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MRCP Endocrine > General > Flashcards

General Flashcards

1
Q

What is the mechanism of acromegaly?

A

Excess growth hormone secondary to a pituitary adenoma in over 95% of cases. A minority of cases are caused by ectopic GHRH or GH production by tumours e.g. pancreatic.

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2
Q

What are the features of acromegaly?

A

Coarse facial features
Spade like hands
Increase in shoe size
Excessive sweating
Large tongue - interdental space
Pituitary tumour –> Headahce, hypopituitarism
Galactorrhea - prolactin rated in 1/3 of cases

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3
Q

What is acromegaly associated with?

A

Hypertension
Daibetes
Cardiomyopathy
Colorectal cancer
MEN -1

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4
Q

How should acromegaly be investigated?

A

IGF-1 (insulin growth factor 1 levels) + serial GH measurements
Oral glucose tolerance test used to confirm diagnosis

MRI may demonstrate pituitary tumour

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5
Q

How can a oral glucose tolerance test be used to diagnose acromegaly?

A

Normal patients GH is suppressed < 2 with hyperglycaemia
In acromegaly there is no suppression

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6
Q

Management of acromegaly?

A

Surgery - if possible

If not possible:
1. Somatostatin analogue - directly inhibitors growth hormone
e.g. octreotide
2. Pegvisomant - GH receptor antagonist
3. Dopamine agonists - example bromocriptine

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7
Q

What test can be used to monitor acromegaly treatment?

A

IGF-1

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8
Q

What are examples of acute phase proteins?

A

CRP*
procalcitonin
ferritin
fibrinogen
alpha-1 antitrypsin
caeruloplasmin
serum amyloid A
serum amyloid P component**
haptoglobin
complement

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9
Q

In acute phase response what does the liver decrease production of?

A

albumin
transthyretin (formerly known as prealbumin)
transferrin
retinol binding protein
cortisol binding protein

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10
Q

How does CRP work in acute phase?

A

binds to phosphocholine in bacterial cells and on those cells undergoing apoptosis. In binding to these cells it is then able to activate the complement system.

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11
Q

What are the features of Addison’s disease?

A

lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia

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12
Q

What are primary causes of hypoadrenalism?

A

tuberculosis
metastases (e.g. bronchial carcinoma)
meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
HIV
antiphospholipid syndrome

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13
Q

Secondary causes of Addisons disease?

A

Secondary causes
pituitary disorders (e.g. tumours, irradiation, infiltration)
Exogenous glucocorticoid therapy

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14
Q

How to test for Addisons

A
  1. Short synacthen test
    - Measure plasma cortisol 30 minutes before and after given 250 micrograms IM of synacthen
  2. Anti -21 hydroxyls may also be demonstrated
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15
Q

What test can be done if a synthacthen test cannot be done? Results?

A

9 am cortisol level
>500 nmol/L - Addison unlikely
<100 nmol/L - VERY ABNORMAL
100-500 a short synacthen test should be done

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16
Q

What electrolyte / metabolic issues are seen in Addisons?

A

hyperkalaemia
hyponatraemia
hypoglycaemia
metabolic acidosis

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17
Q

What are causes of Addisons crisis?

A
  1. Sepsis or surgery causing an acute exacerbation of chronic
  2. Insufficiency (Addison’s, Hypopituitarism)
    adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
  3. Steroid withdrawal
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18
Q

Management of Addison crisis?

A
  1. Hydrocortisone 100 mg IM or IV
  2. Rehydrate with saline or dextrose if hypoglycaemia
  3. Continue hydrocortisone 6 hourly
  4. Begin oral replacement after 24 hours
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19
Q

Causes of ALP rise?

A

liver: cholestasis, hepatitis, fatty liver, neoplasia
Paget’s
osteomalacia
bone metastases
hyperparathyroidism
renal failure
physiological: pregnancy, growing children, healing fractures

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20
Q

Rasied ALP with raised calcium

A

Bone metastases
Hyperparathyroidism

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21
Q

Raised ALP and low calcium?

A

Osteomalacia
Renal failure

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22
Q

What is primary amenorrhoea?

A

defined as the failure to establish menstruation by 15 years of age in girls with normal secondary sexual characteristics (such as breast development), or by 13 years of age in girls with no secondary sexual characteristics

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23
Q

What is secondary amenorrhoea?

A

cessation of menstruation for 3-6 months in women with previously normal and regular menses, or 6-12 months in women with previous oligomenorrhoea

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24
Q

Causes of primary amenorrhea?

A

gonadal dysgenesis (e.g. Turner’s syndrome) - the most common causes
testicular feminisation
congenital malformations of the genital tract
functional hypothalamic amenorrhoea (e.g. secondary to anorexia)
congenital adrenal hyperplasia
imperforate hymen

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25
Q

Causes of secondary amenorrhoea?

A

hypothalamic amenorrhoea (e.g. secondary stress, excessive exercise)
polycystic ovarian syndrome (PCOS)
hyperprolactinaemia
premature ovarian failure
thyrotoxicosis*
Sheehan’s syndrome
Asherman’s syndrome (intrauterine adhesions)

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26
Q

What investigations should be completed for amenorrhea?

A
  1. Exclude pregnancy with urinary or serum bHCG
  2. Coeliac screen
  3. Thyroid function tests
  4. Gonadotrophins
    - low levels indicate a hypothalamic cause where as raised levels suggest an ovarian problem (e.g. Premature ovarian failure)
    - raised if gonadal dysgenesis (e.g. Turner’s syndrome)
    prolactin
  5. Androgen levels
    - raised levels may be seen in PCOS
  6. Oestradiol
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27
Q

What is the genetics behind androgen insensitivity syndrome

A

X linked recessive
46 XY male - has a female phenotype
Due to testosterone resistance

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28
Q

What was the other name (old name) for complete androgen insensitivity syndrome?

A

Testicular feminisation

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29
Q

Features of androgen insensitivity syndrome?

A

‘primary amenorrhoea’
little or no axillary and pubic hair
undescended testes causing groin swellings
breast development may occur as a result of the conversion of testosterone to oestradiol

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30
Q

How is androgen insensitivity syndrome diagnosed?

A

Buccal smear - 46 XY
Testosterone levels: High normal range compared to post pubertal boys

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31
Q

What is the management of androgen insensitivity syndrome

A

bilateral orchidectomy (increased risk of testicular cancer due to undescended testes)
oestrogen therapy

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32
Q

What HLA type is autoimmune polyendocrinopathy syndrome associated with?

A

HLA DR3 and DR4

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33
Q

What is autoimmune polyendocrinopathy syndrome ?

A

Addison’s disease (autoimmune hypoadrenalism) is associated with other endocrine deficiencies in approximately 10% of patients. There are two distinct types of autoimmune polyendocrinopathy syndrome

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34
Q

What is autoimmune polyendocrinopathy syndrome type 1?

A

referred to as Multiple Endocrine Deficiency Autoimmune Candidiasis (MEDAC). It is a very rare autosomal recessive disorder caused by mutation of AIRE1 gene on chromosome 21

chronic mucocutaneous candidiasis (typically first feature as young child)
Addison’s disease
primary hypoparathyroidism

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35
Q

What is the genetics behind bartter’s syndrome?

A

Autosomal recessive
Defective Na+ K+ 2CL- cotransporter in ascending loop of hence

oop diuretics work by inhibiting NKCC2 - think of Bartter’s syndrome as like taking large doses of furosemide

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36
Q

What are the features of Barter’s syndrome?

A

usually presents in childhood, e.g. Failure to thrive
polyuria, polydipsia
hypokalaemia
normotension
weakness

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37
Q

How does Barter’s Syndrome differ from other hypokalaemia conditions?

