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Renal

Anna Walker Englisch 121 Karten

Karten in diesem Stapel (121)

  1. 1What are the roles of the kidney?Glomerular filtration and tubular reabsorption: Excretes waster products of metabolism, e.g. Ur, Cr, urate, drugs etc., and removes excess water and salts. Controls renin-angiotensin system to maintain blood pressure. Produces EPO which stimulates red cell production from bone marrow. Conserves essential nutrients: calcium and phosphate. Maintains blood in a pH neutral state.
  2. 2List some signs and symptoms of CKD.Polyuria(/anuria in end stage), proteinuria (decreased immunity as Ig is lost), hypoalbuminaemia, anaemia (decreased EPO production), hypertension, haematuria, osteoporosis (losing calcium and phosphates), hyperkalaemia.
  3. 3What are the three endocrine roles of the kidney?The kidneys secrete RENIN on decreased glomerular flow, and this activates the RAAS which helps to regulate BP, Na and K balance. CALCITRIOL is also secreted by the kidneys, and this is important for the normal absorption of Ca by the GI tract and for its deposition in bone. Decreased calcitriol production contributes to bone formation abnormalities in chronic renal disease. The kidneys also secrete EPO, which stimulates RBC formation by the bone marrow. Decreased RBC production contributes to the anaemia seen in chronic renal failure.
  4. 4What process happens at the Bowman's capsule?Collection of glomerular filtrate.
  5. 5What process happens at the proximal convoluted and straight tubule?Re-absorption of water, proteins and amino acids, glucose and carbohydrates.
  6. 6What process happens at the Loop of Henle?Creation of hypertonicity gradient between collecting ducts and interstitium.
  7. 7What process happens at the distal straight and convoluted tubule?Acid-base and water balance. Absorption of water, Na and HCO3-. Excretion of K and H.
  8. 8What process happens at the collecting tubule and collecting ducts?Controlled reabsorption of water under influence of ADH.
  9. 9What are the four types of partial renal failure?Asymptomatic haematuria, persistent proteinuria, nephrotic syndrome, nephritic syndrome.
  10. 10What is asymptomatic haematuria?Suggests minor glomerular damage as an early sign of a progressive glomerular disease such as IgA nephropathy.
  11. 11What is persistent proteinuria?Also usually asymptomatic, indicative of an early abnormality involving the basement membrane of mesangium, or both. May progress to nephritic syndrome.
  12. 12What is nephrotic syndrome?Abnormality in basement membrane or mesangium such that proteins cannot be retained in blood. Leads to triad of proteinuria, hypoalbuminuria, and oedema. This also results in increased susceptibility to infection (low Ig and complement), susceptibility to thrombosis (decreased levels of antithrombin III) and hyperlipidaemia. >80% are caused by glomerulonephritis.
  13. 13What is nephritic syndrome?Result of disturbance of glomerular structure that involves reactive cellular proliferation. Leads to reduced glomerular flow, leading to oliguria, leakage of red cells from damaged glomeruli (haematuria), and retention of waste products (uraemia). Low renal blood flow activates RAAS leading to fluid retention and mild hypertension. Small amount of protein are lost in urine, and haematuria is not gross and usually manifests as a smoky brown discolouration of urine.
  14. 14When might a mixed nephrotic/nephritic syndrome be seen?If there is both damage to the basement membrane AND cell proliferation.
  15. 15What are the two types of renal failure?Acute - sudden cessation of nephron function, affecting all of the nephrons at the same time. Chronic - nephrons are destroyed one by one over an extended period of time. Deterioration is slowly progressive and therefore the pt may be asymptomatic as residual undamaged nephrons work harder to compensate for the lost nephrons, although the deterioration may be detected by lab testing of GFR.
  16. 16What are the 3 categories of acute renal failure aetiology?PRE-RENAL: Systemic - Heart failure, blood or fluid loss. Local - renal artery occlusion/stenosis, diseases affecting arteries. Under-perfusion initially causes reversible changes. Subsequently, 'acute tubular necrosis' or other changes cause longer-lasting, but usually temporary, intrinsic renal failure.
    INTRINSIC RENAL DISEASE: Acute tubular necrosis/septic/toxic renal failure (85%), Glomerular disease - either primary or component of systemic disease (5%), Interstitial disease (10%). POST-RENAL: Obstruction - stones, cancer, prostatic enlargement.
    Can be more helpful to think - kidneys first, or kidneys second?
  17. 17What is the breakdown of chronic renal failure aetiology?Diabetes (20-40%), Hypertension (5-25%), Glomerular disease (10-20%. IgA nephropathy is most common), Chronic pyelonephritis (15%), Interstitial nephritis, Renal artery stenosis, Renal stones, benign prostatic hyperplasia, Polycystic kidmey disease, Systemic inflamm/connective tissue diseases (SLE, vasculitis, sarcoidosis, scleroderma), Renal tumour, Haemolytic uraemic syndrome, Myeloma, Alport's syndrome (X-linked defect in type IV collagen which is a vital component in basement membranes), Fabry's disease (X-linked lysosomal storage disorder leading to an accumulation of glycosphingolipids).
  18. 18What is the effect of hypovolaemic, septicaemic or cardiogenic shock on the kidneys?Central perfusion failure due to hypovolaemic shock as a result of, say, masssive haemorrhage or central pump failure due to MI, leads to inadequate perfusion of the kidneys, The most sensitive components of the nephron to poor perfusion and anoxia are the proximal and distal convoluted tubules, which may undergo extensive necrosis termed Acute Tubular Necrosis. Combined with insufficient glomerular perfusion for ultrafiltration to take place, this leads to failure of the nephron. This is the most common cause of acute renal failure.
  19. 19What are the three stages of acute tubular necrosis?A damaging stimulus causes necrosis of renal tubular epithelium. There is a blockage of renal tubules by necrotic cells, and a secondary reduction in glomerular blood flow caused by arteriolar constriction, which reduces glomerular filtration. Pts develop acute renal failure and oliguria. Supportive measures are required to prevent hyperkalaemia and fluid overload. POLYURIC PHASE: Over 1-3 weeks, regeneration of tubular epithelium takes place with removal of dead material by phagocytes, as well as in the form of casts in the urine. As tubules open up and blod flow increases, pts develop polyuria as the regenerated tubular cells are undifferentiated and have not developed specialisations needed for the reabsorption of water. Replacement fluid and electrolytes are needed to compensate for the excessive loss. RECOVERY PHASE: Tubular cells differentiate and there is restoration of homeostatic renal function.
