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Phase 3 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is the role of LH?

A

Interacts with theca interna cells which results in androgen production

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2
Q

What is the role of FSH?

A

Stimulates aromatase synthesis which catalyses formation of oestrogens
Stimulates ovum and follicle development

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3
Q

What is sex hormone binding globulin?

A

B globulin that transports testosterone, dihydrotestosterone and oestradiol in plasma

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4
Q

Where is sex hormone binding globulin produced?

A

Liver

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5
Q

What might cause a decrease in sex hormone binding globulin levels?

A 
Androgenic things 
Obesity
Hypothyroidism
Androgen use
Nephrotic syndrome
Cushings disease
Acromegaly 
PCOS
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6
Q

What can cause and increase in sex hormone binding globulin levels?

A 
Oestrogenic states 
Hepatic cirrhosis 
Hyperthyroidism
Oestrogen use 
Pregnancy 
Oral contraceptives 
Anorexia
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7
Q

What can cause pseudohyponatraemia?

A

Severe hyperlipidaemia
Paraproteinaemia
Iso osmotic non sodium containing fluids to extracellular space - sorbitol/glycine flushing solutions used in urology

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8
Q

What is pseudohyponatraemia?

A

Low measured serum sodium

Normal serum osmolality

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9
Q

What is Kallmann syndrome?

A

Congenital disorder of hypothalamic function and reduced pituitary gonadotropic activity

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10
Q

What are the main features of kallmann syndrome?

A

Hypogonadism
Eunuchoidism
Anosmia

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11
Q

In what disease do you find autoantibodies to glutamic acid decarboxylase?

A

Diabetes mellitus

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12
Q

What can cause adrenal hypertension?

A

Primary aldosteronism
Cushing’s syndrome
Phaechromocytoma

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13
Q

What are features of haemochromatosis?

A 
New diagnosis diabetes
Hypogonadism
Deranged liver function
Pigmentation 
Elevated serum ferritin
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14
Q

A 32 year old lady with BMI of 34 attends clinic complaining of two month history of amenorrhoea. She is noted to have glycosuria and fasting plasma glucose of 12.5. Her oestrogen and prolactin levels are high while LH and FSH concentrations are low. What is the likely diagnosis?

A

Pregnancy

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15
Q

A 42 year old man with a history of cholecystitis and recurrent abdo pain develops diabetes mellitus. What is the underlying diagnosis?

A

Chronic pancreatitis

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16
Q

What is the most useful test for assessing the appropriateness of thyroid hormone replacement in primary hypothyroidism?

A

TSH

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17
Q

What are characteristics of active acromegaly?

A

Increased sweating
Glucose intolerance
Hypertension

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18
Q

What hormone levels are typical of PCOS?

A

Elevated testosterone

High LH

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19
Q

What are the Rotterdam criteria for diagnosis of PCOS?

A

Diagnosis if 2/3:
Oligomenorrhoea or anovulation
Clinical and/or biochemical evidence of hyperandrogenism
Polycystic ovaries on ultrasonography

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20
Q 
A 50 year old male with T2DM has a spot urinary albumin:creatinine ratio of 3.4mg/mmol
Which drug class should be used to retard progression of his renal disease? Why?
A

ACE inhibitor
Urinary ACR over 2.5 in man suggests microalbuminuria
First manifestation of diabetic nephropathy and predicts development of overt nephropathy

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21
Q

On which chromosome is the problem in neurofibromatosis type 1?

A

17

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22
Q

What are characteristics of neurofibromatosis type 1?

A 
Cafe au lait spots
Axillary freckling
Dermal neurofibromas
Nodular neurofibromas
Lisch nodules on iris
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23
Q

What are complications of neurofibromatosis?

A

Nerve compression
Phaechromocytoma
Mild learning disability
Epilepsy

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24
Q

What are features of neurofibromatosis type 2?

A

Cafe au lait spots
Vestibular schwannomas
Premature cataract

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25
Q

If there is a goitre over which there is a bruit, what is the diagnosis? Why?

A

Graves’ disease

Associated with angiogenesis and thyroid follicular hypertrophy

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26
Q

What are Graves eye signs?

A 
Conjunctival oedema (chemosis)
Exopthalmos
Proptosis 
Lid retraction
Lid lag 
Periorbital puffiness
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27
Q

What is a dermatological manifestation of Graves’ disease?

A

Pretibial myxoedema

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28
Q

What are biochemical features of conns syndrome?

A

Hypokalaemia
Alkalosis
Low renin
HTN

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29
Q

What are causes of conns syndrome?

A

Adrenal adenoma

Bilateral adrenal hyperplasia

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30
Q

What are some causes of SIADH?

A 
Hypothyroidism 
Bronchial Ca
Pneumonia
Head injury
Subarachnoid haemorrhage
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31
Q

How do you calculate plasma osmolality?

A

(2 [sodium + potassium] + glucose + urea)

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32
Q

What problems are associated with GH therapy?

A

Pituitary derived GH: CJD

Recombinant GH: IIH

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33
Q

How is a diagnosis of Addison’s disease made?

A

Demonstrating low cortisol levels without diurnal variation with a raised ACTH
Synacthen test shows failure of cortisol secretion following subcutaneous admin of ACTH

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34
Q

A 62 year old is reviewed complaining of lethargy and fatigue. He smokes 10 cigarettes a day and drinks 15 units of alcohol a week. His blood tests show a hyponatraemia of 128. What are 2 appropriate investigations for this patient? Why?

A

Chest X-ray - bronchial Ca with SIADH

TFTs - hypothyroidism

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35
Q

A 59 year old male attends clinic for his first annual review of type 2 diabetes. Most recently he had problems with OA affecting hips and 2nd/3rd metacarpophalangeal joints. Currently he takes aspirin and metformin. When his LFTs are checked prior to commencing a statin, he is found to have AST 78, ALT 88, ALP 210, bilirubin 10. He doesn’t drink, his BMI is 24, he is negative for hep B and C, he is negative for ANA, ASMA, LKM and AMA. His caeruloplasmin is normal. What is the likely cause?

