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Focused 1 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

T1DM Ix?

A
  1. Urine = glucose and ketones
  2. Bloods = fasting glucose, random glucose, HbA1c, C-peptide, Diabetes-specific antibodies

*C-peptide is a byproduct of insulin production. When the pancreas produces insulin, it splits proinsulin into insulin and C-peptide. Measuring C-peptide can provide an indirect assessment of endogenous (self-produced) insulin levels.

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2
Q

T1DM Antibodies?

A
  1. anti-GAD (80%)
  2. anti-ICA (70%)
  3. IAA (insulin autoantibodies)
  4. Insulinoma-associated-2 autoantibodies (IA-2A)
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3
Q

Insulin autoantibodies (IAA) mushkies?

A

Presence in T1DM correlates strongly with age, found in over 90% of young children with T1DM but only 60% of older patients

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4
Q

T1DM diagnostic criteria?

A
  1. Fasting glucose greater than or equal to 7.0 mmol/l
  2. Random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)
  3. (If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions)
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5
Q

When is polydipsia seen?

A

Fasting plasma glucose >16.6mmol/L

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6
Q

How often should HbA1c be checked in T2DM?

A

Every 3-6 months until stable, then 6 monthly

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7
Q

HbA1c targets in T2DM for lifestyle/single drug treatment?

A
  1. Lifestyle = 48mmol/L (6.5%)
  2. Lifestyle + metformin = 48mmol/mol (6.5%)
  3. Includes any drug which may cause hypoglycaemia e.g. sulfonylurea = 53mmol/mol (7.0%)
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8
Q

HbA1c targets in T2DM for patient already on one drug, but HbA1c has risen to 58mmol/L (7.5%)?

A

53 mmol/mol

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9
Q

First-line management of T2DM?

A
  1. Assess cardiovascular risk –> high risk of CVD or established CVD or chronic HF?
  2. No –> Metformin
  3. Yes –> Metformin –> Once established at SGLT2 inhibitor
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10
Q

If metformin not tolerated due to GI s/e?

A

Switch to modified release metformin

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11
Q

If metformin is C/I and pt has high risk of CVD or established CVD or chronic HF?

A

SGLT2 monotherapy

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12
Q

If metformin is C/I and pt is at low risk of CVD or established CVD or chronic HF

A
  1. DPP4 inhibitor OR Pioglitazone OR Sulfonylurea
  2. SGLT2 may be used if certain NICE criteria are met
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13
Q

2nd line Rx of T2DM?

A

Add one of: DPP4i/Pioglitazone/Sulfonylurea/SGLT2i

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14
Q

3rd line Rx of T2DM?

A
  1. Add another one of: DPP4i/Pioglitazone/Sulfonylurea/SGLT2i OR
  2. Start insulin-based treatment
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15
Q

Further therapy of T2DM?

A

If triple therapy is not effective or tolerated consider switching one of the drugs for a GLP-1 mimetic if BMI >35 or insulin would have occupational implications (GLP-1 mimetics should only be added to insulin under specialist care)

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16
Q

At what HbA1c level is further treatment indicated for T2DM?

A

58mmol/mol (7.5%)

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17
Q

Starting insulin recommendation?

A
  1. Start with human NPH insulin (isophane, intermediate-acting) taken at bed-time or twice daily according to need
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18
Q

Thiazolidinediones MOA?

A

PPAR-gamma receptor agonists, reduce peripheral insulin resistance (glitazones, e.g. pioglitazone)

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19
Q

Thiazolidinedione s/e?

A
  1. Weight gain
  2. Liver impairment (monitor LFTs)
  3. Fluid retention (therefore C/I in HF)
  4. Fractures
  5. Bladder cancer
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20
Q

When is thyroxine starting dose 25mcg?

A
  1. Cardiac disease
  2. Severe hypothyroidism
  3. > 50 y/o
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21
Q

Change in thyroxine dose TFT check time?

A

8-12 weeks later

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22
Q

Hypothyroid women become pregnant dose increase?

A

By at least 25-50mcg

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23
Q

Levothyroxine s/e?

A
  1. Hyperthyroidism
  2. Reduced bone mineral density
  3. Worsening of angina
  4. AF
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24
Q

Levothyroxine interactions?

A

Iron and calcium carbonate (absorption of levothyroxine reduced, give at least 4 hours apart)

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25
Q

Subclinical hypothyroidism bloods?

