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Finals Bible: Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Antibodies associated with T1DM?

A

Anti-islet and anti-GAD

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2
Q

Diagnosis for diabetes on blood sugars?

A

Fasting > 7 / HbA1c >48mmol/L (6.5%)

2-hours post OGTT / Random glucose > 11.1mmol/L

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3
Q

What is the definition of impaired fasting glucose?

A

6.1 - 7.0

Offer these OGTT, If this is 7.8 - 11.1 = IMPAIRED GLUCOSE TOLERANCE

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4
Q

Conservative management of diabetes?

A

MDT

The 4 C’s? = Control, compilations, competency and coping

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5
Q

Diabetes conservative management - Control?

A

Record of complications e.g. DKA, HONK and hypo’s

CBG - target of 5-7 on waking and 4-7 pre-meal

HbA1c <6.5% or 48mmol/L
Check every 3-6 months then 6-monthly when stable

Control HTN - <140/80 if no end organ damage
<130/80 if end organ damage

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6
Q

What are BP targets for diabetics?

A

Control HTN - <140/80 if no end organ damage

<130/80 if end organ damage

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7
Q

Conservative management of diabetes - Complications?

A

Macro = Pulses, BP, cardiac

Micro = Fundoscopy, U&E’s and sensory testing

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8
Q

Conservative management of diabetes - Competency?

A

With insulin injections, checking injection sites and BM monitoring

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9
Q

Conservative management of diabetes - coping?

A

Psychological, occupational and domestic

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10
Q

Sick day rules for diabetes?

A

Increase frequency of blood sugars

Aim for at least 3 litres of fluid a day

Access to mobile and emergency food supplies

Continue all medication

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11
Q

Medical management of T1DM?

A

Always need insulin

Biphasic = first line = Twice daily insulin detemir

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12
Q

Management of type 2 diabetes - metformin tolerated?

A

If metformin tolerated it is 1st line

2nd line once HbA1c > 58mmol/L (7.5%) =
Add in gliptin / sulfonylurea / pioglitazone / SGLT-2 inhibitor

3rd line once HbA1c > 58mmol/L (7.5%) = metformin plus:

Sulfonylurea + gliptin
Sulfonylurea + pioglitazone
Sulfonylurea + SGLT-2 inhibitor
Pioglitazone + SGLT-2 inhibitor

3rd line = insulin
OR
Metformin + sulfonylurea + GLP-1 mimetic

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13
Q

When should you not use metformin?

A

End stage renal disease

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14
Q

Management of type 2 diabetes - metformin not tolerated?

A

1st line = gliptin or sulfonylurea or pioglitazone

2nd line once HbA1c >58mmol/L (7.5%):

Gliptin + pioglitazone
Gliptin + sulfonylurea
Pioglitazone + sulfonylurea

3rd line = insulin

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15
Q

When HbA1c hits what level do you move onto the next treatment in T2DM?

A

58 mmol/L or 7.5%

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16
Q

When can you use metformin + sulfonylurea + GLP-1 mimetic?

A

When normal triple therapy not effective (3rd line), then use this if BMI >35, or BMI<35 but weight loss or using insulin would have a big impact

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17
Q

Metformin - MOA, SE’s and CI’s?

A

Increases insulin sensitivity + decreases hepatic neogenesis

Nausea, diarrhoea, abdominal pain, lactic acidosis

Cannot use if eGFR <30ml/minute

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18
Q

Sulfonylureas - Examples, MOA, SE’s?

A

Gliclazide or Glimepiride

Stimulate pancreatic beta cells to stimulate insulin

SE’s = hypoglycaemia, WEIGHT GAIN, hyponatraemia

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19
Q

Thiazolidinediones - Example, MOA, SE’s?

A

Pioglitazone (contraindicated in blander cancer and heart failure)

Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid reuptake, reducing peripheral insulin resistance

SE’s = Weight gain and fluid retention

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20
Q

DPP-4 inhibitors / Gliptins - examples, MOA and SE’s?

