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Healthcare Of Children > Alterations In Genitourinary Function > Flashcards

Alterations In Genitourinary Function Flashcards

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1
Q

What are the nursing considerations for hypospadias?

A

Provide emotional support, protect surgical site, usually has a Foley or stent in place, accurate I and O. Encourage intake, pain management.

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2
Q

What is vesicoureteral reflux?

A

Urine backed up from the bladder into ureter’s, may go as far as the kidneys. This causes infection. Increased pressure in kidneys causes renal scarring, hypertension, possible renal failure. It is often familial

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3
Q

What are diagnostic tests and treatment for vesicoureteral reflux?

A

Voiding cystourethrogram determines if there is reflux. Surgical treatment (Pyeloplasty), reimplant ureter at another place in bladder

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4
Q

What is cystitis?

A

Infection involving urethra or bladder

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5
Q

What is Pyelonephritis?

A

And upper infection involving ureter’s, renal pelvis, and renal parenchyma

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6
Q

What is that etiology for urinary tract infections

A

Contamination from stool or hands, urinary stasis, structural abnormalities, constipation, chemical irritations such as bubble baths, sex or sexual abuse

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7
Q

What are clinical manifestations of urinary tract infections?

A

40% of UTIs are asymptomatic. Infants: nonspecific, fever, vomiting, diarrhea, irritability, poor feeding, FTT, strong smelling urine. Children: enuresis, fever, strong smelling urine, frequency,urgency, dysuria, abdominal or flank pain, hematuria, vomiting, diarrhea. Adolescents: fever, chills, frequency, dysuria, urgency, abdominal or flank pain, he atria

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8
Q

What are diagnostic tests and treatments for urinary tract infection?

A

Dipstick test for nitrates and/or WBC. This is up to 90% productive. You’re in culture: greater than 100,000 organisms equals positive, less than 100,000 or mixed equals contamination, most UTIs caused by E. coli, Need to obtain culture before antibiotics

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9
Q

What is the treatment for a UTI?

A

PO or IV antibiotics

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10
Q

Bladder control

A

One and a half years: Passes urine at regular intervals. Two years: announces one voiding. 2 1/2 years: makes known need to void, can’t hold urine. 2 to 3 years: daytime control. Three years: can’t go to bathroom by self, can hold is involved. 2 1/2 to 3 1/2 years: achieves night time control. Four years: good night time control. Five years: voids about seven times a day, likes privacy. Age in years +2 equals bladder capacity in ounces

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11
Q

What is enuresis?

A

Involuntary voiding after child usually has bladder control. Often familial, more common in boys. Can be diurnal, 10%. Knock to urinal, 50%. Or both, 40%. Can be primary, intermittent, or secondary. Often children have enuresis and hospital due to stress and strange environment

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12
Q

What is the treatment for enuresis?

A

Needed to rule out infection or other disorder. Multi treatment approach is most effective.: Restrict fluid, bladder stretching exercises, wake child up to void, alarms, reward system, drug treatment: desmopressin, oxybutynin, imaprimine

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13
Q

What is minimal change nephrotic syndrome?

A

The cause is unknown, but that there is an alteration in the glomerular membrane which makes it permeable to proteins. Proteins are lost in urine (proteinurea) which causes a decrease in the blood albumin (hypoalbuminemia). The protein urea changes the oncotic pressure causing fluid to move into the interstitial spaces and body cavities (severe edema)

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14
Q

What is the usual age for minimal change nephrotic syndrome

A

2 to 7 years the occurrence is two and 100,000 (more males)

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15
Q

What is hypospadias?

A

A congenital malformation where the opening of the Aretha is in an abnormal place on the penis. treatment is usually repaired during the first year of life, the child is not circumcised as skin is used for a pair

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16
Q

What is the pathophysiology of minimal change nephrotic syndrome?

A

Fluid shift causes hypovolemia it’s secretion of ADH. Secretion of ADH causes reabsorption of sodium and water which adds to edema. Hypoproteinemia causes increased liver synthesis of proteins and lipids (hyperlipidemia). Immunoglobulins are lost in urine causing altered immunity

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17
Q

What are the clinical manifestations of minimal change nephrotic syndrome?

A

Child begins to gain weight over a period of days and weeks. Edema develops, morning Orbital edema but moves into ascites and lower extremities. Severe pallor, irritability and on my way, oliguria: urine dark, frothy, iridescent. Hypertension, tachycardia, skin breakdown or infection, anorexia, abdominal pain, nausea and vomiting, diarrhea, respiratory distress and pulmonary congestion

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18
Q

What are diagnostic test for minimal change nephrotic syndrome

A

Your analysis: severe proteinurea, increased specific gravity. Blood,: hypoproteinemia, hyperlipidemia, increased platelet count, sedation rate increased, bun and creatinine maybe increased. May do renal biopsy to determine type of NS and kidney function

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19
Q

What is the medical treatment for minimal change nephrotic syndrome?

