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Endocrinology Flashcards

1
Q

In T1DM, what HbA1c targert should be used?

A

48 mmol/mol (6.5%)

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2
Q

What investigation should be done in a suspected pheochromocytoma?

A

24hr urinary metanephrines

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3
Q

What is an important side effect of thiazide diuretics?

A

Hypercalcaemia

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4
Q

What test is used to diagnose Addison’s?

A

Short synacthen test

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5
Q

What is the treatment for Addisons? What should the pt do when they’re ill?

A

Hydrocortisone + fludrocortisone

double hydro when ill

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6
Q

Give some causes of raised prolactin

A 
*The Ps
Pregnancy
Prolactinoma
Physiological
PCOS
Primary hypothyroid
Phenothiazines, metoclopramide, domperidone
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7
Q

What drug may decrease the absorption of thyroxine?

A

Ferrous fumarate/sulphate

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8
Q

What is the treatment for galactorrhoea?

A

Bromocriptine

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9
Q

What ABG result is seen in Cushing’s syndrome?

A

Hypokalaemia

Metabolic alkalosis

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10
Q

What is the action of metformin?

A

Inc insulin sensitivity

Dec hepatic gluconeogenesis

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11
Q

What are the SEs of metformin?

A

GI upset

Lactic acidosis

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12
Q

When is metformin C/I?

A

eGFR < 30 (Stage 3/4)

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13
Q

What is the action of sulphonylureas?

A

Inc insulin secretion

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14
Q

Give an example of a sulphonylurea

A

Gliclazide

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15
Q

What are the SEs of sulphonylureas?

A

Hypos
Weight gain
Hyponatraemia

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16
Q

What is the action of pioglitazone?

A

Inc adipogenesis

Inc fatty acid uptake

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17
Q

Give an example of a thiazolidinediones

A

Pioglitazone

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18
Q

What are the SEs of pioglitazone?

A

Weight gain

Fluid retention

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19
Q

What is the action of DPP-4i?

A

Inc incretin -> dec glucagon

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20
Q

Give an example of a DPP-4i

A

Sitagliptin

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21
Q

What are the SEs of DPP-4i?

A

Well tolerated - inc risk pancreatitis

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22
Q

What is the action of GLP-1 agonists?

A

Incretin mimetic -> dec glucagone

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23
Q

What is different about GLP-1 agonists?

A

Given SC

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24
Q

Give an example of a GLP-1 agonist

A

Exenatide

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25
Q

What are the SEs of GLP-1 agonists?

A

N-V

Pancreatitis

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26
Q

What are the benefits of GLP-1 agonists?

A

Typical W/L

Dec risk hypos

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27
Q

What is the action of SGLT-2i?

A

Inhibits reabsorption of glucose in kidney -> inc glucose in urine

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28
Q

Give an example of a SGLT-2i

A

Dapagliflozin

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29
Q

What are the SEs of SGLT-2i?

A

UTIs

Thrush

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30
Q

What investigations are important in DKA?

A

Bedside - ECG, cap glucose, urine dip
Lab - blood gluc + ketones, FBC, U+E (in Na, in K), ABG (met acid)
Imaging - AXR, CXR, CT/MRI (if impaired consciousness)

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31
Q

Outline the management of DKA

A 
Immediate resus
SaO2 monitor, continuous ECG
Large-bore IV access
Urinary catheterisation
Fluid replacement
Insulin at 0.1 units/kg/hr
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32
Q

When treating DKA, what change in blood results are we aiming for?

A

1) Dec ketones by 0.5mmol/L/hr
2) Inc bicarb by 3mmol/L/hr
3) Dec cap gluc by 3mmol/L/hr

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33
Q

Give some causes of primary adrenal failure

A

Anatomic destruction of the gland (Addison’s disease, surgery, trauma. infection etc)
Metabolic failure in hormone production (congenital adrenal hyperplasia, ACTH resistance)
Other (ACTH-blocking antibodies, familial adrenal insufficiency)

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34
Q

Give some causes of secondary adrenal insufficiency

A

Hypothalamic: congenital, CRH deficiency, trauma, radiotherapy, surgery, neoplasm
Suppression of HPA: exogenous steroids, antipsych, steroid producting tumours
Pituitary: congenital, tumours, panhypopituitarism, infection, radio, trauma, surgery etc

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35
Q

What conditions may precipitate adrenal insufficiency?

