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Adult Health > AH1 Exam 3 Urinary/Renal > Flashcards

AH1 Exam 3 Urinary/Renal Flashcards

1
Q

10^5 CFU/mL

A

clinically significant UTI, symptoms arise at 10^2-10^3

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2
Q

typically identified as the causative microorganism for UTI associated with broad spectrum antimicrobial antibiotic therapy or indwelling catheter

A

candida albicans

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3
Q

fever, chills, and flank pain

A

indicated UTI in upper urinary tract (involving renal parenchyma, pelvis, and ureters)-pyelonephritis

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4
Q

inflammation of renal parenchyma and collecting system

A

pyelonephritis

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5
Q

inflammation of the bladder wall

A

cystitis

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6
Q

inflammation of the urethra

A

urethritis

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7
Q

A UTI that has spread into the systemic circulation and is a life threatening condition requiring emergency treatment

A

Urosepsis

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8
Q

infections that occur in an otherwise normal urinary tract and usually only involve the bladder

A

uncomplicated UTI

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9
Q

infections with coexisting presence of obstruction, stones, or catheters, existing diabetes or neurologic disease, pregnancy induced changes, of a recurrent infection

A

complicated UTI

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10
Q

complications associated with a complicated UTI

A

pyelonephritis, urosepsis, and renal damage

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11
Q

term for a UTI due to original infection not being eradicated

A

unresolved bacteriuria or bacterial persistance

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12
Q

Lower ________ levels cause vaginal atrophy, a decrease in vaginal lactobacilli, and an increase in vaginal pH

A

estrogen
Giving women low dose intravaginal estrogen replacement acidifies the vagina and may be effective in treating recurrent UTI

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13
Q

dysuria, frequent urination (+than q2h), urgency, and suprapubic discomfort or pressure
Urine may have blood or sediment

A

LUT (lower Urinary Tract) infection

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14
Q

nonspecific symptoms of UTI

A

fatigue, anorexia

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15
Q

characteristic symptoms of UTI are often absent in which population?

A

older adults who instead experience non localized abdominal discomfort, cognitive impairment, or generalized clinical deterioration

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16
Q

diagnostic study that identifies presence of nitrates, WBCs, and leukocyte esterase in urine

A

dipstick urinalysis

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17
Q

an enzyme present in WBCs that indicates pyuria

A

leukocyte esterase

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18
Q

a voided midstream technique yielding a clean catch urine sample is preferred for obtaining which diagnostic test?

A

urine culture

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19
Q

what do you do with urine after collecting it?

A

refrigerate it immediately!! and it should be cultured w/in 24 hrs of collection

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20
Q

two tests used when obstruction of the urinary system is suspected of causing UTI

A

intravenous pyelogram (IVP)
Cytoscopy
Renal ultrasound is preferred urinary tract imaging technique if recurrent UTI, bc it is noninvasive, easy to perform, and relatively inexpensive

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21
Q

Uncomplicated UTI antibiotics

A

Bactrim, Septra (trimethoprim-sulfamethoxazole)
Nacrodantin, Macrobid (nitrofurantoin)
short-term 1-3 days

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22
Q

Antibiotics 7-14 days or longer
Bactrim or Macrobid
Ampicillin, amoxicillin, first gen cephalosporin, fluoroquinolone
consider 3-6 mons trial of suppressive or prophylactic antibiotic regimen
consider post coital antibiotic prophylaxis (Bactrim, Macrobid, or Cephalexin)
adequate fluid intake

A

Complicated UTI treatment

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23
Q

Nitrofurantoin (Macrodantin, Macrobid) patient teaching

A

avoid sunlight, notify HCP if fever, chills, cough, chest pain, dyspnea, rash or numbness or tingling of fingers or toes develops

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24
Q

debilitated persons, older adults, patients who are immune compromised due to co-morbid disease (CA, HIV, DM), and patients treated with immunosuppressive agents or corticosteriods

A

Are at increased risk of UTI

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25
Q

hyper/hypothermia, decreasing BP, rapid pulse and RR, warm flushed skin

A

report to HCP as these may indicate septic shock r/t urosepsis

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26
Q

benefits of increased fluid intake during UTI, pyelonephritis

A

fluids will increase frequency of urination at first, but will also dilute the urine, making the bladder less irritable. Fluids will help flush out bacteria before they colonize in the bladder.