A

Main treatment steroids (prednisones). May also use immunosuppressant therapy (Cytoxan). May give Lasix for severe edema, make it I’ll be a mentor replace losses, antibiotics if infection present, antihypertensives if needed

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20
Q

What is the clinical course for minimal change nephrotic syndrome?

A

After the start of steroids, diuresis occurs and proteinemia decreases: 7 to 21 days. Edina begins to decrease and child feels better. Appetite improved and child is less irritable. Urine is normal by four weeks and 85% of cases. Often has remission and exacerbations over years. Maybe steroids for prolonged periods

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21
Q

What is acute postinfection glomerulonephritis

A

A noninfectious immune complex disease that usually follows group a beta hemolytic strep infection (8 to 14 days). It does not matter if the infection was treated or not

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22
Q

What is the usual source of infection for a cute postinfection glomerulonephritis? (And younger children, and older children)

A

In younger children it is impetigo, and older children it is strep throat

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23
Q

What is the pathophysiology in acute postinfection glomerulonephritis?

A

Antigen antibody complexes accumulate in the glomeruli causing the renal bloodflow and glomerular filtrate Chin to decrease therefore causing retention of water and sodium resulting in edema. Damage to the glomerular membrane allows red blood cells to pass into urine causing hemateria

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24
Q

When is acute postinfection Glomerulonephritis most common

A

In the winter

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25
Q

What is the peak age of acute postinfection glomerulonephritis, and what sex is it most common in?

A

The peak ages 2 to 12 years and it is more common in boys

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26
Q

What are the clinical manifestations of acute postinfection glomerulonephritis?

A

One half are asymptomatic. Sudden onset of hemateria and 50% of cases. Abdominal/flank pain/costovertebral tenderness. Irritability, malaise, fever, dysuria, edema, usually in the face especially in the a.m. but may spread. Oliguria, hypertension leading to encephalopathy, respiratory difficulty.

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27
Q

What are the two diagnostic test used to determine if a patient has acute postinfection glomerulonephritis?

A

Urinalysis and blood count

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28
Q

For acute postinfection glomerulonephritis, what are you looking for in the urinalysis?

A

He materia: microscopic if not obvious. Protein urea: 3+ or 4+ but not as much as MCNS. Increased specific gravity, negative culture

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29
Q

In a cute postinfection glomerulonephritis what are you looking for in the complete blood count?

A

Increased B UN, creatinine, sed rate, serum lipids. Positive ASO tighter. Reduced Seum c3. decreased H and H

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30
Q

And a cute postinfection glomerulonephritis is the throat culture usually positive or negative?

A

Negative

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31
Q

What is the medical treatment for acute postinfection glomerulonephritis?

A

No specific medical treatment, management is mainly supportive and monitoring for complications of increased BP. Maybe given meds if BP is elevated: Lasix, apresoline, labetalol. It is important to watch for signs of hypertensive encephalopathy

32
Q

What are signs of hypertensive encephalopathy?

A

Headache, dizziness, blurred vision, vomiting, decreased level of consciousness’s, confusion, seizures

33
Q

What is the clinical course for acute postinfection with Glomerulonephritis

A

Children with a normal BP and adequate output may be cared for at home. Those with edema, hypertension, gross hematuria, and/or significant oliguria may be hospitalized due to the need for bedrest

34
Q

How long does the acute phase last in acute postinfection glomerulonephritis?

A

4 to 10 days

35
Q

In acute postinfection glomerulonephritis what is the first sign of improvement?

A

Diuresis. Child begins to feel better and BP and edema decreases, appetite improves, urine clears, B UN and creatinine decrease

36
Q

In a cute postinfection glomerulonephritis how long does it take a child to recover in most cases?

A

14 to 21 days

37
Q

What are two complications that can arise from a cute postinfection glomerulonephritis

A

Some may have chronic or progressive diseases. 2% develop ESRD

38
Q

What are the Kubler Ross stages?

A

Denial, anger, bargaining, depression, acceptance

39
Q

What are the ends of the long bones called?

A

Epiphyses

40
Q

What occurs at epiphyseal plate

A

Growth

41
Q

How are bones different in children than adults?

A

Children’s bones are more poorest and less dense than adults

42
Q

Until puberty how are ligaments, tendons, and bones different than adults

A

Until puberty, both ligaments and tendons are stronger than bone

43
Q

What are ligaments?

A

Structural support connecting bones

44
Q

What are tendons?

A

Connect bones to muscle

45
Q

What is congenital clubfoot?

A

A deformity readily apparent at birth. The midfoot is directed downward the hind foot turned inward and the forefoot crawled towards the heel and turns upward and partial supination

46
Q

In congenital clubfoot how is the Achilles tendon affected, the muscles in the lower leg, and leg lengths?

A

The Achilles tendon is usually shortened, muscles in the lower leg are atrophied, leg lengths are generally normal

47
Q

What is the treatment of choice for congenital clubfoot

A

Serial casting. Timing is critical because short bones of foot are primarily cartilage at birth however they begin to ossify soon

48
Q

In serial casting for congenital clubfoot how often are the cast changed and how long is this continued?

