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Y3 med old > ENDOCRINOLOGY > Flashcards

ENDOCRINOLOGY Flashcards

1
Q

What does diabetes predispose you to?

A

Atheroscerlosis which leads to CVD

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2
Q

How does diabetes affect your chance of getting renal disease?

A

1 in 3 T2Dm develops overt kidney disease and diabetes is the most common causes of ESRD.

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3
Q

What is the risk of amputation in a patient with diabetes?

A

15% lifetime risk of amputation

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4
Q

How is the life expectancy affected by diabetes?

A

Reduced by 5-10 years

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5
Q

What is the normal plasma glucose concentration?

A

4-6 mmol/l

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6
Q

How do you define diabetes?

A

Abnormally elevated plasma glucose concentration

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7
Q

How do you diagnose diabetes?

A

Symptoms + one abnormal result OR 2 abnormal results of ideally the same (but can be different) tests at least week apart.

Fasting glucose greater than or equal to 7mmol/l and/or
OGTT of 75g glucose, 2 hours after greater than or equal to 11.1mmol/l
Hba1c greater than or equal 6.5%

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8
Q

If the patient is asymptomatic, how far apart do diagnostic tests for diabetes have to be?

A

1 week

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9
Q

What is the classic triad of symptoms for diabetes

A

polyuria, polydipsia and weight loss

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10
Q

What is the treatment basis for T1DM?

A

ALWAYS be treated with insulin, always need insulin cover

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11
Q

What other diseases is T1DM associated with?

A

Thyroid disease and adrenal insufficiency, due to its autoimmune nature

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12
Q

What is LADA syndrome?

A

Latent autoimmune diabetes adult, patient who has positive antibodies to beta cell function, indicative of T1DM, but insidious presentation with mild hyperglycaemia

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13
Q

Why don’t healthy people have ketone production?

A

It is suppressed by insulin, absence of insulin leads to gluconeogenesis and fat breakdown—> free fatty acid

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14
Q

What is the mechanism of ketone production in T1DM?

A

No insulin, therefore production of ketones by beta oxidation of free fatty acids.

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15
Q

What is the relevance of a diabetic patient with ketones in their urine?

A

Immediate insulin therapy needs to be started NOW

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16
Q

How is T1DM managed?

A

Insulin- SC injection–> different types of insulin available

Patient education
Lifestyle–> accurate carbohydrate counting -DAFNE course
Home blood glucose monitoring
Regular HbA1c testing and complications- foot check, renal assessment and retinal screening assessment

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17
Q

How is T2DM managed?

A 
Lifestyle 
Anti-obesity drugs 
Oral hypoglycaemic drugs 
GLP 1 agonists 
Insulins 
SGLT2s
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18
Q

What is first line therapy for T2DM?

A

Metformin

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19
Q

What is the main contraindication of metformin?

A

eGFR<30mL/min

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20
Q

How does metformin work?

A

Decrease hepatic glucose production by inhibiting gluconeogenesis

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21
Q

What are the ADRs of metformin?

A

GI upset, nausea, vomitting, diarrhoea

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22
Q

What are the drug-drug interactions with metformin?

A

ACEi, diuretics, NSAIDs- drugs that may impair renal function
loop and thiazide like diuretics- increase glucose so can reduce metformin action

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23
Q

A patient complains of diarrhoea with metformin, what would you suggest?

A

modified release preparations or temporarily decrease the dose.

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24
Q

How do sulphonylureas work?

A

Stimulate the beta cells to release insulin by blocking ATP dependent K+ channels

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25
Q

What are the side effects of sulphonylureas?

A

Weight gai, mild GI upset, hypoglycaemia

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26
Q

What is GLP-1?

A

incretin hormone

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27
Q

What are the effects of GLP-1

A

Pancreas- Increase insulin secretion, decrease glucagon secretion, increase insulin biosynthesis

Liver- decrease glucose production

Stomach- decreases gastric emptying

Muscle- increase glucose uptake

Brain- increase satiety

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28
Q

When is GLP-1 release?

A

From the intestinal L cells, during meals

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29
Q

When do you use GLP-1 agonists?

A

NICE suggest add-on if triple therapy is ineffective, but evidence for their use is vey strong

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30
Q

What are the benefits of GLP-1 agonists?

A

Weight loss

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31
Q

When is using GLP-1 agonists contraindicated?

A

Renal impairment

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32
Q

When do you use sulphonyureas in diabetes management?

A

Used less now, but often used if patient with T2DM has low weight, to increase their weight.

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33
Q

What are DPP-4 inhibitors?

A

They inhibit DPP-4 activity which increases GLP-1 concentrations

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34
Q

What are the side effects of DPP-4 inhibitors?

A

GI symptoms, but quite well tolerated
Acute pancreatitis
Hypoglycaemia when prescribed with other hypoglycaemic drugs - SU, insulin

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35
Q

When are SGLT-2 inhibitors used?

A

In diabetes but also people who have comorbities such as congestive cardiac failure and CKD

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36
Q

What are the acute complications of type 1 DM?

A

DKA

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37
Q

How is DKA defined?

A

Hyperglycaemia, ketonaemia and acidosis

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38
Q

How is DKA diagnosed ?

A 
Needs to have 
Ketonaemia greater than or equal to 3 mmol/L 
Blood glucose > 11mmol/L 
Bicarb < 15mmol/L 
and/or pH<7.3
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39
Q

What are the key issues in DKA?

A 
Hyperglycaemia 
Acidosis 
Dehydration due to osmotic diuresis and vomitting 
Electrolyte loss 
Cerebral oedema 
Hyperkalaemia
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40
Q

How do you manage DKA?