  20. 20Describe the features of renal artery sclerosis.In general, slowly progressive disease of the vessels leads to slowly progressive destruction of the nephrons, ischaemic glomerular filtration failure and ischaemic tubular atrophy, culminating in chronic failure and a small, shrunken end-stage kidney. Generalised atherosclerosis tends to affect the aorta and the origin of the renal artery, causing the aforementioned chronic ischaemia and an end-stage, shrunken kidney on the affected side. The unaffected kidney undergoes compensatory hypertrophy so renal function is largely unaffected in most cases.
    Renal artery stenosis is also caused by arterial fibromuscular dysplasia, which is abnormal fibromuscular lining of an artery, leading to webs that restrict blood flow, classical appearance of "beads on a string" at imaging - usual cause in children and young women; responds well to balloon dilatation.
    Renal artery sclerosis may lead to renovascular hypertension, thought to result from abnormal activity of the RAAS in the chronically ischaemic kidney. This is an important cause of hypertension that may be amenable to surgical correction.
  21. 21What is glomerulonephritis?The group of diseases in which the primary pathology is structural abnormality in the glomerulus. Despite the suffix -itis, most are not characterised by inflammation. Damage may be severe, resulting in scarring and atrophy of that tubule, or may produce a temporary abnormality and following resolution there is a restoration of nephron function.
  22. 22What could cause damage to the glomerulus?Can be damaged by: Generalised vascular disease, particularly hypertension; immunological disorders, particularly where immune complexes are deposited in glomerular capillary walls; depositions of foreigh material, e.g. amyloid.
  23. 23What are the most common patterns of glomerular disease?Diffuse global (the whole of the glomerulus is affected in all glomeruli in both kidneys) and focal segmental (only some glomeruli are affected, and only small parts are affected).
  24. 24List the important types of glomerulonephritis.IgA (Berger) nephropathy - most common cause of glomerulonephritis in adults. Acute diffuse proliferative glomerulonephritis (presents as nephritic syndrome). Membranous nephropathy (presents as proteinuria and nephritic syndrome). Diffuse membranoproliferative glomerulonephritis (presents as mixed nephrotic/nephritic). Goodpasture's is a rare cause.
  25. 25What is chronic pyelonephritis?Chronic inflammation and scarring, which destroys nephrons and distorts the pelvicalyceal system. Renal induced hypertension may develop and hypertension induced vascular damage may increase renal damage. The kidneys have irregular areas of scarring and histologically the kidney has chronic inflammatory cell infiltrate. Tubules are atrophic or dilated and contain proteinaceous material. Glomeruli show fibrosis.
  26. 26What are the two forms of chronic pyelonephritis?Reflux-associated chronic pyelonephritis: reflux of urine from bladder up ureters due to incompetent vesicouretic valve mechanism predisposes to inflammation and scarring - this occurs in childhood and presents in early adulthood with progressive impairment of renal function.
    Obstructive chronic pyelonephritis: Recurrent episodes of infection leading to obstruction which may be due to either anatomical abnormality or a stone.
  27. 27What is interstitial nephritis?Inflammatory disease of the renal interstitium and tubules, associated with tubular atrophy/damage. Types include: Drug-induced acute interstitial nephritis (presents 2-3 weeks after exposure to agent with fever, haematuria, proteinuria and elevated blood urea. There is oedema of interstitium and inflammatory infiltration. Recovery upon withdrawal of causative agent). Drug-induced chronic interstitial nephritis (development of chronic renal failure after exposure. Fibrosis, inflammation and atrophy of tubules). Analgesic neuropathy (often caused by NSAIDs, leads to renal tubular failure, polyuria, metabolic acidosis and ultimately chronic renal failure). Radiation nephritis (following radiotherapy. Hyalinisation of glomeruli and small vessels, ischaemia and interstitial fibrosis).
  28. 28What are the three classifications of diabetic nephropathy?Lesions affecting arterial supply to kidney (types 1 and 2). Lesions of tubules and interstitium (types 1 and 2). Lesions of the glomerulus (mostly type 1). Diabetics have particularly severe atherosclerosis which extends to the smaller arteries moreso than in non-diabetics. The reduction in luminal size leads to initially poor glomerular perfusion by blood with reduced GFR and ultimately glomerular ischaemia.
  29. 29What are Kimmelstiel-Wilson nodules?Spherical sclerotic masses that form on the mesangium; only seen in advanced diabetic kidney disease.
  30. 30What 2 structural changes that occur in long-standing benign hypertension could lead to reduced glomerular flow?1. Renal artery branches within the kidney show a thickening of their wall due to fibroelastic intimal proliferation, elastic lamina reduplication and muscular hypertrophy of the media.
    2. Afferent arterioles undergo hyalinisation, their muscular walls being replaced by amorphous material, which is inelastic.
    There are no clinical symptoms of this except a steadily decreasing GFR until gradually the blood levels of urea and creatinine begin to rise. Eventually enough nephrons stop working for the symptoms of chronic renal failure to develop. This is called Benign Hypertensive Nephrosclerosis and is an important complication of long standing hypertension.
  31. 31What is the effect on the kidney is accelerated malingnant hypertension?The large muscular vessels respond with loose fibroelastic proliferation of the intima, and the afferent arterioles exposed to sudden high pressures may undergo necrosis (often with fibrin in their damaged walls, this is 'fibrinoid necrosis'). The glomerular capillary network may also undergo segmental tuft necrosis. When sufficient nephrons are dysfunctioning, the pt may develop acute renal failure.
  32. 32What is the effect of vasculitis on the kidney?Leads to focal segmental glomerulonephritis. Pathological mechanism is thought to be immunological, so the appearance of the kidney largely overlaps with those of IgA nephropathy. ~20% of infective endocarditis show focal segmental glomerulonephritis, with immune complex deposits. It is also a feature of some of the connective tissue disorders, such as SLE and progressive systemic sclerosis. Fibrinoid tuft necrosis is a frequent feature.