A

TSH raised but normal T3/T4

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26
Q

Significance of subclinical hypothyroidism?

A
  1. Risk of progressing to overt hypothyroidism 2-5% per year (higher in men)
  2. Risk increased by the presence of thyroid autoantibodies
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27
Q

Subclinical hypothyroidism Rx classification?

A
  1. TSH 4-10 and normal thyroxine
  2. TSH >10 and normal thyroxine
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28
Q

TSH 4-10 and normal thyroxine Rx?

A
  1. < 65 y/o with symptoms suggestive of hypothyroidism –> give a trial of levothyroxine, if no improvement then stop
  2. > 80 y/o = watch and wait
  3. If asymptomatic observe and repeat TFTs in 6m
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29
Q

TSH >10 and normal thyroxine Rx?

A
  1. < 70 y/o = start treatment even if asymptomatic
  2. > 80 y/o = watch and wait
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30
Q

HHS or DKA has higher mortality?

A

HHS

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31
Q

HHS pathophysiology?

A
  1. Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium
  2. Severe volume depletion results in a significant raised serum osmolarity (typically > than 320 mosmol/kg), resulting in hyperviscosity of blood.
  3. Despite these severe electrolyte losses and total body volume depletion, the typical patient with HHS, may not look as dehydrated as they are, because hypertonicity leads to preservation of intravascular volume.
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32
Q

HHS Dx?

A
  1. Hypovolaemia
  2. Marked hyperglycaemia (>30mmol/L) without significant ketonaemia or acidosis
  3. Serum osmolality > 320 mosmol/kg
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33
Q

HHS management goals?

A
  1. Normalise the osmolality gradually (the key parameter)
  2. Replace fluid and electrolyte losses
  3. Normalise blood glucose gradually
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34
Q

Serum osmolality estimation?

A

2Na + Glucose + Urea

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35
Q

Fluid losses in HHS estimation?

A

100-220ml/kg (10-22 litres in an individual weighing 100kg)

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36
Q

HHS If the serum osmolarity is not declining despite positive balance with 0.9% sodium chloride?

A

Switch to 0.45% NaCl which is more hypotonic relative to HHS patient serum osmolality

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37
Q

HHS fluid replacement goals?

A

Aim for a positive balance of 3-6 litres by 12 hours and the remaining replacement of estimated fluid losses within the next 12 hours (aim of treatment should be to replace approximately 50% of estimated fluid loss within the first 12 hours and the remainder in the following 12 hours)

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38
Q

When is rising serum Na+ a concern during HHS fluid replacement?

A

Only a concern if the osmalility is not declining concurrently

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39
Q

Plasma glucose fall rate during HHS fluid replacement?

A

4-6mmol/hr, rate of fall should not exceed 10mmol/L in 24 hours

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40
Q

Target blood glucose during HHS treatment?

A

10-15mmol/L

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41
Q

Mixed HHS/DKA picture insulin treatment?

A

(I.e. if significant ketonaemia is present) –> 0.05 units/kg/hr fixed rate

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42
Q

Two conditions accounting for 90% of cases of hypercalcaemia?

A
  1. Primary hyperparathyroidism = commonest cause in non-hospitalised patients
  2. Malignancy = most common cause in hospitalised patients
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43
Q

Mechanisms by which malignancy can cause hypercalcaemia?

A
  1. PTHrP from tumour e.g. SCLC
  2. Bone metastases
  3. Myeloma = due primarily to increased osteoclastic bone resorption caused by local cytokines (e.g. IL-1, tumour necrosis factor) released by the myeloma cells
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44
Q

Diuretic causing hypercalcaemia?

A

Thiazides

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45
Q

How to assess for diabetic neuropathy in the feet?

A

10g monofilament

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46
Q

Diabetic foot screening?

A

Annually
1. Ischaemia = palpating dorsalis pedis and posterior tibial artery
2. Neuropathy = 10g monofilament on various parts of the sole of the foot

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47
Q

Risk stratification of diabetic feet?

A
  1. Low = no risk factors except callus alone
  2. Moderate = deformity/neuropathy/non-critical limb ischaemia
  3. High = previous ulceration/amputation, on renal replacement therapy, neuropathy + non-critical limb ischaemia, neuropathy + callus/deformity, non-critical limb ischaemia + callus/deformity
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48
Q

Who should be followed up by local diabetic foot centre?

