Medicine - Endocrinology Flashcards

1
Q

What are the criteria for diagnosis of type 2 diabetes?

A
Either symptoms + 1 pos test result or no symptoms + 2 pos test results
Pos test thresholds: 
- Fasting glucose >7.0
- OGTT >11.1
- Random glucose >11.1 
- HbA1c > 6.5%/ 48mmol/L
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2
Q

What are the test ranges for impaired gluose tolerance and impaired fasting glucose?

A

IGT: OGTT/random = 7.8-11.1; HbA1c = 42-47

IFG = 6.1-7.0

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3
Q

What is the classic triad of symptoms of type 2 diabetes?

A

Polydipsia
Polyuria
Fatigue

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4
Q

Recall 2 possible consequences of diabetic neuropathy and drugs that can be used to manage each of these possibiities

A
  1. Vagal neuropathy –> gastroparesis: domperidone/ metoclopramide
  2. Neuropathic pain: amitryptiline, duloxetine, gabapentin, pregabalin
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5
Q

Summarise the pathogenesis of diabetic foot

A
  1. Peripheral arterial disease reduces O2 delivery –> intermittent claudication
  2. Neuropathy –> loss of sensation, eventually Charcot’s foot
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6
Q

What is Charcot’s foot?

A

Rare consequence of T2DM in which foot becomes rocker-bottomed

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7
Q

Recall some ways in which diabetic foot can be screened for, and the frequency with which these tests should be done

A

Screening should be done annually
Test for ischaemia: palpate the dorsalis pedis and posterior tibial pulse
Test for neuropathy with 10g monofilament test

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8
Q

How should diabetic nephropathy be screened for?

A

Yearly albumin:creatinine ratio

Microalbuminuria is the first sign of diabetic nephropathy

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9
Q

What is the best management for diabetic nephropathy?

A

ACE inhibitors

However, these are toxic in AKI so eGFR needs to be monitored

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10
Q

How big a drop in eGFR would warrant stopping an ACE inhibitor in a diabetic patient?

A

> 20%

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11
Q

Why is an initial drop in eGFR expected when starting patients on an ACE inhibitor?

A

Dilate the efferent arteriole

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12
Q

Recall 3 things that may cause a falsely high HbA1c

A

Alcoholism
B12 deficiency
Iron deficiency anaemia

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13
Q

What is the BM target for T1DM patients who are monitoring BMs throughout the day?

A

Waking target: 5-7mmol/L

Rest of the day: 4-7mmol/L

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14
Q

Recall the names of 2 long-acting insulins

A

Lantus

Glargine

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15
Q

When are BD mixed regimens of insulin given?

A

Breakfast and dinner

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16
Q

Name a diabetes prevention programme

A

DESMOND

Diabetes education + self-management: ongoing and newly diagnosed

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17
Q

Recall some possible risk-factor modifying therapies that can be used in diabetes mellitus

A

Aspirin 75mg OD
Atorvastatin 20mg OD
Antihypertensives

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18
Q

What is the maximum dose of metformin?

A

2g/day

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19
Q

Recall 4 important side effects of metformin

A

Appetite suppression
B12 deficiency (due to reduced absorption)
Lactate acidosis
GI upset

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20
Q

How can you manage GI upset that is due to metformin?

A

Change immediate release to a modified release mechanism

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21
Q

When should dual therapy be considered in type 2 diabetes?

A

If HbA1c >58/ 7.5%

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22
Q

What are the options for dual therapy for type 2 diabetes?

A

Metformin + 1 of:

  • Sulphonylurea
  • Thiazolidinediones
  • Gliptins
  • SGLT2 inhibitors
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23
Q

Recall 2 examples of sulphonylureas

A

Glibenclamide

Gliclazide

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24
Q

Recall an example of a thiazolidinedione

A

Pioglitazone

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25
Q

Recall an example of a gliptin drug

A

Sitagliptin

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26
Q

What is the mechanism of action of gliptins?

A

DPP4 inhibitors

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27
Q

Recall an example of a SGLT2 inhibitor

A

Empagliflozin

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28
Q

Recall 2 important side effects of sulphonylureas

A

Weight gain

Hypoglycaemia

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29
Q

What sort of diabetes drug is MODY most sensitive to?

A

Sulphonylureas

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30
Q

What is the inheritance pattern of MODY?

A

Autosomal dominant

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31
Q

MODY must be diagnosed before what age?