A

endocrine causes of hypokalaemia such as Conn’s, Cushing’s and Liddle’s syndrome which are associated with hypertension).

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38
Q

What is the mechanism of action of carbimazole?

A

blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production

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39
Q

How long should a patient be on carbimazole?

A

High dose for 6 weeks
Patient becomes euthyroid before being reduced

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40
Q

How does propylthiouracil differ from carbimazole?

A

propylthiouracil has a central and peripheral action by inhibiting 5’-deiodinase which reduces peripheral conversion of T4 to T3

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41
Q

What are the adverse effects of carbimazole?

A

agranulocytosis
crosses the placenta, but may be used in low doses during pregnancy

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42
Q

HPV virus implicated in cervical cancer?

A

Human papillomavirus (HPV), particularly serotypes 16,18 & 33

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43
Q

Mechanism of HPV causing cervical cancer?

A

HPV 16 & 18 produces the oncogenes E6 and E7 genes respectively
E6 inhibits the p53 tumour suppressor gene
E7 inhibits RB suppressor gene

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44
Q

Cervical cancer risk factors?

A

smoking
human immunodeficiency virus
early first intercourse, many sexual partners
high parity
lower socioeconomic status
combined oral contraceptive pill*

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45
Q

What is congenital adrenal hyperplasia?

A

Autosomal disorders
Affect adrenal steroid biosynthesis
Results in low cortisol
Pituitary secretes extra ACTH
ACTH stimulated adrenal androgens –> virtualise female infant

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46
Q

Enzyme deficiencies in congenital adrenal hyperplasia?

A

21-hydroxylase deficiency (90%)
11-beta hydroxylase deficiency (5%)
17-hydroxylase deficiency (very rare)

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47
Q

Features of congenital adrenal hyperplasia - 21 hydroxylase deficiency feature?

A

virilisation of female genitalia
precocious puberty in males
60-70% of patients have a salt-losing crisis at 1-3 wks of age

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48
Q

Features of congenital adrenal hyperplasia - 11 beta hydroxylase deficiency feature?

A

virilisation of female genitalia
precocious puberty in males
hypertension
hypokalaemia

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49
Q

Features of congenital adrenal hyperplasia - 17 hydroxylase deficiency feature?

A

non-virilising in females
inter-sex in boys
hypertension

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50
Q

Steroid with minimal glucocorticoid activity and very high mineralocorticoid activity?

A

Fludrocortisone

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51
Q

Steroid with high glucocorticoid activity and high mineralocorticoid activity?

A

Hydrocortisone

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52
Q

Predominant glucocorticoid activity and low mineralocorticoid activity?

A

Prednisolone

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53
Q

Endocrine side effects of corticosteroids?

A

endocrine

impaired glucose regulation
increased appetite/weight gain
hirsutism
hyperlipidaemia

Cushing’s syndrome
moon face
buffalo hump
striae

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54
Q

Musculoskeletal side effects of corticosteroids

A

osteoporosis
proximal myopathy
avascular necrosis of the femoral head

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55
Q

Psychiatric side effects of corticosteroids?

A

insomnia
mania
depression
psychosis

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56
Q

Gastrointersinal side effects of corticosteroids?

A

peptic ulceration
acute pancreatitis

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57
Q

Ophthalmic side effects of corticosteroids?

A

Glaucoma
Cataracts

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58
Q

Side effects of mineralocorticoids?

A

FLuid retention
Hypertension

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59
Q

Who would be gradual withdrawn from steroids?

A
  1. Received more than 40 mg prednisolone daily for more than one week
  2. Received more than 3 weeks of treatment
  3. Recurrent repeat courses
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60
Q

Most common cause of Cushings?

A

Exogenous steroid therapy

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61
Q

What are the types of ACTH dependent Cushings?

A
  1. Cushing disease - pituitary tumour secreting ACTH
  2. Ectopic ACTH production - small cell lung cancer
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62
Q

What are ACTH independent causes of Cushing syndrome?

A

iatrogenic: steroids
adrenal adenoma (5-10%)
adrenal carcinoma (rare)
Carney complex: syndrome including cardiac myxoma
micronodular adrenal dysplasia (very rare)

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63
Q

What is Pseudo-Cushing’s?

A

mimics Cushing’s
often due to alcohol excess or severe depression
causes false positive dexamethasone suppression test or 24 hr urinary free cortisol
insulin stress test may be used to differentiate

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64
Q

What are general investigation findings consistent with Cushing’s syndrome?

A

Hypokalaemmic metabolic alkalosis
Impaired glucose tolerance
Ectopic ACTH secretion - associated with hypokalaemia

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65
Q

How should Cushing’s syndrome be tested?

A
  1. Overnight dexamethasone suppression test:
    - Most sensitivity
    - Patients with Cushing syndrome do not have their morning cortisol spike
  2. 24 hour urinary free cortisol
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66
Q

To test if Cushings is ACTH or ACTH independent, what test should be done?

A

High dose dexamethasone test

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67
Q

High dose dex test: Cortisol not suppressed + ACTH suppressed

A

ACTH independent causes ( e.g. adrenal adenoma)

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68
Q

High dose dex test: Suppressed cortisol + Suppressed ACTH?

A

Cushing disease (i.e. pituitary adenoma –> acth secretion)

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69
Q

High dose dex test: Cortisol and ACTH not suppressed?

A

Ectopic ACTH syndrome
e.g. small cell lung cancer

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70
Q

What test is used to differentiate between true Cushing’s disease and pseudo-cushings?

A

Insulin stress test

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71
Q

Diagnostic criteria for type 2 diabetes?

A
  1. fasting glucose greater than or equal to 7.0 mmol/l
  2. random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)
  3. a HbA1c of greater than or equal to 48 mmol/mol (6.5%) is diagnostic of diabetes mellitus
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72
Q

What may cause a misleading HbA1c result?

A

Increased red cell turnover

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73
Q

What conditions can HbA1c not be used for a diagnosis of type 2 diabetes mellitus?

A

haemoglobinopathies
haemolytic anaemia
untreated iron deficiency anaemia
suspected gestational diabetes
children
HIV
chronic kidney disease
people taking medication that may cause hyperglycaemia (for example corticosteroids)

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74
Q

Criteria for impaired oral glucose tolerance?

A

Glucose less than 7 before test (they fast before)
OGTT 2 hour value: Greater than 7.8 but less than 11.1

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75
Q

Criteria for impaired fasting glucose?

A

Equal to 6.1 but less than 7.0

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76
Q

Basics of T2DM?

A

relative deficiency of insulin due to an excess of adipose tissue. In simple terms there isn’t enough insulin to ‘go around’ all the excess fatty tissue, leading to blood glucose creeping up.

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77
Q

Basics of T1DM?

A

Autoimmune disorder where the insulin-producing beta cells of the islets of Langerhans in the pancreas are destroyed by the immune system
This results in an absolute deficiency of insulin resulting in raised glucose levels

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78
Q

Features of pre diabetes?

A

term is used for patients who don’t yet meet the criteria for a formal diagnosis of T2DM to be made but are likely to develop the condition over the next few years. They, therefore, require closer monitoring and lifestyle interventions such as weight loss

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79
Q

Basics of gestational diabetes?

A

Some pregnant develop raised glucose levels during pregnancy. This is important to detect as untreated it may lead to adverse outcomes for the mother and baby

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80
Q

Basics of maturity onset diabetes of the young (MODY) ?

A

group of inherited genetic disorders affecting the production of insulin. Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis

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81
Q

Basics of latent autoimmune diabetes of adults?

A

Autoimmune related diabetes presenting as adults

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82
Q

Features of T1DM?

