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Endocrinology / Renal Medicine > Endo for Finals > Flashcards

Endo for Finals Flashcards

1
Q

What affect does aldosterone have on sodium and potassium?

A

Sodium retention

Urinary potassium loss

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2
Q

What affect does aldosterone have on blood pressure?

A

Drives it up due to sodium and water retention

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3
Q

What are the causes of primary hyperaldosteronism?

A

Bilateral adrenal hyperplasia

Adrenal adenoma

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4
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism

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5
Q

What investigations might you do in suspected hyperaldosteronism?

A

U+E

Plasma aldosterone : renin ratio (will be raised)

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6
Q

What must you ensure before testing plasma aldosterone : renin ratio in suspected Conn’s?

A

Aldosterone antagonists (spironolactone and eplenerone) 6 weeks before test

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7
Q

‘Tea-coloured urine’ might lead you to be suspicious of what?

A

Rhabdomyolysis (due to myoglobinuria)

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8
Q

What might investigation results find in rhabdomyolysis?

A

Raised CK
Hyperkalaemia
Hypocalcaemia
Myoglubinuria (Dipstick +ve for blood)

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9
Q

Why might calcium be low in rhabdomyolysis?

A

Calcium is deposited in dead muscle cells so reduced in the circulation

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10
Q

What type of drug is metformin and what is it’s mechanism of action?

A

Biguanide - Increased peripheral insulin sensitivity, reduces hepatic glucose formation

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11
Q

What are the causes of a raised anion gap metabolic acidosis?

A 
Methanol
Uraemia
Diabetic ketoacidosis
Paraldehyde
Isoniazid, infection, ischaemia
Lactic acidosis e.g. from Metformin
Ethalene glycol
Salicylates e.g. aspirin overdose
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12
Q

What are the causes of a metabolic acidosis with a normal anion gap?

A

Renal tubular acidosis

Diarrhoea, vomiting

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13
Q

What is the mechanism behind a normal anion gap metabolic acidosis?

A

Loss of bicarbonate which is buffered by chlorine, so more accurately termed a hyperchloraemic metabolic acidosis

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14
Q

In a patient being treated for DKA, how should you go about restarting their normal insulin?

A

If the patient was on a basal bolus regime:
- Give short acting with a meal and stop the insulin infusion 30-60 minutes later
- The long acting insulin should not have been stopped throughout the episode of DKA
If the patient was using a mixed insulin regime, give a dose with morning or evening meal, then stop the insulin infusion 30-60 minutes later

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15
Q

What is an Addisonian Crisis?

A

Acute adrenal insufficiency

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16
Q

What is the most common cause of an Addisonian Crisis?

A

Iatrogenic i.e. abrupt withdrawal of steroids

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17
Q

How might a patient with an Addisonian Crisis present?

A

Hypovolaemic shock: Tachycardia, hypotension, oliguria, weakness, reduced GCS, comatose

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18
Q

What electrolyte disturbances might be present in an Addisonian Crisis? Why?

A

Hyperkalaemia
Hyponatraemia
Steroids usually increase sodium so lack of steroids will cause low sodium and raised K+ as a consequence

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19
Q

What is the management of Addisonian Crisis?

A

DR ABCDE approach

  • Take bloods, particularly ACTH, cortisol, U+E
  • Hydrocortisone 100mg IV stat
  • Supportive i.e. fluids
  • Monitor glucose (risk of hypoglycaemia) and treat accordingly
  • Look for underlying cause e.g. infection
  • Switch to oral steroids after 72 hours if BP stabilised
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20
Q

What is the inheritance pattern of multiple endocrine neoplasia?

A

Autosomal dominant

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21
Q

What is multiple endocrine neoplasia?

A

Rare condition where there is formation of tumours in several endocrine glands - this may happen at the same time or at different times. Treatment is by removal of the tumours if possible. There are different types depending on the clinical manifestation of the tumours.

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22
Q

Give some features of multiple endocrine neoplasia Type 1

A

All the ‘Ps’:

  • Parathyroid adenoma / hyperplasia
  • Pancreatic tumours: Gastrinoma, insulinoma, glucagonoma, somatostatinoma
  • Pituitary adenoma: Prolactin secreting, GH secreting
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23
Q

What is the most common presentation of multiple endocrine neoplasia Type 1?

