NR 507 Advanced Pathophysiology Midterm Study Guide
I I I I I I
Pulmonary:
▪ Review Iconcepts Irelated Ito Ianticholinergic Idrugs Iand Ithe Itreatment IforIasthma
o (Block Iacetylcholine Ibinding I(primarily Iin Ilung) I-> Ibronchodilation
I through I decreased I parasympathetic I response
▪ Tiotropium, IIpratropium
o Short-acting Ibeta-adrenergic Iagonists I(SABA) I– Iactivate Ibeta
Ireceptors Iprimarily Iin Ithe Ilung I-> Ibronchodilation Ithrough
Iincreased Isympathetic Iresponse
▪ Albuterol
o Oral Icorticosteroids I– Iinhibit I inflammatory Icells Iand Ichemical
Iproduction I-> Ireduce Iinflammatory Iprocess
▪ Prednisone, I prednisolone, I methylprednisolone
o Long I acting:
▪ Inhaled I corticosteroids
• Beclomethasone, I triamcinolone
▪ Mast Icell Istabilizers
• Cromolyn
▪ Leukotriene Imodifiers
• Zafirlukast, I Montelukast
▪ Long Iacting Ibeta2 Iadrenergic Iagonists
• Salmeterol
▪ Methylxanthines
• Theophylline
▪ Monoclonal I antibodies
• Omalizumab
▪ Bronchitis Iand Iassociated Ipathogenesis
o In Ibronchitis, Iinspired Iirritants Ipromote Ibronchial Iinflammation,Icausing
I bronchial I edema, I increases I the I size I and I number I of
, mucous I glands I and I goblet I cells I in I the I airway I epithelium, I smoothImuscle
Ihypertrophy I with I fibrosis, Iand Inarrowing Iof Ithe I airways.
o Hypersecretion I of I thick, I tenacious I mucus I occurs I and I cannot I be Icleared
Ibecause Iof Iimpaired Iciliary Ifunction. IThe Ilung’s Idefense Imechanisms I are
I therefore I compromised, I increasing I susceptibilityIto Ipulmonary Iinfection,
Iwhich Icontributes Ito Iairway Iinjury Iand Iineffective Irepair.
o Frequent Iinfectious Iexacerbations Ifrom Ibacterial Icolonization IofIdamaged
I airways I are I complicated I by I bronchospasm I with Idyspnea Iand
Iproductive Icough.
▪ Chronic Ibronchitis I and Irelated Iacid/base Idisturbances, Iperfusion, Iblood Iflow
Ibetween Ithe Iheart Iand Ilungs
o Characterized Iby Ibronchial Iinflammation, Ihypersecretion IofImucus,
Ichronic I productive I cough, I persisting Ifor I at Ileast I 3 Iconsecutive
I months I for I at I least I 2 I successive I years.
o Symptoms: I productive I purulent I cough, I copious I sputum Iproduction,
I shortness I of Ibreath, Iwheezing, I rhonchi, Icyanosis,Iperipheral Iedema.
o Ventilation Iis Idecreased Iresulting Iin Ialveolar Ihyperinflation Iand
Ihypercapnia Iresulting Iin Irespiratory Iacidosis.
o The I high I concentration I of I CO2 I creates I an I unfavorable I condition Ifor I gas
I exchange I thus I causing I a I ventilation/perfusion I mismatch.
o Decreased Iperfusion Iof Ithe Ipulmonary Icapillaries Iwith Ioxygenated
Iblood Iresults Iin Ichronic Ipulmonary Ihypoxia. IRight Iand ILeft Ishunting I=
Iblood Ipasses Ifrom Ithe IRV Ito Ithe Ilungs Ito ILVIwithout Iperfusion I(gas
Iexchange)
▪ Asthma Isigns Iand Isymptoms
o Coughing
o Wheezing
o Shortness I of I breath
o Rapid I breathing
o Chest Itightness
▪ Bronchioles
o 3 Ilayer Itube-like Istructure Isurrounding Ithe Ilumen Ior Iair
Ipassageway
, o Inner I most I layer
▪ Closest Ito I the Ilumen, Iis Icomposed Iof Icolumner I epithelialIcells
Iand Imucus Iproducing Igoblet Icells
o Outermost I layer
▪ Composed I of I smooth I muscle I cells, I responsible I for I the
Iability Iof Ithe Iairways Ito Iconstrict Iand Idilate
o Middle Ilayer I(lamina Ipropria)
▪ Embedded I with I connective I tissue I cells I as I well I as I immuneIcells.