A

Haemochromatosis

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36
Q

Where is leptin produced?

A

Adipocyte

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37
Q

Where are receptors for leptin located? What is it’s effect?

A

Arcuate nucleus in the hypothalamus

Produces satiety

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38
Q

What are clinical features of acromegaly?

A 
Spade like hands
Prominent supraorbital ridge
Prognathism
Macroglossia
Carpal tunnel syndrome
Oily skin
Paraesthesia 
Visual field disturbance 
Hypopituitarism
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39
Q

What are complications of acromegaly?

A

Hypertension
Cardiomyopathy
Hyperglycaemia/diabetes mellitus
Bowel tumours

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40
Q

What is whipples triad?

A

Diagnosis of hypoglycaemia requires:
Evidence of plasma hypoglycaemia <3
Associated symptomatology
Resolution of sequelae with correction of hypo

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41
Q

What is the management of hypoglycaemia in an inpatient who has reduced consciousness?

A

100ml 20% dextrose IV

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42
Q

What causes of hypoglycaemia should be investigated if the episode cannot be explained?

A 
EXPLAIN
EXogenous insulin administration
Pituitary insufficiency 
Liver failure
Alcohol/autoimmune/Addisons
Insulinoma
Neoplasia
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43
Q

What can cause Thyrotoxicosis?

A

Graves’ disease
Multinodular goitre
Drug induced - Amiodarone

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44
Q

A 13 year old girl starting wetting the bed after being dry from the age of 3. Mother notices she is drinking large volumes of fluids. Two days later she has difficulty breathing and loses consciousness. What is going on?

A

Diabetes mellitus

May initially present as enuresis

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45
Q

An 8 month old infant boy is failing to thrive. He is vomiting, dehydrated, polyuric and is irritable. His blood sugars are normal and he doesn’t have a UTI. What’s going on?

A

X linked recessive nephrogenic diabetes insipidus

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46
Q

What conditions make up sipple syndrome?

A

MEN2A
Bilateral medullary carcinoma of thyroid or C cell hyperplasia
Phaeochromocytoma
Hyperparathyroidism

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47
Q

At what HbA1c level should you add in a second antidiabetic drug after Metformin has been titrated?

A

58 (7.5%) and above

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48
Q

What is the target HbA1c for patients with diabetes using lifestyle changes alone or lifestyle and Metformin?

A

48 (6.5%)

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49
Q

What is the target HbA1c for patients with diabetes using any drug which may cause hypoglycaemia?

A

53 (7%)

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50
Q

What drugs can be added in if Metformin is not adequately controlling diabetes and HbA1c remains above 58?

A

Gliptin
Sulfonylurea
Pioglitazone
SGLT2 inhibitor

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51
Q

What is the therapy of choice if triple therapy (Metformin plus 2 others) are not effective, not tolerated or contraindicated and the patient has a BMI of over 35?

A

Metformin and sulfonylurea and GLP1 mimetic (exanatide)

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52
Q

What risk factor modifications are important in diabetes?

A

Blood pressure target <140/80 or <130 if end organ damage present. ACEi first line
Antiplatelets only if existing CV disease
Statin if QRISK2 score >10%

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53
Q

What are diagnostic criteria for diabetes?

A

If symptomatic:
Fasting glucose 7 or more
Random glucose/OGTT 11.1 or more
Asymptomatic: same but on two separate occasions

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54
Q

In what conditions can HbA1c not be used for diagnosis?

A 
Haemaglobinopathies
Haemolytic anaemia 
Untreated Iron deficiency anaemia
Suspected gestational diabetes 
Children
HIV
CKD
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55
Q

What HbA1c value is diagnostic of diabetes?

A

48 or more

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56
Q

How do you diagnose impaired fasting glucose?

A

Fasting glucose 6.1 or more but less than 7

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57
Q

How do you diagnose impaired glucose tolerance?

A

Fasting plasma glucose less than 7

OGTT 7.8 or more, less than 11.1

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58
Q

What is McCune Albright syndrome? What are features?

A

Genetic condition affecting bone, skin and endocrine systems
Early puberty in girls, bone fractures, gigantism, cafe au lait spots

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59
Q

What are features of an Addisonian crisis?

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia

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60
Q

What can cause an Addisonian crisis?

A

Sepsis or surgery causing an acute exacerbation of chronic insufficiency
Adrenal haemorrhage (Waterhouse friderichsen syndrome)
Steroid withdrawal

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61
Q

What is the management of Addisonian crisis?

A

Hydrocortisone 100mg IM or IV
1L normal saline infused over 30-60 mins, with dextrose if hypoglycaemic
Continue hydrocortisone every 6h until stable
Oral replacement may begin after 24h and reduce to maintenance over 3-4 days

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62
Q

What are some causes of Gynaecomastia?

A

Physiological: normal in puberty
Syndromes with androgen deficiency: Kallman’s, Klinefelter’s
Testicular failure: e.g. mumps
Liver disease
Testicular cancer e.g. seminoma secreting hCG
Ectopic tumour secretion
Hyperthyroidism
Haemodialysis
Drugs: spironolactone, cimetidine, digoxin, cannabis, finasteride, gonadorelin analogues e.g. Goserelin, buserelin, oestrogens, anabolic steroids

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63
Q

What are some contraindications for Metformin use?

