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Endocrine - Level 2 Flashcards

1
Q

Definition of T1DM?

A

o Absolute insulin deficiency causing persistent hyperglycaemia
o Most common is immune for 1A
o Some slower progression form occur later in life (LADA)

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2
Q

Pathology of T1DM?

A

o Islet cell antibodies lead to insulitis and destruction of B cells in Islet of Langerhans causing insulin deficiency

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3
Q

Epidemiology of T1DM?

A
  • Peak age is puberty but can be any age
  • Usually lean
  • Associated with autoimmune diseases of thyroid, blood, etc
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4
Q

Aetiology of T1DM?

A

o HLA-DR3/4

o Family history of Type 1

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5
Q

Environmental triggers of T1DM?

A

o Autoantibodies appear early (Glutamic acid decarboxylase)
o Diet
o Coxsackie virus

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6
Q

Acute symptoms of T1DM?

A
  • Young people with 2-6 week history of thirst, polyuria, weight loss
  • Ketoacidosis
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7
Q

Subacute symptoms of T1DM?

A
  • Over month/years (type 2 commonly)

- Thirst, polyuria, weight loss, fatigue, visual blurring, infections

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8
Q

Diagnosis of T1DM?

A

Symptoms of hyperglycaemia

Fasting PG (8-hours) of ≥7mmol/L or random PG ≥11.1mmol/L
	1 abnormal reading if symptomatic, 2 if asymptomatic

One or more of:
 Ketosis, rapid weight loss, age <50, BMI <25, family history of autoimmune disease

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9
Q

Management if T1DM diagnosed?

A
  • If type 1 diagnosed – refer same-day to diabetes specialist team
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10
Q

Initial care of newly diagnosed T1DM?

A
  • Offer structured education programme – DAFNE programmed 6-12 post-diagnosis
  • Teach self-monitoring of blood glucose
  • Lifestyle changes – stop smoking, strict diet (low fat, sugar, high carbs), regular exercise and low alcohol intake
  • Yearly influenza and pneumococcal vaccine
  • Inform DVLA/insurance if having insulin
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11
Q

Drug treatment in T1DM?

A

Insulin

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12
Q

Advice on self-monitoring in insulin management of T1DM?

Targets?

When to give real time glucose monitoring?

When is sensor pump therapy given?

A

At least 4 times a day, before meals and before bed
• Encourage 10x/day if – poor control, hypo frequency increases, period of illness, around sport

Targets
• FPG 5-7 on waking, PG 4-7 before meals, PG 5-9 at least 90 mins after eating

Real time glucose monitoring used when patient has:
• >1 severe hypoglycaemia, loss of awareness of hypoglycaemia, frequent (>2/week) hypoglycaemias affecting ADLs, fear of hypoglycaemia, hyperglycaemia persistently (HbA1c >75)
• Can have multiple daily injection insulin or CSC insulin pump

Sensor-pump therapy given when:
• Episodes of hypoglycaemia despite continuous SC monitoring

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13
Q

Insulin regimens in T1DM?

A

 Offer Basal-bolus regimen 1st line
 Continuous insulin SC infusion (pump)
 2x day pre-mixed 70:30

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14
Q

Basal-bolus regimen in T1DM?

A

 Basal-bolus regimen 1st line

Long-acting insulin detemir BD 1st line
o Alternative: OD insulin glargine or insulin detemir

Offer rapid-acting insulin analogues before meals (Humalog/Novorapid)

Can adjust for meals and infections better
Need to test sugars more, at school inject (psychological)

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15
Q

Continuous insulin SC infusion in T1DM?

A

Continuous insulin SC infusion (pump)

  • Recommended (children >12 and adults) if multiple daily injections result in disabling hypoglycaemia (repeated and unpredictable hypos that results in persistent anxiety about recurrence and effecting ADLs) OR HbA1c >69mmol/mol on MDI therapy
  • Gives basal infusion and bolus when eat
  • Needle changed every 2-3 days
  • Cannot use in sports, swimming, baths (if disconnected – DKA)
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16
Q

Pre-mixed insulin in T1DM?

A

2x day pre-mixed 70:30
• Consider BD human mixed insulin if MDI basal-bolus regimen not possible
• Not suitable for kids’ normal daily activity
• Difficult to control/change insulin dosages

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17
Q

Adjunctive treatments if insulin not achieving adequate glycaemic control in T1DM?

A

 Sotagliflozin/Dapagliflozin with insulin
• If BMI >27, when insulin does not provide adequate glycaemic control
• On >0.5u/kg/day of insulin
• Stop if not a sustained improvement (>3mmol/mol) of HbA1c in 6 months

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18
Q

Sick day rules in T1DM?

A

 Increases insulin need
 Monitor blood glucose more regularly (up to 10x/day)
 Consider ketone monitoring
 Keep hydrated
 Seek medical attention if unable to keep fluids down

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19
Q

Management of T1DM in hospital?

A

 Aim for 5-8mmol/litre during surgery or acute illness
 IV insulin if – unable to eat or predicted to miss more than 1 meal or acute situation (major surgery, high-dose steroids, inotropes, sepsis) or circulatory compromise
 Use SC insulin (including rapid acting insulin before meals) if eating – enable self-administration if willing

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20
Q

Accessories needed in insulin therapy of T1DM?

A

 Insulin injection device
 Needles
 Blood glucose meter, test strips and lancets
 Urine ketones
 Blood ketones meter, test strips and lancets
 Sharps bin
 Glucagon oral gel/injection

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21
Q

Other drug management given in T1DM?

A
  • Statin
    o Atorvastatin 20mg
     If >40, diabetes for >10 years, established nephropathy, CVD risk factors (obesity, hypertension)
  • Antihypertensive (intervention if no risk >135/85, if albuminuria or 2 features of metabolic syndrome >130/80)
    o ACEi
    o Others: BB, low-dose thiazides, CCB
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22
Q

When to refer to nephrologist in T1DM?

A
  • To nephrologist if eGFR <30
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23
Q

Follow ups in T1DM?

A
  • Measure HbA1c every 3-6 months – target 48mmol/mol
  • Annually
    o HbA1c
    o Height, weight, waist circumference, BMI
    o Smoking status
    o Assess erectile dysfunction (offer PDE-5i)
    o Monitor for neuropathy
    o Check injection sites
    o Assess awareness of hypoglycaemia with Gold/Clarke score
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24
Q

How to screen for retinopathy in T1DM?

A

GP referral on diagnosis and annually

Emergency review by ophthalmologist if:
o Sudden loss of vision, rubeosis iridis, pre-retinal/vitreous haemorrhage, retinal detachment

Refer to ophthalmologist if:
o Maculopathy (exudates near fovea, macula)
o Pre-proliferative retinopathy (venous bleeding, reduplication, multiple round or blot haemorrhages)

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25
Q

How to screen for diabetic foot problems in T1DM?

A

 Diabetic foot problems (foot checks annually, monthly-weekly if at risk)
• Assess neuropathy (10g monofilament), ischaemia, ulcers, callus, infection, deformity, ABPI
• If active diabetic foot problem – refer within 1 working day

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26
Q

How to screen for nephropathy in T1DM?

