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MRCP Part 1 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the cause of excessive sweating and oily skin in acromegaly?

A

caused by sweat gland hypertrophy

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2
Q

4 Complications of acromegaly

A
  1. HTN
  2. DM
  3. CARDIOMYOPATHY
  4. COLORECTAL CANCER
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3
Q

What is the confirmatory test of acromegaly if IGF-1 LEVEL is raised ?

A

Oral glucose tolerance test

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4
Q

In Oral glucose tolerance test
in normal patients GH is suppressed to < …….. mu/L with hyperglycaemia

A

< 2

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5
Q

Acromegaly: management

A

Trans-sphenoidal surgery is the first-line treatment for acromegalyin the majority of patients.

If a pituitary tumour is inoperable or surgery unsuccessful then medication may be indicated:

  1. somatostatin analogue : octreotide
  2. pegvisomant
  3. dopamine agonists : bromocriptine

External irradiation is sometimes used for older patients or following failed surgical/medical treatment

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6
Q

somatostatin analogue directly inhibits ……

A

the release of growth hormone

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7
Q

GH receptor antagonist ( pegvisomant ) - prevents ….

A

dimerization of the GH receptor

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8
Q

10 Acute phase proteins

A
  1. CRP
  2. procalcitonin
  3. ferritin
  4. fibrinogen
  5. alpha-1 antitrypsin
  6. caeruloplasmin
  7. serum amyloid A
  8. serum amyloid P component**
  9. haptoglobin
  10. complement
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9
Q

During the acute phase response the liver decreases the production of other proteins ( negative acute phase proteins)
(5)

A

albumin

transthyretin (formerly known as prealbumin)

transferrin

retinol binding protein

cortisol binding protein

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10
Q

causes of hypoadrenalism

A

Primary causes
1. tuberculosis
2. metastases(e.g. bronchial carcinoma)
3. meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
4. HIV
5. antiphospholipid syndrome

Secondary causes
- pituitary disorders (e.g. tumours, irradiation, infiltration)

Exogenous glucocorticoid therapy

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11
Q

Management of addisonian crisis

A
  1. hydrocortisone 100 mg im or iv continue 6 hourly until the patient is stable.
  2. oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
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12
Q

Causes of raised alkaline phosphatase (ALP)

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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13
Q

2 Causes of Raised ALP and raised calcium

A

Bone metastases
Hyperparathyroidism

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14
Q

Children are screened for Congenital hypothyroidism at …. days using …….. test

A

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

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15
Q

In Toxic multinodular goitre
The treatment of choice is …..

A

radioiodine therapy.

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16
Q

painful goitre and raised ESR

A

Subacute thyroiditis (de Quervain’s)

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17
Q

Management of Thyroid eye disease

A

smoking cessation

topical lubricants may be needed to help prevent corneal inflammation caused by exposure

steroids

radiotherapy

surgery

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18
Q

4 phases of Subacute 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

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19
Q

thyroid scintigraphy:globally reduced uptake of iodine-131

In which condition?

A

Subacute thyroiditis

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20
Q

Riedel’s thyroiditis is associated with ……..

A

retroperitoneal fibrosis.

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21
Q

SGLT-2 inhibitors reversibly inhibit ……..

A

sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion

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22
Q

Side effects of SGLT2

A

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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23
Q

women with established hypothyroidism who become pregnant should have their dose increased ‘by

A

At least 25 - 50 mcg levothyroxine

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24
Q

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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25
Q

Adverse effects of carbimazole

A

agranulocytosis

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

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26
Q

Autoantibodies of Graves’ disease

A

TSH receptor stimulating antibodies(90%)

anti-thyroid peroxidase antibodies (75 %)

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27
Q

Thyroid scintigraphy

diffuse, homogenous, increased uptakeof radioactive iodine

In which condition?

A

Graves’ disease

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28
Q

Radioiodine treatment is contraindicated in

A
  1. pregnancy (should be avoided for 4-6 months following treatment)
  2. age < 16 years. T
  3. Thyroid eye disease is a relative contraindication, as it may worsen the condition
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29
Q

Hashimoto’s thyroiditis is associated with the development of……lymphoma

A

MALT lymphoma

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30
Q

Management of papillary and follicular cancer

A

total thyroidectomy

followed by radioiodine (I-131) to kill residual cells

yearly thyroglobulin levels to detect early recurrent disease

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31
Q

What is the most commonly can cause ectopic ACTH production

A

small cell lung cancer

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32
Q

ACTH independent causes of Cushing’s 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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33
Q

What is Pseudo-Cushing’s?

