Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
30 Cards in this Set
- Front
- Back
|
Acute renal failure
|
-Is a clinical syndrome in which there is a sudden loss of renal function
-It results in derangements in fluid and electrolyte balance, BP regulation, and erythropoiesis -The hallmark of acute renal failure is a decreased GFR, reflected by an accumulation of BUN, and serum creatinine, a condition termed azotemia -Urine output patterns in acute renal failure can manifest as oliguria <400 ml/day, nonoliguria >400 ml/day, or anuria <50 ml/day |
|
|
Creatinine and creatinine clearance
|
-Creatinine is a byproduct of normal muscle metabolism and is excreted in the urine primarily as a result of glomerular filtration
-Creatinine is the most important indicator of GFR -The amount of creatinine excreted in the urine is directly related to muscle mass and normally remains constant unless significant muscle wasting occurs -Normal serum values for creatinine are 0.6 – 1.2 mg/dl -Creatinine clearance is the amount of blood that is cleared of creatinine is 1 minute, excellent indicator of renal function -As renal function diminishes creatinine clearance decreases |
|
|
Causes of acute renal failure
|
-Acute renal failure is organized into three general categories according to precipitating factors and the symptoms manifested
|
|
|
Pathophysiology of prerenal acute renal failure
|
-A decrease in renal perfusion results in the release of the enzyme renin, this activates the renin Angiotensin aldosterone cascade
-Angiotensin II causes profound systemic vasoconstriction and aldosterone induces Na and water retention -With moderate Hypovolemia or CHF, certain drugs like ACE inhibitors and NSAIDs can overwhelm the kidneys ability to autoregulate -Predisposing factors for NSAID and ACE inhibitor induced prerenal failure are Hypovolemia, baseline renal insufficiency, liver disease, heart failure, and disease of the renal arteries |
|
|
Prerenal ARF cont
|
-Urinary volume is reduced to less than 400 ml/day, and increased urine specific gravity (concentrated urine)
-An increase in systemic BP does not necessarily imply improvement in renal perfusion -Norepinephrine used to correct the hypotension associated with states of volume depletion may be associated with further reduction in renal blood flow as a consequence of constriction of the renal arteries -If the hypoperfusion is treated by replacement of volume, improvement of CO or a combination the improved renal perfusion will be manifested as an increased urinary volume and urine Na concentration and as a decreased urine specific gravity |
|
|
Pathophysiology of intrarenal acute renal failure
|
-ATN is the most common hospital acquired form of intrarenal acute renal failure
-Ischemia and nephrotoxicity are two major underlying causes of ATN |
|
|
Ischemic acute tubular necrosis
|
-Results from prolonged hypoperfusion
-When renal hypoperfusion persists for a sufficient time, renal tubular epithelia sustain damage to the point that restoration of renal perfusion no longer effects an improvement in GFR -Electrolyte disturbances from ischemia are decreased intracellular K, Mg, P, and increased intracellular Na, Cl, and Ca -Cellular insults cause the tubular cells to swell and become necrotic -Then they slough off and obstruct the tubular lumen -A final contributor to the pathophysiology of ischemic ATN is profound renal vasoconstriction from vasoconstrictors |
|
|
Toxic acute tubular necrosis
|
-Begins with a concentration of a nephrotoxin in the renal tubular cells, which causes necrosis
-These necrotic cells then slough off into the tubular lumen causing obstruction and impairing GFR -Nonoliguria occurs more often with toxic ATN -Aminoglycoside antibiotics and radio contrast dye deserve special attention -An important way to reduce the risk of this type of acute renal failure is by aggressive hydration with IV saline before and after contrast dye administration |
|
|
Pathophysiology Postrenal acute tubular necrosis
|
-When urine cannot get around the obstruction, resulting congestion causes retrograde pressure through the collecting system and nephrons
-This slows the rate of tubular fluid flow and lowers GFR -The development of acute renal failure from obstruction requires blockage of both kidneys or unilateral ureteral obstruction in pt with a single kidney |
|
|
Onset phase of ATN
|
-Initiating phase begins with an initial insult, injury is evolving
-Heralded by appearance of signs of renal failure, decreased UO and increased serum creatinine |
|
|
Oliguric or nonoliguric phase of ATN