A

 Nephropathy (EMU for ACR, eGFR check)

• Start ACEi if confirmed nephropathy and T1DM

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27
Q

Prognosis of T1DM?

A
  • Without insulin replacement – would die within days/weeks
  • With insulin – live normal life and complication risk reduced by adherence to effective treatment
  • Life expectancy is reduced by 10 years on average
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28
Q

Complications of T1DM?

A

o Macrovascular
 Atherosclerosis – stroke, MI, PVD

o Microvascular
 Affects all small vessels – particularly in retina and nerve sheath

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29
Q

Classes of diabetic eye disease in T1DM?

A

Diabetic retinopathy
 1. Background – capillary microaneurysms, dot & blot haemorrhages, hard exudates
 2. Pre-proliferative – soft “cotton wool” spots
 3. Proliferative – New blood vessels, vitreous/retinal haemorrhages
 4. Maculopathy – Bleeds/exudates encroach on macula causing decreased visual acuity

Cataracts

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30
Q

Nephropathy complications in T1DM?

A

o Damages by glomerular disease – thickening of basement membrane and glomerulosclerosis – microalbuminuria and decreased eGFR

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31
Q

Neuropathy complications in T1DM?

A

o Symmetrical sensory polyneuropathy
o Acute painful neuropathy
o Mononeuritis

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32
Q

Diabetic foot complications in T1DM?

A

o Ulcers due to neuropathy and vascular disease

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33
Q

Skin complications in T1DM?

A

o Lipohypertrophy
o Necrobiosis Lipoiditica – red plaques on skin
o Vitiligo – white patches
o Granuloma annulare – flesh coloured rings over extensor surface of fingers

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34
Q

Other complications in T1DM?

A
  • Infection – especially UTI and skin

- Gastroparesis

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35
Q

Definition of T2DM?

A
  • Type 2 diabetes defined as persistent hyperglycaemia (RPG >11) caused by deficient insulin secretion and resistance to action of insulin
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36
Q

Pathology of T2DM?

A

o Partial insulin deficiency and insulin resistance
o Body unable to secrete enough insulin to meet demands, insulin less able to bind to receptors due to resistance
o Beta cell mass <50% - hyperglycaemia worsens disease and progression to impaired fasting glucose

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37
Q

Epidemiology of T2DM?

A
  • 2-4x more common in Asians, Africans

- One of most common chronic diseases in UK, prevalence increasing

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38
Q

Risk factors of T2DM?

A
  • Older age
  • FHx
  • Hx of gestational diabetes
  • Ethnicity – Asian, African
  • Obesity
  • Diet - High GI index food
  • Hypertension/hyperlipidaemia
  • Low birth weight
  • Alcohol excess
  • Drugs (steroids, statins, thiazide diuretic)
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39
Q

Symptoms of T2DM?

A
  • Subacute with complications – infections, etc
  • Polydipsia, polyuria, weight loss and fatigue
  • Can be asymptomatic
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40
Q

What risk assessment is used in T2DM?

A
  • Tool from Diabetes UK – gender, age, ethnicity, FHx, waist circumference, BMI, BP
  • Gives risk score – low, intermediate, high
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41
Q

When is risk assessment offered in T2DM?

A
  • Offer to:
    o >40
    o 25 and over in South Asian and Afro-Caribbean origin
    o Adults with CVD, hypertension, stroke, obesity, PCOS, Hx of GDM
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42
Q

What to do if risk assessment shows low or intermediate risk score in T2DM?

A

lifestyle and reassess in at least next 5 years

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43
Q

What to do if risk assessment shows high risk score in T2DM?

A

HbA1c testing

o If FPG<5.5 or HbA1c <42 – reassess after 3 years
o If FPG 5.5-6.9 or HbA1c 42-47 – offer lifestyle advice, intensive lifestyle-change programme and reassess at least 1x per year
o If FPG>7.0 or HbA1c >48 – carry out second HbA1c and if confirmed – treat according to guidelines, if <48 offer lifestyle-change programme

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44
Q

HbA1c test - definitions and when to diagnose T2DM?

A
  • Pre-diabetes 42mmol/mol-47mmol/mol
    o Lifestyle advice only
  • Diagnosed when ≥48mmol/mol (or fasting PG ≥7.0mmol/L):
    o Asymptomatic – two abnormal readings
    o Symptomatic – one abnormal reading
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45
Q

Initial management in T2DM?

A
  • Structured group education programme – DESMOND programme
  • Lifestyle modifications – stop smoking, lose weight, foot care, regular exercise, treat risk factors
    o Low glycaemic index foods, low fatty foods, high fibre
    o Over a week, at least 150 minutes of moderate intensity physical activity (such as brisk walking or cycling) in bouts of 10 minutes or more
    o Sick day rules – see diabetic teams
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46
Q

Drug treatment in T2DM - aims?

A

o Aim for 48 - if managed by lifestyle or one drug not associated with hypoglycaemia
o Aim for 53 - if drug associated with hypoglycaemia
o If HbA1c ≥58 - reinforce lifestyle advice, intensify drug treatment

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47
Q

Drug treatment in T2DM - self-monitoring?

A

o Only offer if on insulin, evidence of hypoglycaemic episodes, OHA with risk of hypoglycaemia while driving or operating heavy machinery or pregnant

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48
Q

Drug treatment in T2DM - when metformin appropriate - 1st line?

A

SR Metformin, titrate dose over weeks - 500mg OD with breakfast for at least 1 week, then 500mg BD for at least 1 week, then 500mg TDS to maximum 2g/day

Monitor renal function
 Before (do not start if eGFR <30), annually if normal renal function, biannually if renal impairment
 Stop if eGFR<30, caution if <45

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49
Q

Drug treatment in T2DM - when metformin appropriate - 1st intensification?

A

• Metformin + DPP-4 inhibitor (gliptins)OR
• Metformin + Pioglitazone OR
o Do not use pioglitazone if HF, hepatic impairment, DKA, current or Hx of bladder cancer, uninvestigated macroscopic haematuria
• Metformin + Sullfonylurea

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50
Q

Drug treatment in T2DM - when metformin appropriate - 2nd intensification?

A

• Metformin + DPP-4 inhibitor + sulfonylurea OR
• Metformin + pioglitazone + sulfonylurea OR
• Starting insulin-based treatment OR
• Metformin + sulfonylurea + GLP-1 mimetic (liraglutide)
o If – BMI >35 and psychological or medical problem associated with obesity or BMI<35 where insulin would have significant occupational implications or weight loss would benefit
• Metformin + DPP-4 inhibitor + ertugliflozin
• Metformin + sulfonylurea/thiazolidinedione + empagflozin/canagliflozin

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51
Q

Drug treatment in T2DM - when metformin not appropriate - 1st line?

A

• DPP-4 inhibitor OR pioglitazone OR sulfonylurea

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52
Q

Drug treatment in T2DM - when metformin not appropriate - 1st intensification?

A
  • DPP-4 inhibitor + pioglitazone OR
  • DPP-4 inhibitor + sulfonylurea OR
  • Pioglitazone + sulfonylurea
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53
Q

Drug treatment in T2DM - when metformin not appropriate - 2nd intensification?

