HTN, CKD and Hyperlipidaemia - prework Flashcards

1
Q

CKD - risk factors and aetiology

A
  • Diabetic nephropathy
  • Chronic glomerulonephritis
  • Chronic pyelonephritis
  • HTN
  • Adult PCKD
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2
Q

Clinical features of CKD - early

A
  • Fatigue - build up of toxins and anaemia
  • Polyuria/nocturia
  • HTN - dysregulated fluid volume ratio and RAAS
  • Puffiness/swelling - eyes/ankles due to fluid retention
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3
Q

Clinical features CKD - later

A
  • Decreased urine output
  • Fluid overload symptoms - SOB, peripheral oedema, HTN
  • Uraemic symptoms - N+V, pruiritis, metallic taste in mouth
  • Neurological - difficult conc, coma/seizures
  • CV symptoms - chest pain/SOB
  • Anaemia
  • Bone mineral disease - bonepain and fractures
  • Metabolic acidosis - rapid breathing, confused
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4
Q

Clinical signs of CKD

A
  • Foamy/proteinuria
  • Pallor - anaemia
  • Peripheral oedema
  • HTN
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5
Q

Investigations for CKD

A
  • UACR - first pass morning, 3mg/mmol or more = proteinuria
  • eGFR
  • Urine dip - haematuria?
  • Renal USS - obstruction?
  • BP, HbA1C and lipid profile - assess
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6
Q

Complications of CKD

A
  • CVD
  • Bone mineral disease
  • Anaemia
  • Peripheral neuropathy (toxic waste accumulation)
  • End stage kidney disease
  • Dialysis related complications
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7
Q

Equation for CKD

A

Kidney failure risk equation - estimates likelihood of progression to ESRF with need of dialysis within 5 years

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8
Q

When to refer to nephrologist?

A
  • eGFR less than 30ml/min/1.73m2
  • UACR more than 70mg/mmol
  • Accelerated reduction in eGFR (25% or 15ml within 12 months)
  • 5 year risk requiring dialysis of over 5%
  • Uncontrolled HTN despite 4 or more antihypertensives
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9
Q

BP targets CKD

A
  • Under 130/80 in patients under 80 with CKD and an ACR of more than 70mg/mmol
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10
Q

Management principles CKD

A
  • Control HTN
  • Optimise diabetic control
  • Avoid nephrotoxic drugs
  • Treat GN if cause
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11
Q

Medications for CKD that slow disease progression

A
  • ACEi or ARBs
  • SGLT2 inhibitors - specifically dapagliflozin
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12
Q

Reducing risk of CVD complications in CKD

A
  • Smoking cessation
  • Exercise
  • Healthy, balanced diet
  • Atorvastatin 20mg - in all patients with CKD
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13
Q

Managing complications of CKD

A
  • Oral sodium bicarbonate for metabolic acidosis
  • Iron and erythopoesis stimulating agents for anaemia (optimise iron levels first)
  • Vitamin D (eg alfacalcidol), low phosphate diet and phosphate binders for renal bone disease
  • Sometimes parathyroidectomy is needed
  • Osteoporosis can exist alongside and may be treated with bisphosphonates
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14
Q

Management of ESRD

A
  • Dialysis - many patients require IV iron when get to this stage
  • Special diet advice
  • Transplant
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15
Q

Phosphate binders used in CKD

A
  • Calcium based binders - problem is can cause hypercalcaemia and vascular calcification
  • Sevelamer - non calcium based binder, binds to diet phosphate and prevents absorption, also seems to reduce uric acid levels and improve lipid profile in those with CKD
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16
Q

Fluid overload in CKD

A
  • Sometimes furosemide is needed to control BP
  • Higher doses are sometimes needed
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17
Q

When is dapagliflozin offered in CKD?

A
  • Diabetes plus urine ACR above 30mg/mmol
  • Also considered if diabetes + ACR 3-30mg/mmol and non diabetics with ACR 22.6mg/mmol or more
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18
Q

What happens in renal bone disease?