|
-Second phase of ATN
-Pt with oliguric ATN require renal replacement therapy -Is most commonly the result of ischemic insult -It is marked by fluid overload, azotemia, electrolyte abnormalities, and metabolic acidosis -Nonoliguric is associated with toxic injury |
|
|
Diuretic phase of ATN
|
-Characterized by a gradual increase in UO as renal function starts to return
-Renal concentrating ability is still impaired -Goals during this stage are to maintain hydration, prevent electrolyte depletion, and continue to support renal function |
|
|
Recovery phase of ATN
|
-Time it takes for renal function to return to normal
-Residual renal impairment my result |
|
|
Prerenal (acute renal failure)
|
-Oliguria, increased urine osmolality >500 (concentrated urine), increased urine specific gravity >1.020 (concentrated urine), decreased urine Na <20, increased BUN:Cr >20:1 – dehydration
|
|
|
Postrenal (acute renal failure)
|
-Anuria and polyuria, increased or equal to serum urine osmolality, BUN:Cr 10:1 to 15:1
|
|
|
ATN (acute renal failure)
|
-Anuria, oliguria, nonoliguria, urine osmolality 250-300, urine specific gravity 1.010, urine Na >40, BUN:Cr 10:1 to 15:1
|
|
|
Urinary values (urinary values)
|
-Urine Na concentration, osmolality, and specific gravity are helpful in distinguishing between prerenal and ATN because these values reflect the concentrating ability of the kidney
|
|
|
BUN and creatinine levels (acute renal failure)
|
-In prerenal, the BUN-creatinine ratio is increased from the normal of 10:1 to more than 20:1, caused by a state of dehydration
-ATN and postrenal, the BUN and creatinine increase proportionally, maintaining the normal 10:1 -Creatinine levels change only in response to kidney function -BUN levels change in response to dehydration or protein breakdown |
|
|
Pathophysiology of chronic renal failure
|
-Slow, progressive, irreversible deterioration in renal function
-As renal disease progresses, nephrons can lose function at different times -When an individual nephrons becomes diseased, nephrons close in proximity increase their individual filtration rates by increasing the rate of blood flow and hydrostatic pressure in their glomerular capillaries -Eventually the intact nephrons reach a point of maximal filtration and any additional loss of glomerular mass is accompanied by an increased loss in GFR and subsequent accumulation of filterable toxins -In addition to the primary and potential secondary insults, nephron loss can be accelerated by the hyperfiltration mechanism itself |
|
|
Hypertensive nephrosclerosis
Diabetic nephropathy |
Hypertensive nephrosclerosis
-Involves the development of sclerotic lesions in the renal arterioles and glomerular capillaries that cause them to become thickened and narrowed and eventually necrotic -Patients often remain asymptomatic until extensive damage is done -BP control is essential Diabetic nephropathy: -In DM the microvasculature in the organ system is damaged -Primarily the afferent and efferent arterioles and the glomerular capillaries |
|
|
Preventing the progression of chronic renal failure
|
-Secondary insults can accelerate progression, so monitoring for and avoiding these insults is paramount
-Avoiding nephrotoxins like aminoglycoside antibiotics and IV radio contrast dye -Strict control of blood glucose levels is critical to preventing and retarding the progression of renal failure -BP control is also essential for preventing the progression of renal failure -ACE inhibitors can slow the progression of diabetic nephropathy, they decrease intraglomerualar pressure by blocking the effect of Angiotensin II on the afferent and efferent arterioles -Angiotensin receptor blockers block the effect of Angiotensin II slow the progression of diabetic nephropathy -Protein restricted diet of 0.8 g/kg/day in pt may help |
|
|
Renal insufficiency
|
Renal insufficiency:
-Solute clearance, the ability to concentrate urine and hormone secretion are compromised -Signs of renal failure manifest, fatigue, polyuria, nocturia Decreased renal reserve: -Kidneys are still able to maintain excretory and regulatory functions ESRD: -Characterized by a residual renal function of less than 15% -All the normal regulatory, excretory, and hormonal function are severely impaired -Evidenced by elevation in BUN and creatinine levels, anemia, electrolyte imbalances, and fluid overload -Pt will be oliguric with urine osmolality similar to plasma osmolality |
|
|
Managing fluid balance alterations
Acute RF |
