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;
44 Cards in this Set
- Front
- Back
|
what is polycystic kidney disease?
|
congenital disorder.
-fluid-filled cysts develop in nephrons -dominant form- few nephrons have cysts until 30's -recessive form-100% nephrons have cysts from birth -cysts develop anywhere in nephron from cell division, altered secretion, abn cell matrix biology -usually collects in ducts -become larger over time and widely distributed -damage glomerular and tubular membranes -risk for rupture, infection, bleeding -pts have high BP (renal ischemia) -may reduce liver function -possible bleeding into brain |
|
|
etiology of PKD
|
autosomal dominant pkd (adult form)-one parent w/ gene
-adpkd1-more severe form -adpkd2-slower rate of cystic formation autosomal recessive pkd-less common- both parents have gene, poor prognosis-usually die in childhood -no way to prevent pkd can slow progression through HTN mgt -more common in white ppl |
|
|
key features of PKD
|
abdominal or flank pain-usually first manifestation
HTN nocturia inc abd girth (distended) palpate lightly constipation bloody/cloudy urine kidney stones freq. UTIs proteinuria (once glomeruli involoved) As renal function further declines, pt has increasing HTN, edema, uremic problems: anorexia, N/V, pruritus, fatigue sharp intm pain-rupture or stone red urine-rupture |
|
|
lab findings w/ PKD
|
proteinuria
hematuria bacteruria elevated BUN, crt (as kidney function deteriorates) dec GFR small cysts per US, CT, MRI |
|
|
Nursing Dx for PKD
|
-Acute pain r/t cyst rupture/stone
-chronic pain r/t enlarging kidneys compressing abd contents -constipation r/t compression of intestinal tract -risk for infection r/t presence of cysts and dec renal blood flow -potential for HTN -potential for stone formation -potential for renal failure |
|
|
Nursing Intv for PKD
|
pain mgt-caution w/ NSAIDS, no ASA
-UTI-Bactrim, septra, trimpex, cipro -apply dry heat to abd or flank for comfort -monitor crt levels (antib can be nephrotoxic) -severe pain- cysts reduced by percutaneous needle aspiration and drainage -enhance relaxation techniques -drink at leat 2L fluid/day -avoid dehydration, constipation -lower Na in diet HTN mgt-ACE, Ca blockers, beta blockers, vasodilators -exercise-avoid potential renal trauma ESRD-r/t HTN, lupus, diabetic pts by age 60: 50% inc risk: men, adpkd pts, htn, women w/ >3 preg healthy lifestyle-no contact sports |
|
|
Problems that obstruct urine outflow
|
hydronephrosis, hydroureter, urethral stricture
|
|
|
hydronephrosis
|
kidney enlarges
-kidney pressure increases-blood vessels and renal tubules can be damaged. Drainage impaired normal renal pelvis capacity: 5-8 ML |
|
|
hydroureter
|
obst of ureter
-ureter dilation occurs above obst |
|
|
urethral stricture
|
obst very low in urinary tract, causing bladder distention before hydroureter and hydronephrosis.
|
|
|
when does urinary obst cause damage?
|
when pressure builds up directly on tissue. tubular filtrate pressure also increases in the nephron as drainage through the collection system is impaired. GFR decreases or ceases and renal failure results
|
|
|
causes of hydronephrosis or hydroureter include
|
tumors, stones, trauma, congenital structural defects and fibrosis. in pts w/ cancer-from pelvic radiation or surgical intv.
|
|
|
assessment for urinary obst
|
flank pain, fever
UTI, BUN, crt incr, GFR dec -dilation of ureters/renal pelvis Hx: childhood urinary tract problems -pattern of urination-color, amt, freq, clarity, odor -ask about recent flank/abd pain -chills, fever, malaise (w/ UTI) -inspect each flank for asymm (renal mass) -gently palpate abd-locate ares of tenderness -palpate and percuss the bladder to detect distention UA-bact, WBC w/ infection tubular epithelial cells-prolonged obst -blood chemistries normal unless decreased GFR . -IV urography -shows dilation US, CT-urine obst |
|
|
priority problems for urinary obst
|
urinary retention and infection
urinary retention-privacy, crede maneuver, double-voiding technique, insert urinary cath, monitor degree of bladder distention, catheterize for residual, intm cath as app urologic intv-stricture due to stone-can be located and retrieved using cystoscopic or retrograde pyelogram procedures. radiologic intv-when stricture is causing hydronephrosis and cannot be corrected w/ urologic procedures, a nephrostomy is performed. diverts urine externally. |
|
|
nephrostomy care
|
-npo, clotting studies, mod sedation
-pt in prone position, cath in renal pelvis,ext end connected to drainage bag. Immediately relives the pressure in the kidneys, nephrostomy tube remains in place until blockage resolved. follow-up care: assess amt of drainage in bag hourly tube may be disloged or clogged if amt suddenly decreases/pt has back pain-call dr. -monitor site for leakage or urine/blood. -urine drainage red tinged for first 12-24 H after procedure, should gradually clear. Assess pt for manifestations of infection, including fever, urine character change. |
|
|
pyelonephritis?