A

Chronic kidney disease: NICE recommend dose should be reviewed if creatinine is > 130 micromol/l (or eGFR < 45 ml/min) and stopped if the creatinine is > 150 micromol/l (or eGFR < 30 ml/min)
Metformin may cause lactic acidosis if taken during a period where there is tissue hypoxia - recent MI, sepsis, AKI and severe dehydration
Iodine-containing x-ray contrast media: peripheral arterial angiography, coronary angiography, intravenous pyelography (IVP); there is an increasing risk of provoking renal impairment due to contrast nephropathy; metformin should be discontinued on the day of the procedure and for 48 hours thereafter
Alcohol abuse is a relative contraindication

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64
Q

Why does refeeding syndrome occur? What changes are seen?

A

Exogenously administered glucose results in insulin release and therefore rapid uptake of glucose, potassium, phosphate and magnesium into cells. Fluid is also retained into the extracellular space.
Abnormal fluid balance, vitamin deficiency, hypophosphataemia, hypomagnesaemia, hypokalaemia

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65
Q

What are the most common causes of hypercalcaemia?

A

Malignancy: bone mets, myeloma, PTHrP

Primary hyperparathyroidism

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66
Q

What are some less common causes of hypercalcaemia to consider beside malignancy and hyperpararhyroidism?

A 
Sarcoidosis 
TB
Vitamin D intoxication
Acromegaly
Thyrotoxicosis
Milk alkali syndrome
Thiazides
Calcium containing antacids
Dehydration
Addison's disease
Paget's disease of bone
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67
Q

How is Addison’s disease likely to present?

A

Weight loss
Abdominal pain
Lethargy
Nausea and vomiting

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68
Q

What are causes of hyoadrenal crisis?

A 
Addison's disease
TB
HIV
Adrenal haemorrhage
Anterior pituitary disease
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69
Q

What biochemical changes will you see with Addison’s disease?

A

Hypoglycaemia
Hyponatraemia
Hyperkalaemia

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70
Q

Why is Addison’s disease associated with pigmentation?

A

Excess ACTH and therefore MSH (melanocyte stimulating hormone)

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71
Q

What effect does the administration of GnRH have on levels of oestrogen and how is this beneficial in endometriosis?

A

Induce a state of hypogonadotrophic hypogonadism or psuedomenopause with low circulating levels of oestrogen

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72
Q

What is the management for hypoadrenal crisis due to Addison’s disease?

A

Fluid resuscitation
Urgent cortisol measurement
Steroid administration
Search for occult infection

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73
Q

What are the most common causes of hypertriglyceridaemia?

A 
Obesity
Alcohol intake
Hypothyroidism
Insulin resistance
Poorly controlled diabetes 
Pregnancy 
Familial hypertriglyceridaemia
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74
Q

At what level of GFR should liraglutide (GLP1 agonist) be avoided?

A

If GFR <60

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75
Q

At what level of GFR should saxagliptin (DPP4 inhibitor) be prescribed at half dose?

A

<50

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76
Q

What are some causes of SIADH?

A

Malignancy: small cell lung cancer, pancreas, prostate
Neuro: stroke, SAH, subdural, meningitis
Infections: TB, pneumonia
Drugs: sulfonylureas, SSRI, TCA, carbamazepine, vincristine, cyclophosphamide
PEEP
Porphyria

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77
Q

How is SIADH managed?

A

Correction slowly to avoid central pontine myelinolysis
Fluid restriction
Demeclocycline
Vasopressin antagonist

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78
Q

How is Addison’s disease managed?

A

Hydrocortisone: 20-30mg/day, majority in morning dose
Fludrocortisone
Education on importance of not missing doses
MedicAlert bracelet/steroid card
Intercurrent illness, dose should be doubled

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79
Q

What are causes of an Addisonian crisis?

A

Sepsis or surgery causing acute exacerbation of chronic insufficiency
Ardrenal haemorrhage (waterhouse friderichsen syndrome)
Steroid withdrawal

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80
Q

What is management for an Addisonian crisis?

A

Hydrocortisone 100mg IM or IV
1L normal saline infused over 30-60 mins, or dextrose if hypoglycaemic
Continue hydrocortisone 6h until patient is stable
Oral replacement after 24h and reduce to maintenance over 3-4 days

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81
Q

What is maturity onset diabetes of the young?

A

Development of type 2 diabetes in patients under 25
Autosomal dominant condition
Usually responsive to sulfonylureas

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82
Q

What are the 3 Ds of pellagra (niacin deficiency)?

A

Dementia
Diarrhoea
Dermatitis

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83
Q

What are causes of hypercalciuria?

A

Vitamin D excess
High rates of skeletal turnover eg hyperparathyroidism
Renal tubular acidosis
Treatment with loop diuretic

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84
Q

Why is skin pigmentation seen with primary adrenal failure but not with secondary insufficiency?

A

Primary: problem in adrenal gland, lack of cortisol so compensatory increase in ACTH. This is made from POMC precursor which also is broken down to MST. This stimulates melanocytes so giving hyperpigmentation
Secondary: hypopituitarism and so lack of ACTH

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85
Q

What is thyroid acropachy?

A 
Clubbing of fingers
Painless
Periosteal bone formation 
Periosteal proliferation 
Soft tissue swelling, pigmented and hyperkeratotic
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86
Q

What is pre tibial myxoedema?

A

Slightly raised pinkish indurated patches usually on fronts of shins or dorsum of foot
Associated with Graves’ disease

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87
Q

What are some features of diabetic autonomic neuropathy?

A 
Tachycardia 
Constipation 
Impotence
Urinary retention 
Gastroparesis
Anhydrosis
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88
Q

What is the most appropriate treatment for diabetic gastroparesis?

A

Metoclopramide

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89
Q

Which anti diabetic mediation is associated with fluid retention and weight gain?

A

Pioglitazone

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90
Q

Why should metformin not be prescribed in patients with renal, hepatic or heart failure?

A

Lactic acidosis risk

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91
Q

What can form at the injection site of insulin?

A

Lipodystrophy

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92
Q

What is a problem with using porcine insulin?

A

Development of anti insulin antibodies

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93
Q

Which disease processes can cause salivary/parotid enlargement?