A 
Sepsis
Severe pneumonia
Adult resp stress syndrome
Trauma
HIV infection
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36
Q

How does Addison’s usually present?

A 
Hypotension + hypovolaemic shock
Acute abdo pain + vomiting, diarrhoea
Low-grade fever
Fatigue, weakness, anorexia, W/L
Syncope, confusion, irritability
Craving salty foods
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37
Q

What signs might you see in Addisons?

A

Hyperpigmentation (buccal mucosa, lips, palmar creases, new scars)
Hypotension
Postural hypotension
Low sodium, high potassium

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38
Q

What laboratory investigations should you do if you suspect Addisons?

A 
U+E (Na, K, Ca often high)
LFTs (inc transaminases) 
FBC (may be anaemia + lymphocytosis) 
cortisol (usually inc)
ACTH (inc in 1', dec in 2')
renin + aldosterone levels
synacthen test
adrenal autoantibodies
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39
Q

What imaging investigations would you do in Addisons?

A

CXR (excl lung neo)
AXR (adrenal calcification if prev TB),
CT adrenal
MRI pit

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40
Q

What blood results would suggest an adrenal crisis?

A 
Na moderately dec (could be normal)
K slightly inc or normal 
Creatinine raised
Hypoglycaemia
Ca slightly raised
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41
Q

How do you manage an adrenal crisis?

A

1) Hydrocortisone IV or IM (100mg)
2) Cardiac monitoring
3) Saline infusion
4) After infusion, give 100mg hydrocortisone in 5% glucose over 24hrs
5) Treat precipitating disorder

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42
Q

Outline the symptoms of a phaeochromocytoma

A 
Headache
Sweating, palpitations, tremor
Nausea. epigastric pain, constipation
Weakness
Anxiety
Flank pain
W/L
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43
Q

Outline the signs of a phaeochromocytoma

A 
HTN (may be paroxysmal)
Postural hypotension
Tremor
Hypertensive retinopathy
Pallor
Fever
May have bradycardia
Cafe au lait patches
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44
Q

What laboratory investigations would you do in phaeochromocytoma?

A 
Blood gluc (raised)
Calcium (raised)
Hb (raised due to dec circulating vol)
Plasma catecholamines and metanephrines
Urine creatinine, catecholamines, VMA and metanephrine
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45
Q

What imaging would you do in phaeochromocytoma?

A

CT - tumours can be anywhere from base of brain to urinary bladder
MRI - good at locating mets

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46
Q

Give some examples of risk factors for a hypertensive crisis in phaeochromocytoma

A 
Induction of anaesthesia
Opiates
Dopamine antagonists
Decongestants
Tricyclic antidepressants
Cocaine
XR contrast media
Childbirth
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47
Q

How do you manage a phaeochromocytoma?

A

Surgical resection is the treatment of choice.

Pre-op -> alpha blockade, then add B-blocker, CCB

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48
Q

What tumours are associated with MEN1?

A 
Parathyroid (95%)
Pancreatic endocrine (gastrinomas, insulinomas) (30-80%)
Ant pit (15-90%)
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49
Q

What is the inheritance pattern of MEN1?

A

Autosomal dominant (high degree of penetrance)

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50
Q

How does MEN1 usually present?

A

Parathyroid -> H-PTH (hypercalcaemia)
Pancreatic -> Zollinger-Ellioson syndrome
Ant pit -> prolactinoma, acromegaly, cushing’s
Skin lesions -> multiple angiofibromas
Carcinoid tumours of gut and thymus

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51
Q

How is MEN1 managed?

A

Depends on tumours (e.g. diazoxide in insulinomas, PPI in gastrinomas)
Surgery is controversial - cure is achieved via removing pancreas, duodenum + lymph nodes (high rate of recurrence)
Pit tumours - surgery
Parathyroidectomy

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52
Q

What is the prognosis for MEN1?

A

Poor - life expectancy M-55. F-46

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53
Q

What would suggest MEN2A over B?

A

Medullary thyroid cancer is usually the first manifestation (less virulent than B)
Phaeochromocytoma in 30-50%
PT hyperplasia common, H-PTism rare

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54
Q

What would suggest MEN2B over A?