IThese Iimmune Icells Iinclude Ia Inumber Iof Idifferent Ikinds Iof
IWBCs Ilocated Ihere Ito Iprotect Ithe Iairways.
▪ Alveolar Ihyperinflation Iwith I asthma
o Mast I cell I degranulation I triggered I by I excessive I amts I of I IgE I that Ihave
Iairingly Iformed Ithis Iindividual Ithat Iwill Ibind Ithat Iallergen IasIit Ienters Ithe
Iairway Ithat Imast Icell Idegranulation Ireleases Ichemicals I that I releases
I mucus I production I and I accumulation I as Iwell Ias Ichemicals Ito Icontribute
Ito Ismooth Imuscle Iconstriction. IWith Ithat Iand Imucus Iplugs Ithat Iform
Iresult Iin Ihyperinflation Iof Ithe Ialveoli Iand Ieventual Ierosion Iof Iairway
Itissue.
▪ Polycythemia I vera
o A I chronic I neoplastic, I nonmalignant I condition I characterized I by
Ioverproduction Iof Ired Iblood Icells Iand Iplatelets Iand Isplenomegaly.
o Erythrocytosis Iis Ithe Iessential Icomponent Iof IPV. IClonal Iproliferation Iof
Ierythroid Iprogenitors Ioccurs Iin Ithe Ibone ImarrowIindependent Iof
Ierythropoietin, Ialthough Ithe Icells Iexpress Ia Inormal Ierythropoietin
Ireceptor.
o More I than I 95% I of I individuals I with I PV I possess I an I acquired I point
Imutation I in Ithe I Janus Ikinase I2 I gene, Ia I cytoplasmic Ityrosine Ikinase, Ion
Ichromosome I9. IJAK2 Iincreases Ithe Iactivity Iof Ierythropoietin Ireceptor Iand
Iis Iself-regulatory Iso Ithat IJAK2 IactivityIdiminishes Iover Itime.
o Manifestations:
▪ Present Iinitially Iwith Ilarge Ispleen, Ifrequently Iabd Ipain Iand
Idiscomfort.
▪ Increased Iviscosity, Ias Iwell Ias Ithrombocythemia Iand Iincreased
I platelet I dysfunction, I leads I to I a I hypercoagulable
I I I I I I
Pulmonary:
▪ Review Iconcepts Irelated Ito Ianticholinergic Idrugs Iand Ithe Itreatment IforIasthma
o (Block Iacetylcholine Ibinding I(primarily Iin Ilung) I-> Ibronchodilation
I through I decreased I parasympathetic I response
▪ Tiotropium, IIpratropium
o Short-acting Ibeta-adrenergic Iagonists I(SABA) I– Iactivate Ibeta
Ireceptors Iprimarily Iin Ithe Ilung I-> Ibronchodilation Ithrough
Iincreased Isympathetic Iresponse
▪ Albuterol
o Oral Icorticosteroids I– Iinhibit I inflammatory Icells Iand Ichemical
Iproduction I-> Ireduce Iinflammatory Iprocess
▪ Prednisone, I prednisolone, I methylprednisolone
o Long I acting:
▪ Inhaled I corticosteroids
• Beclomethasone, I triamcinolone
▪ Mast Icell Istabilizers
• Cromolyn
▪ Leukotriene Imodifiers
• Zafirlukast, I Montelukast
▪ Long Iacting Ibeta2 Iadrenergic Iagonists
• Salmeterol
▪ Methylxanthines
• Theophylline
▪ Monoclonal I antibodies
• Omalizumab
▪ Bronchitis Iand Iassociated Ipathogenesis
o In Ibronchitis, Iinspired Iirritants Ipromote Ibronchial Iinflammation,Icausing
I bronchial I edema, I increases I the I size I and I number I of
, mucous I glands I and I goblet I cells I in I the I airway I epithelium, I smoothImuscle
Ihypertrophy I with I fibrosis, Iand Inarrowing Iof Ithe I airways.
o Hypersecretion I of I thick, I tenacious I mucus I occurs I and I cannot I be Icleared
Ibecause Iof Iimpaired Iciliary Ifunction. IThe Ilung’s Idefense Imechanisms I are
I therefore I compromised, I increasing I susceptibilityIto Ipulmonary Iinfection,
Iwhich Icontributes Ito Iairway Iinjury Iand Iineffective Irepair.
o Frequent Iinfectious Iexacerbations Ifrom Ibacterial Icolonization IofIdamaged
I airways I are I complicated I by I bronchospasm I with Idyspnea Iand
Iproductive Icough.
