1
NR 507 Advanced Pathophysiology Midterm Study Guide
Pulmonary:
▪ Review concepts related to anticholinergic drugs and the treatment forasthma
o (Block acetylcholine binding (primarily in lung) -> bronchodilation
through decreased parasympathetic response
▪ Tiotropium, Ipratropium
o Short-actingbeta-adrenergicagonists(SABA)– activatebeta
receptors primarily in the lung -> bronchodilation through
increased sympathetic response
▪ Albuterol
o Oral corticosteroids – inhibit inflammatory cells and chemical
production -> reduce inflammatory process
▪ Prednisone, prednisolone, methylprednisolone
o Long acting:
▪ Inhaled corticosteroids
• Beclomethasone, triamcinolone
▪ Mast cell stabilizers
• Cromolyn
▪ Leukotriene modifiers
• Zafirlukast, Montelukast
▪ Longactingbeta2 adrenergicagonists
• Salmeterol
▪ Methylxanthines
• Theophylline
▪ Monoclonal antibodies
• Omalizumab
▪ Bronchitisandassociatedpathogenesis
o In bronchitis, inspired irritants promote bronchial inflammation,causing
bronchial edema, increases the size and number of
Page 1 of 16
,2
mucous glands and goblet cells in the airway epithelium, smoothmuscle
hypertrophy with fibrosis, and narrowing of the airways.
o Hypersecretion of thick, tenacious mucus occurs and cannot be cleared
because of impaired ciliary function. The lung’s defense mechanisms are
therefore compromised, increasing susceptibilityto pulmonary infection,
which contributes to airway injury and ineffective repair.
o Frequent infectious exacerbations from bacterial colonization ofdamaged
airways are complicated by bronchospasm with dyspnea and
productive cough.
▪ Chronic bronchitis and related acid/base disturbances, perfusion, blood flow
between the heart and lungs
o Characterized by bronchial inflammation, hypersecretion ofmucus,
chronic productive cough, persisting for at least 3 consecutive
months for at least 2 successive years.
o Symptoms: productive purulent cough, copious sputum production,
shortness of breath, wheezing, rhonchi, cyanosis,peripheral edema.
o Ventilation is decreased resulting in alveolar hyperinflation and
hypercapnia resulting in respiratory acidosis.
o The high concentration of CO2 creates an unfavorable condition for gas
exchange thus causing a ventilation/perfusion mismatch.
o Decreased perfusion of the pulmonary capillaries with oxygenated
blood results in chronic pulmonary hypoxia. Right and Left shunting =
blood passes from the RV to the lungs to LVwithout perfusion (gas
exchange)
▪ Asthma signs and symptoms
o Coughing
o Wheezing
o Shortness of breath
o Rapid breathing
o Chest tightness
▪ Bronchioles
o 3 layer tube-like structure surrounding the lumen or air
passageway
Page 2 of 16
, 3
o Inner most layer
▪ Closest to the lumen, is composed of columner epithelialcells
and mucus producing goblet cells
o Outermost layer
▪ Composed of smooth muscle cells, responsible for the
ability of the airways to constrict and dilate
o Middle layer (lamina propria)
▪ Embedded with connective tissue cells as well as immuneIcells.
These immune cells include a number of different kinds of
WBCs located here to protect the airways.
▪ Alveolar hyperinflation with asthma
o Mast cell degranulation triggered by excessive amts of IgE that have
airingly formed this individual that will bind that allergen asit enters the
airway that mast cell degranulation releases chemicals that releases
mucus production and accumulation as well as chemicals to contribute
to smooth muscle constriction. With that and mucus plugs that form
result in hyperinflation of the alveoli and eventual erosion of airway
tissue.
▪ Polycythemia vera
o A chronic neoplastic, nonmalignant condition characterized by
overproduction of red blood cells and platelets and splenomegaly.
o Erythrocytosis is the essential component of PV. Clonal proliferation of
erythroid progenitors occurs in the bone marrowindependent of
erythropoietin, although the cells express a normal erythropoietin
receptor.
o More than 95% of individuals with PV possess an acquired point
mutation in the Janus kinase 2 gene, a cytoplasmic tyrosine kinase, on
chromosome 9. JAK2 increases the activity of erythropoietin receptor and
is self-regulatory so that JAK2 activitydiminishes over time.
o Manifestations:
▪ Present initially with large spleen, frequently abd pain and
discomfort.
