HTN, CKD and Hyperlipidaemia - prework Flashcards
1
Q
CKD - risk factors and aetiology
A
- Diabetic nephropathy
- Chronic glomerulonephritis
- Chronic pyelonephritis
- HTN
- Adult PCKD
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
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
4
Q
Clinical signs of CKD
A
- Foamy/proteinuria
- Pallor - anaemia
- Peripheral oedema
- HTN
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
6
Q
Complications of CKD
A
- CVD
- Bone mineral disease
- Anaemia
- Peripheral neuropathy (toxic waste accumulation)
- End stage kidney disease
- Dialysis related complications
7
Q
Equation for CKD
A
Kidney failure risk equation - estimates likelihood of progression to ESRF with need of dialysis within 5 years
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
9
Q
BP targets CKD
A
- Under 130/80 in patients under 80 with CKD and an ACR of more than 70mg/mmol
10
Q
Management principles CKD
A
- Control HTN
- Optimise diabetic control
- Avoid nephrotoxic drugs
- Treat GN if cause
11
Q
Medications for CKD that slow disease progression
A
- ACEi or ARBs
- SGLT2 inhibitors - specifically dapagliflozin
12
Q
Reducing risk of CVD complications in CKD
A
- Smoking cessation
- Exercise
- Healthy, balanced diet
- Atorvastatin 20mg - in all patients with CKD
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
14
Q
Management of ESRD
A
- Dialysis - many patients require IV iron when get to this stage
- Special diet advice
- Transplant
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
16
Q
Fluid overload in CKD
A
- Sometimes furosemide is needed to control BP
- Higher doses are sometimes needed
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
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
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
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
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
26
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
27
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
28
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
29
BP algorithm management
30
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
31
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
32
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
33
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)
34
Signs of familial hypercholesterolaemia
* Tendon xanthomas
* Premature arcus senilis
35
Familial hypercholestrolaemia treatment vs normal
* High intensity lipid lowering treatment due to high risk of CVD
* Genetic counselling
* Specialist involvement needed
36
Causes of secondary hyperlipidaemia
* nephrotic syndrome
* Hypothyroidism
* Biliary obstruction
* Pregnancy
* Diabetes mellitus
Drugs:
* Steroids
* Beta blockers
* Excess alcohol intake
* Thiazide diuretics
* Oral contraceptives
37
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
38
How are statins grouped?
* High medium and low intensity
* How much effect they have on non-HDL cholesterol
39
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
40
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
41
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
42
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
43
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 `
44
What else to ensure you record before commencing statin?
* Alcohol consumption
* BP
* BMI
* Smoking status
* Diabetes status
45
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
46
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
47
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
48
First line statin primary prevention vs secondary
* Atorvastatin 20mg
* Atorvastatin 80mg
49
