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Year 3 > Endo conditions > Flashcards

Endo conditions Flashcards

1
Q

What symptoms will someone with Addison’s disease classically present with?

A 
Hyperpigmentation
Lethargy 
Anorexia
Weight loss 
Nausea/vomitting 
Hypotension
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2
Q

How does Addison’s disease arise?

A

Adrenocortical failure due to destruction of the adrenal cortex which results in a lack of aldosterone, cortisol and DHEA

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3
Q

Which 3 hormones are not produced in Addison’s disease?

A

Cortisol
Aldosterone
DHEA

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4
Q

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

A

Synacthen test which is when a synthetic version of ACTH is given and cortisol levels are measured half an hour before and after- if they aren’t raised after then it is likely the patient has Addison’s

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5
Q

What investigations would you do if you suspect someone has Addison’s disease?

A

Synacthen test
Electrolytes
FBC

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5
Q

What investigations would you do if you suspect someone has Addison’s disease?

A

Synacthen test
Electrolytes
FBC

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6
Q

What electrolyte imbalance is someone with Addison’s likely to have?

A

Hyponatraemia

Hyperkalemia

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7
Q

How is Addison’s disease managed?

A

Cortisol replacement- hydrocortisone or prednisolone
Aldosterone replacement- fludrocortisone
DHEA replacement if low libido or lethargy

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8
Q

What class of hormones is cortisol?

A

Glucocorticoids

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9
Q

What class of hormones is aldosterone?

A

Mineralocorticoids

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10
Q

What are the main complications of Addison’s disease?

A

Secondary Cushing’s syndrome

Osteopenia/osteoporosis (from prednisolone)

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11
Q

What symptoms will someone with hypoglycaemia present with classically?

A 
Diaphoresis 
Tremor 
Confusion
Hunger
Anxiety
Tingling
Nausea
Drowsiness
Blurred vision
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12
Q

What are some common causes of hypoglycaemia?

A

Incorrect insulin usage

Insulinoma

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13
Q

How is hypoglycaemia managed?

A

If they are conscious and able to swallow give them fast acting carbohydrates eg glucose gel, glucose pills etc and then after a while long acting carbs eg a slice of bread

If they cannot swallow or are unconscious give IM glucagon

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14
Q

What symptoms will someone with Cushing’s disease classically present with?

A 
Weight gain
Facial rounding
Striae
Hyperglycaemia
Hypertension
Menstrual irregularity
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15
Q

How does Cushing’s disease arise?

A

Any pathological cause of hypercortisolism eg pituitary tumour, tumour of the adrenals

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16
Q

What are the 2 types of Cushing’s disease? What is the difference in pathophysiology?

A

ACTH dependent- higher levels of ACTH lead to higher levels of cortisol
ACTH independent- high levels of cortisol but normal/low levels of ACTH

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17
Q

Who is most likely to get Cushing’s disease?

A

Women

People on glucocorticoids

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18
Q

What are some common causes of Cushing’s disease?

A

Pituitary tumor
Adrenal tumor
Exogenous steroid use

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19
Q

What is the difference between Cushing’s disease vs Cushing’s syndrome?

A

Cushing’s disease= pituitary tumor leading to excess cortisol (due to excess ACTH)
Cushing’s syndrome= any pathological reason for hypercortisolism

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20
Q

What symptoms will someone with hyperthyroidism present with classcially?

A 
Heat intolerance
Fatigue
Weakness
Palpitations
Tremor 
Weight loss (unexplained and non intentional) 
Anxiety
Diarrhoea
Oligomenorhea 
Orbitopathy if its due to Grave's
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21
Q

Who is more likely to present with hyperthyroidism?

A

Those with family history

Females

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22
Q

How is hyperthyroidism investigated?

A

TSH is measured (usually it will be low)
If its high or normal measure FT4
If its low measure FT4 and FT3

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23
Q

What are some causes of hyperthyroidism? Explain the hormone levels in each one

A

Grave’s disease= autoimmune disease where antibodies stimulate TSH receptors on the thyroid gland, low TSH, high FT3 and FT4

Pituitary tumor= tumor of the pituitary secretes TSH and raises thyroid hormone levels, high TSH, high FT4 and FT3

Thyroid nodule= nodule of the thyroid is overactive resulting in high FT4 and FT3 but low TSH

Thyroiditis= inflammation of the whole thyroid gland resulting in high FT4 and FT3 but low TSH

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24
Q

How is hyperthyroidism managed?