A

Weight loss
Polydipsia
Polyuria

DKA:
abdominal pain
vomiting
reduced consciousness level

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83
Q

Features of T2DM

A

Often picked up incidentally on routine blood tests
Polydipsia
Polyuria

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84
Q

How many months does HbA1c represent the average blood glucose?

A

2-3 months

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85
Q

How is a oral glucose tolerance test (OGTT) completed?

A

a fasting blood glucose is taken after which a 75g glucose load is taken. After 2 hours a second blood glucose reading is then taken

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86
Q

Diagnosis of T2DM from OGTT? - In symptomatic patient

A

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

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87
Q

Diagnosis of T2DM from OGTT - in asymptomatic patient ?

A

OGTT needs to show diagnostic criteria on two occasions

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88
Q

Side effect of insulin?

A

Hypoglycaemia
weight gain
Lipodystrophy

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89
Q

Mechanism of metformin?

A

Increases insulin sensitivity
Decreases hepatic gluconeogenesis

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90
Q

Side effects of metformin?

A

Gastrointestinal upset
Lactic acidosis

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91
Q

When can metformin not be used?

A

eGFR < 30

Do not use post heart attack - tissue hypoxia

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92
Q

Mechanism of sulfonylureas?

A

Stimulate pancreatic beta cells to secrete insulin

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93
Q

Side effects of sulfonylureas?

A

Hypoglycaemia
Weight gain
Hyponatraemia

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94
Q

Mechanism of thiazolidinediones?

A

Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake

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95
Q

Side effect of thiazolidinediones?

A

weight gain
Fluid retention

Do not use in heart failure

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96
Q

Mechanism of DPP-4 inhibitors? (The gliptans)

A

Increase incretin levels - inhibit glucagon secretion

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97
Q

Side effect of DPP4 inhibitors?

A

Pancreatitis

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98
Q

Mechanism of SGLT2 inhibitors ?

A

Inhibit reabsorption of the glucose in the kidney

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99
Q

Side effect of SGLT2 inhibitors?

A

Urinary tract infections
Typically cause weight loss

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

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100
Q

Mechanism of GLP-1 agonist ( the Tides)?

A

Incretin mimetic
Inhibits glucagon secretion

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101
Q

Side effect of GLP-1 inhibitors (tide)?

A

N+V
Pancreatitis
Typically cause weight loss

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102
Q

Treatment algorithm for T2DM?

A
  1. Metformin

HbA1c > 58
2. Metformin plus:
- Glipten
- Sulphonyurea
- TZD
- SGLt2

HbA1c > 58
3. Consider a triple agent
OR INSULIN

If triple therapy and BMI > 35
4. Metformin + Suphonylurea + GLP1

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103
Q

When should a GLP-1 agonist be considered?

A

Triple therapy
BMI > 35

Start:
Metformin + Sulfonylurea + GLP-1 minimetic

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104
Q

T2DM - cannot tolerate metformin?

A

Try:
Gliptan (DPP4)
Sulfonylurea
Pioglitazone

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105
Q

What does a GLP-1 inhibitor stand for?

A

Glucagon like peptide 1 mimetic

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106
Q

What does the glucose like peptide do?

A

Hormone released by small intestine in respond to an oral glucose load
Oral glucose load results in higher release of insulin, compared to IV
This is mediated by GLP-1

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107
Q

How should eventide be given?

A

Scut injection 60 minutes before morning and evening meal
NOT GIVEN WITH MEAL

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108
Q

What criteria must a patient meet to qualify for repeat prescription of exenatide?

A

> 11 mmol/mol (1%) reduction in HbA1c and 3% weight loss after 6 months to justify the ongoing prescription of GLP-1 mimetics.

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109
Q

How do DPP4 inhibitors increase GLP1 ?

A

Decreasing peripheral breakdown

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110
Q

What are the blood glucose targets for T1DM?

A

5-7 on waking
4-7 before meals or other times

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111
Q

Dietary advice for T2DM?

A

Increase fibre - low glycemic index
Include low fat dietary products
Discourage use of foods marketed specifically at diabetics
Aim for a weight loss of 5-10 %

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112
Q

HbA1c target for T2DM on lifestyle changes only?

A

48

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113
Q

HbA1c target for T2DM on lifestyle changes and metformin

A

48

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114
Q

HbA1c target for T2DM on drugs that may cause hypoglycaemia?

A

53

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115
Q

What would prompt immediate introduction of SGLt2 inhibitors in T2DM?

A

Diagnosis of CVD, QRISK score > 10%

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116
Q

What should be done with metformin before adding in other agent?

A

Increase to maximum dose

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117
Q

Management of T2DM, cannot tolerate metformin, ischaemic heart disease?

A

SGLT2 mono therapy

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118
Q

Management of T2DM, cannot tolerate metformin, no heat disease?

A

DPP‑4 inhibitor or pioglitazone or a sulfonylurea
SGLT-2 may be used if certain NICE criteria are met

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119
Q

What blood pressure targets should be used for T2DM < 80?

A

Clinic: 140/90
Ambulatory /Home blood pressure: 135/85

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120
Q

What blood pressure should be used for T2DM > 80?

A

Clinic: 150/90
Ambulatory /Home blood pressure: 145/85

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121
Q

Pathophysiology of T1DM?

A

autoimmune disease
antibodies against beta cells of pancreas
HLA DR4 > HLA DR3

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122
Q

What antibodies are seen in T1DM?

A

Anti-islet associated antigen
Glutamic acid decarboxylase

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123
Q

Mechanism of diabetic foot disease?

A
  1. Neuropathy
  2. Peripheral arterial disease
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124
Q

Presentation of diabetic foot disease?

A

neuropathy: loss of sensation
ischaemia: absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication
complications: calluses, ulceration, Charcot’s arthropathy, cellulitis, osteomyelitis, gangrene

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125
Q

Risk stratification of diabetic foot disease?

A

Low risk: No risk factors, except callus

Moderate risk: Deformity or Neuropathy or non-critical limb ischaemia

High risk: Previous significant disease or combination of vascular and neuropathy

High risk - should be monitored at diabetic foot centre

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126
Q

What is the pathophysiology of Diabetic Ketoacidosis?

A

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

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127
Q

Biochemical diagnosis of DKA?

A

glucose > 11 mmol/l or known diabetes mellitus
pH < 7.3
bicarbonate < 15 mmol/l
ketones > 3 mmol/l or urine ketones ++ on dipstick

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128
Q

Features of DKA?

A

abdominal pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
Acetone-smelling breath (‘pear drops’ smell)

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129
Q

Management of DKA?

A
  1. Fluids replacement with isotonic saline - normally deplete 5-8 litres
  2. Insulin 0.1 unit per kg PER HOUR
  3. Once BM < 15 - COMMENCE DEXTROSE FLUIDS
  4. Serum potassium is often high on admission, falls quickly, Potassium will lower potassium. Therefore add potassium
  5. Continue long act insulin
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130
Q

Describe the fluid choice over first 6 hours

A

0.9% sodium chloride 1L 1000ml over 1st hour
0.9% sodium chloride 1L with potassium chloride 1000ml over next 2 hours
0.9% sodium chloride 1L with potassium chloride 1000ml over next 2 hours
0.9% sodium chloride 1L with potassium chloride 1000ml over next 4 hours
0.9% sodium chloride 1L with potassium chloride 1000ml over next 4 hours
0.9% sodium chloride 1L with potassium chloride 1000ml over next 6 hours

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131
Q

Guidance of potassium in fluids for DKA?

A

Over 5.5 Nil
3.5-5.5 40
Below 3.5 Senior review as additional potassium needs to be given

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132
Q

What is biochemical resolution of DKA?

A

pH >7.3 and
blood ketones < 0.6 mmol/L and
bicarbonate > 15.0mmol/L

IF EATING - can then switch to subcutaneous insulin

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133
Q

Complications of DKA?

