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Endocrinology Flashcards

1
Q

What is raised in Cushing’s syndrome?

A

Glucocorticoids

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2
Q

Name 2 types of corticsteroid hormone and an example of each

A

Glucocorticoid (cortisol)

Mineralocorticoids (aldosterone)

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3
Q

How might a pituitary adenoma increase cortisol levels?

A

Pituitary ^ACTH secretion, stimulating XS cortisol release from the adrenal glands

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4
Q

How does Cushing’s disease differ from Cusihng’s syndrome?

A

Cushing’s disease is caused specifically by a pituitary adenoma

Cushing’s syndrome is just the symptoms and may have many causes

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5
Q

Name 5 metabolic effects of Cushing’s disease

A

HTN
Cardiac hyptertrophy
T2DM
Dyslipidaemia
Osteoporosis

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6
Q

What is raised in dyslipidaemia?

A

Cholesterol
Triglycerides

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7
Q

What are the causes of Cushing’s Syndrome?

A

CAPE

Cushing’s disease (pituitary adenoma)
Adrenal adenoma
Paraneoplastic syndrome
Exogenous steroids

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8
Q

What is the most common paraneoplastic syndrome causing Cushing’s syndrome?

A

Small cell lung cancer

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9
Q

What are the 5 types of functioning pituitary tumour?

A

Prolactinoma
Cushing’s disease (ACTH)
Acromegaly (GH)
TSH-oma
Gonadotrophinoma (LH/FSH

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10
Q

What 2 tests might be used to diagnose Cushing’s disease?

A

Dexamethasone suppression test

24-hour urinary free cortisol

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11
Q

What are the 3 types of dexamethasone suppression test?

A

Low-dose overnight
Low-dose 48 hour
High-dose 48 hour

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12
Q

What is Nelson’s syndrome?

A

Development of an ACTH-producing pituitary tumour after the surgical removal of both adrenal glands due to a lack of cortisol and negative feedback

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13
Q

Where is GH produced?

A

Anterior pituitary gland

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14
Q

What are the 3 methods of investigation used in Acromegaly?

A

IGF-1 on blood
GH supprssion test
MRI pituitary

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15
Q

What are the aims of management of Acromegaly?

A

To achieve normal levels of IGF-1 and random GH< 1 microg/L

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16
Q

What medical options are available for managing Acromegaly?

A

Pegvisomant (GHR antagonist)

Somatostatin analogues (block GH release)

Dopamine agonists (block GH release)

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17
Q

Name an example of a Somatostatin analogue

A

Octreotide

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18
Q

Name an example of a Dopamine agonist

A

Bromocriptine

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19
Q

How do you investigate a prolactinoma?

A

MRI pituitary

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20
Q

How do you manage prolactinoma?

A

Dopamine agonits

may need to excise it

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21
Q

Name 4 causes of hypopituitarism

A

Large pituitary adenoma
Iatrogenic
Sheehan’s syndrome
Periartum pituitary necrosis (DM)

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22
Q

What is Sheehan’s syndrome?

A

post-partum pituitary infarction

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23
Q

Why is hyperthyroidism?

A

Over-production of T3 and T4 by the thyroid gland

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24
Q

What is thyrotoxicosis?

A

Efects of abnormal and XS thyroid hormones

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25
Q

What organs my be dysfunctional in Secondary hyperthyroidism?

A

Hypothalamus
Pituitary

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26
Q

What is subclinical hyperthyroidism?

A

T3 and T4 normal, TSH suppressed

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27
Q

What is Grave’s disease?

A

AI condition
TSHR Abs cause primary hyperthyroidism

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28
Q

What is Plummer’s disease?

A

Toxic multinodular goitre, producing XS thyroid hormones

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29
Q

What is pretibial myxoedema?

Who gets it?

A

Glycosaminoglycan deposits as a reaction to TSHR Abs

Grave’s disease

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30
Q

What are the causes of hyperthyroidism?

A

GIST

Grave’s
Inflammation (thyroiditis)
Solitary toxic thyroid nodule
Toxic multinodular goitre

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31
Q

What are the phases of thyroiditis?

A

Initial hyperthyroidism
Then hypothyroidism

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32
Q

What are the causes of thyroiditis?

A

De Quervain’s thyroiditis
Hashimoto’s thyroiditis
Postpartum thyroiditis
Drug-induced thyroiditis

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33
Q

What features are specific to Grave’s disease?