A

25

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32
Q

What is the best investigation to confirm the diagnosis of MODY?

A

C peptides

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33
Q

What is the most common type of MODY, and which gene mutation causes it?

A

MODY 3

Mutated HNF-1 alpha

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34
Q

What is LADA?

A

Latent autoimmune diabetes in adults

Late onset T1DM in 20-50yo, no family history

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35
Q

What are the 2 best investigations for confirming the diagnosis of LADA?

A
GAD Abs 
C peptide (will be low)
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36
Q

What 3 things are required to diagnosis DKA?

A

Diabetes, Ketones, Acidosis
Diabetes - BM >11.1
Ketones - >3
Acidosis - pH <7.3

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37
Q

Recall 4 common causes of DKA

A

Missed insulin
Trauma
Infection
EtOH

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38
Q

What 3 investigations are most useful for assessing the extent of the damage done by a DKA acutely?

A

ABG
ECG
U&Es

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39
Q

Recall the 5 main principles of managing DKA acutely

A
  1. Fluids
  2. Insulin
  3. Potassium (run KCl in NaCL bag)
  4. 10% dextrose (when BM < 15)
  5. VTE prophylaxis (very dehydrated)
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40
Q

What dose of insulin should be started in DKA vs HHS?

A

DKA: 0.1U/kg/hr
HHS: 0.5U/kg/hr

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41
Q

Recall the 3 biochemical criteria used to diagnose HHS

A

pH >7.3
Osmolarity >320mmol/L
BM >30

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42
Q

Over what time period does HHS develop?

A

Over a few days

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43
Q

Recall the 3 components of HHS management

A
  1. Fluids
  2. Monitoring (ensure Na+ is not corrected too quickly)
  3. Insulin
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44
Q

Recall 2 differentials for someone whose TFTs show low TSH and low T4

A

Secondary hypothyroidism

Sick euthyroid

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45
Q

Recall the Thy classification

A

Thy 1 = unsatisfactory sample (1c = cyst)
Thy 2 = benign
Thy 3 = atypia of undetermined significance
Thy 4 = Suspicious of malignancy
Thy 5 = malignancy

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46
Q

What classification system is used to classify thyroid nodules?

A

Thy classification

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47
Q

What are the 4 histological types of thyroid cancer

A

Anaplastic
Medullary
Papillary
Follicular

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48
Q

Which type of thyroid cancer is associated with a raised calcitonin?

A

Medullary

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49
Q

Recall 2 differentials for low uptake hyperthyroidism

A

Sub-acute (De Quervain’s) thyroiditis

Postpartum thyroiditis

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50
Q

Recall 3 differentials for high uptake hyperthyroidism

A

Grave’s disease
Toxic multinodular goitre
Single toxic adenoma

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51
Q

Recall 7 signs of thyroid eye disease

A
Mnemonic = NO SPECS 
No signs or symptoms sometimes OR
Only signs (eg upper lid retraction) OR 
Signs AND symptoms: 
Proptosis 
Extra-ocular muscle pathology 
Corneal involvement 
Sight loss due to optic nerve involvement
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52
Q

Why might eye movement be restricted in thyroid eye disease?

A

Rectus thickening restricts movement

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53
Q

What is the best preventative measure to prevent Grave’s disease?

A

Stop smoking

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54
Q

Which subtypes of MEN are associated with medullary thyroid cancer?

A

2A and 2B

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55
Q

Recall the management of Grave’s disease

A

1st line:

  • Propranolol (NOT bisoprolol)
  • Anti-thyroid drug eg carbimazole or propylthiouracil OR
  • If unlikely to respond to ATDs, radioiodine (I-131)
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56
Q

Recall 2 possible side effects of radioiodine

A

Hypothyroidism

Thyroid storm

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57
Q

Recall how a patient should be prepared for thyroidectomy

A
  1. Need to be euthyroid on medication
  2. Laryngoscopy to check vocal cords
  3. Either thionamides or propranolol
    Stop thionamides (PTU) 10 days before surgery as it increases vascularity
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58
Q

Recall some symptoms of a thyroid storm

A
Hyperthermia 
Tachycardia 
Jaundice
Altered mental state
Cardiac (AF/high-output CF)
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59
Q

How should a thyroid storm be managed?

A

IV propranolol –> Thionamides (PTU)

Hydrocortisone –> iodine

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60
Q

What is the most common cause of primary hypothyroidism in the UK?