A

gastric stasis
thromboembolism
arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
acute respiratory distress syndrome
acute kidney injury

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134
Q

Features of androgen insensitivity syndrome?

A

46 XY
X linked recessive
Defect in androgen receptor
Resistance to testosterone
Phenotypically female
Rudimentary vagina and testes present

Testosterone - elevated
Oestrogen - elevated
LH - elevated

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135
Q

Features of 5 alpha reductase deficiency ?

A

46 XY
Auotsomal recessive
Males unable to convert testosterone to dihydrotestosterone
Ambiguous genitalia
Hyposadias
Virilisation at puberty

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136
Q

What is male pseudohermaphroditism?

A

46XY
Individual has testes but external genitalia are female or ambiguous. may be secondary to androgen insensitivity syndrome

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137
Q

What is female pseudohermaphroditism?

A

46 XX
Individual has ovaries but external genitalia are male (virilized) or ambiguous. May be secondary to congenital adrenal hyperplasia

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138
Q

True hermaphroditism?

A

46 XX or 47 XXY
Very rare, both ovarian and testicular tissue are present

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139
Q

Sex hormone is primary hypogonadism (klinefelters) ?

A

LH - high
Testosterone - low

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140
Q

Sex hormone in hypogonadtrophic hypogonadism ( Kallman’s)

A

LH low
Testoestone low

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141
Q

Androgens insensitivity syndrome sex hormones?

A

High LH
High Testosterone

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142
Q

Testosterone secretin tumour sex hormones?

A

Low LH
High testosterone

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143
Q

What does LH do in males?

A

Makes testosterone from testes

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144
Q

Features klinefelters syndrome (primary hypogondism) ?

A

47 XXY
Often taller than average
Lack of secondary characteristics
Small firm testes
Infertile
Gynaecostmia
Elevated gonadotrophin levels - high LH, low testosterone

145
Q

Features of kallman’s syndrome ? - Hypogonadotrophic hypogonadism

A

X linked trait - lack of GnRH secreting neurones
‘delayed puberty’
hypogonadism, cryptorchidism (unable to descend)
anosmia
sex hormone levels are low
LH, FSH levels are inappropriately low/normal
patients are typically of normal or above average height

146
Q

Features of androgen insensitivity syndrome?

A

‘primary amenorrhoea’
undescended testes causing groin swellings
breast development may occur as a result of conversion of testosterone to oestradiol
46 XY

147
Q

Management of androgen insensitivity syndrome?

A

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

148
Q

Requirements for a T2DM to drive HGV liscence?

A

there has not been any severe hypoglycaemic event in the previous 12 months
the driver has full hypoglycaemic awareness
the driver must show adequate control of the condition by regular blood glucose monitoring*, at least twice daily and at times relevant to driving
the driver must demonstrate an understanding of the risks of hypoglycaemia
here are no other debarring complications of diabetes

149
Q

Diabetics and driving requirement

A

If on insulin: Hypoglycaemia awareness. Not more than one episode of hypoglycaemia requiring assistance in 12 hours
If on tablets: Not more than one episode of hypoglycaemia requiring assistance from another person within 12 months

150
Q

How to dynamically test the pituitary?

A

Give insulin, TRH and LHRH

Measure glucose, cortisol, growth hormone, TSH LH, FSH

Normal function:
GH level rises > 20mu/l
cortisol level rises > 550 mmol/l
TSH level rises by > 2 mu/l from baseline level
LH and FSH should double

151
Q

Risk factors of endometrial cancer?

A

obesity
nulliparity
early menarche
late menopause
unopposed oestrogen.
diabetes mellitus
tamoxifen
polycystic ovarian syndrome
hereditary non-polyposis colorectal carcinoma

152
Q

Features of endometrial cancer?

A

postmenopausal bleeding is the classic symptom
usually slight and intermittent initially before becoming more heavy
premenopausal women may have a change intermenstrual bleeding
pain is not common and typically signifies extensive disease
vaginal discharge is unusual

153
Q

Investigations for endometrial cancer

A

first-line investigation is trans-vaginal ultrasound - a normal endometrial thickness (< 4 mm) has a high negative predictive value
hysteroscopy with endometrial biopsy

154
Q

Protective factors for endometrial cancer?

A

OCP
Smoking

155
Q

Mnx of endometrial cancer?

A

localised disease is treated with total abdominal hysterectomy with bilateral salpingo-oophorectomy. Patients with high-risk disease may have postoperative radiotherapy
progestogen therapy is sometimes used in frail elderly women not considered suitable for surgery

156
Q

Mechanism of ezetimibe?

A

inhibits cholesterol receptors on enterocytes, decreasing cholesterol absorption in the small intestine.

157
Q

When can ezetimibe mono therapy be used?

A

If statin therapy has failed:
- It is contraindicated
- It is not tolerated

158
Q

How should ezetimibe be used in primary heterozygous familial / non-familial hypercholesterolaemia

A

Co-administered with statin therapy
Or when Serum total or LDL cholesterol concentration not appropriately controlled

159
Q

What is familial hypercholesterolaemia?

A

Autosomal dominant condition
High levels of LDL cholesterol

Caused by mutations in LDL receptor protein

160
Q

When should familial hypercholesterolaemia be suspected?

A

Total cholesterol > 7.5
Personal or family history of premature coronary heart disease

161
Q

If one parent is affected with familial hypercholesterolaemia, when should they be tested? - what about both parents?

A

One parent: By age 10
Both parents: By age 5

162
Q

Familial hypercholestaemia criteria?

A

Adults:
- total cholesterol > 7.5
- LDL > 4.9
- Tendon xanthoma

Consider testing in history of myocardial infarction < 50 if second degree relative, below 60 if first degree relative

163
Q

When should statins be discontinued before becoming pregnant?

A

3 months

164
Q

Mechanism of Fibrates?

A

activating PPAR alpha receptors resulting in an increase in LPL activity reducing triglycereride levels.

165
Q

Side effect of fibrates?

A

GI side effects
Thromboembolism

166
Q

What is galactosaemia?

A

Autosomal recessive condition
Absence of galactose 1 phosphate uridyl transferase
Results in accumulation of galactose 1 phosphate

167
Q

Features of galactosaemia?

A

jaundice
failure to thrive
hepatomegaly
cataracts
hypoglycaemia after exposure to galactose
Fanconi syndrome

168
Q

Management of galactosaemia?

A

Galactose free diet

169
Q

Risk factors of gestational diabetes?

A

BMI of > 30 kg/m²
previous macrosomic baby weighing 4.5 kg or above
previous gestational diabetes
first-degree relative with diabetes
family origin with a high prevalence of diabetes (South Asian, black Caribbean and Middle Eastern)

170
Q

Screening for gestational diabetes?

A

Oral glucose tolerance test
- women who have had previous gestational diabetes should be tested
- preform after booking at 24-28 weeks

171
Q

What are the diagnostic thresholds for gestational diabetes?

A

fasting glucose is >= 5.6 mmol/L
2-hour glucose is >= 7.8 mmol/L

172
Q

Management of gestational diabetes?

A
  1. <7 - trial of diet and exercise
  2. If trial of diet does not work start metformin
  3. If at booking >7 - starting insulin
  4. If 6-6.9 and evidence of macrosomia - start insulin

*if cannot tolerate metformin start glibenclomide

173
Q

What is gitelman’s syndrome?

A

defect in the thiazide-sensitive Na+ Cl- transporter in the distal convoluted tubule.

Features:
normotension
hypokalaemia
hypocalciuria
hypomagnesaemia
metabolic alkalosis

174
Q

What is the glycemic index?

A

Capacity of food to raise blood glucose in diabetes compared with normal glucose tolerance individuals

175
Q

What foods have a high glycemic index?

