NR 507
ADVACNED PATHOPHYSIOLOGY
WEEK 1 – 4
MIDTERM EXAMS
QNS & ANS
2025
,Pulmonary
1. Concepts of anticholinergic drug and asthma:
Anticholinergic drugs: block acetylcholine binding (primarily in the lungs) -promotes bronchiole
dilation through decrease in the parasympathetic response (tiotropium & ipratropium) is fast
acting
2. Bronchitis & associated pathogenesis:
Begins with an exposure to an irritant (tobacco smoke) – activates bronchiole smooth muscle
constriction- mucus secretion- release of inflammatory mediators(histamine, prostaglandins &
leukotrienes) normal response to occasional airborne site irritants- over bronchitis is over long
term 3 months for over 2 consecutive years- = smooth muscle hypertrophy = increase
bronchoconstriction, hypertrophy and hyperplasia of goblet cells= mucus hypersecretion,
epithelia cell metaplasia = non-ciliated squamous cells, migration of more WBCs to site =
inflammation and fibrosis in bronchial wall, thickening and rigidity of bronchial basement
membrane= narrowing of bronchial passageways : Increased mucus production- inflammation
process = weight loss, loss of appetite, muscle weakness (interleukin controls appetite) increases
protease activity= breakdown of elastin in the connective tissues of the lung= destruction of the
wall between the alveoli and lungs = large ineffective air sacs develop-elastic recoil of bronchial
wall -destroys bronchi and cant dilate and they stay constricted =air trapping : Chronic bronchitis
=Dyspnea- air trapping increased mucus, increase WOB r/t chronic bronchoconstriction
Cough- irritated and inflamed bronchial epithelia membrane Hypoxia & Hypercapnia -from
impaired gas exchange
3. Chronic bronchitis and related acid/base disturbance:
Hypercapnia (CO2 retention) = Respiratory acidosis
r/t anatomical changes ventilation is compromised esp. exhalation = alveolar hyperinflation)
expanded thorax) hypercapnia CO2 retention = respiratory acidosis\
4. Perfusion:
the actual exchange of O2 and CO2 in the bloodstream occurs via the alveoli and pulmonary
capillaries: the passage of fluid to an organ or a tissue usually referring to delivery of blood to an
area
5. Blood flow between the heart and lungs in chronic bronchitis:
Poor ventilation leads to r to l shunting to occur= deoxygenated blood passes from r ventricle to
the lungs to the l ventricle without adequate perfusion (gas exchange) the kidneys respond by
secreting erythropoietin increasing RBC production the increase in RBC increase O2 carrying
capacity -the increase blood volume increases the workload of the pulmonary and cardiovascular
systems increasing blood volume and vasoconstriction = pulmonary HTN= increase workload on
the R ventricle =cardiac hypertrophy= R side HF or Cor Pulmonale
6. Asthma signs and symptoms:
Coughing esp. at night, chest tightness, shortness of breath, wheezing on exhalation, and rapid
breathing: Characteristics: airway inflammation, bronchial hyperactivity, smooth muscle spasms, =
excessive mucus production, hypertrophy of bronchial smooth muscle -obstruction and decrease
alveolar ventilation
7. Bronchioles in asthma:
There are 3 layers of the bronchiole which is a tube-like structure surrounding the lumen or airway
, passageway: innermost layer is composed of columnar epithelial cells and goblet cells-
The outermost layer is composed of smooth muscle cells responsible for the ability of the airway
to constrict and dilate – the middle layer is the laminar propria and it is embedded with connective
tissue and immune cells: in asthma these protective features go overactive =inflammation
response= damage to host tissue=hypertrophy of the bronchioles smooth muscle and excessive
mucus production: bronchioles spasm-mucus production-obstruction
8. Alveolar hyperinflation with asthma:
Increase mucus production from the goblet cells in the inflammation process forms plugs of mucus
and pus and block alveolar passageways leading to air trapping and hyperinflation = erosion of
airway tissue
9. Polycythemia Vera:
a rare blood disease in which the body makes too many RBCs making the blood thicker than
normal causing blood clots; is often a result of chronic low levels of O2 in the blood, the kidney
compensates by increase secretion of erythropoetin, the primary hormone responsible for
stimulating RBC production= as a result patients with chronic bronchitis will often exhibit
increased HCT levels and can develop a condition called secondary polycythemia vera.