A

alcohol excessor 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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34
Q

Tests to confirm Cushing’s syndrome

L

A
  1. overnight (low-dose) dexamethasone suppression test

this is the most sensitive test and is now used first-line to test for Cushing’s syndrome

  1. 24 hr urinary free cortisol

two measurements are required

  1. bedtime salivary cortisol

two measurements are required

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35
Q

Causes of Decreased excretion of Uric acid

A

drugs: low-dose aspirin, diuretics, pyrazinamide

pre-eclampsia

alcohol

renal failure

lead

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36
Q

Increased synthesis of Uric acid

A

Lesch-Nyhan disease

myeloproliferative disorders

diet rich in purines

exercise

psoriasis

cytotoxics

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37
Q

4 Causes of Hypokalaemia with hypertension

A

Cushing’s syndrome

Conn’s syndrome (primary hyperaldosteronism)

Liddle’s syndrome

11-beta hydroxylase deficiency*

  • 2CL11
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38
Q

5 causes of hypokalaemia without hypertension

A
  1. Diuretics
  2. Bartter’s syndrome
  3. Gitelman syndrome
  4. GI loss ( diarrhoea, vomiting)
  5. RTA ( type 1 & 2)
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39
Q

Bartter’s syndrome is autosomal ………

A

autosomal recessive

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40
Q

Bartter’s syndrome cause severe hypokalaemia due to defective ………..

A

chloride absorption at theNa+K+2Cl- cotransporter (NKCC2) in the ascending loop of Henle

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41
Q

Features of Bartter’s syndrome

A
  1. usually presents in childhood, e.g. Failure to thrive
  2. polyuria, polydipsia
  3. hypokalaemia
  4. normotension
  5. weakness
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42
Q

Autoimmune polyendocrinopathy syndrome type 1

A

(2 out of 3 needed)

  1. chronic mucocutaneous candidiasis (typically first feature as young child)
  2. Addison’s disease
  3. primary hypoparathyroidism
  • Vitiligo can occur
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43
Q

Autoimmune polyendocrinopathy syndrome type 2

A

Addison’s disease plus either:

  1. T1DM
  2. autoimmune thyroid disease
  • Vitiligo can occur
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44
Q

Management of Diabetic neuropathy

A

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 clinicsmay be useful in patients with resistant problems

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45
Q

Management of Gastroparesis

A

metoclopramide or

domperidone or

erythromycin

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46
Q

3 Causes of higher than expected levels of HbA1c

A

Vitamin B 12 / folic acid deficiency

IDA

Splenectomy

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47
Q

glycaemic index (GI) describes ….

A

capacity of a food to raise blood glucose compared with glucose in normal glucose-tolerant individuals

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48
Q

Mechanism of action of Metformin

A
  1. Increases insulin sensitivity
  2. Decreases hepatic gluconeogenesis
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49
Q

Metformin is contraindicated if GFR

A

< 30

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50
Q

Sulfonylureas Stimulate

A

pancreatic beta cells to secrete insulin

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51
Q

Mechanism of action of Thiazolidinediones

A

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

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52
Q

DPP-4 inhibitors (-gliptins) Increases

A

incretin levels which inhibit glucagon secretion

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53
Q

SGLT-2 inhibitors (-gliflozins) Inhibits

A

reabsorption of glucose in the kidney

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54
Q

Mechanism of action of GLP-1 agonists(-tides)

A

Incretin mimetic which inhibits glucagon secretion

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55
Q

adverse effects of sulfonylureas

A
  1. Hypoglycemia
  2. Weight gain
  3. Hypo Na
  4. bone marrow suppression
  5. hepatotoxicity(typically cholestatic)
  6. peripheral neuropathy
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56
Q

Sulfonylureas vs breastfeeding

A

should be avoided

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57
Q

Sulfonylureas

On a molecular level they bind ……..?……..on the cell membrane of pancreatic beta cells.

