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MRCP > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Which HLA is usually present in T1 DM?

A

HLA DR4 +/- HLA DR3

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2
Q

What is the simple pathophysiology in T1 DM?

A

Insulin-producing ß cells of the islets of Langerhans in the pancreas are destroyed (auto-immune process)

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3
Q

What is the typical demographic for the onset of T1 DM?

A

Typically in a patient <25, lean body, acute

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4
Q

Why does polyuria and polydipsia occur in DM?

A

glucose spills into the urine and water follows, making glycosuria and dehydration

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5
Q

What are the three ways to diagnose diabetes?

A
  • Symptoms + raised venous glucose (fasting ≥7, random ≥11.1)
  • Raised venous glucose on 2 occasions (fasting ≥7, random ≥11.1)
  • HbA1c ≥48 mmol/L (excluding pregnancy, children, haemoglobinopathy)
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6
Q

What are the SEs of S/C insulin?

A

SE: hypoglycaemia, weight gain, lipodystrophy

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7
Q

What lifestyle modifications can be given to a new T1 diabetic?

A

DAFNE course, smoking cessation, diet advice, test before driving

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8
Q

Baseline glucose monitoring is 4 times a day (before meals and bedtime). When should you monitor more frequently?

A

during illness, sport, planning preg

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9
Q

What is an example of a type of rapid-acting insulin, how long does it take to work and how long does its effects last?

A

NovoRapid
Takes 5 mins, lasts 3-5hrs
May be used as a bolus dose

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10
Q

What is an example of a type of short-acting insulin, how long does it take to work and how long does its effects last?

A

Actrapid
Takes 30 mins, lasts 6-8hrs
May be used as a bolus dose

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11
Q

What is an example of a type of intermediate-acting insulin, how long does it take to work and how long does its effects last?

A

Isophane insulin
Takes 2 hrs, lasts 12-18hrs

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12
Q

What is an example of a type of long-acting insulin, how long does it take to work and how long does its effects last?

A

Insulin determir/glargine – given 1-2 times/day
Takes 1-2hrs, lasts up to 24hrs

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13
Q

What is the simplified pathophysiology of T2 DM?

A

Relative deficiency of insulin d/t excess adipose tissue – there isn’t enough insulin to go around all the excess fatty tissue meaning blood glucose builds up

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14
Q

What does metformin do? What are its SEs and CIs?

A

increases insulin sensitivity + helps with weight, decreases hepatic gluconeogenesis
o SE: GI upset, lactic acidosis
o CI: stage 4 renal failure

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15
Q

What do Sulfonylureas (gliclazide) do? What are their SEs?

A

increases insulin secretions
o SE: weight gain, can cause hypoglycaemia, SIADH
If you have no pancreas function, won’t work

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16
Q

What do Thiazolidinediones (pioglitazone) do? What are their SEs and CIs?

A

increases insulin sensitivity
o SE: weight gain, fluid retention (worse in patients also on insulin), fractures
o CI: osteoporosis, CCF

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17
Q

What do DPP-4 inhibitors (-gliptins) do? What are their SEs?

A

increases incretin levels which inhibit glucagon secretion
o SE: increased risk of pancreatitis
o Good for patients who are obese

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18
Q

What do SGLT2 inhibitors (dapagliflozin) do? What are their SEs and CIs?

A

newer drug, prevents the resorption of glucose from the proximal renal tubules causing more glucose to be secreted in the urine
o SE: urinary/genital infections, weight loss, risk of Fournier’s Gangrene
o CI: recurrent thrush

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19
Q

What is the ‘simple measures’ sick day rules for diabetics?

A
  • Increase frequency of blood glucose monitoring
  • Encourage fluid intake (at least 3 litres in 24hrs)
  • May need sugary drinks to maintain carb intake
  • Patients should have box of ‘sick day supplies’
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20
Q

What should diabetics do about their medication on sick days?

A

• Continue medication even if not eating much (cortisol stress response increases blood sugar levels even without much oral intake)
o Except metformin which should be stopped if patient is becoming dehydrated – risk of renal damage
o Don’t stop insulin, risk of DKA

Patients should check ketone levels and give corrective insulin doses as required

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21
Q

Causes of lower than expected HbA1c?

A
  • Sickle-cell anaemia
  • GP6D deficiency
  • Hereditary spherocytosis
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22
Q

Causes of higher than expected HbA1c?

A
  • Vitamin B12/folic acid deficiency
  • Iron-deficiency anaemia
  • Splenectomy
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23
Q

In T2 DM, what HbA1c should you aim for and above what level would you consider adding in another agent?

A

Aim = <48mmol/L
Add Tx = >58mmol/L

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24
Q

Causes of raised prolactin?

A

The p’s

pregnancy
prolactinoma
physiological
polycystic ovarian syndrome
phenothiazines, metocloPramide, domPeridone
primary hypothyroidism (because TRH from hypothalamus stimulates prolactin release. In hypothyroidism there is a reactive increased in TRH, therefore prolactin)

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25
Q

What is secreted in the posterior pituitary?

A

ADH + oxytocin

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26
Q

What is secreted in the anterior pituitary?

A

GH, ACTH, FSH/LH, TSH, prolactin

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27
Q

Features of excess prolactin in men + women?

A

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

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28
Q

What occurs in Addison’s disease?

A

Autoimmune destruction of the adrenal glands -> primary hypoadrenalism
Responsible for 80% of cases

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29
Q

Other causes of primary hypoadrenalism?

A

TB
HIV
metastases (e.g. bronchial carcinoma)
meningococcal septicaemia (Waterhouse-Friderichsen syndrome - bleeding occurs into the glands (acute haemorrhagic necrosis)
antiphospholipid syndrome

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30
Q

Symptoms of Addison’s disease?

A

Bronze skin
Hypoglycaemia, WL, weakness, low mood
Postural hypotension
GI upset - N&V, abdo pain, diarrhoea/constipation

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31
Q

Investigations for Addison’s disease?

A 
HIGH K+, LOW Na- (as a result of decreased aldosterone) 
Low glucose (as a result of decreased cortisol) 
Can do morning cortisol first: if \>500 - normal, \<100 - addison's, 100-500, do synacthen test 
Short ACTH stimulation test (synacthen test) 
-\> given synacthen (synthetic ACTH), cortisol levels should at least double, if not = addison's
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32
Q

Which antibodies are often positive in Addison’s disease?