A 
Early development of aggressive MTC
Multiple + bilat phaeochromocytoma in 1/2
Present much earlier than A
Almost all have Marfan's-like habitus
Multiple mucosal neuromas
Skeletal abnormalities
Delayed puberty
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55
Q

What is the treatment of MEN2A?

A

Bilat adrenalectomy
Total thyroidectomy
Subtotal parathyroidectomy if H-PTism

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56
Q

What is the treatment of MEN2B?

A

Total thyroidectomy

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57
Q

What is the prognosis of MEN2?

A

B worse than A as MTC more aggressive in B

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58
Q

Outline the NICE guidelines for the management of T2DM

A

1) Lifestyle modification
2) Metformin
3) + pioglitazone, DPP4i (sitagliptin), sulphonylurea (SU), SGLT2i (ONLY + SGLT2i if SU C/I, or hypos to be avoided)
4) Met + SU + DPP4i / Met + SU + Pio / Met + SU/pio + SGLT2i / insulin

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59
Q

A 34-year-old female presents with a thyroid nodule. She has a family history of thyroid disease and both her sisters have undergone total thyroidectomies. Her past medical history includes hypertension which has been difficult to manage. What is the likely diagnosis?

A

Medullary carcinoma - part of MEN syndrome (Thyroid cancer with likely phaeochromocytoma)

60
Q

A 52-year-old woman presents with a neck swelling. Her GP reports that her TSH value is low at 0.01 mu/l. A scintigraphy demonstrates a hot nodule. What’s the likely diagnosis?

A

Toxic adenoma - This lady has thyrotoxicosis (low TSH) and a hot solitary nodule indicating a toxic adenoma. Thyroid cancer rarely causes thyrotoxicosis or hot nodules.

61
Q

An 18-year-old female presents with 3 nodules in the right lobe of the thyroid. Clinically she is euthyroid and there is associated cervical lymphadenopathy. She has no family history of thyroid disease. What is the likely diagnosis?

A

Papillary thyroid cancer is the most common type of thyroid cancer and are the more common in females (M:F=1:3). Papillary tumours are more likely to develop lymphatic spread than follicular tumours.

62
Q

Describe papillary thyroid cancers

A

Most common thyroid cancer
Younger pts
Spreads to lymph nodes and lung

63
Q

Describe follicular thyroid cancer

A

Middle age

Spreads via blood (bone, lungs)

64
Q

Describe medullar thyroid cancer

A

May be sporadic or part of MEN syndrome

65
Q

What blood results would be diagnostic of DM?

A

fasting > 7.0, random > 11.1 at any time

if asymptomatic need two readings

66
Q

Causes of hyponatraemia with dehydration and hypertonic urine (Na >20)

A

Na + H2O are lost via kidneys:

  • Addisons
  • AKI
  • diuretic excess
67
Q

Causes of hyponatraemia with dehydration and normal urine osmolality (Na <20)

A

Na + H2O are lost from elsewhere (not kidney)

  • diarrhoea, vomiting
  • fistulae
  • burns
  • SB obstruction
  • CF
68
Q

Causes of hyponatraemia without dehydration but pt is oedematous

A

Nephrotic
CCF
Liver cirrhosis
Renal failure

69
Q

Causes of hyponatraemia without dehydration with urine osmolality >100

A

SiADH - requires conc urine, hyponatraemia, low plasma osmolality, absence of hypovolaemia, oedema or diuretics.

70
Q

Causes of hyponatraemia without dehydration with urine osmolality <100

A

Water overload
Severe hypothroidism
Gluco-corticoid insufficiency

71
Q

What are the causes of SiADH?

A 
Malignancy - SC lung, pancreas, prostate
CNS - injury, haemorrhage
Chest disease - TB, pneumonia
Endocrine - hypothyroid
Drugs - opiates, SSRIs
72
Q

What is the treatment of SiADH?

A

Treat cause and restrict fluids

73
Q

What are the signs and symptoms of hyponatraemia?

A

Anorexia, nausea, malaise

Headache, irritability, confusion, weakness, dec GCS, seizures

74
Q

What are the signs and symptoms of hypernatraemia?

A

Lethargy, thirst, weakness, irritability, confusion, coma, fits, signs of dehydration

75
Q

Give some causes of hypernatraemia?