A

Vildagliptin and sitagliptin

Increases incretin levels which inhibit glucagon secretion

SE = increased risk of pancreatitis

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21
Q

SGLT-2 inhibitors - MOA, SE’s?

A

-Gliflozins

Inhibit resorption of glucose in the kidneys - typically results in WEIGHT LOSS

SE’s = UTI as more glucose in the urine

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22
Q

GLP-1 agonists - How do you take it, MOA and SE’s?

A

Exanitide

Subcut

Incretin mimetic which inhibits glucagon secretion - typically results in WEIGHT LOSS

SE’s = N&V, pancreatitis

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23
Q

Macrovascular complications of diabetes?

A

MI/CVA

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24
Q

Microvascular complications of diabetes?

A

Diabetic foot
Nephropathy
Retinopathy
Neuropathy

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25
Q

Microvascular complications of diabetes - diabetic foot?

A

ISCHAEMIA = hyperglycaemia damages blood vessels = critical toes, absent pulses and painful punched out ulcers

NEUROPATHY = hyperglycaemia can cause damage to nerves = loss of protective sensation = CHARCOTS FOOT = painless ulcers

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26
Q

Management of diabetic foot?

A

Conservative = regular inspection, comfortable therapeutic footwear. Regular chiropody

Medical = treat any infections and pain management e.g. amitriptyline

Surgical = abscesses, cellulitis or gangrene

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27
Q

Microvascular complications - nephropathy?

A

Hyperglycaemia = nephron loss and glomerulosclerosis

Clinical features = Microalbuminaemia - urine albumin:creatinine ratio > 30

Management = ACEI’s and ARBS

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28
Q

Microvascular complications - Retinopathy?

A

Leading cause of blindness <60

Due to small vessel damage = ischaemia = VEGF = neovascularisation

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29
Q

Classification of diabetic retinopathy

A

Mild NPDR = 1 or more microaneurysm

Moderate NPDR:
Microaneurysms
Blot haemorrhages
Hard exudate
Cotton wool spots, venous bleeding

Severe NPDR:
Blot haemorrhages and micro aneurysms in all quadrants
Venous bleeding in two quadrants

PROLIFERATIVE = neovascularisation

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30
Q

Microvascular complications of diabetes - neuropathy

A

Nerve damage due to hyperglycaemia

Symmetrical sensory loss = polyneuropathy
Mononeuropathy = CN3 and 6 palsies
Autonomic neuropathy = postural hypotension, diarrhoea, urinary retention

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31
Q

Physiology of DKA?

A

Reduced insulin means cannot utilise glucose = B-oxidation of fats = Ketones

Dehydration due severe hyperglycaemia causing osmotic diuresis. Also ketones cause vomiting

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32
Q

Diagnostic criteria of ketoacidosis?

A

Glucose >11mmol or known diabetic

pH <7.3

Bicarbonate <15mmol/L

Ketones >3mmol/L or urine ketones ++ on dipstick

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33
Q

Management of DKA?

A 
ABC
Fluids until systolic >90 then:
1L over 2 hours
1L over 2 hours
1L over 4 hours
1L over 4 hours
1L over 6 hours

Start potassium in the second bag of fluids:
>5.5 = none needed
3.5-5.5 = 40mmol/L
<3.5 = consult senior

Insulin act rapid 0.1unit / kg / hour. Once glucose >15 start 5% dextrose infusion

LMWH

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34
Q

At what rate do we want to improve in DKA, and when is resolution?

A

Continuous monitoring aiming to reduce ketones by >0.5 per hour, or increase bicarb by >3 per hour

Ketones <0.3mmol/L venous pH >7.3, or bicarb >15

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35
Q

What are the criteria for HHS?

A

Profound hyperglycaemia > 33
Hyperosmolarity = serum osm > 320
Dehydration in the absence ketoacidosis = pH >7.3 and ketones <0.3mmol/L

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36
Q

Management of HSS?