A

Hashimoto’s

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61
Q

What is Riedel’s thyroiditis

A

Hypothyroidism caused by chronic inflammatory thyroid gland fibrosis

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62
Q

Recall 2 drugs that can cause hypothyroidism

A

Lithium

Amiodarone

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63
Q

What is the starting dose of levothyroxine?

A

50-100mcg

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64
Q

How long after starting levothyroxine should the TFTs be checked?

A

8-12 weeks

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65
Q

Recall 2 medications that interact with levothyroxine

A

Iron

CaCO3

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66
Q

Recall 4 features of myxoedema coma

A

Hypothermia
Hyporeflexia
Bradycardia
Seizures

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67
Q

How should myxoedema coma be managed?

A

IV thyroxine
IV hydrocortisome
IV fluids

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68
Q

What are the most common causes of Addison’s disease?

A

In the UK: autoimmune adrenal failure

Worldwide: TB

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69
Q

Recall 2 ways that Addison’s/adrenal failure can be investigated for

A
  1. 9am cortisol

2. Short synACTHen test

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70
Q

Recall 3 possible cause of an Addisonian crisis (different from Addison’s disease)

A
  1. Adrenal haemorrhage (Waterhouse-Friderichson syndrome from meningococcaemia)
  2. Steroid withdrawal
  3. Sepsis/ surgery causing an acute exacerbation of chronic insufficiency (autoimmune/ TB)
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71
Q

How should an Addisonian crisis be managed?

A

Immediately:

  • IM hydrocortisone 100mg STAT
  • IV fluid bolus with glucose

Continuing management:

  • IV fluids
  • IV/IM hydrocortisone
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72
Q

What is the most common cause of Cushing’s syndrome?

A

Glucocorticoid therapy

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73
Q

What are some differentials for ACTH-dependent Cushing’s?

A

Cushing’s disease (80% pituitary tumour)

Ectopic ACTH production

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74
Q

What are the possible causes of pseudo-Cushing’s?

A

Alcoholism or severe depression

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75
Q

How can Cushing’s and pseudo-Cushing’s be differentiated?

A

Both will give a positive LDDST and 24hr free urinary cortisol
Can tell the difference between them with insulin stress test

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76
Q

Recall 2 screening tests for Cushing’s

A
  1. 11pm salivary cortisol (if low the cause is NOT Cushing’s)
  2. LDDST
77
Q

How can the cause of Cushing’s syndrome be confirmed?

A

Inferior petrosal sinus sampling

Catheter is fed into the jugular vein

78
Q

What is Nelson’s syndrome?

A

Possible complication of adrenalectomy

Removal of adrenal gland –> pituitary enlargement and very high ACTH

79
Q

What is the most common electrolyte disturbance in Conn’s syndrome?

A

Hypokalaemia

80
Q

What is the best initial investigation in suspected Conn’ syndrome?

A

Aldosterone: renin ratio

81
Q

What are the best tests to determine the cause of hyperaldosteronism?

A

HR-CT and adrenal vein sampling

82
Q

What are the possible causes of hyperaldosteronism?

A
  1. Conn’s syndrome

2. Renal artery stenosis

83
Q

What will be the aldosterone: renin ration in Conn’s syndrome vs renal artery stenosis?

A

Conn’s: high

Renal artery stenosis: normal

84
Q

What medications can be used to manage hyperaldosteronism?

A

Spironolactone and epleronone

85
Q

What test can be used to diagnose diabetes insipidus?

A

Water deprivation test

86
Q

Recall 2 possible renal and 2 non-renal causes of hypernatraemia

A

Renal: osmotic diuresis (T2DM) or diabetes insipidus

Non-renal: GI losses or sweat losses of water

87
Q

What is the possible complication of correcting hypernatraemia too quickly?

A

Cerebral oedema

88
Q

What is the possible complication of correcting hyponatraemia too quickly?

A

Central pontine myelinolysis

89
Q

In which patients is a urine sodium measurement not reliable?

A

Those on diuretics

90
Q

Recall some drugs that can cause SIADH

A

“Serotonin’s TCA Car Sulks, People Oversee Opiates.”