A

21-hydroxylase adrenal auto-Abs

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33
Q

Treatment of Addison’s?

A

Replace steroids
- fludrocortisone + hydrocortisone
Give steroid card/bracelet

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34
Q

Causes of secondary hypoadrenalism?

A

Pituitary surgery
Infection
Sheehan’s syndrome

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35
Q

Causes of tertiary hypoadrenalism?

A

Iatrogenic d/t long-term steroid therapy

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36
Q

What should you do if someone with addison’s becomes sick?

A

Double to doses of both steroids

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37
Q

What occurs in an addisonian crisis?

A

Drop in steroid levels, may be due to:

1) First presentation of addison’s
2) Infection/trauma/acute illness
3) Sudden steroid withdrawal

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38
Q

How to treat an addisonian crisis?

A

IV hydrocortisone
IV fluids
Correct hypoglycaemia
Careful monitoring

Keep fludrocortisone the same - because high cortisone levels (from hydrocortisone) exert weak mineralocorticoid action

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39
Q

Can you take sulfonylureas when pregnant/breastfeeding?

A

No

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40
Q

What is the MOA of sulfonylureas?

A

Blockage of ATP-sensitive potassium channels

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41
Q

How common are each type of thyroid cancer?

A

Papillary (60%)
Follicular (25%)
Medullary (5%)
Anaplastic (1%) - present with compression symptoms e.g. stridor
Lymphoma

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42
Q

Who usually gets papillary thyroid Ca, what do you see on biopsy and how does it spread?

A

Younger patients (female)
Spreads to LNs
Light microscopy - orphan annie eyes

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43
Q

Who usually gets follicular thyroid Ca and how does it spread?

A

Women >50
Haematogenous -> bone, lungs

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44
Q

What tumour markers can be used for thyroid cancers?

A

Thyroglobulin - papillary + follicular
Calcitonin - medullary

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45
Q

Symptoms of thyroid cancer?

A

Painless, hard, immobile nodule
May be hoarseness/trouble swallowing with invasion of surrounding structures

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46
Q

What is sick euthyroid syndrome?

A

Occurs in systemic illness
Changes are reversible, no treatment needed
TSH (low or normal), T3/T4 (low)

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47
Q

What is subacute (De Quervain’s) thyroiditis?

A

Occurs following viral infection
Painful goitre
Typically in patients with hyperthyroidism
Usually self-limiting

Get an initial surge in thyroxine, then a drop
Tx = NSAIDS

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48
Q

What are the 3 defining features of Hashimoto’s thyroiditis?

A

Hypothyroidism
Goitre
Anti-thyroid peroxidase Ab (+ anti-thyroglobulin (Tg) Abs)

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49
Q

What are the levels of the adrenal gland and what do they produce?

A

Zona glomerulosa -> mineralocorticoids (aldosterone)
Zona fasciculata -> glucocorticoids (cortisol)
Zona reticularis -> androgens
Medulla -> NAd, Ad

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50
Q

What are the three causes of cushings syndrome?

A

Cushings disease (70%) - pituitary adenoma, causes bilateral adrenal hyperplasia
Ectopic ACTH secretion (10%) - especially from lung SCLC + carcinoid
Primary adrenal disease - from a Ca/nodular hyperplasia

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51
Q

Symptoms of cushings syndrome?

A

Buffalo hump
Round face
Thin skin, easy bruising
Abdominal striae
Osteoporosis
Muscle weakness
HTN
DM

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52
Q

What investigation for cushings?

A

Firstly, collect 24hr urine free cortisol OR do overnight dexamethasone suppression test (low-dose) and measure serum cortisol in the morning

Dexamethasone suppression test
Low-dose test:
Low cortisol -> normal
High/normal cortisol -> confirms cushings syndrome

High-dose test:
Low cortisol -> cushings disease
High/normal - measure ACTH
ACTH raised -> ectopic ACTH production
ACTH low -> adrenal cushings

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53
Q

Treatment of cushings syndrome?

A

Cushings disease:

  • trans-sphenoidal tumour resection
  • may choose bilateral adrenelectomy
  • metyrapone/ketoconazole may lower serum cortisol pre-op

Adrenal tumour: unilateral adrenalectomy

Ectopic secretion: surgical resection

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54
Q

What is inferior petrosal sinus sampling and when is it used

A

Invasive procedure in which ACTH levels are sampled from the veins that drain the pituitary gland
Then compared with the ACTH levels in the peripheral blood to determine whether a pituitary tumor is responsible for ACTH-dependent Cushing syndrome (or if there is an ectopic source)

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55
Q

What tests to do if someones fasting glucose is between 6.1-7.0?

A

Should then be offered an oral glucose tolerance test to rule out a diagnosis of diabetes
A result between 7.8 - 11.1 mmol/l indicates that the person doesn’t have diabetes but does have IGT

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56
Q

What causes acromegaly?

A 
Pituitary tumour (99%) 
Hyperplasia
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57
Q

Symptoms of acromegaly?

A

SOL -> headaches, bitemporal hemianopia
Prominent forehead (frontal bossing)
Large nose, hands, feet
Large tongue + protruding jaw
Organ dysfunction -> cardiomegaly, HTN, T2DM, CC
Carpel tunnel syndrome

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58
Q

Investigations in acromegaly?

A

First-line: Serum IGF-1 levels

If IGF-1 raised, do:
OGTT - measure every half hour for 2.5hrs
- glucose usually suppresses GH, not in acromegaly
Also do serial GH measures

MRI
Old photos

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59
Q

Management of acromegaly?

A

1) Trans-sphenoidal surgery

2) Somatostatin analogues - octreotide
3) Dopamine agonists - cabergoline, bromocriptine
4) GH receptor antagonists - pegvisomant

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60
Q

What does GH metabolise into in the liver?

A

Insulin-like growth factor 1 (IGF-1)

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61
Q

What are the two histological types of cervical cancer?

A

squamous cell cancer (80%)
adenocarcinoma (20%)

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62
Q

RFs for cervical cancer?

A

HPV 16, 18, 33
Smoking
High parity
Early first intercourse/many sexual partners
cOCP

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63
Q

Symptoms of hyperthyroidism?

