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1 - MSRA > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Mechanism of action of metformin

A

Increases insulin sensitivity
Decreases glucose production by the liver

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2
Q

SEs metformin

A
  • GI symptoms, including pain, nausea, and diarrhoea
  • Lactic acidosis
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3
Q

SGLT-2 inhibitors naming

A

End in -gliflozin

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4
Q

Mechanism of action of SGLT-2 inhibitors

A

Inhibit sodium-glucose co-transporter 2 protein found in proximal tubules of kidneys, causing glucose to be lost to urine

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5
Q

Can SGLT-2 inhibitors cause hypoglycaemia?

A

Yes if combined with insulin or sulfonylureas

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6
Q

Use of SGLT-2 inhibitors in heart failure

A

Reduce risk of cardiovascular disease, empagliflozin and dapagliflozin licensed for heart failure

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7
Q

Use of SGLT-2 inhibtors in CKD

A

Dapagliflozin licensed in CKD

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8
Q

SEs SGLT2 inhibitors

A
  • Glycosuria
  • Increased UO and frequency
  • Genital and urinary tract infections
  • Weight loss
  • DKA (with only moderately raised glucose)
  • Lower-limb amputation (with canagliflozin)
  • Fournier’s gangrene
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9
Q

Thiazolidinedione e.g.

A

Pioglitazone

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10
Q

Mechanism of action of pioglitazone

A
  • Increases insulin sensitivity
  • Decreases liver production of glucose
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11
Q

SEs pioglitazone

A
  • Weight gain
  • Heart failure
  • Increased risk of bone fractures
  • Small increase risk of bladder cancer
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12
Q

Sulfonylurea e.g.

A

Gliclazide

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13
Q

Mechanism of action of sulfonylureas

A

Stimulate insulin release from pancreas

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14
Q

SEs sulfonylureas

A

Weight gain
Hypoglycaemia

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15
Q

DPP-4 inhibitors e.g.

A

Sitagliptin
Alogliptin

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16
Q

SEs DPP-4 inhibitors

A

Headaches
Acute pancreatitis

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17
Q

GLP-1 mimetics e.g.

A

Exenatide
Litaglutide

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18
Q

Route of administration GLP-1 mimetics

A

SC injection

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19
Q

Other use of litaglutide

A

Weight loss in non-diabetic obese patients

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20
Q

SEs GLP-1 mimetics

A

Reduced appetite
Weight loss
GI symptoms, including discomfort, nausea, and diarrhoea

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21
Q

Rapid acting insulin e.g.

A

NovoRapid

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22
Q

Cause acromegaly

A

Excess GH secreted by pituitary adenoma in 95% cases
Minority cases caused by ectopic GNRH or GH production by tumours, e.g. pancreatic

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23
Q

Features acromegaly

A

Coarse facial appearance, spade-like hands, increase in shoe size
Large tongue, prognathism, interdental spaces
Excessive sweating and oily skin

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24
Q

Features of pituitary tumour

A

Hypopituitarism
Headaches
Bitemporal hemianopia

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25
Q

Complications acromegaly

A

Hypertension
Diabetes
Cardiomyopathy
Colorectal cancer

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26
Q

Prolactin in acromegaly

A

1/3 of patients have raised prolactin → galactorrohoea

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27
Q

First line investigation acromegaly

A

Serum IGF-1 levels

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28
Q

What to do if serum IGF-1 raised

A

OGTT

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29
Q

Interpretation of OGTT in acromegaly

A

In normal patients, GH suppressed to <2mu/L with hyperglycaemia
In acromegaly no suppression of GH

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30
Q

Further investigations acromegaly

A

Pituitary MRI may demonstrate pituitary tumour

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31
Q

What is Addison’s disease

A

Autoimmune destruction of adrenal glands, leading to reduced cortisol and aldosterone - accounts for 80% of cases of primary hypoadrenalism

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32
Q

Features Addison’s disease

A

Lethargy
Weakness
Anorexia, nausea and vomiting, weight loss
Salt craving
Hyperpigmentation, esp palmar creases
Vitiligo
Loss of pubic hair in women
Hypotension
Hypoglycaemia
Hyponatraemia and hyperkalaemia

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33
Q

Features Addisonian crisis

A

Collapse
Shock
Pyrexia

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34
Q

Other cause of primary hypoadrenalism

A

TB
Metastases, e.g. bronchial carcinoma
Meningococcal septicaemia
HIV
Antiphospholipid syndrome

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35
Q

Secondary causes hypoadrenalism

A

Pituitary disorders - tumours, irradiation, infiltration

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36
Q

First line investigation Addison’s disease

A

ACTH stimulation test (short Synacthen test)