A
  • Low calcium
  • High phosphate
  • Low vitamin D
  • Increased PTH
    Due to:
  • Reduced phosphate excretion
  • Lack of active vitamin D = less Ca2 absorbed from gut
  • Low Ca and high PO4 stimulate PTH to be released = increased bone turnover = osteomalacia
  • Osteosclerosis then occurs due to osteoblasts matching osteoclast activity but low Ca2+ means bone is not properly mineralised
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19
Q

Spinal X-ray finding of renal mineral bone disease

A
  • Rugger jersey spine
  • Sclerosed both ends of each vertebral body (whiter) with osteomalacia in centre of body (less white)
  • Like stripes on rugby shirt
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20
Q

Follow up for CKD

A
  • Depends on clinical severity of CKD
  • At least annually
    *
21
Q

Risk factors HTN - primary

A
  • Age
  • Obesity
  • FH
  • High salt intake
  • Sedentery lifestyle
  • Alcohol consumption
22
Q

Causes of secondary HTN

A
  • Renal disease
  • Endocrine disease eg phaechromocytoma, primary hyperaldosteronism
  • Others: pregnancy, glucocorticoids, COCP, NSAIDs
23
Q

Symptoms HTN

A
  • Usually none unless BP is over 200/120
  • Can then get headaches, seizures or visual disturbances
24
Q

Investigations HTN

A
  • 24hr BP monitoring
  • Fundoscopy
  • Urine dip and UACR
  • ECG - LVH or ischaemic HD
  • Bloods - U&Es, Lipids, HbA1C
25
Q

Diagnosing and deciding whether to treat HTN

A
  • If BP between 140/90 and 180/120 - need to have 24 hr ambulatory or home readings submitted
  • Take readings from both arms - if higher than 140/90 rpt
  • Rpt if more than 20mmHg between each arm, consider causes for this
26
Q

When to consider immediate BP treatment?

A
  • When BP is 180/110 or more
  • If signs of papilloedema or retinal haemorrhages need same day specialist assessment
27
Q

Ambulatory vs home monitoring recommendation

A

Home:
* Take twice in morning and twice at night for 7 days (at least 4 days)
* Take at least 1 minute apart
* Discard first day and calculate average

Ambulatory:
* Use at least 14 readings to calculate average
* At least 2 measurements per hour during persons waking hours

28
Q

Lifestyle advice for HTN

A
  • Reduce salt intake - aiming for less than 6g/day but ideally less than 3g
  • Reduce caffeine intake
  • Stop smoking
  • Drink less alcohol
  • Balanced diet rich in fruit and veg
  • Exercise
  • Lose weight if overweight
29
Q

BP algorithm management

A
30
Q

BP targets dependent on age

A
  • If under 80 - below 140/90
  • 80 and over - below 150/90
    Ambulatory:
  • Under 80 - below 135/85
  • 80 and over - below 145/85
31
Q

Preventing AKI in CKD

A
  • Regular monitoring of Crt
  • Regular monitoring of renal function
  • Caution with nephrotoxic medications - esp if eGFR less than 60
  • Temporarily stop medications if at risk of AKI eg in acute illness with large fluid losses
  • Provide information leaflets to patinets eg Kidney Care UK
32
Q

Drugs which can cause AKI

A

Pre-renal:
* ACEi/ARBs
* NSAIDs
* Loop diuretics
* MRA eg spironolactone

Intrinsic/nephrotoxic:
* Abx
* NSAIDs
* PPIs
* Allopurinol
* Iodine based contrast
* Chemotherapy

33
Q

When should familial hypercholestrolaemia be suspected?

