renal disorders

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  1. renal failure
    • 2 types acute and chronic
    • early detection can prevent progression of CKD from stage 1 to 5 (CKD/ESRD/ESKD)
    • Increase risk:
    • - ** DM
    • - ** HTN
    • - ** family history
    • - african americans. hispanic, native am, elders
  2. renal failure 2
    • renal impairment
    • - small dec in function
    • - asymptomatic
    • renal insufficiency
    • - 75-80% lost of nephrons
    • - mild anemia, fatigue, chx in urine output, dec erythopoiten, BUN/Crt inc
    • renal failure
    • - > 80%
    • ESRD
    • - almost lost all renal function
  3. acute renal failure/acute kidney injury
    • sudden loss of kidney's ability to excrete wastes, balance fluid & lytes
    • GFR dec over houts to days, BUN & Crt inc "azotemia" dec clearance of waste products- makes you feel bad, N/V, fatigue
    • common, treatable, often reversible
    • - *** if recognized & tx early
    • norm GFR 125
  4. Acute renal failure/acute kidney injury- categories of cause
    • prerenal- "to" the kidneys
    • renal/intrarenal- "in" the kidney
    • postrenal- "out" the kidney
  5. Prerenal
    • *** most common cause of AKI
    • interference with blood supply- 25% of CO- if CO dec kidneys perfusion dec
    • kidneys require minimum MAP 60 mmHg
    • Dec GFR cayses inc proximal tubular reabsorption of Na & H2o via RAAS
  6. prerenal- causes/manifestations
    • Causes:
    • - dehydration
    • - dec BP
    • - renovascular obstuction
    • (think dec perfusion d/t dec blood supply)
    • Manifestations:
    • - dec u/o & concentrated urine
    • - inc BUN: Crt ratio (20:1)
    • - inc urine SG, osmo
    • - absent urine protein- not tubular damage
    • Treatment:
    • - IV fluifs
    • - may do bolus
    • - need to jump start the kidneys
    • - urine out put is the indicator
  7. Intrarenal
    • destruction of glomeruli or tubular structures
    • ** ATN (acute tubular necrosis) most common due to:
    • - ischemia
    • - exposure to nephrotoxic agents
    • - hemolysis of RBC- pluggin
    • - muscle necrosis: breakdown of myoglobin
    • occurs in nephrons- damage
  8. Patho ATN
    • causative factor leads to death of tubular epithelial cells. these cells slough off plug tubules (Hgb & myoglobin can clog tubules as well
    • GFR dec, oliguria follows
  9. manifestations of ATN
    • oliguria
    • proteinuria- kidney and tubular damage
    • progressively inc BUN and Crt
    • "casts" in urine- kidney/tubular damage
    • systemic chx- edema, wt gain, HTN
    • - think holding on to water
  10. Postrenal- causes and manifestations
    • Causes:
    • - mechanical/function al obstruction of urine
    • - ureteral- calculi, stricture
    • - bladder- anticholinergics, infection
    • - urethral- BPH
    • Manisfestation:
    • - depends on obstruction site
    • - ie below level of bladder causes bladder distention
    • - inc BUN/Crt
    • think- obstruction after the kidney, develop hydonephrosis
  11. diagnostic test- aki
    • urine and blood studies
    • US
    • renal angiography
    • inc BUN/Crt
    • inc K
    • dec Na, Hgb/Hct, Ca (bc vita D is activated in the kidney- need vita d to reabsorb)
    • ABG- metabolic acidosis
    • - excreting bicarb
  12. phases of AKI- onset
    • initial phase of injury
    • immediate intervention of prevent damage
    • last from hours to days
  13. phases of AKI- oliguric
    • < 500 ml/d
    • last 10-20 d
    • incr BUN/crt, lyte chx, s/s (n/v, fatigue holding on to waste)
    • ** recognize oliguria & determine cause
    • therapeutic fluid challenge
    • longer the oliguric phase the poorer the outcome
  14. phases of AKI- Diuretic
    • begins when u/o inc to 500cc/24h
    • may last 1-2 wks
    • urine dilute w/ low SG- difficulty urine concentration
    • BUN& Crt may cont to risk
    • ** report massive diuresis (>3000cc/24hr)
    • FVD
    • urine output tells us healing is occuring
    • will start to put off large amts
    • @ end of phase BUN/crt normalize
  15. phases of AKI- recovery
    • begins when BUN stable, may last months to yr
    • protect kidney from another insult
    • ** avoid excessive protein intake
    • may be some residual damage
    • GRF 80% of what it should be
  16. management- oliguric phase
    • monitor I&O, wt
    • careful fluid replacement
    • diuretics- cautiously
    • - loop diuretics
    • - FVO
    • with some renal function
  17. management- oliguric phase 2
    • lytes replacement/adjustment
    • - hyperkalemia- EKG, dietary restriction, Kayexalate (pulls K in the GI), IV D50 & insulin (regular), Ca gluconate (dysrhthmia- PVC, QRS wave wide, loss p wave, high T wave, cardiac arrest)
    • hyponatremia- fluid restri, esp. free H2o)
    • - how much fluid to give: output past 24 hr + 600 ml
  18. management- oliguric dietary/dialysis
    • dietary:
    • - inc cal (for energy), fats, CHO
    • - dec Na++, K+, +/- protein
    • Dialysis:
    • -w/anuria, severe acidosis
    • - FVO
    • remember no added salt bc it holds on to water
    • protein depends on renal fx