  • Serotonin’s: SSRIs
  • TCA: TCAs
  • Car: Carbamazepine
  • Sulks: Sulphonylureas
  • People: PPIs
  • Oversee: Opiates
91
Q

Recall 2 causes of pseudohyponatraemia

A

Hyperlipidaemia

Hyperproteinaemia

92
Q

Recall 2 drugs that can be used to treat SIADH

A

Demeocycline

Vaptans (eg tolvaptan)

93
Q

Recall 3 classes of drugs that could cause hyperkalaemia

A

ARBs
ACE inhibitors
Aldosterone antagonists

94
Q

Recall one antibiotic that can cause hyperkalaemia

A

Tacrolimus - it can reduce K+ excretion

95
Q

Which type of renal tubular acisosis can cause hyperkalaemia

A

Type 4

96
Q

Recall the management of hyperkalaemia

A
10mls 10% calcium gluconate 
120mls 20% dextrose
Maybe:  
10U insulin 
nebulised salbutamol 
If really bad: 
Calcium risonium
97
Q

For each of the following endocrine conditions, say whether they can cause hypo or hyperkalaemia:

  • Addisson’s
  • Conn’s
  • Cushing’s
A

Adisson’s: Causes hyperkalaemia
Conn’s: Causes hypokalaemia
Cushing’s: Causes hypokalaemia

98
Q

Which types of renal tubular acidosis can cause hypokalaemia (rarely)?

A

Types 1 and 2

99
Q

Which hormone will likely be high in renal artery stenosis?

A

Renin

100
Q

Describe the symptoms of hyper vs hypoclacaemia

A

Hypercalcaemia: bones, stones, abdominal groans, psychiatric moans

Hypocalcaemia: paraesthesia, muscle cramps, long QT

101
Q

What is a ‘pepperpot skull?

A

Radiological sign: Multiple tiny well-defined lucencies in the calvaria (top part of the skull) caused by resorption of trabecular bone in hyperparathyroidism

102
Q

How should hypercalcaemia be managed?

A

IV fluids –> bisphosphonates

103
Q

Recall the progression of multiple myeloma

A

(1) MGUS
(2) Smouldering myeloma
(3) Multiple myeloma
(4) B cell leukaemia

104
Q

At what point in the myeloma progression does a patient get the symptoms of CRAB?

A

Not until it gets to multiple myeloma

105
Q

What is the limit for monoclonal serum protein in MGUS?

A

Must be <30g/L

106
Q

What is the limit for bone marrow plasma cells in MGUS?

A

<10%

107
Q

Which type of immunoglobin will be high in myeloma?

A

IgG or IgA

If Waldenstrom’s - IgM

108
Q

What is the most useful form of imaging in myeloma?

A

Whole body low dose CT

109
Q

Which CD markers are positive in immunotyping in myeloma?

A

CD38
CD138
CD56/58

110
Q

What is the pathophysiology of refeeding syndrome?

A

Refeeding –> rise in insulin –> intracellular shift in phosphate –> hypophosphataemia

111
Q

What are some symptoms of the refeeding syndrome?

A
Rhabdomyolysis 
Low RR
Arrhythmia 
Shock
Seizures
Coma
112
Q

What is fibromuscular dysplasia?

A

Idiopathic, non-atherosclerotic, non-inflammatory disorder of arteries
2 subtypes:
- Renal artery
- Cervical artery

113
Q

What are the symptoms of fibromuscular dysplasia?

A

Renal artery FMD: resistant hypertension

Cervical artery FMD: chronic migraines

114
Q

What is the best investigation for assessing fibromuscular dysplasia?

A

Catheter angiography

115
Q

What is the mainstay of management of fibromuscular dysplasia?

A

Stop smoking
Anti-platelets (clopidogrel)
Anti-hypertension (ACEi or ARB)
Surgery (surgical stenting)

116
Q

Recall some causes of vitamin B12 deficiency

A

Autoimmunity
Atrophic gastritis
Gastrectomy
Malnutrition

117
Q

Recall 2 drugs that can treat vitamin B12 deficiency

A

Cyanocobalamin IM

Hydroxocobalamin IM

118
Q

Recall some causes of hypomagnesaemia

A
Diuretics/ PPIs
Diarrhoea 
TPN
EtOH
Gitelman's/Barter's
Hypokalaemia, hypocalcaemia
119
Q

What are the symptoms of hypomagnesaemia most similar to?

A

Hypocalcaemia

120
Q

What are the ECG features of hypomagnesaemia most similar to?

