-critical limb ischaemia
  3. high risk: previous ulceration / amputation / renal replacement therapy / neuropathy and non-critical limb ischaemia together / neuropathy with callus and/or deformity / non-critical limb ischaemia with callus and/or deformity
99
Q

How should patients who are moderate or high risk diabetic foot disease be managed (anything other than callus alone)?

A

followed up regularly by local diabetic foot centre

100
Q

Which type of thyroid cancer is associated with a rise in serum calcitonin?

A

medullary thyroid cancer

101
Q

What is the mechanism of action of pioglitazone?

A

thiazolidinedione - agonst to PPAR-gamma receptor (intracellular nuclear receptor), natural ligands are free fatty acids, receptor thought to control adipocyte function. reduces peripheral insulin resistance

102
Q

What are 5 adverse effects of pioglitazone?

A
  1. weight gain
  2. liver impairment (need to monitor LFTs)
  3. fluid retention - CI in heart failure
  4. increased risk of fractures
  5. bladder cancer
103
Q

What are 6 causes of hypoglycaemia?

A
  1. self-administration of insulin/sulphonylureas
  2. insulinoma (increased ratio proinsulin to insulin)
  3. liver failure
  4. Addison’s disease
  5. alcohol
  6. nesidioblastosis - beta cell hyperplasia
104
Q

How can alcohol cause hypoglycaemia?

A

exaggerated insulin secretion, thought to be due to effect of alcohol on pancreatic circulation - redistribution of pancreatic blood flow from exocrine into endocrine parts, increased insulin secretion

105
Q

What are 5 hormonal responses to hypoglycaemia?

A
  1. decreased insulin secretion
  2. increased glucagon secretion
  3. growth hormone release
  4. cortisol release
  5. increased catecholamine and acetylcholine mediated neutotransmission in autonomic nervous system + CNS
106
Q

Below which capillary blood glucose level are neuroglycopenic symptoms due to inadequate glucose supply to the brain seen?

A

<2.8 mmol/L

107
Q

What are 4 causes of primary hyperparathyroidism and their relative frequencies?

A
  1. solitary adenoma - 85%
  2. hyperplasia - 10%
  3. multiple adenoma - 4%
  4. carcinoma - 1%
108
Q

What will bloods show in primary hyperparathyroidism?

A
  • raised calcium, low phosphate
  • PTH may be raised or (inappropriately) normal
109
Q

What are 2 investigations that may be performed in primary hyperparathyroidism?

A
  1. technetium-MIBI subtraction scan
  2. xray: pepperpot skull, osteitis fibrosa cystica
110
Q

What is the definite management of primary hyperparathyroidism?

A

total parathyroidectomy

111
Q

When may conservative management be offered in primary hyperparathyroidism?

A

if calcium <0.25 mmol/L above the ULN AND patient is >50 years AND no evidence of end-organ damage

112
Q

What is a medical option for treatment patients with primary hyperparathyroidism who are not suitable for surgery?

A

cinacalcet - calcimimetic, allosteric activation of calcium-sensing receptor

113
Q

What is myeloma?

A

plasma cell proliferation - genetic mutation occurs as B-lymphocytes differentiate into mature plasma cells

114
Q

What is the primary factor causing hypercalcaemia in myeloma?

A

increased osteoclastic bone resorption caused by local cytokines (e.g. IL-1, TNF) released by myeloma cells

115
Q

What will peripheral blood film show in myeloma?

A

rouleaux formation

116
Q

What will protein electrophoresis show in myeloma?

A

raised concentations of monoclonal IgA/IgG proteins (Bence-Jones proteins in urine)

117
Q

What confirms the diagnosis of myeloma?

A

Bone marrow aspiration - raised number of plasma cells

118
Q

How is skeletal survey carried out in myeloma?

A

whole body MRI

119
Q

What are 3 major criteria for myeloma?

A
  • Plasmacytoma (as demonstrated on evaluation of biopsy specimen)
  • 30% plasma cells in a bone marrow sample
  • Elevated levels of M protein in the blood or urine
120
Q

What are 4 minor criteria for myeloma?

A
  • 10% to 30% plasma cells in a bone marrow sample.
  • Minor elevations in the level of M protein in the blood or urine.
  • Osteolytic lesions (as demonstrated on imaging studies).
  • Low levels of antibodies (not produced by the cancer cells) in the blood.
121
Q

Of the major and minor criteria, what constitutes a diagnosis of myeloma?

A

1 major and 1 minor, or 3 minor

122
Q

What causes secondary hyperparathyroidism?

A
  • caused by chronic hypocalcaeia e.g. chronic kidney disease
  • serum calcium will be low or normal, causing high PTH
123
Q

What is tertiary hyperparathyroidism?

A

develops from secondary hyperparathyroidism and results in autonomous parathyroid production - seen in end-stage renal disease

124
Q

How does androgen insensitivity syndrome present at puberty?

