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MRCP > Endocrine > Flashcards

Endocrine Flashcards

1
Q

what is the cause of majority of acromegaly cases?

A

pituitary adenoma

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2
Q

what are the features of acromegaly?

A

coarse facial appearance, spade-like hands, big feet.
large tongue, prognathism, interdental spaces
excessive sweating and oily skin: caused by sweat gland hypertrophy
features of pituitary tumour: hypopituitarism, headaches, bitemporal hemianopia
raised prolactin in 1/3 of cases → galactorrhoea

hypertension
diabetes (>10%)
cardiomyopathy
colorectal cancer

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3
Q

how is acromegaly investigated?

A

Serum IGF-1 levels (when first suspected and also used for monitoring)
oral glucose tolerance test (OGTT) - confirms if IGF1 is raised
pituitary MRI

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4
Q

how does oral glucose tolerance test confirm acromegaly?

A

give glucose, if GH does not become supressed to <1 , then confirms diagnosis

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5
Q

how is acromegaly treated?

A 
Trans-sphenoidal surgery as first line
If a pituitary tumour is inoperable or surgery unsuccessful then medication may be indicated:
    somatostatin analogue (octreotide)
    pegvisomant
    dopamine agonist (bromocriptine)
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6
Q

How does a somatostatin analogue work in acromegaly?

A

inhibits release of GH

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7
Q

What is the mechanism of pegvisomant?

A

GH receptor antagonist - prevents dimerization of the GH receptor
once daily s/c administration

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8
Q

what are the acute phase proteins?

A

during inflammation/infection liver increases production of acute phase proteins…
CRP, procalcitonin, ferritin, fibrinogen, alpha-1 antitrypsin, caeruloplasmin, serum amyloid A & P , haptoglobin and complement

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9
Q

which proteins are decreased during acute phase response?

A 
albumin
transthyretin (formerly known as prealbumin)
transferrin
retinol binding protein
cortisol binding protein
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10
Q

what is the function of CRP?

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 is the commonest cause of hypoaldrenalism? what is this called?

A

Autoimmune destruction of the adrenal glands

Addisons - both cortisol and aldosterone reduced

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12
Q

what are the features of addisons?

A

lethargy, weakness, anorexia, nausea & vomiting, weight loss,

‘salt-craving’
hyperpigmentation (especially palmar creases) hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen

vitiligo, loss of pubic hair in women,
crisis: collapse, shock, pyrexia

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13
Q

other than addisons what are the other causes of hypoadrenalism?

A 
tuberculosis
metastases (e.g. bronchial carcinoma)
meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
HIV
antiphospholipid syndrome
Secondary causes
pituitary disorders (e.g. tumours, irradiation, infiltration)

Exogenous glucocorticoid therapy

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14
Q

how is addisons disease diagnosed?

A

ACTH stimulation test (short Synacthen test). Plasma cortisol is measured before and 30 minutes after giving Synacthen 250ug IM.

Adrenal autoantibodies such as anti-21-hydroxylase may also be demonstrated.

If an ACTH stimulation test is not readily available then sending a 9 am serum cortisol can be useful:
> 500 nmol/l makes Addison’s very unlikely
< 100 nmol/l is definitely abnormal
100-500 nmol/l should prompt a ACTH stimulation test to be performed

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15
Q

what are the electrolyte abnormalities in addisons?

A

hyperkalaemia
hyponatraemia
hypoglycaemia
metabolic acidosis

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16
Q

what are the causes of an addisonian crisis?

A

acute exacerbation of chronic hypoadrenalism e.g. surgery or infection
OR
Sudden loss of adrenal - adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
OR
steroid withdrawal

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17
Q

how is addisonian crisis managed?

A

hydrocortisone 100 mg im or iv

1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic

continue hydrocortisone 6 hourly until the patient is stable.

No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action

oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days

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18
Q

causes of raised ALP (Alanine phosphatase)?

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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19
Q

how can the causes of raised ALP be differentiated?