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27
Q

Caffeine, alcohol, citrus juices, chocolate, and highly spiced foods or bevs

A

should be avoided during UTI as they are irritating to the bladder

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28
Q

nonpharmacological relief of UTI

A

heating pad, warm shower, sitz bath

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29
Q

commonly starts in renal medulla and spreads to renal cortex

A

pyelonephritis

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30
Q

mild fatigue, sudden onset of chills, fever, vomiting, malaise, flank pain, and the LUTs of cystitis (dysuria, urgency, frequency).
Costovertebral tenderness is usually present on the affected side
these manifestations usually subside within a few days (even without treatment) but bacteriuria and pyuria persist

A

Acute pyelonephritis

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31
Q

CBC shows leukocytosis and a shift to the left with an increase in immature neutrophils (bands)

A

acute pyelonephritis

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32
Q

kidneys have become small, atrophic, and shrunken and have lost fxn owing to scarring or fibrosis. Usually the outcome of recurrent infections of upper urinary tract

A

Chronic pyelonephrits (AKA interstitial nephritis, chronic atrophic pyelonephritis, or reflux nephropathy)

*if both kidneys are involved, often progresses to ESRD

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33
Q

how do you diagnose chronic pyelonephritis?

A
  • radiologic imaging-indicate small, contracted kidney with thinned parenchyma; collecting system may be small or hydronephrotic
  • histologic testing-
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34
Q

trichomona, monilial infection, chlamydial infection and gonorrhea

A

typical causes of urethritis

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35
Q

trimethoprim/sulfamethoxazole and nitrofurantoin

A

drugs for bacterial infections of urologic origin

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36
Q

Flagyl and Mycelex

A

treat Trichomonas

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37
Q

nystantin (Mycostatin), Diflucan

A

monilial infections

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38
Q

doxycycline (Vibramycin)

A

chlamydial infection

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39
Q

teach patients with sexually transmitted urethritis to refer their sexual partner(s) for evaluation and testing if they have had sexual contact in the last ____ days

A

60

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40
Q

the result f obstruction and subsequent rupture of the periurethral glands into the urethral lumen with epithelization over the opening of the resulting periurethral cavity

A

urethral diverticula (mostly occurs near Skene’s glands which are the largest and most distal glands along the urethra)

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41
Q

dysuria, post void dribbling, frequent urination, urgency, suprapubic discomfort or pressure, dyspareunia, and a feeling of incomplete bladder emptying; urinary incontinence is common; urine may contain gross hematuria and sediment (cloudy); an anterior vaginal wall mass may be noted on physical exam and the mass may be tender and expel purulent discharge through urethra when palpated.

A 
urethral diverticula (1:4 women will have no symptoms)
Voiding Cystourethrography (VCUG)
UA, MRI to determine size of diverticulum
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42
Q

condition suspected whenever a pt experiences symptoms of a UTI but tests are neg for bacteria or pyuria

A

IC/PBS

Interstitial Cystitis/Painful Bladder Syndrome:

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43
Q

avoid acidic foods: citrus, aged cheese, nuts, vinegar, curries, hot peppers +tea, coffee, alcohol, soda
take calcium phosphorus supplements

A

bladder irritating foods and dietary recommendations (esp for IC/PBS)

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44
Q

Elavil and Aventyl are used to decrease burning pain and urinary frequency
Pentosan (Elmiron) is only oral agent approved for tx of IC-enhances protective effects of glycosaminoglycan layer of the bladder
drugs do not provide immediate relief!!** for that, give opioid analgesics!
instill Dimethylsulfoxide (DMSO) directly into bladder to desinsitize pain receptors in the bladder wall.
Heparin and hyaluronic acid may also be instilled in bladder
Instillations are often administered with Lidocaine
Bacille Calmette-Guerin is an attenuated form of Mycobacterium bovis, and is another common tx.

A

medication mgmt IC/PBS

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45
Q

affects both kidneys equally and is the third leading cause of renal failure in US

A

glomerulonephritis

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46
Q

SLE, systemic sclerosis (scleroderma), streptococcal infection

A

common causes of glomerulonephritis

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47
Q

accumulation of antigen, antibody, and complement in the glomeruli:
Anti-GBM antibodies
lumpy bumpy deposits in renal tissue

A

glomerulonephritis

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48
Q

hematuria and urinary excretion of RBCs, WBCs, and casts. Proteinuria, and elevated BUN/Cr

A

clinical manifestations of glomerulonephritis

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49
Q

develops 5-21 days after infection of the tonsils, pharynx, or skin (streptococcal sore throat, impetigo) (group A beta hemolytic strep)

A

Acute Poststreptococcal glomerulonephritis-due to complement clogging glomerulus

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50
Q

generalized body edema, hypertension, oliguria, hematuria with a smoky or rust appearance (indicative of bleeding in upper urinary tract), and proteinuria. Fluid retention (due to decreased glomerular filtration); abdominal or flank pain possible

