Urinary Term 3
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| AKI definition | AKI is defined as any one of the following: Increase in Serum Creatinine by 26.5 μmol/l within 48 hours or Increase in Serum Creatinine to ≥ 1.5 times baseline, known/presumed to have occurred within the prior 7 days or Urine volume < 0.5 ml/kg/h for 6 hours. |
| Risk factors for AKI | Age Diabetes immunosuppression polypharmacy dehydration infection CKD Renal stones BPH |
| Classification of AKI | Stage 1: 1.5-1.9 times baseline serum creatinine, urine output of less than 0.5 ml/kg/h for 6-12 hours Stage 2: 2-2.9 times baseline serum creatinine, urine output of less than 0.5 ml/kg/h for 12 hours or greater Stage 3: 3times baseline serum creatinine, urine output of less than 0.3 ml/kg/h for 24 hours or greater or anuria for 12 hours or more |
| Causes of Prerenal AKI | Hypovolemia Decreased Cardiac Output Decreased Effective circulating volume (caused by CHF and liver failure) Impaired Renal Autoregulation (caused by NSAIDS, Angiotensin receptor Blockers, ACE inhibitors, Cyclosporine) |
| Drug induced Pre-renal AKI pathophysiology | Decreased Renal blood flow -> leads to increase in vasodilating prostaglandins to dilate the afferent arteriole. Blunted by NSAIDS that inhibit prostaglandin production Decreased Renal blood flow-> leads to Angiotensin 2 constricting the efferent arteriole. Blunted by ACE inhibitors/ARBs that inhibit angiotensin 2 production Both processes overcome by sever hypovolaemia |
| Intrinsic Renal AKI causes | Acute Glomerulonephritis Tubular Damage (caused by Ischaemia, Sepsis, Nephrotoxins) Vascular (caused by Vasculitis, thrombotic thrombocytopenic purpura/Hemolytic uremic syndrome, Malignant hypertension) |
| Glomerular diseases (Nephrotic vs Nephritic) | Nephrotic Injury to podocytes Changed architecture: Scarring, Deposition of matrix or other elements Proteinuria Nephritic Inflammation Reactive cell proliferation Breaks in GBM Crescent formation Haematuria |
| Postrenal AKI causes | Bilateral uretopelvic obstruction Bladder outlet obstruction |
| AKI signs and symptoms | Nausea and lethargy Decreased urine output Fluid overload Electrolyte abnormalities Acid base disturbance |
| Risk factors for AKI | Age 65+ CKD Cardiac Failure Liver disease Diabetes Vascular disease Nephrotoxic medications ACUTE 'STOP' Sepsis and hypoperfusion Toxicity Obstruction Parenchymal kidney disease |
| AKI Prevention | Monitor patient Maintain circulation Minimise kidney insults Manage the acute illness |
| Anaemia complications | Imbalance of homeostatis Since no |
| Function of Kidneys | Acid base balance Electrolyte & balance Remove toxins and waste products Control BP Produce Erythropoietin/renin/calcitriol |
| Definition of CKD | Abnormalities of kidney structure or function, present for ≥3 months, with implications for health such as: A glomerular filtration rate less than 60 mL/minute/1.73 m², or the presence of one or more of the following markers of kidney damage: albuminuria/proteinuria, Urine sediment abnormalities (e.g., haematuria) Abnormalities (Electrolyte, histology, imaging) History of kidney transplantation. |
| Range of CKD classification (GFR & Albumin) | G1 90+ ml/min/1.73m^2 G2 60-89 G3a 45-59 G3b 30-44 G4 15-29 G5 less than 15 Albumin A1 lower than 30 mg/g A2 30-300 A3 300 + |
| Renal Causes of CKD | Glomerulonephritis Inherited diseases, such as polycystic kidney disease Chronic pyelonephritis Interstitial nephritis Outflow obstruction Myeloma |
| Systemic causes of CKD | Heart failure Reno vascular disease SLE (Lupus) Vasculitis |
| Drug causes of CKD | NSAIDs Lithium Antibiotics Diuretics LMW Heparin |
| Complications of CKD | Cardiovascular disease Peripheral neuropathy Renal mineral and bone disorder ( bone pain/disturbed Vitamin D, Calcium, PTH and phosphate metabolism) Renal anaemia |
| Cardiovascular complications | Hypertension and dyslidaemia, which in turn can contribute to the progression of renal failure, activation of inflammatory mediators and RAAS system, leading to accelerated atherosclerosis. |
| Cardiovascular management | Aspirin, statins, ACE inhibitors or angiotensin receptors blockers and beta blockers. For Optimal control of glycaemia and blood pressure. |
| Neuropathy complications | Stroke, cognitive dysfunction, encephalopathy, through to autonomic and peripheral neuropathies. (affects the level of electrolytes) Peripheral neuropathy as a result of kidney disease is referred to as uremic neuropathy. |
| Neuropathy management | Renal replacement therapy Risk factors Complications |
| Renal mineral and bone disorder complications | Mineral bone disorder Decreased Calcitriol (Vit D-absorb Ca) Low calcium, high phosphate Hight PTH- increase calcium from bones (pain, shape) |