A

Calcium levels..

if high ALP and high CA - bone mets/ hyperparathyroid
if high ALP and low Ca - osteomalacia/renal failure

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20
Q

define primary amenorrhoea.

A

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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21
Q

define 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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22
Q

what are the causes of primary amenorrhoea?

A

gonadal dysgenesis (e.g. Turner’s syndrome) - the most common causes

testicular feminisation

congenital malformations of the genital tract
imperforate hymen

functional hypothalamic amenorrhoea (e.g. secondary to anorexia)

congenital adrenal hyperplasia

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23
Q

what are the causes of secondary amenorrhoea?

A

hypothalamic amenorrhoea (e.g. secondary stress, excessive exercise)

polycystic ovarian syndrome (PCOS)
hyperprolactinaemia
thyrotoxicosis / hypothyroid

premature ovarian failure

Sheehan’s syndrome
Asherman’s syndrome (intrauterine adhesions)

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24
Q

how is amenorrhoea investigated?

A

Exclude pregnancy with urinary or serum bHCG

full blood count, urea & electrolytes, coeliac screen, thyroid function tests

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
androgen levels - raised levels may be seen in PCOS
oestradiol

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25
Q

what is androgen insensitivity syndrome?

A

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

Complete androgen insensitivity syndrome is the new term for testicular feminisation syndrome

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26
Q

what are the features of androgen insensitivity syndrome?

A

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

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27
Q

how is androgen insensitivity diagnosed?

A

buccal smear or chromosomal analysis to reveal 46XY genotype

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28
Q

how is androgen insensitivity managed?

A

couselling - raise child as female
oestrogen therapy
bilateral orchidectomy - risk of testicular cancer from undescended testes

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29
Q

what is autoimmune polyendocrinopathy syndrome (APS)?

A

Addison’s disease is associated with other endocrine deficiencies in approximately 10% of patients.
There are two distinct types of autoimmune polyendocrinopathy syndrome (APS), with type 2 (sometimes referred to as Schmidt’s syndrome) being much more common.

vitiligo can happen with either APS 1 or 2

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30
Q

what is APS type 2? what allele is it linked to?

A

APS type 2 linked to HLA DR3/DR4.

Patients have Addison’s disease plus either:
type 1 diabetes mellitus
autoimmune thyroid disease

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31
Q

what is APS type 1? what is it also known as? genetics?

A

APS type 1 is occasionally referred to as Multiple Endocrine Deficiency Autoimmune Candidiasis (MEDAC).
very rare autosomal recessive disorder caused by mutation of AIRE1 gene on chromosome 21

Features of APS type 1 (2 out of 3 needed)
chronic mucocutaneous candidiasis (typically first feature as young child)
Addison’s disease
primary hypoparathyroidism

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32
Q

what is bartters syndrome? how does bartters differ from other endocrine causes of hypoK?

A

autosomal recessive cause of severe hypokalaemia due to defective chloride absorption at the Na+ K+ 2Cl- cotransporter (NKCC2) in the ascending loop of Henle.

It should be noted that it is associated with normotension (unlike other endocrine causes of hypokalaemia such as Conn’s, Cushing’s and Liddle’s syndrome which are associated with hypertension).

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33
Q

How does Bartters present?

A 
usually presents in childhood, e.g. Failure to thrive
polyuria, polydipsia
hypokalaemia
normotension
weakness
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34
Q

what is the function of carbimazole? How does this compare to propylthiouracil?

A

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

in contrast propylthiouracil as well as this central mechanism of action also has a peripheral action by inhibiting 5’-deiodinase which reduces peripheral conversion of T4 to T3

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35
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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36
Q

what type of cancer are the majority of cervical cancers?

A

squamous cell

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37
Q

which HPVs are most linked to cervical cancer?

A

16, 18, 33

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38
Q

whats the function of E6/7?