A
  • ‘primary amenorrhoea’ no period in female presenting adolescent
  • little or no axillary and pubic hair
  • undescended testes causing groin swellings
  • breast development may occur as a result of conversion of testosterone to oestradiol
125
Q

What causes androgen-insensitivity syndrome?

A

X-linked recessive condition due to end-organ resistance to testosterone causing genotypically male children (46XY) to have a female phenotype

new term for tesicular feminisation syndrome

126
Q

How is a diagnosis of androgen insensitivity syndrome made?

A
  • buccal smear or chromosomal analysis to reveal 46XY genotype
  • testosterone concernations - high-normal to slightly elevated range for postpubertal boys
127
Q

What is the management of androgen insensitivity syndrome?

A
  • counselling - raise child as female
  • bilateral orchidectomy (risk of testicular cancer due to undescended testes)
  • oestrogen therapy
128
Q

What is the presentation fo congenital adrenal hyperplasia?

A
  • primary amenorrhoea
  • development of male secodnary sexual characteristics in females (e.g. deep voice and hirsutism) - due to impaired cortisol synthesis leading to surplus progesterone
129
Q

```

~~~

What should be prescribed prior to moderate-major surgery for patients taking long term steroid therapy?

A

hydrocortisone -
* moderate: 50mg before induction and 25mg every 8h for 24h
* major: 100mg hydrocortisone before induction, 50mg every 8h for 24h, thereafter halving dose every 24h until maintenance reached

130
Q

What are 2 groups that the causes of Cushing’s syndrome can be split into?

A
  1. ACTH-dependent causes
  2. ACTH-independent causes
131
Q

What are 2 examples of ACTH-dependent causes of Cushing’s syndrome?

A
  1. Cushing’s disease i.e. pituitary adenoma -> ACTH secretion
  2. ectopic ACTH secretion secondary to malignancy
132
Q

What is an ACTH-independent cause of Cushing’s syndrome?

A

adrenal adenoma

133
Q

What key electrolyte / metabolic disturbance is seen in Cushing’s syndrome?

A

hypoakalaemic metabolic alkalosis (+ impaired glucose tolerance)

134
Q

Which cause of Cushing’s syndrome is characteristically associated with very low potassium levels?

A

ectopic ACTH secretion e.g. small cell lung cancer

135
Q

What are the 3 most commonly used tests to confirm Cushing’s syndrome?

A
  1. Overnight (low-dose) dexamethasone suppression test (first line)
  2. 24h urinary free cortisol - 2x measurements
  3. bedtime salivary cortisol - 2x measurements
136
Q

What is the first line localisation test for Cushing’s syndrome?

A
  • 9am and midnight plasma ACTH (and cortisol) levels
  • if ACTH is suppressed, then a non-ACTH dependent cause is likely, such as an adrenal adenoma
137
Q

In addition to 9am and plasma ACTH levels, what are 4 other tests that can help localise the cause of Cushing’s syndrome?

A
  1. High-dose dexamethasone suppression test
  2. CRH stimulation - if pituitary source, cortisol rises, if ectopic/adrenal no change
  3. Petrosal sinus sampling of ACTH
  4. Insulin stress test - true Cushing’s vs pseudo-Cushing’s
138
Q

How can the high-dose dexamethasone suppression test be used to help localise the cause in Cushing’s syndrome?

A
  • Cortisol not suppressed, ACTH suppressed: Adrenal adenoma
  • Cortisol suppressed, ACTH suppressed: Cushing’s disease i.e. pituitary adenoma
  • Cortisol not suppressed, ACTH not suppressed: ectopic ACTH syndrome
139
Q

What is the difference between sick euthyroid syndrome and subclinical hypothyroidism?

A
  • subclinical hypothyroidism - raised TSH with normal thyroxine
  • sick euthyroid - low thyroxine, low or normal TSH - seen in acute illness
140
Q

What type of peripheral neuropathy is typically seen in diabetes?

A

sensory - glove and stocking distribution

141
Q

What are 4 options for the first-line treatment of diabetic peripheral neuropathy causing neuropathic pain?

A
  1. amitriptyline
  2. duloxetine
  3. gabapentin
  4. pregabalin
142
Q

What can be used as rescue therapy for exacerbation of diabetic neuropathic pain?

A

tramadol

143
Q

What can be used for localised diabetic neuropathic pain e.g. post-herpetic neuralgia?

A

topical capsaicin

144
Q

What are 3 types of GI autonomic neuropathy seen in diabetes?

A
  1. gastroparesis
  2. chronic diarrhoea
  3. GORD
145
Q

What are 3 management options for gastroparesis?

A
  1. metoclopramide
  2. domperidone
  3. erythromycin
146
Q

What is used an initial treatment for Graves disease?