A 
Lymphoma
Sarcoidosis
Parotid tumour
Calculi
Virus: mumps 
Alcohol excess 
Anorexia nervosa/ bulimia
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5
Perfectly
94
Q

Deficiency of which other electrolyte can result in treatment unresponsive hypocalcaemia?

A

Magnesium as it is required for action of PTH

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95
Q

What are causes of raised prolactin?

A 
Pregnancy 
Prolactinoma
Physiological
PCOS
Primary hypothyroidism 
Phenothiazines, metoclopramide, domperidone
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96
Q

What are causes of peripheral neuropathy?

A 
Diabetes 
Alcohol
Vitamins (B)
Infection (Guillain Barre) 
Drugs: amiodarone, anticonvulsants, isoniazid, nitrofurantoin
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97
Q

What are complications of pagets?

A 
Hypercalcaemia 
High output failure
Pathological fractures
Platybasia (malformed relationship between occipital bone and cervical spine)
Sarcoma
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98
Q

What is the most common cause of hirsutism in women?

A

PCOS

99
Q

What is hitsutism?

A

Androgen dependent hair growth in women

100
Q

What are causes of hirsutism?

A 
PCOS
Cushing's syndrome
Congenital adrenal hyperplasia
Androgen therapy
Obesity (peripheral conversion oestrogen to androgen)
Adrenal tumour
Androgen secreting ovarian tumour
Phenytoin
101
Q

What is the Ferriman-Gallwey scoring system?

A

Assessment of hirsutism

9 body areas assigned a score 0-4. Score >15 indicates moderate to severe

102
Q

What is the management of hirsutism?

A

Weight loss
Waxing/bleaching
COCP - dianette or Yasmin
Facial: topical eflornithine (not in preg or breast feeding)

103
Q

What are risk factors for scurvy?

A 
Elderly patients particularly if live alone
Patients in developing world
Alcohol dependent
Smokers
Unbalanced diet
Peritoneal dialysis or haemodialysis
104
Q

What is the appropriate test for suspected phaeochromocytoma?

A

24 hour urinary vanillymandelic acid measurement (VMA)

105
Q

Which is the most appropriate test for suspected Addisons?

A

Synacthen test

106
Q

What are appropriate screening tests for Cushing’s syndrome?

A

1mg overnight dexamethasone suppression test (given at 11pm and cortisol measured at 9am)
24 hour urine free cortisol collection

107
Q

Why does a VIPoma lead to hypokalaemic acidosis?

A

Loss of alkaline secretions

108
Q

Why does thyrotoxicosis lead to hypercalciuria and elevated alk phos?

A

Increased bone turnover

109
Q

What are features of vitamin A deficiency?

A 
Night blindness
Dry skin
Dry conjunctiva
Xerophthalmia 
Bitots spots (white plaques of keratinised epithelial cells in conjunctiva)
110
Q

How does vitamin C deficiency present?

A

Bleeding gums
Muscle pain
Periosteal and perifollicular haemorrhages

111
Q

What are clinical features of osteomalacia?

A

Bone pain
Waddling gait due to proximal myopathy
Fractures

112
Q

What are features of pellagra?

A 
Diarrhoea
Dementia
Dermatitis 
Neuropathy
Ataxia 
Fits
113
Q

What is pellagra?

A

Lack of nicotinic acid

114
Q

Which hormones are released from the adrenal gland?

A

Mineralocorticoids
Glucocorticoids
Androgrens
Stress hormones

115
Q

What is the role of glucocorticoids in the body?

A

Facilitates hepatic gluconeogenesis
Inhibition of glucose uptake in muscle
Inhibition of protein synthesis
Reduces inflammatory processes

116
Q

Which zones of the adrenal gland are responsible for making each hormone?

A

Zona glomerulosa: mineralocorticoids
Zona fasciculata: glucocorticoids
Zona reticularis: androgens
Medulla: catecholamines

117
Q

What controls CRH release from the hypothalamus?

A

Circadian rhythm

Stress

118
Q

What are the biochemical abnormalities seen with Addison’s disease?

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia

119
Q

How is a diagnosis of Addisons made?

A

Short Synacthen Test (SST): IV or IM injection of synthetic ACTH (tetracosactide), If cortisol level after 30 mins fails to rise above 550nmol/L = adrenal insufficiency

120
Q

What is the management for addisons?

A

Long-term corticosteroid and mineralocorticoid replacement
Hydrocortisone: 20mg daily – 10mg on waking, then 10mg mid-afternoon or 5mg midday and 5mg mid-late afternoon
Replaces circadian rhythm
Fludrocortisone: Longer acting therefore only require 100 microgram OD
Patients entirely dependent on tablet replacement
Sick day rules
Steroid card

121
Q

What are signs and symptoms of Cushing’s?

A 
Hyperglycaemia
Moon face
Gynaecomastia
Fat deposit on face and back of shoulders
Osteoporosis
Sodium and fluid retention
Amenorrhoea
Hirsutism 
Thin skin
Purple striae 
Bruises
122
Q

How do you diagnose Cushing’s?

A

Dexamethasone suppression test - potent synthetic glucocorticoid that inhibits normal ACTH production
Low-dose dexamethasone suppression test: Defines glucocorticoid excess, Single 1mg dose at midnight, Failure to suppress 9am serum cortisol (<50nmol/L) = Cushing syndrome
High-dose dexamethasone suppression test: Localises glucocorticoid excess, 2mg x 8 doses 6hrly ending at midnight, >50% suppression at 9am of cortisol = Anterior pituitary source, <50% suppression at 9am = Extrapituitary ‘ectopic’ source

123
Q

What is the management of Cushing’s?

A

Surgical: Adrenal adenoma = adrenalectomy, Pituitary adenomas = transsphenoidal surgery
Rapid removal of cause can cause relative adrenal insufficiency so may need hydrocortisone cover until return to normal
Not fit for surgery: Radiotherapy, Metryrapone – inhibit glucocorticoid secretion

124
Q

What are causes of conns syndrome?