A
  • E6 inhibits the p53 tumour suppressor gene

* E7 inhibits RB suppressor gene

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39
Q

what is congenital adrenal hyperplasia? (genetics and pathogenesis)

A

•group of autosomal recessive disorders - mainly 21-hydroxylase deficiency

  • affect adrenal steroid biosynthesis
  • in response to resultant low cortisol levels the anterior pituitary secretes high levels of ACTH
  • ACTH stimulates the production of adrenal androgens that may virilize a female infant
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40
Q

what are the features of CAH caused by 21 hydroxylase deficiency?

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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41
Q

what are the features of CAH caused by 11 beta hydroxylase deficiency?

A 
11-beta hydroxylase deficiency features
•virilisation of female genitalia
•precocious puberty in males
•hypertension
•hypokalaemia
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42
Q

what are the features of CAH caused by 17 hydroxylase deficiency? (very rare)

A

17-hydroxylase deficiency features
•non-virilising in females
•inter-sex in boys
•hypertension

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43
Q

what are the problems of congenital hypothyroid?

A

if not treated within 4 weeks - irreversible cognitive delay

  • prolonged neonatal jaundice
  • delayed mental & physical milestones
  • short stature
  • puffy face, macroglossia
  • hypotonia
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44
Q

when are children screened for congenital hypothyroidism?

A

Children are screened at 5-7 days using the heel prick test

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45
Q

which steroids have glucocorticoid/mineralocorticoid activity?

A

fludrocortisone - mineralocorticoid
hydrocortisone - both (high mineralo)
prednisolone - both (mainly gluco)
Dexamethasone/bethamethasone - glucocorticoid

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46
Q 
what are the side effects of steroids for the... 
MSK system?
psych?
GI?
Opthal?
A
  • musculoskeletal: osteoporosis, proximal myopathy, avascular necrosis of the femoral head
  • psychiatric: insomnia, mania, depression, psychosis
  • gastrointestinal: peptic ulceration, acute pancreatitis
  • ophthalmic: glaucoma, cataracts
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47
Q

when do patients require gradual withdrawal of steroids?

A

•the BNF suggests gradual withdrawal of systemic corticosteroids if patients have: received more than 40mg prednisolone daily for more than one week, received more than 3 weeks treatment or recently received repeated courses

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48
Q

what is the most common cause of cushings syndrome?

A

exogenous use

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49
Q

what are the causes of cushings?

A

ACTH dependent causes
•Cushing’s disease (80%): pituitary tumour secreting ACTH producing adrenal hyperplasia
•ectopic ACTH production (5-10%): e.g. small cell lung cancer is the most common causes

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

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50
Q

what is carney complex ?

A

syndrome of cushings and cardiac myxoma

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51
Q

what is pseudo cushings?

A

mimics cushings
•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

52
Q

what metabolic lab result is found in cushings?

A

hypokalaemic metabolic alkalosis may be seen, along with impaired glucose tolerance.

(ectopic ACTH is associated with very low K+ levels)

53
Q

how is cushings tested for?

A

overnight dexamethasone suppression test
- this is the most sensitive test and is now used first-line to test for Cushing’s syndrome
◦patients with Cushing’s syndrome do not have their morning cortisol spike suppressed

•24 hr urinary free cortisol

54
Q

how can we investigate the cause of cushings (source of issue)?

A

localization tests e.g. finding out where the problem is..

first one
9am and midnight plasma ACTH (and cortisol) levels. If ACTH is suppressed then a non-ACTH dependent cause is likely such as an adrenal adenoma

second
High-dose dexamethasone suppression test

CRH stimulation
•if pituitary source then cortisol rises
•if ectopic/adrenal then no change in cortisol

55
Q

how are results of high dose dexamethasone test interpreted for cushings?

A

cotisol not supressed, ACTH supressed - adrenal issue

Cortisol and ACTH supressed - pituitary issue.

neither supressed - ectopic ACTH release

56
Q

how can you differentiate between real cushings and pseudocushings?

A

An insulin stress test is used to differentiate between true Cushing’s and pseudo-Cushing’s.

57
Q

how is T2D diadnosed?

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)

If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.

HbA1c >6.5%

58
Q

How is prediabetes defined?

A

HbA1c - 6-6.4%

fasting gluc - 6.1-6.9

59
Q

when can HbA1c not be used for diagnosis?

