N254

1. N254 Renal Nursing Care Mary Moon, RNC, FNP Fall 2009

2. Renal Circulation

3. Bowman’s Capsule

9. Coffee Sugar Perfume Room Diffusion Small molecules make easily movement by diffusion in a cell limited by the cell’s semi permeable membrane In liquid: Equally sweet In air: Equally smell

10. O.9% NaCl 99.1% H20 0.9% Plasma NaCl 99.9% H20 Ex. RBC Isotonic=In Equilibrium Solutes: materials-- sugar, salt. Solvent: Liquid material that dissolve--water Solution: A mixture of two. Tonicity: A state of amount of dissolved material in them.

11. 99.1 H20 0.9 NaCl 0% NaCl 100% H20 Tonicity: By NaCl Osmosis: From: 0.9% NaCl 99.1% H20 To: 3% NaCl 97% H20 Osmosis: [H20] [H20] So, H20 will move into RBC. So., RBC will rupture Hyper tonic Hypo tonic

12. Osmosis A special type of diffusion between NACl & water. Water: Small, unchanged molecules NaCl: Changed molecules *** Changed molecules are hard to move--- H20 move freely from a weaker solution to a more concentrated one. NaCl: Electrolytes that regulate vascular osmotic pressure.

13. Kidney Purify (Filter) and reabsorb 5 inches long, level with T12 and L1~L3 Urine: collected by the pelvis 20% to 25% of the resting cardiac output (approx. 1200 mL per Min.) passes through kidney. Liver: 27% Brain: 14% Heart: 4% Skeletal: 15% Skin: 6% Bone: 6% Miscellaneous: 7%

14. Each region of the nephron: filtration, re absorption, and secretion. (Bowman’s Capsule) (Tubules and Collecting Duct) 180 liters of filtrate a day upper limit (transport maximum): glucose 225 mg/min (BS: 180 mg/dl) at higher concentration, glucose begins to be lost in urine. Right one more volunable Nephron: Functional unit of Kidney. 1/4 of nephron needed for living.

15. Excretion of waste nitrogen (urea, uric acid, creatin) protein--> ammonia--> harmless urea--> kidney American food ( protein) Detoxification of ammonia --> ¤ Liver, Kidney failure H20 and electrolytes Hypothalamus (Osmoreceptor) Sense blood ¤ [ ] = H20, lytes.

16. A.R.F Is a clinical syndrome characterized by a renal shut down--> acute tubular necrosis, obstruction, acute tubular insufficiency--> Most occur in previously healthy individuals. Generally follows an identifiable trauma contact with a nephrotoxic agent. The most cause of ARF is related to surgical procedures.

19. Pre Renal Causes---> Consists of factors outside the kidneys that impair renal blood flow and lead to decreased glomerular perfusion Problem corrected --> no ARF

20. Prerenal • 55-70% • Intravascular volume depletion, decreased CO, vascular failure secondary to vasodilation or obstruction---HTN, MI, severe dehydration, & shock ( not enough volume circulating). • Reversible—can be corrected by establishing renal perfusion & preventing necrotic renal damage by fluid challenge • Irreversible ischemia

21. Intra Renal Conditions of actual damage to the renal tissue leading to malfunctioning of nephrons---> APN may lead ARF Ex) acute tubular necrosis- renal ischemia Nephrotoxic drugs Glomerulonephritis

22. Intrarenal • 25-40% • Kidney itself damaged to the kidney tissues and structures & includes tubular necrosis, nephrotoxicity & alterations in renal blood flow • Injuries @kidney glomeruli or tubules—90% due to ATN--- glomerulonephrits, toxins, trauma, crushing injuries, surgery, sepsis, CV collapse, MOF, ABX like aminoglycosides, street drugs, chemo, nephrotoxic drugs • Don’t get confused w/ prerenal caused by blood volume—dehydration & hypovolemia

23. Post Renal Mechanical Obs. Of urinary outflow. As the flow of urine is blocked. Urine backs up into the renal pelvis. The most common causes are renal calculi, trauma, tumors.--> usually anuria rather than oliguria Ex) Calculi, bladder tumor. Stricture (Compression)--BPH Basement membrane is not destroyed. Trauma to back, pelvis, perineum strictures, spinal cord disease.