A

Diarrhoea
Weight loss/muscle wasting
Increased appetite
Overactive/tremor
Oedema
Sweating/intolerance to heat
Proptosis
Goitre
Tachycardia/HTN

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64
Q

Three characteristic symptoms in Graves?

A

1) Eye disease
2) Pretibial myxoedema (orange peel skin)
3) Thyroid acropathy (clubbing/swelling)

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65
Q

Cause + RF for thyroid eye disease and Tx if severe?

A

Swelling in extra ocular muscles most likely d/t autoantigen in muscles that reactive with thyroid autoantigen
RF = Smoking
IV methylprednisolone/surgical decompression

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66
Q

Treatment of hyperthyroidism?

A

1) B-blockers
2) Anti-thyroid medications - carbimazole (inhibit production of thyroid hormones by blocks thyroid peroxidase)/propylthiouracil (inhibits T4->T3)
3) Radioiodine (damaged DNA/enzympes)
4) Thyroidectomy

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67
Q

Other than Graves what can cause hyperthyroidism?

A

Toxic multinodular goitre - nodules in goitre produce thyroxine irrespective of TSH levels
Toxic adenoma (solitary goitre)
Drug-Induced - amiodarone, iodine

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68
Q

Pathophysiology of Graves disease?

A

Circulating thyroid stimulating IgG antibodies cause activation of G-protein coupled thyrotropin receptors

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69
Q

What can happen to the foetus and mother if a mother has untreated thyrotoxicosis?

A

fetal loss, maternal heart failure and premature labour

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70
Q

What will happen to the levels of TBG/free T3 + T4 in pregnancy?

A

Thyroid binding globulin (TBG) levels rise during pregnancy in response to elevated estrogen levels. Because the majority of T4 and T3 circulates bound to TBG the total T4 and total T3 measurements will also rise, but the levels of free T4 and free T3 will not be affected.

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71
Q

Which drugs should be used to treat hyperthyroidism in pregnancy?

A

Propylthiouracil i-> first trimester of pregnancy
Carbimazole -> beginning of the second trimester
(Carbimazole in 1st trim may be associated with an increased risk of congenital abnormalities)

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72
Q

What should the target thyroxine levels be for pregnant women?

A

maternal free thyroxine levels should be kept in the upper third of the normal reference range to avoid fetal hypothyroidism
Women may therefore require an extra doses of thyroxine during pregnancy (by up to 50% as early as 4-6 weeks of pregnancy)

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73
Q

When should you measure TSH in pregnancy?

A

serum TSH measured in each trimester and 6-8 weeks post-partum

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74
Q

What is the male:female ratio in Hashimoto’s?

A

M:F 1:10

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75
Q

Which cancer is Hashimoto’s associated with?

A

MALT lymphoma
Biopsy: extranodal marginal B-cells

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76
Q

What is the inheritance pattern for MEN?

A

AD

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77
Q

What occurs in MEN type 1?

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

Common symptoms: peptic ulceration, galactorrhoea, hypercalcaemia

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78
Q

What occurs in MEN type 2a?

A 
Parathyroid hyperplasia (60%)
Phaeochromocytoma

Medullary thyroid carcinoma

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79
Q

What occurs in MEN type 2b?

A

Phaeochromocytoma

Marfanoid body habitus
Mucosal neuromas
Medullary thyroid carcinoma

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80
Q

Which genes are responsible for MEN 1/2a/2b?

A 
1 = MEN1 gene 
2a/b = RET oncogene
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81
Q

Most common presentation of MEN1?

A

Hypercalcaemia

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82
Q

What is von-hippel lindau syndrome?

A

Von Hippel-Lindau syndrome is an inherited disorder characterized by the formation of tumors and fluid-filled sacs (cysts) in many different parts of the body

Affecting the CNS, kidneys, pancreas, adrenal glands, liver and lung. The most common presenting features are haemangioblastomas are seen in the brain, spinal cord and retina causing headaches, neurological disturbance and visual changes

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83
Q

What is a phaeochromocytoma?

A

A rare catecholamine secreting tumour that grows from chromaffin cells in the adrenals

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84
Q

Rule of 10%s in phaeochromocytomas?

A

10% familial
10% bilateral
10% malignant
10% extra-adrenal

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85
Q

Symptoms of phaeochromocytomas?

A

Episodic features of:
HTN
headaches
palpitations
sweating
anxiety
(symptoms of increased adrenaline)

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86
Q

Investigations for phaeochromocytomas?

A

24hr urinary collection of metanephrines

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87
Q

Management of phaeochromocytomas?

A

First stabilise with medical treatment:
- alpha-blockers (phenoxybenzamine)
- then beta-blockers (propranolol)
Then surgical intervention

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88
Q

Why do you give alpha-blockers before beta-blockers in the treatment of phaeochromocytomas?

A

Because B-blockers prevent the vasodilatory effects of peripheral B-2 adrenoceptors, potentially leading to unopposed alpha-adrenoreceptor stimulation causing vasoconstriction and ultimately a hypertensive crisis

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89
Q

What is a dynamic pituitary function test?

A

Used to assess for suspected primary pituitary dysfunction
Insulin, TRH and GnRH are given to the patient following which the serum glucose, cortisol, growth hormone, TSH, LH and FSH levels are recorded at regular intervals

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90
Q

In an OD of anti-glycaemic medications, which molecule is produced first?

A

the first response of the body is to decrease the production of insulin and then to increase glucagon secretion. Glucagon promotes gluconeogenesis in an attempt to raise blood glucose levels.

GH and cortisol are also released but later.

sympathoadrenal response: increased catecholamine-mediated (adrenergic) and acetylcholine-mediated (cholinergic) neurotransmission in the PNS and in the CNS

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91
Q

What is galactosaemia?

A

Raised galactose in the blood

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92
Q

What are the symptoms of galactosaemia?

A

Liver, eyes, kidney, brain
Brain damage, cataracts, jaundice, hepatomegaly, kidney damage

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93
Q

What causes galactosaemia?

A

The absence of galactose-1-phosphate uridyl transferase

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94
Q

In alcoholics with hypoglycaemia, what do you need to remember to give at the same time as glucose?

A

In alcoholic patients, thiamine supplementation should be given with, or following, the administration of intravenous glucose to minimise the risk of Wernicke’s encephalopathy

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95
Q

Which type of glucose preparation should be given to alcoholics with hypoglycaemia?