A

Hypercalcaemia - This is because a parathyroid tumour is the most common tumour type in MEN1

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24
Q

Which tumour type is seen both in MEN1 and MEN2a?

A

Parathyroid adenoma

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25
Q

Which tumour types are seen in MEN2a?

A

Parathyroid adenoma
Thyroid medullary cancer
Adrenal tumour i.e. phaeochromocytoma

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26
Q

Which type of multiple endocrine neoplasia does NOT have parathyroid adenomas as a feature?

A

MEN2b

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27
Q

Which type of multiple endcrine neoplasia might present with a patient with a Marfanoid appearance?

A

MEN2b

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28
Q

Which tumour types are seen in MEN2b?

A

Thyroid medullary cancer
Adrenal - Phaeochromocytoma
Neuromas
(Patients also have Marfanoid appearance)

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29
Q

Which type(s) of multiple endocrine neoplasia are caused by the RET oncogene?

A

MEN2a and MEN2b

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30
Q

Give some causes of primary adrenal insufficiency (Addison’s disease)

A 
Autoimmune: Antibodies to 21-hydroxylase
Neoplastic: Adrenal metastasis, lymphoma
Infective: TB, histoplasmosis
Haemorrhage: Waterhouse-Friedrichsen's Syndrome
Infarction
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31
Q

Give some causes of secondary adrenal insufficiency

A

Hypothalamic or pituitary disease

Iatrogenic: Withdrawal of steroid therapy

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32
Q

What is Addison’s Disease?

A

Adrenal insufficiency - This is usually autoimmune destruction of the adrenal cortex, which results in insufficiency of glucocorticoids and mineralocorticoids

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33
Q

List some clinical features of Addison’s disease

A
  • Insidious onset, usually with non-specific symptoms (lethargy, depression, weight loss)
  • Postural hypotension
  • Nausea, vomiting, abdominal pain, diarrhoa, constipation
  • Hyperpigmented skin, especially buccal mucosa and skin creases - Due to stimulation of melanocytes by excess ACTH
  • Vitiligo
  • Loss of body hair in women
  • Addisonian crisis
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34
Q

What initial screening tests can you do for Addison’s disease? What would they show?

A

9am cortisol and ACTH
Primary hypoadrenalism = ACTH high
Secondary hypoadrenalism = ACTH low

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35
Q

What is the diagnostic test for Addison’s disease?

A

Short Synacthen Test

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36
Q

What happens in the Short Synacthen Test?

A

Demonstrate’s body’s response to ACTH administration for investigation of Addison’s Disease: Measure cortisol then administer 250ug of Synacthen (synthetic ACTH), and remeasure cortisol after 30 minutes. Cortisol should rise by more than 550umol/L. Addison’s confirmed if this risk is not seen.

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37
Q

What is the treatment for Addison’s?

A

Replace steroids: Daily hydrocortisone
Replace mineralocorticoids to maintain BP and electrolyte balance: Daily fludrocortisone
Investigate for causes
Education about adrenal crisis i.e. don’t stop steroids!

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38
Q

What class of drug are exanatide and liraglutide?

A

GLP-1 analogues

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39
Q

Give 2 examples of GLP-1 analogues

A

Exenatide

Liraglutide

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40
Q

What is the importance of GLP-1?

A

It stimulates insulin production in response to an oral glucose load - the ‘incretin effect’. This is known to be decreased in diabetes and so increasing GLP-1 levels will help with insulin production and thus lowering glucose levels.

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41
Q

True / False: GLP-1 analogues typically cause weight gain

A

False - They cause no increase in weight, in fact they often cause weight loss

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42
Q

How do DPP-4 inhibitors work?

A

They prevent the breakdown of GLP-1, thus increasing it’s availability and increasing insulin via the incretin effect

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43
Q

Give 2 examples of DPP-4 inhibitors

A

The ‘gliptin’s:

  • Sitagliptin
  • Linagliptin
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44
Q

By what route are GLP-1 analogues administered? By what route are DPP-4 inhibitors administered?

