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Peds Exam 2 > Renal > Flashcards

Renal Flashcards

1
Q

Full term infant have the same number of…

A

nephrons as adults

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2
Q

GFR in the newborn

A

30% that of the adult

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3
Q

GFR does not reach adult level until…

A

3-5 years old

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4
Q

Kidney’s and tubular system reach full size by…

A

adolescence

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5
Q

Fluid turnover is..

A

7x greater than that of an adult

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6
Q

Greater insensible H2O loss with illness such as…

A
  • increaesed RR
  • fever
  • vomiting
  • diarrhea
  • and drainage from blood loss or tubes
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7
Q

Altered fluid balance..

A

catastrophic consequences

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8
Q

Until age 2…

A
  • immature glomeruli, tubules, and nephrons of the kidney
  • unable to conserve or excrete water and solutes effectively
  • decreases ability to retain and concentrate urine
  • immature homeostatic regulation (buffer) system
  • weaker transport system for ions and bicarb equals risk for acid base imbalance
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9
Q

Bladder capacity…

A

increases from 20-50 mls at birth to 700 mls by adulthood

-no bladder control under age 2 years due to immature nerves

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10
Q

Renal excretion is dependent on

A

glomerular filtration, active tubular secretion, and passive tubular reabsorption

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11
Q

Drugs dependent on…

A

renal excretion, like Pancuronium and Dig, can be markedly affected by immature kidney fx

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12
Q

Kidneys receive a ______ percentage of CO than in adults

A

lower

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13
Q

Hypodpadius

A

-urethral meatus located on ventral surface

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14
Q

Epispadius

A

urethral opening located on dorsal surface

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15
Q

Causes of hypospadius and epispadias

A

urethral folds fail to fuse completely over the urethral groove

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16
Q

Medical Management of misplaced urethra

A

surgical repair

  • usually during 1st year of life
  • usually an outpatient procedure
  • caudal nerve block
  • anticholinergics
  • urethral stent
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17
Q

Nursing Management

A
  • avoid stent removal
  • I and O every hour
  • pain control
  • antibiotics until stent is removed
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18
Q

UTI

A

-infection of bacterial, viral, or fungal origin that occurs in the urinary tract

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19
Q

cystitis

A

lower UTI that involves the urethra or bladder

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20
Q

pyleonephritis

A

upper UTI that involves the ureters, renal pelvis, renal parenchyma

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21
Q

bacteriuria

A

presence of bacteria in the urine

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22
Q

organisms causing UTIs

A
  • E. coli most common
  • staph aureus
  • klebsiella
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23
Q

Neonates

A

urinary tract more likely to be infected via the blood stream (boys more than girls)

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24
Q

Older infants and children

A

(girls more than boys)

  • peak age 2-6 years
  • bacteria ascends the urethra
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25
Q

Causes of UTIs

A
  • shorter urethra in females
  • urinary stasis
  • infrequent voiding
  • incomplete emptying of the bladder
  • vesicoureteral reflux
  • poor personal hygiene
  • indwelling catheter placement
  • antimicrobial agents that alter the normal urinary tract flora
  • sexually active adolescent females/sexually abused children
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26
Q

Clinical manifestations of UTI in infants

A
  • unexplained fevers
  • poor feeding
  • failure to thrive
  • vomiting
  • strong-smelling urine
  • irritable
  • all children under 2 years with FUO should be tested for UTI
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27
Q

Clinical manifestations of UTI in older children

A
  • dysuria
  • urgency
  • enuresis
  • abdominal pain
  • strong-smelling urine
  • CVA tenderness
  • chills
  • high fevers with pyelonephritis
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28
Q

Urine C/S

A
  • presence of bacteria
  • collected via clean catch midstream, sterile cath, or suprapubic
  • bagged urine only reliable when culture negative
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29
Q

Dipstick test (UA)

A
  • leukocytes
  • blood
  • nitrite
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30
Q

If culture is positive,

A
  • renal and bladder U/S (r/o scarring)

- voiding cystourethrogram to r/o reflux

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31
Q

IVP

A
  • IV pyleogram
  • rare
  • to r/o obstruction such as kidney stones
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32
Q