A

Anti thyroid drugs eg carbimazole, thiamizole
Radioiodine therapy where the thyroid cells are damaged to stop them making excess hormones
Surgery to remove part or all of the thyroid

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25
Q

What are complications of hyperthyroidism?

A

Thyroid storm
Problems in pregnancy eg pre eclampsia, miscarriage
Eye problems

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26
Q

What are the first line investigations you shoudl order if you think someone has hyperthyroidism?

A

Serum TSH

Can also measure FT4 and T3

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27
Q

What symptoms will someone with hypothyroidisim present with classically?

A 
Fatigue
Weight gain
Depression
Cold intolerance 
Constipation
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28
Q

What are the first line investigations when you suspect someone has hypothyroidism?

A

Serum TSH (will be high)
Can also measure FT4 and T3
FBC (check for anaemia)
Cholesterol (check due to weight gain)

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29
Q

How is hypothyroidism managed?

A

Levothyroxine

If they are young measure their TSH and FT4 to monitor them

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30
Q

How long does treatment for hypothyroidism take to work?

A

It can take up to 6 months for TSH levels to return to normal

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31
Q

What is the difference between primary and secondary hypothyroidism and how do hormone levels differ?

A 
Primary= thyroid gland doesn't make enough T4 and T3, this causes high TSH levels
Secondary= TSH levels are low which insufficient T3 and T4 production from the thyroid
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32
Q

What is Hashimoto’s thyroiditis?

A

Autoimmune hyperthyroidism

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33
Q

What are hormone levels over the course of Hashimoto’s thryoiditis?

A

Hyperthyroidism to start with (inflammation of the thyroid)
Hypothyroidism following this due to thyroid cells unable to take in iodine
Normal thyroid levels

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34
Q

Are thyroid gland lumps deep or surperficial?

A

Deep

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35
Q

What does diffuse and smooth enlargement of the thyroid indicate?

A

Hashitmoto’s, Grave’s physiologoica goitre

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36
Q

What can you ask the patient to do to try and ascertain if the nodule is on the thyroid? What will you see?

A

Get them to swallow, the nodule will move

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37
Q

What can you ask the patient to do to try and ascertain if the nodule is a thyroglossal cyst? What will you see?

A

Tell them to stick their tongue out and it will move when they do this

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38
Q

What are hand signs of hyperthyroidism?

A 
Fine tremor
Palmer erythema
Clubbing 
Sweating
Tachycardia 
Onycholysis
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39
Q

What is onycholysis?

A

Separation of the nail from the nail bed

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40
Q

What are eye signs in hyperthyroidism?

A

Lid lag

Exopthalamos

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41
Q

What signs are specific to Grave’s disease?

A

Exopthalamos

Pretibial myxoedema

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42
Q

What are some general signs of hypothyroidism?

A

Deepening or voice
Coarse skin
Oedematous looking face
Slow reflexes

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43
Q

What will thyroid levels be in someone with goitre?

A

You can’t tell you have to test them biochemically

They could be hypo hyper or euthyroid

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44
Q

What are thyroid levels in someone with malignancy/

A

They can be anything, most commonly they are euthyroid

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45
Q

What antibody is tested if someone has high TSH? Why?

A

Thyroid peroxidase antibody to check for Hashimoto’s thyroiditis

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46
Q

If someone has a neck lump and thyroid function is measured, who should they be reffered to if thyroid levels aren’t normal vs are normal

A 
Normal= surgeon as it could be malignant (such patients are often euthyroid)
Deranged= endocrinologist (thyroid issue that likely isn't to do with malignancy)
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47
Q

What is thyroid eye disease?

A

Changes to the orbital tissue due to thyroid dysregulation

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48
Q

What are some classical symptoms of thyroid eye disease?

A 
Soreness of the eyes
Bulging out of the eyes (exopthalamos) 
Diplopia
Increased watering of the eye 
Visual problems due to compression of the optic nerve
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49
Q

What thyroid problems cause thyroid eye disease?

A

Hyperthyroidism (Grave’s disease)

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50
Q

How is thyroid eye disease managed?

A

Conservative management is ideal
If severe, corticosteroids may eb prescribed first
Radiation therapy can be used to reduce inflammation at the back of the eye
Surgery can be used for decompression if the optic nerve is compromised

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51
Q

What is the pathophysiology of thyroid eye disease?