A

Rehydrate the same as DKA

Wait 1 hour prior to starting insulin as many may not need it

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37
Q

What are the causes of thyrotoxicosis?

A

Most common = graves

Toxic nodular goitre (Hot nodules)

Acute phase of hashimotos / de Quervains (decreased iodine uptake)

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38
Q

Graves specific signs ?

A

Diffuse goitre and increased uptake

Ophthalmopathy = Exophthalmos and ophthalmoplegia

Pre-tibial myxoedema

Thyroid acropachy

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39
Q

Management of thyrotoxicosis?

A

Anti-thyroid drugs = Carbimazole 40mg
SE = agranulocytosis

Symptomatic = propranolol to ameliorate the adrenergic symptoms

Refractory = radioiodine

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40
Q

Clinical features of a thyroid storm?

A

Raised temperature
Tachycardia and AF
Acute abdomen / heart failure
Agitated and confused

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41
Q

Management of thyroid storm?

A

Fluids and NGT
Propranolol
Carbimzaole and lugs iodine
Hydrocortisone

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42
Q

Causes of hypothyroid?

A

Hashimotos thyroiditis commonest in UK = anti-TPO and anti-Tg

Atrophic thyroiditis = similar to hashimotos but antibodies vs TSH and TPO

Post-partum

De Quervains

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43
Q

Management of hypothyroid?

A

Levothyroxine:
Start dose low in elderly / IHD
Normal dose 50-100ug OD
Therapeutic goal is TSH 0.5-2.5

SE’s:
Hyperthyroid, reduced BM density, worsening of angina

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44
Q

What reduces levothyroxine absorption?

A

When taken with iron

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45
Q

What is simple colloid goitre?

A

A benign diffuse multinodular goitre

Mass effect = Dysphagia, stridor and SVC obstruction

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46
Q

What is hashimotos?

A

Autoimmune disease vs anti-TPO

Clinical features = Middle aged women, diffuse NON-TENDER goitre

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47
Q

Management of hashimotos?

A

Levothyroxine

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48
Q

Most common cause of hypothyroid in developing world?

A

Iodine deficiency

= diffuse massive thyroid enlargement

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49
Q

What is subacute thyroiditis?

A

Often following viral infection, typically presents with:

  • 4 weeks of hyperthyroidism + PAINFUL goitre
  • 2 weeks of euthyroid
  • Months of hypothyroid
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50
Q

What is the scan uptake for subacute thyroiditis?

A

Globally reduced uptake on iodine scan

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51
Q

Management of subacute thyroiditis?

A

Usually self-limiting

More severe may need steroids

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52
Q

What is Riedels thyroiditis?

A

Rare cause of hypothyroidism where dense fibrous tissue replaces the normal thyroid parenchyma

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53
Q

Clinical features of Riedels thyroiditis?

A

Hard, fixed painless goitre

Associated with retroperitoneal fibrosis

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54
Q

Management of Riedels thyroiditis?

A

Corticosteroids

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55
Q

What is graves disease?

A

Autoantibodies to TSH receptor antibodies and TPO antibodies

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56
Q

What is toxic multi nodular goitre / Plummer’s?

A

Gland contains a number of autonomously functioning thyroid nodules

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57
Q

what is the uptake in Plummer’s?

A

Patchy uptake on the iodine scan

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58
Q

Management of plumbers?

A

Radioiodine

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59
Q

What is the commonest thyroid malignancy?

A

Papillary carcinoma

Branching papillary structure with fibrous stroma and psammoma bodies

60
Q

Clinical features of thyroid papillary carcinoma?

A

20-40 years

Slow growing solitary thyroid nodule
Commonly enlarged cervical LN’s
Euthyroid

Scanning shows NO UPTAKE

61
Q

Management of thyroid papillary carcinoma?

A

Thyroidectomy
- remove any palpable cervical LN’s at the same time

Total thyroidectomy has slightly increased risk of post-op hyperparathyroidism but means any recurrence can be treated with radioiodine

Give levothyroxine too……
Tumour / mets need high TSH, which only occurs if normal tissue left - so give levothyroxine to keep TSH low

62
Q

How do you check for recurrence of papillary carcinoma?

