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NUR 3020 exams > renal > Flashcards

renal Flashcards

1
Q

polycystic kidney disease (PKD) (what (3), early sx., _________ _______ -> CKD)

A

inherited disorder in which fluid-filled cysts develop in the nephrons
- growing cysts damage the glomerular and tubular membranes
- as the cysts fill with fluid and enlarge, the nephron and kidney function become less effective
- early: wasting Na/H2O
- decreased GFR -> CKD (retain H2O/Na)

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2
Q

polycystic kidney disease s/sx (5)

A
  • abdominal or flank pain
  • HTN
  • hematuria, polyuria, proteinuria, nocturia
  • kidney stones, UTIs
  • progression to kidney failure with anuria (no UO)

tips:
- uremic s/sx: anorexia, N/V, pruitis, fatigue

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3
Q

polycystic kidney disease diagnostic labs (2)/tests (3)

A

labs:
- urinalysis (protein - glomerular), hematuria, bacteria (infection)
- BUN, Cr.

tests:
- renal US (screening PKD)
- CT (F/U)
- MRI (F/U)

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4
Q

polycystic kidney disease interventions (6)

A
  • pain mgmt
  • prevention of infection (bactrim/cipro if cyst infection causes discomfort)
  • control of other comorbidies (ACE inhibitors -> HTN prevention, CKD) -> control cell growth, decreased albuminuria, salting wasting
  • diet changes: no sodium restrict diet unless Na. retention to control BP
  • hemodialysis
  • kidney transplant (education: self mgmt)
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5
Q

glomerulonephritis (GN) (what, leads to (5))

A

1) group of diseases that injure the part of the kidney from an antibody reaction with antigens can cause immune complexes to form and become deposited in glomerular tissue, leading to inflammation
2) inflammation causes damage to kidney tissue and leads to:
- proteinuria
- hematuria
- decreased GFR
- edema
- HTN

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6
Q

acute glomerulonephritis (acute nephritic syndrome) (what, s/sx (5))

A
  • an acute inflammation and subsequent damage to the glomeruli leading to hematuria, proteinuria, and azotemia

s/sx:
- edema, esp. in face, eyelids, and hands
- fluid overload, HTN
- hematuria, dysuria, oliguria (decreased UO)
- wt. gain
- fatigue, anorexia, n/v

tips:
- toxins accumulate + can’t be excreted -> acute glomerulonephritis (AGN)
- recover quickly and complete (treatment cause -> infectious cause (strept., group A beta staphylococcus, staph. (-) bacteremia, pneumonia (bacteria), syphilis)
- effects endo., hep B, cytomegaly, mumps/measles/varicella, infectious mono, spotting fever

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7
Q

chronic glomerulonephritis (chronic nephritic syndrome) (what, s/sx (6))

A
  • group of kidney diseases characterized by long term inflammation and scarring of the glomeruli

s/sx:
- mild proteinuria
- hematuria
- HTN
- fatigue
- occasional edema
- uremia

tips:
- exact cause: unknown
- changes to kidney tissue, number of functioning nephrons decrease -> ESKD

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8
Q

glomerulonephritis diagnostic labs (5)/tests (3)

A

labs:
- urinalysis: protein, hematuria
- specific gravity: constant level 1.010 (dilution)
- GFR: Cr clearance (low)
- BUN/Cr. (increased, >100-200mg/dL (BUN), >6mg-30mg/dL(Cr.))
- BMP: fluid/electrolyte disturbances

tests:
- XR
- CT
- kidney biopsy (precise diagnosis, outcome tx.)