A

IV glucose
They have depleted glycogen stores, therefore, treatment with glucagon does not improve blood glucose
(because IM glucagon works by breaking down glycogen into glucose)

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96
Q

Causes of hypoglycaemia?

A

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

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97
Q

What are the symptoms of hypogylcaemia?

A

BM <3.3 mmol/L cause autonomic symptoms d/t the release of glucagon and adrenaline:
Sweating, shaking, hunger, anxiety, nausea

BM <2.8 mmol/L cause neuroglycopenic symptoms due to inadequate glucose supply to the brain:
Weakness, vision changes, confusion, dizziness

Severe and uncommon features of hypoglycaemia include:
Convulsion + coma

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98
Q

Skin conditions associated with hyper- and hypothyroidism?

A

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

Skin manifestations of hyperthyroidism
pretibial myxoedema
clubbing
scalp hair thinning
increased sweating

Pruritus can occur in both hyper- and hypothyroidism

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99
Q

What is MODY?

A

Maturity onset diabetes of the young, usually <25yo

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100
Q

What is the inheritance pattern of MODY?

A

Autosomal dominant

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101
Q

What two things might you find in the stem of a question with a patient presenting with undiagnosed MODY?

A

FH of early onset T2 DM
No ketosis

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102
Q

What do you use to treat MODY?

A

Sulfonylureas, usually don’t need insulin

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103
Q

Most common sub-classification of MODY and what are they more at risk of?

A

MODY 3
At increased risk of HCC

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104
Q

Which patients may develop myxoedema coma and how do you treat?

A

Hypothyroidism
Hydrocortisone and levothyroxine

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105
Q

What is the most common cause of hyperaldosteronism (2/3 of cases)?
And the other cause (1/3)?

A

Most common: Bilateral adrenocortical hyperplasia
Conn’s syndrome (solitary aldosterone-producing adrenal adenoma)
May also be familial

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106
Q

What is the mechanism by which hyperaldosteronism causes electrolyte abnormalities?

A

Aldosterone stimulates Na/K ATPase channels to be inserted into the distal convoluted tubules
This causes hypernatraemia (and secondary retention of water) + hypokalaemia

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107
Q

Causes of secondary hyperaldosteronism?

A

RAS
Renal artery obstruction
HF
-> all result in drop in BP in kidneys, therefore increased renin release and increased aldosterone

108
Q

Management of hyperaldosteronism?

A

adrenal adenoma: surgery
bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone

109
Q

Main features at diagnosis of hyperaldosteronism?

A

HTN
Hypokalaemia/hypernatraemia
Alkalosis

110
Q

How to investigate for hyperaldosteronism?

A

1st line - aldosterone/renin ratio (high aldosterone, low renin) - renin -> increased Angiotensin 1->2, increases aldosterone and causes increased BP (which has a negative feedback on renin). Therefore ++ aldosterone from tumour/hyperplasia will cause suppression on renin.
2nd line - High-res CT
3rd line - adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia

111
Q

What causes hypokalaemia with alkalosis?

A

vomiting
thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)

112
Q

What causes hypokalaemia with acidosis?

A

diarrhoea
renal tubular acidosis
acetazolamide
partially treated diabetic ketoacidosis

113
Q

What level of CRP would concern you post-surgery?

A

Levels of greater than 150 at 48 hours post operatively are suggestive of evolving complications

114
Q

Which blood tests can act as an acute phase reactant?

A

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

115
Q

What effect does vitamin D have in the body?

A

Increases absorption of Ca from kidneys, gut and bones
Increases absorption of PO4 from gut and bones
Increases excretion of PO4 from kidneys

116
Q

What is the overall effect of PTH?

A

Increases Ca
Decreases PO4

117
Q

What does primary hyperparathyroidism look like biochemically and what is the main cause?

A

Increased PTH + Ca, decreased PO4
Common cause = solitary adenoma
Also causes by multifocal disease/hyperplasia

118
Q

What does secondary hyperparathyroidism look like biochemically and what is the main cause?

A

Increased PTH + PO4, low or normal Ca
Caused by: almost always d/t CKD, low Ca causes parathyroid gland hyperplasia

119
Q

What does tertiary hyperparathyroidism look like biochemically and what is the main cause?

A

Increased PTH, high or normal Ca + low or normal PO4
Caused by: ongoing hyperplasia of PTH glands after correction of underlying renal disorder

120
Q

What is the stereotypical stem for a patient with primary hyperparathyroidism?

A

elderly females with an unquenchable thirst and an inappropriately normal or raised parathyroid hormone level

121
Q

What is the characteristic XR finding in hyperparathyroidism?

A

Pepperpot skull

122
Q

Management of hyperparathyroidism?

A

Parathyroidectomy
Or conservative if the calcium level is less than 0.25 mmol/L above the upper limit of normal AND the patient is > 50 years AND there is no evidence of end-organ damage AND asymptomatic
Treat with cinacalcet

123
Q

Symptoms of hypocalcaemia?

A

CATS GO NUMB
Chvostek’s sign
Arrhythmia
Tetany/Trousseau’s sign
Seizures
Perioral paraesthesia

124
Q

Management of hypocalcaemia?

A

Severe: IV calcium gluconate 10ml of 10% solution over 10 minutes

125
Q

ECG changes in hypocalcaemia?

A

Long QT interval

126
Q

In patients with hypocalcaemia, what is the most useful test in determining the cause?

A

PTH

127
Q

Causes of gynaecomastia?

A

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 (in up to 1/3 of men)
haemodialysis
drugs: spironolactone (most common)
digoxin, cannabis, finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids

128
Q

What is Kallman’s syndrome?

A

recognised cause of delayed puberty secondary to hypogonadotropic hypogonadism
Usually inherited as an X-linked recessive trait

129
Q

Features of Kallman’s syndrome?

A

‘delayed puberty’
hypogonadism, undescended testes
anosmia
sex hormone levels are low
LH, FSH levels are inappropriately low/normal
patients are typically of normal or above average height

130
Q

What is the genetic pattern for Kleinfelter’s syndrome?

A

karyotype 47, XXY

131
Q

Features of Kleinfelter’s syndrome?