A

GLP-1 analogues = Subcutaneous injection before a meal

DPP-4 inhibitors = Orally

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45
Q

True / False: DPP-4 inhibitors cause weight gain

A

False - DPP-4 inhibitors do not cause weight gain

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46
Q

Give 1 example of a thiazolidinedione

A

Pioglitazone

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47
Q

List some side effects of thiazolidinediones e.g. pioglitazone

A

Weight gain
Fractures
Deranged LFTs
Bladder cancer

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48
Q

Give an example of a sulphonylurea

A

Gliclazide

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49
Q

Give some side effects of sulphonylureas

A

Hypoglycaemia
Weight gain
SIADH
Deranged LFTs

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50
Q

Give an example of a biguanide drug

A

Metformin

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51
Q

What type of drug is gliclazide?

A

Sulphonylurea

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52
Q

What type of drug is pioglitazone?

A

Thiazolidinedione

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53
Q

What type of drug are sitagliptin and linagliptin?

A

DPP-4 inhibitors

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54
Q

What type of drug is Metformin?

A

A biguanide

55
Q

What are the key side effects of metformin?

A

GI upset: Diarrhoea

Lactic acidosis

56
Q

What is the target HbA1c for patients with TIIDM on metformin only?

A

48mmol/L (6.5%)

57
Q

What is the target HbA1c for patients with TIIDM on gliclazide?

A

53mmol/L (7.0%) due to risk of hypoglycaemia on this drug

58
Q

What is the mechanism of SGLT2-inhibitors?

A

They inhibit glucose uptake in the renal tubule, thus causing renal excretion of glucose to reduce systemic levels

59
Q

Give an example of an SGLT-2 inhibitor

A

Dapaglifloxin

60
Q

What is the target HbA1c for a patient on metformin and another drug?

A

53mmol/L (7.0%)

61
Q

After lifestyle modification, what is the first line for patients with TIIDM?

A

Metformin

62
Q

What is the next step in the management of a patient with TIIDM on metformin who has an HbA1c greater than 58mmol/L?

A 
Continue metformin and add one of the following:
DPP-4 inhibitor e.g. Sitagliptin
Sulphonylurea e.g. Gliclazide
Pioglitazone
SGLT-2 inhibitor e.g. Dapagliflozin
63
Q

What is the next step in the management of a patient with TIIDM on metformin and another drug (dual therapy) who has an HbA1c greater than 58mmol/L?

A

Try one of the following triple therapies:

  • Metformin, DPP-4 inhibitor, sulphonylurea
  • Metformin, pioglitazone, sulphonylurea
  • Metformin, pioglitazone, SGLT-2 inhibitor
  • Metformin, sulphonylurea, SGLT-2 inhibitor
64
Q

What is the next step in the management of a patient with TIIDM on triple therapy who has an HbA1c greater than 58mmol/L?

A

In patients who have BMI more than 35 or who cannot tolerate insulin, add a GLP-1 analogue.

In all other patients consider insulin.

65
Q

What is the management of patients with TIIDM who cannot tolerate metformin (or for whom it is contraindicated)?

A

DPP-4 inhibitor (sitagliptin) OR sulphonylurea OR pioglitazone

66
Q

What is the diagnostic criteria for diabetes?

A
  • One hyperglycaemic reading i.e. fasting glucose over 7mmol/L or non-fasting over 11.1mmol/L in a patient with symptoms
  • Two hyperglycaemia readings OR a 2 hour OGTT result over 11.1mmol/L
  • HbA1c more than 48mmol/L (6.5%)
67
Q

What is the diagnostic criteria for impaired fasting glucose?

A

Fasting glucose more than 6.1mmol/L but less than 7mmol/L

68
Q

What is the diagnostic criteria for impaired glucose tolerance?

A

Fasting glucose less than 7mmol/L but OGTT 2 hour result more than 7.8mmol/L but less than 11.1mol/L

69
Q

What are the main complications of insulin?

A

Hypoglycaemia
Injection site lipo-atrophy
Injection site lipo-hypertrophy
Weight gain

70
Q

Is metformin discontinued peri-operatively?

A

It depends!

  • Continue pre-operatively, do not need to stop
  • Likely to be continued on the day of the surgery depending on the length of the surgery and how long the patient is NBM for
  • Continue after surgery but check U+E to ensure it’s safe to restart
71
Q

Is gliclazide discontinued peri-operatively?