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37
Q

How is short synacthen test carried out

A

Plasma cortisol measured before and 30 mins after 250ug IM synacthen

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38
Q

Investigations of Addison’s when SST not available

A

9am serum cortisol

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39
Q

Interpretation 9am serum cortisol in Addisons

A

> 500nmol/L makes Addison’s very unlikely
<100nmol/L definately abnormal
100-500nmol needs ACTH stimulation

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40
Q

Electrolyte abnormalities in Addison’s

A

Hyperkalaemia
Hyponatraemia
Hypoglycaemia
Metabolic acidosis

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41
Q

Management Addison’s disease

A

Hydrocortisone - 2 to 3 divided doses, typically need 20-30mg/day
Fludrocortisone

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42
Q

Management Addison’s during intercurrent illness

A

Glucocorticoid dose should be doubled, fludrocortisone dose stays the same

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43
Q

Use of carbimazole

A

Used in thyrotoxicosis - typically given in high doses for 6 weeks until patient becomes euthyroid before being reduced

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44
Q

Adverse effects carbimazole

A

Agranulocytosis
Crosses placenta (can be used in low doses during pregnancy)

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45
Q

Glucocorticoid vs mineralocorticoid activity fludrocortisone

A

MInimal gluco
Very high mineralo

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46
Q

Glucocorticoid vs mineralocorticoid activity hydrocortisone

A

Some gluco
High mineralo

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47
Q

Glucocorticoid vs mineralocorticoid activity prednisolone

A

Predominant glucoco
Low mineralo

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48
Q

Glucocorticoid vs mineralocorticoid activity dexamethasone/betmethasone

A

Very high gluco
Minimal mineralo

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49
Q

Endocrine SEs glucocorticoids

A

Impaired glucose regulation
Increased appetite/weight gain
Hirsuitism
Hyperlipidaemia
Cushing’s

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50
Q

MSK SEs glucocorticoids

A

Osteoporosis
Proximal myopathy
Avascular necrosis of femoral head

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51
Q

Immunosuppressive SEs glucocorticoids

A

Increased susceptibility severe infection
Reactivation of TB

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52
Q

Psychiatric SEs glucocorticoids

A

Insomnia
Mania
Depression
Psychosis

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53
Q

GI SEs glucocorticoids

A

Peptic ulceration
Acute pancreatitis

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54
Q

Opthalmic SEs glucocorticoids

A

Glaucoma
Cataracts

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55
Q

Other SEs glucocorticoids

A

Suppression of growth in children
Intracranial HTN
Neutrophilia

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56
Q

SEs mineralocorticoids

A

Fluid retention
Hypertension

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57
Q

When is gradual withdrawal of steroids required

A

More than 40mg pred daily for more than 1 week
More than 3 weeks of treatment
Recently received repeated courses

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58
Q

ACTH dependant causes Cushing’s syndrome

A

Cushing’s disease
Ectopic ACTH production, e.g. SCLC

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59
Q

What is Cushing’s disease

A

Pituitary tumour secreting ACTH → adrenal hyperplasia

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60
Q

ACTH independent causes Cushin’s syndrome

A

Iatrogenic - steroids
Adrenal adenoma
Adrenal carcinoma
Carney complex (syndrome including cardiac myxoma)
Micronodular adrenal dysplasia

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61
Q

Causes pseudo-Cushing’s

A

Alcohol excess
Severe depression

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62
Q

How to differentiate Cushings syndrome and pseudocushings

A

Insulin stress test

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63
Q

Features Cushing’s

A

Round face
Central obesity
Abdominal striae
Buffalo hump
Proximal limb muscle wasting
Hirsuitism
Easy bruising, poor skin healing

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64
Q

Findings on gas Cushings

A

Hypokalaemic metabolic alkalosis

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65
Q

First line test Cushing’s syndrome

A

Overnight dexamethasone suppression test

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66
Q

Other tests to confirm Cushing’s syndrome

A

24 hr urinary free cortisol
Bedtime salivary cortisol

Both need 2 measurements

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67
Q

Finding on overnight dexamethasone supression test in Cushing’s

A

Patients with Cushing’s do not have their morning cortisol spike suppressed

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68
Q

First line localisation tests Cushing’s syndrome

A

9am and midnight plasma ACTH and cortisol

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69
Q

Interpretation 9am and midnight ACTH in Cushing’s

A

If ACTH suppressed, non-ACTH dependent cause likely

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70
Q

Other localisation tests Cushing’s syndrome

A

High-dose dexamethasone suppression test
CTH stimulation
Petrosal sinus sampling of ACTH
Insulin stress test