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9
Q

glomerulonephritis interventions acute (pharm (4) + 3)

A

1) pharmacological:
- corticosteroids
- antibiotics for infections
- diuretics may be needed for fluid overload
- antihypertensives to control BP
2) fluid restrictions, monitor I/Os (oliguria, increased K + BUN)
3) dietary restrictions (Na, K, decrease protein intake (restrict))
4) dialysis if uremia occurs

tips:
- N/V/A = uremia present
- fluid volume excess can’t be controlled

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10
Q

glomerulonephritis interventions chronic (7)

A
  • slow progression of disease
  • prevent complications
  • diet changes, monitor weight
  • drug therapy to control the problems from uremia (N/V/anorexia)
  • manage HTN
  • hemodialysis
  • kidney transplantation
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11
Q

nephrotic syndrome (NS) (what, occurs with, causes, main feature)

A
  • condition of increased glomerular permeability that allows larger molecules to pass through the membrane into the urine and then be excreted
  • occurs with many intrinsic kidney diseases and systemic diseases that cause glomerular damage -> not specific glomerular disease but a constellation of clinical findings that result from the glomerular damage
  • this process causes massive loss of protein into the urine, edema formation, and decreased plasma albumin levels
  • main feature of nephrotic syndrome: severe proteinuria (w/ more than 3.5g of protein in a 24 hour urine sample)
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12
Q

nephrotic syndrome s/sx (8)

A
  • massive proteinuria
  • hypoalbuminemia
  • edema (esp. facial, periorbital, dependent areas, ascites) (anasarca)
  • HLD
  • reduced kidney function
  • irritability
  • headache
  • malaise

tips:
- all sx. d//t retain fluids/toxins

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13
Q

nephrotic syndrome interventions (pharm (4) + 1)

A

1) pharm:
- immunological processes may improve w/ suppressive therapy using steroids and cytotoxic or immunosuppressive agents
- ACE inhibitors -> decrease protein loss in the urine
- cholesterol-lowering drugs -> improve blood lipid levels
- mild diuretics, sodium restriction -> control edema, HTN

2) diet changes are often prescribed: decrease Na intake, most limit protein (except nephrotic syndrome), increase protein intake typically

tip:
- early stages: nurse mgmt similar to acute glomerulonephritis, as progress -> ESKD treatment

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14
Q

kidney dysfunction (3)

A

1) kidney function loss
2) acute kidney injury (AKI)
3) chronic kidney disease (CKD)

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15
Q

kidney function loss

A

interrupts the activity of every organ system, particularly the immune, endocrine, and skeletal, and cardiovascular systems

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16
Q

acute kidney injury (AKI)

A

kidney declines SUDDEN, functioning nephrons are overworked and kidney failure may develop with the loss of 50% of functioning nephrons

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17
Q

chronic kidney disease (CKD)

A

AKA chronic renal failure (CRF)
- when kidney function declines gradually, where the patient may have many years of abnormal serum BUN and Cr. values, sometimes called renal insufficiency, before the uremia of ESDK develops

tip:
- acute = sudden
- chronic = gradual
- both can result in ESKD -> tx: dialysis, decreased independence, quality of life, longevity of life
- acute + chronic = acute on chronic kidney injury -> accelerates loss of kidney function, decreasing nephron numbers from CKD contributes to progression of KD

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18
Q

acute kidney injury (what, severity, classified using (2))

A

rapid reduction in kidney function resulting in failure to maintain fluid and electrolyte balance and acid base balance
- severity of AKI: based on increases in serum creatinine, decreased urine output
- classified using: RIFLE classification (risk, injury, failure, loss, ESRD/ESKD) or KDIGO classification (kidney disease: improving global outcomes)

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19
Q

what is the KDIGO criteria for AKI (3)

A

1) increase in Cr >/= 0.3mg/dL within 48H
2) increase in Cr >/= 1.5 x baseline within 7D
3) urine volume <0.5 mL/kg/hr for more than 6 consecutive hours

tip:
- 50% increase Cr above baseline
- 40-90% inpatient mortality rate

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20
Q

causes of AKI (pre-renal/due to (7), intrinsic/due to (6), post-renal/due to (7))

A

1) pre-renal: from perfusion reduction (blood can’t go into kidney for perfusion)
- d/t blood or fluid loss, hTN, MI, HF, infection, liver failure, atherosclerosis

2) intrinsic/intra-renal: from kidney damage (inside)
- d/t glomerulonephritis, pyelonephritis, lupus, drugs, hemolytic uremic syndrome (N/V/A), vasculitis