A
  • Continue until day of surgery

- Withold on day of surgery as patient is NBM and it’s a hypoglycaemic drug

72
Q

Describe the rules about insulin administration peri-operatively

A
  • Continue until day of surgery
  • Take long-acting insulin on day of surgery but omit short-acting
  • Recommence short-acting when the patient is eating and drinking
  • Consider prescribing rescue medication for hypoglycaemia in a diabetic patient peri-operatively
  • Start variable rate insulin infusion in: Poorly controlled DM patients, patients who are having large operations and who are likely to miss more than 1 meal, diabetic patients undergoing emergency surgery
73
Q

What is tested at a diabetic patient’s annual review?

A 
Bloods:
- U+E, eGFR
- Cholesterol
- HbA1c
Urine for ACR
Feet for neuropathy
Compliance to medication etc.
74
Q

Give examples of 2 long-acting insulins

A

Lantus

Levemir

75
Q

What is the diagnostic criteria for diabetic ketoacidosis?

A

pH less than 7.3 ± bicarbonate less than 18mmol/L
Hyperglycaemia: Blood glucose more than 11.1mmol/L
Presence of ketones: 2+ ketones on urine dip, or more than 3mmol/L in blood

76
Q

What might be the cause of diabetic ketoacidosis?

A

Previously undiagnosed diabetes
Poor-compliance with insulin
Intercurrent infection

77
Q

What is the management of DKA?

A

DRABCDE approach

  • IV access: Take bloods for FBC, U+E, CRP, ketones
  • ABG
  • Fluid resuscitation if BP low
  • IV fluids…1L 0.9% sodium chloride in 1 hour, then 1L in 2 hours, 1L in 2 hours, 1L in 4 hours, 1L in 4 hours, 1L in 6 hours
  • Start fixed rate insulin infusion with ActRapid insulin 50 units in 50mL 0.9% NaCl at a rate of 0.1units/kg/hr added to 2nd bag of fluids
  • Continuous cardiac monitoring
  • Add K+ if levels below 5.5mmol/L
  • LMWH in all patients
  • Consider NG tube if patient vomiting, consider catheter to monitor urine output
  • Give 10% glucose alongside saline if glucose levels drop below 14mmol/L
  • Continue fixed rate insulin until ketones less than 0.3mmol/L, pH more than 7.3 and bicarbonate more than 18mmol/L
78
Q

How do you measure the serum osmolality?

A

[2 x Na] + K + glucose + urea

Although K+ not always included

79
Q

What are the features of hyperosmlar hyperglycaemic state?

A 
Only seen in TIIDM
Hyperglycaemia
Hypovolaemia
Hyperosmolality (more than 320mosmol/kg)
Hypernatraemia due to dehydration
Normal pH
Normal bicarbonate
Normal pCO2
Normal K+
No (or minimal) ketones
80
Q

How is hyperosmolar hyperglycaemic state treated?

A

Insulin infusion
Rehydration
LMWH

81
Q

What is HHS?

A

Hyperosmolar hyperglycaemic state

82
Q

What is the most common form of secretory pituitary adenoma?

A

Prolactinoma

83
Q

What test might be done in the initial screening for acromegaly?

A

IGF-1 level

If normal, acromegaly is unlikely

84
Q

What is the definitive test for acromegaly?

A

Oral glucose tolerance test

Normally, high level of glucose suppresses the production of growth hormone. If GH remains high despite high levels of glucose, this confirms acromegaly diagnosis

85
Q

What is the definitive test for growth hormone deficiency?

A

Insulin tolerance test

Administering insulin causes hypoglycaemia which should normally stimulate a stress response resulting in the release of cortisol and growth hormone. If GH remains low despite insulin administration, this indicates GH deficiency

86
Q

What is the treatment for growth hormone deficiency?

A

Recombinant growth hormone

87
Q

List some causes of hyperprolactinaemia

A

Pituitary adenoma i.e. prolactinoma
Dopamine antagonists e.g. metoclopramide, domperidone, anti-psychotics (haloperidol)
Compression of the pituitary stalk which reduces dopamine thus removing the inhibition of prolactin
Physiological: Pregnancy, breast-feeding
Acromegaly
Polycystic ovarian syndrome
Hypothyroidism

88
Q

What effect does dopamine have on prolactin levels?