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71
Q

Interpretation high-dose dexamethasone suppression test

A

If cortisol suppressed and ACTH suppressed, Cushing’s disease (pituitary adenoma → ACTH secretion
If cortisol not suppressed but ACTH is, Cushing’s syndrome due to other causes
If neither cortisol or ACTH suppressed, ectopic ACTH syndrome

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72
Q

Interpretation CRH stimulation in Cushings

A

If pituitary source, cortisol rises
If ectopic/adrenal, no change in cortisol

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73
Q

Use of petrosal sampling in Cushing’s

A

Differentiate between pituitary and ectopic ACTH secretion

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74
Q

Use of insulin stress test in Cushing’s

A

Differentiate between Cushing’s and pseudo-Cushings

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75
Q

C-peptide in T1DM

A

Typically low

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76
Q

Use of antibodies in diagnosis of diabetes mellitus

A

Useful to distinguish between T1DM and T2DM

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77
Q

Antibodies in T1DM

A

Anti-GAD
Islet cell antibodies
Insulin autoantibodies
Insulinoma associated 2 autoantibodies (IA-2A)

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78
Q

Diagnostic criteria T1DM

A

If symptomatic:
- Fasting glucose greater than or equal to 7.0mmol/L
- Random glucose greater than or equal to 11.1mmol/L

If asymptomatic, above criteria on 2 seperate occasions

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79
Q

Features favouring T1DM over T2DM

A

Ketosis
Rapid weight loss
Age of onset below 50
BMI below 25
Personal and/or family history autoimmune disease

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80
Q

When to consider further tests to distinguish T1DM from T2DM

A

If T1DM suspected, but clinical presentation involves some atypical features, e.g. over 50, BMI over 25, slow evolution of hyperglycaemia

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81
Q

Features favouring T2DM over T1DM

A

Over 40
Respond well to oral hypoglycaemic

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82
Q

Criteria for diagnosis of T2DM

A

If symptomatic:
- Fasting glucose greater than or equal to 7.0mmol/L
- Random glucose greater than or equal to 11.1mmol/L
- HbA1c ≤48mmol/mol (6.5%)

If asymptomatic, above criteria on 2 seperate occasions

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83
Q

When can’t HbA1c be used to diagnose diabetes

A

Haemoglobinopathies
Haemolytic anaemia
Untreated iron deficiency anaemia
Suspected gestational diabetes
Children
HIV
CKD
Taking medications that may cause hyperglycaemia, e.g. corticosteroids

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84
Q

Criteria impaired fasting glucose

A

Fasting glucose ≥6.1 but <7.0

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85
Q

Criteria impaired glucose tolerance

A

Fasting plasma glucose less than 7.0, OGTT value ≥7.8mmolL but less than 11.1

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86
Q

Diabetic drug adjustments for Ramadan

A

For patients taking metformin, dose split 1/3 before sunrise and 2/3 after sunset
For patients on OD sulfonylureas, change to after sunset. For BD, larger proportion of dose taken after sunset

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87
Q

Screening for diabetic foot disease

A

At least annually
Ischaemia - palpating for dorsalis pedis and posterior tibial pulse
Neuropathy - 10g monofilament various parts of sole of foot

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88
Q

Low risk diabetic foot disease criteria

A

No risk factors except callus alone

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89
Q

Moderate risk diabetic foot disease criteria

A

Deformity
Neuropathy
Non-critical limb ischaemia

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90
Q

High risk diabetic foot disease criteria

A

Previous ulceration
Previous amputation
Renal replacement therapy
Neuropathy and non-critical limb ischaemia
Neuropathy with callus and/or deformity
Non-critical limb ischaemia with callus and/or deformity

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91
Q

Diagnostic criteria DKA

A

Glucose >11 or known diabetes
pH >7.3
Bicarb <15
Ketones >3mmol/L or urine ketones ++

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92
Q

Management DKA

A
  • Fluid replacement
  • Insulin
  • Correcting electrolyte disturbance
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93
Q

Insulin regime in DKA

A

IV insulin infusion started at 0.1unit/kg/hour
Once glucose <14, infusion of 10% dextrose should be started at 125ml/hour in addition to 0.9% NaCl regime

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94
Q

Management of potassium in DKA

A

Serum potassium often high on admission, but quickly falls with insulin treatment, resulting in hypokalaemia, so potassium added to replacement fluids
If rate of K infusion greater than 20mmol/hour, cardiac monitoring

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95
Q

Management of regular insulin in DKA

A

Long acting insulin continued, short acting insulin stopped

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96
Q

How much potassium to add to replacement fluids in DKA

A

If K over 5.5, none
If K 3.5-5.5, 40mmol/L
If K below 3.5, senior review

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97
Q

DKA resolution defined as

A

pH >7.3
Blood ketones <0.6mmol/L
Bicarb >15

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98
Q

When should DKA resolution be achieved by

A

Within 24 hours - if not, senior review from endocrinologist

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99
Q

When can patient switch to SC insulin in DKA

A

Once resolution criteria met and patient eating and drinking

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100
Q

Complications DKA

A
  • Gastric stasis
  • Thromboembolism
  • Arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
  • ARDS
  • AKI