A

Thyroglobulin levels

63
Q

Histology of follicular carcinoma?

A

Well developed follicular pattern

64
Q

Management of follicular carcinoma?

A

RARE, 40-50 years

Subtotal / total thyroidectomy

May opt for a total as allows for better uptake of radioiodine for mets

65
Q

Endocrine features of medullary carcinoma?

A

Arises from parafollicular / C-cells = excess calcitonin

May also secrete serotonin and ACTH

66
Q

Clinical features of medullary carcinoma?

A

RARE

Stony hard tumour
Secondaries in cervical nodes and poor prognosis

67
Q

Management of medullary carcinoma?

A

Need aggressive surgery, won’t take up radioiodine

68
Q

What is anaplastic thyroid carcinoma?

A

Extremely aggressive tumour, appalling prognosis

Histology = sheets of differentiated cells

Will rapidly invade local structures = Recurrent laryngeal, early mets, oesophageal obstruction

69
Q

Complications of thyroid surgery?

A

Laryngeal oedema

Recurrent laryngeal nerve damage = right sided more common due to oblique ascent

Hypocalcaemia = due to parathyroid dysfunction
PC:
- Tingling lips and fingers
- Wheeze and stridor
- Chvosteks and trousseaus

Thyroid storm

70
Q

Mechanism of PTH?

A

Secreted in response to low calcium

Causes osteoclast activity up and increased calcium reabsorption

71
Q

Causes of primary hyperparathyroidism?

Biochem?

A 
80% = solitary adenoma
20% = hyperplasia

Raised calcium and PTH, low phosphate

72
Q

Management of primary hyperPTH?

A

Increased fluid intake
Avoid dietary calcium and thiazides

Surgical excision if hypercalcaemia, <50 years, low T-score

73
Q

Causes of secondary hyperparathyroidism?

Biochem?

A

Vitamin D deficiency
Chronic renal failure
Malabsorption e.g. Coeliacs

Calcium low, PTH and phosphate raised

74
Q

Management of secondary hyperparathyroidism?

A

Correct causes

Medical = phosphate binders e.g. calcichew
Vitamin D supplementation

Surgical for renal if:

  • Bone pain
  • Persistent pruritus
  • Soft tissue calcifications
75
Q

Causes of tertiary hyperparathyroidism?

biochem?

A

Prolonged secondary, leads to autonomous PTH secretion

Calcium and PTH raised, low phosphate

76
Q

Features of low calcium?

A

SCAPS:

Spasma = Trousseaus and Chvosteks
Confused
Anxious and irritable
Prolonged QT
Seizures
77
Q

Causes of hypoparathyroidism?

A

Autoimmune

Congenital = Di George:
Cardiac abnormality
Abnormal facies
Thymic aplasia
Cleft palate
Hypocalcaemia
Chr22

Iatrogenic = surgery or radiation

78
Q

management of hypoparathyroidism?

A

Calcium supplementation

79
Q

What is pseudohypoparathyroidism?

Biochem?

A

Failure of the target organ to respond to PTH = abnormality in G protein

Low calcium, raised PTH and phosphate

80
Q

How to diagnose pseudohypoparathyroidism?

A

Measure urinary cAMP and phosphate levels following PTH infusion.

If type 1 neither will rise
Type two only cAMP will rise

81
Q

What is Cushing’s syndrome?

A

Clinical state produced by excess glucocorticoid

82
Q

Causes of Cushing syndrome?

A

ACTH dependant = High ACTH:

  • Cushings disease 80% = Pituitary tumour secreting ACTH, causes adrenal hyperplasia
  • Ectopic ACTH from small cell lung cancer or carcinoid tumour

ACTH independent = low ACTH:

  • Adrenal adenoma 15%
  • Iatrogenic steroids
  • Carney complex = syndrome including cardiac myxoma

Pseudo cushings = Due to alcohol and stress

83
Q

Clinical features of Cushing’s?

