NR 507: Advanced Pathophysiology Midterm With 100% correct answers + rationales 2026

Asthma

Chronic disease due to bronchoconstriction and an excessive inflammatory response in the bronchioles

What are 5 s/s of asthma

coughing

wheezing

shortness of breath

rapid breathing

chest tightness

Pathophysiology of asthma (5)

-airway inflammation, bronchial hyper-reactivity and smooth muscle spasm

-excess mucus production and accumulation

-hypertrophy of bronchial smooth muscle

-airflow obstruction

-decreased alveolar ventilation

Bronchioles

smaller passageways that originate from the bronchi that become the alveoli

3 layers of the bronchioles

innermost layer

middle layer - lamina propria

outermost layer

lamina propria

the middle layer of the bronchioles

structure of the lamina propria

embedded with connective tissue cells and immune cells

purpose of the lamina propria

white blood cells are present to help protect the airways

How does the lamina propria effect the lungs in regards to asthma

the WBCs protective feature goes into overdrive causing an inflammatory response that damages host tissue

What does the innermost layer of the bronchioles contain

columnar epithelial ells and mucus producing goblet cells

What does the outermost layer of the bronchioles contain

smooth muscle cells

what does the outermost layer of the bronchioles do

control the airways ability to constrict and dilate

alveolar hyperinflation

When air is unable to move out of the alveolar like it should due to bronchial walls collapsing around possible mucus plug thus trapping air inside

how does hyperinflation occur?

the ongoing inflammatory process of asthma produces mucus and pus plug that the bronchial walls collapse around

Effect of hyperinflation of the alveolar

-expanded thorax and hypercapnia (retention of CO2)

- respiratory acidosis

What are two anticholinergic drugs used for asthma

tiotropium and ipratropium

What do anticholinergics do in the lungs?

These drugs block the effects of the parasympathetic nervous system

- increasing bronchodilation

MOA of anticholinergic drugs for asthma

the parasympathetic system is stimulated by the vagal nerve to release acetylcholine which binds to the cholinergic receptors of the respiratory tract to cause bronchial constriction = decreased airflow

- blocking the cholinergic receptors prevents acetylcholine binding preventing the bronchial constriction

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

-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 bronchials

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 bronchials 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

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

What can cause decreased preload

cardiac tamponade and hypovolemia

What are two common causes of hypovolemia

dehydration and hemorrhage

Afterload

the amount of resistance to open the semilunar valves and eject of blood from the ventricle

what influences afterload (3)

ventricle wall thickness (muscle strength)

arterial pressure (resistance to ejection)

ventricle chamber size (blood volume capacity)

what can cause an increase in afterload

systemic hypertension

valve disease

COPD (pulmonary hypertension)

what can decrease afterload

hypotension or vasodilation

what influences cardiac contractility (inotropic state)

levels of electrolytes

High levels of ATP

level of oxygen available

synchronous muscle contraction

What electrolytes are used for cardiac muscle contraction?

sodium potassium and calcium

What increases cardiac muscle contraction

sympathetic stimulation; fear anxiety and increased thyroxine

what decreases cardiac muscle contraction

low ATP levels; ischemia hypoxia or acidosis

Stimulation of what set a resting HR (chronotropic state)

parasympathetic system

what stimulates the parasympathetic system

the vagus nerve

What does the parasympathetic system do?

It releases acetycholine which decreases heart rate and causes vasodilation

What can extreme vagal response result in?

life threatening bradycardia

What mediates the sympathetic system

epinephrine and norepinephrine

What does the sympathetic system promote in the cardiac system

vasoconstriction and increased HR

What can uncontrolled tachycardia lead to?

reduced stroke volume and fatigue

What are the two parts of the cardiac cycle?

diastole and systole

What causes blood to move from the atria to the ventricles

gravity and atriole systole

What causes the S1 heart sound?

Bicuspid/Mitral and Tricuspid valves closing

What are the atrioventricular valves?

tricuspid and bicuspid (mitral) valves

What are the semilunar valves?

pulmonary and aortic valves

What causes the semilunar valves to open?