Iatrogenic due to incorrect fluids - cerebral oedema, hypokalaemia, hypoglycaemia

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101
Q

Who is at most risk from cerebral oedema in DKA treatment

A

Children/young adults

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102
Q

Presentation cerebral oedema in DKA treatment

A

Headache
Irritability
Visual disturbance
Focal neurology

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103
Q

When does cerebral oedema occur in DKA treatment

A

4-12 hours after commencing treatment

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104
Q

Investigation suspected cerebral oedema in DKA treatment

A

CT head

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105
Q

Presentation diabetic peripheral neuropathy

A

Typically sensory loss not motor - glove and stocking distribution

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106
Q

First line treatment pain from diabetic peripheral neuropathy

A

Amitriptyline, duloxetine, gabapentin, or pregabalin

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107
Q

‘Rescue therapy’ for exacerbation of pain diabetic peripheral neuropathy

A

Tramadol

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108
Q

Treatment localised neuropathic pain in diabetes

A

Topical capsaicin

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109
Q

GI autonomic neuropathy in diabetes causes…

A

Gastroparesis
Chronic diarrhoea
GORD

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110
Q

Symptoms gastroparesis diabetes

A

Erratic glucose control
Bloating
Vomiting

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111
Q

Management gastroparesis diabetes

A

Metoclopramide
Domperidone
Erythromycin

112
Q

Features chronic diarrhoea caused by diabetic neuropathy

A

Often occurs at night

113
Q

Causes of falsely low HbA1c

A

Sickle cell anaemia
G6PD deficiency
Hereditary spherocytosis
Haemodialysis

114
Q

Causes of falsely high HbA1c

A

Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy

115
Q

What is Graves disease

A

Autoimmune thyroid disease in which body produces IgG antibodies to TSH receptor, stimulating it

116
Q

Features specific to Graves disease

A

Eye signs - exopthalmos, opthalmoplegia
Pretibial myxoedema
Thyroid acropachy - digital clubbing, soft tissue swelling of hands and feet, periosteal new bone formation

117
Q

Autoantibodies seen in Graves

A

TSH receptor stimulating antibodies (90%)
Anti-thyroid peroxidase antibodies (75%)

118
Q

Thyroid scintigraphy in Graves

A

Diffuse, homogenous, increased uptake of radioactive iodine

119
Q

Initial treatment to control symptoms in Grave’s diseasea

A

Propanolol

120
Q

First line definitive treatment Grave’s disease

A

Anti-thyroid drugs

121
Q

Anti-thyroid drug therapy in Graves

A

Carbimazole - started at 40mg and reduced gradually to maintain euthyroidism

122
Q

How long is carbimazole continued for in Grave’s

A

Typically 12-18 months

123
Q

Major complication of carbimazole therapy

A

Agranulocytosis

124
Q

Second line definitive treatment Grave’s disease

A

Radioiodine treatment

125
Q

Indications radioiodine treatment in Graves

A

Relapse following or resistance to anti-thyroid drug treatment

126
Q

Contraindications radioiodine treatment for Graves

A

Pregnancy (should be avoided for 4-6 months after)
Age <16

Thyroid eye disease relative contraindication - may worsen condition

127
Q

Aftermath of radioiodine treatment

A

Majority of patients need thyroxine supps after 5 years

128
Q

Pathophysiology gynaecomastia

A

Due to increased oestrogen:androgen ratio

129
Q

Causes of gynaecomastia

A

Physiological - normal in puberty
Syndromes with androgen deficiency - Kallmans, Klinefilters
Testicular failure, e.g. mumps
Liver disease
Testicular cancer
Ectopic tumour secretion of oestrogen
Hyperthyroidism
Haemodialysis
Drugs

130
Q

Drugs causing gynaecomastia

A

Spironolactone
Cimetidine
Digoxin
Cannabis
Finasteride
GnRH agonists, e.g. goserelin, buserelin
Oestrogens, anabolic steroids

131
Q

What is Hashimoto’s thyroiditis

A

Autoimmune disorder of thyroid gland, typically associated with hypothyroidism but may be transient thyrotoxicosis in acute phase

132
Q

Features Hashimoto’s thyroiditis

A

Features of hypothyroidism
Firm, non-tender goitre

133
Q

Antibodies in Hashimoto’s thyroiditis

A

Anti-thyroid peroxidase (TPO)
Anti-thyroglobulin (Tg) antibodies

134
Q

Conditions associated with Hashimoto’s thyroiditis

A

Other autoimmune conditions, e.g. coeliac, T1DM, vitiligo
MALT lymphoma

135
Q

Most common causes hypercalcaemia (90% of cases)