A

All moderate and high risk patients

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49
Q

Most common cause of thyrotoxicosis in UK?

A

Graces

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50
Q

Thyrotoxicosis causes?

A
  1. Graves’ disease
  2. Toxic nodule goitre
  3. Acute phase = subacute, post-partum, Hashimoto’s thyroiditis
  4. Amiodarone
  5. Contrast
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51
Q

DKA pathophysiology?

A

Uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies

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52
Q

Most common causes of DKA?

A
  1. Infection
  2. Missed insulin doses
  3. MI
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53
Q

DKA diagnosis?

A
  1. BM > 11
  2. pH < 7.3
  3. Bicarb < 15
  4. Ketones >3 or ++
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54
Q

DKA Rx?

A
  1. Fluid replacement (1h, 2h, 2h, 4h, 4h, 5h)
  2. 0.1 units/kg/hr fixed rate
  3. Once BM <15mmol/l, start 5% dextrose infusion
  4. Continue long acting insulin, stop short acting insulin
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55
Q

DKA potassium replacement?

A
  1. Over 5.5 = Nil
  2. 3.5-5.5 = 40mmol/L
  3. <3.5 = senior review as additional potassium needs to be given
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56
Q

DKA resolution?

A
  1. pH > 7.3
  2. Ketones < 0.6
  3. Bicarb > 15
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57
Q

If ketonaemia and acidosis hasnt resolved within 24 hours DKA?

A

Senior review from endocrinologist

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58
Q

Suspicion of cerebral oedema during fluid resuscitation in DKA?

A

CT head and senior review

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59
Q

Most common cause of hypothyroidism?

A

Hashimoto’s (autoimmune) thyroiditis

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60
Q

Hashimoto’s thyroiditis features?

A
  1. 10F:1M
  2. Goitre: firm, non-tender
  3. Anti-TPO (thyroid peroxidase) and anti-thyroglobulin (anti-Tg) antibodies
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61
Q

What lymphoma is associated with Hashimoto’s?

A

MALT lymphoma

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62
Q

Addison’s disease management?

A
  1. Hydrocortisone = given in 2 or 3 divided doses, patients typically require 20-30 mg per day, with the majority given in the first half of the day
  2. Fludrocortisone
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63
Q

Addison’s disease intercurrent illness management?

A
  1. Double glucocorticoid dose, fludrocortisone dose remains the same
64
Q

A person with Addison’s who vomits?

A

Should take IM hydrocortisone until vomiting stops

65
Q

Addisons disease Dx?

A

Short Synacthen test

66
Q

Short synacthen test meethod?

A

Plasma cortisol is measured before and 30 minutes after giving Synacthen 250ug IM. Adrenal autoantibodies such as anti-21-hydroxylase may also be demonstrated.

67
Q

9am serum cortisol interpretation for Addisons if ACTH stimulation test is not readily available?

A
  1. > 500 = unlikely
  2. < 100 = abnormal
  3. 100-500 = Synacthen test to be performed
68
Q

Very high mineralocorticoid activity steroid?

A

Fludrocortisone

69
Q

High gluco and mineralocorticoid activity steroid?

A

Hydrocortisone

70
Q

Predominant glucocorticoid activity?

A

Prednisolone

71
Q

Very high glucocorticoid activity?

A

Dexamethasone

72
Q

Mineralocorticoid s/e?

A
  1. Fluid retention
  2. Hypertension
73
Q

When should systemic steroids be gradually withdrawn?

A
  1. Received more than 40mg prednisolone daily for one week
  2. Received more than 3 weeks of treatment
  3. Recently received repeated courses
74
Q

Pituitary adenoma classification?

A
  1. Size (micro <1cm and macro >1cm)
  2. Hormonal statues (secretory/non-secretory)
75
Q

Most common type of pituitary adenoma?

A

Prolactinoma

76
Q

Prolactinoma Dx?

A

MRI

77
Q

Prolactinoma Rx?

A
  1. Medically = Dopamine agonists e.g. cabergoline, bromocriptine –> inhibit release of prolactin from the pituitary gland
  2. Surgery = if cannot tolerate/fails medical therapy. Usually trans-sphenoidal approach.
78
Q

Octreotide use?