A

Rapid fluid administration 0.9% NaCl and insulin
Restoration of circulatory volume
Clearance of ketones
Correct any electrolyte imbalance using crystalloids

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41
Q

What insulin therapy do you use for DKA?

A

Fixed rate IV infusion 0.1 units per kilo body weight per hour

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42
Q

What are your metabolic treatment targets for DKA?

A

Reduce ketones by 0.5mmol/l/hour
Increase venous bicarb by 3.0mmol/l/hour
Maintain potassium between 4-5.5mmol/l

If blood glucose falls below 14mmol/l introduce dextrose with N saline until patient is eating

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43
Q

What do you measure hourly in patients admitted with DKA?

A

Blood glucose

Hourly ketones

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44
Q

What initial investigations should you do for a patient with DKA?

A 
Blood ketones 
Cap blood glucose 
Venous plasma glucose 
Urea and electrolytes 
VBG 
FBC 
Blood cultures 
ECG 
continuous cardiac monitoring 
Urianalysis and culture
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45
Q

How many mmol/L in the blood do you start potassium therapy in patients with DKA?

A

Between 3.5-5.5mmol/L you add 40mmol/L of potassium into the infusion, any less than 3.5mmol/L need senior review

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46
Q

What must be done/considered in the first 6 hours of DKA treatment?

A 
At least hourly review 
Clear blood of ketones and surprise ketogenesis, reduce at rate of 0.5mmol/l/hour 
Avoid hypoglycaemia 
Consider catheterisation 
Consider NG tubing 
Continuous cardiac monitoring 
Treat co-morbities
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47
Q

When can you stop the fixed rate insulin infusion (FRII) and convert back to subcut insulin in a patient with DKA?

A

Ketones <0.6mmol/L and ready to eat

No evidence of acidosis

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48
Q

What is hyperosmolar hyperglycaemic syndrome?

A

Marked water loss due to hyperglycaemia, without ketonaemia or acidosis.

High osmolality–> v dehydrated

Usually you get a mixed picture of both HHS and DKA

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49
Q

How do you diagnose HHS?

A

Hypovolaemia
Marked hyperglycaemia (30mmol/L or more) with significant hyperkenonaemia (<3mmol/L) or without acidosis
Osmolality usually 320 mosmol/kg or more

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50
Q

Who is most affected by HHS?

A

Elderly and frail people

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51
Q

What can trigger HHS?

A

Usually precipitated by something e.g. infection

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52
Q

How can you calculate plasma osmolality?

A

2Na + glucose +urea

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53
Q

What are the treatment goals for HHS?

A

Normalise osmolality
Replace fluid and electrolyte losses
Normalise blood glucose

We also want to prevent
Arterial or venous thrombosis
Other potential complications e.g. Cerebral oedema, central pontine mylinolysis
Foot ulceration

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54
Q

How do you treat HHS?

A 
Crystalloids
Aim to replace 50% of loss within first 12 hours 
FRIII 0.05units/Kg/hour 
Monitor potassium and renal function 
Glucose fall 4-6mmol/hour 
Co-morbities 
Anticoagulation
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55
Q

Name 5 RF for hypoglycaemia?

A
  • Increased exercise (relative to usual),
  • renal failure,
  • strict glycemic control,
  • previous hx of severe hypoglycaemia,
  • long duration of type 1 diabetes,
  • food malabsorption,
  • inadequate glucose monitoring
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56
Q

What are the causes of inpatient hypoglycaemia?

A

acute discontinuation of long term steroid therapy, recovery from acute illness, mobilisation after illness, missed or delayed meals, less carbs than normal, reduced appetite

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57
Q

How do you treat hypoglycaemia in an adult who is conscious, orientated and able to swallow?

A

15-20g quick acting carbohydrate of patients choice e.g. 90-120ml go original lucozade, 3-4 heaped teaspoons of sugar dissolved in water, 150-200ml pure fruit juice

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58
Q

How do you treat hypoglycaemia in a patient who is confused but able to swallow?

A

1.5-2 tubes glycogen/dextrogel squeezed between teeth and gum OR give glucagon IM (less effective in pts prescribed sulfonylurea therapy or under influence of alcohol)

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59
Q

What are the chronic complications of diabetes?

A

neuropathy
nephropathy
retinopathy
CVS

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60
Q

What 3 groups can the symptoms of hypoglycaemia be divided into?

A

Autonomic
Neuroglycopenic
General malaise

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61
Q

What are some autonomic symptoms of hypoglycaemia?

A

Sweating
palpitations
shaking
hunger

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62
Q

What are some neuroglycopenic symptoms of hypoglycaemia?

A

Confusion
Drowsiness
Odd behaviour
Speech difficulty

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63
Q

What are some general malaise symptoms related to hypoglycaemia?

A

Headache and nausea

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64
Q

What is charcots foot?

A

Osteoarthropathy associated with neuropathy

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65
Q

A patient with T2DM has a dusky and painful foot, what are you thinking?

A

Peripheral vascular disease associated with diabetes- not neuropathic but ischaemic, referral to the vascular surgeons

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66
Q

What are the physiological effects of thyroid hormone?

A 
Increase HR and CO 
Increase bone resorption 
increases gut motility 
Increases gluconeogenesis 
Maintains normal hypoxic and hypercapnic drive
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67
Q

Outline the normal thyroid hormone axis?

A

TRH released from hypothalamus–> TSH secreted from ant pit–> thyroid to release T3 and T4

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68
Q

What is Graves disease?

A

A type of HYPERthryoidism where TSH-receptor stimulating antibodies cause excess T3/T4

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69
Q

Apart from Graves disease, outline another autoimmune cause of thyrotoxicosis?

A

Nodular, either toxic nodule on the thyroid or a multiple nodules, secreting T3/T4

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70
Q

What is thyroiditis?