A

Dopamine inhibits prolactin

89
Q

List some features of hyperprolactinaemia

A

Females: Oligo/Amenorrhoea, galactorrhoea, reduced libido, weight gain, vaginal dryness, infertility
Males: Impotence, galactorrhoea
May present late e.g. osteoporosis or mass effect from tumour (headache, visual disturbances)

90
Q

What is the treatment for hyperprolactinaemia

A

Remove drugs which might be causing it
Correct thyroid dysfunction
Dopamine agonist e.g. Bromocriptine
Specialist input regarding surgery

91
Q

Give some causes of Cushing’s

A

Exogenous i.e. steroid use
Cushing’s disease i.e. ACTH-producing tumour
Ectopic ACTH secretion: Small cell lung cancer, carcinoid tumour
Ectopic CRH production in thyroid cancer
Adrenal causes: Adrenal adenoma, adrenal nodular hyperplasia

92
Q

What might be a useful initial investigation in Cushing’s?

A

ACTH level

If high, continue to the dexamethasone suppression test. If low, this indicates an ‘ACTH independent’ cause of Cushing’s i.e. an adrenal cause

93
Q

What is the definitive investigation in Cushing’s?

A

Dexamethasone suppression test

On administration of dexamethasone, cortisol levels should fall.
Pituitary causes of Cushing’s = Suppression
Ectopic causes of Cushing’s = No suppression

94
Q

Give some side effects of steroids

A

Weight gain: Central distribution of weight, buffalo hump, moon face
Hypertension
Raised glucose
Oral / vaginal candidiasis
Skin atrophy, easy bruising
Osteoporosis
Cataracts
Psychiatric symptoms: Depression, insomnia
Addisonian crisis on abrupt withdrawal of steroids

95
Q

What is a phaeochromocytoma?

A

A rare catecholemine producing tumour of the sympathetic nervous system (chromaffin cells), usually found in the adrenal medulla

96
Q

Give some familial causes of phaeochromocytoma

A

von Hippel Lindau
MEN2
Neurofibromatosis

97
Q

Give some features of a phaeochromocytoma

A 
Palpitations
Tremor
Sweating
Anxiety
Headache
Nausea
Weight loss
Uncontrolled hypertension
98
Q

What investigations would you do in phaeochromocytoma?

A

Plasma metanephrines
24 hours urinary metanephrines, catecholamines, VMA (a metabolite of adrenaline)
CT abdomen

99
Q

What is the management of phaeochromocytoma?

A

Surgical excision of the tumour
Needs medical stabilisation before surgery:
- Alpha blocker e.g. phenoxybenzamine
- Beta blocker e.g. propranolol

100
Q

Why is it important to block alpha action before beta in the management of a phaeochromocytoma

A

It prevents there from being unopposed alpha action which would lead to refractory hypertension

101
Q

Why is there no dynamic testing for thyroid function?

A

Thyroid hormones have a half life of 7 days so static testing is sufficient

102
Q

Which is a more potent suppressor of TSH…T3 or T4?

A

T3

103
Q

Low TSH, high T4 indicates what underlying pathology?

A

Primary hyperthyroidism:

  • Grave’s disease
  • Toxic multinodular goitre
  • Solitary toxic adenoma
104
Q

What antibodies are present in Grave’s disease?

A

TSH-receptor antibodies…which act to STIMULATE the thyroid

105
Q

Why is T4 a preferred test for thyroid function than T3?

A

T4 is a precursor to T4

106
Q

What is the treatment for Grave’s disease?

A

Propranolol may help symptoms e.g. tremor
Carbimazole: Give for 18/12, in which time 50% will be in remission
Radio-iodine
Surgery: Considered for those whom carbimazole was ineffective

107
Q

What are the indications for surgery of a thyroid goitre?

A

Failure of medical management
Patient choice
Large goitre - These are more likely to relapse

108
Q

What is the key side effect of carbimazole and what should patients be advised?

A

Agranulocytosis

Advise patient if symptoms of rash, sore throat, fever, stop the medication and consult medical help. Check FBC.

109
Q

Normal to high TSH, with high T4, indicates what underlying pathology?