| Renal mineral and bone disorder management | Gut phosphate binders/diet/dialysis Calcitriol (1,25 (OH) Vitamin D) analogues- increase calcium absorption and suppress PTH Calcimimetic agents- reduce calcium by acting on calcium sensing receptors in parathyroid to reduce PTH. |
| Anaemia complications | Imbalance of homeostatis Since decreased eythropoietin, so lower red bone marrow, decreased RBC count |
| Anaemia management | Hb 100- 120g/L Check B12, Folate, Iron Supplement Iron poorly absorbed in CKD ESAs improves QOL Avoids blood transfusion |
| Stages of CKD management | 1/2- ACE inhibitor, Statin, Bp control, Glycaemic control 3/4- Education-Renal replacement Therapy, Anaemia- epo stimulating agent/Iron 2' Hyperparathyroidism- Diet/phosphate and calcium control Metabolic acidosis- Sodium bicarbonate 5- Renal replacement therapy, Haemodialysis, Peritoneal dialysis, Renal transplant |
| Haemodialysis vs Peritoneal Dialysis | HD Staff required Has to happen in HD unit Cardiac Risk 6 weeks Difficult to access with veins PD No staff required Can happen anywhere Safer for Cardiac risk 2 weeks Difficult to access with adhesions |
| What does Dialysis help maintain | Maintain Euvolaemia (sodium & water) maintains electrolytes Dialysate bicarbonate diffuses blood into correct acidosis |
| Renal transplant benefits | Improved patient survival Correct symptoms and metabolism improved QOL and Family QOL |
| Glomerulonephritis Definition | Glomerulonephritis (GN) is a renal disease characterised by inflammation and damage to the glomeruli. |
| Nephrotic Syndrome Definition | The definition of nephrotic syndrome includes both massive proteinuria (≥3.5 g/day) and hypoalbuminaemia (serum albumin ≤30 g/L). Increased permeability of the glomerulus leading to loss of proteins into the tubules. This leads to the loss of significant volumes of protein via the kidneys (proteinuria) which results in hypoalbuminaemia. |
| Symptoms of Nephrotic syndrome | Peripheral oedema (more common in adults) Facial oedema (more common in children) Frothiness of urine (proteinuria in urinalysis) Fatigue Poor appetite Recurrent infections (due to immune dysfunction) Venous or arterial thrombosis (e.g. myocardial infarction, deep vein thrombosis) due to hypercoagulability |
| Signs of Nephrotic syndrome | Oedema (e.g. peri-orbital, lower limb, ascites) Xanthelasma and/or xanthoma Leukonychia (white dots on nails) Shortness of breath (with associated chest signs of pleural effusion – e.g. stony dullness in lung bases) |
| Nephritic Syndrome definition | Damage to the thin glomerular basement membrane with pores that allow protein and blood into the tubule. This involves Haematuria / Red cell casts Proteinuria - mild to moderate(typically less than 3.5g/L/day) Hypertension (mild) Oliguria Uraemia |
| Nephritic syndrome symptoms | Haematuria (can be frank haematuria or microscopic) In urinalysis red cell casts would be found, which is a distinguishing factor from nephrotic Oedema (to a lesser extent compared to nephrotic syndrome) Reduced urine output Uraemic symptoms (e.g. reduced appetite, fatigue, pruritus, nausea) |
| Risk factors of Malignancy | Occupational Environmental Genetic Age Sex Smoking Alcohol Obesity |
| Renal adenocarcinoma (RCC) Triad | Haematuria (may produce iron deficient anaemia 60%) Flank pain (40%) Flank mass (25%) |
| RCC treatment | Established – Surveillance – Radical nephrectomy – Partial nephrectomy Developmental – Ablation |
| What is Nephroblastoma (Wilms' Tumour) | Abnormality in chromosome 11 (children), leading to Large abdominal mass, abdominal pain, anaemia, incidental finding, hypertension, haematuria, weight loss. |
| Most common bladder carcinoma | Transitional cell carcinoma (90%) |
| Signs and symptoms of Bladder carcinoma | Painless haematuria must be treated as urinary tract malignancy until proven otherwise LUTS, loin/suprapubic/urethral/penile tip pain |
| Prostate cancer Grading | Grade Group 1 The cells look similar to normal prostate cells. The cancer is likely to grow very slowly, if at all. Grade Group 2 Most cells still look similar to normal prostate cells. The cancer is likely to grow slowly Grade Group 3 The cells look less like normal prostate cells. The cancer is likely to grow at a moderate rate Grade Group 4 Some cells look abnormal. The cancer might grow quickly or at a moderate rate Grade Group 5 The cells look very abnormal. The cancer is likely to grow quickly |
| Tests for Prostate cancer | PSA is a protein produced by normal and cancerous prostate cells. PSA is secreted by prostate epithelial cells into prostatic fluid, where its function is to liquefy semen and thus allow spermatozoa to move more freely. Cancer can be present without increased PSA levels, and there are many other causes of increased PSA levels (for example, benign prostatic enlargement, prostatitis, and urinary tract infection). Digital Rectal Examination MRI Biopsy |