A

Diffuse goitre
Exophthalmos
Pretibial myxoedema
Thyroid acropachy

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34
Q

Who is at risk of post-partum thyroiditis?

A

Associated with T1DM

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35
Q

How long post-partum might someone develop post-partum thyroiditis for?

A

12 months

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36
Q

How do you grade toxic multinodular goitre?

A

1 - only palpable
2 - palpable + just visible
3 - clearly visible

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37
Q

What are the 2 main physiologicla features of thyrotoxicosis?

A

^ metabolic rate
^ sympathetic drive

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38
Q

What is thyroid storm?

How might it present?

A

Really severe thyrotoxicosis

Fever, ^HR, delirium

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39
Q

How might you manage a thyroid storm?

A

Fluids
Anti-arrhythmics
BBs

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40
Q

What is the 1st line anti-thyroid drug?

How long is it taken for?

A

Carbimazole

12-18 months

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41
Q

What are the 3 main risks associated with Carbimazole?

Can you give a bonus one?

A

Agranulocytosis
Hepatotoxicity
Teratogenicity

Acute pancreatitis

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42
Q

What is the 2nd line anti-thyroid drug?

Why is it 2nd and not 1st line?

A

Propylthiouracil

Small risk of severe liver reactions, including death

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43
Q

What problem is associated with Radioactive iodine therapy?

A

Remission can take 6 months

May be hypothyroid for a while after and require levothyroxine therapy

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44
Q

What BBs might you use for hyperthyroidism?

A

NSBBs like propranolol

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45
Q

What are the 2 most common causes of primary hypothyroidism?

A

Hashimoto’s - deveoped worls
Iodine deficiency - developing world

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46
Q

What Abs are associated with Hashimoto’s thyroiditis?

A

anti-TPO Abs
anti-Tg Abs

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47
Q

Which drugs might cause primary hypothyroidism?

A

Hyper - treatments (carbimazole, propylthiouracil, iodine therapy, surgery)

LIthium

Amiodarone (contains iodine)

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48
Q

How might lithium cause hypothyroidism?

A

Inhibits production of thyroid hormones

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49
Q

How might amiodarone cause hypothyroidism?

A

Interferes with thyroid hormone production and metabolism

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50
Q

How might you differentiate primary and secondary hypothyroidism?

A

1 - ^TSH
2 - low TSH

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51
Q

What is the core treatment of hypothyroidism?

A

Oral levothyroxine

(synthetic T4, metabolises to T3 in the body)

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52
Q

How often (initially) is levothyroxine titrated?

A

Every 4 weeks based on TSH level

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53
Q

What 2 drugs may interact with levothyroxine?

A

Questran
Warfarin

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54
Q

What is Addison’s disease?

Which hormones are affected?

A

Primary adrenal insufficiency

Reduced cortisol and aldosterone

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55
Q

What is secondary adrenal insufficiency?

What is tertiary adrenal insufficiency?

A

2 - low ACTH release from pituitary gland

3 - Low CRH release by hypothalamus

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56
Q

Who tends to get tertiary adrenal insufficiency?

A

Those on long term oral steroids (>3 weeks), suppressing the hypothalamus by negative feedback

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57
Q

What are the 2 main signs of adrenal insufficiency?

A

Bronze hyperpigmentation

Hypotension (particularly postural)

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58
Q

Why do those with adrenal insufficiency get Bronze hyperpigmentation?

A

ACTH stimulates melanocytes to produce melanin

59
Q

What is the key biochemical finding of adrenal insufficiency?

A

Hyponatraemia

60
Q

What is the investigation of choice for diagnosing adrenal insufficiency?

A

Short Synacthen Test

61
Q

How might you differentiate primary and secondary adrenal insufficiency?

A

Measure ACTH

62
Q

How is the short synacthen test conducted?

A

250mcg Synacthen (synthetic ACTH) IV

BLood collected at 0, 30, and 60 minutes

Normal response >450nmol/l

63
Q

How is cortisol replaced in adrenal insufficiency?

A

Hydrocortisone (total 15-25mg daily

10mg on waking
5mg at lunch
5mg late afternoon

64
Q

When should you increase hydrocortisone doses?

A

Double it in times of stress

65
Q

How might you replace aldosterone in adrenal insufficiency?