A

Discrete adenoma - tumour of the zona glomerulosa

Bilateral hyperplasia

125
Q

What are signs and symptoms of conns syndrome?

A

Hypokalaemia: Muscle fatigue, Tiredness
Hypertension: Headaches, Visual disturbances

126
Q

How is a diagnosis of conns made?

A

Evidence of features suggestive: Severe hypertension BP >180/100 mmHg, Difficult to control HTN despite use of multiple anti-hypertensive agents, Hypertension at a young age, Hypertension with spontaneous or diuretic induced hypokalaemia
Hypertension in patients with coexisting adrenal adenoma or hyperplasia
Calculation of the aldosterone:renin ratio – increased in disease
Confirmation of adrenal tumour on CT

127
Q

What are some side effects of treatment with recombinant human growth hormone?

A 
Raised ICP with normal MRI: results from antidiuretic effect, most common in those with impaired renal function
SUFE
Malignancy
Gynaecomastia 
Impaired glucose metabolism
128
Q

Which test is most appropriate for diagnosing acromegaly?

A

Oral glucose tolerance test

129
Q

What is the gold standard test for assessment of dynamic pituitary function including cortisol and growth hormone secretory capacity?

A

Insulin tolerance test

130
Q

What is diabetic nephropathy?

A

Persistent albuminuria >300 mg/day or >200 micrograms/min
Confirmed on at least 2 occasions 3-6 months apart
Relentless decline in GFR
Elevated BP

131
Q

What are signs of hyperprolactinaemia?

A 
Reduced libido and arousal 
Gynaecomastia 
Menstrual irregularities 
Amenorrhoea 
Galactorrhoea
132
Q

What are features of acromegaly?

A 
Coarse facial appearance 
Spade hands
Increase shoe size
Large tongue 
Prognathism 
Interdental spaces
Excessive sweating and oily skin
Hypopituitarism 
Headaches
Bitemporal hemianopia 
Galactorrhoea
133
Q

What are complications of acromegaly?

A

HTN
Diabetes
Cardiomyopathy
Colorectal cancer

134
Q

What is the management of conns syndrome?

A

Surgical management: Unilateral adrenalectomy in presence of adenoma
Medical management: Spironolactone – mineralocorticoid receptor antagonist, Will result in rapid fall in refractory high blood pressure

135
Q

What is Phaeochromocytoma?

A

Tumour of the adrenal medulla secreting excessive catecholamines: Adrenaline / noradrenaline / dopamine

136
Q

What are signs and symptoms of Phaeochromocytoma?

A 
Intermittent due to paroxysmal release 
Anxiety / headache 
Palpitations / tachycardia 
Hypertension 
Sweating
137
Q

How is a diagnosis of Phaeochromocytoma made?

A

Urine collections of catecholamines or metabolites
24-hour urine metadrenaline and normetadrenaline collection due to variable production of catecholamines throughout day
Total urinary levels elevated in phaeochromocytoma
Plasma tests for metabolites higher sensitivity

138
Q

What is the management of Phaeochromocytoma?

A

Prevention of hypertensive crisis
Stabilise on medical therapy prior to any definitive surgical intervention
Medical: Blockade of alpha-adrenoceptors (doxazosin), Control peripheral vasoconstriction and hypertension, Control blood pressure
Followed by beta-adrenoceptor blockade (bisoprolol), Control pulse rate
Surgical removal of tumour

139
Q

What percentage weight loss should a patient be aiming for if they are put on orlistat?

A

5% weight loss in 3 months

140
Q

What levels of HBA1c are diagnostic for diabetes?

A

One off reading 48 if symptomatic

If no symptoms, 2 readings of 48 or more 3 months apart

141
Q

How often should women who have gestational diabetes be screened post partum?

A

Check initially post partum then repeat annually

142
Q

What should the HbA1c target of a diabetic controlled with diet alone be?

A

48

143
Q

What should the HbA1c target be for a diabetic patient on any drugs which may cause hypoglycaemia?

A

53

144
Q

Why should metformin be stopped in a patient with an MI?

A

Risk of lactic acidosis

145
Q

How does diabetic amyotrophy present?

A

Asymmetrical painful wasting of quadriceps and areflexia

146
Q

What are some manifestations of autonomic neuropathy?

A

Postural hypotension
Impotence
Gastroparesis
Neuropathic bladder

147
Q

What is the treatment for acromegaly?

A

Somatostatin analogues

Surgery

148
Q

What is the treatment for a prolactin secreting tumour?

A

Bromocriptine or cabergoline (dopamine agonists)

Surgery

149
Q

In a patient presenting with cushingoid features, what does a lack of suppression of cortisol levels with high dose dexamethasone suggest?

A

Ectopic source of ACTH for example from a small cell lung cancer

150
Q

What are the features of metabolic syndrome?

A 
Increased waist circumference: >94cm men, 80cm women. Or BMI over 30
Raised triglycerides: >1.7
Reduced HDL: <1.03, <1.29 in women
Raised BP: >130/85 or treated HTN
Raised fasting plasma glucose: >5.6
151
Q

Why does a hydatidiform mole lead to high levels of thyroxine?

A

Beta HCG is very similar in structure to LH, FSH and TSH so high levels can lead to production of T4 and T3

152
Q

Which diabetic patients should be offered statin therapy?

A

Type 1 who do not have established CVD risk factors but are:
Older than 40
Have had diabetes for more than 10 years
Have established nephropathy
Have other CVD risk factors such as obesity and HTN

153
Q

What are some causes of predominantly hypercholesterolaemia as opposed to hypertriglceridaemia?

A

Nephrotic syndrome
Cholestasis
Hypothyroidism

154
Q

Which antibodies are likely to be present in type 1 diabetes?

