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Endocrine > Passmedicine > Flashcards

Passmedicine Flashcards

1
Q

Name 5 kinds of thyroid cancer

A 
Papillary
Follicular
Medullary 
Anaplastic
Lymphoma
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2
Q

Which thyroid cancer is most common?

A

Papillary

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3
Q

In which age group/gender is papillary thyroid cancer most common?

A

Young females

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4
Q

Where does papillary thyroid cancer tend to metastasise to?

A

Cervical lymph nodes

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5
Q

What can be used as a tumour marker in papillary thyroid cancer?

A

Thyroglobulin

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6
Q

What do you see in light microscopy of papillary thyroid cancer cells?

A

Orphan Annie eyes

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7
Q

What is the prognosis of papillary thyroid cancer?

A

Good

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8
Q

In what age group does follicular cancer tend to occur?

A

> 50 year women

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9
Q

Where does follicular thyroid cancer tend to metastasise to?

A

Lungs

Bone

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10
Q

What can be used as a tumour marker in follicular thyroid cancer?

A

Thyroglobulin

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11
Q

What is the prognosis of follicular thyroid cancer?

A

moderate

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12
Q

What are the two ways in which a medullary thyroid cancer can arises?

A

Spontaneous or as part of MEN2

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13
Q

From what cells does a medullary thyroid cancer arise?

A

Parafollicular cells (which make calcitonin hence this can be a tumour marker)

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14
Q

Which group of individuals tend to get anaplastic thyroid cancer?

A

It is very rare! But mostly occurs in elderly patients

NB has really poor prognosis

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15
Q

How might a lymphoma in the thyroid gland present?

A

Dysphagia

Stridor

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16
Q

What conditions comprise MEN1?

A

Pituitary adenoma
Parathyroid hyperplasia
Pancreatic tumours

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17
Q

What conditions comprise MEN2A?

A

Parathyroid hyperplasia, medullary thyroid carcinoma, pheochromocytoma

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18
Q

What conditions comprise MEN2B?

A

Mucosal neuroma, marfanoid appearance, medullary carcinoma, phaeochromocytoma

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19
Q

With which condition is lymphoma of the thyroid gland associated?

A

Hashimoto’s thyroiditis

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20
Q

How do you manage papillary/follicular cancer?

A

Total thyroidectomy
Radioiodine to kill residual cells
Yearly thyroglobulin levels to detect recurrent dx

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21
Q

What lab results would you see in thyrotoxicosis?

A

TSH: low

Free T4: high

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22
Q

What lab results would you see in primary hypothyroidism?

A

TSH: high

Free T4: low

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23
Q

What lab results would you see in secondary hypothyroidism?

A

TSH: low

Free T4: low

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24
Q

What must you give to individuals with secondary hypothyroidism before they get thyroxine?

A

Steroid replacement therapy

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25
Q

What lab results would you see in sick euthyroid syndrome?

A

TSH: low
Free T4: low

This is common in inpatients

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26
Q

What lab results would you see in subclinical hypothyroidism?

A

TSH: high

Free T4: normal

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27
Q

What lab results would you see in poor compliance with thyroxine?

A

TSH: high

Free T4: normal

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28
Q

What lab results would you see in steroid therapy?

A

TSH: low

Free T4: normal

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29
Q

What are the lab results for primary hyperparathyroidism?

A

PTH elevated
Ca elevated
Phosphate low
Urine Ca:creatinine clearance ratio >0.01

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30
Q

What are the clinical features of primary hyperparathyroidism?

A

Asymptomatic if mild
Abdominal pain - pancreatitis, renal colic
Changes to emotional/cognitive state

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31
Q

What is the most common cause of primary hyperparathyroidism?

A

Solitary adenoma

Less common: multifocal disease or parathyroid carcinoma in <1%

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32
Q

What are the lab results in secondary hyperparathyroidism?

A

PTH: elevated
Ca: normal or low
Phosphate: elevated
Vit D: low

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33
Q

What causes secondary hyperparathyroidism?

A

Parathyroid gland hyperplasia as a result of low Ca, usually in setting of chronic renal failure

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34
Q

What are the clinical features of secondary hyperparathyroidism?

A

May have symptoms

May eventually develop bone disease + soft tissue calcification

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35
Q

What are the lab results in tertiary hyperparathyroidism?

A 
PTH elevated
Ca normal or high 
Phosphate normal or low
Vit D normal or low
ALP elevated
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36
Q

What causes tertiary hyperparathyroidism?

A

Due to ongoing hyperplasia of the parathyroid glands after correction of renal disorder

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37
Q

What are the clinical features of tertiary hyperparathyroidism?

A

Metastatic calcification
Bone pain/fractures
Nephrolithiasis
Pancreatitis

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38
Q

How do you distinguish between primary hyperparathyroidism and benign familial hypocalcuric hypercalcaemia?

A

Diagnosis by genetic testing and urine calcium:creatinine clearance ratio <0.01

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39
Q

How is benign familial hypocalcuric hypercalcaemia inherited?

A

Autosomal dominant

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40
Q

What are the indications for surgery in primary hyperparathyroidism?

A 
Elevated serum Ca >1mg/dL above normal 
Hypercalciuria >400mg/day 
Cr clearace <30% normal 
Episode of lifethreatening hypercalcaemia
Nephrolithiasis
Age <50
Neuromuscular symptoms
Reduction in BMD of femoral neck, lumbar spine or distal radius <2.5SD below peak bone mass
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41
Q

How is secondary hyperparathyroidism usually managed?

A

Medical therapy

Surgery only if bone pain, persistent pruritus, soft tissue calcifications

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42
Q

How should you manage tertiary hyperparathyroidism?

A

Wait 12m after Tx as many cases resolve

May req. surgery (e.g. total parathyroidectomy + reimplantation of part of the gland)

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43
Q

What is the pathophysiology of DKA?

A

Uncontrolled lipolysis which results in excess of FFAs that are converted to ketone bodies

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44
Q

What are the most common precipitating factors of DKA?

A

Infection
Missed insulin doses
MI

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45
Q

What are the clinical features of DKA?

A

Abdominal pain
Polyuria, polydipsia, dehydration
Kussmaul respiration
Acetone smelling breath

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46
Q

What is Kussmaul respiration?

A

Deep hyperventilation in an attempt to blow of CO2 in a metabolic acidosis

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47
Q

What is the diagnostic criteria for DKA?

A

Glucose >11mmol or known DM
pH <7.3
Bicarb <15mmol/l
Ketones >3mmol/l or urine ketones ++ on dipstick

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48
Q

How do you manage DKA?

A
  1. Fluid replacement with isotonic saline
  2. Insulin: IV fixed rate 0.1units/kg/h
    (once glucose <15mmol/l 5% dextrose infusion should be started)
  3. Correct of hypokalaemia

CONTINUE LONG ACTING INSULIN, STOP SHORT ACTING INSULIN

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49
Q

What fluids should you use in DKA?

A

0.9% NaCl

with 0.9% NaCl with K depending on K levels

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50
Q

In which patients is slower infusion recommended in DKA and why?

A

Young adults (18-25) as they are at greater risk of cerebral oedema

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51
Q

How much potassium replacement should be given in DKA if the potassium is over 5.5?

A

None

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52
Q

How much potassium replacement should be given in DKA if the potassium is 3.5-5.5?

A

40mmol/l

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53
Q

How much potassium replacement should be given in DKA if the potassium is less than 3.5?

A

Seek senior review as additional potassium must be given

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54
Q

What are complications that can occur due to DKA treatment?

A

Cerebral oedema, hypokalaemia, hypoglycaemia due to incorrect fluid therapy

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55
Q

What are complications of DKA?

A 
Gastric stasis
TE
Arrhythmias due to hypokalaemia/hyperkalaemia
Acute respiratory distress syndrome
AKI
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56
Q

As children are particularly vulnerable to cerebral oedema in DKA what is usually required?

A

1:1 nursing to monitor neuro-obs, headache, irritability, visual disturbance, focal neurology

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57
Q

When will cerebral oedema usually present in DKA?

A

4-12h after starting treatment

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58
Q

What should you do if you suspect cerebral oedema in DKA?

A

CT head, senior review

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59
Q

What is the target HbA1c for a type 2 diabetic on just metformin/diet + lifestyle changes?

A

48mmol/mol

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60
Q

At what HbA1c should you add a second drug to metformin in a type 2 diabetic?

A

> 58mmol/mol

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61
Q

What dietary advice should be given to type 2 diabetics?

A 
High fibre, low glycaemic index sources of carbs
Low fat diary productions, oily fish 
Low sat/trans fats
Avoid energy excess
Target weight loss if overweight 5-10%
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62
Q

How often should HbA1c be check in a type 2 diabetic?