A

to an ATP-dependent K+(KATP) channel

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58
Q

5 Side effects of Thiazolidinediones

A
  1. Weight gain
  2. Liver Impairment
  3. Fluid retention
  4. Increase risk of fractures
  5. Bladder cancer
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59
Q

prediabetes

  1. FBG
  2. HbA1C
A
  1. 6.1-6.9 mmol/l
  2. 42-47 mmol/mol (6.0-6.4%)
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60
Q

Phaeochromocytoma may be associated with

A

MEN type II,

neurofibromatosis and

von Hippel-Lindau syndrome

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61
Q

Tests of Phaeochromocytoma

A
  1. 24 hr urinary collection of metanephrines(sensitivity 97%*)
  2. 24 hr urinary collection of catecholamines (sensitivity 86%)
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62
Q

Management of Phaeochromocytoma

A

Surgery is the definitive management. The patient must first however be stabilized with medical management:

alpha-blocker (e.g. phenoxybenzamine), given before a

beta-blocker (e.g. propranolol)

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63
Q

the most common cause of Primary hyperaldosteronism

A

bilateral idiopathic adrenal hyperplasia: the cause of around 60-70% of cases

64
Q

Investigations of Primary hyperaldosteronism

A
  1. plasma aldosterone/renin ratio is the first-line investigationin suspected primary hyperaldosteronism
  • should show high aldosterone levels alongside low renin levels
  1. following this a high-resolution CT abdomen and adrenal vein sampling is used to differentiate between unilateral and bilateral sources of aldosterone excess
  • if the CT is normal adrenal venous sampling (AVS)can be used to distinguish between unilateral adenoma and bilateral hyperplasia
65
Q

Management of Primary hyperaldosteronism

A

adrenal adenoma: surgery (laparoscopic adrenalectomy)

bilateral adrenocortical hyperplasia:aldosterone antagonist e.g. spironolactone

66
Q

Drugs causing SIADH

A

sulfonylureas*

SSRIs, tricyclics

carbamazepine

vincristine

cyclophosphamide

67
Q

Causes of SIADH

A
  1. Malignancy
    small cell lung cancer

also: pancreas, prostate

  1. Neurological
    Stroke
    SAH
    SUBDURAL HEMORRHAGE
  2. Infections
    TB
    Pneumonia
  3. Other causes
    positive end-expiratory pressure (PEEP)

porphyrias

68
Q

Investigations of SIADH

A

Urine osmolality: Urine osmolality is inappropriately high (>100 mOsm/kg) in relation to serum osmolality, as the kidneys should normally dilute urine in the setting of low serum osmolality.

Urine sodium concentration: >40 mmol/L)

69
Q

Management of SIADH

A

correction must be done slowly to avoid precipitating central pontine myelinolysis

fluid restriction

demeclocycline: reduces the responsiveness of the collecting tubule cells to ADH

ADH (vasopressin) receptor antagonists have been developed

70
Q

3 Contraindications of insulin stress test

A
  1. Epilepsy
  2. IHD
  3. ADRENAL INSUFFICIENCY
71
Q

Risk factors for 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)

72
Q

Screening for gestational diabetes with

A

OGTTis the test of choice

73
Q

Pregnant women with any of the other risk factors should be offered an OGTT at…..?

A

at 24-28 weeks

74
Q

Diagnostic thresholds for gestational diabetes

A

FBG >= 5.6 MMOL / L

2Hr GLUCOSE >= 7.8 MMOL / L

75
Q

Management of gestational diabetes

A
  1. if the fasting plasma glucose level is< 7 mmol/l a trial of diet and exercise should be offered

if glucose targets are not met within 1-2 weeks of altering diet/exercise metformin should be started

if glucose targets are still not met insulin should be added to diet/exercise/metformin

gestational diabetes is treated short-acting, not long-acting, insulin

  1. if at the time of diagnosis the fasting glucose level is >= 7 mmol/l insulin should be started
  2. if the plasma glucose level is between 6-6.9 mmol/l, and there is evidence of complications such as macrosomia or hydramnios, insulin should be offered
76
Q

Targets for self monitoring of pregnant women (pre-existing and gestational diabetes)

Fasting …….?

1 hr after meal …….?

2 hr after meal …….?

