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Urinary Term 3


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Satvika Sinha


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AKI definition
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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.

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Urinary Term 3 - Detalles

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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