A

3-6m until stable

6 monthly thereafter

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63
Q

What is the HbA1c target for someone on a drug that may cause hypoglycaemia?

A

53mmol/mol

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64
Q

What is the HbA1c target for someone who is already on 1 drug but HbA1c has risen to 58mmol/mol?

A

53mmol/mol

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65
Q

What is the first line drug for the management of T2DM?

A

Metformin

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66
Q

If HbA1c rises to 58mmol/mol on metformin what can you add?

A

SU
Gliptin
Pioglitazone
SGLT-2 inhibitor

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67
Q

If Hba1c rises to or remains above 58mmol/mol on double therapy, what should be offered?

A

→ metformin + gliptin + sulfonylurea
→ metformin + pioglitazone + sulfonylurea
→ metformin + sulfonylurea + SGLT-2 inhibitor
→ metformin + pioglitazone + SGLT-2 inhibitor
→ OR insulin therapy should be considered

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68
Q

If triple therapy if not effective or tolerated or CI then what drug therapy should you consider T2DM?

A

Metformin, SU, GLP1 mimetic (e.g. exenatide) if BMI 35+ if psychological/medical problems assoc. w. obesity or <35 whom insulin therapy would have significant occupational implications or if wt loss would benefit significant co-morbs (+ they reduce Hb1Ac by 11mmol/mol + lose 3% body wt in 6m)

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69
Q

If someone cannot tolerate metformin or it is CI what drugs can you offer them for treatment of T2DM?

A

SU, gliptin, pioglitazone

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70
Q

If someone cannot have metformin and is not able to keep HbA1c <58mmol/mol on single drug therapy what can you offer them?

A

Gliptin + pioglitazone
Gliptin + SU
Pioglitazone + SU

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71
Q

If HbA1c rises to or remains above 58mmol/mol on double therapy (without metformin) what should you consider?

A

Insulin therapy

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72
Q

What drugs should be continued when a T2DM starts taking insulin?

A

Metformin can be continued, review need for others

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73
Q

What insulin should T2DM be started on?

A

Human NPH insulin (isophane), intermediate acting

Taken at bed time or twice daily according to need

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74
Q

What is the first line treatment of HTN in diabetics?

A

ACEi

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75
Q

What is the BP target for diabetics?

A

< 140/80 if no end organ damage

< 130/80 if end organ damage

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76
Q

When should diabetics be given statins?

A

If 10 year CV risk >10%

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77
Q

What is the first line statin for primary prevention in diabetics?

A

Atorvastatin 20mg

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78
Q

What is the first line statin for secondary prevention (e.g. IHD, CV dx, PAD) in diabetics?

A

Atorvastatin 80mg

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79
Q

What can cause an Addisonian crisis?

A

Sepsis/surgery causing an acute exacerbation of insufficiency (e.g. Addisons, hypopituitism)
Adrenal haemorrhage
Steroid withdrawal

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80
Q

What is Water-house friderichsen syndrome?

A

Adrenal haemorrhage

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81
Q

How do you manage an Addisonian crisis?

A

Hydrocortisone 100mg IM/IV
1L normal saline infused over 30-60m w. dextrose if hypoglycaemic
Continue hydrocortisone 6hrly until patient stable
Oral replacement may begin after 24h and be reduced to maintenance over 3-4 days

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82
Q

What are the clinical features of an Addisonian crisis?

A

Low sodium, high potassium, low glucose

Hx of steroid use may be there

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83
Q

What are clinical features of hypercalcaemia?

A

Fatigue, anorexia, thirst, constipation, general aches and pains

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84
Q

How do you diagnose T2DM?

A

Symptoms + fasting glucose of 7mmol/l+ or random glucose/OGTT 11.1mmol/l+

OR asymptomatic + high BG demonstrated on two different occasions

OR HbA1c 48mmol/mol+ (on 2 occasions or symptomatic + 1 reading)

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85
Q

In which conditions may HbA1c not be used for diagnosis?

A 
Haemoglobinopathies
Haemolytic anaemia
Untreated iron deficiency anaemia
Suspected gestational diabetes
Children 
HIV
CKD
People taking meds that may cause hyperglycaemia (e.g. steroids)
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86
Q

Define impaired fasting glucose

A

Fasting glucose 6.1-7mmol/l

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87
Q

Define impaired glucoses tolerance

A

Fasting glucose less than 7mmol/l and OGTT 2h value of 7.8mmol/l-11.1mmol/l

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88
Q

If someone has IFG what should they be offered?

A

Oral glucose tolerance test to rule out diabetes

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89
Q

What is a typical history of primary hyperparathyroidism?

A

Elderly female with an unquenchable thirst

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90
Q

What are the features of primary hyperparathyroidism?

A

Bones, stones, abdominal groans and psychic moans

Polydipsia, polyuria
Peptic ulceration, constipation, pancreatitis
Bone pain/fractures
Renal stones
Depression 
HTN
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91
Q

What is primary hyperparathyroidism associated with?

A

HTN

MEN 1 and 2

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92
Q

What investigations should you do in primary hyperparathyroidism?

A

Ca, phosphate, PTH

Technectium MIBI substraction scan

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93
Q

What is the characteristic X-Ray finding in hyperparathyroidism?

A

Pepperpot skull

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94
Q

What is the definitive management of primary hyperparathyroidism?

A

Total parathyroidectomy

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95
Q

When can patients be offered conservative management of primary hyperparathyroidism?

A

If Ca <0.25mmol/L above upper limit and patient >50 AND no evidence of end organ damage

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96
Q

What drugs may be used for primary hyperparathyroidism in patients unsuitable for surgery?

A

Calcimemtics, e.g. cinacalcet

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97
Q

What findings may you see on hand-Xray of someone with primary hyperparathyroidism?

A

Generalised osteopenia
Erosion of terminal phalangeal tufts
Subperiosteal resorption of bone

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98
Q

How often should HbA1c be monitored in T1DM?

A

3-6mthly

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99
Q

What is the target HbA1c for adults with T1DM?

A

48mmol/mol (but take into account likelihood of complications, hx of hypos, occupation, comorbs etc.)

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100
Q

How often should T1DM monitor their BG?

A

At least 4 times a day - before each meal and before bed

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101
Q

When might more frequent monitoring of bloods be required in T1DM?

A

Frequency of hypos increases, during periods of illness, before, during and after sport, when planning pregnancy, during pregnancy, during breast feeding

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102
Q

What are the BG targets for type 1 diabetics?

A

5-7mmol/l on waking

4-7mmol/l before meals and at other times of the day

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103
Q

What is the treatment regimen of choice in T1DM?

A

Basal bolus regimens + twice daily detemir/once daily glargine/determir

Rapid acting insulin before meals

Consider adding metformin if BMI is 25+

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104
Q

What is Addison’s disease?

A

Autoimmune destruction of the adrenal glands

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105
Q

What is the commonest cause of primary hypoadrenalism in the UK?

A

Addison’s disease

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106
Q

Addison’s disease results in a reduced level of which two hormones?

A

Cortisol

Aldosterone

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107
Q

What are features of Addison’s disease?

A

Lethargy, weakness, nausea, vomiting, wt loss, salt craving
Hyperpigmentation (esp. palmar creases), vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
Hyponatraemia, hyperkalaemia

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108
Q

What are primary causes of hypoadrenalism?

A 
TB
Mets
Meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
HIV
Antiphospholipid syndrome

Exogenous glucocorticoid therapy

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109
Q

What are secondary causes of hypoadrenalism?

A

Pituitary disorders, e.g. tumours, irradiation, infiltration

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110
Q

What electrolyte abnormalities are seen in Addison’s disease?

A

Hyponatraemia

Hyperkalaemia

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111
Q

What is the first line treatment of cerebral mets?

A

High dose dexamethasone to reduce cerebral oedema

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112
Q

For each of the following commonly used steroids comment on their glucocorticoid and mineralocorticoid activity

a. Fludrocortisone
d. Hydrocortisone
c. Prednisolone
d. Dexamethasone, Betamethasone

A

a. V. high mineralocorticoid
b. Bit of glucocorticoid, mostly mineralo
c. Mostly glucocorticoid
d. V. high glucocorticoid

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113
Q

What are SEs of glucocorticoids?