A

Catabolic state = Proximal myopathy, striae and bruising

Glucocorticoids = DM, obesity

MR affects = HTN and hypokalaemia

84
Q

Investigations to confirm Cushings?

A

Overnight dexamethasone suppression test and urinary 24 hour cortisol

Then we need to localise:

1st line = 9am and midnight ACTH. if suppressed then non-ACTH cause

Next do a high dose dexamethasone suppression test - pituitary source (cushings disease) will be supressed, ectopic / adrenal will not

85
Q

Management of Cushings?

A

Treat the cause:

Cushings disease = Trans=sphenoidal excision
- may also need bilateral adrenalectomy to control excess cortisol

Adrenal adenoma = adrenalectomy

Ectopic ACTH = tumour excision and metyrapone can inhibit cortisol synthesis

86
Q

What is Nelson’s syndrome?

A

Rapid enlargement of a pituitary adenoma following bilateral adrenalectomy for Cushings syndrome

= Bitemporal hemianopia and hyper pigmentation

87
Q

Primary causes of hyperaldosteronism?

A

Bilateral adrenal hyperplasia 70%

Adrenocortical adenoma (CONNS) 30%

88
Q

Clinical features of hyperaldosteronism?

A

HYPOKALAEMIA = weakness, hypotonia, hyporeflexia and cramps

Paraesthesia

HTN

89
Q

What does aldosterone do?

A

Absorbs sodium and water, excreting potassium by acting on the MR receptors in the collecting duct and DCT

90
Q

Biochemistry and ECG changes in hyperaldosteronism?

A

Low potassium, high sodium
HYPOKALAEMIC ALKALOSIS

High serum aldosterone, low serum renin
Can do adrenal vein sampling

ECG = flat t-waves, depressed ST

91
Q

Management of primary hyperaldosteronism?

A

Adrenal adenoma = surgery

Bilateral hyperplasia = Aldosterone antagonist = spironolactone

92
Q

Secondary causes of hyperasldosteronism?

A

Due to increased renin from reduced renal perfusion:

Renal artery stenosis
Diuretics
CCF
Nephrotic syndrome

NORMAL ALDOSTERONE TO RENIN RATIO

93
Q

What is barters syndrome?

A

Autosomal recessive condition associated with severe hypokalaemia

Defective chloride absorption at the Na K 2Cl co-transporter in ascending loop of Henle

94
Q

Causes of adrenal insufficiency?

A

Primary = Addisons = destruction of there adrenal cortex so no glucocorticoids or mineralcorticoids:

  • Autoimmune 80%
  • TB commonest worldwide
  • Metastases
  • CAH

Secondary = hypothalamus or pituitary failure:

  • Chronic steroid use
  • Pituitary apoplexy / Sheehan’s
  • Pituitary macroadenoma
95
Q

clinical features of adrenal failure?

A 
Weight loss
N&amp;V
Hyperpigmentation
Postural hypotension 
Vitiligo
Hypoglycaemia
96
Q

Which type of adrenal insufficiency will NOT give you hyper pigmentation?

A

Secondary as you still have normal mineralocorticoid production = low ACTH

97
Q

Biochemistry for adrenal insufficiency?

A

Low sodium and high potassium

ACTH stimulation test:

  • Plasma cortisol measured before and 30 minutes after giving 250ug IM Synacthen
  • excludes Addison’s if raised cortisol
98
Q

Management of adrenal insufficiency?

A

Hydrocortisone and fludrocortisone

Don’t stop steroids suddenly during illness, double dose!

99
Q

What is addisonian crisis?

A

Shocked = tachycardia, postural BP, oliguria and confused

Management = Hydrocortisone
Fluids
Septic screen and treat underlying cause

100
Q

What is a phaeochromocytoma?

A

Catecholamine producing tumour arising from sympathetic paraganglia, usually in the adtrenal medulla

101
Q

Clinical features of phaeochromocytoma?