  19. management- diuretic phase
    • monitor u/o, wt, orthostatic VS
    • avoid repeat insult
    • ** AKI may lead to CKD
  20. nursing interventions
    • as above and:
    • oral hygiene
    • help with fluid restriction
    • good skin care
    • good cath care
    • psychological support
    • complete recovery
  21. Chronic renal/failure/esrd
    • 5th and final stage of CKD
    • progressive, irreversible deterioration in renal function, with failure to maintain fluid & electrolyte balance
    • affects every body system
    • results fatally in uremia
    • cant maintain lytes
  22. common causes pf CRF
    • ** DM
    • un/poorly controlled HTN
    • HLD, smoking
    • fam hx of renal dx
    • ARF
    • Nsaids over use
    • glomphephritis
    • lysis?
  23. Patho CRF
    • progressive renal function dec with deterioration and destruction of nephrons
    • as total GFR fails, serum BUN/crt inc
    • remaining nephrons hypertrophy- try to work harder and harder
    • kidneys cant concentrate urine adequately
    • large volume of urine made
  24. patho CRF
    • tubules gradually lost ability to reabsorb lytes-acidosis, inc PO4 (phosphate inreverse relationship with Ca), K+, Mg, dec Ca
    • as renal damage cont & functioning # nephrons dec, GFR dec more
  25. patho CRF
    • body is unable to rid itself of H2O, salt, and other wastes
    • anemia and htn develops- reabsorbing fluid
    • w/GFR < 10-20 ml/min, clinical uremia seen
    • result of CRF is uremia & death unless tx
  26. diagnostic test CKD
    • dec NA++. Ca++, Ph
    • inc K+, PO4, mg, BUn/crt
    • U/A- proteinuria
    • dec urine creatinin clearance- 24 hrs
    • CBC- normochromic normocytic anemia- MCV, MCH, MHCH norm
    • elev trig
    • dec plat- risk for petechia
    • metabolic acidosis- dec ph, bicarb
    • may have chx in BS- DM must need less insulin bc not excreting
  27. diagnostic test CKD 2
    • KUB, IVP, CT
    • renal angiography
  28. management-CKD conservative
    • maintain/restore fluid balance
    • - Na++/fluid restriction (daily u/o + 600 ml)
    • - diuretics- loop need some renal fx
    • - antihtn
    • - strict I&O, daily wt
    • assess FVO
    • 1L of fluid- 1Kg
    • remember 1 kg- 2.2 lbs
  29. management- CKD electrolyte balance
    • K+ diet restriction, kayexalate
    • PO4- dietary restriction- 800-1000 mg/d
    • phosphate binders if diet not successful
    • - amophogel, CaCO3, Ca gluconate, sevelamer (renagel)
    • Ca++= calcitriol, calcitonin- surpress parathyroid hormone- pt ca in bloodstream
    • mg++ avoid laxatives, anacids w/mg (mile of mg)
  30. management- ckd metabolic acidosis
    • symptoms if serum bicarb < 15 mEq/L
    • H/A, malaise, change in resp, to stupor coma
    • treated with IV bicarb or dialysis
  31. management CKD- diet
    • protein restriction= at least 50 % high (not too much) but eggs, diary, fish
    • inc CHO, fats, cal for energy
    • Na++, K+ restriction- watch seasonings
    • PO4 restrictions (most foods have both po4 and ca)
    • water soluble vitas, high iron foods
    • K- orange juice, banana, protein
  32. management- anemia, htn
    • anemia-- if Hct is < 30, to dec S&S
    • Epogen ** primary tx- viscosity clots
    • - IV/Sc
    • - 2-6 wks before improvement seen
    • Blood infusion
    • HTN
    • antihtn
    • ace-i, ca channel blockers and statins (hld dec chol)
  33. Management ckd integumentary
    • dec itching
    • uv light
    • soothing skin lotions-temporary
    • coping
    • stress management
    • support groups
    • skin issue
    • grayish
    • look sick
    • pale- anemia
    • uremic frost- crystals- form on skin itchy
    • petechia- dec plat
  34. management ckd more aggressive
    • dialysis
    • transplantation
  35. dialysis
    • eliminates wastes, lytes, water
    • hemodialysis or peritoneal (artifical kidney)
    • either may temp or permanent
    • "artificial kidney"- semipermable membrane thru which dialysis occurs ultrafiltration & diffusion
    • dialysate- specially prepared lyte solution that runs on other side of membrane
    • remind- trying to replace kidney that is not working
  36. dialysis indications
    • S&S progressive uremia
    • BUN > 99mg/dl, Crt >10
    • toxic level certain meds
    • - cant excrete meds
    • significant acidosis dec ph, dec GFR (norm 125) < 10
  37. peritoneal dialysis
    • dialysate insilled at regular intervals into peritoneal cavity
    • wastes, excess fluid, lytes pass thru via osmosis & diffusion (peritoneum- artificial kidney)
    • drained at regular intervals
    • you have to have intact peritonum - can't have abd surgeries, multi obesity with large walls
  38. peritoneal dialysis 3
    • fill
    • - room temp sterile dialystate- hypertonic pull solution
    • dwell
    • - remain in abd- diffusion & osomosis 2-8 hrs
    • drain
    • - by gravity into sterile bag or pump
    • pt will have feeling of fullness
    • solution clear- yellowish

Card Set Information

Author:
Prittyrick
ID:
330729
Filename:
renal disorders
Updated:
2017-04-25 03:41:14
Tags:
kidneys
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