10. Mechanism of action of anticholinergic drugs to treat asthma:
Anticholinergic drugs bind to muscarine receptors and block the action of acetylcholine They
reduce Broncho motor tone =bronchodilation: block acetylcholine binding, bronchodilation,
decrease parasympathetic response
Cardiovascular:
11. Review concepts of Cardiac Output:
Cardiac Output= Heart rate x Stroke volume\
Cardiac output: is the volume of blood ejected by each ventricle per minute
(75 bpm x 70ml = 5.25 L/min) 5 L of blood in the body= every drop of blood circulates the body
-per heartbeat per minute
Cardiac output decrease with age at a rate of 1% per year after the age of 30 (other factors can
accelerate the rate of decline)
Cardiac output is a key component of HF and is important to understand the connection b/t HR &
SV:
DECRESE in HR (longer filling time) INCREASE in SV
INCREASE in HR (shorter fill time) DECREASE in SV
12. Concepts of cardiac contractility:
Contractility (ionotropic state)
Contractility is determined by Calcium availability and its interaction with actin and myosin
Contractility INCREASES by sympathetic stimulation (fever, anxiety, increased thyroxine levels;
factors that increase the cellular metabolic rate will increase strength of muscle cell at least
temporarily)
Contractility DECREASES by low levels of ATP (ischemia, hypoxia, acidosis;
Factors that decrease the amount of energy available to the muscle cell will decrease strength of
contraction)
13. Preload and Afterload Concepts:
PRELOAD: is the degree of myocardial fiber length stretch before contraction; the degree of
stretch will be influenced by the end diastolic ventricular volume (EDV) [edv= is the amount of
blood entering each ventricle during diastoles {approx. 120- 130 ml}] PRELOAD IS LOADING
, THE HEART WITH BLOOD
Preload can be INCREASED by CHF, hypervolemia, (increased BV)
Preload can be DECREASED by cardiac tamponade, hypovolemia (hemorrhage or dehydration)
AFTERLOAD is the amount of tension the ventricle must develop during systole to open the
semilunar valves and eject blood into circulation:
Afterload is influenced by: Ventricular wall thickness= muscle strength
Arterial pressure= resistance to ejection
Ventricle chamber size= blood volume capacity
Ventricular wall thickness: muscle strength (increase thickness the more muscle mass decrease
tension force required for ejection)
Arterial pressure: resistance to ejection (increase pressure within the pulmonary or systemic
vessels = increase tension required for ejection)
Ventricle chamber size: increased blood volume (increase tension required for ejection)
AFTERLOAD INCREASED by systemic HTN, valve disease, COPD = pulmonary HTN
AFTERLOAD DECREASED by hypotension or vasodilation, such as SHOCK
LAPELACE LAW: THE HEART MUST WORK HARDER (INCREASE TENSION) WHEN
HEART MUSCLE IS WEAK: VENTRICLES ARE HYPERTROPHIED (HOLD MORE
VOLUME) AND OR PULMONARY OR SYSTEMIC BP IS ELEVATED
14. Systole and Diastole:
Systole and Diastole are two phases of the cardiac cycle: they occur as the heart beats, pumping
blood through the body.