A

Inflammation of the thyroid gland causing release of thyroxine (T4)

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71
Q

What can cause thyroiditis?

A

Viral infection, medication (amiodarone) or following pregnancy

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72
Q

What is Addisons disease?

A

Primary adrenal insufficiency. Destruction of the adrenal gland or genetic defects in steroid production

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73
Q

What are the symptoms of Addison’s disease?

A 
Very non-specific:
Nausea
Abdo pain 
Weight loss 
Fatigue 
Weakness
Cramps
Reduced libido

Dizziness and hypotension due to mineralocorticoid deficiency (aldosterone)
Hypoglycaemia due to glucocorticoid deficiency
Pigmentation due to ACTH excess from reduced cortisol

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74
Q

How do you treat an Addisonian Crisis?

A

IV fluids and hydrocortisone

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75
Q

What is the relevance of hyponatraemia?

A

Very commonly affects hospital patients, up to 30% of hosp patients will have hyponatraemia

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76
Q

What are the symptoms of hyponatraemia?

A 
Early symptoms:
headache 
nausea 
vomitting 
general malaise

Later signs:
confusion
agitation
drowsiness

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77
Q

What serious symptoms can acute severe hyponatraemia cause?

A

Seizures
Resp depression
Coma
Death

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78
Q

What common medication can cause hyponatraemia?

A

thiazide like diuretics

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79
Q

What is osmolality?

A

How salty the blood is, low osmolality means less salt

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80
Q

What is a complication of acute severe hyponatraemia?

A

cerebral oedema

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81
Q

In patient with severe acute hyponatraemia what would always prescribe?

A

Hypertonic saline

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82
Q

What is the most common cause of Addison’s disease in the UK?

A

Autoimmune

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83
Q

What is the relevance of TB to Addison’s disease?

A

TB can cause Addison’s- most common cause in developing countries

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84
Q

What is a known medication that can worsen blood sugar levels?

A

Bendroflumethiazide

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85
Q

What are the symptoms of hypothyroidism?

A 
dry thick skin 
brittle hair 
macroglossia 
puffy face 
loss of lateral 1/3 eyebrow 
weight gain 
carpal tunnel syndrome 
peripheral neuropathy 
bradycardia
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86
Q

What is the first line investigation for Addison’s disease?

A

Morning cortisol

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87
Q

What is a thyroid storm?

A

Severe form of thyroid disease.

Can occur in thyroxic patients who experience an acute stressor e.g. illness, trauma, surgery

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88
Q

How do you treat a thyroid storm?

A 
symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
HDU 
Strong dose of anti-thyroid medication e.g methimazole or propylthiouracil
Beta blockers (IV propranolol) 
Potassium iodide aka Lugol's iodine (to inhibit production of anymore thyroid hormone) 
High dose steroids: dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3
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89
Q

What is the pathological mechanism that leads to peripheral neuropathy in diabetes?

A

Hyperglycaemia leads to advanced glycation end products- these act on specific cells such as endothelial cells and monocytes, this leads to increased production of cytokines and adhesion molecules. This has been shown to have an effect on matrix metalloproteinases, which damaged nerve fibres

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90
Q

What are the effects of a prolactinoma in a) women and b) men

A

a) Women- amenorrhea, galactorrhea and infertility

b) Men- erectile dysfunction, gynocomastia, reduced sex drive and less body hair

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91
Q

What are the risk factors of osteomyelitis?

A 
DM
Peripheral vascular disease 
Malnutrition 
Immunosuppression 
Malignancy
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92
Q

What is the most common cause of primary adrenal failure?

A

Autoimmune, usually have positive adrenal antibodies present

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93
Q

What are the hallmark biochemical features of primary adrenal failure?

A

Hyperkalaemia, hyponatraemia, raised urea and mild anaemia, hypoglycaemia

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94
Q

What biochemical investigations would you do in a patient with hyponatraemia?

A

Serum osmolality, urine osmolality, urine sodium, thyroid function and assessment of cortisol response

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95
Q

What is the first thing to do if a patient presents with low serum osmolality?

A

Rule out non-hypo- osmolar hyponatraemia e.g. hyperglycaemia

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96
Q

What would a low serum osmolality and urine osmolality of less than 100mosmol/kg indicate?

A

primary polydipsia or inappropriate IV fluid administration

97
Q

What is the next steps in investigation if a patient has low serum osmolality and a urine osmolality of greater than 100mosmol/kg?

A

You need to measure their urine sodium

98
Q

What would a low serum osmolality and a urine osmolality of greater than 100mosmol/kg (100= concentrated) and urine sodium of less than 30mmol/kg?

A

True dehydration e.g. GI salt loss
OR
clinically overloaded but intravascular depletion e.g. in congestive cardiac failure, cirrhosis or nephrotic syndrome

Urine sodium of <30 mmol/L suggests low effective arterial volume

99
Q

What would a patient with SIADH look like biochemically (serum osmolality, urine osmolality, urine sodium and their fluid balance)

A

Low serum osmolality
Urine osmolality> 100mosmol/kg
Urine sodium> 30mmol/L
Euvolaemic

100
Q

What is the next steps in investigation if a patient has low serum osmolality and a urine osmolality of greater than 100mosmol/kg and urine sodium of greater than 30mmol/kg?

A

Need to work out - are they EUVOLAEMIC or DEHYDRATED?

101
Q

A patient low serum osmolality and a urine osmolality of greater than 100mosmol/kg and urine sodium of greater than 30mmol/kg and they are dehydrated, what do you need to consider?

A

Addison’s disease, renal or cerebral salt wasting or does the patient have a history of vomitting

102
Q

What do you need to rule out before you make a diagnosis of SIADH?