A

Fasting 5.3

1 hr after meal 7.8

2 hr after meal 6.4

77
Q

Meglitinides increase

A

pancreatic insulin secretion like sulfonylureas theybind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells

78
Q

MODY associated with HNF1A often respond well to treatment with ……?

A

low-dose sulfonylureas

79
Q

The most common types of MODY

A

MODY2 (GCK mutation)

80
Q

Causes of hypoglycemia

A

insulinoma - increased ratio of proinsulin to insulin

self-administration of insulin/sulphonylureas

liver failure

Addison’s disease

alcohol

nesidioblastosis - beta cell hyperplasia

81
Q

Physiological response to hypoglycaemia

A

hormonal response: the first response of the body is decreased insulin secretion. This is followed byincreased glucagon secretion. Growth hormone and cortisol are also released but later

sympathoadrenal response: increased catecholamine-mediated (adrenergic) and acetylcholine-mediated (cholinergic) neurotransmission in the peripheral autonomic nervous system and in the central nervous system

82
Q

Very high glucocorticoid activity, minimal mineralocorticoid activity

Which preparation?

A

Dexamethasone

Betmethasone

83
Q

Glucocorticoid activity, high mineralocorticoid activity,

Which preparation?

A

Hydrocortisone

84
Q

Predominant glucocorticoid activity, low mineralocorticoid activityVery high glucocorticoid activity, minimal mineralocorticoid

Which preparation?

A

Prednisolone

85
Q

Minimal glucocorticoid activity, very high mineralocorticoid activity,

Which preparation?

A

Fludrocortisone

86
Q

theBNF suggests gradual withdrawal of systemic corticosteroids if patients have:
(3)

A
  1. received more than 40mg prednisolone daily for more than one week
  2. received more than 3 weeks of treatment
  3. recently received repeated courses
87
Q

Mineralocorticoid side-effects

A

fluid retention

hypertension

88
Q

ophthalmic Glucocorticoid side-effects

A

glaucoma

cataracts

89
Q

psychiatric Glucocorticoid side-effects

A

insomnia

mania

depression

psychosis

90
Q

Causes of Hypokalaemia with alkalosis

A

vomiting

thiazideand loop diuretics

Cushing’s syndrome

Conn’s syndrome (primary hyperaldosteronism)

91
Q

6 Causes of Hypophosphataemia

A

alcohol excess

acute liver failure

diabetic ketoacidosis

refeeding syndrome

primary hyperparathyroidism

osteomalacia

92
Q

Liddle’s syndrome is

A

HTN
HYPOKALAEMIC ALKALOSIS

93
Q

Treatment of Liddle’s syndrome

A

Treatment is with either amiloride or triamterene

94
Q

Causes of primary hyperparathyroidism

A

85%: solitary adenoma

10%: hyperplasia

4%: multiple adenoma

1%: carcinoma

95
Q

Pendred’s syndrome

A

bilateral sensorineural deafness, with mild hypothyroidism and a goitre

96
Q

Treatment of Pendred’s syndrome

A

Treatment is with thyroid hormone replacement and cochlear implants.

97
Q

Pseudohypoparathyroidism
Associated with

Labs ?

A

associated with low IQ, short stature, shortened 4th and 5th metacarpals

low calcium, high phosphate, high PTH

diagnosis is made by measuring urinary cAMP and phosphate levels following an infusion of PTH

98
Q

What’s Pseudopseudohypoparathyroidism?

A

similar phenotype to pseudohypoparathyroidism but normal biochemistry

99
Q

Pseudohypoparathyroidism is caused by

A

target cell insensitivity to parathyroid hormone (PTH) due to a mutation in a G-protein.

100
Q

Investigations of Pseudohypoparathyroidism

A

↑ PTH

↓ calcium

↑ phosphate

infusion of PTH followed by measurement of urinary phosphate and cAMP measurement - this can help differentiate between type I (neither phosphate or cAMP levels rise) and II (cAMP rises but phosphate levels do not change)

101
Q

Type 1 vs type 2 of pseudohypoparathyroidism

A

Type 1 &raquo_space;> complete receptor defect

type 2»> the cell receptor is intact

102
Q

Drug causes of raised prolactin

A

metoclopramide, domperidone

phenothiazines

haloperidol

very rare: SSRIs, opioids

103
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)

Drugs

104
Q

Pituitary adenomas can be classified according to size

A

microadenoma is <1cm

macroadenoma is ≥1cm)

105
Q

Orlistat is a…………………… inhibitor

A

pancreatic lipase inhibitor

106
Q

criteria for use Liraglutide in obesity

A
  1. BMI >= 35
  2. Pre diabetes
107
Q

Galactosaemia is a rare autosomal …1…….. condition caused by …..2…..