▪ Increased viscosity, as well as thrombocythemia and increased
platelet dysfunction, leads to a hypercoagulable
Page 3 of 16
NR 507 Advanced Pathophysiology Midterm Study Guide
Pulmonary:
▪ Review concepts related to anticholinergic drugs and the treatment forasthma
o (Block acetylcholine binding (primarily in lung) -> bronchodilation
through decreased parasympathetic response
▪ Tiotropium, Ipratropium
o Short-actingbeta-adrenergicagonists(SABA)– activatebeta
receptors primarily in the lung -> bronchodilation through
increased sympathetic response
▪ Albuterol
o Oral corticosteroids – inhibit inflammatory cells and chemical
production -> reduce inflammatory process
▪ Prednisone, prednisolone, methylprednisolone
o Long acting:
▪ Inhaled corticosteroids
• Beclomethasone, triamcinolone
▪ Mast cell stabilizers
• Cromolyn
▪ Leukotriene modifiers
• Zafirlukast, Montelukast
▪ Longactingbeta2 adrenergicagonists
• Salmeterol
▪ Methylxanthines
• Theophylline
▪ Monoclonal antibodies
• Omalizumab
▪ Bronchitisandassociatedpathogenesis
o In bronchitis, inspired irritants promote bronchial inflammation,causing
bronchial edema, increases the size and number of
Page 1 of 16
,2
mucous glands and goblet cells in the airway epithelium, smoothmuscle
hypertrophy with fibrosis, and narrowing of the airways.
o Hypersecretion of thick, tenacious mucus occurs and cannot be cleared
because of impaired ciliary function. The lung’s defense mechanisms are
therefore compromised, increasing susceptibilityto pulmonary infection,
which contributes to airway injury and ineffective repair.
o Frequent infectious exacerbations from bacterial colonization ofdamaged
airways are complicated by bronchospasm with dyspnea and
productive cough.
▪ Chronic bronchitis and related acid/base disturbances, perfusion, blood flow
between the heart and lungs
o Characterized by bronchial inflammation, hypersecretion ofmucus,
chronic productive cough, persisting for at least 3 consecutive
months for at least 2 successive years.
o Symptoms: productive purulent cough, copious sputum production,
shortness of breath, wheezing, rhonchi, cyanosis,peripheral edema.
o Ventilation is decreased resulting in alveolar hyperinflation and
hypercapnia resulting in respiratory acidosis.
o The high concentration of CO2 creates an unfavorable condition for gas
exchange thus causing a ventilation/perfusion mismatch.
o Decreased perfusion of the pulmonary capillaries with oxygenated
blood results in chronic pulmonary hypoxia. Right and Left shunting =
blood passes from the RV to the lungs to LVwithout perfusion (gas
exchange)
▪ Asthma signs and symptoms
o Coughing
o Wheezing
o Shortness of breath
o Rapid breathing
o Chest tightness
▪ Bronchioles
o 3 layer tube-like structure surrounding the lumen or air
passageway
Page 2 of 16
, 3
o Inner most layer
▪ Closest to the lumen, is composed of columner epithelialcells
and mucus producing goblet cells
o Outermost layer
▪ Composed of smooth muscle cells, responsible for the
ability of the airways to constrict and dilate
o Middle layer (lamina propria)
▪ Embedded with connective tissue cells as well as immuneIcells.
These immune cells include a number of different kinds of
WBCs located here to protect the airways.
▪ Alveolar hyperinflation with asthma
o Mast cell degranulation triggered by excessive amts of IgE that have
airingly formed this individual that will bind that allergen asit enters the
airway that mast cell degranulation releases chemicals that releases
mucus production and accumulation as well as chemicals to contribute
to smooth muscle constriction. With that and mucus plugs that form
result in hyperinflation of the alveoli and eventual erosion of airway
tissue.
▪ Polycythemia vera
o A chronic neoplastic, nonmalignant condition characterized by
overproduction of red blood cells and platelets and splenomegaly.
o Erythrocytosis is the essential component of PV. Clonal proliferation of
erythroid progenitors occurs in the bone marrowindependent of
erythropoietin, although the cells express a normal erythropoietin
receptor.
o More than 95% of individuals with PV possess an acquired point
mutation in the Janus kinase 2 gene, a cytoplasmic tyrosine kinase, on
chromosome 9. JAK2 increases the activity of erythropoietin receptor and
is self-regulatory so that JAK2 activitydiminishes over time.
o Manifestations:
▪ Present initially with large spleen, frequently abd pain and
discomfort.
▪ Increased viscosity, as well as thrombocythemia and increased
platelet dysfunction, leads to a hypercoagulable
Page 3 of 16