A

Acute Poststreptococcal glomerulonephritis-

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51
Q

an immune response to streptococcus is usually demonstrated by assessment of

A 
ASO titers (antistreptolysin-O)
which will reflect a decrease in complement componenets of C3 and CH50
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52
Q

renal biospy

A

to confirm Acute Poststreptococcal glomerulonephritis-

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53
Q

erythrocyte casts are usually indicative of __________ if found in dipstick urinalysis

A

Acute Poststreptococcal glomerulonephritis-

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54
Q

rest (address proteinuria, hematuria), sodium and fluid restriction (to address edema), diuretics (to address edema), anti-HTN therapy, adjustment of dietary protein (if BUN is elevated-to decrease nitrogenous waste in urine)

A

tx for Acute Poststreptococcal glomerulonephritis-

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55
Q

a cytotoxic autoimmune disease characterized by the presence of circulating antibodies against glomerular and alveolar basement membrane

A

Good Pasture Syndrome-seen mostly in young male smokers

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56
Q

flulike symptoms with pulmonary symptoms of cough, milk SOB, hemoptysis, crackles, rhonchi, and pulmonary insufficiency. hematuria, weakness, pallor, anemia, and renal failure

A

clinical manifestations of Good Pasture’s Syndrome

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57
Q

corticosteroids, immunosuppressive drugs (Cytoxan, Imuran), plasmapheresis, and dialysis

A

tx for good pasture syndrome, rapidly progressive glomerulonephritis

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58
Q

HTN, edema, proteinuria, hematuria, and RBC casts

A

rapidly progressive glomerulonephritis

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59
Q

proteinuria, hematuria, and slow development of uremia

A

Chronic glomerulonephritis: protein and phosphate restrictions may slow disease progression

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60
Q

when the glomerulus is excessively permeable to plasma protein, causing proteinuria that leads to low plasma albumin and tissue edema

A

Nephrotic Syndrome

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61
Q

peripheral edema, massive proteinuria, HTN, hyperlipidemia, hypoalbuminemia, decreased serum albumin, decreased total serum protein, and elevated serum cholesterol; hypocalcemia, blunted calcemic response to parathyroid hormone, hyperparathyroidism, and osteomalacia

A

Nephrotic Syndrome

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62
Q

What causes hyperlipidemia?

A

the diminished plasma oncotic pressure from the decreasaed serum proteins (nephrotic syndrome) stimulates hepatic lipoprotein synthesis–>hyperlipidemia

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63
Q

nephrotic proteinuria (nephrotic syndrome) leads to

A

loss of clotting factors resulting a hypercoagulable state

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64
Q

serious complication of nephrotic syndrome

A

hypercoagulability with thromboembolism

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65
Q

ACEI’s, NSAIDS, low sodium, low protein

if severe, consider corticosteriods and cyclophosphamide

A

tx for nephrotic syndrome

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66
Q

Nursing interventions r/t edema

A

weight pt daily, monitor I&Os, measure abdominal girth or extremity size

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67
Q

risk for imbalanced nutrition: less than body requirements

A

nephrotic syndrome from excessive loss of protein in the urine. serve small, frequent meals in a pleasant setting

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68
Q

struvite

A

stones assoc with UTI (magnesium ammonium phosphate)

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69
Q

abnormalities that result in increased urine levels of calcium, oxaluric acid, uric acid, or citric acid

A

metabolic risk factors for the development of urinary tract calculi

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70
Q

large intake of dietary proteins that increases uric acid excretion
excessive amounts of tea or fruit juices that elevate urinary oxalate level
large intake of calcium and oxalate

A

dietary risk factors for the development of urinary tract calculi

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71
Q

abdominal or flank pain, hematuria, and renal colic

A

clinical manifestations of urinary stones

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72
Q

sardines, herring, mussels, liver, kidney, goose, venison, meat soups, sweetbreads

A

foods high in purine (avoid if uric acid stones)

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73
Q

milk, cheese, ice cream, yogurt, all beans except green beans, lentils, fish with fine bones (sardines, kippers, herring, salmon), dried fruits, nuts, ovaltine, chocolate, cocoa

A

food high in calcium (avoid if calcium stones)

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74
Q

drak roughage, spinach, rhubarb, asparagus, cabbage, tomatoes, beets, buts, celery, parsley, runner beans, chocolate, cocoa, instant coffee, ovaltine, worcestershire sauce, tea

A

food high in oxalate

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75
Q

all voided urine should be strained through gauze or urine strainer

A

pts with urinary stones

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76
Q

hypertension, hematuria, feeling of heaviness in the back, side or abdomen, chronic pain, bilateral, enlarged kidneys are palpable

A

polycystic kidney disease, a hereditary renal disease characterized by a cortex and medulla filled with large, thin walled cysts that enlarge and destroy surrounding tissue by compression.