A

Secondary hyperthyroidism:

  • TSH secreting tumor (TSHoma)
  • Ectopic thyroid tissue e.g. follicular thyroid cancer
  • Exogenous thyroid production e.g. iodine excess
  • Drugs e.g. amiodarone, too much thyroxine!
110
Q

Which patients are not suitable for radio-iodine treatment?

A

Thyroid eye disease patients - Radioiodine can make symptoms worse due to antigen release

111
Q

What investigation results would you expect in subclinical hypothyroidism?

A

High TSH, normal T4

112
Q

High TSH, Low T4 indicates what underlying pathology?

A

Primary hypothyroidism

  • Hashimoto’s thyroiditis
  • Post-treatment for hyperthyroidism
  • Primary atrophic hypothyroidism
113
Q

Which antibodies are present in Hashimoto’s thyroiditis?

A

Anti-TPO antibodies (thyroid peroxidase)

114
Q

A patient is started on levothyroxine for hypothyroidism. 6/52 later their thyroid is checked and the TSH levels are low, while T4 is towards the upper limit of normal. What is the cause?

A

Likely over-treatment. Consider reducing thyroxine replacement.

115
Q

A patient has a painful thyroid goitre - what is the likely cause?

A

Subacute (de Quervain’s) thyroiditis

116
Q

List some complications of thyroid surgery

A

Acute / rare: Bleeding into thyroid bed (leads to airway compromised), thyroid crisis
Damage to local structures: Hypoparathyroidism, recurrent laryngeal nerve palsy
Late complications: Hypothyroidism, recurrent hyperthyroidism

117
Q

List 2 drugs which might cause hypothyroidism

A

Lithium

Amiodarone

118
Q

What are they types of thyroid tumours?

A 
Benign: Follicular adenoma
Malignant:
- Papillary carcinoma
- Medullary carcinoma
- Anaplastic carcinoma
119
Q

What is the most common type of thyroid cancer?

A

Papillary carcinoma

120
Q

Which thyroid cancer has the worst response to treatment?

A

Anaplastic carcinoma

121
Q

Which thyroid cancer is associated with a tumour marker? What is it?

A

Medullary carcinoma - Produces calcitonin so useful marker of the disease

122
Q

Which thyroid cancer might be seen in MEN2?

A

Medullary carcinoma

123
Q

What are the differentials for a midline neck swelling?

A

Thyroid goitre
Thyroiglossal cyst
Thyroid cancer

124
Q

What are the differentials for a lateral neck lump?

A 
Lymph node
Solitary thyroid nodule
Vascular cause: Carotid aneurysm, carotid body tumour
Sebaceous cyst
Lipoma
Cystic hygroma
Branchial cyst
Salivary glands
Neurofibroma
125
Q

How might you differentiate a sebaceous cyst from a lipoma?

A

Sebaceous cyst = Attached to skin at punctum

Lipoma = Mobile, no punctum

126
Q

Give 2 differences between a cystic hygroma and a branchial cyst

A

Cystic hygroma = Posterior triangle, present from birth

Branchial cyst = Anterior triangle, generally appears in teenage / young adulthood

127
Q

What investigation results would you expect to see in primary hyperparathyroidism?

A

High PTH
High calcium
Low phosphate
High ALP

128
Q

What investigation results would you expect to see in secondary hyperparathyroidism?

A

High PTH
Normal or low calcium
High phosphate in CKD, low phosphate in Vitamin D deficiency

129
Q

What investigation results would you expect to see in tertiary hyperparathyroidism?

A

High PTH
High calcium
High PTH
High ALP

130
Q

What are the causes of primary hyperparathyroidism?

A

Parathyroid adenoma / hyperplasia
Drugs: Thiazide diuretics, lithium
Pancreatic neuroendocrine tumours

131
Q

What is the cause of secondary hyperparathyroidism?

A

Chronic kidney disease

Vitamin D deficiency

132
Q

What is the treatment for tertiary hyperparathyroidism?

A

Parathyroidectomy

133
Q

What is the treatment for primary hyperparathyroidism?

A

IV fluids
Avoid drug causes e.g. thiazide diuretics
Parathyroidectomy

Endocrinology / Renal Medicine (6 decks)

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