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Year 3 Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are symptoms of hyperthyroidism?

A 
Weight loss with increased appetite 
Diarrhoea 
Heat intolerance 
Anxiety 
Amenorrhoea
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2
Q

What are some signs of hyperthyroidism?

A 
Tachycardia 
Palmar erythema 
Goitre 
Thin hair 
Lid lag
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3
Q

What signs are specific to Graves’ disease?

A

Eye disease - exophthalmos, ophthalmoplegia
Pretibial myxoedema
Thyroid acropachy - clubbing, painful swelling of toes and fingers

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4
Q

What test results indicate hyperthyroidism?

A

Elevated T3 and T4 with undetectable TSH

Subclinical hyperthyroidism - low TSH with normal T3 and T4

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5
Q

What are some causes of hyperthyroidism?

A 
Graves’ disease 
Toxic multinodular goitre 
Toxic adenoma 
Post-partum 
Subacute de Quervians thyroiditis - post viral, self limiting
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6
Q

What is the pathophysiology of Graves’ disease?

A

Due to presence of TSH stimulating antibodies

This causes thyroid enlargement and increased hormone production

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7
Q

What antibodies can be measured in hyperthyroidism?

A

Anti-thyroid peroxidase
Anyithyroglobulin
TSH receptor antibodies

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8
Q

What imaging can be done to assess hyperthyroidism?

A

USS

Thyroid uptake scan - to assess areas of overactivity

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9
Q

What is the medical treatment of hyperthyroidism?

A

Carbimazole - reduce according to TFTs after 4 weeks

Also needs propanolol to control Sx until this works

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10
Q

What should pts be told about when taking thionamides (carbimazole)?

A

Risk of agranulocytosis - decreased WBC
Stop taking if they develop sore throat, fever, mouth ulcers
Requires urgent FBC

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11
Q

What is the definitive treatment of hyperthyroidism?

A

Radioactive iodine

Thyroidectomy

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12
Q

What are some complications of hyperthyroidism?

A 
Heart failure 
Angina 
AF 
Ophthalmopathy 
Thyroid storm
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13
Q

What are symptoms of hypothyroidism?

A 
Tiredness 
Weight gain with decreased appetite 
Cold intolerance 
Dry skin 
Hair loss
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14
Q

What are signs of hypothyroidism?

A

Dry skin and hair
Myxoedema
Bradycardia
Carpal tunnel

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15
Q

What test results are seen in primary hypothyroidism?

A

Elevated TSH

Low T3 and T4

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16
Q

What test results are seen in secondary hypothyroidism?

A

Low TSH
Low T3 and T4

Due to hypopituitarism

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17
Q

What are some causes of hypothyroidism?

A

Primary atrophic hypothyroidism
Hashimoto’s disease
Iodine deficiency
Iatrogenic - post thyroidectomy, radioactive iodine

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18
Q

What is the treatment of hypothyroidism?

A

50-100 mcg of levothyroxine
Adjust at 6 weeks according to TFTs

Elderly - 25mcg levothyroxine
Adjust at 4 weeks according to TSH

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19
Q

What is the treatment of hypothyroidism?

A

50-100mcg levothyroxine - adjust according to TSH levels

Elderly/ischaemic heart disease - start on 25mcg

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20
Q

What is Cushing’s syndrome?

A

Chronic glucocorticoid excess

Loss of the normal negative feedback mechanisms, and loss of normal circadian rhythm release of steroids

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21
Q

What are ACTH dependent causes of Cushing’s?

A

Cushing’s disease - bilateral adrenal hyperplasia due to an ACTH secreting pituitary adenoma
Ectopic ACTH secretion - eg from small cell lung ca

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22
Q

What are some ACTH independent causes of Cushing’s?

A

Iatrogenic - steroid treatment

Adrenal adenoma

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23
Q

What are symptoms of Cushing’s syndrome?

A

Central weight gain
Mood change - depression
Proximal muscle weakness
Acne

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24
Q

What are signs of Cushing’s disease?

A 
Dorso-cervical fat pad 
Round shaped face
Hypertension 
Abdominal striae 
Bruising 
Thin skin
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25
Q

What investigations can be done for Cushing’s syndrome?

A

Overnight dexamethasone suppression test

24hr urinary cortisol

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26
Q

What is the overnight dexamethasone suppression test?

A

Give 1mg dexamethasone at midnight
Measure serum cortisol at 8am
If levels aren’t suppressed this indicates Cushing’s

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27
Q

What can confirm a pituitary cause of Cushing’s?