A

Endocrine - impaired glucose regulation, increased appetite/wt gain, hirsutism, hyperlipidaemia
Cushing’s syndrome - moon face, buffalo hump, striae
MSK - osteoporosis, proximal myopathy, AVN of head of femur
Immunosupression - inc. risk of infections/reactivation of TB
Psychiatric - insomnia, mania, depression, psychosis
GI - peptic ulceration, acute pancreatitis
Ophthlamic - glaucoma, cataracts
Supression of growth in children
Intracranial HTN
Neutrophilia

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114
Q

What are SEs of mineralocorticoids?

A

Fluid retention

HTN

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115
Q

What are some really important things to remember about people who are taking steroids long term?

A

Double doses during intercurrent illness
Gradually withdraw corticosteroids if pts have received >40mg pred daily for >1 week, received more than 3 weeks of treatment or recently received repeated courses

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116
Q

What are common adverse events with SUs?

A

Hypoglycaemic episodes

Wt gain

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117
Q

What are rarer AEs seen with SUs?

A

SIADH
Bone marrow suppression
Cholestatic liver damage
Peripheral neuropathy

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118
Q

What is the mechanism of action of glicazide?

A

Releases vesicles of stored within the pancreas containing insulin + c-peptide

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119
Q

What can glicazide OD lead to?

A

Hyperinsulinaemia and raised c-peptide –> hypoglycaemia

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120
Q

What acid-base abnormality may be seen in cushing’s syndrome?

A

Hypokalaemic metabolic alkalosis

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121
Q

Is impaired glucose tolerance seen in Cushing’s?

A

Yes

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122
Q

Ectopic ACTH secretion (e.g. secondary to small cell lung cancer) is characteristically seen with very low levels of what electrolyte?

A

K

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123
Q

What test is used to differentiate between true Cushing’s and pseudocushing’s?

A

Insulin stress test

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124
Q

What two tests are most commonly used to confirm a diagnosis of Cushing’s?

A

Overnight dexamethasone supression test (most sensitive)

24hr urinary free cortisol

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125
Q

What is the first line localisation test for cushing’s?

A

9am and midnight plasma ACTH (and cortisol) levels

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126
Q

If on doing a 9am and midnight plasma ACTH (and cortisol) level you find ACTH is suppressed, what does this mean?

A

The cause is non-ACTH dependent and is likely something like an adrenal adenoma

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127
Q

What other tests may be used to localise the cause of cushing’s syndrome?

A

Low and high dose dexamethasone suppression tests

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128
Q

If cortisol is not suppressed by a low dose dexamethasone test what does this mean?

A

Cushing’s syndrome not due to primary causes, e.g. likely secondary to corticosteroid therapy

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129
Q

If cortisol is not suppressed by low dose but is suppressed by high dose dexamethasone then what does this mean?

A

Cushing’s disease

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130
Q

If cortisol is not suppressed by low or high dose dexamethasone what does this mean?

A

Ectopic ACTH likely

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131
Q

How might you interpret the results of CRH stimulation to localise the cause of cushing’s syndrome?

A

If pituitary source then cortisol rises

If ectopic/adrenal then no change in cortisol

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132
Q

What investigation may be required to distinguish between pituitary and ectopic ACTH secretion?

A

Petrosal sinus sampling of ACTH

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133
Q

How is the dexamethasone suppression test carried out?

A

Give dexamethasone at night (10pm) and measure cortisol level at 9am

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134
Q

What is the low dose dexamethasone test used for?

A

Confirm if they have a normal adrenal axis or to confirm they have cushing’s syndrome

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135
Q

What is the high dose dexamethasone test used for?

A

To see what the cause of cushing’s syndrome is

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136
Q

What does the dexamethasone do?

A

Acts on hypothalamus to suppress CRH
Acts on pituitary to suppress ACTH
–> reduced cortisol
(Normal response)

If you have high cortisol already - low dose dex (1mg) not going to do anything to pituitary/hypothalamus

Giving high dose dex (8mg) - big dose is enough to cause suppression of the pituitary even if there is an adenoma there

In ectopic ACTH production or adrenal adenoma, high dose dex does not cause suppression

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137
Q

What is acromegaly?

A

Condition where there is xs growth hormone secondary to a pituitary adenoma in 95% of cases

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138
Q

What are a minority of acromegaly cases caused by?

A

Ectopic GHRH or GH production by tumours, e.g. pancreatic

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139
Q

What are features of acromegaly?

A

Coarse facial appearance, spade like hands, increase in shoe size
Large tongue, prognathism, interdental spaces
Excessive sweating + oily skin (due to sweat gland hypertrophy)
Features of pituitary tumour (hypopituitism, headaches, bitemporal haemianopia)
Raised prolactin in 1/3rd cases –> galactorrhoea

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140
Q

What complications are associated with acromegaly?

A

HTN
DM
Cardiomyopathy
Colorectal cancer

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141
Q

What two conditions account for 90% of cases of hypercalcaemia?

A

Primary hyperparathyroidism

Malignancy (e.g. due to bone mets, myeloma, PTHrP from squamous cell lung cancer)

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142
Q

What are other causes (apart from the big 2) of hypercalcaemia?

A 
Sarcoidosis
Vit D intoxication 
Acromegaly
Thyrotoxicosis
Milk-alkali syndrome
Drugs - thiazides, calcium containing antacids
Dehydration 
Addison's
Paget's disease of the bone
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143
Q

What is the most common cause of thyrotoxicosis?

A

Grave’s disase

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144
Q

In which group of people is Grave’s disease typically seen?

A

Women aged 30-50 years old

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145
Q

What are features of Grave’s disease?

A

Thyrotoxicosis
Eye signs (30% pts) - exophthalmos, ophthalmoplegia
Pretibial myxoedema
Thyroid acropachy (triad of digital clubbing, soft tissue swelling of hands + feet, periosteal new bone formation)

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146
Q

What autoantibodies are most commonly found in Grave’s disease?

A

TSH receptor stimulating antibodies (90%)

Anti-thyroid peroxidase antibodies (75%)

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147
Q

What mnemonic can be used to grade the severity of Grave’s eye disease?

A 
NOSEPCS - 
No signs/symptoms
Only signs, e.g. upper lid retraction 
Signs and symptoms (incl. soft tissue involvement) 
Proptosis
Extra-ocular muscle involvement
Corneal involvement
Sight loss due to optic nerve involvement
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148
Q

What x-ray findings (of the hands) are associated with hyperparathyroidism?

A

Generalised osteopenia
Erosion of terminal phalyngeal tufts
Sub-periosteal resportion of bones

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149
Q

What are features of hypothyroidism?

A 
Wt gain 
Lethargy 
Cold intolerance
Dry, cold, yellowish skin
Non-pitting oedema 
Dry, coarse, scalp hair, loss of lateral aspect of eyes
Constipation
Menorrhagia
Decreased deep tendon reflexes
CTS
Hoarse voice
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150
Q

What are features of a myxoedemic coma?

A

Hypothermia
Hypotension
Bradycardia
Thin, brittle hair, peritorbital oedema, reduced reflexes

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151
Q

What is a myxoedemic coma?

A

Severe hypothyroidism leading to decreased mental status, hypothermia, and other symptoms related to slowing of function in multiple organ

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152
Q

How many types of MEN are there?

A

MEN I
MEN 2a
MEN 2b

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153
Q

What is MEN?

A

Inherited AD disorder

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154
Q

What are the neoplasias are found in MEN I?

A

3Ps -
Parathyroid - hyperparathyroidism due to parathyroid hyperplasia

Pituitary

Pancreas, e.g. insulinoma, gastrinoma

Also - adrenal + thyroid

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155
Q

What neoplasias are found in MEN IIa?

A

2Ps -
Parathyroid
Phaeochromocytoma

Medullary thyroid cancer

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156
Q

What neoplasias are found in MEN IIb?

A 
1P - 
Phaeochromocytoma
Medullary thyroid cancer
Marfanoid body habitus
Neuromas
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157
Q

MEN Ia is due to a mutation in which gene?

A

MEN1 gene

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158
Q

What is the most common presentation of MEN1?

A

Hypercalcaemia

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159
Q

MEN IIa is due to a mutation in which gene?

A

RET oncogene

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160
Q

MEN IIb is due to a mutation in which gene?

A

RET oncogene

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161
Q

How does subacute (De Quervain’s) thyroiditis tend to present?

A

Hyperthyroidism

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162
Q

What does subacute (De Quervain’s) thyroiditis tend to follow?

A

A viral infection

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163
Q

What are the classical 4 phases of subacute (De Quervain’s) thyroiditis?

A

Phase 1 - 3-6w - hyperthyroidism, painful goitre, raised ESR
Phase 2 - 1-3w - euthryoid
Phase 3 - weeks-months - hypothyroidism
Phase 4 - thyroid structure + function returns to normal

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164
Q

What investigations can be done for suspected subacute (De Quervain’s) thyroiditis and what will they show?

