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33 Cards in this Set
- Front
- Back
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Discuss the kidney's role in acid-base balance of the blood...
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Blood is normally basic.
• Role of lungs - release CO2 (fast) • Role of kidneys - excrete excess acids or bases (slower) |
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What are some of the roles of the kidney?
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• Filter metabolic waste products
• Fluid balance • Electrolyte balance • Acid-base homeostasis |
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What are some signs and symptoms of renal damage?
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• Presence of urinary tract discomfort and/or frequency changes
• Other physical findings related to body volume (change in weight, HR, BP, peripheral/pulmonary oedema, ascites) • Change in urinary volume • Azotemia • Abnormal components in a urinalysis (e.g. proteinuria, hematuria, casts, pH, epithelial cells, crystals) • Urine sodium excretion & osmolality change • GFR and creatinine clearance decrease |
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What is the Cockroft-Gault equation?
When should you be cautious in using this equation? |
CrCl (mL/min) = (140 - Age in yrs) x IBW (kg) divided by SeCr (micromol/L)
Multiply by 1.04 (females) or 1.23 (males) Caution: Decreased muscle mass, advanced liver disease, non-vegetarians. |
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What is the eGFR calculation based upon, and when can/can't it not be used?
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• Requires age, sex & serum creatinine only
• NO use of body weight • Valid in 18 yrs or older • Can't be used to detect mild renal impairment • Results > 60 mL/min/1.73m2 do not necessarily indicate normal renal function • Not validated in Aboriginals, Pacific Islanders or Chinese people • In African Americans multiply result by 1.21 • Less reliability in exceptional dietary intake, extremes of body composition or severe liver disease |
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What are some additional methods of assessing renal failure?
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X-ray of abdomen
• Determine kidney size & shape Ultrasonography & CT scan • Non-invasive image of kidney • Evaluate for masses, obstructions, stones IV pyelogram • Injection of radiocontrast • Determine kidney size, shape & calyceal anatomy, obstructions, screen for renovascular hypertension Radionuclide studies • Screen for renovascular hypertension, renal thromboemboli Renal arteriography • Detect renovascular hypertension, thromboemboli or masses Biopsy |
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What is acute renal failure?
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Abrupt and sustained decline in renal function, & an accumulation of nitrogenous waste products (azotemia)
• Assoc. with anuria or oliguria • Serum urea, K+ and serum creatinine rise |
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What are the causes of prerenal ARF?
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• Decreased renal blood flow
• Decreased cardiac output • Hypovolemia • Increased renal vascular resistance • Systemic vasodilation • Renovascular obstruction |
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What are the compensatory mechanisms that occur in prerenal ARF?
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• Kidneys attempt to increase intravascular volume (conserve water by increasing reabsorption, increased ADH)
• GFR maintained initially • Small amounts of concentrated urine • Increased urea reabsorption leads to increased BUN:SeCr |
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What are some symptoms of prerenal ARF?
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• Dizziness
• Dry mouth • Low BP • Rapid HR • Slack skin • Thirst • Weight loss |
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What is intrinsic ARF and how is it caused?
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• Results from severe or prolonged ischaemic, toxic or immunologic mechanisms
• Follows prerenal or postrenal azotemia • Structural damage to glomeruli, tubules, vascular supply, or interstitial tissue • Acute tubular necrosis (ATN) • Nephrotoxic agents • Reversibility depends on degree of insult, duration of hypoperfusion/obstruction (usually 10-14 days for recovery) |
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What is Acute Tubular Necrosis and what agents are associated with it?
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• Non-specific response to ischaemia/direct toxic insult
• Often arises after multiple insults Tubular necrosis -> cellular debris -> obstruction of proximal tubule -> intratubular pressure -> decreased GF -> leaking across transtubular membranes -> filtered wastes re-enter circulation • Antibiotics (aminoglycosides, amphotericin B, cephalosporins, sulfonamides, polymixins) • Metals (bismuth, mercurials, platinum) • Radiocontrast media • Others (paracetamol, cisplatin, CyA, MTX) |
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What is Acute Tubulointerstitial Disease caused by and is it reversible?
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• Interstitial oedema, renal cellular infiltrates
• Agent associated (antibiotics, metals, others) • Hypersensitivity reaction • Systemic signs of allergic reaction • Less common causes (autoimmune disease, infectious agents) Reversible: • Treat underlying problem • Corticosteroids accelerate recovery (exclude infection) |
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What is glomerulonephritis caused by and what should prompt treatment be?
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• Immunologic reactions
• Drugs may act as antigens • Damage/alteration of glomerular basement membrane -> proteinuria; nephrotic syndrome Prompt treatment with immunosuppressants to reduce risk for ESRD. |
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What is postrenal ARF caused by?
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~10% of cases due to urine flow obstruction - consider if alternating polyuria and oliguria.
Often easily corrected preventing progression to intrinsic renal damage. • Bilateral ureteral obstruction • Bladder obstruction • Urethral obstruction • Drug causes (rare) |
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Discuss the fraction of Na excreted in urine...
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99% Na is usually reabsorbed (renal tubule)
• Fe(Na) < 1% in pre-renal azotemia (there's no prob in renal tubule) • Fe(Na) > 2% in acute tubular necrosis • Fe(Na) > 1% in postrenal obstruction • Fe(Na) elevated in patients on diuretics |
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What is the renal failure index?
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RFI = Urine Sodium Conc. divided by Urine:Plasma Cr ratio
• RFI < 1 in pre-renal ARF • RFI > 4 in ATN (intrarenal ARF) |
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What is the BUN:SeCr in prerenal ARF, ATN, and postrenal obstruction?
