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NR283 Pathophysiology Exam Questions & Answers - Nursing Study Guide

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Prepare for Chamberlain College of Nursing NR 283 Pathophysiology with this comprehensive study resource designed to reinforce essential pathophysiology concepts and support nursing exam preparation. Review major topics involving cellular injury and adaptation, inflammation, fluid and electrolyte balance, acid-base regulation, cardiovascular, respiratory, renal, gastrointestinal, neurological, endocrine, immune, and musculoskeletal disorders, along with disease processes, clinical manifestations, complications, and nursing considerations. Ideal for NR 283 exam review, practice questions, study preparation, and final exam revision for the academic year. Current Stuvia listings confirm strong relevance for the search terms NR283, NR 283, Pathophysiology, Chamberlain, Exam Questions, and Study Guide.

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NR283 Pathophysiology Final Exam
inflammation a localized, immunologic defense against tissue injury, infection, or an allergy;
involves white blood cells and a number of different chemicals that serve to
protect the body against invading pathogens or cellular/tissue trauma.


clinical manifestations of inflammation heat, redness, pain, swelling, loss of function




Which immune chemical mediators contribute to the -kinins
swelling associated with acute inflammation? -prostaglandins
-histamine
-leukotrienes


what can cause chronic inflammation? foreign material left in the body




acute inflammation has an immediate onset, a relatively short duration (several days), and is usually
caused by injury or an invading pathogen



recap of acute inflammation cause: pathogens, allergy, injury
duration: immediate, lasts for several days
chemical mediators: Complement system, Kinins, Leukotrienes, Interferon-
gamma
immune cells: Infection (neutrophils, monocytes, macrophages) or Allergy
(eosinophils, mast cells)
lesion: Rash, Pus, Abscess
outcomes: Resolution, Abscess formation, Chronic inflammation
examples: Abscess (skin, organ); Allergic reaction (anaphylaxis)


steps of inflammation 1. Injury to capillaries and tissue cells
2. Release of bradykinin from injured cells
3. Bradykinin stimulates pain receptors.
4. Pain causes mast cells and basophils to release histamine.
5. Bradykinin and histamine cause capillary dilation, which increases the blood
flow to and capillary permeability in the injured area
6. Break in skin allows bacteria to enter tissue
7. Neutrophils phagocytize bacteria (monocytes activated later)
8. Macrophages (mature monocytes) leave the bloodstream and phagocytose
microbes.




why do redness and warmth occur in inflammation? Proinflammatory hormones (e.g., prostaglandins, cytokines, histamines) increase
blood flow to the injured area



why does swelling occur in inflammation? it is the result of a combination of increased blood flow and extravasation of white
blood cells (WBCs), fluids, and other substances out of the vascular system into
the injured area.


why does pain occur in inflammation? results from the pressure of swollen tissues that stimulate pain receptors.




why does loss of function occur in inflammation? occurs as a result of swelling. For example, swelling can impede muscle and
joint movement. Pain can also cause guarding and avoidance of painful voluntary
movement, which also contributes to loss of function.


exudate collection of interstitial fluid in the area of inflammation (pus)

, NR283 Pathophysiology Final Exam
serous exudate consists of fluid with small amounts of protein and white blood cells; commonly
seen in allergic reactions or burns



fibrinous exudate thick, sticky, and high cell and fibrin content that causes more risk for scar tissue
at the site.



purulent exudate thick, yellow-green substance that contains leukocytes, cell debris, and
microorganisms; commonly seen in bacterial infections and known as pus



abscess a localized pocket of pus in a solid tissue




hemorrhagic exudate occurs when blood cells have been damaged.




systemic inflammation manifestation -mild fever (pyrexia)
-malaise (feeling unwell)
-fatigue
-headache
-anorexia (loss of appetite)


fever a result of pyrogens, white blood cells (WBCs), or macrophages. As the
pyrogens circulate in the bloodstream, the body temperature resets at a higher
level


-itis inflammation




diagnostic testing for inflammation -Complete blood count (CBC) test: elevated WBC is an indicator of inflammation.
-C-reactive protein (CRP): identifies if the protein is in the blood which indicates
acute inflammation and necrosis within 24-48 hours
-Erythrocyte sedimentation rate (ESR) determines if there are elevated plasma
proteins which indicates the rate at which red blood cells (RBC) settle in a
sample.
-Differential count identifies the proportion of each type of WBC altered based on
the cause.
-aspartate aminotransferase (AST): prescribed if a client has liver disease or is in
an acute stage of a myocardial infarction.
-Creatine kinase with myocardial component (CK-MB) is specific for myocardial
infarctions
-Alanine aminotransferase (ALT) is specific for the liver.


complications of inflammation lungs: impairs oxygenation
heat: can cause heart attack
joints: prevents range of motion
muscles: spasms


chronic inflammation develops slowly and has a relatively long duration (months/years/lifetime); can
result from prolonged acute inflammation, a foreign substance that remains in the
body, or as part of an autoimmune condition


recap of chronic inflammation cause: Persistent acute inflammation, Persistent foreign body, Autoimmune
reaction
duration: delayed, lasts up to months or years
chemical mediators: Cytokinins
immune cells: Monocytes, Macrophages, Lymphocytes, Fibroblasts
lesion: Rash, Fibrosis, Granuloma
outcomes: Tissue destruction, Fibrosis
examples: Autoimmune disorders (rheumatoid arthritis); Cystic fibrosis

, NR283 Pathophysiology Final Exam
acute vs chronic inflammation chronic inflammation includes less swelling and exudate with an increased
number of lymphocytes, macrophages, and fibroblasts. Patients with chronic
inflammation experience more tissue destruction and fibrous scar tissue
formation that contributes to ongoing pain and alterations in the function of the
impacted tissue


treatments for inflammation mild exercise, physiotherapy, occupational therapy, good nutrition, hydration

-medications: anti-inflammatory drugs, analgesic drugs, nonsteroidal anti-
inflammatory drugs (NSAIDS), corticosteroids

-RICE: rest, ice, compression, elevation


healing by primary/first intention In an area with small amounts of tissue loss, tissue regenerates with little to no
scarring (stitches or staples can be used)



healing by secondary/second intention When a lot of tissue is missing, much of it is replaced by scar tissue




steps of the healing process 1. injury and inflammation
2. granulation and epithelial tissue growth
3. scar (fibrous tissue remains)


factors that affect wound healing age
nutritional deficiencies
hemoglobin levels
circulation problems
presence of additional medical conditions
chronic disease
radiation or chemotherapy exposure
long-term use of glucocorticoids (steroids)


A client is seen in the emergency clinic after jumping off wrap the ankle, elevate the injured leg, apply an icepack, rest the affected area
a ski lift and injuring their ankle. Which steps can the
client take to reduce inflammation and pain?


why are young children at risk for inflammation? immature immune systems




why are elderly patients at risk for inflammation? less able to adapt to foreign pathogens




why are those who are underinsured at risk for might not have access to services that provide early intervention
inflammation?



why is good hand hygiene important? decreases the risk of pathogen transmission, which can reduce the potential for
an inflammatory response



how does safety equipment use affect inflammation? reduces injury and subsequent inflammatory response




how does safe food handling affect inflammation? reduces contamination and the spread of pathogens that can cause inflammation
and associated immune responses



scar tissue fibrous connective tissue that binds damaged tissue; non elastic and shrinks over
time

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