A

Primary hyperparathyroidism
Malignancy

136
Q

Causes of hypercalcaemia in malignancy

A

PTHrP from tumour, e.g. squamous cell lung cancer
Bone mets
Myeloma

137
Q

Other causes hypercalcaemia

A

Sarcoidosis
Vitamin D intoxication
Acromegaly
Thyrotoxicosis
Milk-alkali syndrome
Thiazides, calcium containing antacids
Dehydration
Addison’s disease
Paget’s disease of bone

138
Q

HHS precipitating factors

A

Intercurrent illness
Dementia
Sedative drugs

139
Q

Presentation HHS

A

Comes on over many days, so dehydration and metabolic distubances may be worse than DKA
Dehydration, polyuria, polydipsia
Lethargy, N&V
Altered consciousness, focal neurological deficits
Hyperviscosity - MI, stroke, thrombosis

140
Q

HHS not diagnostic criteria but what you see

A

Hypovolaemia
Marked hyperglycaemia (>30mmol/L)
Significantly raised serum osmolarity (>320mosmol/kg)
No significant hyperketonaemia
No significant acidosis

141
Q

Management HHS

A

Fluid replacement
VTE prophylaxis

142
Q

Fluid losses in HHS estimation

A

100-220ml/kg

143
Q

Fluid used for replacement HHS

144
Q

Role of insulin in HHS

A

Should not be given unless blood glucose stops falling while giving IV fluids

145
Q

Causes hypoglycaemia

A

Insulinoma
Insulin/sulphonylureas
Liver failure
Addison’s disease
Alcohol

146
Q

Effects of glucose <3.3

A

Causes autonomic symptoms due to release of glucagon and adrenaline, causing:
- Sweating
- Shaking
- Hunger
- Anxiety
- Nausea

147
Q

Effects of glucose <2.8

A

Cause neuroglycopenic symptoms due to inadequate glucose supply to brain:
- Weakness
- Vision changes
- Confusion
- Dizziness

148
Q

Investigation hypoglycaemia

A

If cause of hypoglycaemia unclear, measure insulin and c-peptide

149
Q

High insulin and high c-peptide interpretation

A

Endogenous insulin production - insulinoma, sulphonylurea use/abuse

150
Q

High insulin, low c-peptide interpretation

A

Exogenous insulin administration - exogenous insulin overdose, factitious disorder

151
Q

Low insulin, low c-peptide interpretation

A

Non-insulin related cause, e.g. alcohol-induced hypoglycaemia, critical illness, adrenal insufficiency, GH deficiency, fasting/starvation

152
Q

Community management hypoglycaemia

A

Oral glucose 10-20g in liquid, gel, or tablet form

153
Q

Hospital management hypoglycaemia

A

If patient alert, quick acting carbohydrate
If patient unconscious or unable to swallow, SC or IM injection glucagon, or IV 20% glucose solution

154
Q

Bloods in primary hypoparathyroidism

A

Low calcium, high phosphate

155
Q

Treatment primary hypoparathyroidism

A

Alfacalcidol

156
Q

Symptoms of hypoparathyroidism

A

Secondary to hypocalcaemia:
- Tentany - muscle twitching, cramping, spasm
- Perioral paresthesia
- Trousseau’s sign
- Chvostek’s sign
- Depression
- Cataracts

157
Q

What is Trousseau’s sign

A

Carpal spasm if brachial artery occluded by BP cuff and pressure maintained above systolic

158
Q

What is Chvostek’s sign

A

Tapping parotids causes facial muscles to twitch

159
Q

ECG findings hypoparathyroidism

A

Prolonged QT interval

160
Q

Cause pseudohypoparathyroidism

A

Target cells insensitive to PTH

161
Q

Other features associated with pseudohypoparathyroidism

A

Low IQ
Short stature
Shortened 4th and 5th metacarpals

162
Q

Bloods pseudohypoparathyroidism

A

Low calcium
High phosphate
High PTH

163
Q

Diagnosis pseudohypoparathyroidism

A

Measuring urinary cAMP and phosphate levels following infusion of PTH - in hypoparathyroidism, this will cause increase in cAMP and phosphate. In pseudohypoparathyroidism type I, neither rise. In type II, only cAMP rise

164
Q

Most common cause hypothyroidism

A

Hashimoto’s thyroiditis

165
Q

Other causes hypothyroidism

A

Subacute (de Quervain’s) thyroiditis
Riedel thyroiditis
After thyroidectomy or radioiodine treatment
Drug therapy
Dietary iodine deficiency

