HTN, CKD and Hyperlipidaemia - prework Flashcards
CKD - risk factors and aetiology
- Diabetic nephropathy
- Chronic glomerulonephritis
- Chronic pyelonephritis
- HTN
- Adult PCKD
Clinical features of CKD - early
- Fatigue - build up of toxins and anaemia
- Polyuria/nocturia
- HTN - dysregulated fluid volume ratio and RAAS
- Puffiness/swelling - eyes/ankles due to fluid retention
Clinical features CKD - later
- 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
Clinical signs of CKD
- Foamy/proteinuria
- Pallor - anaemia
- Peripheral oedema
- HTN
Investigations for CKD
- UACR - first pass morning, 3mg/mmol or more = proteinuria
- eGFR
- Urine dip - haematuria?
- Renal USS - obstruction?
- BP, HbA1C and lipid profile - assess
Complications of CKD
- CVD
- Bone mineral disease
- Anaemia
- Peripheral neuropathy (toxic waste accumulation)
- End stage kidney disease
- Dialysis related complications
Equation for CKD
Kidney failure risk equation - estimates likelihood of progression to ESRF with need of dialysis within 5 years
When to refer to nephrologist?
- 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
BP targets CKD
- Under 130/80 in patients under 80 with CKD and an ACR of more than 70mg/mmol
Management principles CKD
- Control HTN
- Optimise diabetic control
- Avoid nephrotoxic drugs
- Treat GN if cause
Medications for CKD that slow disease progression
- ACEi or ARBs
- SGLT2 inhibitors - specifically dapagliflozin
Reducing risk of CVD complications in CKD
- Smoking cessation
- Exercise
- Healthy, balanced diet
- Atorvastatin 20mg - in all patients with CKD
Managing complications of CKD
- 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
Management of ESRD
- Dialysis - many patients require IV iron when get to this stage
- Special diet advice
- Transplant
Phosphate binders used in CKD
- 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
Fluid overload in CKD
- Sometimes furosemide is needed to control BP
- Higher doses are sometimes needed
When is dapagliflozin offered in CKD?
- 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
What happens in renal bone disease?
- 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
Spinal X-ray finding of renal mineral bone disease
- Rugger jersey spine
- Sclerosed both ends of each vertebral body (whiter) with osteomalacia in centre of body (less white)
- Like stripes on rugby shirt
Follow up for CKD
- Depends on clinical severity of CKD
- At least annually
*
Risk factors HTN - primary
- Age
- Obesity
- FH
- High salt intake
- Sedentery lifestyle
- Alcohol consumption
Causes of secondary HTN
- Renal disease
- Endocrine disease eg phaechromocytoma, primary hyperaldosteronism
- Others: pregnancy, glucocorticoids, COCP, NSAIDs
Symptoms HTN
- Usually none unless BP is over 200/120
- Can then get headaches, seizures or visual disturbances
Investigations HTN
- 24hr BP monitoring
- Fundoscopy
- Urine dip and UACR
- ECG - LVH or ischaemic HD
- Bloods - U&Es, Lipids, HbA1C
Diagnosing and deciding whether to treat HTN
- 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
When to consider immediate BP treatment?
- When BP is 180/110 or more
- If signs of papilloedema or retinal haemorrhages need same day specialist assessment
Ambulatory vs home monitoring recommendation
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
Lifestyle advice for HTN
- 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
BP algorithm management
BP targets dependent on age
- If under 80 - below 140/90
- 80 and over - below 150/90
Ambulatory: - Under 80 - below 135/85
- 80 and over - below 145/85
Preventing AKI in CKD
- 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
Drugs which can cause AKI
Pre-renal:
* ACEi/ARBs
* NSAIDs
* Loop diuretics
* MRA eg spironolactone
Intrinsic/nephrotoxic:
* Abx
* NSAIDs
* PPIs
* Allopurinol
* Iodine based contrast
* Chemotherapy
When should familial hypercholestrolaemia be suspected?
- 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)
Signs of familial hypercholesterolaemia
- Tendon xanthomas
- Premature arcus senilis
Familial hypercholestrolaemia treatment vs normal
- High intensity lipid lowering treatment due to high risk of CVD
- Genetic counselling
- Specialist involvement needed
Causes of secondary hyperlipidaemia
- nephrotic syndrome
- Hypothyroidism
- Biliary obstruction
- Pregnancy
- Diabetes mellitus
Drugs:
* Steroids
* Beta blockers
* Excess alcohol intake
* Thiazide diuretics
* Oral contraceptives
Special circumstances to consider statin regardless of QRISK
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
How are statins grouped?
- High medium and low intensity
- How much effect they have on non-HDL cholesterol
Follow up for people on statins
- 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
What age is QRISK valid for? Who to not use it for?
- Up to and including aged 84
- Do not use in T1DM, eGFR less than 60 +/- albuminuria and familial hypercholsterolaemia family history
When may QRISK underestimate CVD risk?
- 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
Lifestyle advice for hypercholestrolaemia - diet
- 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
Baseline bloods before commencing statin
- Full lipid profile - non fasting
- Creatine kinase
- LFTs
- Renal function inc eGFR
- HbA1c
- TSH - symptoms of under/over active thyroid `
What else to ensure you record before commencing statin?
- Alcohol consumption
- BP
- BMI
- Smoking status
- Diabetes status
Aim of primary vs secondary prevention of statin use
- 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
Follow up after prescribing primary prevention statin
- 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
Primary prevention of hypercholesterolaemia for those aged 85 and above
- 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
First line statin primary prevention vs secondary
- Atorvastatin 20mg
- Atorvastatin 80mg