24. Postrenal 5% Obstruction of urine between the kidney and the urethral meatus Calculi BPH Tumors strictures B/C the obstruction, urine backflows

25. Prevention A. High Risk Hospital Pt. --> Massive trauma, major surgical procedure, extensive burns, sepsis. B. Industrial chemicals and nephrotoxic drugs.

26. A.R.F PhasesA. Onset phase begins with precipitating event-- Hypovolemia, or nephrotoxin exposure Ends when the oliguric-anuric phase begins. Time Span: Up to two days urine output: 20% of normal.

27. A. Onset Phase • Initial injury to the kidney • Reversible • Preventable with early intervention • UO:20% of normal • Unable to regulate electrolytes

28. B. Oliguric Phase Spans the period when urine is less than 400 cc/d Time Span: 8-14 days (1-2 wks) urine output: 5% of normal. Can not excrete fluid or waste products Oliguria--> caused by reduction in the GFR

29. urea H20 H20 H20 H20 H20 H20 C. Diuretic Phase Gradual increase in urine output of 1-3L up to 4-5 L/day. The high vol. Is due to osmotic diuresis from high urea concentration Capillary cells and the adequate concentrating ability of tubules.

30. Lab. Value stop rising, decreased SG: Diluted urine and poss. Excessive diuresis when lab value stops dropping. Ends when they stabilize. Time span: 10 days U.O: Early 150% Late: 200%

31. Diuretic Phase Electrolytes are lost—deficit in concentrating ability of tubules and osmotic diuretic effect of increased BUN, slowly increased excretion of metabolic wastes, hypovolemia, loss of Na, K, increased BUN initially then gradually return to baseline

32. Diuretic Phase S/S: postural hypotension, tachycardia, improving mental alertness and activity, weight loss, thirsty, dry mucous membrane, decreased skin turgor K replacement may require

33. D. Recovery Phase (convalescent phase) Begins when lab. Values stabilize, ends when renal function returns to normal. Time Span: 4-6 mo. Up to 12 mo. U.O: 100%

34. Recovery Phase Increased GFR Increased concentrating ability. Urine SG -- 1.003-1.030 Urine osmolarity: Normal 300-1300 Mortality Rate: 30% to 60% Most common cause of death secondary to infection

35. Prevention of ARF CHF, dehydration, shock. To minimize the risk. 1. Keep the patient hydrated (esp. before and after OR) 2. Continuously monitor the dosages and effects of ABX and other drugs (nephrotoxic) 3. Assess renal function regularly

36. Treatment Goals 1. Correcting the underlying problem 2. Preventing infection 3. Treating fluid and electrolytes imbalance 4. Correcting metabolic acidosis 5. Treating clinically significant anemia.

37. How does one differentiate acute from chronic renal failure? 1. History-medical records. 2. Hypo calcemia, hyper phosphatemia, anemia. --> has been associated more often with CRF. * Calcium, phosphorous, acid-base derangement are often seen in ARF as early as 48-72 hours after onset of illness. * Anemia: nonspecific indicator. 3. Reliable indicator of CRf Small kidney with a decreased or absence of renal cortex as assessed by UTZ (0.5 cm) Abnormal: Kidney length of less than 9 cm --> CRF or significant renal dz. > 1.5 cm in renal length: unilateral/asymmetric renal dz.

38. CRF

39. CRF Slow, progressive, irreversible damage 4 stages Diminished Renal Reserve ---50% of nephrones are lost, asymptomatic, no S/S Renal Insufficiency---75% nephrones lost, azotemia, anemia, polyuria, nocturia Renal Failure---pt needs temporary or permanent dialysis End Stage Renal Disease

40. CRF An irreversible loss of nephrons. A symptomatic until 70-90% of the nephron is destroyed. (Divided into four stages) 1. Diminished renal reserve: nephron loss without the loss of measured renal function. Normal BUN, CR, no sxs. 2. Renal insufficiency: a measurable decline in renal function. Loss of ability to concentrate urine --> nocturia, polyuria, often associated HTN fatigue, weak. Ha. 3. Renal failure /ESRD 4. Uremia: a clinical syndrome with severe decline in renal function, associated with dysfunction of multiple organ systems.