A

• Consider insulin-based treatment

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54
Q

When insulin indicated in T2DM - what regimen is used?

A

 Continue metformin

 Regimens:
• Offer NPH (isophane) insulin OD/BD
• Consider both NPH and short-acting either separately or pre-mixed
• Consider insulin detemir/glargine as alternative to NPH
• If metformin not used – gliptin plus sulfonylurea/pioglitazone or together

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55
Q

Other drug management in T2DM?

A
  • Statin
    o If QRISK2 is ≥10% and <84 years, atorvastatin 20mg
  • Antihypertensive
    o Aim for <140/90
    o Lifestyle advice for 2 months
    o ACEi OD (ACEi + diuretic/CCB for Afro-Caribbean)
     Add CCB
     Add thiazide like diuretic
     Alpha-blocker, Beta-blocker or spironolactone
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56
Q

Follow up in T2DM?

A
  • Every review
    o Measure height, weight, waist circumference, BMI
    o Smoking status
    o Assess neuropathy
  • Every 6 months
    o Measure HbA1c every 3-6 months until stable and then 6-monthly
    o If BP stable on medication (1-2 months until stable)
-	Yearly
o	Retinopathy
o	Diabetic foot problems (foot checks monthly-weekly if at risk)
o	Nephropathy (EMU for ACR, eGFR check)
o	CVD (lipids, BP)
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57
Q

Names of gliptins?

A
  • DPP-4 inhibitor

- Sitagliptin, vildagliptin, saxagliptin, linagliptin

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58
Q

names of thiazolidinediones?

A
  • Stimulates nuclear receptor PPAR-Gamma
  • Can cause fluid retention, anaemia
  • Pioglitazone, rosiglitazone
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59
Q

Names of flozins, SE?

A
  • SGLT2 inhibitor

- Common SE UTIs, joints pains, fungal infection

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60
Q

Names of GLP-1 mimetics?

A
  • Glucagon-like peptide 1 receptor agonists (GLP-1 receptor agonists)
  • Liraglutide
  • Used if insulin cannot be used or need weight loss
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61
Q

Prognosis of T2DM?

A
  • Optimal management, usually patients live normal life but may have complications
  • Reduced life expectancy by average of 10 years
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62
Q

How to assess diabetic foot infection in diabetes?

A 
o	Neuropathy (10g monofilament as part of sensory foot exam)
o	Limb ischaemia (pulses, CRT)
o	Ulcers
o	Callus
o	Infection
o	Deformity
o	Gangrene
o	Charcot arthropathy
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63
Q

Management of low risk diabetic foot disease?

A

annual foot assessments, emphasise foot care importance

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64
Q

Management of moderate-to-high risk diabetic foot disease?

A

Refer to foot protection services

 Assess within 2-4 weeks (high) or 6-8 weeks (moderate)

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65
Q

Assessment in foot protection services?

A
  • Assess feet
  • Advice, skin and nail care
  • Biomechanical status of feet, specialist footwear provision
  • Vascular status
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66
Q

When to reassess diabetic foot problems?

A
  • Annual – low risk
  • 3-6 months – moderate risk
  • 1-2 months – high risk (no immediate concern)
  • 1-2 weeks – high risk (immediate concern)
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67
Q

When to refer diabetic foot problems to hospital?

A

 Ulcer with fever or signs of sepsis
 Ulcer with limb ischaemia
 Deep-seated soft tissue or bone infection
 Gangrene

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68
Q

Management of Charcot arthropathy?

A

o Suspect Charcot arthropathy if red, warm, swollen and deformed foot
 Refer within 1 working day to MDT foot care service for triage

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69
Q

Definiton of Charcot’s arthropathy?

A

 Deformed foot
 Rocker bottom foot
 Collapsed medial arch

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70
Q

Investigations of Charcot’s arthropathy?

A

 Weight-bearing X-ray of foot and ankle

 MRI if X-ray normal but still suspected

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71
Q

Management of Charcot’s arthropathy?

A

 Non-removable/Removable offloading device

 Monitor with foot-skin temperature difference and X-rays until resolves

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72
Q

Investigations in diabetic foot infections?

A

 Soft tissue or bone sample from base of debrided wound for microbiology
 FBC/ESR/CRP/blood cultures
 X-ray of foot
 MRI

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73
Q

Management in diabetic foot infections?

A

Antibiotics
• Mild – Oral flucloxacillin 500mg-1g QDS for 7 days (clarithromycin/doxycycline/erythromycin)

• Moderate/Severe

  1. IV flucloxacillin 1g QDS +/- Gentamicin +/- Metronidazole
  2. IV Co-amoxiclav +/- Gentamicin
  3. IV Co-trimoxazole +/- Gentamicin +/- Metronidazole
  4. IV Ceftriaxone +/- Metronidazole

• Pseudomonas aeruginosa
1. Tazocin 4.5g TDS IV

• MRSA
1. Vancomycin/Teicoplanin/Linezolid
o Review after 48 hours and consider oral switch

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74
Q

Investigations of diabetic foot ulcer?

A

 Document size, depth and position of ulcer

 Use SINBAD (Site, ischaemia, neuropathy, bacterial infection, area and depth) to classify

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75
Q

Management of diabetic foot ulcer?

A

 Offloading (plantar, forefoot and midfoot)
 Control infection/ischaemia
 Wound debridement & dressing
• UrgoStart dressings

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76
Q

Description of Graves’ disease?

A
  • Excess circulating thyroid hormones produced by overactive thyroid gland
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77
Q

Types of hyperthyroidism?

A

o Primary – causes by abnormal thyroid gland
 Overt – TSH is low and T3/T4 high
 Subclinical – TSH low and T3/T4 normal

o Secondary – abnormal stimulation of thyroid gland

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78
Q

Epidemiology of Graves’ disease?

A
  • 10x more common in women
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79
Q

Risk factors of Graves’ disease?

A 
o	Women 10x
o	FHx of thyroid disease
o	Smoking
o	Low iodine intake
o	T1DM
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80
Q

Causes of primary hyperthyroidism?

A

 Graves’ Disease
 Toxic Multinodular Goitre
 Toxic thyroid adenoma
 Drugs

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81
Q

Definition of Grave’s disease?

A
  • Most common cause, 75%
  • Autoimmune disorder, antibodies that stimulate TSH leading to excessive secretion of thyroid hormones and hyperplasia of thyroid cells
  • Causes toxic diffuse goitre
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82
Q

Definition of toxic multinodular goitre?

A
  • Thyroid with >2 autonomously functioning thyroid nodules that secrete excess thyroid hormones (benign follicular adenomas)
  • People >60, iodine deficient areas (Denmark)
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83
Q

Definition of toxic thyroid adenoma?

A

• Nodule produces enough hormone to supress TSH from pituitary and contralateral thyroid lobe

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84
Q

What drugs cause hyperthyroidism?

A

• Iodine (amiodarone, IV contrast), lithium, IFN-alpha

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85
Q

Causes of secondary hyperthyroidism?

A

 High hCG (gestational, multiple pregnancy, choriocarcinoma, hydatidiform mole)
 Pituitary adenoma

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86
Q

What causes thyrotoxicosis without hyperthyroidism?