|
bacterial infection in kidney & renal pelvis, causes inflamm, inc WBCs
--acute or chronic -scarring can occur upon healing, may lead to decreased renal function acute-active bacterial infection (contamination of urethra, instruments, pregnancy, obst)usually brief, may lead to bacteremia, more diff to eradicate than bladder mucosal infections chronic-repeated/continued upper urinary tract infections, vesicoureteral urine reflex -bact enter renal pelvis-inflammation, inc WBCs. -scarring may occur upon healing; can lead to decreased renal function possible abscess formation-capsule, cortex, medulla -reflux of infected urine responsible for most chronic pyelonephritis can occur when some papillae don't close properly. |
|
|
clinical manifestations of acute pyelonephritis
|
-high fever
-chills -nausea -flank pain on affected side -headache -muscle pain -tenderness upon percussion -dysuria, freq, urgency for days -urine:blood, foul smelling, WBCs, pus, casts tachycardia, tachypnea malaise chronic-HTN, inability to conserve Na, nocturia, hyperkalemia, acidosis |
|
|
diagnostics of pyelonephritis
|
C&S-shows bacterial species, any resistance to antibiotics
UA- +leukocyte esterase, nitrite, WBCs, bacteria cytourethrogram-define urinary tract structures and ID any defects (stones, tumor, urine reflux) c-reactive protein erythrocyte sedimentation rate KUB/IVP-stones, obst |
|
|
collaboration mgt in pyelonephritis
-goals, antib therapy |
goals-eliminate pathogens, remove cause of decreased host resistance
antibiotic therapy- sufa or sulfa w/ trimethoprim, cipro or levaquin, gentamycin w/ or w/o ampicillin, 3rd generation cephalosporins may be used. unasyn, macrodantin. OP require 2 wks of tx, follow-up urine culture done. increase fluid intake 2-3 L/day possible surgical mgt-pyelolithotomy (remove lg stone) nephrectomy, ureteral diversion. |
|
|
renal absccess
|
collection of fluid/cells r/t inflammation response to bacteria.
Can occur in kidney tissue, gerota's fascia or flank. Dx by CT, fever not relieved by antobiotics manifestaions-fever, flank pain, gen. malaise, possible edema/redness drainage by incision, needle aspiration broad spectrum antibiotic |
|
|
renal tuberculosis
|
myobacterium TB reaches kidney, via bloodstream from another source in body. Inflammation resp triggered and forms scar tissue (granuloma) replaces normal kidney tissue.
-clinical manifestations: early disease involves cortex/medulla -symptoms of cystitis (freq, dysuria, hematuria, proteinuria,renal colic,flank pain w/ passage of clots, stones, pyuria, htn) -growth of TB in urine confirms Dx.(3 clean catches) -Treated with combination of meds (antitubercular therapy 2 months: rifampin, soniazid, purazinamide) comps: renal failure, kidney stones, obst, bact superinfection |
|
|
renal candidias
|
increasing in women w/ diabetes
clinical manifestations: -progressive oliguria alternating w/ diuresis -ureter colic -pyuria -progressive renal failure -fungi noted in urine cultures meds -amphotericin: requires close monitoring to prevent toxicity |
|
|
renal cancer
|
most all renal tumors are malignant
-occurs 2:1 in men ages 50-70 -possible link to smoking and chemicals -lungs common site of metastasis |
|
|
manifestations of renal cancer
|
palpable abd mass may be first symptom
triad of symptoms: -hematuria (late sign) -dull flank pain -flank mass other symptoms: -wt loss, anemia, fatigue, fever |
|
|
diagnostics for renal cancer
|
explore renal mass: IVP, US, CT, MRI
Renal biopsy H/H decreased UA: possibly RBCs, increased calcium, inc erythrocyte sed rate, incadrenocorticotropic hormone, parathyroid hormone, corisol |
|
|
collaborative mgt of renal cancer
|
staging of tumor-4 stages
coms-metastasis, urinary obst. radiation therapy, radiofrequency ablation during MRI. chemotherapy-limited effects. Use of biological resp. modifiers incr survival time. immunotherapy |
|
|
surgical mgt for renal cancer
|
nephrectomy-blood loss is a concern
may give blood/fluids before thoraco-lumbar incision used; lap approach may be used complications: -hemorrhage -atelectasis/pneumonia thromboembolism post-op assessment: VS, npo 24-48 H urine output, bleeding (may appear distended), pneumothorax, ileus an acceptable UO is 30-50 ML pain mgt: -pca, epidural- 3-5 days -splint incision during respiratory exercises |
|
|
renal trauma
|
concern in penetrating wounds, blunt injuries (85%)
minor-contusions (bruising), sm lacerations (falls, sports, blows to back) major-laceration to cortex, medulla, A/V-extensive bleeding (abd, back, flank wounds, gunshots, knife, MVA) pedicle- laceration/disruption of renal A/V-extensive bleeding, rapid, emergent (breaks in renal artery, vein) H/H decreases w/ blood loss diagnostics: IV urography, CT, VS q 10-15 minutes, UO hourly (should be greater than 25-30 ml/hr) -possible nephrectomy/partial IV dopamine promotes renal perfusion possibly may need vitK and platelets, fluids |
|
|
nephrosclerosis
|
thickening and narrowing in the sm arteries and arterioles in the nephron
-renal blood flow decreases -kidney becomes hypoxic; ischemia occurs -associated with HTN, diabetes, atherosclerosis -rarely seen when BP consistently below 160/110. treatment goals: control HTN, preserve renal function |
|
|
renal artery disease
|
cause: atherosclerosis or FMD
-if untreated, cause ischemia or renal atrophy -decreased renal blood flow -suspected w/ sudden onset of HTN w/ no family Hx. Tx: anti-HTN, balloonangioplasty, renal artery bypass surgery. key features: diff to control BP, elevated crt, dec crt clearance |
|
|
diabetic nephropathy
|
pathologic change in kidney that reduces kidney function and leads to renal failure.