A

Normal or high ACTH
Some cortisol suppression in high dose DST
Should also have an MRI of pituitary gland

Can do inferior petrosal sinus sampling

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28
Q

What can confirm adrenal causes of Cushing’s?

A

Low ACTH
CT of adrenal glands

Adrenal vein sampling

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29
Q

What is the treatment of Cushing’s disease?

A

Trans-sphenoidal removal of pituitary adenoma

May require adrenalectomy - requires lifelong hydrocortisone and fludrocortisone

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30
Q

What is primary adrenocortical insufficiency (Addisons disease)?

A

Autoimmune destruction of the adrenal cortex => glucocorticoid and mineralocorticoid insufficiency

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31
Q

What are symptoms of Addisons disease?

A 
Lethargy and fatigue 
Weakness 
Weight loss
Tanned
Myalgia/arthralgia 
Abdo pain, vomiting
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32
Q

What are the effects of low mineralocorticoids in Addisons?

A

Postural hypotension

Dizziness

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33
Q

What are the effects of low glucocorticoids in Addisons?

A

Hypoglycaemia

Skin pigmentation - synthesis of ACTH results in production of hormone which increases melanin production

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34
Q

What is the effect of low androgen production in Addisons?

A

Reduced libido and loss of axillary and pubic hair in women

Not as much of an effect in men - androgens produced in testes

35
Q

What are the investigations for Addisons disease?

A

Hyponatraemia, hyperkalaemia
Raised urea
Hypoglycaemia
Mild anaemia

Low 9am cortisol
Positive synacthen test

36
Q

What is the synacthen test (short ACTH simulation test)?

A

Measure plasma cortisol
Give IM synacthen - ACTH analogue

Addisons is excluded with cortisol rise of >550nmol/L

37
Q

What is the treatment for Addisons?

A

Steroid replacement

Hydrocortisone - glucocorticoid replacement
Fludrocortisone - mineralocorticoid replacement

38
Q

How would a pt with an Addisonian crisis present?

A

Shock - tachycardia, hypotension, oliguria, confused, comatose

39
Q

What are some precipitating factors of an Addisonian crisis?

A

Infection, trauma, surgery, missed medication

40
Q

What is the initial management of an Addisonian crisis?

A

Bloods - cortisol, ACTH, U&Es (hyperkalaemia, hyponatraemia)
100mg IV hydrocortisone
IV fluid bolus - 500ml 0.9% saline
Monitor BMs
Blood, sputum or urine culture if suspecting infection

41
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism
Excess release of aldosterone outside of RAAS => Na retention and therefore water retention
Causes hypertension

42
Q

When should you suspect Conn’s syndrome?

A

Hypertension in a pt <40 yrs
Hypertension which doesn’t respond to treatment
Hypertension associated with hypokalaemia

43
Q

What is a Phaeochromocytoma?

A

Cathecholamine secreting tumour of the chromaffin cells in the adrenal medulla

44
Q

How does a Phaeochromocytoma present?

A

Fight or flight response - palpitations, sweating, anxiety, hypertension

45
Q

What are some complications of a Phaeochromocytoma?

A

Hypertensive crisis
Hyperglycaemia
Arrhythmias
Sudden death

46
Q

What investigations are done for a Phaeochromocytoma?

A

24 hr urinary metanephrines

Localise with CT abdomen, can also do MIBG scan to locate

47
Q

What is the treatment for a Phaeochromocytoma?

A

Needs to be removed

Requires alpha blocker (eg phenoxybenzamine) at diagnosis
Do this before beta blocker to avoid hypertensive crisis. Beta blockers can be used to control reflex tachycardia

48
Q

What is type 1 diabetes?

A

Insulin deficiency as a result of autoimmune destruction beta islet cells
Often presents before puberty

49
Q

What is type 2 diabetes?

A

Insulin resistance

Typically occurs in older, overweight pts

50
Q

How is diabetes diagnosed?

A

Symptoms of hyperglycaemia with a single raised venous glucose (fasting - >7mmol, random >11mmol)
Raised venous glucose on two separate occasions
HbA1c >48mmol/6.5%

51
Q

What are symptoms of hyperglycaemia?

A

Polydipsia, polyuria, weight loss, lethargy

52
Q

What lifestyle advice should be given for diabetes?

A

Exercise => inc insulin sensitivity

Healthy diet

53
Q

What is the general management of T2DM?

A

1) Lifestyle modification, diet controlled
2) Metformin
3) Dual therapy
4) Triple therapy
5) Use insulin, or metformin+SU+GLP1 mimetic

54
Q

What are some oral hypoglycaemic agents?

A 
Metformin 
Gliptin - sitagliptin
Sulphonylurea - gliclazide
Glitazone
SGLT inhibitors - glifozin
55
Q

What is the MOA of metformin?