A

 Drugs – levothyroxine, amiodarone, corticosteroids

 Thyroiditis (release of thyroid hormones into circulation due to inflammation of follicles)

87
Q

Types of thyroiditis?

A

• Postpartum
o Autoimmune, usually painless, occurs 2-6 months after delivery
o Thyrotoxicosis followed by hypothyroidism within 1 year of giving birth in previously euthyroid women
o Most becomes euthyroid within 12 months

• Acute
o Bacterial infection of thyroid gland via pyriform sinus connecting gland with oropharynx

• Subacute (De Quervain’s) thyroiditis
o Self-limiting, post-viral painful goitre, high temp, high ESR
o Rx NSAIDs

88
Q

Symptoms of hyperthyroidism?

A

o Malaise, fever
o Thyroid pain
o Hyperactivity, insomnia, irritability, anxiety, palpitations
o Heat intolerance, sweating
o Increased appetite, weight loss, diarrhoea
o Infertility, oligomenorrhoea, amenorrhoea
o Reduced libido

89
Q

Signs of hyperthyroidism?

A 
o	Agitation
o	Fine tremor 
o	Moist skin
o	Palmar erythema
o	Sinus tachycardiac, AF
o	Thin hair
o	Goitre
o	Muscle wasting
o	Hyperreflexia
90
Q

Features of goitres in Graves’, toxic multinodular goitre, toxic adenoma, subacute de Quervains?

A

 Grave’s – diffusely enlarged and pyramidal lobe palpable, may be bruit, soft and symmetrical
 Nodules – toxic multinodular goitre
 Unilateral non-tender – toxic adenoma
 Tender, enlarged, firm, irregular gland – subacute de Quervain’s thyroiditis

91
Q

Signs in Graves’ disease?

A

o Eye disease – exomphalos, proptosis, ophthalmoplegia
o Pretibial myxoedema (swelling above lateral malleoli)
o Thyroid acropachy – clubbing, painful finger and toe swelling

92
Q

Blood tests to perform in hyperthyroidism?

A

TFTs (TSH, T3/4)

93
Q

What to do if TSH within normal range in hyperthyroidism?

A

further investigations not usually needed

94
Q

What to do if TSH low (but over 0.1) in hyperthyroidism?

A

recheck along with FT4 &FT3 after 1-2 months

95
Q

What to do if TSH <0.1 in hyperthyroidism?

A

check FT4 and FT3

96
Q

Definitions of hyperthyroidism according to TSH and T3/4?

A

 Low TSH and raised T3/4 = overt hyperthyroidism (Graves’, amiodarone)

 Low TSH with thyroid pain = thyroiditis

 Low TSH but normal T3/4 = subclinical hyperthyroidism

 Low TSH on levothyroxine = over-treatment

 High TSH & T3/4 = TSH-secreting pituitary adenoma

97
Q

Investigations to perform if thyroiditis suspected?

A

CRP/ESR

98
Q

Management of overt hyperthyroidism?

A

Refer overt hyperthyroidism to endocrinology

Whilst awaiting specialist assessment:
 Beta-blockers (propranolol) to control tremor and tachycardia

99
Q

Specialist management in hyperthyroidism - testing?

A
  • Thyroid-stimulating hormone receptor antibodies (TSH-RAb) – Grave’s disease
  • Radionucleotide thyroid uptake – diffuse in Grave’s, one or more hot nodule
100
Q

Specialist management in hyperthyroidism - drug treatment?

A
  • Radioiodine

* Carbimazole (or propylthiouracil)

101
Q

Management with radioiodine in hyperthyroidism?

A

o First line in toxic nodular goitre & Grave’s disease

o For 18 months

102
Q

Management with carbimazole (or propylthiouracil) in hyperthyroidism?

A

o After euthyroidism achieved:

 Titration-block regime – carbimazole used and dose adjusted every 4-6 weeks, allow endogenous synthesis of thyroid hormone to continue
 Block and replace regime – carbimazole used to block synthesis of thyroid hormone and levothyroxine added

o Both continued for 6-18 months

103
Q

Surgical management in hyperthyroidism?

A

• Total or near-total thyroidectomy

o Second-line in multiple nodules

104
Q

Management of subclinical hyperthyroidism?

A

o Repeat TFTs in 3-6 months
o Refer to endocrinologist if persistent subclinical hyperthyroidism
 Treatment given if TSH <0.1, >65, postmenopausal, or risk of osteoporosis/CVD

105
Q

Management of Graves’ orbitopathy?

A

o Admit immediately – if suspected optic neuropathy, corneal opacity or Hx of globe subluxation
o Refer to ophthalmology

106
Q

General advice given in hyperthyroidism/Graves’ disease?

A

 Smoking cessation
 Artificial tears to lubricate eyes
 Avoid damage to eyes
 Elevate head of bed

107
Q

Follow up in hyperthyroidism - if on carbimazole/propylthiouracil?

A

 Before – FBC, LFT

 Every 6 weeks – TSH, FT4, FT3

 Every 3 months – TSH

 After stopping – TSH within 8 weeks, then every 3 months for a year then once a year

108
Q

Follow up in hyperthyroidism - after radioactive iodine treatment?

A

 Every 6 weeks – TFTs

109
Q

Follow up in hyperthyroidism - after surgery?

A

 TSH and FT4 at 2 and 6 months, then TSH annually

110
Q

Follow up in hyperthyroidism - if in remission?

A

 TFTs annually

111
Q

Follow up in hyperthyroidism - if untreated subclinical hyperthyroidism?

A

 Check TFTs every 6-12 months

112
Q

Prognosis of hyperthyroidism?

A

 Remission in up to 30% without treatment in Grave’s

 Risk of relapse if anti-thyroid drug stopped

113
Q

Complications of Graves’ disease - orbitopathy?

A

 Autoimmune disorder in 90% of Graves disease
 Eye irritation, photophobia, watering of eyes, swelling of eyes
 Lid lag, troubled eyelid retraction
 Double vision, low visual acuity

114
Q

Symptoms of thyrotoxic storm?

A

tachycardia, fever, AF, HF, fever, diarrhoea, vomiting, dehydration, delirium, coma

115
Q

Tests in thyrotoxic storm?

A

 Tests – TFTs, technetium uptake if possible

116
Q

Management of thyrotoxic storm?

A
  • IV access, fluids if dehydrated and NG tube if vomiting
  • Bloods – TFTs, cultures if infection, TRAbs
  • Sedation (chlorpromazine)
  • Propranolol 40mg/8h PO
  • If CI: diltiazem
  • High-dose digoxin to slow heart – ECG monitoring
  • Carbimazole 15-25mg/6h PO
  • Hydrocortisone IV or dexamethasone PO to prevent peripheral conversion of T4 into T3
  • If infection – co-amoxiclav
117
Q

Other complications in hyperthyroidism?

A 
o	AF
o	Heart failure
o	Reduced bone mineral density
o	Anxiety/Depression
o	In pregnancy – miscarriage, pre-eclampsia, prematurity, IUGR, low birthweight
118
Q

Definition of adrenal insufficiency? Epidemiology?