A

White rice, baked potatoes, white bread

176
Q

What conditions give a lower than expected HbA1c?

A

Sickle-cell anaemia
GP6D deficiency
Hereditary spherocytosis
Haemodialysis

177
Q

What conditions gives a higher than expected HbA1c?

A

Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy

178
Q

Most common cause of thyrotoxicosis?

A

Graves

179
Q

Features of grave’s disease?

A

eye signs (30% of patients)
exophthalmos
ophthalmoplegia
pretibial myxoedema

thyroid acropachy, a triad of:
1. digital clubbing
2. soft tissue swelling of the hands and feet
3. periosteal new bone formation

180
Q

Antibodies behind graves?

A

TSH receptor stimulating antibodies (90%)
anti-thyroid peroxidase antibodies (75%)

181
Q

What does thyroid scintigraphy show in graves?

A

diffuse, homogenous, increased uptake of radioactive iodine

182
Q

Management of Graves?

A

Symptoms: Propanolol

Anti-thyroid drugs:
1. Carbimazole 40 mg

Alternative regimen - “ block and replace”
1 Carboxmoazle, when euthyroid, give thyroxine
(Less side effects)

Consider radio iodine treatment in patients who relapse following ATD

183
Q

Contraindications of radio-iodine treatment?

A

Thyroid eye disease ( may make worse)
Pregnant - avoid 4-6 months prior to conception
Age < 16

184
Q

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: see below

185
Q

Drugs causes of gynaecomastia?

A

spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids

186
Q

What is Hashimoto’s thyroiditis?

A

Chronic autoimmune thyroiditis
Typically associated with hypothyroidism
May be transit thyrotoxicosis

187
Q

Features of Hashimoto’s thyroiditis?

A

features of hypothyroidism
goitre: firm, non-tender
anti-thyroid peroxidase (TPO) and also anti-thyroglobulin (Tg) antibodies

188
Q

Associations of Hashimoto’s thyroiditis?

A

autoimmune conditions e.g. coeliac disease, type 1 diabetes mellitus, vitiligo
Hashimoto’s thyroiditis is associated with the development of MALT lymphoma

189
Q

Antibodies in Hashimoto’s thyroiditis?

A

anti-thyroid peroxidase (TPO)
anti-thyroglobulin (Tg) antibodies

190
Q

What is the composition of hormone replacement therapy ?

A

Small dose of oestrogen
If has a uterus - include progesterone

191
Q

Complications of HRT?

A

Breast cancer - if progesterone included
Endometrial cancer - oestrogen should not be given mono therapy if have womb
Increase VTE
Increased stroke
Increased risk of ischaemic heart disease

192
Q

What is hungry bone syndrome?

A

Occurs parathyroidectomy - if hyperparathyroidism has been longstanding
High levels of PTH provide constant stimulus for osteoclasts
Creates a hypercalcaemic state by demineralising bones
Removal of gland causes hormone levels to fall rapidly
Causes osteoclasts to RE-MINERALISE bone

Can be painful
Causes hypocalcaemia

193
Q

What are the two types of hypercalcaemia?

A
  1. Primary hyperparathyroidism - commonest cause
  2. Malignancy

Others:
Squamous cell lung cancer - ectopic PTH
Bone metastasis
Myeloma
Sarcoidosis
Acromegaly
Thyrotxicosis
Vitamin D intoxication
Thiazides
Addison’s disease
Paget’s disease

194
Q

Management of hypercalcaemia?

A
  1. Rehydration with normal saline
  2. Following rehydration bisphonates may be used

*If patient cannot tolerate fluid rehydration
- Try using loop diuretic

195
Q

Causes of hyperkalaemia ?

A

acute kidney injury
drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
metabolic acidosis
Addison’s disease
rhabdomyolysis
massive blood transfusion

196
Q

ECG changes in hyperkalaemia?

A

Small P waves
QRS widening
Tented Tall T waves

197
Q

Why is metabolic acidosis associated with hyperkalaemia?

A

Hydrogen and potassium compete for same exchanger in distal tubule

198
Q

When should a statin be offered to a T1DM?

A

older than 40 years, or
have had diabetes for more than 10 years or
have established nephropathy or
have other CVD risk factors

199
Q

Causes of hypertrigylceridaemia?

A

Causes of predominantly hypertriglyceridaemia
diabetes mellitus (types 1 and 2)
obesity
alcohol
chronic renal failure
drugs: thiazides, non-selective beta-blockers, unopposed oestrogen
liver disease

200
Q

Causes of predominately hypercholesterolaemia?

A

Nephrotic syndrome
Cholestasis
Hypothyroidism

201
Q

Causes of predominately hypercholesterolaemia?

A

Nephrotic syndrome
Cholestasis
Hypothyroidism

202
Q

Causes of hypernatraemia?

A

Causes of hypernatraemia
dehydration
osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma
diabetes insipidus
excess IV saline

203
Q

What is the maximum reduction of sodium per hour?

A

0.5 mmol/hour

204
Q

Pathophysiology of HHS ?

A

Hyperglycaemia results in osmotic diuresis and elecroylte deficiencies
Severe dehydration
Loss of sodium and potassium
Raises serum osmolarity to > 320 mosmol/kg
Hyperviscoity of blood

205
Q

Why may HHS not look dehydrated?

A

Due to hypertonicity leads to preservation of intravascular volume

206
Q

Clinical features of HHS?

A

General: fatigue, lethargy, nausea and vomiting
Neurological: altered level of consciousness, headaches, papilloedema, weakness
Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
Cardiovascular: dehydration, hypotension, tachycardia

Diagnosis
1. Hypovolaemia
2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
3. Significantly raised serum osmolarity (> 320 mosmol/kg)

*May be complicated by vascular complications

207
Q

How can osmolality be estimated?

A

2* Na + Glucose + Urea

208
Q

Management of HHS?

A
  1. Replace fluid losses - 100 ml/kg
    - Use 0.9% NaCl (will be hypotonic in comparison to patient)
    - If osmolarity is not decline delisted positive balance switch to 0.45% NaCl
209
Q

How quickly should fluids be administered in HHS?

A

50% within first 12 hours
Remained in next 12 hours s

210
Q

What should be monitored in HHS and how often?

A

1 hourly
- Osmolarity
- Glucose
- Sodium

211
Q

Causes of hypruricaemia?

A

Increased synthesis:
Lesch-Nyhan disease
myeloproliferative disorders
diet rich in purines
exercise
psoriasis
cytotoxics

Decreased excretion:
drugs: low-dose aspirin, diuretics, pyrazinamide
pre-eclampsia
alcohol
renal failure
lead

212
Q

Causes of hypocalcaemia?

A

vitamin D deficiency (osteomalacia)
chronic kidney disease
hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
pseudohypoparathyroidism (target cells insensitive to PTH)
rhabdomyolysis (initial stages)
magnesium deficiency (due to end organ PTH resistance)
massive blood transfusion
acute pancreatitis

213
Q

Severe hypocalcaemia management ?

A

the preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes
intravenous calcium chloride is more likely to cause local irritation
ECG monitoring is recommended

214
Q

Features of hypocalcaemia?

A

tetany: muscle twitching, cramping and spasm
perioral paraesthesia
if chronic: depression, cataracts
ECG: prolonged QT interval

Trousseau’s sign
carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
wrist flexion and fingers are drawn together

Chvostek sign:
tapping over parotid causes facial muscles to twitch
seen in around 70% of patients with hypocalcaemia and around 10% of normocalcaemic people

215
Q

Causes of hypoglycaemia?

A

insulinoma - increased ratio of proinsulin to insulin
self-administration of insulin/sulphonylureas
liver failure
Addison’s disease
alcohol
Nesidoblastsis - beta cell hyperplasia

216
Q

How does alcohol cause hypoglycaemia?