A

Thyroid dysregulation causes the eye muscles to enlarge and fatty tissue to build up behind the eyes

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52
Q

What is a notable side effect of medications for hyperthyroidism that you must warn patients about?

A

Agranulocytosis- this means their immune system may not be as strong so they are more at risk of infections etc

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53
Q

What is diabetes insipidus?

A

A metabolic disorder where there is inability to concentrate urine due to either lack of AVP production or insensitivity to AVP by renal cells

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54
Q

What are the 2 types of diabetes insipidus and how do they differ in terms of pathophysiology?

A 
Cranial= problem in the hypothalo-pituitary axis results in lack of AVP production
Nephrogenic= renal cells are not sensitive to AVP
55
Q

What is another name for AVP?

A

ADH

56
Q

What are some causes of cranial diabetes insipidus?

A

Damage to the pituitary eg haemorrhage, trauma, tumor

Autoimmune disorders

57
Q

What are some causes of nephrogenic diabetes insipidus?

A 
Long term lithium use
Nephrotoxicity from other drugs 
CKD
Chronic hypercalcaemia 
Hypokalemia
58
Q

What are some risk factors for diabetes insipidus?

A 
Family history 
Having an existing autoimmune condition
Having an existing pituitary disorder
Being on long term lithium 
Being on long term nephrotoxic drugs
59
Q

What is the first line investigation when you suspect diabetes insipidus?

A

Water deprivation test- measure serum and urine osmolality every hour (normal people will have a reduction in urine volume, higher urine osmolality and lower serum osmolality, does with DI will continue to have a high urine vol, serum osmolality and low urine osmolality)

AVP/desmopressin injection- to see what type of DI they have, if its nephrogenic there will be no change in urine vol, if its cranial there will be a reduction in urine vol

Cranial MRI- if damage to the pituitary gland is suspected

60
Q

What symptoms will someone with diabetes insipidus classically present with?

A

Polyuria
Polydipsia
Nocturia
Hypernatraemia symptoms (lethargy, irritability, hyperreflexia, spasticity)

61
Q

What electrolyte imbalance is common in diabetes insipidus and why?

A

Hypernatreamia- AVP helps sodium excretion in the urine so lack of it means there are higher levels in the body

62
Q

How is cranial diabetes insipidus treated?

A

If mild no treatment is needed
If more acute give desmopressin which is an AVP analogue
Treat acute hypernatreamia with IV or oral fluids

63
Q

How is nephrogenic diabetes insipidus treated?

A

Stop lithium/ nephrotoxic drugs
Correct electrolyte imbalances eg hypercalcaemia/ hypokalemia
Advise them to maintain a low sodium diet and have a high fluid intake
Thiazide duiretics or NSAIDs if pharmacological treatment is needed

64
Q

What is primary hyperparathyroidism?

A

High PTH levels most commonly due to an adenoma of one hyperparathyroidism

65
Q

What symptoms will someone with primary hyperparathyroidism classically present with?

A 
Fatigue
Anxiety
Depression
Poor sleep
Myalgia
66
Q

What are the first line investigations for primary hyperparathyroidism? What would you see?

A

Serum calcium- high
Serum PTH- high
DEXA scan- may show osteopenia or osteoporosis
Vitamin D- often low
Ultrasound neck- done to image and see size of adenoma

67
Q

How is primary hyperparathyroidism managed?

A

First line parathyroidectomy

Give vitamin D supplements

68
Q

What is the main complication for hyperparathyroidism? Explain why

A

Osteoporosis or osteopenia
Occurs because high PTH causes activation of osteoclasts
This leads to bone resorption

69
Q

What is secondary hyperparathyroidism?

A

High PTH levels due to insufficient calcium levels

70
Q

What symptoms will someone with secondary hyperparathyroidism classically present with?

A

Bone pain
Muscle aches
Features of CKD: fluid overload, deranged electrolytes, rash, bruising, high BP, nausea

71
Q

Who is more likely to get secondary hyperparathyroidism?

A

Low vitamin D/ sunlight
Low dietary calcium
CKD

72
Q

What chronic underlying condition is commonly associated with secondary hyperparathyroidism? Why?

A

CKD- when someone has CKD their kidneys have impaired vitamin D metabolism. This means they can’t absorb calcium like they normally would and this causes PTH to rise. They also have impaired phosphate metabolism which makes phosphate levels high

73
Q

What are the first line investigations for secondary hyperparathyroidism? What would you expect to see?