3) post-renal: from urine flow obstruction (urine can’t be excreted from kidneys)
- d/t bladder ca., cervical ca., colon ca., prostate ca., BPH, kidney stones, neurogenic bladder

tip:
- kidney compensates by: (1) constrict kidney BV, (2) activate aldosterone pathways, (3) release ADH -> increased BV and kidney perfusion -> decreased U/O (oliguria, retention/build up nitrogenous waste)
- can all occur together
- radiocontrast induced neuropathy (RCIN): major cause hospital acquired AKI, common experience amongst patients leading to need for dialysis/prolonged hospital stay (most common cause in AKI)
- baseline Cr: >2mg/dL
- limit exposure to contrast + nephrotoxins to decrease risk RCIN
- sodium bicarb: helps to decrease risk c/ contrast
- prehydration c/ NS: PREVENTION #1

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21
Q

AKI nursing interventions early (6)

A
  • evaluate fluid status (fluid volume, Na, K issues)
  • measure I/O (0.5mg/kg/hr)
  • check body weight every day
  • note characteristics of urine
  • monitor lab values and vital signs (esp. MAP -> perfusion, adequate is 65)
  • prevent and treat infections promptly
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22
Q

AKI s/sx (7)

A
  • fluid overload
  • pulmonary crackles
  • generalized edema
  • decreased oxygenation
  • increased RR
  • dyspnea
  • decreased U/O

tip:
- not all patients experience oliguria, think about inflammatory response to increase protein in glomerulus, hold fluid in filtrate -> polyuria -> hypovolemia + electrolyte loss (main issue AKI)

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23
Q

AKI diagnostic labs (3)/tests(3)

A

1) labs:
- serum Cr: 1-6 mg/dL/<1 week OR 1-2mg/dL/24-48H
- BUN: increased, 10-20mg/dL, 80-100 mg/dL/wk.
- BMP: increased K, Mg, Phos (acid/base/electrolyte imbalance), decreased Ca, bicarb, pH, HgB/HcT (not enough EPO)

2) tests:
- U/S: dx. kidney/urinary tract obstruction
- XR: initial screen urinary tract
- CT (w/o contrast): adequate kidney BF, obstruction/tumor identification

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24
Q

AKI pharm interventions (5)

A

1) diuretics to rid the body of retained fluid/electrolytes
- DOES NOT preserve kidney function or STOP AKI

2) fluid challenges to promote kidney perfusion
- 500-1000mL of NS infused over 1 hour (bolus)
- monitor CVP, PAP, hemodynamics status, and respiratory status

3) calcium channel blockers to treat AKI resulting from nephrotoxins
- prevents the movement of calcium into the kidney cells, maintains kidney cell integrity, and improves kidney blood flow

4) medication to correct electrolytes

5) dialysis with dialysate to purify blood
- symptomatic uremia: precarditis, anemia, neuropathy, cognition deficit, persistent/rapid rise potassium (>6-6.5), severe metabolic acidosis (pH: >7.1), fluid overload, drug intoxication

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25
Q

AKI nutritional interventions (3)

A

1) patients who have AKI often have a high rate of catabolism
2) nutrition support can include oral supplements, enteral nutrition, or parenteral nutrition
3) obtain a dietitian consult to regulate protein, fluids and electrolytes
- non-dialysis protein need: 0.6g/kg of body weight (40g protein daily)
- dialysis protein needs: 1-1.5g/kg of body weight
- sodium: 60-90 mEq/kg (135-145)
- potassium: 60-70 mEq/kg (3.5-5.0) (potassium low diet)
- fluid: equals the urine volume + 500mL)

tips:
- assess I/O QH!!
- caloric intake adequate

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26
Q

AKI post hospital care (resolved vs. unresolved)

A

1) AKI resolved:
- follow up with nephrologist and primary care provider frequently
- dietician
- fluid restrictions and daily weights during recovery

2) AKI NOT resolved:
- require life long intermittent dialysis
- renal transplant
- home care or social work assistance