A

Exaggerated insulin secretion
Redistribution of pancreatitis blood flow into endocrine components
Increased insulin secretion

217
Q

What is the physiological response in hypoglycaemia?

A

Decreases insulin secretion
Increased glucagon secretion
Growth hormone and cortisol released later
Increased catecholamine mediated and Ach neurotransmission

218
Q

Features of blood glucose concentrations < 3.3 mmol/L

A

Causes autonomic symptoms
- sweating
- shaking
- hunger
- anxiety
- nausea

219
Q

Features of glucose concentrations < 2.8

A

Neuroglycopaenic symptoms

  • weakness
  • vision
  • confusion
  • dizziness
220
Q

Causes of hypokalaemia with alkalosis ?

A

Vomiting
Thiazides
Cushing syndrome
Conn’s syndrome

221
Q

Causes of hypokalaemia with acidosis?

A

Diarrhoea
Renal tubular acidosis
Acetazolmide
DKA

222
Q

Hypokalaemia with hypertension?

A

Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
Liddle’s syndrome
11-beta hydroxylase deficiency*

223
Q

Hypokalaemia without hypertension?

A

diuretics
GI loss (e.g. Diarrhoea, vomiting)
renal tubular acidosis (type 1 and 2**)
Bartter’s syndrome
Gitelman syndrome

21 - hydroxylase deficiency

224
Q

Hyponatraemia caused by high urinary sodium?

A

Urinary sodium > 20

Hypovolaemic patients
- Diuretics
- Addisons
- Renal failure

Euvolaemic
- SIADH
- Hypothyroidism

225
Q

Hyponatraemia caused by low urinary sodium?

A

Urinary sodium < 20

Sodium depletion, extra-renal loss
- diarrhoea, vomiting, sweating
- burns, adenoma of rectum

Water excess (patient often hypervolaemic and oedematous)
- secondary hyperaldosteronism: heart failure, liver cirrhosis
- nephrotic syndrome
- IV dextrose
- psychogenic polydipsia

226
Q

Biochemical features of hypoparathyroidism?

A

decrease PTH secretion
e.g. secondary to thyroid surgery*
low calcium, high phosphate

227
Q

Clinical features of hypoparathyroidism ?

A

Features of hypocalcaemia

tetany: muscle twitching, cramping and spasm
perioral paraesthesia
Trousseau’s sign: carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
Chvostek’s sign: tapping over parotid causes facial muscles to twitch
if chronic: depression, cataracts
ECG: prolonged QT interval

228
Q

What is pseudohypoparathyroidism

A

Genetic condition
Cells insensitive to PTH due to G protein abnormality
Low IQ
Short stature
Shortened 4’th and 5’th metacarpals
Low calcium, high phosphate, high PTH

229
Q

How to differnaite between pseudohypoparthyroidism and hypoparathyroidism?

A

1.PTH infusion - Measuring urinary cAMP and phosphate

Should cause increase in both cAMP and phosphate

230
Q

What is pseudopseudohypoparathyroidism ?

A

similar phenotype to pseudohypoparathyroidism but normal biochemistry

231
Q

Causes of hypophosphataemia?

A

Causes
alcohol excess
acute liver failure
diabetic ketoacidosis
refeeding syndrome
primary hyperparathyroidism
osteomalacia

232
Q

Consequences of hypophosphateaemia?

A

red blood cell haemolysis
white blood cell and platelet dysfunction
muscle weakness and rhabdomyolysis
central nervous system dysfunction

233
Q

Causes of hypothyroidism?

A

Hashimoto’s thyroiditis - most common
Subacute thyroidisits - de quervains
Ridel thyroiditis
Drug therapy: Lithium, amiodarone
Dietary iodine

234
Q

Causes of secondary hypothyroidism?

A

From pituitary failure

Down syndrome
Turner’s
Coeliac

235
Q

Interactions of thyroxine ?

A

Iron
Calcium carbonate

Reduced absorption
Take at least 4 hours apart

236
Q

How does a insulin stress test work?

A

IV insulin given, GH and cortisol levels measured
with normal pituitary function GH and cortisol should rise

237
Q

Features of insuloma?

A

hypoglycaemia: typically early in morning or just before meal, e.g. diplopia, weakness etc
rapid weight gain may be seen
high insulin, raised proinsulin:insulin ratio
high C-peptide

238
Q

How should a insuloma be diagnosed?

A

CT pancreas
Supervised prolonged fasting - up to 72 hours

239
Q

Management of insuloma?

A

surgery
diazoxide and somatostatin if patients are not candidates for surgery

240
Q

Associations of insuloma?

A

most common pancreatic endocrine tumour
10% malignant, 10% multiple
of patients with multiple tumours, 50% have MEN-1

241
Q

Management of kallman’s syndrome?

A

Testoestone supplement
Gondaotrophin supplement

242
Q

What is Liddles syndrome?

A

Autosomal dominant
Hypertension + hypokalaemia
Disordered sodium channels in DCT
Increased reabsorption of sodium

Try: Amiloride

243
Q

Days of the menstrual cycle?

A

Days
Menstruation 1-4
Follicular phase (proliferative phase) 5-13
Ovulation 14
Luteal phase (secretory phase) 15-28

244
Q

What are the criteria for metabolic syndrome?

A

3 from:

elevated waist circumference: men > 102 cm, women > 88 cm
elevated triglycerides: > 1.7 mmol/L
reduced HDL: < 1.03 mmol/L in males and < 1.29 mmol/L in females
raised blood pressure: > 130/85 mmHg, or active treatment of hypertension
raised fasting plasma glucose > 5.6 mmol/L, or previously diagnosed type 2 diabetes

245
Q

What is the inheritance of MODY? What is MODY?

A

Autosomal dominant
Development of T2DM <25

245
Q

What is the inheritance of MODY? What is MODY?

A

Autosomal dominant
Development of T2DM <25

246
Q

Features of MEN type 1?

A

There 3 P’s

Parathyroid (95%): hyperparathyroidism due to parathyroid hyperplasia
Pituitary (70%)
Pancreas (50%): e.g. insulinoma, gastrinoma (leading to recurrent peptic ulceration)

Also: adrenal and thyroid

247
Q

Genetic mutation in MEN type 1?

A

MEN 1 gene

248
Q

Features of MEN 2a?

A

Medullary thyroid cancer + 2 P’s

Parathyroid (60%)
Phaeochromocytoma

249
Q

Genetic mutation in MEN 2a?

A

RET oncogene

250
Q

Features of MEN 2b?

A

Medullary thyroid cancer + 1 P

Phaeochromocytoma

Marfanoid body habitus
Neuromas

251
Q

Where does a neuroblastoma arise from?

A

Neural crest tissue of the adrenal medulla

252
Q

Features of neuroblastoma?

A

abdominal mass
pallor, weight loss
bone pain, limp
hepatomegaly
paraplegia
proptosis

253
Q

Investigation of neuroblastoma?

A

raised urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) levels
calcification may be seen on abdominal x-ray
biopsy

254
Q

How does orilstat work?

A

Pancreatic lipase inhibit

255
Q

What is pended’s syndrome ?

A

Autosomal recessive syndrome
PDS gene on chromosome 7

Bilateral sensorineural deafness
Mild hypothroidism
Goitre
Sensorineural heading loss worse on head trauma

MRI: Less turns on cochlea - characteristic one and a half, rather than 2 and a half

256
Q

What is pheochromocytoma?

A

Rare catecholamine secreting tumour

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

257
Q

Features of phaechromocytoma?

A

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

258
Q

Investigation for phaechromocytoma?

A

24 hr urinary collection of metanephrines (sensitivity 97%*)
this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%)

259
Q

Management of phaechromocytoma?