A

1) Pure water loss:
- inadequate intake -> thirst impairment (dementia)
- Diabetes insipidus

2) Hypotonic fluid loss (dehydration + hypovolaemia)
- dermal -> burns, hyperhydrosis
- GI
- urinary -> diuretics, ATN

3) Hypertonic Na gain (pure inc in Na)
- iatrogenic (hypertonic saline, tube feeds)
- excess salt intake
- hyperaldosteronism

76
Q

What is the management of hypernatraemia?

A

Water orally if possible, otherwise IV glucose 5% slowly (1L/6h)
If hypovolaemic, give 0.9% saline

77
Q

Complication of rapid correction of hyponatraemia

A

Centrol pontine myelinolysis

  • demyelination syndrome
  • may lead to quadriparesis + bulbar palsy
78
Q

Drugs causing hyperkalaemia

A 
K-sparing diuretics
ACEi
A2RB
Spironolactone
Ciclosporin
Heparin
79
Q

Causes of hyperkalaemia

A 
AKI
Drugs
Metabolic acidosis
Addison's
Rhabdo
Massive blood transfusion
80
Q

Cause of thyrotoxicosis with tender goitre

A

Subacute (de Quervain’s) thyroiditis

81
Q

Cause of peptic ulcer in MEN IIa

A

Hypercalcaemia (hyperparathyroid tumour)

82
Q

Diagnostic criteria for hyoerosmolar hyperglycaemic state (HHS)

A

Dehydration
Osmolality >320
Hyperglycaemia >30 with pH >7.3, bicarbonate >15 and NO significant ketonaemia (<3)

83
Q

Outline what defines impaired fasting glucose

A

Fasting glucose between 6.1 and 7

84
Q

Outline impaired glucose tolerance

A

Fasting plasma glucose <7 and oral glucose tolerance test (2hrs) >7.8 but less than 11.1

85
Q

Treatment of acromegaly

A

Trans-spenoidal resection of tumour

Bromocriptine - reduce GH synthesis

86
Q

Differential diagnoses for acromegaly

A

Pseudo-acromegaly - similar appearance in absence of elevated GH or IGF-1 (causes incl insulin resistance)
Other causes of symptoms - T2DM, other cardiomyopathy

87
Q

Important complication of fluid resus in DKA

A

Cerebral oedema

88
Q

XR features of hyperparathyroidism

A

Generalised osteopenia
Erosion of terminal phalyngeal tufts
Sub-periosteal reabsorption of bone

89
Q

HbA1c threshold for initiating a second drug in T2DM

A

7.5%

90
Q

Outline the short Synacthen test results in Addison’s

A

Serum cortisol <500nmol/L 1/2 hr after synthetic ACTH given (250mcg IM)

91
Q

Causes of Cushing’s syndrome

A

High ACTH - pit adenoma (Cushing’s disease), ectoptic ACTH (SCLC)
Low ACTH - adrenal adenoma or carcinoma, iatrogenic

92
Q

Inc ACTH, dec cortisol

A

Addison’s disease

93
Q

Inc ACTH, inc cortisol

A

Pit adenoma - Cushing’s disease

Ectopic ACTH - SCLC

94
Q

Dec ACTH, inc cortisol

A

Adrenal adenoma or carcinoma

Iatrogenic

95
Q

How would confirm a diagnosis of Cushing’s syndrome?

A

Overnight dexamethasone suppression test, or 24hr urinary free cortisol measurement
Then 48hr dexa supp test
Plasma ACTH
Imaging: CT (chest/adrenals), MRI (pit fossa)

96
Q

How would you differentiate between Cushing’s disease and ectopic ACTH production?

A

CRH test - cortisol will inc in pit disease, but not with ectopic ACTH
Image pituitary

97
Q

Causes of a goitre

A 
Multinodular goitre
Graves'
Solitary nodule (adenoma/carcinoma)
Hashimoto's thyroiditis
Subacute thyroiditis
98
Q

Risk associated with fast correction of hypernatraemia

A

Cerebral oedema

99
Q

How would you manage hyperglycaemic hyperosmolar state?

A

Give LMWH prophylaxis unless C/I (risk of occlusive events)
Rehydrate slowly with saline IV over 48hrs
Replace K when urine output begins to return
If blood glucose not falling by 5mmol/L/hr then use insulin

100
Q

HbA1c diagnostic of T2DM?