A

Thyroid scintigraphy (globally reduced uptake of iodine-131)

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165
Q

How is subacute (De Quervain’s) thyroiditis managed?

A

Usually self-limiting + does not req. treatment

Thyroid pain may respond to aspirin/ other NSAIDs

In more severe cases steroids can be used (esp if hypothyroidism develops)

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166
Q

What is the mechanism of action of the SGLT-2 inhibitors?

A

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

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167
Q

What are e.g.s of SGLT-2 inhibitors?

A

Canagliflozin, dapagliflozin and empagliflozin

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168
Q

What are AEs of SGLT-2 inhibitors?

A

Urinary + genital infections (secondary to glycosuria)
Normoglycaemia ketoacidosis
Increased risk of lower limb amputation

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169
Q

What is a benefit of taking SGLT-2 inhibitors?

A

Often cause wt loss

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170
Q

What is the first line test for acromegaly?

A

Serum IGF-1 levels with serial GH measurements

OGTT recommended to confirm diagnosis if IGF-1 is raised

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171
Q

What parameter can be used to measure disease progression in acromegaly?

A

Serum IGF-1

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172
Q

What does the OGTT show in normal patient vs acromegalic patients?

A

Normal - GH supressed to <2mu/l with hyperglycaemia

In acromegaly - no suppression of GH

May also demonstrate impaired glucose tolerance which is associated with acromegaly

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173
Q

What investigation may you consider in confirmed acromegaly?

A

MRI pituitary to see pituitary tumour

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174
Q

What is a phaeochromocytoma?

A

Catecholamine secreting tumour

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175
Q

What conditions are phaeochromocytomas commonly associated with?

A

MEN II, neurofibromatosis, vHL syndrome

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176
Q

What is the rule of 10%s for phaeochromocytomas?

A

10% bilateral
10% malignant
10% extra-adrenal (most common site = organ of Zuckerkandl, adjacent to bifurcation of aorta)

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177
Q

What are features of phaeochromocytomas?

A

Episodic HTN, headaches, palpitations, sweating, anxiety

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178
Q

What test is used to diagnose phaeochromocytoma?

A

24hr urinary collection of METAnephrines

CT chest, abdo, pelvis would be done if this came back raised

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179
Q

What is the definitive management of phaeochromocytoma?

A

Surgery

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180
Q

What medications are given to stabilise patients with phaeochromocytomas?

A

Alpha blocker (e.g. phenoxybenzmine) given before a beta blocker e.g. propanolol

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181
Q

What HbA1c is indicative of prediabetes?

A

42-47mmol/mol

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182
Q

What is the management of prediabetes?

A

Encourage to increase physical activity, lose weight and improve diet

Consider metformin at 500mg and arrange repeat HbA1cs at regular intervals

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183
Q

What kind of neuropathy is diabetic neuropathy most commonly?

A

Sensory loss but not motor loss in peripheral neuropathy

Painful diabetic neuropathy a common issue

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184
Q

What is first line treatment of diabetic neuropathy (neuropathic pain)?

A

Amitriptyline, duloxetine, gabapentin or pregabalin

Tramadol as rescue therapy for exacerbations

Topical capsaicin for localised neuropathic pain

Pain management clinics for resistant problems

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185
Q

What conditions can result from GI autonomic diabetic neuropathy?

A

Gastroparesis
Chronic diarrhoea
GORD

186
Q

What are features of gastroparesis?

A

Erratic blood glucose control
Bloating
Vomiting

187
Q

What are management options for gastroparesis?

A

Metoclopramide, domperidone or erythromycin

188
Q

What causes GORD in GI autonomic neuropathy?

A

Decreased LES pressure

189
Q

What karotype is associated with Klinefelter’s syndrome?

A

47 XXY

190
Q

What are features of Klinefelter’s syndrome?

A

Tall
Lack of secondary sexual characteristics
Small firm testes
Infertile
Gynaecomastia (inc. incidence of breast ca)
Elevated gonadotrophin levels but low testosterone

191
Q

How is Klinefelter’s syndrome diagnosed?

A

Karotyping

192
Q

Who does hyperosmolar hyperglcyaemia state tend to occur in?

A

Elderly with T2DM

193
Q

What is hyperosmolar hyperglcyaemia state?

A

Hyperglycaemia resulting in osmotic diuresis, severe dehydration + electrolyte deficiencies

194
Q

What things may complicate hyperosmolar hyperglcyaemia state?

A

MI
Stroke
Peripheral arterial thrombosis

195
Q

Over how long does hyperosmolar hyperglcyaemia state tend to come on?

A

Over many days, so dehydration + electrolyte disturbances often more pronounced than in DKA

196
Q

What is the pathophysiology of hyperosmolar hyperglcyaemia state?

A

Hyperglycaemia –> osmotic diuresis + loss of Na and K –> hyperviscosity of blood

Despite this, pt may not look as dehydrated as they are as hypertonicity –> preservation of intravascular volume

197
Q

What are clinical features of hyperosmolar hyperglcyaemia state?

A

Fatigue, lethargy, nausea, vomiting
Altered level of consciousness, headaches, papilloedema, weakness
Hyperviscosity
Dehydration, hypotension, tachcardia

198
Q

What 3 criteria are useful in helping to distinguish HHS from DKA?

A 
Hypovolaemia
Marked hyperglycaemia (>30mmol/L) without significant ketonaemia/acidosis
Significantly raised serum osmolarity (>320mosmol/kg)
199
Q

What are the aims of management of HHS?

A

Normalise osmolality
Replace fluid + electrolyte losses
Normalise BG

200
Q

What is the first line fluid used in HHS?

A

IV 0.9% sodium chloride solution

if serum osmolality not decreasing with this switch to 0.45% NaCl

201
Q

Should insulin be used in the treatment of HHS?

A

NOOOOOOO - may cause CV collapse as water moves out of intravascular space –> decline in IV volume

Only start insulin if significant ketonaemia demonstrated as this may indicate mixed DKA/HHS picture

202
Q

What are the two main factors responsible for diabetic foot disease?

A

Neuropathy - reduced protective sensation, Charcot’s arthropathy, dry skin
Peripheral arterial disease (DM is a RF for macro and microvascular ischaemia)

203
Q

How does diabetic foot disease present?

A

Neuropathy - loss of sensation
Ischaemia - absent foot pulse, reduced ABPI, intermittent claudication
Complications - calluses, ulceration, Charcot’s arthropathy, cellulitis, OM, gangrene

204
Q

How often should diabetic patients have their feet screened?

A

Yearly

205
Q

How is screening for neuropathy in the feet done?

A

10g monofilament on various parts of sole of foot

206
Q

What diabetics are at low risk of diabetic foot issues?

A

No risk factors except callus alone

207
Q

What diabetics are at moderate risk of diabetic foot issues?

A

Deformity or neuropathy or non-critical limb ischaemia

208
Q

What diabetics are at high risk of diabetic foot issues?

A

Prev ulceration/gangrene
On RRT
Neuropathy + non-critical limb ischaemia together or neuropathy + callus/deformity
Non-critical limb ischaemia + callus/deformity

209
Q

All patients at moderate/high risk of diabetic foot problems should be followed up by who?

A

Local diabetic foot centre

210
Q

What are treatment options for Grave’s disease?

A 
Antithyroid drugs
Block + replace regimens
Radioiodine treatment 
Surgery 
Propanolol for symptom control
211
Q

What is the most commonly used anti-thyroid drug?

A

Carbimazole (started at 40mg and titrated upwards)

212
Q

How long is a course of carbimazole usually continued for?

A

12-18 months

213
Q

What does block + replace therapy for Grave’s disease consist of?

A

Carbimazole started at 40mg, thyroxine added when patient is euthyroid

214
Q

What is a major complication of carbimazole therapy?

A

Agranulocytosis

215
Q

What are CIs to the use of radioiodine?

A

Pregnancy (avoid for 4-6 m after treatment)
Age <16
Thyroid eye disease (relative CI as may worsen condition)

216
Q

Majority of patients will require what after radioiodine therapy for the treatment of Grave’s disease?

A

Thyroxine

217
Q

Where is PTH secreted from?

A

Chief cells in the parathyroid glands

218
Q

What is the role of PTH?

A

Calcium homeostasis

219
Q

How does calcium enter the body?

A

Intestines

220
Q

How does calcium leave the body?

A

In urine + faeces

221
Q

What is the main reservoir of calcium in the body?

A

In bone

222
Q

What are the three forms that calcium exists as in the bone?

A

Free calcium
Bound to albumin
Complexed with anions

223
Q

What form of calcium is physiologically active?