  33. 33What are most post-renal causes of kidney failures due to, and where does this most often occur?Most are due to obstruction of drainage of urine, which causes hydronephritis. This may occur at any point in the urinary tract: Renal pelvis (calculi, tumours), Pelviureteric junction (stricture, calculi, extrinsic compression), Ureter (calculi, extrinsic compression due to pregnancy/tumour/fibrosis), Bladder (tumour, calculi), Urethra (prostatic hyperplasia/cancer, urethral valves, urethral stricture).
  34. 34What happens if there is a urethral blockage?The bladder will dilate and the muscle in its wall will develop secondary hypertrophy, which predisposes to outpouching of the bladder mucosa (diverticula).
  35. 35What is megaureter?This is dilatation of the ureter proximal to a blockage. This usually leads to progressive dilatation of the renal pelvicalyceal system, termed hydronephrosis.
  36. 36What is actually happening in benign prostatic hyperplasia?The area of prostate which undergoes hyperplasia is not actually the true prostatic glands (at the periphery) but the periurethral group of prostatic glands which surround the urethra. Continuing enlargement of these glands compresses the true prostate and leads to peripheral collapse, leaving only their supporting stroma behind. Also, muscular hypertrophy occurs at the bladder neck.
  37. 37Describe the features of prostate carcinoma.Second most common cancer in men, esp in men >55yrs. Adenocarcinoma originating in the periphery of the prostate, thus local involvement outwards is more likely before the tumour invades the urethra. Therefore, diagnosis is better made using the transrectal approach as the transurethral approach is likely to give a false negative. No causative factors - screen for PSA in the blood. Raised testosterone and family history may predispose. Tumour often well established and may well have mets by the time urethral symptoms manifest.
  38. 38What are the 3 clinical groups of prostatic cancer?Invasive prostatic carcinomas - invade locally and metastasise. Latent prostatic carcinomas - small, well-differentiated foci in prostate, incidental finding as they remain localised to the prostate for a long time. Occult carcinomas - not clinically apparent at primary site but present as metastatic disease.
  39. 39Why do renal calculi develop?Due to an increased concentration of solute in the urine OR reduced solubility of product in urine. Main underlying causes are: Infection, Stasis and Metabolic abnormalities.
  40. 40What are renal stones usually made up of?Calcium oxalate and phosphate, which some being caused by hypercalciuria or hyperoxaluria. The second most common are triple-phosphate stones caused by chronic infections.
  41. 41Name three complications that renal stones may predispose to.Infection, perinephritic abscess, and the development of squamous metaplasia in the urothelium. NB: Squamous cell carcinoma may occasionally occur in metaplastic areas.
  42. 42What is Retroperitoneal Fibrosis?Retroperitoneal fibrosis or Ormond's disease is a disease featuring the proliferation of fibrous tissue in the retroperitoneum, the compartment of the body containing the kidneys, aorta, renal tract, and various other structures, which causes unilateral or bilateral ureteric obstruction. Condition may spread from L2 to the pelvic brim. It is an autoallergic response to leakage of material, probably ceroid (a pigment). Malaise, back pain, normochromic anaemia, uraemia and a raised ESR are typical features. Biopsy should be performed to rule out lymphoma/carcinoma. CT may reveal periaortic mass. Obstruction is relieved surgically by ureterolysis (freeing of ureters from surround structures), although corticosteroids may be of benefit. A stent is another option. Bilat. ureterolysis is a big op so they usually only do one.
  43. 43What is the definition of Acute Renal Failure (ARF) and how does it manifest clinically?An abrupt deterioration in parenchymal renal function whic is usually (but not invariably) reversible over a period of days to weeks. Clinically manifests as an abrupt and sustained rise in serum urea and creatinine. Acute renal failure may cause sudden, life-threatening hyperkalaemia, volume overload and metabolic acidosis, and this is a medical emergency. It mosy commonly occurs in the setting of circulatory disturbance, or nephrotoxic drugs in pts with DM, hypertension, or the elderly.
  44. 44What kind of metabolic abnormalities are likely to be seen in ARF?Rapidly progressive uraemia, dependent upon rate of tissue breakdown. Symptoms of uraemia include: anorexia, nausea, vomiting, pruritis, intellectual clouding, drowsiness, fits, coma, haemorrhagic episodes. Hyperkalaemia, particularly following muscle trauma and in haemolytic states. Matebolic acidosis usual, unless vomiting or aspiration of gastric contents. Hyponatraemia due to fluid overload OR hypernatraemia due to shock. Pulmonary oedmea due to salt and water retention. Hypocalcaemia due to underproduction of calcitriol. Hyperphosphataemia due to phosphate retention.
  45. 45What is the emergency management of hyperkalaemia (6)?The danger here is ventricular fibrillation. K >7mmol/L will usually require urgent treatment, as do lower values with ECG changes (e.g. Tented T waves +/- flat P waves +/- increased PR interval, widening og QRS, sinusoidal pattern of VF/VT). Management:
    MONITOR ECG. 10ml CALCIUM GLUCONATE (10% IV over 2 mins, repeated as necessary if severe ECG changes). This provides cardio-protection by raising the threshold potential. It does no alter serum K levels. (NB: skin necrosis if extravasation so avoid peripheral cannulae). INSULIN + GLUCOSE, e.g. 50ml or 50% glucose with 10U of rapidly acting insulin given into large vein (unless hyperglycaemic). over 30 mins. Monitor for hypoglycaemia. This regimen may need repeating. Insulin moves K into cells. NEBULISED SALBUTAMOL 2.5mg moves K into cells. POLYSTYRENE SULFONATE resin orally, or if vomiting, as an enema followed by colonic irrigation after 9h to remove potassium. DIALYSIS.
  46. 46How would you assess whether a pt with renal failure has acute or chronic failure?Suspect chronic renal failure if history of comorbidity (DM, HTN), long duration of symptoms, previously abnormal blood results (GP records, lab results), small kidneys on USS (<9cm) with increased echogenicity. the presence of anaemia, hypocalcaemia or hyperphosphataemia may not help to distinguish ARF from CRF, as these can occur within days, but their absence indicates ARF.