A

Hypothyroidism - elevated ADH due to decreased Cardiac output
Total salt depletion
ACTH deficiency- check serum cortisol as low cortisol causes less -ve feedback on CRH and Cortisol directly suppresses ADH secretion )

103
Q

Why does ACTH deficiency present like SIADH?

A

Cortisol deficiency leads to increased ADH secretion

104
Q

What are the causes of SIADH?

A

Underlying malignancy
Resp/CNS pathology- CXR to rule out any lung pathology needs to be done
Drugs e.g. anticonvulsants

105
Q

What malignancy is know to cause SIADH?

A

small cell lung cancer

106
Q

How do you treat SIADH?

A

Fluid restriction- however in practice this is quite poorly tolerated
ADH antagonists- Tolvaptan
Demeclocycine- tetracycline antibiotic that inhibits ADH

107
Q

How do you treat hyponatraemia?

A

Hypovolaemic hyponatraemia- normal saline

Hypervolaemic hyponatraemia- needs specialist treatment to treat the underlying cause of CCF, nephrotic syndrome or cirrhosis

108
Q

What is diabetes insipidus caused by?

A

Vasopressin deficiency - cranial DI,

or vasopressin resistance - nephrogenic DI.

109
Q

What is seen in biochemistry of DI?

A

High serum osmolality, low urine osmolality and high urine volume

110
Q

What is cranial DI caused by?

A 
Pituitary disease 
Brain tumours 
Head injury 
Brain malformation 
Brain infections 
Genetic causes - strong FHx
111
Q

What is nephrogenic DI caused by?

A

Metabolic and electrolyte disturbance
Renal disease
Drugs affecting the kidney e.g. lithium

112
Q

What values of urine volume confirm DI?

A

> 3L in 24hrs in the presence of high serum osmolality and low urine osmolality

113
Q

What values of serum osmolality and urine osmolality confirm DI?

A

serum osmolality >295mosmol/kg and urine osmolality <300mosmol/kg

114
Q

What value of urine osmolality or serum osmolality can exclude diagnosis of DI?

A

Urine osmolality >600mosmol/kg

Double serum osmolality

115
Q

What investigation might you do for suspected DI?

A

Water deprivation test

116
Q

How do you conduct the water deprivation test?

A

Patient fluid deprived for 8 hours
Then urine osmolality is measured
Synthetic ADH is administered
8 Hours later urine osmolality is measure again

117
Q

What results would you expect on the water depravation test for cranial DI?

A

Initially low urine osmolality, then post-ADH administration high urine osmolality as cells of collecting duct are responding to the synthetic ADH

118
Q

What results would you expect on the water depravation test for nephrogneic DI

A

Low urine osmolality both pre and post ADH, due to the cells of the collecting duct not being able to respond to ADH

119
Q

How is cranial DI managed?

A

Investigate for pituitary disease

Give synthetic vasopressin - desmopressin

120
Q

How does overtreatment of DI with desmopressin present?

A

Get dilutional hyponatrameia - so get headaches, reduced cognitive ability, seizures

N.B.desmopressin= synthetic ADH, overtreatment leads to increased reabsorption of water therefore leading to the dilutional hyponatraemia

121
Q

How does undertreatment of DI with desmopressin present?

A

Excessive thirst, polyuria

122
Q

How is nephrogenic DI managed?

A

Find cause and reverse if possible.
Use of low salt, low protein diet, diuretics, NSAIDs
Keep on top of the thirst and replace water lost

123
Q

Where is the pituitary gland situated?

A

In pituitary fossa at the base of the brain

124
Q

What anatomy lies a) superior and b) laterally to the pituitary gland?

A

a) Superior - optic chiasm. b) Laterally - cavernous sinus

125
Q

What nerves/ blood vessels are in the cavernous sinus?

A

Occulomotor, Trochlear , trigeminal Va, Vb, abducens, internal carotid artery.

126
Q

How is growth hormone secreted?

A

Pulsatile manner. Peak pulses during REM sleep

127
Q

Name the hormones positively and negatively controlling GH

A

Positive = GHRH. Negative = somatostatin

128
Q

Describe the adrenal axis

A

CRH stimulates ACTH release. ACTH release is circadian - peak pulses early in the morning and lowest at midnight. ACTH stimulates cortisol release. Cortisol has negative feedback on ACTH

129
Q

What are LH and FSH stimulated by and inhibited by?

A

Pulsatile GnRH stimulates. Testosterone and oestrogen inhibit

130
Q

What hormones does prolactin inhibit?

A

LH and FSH - directly inhibit.

131
Q

What are the 2 ways that pituitary tumours can present?

A

Compressive - compress surrounding structures - vision, cranial nerves, all hormones can be reduced. (non-functional pituitary tumour).

Excessive hormone production (functional pituitary tumours).

132
Q

How is prolactin predominantly controlled?

A

Mostly under negative control by dopamine and weak stimulatory control by TRH

133
Q

How can functional pituitary tumours present?

A

Acromegaly. Cushing’s disease. Prolactinoma. TSHoma.

134
Q

Pituitary tumours compressing optic chiasm cause which visual defect?

A

Bi-temporal hemianopia

135
Q

What should be assessed in pt with suspected pituitary tumour?

A

Assessment of visual fields
Biochemical assessment- divided into basal (prolactin, TSH, LH and FSH) and dynamic tests (synacthen test and insulin tolerance test)

136
Q

What time of day should LH, FSH and basal testosterone be checked in men?

A

0900 when deficiency is suspected.

137
Q

When should LH, FSH be tested in women?

A

Measured within 1st 5 days of the menstrual cycle

138
Q

IGF-1 is a marker of GH. What do a) low levels and b) high levels of IGF-1 show?