-In prerenal acute renal failure and the early stages of ischemic ATN, the cause of the renal failure is inadequate renal perfusion
-Therapy involves prompt administration of replacement fluids -Fluid administration in acute renal failure is also indicated in the diuretic phase of ATN, and for the prevention or alleviation of tubular obstruction seen in obstructive causes of acute renal failure, including ATN -In a sustained oliguric state, fluid restricted to the previous days urine output amount plus 500-800ml to account for insensible losses -Diuretics are often used in acute renal failure to increase urinary flow to prevent or reverse oliguria, to help alleviate condition of fluid overload, to prevent tubular obstruction, or a combination of these goals -Tinnitus and hearing impairment have been reported after IV lasix -Ototoxicity is associated with rapid injection, excessively high doses, or concomitant therapy with other ototoxic drugs |
|
|
Managing fluid balance alterations
Chronic renal failure |
-Fluid and salt restriction I a mainstay of therapy to prevent fluid overload
-Diuretics are also used to delay the need for dialysis |
|
|
Managing acid base alterations
|
Managing acid base alterations:
-Typically results in metabolic acidosis because of the nephrons inability to secrete and excrete H ions and reabsorb HC03 ions -IV NaHC03 is reserved for severe acidosis, pH <7.2 or a plasma HC03 <12-14 HTN: -As a complication of renal failure results from excess retention of water and Na, overactivation of the sympathetic nervous system, and stimulation of the RAAS |
|
|
Hyperkalemia
|
-As the GFR decreases, the ability of the kidneys to excrete excess K diminishes
-When the serum K level is about 6-7, the T waves become peaked, PR interval is prolonged and ST segment is depressed -About 8-9 the P wave is lost -At about 10-11 the QRS complex widens followed by v-fib -Mild hyperkalemia may be treated with dietary K restriction, diuretics and K-binding resins -Sodium polystyrene is given orally -Treatment of life threatening hyperkalemia entails taking steps to antagonize the effects of K on the heart, promote intracellular shifting of K, and remove K from the body -Antagonizing the effects of K on the heart is achieved with IV calcium gluconate or calcium chloride and is the first priority for pt with substantial ECG changes -Means to shift K into the cell include IV insulin and dextrose administration and IV HC03 administration -Removal of K from the body entails diuretic administration and the use of K exchanging resins |
|
|
Increased bleeding tendency
|
-Is attributable to a decrease in clotting factors, impaired platelet aggregation and adhesion and prothrombin consumption
-Anemia is associated with erythropoietin deficiency, decreased red blood cell survival time, and blood loss due to an increased bleeding tendency -Erythropoietin is produced in the kidney -As kidney disease progresses and nephrons are damaged, this hormone is inadequately synthesized -Iron studies also need to be obtained because iron deficiency itself can cause anemia and because adequate iron stores are needed for erythropoietin to be effective -Management includes minimizing blood loss, administering oral or IV iron supplements, providing vitamin supplementation, aggressively treating infection, ensuring adequate nutrition, and administering erythropoietin, blood production or both |
|
|
Managing alteration in drug elimination
|
-Depending on the pt GFR adjustments may need to be make in drug dosage
|
|
|
Managing skeletal alterations
|
-As GFR decreases, glomerular filtration of P also decreases and serum P levels begin to rise
-This results in decreased serum ionized Ca levels because of binding of the Ca with the P -Ca levels also decrease owing to the failing kidneys inability to convert vitamin D it its active form -In response to decreased ionized Ca levels, the parathyroid gland secretes PTH which causes the reabsorption of Ca and P salts from the bone -Measures to control P levels include dietary restrictions and P-binding medications -Calcium acetate, tums, and renagel are commonly used P-binders -Active vitamin D supplements are administered to increase serum Ca levels in hypocalcemic pt -Active vitamin D should be given only when the Ca-P product is <65 mg/dl |
|
|
Managing alterations in dietary intake
|
-Patient with renal disease need a high calorie diet with a total of 30-44 Kcal/kg/day
-Most of which should come from a combination of carbohydrates and lipids -Moderate protein restriction of 0.8 g/kg/day in pt not receiving dialysis and up to 1.5 g/kg/day in patients on dialysis |