microvascular complication of DM -persistent albuminuria (1st symp) pt may require less insulin risk factors: 10-15yrs diabetic, diabetic retinopathy, poor BS control, uncontrolled HTN. chronic high BP causes HTN in kidney vessels. Vessels become leaky, allows filtration of lg particles forming deposits that narrow vessels. |
|
|
stages of diabetic renal disease
|
stage 1: kidney size increases, GFR increase reversible (at dx of DM)
stage 2: microscopic changes loss of filtration surface area, glomerulosclerosis (2-3 yrs after dx) stage 3: microalbuminura, GFR dec or normal (7-15 yrs after Dx) stage 4: albuminuria, GFR dec, HTN stage 5: GFR decreases to 10 ml/min |
|
|
uncorrected renovascular diseases such as renal artery stenosis, atherosclerosis, or thrombosis causes what?
|
ischemia and atrophy of renal tissue
|
|
|
glomerulonephritis
|
3rd leading cause of ESRD
-variety of diseases caused by immunologic rxn -result:inflammatory changes in glomerulus -may have primary or secondary cause |
|
|
glomerulonephritis causes
|
primary-AGN
-post-infectious glomerulonephritis group a beta-hemolytic strep secondary causes-due to systemic disease -diabetic nephropathy -SLE (lupus) -goodpasture's |
|
|
pathophysiology of AGN
|
an immunologic disorder:
inflammation & increase cells in glomeruli in both kidneys triggered by: disease, immunologic rxns antigen-antibody complexes trapped in glomerulus protein leaks through glomeruli-proteinuria inflammation of glomeruli leads to hematuria |
|
|
clinical manifestations of AGN
|
hematuria
proteinuria fever chills N/V generalized edema (facial, periorbital) HTN headache oliguria |
|
|
Diagnostic Findings in AGN
|
UA
-fixed specific gravity -proteinuria -WBC's -RBC's -dark, smoky color -low pH elevated BUN & crt, dec GFR decreased Crt clearance dec Hgb & Hct |
|
|
collaborative mgt in AGN
|
reduce inflammation:
-plasmapherisis (removal and filtering of plasma to eliminate antibodies) -steroids maintain fluid & lyte balance: -diuretics -anti-HTN agents -restriction of dietary Na & H20 maintain rest prevent imp skin integrity |
|
|
chronic glomerulonephritis
|
develops over 20-30 yrs or longer
cause usually unknown -mild proteinuria, hematuria, HTN, occasional edema changes in the renal tissue result from HTN, infections, inflammation, or alt metb and poor blood flow to kidneys. -loss of nephrons reduces GFR. HTN and renal arteriole sclerosis are often present. this damage allows urine to enter urine. eventually leads to renal failure. |
|
|
nephrotic syndrome
|
condition of increased glomerular permeability resulting in:
-proteinuria -hypoalbuminemia (serum alb <3G/DL) -edema -hyperlipidemia -incr susceptibility to infection coagulation -HTN (renin-angiot-aldos cycle as a result of ECF to interstitial shift of fluids) |
|
|
goals of tx:
nephrotic syndrome |
-heal leaking basement membrane, halt loss of protein in urine, eliminate edema
interventions: -reduce inflammation: steroids -prevent thrombosis: anticoagulants -minimize protein loss: incr protein intake (1gm/kg/day), albumin-to raise oncotic pressure maintain fluid and lyte balance |
|
|
nephrotic syndrome: maintaining fluid/lyte balance
nursing interventions |
daily weights
strict I & O mild NA restricted diet meticulous skin care administration of diuretics -loop, thiazide, k sparing, osmotic |
|
|
diuretic therapy
|
loop: Lasix, bumex, edecrin
-act on ascending loop of henle to inhibit Na & water reabsorption thiazid: Diuril, hydrodiuril, hygroton, zaroxlyn -inhibit Na reabsorption in ascending loop and decrease h20 reabsorption -less potent than loop diuretics k-sparing: aldactone, dyrenium, midamor -blocks Na and K exchange in distal tubule casuing Na and water retention osmotic: mannitol -expands intravascular volume and increases GFR; decreases Na and water reabsorption |