A

Only free calcium

224
Q

What is PTH generated in response to?

A

Low calcium levels in the blood

225
Q

Which two organ/tissues does the PTH mainly act on?

A

Bone

Kidney

226
Q

What is the effect of PTH on bone?

A

Increases osteoclastic activity (increased boen resportion –> Ca and phosp released into bloodstream)

227
Q

What is the effect of PTH on the kidney?

A

Increases hydroxylation + activation of vitamin D in PCTs

Increases calcium reabsorption from DCT + increase phosphate excretion

228
Q

What kind of hormone is activated vitamin D?

A

Steroid hormone

229
Q

What is the action of vitamin D?

A

Increases dietary calcium absorption from intestine by increasing expression of calcium-binding hormone

230
Q

How are the levels of PTH regulated in the body?

A

Negative feedback loop

231
Q

What is primary hyperparathyroidism?

A

A condition where the parathyroids are overactive (usually due to dysplasia/adenoma/malignancy)

232
Q

What are the symptoms of primary hyperparathyroidism?

A

Hypercalcaemia (renal calculi, constipation, polyuria, ab pain, low mood)

233
Q

What a common treatment of primary hyperparathyroidism?

A

Surgical removal of the glands

234
Q

What is PTHrP?

A

A polypeptide which is similar in structure to PTH that is secreted from cancer cells causing hypercalcaemia

235
Q

What is the only difference in the functional capabilities of PTHrP when compared to PTH?

A

It is unable to activate vitamin D

236
Q

What cancer is PTHrP mostly associated with?

A

Squamous cell bronchial carcinoma

237
Q

What is an adrenal adenoma causing primary aldosteronism known as?

A

Conn’s syndrome

238
Q

What are causes of primary hyperaldosteronism?

A

Conn’s syndrome
Bilateral idiopathic adrenal hyperplasia
Adrenal carcinoma (rare)

239
Q

What are features of primary hyperaldosteronism?

A

HTN
Hypokalaemia (e.g. muscle weakness)
Hypernatraemia
Alkalosis

240
Q

What is the first line investigation for suspected primary hyperaldosteronism?

A

Plasma aldosterone/renin ratio

(Which should show high aldosterone levels alongside low renin levels - negative feedback due to Na retention from aldosterone)

241
Q

After a plasma aldosterone/renin ratio what test should be done in suspected primary hyperaldosteronism?

A

High resolution CT + adrenal vein sampling to differentiate between unilateral + bilateral sources of aldosterone excess

242
Q

What is the management of an adrenal adenoma?

A

Surgery

243
Q

What is the management of bilateral adrenocortical hyperplasia?

A

Aldosterone antagonist, e.g. spirnolactone

244
Q

What is the pathophysiology of thyroid eye disease?

A

Autoimmune response against an autoantigen (possibly the TSH receptor –> retro-orbital inflammation –> glycosaminoglycan + collagen deposition in muscles)

245
Q

What is the most important modifiable risk factor for the development of thyroid eye disease?

A

Smoking

246
Q

What may help reduce the risk that someone who has thyroid eye disease that undergoes radioiodine treatment will develop worsening eye disease?

A

Prednisolone

247
Q

What are features of thyroid eye disease?

A 
Exophthalmos 
Conjunctival oedema
Optic disc swelling
Ophthalmoplegia
Inability to close eyelids --> sore, dry eyes (at risk of keratopathy)
248
Q

What is involved in the management of thyroid eye disease?

A

Topical lubricants to prevent corneal inflammation
Steroids
Radiotherapy
surgery

249
Q

For those with established thyroid eye disease, what signs/symptoms indicate need for urgent review by an ophthalmologist?

A

Unexplained deterioration in vision
Awareness of change in intensity/quality of colour vision in 1/both eyes
Hx of eye suddenly popping out (globe subluxation)
Obvious corneal opacity
Cornea still visible when eyelids close
Disc swelling

250
Q

Why do patients with addison’s disease sometimes get hyperpigmentation in skin creases, buccal mucosa + scars?

A

ACTH has the same precursor molecule as melanocyte stimulating hormone so overproduction of ACTH has the same SEs as raising MSH levels

251
Q

What is the definitive investigation in Addison’s disease?

A

ACTH stimulation test (short Synacthen test)

252
Q

How is the short Synacthen test carried out?

A

Plasma cortisol is measured before and 30 minutes after giving Synacthen 250ug IM

253
Q

What autoantibodies may be found in addison’s disease?

A

Anti-21 hydroxylase

254
Q

If a short Synacthen test is not available (e.g. in primary care) that investigation should you consider to help diagnose Addison’s?

A

9am serum cortisol
>500nmol/l makes Addison’s very unlikely
<100nmol/l is definitely abnormal
100-500nmol.l should prompt a ACTH stimulation test to be performed

255
Q

What electrolyte abnormalities are seen in Addison’s disease?

A

Hyperkalaemia
Hyponatraemia
Hypoglycaemia
Metabolic acidosis

256
Q

Addison’s disease leads to an insufficiency of what hormones?

A

All of those produced by the adrenal cortex (mineralocorticoids (e.g. aldosterone), glucocorticoids (e.g. cortisol), androgens)

257
Q

What is the function of the mineralocorticoids?

A

Retention of sodium and water –> increased BP

258
Q

What is the function corticosteroids?

A 
Immunosupression, anti-inflammatory
Weight gain 
Insulin resistance
Skin thinning
Increased osteoclastic activity in bones 
Cortisol increases BP
259
Q

What is the most common cause of Addison’s disease?

A

Autoantibodies directed at adrenal cortical cells + 21-hydroxylase –> damage to adrenals –> reduced levels of adrenal hormones

260
Q

To have a HGV license, what criteria must diabetics on insulin/other hypoglycaemics meet?

A

No severe hypo in last 12m
Pt has full hypoglycaemic awareness
Adequate control of condition w. regular BG monitoring
Driver demonstrates understanding of risks of hypos
No debarring complications of DM

261
Q

What form do T1 diabetics have to fill out to get a group 2 (HGV) license?

A

VDIAB1I form

262
Q

What are the rules for diabetics on insulin having a group 1 license?

A

Hypoglycaemic awareness
Not >1 episode of hypo req. assistance from another in the last 12m
No visual impairment

263
Q

What is congenital adrenal hyperplasia?

A

Group of AR conditions affecting adrenal steroid biosynthesis

264
Q

Abnormally high levels of what hormone are found in congenital adrenal hyperplasia? What is the consequence of this?

A

ACTH due to low cortisol levels

ACTH stimulates production of adrenal androgens that may virulize a female infant

265
Q

What are the causes of congenital adrenal hyperplasia?

A

21-hydroxylase deficiency (90%)
11-beta hydroxylase deficiency
17-hydroxylase deficiency

(good video on PM notes about this!)

266
Q

What is the 21-hydroxylase enzyme responsible for?

A

Biosynthesis of aldosterone + cortisol

267
Q

What is Hashimoto’s thyroiditis?

A

Autoimmune disorder of the thyroid gland, typically associated with hypothyroidism

NB may be transient thyrotoxicosis in acute phase

268
Q

What are the features of Hashimoto’s thyroiditis?

A

Hypothyroidism
Firm, non-tender goitre
Anti-thyroid peroxidase and anti-thyroglobulin (Tg) antibodies

269
Q

What things are associated with Hashimoto’s thyroiditis?

A

Autoimmune conditions - coeliac, T1DM, vitiligo

MALT lymphoma

270
Q

Gastroparesis occurs in diabetics due to neuropathy of what nerve?

A

Vagus

271
Q

What is the mechanism of action of thiazolidinediones?

A

Agonists to the PPAR-gamma receptor (a receptor thought to control adipocyte differentiate + function) + reduce peripheral insulin resistance

272
Q

What AEs are associated with thiazolidinediones?

A 
Wt gain 
Liver impairment - monitor LFTs
Fluid retention 
Increased fracture risk 
Bladder cancer (pioglitazone)
273
Q

When are the use of thiazolidinediones CI?

A

Heart failure (due to fluid retention)

274
Q

What is DM?

A

Chronic condition characterised by abnormally raised levels of blood glucose

275
Q

What is the main aim of treating DM?

A

Reducing incidence of macrovascular (IHD, stroke) + microvascular (eye, nerve, kidney damage) complications

276
Q

What is type 1 DM?

A

Autoimmune disorder where the insulin producing beta cells of the islets of Langerhans are destroyed by the immune system –> absolute insulin deficiency –> raised BG

277
Q

How do T1DM tend to present?

