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NR 507 Week 4 Parts 1–3 Discussion Responses (2026) PDF | Chamberlain Pathophysiology

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Stay ahead in NR 507 Pathophysiology at Chamberlain University with these Week 4 Discussion Responses (Parts 1, 2 & 3). This PDF focuses on Alterations in Renal Function, presented in a clear, academically structured format aligned with discussion board expectations and grading rubrics. Ideal for reinforcing key renal concepts, improving participation scores, and saving valuable study time. ️ Well-written, course-aligned discussion responses ️ Topic-focused: renal function alterations ️ Excellent reference for discussion posts and replies Instant digital PDF download – no physical item shipped NR 507 week 4, NR 507 discussion, renal function alterations, pathophysiology responses, Chamberlain NR 507, renal disorders nursing, discussion board answers, nursing discussion help, NR 507 study guide, graduate nursing notes, pathophysiology study notes, exam prep nursing, online class support, Chamberlain University nursing, NR 507 PDF, nursing school success, Week 4 discussion responses, renal pathophysiology

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NR 507
Week 4 Part 1, 2 & 3
Discussion Responses
Alterations in Renal Function

,Week 3: Cardiovascular, Cellular, and Hematologic Disorders -
Discussion Part Three


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Discussion
This week's graded topics relate to the following Course Outcomes (COs).


1 Analyze pathophysiologic mechanisms associated with selected
disease states. (PO 1)



2
Differentiate the epidemiology, etiology, developmental
considerations, pathogenesis, and clinical and laboratory
manifestations of specific disease processes. (PO 1)


3
Examine the way in which homeostatic, adaptive, and
compensatory physiological mechanisms can be supported and/or
altered through specific therapeutic interventions. (PO 1, 7)


4 Distinguish risk factors associated with selected disease states.
(PO 1)



5 Describe outcomes of disruptive or alterations in specific
physiologic processes. (PO 1)



6 Distinguish risk factors associated with selected disease states.
(PO 1)



7 Explore age-specific and developmental alterations in physiologic
and disease states. (PO 1, 4)




Discussion Part Three (graded)

,A new patient is brought into the office for their annual evaluation. The child is a 6-year-old and
appears a bit small for their age but not so small that any alarm bells are set off. The vitals are: P
= 116, R = 22, T = 98.6 F, BP = 110/50. (The normal vitals in a 6-year-old are P = 75 – 120, R =
16 – 22, T = 98.6 , BP = (85-115)/(48-64). Examination of the lungs is normal, HEENT is normal,
as is the abdominal exam. The heart however, seems laterally displaced and there appears to be
only a continuous murmur which can be described as crescendo/decrescendo systolic murmur
that extends into diastole. Because, you were trained at Chamberlain College of Nursing you
immediately know that this is probably a patent ductus arteriosus.

Explain the murmur from a mechanistic view of the hearts physiological functioning?

What is the epidemiology of a patent ductus arteriosus?

How is a patent ductus arteriosus treated?