A

Islet cell

Glutamic acid decarboxylase

155
Q

What are features of diabetic autonomic neuropathy?

A 
Impotence
Postural hypotension 
Gastroparesis 
Steatorrhoea (bacterial overgrowth)
Atonic distended bladder
156
Q

What features confirm hyperosmolar hyperglycaemic state?

A

Dehydration
Osmolality >320
Hyperglycaemia >30 with pH >7.30, bicarbonate >15 and no significant ketonaemia <3

157
Q

What 2 differentials account for 90% of hypercalcaemia cases?

A

Primary hyperparathyroidism

Malignancy

158
Q

In which condition are Kimmelstiel Wilson nodules seen in the kidney?

A

Diabetic nephropathy

159
Q

What are 3 ways of monitoring glucose control over time?

A

HbA1c
Fructosamine
Log book of blood sugar levels

160
Q

What does dexa stand for?

A

Dual energy X-ray absorptiometry

161
Q

What is maturity onset diabetes of the young?

A

Development of type 2 diabetes mellitus in patients under 25
Inherited as autosomal dominant

162
Q

What is the most common presentation of men 1?

A

Hypercalcaemia

163
Q

Which gene causes men 2?

A

RET oncogene

164
Q

At what level of HbA1c does an additional medication need to be added for glycaemic control?

A

58

165
Q

What biochemical abnormalities are seen in congenital adrenal hyperplasia?

A

Increased plasma 17 hydroxyprogesterone
Increased plasma 21 deoxycortisol
Increased urinary adrenocorticosteroid metabolites

166
Q

What is congenital adrenal hyperplasia?

A

Autosomal recessive inherited condition

Deficiency of 21 hydroxlase enzyme which is responsible for synthesis of aldosterone and cortisol

167
Q

How does congenital adrenal hyperplasia present?

A

Due to inadequate mineralocorticoids: vomiting due to salt-wasting leading to dehydration and death
Due to excess androgens: azoospermia, ambiguous genitalia in some females, such that it can be difficult to identify external genitalia as male or female, early pubic hair and rapid growth in childhood, precocious puberty or failure of puberty to occur, excessive facial hair, virilization, and/or menstrual irregularity in adolescence, infertility due to anovulation, clitoromegaly, enlarged clitoris and shallow vagina
Due to insufficient androgens and estrogens: Undervirilization in XY males with female external genitalia, In females, hypogonadism, sexual infantilism or abnormal pubertal development, infertility

168
Q

What are causes of hirsutism?

A 
PCOS
Cushings
CAH
Androgen therapy
Obesity
Adrenal tumour
Androgen secreting ovarian tumour
Phenytoin
169
Q

What scoring system is used to assess hirsutism?

A

Ferriman Gallwey score: 9 body areas assigned a score 0-4

Score >15 is moderate to severe hirsutism

170
Q

What is the management of hirsutism?

A

Advise weight loss if overweight
Cosmetic techniques: waxing/bleaching
Dianette (co-cyprindiol) or Yasmin (drospirenone)
Facial: topical eflornithine

171
Q

What are causes of hypertrichosis?

A

Drugs: minoxidil, ciclosporin, diazoxide
Congenital hypertrichosis lanuginosa
Anorexia nervosa
Porphyria cutanea tarda

172
Q

What is nelsons syndrome?

A

Rapid enlargement of a pituitary corticotroph adenoma that occurs after removal of both adrenal glands

173
Q

What investigation should be done for suspected phaeochromocytoma?

A

24 hr urinary collection of metanephrines

174
Q

What are sick day rules for diabetics?

A

Increase frequency of glucose monitoring to 4 hourly or more frequently
Encourage fluid intake aiming for at least 3 litres in 24 hours
If unable to eat, sugary drinks to maintain carb intake
Continue to take meds even if not eating much

175
Q

What is the management of Hyperosmolar hyperglycaemic state?

A

Slow rehydration with IV infusion of 0.9% saline over 2 days

176
Q

What are risk factors for diabetes?

A

Modifiable: Obesity, Deprivation, Diet, Physical Activity, Smoking
Non modifiable: Age, Sex, Ethnicity, FH of Diabetes, Gestational Diabetes

177
Q

How does diabetes present?

A 
Thirst
Frequency
Polyuria
Weight Loss 
Tired all the time
178
Q

What are benefits of Metformin?

A

Reduces CVD risk
Optimises control
Weight loss

179
Q

What are important side effects and complications of Metformin?

A

Lactic Acidosis with low eGFR

Gastric upset

180
Q

What is target HbA1c for a patient on a sulfonylurea?

A

53

181
Q

What are side effects and risks of DPP4 inhibitors?

A

Acute Pancreatitis

Derangement of LFTs

182
Q

Which DPP4 inhibitors can be used for diabetes?

A

Alogliptin (first line CCG recommendation)

Linagliptin safe in renal impairment

183
Q

What are problems with pioglitazone?

A

Associated with bladder cancer

Do not use in heart failure

184
Q

What is the mechanism of action of Metformin?

A

Decreased hepatic gluconeogenesis by inhibition of mitochondrial respiratory chain complex 1
Increases insulin sensitivity to enhance peripheral glucose uptake by GLUT4
Decrease glucose absorption from GI tract

185
Q

What is the dose of Metformin?

A

500mg BD

186
Q

What are contraindications to use of Metformin?

A 
Impaired renal function: stop if GFR <30
Cardiac or respiratory insufficiency
Liver disease, alcohol abuse
History of metabolic acidosis
Severe sepsis
Use of IV contrast media: stop couple of days before to prevent AKI
187
Q

What are adverse effects of Metformin?

A

Lactic acidosis: very rare, 0.03 cases / 1000 patient years, 50% mortality
GI symptoms
B12 malabsorption

188
Q

What is the mechanism of action of sulfonylureas?