  47. 47How would you assess whether a pt with renal failure has urinary tract obstruction?Prompt treatment will reverse renal damage, so this is important. Suspect in pts with a single functioning kidney, Hx renal stones, BPH or previous pelvic/retroperitoneal surgery. Examine for palpable bladder, pelvic or abdo masses, or enlarged prostate. Complete anuria suggests renal tract obstruction and is unusual in ARF. Renal USS is the preferred method to detect a dilated tract. Obtruction may be present without dilatation, esp in malignancy.
  48. 48How would you assess whether a pt with renal failure has fluid overload/reduced intravascular volume?REDUCED INTRAVASCULAR VOLUME is suggested by reduced urine output, invisible JVP, poor tissue turgor, hypotension, tachycardia. If in doubt, consider inserting a CVP line. SIGNS OF FLUID OVERLOAD: gallop rhythm on cardiac auscultation, hypertension, raised JVP, lung crepitations, peripheral oedema.
  49. 49What is the definition of chronic kidney disease?CKD = Kidney damage for >3 months based on findings of abnormal structure or function OR GFR <60ml/1.73m^2 for >3 months with or without evidence of kidney damage.
  50. 50What are the clinical features of CKD?Often asymptomatic early on, despite the accumulation of metabolites. Symptoms become more common when serum urea exceeds 40mmol/L. Malaise, loss of appetite, itching, insomnia, nocturia and polyuria (due to impaired concentrating ability), nausea, vomiting, diarrhoea, peripheral + pulmonary oedema due to salt and water retention, anaemic syx, restless legs, bone pain (due to metabolic alterations), paraesthesia and tetany due to hypocalcaemia and polyneuropathy, amenorrhoea in women, ED in men.
  51. 51What would an FBC and U&E show in a pt with CKD?FBC - low Hb (normochromic, normocytic), U&E - high creatinine and high urea. A disproportionate increase in creatinine and K compared to urea indicates rhadomyolysis.
  52. 52How should urine be analysed in ?CKD and what would be seen if they have it?M, C &S: Do early morning samples for TB. WBCs indicate bacterial urinary infection. Sterile pyuria indicates papillary necrosis or renal TB. Eosinophilia suggests allergic tubulointerstitial nephritis or cholesterol embolisation. Casts - granular casts suggest abnormal cells in tubular lumen; red cell casts indicate glomerulonephritis. Red cells may be from anywhere between glomerulus and urethral meatus. Urine osmolality may indicate disease if dilute in hypovolaemia/hypotension. DIPSTICK: Haematuria indicates glomerulonephritis. Proteinuria is strongly suggestive of glomerular disease if heavy. Infection may also cause proteinuria. Glucosuria with normal blood glucose is common in CKD.
  53. 53What would be seen on a CXR in a pt with CKD?Cardiomegaly, pleural/pericardial effusion, pulmonary oedema.
  54. 54List the common causes of CKD.Diabetes, glomerulonephritis, HTN, chronic interstitial nephritis, macrovascular disease, polycystic kidney disease, obstructive uropathy.
  55. 55Describe the features of autosomal dominant polycystic kidney disease (ADPKD).Both kidneys gradually replaced by enlarging fluid cysts which are sometimes haemorrhagic. Renal parenchyma is compressed out of existence over years. Renal failure develops in adult life, unfortunately after the pt has passed on the gene mutation. Pt has systemic HTN, CKD and abdo swelling due to enormously enlarged kidneys. Cysts also occur in liver, lungs and pancreas, but without symptoms.
  56. 56Describe the features of autosomal recessive polycystic kidney disease (ARPKD).Rare. Onset is earlier than ADPKD and runs a more malignant course. There are perinatal, neonatal, infantile and juvenile types, becoming less severe with later onset. Kidneys are enlarged and show radial pattern of elongated cysyts replacing cortex and medulla, causing chronic renal failure and HTN. Cysts also in liver leading to portal hypertension, periportal fibrosis and duct proliferation.
  57. 57Describe the features of Juvenile nephronophthisis (medullary cystic disease).Group of diseases which begin in childhood. Multiple small cysts on corticomedullary junction. Interstitial fibrosis with progressive destruction of cortical and medullary tubules. Presents in childhood with polyuria and polydipsia, progressing to renal failure by age 10. Rare type which presents in adulthood. can be dominant or recessive.
  58. 58Describe how creatinine clearance (GFR) is calculated.Urine is collected over 24 hours for measurement of urinary creatinine. A single plasma level of creatinine is measured in this 24h period. U = urine concentration of creatinine, V = rate of urine flow (ml/min) and P=plasma concentration of creatinine. Creatinine clearance = (U x V)/P. Normal range = 90-140 ml/min in men and 80-125ml/min in women.
  59. 59What is renal osteodystrophy?A mixture of hyperparathyroid bone disease, osteomalacia, osteoporosis, osteosclerosis, adynamic bone disease. Reduced renal production of 1alpha-hydroxylase results in reduced activation of Vitamin D. Lack of activation of Vit D receptors in parathyroids leads to increased PTH secretion. Gut calcium malabsorption occurs. Phosphate retention owing to reduced renal excretion leads to an increase in PTH. Phosphate also lowers ionised calcium. PTH promotes reabsorption of calcium from bone and increased proximal renal tubular reabsorption of calcium. This opposes hypocalcaemia induced by Vit D deficiency and phosphate retention. This leads to osteoclastic activity, cyst formation and marrow fibrosis. This eventually leads to tertiary hyperparathyroidism and hypercalcaemia. This leads to osteosclerosis of the spine and a 'rugger jersey' appearance on XR.
  60. 60What lifestyle advice would you give to someone with CKD?Exercise, healthy weight, stop smoking. Match dietary and fluid intake with excretion. Sodium restriction helps control BP and prevent oedema. Moderate protein diet. K restriction if hyperkalaemia. HCO3 supplements to correct acidosis.
  61. 61When should dialysis be started in CKD?Official guidelines suggest starting when GFR is <15ml/min with symptoms, but optimal timing is debated and data shows that dialysis is started when GFR <8 on average. Dialysis is started earlier for diabetics.