A
  1. autosomal recessive
  2. the absence of galactose-1-phosphate uridyl transferase
108
Q

Features of Galactosaemia

A

jaundice

failure to thrive

hepatomegaly

cataracts

hypoglycaemia after exposure to galactose

Fanconi syndrome

109
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:

110
Q

Drug causes of gynaecomastia

A

spironolactone (most common drug cause)

cimetidine

digoxin

cannabis

finasteride

GnRH agonists e.g.goserelin, buserelin

oestrogens, anabolic steroids

Very rare drug causes of gynaecomastia

tricyclics

isoniazid

calcium channel blockers

heroin

busulfan

methyldopa

111
Q

Causes of predominantly hypertriglyceridaemia

A

diabetes mellitus (types 1 and 2)

obesity

alcohol

chronic renal failure

drugs: thiazides, non-selective beta-blockers, unopposed oestrogen

liver disease

112
Q

Causes of predominantly hypercholesterolaemia

A

nephrotic syndrome

cholestasis

hypothyroidism

113
Q

Water deprivation test

Inpsychogenic polydipsia

  1. Sarting Plasma Osmolality
  2. Final urine osmolality
  3. Urine osmolality post DDAVP
A
  1. Low
  2. > 400
  3. > 400
114
Q

Water deprivation test

Incranial DI

  1. Sarting Plasma Osmolality
  2. Final urine osmolality
  3. Urine osmolality post DDAVP
A
  1. High
  2. <300
  3. > 600
115
Q

Water deprivation test

Innephrogenic DI

  1. Sarting Plasma Osmolality
  2. Final urine osmolality
  3. Urine osmolality post DDAVP
A
  1. High
  2. < 300
  3. < 300
116
Q

Water deprivation test

Innormal

  1. Sarting Plasma Osmolality
  2. Final urine osmolality
  3. Urine osmolality post DDAVP
A
  1. Normal
  2. > 600
  3. > 600
117
Q

Risk factors of Urinary incontinence

A

advancing age

previous pregnancy and childbirth

high body mass index

hysterectomy

family history

118
Q

Immediate release oxybutynin should, however, beavoided in …..?

A

frail older women’

119
Q

theRotterdam criteriastate that a diagnosis of PCOS can be made if 2 of the following 3 are present:

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)
120
Q

Treatment of Hirsutism and acne (PCOS)

A
  1. third generation OCP which has fewer androgenic effects or co-cyprindiol which has an anti-androgen action.
  2. if doesn’t respond then topical eflornithine may be tried
  3. spironolactone, flutamide and finasteride may be used under specialist supervision
121
Q

Treatment of infertility in PCOS

A

metformin is also used, either combined with clomifene or alone, particularly in patients who are obese

gonadotrophins

122
Q

Treatment of Premature ovarian insufficiency

A

hormone replacement therapy (HRT) or a combined oral contraceptive pill should be offered to women until the age of the average menopause (51 years)

it should be noted that HRT does not provide contraception, in case spontaneous ovarian activity resumes

123
Q

Risk factors of ovarian cancer

A

family history: mutations of theBRCA1or theBRCA2 gene

many ovulations*:early menarche,late menopause,

124
Q

Investigations of ovarian cancer

A
  1. CA 125 if >= 35 IU/ML THEN ultrasound of abdomen and pelvis should be ordered
125
Q

Neuroblastoma arises from …….

A

neural crest tissue of the adrenal medulla (the most common site) and sympathetic nervous system.