A

Changed every 1 to 2 weeks for approximately 8 to 12 weeks

49
Q

Serial casting is unsuccessful in congenital clubfoot what is the next step

A

Surgical interventions, the agent varies but mostly between 3 to 12 months. The procedure is the realignment of bones of the foot and releasing of the constricting soft tissue. The foot is held in proper position by steel pins, casting of the foot and leg for 6 to 12 weeks. Severe deformities may require repeated surgical tendon or joint releases

50
Q

What is developmental dysplasia of the hip?

A

The for moral head and acetabulum are improperly aligned

51
Q

In developmental dysplasia of the hip what can that include?

A

Hip instability, dislocation: complete displacement of the bone out of the hip joint (occurs in 1 to 2 in 1000 births). Subluxation: partial this location. Acetabular dysplasia: abnormal cellular or structural development

52
Q

How many births have hip instability?

A

One and 100

53
Q

What percentage of hips affected in developmental dysplasia are unilateral? And which hip is more affected?

A

80% is unilateral. Left hip is affected three times more often

54
Q

What are the causes for developmental dysplasia of the hip?

A

Cause is unknown: possibly intrauterine position, maternal estrogen may cause laxity of the hip joint leading to joint instability, more common in breech babies

55
Q

And developmental dysplasia of the hip which gender is most affected?

A

Females are four times more likely to be affected

56
Q

If a relative has developmental dysplasia of the hip how many times more likely is the. Infants to have it?

A

2250 times more common

57
Q

What are clinical manifestations of developmental dysplasia of the hip?

A

Limited abduction of the affected hip, asymmetric fight and gluteal fat folds. Telescoping or pistoning of the thigh. The extended dais pushed toward the infants head then pulled this silly, the head of the femur can be felts to move up and down in the buttock

58
Q

In the older infant and child what are the clinical manifestations of developmental dysplasia of the hip

A

Affected leg will be shorter than the other, walking is delayed, walk with a limp and toe walking

59
Q

And developmental hip dysplasia what is the Trendelenburg sign

A

Bearing weight on the affected hip, the pelvis tilts down word on the normal side instead of upward as it would with normal stability

60
Q

In developmental dysplasia of the hip, what is the positive Allis’ sign

A

Wendy is lower than the other one the knees are flexed lying on the back

61
Q

What is positive ortolans sign and developmental hip dysplasia

A

Reduces a dislocated hip, hip flexed then abducted the head of the femur will be filed going back into the joint

62
Q

And developmental hip dysplasia a positive Barlow’s test is what

A

The babies thigh is grasped am a ducted with gentle downward pressure. Dislocation is palpable as the for moral head slips out of the acetabulum

63
Q

For developmental hip dysplasia how was it diagnosed if the child is under four months?

A

Ultrasound

64
Q

For developmental hip dysplasia how was it diagnosed in children and older infants?

A

Radiographic examination

65
Q

What is the Pavlik harness?

A

A dynamic splint that allows movement. It ensures hip flexion and abduction and does not allow head extension or adduction

66
Q

What is the goal of the Pavlik harness in developmental dysplasia of the hip?

A

Correct positioning. Involves relocating the for moral head into the acetabulum while gently stretching the restrictive soft tissue. It is one continuously for 3 to 5 months 23 out of the 24 hours except for bathing

67
Q

What is skin traction?

A

Used When adduction contracture is present. Used to slowly and gently stretchy the hip full abduction then wide abduction is maintained until stability is attained

68
Q

What is the most common type of skin traction

A

Bryant skin traction

69
Q

In reference to the application of the Pavlik harness, when is skin traction used

A

Skin traction is used prior to the harness

70
Q

When is hip spica cast used

A

When there is difficulty maintaining stable reduction. It is applied and changed periodically to allow for growth. Generally over 3 to 6 months

71
Q

What is Legg-calve perthes

A

An avascular process of the head of the femoral head. Necrosis is due to an interruption of the blood supply to the femoral epiphysis

72
Q

In legg calve perthes what is thought to be the cause, who is more at risk and when are the peak ages

A

How and why is not understood. It may be genetic. 20% more families with it with history. Boys are four times more likely to have at the girls. Average it’s 2 to 12 years with the peak between 4 to 8 years

73
Q

In legg calve perthes how is diagnosis made?

A

X-ray. bone scans and mri may show process sooner.

74
Q

What are the early symptoms of legg calve perthes

A

Mild pain. limb aggravated by increased activity and relieved by rest. Child favors affected hip and limits movement to avoid discomfort. Medical attention may not be obtained for several months

75
Q

What are worsening symptoms of legg calve perthes

A

ROM becomes limited. Weakness and muscle wasting develop

76
Q

What is the desired outcome for legg calve perthes

A

Pain free hip that functions properly. To promote healing and prevent deformity, femoral head contained in hip socket until ossification is complete

77
Q

What needs to be done for the hip/head of femur to promote healing in legg calve perthes

A

The head of the femur needs to be kept in the socket until new bone former. Hips must be kept in abduction position

Healthcare Of Children (7 decks)

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