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77
Q

which type of urinary incontinence is more common in men?

A

overflow incontinence

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78
Q

which types of urinary incontinence are more common in women?

A

stress and urge incontinence

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79
Q

urinary leakage and post void dribbling

A

overflow

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80
Q

normal PVR (post void residual)

A

50-75 mL

repeat measurement if you get a finding over 100mL

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81
Q

Abnormal PVR in older client

A

> 200mL obtaining on two separate occasions and will require HCP attention

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82
Q

urinary retention is caused by two different dysfunctions of the urinary system:

A

1) bladder outlet obstruction (enlarged prostate)
2) deficient detrusor (bladder) muscle contraction strength (caused by childbirth, DM, overdistention, chronic alcoholism, anticholinergics)

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83
Q

sudden increase in intrabdominal pressure causes involuntary passage of urine (coughing, laughing, sneezing, heavy lifting, exercising

A

Stress Incontinence

tx: Kegels, weight loss if obese, cessation of smoking, topical estrogen

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84
Q

condition occurs randomly when involuntary urination is preceded by urinary urgency. Overactive bladder, nocturnal frequency and incontinence are common

A

urge incontinence
Treat underlying cause
bladder retraining with urge suppression, decrease in dietary irritants, bowel regularity, and kegels
administer anticholinergics, CCBs, or Tofranil at bedtime

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85
Q

what causes urge incontinence?

A

uncontrolled contraction or overactivity of detrusor muscle (CNS d/os, CVA, alzheimers, brain tumor, parkinsons, interstitial cystitis)

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86
Q

condition occurs when the pressure of urine in overfull bladder overcomes sphincter control; bladder remains distended and is usually palpable

A

overflow incontinence
urinary catheterization to decompress bladder
implement Crede or Valsalva maneuver
alpha blockers Cardura, Flomax
bethanechol to enhance bladder contractions

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87
Q

what causes overflow incontinence?

A 
bladder or urethral outlet obstruction or underactive detrusor muscle caused by myogenic or neurogenic causes (herniated disc, diabetic neuropathy)
may occur after anesthesia and surgery
neurogenic bladder (flaccid type)
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88
Q

condition occurs when no warning or stress precedes periodic involuntary urination.

A

Reflex Incontinence
Treat underlying cause
bladder decompression to prevent ureteral reflux and hydronephrosis
intermittent self cath
diazepam and baclofen to relax external sphincter
prophylactic antibiotic

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89
Q

What causes Reflux incontinence?

A

spinal cord lesion above S2 interferes with CNS inhibition resulting in detrusor hyperreflexia and interferes with pathways coordinating detrusor contraction and sphincter relaxation

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90
Q

loss of urine resulting from cognitive, functional or environmental factors

A

functional incontinence

modifications of environment or care plan that facilitate regular, easy access to toilet and promote patient safety

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91
Q

penile compression device

A

must be released hourly to void

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92
Q

drugs to decrease bladder spasms

A

oxybutynin or other oral antispasmodics or belladonna and opium

93
Q

irrigating a nephrostomy tube

A

no more than 5mL sterile saline solution at one time to prevent overdistention of the kidney; infection and kidney stones are complications assoc with nephrostomy tubes

94
Q

inserting a urethral catheter q3-5h; somtimes only twice a day to measure residual volume and to ensure empty bladder

A

intermittent catheterization

95
Q

how frequently do you change a catheter?

A

q7days

96
Q

most common cause of acute kidney injury

A

acute tubular necrosis

97
Q

most common cause of chronic kidney disease

A

diabetic nephropathy

98
Q

diagnostic criteria for acute kidney disease

A

acute reduction in urine output and/or elevation in serum Cr

99
Q

diagnostic criteria for CKD

A

GFR 3mos and/or kidney damamge > 3mos

100
Q

Kidney failure results in an inability to excrete ______ and ____ as well as contributing to disturbances of all body systems

A

metabolic waste and water

101
Q

an accumulation of nitrogenous waste products (urea nitrogen and creatinine) in the blood

A

azotemia

102
Q

AKI develops over hours or days with progressive elevations of ____, ______, and _____

A

BUN, Creatinine, and potassium

103
Q

factors external to the kidneys that reduce systemic circulation causing a reduction in renal blood flow, and lead to decreased glomerular perfusion and filtration of the kidneys.

A

Prerenal causes of AKI

hypovolemia, decreased CO, Decreased PVR, decreased renovascular blood flow

104
Q

Why might renovascular blood flow diminish?