A

Bind to and close ATP sensitive K channels on pancreatic beta cells which depolarises cell leading to opening of voltage gated Ca channels leading to increased fusion of insulin granules with cell membrane and therefore increased secretion of proinsulin

189
Q

What are adverse effects of sulfonylureas?

A 
Hypoglycaemia
Weight gain: 1-4 kg in 6 months
Gastrointestinal symptoms in 3%
Allergic rash
Bone marrow suppression
190
Q

What is the mechanism of action of acarbose?

A

Alpha glucosidase inhibitor

Prevent digestion of carbohydrates

191
Q

What does nice recommend on use of acarbose as an oral hypoglycaemic drug?

A

Use only in individuals intolerant of other OHDs

192
Q

What is the mechanism of action of Thiazolidinediones (glitazones)?

A

PPAR-gamma agonist
Nuclear receptor which leads to transcription of insulin sensitive genes: lipoprotein lipase, GLUT4, fatty acid transport protein

193
Q

What are contraindications to glitazones?

A

Oedema
Anaemia
Impaired liver function
Can worsen macular oedema

194
Q

What are adverse effects of glitazones?

A

Fluid retention : oedema , heart failure , anaemia
Weight gain : 1 – 4 kg in 6 months
Hypoglycaemia in combination with other oral agents
Increased risk of distal fractures
Unforeseen chronic effects
Can induce ovulation - increasd risk of pregnancy

195
Q

What are examples of GLP1 agonists?

A

Exenatide
Liraglutide
Lixisenatide
Dulaglutide

196
Q

What are examples of DPP4 (Dipeptidyl peptidase-4) inhibitors?

A

Sitagliptin, Vildagliptin, Saxagliptin, Linagliptin, Alogliptin

197
Q

What is the mechanism of action of GLP1 agonists?

A 
Incretin mimetics 
Increase insulin sensitivity 
Decrease hepatic glucose production 
Decrease gastric emptying and GI motility 
Decrease appetite, increase satiety
198
Q

What is the mechanism of action of DPP4 inhibitors?

A

DPP4 enzyme inactivates GLP1 so inhibit this to increase GLP1 levels

199
Q

What are advantages of GLP1 agonists?

A

Improves glycemic control – 0.5 to 1%
Promote weight loss
Low risk of hypo on its own
Improves lipid profile

200
Q

What are side effects of GLP1 agonists?

A

GI symptoms
Rare risk of pancreatitis due to islet cell hyperplasia
Risk of hypo when used with insulin or SU

201
Q

What are advantages of gliptins (DPP4 inhibitors)?

A

No weight loss, hypos or slowing of gastric emptying

Adverse events comparable to placebo

202
Q

When should DPP4 inhibitors be prescribed?

A

Consider as 2nd line instead of SFU if : Hypos may be a problem, SFU contraindicated or intolerant
Use as 3rd line therapy
May be preferable to glitazone if : Weight gain may be a problem, Glitazone contraindicated or not tolerated
Stop if A1c reduction at 6 months < 0.5%

203
Q

What is the mechanism of action of dapagliflozin?

A

Selectively inhibits SGLT2 in the renal proximal tubule so blocks reabsorption of glucose back into blood

204
Q

What are complications of dapagliflozin?

A

Vulvovaginitis, balanitis and related genital infections - thrush

205
Q

What are examples of fast acting insulin?

A

Novorapid
Humalog
Apidra

206
Q

What are examples of long acting insulins?

A

Glargine
Levemir
Degludec
Toujeo

207
Q

What are examples of pre mixed insulins?

A

Novomix 30

Humalog Mix

208
Q

What are examples of different insulin regimes?

A

Once-daily regimen: Long acting or intermediate acting insulin administered at bedtime
Twice-daily regimen: A biphasic insulin is injected twice a day (pre-breakfast and pre-evening meal)
Basal-bolus regimen: Intermediate- or long-acting insulin is administered at night, plus short acting insulin at meal times. This regimen provides tight glycaemic control but requires more frequent injections

209
Q

What is the alphabet strategy for improving diabetic health?

A 
Advice: Smoking , diet , exercise
Blood pressure: < 140/80
Cholesterol: TC 4 or less , LDL : HDL 2 or less 
Diabetes control: HbA1c 7% or less 
Eye examination: Annual examination
Feet examination: Annual examination
Guardian drugs: Aspirin, ACEI, statins
210
Q

What are criteria for use of GLP1 mimetics?

A

BMI > 35 and weight related co-morbidities/psychological issues
BMI < 35 and insulin has occupational implications, or weight loss likely to help co-morbidities

211
Q

What are eye signs of Graves’ disease?

A 
Proptosis, lid lag, lid retraction, chemosis, Grittiness
Optic neuropathy (colour vision), Ophthalmoplegia
212
Q

What investigations should be done for a person with suspected Graves’ disease?

A 
TFTs
ECG
Thyroid autoantibodies
Thyroid USS
Radio-iodine uptake scan: If unsure about etiology - graves increased uptake. Thyroiditis decreased
213
Q

What are possible treatments for Graves’ disease?

A 
Carbimazole
Propylthiouracil: use in pregnancy 
Beta-blocker: symptomatic relief 
Radioiodine: not in pregnancy or thyroid eye disease 
Thyroidectomy
214
Q

What changes with thyroid disease in pregnancy?

A

FT4 falls in early pregnancy (increased TBG)
FT3 remains stable
TSH also falls in first trimester
Graves’ disease usually improves, but relapses post-partum
Hypothyroid patients need 50% more thyroxine
Hyperemesis can cause transient mild hyperthyroidism

215
Q

What gamma GT result would be inkeeping with acromegaly?

A

Failure of suppression of gh on GTT

216
Q

What investigations should be done for acromegaly?

A

GTT – growth hormone, IGF1
MRI pituitary
Formal visual fields
Pituitary function test

217
Q

What are features of acromegaly?

