17 - HTN, CKD, Hyperlipidaemia Flashcards
What is the definition of CKD and what is the diagnostic criteria?
Reduction in kidney function or structural damage (or both) present for more than 3 months, with associated health implications
Markers of kidney damage: proteinuria (urinary albumin:creatinine ratio [ACR] greater than 3 mg/mmol), urine sediment abnormalities, electrolyte imbalance, abnormalities detected by histology, structural abnormalities detected by imaging, and a history of kidney transplantation, and/or
Persistent reduction in renal function with eGFR <60ml/min
What are the different classifications of CKD?
Classified based on the underlying cause, GFR, and proteinuria category
Given a G score and an A score
What are some risk factors for developing CKD?
- Hypertension
- Diabetes
- CVD
- AKI
- Nephrotoxic drugs e.g ACEi, bisphosphonates, calcineurin inhibitors, NSAIDs, diuretics, Lithium
- Obstructive uropathy
- Smoking
- Afro-caribbean/Asian
- Family history e.g auto dominant polycystic kidney disease
- Aged over 60
- Kidney transplant
- Obesity
- SLE, Vasculitis, Myeloma
What are some complications of CKD?
- AKI
- Hypertension
- CVD
- Renal anaemia
- Renal mineral and bone disorder
- End-stage renal disease (ESRD)
- Increased all-cause mortality
- Electrolyte imbalances
- Malnutrition
- Infertility, libido loss, impotence, amenorrhea
What are some of the signs and symptoms of CKD that may present to a GP?
Symptoms
- Often asymptomatic or generic/vague
- Lethargy, itch, breathlessness, cramps (often worse at night), sleep disturbance, bone pain, loss of appetite, vomiting, weight loss, taste disturbance (often present with end-stage disease).
- Polyuria (tubular concentrating ability is impaired), oliguria, nocturia, anuria
Signs
- Uraemic breath odour, pallor due to renal anaemia, cachexia, cognitive impairment, dehydration or hypovolaemia (risk of AKI)
- Tachypnoea (may be due to fluid overload, anaemia, or co-morbid ischaemic heart disease), hypertension (may be primary or secondary to CKD itself)
- Palpable bilateral flank masses with possible hepatomegaly (suggests polycystic kidney disease with possible liver cysts).
- Palpable distended bladder (suggests obstructive uropathy).
- Peripheral oedema (may be due to renal sodium retention, hypoalbuminaemia, or co-morbid heart failure).
- Peripheral neuropathy (may present with paraesthesia, sleep disturbance, and restless legs syndrome)
- Frothy urine (proteinuria)
What are some investigations you may do if you suspect a patient has CKD?
- Blood tests for serum creatinine and eGFR and advise not to eat meat for 12 hours before: if less than 60 repeat in 2 weeks and again in 3 months if still less than 60 and no evidence of sudden deterioration
- Early morning urine sample for ACR: if less than 3mg/mmol no action, if above then indicates proteinuria so repeat in 3 months. Can be falsely raised during menstruation, UTI, strenuous exercise and upright posture
- Urine dipstick for haematuria: if 1+ arrange MSU to check for UTI. If isolated persistent haematuria (2 out of 3 dipsticks positive) and no decline in eGFR or proteinuria think about urological cancer
- Check BMI, HbA1c, Lipid profile, BP to assess for CVD risk factors.
- Consider renal US if suspect stones, obstruction, FHx of polycystic kidney disease
- If repeated in 3 months and still the same ACR and eGFR can classify what type of CKD it is to determine the risk of disease progression. (raised serum creatinine by 20% but normal eGFR can indicate CKD)
How should CKD be monitored in primary care to look for disease progression?
- Monitor renal function by looking at eGFR and urine ACR. If decline by 25% and a category or drop by 15ml/min in 12 months this is accelerated progression
- FBC to exclude renal anaemia
- Serum calcium, phosphate, vitamin D, and parathyroid hormone tests to exclude renal metabolic and bone disorder
Which CKD patients should be referred to a nephrology specialist?
- Uncontrolled HTN when has not responded to 4 different drugs
- Complications include renal anaemia as may need EPO, decline in nutrition status, phosphate or other mineral disorders, persistent metabolic acidosis
- Suspect renal artery stenosis if decline in eGFR by 25% within 3 months of starting RAAS antagonist, refractory HTN, pulmonary oedema, renal artery bruit
What lifestyle advice can be given to a patient with CKD?
- Provide sources of info and support e.g patient info, NHS, Kidney Care UK, Think Kidneys
- Healthy lifestyle and diet as CKD can raise lipids and cholesterol e.g alcohol, low protein diet if advised by specialist, smoking, exercise
- Tell patient to avoid NSAIDs, protein supplements and herbal remedies
- Advise on risk of AKI
How are patients with CKD managed in primary care apart from the monitoring for disease progression?