A

6.5%

48mmol/mol

101
Q

Target HbA1c in T1DM

A

6.5%

48mmol/mol

102
Q

ABG result in Conns syndrome

A

Metabolic alkalosis

103
Q

40yo pt with Hx of psych problems complains of polydipsia and polyuria. Normal glucose. What is the likely condition, and what medication may have caused this

A

Nephrogenic DI due to lithium

104
Q

Treatment of nephrogenic DI

A

Chlorothiazide

105
Q

Treatment of cranial DI

A

Desmopressin

106
Q

Causes of cranial DI

A

Idiopathic
Post head injury
Pit surgery

107
Q

Causes of nephrogenic DI

A 
Genetic
Hypercalcaemia
Hypokalaemia
Lithium
Obstruction, sickle cell, pyelonephritis
108
Q

Causes of hypothyroidism

A

AI - 1’ atrophic thyroiditis, Hashimoto’s

Acquired - iodine def, iatrogenic

109
Q

Urea and electrolytes in Cushing’s syndrome

A

Hypokalaemic metabolic alkalosis

110
Q

Most useful test in determining the cause of hypocalcaemia?

A

PTH

111
Q

Differentials for HTN with hypokalaemia. What test would you do after the routine bloods?

A

Conn’s, Cushing’s, renal artery stenosis

Do plasma renin and aldosterone levels

112
Q

Pt on metformin booking to have a CT with contrast. What do you advice them?

A

Discontinue metformin for 48hrs after scan due to risk of renal impairment (with met + contrast)

113
Q

Best drug for MODY

A

Gliclazide

114
Q

Monitoring for pts on gliclazide

A

None required

115
Q

T1DM blood glucose targets on waking

A

5-7 mmol/L

116
Q

T1DM blood glucose targets before meals

A

4-7 mmol/L

117
Q

Criteria for prediabetes

A

Impaired fasting glycaemia (6.1-6.9)

118
Q

First line insulin regime for newly diagnosed T1DM

A

Basal-bolus with twice-daily insulin detemir

119
Q

Inheritance pattern of haemochromatosis

A

Autosomal recessive

120
Q

Raised calcium, normal PTH

A

Primary hyper-PTH (raised calcium should Dec PTH)

121
Q

Management of subclinical hypothyroidism

A

If TSH is 4-10 and normal fT4:
- if <65yo and symptomatic, trial levothyroxine
- if older or asymptomatic, watch and wait
If TSH is >10:
- <70yo, start levothyroxine (even if asymp)
- if older, watch and wait

122
Q

Diagnostic test for Conn’s

A

Renin:aldosterone ratio

123
Q

Very high blood glucose with normal pH

A

Hyperosmolar hyperglycaemic state (T2DM)

124
Q

Management of T1DM with vomiting and diarrhoea. BM 15 and ketones 1+

A

Give extra insulin and maintain a minimum calorie intake each hour

125
Q

Most common cause of primary hyperparathyroidism?

A

Adenocarcinoma

126
Q

Deficiency in which electrolyte could cause persistent hypocalcaemia?

A

Magnesium

127
Q

Causes of hypokalaemia

A

with HTN:

  • hyperaldosteronism -> Conn’s, Cushing’s
  • inadequate K replacement in IV fluids

normotensive:

  • GI losses -> v+d
  • Barrter -> genetic K transport dysfunction in loop on Henle
  • diuretics
  • metabolic/resp alkalosis
128
Q

Management of hypokalaemia

A

Treat cause
Mild - oral K supplements, r/v after 3d
Severe (<2.5, or dangerous symptoms) - cautious IV K replacement (<25mmol/hr, <40mmol/L) NEVER BOLUS

129
Q

Management of hyponatraemia

A

Treat cause
Asymptomatic and chronic -> fluid restrict
Symptomatic or acute -> rehydrate with 0.9% saline

130
Q

Causes of hypocalcaemia

A

with raised phosphate:

  • hormonal -> 2’ hyperPTH, hypoPTH
  • rhabdomyolysis

with normal/low phosphate:

  • malabsorption
  • alkalaemia
  • acute pancreatitis
  • artefactual (over hydrated)
131
Q