A

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

132
Q

What is the genetic pattern for Turner’s syndrome?

A

45, XO

133
Q

What are the features of Turner’s syndrome?

A

short stature
shield chest, widely spaced nipples
webbed neck
bicuspid aortic valve (15%), coarctation of the aorta (5-10%)
primary amenorrhoea
short fourth metacarpal

gonadotrophin levels will be elevated
hypothyroidism is much more common in Turner’s

95% die in utero

134
Q

What is the most common renal abnormality in Turner’s syndrome?

A

horseshoe kidney

135
Q

After 6 months on a GLP-1, what are the parameters for continuing treatment?

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

136
Q

Which alpha blocker do you use in phaeochromocytomas?

A

Phenoxybenzamine

137
Q

What are the criterion for diagnosing a metabolic syndrome?

A

obesity
raised triglycerides level
reduced HDL cholesterol
hypertension
raised fasting plasma glucose

138
Q

What is an insulinoma?

A

a neuroendocrine tumour deriving mainly from pancreatic Islets of Langerhans cells
10% malignant, 10% multiple

139
Q

What are the symptoms of an insulinoma and what might be seen on blood tests?

A

Symptoms of hypoglycaemia
rapid weight gain may be seen
high insulin, raised proinsulin:insulin ratio
high C-peptide

140
Q

Diagnosis of an insulinoma?

A

Supervised, prolonged fasting (up to 72 hours)
CT pancreas

141
Q

Management of an insulinoma?

A

surgery
diazoxide and somatostatin if patients are not candidates for surgery

142
Q

Non-specific symptoms of Addison’s?

A

GI upset - vomiting, abdo pain, diarrhoea/constipation

143
Q

What are the cardinal features of APS type 1?

A

chronic mucocutaneous candidiasis
hypoparathyroidism
adrenocortical insufficiency (addison’s)
(need 2 out of 3)

144
Q

Which type of autoimmune polyendocrinopathy syndrome is most common?

A

type 2

145
Q

Causes of metabolic alkalosis?

A

ABCCDD
A - apiration (and vomiting)
B - Bartter’s syndrome
C - Cushing’s
C - Conn’s
D - diuretics
D - decreased K

146
Q

Causes of metabolic alkalosis?

A

ABCCDD
A - apiration (and vomiting)
B - Bartter’s syndrome
C - Cushing’s
C - Conn’s
D - diuretics
D - decreased K

147
Q

Triad of features in SIADH?

A

Hyponatraemia
Concentrated urine
Low plasma osmolality

148
Q

Causes of SIADH?

A

MIND
Malignancy - SCLC
Infections - TB, pneumonia
Neurological disorders - stroke (SAH)
Drugs - sulfonylureas, carbamazepine, SSRIs, TCAs

149
Q

Treatment of SIADH?

A

Restrict fluid
If severe: salt +/- loop diuretic

150
Q

What is the main risk of correcting Na (increasing it) too quickly?

A

central pontine myelinolysis

151
Q

Causes of predominantly hypercholesterolaemia?

A

nephrotic syndrome
cholestasis
hypothyroidism

152
Q

Causes of predominantly hypertriglyceridaemia?

A

A lcohol
B eta-blockers (non-selective)
C hronic renal failure
D iabetes mellitus/Diuretic (thiazides)
E strogen (unopposed)
F at (obesity)
G -
H epatic disease

153
Q

What are the symptoms of hypercalcaemia?

A

bones, stones, groans and psychic moans
bones - weight loss, weakness
stones - renal
groans - abdo pain, constipation, nausea & vomiting
moans - depression, confusion

154
Q

How to manage hypercalcaemia?

A

1) Fluids + diuretics (immediate)
2) Calcitonin (4-6hrs)
3) Bisphosphonates (1-3 days)

155
Q

ECG changes in hypercalcaemia?

A

Short QT interval

156
Q

What are the possible causes of hyponatraemia?

A

Post-op
Alcoholics
Malnourishment
Elderly
Burns victims

157
Q

Causes of hypernatraemia?

A

dehydration - diarrhoea/burns/vomiting
osmotic diuresis - diabetic coma
diabetes insipidus
excess IV saline

158
Q

Cause of asymptomatic hyponatraemia with normal bloods?

A

pseudohyponatraemia (may be caused by sample taken from drip arm or hyperlipidaemia)

159
Q

Management of DKA?

A

Fluid replacement – start with saline e.g. 1L over 1hr, then 1L over 2hrs x2 etc, usually patients are deplete about 5-8L
(in children you would now delay insulin for 1hour d/t increased risk of cerebral oedema)
Insulin – IV infusion fixed-rate of 0.1 units/kg/hour, once blood glucose is <15 mmol/l an infusion of 5% dextrose should be started
Correction of hypokalaemia
Long-acting insulin should be continued, short-acting insulin should be stopped

160
Q

Diagnostic criteria for DKA?

A
  • Urine Ketones > ++
  • Blood glucose > 11mmol/L and
  • Venous pH <7.3 or
  • serum bicarbonate < 16mmol/L
161
Q

What causes DKA?

A

Three things occur:

1) In the muscles - increased glycogenolysis and proteolysis (generated amino acids), decreased glucose ulitisation
2) In the liver - increased glycogenolysis and gluconeogenesis AND ketogenesis
3) In the adipocytes - increased lipolysis (which generate free fatty acids)

All result in hyperglycaemia and ketoacidosis

162
Q

Symptoms of DKA?

A
  • Abdominal pain
  • Polydipsia, polyuria, dehydration
  • Kussmaul respiration (deep hyperventilation)
  • Acetone-smelling breath (‘pear drops’ smell)
163
Q

Complications of DKA?

A

Gastric stasis
Thromboembolism
Arrythmias secondary to potassium derangement
Cerebral oedema

164
Q

What are the circumstances in which you would increase the rate of the fixed rate insulin infusion in the treatment of DKA?

A

If a patient’s ketone level does not fall by at least 0.5mmol/L/hour or their blood glucose level does not fall by 3mmol/hour then the insulin infusion rate should be increased by 1 unit/hour

165
Q

Symptoms of cerebral oedema?

A

headache, irritability, visual disturbance, focal neurology

166
Q

What lifestyle advice should you give to a patient with hypercalcaemia?