41. Etiology of CRF 1. 30%: Diabetic nephropathy 2. 26%: Hypertension 3. 14%: other urological disease ( hydronephrosis, polycystic kidney.) 4. Congenital malformations 5. Nephropathy associated with the human immunodeficiency virus. 6. Myeloma Kidney

42. Evaluation: To establish the degree of renal impairment. To identify reversible factors -infection, obstruction, volume deficit, nephrotic drugs, less than optimal cardiac output with, without HTN, uncontrolled HTN, hypercalcemia and hyperuricemia -orthostatic Bp. Pulse -U/A with microscope/dipstick, serum electrolyte, BUN, CR, CBC, evaluation of post void residual, UTZ

43. U/A: the simplest, most cost effective evaluation Urine SG: 1.010 or less Urine pH: less than 7.0 8.0: the question of infection Dipstick: glucose in DM or CRF Proteinuria: the hall mark of intrinsic renal disease. Nephrotic-range of proteinuria is seen in glomerular lesions and 1-2 gm of protein excretion in interstitial dzs. RBC: active renal dz of a glomerular or vascular etiology. WBC: infection

44. Medical Treatment A. Most hypervolemic--> kidney can’t eliminate amount of H20 and electrolytes. ** Hypovolemia (Increased HCT) B. Anemia/Bleeding The main cause of anemia--> Decreased production of erythropoietin by the kidney C. Nutritional deficiency Decreased RBC life increased hemolysis of RBC bleeding from G I tract dialyzer may contribute to the anemic state.

45. Folic Acid: Essential for DNA Synthesis and normal maturation of RBC. D. Dialysis 1) Hemodialysis: within 1-2 Hr. bring K+ to normal 2) Peritoneal dialysis: 4-8 hrs. E. Phosphate binders (aluminum or magnesium containing antacids)--> CA-Phos. An inverse relationship to bind excessive CA in ECF--> Decreased serum Ca level phosphate binders--> urinary acidifier to help prevent calcium stones F. Diet the major goal of nutritional management is to decrease catabolism of the body’s protein. No more than 0.8-1 gm of protein/kg/day.

46. F. Diet the major goal of nutritional management is to decrease catabolism of the body’s protein. No more than 0.8-1 gm of protein/kg/day. G. HTN 1. NA-fluid restriction 2. Diuretic--Lasix *3. Anti HTN drugs A. Ace inhibitors-- enalapril, captopril B. beta-adrenergic--inderal (decreased rennin released) C. Calcium channel blockers: diltiazem, verapamil

47. H. Neurologic Function No. TX. Available without dialysis neuro Change--> renal failure progress * contraindicated AntiHTN: triamiterene spironolactone, amiloride * 10 unit regular insulin + D 50 ampule. NaHCO3 bolus or 75~ 100 cc/hr- hyperkalemia tx. * Albuterol: Potassium lowering effect

48. Increased nitrogenous waste products, electrolytes imbalances --> demylination of nerve fiver, axonal atrophy. ** Safety: due to weak muscle general depression of CNS--> lethargy, fatigue, decreased concentration, dialysis dementia due to aluminum toxicity Complications: UGI bleeding a major Cx and 3-7% of deaths. Superficial mucosal abnormalities. Duodenitis and gastritis (10-60%) TX: Cimetidine (H2-receptor antagonist)

49. Death is usually due to infection, G-I bleed, myocardiac infarction. Kidney can no longer remove toxic wastes and water from blood. Two means are mimicking the body’s lost capabilities.

50. Uremia is a clinical situation in which azotemia progress to systematic state. Azotemia; an excess of urea or other nitrogenous compounds in the blood. Fetor: offensive odors halitosis: offensive odors of the breath.