A

Inc insulin sensitivity
Dec hepatic gluconeogenesis
Dec intestinal absorption of glucose

SE: nausea, abdo pain, diarrhoea

56
Q

What is the MOA of gliptins?

A

Inc insulin production

Dec release of glucagon

57
Q

What is the MOA of sulphonylureas?

A

Inc insulin secretion - blocks ATP sensitive K channels

SE: hypoglycaemia, monitor BMs

58
Q

What is the MOA of glitazones?

A

Inc insulin secretion

SE: hypoglycaemia, fluid retention, fractures
Need to monitor LFTs

59
Q

What is the MOA of SGLT inhibitors?

A

Increase urinary excretion of glucose via Na/glucose co-transporter

SE: thrush, UTI, polyuria

60
Q

What advice should be given to someone taking insulin?

A

Modify diet, avoid binge drinking
Measure BMs at least four times a day, inc before meals and before driving
Rotate site of injection before injection
Need to educate on self adjustment on doses according to exercise, calorie intake, finger prick results

61
Q

What are some regimens for insulin?

A

Basal bolus
BD biphasic regimen
Once daily before bed long acting (T2DM)

62
Q

What is the target for fasting glucose when on insulin?

A

4-7mmol

63
Q

What advice should be given to people on insulin when they are ill?

A 
Don't stop taking insulin
Maintain calorie intake 
Increase monitoring of BMs, inc insulin if increasing 
Look for ketonuria 
Admit if vomiting, ketotic or dehydrated
64
Q

What are some chronic complications of DM?

A 
Cardiovascular disease
Nephropathy 
Diabetic neuropathy 
Diabetic foot/ulcers 
Retinopathy
65
Q

What are the stages of diabetic retinopathy?

A

Background retinopathy
Pre-proliferative retinopathy
Proliferative retinopathy
Maculopathy

66
Q

What are the blood pressure targets in DM?

A

T1DM - 135/85
T2DM - 140/ 80

If there is end organ damage => 130/80

67
Q

How should diabetic nephropathy be managed?

A

Start ACE-i/ARB

Refer if UA:CR >7

68
Q

How does diabetic neuropathy present?

A

Decreased sensation in stocking distribution
Absent ankle reflex
Charcot joint

69
Q

How is diabetic neuropathy managed?

A

Paracetamol => tricyclic => duloxetine, pregabalin => opiates

70
Q

What are acute complications of DM?

A

Hypoglycaemia
DKA
Hyperosmolar hyperglycaemic State

71
Q

How does hypoglycaemia present?

A

Confusion, drowsiness

Sweating, tachycardia

72
Q

How is hypoglycaemia managed?

A

Conscious - quick acting carb (orange juice) and recheck BMs after 15mins
Unconscious or not responding - IV glucose

73
Q

What causes DKA?

A

Excess glucose which is unable to be used due to lack of insulin
Only way to provide energy is ketosis
Inefficient, produces acetone

74
Q

How does DKA present?

A

Drowsiness, abdo pain, vomiting, dehydration

Deep breathing - Kussmaul breathing

75
Q

What are some predisposing factors to DKA?

A

Infection

Inadequate insulin - non-compliance or undiagnosed

76
Q

What investigations are needed in DKA?

A

ECG, CXR
Urine dipstick
Bloods - glucose, VBG, U&E,

77
Q

What is the management of DKA?

A

A-E assessment
1L 0.9% saline over 1hr (500ml 15 mins if BP <90 systolic)
Start on fixed rate insulin => aim for fall in blood ketones, or rise in venous bicarb
Check BMs hourly
Continue fluids, assess need for K+

Treat underlying cause

78
Q

What are complications of DKA?

A

Cerebral oedema
Hypokalaemia
VTE
Aspiration pneumonia

79
Q

How does HHS present?

A

One week of dehydration and glucose >30mmol
No ketonaemia, pH >7.3
Osmolality >320

80
Q

How is HHS managed?

A

Slow rehydration with 0.9% saline
Replace K+ when passing urine
Keep blood glucose 10-15mmol for first 24 hrs to avoid cerebral oedema
Treat underlying cause

81
Q

What are symptoms of HHS?

A

Generalised weakness, muscle cramps

Focal neurological signs

82
Q

What are some causes of HHS?

A

Infection
AKI
Hyperthyroidism
Drugs

83
Q

What is the pathophysiology of HHS?

A

Hyperglycaemia => osmotic diuresis => loss of Na and K

Severe volume depletion => raised serum osmolarity

Year 3 Medicine (11 decks)

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