Nursing Management of UTIs

A
  • admin antibiotics (amoxicillin, sulfa, cephalosporins)
  • analgesia, comfort measures
  • education on prevention of future UTIs and diagnostic tests
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33
Q

Enuresis

A
  • repeated involuntary voiding by a child old enough to have bladder control
  • nocturnal, diurnal or both
  • primary: never had a dry night
  • secondary: dry for at least 6 mths before bedwetting
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34
Q

Milestones in the Development of Bladder Control:

1.5 year
2 yrs
2.5 yrs
3 yrs
2.5 to 3.5 yrs
4 yrs
5 yrs
A

1.5 year: passes urine at regular intervals

2 yrs: child announces when he or she is voiding

2.5 yrs: child makes known the need to void and can hold urine

3 yrs: child goes to the bathroom by himself or herself, holds urge if preoccupied with play

2.5 to 3.5 yrs: child achieves nighttime control

4 yrs: child shows great interest in going to bathrooms when away from home

5 yrs: child voids approx. 5-6 times a day prefers privacy and is able to initiate emptying of bladder at any degree fulness

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35
Q

Treatment approaches

A
  • fluid restriction before bed
  • bladder exercises
  • timed voiding
  • enuresis alarms
  • reward system
  • medications
36
Q

Vesicoureteral Reflux

A
  • defined as retrograde flow of urine from bladder to ureters
  • may result from faulty valve in bladder, anatomic implantation abnormality or acquired r/t scarring from recurrent UTIs
  • left untreated, urine can retrograde into renal pelvis causing hydronephrosis and RF
37
Q

VCUG

A
  • examines the urethra and bladder while the bladder fills and empties
  • radiopaque dye is placed in the bladder via catheter
  • pictures are taken when the bladder via catheter
  • reveals abnormalities of the inside of the urethra and bladder
  • also determines whether urine flow is normal as bladder empties
38
Q

Medical Management of Vesicoureteral Reflux

A
  • mild cases: antibiotics, may outgrow or require surgery by endoscopy, STING
  • severe cases: open surgery
  • general anesthesia required for both
39
Q

APIGN

A

acute post-infectious glomerulonephritis

  • inflammation of the glomeruli of the kidneys
  • usually occurs after a streptococcal infection (strep and impetigo)
  • more common in boys
  • highest incidence age 2-12 years
40
Q

Pathophysiology of APIGN

A
  • antibody-antigen complexes enter the glomeruli, leads to inflammation and obstruction
  • glomerular filtration rate decreased
  • vascular permeability increases leading to excretion of RBCs in urine
  • sodium and H2O retained leads to edema
41
Q

Clinical Manifestations of APIGN

A
  • many children asymptomatic
  • flank or mid abdominal pain
  • irritability, malaise, fever
  • HTN
  • edema
  • oliguria
  • hematuria
  • proteinuria
  • fatigue, lethargy, anorexia
42
Q

Nursing Management of APIGN

A
  • fluid balance: monitor I/O, DW, assess edema, monitor electrolytes
  • monitor VS and BP
  • Medications: antihypertensives, diuretics, antibiotics, digitalis
  • dialysis for severe cases
  • diet: sodium, potassium, and fluid restrictions
  • protein restricted if azotemia is severe
  • bed rest during acute phase, prevent skin breakdown
  • prevent infection
  • provide emotional support to parents
  • discharge planning teaching: medication regime, dietary restrictions, signs and symptoms of complications
43
Q

Digitalis used to tx

A

circulatory overload

44
Q

Antibiotics used to tx…

A

existing streptococcal infection, not APIGN

45
Q

Prognosis of APIGN

A
  • good for 90 percent of cases
  • clinical signs resolve within few weeks
  • renal function returns
46
Q

Nephrotic Syndrome

A

-not a specific disease, but a clinical state

  • characterized by:
  • edema
  • massive proteinuria
  • hypoalbuminemia
  • hypoproteinemia
  • hyperlipidemia
  • altered immunity
  • more common in males, AA, hispanics
  • peak age 2-7 years
47
Q