▪ Chronic Ibronchitis I and Irelated Iacid/base Idisturbances, Iperfusion, Iblood Iflow
Ibetween Ithe Iheart Iand Ilungs
o Characterized Iby Ibronchial Iinflammation, Ihypersecretion IofImucus,
Ichronic I productive I cough, I persisting Ifor I at Ileast I 3 Iconsecutive
I months I for I at I least I 2 I successive I years.
o Symptoms: I productive I purulent I cough, I copious I sputum Iproduction,
I shortness I of Ibreath, Iwheezing, I rhonchi, Icyanosis,Iperipheral Iedema.
o Ventilation Iis Idecreased Iresulting Iin Ialveolar Ihyperinflation Iand
Ihypercapnia Iresulting Iin Irespiratory Iacidosis.
o The I high I concentration I of I CO2 I creates I an I unfavorable I condition Ifor I gas
I exchange I thus I causing I a I ventilation/perfusion I mismatch.
o Decreased Iperfusion Iof Ithe Ipulmonary Icapillaries Iwith Ioxygenated
Iblood Iresults Iin Ichronic Ipulmonary Ihypoxia. IRight Iand ILeft Ishunting I=
Iblood Ipasses Ifrom Ithe IRV Ito Ithe Ilungs Ito ILVIwithout Iperfusion I(gas
Iexchange)
▪ Asthma Isigns Iand Isymptoms
o Coughing
o Wheezing
o Shortness I of I breath
o Rapid I breathing
o Chest Itightness
▪ Bronchioles
o 3 Ilayer Itube-like Istructure Isurrounding Ithe Ilumen Ior Iair
Ipassageway
, o Inner I most I layer
▪ Closest Ito I the Ilumen, Iis Icomposed Iof Icolumner I epithelialIcells
Iand Imucus Iproducing Igoblet Icells
o Outermost I layer
▪ Composed I of I smooth I muscle I cells, I responsible I for I the
Iability Iof Ithe Iairways Ito Iconstrict Iand Idilate
o Middle Ilayer I(lamina Ipropria)
▪ Embedded I with I connective I tissue I cells I as I well I as I immuneIcells.
IThese Iimmune Icells Iinclude Ia Inumber Iof Idifferent Ikinds Iof
IWBCs Ilocated Ihere Ito Iprotect Ithe Iairways.
▪ Alveolar Ihyperinflation Iwith I asthma
o Mast I cell I degranulation I triggered I by I excessive I amts I of I IgE I that Ihave
Iairingly Iformed Ithis Iindividual Ithat Iwill Ibind Ithat Iallergen IasIit Ienters Ithe
Iairway Ithat Imast Icell Idegranulation Ireleases Ichemicals I that I releases
I mucus I production I and I accumulation I as Iwell Ias Ichemicals Ito Icontribute
Ito Ismooth Imuscle Iconstriction. IWith Ithat Iand Imucus Iplugs Ithat Iform
Iresult Iin Ihyperinflation Iof Ithe Ialveoli Iand Ieventual Ierosion Iof Iairway
Itissue.
▪ Polycythemia I vera
o A I chronic I neoplastic, I nonmalignant I condition I characterized I by
Ioverproduction Iof Ired Iblood Icells Iand Iplatelets Iand Isplenomegaly.
o Erythrocytosis Iis Ithe Iessential Icomponent Iof IPV. IClonal Iproliferation Iof
Ierythroid Iprogenitors Ioccurs Iin Ithe Ibone ImarrowIindependent Iof
Ierythropoietin, Ialthough Ithe Icells Iexpress Ia Inormal Ierythropoietin
Ireceptor.
o More I than I 95% I of I individuals I with I PV I possess I an I acquired I point
Imutation I in Ithe I Janus Ikinase I2 I gene, Ia I cytoplasmic Ityrosine Ikinase, Ion
Ichromosome I9. IJAK2 Iincreases Ithe Iactivity Iof Ierythropoietin Ireceptor Iand
Iis Iself-regulatory Iso Ithat IJAK2 IactivityIdiminishes Iover Itime.
o Manifestations:
▪ Present Iinitially Iwith Ilarge Ispleen, Ifrequently Iabd Ipain Iand
Idiscomfort.
▪ Increased Iviscosity, Ias Iwell Ias Ithrombocythemia Iand Iincreased
I platelet I dysfunction, I leads I to I a I hypercoagulable