A

Maintaining good hydration (drinking 3-4 L of fluid per day)
Low calcium diet is not necessary
Advise the person to avoid any drugs or vitamin supplements that could exacerbate the hypercalcaemia
Encourage mobilization where possible
Advise the person to report any symptoms of hypercalcaemia

167
Q

What test should you do and when to screen for gestational diabetes?

A

OGTT between wk 24-28
Earlier if history of gestational diabetes.

168
Q

Diagnostic thresholds for gestational diabetes?

A

these have recently been updated by NICE, gestational diabetes is diagnosed if either:
fasting glucose is >= 5.6 mmol/L
2-hour glucose is >= 7.8 mmol/L

169
Q

What is the deficiency in CAH?

A

21-hydroxylase deficiency

170
Q

What is CAH?

A

Most common non-iatrogenic cause of insufficient cortisol and aldosterone secretions

171
Q

What percentage of patient with CAH are unable to produce aldosterone?

A

70-80%

172
Q

How do women present in CAH?

A

Virulisation of the external genitalia
Leads to cliteral hypertrophy + variable fusion of the labia

173
Q

How do men present in CAH?

A

Enlarged penis + scrotal pigmentation (often only noticed when diagnosis made)

174
Q

How do people with CAH present as a baby?

A

A salt-losing adrenal crisis in 80% of males who are salt-losers at 1-3 weeks
Present with vomiting, WL, hypotonia and circulatory collapse
(Less common in females as visualisation is noted early and treatment started)

175
Q

How do people with CAH present if not picked up as a baby?

A

Often tall stature
Develop a muscular build, adult body odour, pubic hair and acne from excess androgen production -> precocious pubarche

176
Q

What would you see on blood results in CAH?

A

Raised levels of 17 alpha-hydroxyprogesterone
In salt-losers: low Na, high K, metabolic acidosis, hypoglycaemia

177
Q

How to manage CAH?

A

Women sometimes require corrective surgery, definite reconstruction usually delayed until late puberty -> cliteromegaly reduction + vaginoplasty
Infants with salt-losing crisis require NaCl, glucose, hydrocortisone IV
Life-long hydrocortisone + fludrocortisone

178
Q

Prognosis in CAH?

A

Death can result from adrenal crisis at the time of illness/injury
Psychosexual problems in women
Prenatal diagnosis possible when couples have had a previous affected child

179
Q

What is the inheritance pattern in CAH?

A

Autosomal recessive

180
Q

What are two rarer deficiencies that can cause CAH?

A

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

181
Q

What is Pendred’s syndrome?

A

Pendred is an AR disorder, characterised by bilateral sensorineural deafness + mild hypothyroidism + goitre. The patients tend to present with progressive hearing loss and delay in academic progression.

182
Q

What do the TFTs usually look like in Pendred’s syndrome?

A

Usually normal

183
Q

What gene is responsible for Pendred’s syndrome and what might you see on MRI head?

A

(PDS) gene, chromosome 7
characteristic one and a half turns in the cochlea, compared to the normal two and a half turns

184
Q

How do you treat Pendred’s syndrome?

A

thyroid hormone replacement and cochlear implants

185
Q

What are the symptoms of a thyroid storm?

A

fever > 38.5ºC
tachycardia + HTN
confusion and agitation
nausea and vomiting
heart failure
abnormal LFTs - jaundice may be seen clinically

186
Q

How do you treat a thyroid storm?

A

Hydrocortisone, propranolol, propylthiouracil

187
Q

What do Hydrocortisone, propranolol + propylthiouracil do to the body when given in the case of a thyroid storm?

A

Hydrocortisone acts to prevent the peripheral conversion of T4 to T3 and is particularly effective in Graves’ disease. Propranolol blocks the effects of thyroid hormones and reduces the heart rate. Propylthiouracil stops the release and production of thyroid hormones and reduces the peripheral conversion of T4 to T3

188
Q

What are the four most common types of pituitary adenomas?

A

1) Prolactinoma
2) non-secreting adenomas (can cause pressure effects)
3) GH secreting adenoma
4) ACTH secreting adenomas

189
Q

What causes a hypovolaemic hyponatraemia with a raised urinary Na?

A

Renal loss

  • diuretics: thiazides, loop
  • Addison’s disease
  • diuretic stage of renal failure
190
Q

What causes a euvolaemic hyponatraemia with a raised urinary Na?

A

SIADH (urine osmolality > 500 mmol/kg)
hypothyroidism

191
Q

What causes a hypervolaemic hyponatraemia with a low urinary Na?

A

secondary hyperaldosteronism: heart failure, liver cirrhosis
nephrotic syndrome
IV dextrose
psychogenic polydipsia

192
Q

What can result from untreated, severe hyponatraemia?

A

Cerebral oedema

193
Q

How to manage hyponatraemia?

A

Acute: hypertonic saline
Chronic:
hypovolaemic -> normal saline
euvolaemia -> fluid restrict
hypervolaemia -> fluid restrict, consider diuretics/vaptans

194
Q

In which patients can vasopressin analoges be dangerous?

A

Patient with underlying liver disease -> induce hepatotoxicity

195
Q

What is central pontine demyelination?

A

Na+ levels are only raised by 4 to 6 mmol/l in a 24-hour period
symptoms usually occur after 2 days and are usually irreversible: dysarthria, dysphagia, paraparesis or quadriparesis, seizures, confusion, and coma
patients are awake but are unable to move or verbally communicate, also called ‘Locked-in syndrome’

196
Q

In which patients would you start primary prevention with atorvastatin?

A

10yr CVS disease risk >10%
OR T1 DM
OR CKD with eGFR <60
(cannot use the QRISK2 score in the above two)

197
Q

In which patients would you start secondary prevention with atorvastatin?

A

IHD OR cerebrovascular disease OR peripheral artery disease

198
Q

In which patients might the QRISK2 score underestimate the risk?

A

HIV, serious MH problems, patients on medications that cause dyslipidaemia - antipsychotics, corticosteroids, immunosuppressants, patients with AI disorders e.g. SLE

199
Q

In which T1 DM patients should atorvastatin be offered?

A

atorvastatin 20 mg should be offered to T1 diabetics who are:
>40 years, or
have had diabetes for more than 10 years or
have established nephropathy or
have other CVD risk factors

200
Q

In which CKD patients should the atorvastatin dose be increased?