A
  • Total cholesterol greater than 7.5mmol/L and/or
  • Personal or FH of premature CHD (event before 60 in first degree relative eg parents, siblings, children)
34
Q

Signs of familial hypercholesterolaemia

A
  • Tendon xanthomas
  • Premature arcus senilis
35
Q

Familial hypercholestrolaemia treatment vs normal

A
  • High intensity lipid lowering treatment due to high risk of CVD
  • Genetic counselling
  • Specialist involvement needed
36
Q

Causes of secondary hyperlipidaemia

A
  • nephrotic syndrome
  • Hypothyroidism
  • Biliary obstruction
  • Pregnancy
  • Diabetes mellitus

Drugs:
* Steroids
* Beta blockers
* Excess alcohol intake
* Thiazide diuretics
* Oral contraceptives

37
Q

Special circumstances to consider statin regardless of QRISK

A

T1DM: Consider in all pts with condition, offer id:
* Over 40 or
* 10 or more years with diabetes or
* Established nephropathy or
* Other CVD RF

CKD:
* All patients
* Increase dose if greater than 40% reduction is achieved and eGFR is still more than 30, if lower consult nephrology

38
Q

How are statins grouped?

A
  • High medium and low intensity
  • How much effect they have on non-HDL cholesterol
39
Q

Follow up for people on statins

A
  • Lipid profile and LFTs at 3 months after commencing
  • If non-HDL cholesterol has not fallen by 40% discuss adherance and lifestyle
  • Consider increasing to 80mg atorvastatin
40
Q

What age is QRISK valid for? Who to not use it for?

A
  • Up to and including aged 84
  • Do not use in T1DM, eGFR less than 60 +/- albuminuria and familial hypercholsterolaemia family history
41
Q

When may QRISK underestimate CVD risk?

A
  • People treated for HIV
  • Serious mental health problems
  • Taking medicines that can cause dyslipidaemia eg antipsychotics, corticosteroids or immunosupressant drugs
  • People with autoimmune disorders/systemic inflammatory disorders eg SLE
42
Q

Lifestyle advice for hypercholestrolaemia - diet

A
  • Total fat should be 30% or less than total energy intake
  • Saturated fats 7% or less than total energy intake
  • Dietary cholesterol intake of less than 300mg/day
  • Replace saturated and monosaturated fats with olive oil, rapeseed oil or spreads with these in
  • Wholegrain varieties of starchy food
  • Reduce intake of sugar and refined sugars inc fructose
  • At least 5 portions of FRV /day
  • 2 portions of fish per week, one being oily fish
  • 4-5 portions of unsalted nuts, seeds or legumes per week
43
Q

Baseline bloods before commencing statin

A
  • Full lipid profile - non fasting
  • Creatine kinase
  • LFTs
  • Renal function inc eGFR
  • HbA1c
  • TSH - symptoms of under/over active thyroid `
44
Q

What else to ensure you record before commencing statin?

A
  • Alcohol consumption
  • BP
  • BMI
  • Smoking status
  • Diabetes status
45
Q

Aim of primary vs secondary prevention of statin use

A
  • Primary - greater than 40% reduction in non-HDL cholesterol levels
  • Secondary - achieve LDL-C of 2mmol/L or less, or non-HDL level of 2.6mmol/L or less
46
Q

Follow up after prescribing primary prevention statin

A
  • Measure total cholesterol, HDL and non-HDL cholesterol, LFTs in all people 2-3 months following change/initiation

If greater than 40% reduction in non-HDL is not acheived:
* Discuss adherance
* Lifestyle
* Consider increasing dose, if still not acheieved then consider ezetimibe

  • Then recheck LFTs again at 12 months
  • Provide annual medication review - consider annual full lipid profile
47
Q

Primary prevention of hypercholesterolaemia for those aged 85 and above

A
  • Consider offering without the need for QRISK assessment esp if smoke or have raised BP
  • Take into account benefits, preference, co-morbids, polypharmacy, frailty and life expectancy
48
Q

First line statin primary prevention vs secondary

A
  • Atorvastatin 20mg
  • Atorvastatin 80mg
49
Q
A