A

Hypokalaemia

121
Q

What is the threshold for giving IV magnesium sulphate as a Mg replacement, rather than just PO tablets?

A

Mg <0.4mmol/L

122
Q

How should suspected SIADH be investigated?

A
  1. Serum corrected calcium - must exclude hypercalcaemia secondary to hyperPTHism
  2. Water deprivation test
123
Q

What is the mechanism of hyponatraemia development in SIADH?

A

Increased water absorption in the collecting duct

124
Q

What would be the main abnormality on TFTs in thyrotoxic crisis?

A

Marked elevation of free T4

125
Q

What change in vision is caused by a lesion in the optic chiasm?

A

Bitemporal hemianopia

126
Q

What change in vision is caused by a lesion in the optic tract?

A

Homonymous hemianopia

127
Q

What change in vision is caused by a lesion in the optic radiation?

A

Superior quandrantopia

128
Q

Give some examples of causes of metabolic acidosis with increased anion gap

A

DKA is a big one

Also: lactate acidosis, uraemia secondary to renal failure and salicylate/biguianide poisoning

129
Q

In DKA, for how long should insulin infusion be continued before switching to SC insulin?

A

Until blood ketones <0.6mmol/L

130
Q

How frequently should potassium be monitored in the acute setting of DKA being treated with an insulin infusion?

A

4 hourly

131
Q

How should a known type 1 diabetic patient’s insulin be managed when they are in DKA and require an insulin infusion?

A

Long acting basal insulin should be continued alongside the infusion as this simplifies the change from infusion to SC insulin in due course

132
Q

Recall 4 side effects of carbimazole

A

Maculopapular rash
Bone marrow suppression leading to agranulocytosis
Pruritis
Jaundice

133
Q

How should primary hyperaldosteronism due to BL adrenal hypertrophy be managed?

A

Spironolactone

134
Q

What is the first drug to give in phaeochromocytoma?

A

Phenoxybenzamine

135
Q

How should once daily insulin regimes be managed pre-operatively?

A

Reduced dose insulin on the day of the op and the day before

136
Q

Why might someone get hyponatraemia post-SAH?

A

SAH can lead to SIADH

137
Q

What is the best test for diagnosing phaeochromocytoma?

A

Plasma and serum catecholamines

138
Q

How can a splenectomy affect blood sugar levels?

A

Can give a falsely high reading due to the increased life span of RBCs

139
Q

What is the immediate management of pituitary apoplexy?

A

IV hydrocortisone

140
Q

What is the treatment for malignant hyperthermia?

A

IV dantrolene

141
Q

If a diabetic type 1 patient is sick what should be done to the insulin dose

A

continue normal regime due to risk of DKA

check glucose more, replace with carb drinks

142
Q

Type 2 diabetic sick day rules

A

stop oral hypoglycaemics - restart after 24-48 hrs of feeling better

met:reduce lactic acidosis
sulf: increase hypo
sglt2: ketones - euglycaemic
glp1: reduce aki risk

insulin - keep the same

143
Q

Why is Pioglitazone contraindicated in diabetics with heart failure

A

can cause fluid retention, also linked with increase risk of bladder cancer & peripheral oedema

give sglt2 if cardiac as well, titrate metformin before tho

144
Q

When should a second drug be added in t2dm

A

HbA1c rises to 58<

check every 3-6 months

145
Q

Metformin not tolerated due to GI side effects

A

modified release metformin

146
Q

If a patient is asymptomatic with a fg of 7 or rg of 11.1 what should be done

A

re test on two separate occasions

147
Q

Give some conditions where HbA1c may not be used for diagnosis

A

haemoglobinpathies
children
HIV
CKD

148
Q

Define impaired glucose tolerance and fasting glucose

A

fasting 6.1 - 7.0

OGTT 7.8 - 11.1

149
Q

First line treatment for diabetic neuropathy

A

TCA, duloxetine, gabapentin etc
try another if not work
pain management if resistant

150
Q

Symptom of GI autonomic neuropathy

A

erratic blood glucose control with bloating
treat with metoclopramide, domperiodone etc

