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Flashcards in Renal Deck (34)
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1

What is chronic kidney disease?

GFR less than 60 mL/min/1.73 m2 for 3 months

2

What is chronic renal failure (CRF)

15 mL/min/1.73m2

3

What is ESRD?

loss of renal function for 3 months or more

  • diabetes accounts for half of cases and HTN for one fourth
  • Polycystic 10% - genetic autosomal dominant

4

What is acute kidney injury?

  • sudden decrease function/UOP

5

Very generic overview of why pt with acute or chronic renal failure may end up in OR?

Acute renal failure- patients requiring surgery are very ill (postop complication or trauma)

Chornic renal failure- often present for AV fistula creation or revision

6

What should you focus ROS on for patient with renal failure?

Issues r/t:

  • uremia
    • toxic condition associated with renal insuffieicny produced by retention in the blood fo nitrogenous substances normally excreted by kidney
    • widespread systemicmanifestations are seen from this syndrome when GFR <25 mL/min
    • At <10mL/min, patient become dependent on dialysis for surivvial. However, overtime, symptoms may not be entirely controlled by dialysis and there are also complications that result directly from dialysis
  • dialysis
    • intermittend HD (av fistula)
    • continuous peritoneal dialysis (implanted catheter)
      • better for patient with issue w/ vascular access or can't tolerate fluid shifts with HD

7

When might dialysis be required?

  • Oliguria
  • Fluid overload
  • hyperkalemia
  • severe acidosis
  • metabolic encephalopathy
  • pericarditis
  • coag
  • refractory GI symptoms
  • drug toxicity

Goals of HD include ensuring adequate nutrition, maintaining vascular access, correcting hormonal deficiencies, minimizing hospitalizations, increasing quality and lifespan

8

Basic for HD?

  • Diffusion of solutes b/w the blood and dialysis solution remove metabolic wastesa nd restore buffers to the blood
  • need vascular access
    • AV fistula= cephalic anastomosed to radial artery
    • jugular or femoral vein for emergency access
  • 25 % of dialysis pt die each year r/t CV causes or infection
  • even if pt doesn't need HD yet, preserve non dominant UE for future vascular access

9

If patient is on dialysis, what should happen sometime before elective surgery?

  • Preop dialysis!
    • either day before or day of. Day before is generally better and less adverse outcomes during procedure
  • Optimize as much as possible
  • Review dialysis flowsheet if available
  • amount of fluid "taken off"
  • pre and post dialysis weights compare with day of sx weight
  • note post dialysis chem. serum K <5.5 mEq/L
    • patient may initially appear hypokalemic until equilibrium is reestablished b/w ICF and ECF

10

What is important to remember about dialysis and meds?

  • General rule: scheduled doses of drugs are administered after dialysis
  • low-molecular weight, water soluble and non protein bound drugs are readily cleared by dialysis
    • exception low-molecular weight heparin is not adequately cleared by dialysis

11

What are some s/s to assess for during neuro assessment of renal patient?

  • Uremic encephalopathy
    • asterixis
    • myoclonus
    • lethargy
    • confusion
    • seizures
    • coma
  • Autonomic neuropathy
    • may be dififcult to control BP, more sensitive to VA, spinal, etc
  • peripheral neuropathy
    • typically sensory and involve distal lower extremities
  • Disequilibrium syndrome (dialysis related) transient CNS disturbance after rapid decrease in ECF osmolality compared with ICF osmolality
  • Dementia

12

Factors in hematological assessment of renal failure patient?

  • Anemia typical Hgb 6-8 g/dL
  1. Decreased erthyropoietin production
  2. decreased RBC prodcution and cell life span
    1. anemia almost always present if GFR <30mL/min- unless they are on aggressive erythropoietin replacement therapy, when they can actually develop polycythemia which then increase M and M (morbiity and mortality?)
  3. GI blood loss, hemodilution, bone marrow suppression
  4. Excess PTH repalces bone marrow with fibrous tissue
  • Most pt tolerate the anemia well (exception CAD)
  1. Increased 2,3 DPG- (diphosphoglycerate)
    1. this causes right shift, releasing O2 more readily
  2. metabolic acidosis also favors rightward shift
  • Impaired PLT (qualitative)- prolonged bleeding time
  1. decreased PLT factor III activity
  2. decreased adhesiveness and aggregation
  • Impaired WBc function- infection
  • release of defective von wilebrand factor
  • dialysis- residual anticoag vs promotion of hypercoagulable state
  • hypocomplementemia with dialysis

13

What to consider with aseptic technique with renal failure patient?