A 
Serum calcium- low
Serum PTH
Serum urea- high due to CKD
Serum creatinine- high due to CKD
Serum phosphate- high due to CKD
74
Q

How is secondary hyperparathyroidism managed?

A

If due to CKD reduce dietary phosphate or give phosphate binders
If due to lack of sunlight or diet then increase exposure to the sun and diet intake

75
Q

What is T1DM?

A

Hyperglycaemia due to immune mediated destruction of beta cells of the pancreas leading to complete lack of insulin production

76
Q

How will someone with T1DM classically present?

A 
Polyuria
Polydipsia
Unintentional weight loss
Fatigue
Blurred vision
Ketosis/ ketonuria
77
Q

How is T1DM diagnosed?

A

Hyperglycaemia (randomn glucose over 11 or hba1c over 48) and the presence of symptoms

78
Q

Who is more likely to get T1DM?

A 
Young children (most commonly presents at 10-14 years but can present at any age) 
Those with family history
79
Q

What is hyperglycaemia defined as in T1 and T2 DM?

A

Randomn glucose= >11 mmol/l

Hba1c= >48 mmol/l

80
Q

How is T1DM managed?

A

First line basal bolus insulin plus dose adjusted insulin for meals
They can be given metformin if hyperglycaemia is not controlled after this
Lifestyle advice to have a heathy diet, do regular exercise, dont smoke, dont drink a lot of alcohol and not on an empty stomach etc and refer them to specialists to monitor treatment and give them carbohydrate counting advice etc

81
Q

What are some complications of T1DM?

A

Ketoacidosis
Hypoglycaemia
Diabetic neuropathy, nephropathy, retinopathy etc etc
Cardiovascular disease

82
Q

What are the sick day rules for T1DM?

A

Keep very well hydrated- 3L fluid/ day
Monitor their blood glucose more regularly
Look for signs of hypoglycaemia or diabetic ketoacidosis
Go to the hospital if they are unwell/ unable to eat or keep hydrated

83
Q

Why does diabetic ketoacidosis arise? Explain why it only occurs in T1DM and not T2

A

It occurs when there is no insulin signal in the body
This means that glucose is not driven into cells and so although there is hyperglycaemia, the body believes it is in a state of starvation as there is no glucose for the cells to use
As a response to this, the liver starts breaking down fats rapidly as a source of energy
This breakdown leads to the production of ketone bodies which are acidic and build up in the blood leading to ketoacidosis
It doesnt occur in T2DM as there is always a small amount of insulin produced which means this state is not triggered

84
Q

What is T2DM?

A

Hyperglycaemia due to impaired insulin secretion and reduced sensitivity to insulin causing impaired glucose metabolism

85
Q

How will someone with T2DM classically present?

A 
Polyuria
Polydipsia
Blurred vision
Unintentional weight loss
Neuropathy if advanced 
Acanthosis nigricans
Infections: urinary, skin, candidal 
They may also be asymptomatic
86
Q

What is a common sign of T2DM? Where do you see it and what does it look like? Explain what it shows

A

Acanthosis nigricans- dark patches of skin (brown in colour) in skin folds eg axilla, groin etc, it is a sign of insulin resistance

87
Q

Who is more likely to get T2DM?

A 
Those with family history
Non white ancestry
Cardiovascular disease
Increasing age 
Those who are overweight or obese
PCOS
Hypertension
Dyslipidaemia
88
Q

How is T2DM diagnosed?

A

Hyperglycaemia (randomn glucose over 11 or hba1c over 48) and symptomatic
If assymptomic 2 tests showing hyperglycaemia (preferably the same test just done at different times)

89
Q

How is T2DM managed?

A

First line lifestyle advice
If this doesnt control hba1c then metformin (slowly increase the dose)- if contraindicated or nto tolerated start with DPP4 inhibitor
If still not controlled add a DPP4 inhibitor or pioglitazone or a sulphonylurea or SGLT2 inhibitor
If not controlled try triple therapy
If not controlled add insulin therapy

90
Q

What must you monitor when someone is on metformin?

A

Kidney function

91
Q

What are some complications of T2DM?

A 
Cardiovascular disease
Congestive heart failure
Stroke
OSA
Depression
Dental problems
Infections
92
Q

What is diabetic eye disease

A

Diabetic retinopathy due to microvascular leakage and occlusion in patients with long term diabetes

93
Q

How will someone with diabetic eye disease classically present?