Pathophysiology of Nephrotic Syndrome

A
  • unknown etiology, but immune system role suspected–preceded by URI
  • increased glomerular permeability allows albumin to cross into urine (proteinuria)
  • proteinuria leads to decreased oncotic pressure and increased edema (fluid stays in interstitial areas, not pulled into vascular space)
  • immunoglobulins lost, altered immunity
  • anti-clotting factors lost, increased risk of blood clots
  • liver increased lipid synthesis–hyperlipidemia
48
Q

Clinical Manifestations of Nephrotic Syndrome

A

-edema develops slowly over several weeks

  • AM: periorbital edema
  • PM: edema in abdomen and ankles
  • other S/S: HTN, irritability, anorexia, hematuria, decreased urine output, frothy urine, weight gain
  • malnourishment results from proteinuria
  • brittle hair
  • pale, shiny skin
49
Q

Criteria for diagnosis for Nephrotic Syndrome

A
  • U/A: massive proteinuria

- Blood: hypoalbuminemia

50
Q

Medical Management of Nephrotic Syndrome

A
  • goal is to decrease proteinuria, decreased edema, improve nutrition, prevent infection
  • corticosteroids main treatment
  • prednisone 2 mg/kg/dose 1-3 times per day until urine is protein free for 5-7 days
  • continue prednisone once daily for 4 weeks, then give once every other day for 8 wks
51
Q

Side effects of steroids

A
  • growth suppression
  • hyperglycemia
  • obesity
  • increased risk of infection
  • HTN
  • increased appetite
  • mood swings
52
Q

tx for patients unresponsive to steroids or with steroid toxicity

A

immunosuppressive therapy

  • cytoxan
  • prograf
  • cyclosporine
53
Q

IV albumin and diuretics for….

A

severe edema, monitor electrolytes

54
Q

Dietary guidelines Nephrotic Syndrome

A
  • decreased sodium
  • decreased fat
  • no need to decrease protein
55
Q

Nursing Assessment for Nephrotic Syndrome

A
  • physiologic assessment is crucial
  • assess hydration status, edema
  • strict I/O, DW
  • abdominal girth
  • V/s q 4 hrs
  • monitor respiratory status
  • test urine for specific gravity, proteinuria
  • monitor for hypovolemia if on diuretics
56
Q

Nursing Management of Nephrotic Syndrome

A
  • admin meds
  • prevent infection
  • prevent skin breakdown
  • dietary education
  • promote rest
  • provide emotional support
  • discharge planning and home care teaching
57
Q

Renal Failure

A
  • occurs when kidney unable to excrete wastes, conserve electrolytes and concentrate urine
    acute: occurs suddenly over days and weeks, may be reversible
    chronic: occurs gradually and permanently over mths or years
  • both types characterized by azotemia and oliguria
  • anuria
58
Q

Acute Renal Failure Clinical Manifestations

A
  • dark urine or gross gematuria
  • HA
  • edema
  • fatigue
  • crackles
  • gallop heart rhythm
  • HTN
  • hematuria
  • lethargy
  • N/V
  • oliguria
  • mass in flank area if a cyst, tumor, or obstructive lesion is present
59
Q

Chronic Renal Failure Clinical Manifestations

A
  • fatigue
  • malaise
  • poor appetite
  • N/V
  • failure to thrive or short stature
  • may have oliguria or polyuria
  • HA
  • decreased mental alertness or ability to concentrate
  • chronic anemia
  • HTN
  • edema
  • fractures with minimal trauma
  • rickets
  • valgus deformity
60
Q

Hyperkalemia in RF Clinical Manifestations

A
  • peaked T waves, widening of QRS waves on ECG
  • dysrhythmias
  • muscle weakness
61
Q

Hyponatremia in RF Clinical Manifestations

A
  • ALOC
  • muscle cramps
  • anorexia
  • abdominal reflexes, depressed DTR
  • Cheyne-Stokes Respirations
  • Sz
62
Q

Hypocalcemia in RF Clinical Manifestations

A
  • muscle tingling
  • changes in muscle tone
  • Sz
  • Muscle cramps and twitching
  • Positive Chvostek sign
63
Q

Acute RF

A
  • kidney fx abruptly diminishes
  • rapid rise in BUN
  • kidneys unable to regulate: extracellular fluid volume, sodium balance, acid-base homeostasis
64
Q