A

Classic triad = headaches, sweating and tachycardia

102
Q

Investigations for phaeochromocytoma?

A

24 hour urinary metanephrines

Abdominal CT/MRI

103
Q

Management of phaeochromocytoma?

A

Often volume depleted = fluids

Surgical adrenalectomy is definitive, but must stabilise first:

alpha blockers first = phenoxybenzamine 10mg PO BD

Beta blockers = propranolol

104
Q

Phaeochromocytoma: Clinical presentation and management of hypertensive crisis?

A

PC = pallor, pulsating headache, feeling of impending doom and raised BP

Phentolamine 5mg IV of Sodium nitroprusside
Followed by elective surgery 4 weeks after alpha blockade

105
Q

What is multiple endocrine neoplasia?

A

Functioning hormone tumours In multiple organs.

Autosomal dominant

106
Q

What is MEN1?

A

Pituitary adenoma = prolactin or GH
Parathyroid adenoma
Pancreatic tumours = Gastrinoma or insulinoma

107
Q

What is MEN2a?

A

Thyroid medullary cancer
Phaeo
Parathyroid

108
Q

What is MEN2b?

A

Thyroid medullary cancer
Phaeo
Marfanoid habitus and neuromas

109
Q

Genes associated with MEN1 vs MEN2?

A

MEN1 = MEN1

MEN2 = RET oncogene

110
Q

Clinical features of MEN?

A

Positive FHx and young age
Kidney stones

MEN1 = Facial angiofibromas and collagenomas

MEN2 = Neuromas = bumpy lips, marfanoid, palpable thyroid nodules

111
Q

Investigations for MEN?

A

PTH levels, calcium
MEN1 = fasting serum gastrin, IGF 1 levels, prolactin
MEN2 = Serum calcitonin and CEA = medullary thyroid, urinary metanephrines

112
Q

management of MEN?

A

HyperPTH = fluids and bisphosphonates / Cincalet

Gastrinoma = PPI
Prolactinoma = Bromocriptine

Phaeo = alpha and BB, adrenalectomy

113
Q

What is Carney complex?

A

LAMES

Lentigenes = spotty pigmentation
Atrial Myxoma
Endocrine tumours = pituitary or adrenal hyperplasia
Schwannomas

114
Q

What is peutz-Jeghers?

A

Autosomal dominant disease characterised by numerous hamartomatous polyps in the GI tract

115
Q

Clinical features of Peutz Jeghers?

A

Mucocutaneous freckling on lips / mucosa / palms and soles

GI hamartomas = obstruction and bleeds

Pancreatic endocrine tumours

116
Q

What is Von Hippel-Lindau?

A

Autosomal dominant condition with an abnormality in the VHL gene located on chromosome 3

117
Q

clinical features of Von hippie-Lindau syndrome?

A

Renal cysts

Bilateral renal cell carcinoma

Haemangioblastomas - often in cerebellum = cerebellar signs

Phaeochromocytoma

118
Q

Clinical features of NFT1?

A 
Cafe au last spots >6, 15mm in diameter
Axillary and groin freckling
Iris hamartomas (lisch nodules) 
Peripheral neurofibromas
Scoliosis
Phaeo
119
Q

clinical features of NFT2?

A

bilateral acoustic neuromas

Multiple schwannomas and meningiomas

120
Q

What does the hypothalamus release, and what does this cause the pituitary to release?

A

TRH - TSH and prolactin

CRH - ACTH

GnRH - LH and FSH

GHRH - GH

121
Q

What do the pituitary hormones act upon?

A

TSH acts on thyroid = thyroxine = HR, temperature and metabolism

ACTH acts upon the liver = cortisol = maintains blood sugar and BP

LH and FSH = testosterone or oestradiol = spermato/oo-genesis

GH acts on liver = IGF1

Prolactin acts upon the breast = MILK

122
Q

What is released from the posterior pituitary?

A

ADH and oxytocin

123
Q

Causes of hypopituitarism?