A

a) low levels - GH deficiency

b) high levels - excess GH.

139
Q

What is synacthen test?

A

Give synthetic ACTH to assess primary adrenal failure. Test how well adrenal glands work by measuring cortisol.

140
Q

What is the Insulin Tolerance Test?

A

Gold standard to test ACTH and GH reserve.

Cause insulin - induced hypoglycaemia. Should see ACTH and GH rise (from the reserve).

141
Q

Which patients should you NOT do insulin tolerance test for?

A

Pt with IHD - can triggery coronary ischemia

Pt with epilepsy - can trigger seizures

142
Q

What imaging would you order for pathology of pituitary gland?

A

MRI

CT if unable to have MRI

143
Q

Distinguish between micro and macro adenomas

A

Micro - less than a cm. More common in women

Macro - more than a cm. More common in men

144
Q

Name ddx for a finding of hyperprolactinaemia

A 
Pregnancy - needs to be excluded first 
Medications - antiemetics, anti-psychotics 
Hypothyroidism (rare)
PCOS 
Large pituitary tumour 
Stress 
Renal failure, adrenal insufficiency.
145
Q

How do micro-prolactinomas present?

A

Menstrual disturbance
Hypogonadism in men
Galactorrhoea
Infertility

146
Q

How is PCOS distinguished from prolactinoma?

A

The presence of androgenic symptoms
Less elevated prolactin (<1,000 miU/L)
Absence of pituitary lesion on MRI

147
Q

How are prolactinomas treated?

A

Dopamine D2 agonists

148
Q

Name a D2 agonist

A

Cabergoline- given once or twice weekly, and better tolerated than bromocriptine
Bromocriptine- given daily

149
Q

Name common side effects of cabergoline

A

Nausea, postural hypotension

Rare - psych disturbance

150
Q

What is risk associated to reducing size of lesion/ tumour bulk of prolactinoma?

A

When size reduces rapidly, can get CSF leak which gives potential risk of meningitis

151
Q

What causes acromegaly?

A

Excessive growth hormone.
Most common cause if unregulated GH secretion by pituitary adenoma

Can also be secondary to malignancy elsewhere e.g lung or pancreatic cancer secreting ectopic GHRH or GH

152
Q

What can untreated acromegaly lead to?

A

Disfiguring features
CVD → premature death
Increased risk of bowel cancer

153
Q

How does acromegaly present?

A

Increased size of hands and feet
Frontal bossing of forehead
Protrusion of chin
Widely spaced teeth
Enlargement of tongue and soft palate due to soft tissue swelling - sleep apnoea, snoring
Puffiness of hands - carpal tunnel syndrome

154
Q

Name specific features of active GH hypersecretion

A

Sweating, headaches, HTN, DM

155
Q

What investigation would you do for suspected acromegaly? And what would you see?

A

Oral glucose tolerance test. Failure to supress GH after OGTT ad elevated IGF-1.

156
Q

List management options available for acromegaly

A

Surgery - remove adenoma
Medical - somatostain analogue or dopamine agonist.
External beam or stereotactic radiotherapy- stereotactic radiotherapy only suitable for lesions well away from the optic chiasm

157
Q

How does the chance of remission differ between patients with pituitary micro-adenomas vs macro-adenoma

A

Micro-adenoma, high chance of remission

Macro-adenoma- only achieved in 60% of patients

158
Q

How is acromegaly monitored?

A

Repeat OGTT after surgery
Long term follow up needed - to control GH and IGF-1 levels.
Periodic screening colonoscopy as there is risk of neoplasia.
Assess for sleep apnoea, DM, CVD risk, symptoms of recurrance

159
Q

What are Non-functioning pituitary adenomas (NFPA)?

A

Biochemically inactive tumours

160
Q

How do non-functioning pituitary adenoma present?

A

Visual field loss, headache, hypopituitarism

161
Q

How does hypopituitarism present?

A

Non specific - lethargy, weight gain, sexual dysfunction
Can present with hypo-adrenal crisis - hyponatraemia, hypotension - MEDICAL EMERGENCY
Short stature in children

162
Q

How is hypopituitarism investigated?

A

Exclusion of adrenal insufficiency
Investigate levels of all hormones.
MRI could show empty fossa or pituitary tumour

163
Q

How is hypopituitarism treated?

A

Depends on the deficiency - ACTH-hydrocortisone replacement
TSH-thyroxine replacement
gonadotropin- Men- testosterone via gel or injection
Women- oestrogen and progesterone via COCP or HRT
GH- daily subcut injection

164
Q

Differentiate between Cushings syndrome and Cushing’s disease

A

Cushing’s syndrome- collection of symptoms

Cushing’s disease- excessive ACTH secretion from a PITUIATARY adenoma, can cause cushings syndrome

165
Q

How does Cushing’s syndrome present?

A

Central obesity
Dorso-cervical fat pad
Increased roundness of the face
Pt has red face, thin skin, proximal myopathy
May be HTN, premature osteoporosis, DM, depression, cardiac hypertrophy (due to too much stress hormone)

166
Q

Why is it dangerous to leave Cushing’s syndrome untreated?

A

Significant morbidity. 5-yr mortality approaching 50%

167
Q

What are the causes of Cushing’s syndrome?

A

Exogenous steroids
Cushing’s disease
Adrenal adenoma
Paraneoplastic Cushing’s (ectopic ACTH secretion e.g. small cell lung cancer)

168
Q

What investigations would you do for suspected Cushing’s syndrome?

A

24hr urine free cortisol, low dose dexamethasone suppression test, overnight dexamethasone suppression test.

Screening tests - alcoholism and severe depression can make pts look like they have cushings syndrome but tests come back as normal

169
Q

Explain the dexamethasone supression tests.