A

Fludrocortisone

66
Q

How would you manage adrenal crisis?

A

IM / IV hydrocortisone (100mg bolus)
IV fluids
IV dextrose (if hypoglycaemic)

67
Q

How do Primary adrenal insufficiency and primary aldosteronism affect K+ levels?

A

^K+ -> primary adrenocortical insufficiency

Low K+ -> primary aldosteronism

Aldosterone causes K+ loss

68
Q

What is Conn’s syndrome?

A

Adrenal adenoma producing too much aldosterone

This is just one form of hyperaldosteronism

69
Q

What is the key presenting feature of hyperaldosteronism?

A

HTN

Always be wary of hyperaldosteronism in HTN pts with ^K+

70
Q

What is the affect of aldosterone on the nephrons?

A

^Na+ resorption in DCT
^K+ secretion in DCT
^H+ secretion in CD

71
Q

Name 3 causes of primary hyperaldosteronism

A

Bilateral adrenal hyperplasia
Conn’s syndrome
Familial hyperaldosteronism

72
Q

What is the most common type of primary hyperaldosteronism

A

Bilateral adrenal hyperplasia

73
Q

What causes secondary hyperaldosteronism?

A

XS renin stimulating XS aldosterone

Normally released due to a disproportionately lower BP in the kidneys;
- Renal artery stenosis
- HF
- Liver cirrhosis + ascites

74
Q

What screening test might be used to investigate hyperaldosteronism?

A

ARR (aldosterone-to-renin ratio)

^A, low R -> primary
^A, ^R -> secondary

75
Q

How would you medically manage hyperaldosteronism?

A

Aldosterone antagonists

Eplerenone
Spironolactone 25-200mg

76
Q

How might you manage idiopathic hyperplasia causing hyperaldosteronism?

A

Spironolactone
Triamerene
Amiloride

77
Q

What in the adrenal gland is adrenaline produced?

A

Chromaffin cells in the medullaWh

78
Q

What genetic disorders are associated with phaeochromocytoma?

What proportion of patients will have a genetic cause?

A

MEN 2
NFM 1
Von Hippel-Lindau disaese

40%

79
Q

What proportion of phaeochromocytoma cause death before diagnosis?

A

1/3

yikes.

80
Q

What are the 2 initial tests used to investigate for phaeochromocytoma?

A

Plasma free metanephrines

24-hour urine catecholamines

81
Q

Why might we measure metanephrines instead of serum adrenaline or catecholamine?

A

Catecholamine levels are unreliable as they fluctuate and have a very short half life of only a minute or so

Metanephrines are a breakdown product of adrenaline with a longer half life so are more stable

82
Q

What do the results of a 24-hour urine catecholamine test tell us?

A

How muh adrenaline is being seceted by a phaeochromocytoma over 24 hours

83
Q

How might you manage Phaeochromocytoma?

A

Alpha-blockers - phenoxybenzamine or doxazocin

BBs

Surgical excision

84
Q

What does parathyroid hormone do to calcium levels?

How?

A

^blood calcium

^osteoclats activity
^calcium renal reabsorption
^vit D, increasing calcium reabsorption in the intestines

85
Q

How might hypercalcaemia present?

A

Bones, moans, and groans

86
Q

How might you manage primary hypercalcaemia?

A

Surgical excision

Clinacalcet

87
Q

How does clinacalcet work?

A

Acts on calcium-sensing receptor, lowering calcium and PTH

88
Q

What migh cause secondary hyperparatyroidism?

A

Vitamin D deficiency
CKD

89
Q

What is tertiary hyparathyroidism?

A

Tertiary hyperparathyroidism happens when secondary hyperparathyroidism continues for an extended period, after which the underlying cause is treated.

Hyperplasia (growth) of the parathyroid glands occurs as they adapt to producing a higher baseline level of parathyroid hormone.

Then, when the underlying cause of the secondary hyperparathyroidism is treated, the baseline parathyroid hormone production remains inappropriately high. In the absence of the previous pathology, this high parathyroid hormone level leads to the inappropriately high absorption of calcium in the intestines, kidneys and bones, causing hypercalcaemia.

90
Q

How would you manage acute hypercalcaemia?

