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NR 507 ADVANCED PATHOPHYSIOLOGY MIDTERM EXAM WITH ACTUAL CORRECT QUESTIONS AND VERIFIED DETAILED ANSWERS|FREQUENTLY TESTED QUESTIONS AND SOLUTIONS|NEWEST|GUARANTEED PASS 2026/2027

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NR 507 ADVANCED PATHOPHYSIOLOGY MIDTERM EXAM WITH ACTUAL CORRECT QUESTIONS AND VERIFIED DETAILED ANSWERS|FREQUENTLY TESTED QUESTIONS AND SOLUTIONS|NEWEST|GUARANTEED PASS 2026/2027

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NR 507 ADVANCED PATHOPHYSIOLOGY
MIDTERM EXAM WITH ACTUAL
CORRECT QUESTIONS AND VERIFIED
DETAILED ANSWERS|FREQUENTLY
TESTED QUESTIONS AND
SOLUTIONS|NEWEST|GUARANTEED
PASS 2026/2027
bronchitis

inflammation of the bronchial tubes

3 characteristics of bronchitis

bronchial inflammation
hypersecretion of mucus
chronic productive cough for at least 3 consecutive months for at least 2 successive years

Perfusion

The supply of oxygen to and removal of wastes from the cells and tissues of the body as a result of the
flow of blood through the capillaries.

results of chronic bronchitis/ low perfusion

cyanosis
right to left shunting
chronic hypoxemia

Why is there cyanosis with chronic bronchitis

there is hypoxia due to unfavorable conditions for gas exchange

Right to left shunting

when blood passes from the right ventricle through the lungs and to the left ventricle without perfusion

Causes of bronchitis

-long term exposure to environmental irritants
-repeated episodes of acute infection (RSV infection in early infancy)
-Factors affecting gestational childhood lung development (preterm birth)

Pathogenesis of bronchitis
1|Page

,-Exposure to airborne irritants
- Irritant activates bronchial smooth muscle constriction and mucus secretion
- Triggers release of inflammatory mediators from immune cells located in the lamina propria

most common irritant with bronchitis is?

tobacco product smoke

what does long term exposure to irritants promote in bronchitis? (5)

- smooth muscle hypertrophy
- hypertrophy and hyperplasia of goblet cells
- epithelial cell metaplasia
- migration of more WBC to site
- thickening and rigidity of bronchial basement membrane

What does smooth muscle hypertrophy do in lungs?

causes increased bronchoconstriction

Hypertrophy and hyperplasia of goblet cells do what in the bronchial

promotes hypersecretion of mucus

What are characteristics of epithelial cell metaplasia?

squamous cells become nonciliated and are less protective; allow passage of toxins and WBCs

What does the migration of WBCs to the bronchial do?

increases inflammation of the cite and causes fibrosis in the bronchial wall

How does the thickening and rigidity of bronchial basement membranes effect the lungs?

leads to further narrowing of the bronchial passageways

What acid-base disorder is seen in chronic bronchitis?

respiratory acidosis

how does chronic bronchitis lead to respiratory acidosis?

hyperinflation of the alveoli causes CO2 retention

Where does air enter the body?

naso and oropharynx (mouth and nose)

Where does air go after it passes through the nose and mouth?

it passes through the trachea

After air passes through the trachea where does it go?

goes into the left or right bronchi

2|Page

, Where does air flow after the bronchi?

into the smaller bronchioles

Where does air flow after the bronchioles?

into the alveoli

Describe how blood flows to become oxygenated

- deoxygenated systemic blood flows from the vena cava to R atrium
- Tricuspid valve opens to flow to R ventricle
-Pulmonary semilunar valve opens and blood flows to the alveolar capillaries for gas exchange from the
pulmonary trunk and L & R pulmonary arteries
- blood goes from alveolar capillaries to pulmonary veins to return oxygenated blood to the left atrium
- bicuspid valve opens to allow blood to go to left ventricle
- aortic semilunar valve opens and blood goes to the aorta
- aorta pushes oxygenated blood out to the body

What is the formula for cardiac output?

CO = HR x SV

cardiac reserve

difference between resting and maximal CO; should be about 4-5x as high but does decrease 1% per
year after age 30

What type of relationship does heart rate and stroke volume have?

inverse
low HR = longer fill time = increase stroke volume
high HR = lower fill time = lower stroke volume

What is preload?

the degree of stretch on the heart before it contracts/ amount of blood entering the ventricles during
diastole

average amount of preload?

120-130 mls

When fibers stretch during diastole how does that effect contraction?

contraction is stronger

What happens when cardiac fibers overstretch during diastole?

decreased contraction due to fibers being unable to snap back

What can cause increased preload

CHF and hypervolemia
3|Page

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