  • Infection common cause of death
  • care with ETT- prone to pulmonary infection
  • IV, line insertion
  • strict aseptic technique with catheters and ET tubes
  • 1/3 become infected with HEP virus and become chronic carriers
  • other flinical features include uremic pericarditis and pericarial effusion, tamponade, increased gastric volume, acid production and delayed emptying (full stomach concerns), accelerated atherosclerosis

14

What to assess from CV standpoint for patient with renal failure?

  • Increased cardiac output
    • compensaiton for decreased O2 carrying capcity
  • HTN- Na retention, renin-angiotensin activation
    • ace inhibitors used cautiously in pt in whom the GFR is dependent on increased efferent arteriolar vasoconstriction (b renal artery stenosis) which is mediated by angiotensin II. If these pt receive ACE they can get efferent arteriolar dilation and decreased GFR- deterioration in function
  • LVH common (d/t HTN)
  • CHF with pulmonary edema after limits of compensaiton reached
    • alteration in capillary membrane make vessels more leaky
  • Depositon of calcium- in the conduction system an on the heart valves
    • can result in stenosis or regurg (or both) or conduciton blocks
  • Arrhythmia- electrolyte imbalances
  • uremic pericarditis- can be asymptomatic, chest pain, tamponade, usually secondayr ti inadequate dialysis
  • Accelerated CAD, PVD
    • Chronic renal disease is sig risk factor for CV moribidity and mortality and is an ACC/AHA intermediate cardiac risk factor considered to be equal to angina, MI, or known CAD
    • Cr of 2 mg/dL, need cardiac speicfic assessment

15

Factors in fluid balance assesment of patient with renal failure?

  • Fluid overload VS intravascular depletion status post dialysis/aggressive diuretic therapy
  • body weight
  •  VS (orthostatic hypotension and tachycardia)
  • atrial filling pressures

16

Pulmonary assessment in renal failure?

  • MV increased to compensate for metabolic acidosis
  • Increased pulmonary extravascular water= interstitial edema= widened alveolar/arterial O2 gradient
  • "Butterfly wings" on cxr secondary to increased permeability of alveolar capillary membrane
    • edema even with nml pulmonary capillary pressures

17

Endocrine asesssment in renal failure?

  • Peripheral resistance to insulin= poor glucose tolerace
  • Hyperparathyroidism= prone to fractures
  • abnormal lipid metabolism= accelerated atherosclerosis
  • kidneys do not degrade hormones and proteins normally= increase ciruclating PTH, insulin, glucagon, GH, LH PL

18

GI/Liver assessment in renal disease?

  • 10-30% of patients will develop GI hemorrhage
  • Anorexia
  • nausea and vomiting
  • hypersecretion of gastric acid + delayed gastric emptyin g(autonomic neuroapthy)
  • high incidence of Hep B and C in these pt (multiple transufions, etc)
  • ascites with dialysis

19

Renal failure and impact on drugs?

Effects altered d/t

  • Anemia
  • Decreased serum protein
  • electrolyte abnormalities
  • fluid retention
  • abnormal cell membrane activity

DRUGS ELIMINIATED BY KIDNEYS UNCHANGED ARE CONTRAINDICATED

  • Gallamine, phenobarb, LMWH
    • LMWH are metabolized or cleared by kidneys and not removed by dialysis- risk of bleeding increased even further

 

20

Which MR are not cleared by the kidney and are probably the safest choice?

Atracurium and Cisatracurium

21

How can you assess fluid status of a patient?

VS, mucous membrane, orthostatic, auscultate the lungs

22

What is normal chem panel?

Na, K, Cl, Sodium bicarb, Ca, phosphate, Mg, serum osmolality values?

  • Sodium 135-145 mEq/L
  • Potassium 3.5-5 mEq/L
  • Chloride 95-105 mEq/L
  • Sodium bicarb (veous 19-25 mEq/L; arterial 22-26mEq/L)
  • Calicum 4.5-5.5 mEq/L
  • Phophate 2.4-4.7 mg/dL
  • Magnesium 1.5-2.5 mEq/L
  • Serum osmolality 280-300 mOsM

23

What are some tests to assess GFR?

  • Blood urea nitrogen (10-20 mg/dl)
  • Plastma creatinine (0.7-1.5) 
    • GFR can decrease 50% w/o rise in creatinine. Not accurate indicator of renal funcitone especially in elderly
  • Creatinine clearance 110-150 mL/min

GFR is most frequently evaluated index of renal function but both GFR and RBF need to be evaluated because a decrease in one will gneeralyl reflect in the other

24

What are some tests to assess renal tubular function

  • Urine speicfic gravity (1.003-1.030)
  • urine osmolarity (38-140mOsM/L)

25

What is BUN useful for in renal failure?