A

propranolol - block adrenergic effects

147
Q

Who should manage Graves disease?

A

should be referred to secondary care - but carbimazole can be considered in primary care if symptoms not controlled with propranolol

148
Q

How is carbimazole prescribed to treat Graves disease?

A
  • start 40mg - reduce gradually to maintain euthyroidism
  • continue 12-18 months
149
Q

What is meant by the block-and-replace anti-thyroid therapy for Graves disease?

A
  • carbimazole started 40mg
  • thyroxine added when patient euthyroid
  • treatment lasts 6-9 months
150
Q

Of block and replace and an ATD titration regime, which has fewer side-effects?

A

ATD titration

151
Q

When is radioiodine treatment used to treat Graves disease?

A

patients who relapse after ATD therapy or reistant to primary ATD treatment

152
Q

What are 3 contraindications to radioiodine treatment of Graves’ disease?

A
  1. pregnancy - avoid pregnancy for 4-6 months after treatment
  2. age < 16
  3. thyroid eye disease - may worsen condition
153
Q

How many patients who have radioiodine treatment become hypothyroid?

A

the majority with require thyroxine supplementation after 5 years

154
Q

What is the commonest cause of secondary hypertension?

A

primary hyperaldosteronism

155
Q

Of the causes of hyperthyroidism, which causes tender goitre and which causes non-tender?

A
  • non-tender goitre: Graves’ disease
  • tender goitre: subacute (de Quervain’s) thyroiditis
156
Q

How can steroid therapy affect TFTs?

A

low TSH, normal free T4

157
Q

How can osmolarity be calculated e.g. in suspected HHS?

A

2x sodium + glucose + urea

158
Q

What fluids should be given and at what rate in HHS?

A

0.9% saline 0.5-1 L / hour

159
Q

What is the underlying pathophysiology of DKA?

A

uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies

160
Q

What are the 3 most common factors precipitating DKA?

A
  1. infection
  2. missed insulin doses
  3. MI
161
Q

What are the thresholds for potassium replacement in DKA?

A
  • > 5.5: no replacement
  • 3.5 - 5.5: 40 mmol / L
  • < 3.5: senior review as additional K+ needed
162
Q

After what time period should DKA be expected to have resolved, otherwise prompting endocrinologist review?

A

24 hours

163
Q

What is the best test for acromegaly?

A

insulin-like growth factor 1 (IGF-1) - better than growth hormone

164
Q

What is the commonset type of diabetes insipidus?

A

neurogenic DI - deficiency of ADH

165
Q

What are 4 causes of acquired nephrogenic diabetes insipidus?

A
  1. Hypokalaemia
  2. Hypercalcaemia
  3. CKD
  4. Drugs: Lithium and demeclocycline
166
Q

What are 3 aspects of management of nephrogenic diabetes insipidus?

A
  1. stop any precipitating drugs
  2. if mild: correct deficits in extracellular fluid volume with oral water intake
  3. more severe: desmopressin, thiazide diuretics, NSAIDs (e.g. indemethacin), sodium restriction
167
Q

What will serum and urine osmolality be in nephrogenic diabetes insipidus?

A
  • serum: high osmolality
  • urine: low osmolality
168
Q

What will serum and urine osmolality be for neurogenic (cranial) diabetes insipidus?

A
  • serum: high
  • urine: low after fluid deprivation; high after exogenous ADH given
169
Q

What are 8 situations when HbA1c should NOT be used to make a diagnosis of diabetes?

A
  1. ALL children and young people
  2. any age suspected of T1DM
  3. symptoms of diabetes < 2 months
  4. at high diabetes risk who are acutely ill e.g. requiring hospital admission
  5. taking medication that may cause rapid glucose rise e.g. steroids, antipsychotics
  6. acute pancreatic damage including pancreatic surgery
  7. pregnancy
  8. genetic, haematologic + illness related factors that influence HbA1c measurement - haemoglobinopathies, haemolytic anaemia, iron deficiency anaemia must be treated first
170
Q

What is the presenting feature of MEN1 in most patients?

A

renal colic from renal stones - tumours hypersecrete hormone -> hyperparathyroidism -> hypercalcaemia

171
Q

What are 6 features of MEN1?

A
  1. hypercalcaemia - hyperparathyroidism
  2. Zollinger-Ellison (hypergastrinaemia)
  3. Hypoglycaemia (hyperinsulinaemia)
  4. Amenorrhoea (hyperprolactinaemia)
  5. Acromegaly (excess growth hormone)
  6. Mass effects from tumours of pituitary
172
Q

How do patients with MEN2 typically present?

A

symptoms related to medullary thyroid cancer, hyperparathyroidism, or phaeochromocytoma

173
Q

Which genetic change causes MEN1?

A

tumour suppressor gene MEN1

174
Q

Which genetic change causes MEN2?

A

RET proto-oncogene

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