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27
Q

chronic kidney disease (CKD) definition + criteria (7)

A

progressive, irreversible disorder and kidney function does not recover

KDIGO criteria for CKS (>3mo):
- albuminuria >30mg/day
- urine sediment abnormalities (hematuria, red cell casts, etc.)
- electrolyte and other abnormalities due to tubular disorders
- abnormalities detected by histology
- structural abnormalities detected by imaging
- history of kidney transplantation
- GFR <60 (EXAM)

tips:
- CKD -> ESKD (increased nitrogenous waste blood)
- cause: T1/2DM, HTN, glomerulonephritis, interstitial nephritis, polycystic disease, prolonged obstructed urinary tract, polynephritis, fascicular reflex disease

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28
Q

CKD: health promotion to prevent or delay CKD (7)

A
  • controlling diabetes
  • controlling HTN
  • diet adjustments
  • weight maintenance: ideal BMI (22-25 kg/m2)
  • stop smoking
  • exercise: safe
  • avoid nephrotoxic drugs

tips:
- caution NSAIDs
- (low dose, short term) -> interfere with BF -> kidney
- (high dose, long term) -> decrease kidney function
- limit ETOH 1-2 drinks daily

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29
Q

CKD s/sx neurological manifestations (8)

A
  • behavior changes, inability to concentrate, decreased LOC
  • weakness and fatigue, lethargy
  • tremors, twitching, or jerky movements, seizures
  • coma
  • slurred speech
  • asterixis (the inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements)
  • ataxia (w/o coordination)
  • paresthesias (numbness/tingling)
30
Q

CKD s/sx cardiovascular manifestations (6)

A
  • cardiomyopathy, HF
  • HTN
  • peripheral edema, peri-orbital edema (increased heart working)
  • hyper-kalemia
  • uremic pericarditis: inflammation by uremic toxins/dysfunctions
  • peri-caridal effusion; friction rub or tamponade

tip:
- increased BP doesn’t mean increased BF

31
Q

CKD s/sx respiratory manifestations (8)

A
  • uremic halitosis: d/t increased uremia waste, smell ammonia
  • tachypnea; SOB
  • kussmaul respirations
  • uremic pneumonitis
  • pulmonary edema
  • pleural effusion
  • depressed cough reflex
  • crackles
32
Q

CKD s/sx hematologic manifestations (2)

A
  • anemia: common in LATER stage, worsen CKD (decreased EPO, RBC survival -> decreased folic acid, bleed risk)
  • abnormal bleeding and bruising
33
Q

CKD s/sx GI manifestations (8)

A
  • anorexia, nausea, vomiting (hiccups, increase BUN/Cr/acidosis, urease -> ammonia -> halitosis stomatitis)
  • metallic taste in the mouth
  • changes in taste acuity and sensation
  • uremic colitis (diarrhea)
  • constipation
  • uremic gastritis (possible GI bleeding)
  • uremic fetor (breath odor)
  • stomatitis

tip:
PUD -> errosion BV

34
Q

CKD s/sx urinary manifestations (6)

A
  • polyuria, nocturia (early)
  • oliguria, anuria (later)
  • proteinuria
  • hematuria
  • diluted, straw-colored urine appearance (early)
  • concentrated and cloudy urine appearance (later)

tip:
- healthy nephrons become larger + work harder
- urine with fixed osmolarity
- increased BUN
- U/O
- risk fluid overload

35
Q

CKD s/sx uremia (10)

A
  • metallic taste in mouth
  • anorexia, nausea, vomiting
  • muscle cramps
  • uremic “frost” on skin
  • itching
  • fatigue and lethargy
  • hiccups
  • edema
  • dyspnea
  • paresthesia

tip:
- increased BUN
- Cr. comes from protein -> skeletal muscles, rate depends on muscle mass, activity, diet, constant
- hypoNA, hypoPHOS (early)
- hyperNA, hyperPHOS, hypoCA (late)
- potassium levels (normal until U.O <500/hr)
- decreased nephrons = decreased acid excretion + metabolic acidosis (kuassmall, increased RR, d/t increased CO2 lvls + want to decreased)