  62. 62Describe the process of haemodialysis. What are the problems associated with it?Blood flows on one side of the semipermeable membrane whilst dialysis fluid flows in the opposite direction on the other side. Solute transfer occurs by diffusion. Small solutes diffuse readily (urea), whereas large solutes diffuse less readily and are not cleared as effectively (can use haemofiltration in criticaly ill pts as it is more haemodynamically stable). Ultrafiltration = the removal of excess fluid by creating a -ve transmembrane pressure. PROBLEMS: Time consuming. Hypotension & arrythmias. Dysequilibrium syndrome (cerebral oedema). Fistula required; thrombosis, stenosis, aneurysm, steal syndrome (vascular insufficiency distal to fistula), ischaemia. Temporary line; infection, blockage.
  63. 63Describe the process of peritoneal dialysis. What are the problems associated with it?Simple to perform, requires less complex equipment that is easier to use at home. More commonly used in children, the elderly and those with CV disease. PD fluid is inroduced into the abdomen via a Tenchkoff catheter and uraemic solutes diffuse from underlying vessels into the peritoneal cavity across the peritoneal membrane. Ultrafiltration is achieved by adding osmotic agents, e.g. glucose. PROBLEMS: Peritonitis (60% staphylococci, 20% gram _ve, <5% fungi). Exit site infection. Catheter malfunction. Loss of membrane function. Obesity (glucose in peritoneal fluids). Hernias. Back pain.
  64. 64What is minimal change nephropathy (a primary renal cause of nephrotic syndrome)?Seen mainly in children <6yrs, presenting with proteinuria and nephrotic syndrome. Less common in adults but still makes up 10-15% of nephrotic syndrome). Associations with Hodgkin's lymphoma, and NSAIDs. Biopsy: characterised by nothing abnormal on light microscopy. On EM there is fusion of podocyte processes and some lipid accumulation. Thought to be an immune process. Treat with steroids which bring remission in 2 weeks, but prone to relapse. Cyclosporin or chlorambucil are used in relapses.
  65. 65What is membranous glomerulonephritis (a primary renal cause of nephrotic syndrome)?Accounts for 20-30% of nephrotic syndrome in adults, rare in children. Risk of renal vein thrombosis. 80-90% are idiopathic (primary/idiopathic membranous nephropathy) 10-20% have an underlying cause: malignancy (Ca lung, lymphoma), drugs (gold, penicillin, captopril), autoimmune (RA, SLE, thyroid disease), infection (HBV, syphilis, leprosy, filiariasis). Biopsy: diffuse thickened glomerular basement membrane with IgG and C3subepithelial deposits in all segments of all glomeruli (diffuse global). Treat with steroids and cyclophosphamide or chlorambucil is renal function deteriorates. 25% go into spontaneous remission, 25% stable, 50% develop chronic renal failure over 10 years.
  66. 66What is proliferative 'mesangiocapillary' glomerulonephritis (a primary renal cause of nephrotic syndrome)?Rare type of glomerulonephritis. Presents with nephrotic syndrome or a mixed nephrotic/nephritic syndrome with proteinuria and haematuria. Mostly idiopathic, divided into types I and II. May also be secondary to complement abnormalities: SLE, IE, malaria, infected CSF shunts. Biopsy: large glomeruli with mesangial proliferation and thickened capillary walls leading to a 'tramline' appearance of a double basement membrane. Type I (90%) - most common in adolescents and young adults. There is mesangial proliferation and excessive lobulation of glomerular segments. There are immune complexes containing IgG, IgM and C3. Type II (10%) - sen in children and young adults. Mesangial thickening is not as prominent. There are dense ribbon-like deposits in the basement membrane. They contain no immune complexes and are purely complement factor C3. May be associated with activation of alternative complement pathway. Treament has no proven benefit, though steroids are tried in children. 50% develop ESRF, high recurrence in transplants.
  67. 67Which investigations are necessary to diagnose nephrotic syndrome?Bloods - FBC, U&E, ESR, CRP, Ig, complement (C3 + C4), autoantibodies, blood culture, HBsAG, anti-HCV, ASOT (group A Strep). Urine - RBC casts, M, C & S, Bence-Jones protein (suggests myeloma), 24hr protein or a spot urine to test protein:creatinine ratio or albumin:creatinine. CXR, Renal US, Renal biopsy in all adults. In children, most will have minimal change nephropathy so steroids are usually tried initially.
  68. 68What is the management for nephrotic syndrome?Treat underlying cause (glomerulonephritis in most). Reduce salt intake to <3g/day and fluid intake to ~1.5L/day. Diuretics often used in adults, e.g. furosemide 80-250mg/24h PO +/- metalozone/spironolactone with monitoring of U7E. Proteinuria is an independent risk factor for CV disease. ACEi/ARBs are mainstay of treatment for this as they reduce proteinuria. Treat infections promptly. Pneumococcal vaccinations are recommended. Treating the underlying cause will improve the hyperlipidaemia. Treat with a statin if persistent. Avoid prolonged bed rest - give prophylactiv anticoagulation if immobile. Treat HTN. ACEi/ARB should be 1st line.
  69. 69What is IgA nephropathy (Berger's disease)?Most common glomerulonephritis in developed world. Affects young males a few days after URTI. Presents with macro/microscopic haematuria +/- nephritic syndrome. Recovery is often rapid after attacks. There is raised IgA, possibly due to infection, which forms immune complexes and deposits in mesangial cells. Biopsy shows mesangial proliferation and immunofluorescence demonstrates IgA and C3 deposits. Treat with steroids to reduce proteinuria and slow down the decline of renal function. Cyclophosphamide may be effective if renal function is deteriorating rapidly. Prognosis is worse if HTN, male, proteinuria or renal failure at presentation. 20% develop ESRF over 20 years.
  70. 70What is Goodpasture's disease (Anti-glomerular basement membrane/GBM disease)?Due to development of autoantibodies to type IV collagen, an essential component of the GBM. Type IV collagen is also found in the lung. Most commonly affects young males, but can occur at any age or in women. Presents with macroscopic haematuria, progressing rapidly oliguria. May also be haemoptysis, esp in smokers. Renal failure may occur within days of onset. Treatment = plasma exchange, corticosteroids +/- cytotoxics. Can be cured if treatment started early and relapses are rare.