Responses

Lorna Durfee 5/18/2016 9:36:07 AM
Discussion Part Three

A new patient is brought into the office for their annual evaluation. The child is a 6-year-
old and appears a bit small for their age but not so small that any alarm bells are set off.
The vitals are: P = 116, R = 22, T = 98.6 F, BP = 110/50. (The normal vitals in a 6-year-
old are P = 75 – 120, R = 16 – 22, T = 98.6 , BP = (85-115)/(48-64). Examination of the
lungs is normal, HEENT is normal, as is the abdominal exam. The heart, however, seems
laterally displaced, and there appears to be only a continuous murmur which can be
described as crescendo/decrescendo systolic murmur that extends into diastole. Because
you were trained at Chamberlain College of Nursing, you immediately know that this is
probably a patent ductus arteriosus.
Doctor Brown and Class:
Explain the murmur from a mechanistic view of the heart's physiological functioning?
Philips (2015) describes ductus arteriosus (DA) as a vascular connection between the main
pulmonary artery and aorta. When the fetus is developing the DA diverts blood from the
pulmonary artery into the aorta. This diversion bypasses the lungs. When the baby is born,
the DA is supposed to undergo constriction and obliteration. A patent ductus arteriosus
results when the ductus fails to close completely after delivery (Philips, 2016).
The murmur in patent ductus arteriosus is a result of pulmonary vascular resistance that has
fallen and reversal of shunting of blood occurs. The blood shunts left to right from aorta to
the pulmonary artery. This condition increases pulmonary blood flow, and venous return to
the LA and LV and places an increased workload on the left side of the heart. It could also
increase right ventricular pressure if there are pulmonary changes that are vascular that
occur in response to the increased flow of blood and can lead to increased pulmonary. If
pulmonary resistance has fallen, infants will have a continuous-machinery type murmur
that is heard at the left upper sternal border through systole and diastole (McCance,
Huether, Brashers, and Rote, 2014, p. 1203).
What is the epidemiology of a patent ductus arteriosus? Baffa (2014) reveals that
patent ductus arteriosus is responsible for 5 to 10% of heart abnormalities. The ratio of
male to female is 1:3. Patent ductus is seen commonly with the birth of premature infants.
It is present in about 45% of premature infants with a weight less than 1750 g, and it rises

, to 80% with a birth weight of less than 1200 g. Patent ductus can cause heart failure in
premature infants with a birth weight of less than 1750 gram and 40 to 50% of infants born
with a weight of less than 1500 g (Baffa, 2014).
Patent ductus arteriosus occurs in about 5% to 10% of all congenital defects (McCance,
Huether, Brashers, & Rote, 2014, pp. 1202-1203).
How is a patent ductus arteriosus treated?
Baffa (2014) explains that in the use of Indomethacin in pre-term infants is used with or
without fluid restriction. For term infants or older children, this treatment is not effective.
If a connection persists between the thoracic descending aorta and the pulmonary artery
then surgery or catheter-based correction is indicated (Baffa, 2014). She also informs us
that transcatheter closure has become the treatment of choice in children great than one
year. In those infants, less than one or who have varieties of the ductus, surgery with
division and ligation may be a better choice versus the trans-catheter approach. If the shunt
is large enough and is causing symptoms of heart failure or pulmonary hypertension,
closing it should be done once there is stabilization. For a persistent PDA without heart
failure and pulmonary hypertension closure can be done at any time as an elective (Baffa,
2014).
Lam, Lopushinsky, Ma, Dicke, and Brindle (2015) did a study using meta-analysis
comparing clinical outcomes for surgical ligation or catheter occlusion treatment to see if
one treatment was better. They searched the literature and randomized control trials
between 1950 and 2014 for information. They excluded adult or premature patients and
those with no comparison. They found that both treatments have comparable outcomes,
but re-intervention is more common with catheter-based treatment. Complications appear
lower, and the hospital stay is shorter. They suggest further studies to help determine the
best and optimal treatment (Lam, Lopushinsky, Ma, Dicke, & Brindle, 2015, pp. 784 and
791).


References

Baffa, J. M. (2014). Patent Ductus Arteriosus (PDA). In Merck Manual online.

Retrieved from https://www.merckmanuals.com/professional/pediatrics/congenital-

cardiovascular-anomalies/patent-ductus-arteriosus-pda

Lam, J. Y., Lopushinsky, S. R., Ma, I. W., Dicke, F., & Brindle, M. E. (2015). Treatment

Options for Pediatric Patent Ductus Arteriosus. Chest, 148(3), 784-793.

doi:10.1378/chest.14-2997

McDaniel, N.L. (2014). Alterations of Cardiovascular Function in Children. In

McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (Eds.)

Pathophysiology: The biologic basis for disease in adults and children (7th ed.,

pp. 1202, 1203). St. Louis, MO: Mosby.

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