A

Somatostatin analogue used in the treatment of acromegaly

79
Q

Pre-diabetes definition?

A
  1. HbA1c 42-47 mmol/mol (6.0-6.4%)
  2. Fasting glucose 6.1-6.9
80
Q

Impaired fasting glucose cause?

A

Hepatic insulin resistance

81
Q

Impaired glucose tolerance cause?

A

Muscle insulin resistance

82
Q

IFG definition?

A

A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l

83
Q

IGT definition?

A

A fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

84
Q

IFG management?

A

Offer OGTT to rule out a diagnosis of diabetes

85
Q

Diabetic neuropathy management?

A
  1. 1st line = amitryptiline, duloxetine, gabapentin or pregabalin
  2. 2nd line = try one of the other 3 drugs
  3. Tramadol rescue therapy for exacerbations
  4. Topical capsaicin for localised neuropathic pain
  5. Pain management clinics for resistant problems
86
Q

GI autonomic neuropathy management?

A

Prokinetics = metoclopramide, domperidone, erythromycin

87
Q

Falsely low HbA1c readings (reduced RBC lifespan)?

A

Sickle cell anaemia, G6PD, Hereditary Spherocytosis

88
Q

What is HbA1c dependent upon?

A
  1. Red blood cell lifespan
  2. Average blood glucose concentration
89
Q

Falsely high HbA1c (increased RBC lifespan)?

A
  1. B12/folic acid deficiency
  2. IDA
  3. Splenectomy
90
Q

Average plasma glucose from HbA1c calculation?

A

(HbA1c x 2) - 4.5

91
Q

Thyrotoxicosis with tender goitre?

A

Subacute (De Quervain’s) Thyroiditis

92
Q

Subacute thyroiditis phases?

A
  1. 3-6 weeks = hyperthyroid, painful goitre, raised ESR
  2. 1-3 weeks = euthyroid
  3. Weeks-months = hypothyroid
  4. Thyroid structure and function returns to normal
93
Q

Subacute thyroiditis Ix?

A

Thyroid scintigraphy: globally reduced uptake of Iodine-131

94
Q

Subacute thyroiditis Rx?

A
  1. Usually self limiting
  2. Thyroid pain may respond to aspirin/NSAIDs
  3. In more severe cases steroids are used, particularly if hypothyroidism develops
95
Q

TSH aim?

A

0.5-2.5

96
Q

T1DM HbA1c aim?

A

48mmol/mol (6.5%)

97
Q

HbA1c monitoring in T1DM?

A
  1. Every 3-6 months
  2. Target <48mmol/mol (6.5%)
98
Q

T1DM self monitoring of glucose?

A
  1. Testing at least 4x a day, including before each meal and before bed
  2. More frequent monitoring is recommended if frequency of hypoglycaemic episodes increases; during periods of illness; before, during and after sport; when planning pregnancy, during pregnancy and while breastfeeding
99
Q

T1DM blood glucose targets?

A
  1. 5-7 mmol/l on waking
  2. 4-7 mmol/l before meals at other times of the day
100
Q

When should metformin be added in T1DM?

A

If BMI >=25

101
Q

Sulfonylurea MOA?

A

They work by increasing pancreatic insulin secretion and hence are only effective if functional B-cells are present. On a molecular level they bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells.

102
Q

Sulfonylurea s/e?

A
  1. Hypoglycaemic episodes
  2. Weight gain
  3. Hyponatraemia due to SIADH
  4. Bone marrow suppression
  5. Hepatotoxicity (typically cholestatic)
  6. Peripheral neuropathy
103
Q

When should sulfonylureas be avoided?

A

Breastfeeding and pregnancy

104
Q

Steroid therapy effect on TSH and T4?

A

Low TSH, Normal T4

105
Q

Poor compliance with thyroxine TSH and T4?

A

High TSH, Normal T4

106
Q

Initial target weight loss in T2DM overweight person?

A

5-10%

107
Q

HbA1c monitoring in T2DM?

A

Every 3-6 months until stable, and then 6 monthly

108
Q

Secondary hypothyroidism associated conditions?

A
  1. Down’s
  2. Turner’s
  3. Coeliac
109
Q

Secondary hypothyroidism Ix?

A

MRI brain and pituitary

110
Q

DM medication contraindicated in HF?