  71. 71Describe the features of Rapidly Progressive Glomerulonephritis.The most aggressive GN with the potential to cause ESRF over days. There are different causes, all have the biopsy finding of crescents affecting most glomeruli (a proliferation of parietal epithelial cells and macrophages in the Bowman's capsule). RPGN is classified into 3 capillaries: Immune Complex Diseases (45%): post-infectious (endocarditis, shunt nephritis), multi-system disease (SLE), IgA nephropathy, HSP. Pauci-Immune Disease (50%): Wegener's granulomatosis (cANCA +ve), microscopic polyangitis (pANCA +ve), Churg-Strauss. Anti-GBM Disease (3%): Goodpasture's.
    All present with signs of renal failure, features of individual systemic disease. Massive pulmonary haemorrhage is most common cause of death in ANCA +ve pts. Mangement = aggressive immunosuppression with high-dose steroids + cyclophosphamide with plasma exchange to remove existing antibodies.
  72. 72List the signs and symptoms of cystitis (LUTI).Most typically: frequency of micturition day and night, dysuria, urgency, strangury (painful, frequent urination of small volumes that are expelling slowly only by straining and despite a severe sense of urgency, usually with a residual feeling or incomplete emptying), suprapubic pain and tenderness, haematuria, smelly urine.
  73. 73List the signs and symptoms of pyelonephritis (UUTI).High fever, rigors, vomiting, loin pain, tenderness, oliguria (if acute renal failure).
  74. 74List some predisposing factors to UTI.More common in women due to shorter urethra. Uncommon in men and children; urinary tract is often abnormal and require investigation. Exposure to spermicide in women. Pregnancy. Menopause. Reduced host defencec (DM, immunosuppression). Stones. Obstruction. Catheter. Tract malformation.
  75. 75How do you distinguish between a relapse and a reinfection in a pt with recurrent UTIs?Relapse = recurrence of infection with the same organism within 7 days of completion of antibacterial treatment and implies failure to eradicate infection, usually in conditions such as stones, scarred kidneys, polycystic disease or bacterial prostatitis.
    Reinfection = bacteruria is absent after treatment for at least 14 days followed be a recurrence of infection with the same or a different organism. This is not due to failure to eradicate infection but reinvasion of a susceptible tract with new organisms.
  76. 76What are the suitable investigations for UTI?If symptomatic then dipstick the urine. Treat empiracally if nitrates or leucocytes are +ve whilst awaiting sensitivities on an MSU. If dipstick -ve, consider sending an MSU for M, C & S to confirm this. Send lab MSU anyway if male, child, pregnant, immunosuppressed or ill.
  77. 77Why might you get a sterile pyuria (WBCs raised but no organisms grown)?Treated UTI <2 weeks before. Inadequately treated UTI. Appendicitis. Calculi, prostatitis. Bladder Ca. UTI with fastidious culture requirements (TB, chlamydia). Papillary necrosis (DM, analgesic excess). Tubulointerstitial nephritis. Polycystic kidney. Chemical cystitis e.g. cyclophosphamide.
  78. 78What is the treatment for a bacterial UTI in non-pregnant women?Empirical treatment in otherwise healthy women who present with a lower UTI: Trimethoprim 200mg/12h PO OR Nitrofurantoin 3-6 days if normal renal function. Cephalexin or co-amoxiclav are alternatives but may cause C. diff issues. Urine culture if no response.
  79. 79What is the treatment for a bacterial UTI in pregnant women?Seek expert help. Treat asymptomatic bacteruria with antibiotic. Culture urine at every visit if previous infection.
  80. 80What is the treatment for a bacterial UTI in adult men?Those with symptoms of upper UTI, recurrent UTI or who fail to respond to antibiotics should all be referred to urology (consider prostatitis, epididymitis and chladmydial infection). Bacterial UTI in men may need a 2 week course of a quinolone such as levofloxacin. If no response, thick prostatitis and treat for 4 weeks.
  81. 81What is the management for recurrent UTI?In relapse a search should be made for the cause (e.g. stones, scarred kidneys), and if possible this should be eradicated. Intense and prolonged treatment - IV or IM aminoglycoside for 7 days/oral antibiotics for 4-6 weeks - is required. If this fails, long-term Abx are needed.
  82. 82What prophylactic measures should pts who have a recurrent UTI take?A 2L daily fluid intake. Voiding at 2-3hr intervals Voiding before bed time and after intercourse. Avoidance of spermicidal jellies and bubble baths etc. Avoidance of constipation, which may impair bladder emptying.
  83. 83List 5 things that could cause renal tract obstruction from within the lumen.Calculus, bloot clot, sloughed papilla, tumour of the renal pelvis/ureter, bladder tumour.
  84. 84List 4 things that could cause renal tract obstruction from within the wall of the lumen.Pelviureteric neuromuscular dysfunction (congenital), ureteric stricture (TB, post-calculus, post-surgery), ureterovesical stricture (congenital, ureterocoele, schistosomiasis), congenital megaureter.
  85. 85List 7 things that could cause renal tract obstruction from outside of the lumen.Pelviureteric compression (bands, aberrant vessels), Tumours (retroperitoneal tumour, Ca colon, Ca in pelvis), Diverticulitis, Aortic aneurysm, Retroperitoneal fibrosis, Accidental ligation of ureter, Retrocaval ureter.
  86. 86Which examinations are essential in a pt presenting with signs and symptoms of urinary tract obstruction?External genitalia, rectum and vagina, since prostatic obstruction and pelvic malignancy are common causes of tract obstruction.
  87. 87What is the management of an upper urinary tract obstruction?Temporary external drainage by nephrostomy (artifical opening between skin and renal pelvis) or stent insertion may be valuable as this allows for further investigations when the site and nature of obstruction are uncertain. Recent, complete obstruction demands urgent relief to preseve kidney function, especially if infection is present. In partial obstruction (especially when spontaneous relief is expected, e.g. from passing a stone), there is no immediate urgency. Surgical management depends on the cause of the obstruction and local expertise. Dialysis may be required in the ill pt prior to surgery. Pyeloplasty, to widen the the pelviureteric junction, may be performed if obstruction is at this level. Beware of a large diuresis following relief, as a salt-losing crisis may occur resulting in loss of several litres of fluid per day - monitor weight and U&Es carefully.
  88. 88Where do renal calculi form and where do they classically get deposited?Formed as crystal aggregates at the collecting ducts. Classically deposited: At pelviureteric junction, pelvic brim, vesicoureteric junction.