Management of hypocalcaemia

A

Treat cause
Mild: PO calcium
Severe: 10% calc gluconate IV over 30min

132
Q

Causes of hypercalcaemia

A

Raised albumin? - dehydration
Normal albumin? Look at phosphate:

Low phosphate (PTH problem):

  • hyperPTH
  • PTHrP (SqCLC)

Raised phosphate:

  • cancer (mets, myeloma)
  • hyperthyroidism
  • sarcoidosis
  • drugs (thiazides, vit D supp)
133
Q

Management of hypercalaemia

A

Treat cause
Maintain hydration
Reduce bone turnover with bisphosphonates

134
Q

Quick way of remembering the symptoms of electrolyte imbalances

A

Ca - muscles
K - heart
Na - neuro

135
Q

Mnemonic for severity of Grave’s eye disease

A 
NOSPECS
No signs/symptoms
Only signs (e.g. upper lid retraction)
Signs + symptoms (incl soft-tissue involvement)
Proptosis
Extra-ocular muscle involvement
Corneal involvement
Sight loss due to optic nerve involvement
136
Q

Mnemonic for remembering causes of hypoglycaemia

A 
EXPLAIN
Exogenous drugs (SUs or insulin)
Pituitary insufficiency
Liver failure
Addison’s disease
Insulinomas
Non-pancreatic neoplasms
137
Q

HTN, hypernatraemia and hypokalaemia, alkalosis

A

Primary hyperaldosteronism

138
Q

Describe pituitary adenomas. How are they classified? What is a typical presentation?

A

Benign tumour of pituitary
Classified according to size (micro if <1cm, macro if >1cm) or hormonal status (secreting or non-secreting)
Prolactinomas are the most common type, then GH secreting, then ACTH

Symptoms:

  • excess hormones -> Cushing’s (inc ACTH), acromegaly (inc GH), amenorrhoea or galactorrhoea (inc prolactin)
  • depletion of hormone due to compression of the normal functioning pit gland
  • stretching of the dura within/around pituitary fossa causing headaches
  • compression of the optic chiasm causing bitemporal hemianopia due to crossing nasal fibres
139
Q

Investigations and management of a pituitary adenoma

A

Investigations:

  • pituitary blood profile (GH, prolactin, ACTH, FH, LSH, TFTs)
  • formal visual field testing
  • MRI brain with contrast

Management:

  • hormone therapy
  • surgery (transsphenoidal transnasal hypophysectomy)
  • radiotherapy
140
Q

Differential diagnoses for pituitary adenoma

A 
Pituitary hyperplasia
Craniopharyngioma
Meningioma
Brain mets
Lymphoma
Hypophysitis
Vascular malformation (e.g. aneurysm)
141
Q

What is Nelson’s syndrome?

A

Occurs due to rapid enlargement of a pituitary corticotroph adenoma (ACTH-producing) that occurs after the removal of both adrenal glands (for Cushing’s syndrome). The removal of both adrenals eliminates the production of cortisol and the lack of cortisol’s -ve FB can allow any pre-existing adenoma to grow unchecked.
The continued growth can cause mass effects due to physical compression of brain tissue.

Inc ACTH -> inc Melanocyte SH -> hyperpigmentation

142
Q

What TFTs would you expect in sick euthyroid syndrome?

A

Usually TSH is normal/low, T3 + 4 are low

143
Q

Which three endocrine parameters are reduced in stress response?

A

Insulin
Testosterone
Oestrogen

144
Q

Management of sub clinical hypothyroidism

A

TSH 4-10:

  • if <65yrs + symptomatic give levothyroxine trial
  • if >80, watch and wait
  • if asymptomatic, observe + repeat TFTs in 6m

TSH >10:

  • start treatment (even if asymptomatic) with levothyroxine if <70
  • in older pts, watch and wait
145
Q

Outline the types of MEN and which malignancies are associated with each.

A 
MEN I (3 Ps) - Pituitary, Parathyroid, Pancreatic
MEN IIa (2Ps, 1M) - Pheochromocytoma, Parathyroid, Medullary Thyroid Ca
MEN IIb (1P, 2Ms) - Pheochromocytoma, Medullary Thyroid Ca, Marfanoid habitus/mucosal neuroma

Finals (25 decks)

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