166
Q

Drug therapy causing hypothyroidism

A

Lithium
Amiodarone
Anti-thyroid drugs, e.g. carbimazole

167
Q

Starting dose levothyroxine

A

50-100mcg OD

25mcg if cardiac disease, 50+, or severe hypothyroidism

168
Q

When to check thyroid after dose change thyroxine

A

8-12 weeks

169
Q

Therapeutic goal of thyroxine therapy

A

Normalisation of TSH (0.5-2.5)

170
Q

Adjustment to levothyroxine in pregnancy

A

Dose increase by at least 25-50mch, TSH monitored carefully aiming for low-normal value

171
Q

SEs thyroxine

A

Hyperthyroidism
Reduced bone mineral density
Worsening of angina
AF

172
Q

Drug interactions levothyroxine

A

Iron, calcium carbonate - reduce absorption, so should give at least 4 hrs apart

173
Q

Inheritance Kallman’s syndrome

A

X linked recessive

174
Q

Features Kallmans syndrome

A

Delayed puberty
Hypogonadism, cryptorchidism
Anosmia

Cleft lip/palate and visual/hearing defects in some patients

175
Q

Blood tests Kallman’s syndrome

A

Sex hormones low
LH/FSH levels low or inappropriately normal

176
Q

Management Kallman’s syndrome

A

Testosterone supplementation
Gonadotrophic supplementation for sperm production if fertility desired

177
Q

Karyotype Klinefilters

178
Q

Features Klinefelter’s

A

Taller than average
Lack of secondary sexual characteristics
Small, firm testes
Infertile
Gynaecomastia

179
Q

Bloods Klinefelter’s

A

Elevated gonadotrophins, low testosterone

180
Q

Examples meglitinides

A

Repaglinide
Nateglinide

181
Q

Mechanism of action meglitanides

A

Increase pancreatic insulin secretion

182
Q

What kind of patients are meglitanides often used for

A

Those with erratic lifestyle

183
Q

Tumours associated with MEN I

A

Parathyroid
Pituitary
Pancreas, e.g. insulinoma, gastrinoma
Adrenal
Thyroid

184
Q

Tumours associated with MEN IIa

A

Medullary thyroid cancer
Parathyroid
Phaeochromocytoma

185
Q

Tumours associated with MEN IIb

A

Medullary thyroid cancer
Pheochromocytoma

Marfanoid body habitus
Neuromas

186
Q

Presentation myxoedema coma

A

Confusion
Hypothermia

187
Q

Causes myxodema coma

A

Severe hypothyroidism

188
Q

Treatment myxoedema coma

A

IV thyroid replacement
IV fluid
IV corticosteroids (until possibility of co-existing adrenal insufficiency excluded)
Electrolyte imbalance correction
Sometimes rewarming

189
Q

BMI underweight

190
Q

Normal BMI

191
Q

Overweight BMI

192
Q

Obese class 1 BMI

193
Q

Obese class 2 BMI

194
Q

Obese class 3 BMI

195
Q

Medical management obesity

A

Orlistat
Liraglutide

196
Q

Adverse effects orlistat

A

Faecal urgency/incontinence
Flatulence

197
Q

Criteria prescription orlistat

A

Part of overall plan for managing obesity in patients wtih:
BMI 28+ with associated risk factors
BMI 30+
Continued weight loss, e.g. 5% at 3 months

198
Q

Duration of use orlistat

199
Q

Criteria prescription liraglutide for obesity

A

BMI 35+
Prediabetic hyperglycaemia 42-47

200
Q

Associations phaeochromocytoma

A

MEN II
Neurofibromatosis
Von Hippel-Lindau syndrome

201
Q

Symptoms phaeochromocytoma

A

Usually episodic

  • Hypertension
  • Headaches
  • Palpitations
  • Sweating
  • Anxiety
202
Q

Investigations phaeochromocytoma

A

24 hour urinary collection of metanephrines

203
Q

Treatment phaeochromocytoma

A

Definitive treatment with surgery, first stabilise with:
Alpha-blocker, e.g. phenoxybenzamine, given before
Beta blocker, e.g. propanolol

204
Q

Diagnostic criteria prediabetes

A

Fasting plasma glucose 6.1-6.9mmol/L
HbA1c 42-47 (6-6.4%)

205
Q

Management prediabetes

A

Lifestyle modification - weight loss, increased exercise, change in diet
At least yearly f/u with blood tests
Metformin if blood tests progressive despite participation in intensive lifestyle-change programme

206
Q

Cause impaired fasting glucose

A

Hepatic insulin resistance

207
Q

Cause impaired glucose tolerance

A

Muscle insulin resistance

208
Q

Whats worse, impaired fasting glucose or impaired glucose tolerance

A

Impaired glucose tolerance more likely to develop T2DM and cardiovascular disease