A

In DKA or very unwell

278
Q

What is T2DM due to?

A

Relative deficiency of insulin due to excess of adipose tissue

279
Q

Define prediabetes

A

Patients who don’t meet the criteria for a formal diagnosis of T2DM but are likely to develop it over the next few years

280
Q

What is maturity onset diabetes of the young?

A

Group of inherited genetic disorders affecting insulin production
Happens in younger patients and tends to cause symptoms similar to T2DM, i.e. asymptomatic hyperglycaemia with progression to DKA

281
Q

What is latent autoimmune diabetes of adults?

A

Autoimmune related diabetes presenting in later life (often misdiagnosed)

282
Q

What other things may cause diabetes?

A

Chronic pancreatitis
Haemachromatosis

Drugs may also impair BG levels, e.g. corticosteroids

283
Q

What are the features of T1DM?

A

Wt loss
Polydipsia
Polyuria
May present with DKA

284
Q

What are features of DKA?

A

Ab pain
Vomiting
Reduced conscious level

285
Q

How does T2DM tend to present?

A

Often incidental finding
Polydipsia
Polyuria

286
Q

What causes polydipsia/polyuria in diabetes?

A

Water being dragged out of the body due to osmotic effects of excess glucose being excreted in the urine

287
Q

What are the four main ways to check blood glucose?

A

Finger prick with bedside glucose monitor
One off blood glucose (fasting/not fasting)
HbA1c
Glucose tolerance test

288
Q

What does HbA1c measure?

A

Amount of glycosylated Hb + represents BG average over past 2-3 months

289
Q

What does a glucose tolerance test involve?

A

Fasting glucose taken after which 75g glucose taken and BG measured 2 hours later

290
Q

How is diabetes diagnosed?

A

If symptomatic
Fasting glucose >=7mmol/l
Random glucose/OGTT >=11.1

If asymptomatic above criteria demonstrated on two separate occasions

291
Q

What HbA1c is diagnostic of diabetes?

A

6.5% (48mmol/mol)

292
Q

In a patient without symptoms but an HbA1c >=48, what should be done?

A

Repeat to confirm diagnosis

293
Q

What are SEs of insulin therapy?

A

Hypoglycaemia
Wt gain
Lipodystrophy

294
Q

What is the mechanism of action of metformin?

A

Increases insulin sensitivity

Decreases hepatic gluconeogenesis

295
Q

What are common SEs of metformin?

A

GI upset

Lactic acidosis

296
Q

When is metformin CI?

A

eGFR <30ml/min

297
Q

What is the mechanism of action of SUs?

A

Stimulate pancreatic beta cells to secrete insulin

298
Q

What are SEs of SUs?

A

Hypoglycaemia
Wt gain
Hyponatraemia

299
Q

Give two examples of SUs

A

Glicazide

Glimepiride

300
Q

What is the only available thiazolidinedione currently?

A

Pioglitazone

301
Q

What is the mechanism of action of DPP-4 inhibitors (-gliptins)?

A

Increases incretin levels which inhibit glucagon secretion

302
Q

What is an AE of DPP-4 inhibitors (-gliptins)?

A

Risk of pancreatitis

303
Q

What is the mechanism of action of SGLT-2 inhibitors (-gliflozins)?

A

Inhibits resportion of glucose in the kidney

304
Q

What are AEs of SGLT-2 inhibitors (-gliflozins)?

A

UTIs

305
Q

What is a benefit of taking SGLT-2 inhibitors (-gliflozins)?

A

Generally cause wt loss

306
Q

What is the mechanism of action of GLP-1 agonists (-tides)?

A

Incretin mimetics which inhibit glucagon secretion

307
Q

What are SEs of GLP-1 agonists (-tides)?

A

Nausea, vomiting, pancreatitis

308
Q

What is a benefit of GLP-1 agonists (-tides)?

A

Typically cause wt loss

309
Q

What is the only T2 diabetic drug that needs to be taken s/c instead of orally?

A

GLP-1 agonists (-tides)

310
Q

Define MODY

A

Onset of type 2 DM in someone <25

311
Q

How is MODY inherited?

A

AD

312
Q

How many types of MODY have been identified?

A

6

313
Q

A defect in what gene causes MODY 3?

A

HNF-1 alpha gene

314
Q

Having MODY 3 is associated with increased risk of what?

A

Hepatocellular carcinoma

315
Q

A defect in what gene causes MODY 2?

A

Glucokinase gene

316
Q

What is the most common type of MODY?

A

MODY 3

317
Q

A defect in what gene causes MODY 5?

A

HNF-1 alpha gene

318
Q

As well as diabetes what do those with MODY 5 commonly get?

A

Liver and renal cysts

319
Q

How are those with MODY usually treated?

A

SUs

Insulin not usually req.

320
Q

What is glucagon-like peptide?

A

A hormone released by the small intestine in response to an oral glucose load

321
Q

What is the incretin effect?

A

An oral glucose load results in a greater release of insulin that if the same load was given IV

322
Q

What hormone largely mediates the incretin effect?

A

GLP-1 (known to be decreased in T2DM)

323
Q

Give an e.g. of a GLP-1 mimetic

A

Exenatide

324
Q

How is exenatide taken?

A

SC injection 60 minutes before morning and evening meals

325
Q

What drugs can GLP-1 be taken with?

A

Metformin SUs

326
Q

When should you consider adding exenatide to metformin and a SU?

A

BMI >35 in people of european descent
BMI <35 + insulin unacceptable due to occupation or wt loss would benefit co-morbs

Pts must have achieved 11mmol/mol reduction in HbA1c + 3% wt loss after 6 months to justify continuing treatment

327
Q

How are DDP-4 inhibitors taken?

A

Orally

328
Q

Give e.g.s of DDP-4 inhibitors

A

Vildagliptin, sitagliptin

329
Q

When might you prescrbe a DDP-4 inhibitor?

A

If a thiazolidinedione would cause further wt gain or significant problems is CI or the person had a poor response to it

330
Q

What is a rare neuropsychiatric complication of steroids?

A

Psychosis

331
Q

What is toxic multinodular goitre?

A

A thyroid gland that contains a number of autologously functioning thyroid nodules causing hyperthyroidism

332
Q

What does nuclear scintigraphy demonstrate in toxic multinodular goitre?

A

Patchy uptale

333
Q

What is the treatment of choice for toxic multinodular goitre?

A

Radioiodine therapy

334
Q

What is gynaecomastia?

A

Abnormal amount of breast tissue in males usually caused by an increase in oestrogen:androgen ratio

335
Q

What are causes of gynaecomastia?

A 
Physiological - in puberty 
Syndromes with androgen deficiency, e.g. Kallman's, Klinefelter's
Testicular failure, e.g. mumps
Liver dsiease
Testicular cancer, e.g. seminoma secreting hCG
Ectopic tumour secretion 
Hyperthyroidism
Haemodialysis
Drugs
336
Q

What drugs can cause gynaecomastia?

A 
Spirnolactone (most common)
Cimetidine
Digoxin
Cannabis
Finasteride
Gonadorelin analogues, e.g. Goserelin, buserelin
Oestrogen, anabolic steroids
337
Q

What are causes of primary hypothyroidism?

A 
Hashimoto's
De Quervian's
Riedel thyroiditis
After thyroidectomy/radioiodine treatment
Drugs, e.g. lithium, amiodarone, ATDs
Dietary iodine deficiency
338
Q

What causes secondary hypothyroidism?

A

Pituitary failure

339
Q

What conditions are associated with secondary hypothyroidism?

A

Down’s
Turner’s
Coeliac disease

340
Q

What should you start the insulin infusion rate at in DKA?

A

0.1 unit/kg/hour

341
Q

Why can hypomagnesaemia lead to hypocalcaemia?

A

Mg req for PTH secretion and action on target tissues so low mg –> patients being unresponsive to ca and vit D supplements

342
Q

Where is mg stored in the body?

A

Half in bone

Rest in muscle, soft tissue, extracellular fluid

343
Q

What hormones affect renal handling of mg?

A

PTH, aldosterone

344
Q

What are causes of hypoglycaemia?

A 
Insulinoma 
Self administration of insulin/SUs
Liver failure
Addison's
Alcohol

in children - nesidioblastosis (beta cell hyperplasia)

345
Q

What is the physiological normal response to hypoglycaemia?

A

Hormonal –> decrease insulin secretion, increase glucagon secretion, GH and cortisol released later

Sympathoadrenal response –> increased catecholamine mediated + ACh mediated neurotransmission in peripheral ANS and CNS

346
Q

How is hypoglycaemia in impaired GCS managed?