A

increase the dose if a greater than 40% reduction in non-HDL cholesterol is not achieved and the eGFR > 30 ml/min. If the eGFR is < 30 ml/min a renal specialist should be consulted before increasing the dose

201
Q

How should patients starting a statin be followed up?

A

At 3 months:
repeat a full lipid profile
if the non-HDL cholesterol has not fallen by at least 40% concordance and lifestyle changes should be discussed with the patient
NICE recommend we consider increasing the dose of atorvastatin up to 80mg

202
Q

Who usually suffers from HHS?

A

Elderly with T2 DM

203
Q

What is the pathophysiology of HHS?

A

Excess glucose in the blood tries to be extracted by the kidneys which causes an osmotic diuresis and loss of Na and K also
Severe volume depletion results in a significant raised serum osmolarity (typically > than 320 mosmol/kg), resulting in hyperviscosity of blood

204
Q

What are the clinical features of HHS?

A

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

205
Q

How to diagnose HHS?

A

No specific criteria

  1. Hypovolaemia
  2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
  3. Significantly raised serum osmolarity (> 320 mosmol/kg)
206
Q

How can you estimate the serum osmolality?

A

2 * Na + glucose + urea

207
Q

How to treat HHS?

A

IV 0.9% saline
Replacement should aim to achieve a positive balance of 3-6 litres by 12 hours and the remaining replacement of estimated fluid losses within the next 12 hours

208
Q

What is pseudohypoparathyroidism + symptoms?

A

Inability of the body to use PTH
low IQ, short stature, shortened 4th and 5th metacarpals

209
Q

How to diagnosis pseudohypoparathyroidism?

A

measuring urinary cAMP and phosphate levels following an infusion of PTH. In hypoparathyroidism this will cause an increase in both cAMP and phosphate levels. In pseudohypoparathyroidism type I neither cAMP nor phosphate levels are increased whilst in pseudohypoparathyroidism type II only cAMP rises

210
Q

What is pseudopseudohypoparathyroidism?

A

Same as pseudohypoparathyroidism (phenotypically) but with normal biochemistry

211
Q

When would you offer radio iodine therapy to patients with Graves disease?

A

If oral therapy hasn’t worked
CI: pregnancy, thyroid eye disease, age <16

212
Q

What should the TSH goal be in patients taking levo?

A

0.5-2.5 mU/l (lower half)

213
Q

What are the SEs of levo?

A

hyperthyroidism: due to over treatment
reduced bone mineral density
worsening of angina
atrial fibrillation

214
Q

Which drugs can interact with levo?

A

iron, calcium carbonate - both lower levo effects as reduce absorption - give at least 4hrs apart

215
Q

What is a pituitary apoplexy?

A

commonly seen in the presence of a pituitary tumour and is caused by bleeding into or impaired blood supply of the pituitary, This generally presents with sudden onset headache, followed by symptoms of non-functioning pituitary

216
Q

What are the two main causes of diabetic foot disease?

A

Neuropathy - something in shoe, charcot’s arthropathy
Peripheral artery disease

217
Q

How often should you screen for diabetic foot disease and how?

A

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

218
Q

How many people in UK have prediabetes?

A

1 in 7

219
Q

What is the difference between impaired glucose tolerance and impaired fasting glucose?

A

impaired fasting glucose (IFG) - due to hepatic insulin resistance
impaired glucose tolerance (IGT) - due to muscle insulin resistance

IFG = fasting glucose 6.1-7 
IGT = fasting glucose \<7 AND OGTT 2-hour value \>7.8 mmol/l but \<11.1 mmol/l
220
Q

Which of IFG and IGT make you more likely to develop diabetes?

A

IGT

221
Q

Which foods have a high glycemic index?

A

White bread, white rice, baked potatoes

222
Q

What is the MOA of Orlistat?

A

inhibits gastric and pancreatic lipase to reduce the digestion of fat

223
Q

What are the SEs of Orlistat?

A

faecal urgency/incontinence and flatulence

224
Q

Which patients should be offered Orlistat?

A

BMI of 28+ with associated RFs, or
BMI of 30+
continued weight loss e.g. 5% at 3 months
orlistat is normally used for < 1 year

Used in conjunction with healthy eating plans

225
Q

How to convert from HbA1c to average blood glucose level?

A

2xHbA1c (in %) - 4.5

226
Q

Which hormone surge causes ovulation and on which day on the cycle?

A

D14, LH
As follicles develop they secrete oestrodiol which at some point cause a surge in LH

227
Q

What does progesterone do in the secretory phase?

A

Rises as is secreted from the corpus luteum

228
Q

What is the first-line Tx for diabetic neuropathy?

A

amitriptyline, duloxetine, gabapentin or pregabalin
tramadol can be used as a ‘rescue therapy’

229
Q

What is GI autonomic neuropathy and how is it treated?

A

Occurs in diabetes
gastroparesis (bloating and vomiting)
Mx options = metoclopramide, domperidone or erythromycin (prokinetic agents)

Also suffer from chronic diarrhoea + GORD

230
Q

What is familial hypercholesterolaemia? Inheritance pattern, cause and symptoms

A

AD
results in high levels of LDL-cholesterol (due to gene mutation which codes for LDL-receptor protein)

231
Q

When to test children for familial hypercholesterolaemia?

A

if one parent is affected by familial hypercholesterolaemia, arrange testing in children by age 10
if both parents are affected by familial hypercholesterolaemia, arrange testing in children by age 5

232
Q

How to diagnose familiar hypercholesterolaemia?

A

in adults total cholesterol (TC) > 7.5 mmol/l and LDL-C > 4.9 mmol/l or children TC > 6.7 mmol/l and LDL-C > 4.0 mmol/l, plus:
for definite FH: tendon xanthoma in patients or 1st or 2nd degree relatives or DNA-based evidence of FH

233
Q

Are statins safe in pregnancy?

A

No, statins should be discontinued in women 3 months before conception due to the risk of congenital defect

234
Q

In which ethnicity are fibroids more common?

A

Afro-Caribbean women

235
Q

Symptoms of fibroids?

A

menorrhagia, can lead to iron-deficiency anaemia
lower crampy abdo pain
bloating
urinary symptoms, e.g. frequency
subfertility
rare features:
polycythaemia secondary to autonomous production of EPO

236
Q

Diagnostic investigation for fibroids?