A
  • Destruction of cortex leads to primary adrenal insufficiency
    o Reduces glucocorticoids (cortisol), mineralocorticoids (aldosterone) and adrenal androgens (dehydroepiandrosterone)
    o Absence of cortisol leads to increased ACTH from pituitary gland
  • Adrenal insufficiency can be caused by long-term corticosteroids or disorders of hypothalamus/pituitary but this is secondary:
    o Pituitary ACTH insufficient and adrenal atrophy
  • 1 in 20000
  • Women 30-50
119
Q

Causes of Primary adrenal insufficiency?

A 
	Addison's Disease (80%)
	TB
	Adrenal metastases/haemorrhage
	Amyloidosis/haemachromatosis
	Infection – histoplasmosis, cryptococcosis, CMV, HIV
	CAH
	Adrenalectomy
120
Q

Causes of Secondary adrenal insufficiency?

A

 Exogenous steroids
 Antipsychotic medication
 Tumours secreting steroids
 Trauma, radiotherapy, surgery, neoplasm to hypothalamus

121
Q

Associated diseases with adrenal insufficiency?

A

o Hypothyroidism

o T1DM

122
Q

Symptoms of Addison’s disease?

A 
o	Lean
o	Tanned (due to increase ACTH – sun-exposed areas, scars, palmar creases, mucous membranes)

o Fatigue, weight loss, anorexia, N&V, abdominal pain
o Muscle weakness, cramps, joint pains
o Postural dizziness (postural hypotension)
o Increased thirst/urination
o Craving soy sauce and liquorice

123
Q

Primary care tests performed in Addison’s disease? What are the findings?

A 
Serum cortisol level
	Specialist advice from endocrinologist before serum cortisol if people work shifts, on long-term corticosteroids, receiving oestrogen treatment
	Obtain 8-9am
	If <100 – admit
	If 100-500 – refer to endocrinologist

o U&Es
 Low Na and High K

124
Q

Secondary care tests performed in Addison’s disease - diagnostic 3?

A
  1. ACTH Stimulation (Synacthen) test - Blood sample to check cortisol before and 30 minutes after 250mcg of tetracosactide (synthetic ACTH) IV or IM
  • Normal – cortisol increase to >500-550nanomol/L after 30-60 minutes
  • Adrenal insufficiency – cortisol does not increase adequately
  1. ACTH levels (high in Addison’s, low in secondary adrenal insufficiency)
  2. Plasma renin and aldosterone levels (renin high, aldosterone low)
125
Q

Secondary care tests performed in Addison’s disease - autoantibodies?

A

 Adrenal cortex autoantibodies

 21-hydroxylase antibodies

126
Q

Secondary care tests performed in Addison’s disease - imaging?

A

 CXR/AXR

 CT scan if TB, infection, haemorrhage or neoplastic disease suspected

127
Q

Management of Addison’s disease - drug therapy?

A

o Steroid Replacement
 Glucocorticoid replacement – hydrocortisone 15-30mg daily (10mg waking, 5mg lunch and 5mg in early evening)
 Mineralocorticoid replacement – fludrocortisone 50-300mcg

o Androgen replacement
 Dehydroepiandrosterone may be used in specialist care

128
Q

Management of Addison’s disease - general management?

A

 Lifelong treatment
 Do not stop abruptly
 Steroid card and MedicAlert bracelet
 Adjusting steroid medication
 Recognise adrenal crisis and give IM hydrocortisone
 If undergoing surgery, endoscopy or dental treatment
• Make team aware and cover glucocorticoid cover

129
Q

Management of Addison’s disease - illness rules?

A

o Double normal dose of hydrocortisone if fever/antibiotics
o If nausea – take 20mg hydrocortisone orally and sip ORS
o If vomited – IM hydrocortisone and seek advice

130
Q

Management of Addison’s disease - Exercise rules?

A 
o	Strenuous (marathon) –  up to double dose
o	Normal exercise – 5-10g hydrocortisone before activity
131
Q

Management of Addison’s disease - follow up?

A

 Primary and secondary care shared
 Annual
• Weight, BP, U&Es
• TFTs, glucose, HbA1c, FBC, VitB12, coeliac

132
Q

Symptoms of adrenal crisis?

A

 Symptoms: malaise, fatigue, N&V, abdominal pain, shock (tachycardia, postural hypotension, oliguria, weak, confused)
 Precipitating factors – infection, trauma, surgery, missed medication

133
Q

Initial management of adrenal crisis?

A 
	IM/IV hydrocortisone
•	100mg adults
•	50-100mg child >6 depending on size
•	50mg child 1-5
•	25mg child <1
	Bloods – cortisol, ACTH, U&amp;Es
	IV fluid bolus
	Monitor ECG, blood glucose
	Blood, urine and sputum culture
	Abx if infection suspected
134
Q

Further management of adrenal crisis?

A

 IV glucose if needed
 IV fluids and correct electrolyte imbalance
 Continue IV hydrocortisone 100mg/8h
 Change to oral steroids after 72 hours if condition good

135
Q

Prognosis of Addison’s Disease?

A

o If untreated – fatal

o Require lifelong treatment

136
Q

Description of hypothyroidism?

A
  • Impaired production of thyroid hormones, thyroxine (T4) and tri-iodothyronine (T3)
137
Q

Types of hypothyroidism?

A

o Primary (95%) – thyroid gland unable to produce thyroid hormones:
 Overt – High TSH and low T4
 Subclinical – High TSH and normal T3/T4

o Secondary – insufficient production of TSH due to pituitary or hypothalamic disorder

138
Q

Epidemiology of hypothyroidism?

A
  • Prevalence 1-2%
  • Women 10x
  • Secondary hypothyroidism is rare
  • Congenital hypothyroidism is screened for in Guthrie test
139
Q

Causes of primary hypothyroidism?

A

o Iodine deficiency (MC worldwide cause)
o Autoimmune thyroiditis (atrophic/Hashimoto’s) – MC in UK
 Atrophic – common, diffuse lymphocyte infiltrate of thyroid, atrophy and NO goitre
 Hashimoto’s – goitre due to lymphocytic and plasma cell infiltration, women 60-70, high autoantibodies
o Post-ablative therapy or surgery
o Drugs – anti-thyroid drugs, iodine, amiodarone, lithium, thalidomide, rifampicin
o Transient thyroiditis (subacute, postpartum)
o Thyroid infiltrative disorders – amyloidosis, sarcoidosis, haemochromatosis, TB, scleroderma
o Congenital hypothyroidism – absence or thyroid, ectopic hypoplastic

140
Q

Causes of secondary hypothyroidism?

A

o Pituitary dysfunction – tumours (pituitary adenoma), surgery, radiotherapy, infarction, Sheehan’s syndrome, infiltrative disorders

o Hypothalamic dysfunction – tumours (glioma), surgery, radiotherapy, infiltrative disorders, drugs (retinoids)

141
Q

Symptoms of hypothyroidism?

A 
o	Tired/Lethargic
o	Low mood
o	Cold intolerance
o	Weight gain
o	Constipation
o	Menorrhagia
o	Dry skin, reduced body hair (eyebrows)
o	Hoarse voice
o	Myalgia, cramps, muscle weakness
142
Q

Signs of hypothyroidism?