A

Neoplastic =

  • Pituitary adenoma (upper fields first)
  • Craniopharyngoma (lower fields first), originates from Rathkes pouch

Vascular = Pituitary apoplexy, or Sheehan’s

Infiltrative = Sarcoidosis or TB

Congenital = Kallmans - delayed puberty, anosmia, tall and hypogonadism

124
Q

Investigations and management for hypopituitarism?

A

Test all the hormones e.g. low 9am cortisol, TFT’s, sex hormones low, prolactin can be raised if prolactinoma, IGF-1 low

Management = replace all the hormones e.g. Hydrocortisone, levothyroxine, gonadotrophin, recombinant human GH and desmopressim

125
Q

Classification of pituitary tumours?

A

<1cm = Microadenoma

> 1cm = Macroadenoma

40% produce prolactin

126
Q

Clinical features of pituitary tumours?

A

Mass effects = headaches, bitemporal hemianopia, CN3/4/5/6 palsies

Hormone effects:
Prolactin = galactorrhoea, low libido

GH = acromegaly

ACTH = cushings

127
Q

Management of pituitary tumours?

A

If prolactin = Cabergoline 0.25mg PO twice weekly

GH = octreotide

ACTH = tran-sphenoidal excision

128
Q

Cabergoline SE’s?

A

Nausea, postural hypotension and fibrosis

129
Q

What is acromegaly?

A

Chronic progressive disease due to excessive secretion of growth hormone.

GH stimulates bone and soft tissue via IGF1

130
Q

Causes of acromegaly?

A

99% = pituitary adenoma

Rarely hyperplasia from GHRH secreting carcinoid tumour

131
Q

Clinical features of acromegaly?

A

Coarse facial appearance
Carpal tunnel
Large tongue and prognathism
Excess sweating and oily skin

features of pituitary tumour e.g. bitemporal hemianopia and headaches

132
Q

Investigations in acromegaly?

A

Visual fields

OGTT with serial GH measurements - normal patient swill suppress to <2

Pituitary MRI

133
Q

Management of acromegaly?

A

First line = aran-sphenoidal excision

2nd line = somatostatin analogues = octreotide 10mg IM ever month for three months

134
Q

What is diabetes insidious?

A

Metabolic disorder characterised by the inability to concentrate urine

135
Q

What causes DI?

A

either an absolute deficiency in ADH from the posterior pituitary, or an insensitivity to the receptors

136
Q

Causes of cranial DI?

A

Idiopathic
Trauma
Post pituitary surgery
DIDMOAD / Wolframs

137
Q

Cause sof nephrogenic DI?

A

Genetic
Electrolytes = Hypercalcaemia and hypokalaemia
Drugs e.g. democlocycline

138
Q

Investigations for DI?

A

High plasma osm, low urine osm (if urine >700 excludes DI)

Water deprivation test = urine osmolality stays low

Desmopressin test = if nephrogenic still won’t respond

139
Q

Management of DI?

A

Fluids
Cranial = desmopressin

Nephrogenic = treat underlying cause, give chlorothiazide

140
Q

Causes of hirsutism?

A

Familial
Idiopathic
Raised androgens e.g. PCOS, Cushings

141
Q

Clinical features of PCOS?

Investigations?

Management?

A

Subfertility / infertility
Oligo / amenorrhoea
Hirsutism / acne
Obesity

USS of ovaries
Raised LH:FSH ratio

Management = Metformin, COCP, clomiphene for infertility

142
Q

Causes of gynaecomastia?

A 
Cirrhosis
Hypogonadism
Hyperthyroid
Oestrogen
Drugs e.g. spironolactonme
143
Q

What is orlistat?

A

weight loss drug, pancreatic lipase inhibitor

144
Q

SE’s of orlistat?

A

Faecal urgency / incontinence and flatus

145
Q

Indications for orlistat?

A

Part of overall weight loss plan
BMI >28 with RF’s
BMI > 30
Continued weight loss

Finals Bible: Medicine (6 decks)

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