36
Q

CKS s/sx integumentary manifestations (8)

A
  • decreased skin turgor
  • yellow gray bronze skin color
  • dry sky
  • pruritus
  • ecchymosis
  • purpura
  • thin, brittle nails, coarse, thinning hair
  • uremic frost (late) (IMPORTANT) -> layer urea crystals from evaporated sweat (face, brows, axilla, groin with advanced uremic syndrome)
37
Q

CKD s/sx musculoskeletal manifestations (4)

A
  • muscle weakness and cramping
  • bone pain
  • fractures
  • renal osteodystrophy (esp. later ESKD d/t increased PHOS/CA -> PTH moves CA bones -> blood -> decreased CA -> weak bones)
38
Q

CKS s/sx reproductive manifestations (6)

A
  • decreased fertility
  • infrequent absent menses
  • decreased libido
  • impotence
  • sexual dysfunction
  • testicular atrophy
39
Q

stages of CKD (4) (what, ___ ml/min, intervention)

A

1) stage 1: at risk, normal kidney function but urine findings or structural abnormalities or genetic trait point to kidney disease
- >90mL/min
- intervention: pregnancy, DM, HTN, HF, slow CKD, nephrotoxic substances

2) stage 2: mild CKD, reduced kidney function, lab values and other findings (structural changes) point to kidney disease
- 60-89mL/min
- intervention: focus on reduction of risk factors (fluid vol., HTN, electrolyte mgmt important)

3) stage 3: moderate CKD
- 30-59mL/min
- intervention: implement strategies to slow disease progression, fluid/protein/electrolyte restrict, nephron damage greater

4) stage 4: severe CKD
- 15-29mL/min
- intervention: manage complications, discuss preferences and values, educate about options and prepare for renal replacement therapy, excessive BUN, severe F/E balance, acid-base imbalance

5) stage 5: end stage kidney disease (ESKD)
- <15mL/min
- intervention: implementation renal replacement therapy or kidney transplantation, w/o renal replacement -> death

40
Q

CKD diagnostic labs (5)/tests(2)

A

labs:
- BUN: r/t diet protein intake
- Cr
- GFR
- BMP
- CBC

tests:
- US
- CT

tip:
- w/o protein restrict, BUN increased 10-20x

41
Q

CKD interventions (8)

A
  • managing fluid volume
  • preventing pulmonary edema
  • increasing cardiac output & controlling BP
  • enhancing nutrition
  • preventing infection
  • preventing injury
  • minimizing fatigue
  • reducing anxiety
42
Q

CKD interventions to manage fluid volume (6 + pharm)

A
  • monitor and control for optimal BP and electrolytes
  • monitor weight every day (2 Ibs overnight, 5 Ibs/wk)
  • intermittent dialysis or peritoneal dialysis
  • maintain fluid restrictions w/ strict I/O
  • monitor s/sx fluid overload Q4H PRN
  • pharm: diuretics to reduce fluid overload (decrease, NO diuretics)

tip:
- 1kg = 1L

43
Q

CKD interventions to prevent or manage pulmonary edema (3, pharm (2))

A
  • maintain optimal fluid balance
  • continue to assess for early indicators of pulmonary edema
  • position the patient for optimal oxygenation

pharm:
- loop diuretics
- morphine

tip:
- L HF d/t fluid output or BV injury -> no elect blood from LV -> LA -> pulmonary BV -> increased pressure -> edema
- injury lung BV d/t uremia -> inflammation, cap leak
- restless, anxiety, crackles base lungs, high fowlers, O2 (increased gas exchange), IV morphine 1-2 mg, decreased myocardial demand, dilate BV

44
Q

CKD interventions to manage adequate cardiac output (2, pharm (2))

A
  • maintain optimal BP
  • monitor weight daily

pharm:
- ACE inhibitors: most effective decrease BP for HTN pts. (adults CKD -> ACE/ARB (improve kidney r/t outcomes)
- calcium channel blockers (increased GFR + BF kidneys)