151
Q

What blood pH does cushing syndrome lead to

A

hypokalaemic metabolic alkalosis due to sodium and water retention

152
Q

How is ACTH release determined between sites

A

Petrosal sinus sampling

153
Q

Graves disease: Mx

A

Propranolol - initial control symptoms
Secondary care (carbimazole if not controlled)
40mg carbimazole - reduce gradually

agranulocytosis

154
Q

Mx of Thyroid storm

A

beta blockers
anti-thyroids - propylthiourail
dexamethasone - blocks t4 to t3

155
Q

how do sglt2 inhibitors work and what are the side effects

A

reversely inhibit SGcotransporter 2 in procximal - reduce gluocse reabsorpition and increase exrection

UTI, fourniers gangrene, ketoacidosis, increase limb amputation, lose weight

156
Q

Cushings disease

A

cortisol no suppressed by low dose but by high

157
Q

Treatment for primary hyperparathyroidism and x ray findings

A

pepperpot skull and osteitis fibros cystica

total parathyroidectomy
if not suitable for surgery - calcimimetic such as cinacalcet

158
Q

Most common cause of primary hyperaldosteronism

A

bilateral idiopathic adrenal hyperplasia

aldosterone/renin ratio
ct/adrenal vein - unilateral vs bilateral

adenoma - surgery
hyperplasia - spironolactone

htn, hypokalaemia (muscle weakness)

159
Q

Alcohol intoxication with glucose

A

hypoglycaemia - check glucose as can be like being drunk

160
Q

Treatment of addisonian crisis

A

fluids, hydrocortisone - no fludro due to alreay high cortisol exerting inhibitor affect

161
Q

Results of Gliclazide (sul) overdose

A

raised insulin and c peptide

162
Q

What is associated with acromegaly?

A

Hypertension, diabetes, cardiomyopathy and colrectal cancer

MEN1

163
Q

What is a common thyroid problem when sick

A

Sick euthyroid - no treatment

164
Q

Causes of lower than expected HbA1c

A

Blood problems

b12, ida, splnectomy, cause higher due to increase red cell lifespan

165
Q

What can reduce the absroption of levothyroxine

A

iron / calcium carbonate tablets - take 4 hrs after

t -reduce bone density, angina

166
Q

What diabetic medication is used for patients who are obese

A

Dpp-4 inhibitors

167
Q

hbA1c target for drugs that may cause hypoglycaemia

A

53 e.g. sulfonylurea

168
Q

Which endocrine hormones are decreased in response to stress

A

insulin, testosterone, oestrogen

169
Q

Causes of pseudo-cushings

A

alcohol excess / depression - use insulin stress test

170
Q

Features of De Quervains thyroiditis

A

viral infection
hyperthyroidism
4 phases - up, eu, hypo, then normal
reduced uptake of iodine -131

171
Q

Why should patients on long term steroid use not be withdrawn quickly

A

addisonian crisis

indications: received more than 40mg prednisolone daily for more than one week
received more than 3 weeks of treatment
recently received repeated courses

172
Q

steroids with illness

A

double the dose

173
Q

MoA orlistat

A

pancreatic lipase inhibitor

faecal urgency and incontinence

174
Q

Existing insulin management in DKA

A

long-acting insulin should be continued, short-acting insulin should be stopped

175
Q

Drugs that cause gynaecomastia

A

spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids

176
Q

Subclinical hypothyroidism

A

Flashcard: Subclinical Hypothyroidism

Basics:
- TSH high, T3, T4 normal
- No symptoms

Significance:
- 2-5% yearly risk of hypothyroidism
- Higher risk with autoantibodies

Management:
- NICE guidelines for treatment
- TSH >10mU/L: Levothyroxine if confirmed
- TSH 5.5-10mU/L:
- <65 and symptomatic: Consider levothyroxine
- >80: ‘Watch and wait’
- Asymptomatic: Monitor, reevaluate in 6 months.

177
Q

Diabetes: Ramadan

A

Flashcard: Diabetes and Ramadan

Points:
- Type 2 diabetes common in UK Muslim population.
- BMJ 2011 review guides Ramadan fasting for diabetes.
- Fasting is personal, exemptions for chronic conditions.
- 79% Muslim type 2 diabetics fast during Ramadan.
- Diabetes UK and Muslim Council provide detailed guidance.

Guidelines:
- Eat long-acting carbs before sunrise (Suhoor).
- Use glucose monitor, especially if unwell.
- Metformin: 1/3 before Suhoor, 2/3 after Iftar.
- Sulfonylureas: Once-daily after sunset, larger dose for twice-daily.
- No adjustment for pioglitazone users.