A

bl renal vein thrombosis
embolism
hepatorenal syndrome
renal artery thrombosis

105
Q

Prerenal azotemia results in

A

a reduction in the excretion of sodium (less than 20 mEq/L) increased salt and water retention, and decreased urine output due to activation of angiotensin II, aldosterone, NE, and ADH

106
Q

Prerenal conditions account for many cases of

A

intrarenal AKI bc if the decreased perfusion persists for an extended period of time, the kidneys lose their ability to compensate and damage to renal tissue occurs

107
Q

What damages intrarenal function?

A

prolonged ischemia, nephrotoxins (aminoglycoside antibiotics, contrast medium), hemoglobin released from hemolyzed RBCs, or myoglobin released from necrotic muscle cells

Primary renal disease such a acute glomerulonephritis, acute tubular necrosis, or SLE may also cause AKI

108
Q

Most common cause of intrarenal AKI

A

Acute tubular necrosis

109
Q

what causes Acute tubular necrosis?

A

ischemia, nephrotoxins, or sepsis

110
Q

what causes postrenal causes of AKI?

A 
mechanical obstruction in the outflow of urine
BPH
bladder CA
Calculi formation
neuromuscular d/o
prostate CA
spinal cord disease
strictures
trauma to back, pelvis, or perineum
111
Q

Where does the urine goes if obstructed?

A

it refluxes into renal pelvis, impairing kidney fxn

112
Q

kidney dilation

A

hydronephrosis (due to BL ureter obstruction and urine builds up in renal pelvis)

113
Q

phases of AKI

A

oliguria-high urine specific gravity, hyperkalemia, hypervolemia *give only enough fluids in oliguric phase to replace losses (400-500mL/24hrs)
diuretic (low urine specific gravity (<1.020g/mL), hypokalemia, hypovolemia
recovery: everything returns to normal

114
Q

RIFLE standardizes the diagnosis of AKI

A

Risk (serum Cr increases X1.5 or GFR decreased by 25%
Injury CrX2 or GFR decreased by 50%
Failure CrX3 or GFR decreased by 75% or Cr>4mg/dL
Loss persistent Acute Kidney Failure; complete loss of kidney fxn if >4wks
End Stage Renal Disease complete loss of kidney fxn > 3 mos

115
Q

less than 400mL/day or urine

A

oliguria; urine specific gravity will be high (>1.020g/mL)

116
Q

typical duration of oliguria phase of AKI

A

10-14 days but can last for months in some cases

117
Q

the longer the oliguric phase

A

the poorer the prognosis for complete recovery of kidney fxn

118
Q

anuria

A

often seen in urinary obstruction (postrenal failure)

119
Q

oliguria

A

often seen in prerenal failure

120
Q

nonoliguric AKi

A

seen with Acute interstitial nephritis and ATN

121
Q

anuria and oliguria can lead to

A

JVD, edema, HTN, fluid overload, HF, pulmonary edema, pleural effusions

122
Q

In kidney failure, the kidneys cannot synthesize

A

ammonia which is needed for hydrogen excretion leading to metabolic acidosis (bicarb is used up trying to neutralize the hydrogen ions that can’t be excreted)–> Kussmaul respirations

123
Q

(with regard to AKI) uncontrolled hyponatremia or water excess can lead to

A

cerebral edema

124
Q

(With regard to AKI) What happens to potassium in AKI?

A

kidneys cannot excrete potassium–> hyperkalemia
compounded by massive tissue trauma bc damaged cells release addt’l potassium into ECF.
PLUS bleeding and blood tranfusions may cause cellular destruction, releasing MORE potassium into ECF
FINALLY, Acidosis worsens hyperkalemia as hydrogen ions enter the cells and potassium is driven out of the cells into the ECF

125
Q

peaked T waves, widening QRS complex, and ST depression

A

hyperkalemia

126
Q

What happens to the blood with AKI?

A

leukocytosis-the most common cause of death with AKI is INFECTION (in urinary and respiratory systems)

127
Q

AKI with leukopenia and thrombocytopenia indicate

A

etiology of SLE or thrombotic thrombocytopenic purpura

128
Q

A CBC with esinophilia in a pt with AKI indicates

A

etiology of allergic response and presence of interstitial nephritis

129
Q

an end product of endogenous muscle metabolism

A

creatinine

130
Q

end product of protein metabolism

A

urea

131
Q

BUN and Cr are __________ in AKI

A

elevated

132
Q

what does an elevated BUN indicate?