45
Q

CKD interventions to enhance nutrition (what, 6)

A

nutrition needs and diet restrictions for the patient with CKD vary according to the degree of kidney function and the type of renal replacement therapy used; so refer to consul dietician
- protein restriction
- fluid restriction
- sodium restriction (edema, HF)
- potassium restriction
- phosphorus restriction (start early CKD prevent renal, bone deficit: take at dinner to control phos., pt. education ESKD (limit K
- monitor blood sugar

tip:
- decreased GFR
- protein breakdown -> main cause uremia
- ESKD: high protein diet necessary (replace lost protein)
- increased vitamin daily, water soluble vitamin remove in dialysis, anemia (CKD): decreased iron, protein, EPO (supp. iron)
- CKD -> DM require decreased insulin dose, fail kidney can’t metabolize drug well)
- PD (nutritional needs) -> can’t k+ restrict, K restriction determine by serum k.

46
Q

CKD interventions to prevent infection (4)

A
  • provide meticulous care to any areas where skin is not intact
  • provide preventative skin care to intact areas
  • for patients with ESRD undergoing dialysis, inspect the vascular access site or peritoneal dialysis catheter insertion site every shift for redness, swelling, pain, and drainage
  • monitor vital signs for manifestations of infection
47
Q

CKD interventions to prevent injury (3, pharm (3))

A

(CA/PHOS levels)
- patients with long standing CKD may have brittle, fragile bones that fracture easily and cause little pain
- use lift sheet rather than pulling the patient
- observe for abnormal ROM, unusual surface bumps or depressions over bony areas

pharm:
- calcium supplements
- vitamin D supplements
- phosphate binders

48
Q

CKD interventions to minimize fatigue (3, pharm (3))

A
  • some causes of fatigue in the patient with CKD include vitamin deficiency, anemia, and buildup of urea
  • treat anemia with goal of HgB around 10g/dL
  • monitor diet intake

pharm:
- Erythropoietin
- iron supplements
- vitamin and mineral supplements PRN

49
Q

CKD interventions to reduce anxiety (6)

A
  • evaluate the support systems, such as the involvement of family and friends w/ the patient’s care
  • explain all procedures, tests, and treatments
  • identify the patient’s knowledge needs about kidney disease
  • facilitate discussions w/ family members about the prognosis and the impact on lifestyle
  • provide continuity of care, whenever possible
  • consult social workers or therapy PRN
50
Q

dialysis therapy (2, indications (5))

A
  • supportive strategy to purify blood, substituting for the normal function of the kidney
  • particles are separated from blood based on the different ability to particles to pass through (diffuse) a membrane

indications:
- symptomatic uremia: pericarditis, neuropathy, cognition dysfunction
- persistent or rapidly rising high K levels
- severe metabolic acidosis
- fluid overload that compromises tissue perfusion
- to remove toxins

tip:
- intermittent, continuous, mixed

51
Q

dialysis: vascular access (what, ____ ml/min, usually for?, types for temporary vs. permanent)

A

needed as dialysis requires the easy availability of a large amount of blood flow
- 300-800 mL/min
- usually for a period of 3-4 hours, normal venous cannulation DOES NOT provide this high rate of blood flow

1) temporary/immediate: dialysis catheter (type of central line)
2) permanent: AV fistula, AV graft

52
Q

hemodialysis (HD) (what, delivered over, _______ is used as fluid, machine also monitors)

A

AKA intermittent dialysis
- remove excess fluids and waste products and restores chemical and electrolyte balance. HD involves passing the patient’s blood through an artificial semipermeable membrane to perform the filtering and excretion functions of the kidney
- delivered over 3-5 hours around 3 or 4 times a week (depends how pt. is)
- dialysate
- the machine also monitors the flow of blood while it is outside of the body and alarms are set to monitor safe and effective

53
Q

continuous renal replacement therapy (CRRT) (what, occurs only in ____ d/t ____)

