Mid Term Study Guide NR 507
Mid Term Study Guide NR 507
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, =
, Mid Term Study Guide NR 507
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
Mid Term Study Guide NR 507
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, =
, Mid Term Study Guide NR 507
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