A

Low dose 1mg- give dexamethasone at 10pm, check free cortisol at 9am. NORMALLY, should be suppressed, in Cushing’s SYNDROME, it will not be suppressed, therefore you now do the HIGH dose to find out the underlying cause

High dose dexamethasone supression test 8mg. Process is same as above:

Cortisol is surpressed- cushing’s disease- pit adenoma

Cortisol is NOT supressed but ACTH is surpressed- adrenal adenoma (secreting cortisol independently)

Neither cortisol or ACTH surpressed- ectopic ACTH

170
Q

Name differential for Cushings syndrome

A

Pituitary, adrenal or ectopic ACTH

171
Q

What may be in pt’s Hx to point towards them having ectopic ACTH secretion, causing Cushings syndrome?

A

Hypokalaemia
SMoking Hx
Weight loss
By lung cancer or other malignancy.

172
Q

What presenting complaint directly points towards adrenal tumour?

A

Significant, accelerated hirsutism

173
Q

How is adrenal tumour managed?

A

Adrenalectomy

174
Q

How is cushings disease managed?

A

Trans-sphenoidal removal of pit adenoma

175
Q

What is Trousseau’s sign? What is relevance?

A

Due to Hypocalcaemia

When inflate BP cuff above systolic pressure. Brachial artery is occluded. Causes carpal spasm (e.g. wrist flexing and fingers abducting)

176
Q

What is Chvostek’s sign? What is its relevance?

A

Due to hypocalcaemia.

Tapping over parotid (CN7) causes facial muscles to twitch

177
Q

Briefly describe hypoparathyroidism

A

decrease PTH secretion
e.g. secondary to thyroid surgery*

low calcium, high phosphate

treated with alfacalcidol

178
Q

What are the main symptoms of hypoparathyroidism?

A

The main symptoms of hypoparathyroidism are secondary to hypocalcaemia:

tetany: muscle twitching, cramping and spasm
perioral paraesthesia

Trousseau’s sign: carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic

Chvostek’s sign: tapping over parotid causes facial muscles to twitch

if chronic: depression, cataracts
ECG: prolonged QT interval

179
Q

What is myxoedemic coma? How would it present? How treated?

A

WHAT? Potentially fatal complication of undiagnosed hypothyroidism or poor adherence to levothyroxine therapy

Present: overweight pt, dry skin, thinning hair, hypotensive, bradycardia, hypothermic

Treat:
IV Thyroxine
IV hydrocortisone - for possibility of adrenal insufficiency
ITU for support

180
Q

What are some side effects of long term steroid use - many think of a few from different systems

A 
endocrine:
impaired glucose regulation
increased appetite/weight gain
hirsutism
hyperlipidaemia

Cushing’s syndrome:
moon face
buffalo hump
striae

musculoskeletal:
osteoporosis
proximal myopathy
avascular necrosis of the femoral head

immunosuppression:
increased susceptibility to severe infection
reactivation of tuberculosis

psychiatric:
insomnia
mania
depression
psychosis

gastrointestinal:
peptic ulceration
acute pancreatitis

ophthalmic:
glaucoma
cataracts

suppression of growth in children

intracranial hypertension

neutrophilia

181
Q

What is Sheenhan’s syndrome? What causes it?

A

What?
Ischaemia of pituitary gland causes necrosis of secretory cells - get panhypopituitarism.
Leads to : amenorrhea, failure to lactate and death

Cause?
Hypotension/ hypovolaemia due to obstetric haemorrhage. Pituitary gland becomes large and vascular during pregnancy so is vulnerable to hypotension and hypoxia.

182
Q

What is a pituitary apoplexy? What causes it? What is commonly lost? Tests?

A

What?
Endocrine Emergency —-> Haemorrhage / infarction of a pituitary tumour

Cause?
Commonly hypertension or surgery

Commonly lost?
Anterior pituitary hormones- especially ACTH.
Causes 2ndary Adrenal Insufficiency

Tests: Electrolytes / Pit hormones / Glucose / MRI or CT if none

183
Q

How would a patient with pituitary apoplexy present?

A

Sudden onset severe headache (thunderclap) retro-orbital

Nausea, vomiting, reduced consciousness

Opthalmoplegia (paralysis / weakness of 1 or more extraocular muscles)

Visual disturbance - bitemporal hemianopia most common

+ deficiency in Ant Pit hormones - especially ACTH

184
Q

Most common functioning tumour of the anterior pituitary gland?

A

Prolactinoma

185
Q

What causes hypopituitaism vs hyper

A
186
Q

What investigations would you do if suspect hypopituitasm

A
187
Q

How large is a macroadenoma of the pituitary? what sign might a patient have ?

A

> 10mm

Bitemporal hemianopia due to compression of optic chiasm

188
Q

What is 1st line treatment for Prolactinomas in men and women? 2nd line?

A

1st line:
Dopamine agonist - Cabgergoline reduce tumour size and prolactin level

2nd line: Trans sphenoidal surgery if medical treatment not tolerated or unsuccessful

189
Q

How does Prolactinoma present in men vs women

A 
Men:
Loss of libido 
Lethargy
Galactorrhea
impotence 
hypogonadism (small testes)

Women:

  1. Menstrual disturbance: Amenorrhea/Oligomenorrhea/Menorrhagia
  2. Infertility
  3. Galactorrhea
190
Q

How does hypercalcaemia present?

A

Non-specific symptoms - tiredness, aches, pains
Specific symptoms - polyuria, polydipsia (nephrogenic DI)
Abdominal pain, constipation. Psychiatric symptoms present. Kidney stones.

191
Q

How might a non-functioning adenoma present?