178
Q

Prolactinoma

A

Flashcard: Prolactinoma

Overview:
- Pituitary adenoma, benign.
- Classified by size and hormonal status.

Features:
- Women:
- Amenorrhoea, Infertility, Galactorrhoea, Osteoporosis
- Men:
- Impotence, Loss of libido, Galactorrhoea
- Macroadenomas:
- Headache, Visual issues, Hypopituitarism symptoms

Diagnosis:
- MRI

Management:
- Medical:
- Dopamine agonists (e.g., cabergoline, bromocriptine)
- Surgery:
- If medical treatment ineffective or intolerable

179
Q

Uptake of iodine in graves

A

diffuse, homogenous, increased uptake of radioactive iodine

180
Q

Cushings tests

A

Flashcard: Cushing’s Syndrome Investigations

Overview:
- Tests for confirmation and localization of Cushing’s syndrome.
- Consider iatrogenic, ACTH-dependent (Cushing’s disease, ectopic ACTH), and ACTH-independent (adrenal adenoma) causes.

General Findings:
- Hypokalemic metabolic alkalosis.
- Impaired glucose tolerance.
- Ectopic ACTH: Very low potassium levels.

Tests to Confirm Cushing’s:
1. Overnight Dexamethasone Suppression Test:
- Most sensitive; used first-line.
- Lack of morning cortisol spike indicates Cushing’s syndrome.

  1. 24hr Urinary Free Cortisol:
    • Two measurements required.
  2. Bedtime Salivary Cortisol:
    • Two measurements required.

Localisation Tests:
- 9am and midnight plasma ACTH (and cortisol) levels.
- Suppressed ACTH suggests non-ACTH dependent cause (e.g., adrenal adenoma).

High-Dose Dexamethasone Suppression Test:
- Interpretation:
- Not suppressed cortisol, suppressed ACTH: Other causes (e.g., adrenal adenomas).
- Suppressed cortisol, suppressed ACTH: Cushing’s disease (pituitary adenoma).
- Not suppressed cortisol, not suppressed ACTH: Ectopic ACTH syndrome.

Other Tests:
- CRH Stimulation:
- Pituitary source: cortisol rises.
- Ectopic/adrenal: no change.

  • Petrosal Sinus Sampling:
    • Differentiate pituitary and ectopic ACTH secretion.
  • Insulin Stress Test:
    • Distinguish true Cushing’s from pseudo-Cushing’s.
181
Q

Klinefelters

A

Flashcard: Klinefelter’s Syndrome

Overview:
- Karyotype: 47, XXY.

Features:
- Taller than average.
- Lack of secondary sexual characteristics.
- Small, firm testes; infertility.
- Gynaecomastia; increased breast cancer risk.
- Elevated gonadotrophin levels, low testosterone.

Diagnosis:
- Method: Karyotype (chromosomal analysis).

182
Q

MEN presentations

A

Note: MEN = Multiple Endocrine Neoplasia.

MEN Type | Features | Common Presentations |
|————–|——————————————————–|—————————————–|
| Type I | - 3 P’s: | - Hypercalcemia. |
| | - Parathyroid (95%): Hyperparathyroidism. | - Pituitary (70%). |
| | - Pituitary (70%). | - Pancreas (50%): insulinoma, gastrinoma.|
| | - Pancreas (50%): insulinoma, gastrinoma. | - Medullary thyroid cancer (70%). |
| | - Also involves adrenal and thyroid. | |
| Type IIa | - 2 P’s: | - Medullary thyroid cancer. |
| | - Parathyroid (60%). | - Phaeochromocytoma. |
| | - Phaeochromocytoma. | |
| Type IIb | - 1 P: | - Medullary thyroid cancer. |
| | - Phaeochromocytoma. | - Marfanoid habitus, Neuromas. |
| | - Marfanoid habitus, Neuromas. | - Involves RET oncogene. |
| | - Involves RET oncogene. | |

183
Q

Kallman syndrome

A

Flashcard: Kallmann’s Syndrome

  • Cause: X-linked recessive inheritance; failure of GnRH-secreting neurons’ migration to hypothalamus.
  • Key Clue: Lack of smell (anosmia) in boys with delayed puberty.

Features:
- Delayed puberty, hypogonadism, cryptorchidism.
- Anosmia.
- Low sex hormone levels.
- LH, FSH levels are inappropriately low/normal.
- Patients are usually of normal or above-average height.
- Some may have cleft lip/palate and visual/hearing defects.