A

MUST BE STABILISED ON MEDICAL THERAPY BEFORE SURGYER

  1. Alpha blocker must be given first before
  2. Beta blocker
260
Q

How to classify pituitary adenoma?

A
  1. Size
    - microadenoma < 1 cm
    - macro adenoma > 1 cm
  2. Hormonal status
    - Secreting function
261
Q

What is the most common pituitary adenoma?

A

Prolactinoma (most) –> nonsecreting –> Growth hormone –> acth ( least)

262
Q

First line treatment for prolactinoma?

A

Hormonal therapy - bromocriptine

263
Q

Features of PCOS?

A

subfertility and infertility
menstrual disturbances: oligomenorrhoea and amenorrhoea
hirsutism, acne (due to hyperandrogenism)
obesity
acanthosis nigricans (due to insulin resistance)

264
Q

Investigations in PCOS?

A

Pelvic ultrasound
Baseline: FSH, LH, Prolactin, TSH, testosterone, sex hormone binding globulin, testosterone
- Raised LH:FSH ratio
- Low SHBG
- High testosterone
Glucose tolerance

265
Q

Rotterdam criteria for PCOS diagnosis?

A
  1. infrequent or no ovulation (usually manifested as infrequent or no menstruation)
  2. clinical and/or biochemical signs of hyperandrogenism (such as hirsutism, acne, or elevated levels of total or free testosterone)
  3. polycystic ovaries on ultrasound scan (defined as the presence of ≥ 12 follicles (measuring 2-9 mm in diameter) in one or both ovaries and/or increased ovarian volume > 10 cm³)
266
Q

Management of PCOS?

A
  1. Weight loss
  2. OCP
    - third generation OCP have anti-androgen action
    - spironolactone, finisher may be tried
  3. Metformin
  4. Clomifene for infertility
    5/ Gonadotrophins if required
267
Q

Thyroid pregnancy changes ?

A

Increased thyroxine binding globulin
Increase in total thyroxine - does not affect free thyroxine level

268
Q

Treatment of thyrotoxicosis in pregnancy?

A

Propylthiouracil

269
Q

Management of hypothyroidism in pregnancy?

A

Thyroxine
Dose increased by up to 50% 4-6 weeks of pregnancy

270
Q

Features of premature ovarian insufficiency ?

A

Elevated gonadotrophin levels before age of 40

climacteric symptoms: hot flushes, night sweats
infertility
secondary amenorrhoea
raised FSH, LH levels
e.g. FSH > 40 iu/l
elevated FSH levels should be demonstrated on 2 blood samples taken 4–6 weeks apart
low oestradiol
e.g. < 100 pmol/l

271
Q

Features of primary hyperaldosteronism ?

A

hypertension
hypokalaemia
e.g. muscle weakness
this is a classical feature in exams but studies suggest this is seen in only 10-40% of patients
alkalosis

272
Q

Investigations in primary hyperaldosteronism?

A

Aldosterone / renin ratio first line investigation
High resolution CT abdomen and adrenal vein sampling

273
Q

Features of hyperparathyroidism?

A

polydipsia, polyuria
depression
anorexia, nausea, constipation
peptic ulceration
pancreatitis
bone pain/fracture
renal stones
hypertension

274
Q

Investigations in hyperparathyroidism?

A

raised calcium, low phosphate
PTH may be raised or (inappropriately, given the raised calcium) normal
technetium-MIBI subtraction scan
pepperpot skull is a characteristic X-ray finding of hyperparathyroidism

275
Q

Management for hyperparathyroidism?

A

total parathyroidectomy
Conservative management:
- calcium < 0.25
- Patient > 50 and no evidence of end organ damage

276
Q

What secretes prolactin?

A

Anterior pituitary
Dopamine acts of releasing inhibitor

277
Q

Features of excess prolactin ?

A

men: impotence, loss of libido, galactorrhoea
women: amenorrhoea, galactorrhoea

278
Q

Causes of raised prolactin?

A

prolactinoma
pregnancy
oestrogens
physiological: stress, exercise, sleep
acromegaly: 1/3 of patients
polycystic ovarian syndrome
primary hypothyroidism (due to thyrotrophin releasing hormone (TRH) stimulating prolactin release)

279
Q

What is pseudohyperkalaemia?

A

rise in serum potassium that occurs due to excessive leakage of potassium from cells

280
Q

Causes of pseudohypekalaemia?

A

haemolysis during venipuncture (excessive vacuum of blood drawing, prolonged tourniquet use or too fine a needle gauge)
delay in the processing of the blood specimen
abnormally high numbers of platelets, leukocytes, or erythrocytes (such as myeloproliferative disorders)
familial causes

281
Q

What are all renal tubular acidosis associated with?

A

hyperchloraemic metabolic acidosis (normal anion gap)

282
Q

What are the features of type 1 renal tubular acidosis?

A

inability to generate acid urine (secrete H+) in distal tubule
causes hypokalaemia
complications include nephrocalcinosis and renal stones

causes include idiopathic, rheumatoid arthritis, SLE, Sjogren’s, amphotericin B toxicity, analgesic nephropathy

283
Q

What are the features of type 2 renal tubular acidosis ?

A

decreased HCO3- reabsorption in proximal tubule
causes hypokalaemia
complications include osteomalacia

causes include idiopathic, as part of Fanconi syndrome, Wilson’s disease, cystinosis, outdated tetracyclines, carbonic anhydrase inhibitors (acetazolamide, topiramate)

284
Q

What are the features of type 3 renal tubular acidosis?

A

extremely rare
caused by carbonic anhydrase II deficiency
results in hypokalaemia

285
Q

What are the features of type 4 RTA?

A

reduction in aldosterone leads in turn to a reduction in proximal tubular ammonium excretion –> hyperkalaemia

causes include hypoaldosteronism, diabetes

286
Q

What are the features of type 4 RTA?

A

reduction in aldosterone leads in turn to a reduction in proximal tubular ammonium excretion –> hyperkalaemia

causes include hypoaldosteronism, diabetes

287
Q

What is riddle’s thyroiditis?

A

Hypothyroidism characterised by dense fibrous tissue replacing the normal thyroid parenchyma

288
Q

Causes of ALP rise?

A

liver: cholestasis, hepatitis, fatty liver, neoplasia
Paget’s
osteomalacia
bone metastases
stthyroidism
renal failure
physiological: pregnancy, growing children, healing fractures

289
Q

Malignancies that cause SIADH?

A

small cell lung cancer
also: pancreas, prostate

290
Q

Neurological conditions that cause SIADH?

A

stroke
subarachnoid haemorrhage
subdural haemorrhage
meningitis/encephalitis/abscess

291
Q

Drugs that cause SIADH?

A

sulfonylureas*
SSRIs, tricyclics
carbamazepine
vincristine
cyclophosphamide

292
Q

Why must SIADH be corrected slowly?

A

Avoid central pontine myelinolysis

293
Q

Management of SIADH?

A

Fluid restriction

294
Q

Findings in sick euthyroid?

A

Low T3
Changes are reversible upon recovery from systemic illness
No treatment needed

295
Q

Skin manifestation of hypothyroidism?

A

dry (anhydrosis), cold, yellowish skin
non-pitting oedema (e.g. hands, face)
dry, coarse scalp hair, loss of lateral aspect of eyebrows
eczema
xanthomata

296
Q

Skin manifestations of hyperthyroidism?

A

pretibial myxoedema: erythematous, oedematous lesions above the lateral malleoli
thyroid acropachy: clubbing
scalp hair thinning
increased sweating

297
Q

Phases of De Quervain thyroiditis?

A

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

298
Q

Management of de quervain’s ?

A

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

299
Q

Molecular mechanism of sulfonylureas?