Systole: occurs when the heart contracts to pump blood OUT
Diastole: occurs when the heart RELAXES after contraction
Systole causes the ejection of blood into the aorta and pulmonary trunk. Systole, period of
contraction of the ventricles of the heart that occurs between the first and the second heart sound
Diastole period of relaxation of the heart muscle accompanied by the filing of the chambers with
blood
15. Heart valves: When they open and close
4 valves of the heart
2 atrioventricular valves/ AV valves: tricuspid and bicuspid
2 semilunar valves/ SL : pulmonary and aortic
Valves are responsible for unidirectional flow of blood through the heart
The valves open and close in response to myocardial contractions and pressure changes within the
heart
As the RV contracts the TRICUSPID valve closes and the PULMONARY valve opens; closure of
the TRUCUSPID valve keeps blood from backing up into the RIGHT ATRIUM and the opening of
the PULMONARY valve allows blood to flow into the pulmonary artery into the Lung
As the LV contracts the BICUSPID (mitral) valve closes, and the (SL) AORTIC valve opens,
closure of the BICUSPID (mitral) valve prevents blood from backing into the LEFT ATRIUM and
the opening of the AORTIC valve allows blood to flow into the aorta and into the Body
ADVACNED PATHOPHYSIOLOGY
WEEK 1 – 4
MIDTERM EXAMS
QNS & ANS
2025
,Pulmonary
1. Concepts of anticholinergic drug and asthma:
Anticholinergic drugs: block acetylcholine binding (primarily in the lungs) -promotes bronchiole
dilation through decrease in the parasympathetic response (tiotropium & ipratropium) is fast
acting
2. Bronchitis & associated pathogenesis:
Begins with an exposure to an irritant (tobacco smoke) – activates bronchiole smooth muscle
constriction- mucus secretion- release of inflammatory mediators(histamine, prostaglandins &
leukotrienes) normal response to occasional airborne site irritants- over bronchitis is over long
term 3 months for over 2 consecutive years- = smooth muscle hypertrophy = increase
bronchoconstriction, hypertrophy and hyperplasia of goblet cells= mucus hypersecretion,
epithelia cell metaplasia = non-ciliated squamous cells, migration of more WBCs to site =
inflammation and fibrosis in bronchial wall, thickening and rigidity of bronchial basement
membrane= narrowing of bronchial passageways : Increased mucus production- inflammation
process = weight loss, loss of appetite, muscle weakness (interleukin controls appetite) increases
protease activity= breakdown of elastin in the connective tissues of the lung= destruction of the
wall between the alveoli and lungs = large ineffective air sacs develop-elastic recoil of bronchial
wall -destroys bronchi and cant dilate and they stay constricted =air trapping : Chronic bronchitis
=Dyspnea- air trapping increased mucus, increase WOB r/t chronic bronchoconstriction
Cough- irritated and inflamed bronchial epithelia membrane Hypoxia & Hypercapnia -from
impaired gas exchange
3. Chronic bronchitis and related acid/base disturbance:
Hypercapnia (CO2 retention) = Respiratory acidosis
r/t anatomical changes ventilation is compromised esp. exhalation = alveolar hyperinflation)
expanded thorax) hypercapnia CO2 retention = respiratory acidosis\
4. Perfusion:
the actual exchange of O2 and CO2 in the bloodstream occurs via the alveoli and pulmonary
capillaries: the passage of fluid to an organ or a tissue usually referring to delivery of blood to an
area
5. Blood flow between the heart and lungs in chronic bronchitis:
Poor ventilation leads to r to l shunting to occur= deoxygenated blood passes from r ventricle to
the lungs to the l ventricle without adequate perfusion (gas exchange) the kidneys respond by
secreting erythropoietin increasing RBC production the increase in RBC increase O2 carrying
capacity -the increase blood volume increases the workload of the pulmonary and cardiovascular
systems increasing blood volume and vasoconstriction = pulmonary HTN= increase workload on
the R ventricle =cardiac hypertrophy= R side HF or Cor Pulmonale
6. Asthma signs and symptoms:
Coughing esp. at night, chest tightness, shortness of breath, wheezing on exhalation, and rapid
breathing: Characteristics: airway inflammation, bronchial hyperactivity, smooth muscle spasms, =
excessive mucus production, hypertrophy of bronchial smooth muscle -obstruction and decrease
alveolar ventilation
7. Bronchioles in asthma:
There are 3 layers of the bronchiole which is a tube-like structure surrounding the lumen or airway
, passageway: innermost layer is composed of columnar epithelial cells and goblet cells-
The outermost layer is composed of smooth muscle cells responsible for the ability of the airway
to constrict and dilate – the middle layer is the laminar propria and it is embedded with connective
tissue and immune cells: in asthma these protective features go overactive =inflammation
response= damage to host tissue=hypertrophy of the bronchioles smooth muscle and excessive
mucus production: bronchioles spasm-mucus production-obstruction
8. Alveolar hyperinflation with asthma:
Increase mucus production from the goblet cells in the inflammation process forms plugs of mucus
and pus and block alveolar passageways leading to air trapping and hyperinflation = erosion of
airway tissue
9. Polycythemia Vera:
a rare blood disease in which the body makes too many RBCs making the blood thicker than
normal causing blood clots; is often a result of chronic low levels of O2 in the blood, the kidney
compensates by increase secretion of erythropoetin, the primary hormone responsible for
stimulating RBC production= as a result patients with chronic bronchitis will often exhibit
increased HCT levels and can develop a condition called secondary polycythemia vera.