A

Compression might cause:

Visual disturbance - bitemporal hemianopia

Headache / vomiting / papilloedema (ICP +)

Oligomenorrohea and amenorrhea in women

Reduced libido and fertility in men

Cranial nerve palsy

192
Q

How might a non functioning pituitary adenoma cause hyperprolactineamia?

A

Non functioning can cause as it removes the dopaminergic inhibition of prolactin release

193
Q

What investigations for Hyperpituitarism ? (4)

A
  1. Visual
    Optic chiasm - bitemporal hemianopia
    Cavernous sinus - diplopia
2. Blood hormones (morning )
TSH / thyroxine
Prolactin
ILGF-1
FSH / LH / oestrogen / testosterone
ACTH / Cortisol
  1. Imaging
    MRI / CT
    radio-labelled dopamine antag. can visualise prolactinoma
  2. SUPPRESSION tests (reduced -ve feedback)

Oral glucose tolerance test - should normally suppress GH

ACTH in response to dexamethesone should suppress CRH and ACTH

194
Q

What drugs can cause hyperprolactinaemia?

A

D2 antagonists

Antipsychotics 1st + 2nd:
Haloperidol 1st
Clazapine 2nd

Cyclic Antidepressants:
Amytryptilline

SSRIs:
Citalopram

Anti emetics:
Domperidone
Metoclopramide

195
Q

How does a prolactinoma lead to infertility?

A

Prolactin interferes with GnRH release. This inhibits the release of LH and FSH causing hypogonadism

196
Q

What outside of the pituitary gland in surrounding tissues could cause hypopituitarism?

A

Tumours of surrounding tissues that could compress.

Gliomas (in optic chiasm)
Meningiomas
Craniopharyngiomas
Mets - breast, bronchus, kidney

197
Q

What is the medical treatment of hyperprituitarism? (4) Risk of treatment?

A

All risk of inducing hypopituitarism

Cabergoline - dopamine antagonist to reduce prolactin

Somatostatin analogue - Octreotide to reduce GH

Surgical removal

Irradiation to prevent recurrence

198
Q

What is a microadenoma?

A

adenoma <10mm

more common

199
Q

Name causes of hypocalcemia?

A

Post - surgical hypoparathyroidism
Vitamin d deficiency
Hypomagnesaemia

200
Q

What are the clinical features of acute severe hypocalcaemia?

A

Laryngospasm
Prolonged QT interval
Seizures

201
Q

How does hypocalcemia present?

A 
Muscle cramps 
Carpo-pedal spasm
Perioral parasthesia 
Peripheral parasthesia 
Neuro-psychiatric symptoms 
Positive Chvostek’s sign
Trousseau’s sign
202
Q

What investigations needed to diagnose hypopituitarism?

A

Visual field assessment
Basal blood tests
MRI or CT

STIMULATION TESTS
GH - does GH rise in response to insulin tolerance test?

Cortisol - does it rise after ACTH (Synacthen)

LH / fSH in response to GnRH or clomifene (anti oestrogen)

203
Q

What is Trousseau’s sign?

A

Carpo-pedal spasm induced after inflation of a sphygmomanometer cuff 20 mmHg over pts systolic BP for 3 mins. Positive when induces latent tetany (spasm) due to hypocalcaemia.

204
Q

How is hypocalcaemia treated?

A

Calcium replacement

205
Q

How is acute hypocalcaemia treated?

A

IV calcium

206
Q

What is dosage given for severe vit d deficiency?

A

Loading dose of cholecalciferol - 20,000IU per week for 7 weeks then maintenance dose of 1-2000 IU per week

207
Q

How is hypoparathyroidism treated?

A

Alfacalcidol or calcitriol - starting dose of 0.25mcg/day 1-alfacalcidol

208
Q

What is the aim in treating hypocalcaemia?

A

Keep calcium levels at lower end of reference to reduce risk of nephrocalcinosis

209
Q

What is pseudo-hypoparathyroidism?

A

Rare condition caused by mutation in G protein coupled to PTH receptor, leading to PTH resistance

210
Q

How does pseudo-hypoparathyroidism present?

A

Bloods - Hypocalcaemia, High phosphate

Signs - Short stature, round face, short 4th and 5th metacarpals

211
Q

A 10 week pregnant patient comes in with heat intolerance and palpitation, upon further investigations it is found she has hyperthyroidism, what drug would you prescribe here?

A

Propylthiouracil as carbimazole crosses the placenta, therefore unable to use in first trimester of pregnancy

212
Q

What is the treatment for Pituitary Apoplexy?

A

High dose IV hydrocortisone

Transsphenoidal surgical decompression w/in 1 week
( Surgery for pts with neuro-opthalmic signs / deteriorating consciousness)

213
Q

Group the major disorders of the anterior pituitary into 2 main categories

A
  1. Hormone excess due to functioning adenomas
    e. g. GH- acromegaly, ACTH- Cushing’s disease
  2. Hormone deficiency due to non functioning adenoma (SOL). Present later as a macroadenoma - compress secretory cells or portal vessels
214
Q

List 4 ways that pituitary tumours can present

A
  1. Visual disturbance / headache
  2. Inappropriate hormone excess ACTH- Cushing’s disease, Prolactinaemia, GH- acromegaly
  3. hormone hypo / hyper secretion due to compression
  4. Amenorrhea or loss of libido
215
Q

What are some infective / inflammatory cause of pituitary failure?

A

Infective:
TB / syphyllis

Inflammatory:
sarcoidosis
haemochromatosis

216
Q

What investigations needed to diagnose hypopituitarism?

A

STIMULATION TESTS

217
Q

What are the differentials of Diabetes Insipidus clinical presentation?