Etiology of Acute RF

A
  • dehydration from gastroenteritis
  • hemorrhage
  • sepsis
  • acute glomerulonephritis
  • hemolytic uremic syndrome
  • poisoning
  • 2 to 3 percent children in PICU
  • 8 percent neonates in NICU
65
Q

Medical Tx for Acute RF

A
  • depends on underlying cause
  • goals: minimize or prevent permanent renal damage and maintain fluid and electrolyte balance
  • emergency tx for hypovolemia
  • pulmonary edema, diuretics, dialysis if diuretics do not work
66
Q

Hyperkalemia tx

A

tx with meds

  • Kayexalate
  • Calcium gluonate
67
Q

Hypocalemia tx

A

-calcium gluconate

68
Q

Metabolic Acidosis

A

sodium bicarb

69
Q

HTN

A

anti-hypertensives

70
Q

Infection tx with Acute RF

A
  • tx with antibiotics

- avoid nephrotoxic drugs–aminoglycosides

71
Q

Hemorrhage/Anemia with Hgb less than 6 with ARF

A

transfuse with PRBCs

72
Q

Chronic Renal Failure

A
  • progressive, irreversible reduction in kidney function
  • ultimately results in ESRD
  • less than 10% renal function
  • uremic syndrome
  • anemia
  • dialysis required for homeostasis
  • higher in black children
73
Q

Etiology of Chronic RF

A
  • Developmental abnormalities of kidney
  • Obstructed urine flow
  • Urinary reflux
  • Polycystic kidney disease
  • Glomerulonephritis
  • Hemolytic Uremic syndrome
74
Q

Pathophys of Chronic RF

A
  • healthy kidneys excrete excess acid body and regulate homeostasis
  • renal failure disrupts the balance
  • metabolic acidosis results
  • retention of H2O and sodium results in HTN
  • anemia results from decreased erythopoietin production
  • osteodystrophy increase risk of fractures and rickets
  • growth retardation secondary to:
  • disturbed metabolism of calcium, phosphorus, and Vit D
  • metabolic acidosis
  • decreased caloric intake
75
Q

Clinical Manifestations of Early RF

A
  • polyuria
  • pallor
  • HA
  • N
  • fatigue
  • decreased mental alertness
  • anemia, resulting in tachycardia, tachypnea
76
Q

Clinical Manifestations of Progressive RF

A
  • HTN
  • Anorexia
  • Pul edema
  • growth retardation
  • osteodystrophy
  • delayed fine and gross motor development
  • delayed sexual maturation
77
Q

Acidosis Medical Management

A
  • sodium bicarb

- sodium citrate

78
Q

Anemia Medical Management

A
  • diet: sufficient sources of iron and folic acid
  • injectable iron may be required
  • recombinant human erythropoietin–epogen, procrit
79
Q

Medical Management HTN

A
  • initial: low sodium diet, fluid restriction, and diuretics: thiazides, fursemide
  • severe HTN–sodium restriction
  • first line anti-hypertensive: ace inhibitors or angiotensin-receptor blockers ARB. both of these have shown a reduction in proteinuria
  • combining the above is recommended for more significant HTN before trying other classes of medications, also shows a further reduction in protein excretion
80
Q

Medical Management of Osteodystrophy

A

bone disease which results from kidneys inability to maintain normal phosphorus and calcium levels

  • slows bone growth and causes deformities (rickets)
  • increased serum phosphorus
  • decreased serum calcium
81
Q

Reduction of phosphorus

A

diet: milk, cheese, peas, beans, nuts, PB
- admin of phosphorus binding agent: calcium carbonate “Tums”
- admin of calcium with vit D

82
Q

Growth Retardation

A

human growth hormone: especially before puberty

83
Q

Nursing Management of RF

A

-identify complications of renal failure

  • HTN
  • Edema
  • poor growth and development
  • osteodystrophy
  • metabolic acidosis
84
Q

Monitor for side effects of medications

A
  • diuretics: electrolyte imbalance, weakness, muscle cramps, dizziness, HA, N/V
  • anti hypertensives: monitor BP, weight
85
Q

Signs of infection

A
  • elevated temp
  • strong-smelling urine
  • dysuria
  • changes in respiratory pattern, productive cough

-good hand washing practice

Peds Exam 2 (5 decks)

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