209
Q

Impaired fasting glucose diagnostic criteria

A

Fasting glucose ≥6.1 but <7

210
Q

Impaired glucose tolerance diagnostic criteria

A

Fasting plasma glucose <7, but OGTT ≥7.8 but <11.1

211
Q

Causes primary hyperaldosteronism

A

Bilateral idiopathic adrenal hyperplasia (most common)
Adrenal adenoma (Conn’s syndrome)
Unilateral hyperplasia
Familial hyperaldosteronism
Adrenal carcinoma

212
Q

Features primary hyperaldosteronism

A

Hypertension
Hypokalaemia
Metabolic alkalosis

213
Q

Who needs screening for primary hyperaldosteronism

A

Hypertension with hypokalaemia
Treatment resistant hypertension

214
Q

First line investigation suspected primary hyperaldosteronism

A

Aldosterone/renin ratio

215
Q

Findings plasma aldosterone/renin ratio in primary hyperaldosteronism

A

High aldosterone levels with low renin levels (negative feedback due to sodium retention from aldosterone)

216
Q

Further investigation if aldosterone/renin ratio suggests primary hyperaldosteronism

A

High resolution CT
Adrenal vein sampling

Tests to differentiate between unilateral adenoma and bilateral hyperplasisa

217
Q

Management adrenal adenoma

A

Laparoscopic adrenalectomy

218
Q

Management bilateral adrenocortical hyperplasia

A

Aldosterone antagonist, e.g. spironolactone

219
Q

Causes primary hyperparathyroidism

A

Solitary adenoma (85%)
Hyperplasia
Multiple adenoma
Carcinoma

220
Q

Symptoms primary hyperparathyroidism

A

Those of hypercalcaemia

Polydipsia, polyuria
Depression
Anorexia, nausea, constipation
Peptic ulceration
Pancreatitis
Bone pain/fracture
Renal stones
Hypertension

221
Q

Associations primary hyperparathyroidism

A

Hypertension
MEN 1 and 2

222
Q

Blood findings primary hyperparathyroidism

A

Raised calcium, low phosphate
PTH may be raised or inappropriately normal

223
Q

X ray findings primary hyperparathyroidism

A

Pepperpot skul
Osteitis fibrosa cystica

224
Q

Definitive management primary hyperparathyroidism

A

Total parathyroidectomy

225
Q

Conservative management primary hyperparathyroidism

A

Cinacalcet

226
Q

Criteria for conservative management primary hyperparathyroidism

A

Calcium level less than 0.25 above upper limit of normal
Patient >50
No evidence of end organ damage

227
Q

Features of high prolactin in men

A

Impotence
Loss of libido
Galactorrhoea

228
Q

Features of high prolactin women

A

Amenorrhoea
Galactorrhoea
Osteoporosis
Infertility

229
Q

Causes of raised prolactin

A

Prolactinoma
Pregnancy
Oestrogens
Physiological - stress, exercise, sleep
Acromegaly
PCOS
Primary hypothyroidism

230
Q

Drugs causing raised prolactin

A

Metoclopramide, domperidone
Phenothiazines
Haloperidol
SSRIs
Opioids

231
Q

Symptoms seen with pituitary macroadenoma

A

Headache
Visual disturbance, classically bitemporal hemianopia or upper temporal quadrantanopia
Signs and symptoms of hypopituitarism

232
Q

Diagnosis prolactinoma

233
Q

Management prolactinoma

A

Majority of symptomatic patients managed with dopamine agonists, e.g. cabergoline, bromocriptine
Surgery if can’t tolerate/fail to respond - trans-sphenoid approach unless significant extra-pituitary extension

234
Q

What is Riedels thyroiditis

A

Rare cause of hypothyroidism characterised by dense fibrous tissue replacing normal thyroid parenchyma

235
Q

Examination findings Riedels thyroiditis

A

Hard, fixed, painless goitre

236
Q

Associations Riedels thyroiditis

A

Retroperitoneal fibrosis

237
Q

Examples SGLT inhibitors

A

Canagliflozin
Dapagliflozin
Empagliflozin

238
Q

Adverse effects SGLT2 inhibiotrs

A

Urinary and genital infection
Fourniers gangrene
Normoglycaemia ketoacidosis
Increased risk of lower limb amputation