A

dehydration, corticosteriods, catabolism r/t infections, fever, severe injury, or GI bleeding, thus elevated Cr is more indicative of AKI

133
Q

fatigue, difficulty concentrating which escalates to seizures, stupor, and coma
Asterixis

A

neurologic changes that occur as nitrogenous wastes accumulate in brain and other nervous tissue

134
Q

flapping tremor when the wrist is extended

A

Asterixis

135
Q

What happens during the diuretic phase of AKI?

A

kidneys have regained ability to excrete waste, but not to concentrate urine in the tubules and thus hypotension and hypovolemia result from the massive fluid losses (3-5L/day!)

136
Q

How long does diuretic phase of AKI last

A

1-3 weeks

137
Q

What happens in the recovery phase of AKI?

A

GFR increases, allowing the BUN/Cr to plateau then decrease. Major improvements occur within 1-2 weeks of this phase, but kidney fxn may take up to 12 mos to stabilize

138
Q

dehydration, blood loss, severe heart disease

A

prerenal causes of AKI

139
Q

nephrotoxic drugs, recent blood transfusion, or radiologic study using contrast media

A

intrrenal causes of AKI

140
Q

stones, BPH, CA of bladder or prostate

A

postrenal causes of AKI

141
Q

Urine sediment (obtained in urinalysis) containing abundant casts, cells, or proteins (hematuria, pyuria, and crystals) suggest

A

intrarenal disorder

142
Q

urine sediment may be normal in

A

prerenal and postrenal AKI

143
Q

assess abnormalities in kidney blood flow, tubular fxn, and the collecting ststem

A

renal scan

144
Q

identify lesions and masses , obstructions or vascular abnormalities in kidney

A

CT scan

145
Q

administration of contrast medium gadolinium (used primarily in MRA) has been associated with the development of

A

nephrogenic systemic fibrosis: cutaneous hyperpigmentation and induration and joint contractures

146
Q

diagnosis of intrarenal cause of AKI

A

renal biopsy

147
Q

during the oliguric phase, monitor fluid intake closely. fluid restrictions often are

A

600mL plus previous 24 hr fluid loss

148
Q

what temporarily shifts potassium back into cels during hyperkalemia?

A

insulin and sodium bicarb

149
Q

what rises threshold at which hyperkalemia related dysrhythmias will occur?

A

calcium gluconate

150
Q

what removes potassium from the body during aki and hyperkalemia?

A

kayexalate and dialysis

151
Q

when is kayexalate contraindicated?

A

paralytic ileus bc bowel necrosis may occur

152
Q

What is RRT?

A

renal replacement therapy
intermittent Hemodialysis
Continuous hemodialysis (CRRT over 24 hours-slowly)
peritoneal dialysis

153
Q

When do you institute RRT?

A

1) volume overload causing compromised cardiac/respiratory fxn
2) elevated serum potassium
3) metabolic acidosis (bicarb 120mg/dL
5) significant change in mental status
6) pericarditis, pericardial effusion, or cardiac tamponade

154
Q

what to consider when giving iv insulin for elevated k+?

A

give glucose iv concurrently to avoid hypoglycemia

155
Q

how do you give kayexalate?

A

by mouth or retention enema; mixed in water with sorbitol to produce osmotic diarrhea, allowing for evacuation of potassium rich stool from the body

156
Q

What might you hear in a heart with aKI

A

s3 gallop, murmurs, pericardial friction rub

157
Q

dont give a patient with renal d/o a contrast medium diagnostic study. If you cant avoid it…

A

ensure optimal hydration using bicarbonate solution or sodium chloride with or without the prophylactic administration of mucomyst

158
Q

1 kg =

A

1000 ml of fluid

159
Q

what causes stomatitis?

A

ammonia excess in saliva irritates mucus membranes

160
Q

stage 1 CKD

A

GFR >90mL/min/1.73^m2

161
Q

Stage 2 CKD

A

GFR 60-89 mL/min/1.73^2

162
Q

Stage 3 CKD

A

GFR 30-59 Moderately decreased GFR

163
Q

Stage 4 CKD: prep for RRT

A

GFR 15-29 severe decrease in GFR

164
Q

Stage 5 CKD

A

GFR <15 or dialysis required KIDNEY FAILURE

165
Q

two main causes of CKD

A

diabetes, HTN

166
Q

a syndrome in which kidney function declines to the point that symptoms develop in multiple body systems

A

Uremia in CKD

GFR <10mL/min

167
Q

n/v, lethargy, fatigue, impaired thought processes and HA

A

elevated BUN

168
Q

CKD: Altered carb metabolism

A

due to impaired glucose use resulting from cellular insensitivity to the normal action of insulin–>hyperglycemia and hyperinsulinemia

169
Q

insulin depends on the kidneys for excretion, therefore, diabetics with CKD may need ______ insulin than before the onset of CKD

A

less

170
Q

hyperinsulinemia stimulates hepatic production of

A

triglycerides
therefore, almost all pts with uremia develop dyslipidemia r/t decreased levels of lipoprotein lipase that is important in the breakdwn of lipoproteins. This means that many pts with CKD die of Cardiovascular disease.