A 
o	Bradycardic
o	Coarse dry skin/hair, hair loss
o	Oedema, ascites and including around eyes
o	Goitre
o	Delayed relaxation of reflexes
o	Paraesthesia – carpal tunnel syndrome
143
Q

Symptoms specifically in secondary hypothyroidism?

A

also with headache, diplopia, pituitary hormone symptoms

144
Q

Symptoms in postpartum hypothyroidism?

A

usually 3-8 months PP and lasts 6 months

145
Q

Bloods taken in hypothyroidism? Interpretation of results?

A

TFTs

	Overt = TSH high, T4 low
	Subclinical = TSH high, T4 normal
•	Measure again 3-6 months
	Secondary = T4 low without raised TSH
	Pregnancy = TSH high
•	Measure thyroid peroxidase antibodies (TPOAb) and if negative, thyroglobulin antibodies (TgAb)
146
Q

Bloods tested if primary hypothyroidism suspected?

A

 FBC – anaemia
 HbA1c – T1DM
 Lipids
 Thyroid peroxidase antibodies (TPOAb)

147
Q

Imaging if goitre present with hypothyroidism?

A

USS

148
Q

When to screen TFTs in people for hypothyroidism - if pregnant or planning?

A

 >30, goitre, lives in iodine deficient area, FHx, symptoms, T1DM, Hx of neck radiotherapy, BMI>40

149
Q

When to screen TFTs in people for hypothyroidism - if not pregnant?

A

 Goitre, T1DM, T2DM, AF, Osteoporosis, Dyslipidaemia, hyperthyroidism surgery/radioiodine, Hx of neck radiotherapy, Down’s/Turners, subfertile, post-partum depression, drugs (lithium, amiodarone)

150
Q

Management of overt hypothyroidism - referral to endocrine?

A

 Suspected subacute thyroiditis, goitre, nodule, endocrine disease, female and planning pregnancy, CVD, drug-induced

151
Q

Management of overt hypothyroidism - drug treatment?

A

Levothyroxine
• 50-100mcg OD, adjusted in steps of 25-50mcg
o Over 65 – 25-50mcg OD
• Review every 3-4 weeks and adjust dose
• Dose taken >30 minutes before breakfast or caffeinated drinks

152
Q

Management of overt hypothyroidism - follow up?

A

o Once stable, TSH every 4-6 monthly and then annually

o Check lipids if elevated initially

153
Q

Management of subclinical hypothyroidism?

A

o Most do not need treatment but if so: levothyroxine
 If TSH >10 – start if <70, if >70 watch and wait
 If TSH 4-10 - <65 start, >65 ‘watch and wait’

154
Q

Follow up of subclinical hypothyroidism?

A
  • Annually if symptoms, thyroid surgery, raised Ab levels

* Every 2-3 years if no features of disease

155
Q

Management of secondary hypothyroidism?

A

o Refer urgently to endocrinologist

156
Q

Management of postpartum hypothyroidism?

A

o If thyrotoxic pattern – refer to differentiate from Grave’s

o TFT every 2 months
 If hypothyroid – if planning another pregnancy then treat, if not reassess in 2 months

o Annual TFTs

157
Q

Symptoms of myxoedema coma?

A

o Symptoms: hypothyroid, hypothermia, hyporeflexia, low glucose, bradycardic, coma, seizures, psychotic (myxoedema madness)

o Signs: goitre, cyanosis, low BP, HF

158
Q

Management of myxoedema coma?

A 
	ICU
	Bloods – TFTs, FBC, U&amp;Es, cultures, cortisol, glucose
	ABG
	High-flow O2 and ventilation if needed
	T3 (liothyronine) IV slowly
	Hydrocortisone 100mg/8h IV
	Antibiotics
	Warming (blankets, fluids)
	Following initial management – levothyroxine PO
159
Q

Prognosis of hypothyroidism?

A

o Good, most recover with levothyroxine for life
o Subclinical may revert spontaneously to euthyroid
o Postpartum usually resolves after 1 year

160
Q

Complications of hypothyroidism?

A 
o	Impaired QoL
o	Dyslipidaemia
o	CHD/Stroke
o	Heart failure
o	Impaired fertility
o	Pregnancy – miscarriage, pre-eclampsia, placental abruption, PPH, stillbirth, premature, LBW, congenital hypothyroidism
o	Deafness, impaired cognitive function
o	Myxoedema coma
	Rare, presents with hypothermia, coma and seizures
	Precipitant usually HF, sepsis, stroke
161
Q

Describe calcium homeostasis - high levels and low levels?

A

o High calcium level leads to thyroid releasing (vitamin D3 – 1, 25-dihydroxy-vitamin D) calcitonin which:
 Promotes osteoblasts deposit calcium in bone
 Reduces absorption of calcium in kidneys

o Low blood calcium level leads to parathyroid releasing PTH which:
 Promotes osteoclasts to release calcium from bones
 Stimulates kidney to absorb calcium
 Kidney converts 25-hydroxy Vitamin D to 1-25 dihydroxy Vitamin D to stimulate bowels to absorb calcium

162
Q

Definition of hyperparathyroidism?

A

excessive of PTH, leads to raised serum Ca and low phosphate

163
Q

Types of hyperparathyroidism?

A

o Primary – one or more parathyroid gland produces excess PTH
o Secondary – increased secretion of PTH in response to low calcium due to kidney, liver or bowel disease
o Tertiary – autonomous secretion of PTH, usually CKD

164
Q

Epidemiology of hyperparathyroidism?

A
  • 3rd most common endocrine disorder

- Primary hyperparathyroidism – common in women 50-60 years old

165
Q

Causes of primary hyperparathyroidism?

A

 Single parathyroid adenoma 80% (may be due to MEN1, 2a)
 Hyperplasia of all glands 20%
 Parathyroid carcinoma <1%

166
Q

Causes of secondary hyperparathyroidism?

A

 CKD – hyperplastic after long-term stimulation due to chronic hypocalcaemia
 Low vitamin D intake
 Malabsorption

167
Q

Causes of tertiary hyperparathyroidism?

A

 Prolonged secondary hyperparathyroidism
• Glands become autonomous, producing excessive PTH even after corrected hypocalcaemia
 CKD most common cause

168
Q

Symptoms of hypercalcaemia?

A 
o	Lethargy
o	Malaise
o	Muscle weakness
o	Anorexia
o	Polyuria
o	Thirst
o	Nausea &amp; vomiting 
o	Constipation
o	Bone pain
o	Confusion
o	Memory problems
o	Drowsiness
o	Fits 
o	Coma
169
Q

Signs of primary hyperparathyroidism?

A

 Hypertension, shortened QT interval
 Peptic ulcers (duodenal 7x)
 Depressed

170
Q

Symptoms of secondary hyperparathyroidism?

A

o CKD
o Oesteomalacia, fracture risk, myopathy
o Bone pain

171
Q

Symptoms of tertiary hyperparathyroidism?

A

o Hypercalcaemia symptoms so similar to primary

172
Q

What incidental findings indicate primary hyperparathyroidism?

A

 Hypercalcaemia

 Hypophosphataemia

173
Q

Diagnostic testing in primary care for primary hyperparathyroidism - when and results?