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)
60
Q

what is MODY?

A

mature onset diabetes of the young
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

61
Q

what is LADA?

A

latent autoimmune diabetes of adults

small group of patients who develop such problems later in life. These patients are often misdiagnosed as having T2DM

62
Q

what are the main side effects of insulin?

A

Hypoglycaemia
Weight gain
Lipodystrophy

63
Q

what is the function of metformin?

A

Increases insulin sensitivity

Decreases hepatic gluconeogenesis

64
Q

what are the side effects of metformin?

A

GI iupset

lactic acidosis

65
Q

when is metformin contraindicated?

A

eGFR <30

66
Q

what is the function of sulphonylureas? (gliclazide and glimepiride)

A

Stimulate pancreatic beta cells to secrete insulin

67
Q

what are the side effects of sulphonylureas?

A

Hypoglycaemia
Weight gain
Hyponatraemia

68
Q

what is the function of pioglitazone (Thiazolidinediones)? what are the side effects?

A

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

Weight gain
Fluid retention

69
Q

what is the function of DPP-4 inhibitors (-gliptins)? what risk is there with these?

A

Increases incretin levels which inhibit glucagon secretion

risk of pancreatitis

70
Q

what is the function of SGLT-2 inhibitors (-gliflozins)? what are the side effects/benefits?

A

Inhibits reabsorption of glucose in the kidney
UTI
result in weight loss

71
Q

what are GLP1 agonists?

how are they given? side effects? benefits?

A

Incretin mimetic which inhibits glucagon secretion Subcutaneous
Nausea and vomiting, Pancreatitis
Typically result in weight loss

72
Q

How is T2D managed (algoithm for drug therapy)?

A

metformin 1st line if HbA1c >7.5 add in antoher, if still about 7.5 , add another for triple therapy OR insulin.

if not tolerated and BMI >35 add GLP1

73
Q

what class of drug is Exenatide? how is it given?

A

glucagon-like peptide-1 (GLP-1) mimetic. These drugs increase insulin secretion and inhibit glucagon secretion.
Exenatide must be given by subcutaneous injection within 60 minutes before the morning and evening meals. It should not be given after a meal.

74
Q

How does Liraglutide compare to exenatide?

A

Liraglutide is the other GLP-1 mimetic

One the main advantages of liraglutide over exenatide is that it only needs to be given once a day.

75
Q

when are GLP1 used?

A

Consider adding exenatide to metformin and a sulfonylurea if:
BMI >= 35 kg/m² OR
BMI < 35 kg/m² and insulin is unacceptable because of occupational implications or weight loss would benefit other comorbidities.

76
Q

How are the use of GLP1s justified according to NICE?

A

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

77
Q

what are the function of gliptins?

A

increase levels of incretins (GLP-1 and GIP) by decreasing their peripheral breakdown

78
Q

how often should HbA1c be monitored in T1DM? what is the target?

A

3-6 months

target of 6.5% or lower

79
Q

How often should blood glucose be monitored in T1dM?

A

4x daily - before each meal and before bed
more frequently during periods of illness; before, during and after sport; when planning pregnancy, during pregnancy and while breastfeeding

80
Q

what should blood glucose targets be?

A

5-7 mmol/l on waking and

4-7 mmol/l before meals at other times of the day

81
Q

when is metformin considered in T1DM?

A

when BMI >25

82
Q

what are the target HbA1c for T2DM and what is the cut off before considering the next drug?

A

target when on no drugs/ metformin alone = 6.5
if on oral hypoglycaemics then 7% target

you can titrate up metformin and encourage lifestyle changes to aim for a HbA1c of 48 mmol/mol (6.5%), but should only add a second drug if the HbA1c rises to 58 mmol/mol (7.5%)

83
Q

what is the management of T2DM (use Hba1c targets)

A

metformin is still first-line and should be offered if the HbA1c rises to 48 mmol/mol (6.5%)* on lifestyle interventions
if the HbA1c has risen to 58 mmol/mol (7.5%) then a second drug should be added from the following list:
sulfonylurea, gliptin, pioglitazone, SGLT-2 inhibitor

if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then triple therapy with one of the following combinations should be offered:
metformin + gliptin + sulfonylurea
metformin + pioglitazone + sulfonylurea
metformin + sulfonylurea + SGLT-2 inhibitor
metformin + pioglitazone + SGLT-2 inhibitor
OR insulin therapy should be considered

84
Q

what is the criteria to continue a GLP 1 analgoe?