171
Q

what serum potassium level is fatal?

A

7-8

172
Q

If you are retaining sodium in renal failure, then why do you have hyponatremia and not hypernatremia?

A

bc of the excessive amount of fluid–dilutional hyponatremia

173
Q

what is the sodium restriction for CKD

A

2g/day

174
Q

absence of reflexes, decreased mental status, cardiac dysrhythmias, hypotension, and respiratory failure

A

hypermagnesemia in CKD

175
Q

which type of anemia is associated with CKD?

A

normocytic, normochromic anemia. due to decreased production of erythropoietin by the kidneys.
nutritional def’s, decreased RBC lifespan, increased hemolysis of RBC, frequent blood samplings, and bleeding from GI tract add to anemia

176
Q

What about PTH and CKD?

A

parathyroid hormone is increased in CKD to compensate for decreased Ca++ and HD. PTH inhibits erythropoeisis, shorten survival of RBCs and cause bone marrow fibrosis
PTH stimulated bone demineralization (increased fractures) to release Ca++ from bones, but this releases phosphate too and phosphate decreases vit D activation by kidneys too.

177
Q

What about iron in CKd?

A

folic acid, essential for RBC maturation, is dialyzable bc it is water soluble. Give folic acid 1mg/day

178
Q

Why is there so much bleeding with uremia and CKD?

A

defect in platelet fxn-impaired platelet aggregation and impaired release of platelet factor III. Alterations in the coagulation system with increased concentrations of factor VIII and fibrinogen=bleeding

179
Q

Why do pts with CKD get so many infections?

A

decreased leukocyte production (enlarged spleen) as well as hyperglycemia and use of catheters, needle insertions, etc

180
Q

which would you expect to see in a HD pt? left or right sided HF?

A

Left sided, esp left ventricular hypertrophy due to so much fluid to overcome to pump out

181
Q

friction rub, chest pain, low grade fever

A

pericarditis

182
Q

why is serum calcium low in CKD?

A

as kidney fxn deteriorates, less vit D is converted to its active form, resulting in decreased serum levels. To absorb Ca++ from GI tract, activated vit D is needed. Thus decreased active vit D levels result in less Ca++ absorption from GI and therefore decreased serum Ca++

183
Q

CKD mineral and bone disorder

A

adds to morbity and mortaltiy risks bc the phosphate and calcium released from bone by PTH bind together and deposit on walls of vasculature (this may occur in the heart and disrupt conduction)

184
Q

what happens to the skin with CKD?

A

pruritis, itchy, dry, uremic frost

185
Q

first indication of kidney damage

A

proteinuria-do dipstick eval of protein in urine or evaluation for microalbuminuria (not detected on routine urinalysis)

186
Q

a ratio greater than 300 mg albumin per 1 g Cr

A

signals CKD

187
Q

meds for CKD

A 
erythropoeitin therapy
calcium supplements and/or phosphate binders, iron
anti-HTN meds
ACEIs or ARBs
statins for hyperlipidemia
188
Q

when do you take phosphate binders?

A

with meals

189
Q

when do you take calcium supplements?

A

on an empty stomach, but NOT with iron

190
Q

when do you take iron?

A

between meals

191
Q

dyspnea, tachypnea, and SOB

A

indicators of fluid excess

192
Q

what is dialysis for

A

to correct fluid and electrolyte imbalances in pts with kidney failure

193
Q

Which dialysis is preferrable for a diabetic CKD patient?

A

Peritoneal dialysis

194
Q

inflow (10 mins) , dwell (20-30 mins), drain (15-30mins)

A

PD

195
Q

why implant an AVG over AVF?

A

history of IV drug abuse, obesity, or PVD

196
Q

when can you use an AVF?

A

4-6 weeks, but recommendation is 3 months

197
Q

when can you use AVG?

A

2-4 weeks

198
Q

what is steel syyndrome

A

development of distal ischemia r/t HD access

199
Q

Where do you access for HD while waiting for AVF or AVG?

A

Internal jugular or femoral percutaneous cannulation

1-3 weeks if in jugular, only 1 week in femoral

200
Q

how do you treat hypotension during dialysis?

A

decrease volume of fluid being removed and infuse NS

201
Q

What two nutritional supplements do you commonly give pts with CKD?

A

calcium and iron (iron causes constipation)

202
Q

What happens to Hgb when dehydrated?