A

TV USS

237
Q

Management of menorrhagia with fibroids?

A

IUS
NSAIDs e.g. mefenamic acid
tranexamic acid
cOCP
oral progestogen
injectable progestogen

238
Q

Management to shrink fibroids?

A

GnRH agonists
Myomectomy/hysteroscopic endometrial ablation/hysterectomy
Uterine artery ablation

239
Q

When do fibroids naturally regress?

A

After menopause

240
Q

What is premature ovarian syndrome?

A

the onset of menopausal symptoms and elevated gonadotrophin levels before the age of 40 years. It occurs in around 1 in 100 women.

241
Q

What can cause premature ovarian syndrome?

A

Idiopathic
Bilateral oophorectomy
chemo/radio
infections e.g. mumps

242
Q

What biochemical changes do you see in premature ovarian syndrome?

A

raised FSH, LH levels
e.g. FSH > 40 iu/l
low oestradiol
e.g. < 100 pmol/l

243
Q

What are the most common causes of primary hyperparathyroidism?

A

80%: solitary adenoma
15%: hyperplasia
4%: multiple adenoma
1%: carcinoma

244
Q

HRT risks?

A

Increased risk of breast Ca + VTE (if given with progesterone)
Increased risk of endometrial Ca (if given as oestrogen alone - should not be given to women with a womb)
Increased risk of stroke/IHD

245
Q

What is the difference between PPAR-α and PPAR-γ agonists?

A

PPAR-α agonists act as cholesterol lowering drugs (fibrates).
PPAR-γ agonists act as antidiabetic agents

246
Q

What is Reidel’s thyroiditis?

A

a rare cause of hypothyroidism characterised by dense fibrous tissue replacing the normal thyroid parenchyma. On examination a hard, fixed, painless goitre is noted. It is usually seen in middle-aged women. It is associated with retroperitoneal fibrosis. Most patients are euthyroid, but hypothyroidism is noted in approximately 30% of cases.

247
Q

What is the diagnostic criteria for gestational diabetes?

A

5678
Fasting glucose: >5.6
OGTT: >7.8

248
Q

Which sign is more sensitive and specific in hypocalcaemia?

A

Trousseau’s sign is more sensitive and specific than Chvostek’s sign

249
Q

Chronic features of hypocalcaemia?

A

Cataracts and depression

250
Q

Treatment of prediabetes?

A

Lifestyle
Metformin for those who are still progressing to T2 DM despite lifestyle changes

251
Q

RFs for urge incontinence?

A

Age
previous pregnancy and childbirth
high BMI
hysterectomy
family history

252
Q

What causes the four different types of urinary incontinence?

A

overactive bladder (OAB)/urge incontinence: due to detrusor overactivity
stress incontinence: leaking small amounts when coughing or laughing
mixed incontinence: both urge and stress
overflow incontinence: due to bladder outlet obstruction, e.g. due to prostate enlargement

253
Q

Investigation for incontinence?

A

Bladder diaries for at least 3 days
Urine dipstick/culture
Cystometry (done to exclude/diagnose urge incontinence after lifestyle changes have failed)
ePAQ questionnaire
Residual bladder volumes

254
Q

Management of urge incontinence?

A

Simple measures - avoid caffeine, review meds
Bladder retraining for 6wks - education, times voiding with systematic delay in voiding, positive reinforcement (aim is to gradually increase the interval between voiding)

Anti-muscarinics -> oxybutynin/tolterodine (immediate release) or darifenacin (once daily preparation)
Mirabegron (beta-3 agonist) - used if concerns of anticholinergic SEs in frail elderly patients
Can also use oestrogens/botox A

255
Q

Management of stress incontinence?

A

Pelvic floor training - >8contractions TDS for 3/12
Mid-urethral sling (tension free vag tape/trans-obturator tape)
Duloxetine (SNRI), enhance urethral sphincter activity
Injectable peri-urethral bulking agents

256
Q

What would HPV infected cells look like under microscopy?

A

Infected endocervical cells may undergo changes resulting in the development of koilocytes. These have the following characteristics:
enlarged nucleus
irregular nuclear membrane contour
the nucleus stains darker than normal (hyperchromasia)
a perinuclear halo may be seen

257
Q

Which HPV subtypes are responsible for genital warts?

A

6 & 11

258
Q

How to investigate for cervical cancer?

A

Smear test
If abnormal cells identified, test for HPV:
- if high-risk HPV present -> colposcopy
- if not present -> enter back to routine screening
If cervical glandular intraepithelial neoplasia (CGIN) present, need to exclude adenocarcinoma -> colposcopy + endocervical curretage

259
Q

When does the UK screening test take place for cervical Ca?

A

25-49 -> every 3yrs
50-64 -> every 5yrs
65+ -> those not screened since 50/those with recent abnormal smears

260
Q

Management of cervical Ca?

A

Microinvasive disease -> cone biopsy
Stage 1 + early stage 2 -> radical abdo hysterectomy
Can do radical trachelectomy (remove 80% of cervix and place cervical suture to prevent preterm labour) - for women wanting to conserve fertility
Late stage 2 (+LNs) -> chemo/radiotherapy

261
Q

What is premature ovarian failure?

A

onset of menopausal symptoms and elevated gonadotrophin levels before the age of 40 years

262
Q

Causes of premature ovarian failure?

A

idiopathic (c)
bilateral oophorectomy
having a hysterectomy with preservation of the ovaries
radio/chemotherapy
infection: e.g. mumps
autoimmune disorders
resistant ovary syndrome: due to FSH receptor abnormalities

263
Q

How do HPV 16-18 cause cervical Ca?

A

Human papilloma virus 16 and 18 produces oncoproteins which causes inhibition of the tumor suppressor genes causing cervical carcinoma (look at notes in gynae book to perfect this explanation)

264
Q

What is androgen insensitivity syndrome and symptoms?

A

46XY

X-linked recessive condition due to end-organ resistance to testosterone

Males look phenotypically female

‘primary amennorhoea’

undescended testes causing groin swellings

breast development may occur as a result of conversion of testosterone to oestradiol

265
Q

What percentage of people with Graves have TSH Abs?

A

TSH antibodies are found in 90% of patients with Graves’ disease

MRCP (14 decks)

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