A

only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months

85
Q

how is T2DM tolerated if metformin is not tolerated?

A

if the HbA1c rises to 48 mmol/mol (6.5%) on lifestyle interventions, consider one of the following:
sulfonylurea, gliptin, pioglitazone
if the HbA1c has risen to 58 mmol/mol (7.5%) then a one of the following combinations should be used:
gliptin + pioglitazone
gliptin + sulfonylurea
pioglitazone + sulfonylurea
if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then consider insulin therapy

86
Q

what is the recommended insulin to start with for T2DM?

A

NICE recommend starting with human NPH insulin (isophane, intermediate-acting) taken at bed-time or twice daily according to need

87
Q

what antibodies are present in t1dm?

A

islet-associated antigen (IAA) antibody and glutamic acid decarboxylase (GAD) antibody

88
Q

how often are patients screen for diabetic foot? and how?

A

Annually.
screening for ischaemia: done by palpating for both the dorsalis pedis pulse and posterial tibial artery pulse
screening for neuropathy: a 10 g monofilament is used on various parts of the sole of the foot

89
Q

what factors give a high risk of diabetic foot ulcer?

A
  • previous ulceration or
  • previous amputation or
  • on renal replacement therapy or
  • neuropathy and non-critical limb ischaemia together or
  • neuropathy in combination with callus and/or deformity or
  • non-critical limb ischaemia in combination with callus and/or deformity.
90
Q

How does ezetimibe work?

A

Ezetimibe is a lipid-lowering drug which inhibits cholesterol receptors on enterocytes, decreasing cholesterol absorption in the small intestine.

91
Q

when does NICE recommnend the use of ezetimibe?

A

use of ezetimibe in primary heterozygous-familial and non-familial hypercholesterolaemia

Ezetimibe monotherapy is recommended as an option for treating primary hypercholesterolaemia in adults in whom initial statin therapy is contraindicated or who cannot tolerate statin therapy
Ezetimibe, coadministered with initial statin therapy, is recommended as an option for treating primary hypercholesterolaemia in adults who have started statin therapy when:
serum total or LDL cholesterol concentration is not controlled despite titrating up / cannot tolerate higher dose

92
Q

when are fibrates used? what is their mechanism of action?

A

Fibrates are used in the management of hyperlipidaemia, particularly raised triglycerides.

Fibrates work through activating PPAR alpha receptors resulting in an increase in LPL activity reducing triglyceride levels.

93
Q

What are the side effects of fibrates?

A

Gastrointestinal side-effects are common

increased risk of thromboembolism

94
Q

what are the triggers of DKA?

A

MI
infection
missed insulin

95
Q

what are the clinical features of DKA?

A

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

96
Q

what is the diagnostic criteria 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

97
Q

what is the management of DKA?

A

fixed rate insulin 0.1units/kg/hr
fluids NaCL + KCL (unless high)
- 1L over 1h, 1L over 2 hour x2, 1L over 4 hours x2, 1 L over 6 hours.
once BMs <15 , dextrose 5% started too

any long acting insulins can continue but short acting stopped.

98
Q

how much K+ is given in DKA?

A

if >5.5 none
if 3.5-5.5 40mM
if <3.5 senior review

99
Q

how is DKA resolution defined?

A

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

100
Q

what are the 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

101
Q

which group of patients are particularly at risk of cerebral oedema?

A

children and young adults.

give a slower fluid regime
following fluid resuscitation in DKA and often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc. It usually occurs 4-12 hours following commencement of treatment but can present at any time. If there is any suspicion a CT head and senior review should be sought

102
Q

how is diabetic painful neuropathy managed?