10. Mechanism of action of anticholinergic drugs to treat asthma:
Anticholinergic drugs bind to muscarine receptors and block the action of acetylcholine They
reduce Broncho motor tone =bronchodilation: block acetylcholine binding, bronchodilation,
decrease parasympathetic response
Cardiovascular:
11. Review concepts of Cardiac Output:
Cardiac Output= Heart rate x Stroke volume\
Cardiac output: is the volume of blood ejected by each ventricle per minute
(75 bpm x 70ml = 5.25 L/min) 5 L of blood in the body= every drop of blood circulates the body
-per heartbeat per minute
Cardiac output decrease with age at a rate of 1% per year after the age of 30 (other factors can
accelerate the rate of decline)
Cardiac output is a key component of HF and is important to understand the connection b/t HR &
SV:
DECRESE in HR (longer filling time) INCREASE in SV
INCREASE in HR (shorter fill time) DECREASE in SV
12. Concepts of cardiac contractility:
Contractility (ionotropic state)
Contractility is determined by Calcium availability and its interaction with actin and myosin
Contractility INCREASES by sympathetic stimulation (fever, anxiety, increased thyroxine levels;
factors that increase the cellular metabolic rate will increase strength of muscle cell at least
temporarily)
Contractility DECREASES by low levels of ATP (ischemia, hypoxia, acidosis;
Factors that decrease the amount of energy available to the muscle cell will decrease strength of
contraction)
13. Preload and Afterload Concepts:
PRELOAD: is the degree of myocardial fiber length stretch before contraction; the degree of
stretch will be influenced by the end diastolic ventricular volume (EDV) [edv= is the amount of
blood entering each ventricle during diastoles {approx. 120- 130 ml}] PRELOAD IS LOADING
, THE HEART WITH BLOOD
Preload can be INCREASED by CHF, hypervolemia, (increased BV)
Preload can be DECREASED by cardiac tamponade, hypovolemia (hemorrhage or dehydration)
AFTERLOAD is the amount of tension the ventricle must develop during systole to open the
semilunar valves and eject blood into circulation:
Afterload is influenced by: Ventricular wall thickness= muscle strength
Arterial pressure= resistance to ejection
Ventricle chamber size= blood volume capacity
Ventricular wall thickness: muscle strength (increase thickness the more muscle mass decrease
tension force required for ejection)
Arterial pressure: resistance to ejection (increase pressure within the pulmonary or systemic
vessels = increase tension required for ejection)
Ventricle chamber size: increased blood volume (increase tension required for ejection)
AFTERLOAD INCREASED by systemic HTN, valve disease, COPD = pulmonary HTN
AFTERLOAD DECREASED by hypotension or vasodilation, such as SHOCK
LAPELACE LAW: THE HEART MUST WORK HARDER (INCREASE TENSION) WHEN
HEART MUSCLE IS WEAK: VENTRICLES ARE HYPERTROPHIED (HOLD MORE
VOLUME) AND OR PULMONARY OR SYSTEMIC BP IS ELEVATED
14. Systole and Diastole:
Systole and Diastole are two phases of the cardiac cycle: they occur as the heart beats, pumping
blood through the body.
Systole: occurs when the heart contracts to pump blood OUT
Diastole: occurs when the heart RELAXES after contraction
Systole causes the ejection of blood into the aorta and pulmonary trunk. Systole, period of
contraction of the ventricles of the heart that occurs between the first and the second heart sound
Diastole period of relaxation of the heart muscle accompanied by the filing of the chambers with
blood
15. Heart valves: When they open and close
4 valves of the heart
2 atrioventricular valves/ AV valves: tricuspid and bicuspid
2 semilunar valves/ SL : pulmonary and aortic
Valves are responsible for unidirectional flow of blood through the heart
The valves open and close in response to myocardial contractions and pressure changes within the
heart
As the RV contracts the TRICUSPID valve closes and the PULMONARY valve opens; closure of
the TRUCUSPID valve keeps blood from backing up into the RIGHT ATRIUM and the opening of
the PULMONARY valve allows blood to flow into the pulmonary artery into the Lung
As the LV contracts the BICUSPID (mitral) valve closes, and the (SL) AORTIC valve opens,
closure of the BICUSPID (mitral) valve prevents blood from backing into the LEFT ATRIUM and
the opening of the AORTIC valve allows blood to flow into the aorta and into the Body