A

Psychogenic polydipsia, DM, Diuretic use, Hypercalcaemia ( as serum calcium is elevated)

218
Q

Acid base balance in addisons/adrenal insufficiency?

A

Hyperkalaemic metabolic acidosis

219
Q

Target HbA1c for patients on a drug the causes hypoglycaemia?

A

The Hba1c target for patients on a drug which may cause hypoglycaemia (eg sulfonylurea) is 53 mmol/mol

220
Q

Causes of hypoglycaemia?

A

Insulinoma
Self-Administered insulin/sulfonyureas
Addisons disease
alcohol

221
Q

Levothryroxine side effects?

A

hyperthyroidism: due to over treatment
reduced bone mineral density
worsening of angina
atrial fibrillation

222
Q

Treatment for ectopic Cushing’s syndrome?

A

Treat underlying malignancy

223
Q

Why are ACTH levels low in an adrenal cause of Cushing’s syndrome?

A

Increased cortisol causes negative feedback.

224
Q

What are levels of ACTH in Cushing’s syndrome caused by pituitary adenoma or paraneoplastic?

A

Normal or high

Pit adenoma= excessive ACTH secretion
Paraneoplastic= tumour secreting ACTH that is NOT pit adenoma

225
Q

What are cortisol levels following high dose dexamethasone suppression test in a pituitary adenoma?

A

Reduced cortisol

226
Q

What are cortisol levels following high dose dexamethasone suppression test in ectopic Cushing’s syndrome?

A

No suppression - cortisol remains high.

227
Q

Following High dose DST for pituitary adenoma secreting ACTH, what is next step in management ?

A

MRI of the pituitary gland.

228
Q

If MRI of pituitary gland in Cushing’s syndrome does not show pituitary adenoma, what is next step?

A

Inferior Petrosal Sinus Sampling = shows clear gradient between central and peripheral ACTH levels after an injection with CRH. (Sampling the veins that drain the pituitary gland)

229
Q

In suspected ectopic ACTH in Cushing’s syndrome, what is next step following High Dose DST?

A

Whole body CT scan or PET imaging - to find carcinoma.

Note: common place = thorax.

230
Q

Medical treatment options for Cushing’s syndrome?

A

Metyrapone - block steroid synthesis pathway
Ketocanazole - adrenolytic agent
Radiotherapy - help reduce size of tumours before surgery. Or mainstay of treatment if tumours are unresectable.

231
Q

What is myxoedema coma?

A

extreme form of hypothyroidism
high mortality

232
Q

Clinical features of myxoedema coma?

A

stupor
hypothermia
respiratory failure
confusion
coma
dry skin
sparse hair
hoarse voice
periorbital oedema

CVS: non-pitting oedema of hands and feet, bradycardia, hypotension refractory to vasopressors, reduced contractility, pericardial effusion
RESP: respiratory depression, impaired respiratory muscle function, hypoxia and hypercapnia
RENAL: bladder atony, urinary retention, urinary Na+ normal or high
ELECTROLYTES: hyponatraemia from increased H2O reabsorption from high levels of ADH
GI: macroglossia, anorexia, abdominal pain, constipation, ileus
CNS: delayed tendon reflexes, slow mentation, depression -> psychosis, seizures

233
Q

Risk factors for myxoedema coma?

A
  • hypothermia
  • CVACHF
  • infections
  • drugs: anaesthetics, sedatives, narcotics, amiodarone, lithium
  • GIH
  • trauma
  • electrolytes: hypoglycaemia, hyponatraemia
  • acidosis
  • hypoxaemia
  • hypercapnia
234
Q

Inv and suspected findings in myxodema coma?

A
  • TSH: markedly elevated in 95% of cases, 5% are caused by central TSH failure
  • low free T4
  • low T3
  • hyponatraemia
  • hypoglycaemia
  • anaemia
  • hypercholesterolaemia
  • high LDH
  • high CK
235
Q

Management for myxoedema coma?

A

RESUSCITATION
* admit to ICU because if high mortality and multi-faceted therapy
* may require intubation for various reasons (respiratory failure, airway obstruction from macroglossia, coma)
* ventilation may be required for several days -> weeks
* IV fluid resuscitation and vasoactive agents until thyroid hormone action begins
* warm patient and pre-empt vasodilation and hypotension

Acid-base and Electrolytes
* supportive care
* glucose
* hyponatraemia: cautious correction over time (<10mmol/L day)

Specific Therapy
* hydrocortisone 100mg Q 6hourly if adrenal or pituitary insufficiency suspected
* replacement of thyroid hormones (T4 or T3 is controversial):
* (1) T4 – loading dose = 500mcg IV -> 50-100mcg OD IV or orally
* (2) T3 – loading dose = 10mcg IV -> 10mcg Q4 hrly for 24 hours then every 6 hours

Underlying Cause
treat precipitant (withdraw drugs, treat infection…)

236
Q

Features of thyroid storm?

A

fever > 38.5ºC
tachycardia
confusion and agitation
nausea and vomiting
hypertension
heart failure
abnormal liver function test - jaundice may be seen clinically

237
Q

What is pseudohypoparathryoidism?

A

due to abnormality in a G protein
associated with low IQ, short stature, shortened 4th and 5th metacarpals

238
Q

Blood results for pseudohypoparathryoidism?

A

low calcium, high phosphate, high PTH

239
Q

How is pseudohypothyroidism diagnosed?

A

diagnosis is made by measuring urinary cAMP and phosphate levels following an infusion of PTH. In hypoparathyroidism this will cause an increase in both cAMP and phosphate levels. In pseudohypoparathyroidism type I neither cAMP nor phosphate levels are increased whilst in pseudohypoparathyroidism type II only cAMP rises.

Y3 med old (8 decks)

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