  89. 89How do the symptoms of renal calculi reflect where the stone is?Pts often present with renal colic - excruciating spasms 'loin to groin' (or genitals/inner thigh)m often with nausea and vomiting. Often cannot lie still (differs from peritonitis in this). RENAL OBSTRUCTION: Felt in the loin between rib 12 and the lateral edge of lumbar muscles, similar to intercostal nerve pain. OBSTRUCTION OF MID-URETER: Mimics appendicitis/diverticulitis. OBSTRUCTION OF LOWER URETER: Leads to symptoms of bladder irritability, pain in scrotum, penile tip or labia majora. OBSTRUCTION IN BLADDER OR URETHRA: Pelvic pain, dysuria, strangury +/- interrupted flow.
  90. 90What is pyonephritis?Infected hydronephritis.
  91. 91What percentage of renal stones are visible on XR? CT?80% and 99% respectively
  92. 92What is a 'dense nephrogram' on IVU?When contrast is unable to flow from the kidney into the ureter.
  93. 93What does the appearance of blunted/clubbed renal calyces on IVU suggest?Back pressure
  94. 94What is the management for renal calculi?Initially analgesia - diclofenac 75mg IV/IM or 100mg suppository. IV fluids if unable to tolerate oral fluids. Antibiotics (cefuroxime IV) if infection. Stones <5mm in lower ureter = 95% pass spontaneously. Increase fluid intake and sieve urine for analysis. Stones >5mm or pain not responding = medical expulsive therapy (nifedipine or alpha-blockers +/- prednisolone). Most will pass within 48h.
    If stones persist then try: Extracorporeal shock wave lithotripsy (ESWL) = US waves shatter stone. Percutaneous nephrolithotomy (PCNL) = Keyhole surgery to remove stones when large, multiple or complex. Open surgery is rare. Urgent intervention is needed if there is infection + obstruction, urosepsis, intractable pain, vomiting, impending acute renal failure, obstruction in a kidney when the other has been removed, or bilateral obstructing stones.
  95. 95Describe the features of Wilm's tumour.This is the most common intra-abdominal tumour of childhood. Undifferentiated mesodermal tumour of the intermediate cell mass. May be sporadic or familial (2%). Associated with Beckwith-Wiedemann syndrome (an overgrowth syndrome), aniridia, GU malformations and retardations. Median age at presentation is 3.5 years. 95% are unilateral. Presents with: fever, flank pain, abdo mass. haematuria is uncommon.
  96. 96Describe the features of renal cell carcinoma.=Hypernephroma/Grawitz tumour. Arise from the proximal tubular epithelium; very vascular tumours. Account for 90% of renal cancer. 15% of haemodialysis pts develop renal cell carcinoma. Bilateral carcinomas are common in Von Hippel-Lindau disease (a mutation in a tumour suppressor gene).
  97. 97What is the clinical presentation of renal cell carcinoma?Mean age 55 years M:F = 2:1. 50% incidental findings. Haematuria. Loin pain. Abdo mass. Anorexia, malaise, weight loss. PUO - often in isolation. Rarely, invasion of left renal vein compresses left testicular vein causing a varicocoele. Spread is direct, haematogenous (bone, liver, lung) or via lymph nodes.
  98. 98What is the management of renal cell carcinoma?Do USS, CT, IVU (filling defect +/- calcification), CXR ('cannon ball' mets) and renal angiography if considering partial nephrectomy or palliative embolisation. Do radical nephrectomy. Consider partial nephrectomy if bilateral or contralateral kidney functions poorly. In low and intermediate risk pts give angiogenesis-targeted agents. Give mTOR inhibitor in pts with a poor prognosis. (NB: Prognosis - 65% 5 year survival if confined to kidney, 25% with lymph node involvement, 5% with distant mets).
  99. 99Describe the features of Transitional Cell Carcinoma.TCCs can occur in the bladder (50%), ureter or renal pelvis. Risk factors: smoking, aromatic amines (rubber industry), chronic cystitis, schistosomiasis, pelvic irradiation. Clinical features are: Age >40yrs, M:F = 4:1. In the kidney/ureter TCCs may present with haematuria and flank pain.
  100. 100Describe the management of Transitional Cell Carcinoma.Manage with nephroureterectomy. Radio and chemotherapy are of little value. Carry out subsequent cystoscopy as 50% will develop subsequent bladder tumours.
  101. 101What is the presentation of ADPKD?Acute loin pain +/- haematuria due to bleeding into cyst, infection or stone formation. Loin/abdo discomfort due to large size. SAH associated with burst berry aneurysm. Complications of HTN. Complications of associated liver cysts. Symptoms of mitral valve prolapse (20%). Symptoms or uraemia/anaemia due to chronic renal failure.
  102. 102What is the management of ADPKD?Manage complications, as well as: Regular monitoring of U&Es and BP. Treat BP with ACEi/ARBs with target of <130/80. Treat infections. Dialysis or transplantation for ESRF. Pain may be helped by laparoscopic cyst removal or partial nephrectomy.
  103. 103What is Medullary Cystic Disease?This is an inheretid disorder with tubular loss and medullary formation. Signs include: Shrunken kidney, cysts restricted to medulla. Salt wasting, polyuria, polydipsia, enuresis. Failure to thrive. Extra renal manifestations include: Retinal degeneration, retinitis pigmentosa, skeletal changes, cerebellar ataxia, liver fibrosis. A disease of childhood; adult form is rare.
  104. 104What is Medullary Sponge Kidney?Characterised by dilatation of the collecting ducts, sometimes with a cystic change. Has a sponge-like appearance in severe cases. Most cases are sporadic. Presents with: Renal colic or haematuria with the passage of small stones. Small calculi develop in the cysts in the papillary zones, visible on excretion urography. May be associated tubular acidosis or hypercalciuria. Renal function is usually well maintained unless there is obstructive nephropathy.
  105. 105What is the management of trauma to the bladder (intraperitoneal and extraperitoneal)?INTRAPERITONEAL BLADDER RUPTURE: treated with laparotomy and suturing of the bladder, with a urethral catheter left in situ for 5-7 days until the defect has healed. EXTRAPERITONEAL BLADDER RUPTURE: is treated conseratively with prolonged urethral/suprapubic catheterisation.