A

IV fluids
IV furosemide
IV bisphosphonates
SC denosumab
SC Salmon calcitonin

91
Q

Name 5 causes of hypocalcaemia

A

Primary hypoparathyroidism
Vit D deficiency
Malabroption syndrome
Acute pancreatitis
Chronic renal failure

92
Q

What is the classic triad of hypoparathyroidism in paediatrics?

A

Carpopedal spasm
Stridor
Convulsions

93
Q

What are the signs of overt tetany?

A

Trousseau’s signs - inflation of the sphygmomanometer suff above systolic blood pressure if followed by a carpal spasm in 3 min

Chvostek’s sign - tapping on the branches of the facial nerve as they emerge fromt he parotid gland causes twitching of the facial muscles

94
Q

From where is ADH secereted?

A

Posterior pituitary

Perhaps ectopic in small cell lung cancer

95
Q

What electrolyte abnormalities does SIADH cause?

A

^ water reabsorption
Hypontraemia

This is a euvolaemic hypontraemia as the ^water isn’t enough to cause fluid overload

96
Q

How might severe hypontraemia present?

A

Seizures
LoC

97
Q

What are the 3 main causes of SIADH?

A

Post-operative
SSRIs
Small Cell Lung Cancer

98
Q

How might you differentiate SIADH and primary polydipsia?

A

Primary polydipsia - low urine Na+ and low urine osmolality

99
Q

What drug might be used to treat SIADH?

A

Tolvaptan

(vasopressin receptor antagonist)

100
Q

What is another name for osmotic demyelination syndrome?

What causes it?

A

Central Pontine Myelinolysis (CPM)

Complication of chronic severe hyponatraemia being treated too quickly

101
Q

What are the 2 phases of osmotic demyelination syndrome?

A

1 - electrolyte imbalance (encephalopathic and confused, seizures, comiting)

2 - demyelination (quadriparesis, pseudobulbar palsy, cognitive and behavioural changes)

102
Q

What is the key difference between T1DM and T2DM?

A

T1DM - pancreas stops being able to produce insulin

T2DM - insulin resistance

103
Q

What are the 3 main physiological consequences of T1DM?

A

DKA
Dehydration
Potassium Imbalance

104
Q

How might T1DM cause DKA?

A

Fatty acids are converted to ketones

This uses up bicarbonate produced by the kidneys

105
Q

How might T1DM cause dehydration?

A

Glucose filtered out in kidneys, water follows

106
Q

How might T1DM cause potassium imbalance?

A

insulin normally puts K+ in cells, therefore serum potassium may be high/normal, but total body potassium is low

107
Q

When is the oral glucose tolerance test used?

A

To test for gestational DM only

108
Q

What is the ‘pre-diabetes’ range?

A

HbA1C 42-47 mmol/mol

109
Q

What are the target HbA1C ranges for DM patients?

A

48 mmol/mol for new T2DM

53 mmol/mol for diabetic that have moved beyond metformin alone

110
Q

What are the diagnostic criteria for T2DM?

A

HbA1c - 48 mmol/mol
Random glucose > 11mmol/L
Fasting glucose > 7mmol/L
OGTT 2 hour result > 11 mmol/L

111
Q

What is the 1st line managment option for T2DM?

A

Metformin

112
Q

What are the 2nd line options for T2DM?

A

Metformin + sulphonylurea, pioglitazone, DPP-4 inhibitor, or SGLT-2 inhibitor

113
Q

What are the 3rd line options for T2DM?

A

Triple therapy with metformin + 2 othes, or metformin + insulin

CVD? -> SGLT-2 inhibitors and GLP-1 mimetics preferential

114
Q

When might you avoid using metformin?

Why?

A

eGFR </= 36mL/min (risk lactic acidosis)

115
Q

When might you want to administer Insulin IV and not SC?

A

DKA
NBM

116
Q

What are the sick day rules with insulin?

A

Stress hyperglycaemia is likely to occur when acutely unwell

There is hence a risk of going into DKA

Do not stop insulin, you can adjust their doses if appropriate however

117
Q

Name 4 types of insulins

A

Rapid-acting
Short-acting
Immediate acting
Long acting

118
Q

How long do rapid-acting insulins take to work, and how long do they last for?

Name 3 types

A

Start after 10mins, last 4 hours

NovoRapid (insulin aspart)
Humalog
Apidra

119
Q

How long do short-acting insulins take to work, and how long do they last for?

