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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

63
Q

Features Cushing’s

A

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

64
Q

Findings on gas Cushings

A

Hypokalaemic metabolic alkalosis

65
Q

First line test Cushing’s syndrome

A

Overnight dexamethasone suppression test

66
Q

Other tests to confirm Cushing’s syndrome

A

24 hr urinary free cortisol
Bedtime salivary cortisol

Both need 2 measurements

67
Q

Finding on overnight dexamethasone supression test in Cushing’s

A

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

68
Q

First line localisation tests Cushing’s syndrome

A

9am and midnight plasma ACTH and cortisol

69
Q

Interpretation 9am and midnight ACTH in Cushing’s

A

If ACTH suppressed, non-ACTH dependent cause likely

70
Q

Other localisation tests Cushing’s syndrome

A

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

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

72
Q

Interpretation CRH stimulation in Cushings

A

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

73
Q

Use of petrosal sampling in Cushing’s

A

Differentiate between pituitary and ectopic ACTH secretion

74
Q

Use of insulin stress test in Cushing’s

A

Differentiate between Cushing’s and pseudo-Cushings

75
Q

C-peptide in T1DM

A

Typically low

76
Q

Use of antibodies in diagnosis of diabetes mellitus

A

Useful to distinguish between T1DM and T2DM

77
Q

Antibodies in T1DM

A

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

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

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

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

81
Q

Features favouring T2DM over T1DM

A

Over 40
Respond well to oral hypoglycaemic

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

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

84
Q

Criteria impaired fasting glucose

A

Fasting glucose ≥6.1 but <7.0

85
Q

Criteria impaired glucose tolerance

A

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

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

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

88
Q

Low risk diabetic foot disease criteria

A

No risk factors except callus alone

89
Q

Moderate risk diabetic foot disease criteria

A

Deformity
Neuropathy
Non-critical limb ischaemia

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

91
Q

Diagnostic criteria DKA

A

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

92
Q

Management DKA

A
  • Fluid replacement
  • Insulin
  • Correcting electrolyte disturbance
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

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

95
Q

Management of regular insulin in DKA

A

Long acting insulin continued, short acting insulin stopped

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

97
Q

DKA resolution defined as

A

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

98
Q

When should DKA resolution be achieved by

A

Within 24 hours - if not, senior review from endocrinologist

99
Q

When can patient switch to SC insulin in DKA

A

Once resolution criteria met and patient eating and drinking

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

101
Q

Who is at most risk from cerebral oedema in DKA treatment

A

Children/young adults

102
Q

Presentation cerebral oedema in DKA treatment

A

Headache
Irritability
Visual disturbance
Focal neurology

103
Q

When does cerebral oedema occur in DKA treatment

A

4-12 hours after commencing treatment

104
Q

Investigation suspected cerebral oedema in DKA treatment

A

CT head

105
Q

Presentation diabetic peripheral neuropathy

A

Typically sensory loss not motor - glove and stocking distribution

106
Q

First line treatment pain from diabetic peripheral neuropathy

A

Amitriptyline, duloxetine, gabapentin, or pregabalin

107
Q

‘Rescue therapy’ for exacerbation of pain diabetic peripheral neuropathy

A

Tramadol

108
Q

Treatment localised neuropathic pain in diabetes

A

Topical capsaicin

109
Q

GI autonomic neuropathy in diabetes causes…

A

Gastroparesis
Chronic diarrhoea
GORD

110
Q

Symptoms gastroparesis diabetes

A

Erratic glucose control
Bloating
Vomiting

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

A

0.9% NaCl

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

1 - MSRA (17 decks)

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