A

type of dialysis also known as HEMOFILTRATION
- alternative method for removing wastes and restoring fluid and electrolyte balance in hospitalized adults with AKI who are too unstable to tolerate the changes in blood pressure that occur with intermittent hemodialysis
- CRRT occurs only in the ICU d/t: need for frequent monitoring and specialized skill set to maintain safety during extracorporeal circulation (blood flow outside the body), need for ongoing replacement of fluid and electrolytes

TIP:
- AKI can’t exist yet
- removes + returns blood over 24 hours
- diffusionL intermittent to remove toxins
- ultra filtration: separation of particles from passage by filtering of very fine pores
- connected transport
- depends on differential diffusion

54
Q

dialysis catheter (what, location, time)

A

specially designed catheter with separate lumens for blood outflow and inflow
- location: subclavian, IJ, femoral vein
- time to initial use: immediately after insertion, XR confirmation of placement

tip:
- dialysis cath: no blood samples
- trained professional for access
- x2 lumens (outflow/inflow), sometimes third lumen for meds, blood, etc.

55
Q

dialysis: AV fistula (what, location, time, adv (3), dis (2))

A

an internal anastomosis of an artery to a vein (surgery)
- location: forearm, upper arm
- time to initial use: 2-3 months or longer

adv:
- lower infection rate
- higher blood flow rates
- lower thrombosis/stenosis rates

dis:
- longer maturation time
- aneurysm formation (d/t repeated needle puncture site loss requires surgical repair)

56
Q

dialysis: AV graft (what, location, time, adv (1), dis (8))

A

synthetic vessel tubing tunneled beneath the skin, connecting an artery and a vein
- location: forearm, upper arm, inner thigh
- time to initial use: 1-2 wks (shorter than fistula)

adv:
- can be used much sooner

dis:
- higher restenosis rates
- higher thombosis rates
- higher infection rates
- pseudoaneuryms
- use when AV fistula can’t develop/complications
- graft: synthetic material for older adults
- most grafts fail d/t increased BF from arteries -> veins
- muscle later react by thickening which occludes BF

57
Q

dialysis: monitoring and caring for AV fistulas or AV grafts (7)

A
  • NO BP readings or USE of the extremity for any venous puncturing
  • check distal pulses and cap refill in the arm with the fistula or graft
  • check for a bruit/thrill
  • encourage routine ROM exercises
  • check for bleeding at insertion site
  • check for signs of an infection at insertion sites
  • TO NOT carry heavy objects or compress the area of the vascular access site

tip:
- NO side sleep d/t vascular access

58
Q

dialysate

A

prescribed by the health care provider as an admixture to restore electrolytes and minerals to normal levels in the blood (neurology)

59
Q

dialysis complications include (6)

A
  • hemolysis, bleeding
  • air embolism
  • dialysate error
  • contamination, infection
  • dysrhythmias
  • hTN
60
Q

post dialysis nursing care (5)

A
  • monitor BP (ortho)
  • promote appropriate pharm therapy (hold til after)
  • weight the patient to comparison w/ pre dialysis weight
  • monitor temp: may be elevated d/t warmer on dialysis machine, infection/sepsis
  • monitor site for bleeding/infection: hold invasive procedures for 4-6H after dialysis

tip:
- assess skin for integrity
- uremia, bleeding risk

61
Q

peritoneal dialysis (PD) (what, adv (3), dis (4))

A

allows exchange of wastes, fluid, and electrolytes to occur in the peritoneal cavity

adv:
- flexible schedule for exchanges
- few hemodynamic changes during and following exchanges
- less dietary and fluid restrictions

dis:
- PD slower than hemodialysis
- protein loss in outflow fluid
- risk for peritoneal injury or peritonitis
- potential discomfort from indwelling fluid

tip:
- CKD can choose hemo/peritoneal
- unstable + no anticoags = peritoneal dialysis
- vascular issues = NO peritoneal dialysis

62
Q

peritoneal dialysis 3 phases

A

1) infusion/fill:
- 1-3L dialysate is infused by gravity (fill) into peritoneal space over 5-10 minutes