A

100ml 20% glucose IV stat or IM glucagon

347
Q

What are causes of thyrotoxicosis?

A 
Grave's disease
Toxic nodular goitre
Acute phase De Quervians
Acute phase post-partum thyroiditis
Acute phase hashimoto's
Amiodarone therapy
348
Q

What is HbA1c dependent on?

A

RBC lifespan

Average BG concentration

349
Q

What things may cause HbA1c to be lower than expected (due to reduced RBC lifespan)?

A

Sickle cell anaemia
G6PD deficiency
Hereditary spherocytosis

350
Q

What things may cause HbA1c to be higher than expected (due to increased RBC lifespan)?

A

Vit B12/folate deficiency
Fe deficient anaemia
Splenectomy

351
Q

Patients with addison’s disease are given ____ and ____ replacement

A

Mineralocorticoid and glucocorticoid

352
Q

What is the typical drugs taken by someone with Addison’s?

A

Hydrocortisone (20-30mg per day)

Fludrocortisone

353
Q

What is essential advice to give to a patient with Addison’s about taking their medication?

A

Do not miss a dose of glucocorticoids!!

In intercurrent illness double hydrocortisone dose, fludrocortisone remains at the same dose

354
Q

In relation to treating hypothyroidism - the initial starting dose of levothyroxine should be lowered in which groups?

A

Elderly (>50)
Those with IHD
Those with severe hypothyroidism

355
Q

What is the usual starting dose of levothyroxine?

A

50-100mcg od

356
Q

Following a change in thyroxine dose, when should TFTs be measured?

A

8-12 weeks

357
Q

What is the primary therapeutic goal when treating hypothyroidism?

A

Normalising the TSH level (0.5-2.5)

358
Q

Does pregnancy impact what dose of thyroxine a women should be on?

A

Yes - increase (by 25-50mcg) during pregnancy due to increased demands of pregnancy

359
Q

What are SEs of thyroxine therapy?

A

Hyperthyroidism due to overtreatment
Reduced BMD
Worsening of angina
AF

360
Q

What DDIs with thyroxine are important to be aware of?

A

Iron, calcium carbonate - absorption of levothyroxine reduced so give at least 4h apart

361
Q

What is sick euthyroid syndrome now referred to as?

A

Non-thyroidal illness

362
Q

What do the TFTs look like in sick euthyroid syndrome?

A

Often said everything is low (TSH low, thyroxine low, T3 is low)
But in most cases TSH is normal

363
Q

How is sick euthyroid syndrome managed?

A

Changes reversible upon recovery from systemic illness + so no Rx usually req.

364
Q

What are the NICE recommended GH therapy indications?

A

Proven GH deficiency
Turner’s syndrome
Prader-Willi syndrome
Chronic renal insufficiency before puberty

365
Q

How is GH therapy administered?

A

Subcut

366
Q

When should GH therapy be discontinued?

A

If there is poor response in the first year

367
Q

What are AEs of GH therapy?

A

Headaches
Benign intracranial hypertension
Fluid retention

368
Q

What is the initial management of hypercalcaemia?

A

Rehydration with normal saline (usually 3-4L/day)

Then bisphosphonates can be used

369
Q

What are other options for the management of hypercalcaemia (apart from bisphosphonates)?

A

Calcitonin (works quicker than bisphosphonates)

Steroids in sarcoidosis

370
Q

What are clinical features of hypercalcaemia?

A 
Bones - bone pain
Stones - renal stones
Groans - ab pain, nausea, vomiting
Thrones - polyuria
Psychiatric undertones (confusion, cognitive dysfunction, depression, anxiety, insomnia, coma)
Corneal calcification 
HTN
371
Q

What is typically found on ECG in hypercalcaemia?

A

Shortened QT interval

372
Q

What is the interaction between dopamine and prolactin?

A

Dopamine is the primary prolactin releasing inhibitory factor

373
Q

What are features of hyperprolactinaemia in men?

A

Impotence
Loss of libido
Galactorrhoea

374
Q

What are the features of hyperprolactinaemia in women?

A

Amenorrhoea

Galactorrhoea

375
Q

What are causes of raised prolactin?

A 
Prolactinoma
Pregnancy
Oestrogen
Physiological - stress, exercise, sleep
Acromegaly
PCOS
Primary hypothyroidism (due to thyrotrophin releasing hormone stimulating prolactin release)
376
Q

What are drug causes of raised prolactin?

A

Metoclopramide, domperidone
Phenothiazines
Haloperidol
SSRIs, opioids (rare)

377
Q

What are ACTH dependent causes of Cushing’s syndrome?

A

Cushing’s disease (primary tumour secreting ACTH –> adrenal hyperplasia)
Ectopic ACTH production, e.g. small cell lung cancer

378
Q

What are ACTH independent causes of Cushing’s?

A 
Steroids
Adrenal adenoma
Adrenal carcinoma
Carney complex (syndrome incl. cardiac myxoma)
Micronodular adrenal dysplasia
379
Q

What is pseudocushing’s?

A

A cushing’s mimic (causes false +ve dexamethasone test or 24hr urinary free cortisol)

380
Q

What is pseudocushing’s often due to?

A

Alcohol excess or severe depression

381
Q

What test can be used to distinguish between Cushing’s and pseudocushing’s?

A

Insulin stress test

382
Q

It is estimated than 1 in how many adults in the UK have prediabetes?

A

7

383
Q

How do you identify patients with prediabetes?

A

NICE recommend using a validated computer based risk assessment tool for all >40, people of South Asian and Chinese descent 25-39 or adults with conditions that predispose to diabetes

If at risk –> blood sample

Fasting glucose 6.1-6.9mmol/l or HbA1c of 42-47 indicates high risk

384
Q

What HbA1c and fasting glucose is considered normal?

A

HbA1c 41 or less

Fasting BG <=6

385
Q

What is involved in the management of prediabetes?

A

Wt loss, increased exercise, change in diet
Yearly follow up with blood tests
Consider metformin in those who look as though they are progressing to having T2DM despite lifestyle changes

386
Q

What are the two main types of IGR?

A

IFG - impaired fasting glucose - due to hepatic insulin resistance

IGT - impaired glucose tolerance - due to muscle insulin resistance

387
Q

Define IFG

A

Fasting BG 6.0-6.9mmol/l

388
Q

Define IGT

A

Fasting plasma glucose <7 and OGTT 2h value greater than 7.8 but less than 11.1

389
Q

What test should be offered to those with IFG?

A

OGTT

390
Q

What are treatments for galactorrhoea?

A

Dopamine agonists, e.g. bromocriptine

391
Q

What is a pituitary adenoma?

A

Benign tumour of the pituitary gland

392
Q

How are pituitary adeomas classified?

A

Size: <1cm microadenoma, >1cm macroadenoma

Hormonal status: secretory/functioning vs non-secretory/functioning

393
Q

What is the most common type of pituitary adenoma?

A

Prolactinomas

then non-secreting adenomas, then GH secreting then ACTH secreting

394
Q

How do pituitary adenomas cause symptoms?

A

Hormone excess, e.g. Cushing’s dx –> xs ACTH, acromegaly –> xs GH, prolactinoma –> xs prolactin)

Depletion of hormone due to compression of normal functioning pituitary (non-functioning tumours often present with hypothyroidism)

Stretching of dura within/around pituitary fossa –> headaches

Compression of optic chiasm –> bitemporal hemianopia

395
Q

What investigations should be done for a suspected pituitary adenoma?

A

Pituitary blood profile incl. GH, prolactin, ACTH, FH, LSH, TFTs
Formal visual field testing
MRI brain with contrast

396
Q

What are differential diagnoses for pituitary adenoma?

A 
Pituitary hyperplasia
Craniopharyngioma
Meningioma
Brain metastases
Lymphoma
Hypophysitis
Vascular malformation (e.g. aneurysm)
397
Q

What does treatment of a pituitary adenoma involve?

A

Hormonal therapy
Surgery (e.g. transsphenoidal transnasal hypophysectomy), e.g. if progression in size
Radiotherapy

398
Q

What is Nelson’s syndrome?

A

Rapid enlargement of pituitary corticotroph adenoma that occurs following bilateral adrenalectomy for Cushing’s syndrome (due to lack of negative feedback)

399
Q

What key messages should be given to diabetics about sick day rules?

A

Increase monitoring of BG (4hrly or more)
Drink 3L+/day
Aware of DKA
Continue oral hypoglycaemics (as cortisol elevates BG even if they are not eating)
Do NOT stop insulin due to DKA risk
Stop metformin if becoming dehydrated due to risk of renal dysfunction

400
Q

What is the first line treatment for acromegaly?