As ventricles contract and intraventricular pressure rises, blood is pushed up against the SL valves, forcing them to open

ejection fraction

measurement of the volume percentage of left ventricular contents ejected with each contraction

What causes the semilunar valves to close?

ventricles relax and intraventricular pressure falls, blood flows back from the arteries, and fill the cusps of the semilunar valves

What causes the S2 heart sound?

closing of semilunar (aortic and pulmonary) valves

What prevents the backflow into the ventricles

semilunar valves

Stenosis of heart valve

A narrowing of the valve opening, causing turbulent flow and enlargement of the emptying chamber

Stenosis of a heart valve, may result in what?

Narrowing of the heart valves means that blood moves with difficulty out of the heart. Results may include chest pain, edema in the feet or ankles, and irregular heartbeat. and hypertrophy

heart failure

cardiac dysfunction caused by the inability of the heart to provide adequate CO resulting in inadequate tissue perfusion

Left sided heart failure characteristic

inability of the left ventricle to provide adequate blood flow into systemic circulation

Causes of left sided heart failure

systemic hypertension

left ventricle MI

LV hypertrophy

Aortic SL valve or bicuspid valve damage

Secondary to right heart failure

How does LV hypertrophy lead to left sided heart failure

The hypertrophy is secondary to cardiac damage resulting in an enlarged by weaker structure that holds more blood

How does Aortic SL valve or bicuspid valve damage lead to heart failure

damage leads to back flow into the left atrium or ventricle after ejection

Biventricular failure

unresolved left sided heart failure will increase pressure on the right side of the heart contributing to right sided heart failure as well

How does heart failure progress from hypertension?

- high systemic vascular pressure causes high after load requires the left ventricle to increase contraction force to eject the blood

- damage causes reduced ejection fraction and left ventricle gets tired and becomes unable to eject normal amount of blood

- increased amount of blood remaining in left ventricle and increased left ventricle preload causes the left atrium unable to eject the normal amount of blood into the left ventricle

- blood volume and pressure backs up into the pulmonary veins

- increased pressure will force fluid from the pulmonary capillaries into the pulmonary tissues

What does fluid in the pulmonary tissue result in

the areas are flooded and results in pulmonary edema and dyspnea

cor pulmonale

right-sided heart failure

right sided heart failure

inability of the right ventricle to provide adequate blood flow into the pulmonary circulation

Causes of right sided heart failure

- pulmonary disease

- pulmonary hypertension

- RV MI

- RV Hypertrophy

- pulmonary SLV or tricuspid valve damage

- secondary to left heart failure

What is the most common cause of right sided heart failure

pulmonary hypertension

Progression of right sided heart failure

- damage causes the right ventricle to increase contraction force to eject/unload the blood

- over time EF is reduced and right ventricle us unable to eject the normal amount of blood

- the blood remaining in the RV increases and RA preload increases until the RA is unable to eject the normal amount of blood into the RA

- the amount of blood remaining in the right atrium increases causing an increase in RA preload

- blood volum enad pressure then backs up into the vena cava and systemic veins

signs and symptoms of right sided heart failure

jugular vein distension

hepatosplenomegaly

peripheral edema

Why does hepatosplenomegaly develop in right sided heart failure

the large volume of blood flow through the liver and spleen causes these areas to be engorged

why does peripheral edema occur in right sided heart failure

Increased pressure forces fluid from the systemic capillaries into the peripheral tissues and flood those areas

High output failure

inability of the heart to pump sufficient amounts of blood to meet the circulatory needs of the body despite normal blood volume and cardiac contractility

causes of high output failure

Severe anemia

Nutritional deficiencies

Hyperthyroidism

Sepsis

Extreme febrile state

Process of high output failure

- impaired oxygen delivery of excessive tissue oxygen demands cause tissue hypoxia

- catecholamines initiation increase HR and stroke volume

- increased cardiac output is produced but depletes cardiac muscle reserve overtime and leads to low output failure over time

Troponin-Calcium Binding

Calcium binds to troponin on the thin filament

sliding filament theory

theory that actin filaments slide toward each other during muscle contraction, while the myosin filaments are still

Hematopoiesis

formation of blood cells