A 
Cotton wool spots
Interetinal haemorrhage 
Blurred vision
Macular thickening 
Lipid exudates 
Microaneurysms 
Retinal detachment
94
Q

Who is more likely to get diabtic eye disease?

A

Those who were diagnosed young
Those who have had diebetes for a long time
Those with poorly controlled hyperglycaemia
Those with hypertension
Those with kidney disease

95
Q

What are the 2 types of diabetic eye disease and how do they differ?

A

Non proliferative= no sign of new blood vessels just leakage and occlusion
Proliferative= more advanced with evidence of new blood vessels

96
Q

What is the first line investigation for diabetic eye disease?

A

Opthalmoscopy

Refer them to opthamology

97
Q

How is diabetic eye disease managed?

A

depends on the level of severity
non proliferative= usually anti VEGF injections and macular laser therapy
proliferative= pan retinal photocoagulation, anti VEGF injections and macular laser therapy
if severe then vitrectomy

98
Q

What are some complications of diabetic eye disease?

A

Cataract
Post pan retinal photocoag= macular oedema and visual field loss
Post vitrectomy= haemorrhage and cataract

99
Q

What is diabetic nephropathy?

A

A microvascular complication of diabetes where due to hypertension and hyperglycaemia there is damage to the glomerular basement membrane and kidney vasculature leading to impaired kidney function

100
Q

How will someone with diabetic nephropathy classically present?

A

Proteinuria
Albuminuria
Reduced eGFR
Visual changes- loss of vision (it is unlikely to have diabetic nephropathy without retinopathy)
Loss of sensation in upper or lower limbs
Foot changes

101
Q

Who is more likely to get diabetic nephropathy?

A 
Those with long term diabetes
Those with poor hyperglycaemic control
Those with hypertension
Those who are overweight/ obese
Those who smoke
102
Q

What are the first line investigations of diabetic nephropathy and what woulf they show?

A

First line urine albumin: creatinine- would be high (over 3g for more than 3 months)
eGFR (done by measuring creatinine)= low (60ml or less for 3 months)
Urinalysis would show proteinuria
Kidney ultrasound may show enlarged kidneys

103
Q

How is diabetic nephropathy managed?

A

First line ACE inhibitor or ARB
If CKD stage 3 give atorvastatin (also give if lipids ​are high)
If BP is not controlled add CCB or beta blocker
Aim for better glycaemic control

104
Q

What are some complications of diabetic nephropathy?

A 
End stage renal disease
Hyperkalemia
Cardiovascular events 
Peripheral vascular disease
Blindness
Bone disease 
Anemia
105
Q

What are sick day rules for diabetic nephropathy?

A

Stop taking certain medications eg ace inhibitor if there is risk of dehydration and to reduce the risk of AKI

106
Q

What is the hyperosmolar hyperglycaemic state?

A

A state where there is hyperglycamia, serum hyperosmolarity and hypovolemia without the presence of ketosis

107
Q

How does the hyperosmolar hyperglycaemic state arise?

A

When there is persistent hyperglycaemia so the body compensates by excreting it in the urine. This leads to polyuria and therefore dehydration because there is excess water loss in the urine

108
Q

How will someone in the hyperosmolar hyperglycaemic state classically present?

A 
Polyuria 
Polydipsia
Nausea and vomitting
Acute cognitive decline
Signs of hypovolemia= tachycardia, dry mucous membranes, low BP
109
Q

What are the causes of hyperosmolar hyperglycaemic state?

A

Most commonly UTI or pneumonia infections
Always check for diabetic foot
Worsening diabetic control
Acute illness like MI, sepsis, stroke (in stroke there is risk of dehydration because of weakness and how it affects swallowing ability)

110
Q

What are the first line investigations for hyperosmolar hyperglycaemic state and what would you see?

A

Blood glucose- raised above 30 mmol/L
Serum osmolarity- raised
Blood ketones- low or normal
Venous blood gas- may show mild acidosis
Serum urea, creatinine and electrolytes- check for kidney injury and have as a baseline
FBC- leukocytosis

111
Q

How is hyperosmolar hyperglycaemic state managed?

A

IV fluids
Potassium if needed- to correct hypokalemia
Treat the underlying cause and manage symptoms
Monitor biochemical markers

112
Q

What are some complications of hyperosmolar hyperglycaemic state?

A

Insulin related hypoglycaemia

Treatment related hyperkalemia

113
Q

What symptoms will someone with hyoparathyroidism classically present with?