A 
Acanthosis nigricans
Blood pressure 
Carpal tunnel
Diabetes
Enlarged organs
Field defect
IGF high
218
Q

What is the management of acromegaly?

A

Surgical – trans-sphenoidal: Potentially curative (70% micro, 50% macro), Risk of impaired pituitary function
Medical: Somatostatin analogues (octreotide), pegvisomant, dopamine
agonists (bromocriptine), Can result in tumour regression, Primary therapy in some cases, Control of GH secretion after debulking large tumours
Radiotherapy: If GH levels not controlled

219
Q

What investigations should be done for Addison’s?

A 
U and ES- 40% might have normal k
BONE- 10% have high calcium
Hypoglycemia 
Random cortisol
B12, folate, TFTS, Iron studies, antibodies
Short synacthen test 
ACTH
RENIN
ALDOSTERONE
220
Q

What is the short synacthen test?

A 
ACTH stimulation test
250 mcg ACTH (Synacthen) I.M /I.V
0 and 30 min plasma cortisol
0 min for ACTH
Normal subjects plasma cortisol > 460nmol/l either at baseline or at 30 min
221
Q

What is the management of Addison’s?

A

Hydrocortisone 15-25mg/day e.g 15mg morning, 5mg evening
Fludrocortisone - in a single dose of 50-200 microg/day
Sick day rules - double dose hydrocortisone

222
Q

Why do steroids worsen diabetic control?

A

Causes insulin resistance in skeletal muscle by directly inhibiting translocation of GLUT4 to plasma membrane
Sensitivity of glycogen synthesis and glucose oxidation decreased

223
Q

What is autoimmune polyglandular syndrome type 1?

A 
Autosomal recessive 
Adrenal insufficiency
Hypoparathyroidism
Chronic mucocutaneous candidiasis
Primary gonadal failure
Primary hypothyroidism
Malabsorption 
Pernicious anaemia
Chronic active hepatitis 
Vitiligo
224
Q

What is the investigation of choice for haemochromatosis?

A 
Serum ferritin raised 
Transferrin saturation (serum iron/total iron binding capacity) raised 
HFE genetic testing
225
Q

What is a short synacthen test?

A

Serum cortisol measured before and 30 mins after 250 micrograms synthetic ACTH
If insufficient response, Addison’s/ atrophy or destruction of adrenal glands

226
Q

What is the PPAR gamma receptor? How is it used in treating diabetes?

A

Intracellular nuclear receptor
Natural ligands are free fatty acids
Controls adipocyte differentiation and function
Thiazolidinediones are agonists at receptor and reduce peripheral insulin resistance

227
Q

What are features of hyperosmolar hyperglycaemic state?

A

Severe hyperglycaemia
Dehydration and renal failure
Mild/absent ketonuria

228
Q

What causes mortality in HHS?

A 
Rhabdomyolysis 
VTE
Lactic acidosis
Hypertriglyceridaemia 
Renal failure
Stroke
Cerebral oedema
229
Q

What are precipitants of HHS?

A 
New diagnosis T2DM
Infection
High dose steroids
MI
Vomiting
Stroke
VTE
Poor treatment compliance
230
Q

What is first line management of diabetic neuropathy pain?

A

Amitriptyline
Duloxetine
Gabapentin
Pregabalin

231
Q

What are management options for gastroparesis?

A

Metoclopramide
Domperidone
Erythromycin
All prokinetic agents

232
Q

What is subacute thyroiditis?

A

Associated with viral infections

Characterised by transient hyperthyroidism and high ESR

233
Q

What is the most common variety of congenital adrenal hyperplasia?

A

21 hydroxylase deficiency

234
Q

What is the function of 21 hydroxylase?

A

Conversion of 17 hydroxyprogesterone to cortisol and aldosterone

235
Q

How can virilisation be prevented in congenital adrenal hyperplasia?

A

Early treatment, in vivo treatment with steroids for mother

236
Q

How can adrenal crisis present in a neonate?

A

Hyponatraemia
Hypotension
Hypoglycaemia

237
Q

What is the most appropriate initial investigation for Cushing’s syndrome?

A

24 hour urine free cortisol concentration

238
Q

What are the rules on driving if a patient has a hypoglycaemic episode?

A

Stop car, treat hypoglycaemia, move out of drivers seat and wait 45 mins after blood glucose has risen above 4

239
Q

What are rules on driving a HGV if insulin dependent diabetic?

A

Can drive if:
No severe episodes hypo in previous 12 months
Has full hypo awareness
Must show adequate control of condition by regular monitoring (at least twice daily)
Must demonstrate understanding of risks
No other debarring complications of diabetes

240
Q

What are rules for non insulin dependent diabetics on driving?

A

2 episodes of hypo needing third party assistance in 12 months or lacking hypoawareness or have has disabling hypos while driving must inform DVLA

241
Q

What are signs of hypothyroidism on examination?

A 
Dry skin/hair
Loss of lateral 1/3 eyebrows
Goitre 
Bradycardia
Ataxia
Mental slowness
Carpal tunnel
Slow reflexes 
Peaches and cream complexion 
Peripheral neuropathy
242
Q

What are causes of hypothyroidism?

A 
Drugs: amiodarone, lithium 
Autoimmune
Cancer
Radiotherapy
Infection 
Hypopituitarism
243
Q

What are signs of hyperthyroidism on examination?

A 
Tachycardia
Fast AF
Warm peripheries
Goitre
Opthalmoplegia 
Pretibial myxoedema
Thyroid acropatchy 
Palmar erythema 
Thinning of hair
Brisk reflexes
Lid lag
Exophthalmos
244
Q

What are non diabetic causes of hypoglycaemia?

A 
Liver failure
Addison’s 
Insulinoma
Alcohol excess
Pituitary insufficiency

Phase 3 (23 decks)

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