  106. 106What are the three causes of bladder stones?Bladder outflow obstruction (urethral stricture, neuropathic bladder, prostatic obstruction), prescence of a FB (catheters, non-absorbable sutures) and stone formation higher up urinary tract.
  107. 107What are the clinical features of bladder stones?Significant bacteruria is usually found in pts with bladder stones. They may present with: Frequency, dysuria, introital (relating to opening of the vagina) or perianal pain may occur if trigonitis (inflammation at the trigone of the bladder) is present, anuria and bladder distension if obstructing.
  108. 108What is the treatment for a Tis (in situ) or T1 (tumour in lamina propria) TCC?80% of TCC pts. Diathermy via cystoscopy or transurethral resection of bladder tumour (TURBT). Consider intravesical chemotherapeutic agents (e.g. mitomycin C) for multiple small tumours or high-grade tumours. Immunotherapy with intravesical BCG (stimulating non-specific immune response) is useful in high grade tumours and carcinoma in situ. 5 yr survival = 95%.
  109. 109What is the treatment for a T2 (superficial muscle involved) or T3 (deep muscle involved) TCC?Radical cystectomy is gold standard. Radiotherapy gives worse 5 year survival rates than surgery but preserves the bladder. 'Salvage' cystectomy may be performed if surgery fails. Post-op chemo is effective. If bladder neck is involved, reconstruction may be performed using ileum rather than forming a urostoma, but do not compromise adequate tumour clearance. 3 yr survival is 40-60% depending on age at operation.
  110. 110What is the treatment for a T4 (invasion beyond bladder) TCC?Usually palliative chemo/radiotherapy. Chronic catheterisation and urinary diversions may relieve pain. 3 yr survival is 6% with pelvic node involvement and 0% with para-aortic node involvement.
  111. 111What should the follow-up for TCC be?Regular cystoscopy, every 3 months for 2 years, then every 6 months (low-risk tumours: first follow up cystoscopy after 9 months, then yearly).
  112. 112What are the intra lumen, intramural and extrinsic causes of bladder outflow obstruction?Within the lumen: Bladder tumour. Within the wall: Congenital bladder neck obstruction, neuropathic bladder, urethral stricture (calculus, gonococcal, post-instrumentation), congenital urethral valve, pinhole meatus, Pressure from outside: Prostatic obstruction, phimosis.
  113. 113What are the symptoms of bladder outflow obstruction?Syx may be minimal. Suprapubic pain. Hesitancy, narrowing, and diminished force of urinary stream. Terminal dribbling. A sense of incomplete bladder emptying. Frequent passing of small volumes occurs if a large residual amount of urine remains int he bladder after urination. Incontinence of small amounts of urine is known as 'overflow incontinence' or 'retention with overflow'. Syx of infection also common.
  114. 114What are the signs of bladder outflow obstruction?Loin tenderness. Enlarged palpable hydronephrotic kidney. Enlarged bladder dull to percussion. Examination of external genitalia, rectum and vagina is essential since prostatic obstruction and pelvic malignancy are common causes of tract obstruction. Size of prostate on PR in a poor guide to prostatic obstruction.
  115. 115What investigations would you order for a pt with likely BPH?Assess severity and PR. MSU. U&E. US (incresed residual volume, hydronephrosis). 'Rule out' cancer: PSA, transrectal US +/- biopsy.
  116. 116What is the management for moderate BPH?(Mild = watchful waiting). Moderate = Alpha-blockers (reduce smooth muscle tone in prostate and bladder), e.g. tamsulosin, alfuzosin, doxazosin, terazosin. SEs: Drowsiness, dizziness, depression, hypertension, dry mouth, ejactulatory failure, extra-pyramidal signs, nasal congestion, weight gain. Inhibitors of 5alpha-reductase (the enzyme which converts testoterone to dihydrotestosterone, the androgen responsible for prostatic growth and and enlargement), although effects on prostate size are limited and slow. e.g. finasteride. SEs: excreted in semen so warn to use condoms, females should avoid handling, impotence, reduced libido. Deterioration in renal function or development of upper tract dilatation requires surgery.
  117. 117What are the surgical options for severe BPH?TURP (Trans-Urethral Resection of Prostate). <14% become impotent. Beware bleeding, clot retention and transurethral resection syndrome (absorption of washout causing hyponatraemia and fits). 20% need repeat procedure in 10 years. TUIP (Trans-Urethral Incision of Prostate): Involves less destruction of prostate and less risk to sexual function but gives similar effect. It achieves this by reducing pressure on urethra. Best for those with small prostate glands. RETROPUBIC PROSTATECTOMY: Open operation used if prostate is very large. TULIP (Trans-Urethral Laser Induced Prostatectomy) may be as good as TURP.
  118. 118What are the appropriate investigations for suspected prostate carcinoma?PSA raised (but normal in 30% of small cancers). Normal = <5ng/L. >10ng/L strongly suggests tumour but many factors influence PSA levels - not a reliable screening method. Transrectal US and biopsy. Bone XR. Bone scan. CT. Contrast enhanced MRI for staging.
  119. 119Compare and contrast the following three management approaches for local prostatic carcinoma: radical prostatectomy with goserelin (suppresses production of sex hormones) OR radiotherapy OR watchful waiting with serial PSA monitoring.Radical prostatectomy only reduces disease mortality in those <75yrs compared with watchful waiting, and doubles erectile dysfunction and incontinence rates. Radiotherapy combined with hormone therapy improves survival rates in advanced local disease. Do transurethral resection for obstruction. Brachytherapy (internal/sealed source radiotherapy) is being assessed for local disease.
  120. 120What is the management for metastatic prostatic carcinoma?Hormonal drugs may give benefit for 1-2 years. Gonadotrophin-releasing analogues (e.g. 12-weekly goserelin) first stimulate and then inhibit pituitary gonadotrophin. Symptomatic treatment: analgesia for bone pain, treat hypercalcaemia, radiotherapy for bone mets/spinal cord compression.
  121. 121How are prostatic tumours graded?By the Gleason score: A score of 1-5 with 5 being the highest grade. Measured by taking 2 separate prostate specimens and adding the scores together to get a score out of 10.
    8-10 = Aggressive. 5-7 = Intermediate. 2-4 = Indolent.

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Karteikarten am Renal, erstellt von Anna Walker am 24/05/2014.
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