2) dwell:
- fluid stays (dwells) in the cavity for a specified time prescribed by the physician (nephrologist)

3) outflow/drain:
- fluid then flows out of the body (drains) by gravity into a drainage bag
- peritoneal outflow contains the dialysate + excess water, electrolytes, nitrogen-based waste products (AKA peritoneal effluent) -> colorless/straw colored, blood -> new PD cath only

63
Q

peritoneal dialysis complications include (5)

A
  • pertonitis: cloudy, opaque fluid
  • pain: flow dialysate (common, x1 week), cold increases discomfort, no microwave, check clamps, inflow/outflow reposition Q2H, supine/low fowlers decrease abd. pressure)
  • dialysate leakage: increased pressure, clear from cath, 1-2 wks. to tolerate 1-2 L (d/t obese, DM, LT steroid, therapy -> most likely leakage)
  • bleeding
  • bowel perforation

tip:
- no brown drain fluid (bowel perforation)

64
Q

post-peritoneal dialysis nursing care (6)

A
  • monitor VS compare to baseline
  • weight the patient for comparison with pre-PD weight
  • monitor electrolytes and glucose
  • assess dressing around PD site for bleeding or wetness
  • observe effluent (drain fluid)
  • observe the outflow flow rate (obstruction, reposition)
65
Q

kidney transplant (what, candidate)

A

1) life sustaining treatment for ESRD; NOT CONSIDERED A CURE
2) candidate selection criteria:
- must be free of medical problems that might increase risk from the procedure
- usual age range 2-70 years
- excluded diseases: uncorrectable cardiac disease, metastatic cancer, acute/chronic infection, severe psychosocial problem

66
Q

kidney transplantation donors (what, 3 types)

A

1) can be from living donors (related/unrelated), non-heart-beating donots (NHBD) and cadaveric donors
- NHBDs are person declared dead by cardiopulmonary criteria. kidneys from NHBD are removed (harvested) immediately after death
- if immediate removal must be delated, organ is preserved by infusing a cool preservation solution into the abdominal aorta after death is declared and until surgery can be performed (gift of life)
- cadaveric donors: people who suffer irreversible brain injury. maintained w/ mechanical ventilation and must have sufficient perfusion for the kidneys to remain viable

67
Q

pre-op nursing care (what, important to know (5)

A

immunologic studies are needed because the major barrier to transplant success after a suitable donor kidney is available the the body’s ability to reject “foreign” tissue
- includes simple blood typing and human leukocyte antigen (HLA) studies, as well as other tests
- teach about procedure and post-op care
- perform an in-depth patient assessment
- coordinate all the diagnostic testing
- dialysis 24 hours post surgery

68
Q

post-op nursing care (6)

A
  • monitor for rejection symptoms
  • monitoring for bleeding
  • evaluate kidney function and assess urine, accurate intake and output (decreased U/O -> AKI, thrombosis, obstruction)
  • maintain good care of urinary catheter care
  • give immunosuppressant drug therapy
  • monitor daily weights

tip:
- catheter, decompression bladder, continuous irrigation -> decreased clots, cath care
- decrease CAUTI -> remove cath ASAP (305 days post surgery)
- urine color: pink d/t surgery resolves within days

69
Q

kidney transplant rejection (what, 3 types, diagnosis (3))

A

rejection is the most serious complication of transplantation and is the leading cause of graft loss

3 types of rejection: days-wks progression
1) hyperacute
2) acute: most common with kidney transplant (immunosuppression therapy, reversible)
3) chronic

diagnosis:
- by manifestations
- CT, Renal scan
- kidney biopsy

70
Q

immunosuppressive drug therapy (3)

A
  • combinations of corticosteroids and medications specifically developed to affect the action of lymphocytes are used to minimize the body’s reaction to the transplanted organ
  • treatment with combinations of new agents has dramatically improved survival rates, and now 90-95% of transplanted kidneys still function after 1 year
  • the patient will require to take some form of immunosuppressive therapy for the entire time that they have the transplanted kidney

NUR 3020 exams (11 decks)

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