A

Albumin-adjusted serum Ca (total) – NOT IONISED CALCIUM
• When - Symptoms of hypercalcaemia, osteoporosis, renal stone, incidental elevated albumin-adjusted serum calcium >2.6mmol/L
• Results - Repeat if 1st measurement 2.6 or above or 2.5-2.6 with features of 1o hyperparathyroidism

Parathyroid Hormone (PTH)
•	When - If calcium 2.6 or above on at least 2 separate occasions OR 2.5 or above on at least 2 separate occasions and 1o hyperparathyroidism suspected
•	Results - Refer to endocrinologist if above midpoint of reference range and primary hyperparathyroidism suspected or below midpoint with Ca >2.6
174
Q

Further testing performed in primary hyperparathyroidism?

A

 Vitamin D

 Urine calcium excretion
• To determine if familial hypocalciuric hypercalcaemia
• 24-hour urinary calcium, renal calcium:creatinine excretion ratio or calcium:creatinine clearance ratio

 Skull XR
• Salt and pepper pot skull

175
Q

Investigations once diagnosis confirmed of primary hyperparathyroidism?

A

 U&Es
 DEXA scan of lumbar spine, distal radius and hip
 US of renal tract

176
Q

Bloods in secondary hyperparathyroidism?

A

 Low-normal calcium
 Raised PTH
 Phosphate (high in CKD, low in Vitamin D deficiency)

177
Q

Bloods in tertiary hyperparathyroidism?

A

 Raised Ca
 Raised PTH
 Phosphate often raised

178
Q

Management of primary hyperparathyroidism - mild, asymptomatic disease?

A

o Mild, asymptomatic disease
 Increase fluids
 Avoid thiazides + high Ca diet
 Check U&Es and calcium every 6 months

o Vitamin D supplements if deficient

179
Q

Management of primary hyperparathyroidism - surgical management - when to refer, imaging before surgery?

A

Refer to surgeon if diagnosed and:
• Symptoms of hypercalcaemia
• End-organ disease (stones, fragility fractures, osteoporosis)
• Albumin-adjusted calcium 2.85 or above

Imaging before surgery (if needed):
• US
• Sestamibi scan

Type of surgery
• 4-gland exploration – if US doesn’t show single adenoma
• Focussed parathyroidectomy – if adenoma

180
Q

Management of primary hyperparathyroidism - surgical management - follow up after surgery?

A

• Before surgery
o Albumin-adjusted serum calcium
o PTH

• 3-6 months after
o Albumin-adjusted serum calcium

181
Q

Management of primary hyperparathyroidism - drug treatment?

A

 Cinacalcet
• Increases sensitivity of parathyroid cells to Ca (lowers PTH)
• If surgery unsuccessful, unsuitable or declined and Ca is:
o 2.85 or above with symptoms of hypercalcaemia
o 3.0 or above with/without symptoms
• Continue until symptoms reduced and hypercalcaemia resolved

 Bisphosphonates
• If increased risk of fractures

182
Q

Monitoring of primary hyperparathyroidism?

A

 Endocrinologist monitoring

 If successful surgery:
• Albumin-adjusted serum calcium annually
• If osteoporosis - DEXA scan according to local guidelines
• If renal stones – US KUB according to local pathways

 If no surgery or not successful:
• U&Es and albumin-adjusted serum calcium annually
• DEXA scan every 2-3 years
• US KUB if stone suspected

183
Q

Management of secondary hyperparathyroidism ?

A 
o	Medical treatment
	Treat vitamin D deficiency
	Calcium supplementation
	Phosphate restriction +/- binders
	Cinacalcet if ESKD and SHPT refractory and not suitable for surgery

o Surgery
 Parathyroidectomy if medical refractory

184
Q

Management of tertiary hyperparathyroidism ?

A

o Cinacalcet

o Total or subtotal parathyroidectomy

185
Q

Management of tertiary hyperparathyroidism ?

A

o Cinacalcet

o Total or subtotal parathyroidectomy

186
Q

Definition of hypercalcaemia?

A
  • Defined as a serum Ca concentration of 2.65 mmol/L or higher, on two occasions, following correction for the serum albumin concentration
187
Q

Describe calcium homeostasis?

A

o High blood calcium level leads to thyroid releasing (vitamin D3 – 1, 25-dihydroxy-vitamin D) calcitonin which:
 Promotes osteoblasts deposit calcium in bone
 Reduces absorption of calcium in kidneys

o Low blood calcium level leads to parathyroid releasing PTH which:
 Promotes osteoclasts to release calcium from bones
 Stimulates kidney to absorb calcium
 Kidney converts 25-hydroxy Vitamin D to 1-25 dihydroxy Vitamin D to stimulate bowels to absorb calcium

188
Q

Pathophysiology of hypercalcaemia of malignancy?

A

o Transforming growth factor Alpha
 Produced by tumours and powerful stimulator of bone resorption
o Parathyroid hormone (PTH) related peptides
 Tumour-associated protein that mimics PTH, stimulates bone reabsorption and increases plasma calcium

189
Q

Causes of hypercalcaemia?

A 
o	Primary Hyperparathyroidism
o	Cancer
	Squamous cell lung cancer
	Breast cancer
	Prostate cancer
	Renal cell carcinoma
	Multiple myeloma/lymphoma
	Head and Neck cancers
o	Drugs
	Thiazide diuretics
	Lithium 
	Vit A &amp; D
o	CKD
190
Q

Symptoms of hypercalcaemia?

A

Bones, stones and psychiatric moans

	Early
•	Lethargy
•	Malaise
•	Anorexia
•	Polyuria
•	Thirst
•	Nausea &amp; vomiting 
•	Constipation
•	Bone pain
	Late
•	Confusion
•	Drowsiness
•	Fits 
•	Coma
191
Q

Signs of hypercalcaemia?

A 
o	Hyporeflexia
o	Weight loss
o	Bradycardia
o	Short QT interval, wide T wave, Prolonged PR
o	BBB
192
Q

Investigations in known malignancy of hypercalcaemia?

A 
o	Bloods
	Serum calcium corrected for albumin
•	Mild – adjusted calcium 2.6-3.0mmol/L
•	Moderate – adjusted calcium 3.01-3.4mmol/L
•	Severe – adjusted calcium >3.4mmol/L
	LFTs, FBC

o ECG
 Shortened QT interval
 Osborn wave

193
Q

Management of severe hypercalcaemia?

A

Rehydration
 0.9% saline 1L 4-hourly for 24 hours, then 6 hourly for 48-72 hours
 Give K+
 May need furosemide if at risk of fluid overload

IV Bisphosphonates (pamidronate or zoledronic acid)
	Response seen in 70% around 6-11 days for 3-4 weeks

Salmon calcitonin SC/IM with oral prednisolone

Stop thiazides and vitamin D

194
Q

Definition of hyperlipidaemia?

A
  • Raised serum levels of one or more of total cholesterol, LDLs or triglycerides
195
Q

Epidemiology of hyperlipidaemia?

A
  • UK has highest serum cholesterol levels in world
  • 2/3rds over 5.2mmol/L
  • Heterozygous familial hypercholesterolaemia
    o 1 in 500 people
196
Q

Inherited causes of hyperlipidaemia?