A

Hgb increases when dehydrated

203
Q

dizziness, weakness, cardiac irregularities, muscle cramps, diarrhea, nausea

A

hyperkalemia (during oliguric phase)–>avoid giving pts with renal insufficiency potassium sparing diuretics, potassium supplements, or salt substitutes
use LASIX instead

204
Q

fatigue, anorexia, dyspnea, nocturia, 1+pedal edema, basilar crackles in both lungs, clear pale urine, yellow gray pallor (due to anemia or uremia) bruising and uremic frost

A

ESRD

205
Q

What is protein restricted in renal patients

A

to reduce the accumulation of waste products associated with protein metabolism, which causes the manifestations of uremia. allowed proteins should be of high biologic value, such as eggs. Fluid allowances should be 500-600mL more than the previous days 24 hr urine output.

206
Q

What is a big risk for HD patients?

A

could get hepatitis
AIR EMBOLUS
hypotension

207
Q

What about weight gain and dialysis patients?

A

weight gain between dialysis should not exceed 1.5 kg

208
Q

Nursing considerations for patient post op for kidney transplant?

A

Priority nursing diagnosis is risk for infection bc immunosuppressant meds are prescribed to decrease organ rejection, but also increase risk for infection. NO FLOWERS in patient room and frequent hand washing performed by all visitors
Azathioprine (Imuran)
Cyclosporine (Sandimmune)
Solu-Medrol

209
Q

kidney pan, oliguria or anuria, HTN, lethargy, fever and fluid retention, increased BUN/Cr, increased Potassium

A

symptoms indicative of organ rejection

210
Q

occurs within the first 48 hours of transplantation and requires immediate removal of transplanted kidney

A

hyperacture rejection

211
Q

occurs up to 2 years after surgery, most commonly within first 2 weeks. It can often be managed effectively with increased doses od immunosuppressice meds

A

acute rejection

212
Q

a gradual process, occurring or a period of months to years. Conservative mgmt, including a careful balance of fluid and protein intake helps control the rejection, but the eventual outcome is the need for dialysis

A

chronic rejection

213
Q

raises BP as a result of angiotensin (local vasoconstriction) and aldosterone (volume expansion) secretion

A

renin produced in kidney

214
Q

regulate intrarenal blood flow by vasodilation or vasoconstriction

A

prostaglandins produced by kidney

215
Q

increase blood flow (vasodilation) and vascular permeabilty

A

bradykinins produced in kidney

216
Q

stimulates bone marrow to make RBC

A

erythropoietin make in kidney

217
Q

promotes absorption of calcium in the GI tract

A

Activated Vit D by kidney

218
Q

makes DCT and CD permeable to water to maximaize reabsorption and produce a concentrated urine

A

ADH aka vasopressin (influenced by renal fxn) comes from posterior pituitary

219
Q

promotes sodium reabsorption and potassium secretion in DCT and CD; water and chloride follow sodium

A

aldosterone (influenced by renal fxn) comes from adrenal cortex

220
Q

cause tubular secretion of sodium

A

natriuretic hormones (influenced by renal fxn but made in cardiac atria and brain)

221
Q

what is a nursing consideration for phosphate binders such as amphogel, alternaGEL?

A

aluminum toxicity may cause bone disease and dementia

222
Q

nausea, vomiting, anorexia, visual disturbances, restlessness, HA, cardiac dysrhythmias, bradycardia

A

digoxin toxicity

223
Q

nursing considerations for Epogen

A

monitor Hct weekly-no more than 4 point increase in less than 2 weeks
explain that pelvic and limb pain should dissipate in 12 hours
dont shake vial as that mat inactivate glycoprotein

224
Q

renal osteodystrophy

A

abnormal calcium metabolism causes bone pathology

225
Q

What diagnostic tests allows you to determine kidney function?

A

IVP Intravenous Puelogram

226
Q

Which diagnostic test allows you to determine bladder function?

A

Cystogram

227
Q

Which diagnostic test allows you to determine bladder or urethral abnormalities?

A

Cystoscopy

228
Q

What is a key patient teaching regarding resolution of aUTI?

A

Tell the client to be diligent about taking antibiotics around the clock and to not skip doses in order to keep blood level of antibiotic constant for optimal effectiveness.

229
Q

a needle or catheter is inserted through the skin into the calyx of the kidney. The stone may be dissolved by percutaneous irrigation with a liquid that dissolves the stone or by ultrasonic sound waves (lithotripsy) that can be directed through the needle or catheter to break up the stone, which can then be eliminated through the urinary tract.

A

percutaneous nephrostomy

Adult Health (18 decks)

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