A

ATP dependent K channel binder

300
Q

Rare side effects of sulfonylureas?

A

hyponatraemia secondary to syndrome of inappropriate ADH secretion
bone marrow suppression
hepatotoxicity (typically cholestatic)
peripheral neuropathy

301
Q

Thyroid cancer with best prognosis

A

Papillary

302
Q

What cell is medullary thyroid cancer derived from?

A

Parafollicular C cells
Secretes calcitonin
Part of MEN - 2

303
Q

Thyroid lymphoma associated with what ?

A

Hashiomoto thyroiditis

304
Q

Pathoology of Papillary thyroid cancer?

A

Usually contain a mixture of papillary and colloidal filled follicles
Histologically tumour has papillary projections and pale empty nuclei
Seldom encapsulated
Lymph node metastasis predominate
Haematogenous metastasis rare

305
Q

Pathology of follicular adenoma

A

Usually present as a solitary thyroid nodule
Malignancy can only be excluded on formal histological assessment

306
Q

Pathology of follicular carcinoma

A

May appear macroscopically encapsulated, microscopically capsular invasion is seen. Without this finding the lesion is a follicular adenoma.
Vascular invasion predominates
Multifocal disease raree

307
Q

Pathology of medullary carcinoma?

A

C cells derived from neural crest and not thyroid tissue
Serum calcitonin levels often raised
Familial genetic disease accounts for up to 20% cases
Both lymphatic and haematogenous metastasis are recognised, nodal disease is associated with a very poor prognosis.

308
Q

Pathology of anapaestic carcinoma?

A

Most common in elderly females
Local invasion is a common feature
Treatment is by resection where possible, palliation may be achieved through isthmusectomy and radiotherapy. Chemotherapy is ineffective.

308
Q

Pathology of anapaestic carcinoma?

A

Most common in elderly females
Local invasion is a common feature
Treatment is by resection where possible, palliation may be achieved through isthmusectomy and radiotherapy. Chemotherapy is ineffective.

309
Q

Thyroid function tests: Graves disease?

A

TSH Low
Free T4 high

T3 thyrotoxicosis - the T4 will be normal

310
Q

Thyroid function tests: Primary hypothyroidism?

A

TSH High
Free T4 low

311
Q

Thyroid function tests: Secondary hypothyroidism

A

TSH low
Free T4 low

Replacement steroid therapy is required prior to thyroxine

312
Q

Thyroid function tests: Sick euthyroid?

A

TSH low
T4 low

313
Q

Thyroid function tests: Sublclinical hypothyroidism

A

TSH high
T4 normal

314
Q

Thyroid function tests: Poor compliance

A

TSH high
T4 normal

315
Q

Features of thyroid storm?

A

Clinical features include:
fever > 38.5ºC
tachycardia
confusion and agitation
nausea and vomiting
hypertension
heart failure
abnormal liver function test - jaundice may be seen clinically

316
Q

Precipitating events of thyroid storm?

A

thyroid or non-thyroidal surgery
trauma
infection
acute iodine load e.g. CT contrast media

317
Q

Management of thyroid storm?

A

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

318
Q

Causes of thyrotoxicosis?

A

Graves’ disease
toxic nodular goitre
acute phase of subacute (de Quervain’s) thyroiditis
acute phase of post-partum thyroiditis
acute phase of Hashimoto’s thyroiditis (later results in hypothyroidism)
amiodarone therapy
contrast

319
Q

Features of toxic multinodular goitre?

A

Toxic multinodular goitre describes a thyroid gland that contains a number of autonomously functioning thyroid nodules resulting in hyperthyroidism.

Nuclear scintigraphy reveals patchy uptake.

320
Q

Treatment of toxic multi nodular goitre?

A

Radioiodone therapy

321
Q

What is a water deprivation test ?

A

Method
prevent patient drinking water
ask the patient to empty their bladder
hourly urine and plasma osmolalities

help evaluate patients who have polydipsia.

322
Q

How to test for insulinoma

A

72 hour fast
t to reach glucose levels below 2 mmol/l with paired c-peptide and insulin levels to be valid test.

323
Q

What is TZD contraindicated in ?

A

Heart failure

324
Q

Most common ECG finding in hypocalcaemia?

A

Prolongation of QT

325
Q

Features of Gieltman’s syndrome?

A

thiazide-sensitive Na+ Cl- transporter in the distal convoluted tubule. It is associated with hypokalaemia and normotension.

326
Q

Treatment of thryoid storm?

A

Beta blocker + Hydrocortisone + Propiothyuracil

327
Q

Features of autoimmune polyendocrinopathy syndrome type 1?

A

chronic mucocutaneous candidiasis (typically first feature as young child)
Addison’s disease
primary hypoparathyroidism

328
Q

Features of autoimmune polyendocrinopathy syndrome type 2?

A

type 1 diabetes mellitus
autoimmune thyroid disease
HLA DR 3 DR 4

329
Q

Drugs that cause SIAH?

A

Carbamazepine
Sulphonyulurea
SSRI
Tricyclic

330
Q

How should hyperparathyroidism be conservatively managed?

A

Cinacalcet

331
Q

What alpha blocker should be used in phaechromcytoma

A

PHenoxybenzamine

332
Q

Management of thyroid storm?

A
  1. Beta blocker
  2. Hydrocortisone
  3. Proppiothiouracil
333
Q

Side effect of sulphyulurea?

A

Weight gain
Hypoglycaemia

334
Q

Side effect of Gliptins?

A

Headaches

335
Q

What SGLT2 inhibitor has increased risk of foot amputations?

A

canaglifozin

336
Q

What does oestrogen and progestoner HRT add an additional risk of?

A

Breast cancer

337
Q

Most common cause of primary aldosteronism?

A

Bilateral adrenal hyperplasia

338
Q

What causes increased sweating in acromegally?

A

Sweat gland hypertrophy

339
Q

What are the associations of hyperuricaemia

A

Hyperlipidaemia
Metabolic syndrome
Hypertension

340
Q

How should MODY be treated?

A

Sulfonylurea

341
Q

Management of stress incontinence?

A
  1. Pelvic floor
  2. Duloxetine
342
Q

Management of urge incontinence?

A
  1. Bladder retaining
  2. Antimuscarinics
  3. Mirabegron
343
Q

What type of drug is mirabegron?

A

Beta 3 agonist

344
Q

What type of drug is mirabegron?

A

Beta 3 agonist

345
Q

Primary hyperthyroidism, best management?

A

Total parathyroidectomy

346
Q

Inheritance of kallman’s?

A

X linked

347
Q

First line treatment for acromegally?

A

Transphenoidal surgery

348
Q

Treatment of choice for toxic mutlinodular goitre?

A

Radio iodine

349
Q

Sulphonylurea mechanism?

A

Bindings to beta cell K+ ATP channels - IT CLOSES THEM

350
Q

How do thyroid hormones change in pregnancy?

A

Increased total level - Free levels rem wins the same

351
Q

What is remnant hyperlipidaemia?

A

mixed hyperlipidaemia (raised cholesterol and triglyceride levels)
associated with apo-e2 homozygosity

yellow palmar creases
palmer xanthomas
tuberous xanthomas

352
Q

Management of remnant hyperlipidaemia?

A

Fibrates

353
Q

Fibrate mechanism?

A

activating PPAR alpha receptors resulting in an increase in LPL activity reducing triglyceride levels

354
Q

When do you need to increase dose of levothyroxine in pregnancy?

A

In week 4-6

355
Q

When do you need to increase dose of levothyroxine in pregnancy?

A

In week 4-6

356
Q

Most common MODY mutaiton and its associations?

A

60% of cases
due to a defect in the HNF-1 alpha gene
is associated with an increased risk of HCC

MRCP Endocrine (2 decks)

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