A

Pioglitazone, can cause fluid retention

111
Q

Recurrent UTIs which DM drug to avoid?

A

SGLT2 inhibitors

112
Q

Cushing’s syndrome cause classification?

A
  1. ACTH dependent
  2. ACTH independent
113
Q

ACTH dependent causes of Cushing’s syndrome?

A
  1. Cushing’s disease (80%) = Pituitary tumour secreting ACTH producing adrenal hyperplasia
  2. Ectopic ACTH production (5-10%) e.g. SCLC is the most common cause
114
Q

ACTH independent causes of Cushing’s syndrome?

A
  1. Iatrogenic = steroids
  2. Adrenal adenoma (5-10%)
  3. Adrenal carcinoma (rare)
  4. Carney complex = incl. cardiac myxoma
  5. Micronodula adrenal dysplasia
115
Q

Pseudo-Cushing’s mushkies?

A
  1. Mimics Cushings
  2. Often due to alcohol excess or severe depression
  3. Causes false positive dexamethasone suppression test or 24 hour urinary free cortisol
  4. Insulin stress test may be used to differentiate
116
Q

Myxoedema coma presentation?

A

Confusion and hypothermia

117
Q

Myxoedema coma Rx?

A
  1. IV thyroid replacement
  2. IV fluid
  3. IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded)
  4. Electrolyte imbalance correction
  5. Sometimes rewarming
118
Q

Hypoglycaemia community Rx?

A
  1. Oral glucose 10-20g
  2. Hypokit = syringe and vial of glucagon for IM or SC injection at home
119
Q

Hypoglycaemia hospital Rx?

A
  1. Given quick acting carbohydrate if pt alert
  2. If unconscious/can’t swallow –> S/C or IM Glucagon
  3. Alternatively 20% glucose through large vein
120
Q

DM medication C/I in bladder cancer?

A

Pioglitazone

121
Q

Primary hyperaldosteronism causes?

A
  1. Bilateral idiopathic adrenal hyperplasia (70%)
  2. Conn’s syndrome (adrenal adenoma)
  3. Adrenal carcinoma (rare)
122
Q

Primary hyperaldosteronism causes?

A
  1. HTN
  2. Hypokalaemia e.g. muscle weakness
  3. Alkalosis
123
Q

Primary hyperaldosteronism Ix?

A
  1. Aldosterone:renin ratio
  2. High resolution CT abdomen and adrenal vein sampling 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)
124
Q

Primary hyperaldosteronism Rx?

A
  1. Adrenal adenoma = surgery
  2. Bilateral adrenocortical hyperplasia = aldosterone antagonist e.g. spironolactone
125
Q

Thyroid storm precipitating events?

A
  1. Thyroidal or non-thyroidal surgery
  2. Trauma
  3. Infection
  4. Acute iodine load e.g. CT contrast media
126
Q

Thyroid storm Rx?

A
  1. BB = IV Propranolol
  2. Antithyroid = Carbimazole/Propylthiouracil
  3. Lugol’s iodine
  4. Dexamethasone e.g. 4mg IV QDS = blocks conversion of T4 to T3
  5. Therapeutic plasma exchange if failed medical therapy
  6. Treat underlying precipitating event
127
Q

Hypertension and hypokalaemia?

A

Primary hyperaldosteronism

128
Q

Graves’ features?

A
  1. Eye signs (30%) = exophthalmos, ophthalmoplegia
  2. Pretibial myxoedema
  3. Thyroid acropachy = triad of digital clubbing, soft tissue swelling of hands and feet, periosteal new bone formation
129
Q

Graves’ autoantibodies?

A
  1. TSH receptor stimulating antibodies (90%)
  2. anti-thyroid peroxidase antibodies (75%)
130
Q

Graves’ thyroid scintigraphy?

A

Diffuse, homogeneous, increased uptake of radioactive iodine

131
Q

Medication causing hypercalcaemia?

A

Thiazides

132
Q

High calcium and inappropriately normal/raised PTH level?

A

Primary hyperparathyroidism

133
Q

Causes of primary hyperparathyroidism?

A
  1. Solitary adenoma (80%)
  2. Hyperplasia (15%)
  3. Multiple adenoma (4%)
  4. Carcinoma (1%)
134
Q

Primary hyperparathyroidism associations?

A
  1. HTN
  2. MEN I and II
135
Q

Primary hyperparathyroidism characteristic X-ray finding?