Name 3 types

A

Start after 30 mins, last 8 hours
* Actrapid
* Humulin S
* Insuman rapid

120
Q

How long do immediate-acting insulins take to work, and how long do they last for?

Name 3 types

A

Work after 1h, last 16 hours
* Insulatard
* Humulin I
* Insuman basal

121
Q

How long do long-acting insulins take to work, and how long do they last for?

Name 3 types

A

Start after 1 hours, last 24 hours
* Lantus
* Levemir (insulin detemir)
* Degludec (lasts over 40 hours

122
Q

What is the 1st line insulin regime in T2DM?

A

NPH inulin on it’s own (intermmediate acting human insulin) OD or BD according to need

123
Q

What is the 2nd line insulin regime in T2DM?

A

Long acting insulin analogue (insulin detemir or insulin glargine) for specific cases

124
Q

How might you alter T2DM insulin regimes in cases where HbA1C > 75mmol/mol

A

Consider both NPH and short-acting insulin either separately or as a biphasic

125
Q

What are the 3 most dangerous aspects of DKA?

A

Dehydration
K+ imbalance
Acidosis

126
Q

How do you diagnose DKA?

A

Hyperglycaemia
Ketosis
Acidosis

127
Q

How do you treat DKA?

A

FIG-PICK

Fluids
Insulin
Glucose
Potassium
Infection
Chart (fluid balance)
Ketones

128
Q

What is the maximum rate of K+ infusion?

A

10 mmol/hour

129
Q

What is the pathophysiology of DKA?

A

Insulin deficiency and icnreased counter-regulatory hormones

This causes enhanced hepatic gluconeogenesis and glyconeogenesis, resulting in hyperglycaemia

Ultimately lipolysis increases FFAs and ketogenesis, causing an acidosis

129
Q

What is Whipple’s triad of hypoglycaemia?

A

1) Low plasma glucose
2) Symptoms consistent with hypo
3) Reslution of symptoms with hypo correction

130
Q

How do you manage a conscious patient with hypoglycaemia?

A

Give 15-20g rapid acting carbohydrate (or 1.5-2 tubes of GlucoGel if uncooperative)

Recheck BGL after 10-15 min. If still < 4, repeat step (max 3 times)

Consider 1mg IM glucagon

If still < 4, IV glucose (i.e. 200ml of 10% over 15 minutes)

Once recovered and BGL > 4, give 20g LA carbohydrate

131
Q

How do you manage an unconscious patient with hypoglycaemia?

A

ABCDE

Give IV glucose: 100ml of 20% over 15 minutes

1mg IM glucagon

Recheck BGL after 10min, If still<4, repeat IV glucose (max 3 times)

Once recovered and BGL >4, give 20g LA carbohydrate

132
Q

What is the pathophysiology of HHS?

A

Hyperglycaemia causes osmotic diuresis -> hyperosmolarity

This leads to an osmotic shift of water into the intravascular compartment, causing intracellular dehydration

They become ketoacidotic, we don’t know why though

133
Q

What are the principles of maagement of HHS?

A

Fluid resucitation
Insulin
K+ replacement
Thromboprophylaxis
Foot protection

134
Q

What is diabetes insipidus?

A

Either a lack of response to ADH (nephrogenic) or a lack of production of ADH (cranial)

135
Q

What is Wolfram’s syndrome?

A

primary polydipsia

136
Q

What is Wolfram’s syndrome associated with?

A

DIMOAD

DI
DM
Optic atrophy
Deafness

137
Q

What are the causes of Nephrogenic DI?

A

Drugs (lithium)
Mutation (AVPR2 on X chromosome coding for ADH R)

Intrinsice renal damage

Electrolyte disturbance

Hereditary Haemochormatosis

138
Q

What tests will confirm a diagnosis of DI?

A

Low urine osmolality

High serum osmolality

Water deprivation test

139
Q

How does DI affect Na+ levels?

A

^Na+

140
Q

How is the water deprivation test conducted?

A

No fluids for 8hours

Measure urine osmolality and administer desmopressin (synthetic ADH)

Measure again after 8 hours

141
Q

How do you manage cranial DI?

A

Desmopressin

142
Q

How do you manage nephrogenic DI?

A

Chlorothiazide

Desmopressin (higher doses under close monitoring)

Medicine (22 decks)

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