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Alterations In Genitourinary Function Flashcards

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
What is the peak age of acute postinfection glomerulonephritis, and what sex is it most common in?
The peak ages 2 to 12 years and it is more common in boys
26
What are the clinical manifestations of acute postinfection glomerulonephritis?
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.
27
What are the two diagnostic test used to determine if a patient has acute postinfection glomerulonephritis?
Urinalysis and blood count
28
For acute postinfection glomerulonephritis, what are you looking for in the urinalysis?
He materia: microscopic if not obvious. Protein urea: 3+ or 4+ but not as much as MCNS. Increased specific gravity, negative culture
29
In a cute postinfection glomerulonephritis what are you looking for in the complete blood count?
Increased B UN, creatinine, sed rate, serum lipids. Positive ASO tighter. Reduced Seum c3. decreased H and H
30
And a cute postinfection glomerulonephritis is the throat culture usually positive or negative?
Negative
31
What is the medical treatment for acute postinfection glomerulonephritis?
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
What are signs of hypertensive encephalopathy?
Headache, dizziness, blurred vision, vomiting, decreased level of consciousness's, confusion, seizures
33
What is the clinical course for acute postinfection with Glomerulonephritis
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
How long does the acute phase last in acute postinfection glomerulonephritis?
4 to 10 days
35
In acute postinfection glomerulonephritis what is the first sign of improvement?
Diuresis. Child begins to feel better and BP and edema decreases, appetite improves, urine clears, B UN and creatinine decrease
36
In a cute postinfection glomerulonephritis how long does it take a child to recover in most cases?
14 to 21 days
37
What are two complications that can arise from a cute postinfection glomerulonephritis
Some may have chronic or progressive diseases. 2% develop ESRD
38
What are the Kubler Ross stages?
Denial, anger, bargaining, depression, acceptance
39
What are the ends of the long bones called?
Epiphyses
40
What occurs at epiphyseal plate
Growth
41
How are bones different in children than adults?
Children's bones are more poorest and less dense than adults
42
Until puberty how are ligaments, tendons, and bones different than adults
Until puberty, both ligaments and tendons are stronger than bone
43
What are ligaments?
Structural support connecting bones
44
What are tendons?
Connect bones to muscle
45
What is congenital clubfoot?
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
In congenital clubfoot how is the Achilles tendon affected, the muscles in the lower leg, and leg lengths?
The Achilles tendon is usually shortened, muscles in the lower leg are atrophied, leg lengths are generally normal
47
What is the treatment of choice for congenital clubfoot
Serial casting. Timing is critical because short bones of foot are primarily cartilage at birth however they begin to ossify soon
48
In serial casting for congenital clubfoot how often are the cast changed and how long is this continued?
Changed every 1 to 2 weeks for approximately 8 to 12 weeks
49
Serial casting is unsuccessful in congenital clubfoot what is the next step
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
What is developmental dysplasia of the hip?
The for moral head and acetabulum are improperly aligned
51
In developmental dysplasia of the hip what can that include?
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
How many births have hip instability?
One and 100
53
What percentage of hips affected in developmental dysplasia are unilateral? And which hip is more affected?
80% is unilateral. Left hip is affected three times more often
54
What are the causes for developmental dysplasia of the hip?
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
And developmental dysplasia of the hip which gender is most affected?
Females are four times more likely to be affected
56
If a relative has developmental dysplasia of the hip how many times more likely is the. Infants to have it?
2250 times more common
57
What are clinical manifestations of developmental dysplasia of the hip?
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
In the older infant and child what are the clinical manifestations of developmental dysplasia of the hip
Affected leg will be shorter than the other, walking is delayed, walk with a limp and toe walking
59
And developmental hip dysplasia what is the Trendelenburg sign
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
In developmental dysplasia of the hip, what is the positive Allis' sign
Wendy is lower than the other one the knees are flexed lying on the back
61
What is positive ortolans sign and developmental hip dysplasia
Reduces a dislocated hip, hip flexed then abducted the head of the femur will be filed going back into the joint
62
And developmental hip dysplasia a positive Barlow's test is what
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
For developmental hip dysplasia how was it diagnosed if the child is under four months?
Ultrasound
64
For developmental hip dysplasia how was it diagnosed in children and older infants?
Radiographic examination
65
What is the Pavlik harness?
A dynamic splint that allows movement. It ensures hip flexion and abduction and does not allow head extension or adduction
66
What is the goal of the Pavlik harness in developmental dysplasia of the hip?
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
What is skin traction?
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
What is the most common type of skin traction
Bryant skin traction
69
In reference to the application of the Pavlik harness, when is skin traction used
Skin traction is used prior to the harness
70
When is hip spica cast used
When there is difficulty maintaining stable reduction. It is applied and changed periodically to allow for growth. Generally over 3 to 6 months
71
What is Legg-calve perthes
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
In legg calve perthes what is thought to be the cause, who is more at risk and when are the peak ages
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
In legg calve perthes how is diagnosis made?
X-ray. bone scans and mri may show process sooner.
74
What are the early symptoms of legg calve perthes
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
What are worsening symptoms of legg calve perthes
ROM becomes limited. Weakness and muscle wasting develop
76
What is the desired outcome for legg calve perthes
Pain free hip that functions properly. To promote healing and prevent deformity, femoral head contained in hip socket until ossification is complete
77
What needs to be done for the hip/head of femur to promote healing in legg calve perthes
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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