  • BUN normal= 10-20 mg/dL
  • Varies inversely with GFR and directly with protein catabolism
  • >50 mg/dl is indicative of drop in GFR (in patients with normal diets)
  • BUN is not sensitive index b/c urea clearance also depends on produciton of urea
  • BUN can be abnormal despite a normal GFR due to
    • high protein diet
      • during catabolism of protein, ammonia is produced from deamination fo amino acids. hepatic conerstion of ammonia--> urea prevents toxic ammonia levels of body
      • BUN is not reliable indicator of GFR unless protein catabolism is normal and constant
      • also, hypovolemia result sin reabsorption of urea by kidneys, which results in inflated BUN result
    • GI bleed
    • febrile illness - switching to protein catabolism
  • The most common cause of increased BUN is CHF secondary to reabsorption of BUN

26

What is creatinine level useful for in renal failure?

  • Plasma creatinine is specific indicator of GFR
  • 8-17 hr lag time after a change in GFR before increase in Cr levels are seen
  • suggestive but not indicative of acute renal failure
  • usually a 50% increase in plasma Cr reflects a corresponding decrease in GFR
  • Skeletal muscle= source of Cr
  • elderly pt- Cr levels stay normal constant d/t":
    • decrease in muscle mass and GFR
    • If Cr increase in elderly, this may be indicative of renal failure

Creatine is product o fmuscle metabolism that is nonenzymatically converted to cretinine. Cretinine production in most persons is relatively constant and related to muscle mass. Creatinine is filtered but not reabsorbed in the kidneys. Serum creatinine is directly related to muscle mass, but inversely related to GFR. Nml is 0.8-1.3 in men and 0.6-1 in women. Each time creatinine doubles there is a 50% reduciton in GFR

27

Creatinine clearance?

  • 24 hours collection most accurate although 2 hour tests also helpful
  • creatinien clearance approximates GFR
  1. Normal 100-120 mL/min
  2. Decreased renal reserve 60-100 mL/min
  3. Mild renal impairment 40-50 mL/min
  4. Moderate insufficiency 25-40 mL/min
  5. Renal failure <25mL/min
  6. ESRD <10 mL/min

Creatinine is engoenous marker of renal filtration. It is freely filtered and not reabsorbe.d Most reliable measure of GFR. Does not require a steady state or corrections for age. Reliabiilty is altered by variability in tubular secretion and inability of most time colelciton of urine samples correctly. Progressive renal dx enhnaces creatinine secretion in proximal tubule. Therefore, as renal disease progresses, creatinine clearance overestimates GFR (patient worse than the creatinine clearnace indicates). Also, in early renal failure, the remaining nephrons compensate by increasing filtraiton and glomerular filtraiton pressure

28

What are common abnormalities in lab tests in patient with renal failure?

  • Assess adquacy of dialysis
  • hyponatremia (hypernatremia rare)
  • hyperkalemia (hypokalmeia with dialysis)
    • peaked T waves, widened QRS, prolong PR, loss of P, vfib, asystole)
  • metabolic acidosis with high anion gap
  • hypermagnesemia-  usually from high antacid intake
  • hypocalcemia (unclear why)
  • hypoalbuminemia (esp with dialysis)
  • hyperglycemia (if insulin resistant)

29

Hyperkalemia treatment if symptomatic or >6.5 mEq/L?

  • Calcium gluconate 10% 10-20 mL
    • MOA- antagonized K effect on cardiac musle
    • Onset- immediate
    • duration- brieft
    • s/e- avoid with dig therapy
  • Sodium bicarb (50-100mEq IV)
    • MOA- shift K into cells
    • onset- prompt
    • duration- short
    • s/e- Na overload
  • Glucose (50 mL of 50% soln + 10 units regular insulin)
    • MOA- shift K into cells
    • onset- prompt
    • duration 4-6 hours
    • s/e- hyperglycemia and hypoglycemia
  • Dialysis
    • MOA- Remove K from body
    • Onset- immediate
    • S/E need vasular acess
  • Ion exchange resin (kayexalate)
    • MOA- remove K from body
    • onset 1-2 hours
    • S/e - Na overload

30

Normal CBC values?

  • RBC 1.6-6.2 million mm3 male
    • 4.2-5.4 million mm3 female
  • HCT 40-54% men; 38-47% women
  • Hgb 13.5-18g/dL; men 12-16 g/dL women
  • RBC indices
    • MVC- mean corpusuclar volume or volume of hgb in eahc RBC
    • MCH- Mean corpuscular hgb or weight of hgb in each RBC
    • MCHC- mean corpuscular hgb concentraiton in a % or proporiton of hgb contained in each RBC
  • WBC 5000-10000/mm3
  •