A

Trans-sphenoidal surgery

401
Q

What drugs may be used in the management of acromegaly?

A

Dopamine agonists, e.g. bromocriptine
Somatostatin analogues, e.g. octreotide (may be used as adjunct to surgery; most effective)
Pegvisomant

402
Q

How do somatostatin analogues work in the management of acromegaly?

A

Directly inhibit GH release

403
Q

What is pegvisomant?

A

GH receptor agonist (prevents dimerization of GH receptor)

404
Q

How is pegvisomant administered?

A

SC

405
Q

What treatment is sometimes used for frailer patients with acromegaly? Or used in surgical/medical treatment has failed?

A

External irradiation

406
Q

What is thyroid storm?

A

Rare, but lifethreatening complication of thyrotoxicosis

407
Q

Who is thyroid storm more typically seen in?

A

Patients with established thyrotoxcisosi

408
Q

What events may precipitate thyroid storm?

A

Thyroid/non-thyroidal surgery
Trauma
Infection
Acute iodine load, e.g. CT contrast media

409
Q

What clinical features are associated with thyroid storm?

A 
Fever >38.5C
Tachycardia
Confusion + agitation 
NV
HTN
Heart failure
Abnormal LFTs, jaundice
410
Q

How is thyroid storm managed?

A

Symptomatic treatment, e.g. paracetamol
Treat underlying precipitating event
Beta blockers - IV propanolol
ATDs, e.g. methimazole or prophylthiouracil
Lugol’s iodine
Dexamethasone (blocks conversion of T4 to T3)

411
Q

What is the action of insulin?

A

Causes cells in liver, skeletal muscles, fat tissue to absorb glucose fro the blood

412
Q

How is insulin synthesised?

A

Pro-insulin is formed by rough ER in the beta cells
Pro insulin cleaved to form insulin + c peptide
Insulin stored in secretory granules + released in response to Ca

413
Q

What are the functions of insulin?

A 
Secreted in response to hyperglycaemia
Glucose utilisation + glycogen synthesis
Inhibits lipolysis
Reduces muscle protein loss
Increases cellular uptake of K (stimulates NaK ATPase)
414
Q

What is Whipple’s triad of features of an insulinoma?

A

Symptoms + signs of hypoglycaemia
Plasma glucose <2.5mmol/L
Reversibility of symptoms on administration of glucose

415
Q

What test can be used to help identify an insulinoma?

A

Exogenous insulin injection checking c peptide levels before + after as c-peptide production does not fall on exogenous insulin injection in those with insulinoma

416
Q

Where does a neuroblastoma arise from?

A

Neural crest tissue of adrenal medulla + sympathetic NS

417
Q

What are features of a neuroblastoma?

A 
Abdominal mass
Pallor, wt loss
Bone pain, limp
Hepatomegaly
Paraplegia
Proptosis
418
Q

What investigation findings will you see in neuroblastoma?

A

Raised urinary vanillylmandelic acid (VMA) + homovanillic acid (HVA) levels
calcification on abdominal x-ray
Biopsy confirms

419
Q

Why should all children with palpable abdominal masses or unexplained enlarged abdominal organs be referred very urgently to be assessed?

A

To ensure they do not have a Wilm’s tumour or neuroblastoma

420
Q

What are causes for hypoglycaemia in a non-diabetic patient?

A 
EXPLAIN - 
Exogenous drugs, e.g. alcohol, aspirin poisoning, pentamidine, quinine sulphate, ACE inhibitors
Pituitary insufficiency
Liver failure
Addison's disease
Islet cell tumours, e.g. insulinomas
Non-pancreatic neoplasms
421
Q

What are common hypo symptoms?

A 
Sweating
Anxiety
Hunger
Tremor
Palpitations
Dizziness
Confusion
Drowsiness
Visual disturbance
Seizures
422
Q

Define hypoglycaemia

A

BG <3 (some say 4)

423
Q

What are features of an addisonian crisis?

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia

424
Q

How do SUs work?

A

Increase pancreatic insulin secretion by binding to ATP dependent K channel on the cell membrane of pancreatic beta cells

425
Q

What are common AEs of SUs?

A

Hypos

Wt gain

426
Q

What are features of thyrotoxicosis?

A 
Wt loss
Manic restlessness
Heat intolerance
Palpitations, tachycardia
Increased sweating
Pretibial myxoedema
Thyroid acropachy - clubbing
Diarrhoea
Oligomenorrhoea
Anxiety
Tremor

High output cardiac failure may develop in elderly patients, a reversible cardiomyopathy can rarely develop

427
Q

What is pretibial myxoedema?

A

Erythematous, oedematous lesions above lateral malleoli

428
Q

What is the significance of subclinical hypothyroidism?

A

Risk of progression to hypothyroidism

Increased risk of presence of thyroid autoantibodies

429
Q

How is subclinical hypothyroidism managed?

A

TSH between 4-10mU/L + free thyroine in normal range –>
<65 + symptomatic - trial levothyroxine, if no improvement stop it
In older people watch and wait
In asymptomatic patients - observe + repeat TFTs in 6 months

TSH >10mU/L + free thyroxine normal - start treatment with levothyroxine if <=70
Watch and wait in older people

430
Q

What is the mechanism of action of carbimazole?

A

Blocks thyroid peroxidase from coupling + iodinating tyrosine residues on thyroglobulin –> reduced TH production

431
Q

What AEs are associated with carbimazole?

A

Agranulocytosis (counsel re if develop sore throat/fever FBC must be done to check neutrophil count)
Crosses placenta, use in low doses during pregnancy

432
Q

What is the step wise approach to treating obesity?

A

Conservative - diet, exercise
Medical
Surgical

433
Q

What drug can be used in the management of obesity?

A

Orlistat

434
Q

What is the mechanism of action of orlistat?

A

Pancreatic lipase inhibitor

435
Q

What AEs are associated with orlistat?

A

Faecal urgency/incontinence + flatulence

436
Q

Who should be prescribed orlistat?

A

BMI 28+ + associated RFs
BMI 30+
Continued wt loss, e.g. 5% at 3 months

437
Q

How long is orlistat generally used for?

A

<1 year

438
Q

Which hormones are increased during the stress response?

A 
GH
Cortisol
Renin
ACTH 
Aldosterone
Prolactin
ADH
Glucagon
439
Q

Which hormones are decreased during the stress response?

A

Insulin
Testosterone
Oestrogen

440
Q

What changes occur in the sympathetic nervous system during the stress response?

A

Increased catecholamine release –> tachycardia + HTN

441
Q

What is the purpose of GH being increased after surgery?

A

Prevents muscle breakdown and promotes tissue repair

442
Q

What BMI is considered underweight?

A

<18.49

443
Q

What BMI is considered normal?

A

18.5-25

444
Q

What BMI is considered overweight?

A

25-30

445
Q

What BMI is considered obese class I?

A

30-35

446
Q

What BMI is considered obese class II?

A

35-40

447
Q

What BMI is considered obese class III?

A

> 40

448
Q

How many units does 1ml of insulin contain?

A

100

449
Q

How is myxoedemic coma treated?

A

Thyroxine and hydrocortisone

450
Q

What electrolyte disturbance is seen in hypoparathyroidism?

A

Low calcium, high phosphate

451
Q

How is hypoparathyroidism treated?

A

Alfacalcidol

452
Q

What is a common cause of hypoparathyroidism?

A

Thyroid surgery

453
Q

What are symptoms of hypoparathyroidism?

A 
(Hypocalcaemia)
Tetany - muscle twitching, cramping, spasm
Perioral paraesthesia
Trousseau's sign
Chvostek's sign
If chronic - depression, cataracts
454
Q

What is a +ve Trosseau’s sign?

A

Carpal spasm if the brachial artery occluded by inflating BP cuff and maintaining pressure above systolic

455
Q

What is a +ve Chvostek’s sign?

A

Tapping over parotids –> facial muscle twitching

456
Q

What is pseudohypothyroidism?

A

Target cell insensitivity to PTH due to abnormality in G protein

457
Q

What is pseudohypothyroidism associated with?

A

Low IQ, short stature, shortened 4th and 5th metacarpals

458
Q

What calcium, phosphate and PTH levels is seen in pseudohypothyroidism?

A

Low calcium
High phosphate
High PTH

459
Q

How is pseudohypothyroidism diagnosed?

A

Measuring urinary cAMP and phosphate levels following infusion of PTH

In hypoparathyroidism would cause increase in cAMP and phosphate

460
Q

What is pseudopseudohypoparathyroidism?

A

Similar phenotype to pseudohypoparathyroidism but normal biochemistry

Endocrine (11 decks)

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