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>20:1 in pre-renal
<20:1 in ATN n/a in postrenal |
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What are some complications that can occur in ARF?
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• Na and water imbalance
• Acid-base imbalance (often acidosis) • Potassium imbalance (hypoK) • Anaemia • Hemostatic defects • Ca and PO4 abnormalities • Hyperuricaemia • Carbohydrate intolerance • HTN • GI disturbances • Neuromuscular imbalances • Renal osteodystrophy • Dermatologic disorders • Psychological disorders |
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What is the clinical course of ARF?
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• Initiation or injury (marked decrease in renal function)
• Oliguric phase (1d to several weeks) • Diuretic phase (a few days) - urine production increases - renal function remains poor - azotemia may persist until concentrating abilities improve • Recovery phase (weeks to months) - gradual improvement - long-term prognosis depends on morphologic involvement of kidney |
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What are the treatment goals in ARF?
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• Recognise ARF early, anticipate & prevent potential problems & further renal injury
• Reverse underlying cause • Correct/maintain euvolemia & restore electrolyte and acid balance • Provide support until pt recovers • Maintain patient's nutritional status • Prevent & treat infectious complications • Enhance urine flow rates (loop diuretics) • Reverse azotemia |
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How can you prevent ARF?
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• Identify pts at risk
• Avoid nephrotoxic agents (esp. combinations) • Use prevention strategies - contrast media (extracellular fluid volume expansion) - rhabdomyolysis (correct intravascular volume, urinary alkalinisation, mannitol infusion - surgical procedures (optimise volume status, avoid multiple insults & hypotension) - tumour lysis syndrome (diuresis, urinary alkalinisation) |
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Discuss fluid management as supportive care in ARF..
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Fluid management
• Based on physical exam, BP, pulse, skin turgor, mucous membrane hydration, evidence of pulmonary congestion, pedal oedema, weight change, daily fluid intake/output • If clinical evidence of fluid overload: intake should be < than daily output • Euvolemic pt: 300-500 mL/day electrolyte free water and Na intake < 2g/day • Increase fluid needs during polyuric recovery phase & for pts with volume depletion |
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When does metabolic acidosis occur and how do you calculate treatment?
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Serum HCO3 < 15 mmol/L
pH < 7.1 Treated using Na bicarbonate and calculated by: HCO3 deficit (mmol & mEq) = (24 - measured HCO3) x Weight(kg) x 0.5 |
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Discuss electrolyte homeostasis as supportive care for ARF?
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• Hyper/hyponatraemia
- Adjust free water intake accordingly • Hyperkalemia - Restrict intake - Decrease K+ in diet (fruits, choc, nuts) and drugs (K salts, K sparing diuretics, NSAIDs, ACEIs) - K binding resin - Na polystyrene sulfonate • Hypocalcaemia and/or hypomagnesaemia - Oral Ca/Mg supplementation • Hyperphosphatemia - Restrict dietary PO4 - PO4 binding antacids (Ca salts) |
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Which diuretics and what other drug are useful in intrinsic ARF, and when should they be started?
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• Loop diuretics or mannitol in 'newly apparent' intrinsic ARF
• No value after 'firmly established' intrinsic ARF • Prevents progression from oliguric ARF -> nonoliguric |
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What mechanisms does mannitol work by?
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• Increased filtration pressure
• Improved urine flow rates • Reduced tubular cell inflammation • Decreased renal vascular resistance |
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Discuss the use of Renal Replacement Therapy and its indications...
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• Temporary support until renal insufficiency resolves
• Early use of dialysis increases survival (decreased infections, better wound healing) Absolute indications - Pericarditis, uraemic symptoms Relative indications - Volume overload, acidosis, hyperK+ • A - Acid base abnormalities • E - Electrolyte imbalance • I - Intoxications • O - Overload (fluid) • U - Uraemia |
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What is chronic renal failure?
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Persistent or progressive deterioration in renal function characterised by uraemia, anaemia, acidosis, osteodystrophy, neuropathy and general debility.
Frequently accompanied by HTN, oedema and susceptibility to infection. Manifestation of SMx when GFR < 15 mL/min |
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What are the stages of CRF?
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• Reduction in 'renal reserve'
• Renal insufficiency - Accumulation of Cr and urea - Electrolyte levels within normal (adaptation) -> acidaemia, bone disease, hormone level change • CRF - Further biochemical or hormonal abnormalities • End-stage renal failure - Uraemia, GI, dermatological, CNS symptoms |
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What are the causes of CRF?
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Decrease in renal function due to damage to kidney infrastructure.
Common causes: • Unknown • Chronic glomerulonephritis • Diabetes • Chronic pyelonephritis • Renovascular disease • Congenital abnormalities • HTN |
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What is diagnosis of CRF based on?
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• Signs and symptoms
• Investigation of other medical problems • Family, drug & social history • Functional assessment of kidney • Urinalysis • Structural assessment • Renal biopsy |
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What are some of the clinical manifestations of CRF?
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Urinary symptoms
• Polyuria, nocturia, proteinuria Fluid retention • Peripheral/pulmonary oedema, ascites • Volume dependent HTN Uraemia • Accumulation of urea, Cr, water • Accumulation of middle molecules • SMx: anorexia, nausea, vomiting, constipation, foul taste, skin discoloration, muddy complexion, severe pruritus Anaemia • Slow insidious fall in Hb along with RF • Normochromic, normocytic anaemia • Major cause of fatigue, breathlessness, lethargy, angina • Sensation of feeling cold, poor concentration, reduced appetite, libido • Compensatory changes - increased CO to increase O2 delivery -> tachycardia, palpitations Electrolyte disturbances • Na relatively normal • Hyperkalaemia • Acidosis |