- Assess for and manage risk factors and co-morbidities of CKD and CVS e.g nephrotoxic drugs, disease progression
- Assess for hypertension and give low cost RAAS antagonist if HTN as antiproteinuric(lisinopril or lorsartan). If ACR less than 70mg/mmol aim for 140/90, if more than or diabetic aim for 130/80
- Prescribe statin but be aware raised risks of myopathy and rhabdomyolysis with lower kidney function. Do not prescribe if eGFR<30
- Ensure offered flu and pneumovax
What is the pathophysiology behind CKD?
- Renal damage (e.g by diabetes or HTN)
- Reduced filtration (oxi stress, glomerulosclerosis, loss of nephrons)
- Increased glomerular pressure so glomerular hypertrophy
- Increased glomerular permeability (inflammartion, fibrosis, scarring)
- Overall loss of kidney function
What are the sick day rules for CKD?
When patient has acute illness (N+V for 12 hours or fever, shaking, shaking) stop any ACEi, ARBs, NSAIDs, diuretics, metformin
This is done to prevent an AKI or any drugs building up in the system due to impaired renal function. Need to inform patient of this risk of AKI on Dx
Mneumonic is DAMN
Diuretics and digoxin
ACE inhibitor / ARB
Metformin and methotrexate
NSAIDs
How do you treat a patient with CKD plus the following:
- metabolic acidosis (due to build up of urea)
- anaemia
- secondary hyperparathyroidism
- Oral sodium bicarbonate
- Iron and EPO injections
- Kidney needed for Vit D synthesis, without PTH increases. Phosphate binding agent, active Vitamin D
How often do CKD patients need monitoring of their FBC, eGFR, ACR, phosphate, PTH, calcium, serum creatinine?
- Every 6-12 months
- If stage 4 every 3-6 months and PTH every 6-12 months
- If stage 5 FBC for anaemia monthly, every 1-3 months check calcium and phosphorous etc, every 3-6 months check PTH
Check lipids anually in all CKD patients
What are the target values for blood pressure?
- Stage 1 >140/90 or >135/85 HBPM
- Stage 2 >160/100 or >150/95 HBPM
- Stage 3 >180/120
What is the definition of hypertension?
Persistently raised arterial blood pressure
Stage 1: >140/90
Stage 2: >160/100
Stage 3: >180/120
Malignant hypertension when over 180/120 with retinal haemorraghe and/or papilloedema
How do you manage blood pressure that is over target in general terms?
MEMORISE IMAGE
- Lifestyle advice includes stopping smoking, cutting down caffeine, cutting down alcohol, low dietary salt intake, healthy diet, regular exercise
- Consider drug treatment in under 60s if Stage 1 HTN and QRISK>10%, in all over 80s with Stage 1 HTN, and referral for all those under 40 with Stage 1 HTN
- Treat all patients with stage 2 regardless of age
- Treat severe hypertension promptly
What antihypertensive drug do you use when patients are over target?
- ACD rule!!!
- Add spironolactone, beta blockers and alpha blockers if necessary
- Give drugs if stage 1 with Q risk >10% or stage 2
What are some of the risk factors for developing hypertension?
- Increasing age
- Male
- Ethnicity (AfroCaribbean)
- Family history
- Social deprivation
- Smoking
- Alcohol
- Obesity
- Lack of physical exercise
- Emotional stress
What are the complications of hypertension?
Single biggest risk factor for CVD (strokes and heart attacks)
What are the causes of hypertension?
- Primary: no identifiable cause
- Secondary: other causes e.g renal artery stenosis, phaeochromocytoma, use of certain drugs, diabetic nephropathy, polycystic kidney disease, renal cell carcinoma, coarctation of the aorta, Cushing’s, acromegaly, hypothyroidism, primary hyperaldosteronism
When do you need to refer someone presenting with hypertension for a same day referral?
- Clinical blood pressure over 180/20 with signs of retinal haemorraghe or papilloedema
- Suspected phaeochromocytoma e.g labile/postural hypertension, headache, palpitations, pallor, abdominal pain, diaphoresis
How is hypertension officially diagnosed?
- Measure BP in both arms with appropriate cuff size. If difference between the two is >15mmHg repeat the measurements.
- If over 140/90 repeat. If still above offer ABPM/HBPM
- Check pulse before taking readings as if irregular will not be accurate so need manual reading
What are the different types of hypertension in pregnancy?
Blood pressure and a dipstick for proteinuria is done at every antenatal visit
Eclampsia is the occurence of one or more seizures in women with pre-eclampsia
If at high risk of pre-eclamsia women should take 75-150mg aspirin daily from 12 weeks gestation
How should a woman with pre existing chronic hypertension be managed once she becomes pregnant?