A

usually they get sensory loss which is painless but sometimes can be painful
first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin
if the first-line drug treatment does not work try one of the other 3 drugs
tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
pain management clinics may be useful in patients with resistant problems

103
Q

what are the features of diabetic autonomic neuropathy?

A

Gastroparesis
symptoms include erratic blood glucose control, bloating and vomiting
management options include metoclopramide, domperidone or erythromycin (prokinetic agents)

Chronic diarrhoea
often occurs at night

Gastro-oesophageal reflux disease
caused by decreased lower esophageal sphincter (LES) pressure

104
Q

Which antibodies are associated with Graves’ disease

A

Anti TSH r - stimulating -90%

Anti thyroid peroxidase - 70%

105
Q

What is the first line for fertility in PCOS

A

Clomifene

106
Q

How is gestational diabetes managed

A

If bm less than 7 can try diet and metformin but if targets are still not met with this then start insulin

If more than 7 - start insulin straight away
If any effects of diabetes e.g. macrosomia - start insulin

107
Q

What is the most common cause of Cushing’s syndrome

A

Iatrogenic - 1st

Cushings disease - pituitary tumour - 2nd

108
Q

Which type of malignancy does hashimotos predispose to ?

A

MALT lymphoma

109
Q

Which genes are mutated in MODY

A

Type 3 - HNF1a - most common
Type 2 - glucokinase
Type 5- HNF1b - associated with cyst

110
Q

how can you distinguish klinefelters and kallmans?

A

klinefelters - high LH/ FSH

Kallmans - normal/ low FSH / LH

111
Q

what is the management for diabetic nephropathy?

A

duloxetine, gabapentin, amitriptyline

tramadol for rescue therapy

112
Q

How is SIADH initially managed?

A

fluid restriction

113
Q

what is the mechanism of action of thiazolinediones (TZDs) and the ADRs

A 
PPARg receptor (intracellular receptor) - increases insulin sensitivity 
e.g. pioglitazone

ADRs - fluid retention - shouldnt be used in HF

  • weight gain
  • increased risk of fractures
  • increased risk of bladder Ca with pioglitazone
  • liver impairment - monitor LFTs
114
Q

what is the most common cause of primary hyperaldosteronism?

A

bilateral adrenal hyperplasia

115
Q

What are the ADRs of SGLT2 inhibitors? what are thes drugs called?

A

Gliflozins

forniers gangrene
UTI
normoglycaemic ketoacidosis
limb amputation

116
Q

what blood abnormality is often seen with fibroids and why?

A

high Hb

fibroids produce EPO

117
Q

who are fibroids more common in?

A

Afrocaribean

118
Q

what is HbA1c of 6% equivalent to?

A

42

each 1% = 11 increase

119
Q

what are the causes of gynaecomastia?

A 
testicular failure - mumps
klinefelters , kallmans 
seminoma - HCG secreting 
haemodialysis
hyperthyroid

drugs = spironolactone, goreselin , digoxin, cimetidine, cannabis, finasteride, steroids

120
Q

what are the complications of acromegaly?

A

HTN, CRC, diabetes, cardiomyopathy

121
Q

what inheritance does familial hyperlipidaemia have?

A

autosomal dominant

122
Q

which electrolyte abnormality is associated with low K

A

low Mg

123
Q

what are the causes of euvolaemic hyponatraemia?

A

SiADH, hypothyroidism

urinary sodium usually high >20

124
Q

what inheritance is kallmans? what are the feature?

A

X linked recessive
small testis, tall , anosmia ,
low/ normal LH/ FSH

125
Q

what are the ADRs of sulphonylureas?

A 
weight gain
hypoglycaemia
SiADH
bone marrow sup
hepatotoxic 
peripheral neuropathy

dont use in preg / breast feeding

126
Q

what blood test suggests poor compliance to levothyroxine?

A

high TSH - has been trying to compensate

normal T3/4 - short term fix before blood test

MRCP (7 decks)

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