239
Q

Blood tests sick euthyroid syndrome

A

TSH, thyroxine, and T3 low

TSH may be inappropriately normal

240
Q

Treatment sick euthyroid syndrome

A

No treatment needed - recovers when better from acute illness

241
Q

Cause subacute (De Quervain’s) thyroiditis

A

Occurs following viral infection

242
Q

Phase 1 subacute (De Quervain’s) thyroiditis

A

Lasts 3-6 weeks - hyperthyroidism, painful goitre, raised ESR

243
Q

Phase 2 subacute (De Quervain’s) thyroiditis

A

Lasts 1-3 weeks - euthyroid

244
Q

Phase 3 subacute (De Quervain’s) thyroiditis

A

Lasts weeks - months - hypothyroidism

245
Q

Phase 4 subacute (De Quervain’s) thyroiditis

A

Thyroid structure and function returns to normal

246
Q

Thyroid scintigraphy subacute (De Quervain’s) thyroiditis

A

Globally reduced uptake iodine-131

247
Q

Management subacute (De Quervain’s) thyroiditis

A

Usually self limiting, most patients don’t need treatment
Thyroid pain may respond to aspirin or other NSAIDs
In more severe cases, steroids used

248
Q

Criteria subclinical hypothyroidism

A

TSH raised, T3/4 normal
No obvious symptoms

249
Q

Significance subclinical hypothyroidism

A

Risk of processing towards overt hypothyroidism

250
Q

When should levothyroxine therapy be considered in subclinical hypothyroidism

A

If TSH >10 on 2 occasions 3 months apart
If TSH 5.5-10, <65 and symptoms of hypothyroidism

251
Q

Management asymptomatic subclinical hypothyroidism with TSH 5.5-10

A

Observe and repeat thyroid function in 6 months

252
Q

Adverse effects sulfonylureas

A

Hypoglycaemic episodes
Weight gain

Less commonly:
Hyponatraemia secondary to SIADH
Bone marrow suppression
Hepatotoxicity
Peripheral neuropathy

253
Q

Sulfonylureas in breastfeeding and pregnancy

254
Q

Example thiazolidinediones

A

Pioglitazone

Rosiglitazone withdrawn due to concerns about CVS side effects

255
Q

SEs pioglitazone

A
  • Weight gain
  • Liver impairment
  • Fluid retention
  • Increased risk of cancer
  • Bladder cancer
256
Q

CIs pioglitazone

A

Heart failure

257
Q

Monitoring pioglitazone

258
Q

Features hypothyroidism

A
  • Weight gain
  • Lethargy
  • Cold intolerance
  • Dry, cold, yellowish skin
  • Non-pitting oedema
  • Dry, coase scalp hair, loss of lateral aspect of eyebrows
  • Constipation
  • Menorrhagia
  • Decreased deep tendon reflexes
  • Carpal tunnel syndrome
259
Q

Features hyperthyroidism

A
  • Weight loss
  • Manic, restlessness
  • Heat intolerance
  • Palpitations
  • Increased sweating
  • Pretibial myxoedema
  • Thyroid acropachy
  • Diarrhoea
  • Oligomenorrhoea
  • Anxiety
  • Tremor
260
Q

What is pretibial myxoedema

A

Erythematous, oedematous lesions above lateral malleoli

261
Q

TSH/T4 in thyrotoxicosis

A

TSH low, T4 high

262
Q

TSH/T4 in primary hypothyroidism

A

TSH low, T4 low

263
Q

TSH/T4 in secondary hypothyroidism

A

TSH low, T4 low

264
Q

TSH/T4 in sick euthyroid syndrome

A

TSH low, T4 low

265
Q

TSH/T4 in subclinical hypothyroidism

A

TSH low, T4 normal

266
Q

TSH/T4 in poor compliance with thyroxine

A

TSH high, T4 low

267
Q

Most common condition TSH receptor antibodies seen in

268
Q

Most common condition anti-TPO antibodies seen in

A

Hashimoto’s thyroiditis

269
Q

What is thyroid storm

A

Rare but life-threatening complication of thyrotoxicosis

270
Q

Thyroid storm precipitating events

A

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

271
Q

Clinical features thyroid storm

A

Fever >38.5
Tachycardia
Confusion and agitation
N&V
Hypertension
Heart failure
Abnormal liver function test

272
Q

Management thyroid storm

A

Symptomatic treatment, e.g. paracetamol
Treatment of underlying precipitating event
Beta blockers, usually IV propanolol
Anti thyroid drugs
Lugol’s iodine
Dexamethasone

273
Q

Anti thyroid drugs used in thyroid storm

A

Methimazole or propylthyiouracil

274
Q

Causes thyrotoxicosis

A

Graves disease
Toxic nodular goitre
Acute phase of hypothyroid conditions
Amiodarone
Contrast

275
Q

Conditions causing thyrotoxicosis in the acute phase

A

Subacute thyroiditis
Post-partum thyroiditis
Hasmimoto’s thyroiditis

1 - MSRA (23 decks)

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