Referral to a specialist and stop ACEi, ARBs and thiazides all need to be stopped due to the risk of congenital abnormalities
Any hypertension in pregnancy should be treated with labetolol first line or nifedipine
If >160/110 mother will need to be admitted to hospital for ongoing monitoring and IV drugs
Review antihypertensives 2 weeks after birth and monitor babies for signs of hypotension if breast fed
When should you suspect familial hypercholesterolaemia?
Autosomal dominant
Suspect when total cholesterol >7.5mmol/L
and/or
Personal/family history of premature CHD (before the age of 60 in first degree relative
How do we manage patients with familial hypercholesterolaemia?
- If homozygous or child managed in secondary care by specialist
- Consider baseline ECG
- Addressing other modifiable CVD risk factors e.g smoking, blood pressure
- Offer individualised advice from dietician
- Address any causes of secondary hyperlipidaemia e.g uncontrolled diabetes, excess alcohol
- Baseline bloods before lipid-modifying treatment
- High intensity statin (e.g atorvastatin 20mg or rosuvastatin 10mg)
- Info and support groups e.g HEART UK
- Genetic counselling
- REVIEW ANUALLY FOR ANY STATIN SIDE EFFECTS AND TO CHECK HBA1C, BP, LIFETSTYLE ADVICE ETC
How can you diagnose familial hypercholesterolaemia?
- If suspected take 2 LDL measurements. If >13 suspect homozygous, if >11 suspect heterozygous
- Look for clinical signs but absence does not rule out diagnosis e.g tendon xanthomas, premature corneal arcus,
xanthelasma
- Exclude any secondary causes e.g look at drug history and history
- Use Simon Broome or DLCN criteria
What lipid modifying drugs are used in familial hypercholesterolaemia?
Atorvastatin 20 mg or Rosuvastatin 10 mg after baseline bloods
Not rosuvastatin if predisposing factors for rhabdomyolysis e.g Asian, stage 3 CKD
- If statins contraindicated ezetimibe 10 mg once daily (provided CK and LFTs are fine). Coprescribe with statin if statins not working
What baseline blood tests need to be done before starting lipid modifying treatment?
- CK if have generalised muscle pains (if five times over limit retest in 7 days and if still raised don’t give, if raised but below five times can give)
- LFTs (can give if blow three times normal limit but need to find cause of raised test)
- Renal function (helps work out dosage)
- HbA1c
- TFTs (hypothyroidism can cause dyslipidaemia and statin-induced myopathy)
How do you follow up someone after starting lipid modification treatment for familial hypercholesterolaemia?
- Measure lipid levels after 3 months, want a 50% reduction in LDL.
- If not appropriate reduction, check adherance and timing and titrate dose up to max. If already max consider coprescription of ezetimibe 10mg or switch to 80mg simvastatin
- If still not reducing refer to secondary care for PCSK9i
- Recheck LFTs after 3 months then 12 months then again only if clinically indicated.
- Annually review patient e.g lifestyle, side effects
What are some medications that can cause secondary hypercholesterolaemia?
- Beta Blockers
- Prednisone
- Amiodarone
- Cyclosporin and other immunosuppressants
- Anabolic Steroids
- Protease Inhibitors (Antiretroviral drugs)
- Diuretics
- Oral oestrogen
- Antidepressants
What are some conditions that can cause secondary hypercholesterolaemia?
- Type 2 DM (high LDL+TGs, low HDL)
- Pregnancy
- Hypothyroidism
- Menopause
- Nephrotic syndrome
- Anorexia nervosa
What are some low, medium and high intensity statins?
- Atorvastatin 10mg is medium intensity
- Atorvastatin 20mg, 40mg, 80mg is high intensity
What is the NHS health check programme?
- Everyone aged 40–74 years, who has not already been diagnosed with CVD, diabetes, or chronic kidney disease, is invited every 5 years for a free health check.
- Includes a CVD risk assessment, assessment of alcohol consumption, physical activity, cholesterol level, body mass index (BMI), an assessment for dementia in those aged 65-74 years, and screening for diabetes mellitus and chronic kidney disease
- Qrisk score should be calculated every 5 years!!!!!!!!
What is the first line statin if a persons QRISK score is >10% and lifestyle changes like weight loss and decreased alcohol consumption have not lowered this? (primary prevention)
Atorvastatin 20mg
After an informed discussion about benefits and harms, after having been provided with lifestyle advice, and if there are no contraindication (e.g grapefruit juice)
When should you offer lipid-modifying drugs for primary prevention of CVD?
- <84 if QRISK>10% and lifestyle modifications not worked
- All type 1 diabetics
- CKD
- Familial hypercholesterolaemia
- >85 especially if smoker or HTN. Take into account life expectancy, polypharmacy, risks and benefits etc
What are the side effects of the following?
What are the side effects of the following?
Metformin metallic taste!!!!!
When should statins be taken?
NIGHTTIME