A 
GI symptoms: malnutrition, diarrhoea, malabsorption 
Muscle twitches, spasms, cramps
Anxiety
Brittle nails 
Parasthesia, numbness, tingling
Cataracts
114
Q

What are some causes of hypoparathyroidism?

A

Chronic alcohol use

Surgery of the PTH glands, thyroid or larynx

115
Q

What are the first line investigations for hypoparathyroidism and what would you expect to see?

A 
Serum calcium- low 
Serum magnesium- may be low
Serum vitamin D- may be low
ECG- prolonged PR interval due to hypocalcaemia 
Serum phosphate levels- raised
116
Q

Why do phosphate levels rise in hypoparathyroidism?

A

PTH usually inhibits reabsorption of phosphate in the kidney so when PTH is low phosphate is reabsorbed more

117
Q

What are some complications of hypoparathyroidism?

A 
Ectopic calcification
Renal insufficiency
Kidney stones 
Cataract 
Hypercalcaemia
118
Q

How is hypoparathyroidism managed?

A

IV calcium
Parenteral magnesium if needed
If there is unsatisfactory response to calcium then inject PTH

119
Q

What is hyposplenism?

A

Loss of integrity and function of the spleen, often due to an underlying condition

120
Q

What are the common causes of hyposplenism?

A

Mainly due to:
Coeliac disease
Sickle cell anaemia

Can also be due to:
UC
Dermatitis herpetiformis
Thrombocythemia

121
Q

What are the first line investigations for hyposplenism and what would they show?

A

Blood film- will show howel jolly bodies, pappenheimer bodies, lymphocytosis, monocytosis, increased platelet counts
Imaging of the pancreas via MRI, ultrasound etc will show atrophy

122
Q

How is hyposplenism managed?

A

Immunisations

Prophylactic antibiotics- given after splenectomy for one year daily and to high risk patients for life

123
Q

What is the main medical concern in patients with hyposplenism?

A

Infection- it often progresses to a fatal infection and the highest cause of mortality is pneumococcal infection that develops to sepsis

124
Q

What immunisation is it important to give those with hyposplenism?

A

Pneumococcal- give them the conjugate vaccine because it relies on the T cell mechanism of immunity not the IgM B cell memory cells

125
Q

What must you warn patients with hyposplenism about?

A

The high risk of getting falciparum malaria. Tell them to take all malaria prophylaxis and avoid travel to areas with high risk of malaria

126
Q

What are some risk factors for obesity?

A

Hypothyroidism
Hypercortisolism
Corticosteroid treatment

127
Q

How is obesity diagnosed?

A

By calculating BMI
Obesity I= 30-34.9
Obesity II- 35- 39.9
Obesity III= 40 or over

If someone is very muscular or you think BMI wouldn’t be a good measure of their adiposity measure their waist circumference instead

128
Q

How is obesity managed?

A

First line lifestyle advice about diet and exercise
Bariatric surgery if their BMI is over 50 first line
Consider bariatric surgery if their BMI is over 40 or if they have recently been diagnosed with T2DM but after lifestyle intervention
Pharmacological management can include orlistat and liraglutiside

129
Q

What are some complications of obesity?

A 
Hypertension
Hyperlipidaemia 
ACS
Non alcoholic fatty liver disease 
Metabolic syndrome
Cancer 
Post restrictive surgery nausea and vomitting 
Post surgery vitamin or protein deficiency
130
Q

What is hyperlipidaemia?

A

High levels of cholesterol or triglycerides

131
Q

How will someone with hyperlipidaemia classically present?

A

They often present with a cardiovascular problem
May have xanthelasma- most often next to the eye
May be overweight or obese

132
Q

Who is more likely to get hyperlipidaemia?

A

Those with a family history of ACS, dyslipidaemia eg FH, CHD
Obese
Hypothyroidism
Cholestatic liver disease

133
Q

What are the first line investigations for hyperlipidaemia and what would they show?

A

Serum cholesterol- high LDL, low HDL
Serum triglycerides- high
Lipoprotein(a)- high

134
Q

How is hyperlipidaemia managed?

A

First line statin- can be high diet if they are symptomatic (up to 80mg daily)
Lifestyle advice- exercise, improve diet

135
Q

What are some complications of hyperlipidaemia?

A 
ACS
Ischaemic heart disease 
Peripheral vascular disease 
Stroke
Erectile dysfunction

Year 3 (104 decks)

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