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WEEK 5:
Overview of chronic kidney disease:
| Question | Answer |
|---|---|
| morphological classification | tells you what part (vascular, glomeruli, tubules and interstitium) |
| clinical classification | includes acute renal failure, chronic renal failure (nephrotic syndrome and nephritic syndrome) |
| CKD | slow loss of renal function over time leading to a decreased ability to remove waste products from body and perform homeostatic functions |
| clinical definition of CKD/ CKD presents with | GFR of less than 60ml/min per 1.73^2 per body surface area, and presence of kidney damage regardless of cause for 3 months |
| duration- how long would you classify cause as CKD | 90 days |
| normal GFR | 120ml/min per 1.73^2 per body surface area |
| glomerular filtration rate | sum of all nephron filtration rates acting as the best index of overall function |
| normal GFR range | 90-120ml/min |
| GFR equates to | percentage kidney function |
| stage 1 CKD | kidney damage with normal/ increased EGFR |
| stage 2 CKD | kidney damage with mild reduction in EGFR |
| stage 3a CKD | moderate decrease in EGFR |
| stage 3b CKD | Severe decrease in EGFR |
| stage 4 CKD | severe decrease in EGFR |
| stage 5 CKD | kidney failure |
| 95% of patients with CKD have what (3) | hypertension, diabetes or coronary heart disease |
| major risk factors for CKD (8) | diabetes, high blood pressure, age over 60 years, smoking, obesity, family history of kidney disease, established cardiovascular disease and black/asian ethnicity |
| causes of CKD | diabetic kidney disease, congenital kidney disease (polycystic), immunological damage to all glomeruli - glomerulonephritis, chronic renal reflux and infection (Hep B, Hep C, malaria, TB and HIV) |
| arteriolosclerosis of renal arterioles causes | ishcaemia in nephrons with progression leading to sclerosis of of nephrons and reduction in proteinuria as glomeruli fail leading to CKD |
| treatment of CKD caused by hypertension (2) | dialysis and transplantation |
| glomerulus is vulnerable to (3) | vascular disease, immunological disorders, and deposition of foreign material (amyloid) |
| glomerulus reacts to things its vulnerable by (2) | inflammation and thickening of glomerular basement of membrane/ alteration in podocyte processes |
| how does glomerulus react via inflammation | proliferation of endothelial cells (decreased flow-oliguria, uremia) and proliferation of mesangial cells and or matrix |
| nephritic CKD | proliferation of mesangium and endothelial of glomerulus leading to inflammation (influx of cells and inflammatory exudate) |
| nephritic CKD leads to | occlusion of glomerular capillaries leading to low renal blood flow which activates RAAS leading to fluid retention and hypertension, oliguria, retention of waste products (uraemia) and haematuria |
| nephrotic CKD | severe damage to BM and mesangium of glomerulis leading to increased permeability (leakiness) |
| leakiness in nephrotic CKD includes | proteinuria (heavy mostly albumin), hypoalbuminaemia, loss of albumin (oedema), hyperlipidaemia, low IGs and complement in blood (increased risk of infection), and increased fibrinogen in blood (risk of thrombosis) |
| consequences of loss of protein | oedema, dyspnoea, increased infection, increased atherosclerosis, low levels of hormones and ions, and thromboembolic events |
| why does oedema occur due to loss of protein | hypoalbuminaemia and consequent reduction in colloid osmotic pressure allowing accumulation of fluid in interstitium and activation of RAAS the SNS and reduction of natriuretic factors to increase Na+ and water retention as a result of decreased blood vol |
| why does dyspnoea occur due to loss of protein | due to pleural oedema and effusion; ascites |
| why does increased infection occur due to loss of protein | due to loss of immunoglobulin and complement in urine |
| why does increased atherosclerosis occur due to loss of protein | due to hyperlipidaemia - LDL and triglycerides |
| how does low levels of hormones and ions occur due to loss of protein | low levels (thyroid) and ions (iron and zinc) due to decrease in binding proteins |
| why does thromboembolic events occur due to loss of protein | due to loss of balance of coagulation and anticoagulation factors |
| general symptoms related to renal failure (3) | tiredness/lethargy/fatigue (often related to renal anaemia), salt and water retention (oedema, hypertension, SOB/ pulmonary oedema) and itching (uraemia and phosphate retention usually filtered and excreted away) |
| management | establish aetiology if possible, establish severity, treat reversible factors, changes in lifestyle, avoid or treat factors causing progression, treat complications, assess options for renal replacement therapy, and end of life care |
| decisions in renal replacement therapy (4) | pre-dialysis care, active treatment, supportive (non-dialytic) care, and end of life care |
| active treatment for renal replacement therapy includes (3) | haemodialysis (HD), peritoneal dialysis (PD), and transplantation |
| how to delay progression in CKD | tight BP control, ACE-I and ARB, diet, stop smoking, treat underlying disease |
Created by:
22tango
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