Management:
- Testosterone supplementation.
- Gonadotrophin supplementation may induce sperm production for future fertility.

184
Q

What condition should TCA not be used in

A

BPH

185
Q

Side effects of thyroxine therapy

A

Side-effects of thyroxine therapy
* hyperthyroidism: due to over treatment
* reduced bone mineral density
* worsening of angina
* atrial fibrillation

186
Q

GLP-1 drugs

A

Diabetes Mellitus: GLP-1 Drugs

  • GLP-1 Overview:
    • GLP-1 is a hormone released by the small intestine in response to oral glucose.
    • Incretin effect, mediated by GLP-1, is reduced in type 2 diabetes mellitus (T2DM).
  • Drug Classes:
    • GLP-1 Mimetics (e.g., Exenatide):
      • Increase insulin secretion, inhibit glucagon secretion.
      • Result in weight loss, unlike some other diabetes medications.
      • Administered subcutaneously before meals.
      • Exenatide and Liraglutide are examples.
    • DPP-4 Inhibitors (e.g., Vildagliptin, Sitagliptin):
      • Increase GLP-1 and GIP levels by decreasing peripheral breakdown.
      • Oral preparation.
      • Well-tolerated, no increased hypoglycemia risk.
      • Do not cause weight gain.
  • GLP-1 Mimetics (Exenatide):
    • Given before morning and evening meals via subcutaneous injection.
    • Leads to weight loss, used in combination with other medications.
    • Nausea and vomiting are common adverse effects.
    • Liraglutide requires once-daily administration.
  • Indications and Considerations:
    • NICE recommends considering exenatide with metformin and sulfonylurea in specific BMI conditions.
    • Criteria for ongoing GLP-1 mimetics prescription: > 11 mmol/mol (1%) HbA1c reduction, 3% weight loss after 6 months.
  • Adverse Effects:
    • Major adverse effect: Nausea and vomiting.
    • Exenatide linked to severe pancreatitis, as warned by regulatory agencies.
  • DPP-4 Inhibitors:
    • Increase incretin levels, oral administration.
    • Well-tolerated with no increased hypoglycemia risk.
    • Preferable if further weight gain is problematic or contraindicated thiazolidinedione.
  • NICE Guidelines:
    • NICE suggests DPP-4 inhibitors if weight gain poses issues or thiazolidinedione response is poor.

Note: Always refer to the latest guidelines and consult medical professionals for personalized advice.

187
Q

Pregnancy: Thyroid

A
  • Thyrotoxicosis:
    • Propylthiouracil in 1st trimester, switch to carbimazole later.
    • Monitor maternal free thyroxine, check antibodies at 30-36 weeks.
  • Hypothyroidism:
    • Thyroxine safe during pregnancy; adjust dose (up to 50%).
    • Monitor thyroid-stimulating hormone.
    • Safe for breastfeeding.
188
Q

Drugs that cause a rasied prolactin

A

metoclopramide, domperidone
phenothiazines
haloperidol
very rare: SSRIs, opioids

189
Q

Thyroid Cancer

A

Thyroid Cancer: Key Points

  • General Features:
    • Thyroid malignancies rarely cause hyperthyroidism or hypothyroidism due to hormone secretion.
  • Types and Percentages:
    • Papillary (70%): Excellent prognosis, common in young females.
    • Follicular (20%):
    • Medullary (5%): Associated with MEN-2, C cells, secretes calcitonin.
    • Anaplastic (1%): Unresponsive to treatment, may cause pressure symptoms.
    • Lymphoma (Rare): Linked to Hashimoto’s thyroiditis.
  • Management (Papillary and Follicular):
    • Total thyroidectomy.
    • Radioiodine (I-131) for residual cell destruction.
    • Yearly thyroglobulin levels for early recurrent disease detection.
  • Further Information (Types):
    • Papillary Carcinoma: Papillary projections, pale empty nuclei, lymph node metastasis common.
    • Follicular Adenoma: Usually solitary nodule, malignancy ruled out with histological assessment.
    • Follicular Carcinoma: Capsular invasion seen, vascular invasion predominant.
    • Medullary Carcinoma: C cells origin, elevated calcitonin, familial cases possible.
    • Anaplastic Carcinoma: Common in elderly females, local invasion, resection for treatment, chemotherapy ineffective.