A

Pepperpot skull

136
Q

Primary hyperparathyroidism Rx?

A
  1. Definitive = Total parathyroidectomy
  2. Conservative = If Ca < 0.25mmol/L upper limit of normal AND patient > 50 y/o AND no evidence of end-organ damage
  3. Not suitable for surgery = Cinacalcet (calcimimetic)
137
Q

SGLT2 inhibitor MOA?

A

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

138
Q

SGLT2 inhibitor examples?

A
  1. Canagliflozin
  2. Empagliflozin
  3. Dapagliflozin
139
Q

SGLT2 inhibitor adverse effect?

A
  1. Urinary and genital infection, Fournier’s gangrene
  2. Normoglycaemic ketoacidosis
  3. Increased risk of lower-limb amputation, feet should be closely monitored
140
Q

What inhibits prolactin release?

A

Dopamine, so dopamine agonists e.g. bromocriptine can be used

141
Q

Features of raised prolactin?

A
  1. Men = impotence, loss of libido, galactorrhoea
  2. Women = amenorrhoea, galactorrhoea
142
Q

Causes of raise prolactin?

A
  1. Prolactinoma
  2. Pregnancy and oestrogens
  3. Physiological = stress, exercise, sleep
  4. Acromegaly = 1/3rd of pts
  5. PCOS
  6. Primary hypothyroidism (due to TRH stimulating prolactin release)
143
Q

Drug causes of raised prolactin?

A
  1. Metoclopramide, domperidone
  2. Phenothiazines
  3. Haloperidol
  4. Very rare = SSRIs, opioids
144
Q

Cushing’s syndrome blood gas?

A

Hypokalaemic metabolic acidosis

145
Q

Cushing’s syndrome Ix?

A
  1. Overnight dexamethasone suppression test = 1st line, most sensitive, pts with Cushing’s syndrome do not have their morning cortisol spike suppressed
  2. 24 hour urinary free cortisol
146
Q

Cushing’s syndrome localisation tests?

A
  1. 9am and midnight plasma ACTH (and cortisol) tests (If ACTH is suppressed then a non-ACTH dependent cause is likely e.g. adrenal adenoma)
  2. High dose dexamethasone suppression test
147
Q

Carbimazole dosing?

A

Given in high doses for 6 weeks until the patient becomes euthyroid before being reduced

148
Q

Carbimazole MOA?

A
  1. Blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production
  2. In contrast propylthiouracil as well as this central mechanism of action also has a peripheral action by inhibiting 5’-deiodinase which reduces peripheral conversion of T4 to T3
149
Q

Carbimazole s/e?

A
  1. Agranulocytosis
  2. Crosses the placenta, but may be used in low doses during pregnancy
150
Q

Lithium effect on thyroid?

A

Hypothyroidism

151
Q

Primary hypoadrenalism causes?

A
  1. Addisons = autoimmune, commonest cause in UK
  2. TB, HIV
  3. Metastases
  4. Antiphosphoplipid syndrome
152
Q

GLP1 receptor agonist example?

A

Liraglutide

153
Q

Acromegaly mushkies?

A
  1. Excess GH secondary to pituitary adenoma in >95% cases
  2. Minority of cases caused by ectopic GRG or GH production by tumours e.g. pancreatic
154
Q

Acromegaly complications?

A
  1. HTN
  2. DM
  3. Cardiomyopathy
  4. Colorectal cancer
155
Q

Graves’ disease ATD therapy?

A
  1. Carbimazole is started at 40mg and reduced gradually to maintain euthyroidism
  2. Typically continued for 12-18 months
  3. Alternative regimen is termed block and replace
156
Q

Block and replace Graves’ therapy?

A
  1. Carbimazole started at 40mg
  2. Thyroxine added when patient is euthyroid
  3. Treatment typically lasts for 6-9 months
157
Q

Graves’ radioiodine treatment?

A
  1. Used in patients who relapse following ATD therapy or are resistant to primary ATD treatment
  2. C/I = Pregnancy (should be avoided for 4-6 months following treatment) and age < 16 years. Thyroid eye disease is a relative contraindication, as it may worsen the condition
  3. Proportion of patients who become hypothyroid depends on the dose given, but as a rule the majority of patient will require thyroxine supplementation after 5 years

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