A

 Familial dyslipidaemia, hypercholesterolaemia, combined hyperlipidaemia
 Apoprotein disorders

197
Q

Secondary causes of hyperlipidaemia?

A

 Medical – hypothyroidism, obstructive jaundice, Cushing’s syndrome, anorexia, diabetes, CKD
 Drugs – thiazide diuretics, glucocorticoids, ciclosporin, ART, beta-blockers, COCP, atypical antipsychotics
 Pregnancy
 Obesity
 Alcohol Abuse

198
Q

Risk factors of hyperlipidaemia?

A

o Non-modifiable
 Age, men, FHx, South Asian or sub-Saharan Africa

o Modifiable
 Smoking, low HDL, high non-HDL, sedentary lifestyle, unhealthy diet, alcohol excess, overweight
 Socio-economic status

o Co-morbidities
 Hypertension, DM, CKD, AF, RA, SLE

199
Q

What is the risk assessment performed in primary care for hyperlipidaemia?

A

o QRISK2 in primary care
 For patients up to and including 84 years and patients with T2DM
• People aged 40-74 – offered an NHS health check every 5 years
• Repeat every 5 years
 DO NOT USE WITH T1DM, eGFR<60, PRE-EXISTING CVD, FAMILIAL HYPERCHOLESTEROLAEMIA

200
Q

How to take lipid measurement of hyperlipidaemia? When to refer?

A

Measure total and HDL cholesterol – before primary prevention of CVD, take at least 1 sample to measure full lipid profile

Consider familial hyperholesterolaemia if:
 TChol >7.5 and FHx of premature coronary heart disease

Refer to specialist if:
 Urgent if TG >20mmol/L, TChol >9.0mmol/L or non-HDL-C >7.5mmol/L

If TG 10-20 – repeat with fasting test within 2 weeks, refer is above 10

201
Q

Management of hyperlipidaemia - primary prevention - lifestyle modifications?

A

 Avoid exceeding alcohol limits and avoid binges
 Total fats <30% total energy intake, cholesterol <300mg/day, reduce saturated fats, increase mono-unsaturated fats (olive oil, rapeseed oil), choose wholegrain food, reduce sugar, eat 5-a-day
 150 minutes of moderate exercise per week
 Stop smoking
 Healthy body weight

202
Q

Management of hyperlipidaemia - primary prevention - statin treatment - tests done before starting?

A

 Smoking status, alcohol status, BP, BMI
 Lipid profile, HbA1c, LFT (fine if <3x normal limit), U&E, TFTs
 If generalise muscle pain – measure CK – if >5x limit of normal, re-measure after 7 days – if <5x then start statin at lower dose
 Avoid grapefruit juice

203
Q

Management of hyperlipidaemia - primary prevention - statin treatment?

A

 Atorvastatin 20mg OD

• When to offer:
o QRISK2 >10% (<84 years, >84 decide clinically)
o Type 1 diabetic who: >40, diabetes for >10 years, established nephropathy, other CVD risk factors
o Type 2 DM – if QRISK2 >10%
o CKD – all patients
 eGFR >30 (if under seek specialist)
 Increase dose if <40% reduction in non-HDL cholesterol
o Familial hypercholesterolaemia

204
Q

Management of hyperlipidaemia - secondary prevention - statin treatment - when to offer it and how much?

A

 Atorvastatin 80mg OD
• When to offer:
o CVD (MI, angina, stroke, TIA, PAD) event

 Atorvastatin 20mg OD
• Offer after CVD event in CKD
o eGFR >30 (if under seek specialist)
o Increase dose if <40% reduction in non-HDL cholesterol

205
Q

Management if statin intolerance in hyperlipidaemia?

A

 Aim to treat with maximum tolerated dose – any dose reduces CVD
 Strategies:
• Stop and start again, reduce dose, change statin

206
Q

Monitoring statin therapy in hyperlipidaemia?

A

o LFTs – baseline, 3 months of starting treatment and 12 months
o Lipid profile – baseline, 3 months
 Aim for >40% reduction in non-HDL cholesterol
 If not – consider adherence, diet and lifestyle and increasing dose
o Annual medication review
o If muscle pain or weakness on a statin:
 Measure CK - if >5x limit of normal, re-measure after 7 days – if <5x then start statin

207
Q

Definition of familial hypercholesterolaemia?

A
  • Inherited autosomal dominant condition characterised by high cholesterol concentration in blood
    o Can be heterozygous or homozygous
  • Heterozygous is common – estimated between 1 in 250 and 1 in 500
208
Q

Identifying people with familial hypercholesterolaemia?

A

o Suspect if TChol >7.5 +/- FHx of premature CHD
o If FHx of premature CHD – offer TChol
o In children with parent with FH – refer for DNA test

209
Q

Assessment of people of familial hypercholesterolaemia?

A 
o	2 LDL cholesterol measurements
	Diagnosis if: adults >13, children >11
o	Clinical signs – tendon xanthomas
o	Exclude secondary causes:
	Medical – hypothyroidism, obstructive jaundice, Cushing’s syndrome, anorexia, diabetes, CKD
	Drugs – thiazide diuretics, glucocorticoids, ciclosporin, ART, beta-blockers, COCP, atypical antipsychotics
	Pregnancy
	Obesity
	Alcohol Abuse
210
Q

What is the Simon Broome criteria for familial hypercholesterolaemia?

A

 Definite – Tchol >6.7 or LDL >4 in children, TChol >7.5 or LDL>4.9 in adults with tendon xanthomas and DNA mutation
 Possible - – Tchol >6.7 or LDL >4 in children, TChol >7.5 or LDL>4.9 in adults with FHx of premature CHD

211
Q

Management of familial hypercholesterolaemia - general advice?

A

o Adults with heterozygous
o Refer very high risk (established CHD, FHx of premature CHD, >2 CVD RF)
o Routine referral to cardiologist if FHx of CHD in early adulthood
Baseline ECG

212
Q

Management of familial hypercholesterolaemia - lifestyle advice?

A

 Avoid exceeding alcohol limits and avoid binges
 Total fats <30% total energy intake, cholesterol <300mg/day, reduce saturated fats, increase mono-unsaturated fats (olive oil, rapeseed oil), choose wholegrain food, reduce sugar, eat 5-a-day
 150 minutes of moderate exercise per week
 Stop smoking
 Healthy body weight

213
Q

Management of familial hypercholesterolaemia - statin treatment?

A

 Before
• Smoking status, alcohol status, BP, BMI
• Lipid profile, HbA1c, LFT (fine if <3x normal limit), U&E, TFTs
• If generalise muscle pain – measure CK – if >5x limit of normal, re-measure after 7 days – if <5x then start statin
• Avoid grapefruit juice

 Primary Prevention
• Atorvastatin 20mg OD
o Aim for 50% reduction in LDLs
• If CI or statin therapy fails to achieve target – Ezetimibe 10mg OD or Simvastatin 80mg OD

214
Q

Complications of familial hypercholesterolaemia?

A

o Without treatment – heterozygous FH leads to >50% risk of CHD in men by 50 and >30% in women
o If treated early – normal life expectancy

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