126
Q

MEN tpye 1

A

3 Ps

  1. Pituitary tumour: prolactinoma
  2. Primary hyperparathyroidism
  3. Pancreatic tumour: gastrinoma , insulinoma
127
Q

MEN type 2a

A

2Ps

  1. Primary hyperparathyroidism
  2. Phaeochromocytoma
  3. Medullary thyroid cancer
128
Q

MEN TYPE 2b

A

1P

  1. Phaeochromocytoma
  2. Medullary thyroid cancer
  3. Marfanoid body habitus
129
Q

The most common presentation of MEN1

A

Hypercalcaemia

130
Q

RET oncogene can be found in

A

MEN type 2a & 2b

131
Q

For a diagnosis of metabolic syndrome at least 3 of the following should be identified:

A
  1. FBG > 5.6 mmol / L
  2. BP > 130 / 85 or active treatment of HTN
  3. HDL < 1.03 in males or < 1.29 in females
  4. Waist circumference : men > 102 cm , women > 88 cm
132
Q

Potential complications of Hormone replacement therapy

A
  1. increased risk of breast cancer
  2. increased risk of endometrial cancer
  3. increased risk of venous thromboembolism
  4. increased risk of stroke
  5. increased risk of IHD
133
Q

Fibrates work throughactivating ………..resulting in an increase in ………….. reducing triglyceride levels.

A

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

134
Q

Fibrates side effects

A

gastrointestinal side-effects are common

increased risk of thromboembolism

135
Q

Ezetimibe is a lipid-lowering drug which inhibits ………….., decreasing cholesterol absorption in …………

A

inhibits cholesterol receptors on enterocytes,

decreasing cholesterol absorption in the small intestine.

136
Q

for treating primary hypercholesterolaemia in adults in whom initial statin therapy is contraindicated or who cannot tolerate statin therapy, recommended to start …..

A

Ezetimibe

137
Q

one parent is affected by familial hypercholesterolaemia, arrange testing in children by age ….?

A

by age 10

138
Q

if both parents are affected by familial hypercholesterolaemia, arrange testing in children by age …..?

A

by age 5

139
Q

statins should be discontinued in women ……. months before conception due to the risk of congenital defects

A

3 months

140
Q

insulinoma is a neuroendocrine tumour deriving mainly from ………?

A

from pancreatic Islets of Langerhans cells

141
Q

Diagnosis of insulinoma

A

supervised, prolonged fasting (up to 72 hours)

CT pancreas

142
Q

Management of insulinoma

A

surgery

diazoxide and somatostatin if patients are not candidates for surgery

143
Q

Klinefelter’s syndrome is associated withkaryotype ……..

A

karyotype 47, XXY.

144
Q

Diagnosis of Klinefelter’s syndrome by

A

By karyotype ( chromosomal analysis )

145
Q

Features of which condition?

often taller than average

lack of secondary sexual characteristics

small, firm testes

infertile

gynaecomastia- increased incidence of breast cancer

elevated gonadotrophin levels but low testosterone

A

Klinefelter’s syndrome

146
Q

Managment of Klinefelter’s syndrome

A

testosterone supplementation

gonadotrophin supplementation may result in sperm production if fertility is desired later in life

147
Q

4 Risk factors of Endometrial cancer

A
  1. hereditary non-polyposis colorectal carcinoma
  2. Metabolic syndrome
  3. tamoxifen
  4. excess oestrogen ( early menarche, late menopause)
148
Q

3 Protective factors of endometrial cancer

A

multiparity

combined oral contraceptive pill

smoking(the reasons for this are unclear)

149
Q

What is the most important factor in the development of cervical cancer

A

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

150
Q

Cervical cancer may be divided into :

A

squamous cell cancer (80%)

adenocarcinoma (20%)

151
Q

7 Risk factors of cervical cancer

A
  1. Smoking
  2. HIV
  3. HPV
  4. early first intercourse,many sexual partners
  5. High parity
  6. Combined OCP
  7. Lower socio-economic status
152
Q

Causes of Congenital adrenal hyperplasia

A

21-hydroxylase deficiency (90%)

11-beta hydroxylase deficiency (5%)

17-hydroxylase deficiency (very rare

  • 11, 17 , 21
153
Q

Androgen insensitivity syndrome is condition due to end-organ resistance to testosterone causing genotypically male children (…..XY) to have a female phenotype.

A

(46XY)

154
Q

Management of androgen insensitivity syndrome

A

counselling - raise the child as female

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

oestrogen therapy

155
Q

Metabolic syndrome associated with

A
  1. High uric acid
  2. NAFLD
  3. PCOS
156
Q

Serum osmolality in HHS

A

> 320 mosmol/kg

MRCP Part 1 (17 decks)

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