Week 27-Ronan Parker-COPD/Emphysema

Gas Exchange
1) External respira@on—gas exchange between Respiratory Histology
alveoli and pulmonary capillary blood. Upper Airway
-O2 diffuses from alveolar air -Nose & pharynx —pseudostra@fied ciliated
(PO2=105mmHg) to pulmonary capillaries Trachea columnar, goblet cells
(PO2 =40mmHg). -Oropharynx & laryngopharynx—nonkera@nized
Main Bronchus
-CO2 diffuses opposite from pulmonary stra@fied squamous epithelium
capillaries (PCO2=45mmHg) to alveolar air Lobar
Lower Airway
Bronchus
(PO2=40mmHg). -Larynx—nonkera@nized stra@fied squamous
-Exchange occurs un@l equal on both sides. (above vocal folds), pseudostra@fied ciliated
Segmental
-Exchange influenced by par@al pressure columnar/goblet (below vocal folds)
Bronchus
gradients, small diffusion distance, large -Trachea & bronchi—pseudostra@fied ciliated
surface area, solubility of gases. Terminal Bronchiole columnar, goblet cells.
-Short membrane distance & large surface -Bronchioles, terminal, & respiratory bronchioles
Respiratory Bronchiole
area=efficient gas exchange. —simple ciliated columnar, goblet, Clara cells
2) Internal respira@on—gas exchange at the Alveolar Duct
-Alveolar ducts/sacs—simple squamous.
@ssue level. Alveolar Sac Alveoli -Alveoli—simple squamous (TI) & cuboidal (TII)

Arterial Hypoxemia from Gas Exchange Failure

Key Symptoms of Respiratory Disease
-Arterial hypoxemia is O2 deficiency in arterial blood.
-Dyspnea—SOB and difficulty breathing.
-4 causes
-Cough & sputum
1) Alveolar hypoven,la,on
-Hemoptysis—coughing up blood/bloody sputum.
-Poor ven@la@on to alveoli from defect along respiratory path, thoracic cage
-Chest pain/@ghtness; **differen@ate from angina**
abnormali@es, or upper airway obstruc@on.
-Expiratory wheeze.
-Nocturanal hypoxemia in COPD=intercostal & accessory muscle inhibi@on with
-Nasal symptoms—runny, blocked nose & sneezing.
shallow breathing during sleep.
Respiratory Failure & Headaches 2) Alveolar Diffusion Defect
-Resp. failure: inadequate gas -Alveolar membrane thickness change (fibrosis)/reduc@on in alveolar surface area
exchange by respiratory system. (emphysema) result in slowing of O2 diffusion into blood; PO2 equilibrium doesn’t
-Morning headaches are occur.
expression of poor ven@la@on 3) Ven,la,on:Perfusion Mismatch
(hypercapnia) during sleep. -Ven@la@on and perfusion in different areas aren’t equal thus inefficient gas transfer.
-Hypercapnia & low O2 in the -High V:Q=lung well ven@lated, aren’t many capillaries supplying blood to area;
brain cause vessel perfusing blood well-oxygenated.
dila@on thus -Low V:Q=good blood supply, but poor ven@la@on; blood perfusing poorly oxygenated.
increased blood 4) Shunt (V:Q ra,o=0)
flow & ICP. -2 types:
-Headache is from a) Anatomical CVS abnormality—mixed venous blood bypasses ven@lated alveoli
nerves, muscles, meninges in passing from RT to LT side of heart
& vessels of head/neck b) Intrapulmonary Defect—mixed venous blood perfuses under ven@lated alveoli.
compressed with increased
cranial volume.
 Histopathology
Histopathology
-Primarily effects bronchi with mucous gland -Primarily alters acinus (distal to terminal bronchioles)
hypertrophy, hyperplasia, & hypersecre@on. w alveolar wall destruc@on w/o fibrosis (enlarged air
-Goblet cells lining airways increase resul@ng in space).
excessive mucus produc@on. -Permanent bronchiole dila@on & enlargement.
-Too few ciliated cells for proper removal -Loss of alveolar capillaries w/ alveoli loss
contributes to airway obstruc@on. -Deforma@on of terminal and respiratory bronchioles
-Ciliated pseudostra@fied columnar line bronchi;
due to septa loss normally suppor@ng structures.
with smoking, can morph into stra@fied -Elas@c @ssue surrounding alveolar septa lost; reduces
squamous via metaplasia. trac@on of small airways leading to collapse on
Pathogenesis expira@on.
-3 month chronic produc@ve cough in 2 successive Pathogenesis
years when other causes have been excluded. -Permanent airway space enlargement distal to
-Tracheal & bronchi mucous gland hypertrophy Breathing Control terminal bronchioles & alveolar wall destruc@on
Chemoreceptor RegulaTon
induced by air irritants Parts & Func,ons without fibrosis.
-Respiratory system responds to -Inflamma@on & neutrophil accumula@on from toxic
-Mucous hyper-secre@on reflects bronchial 1) Medullary Rhythmicity Centre changes in H+, CO2 and O2
involvement; airway obstruc@on is small airway -Controls inhala@on & exhala@on substance exposure.
levels in CNS
disease & coexis@ng emphysema. -Inhala@on=2 sec; exhala@on=3 sec. -Epithelial injury & ECM proteolysis from neutrophils
-Peripheral chemoreceptors are (release elastase), cytokines (IL-8), & oxidants.
-Impulse in inspiratory centre sent to in aor@c bodies in aor@c arch
COPD Airway ObstrucTon Pathophysiology intercostal muscles/diaphragm s@mula@ng and caro@d bodies in caro@d Cor Pulmonale & COPD
-COPD—chronic recurrent airflow obstruc@on where contrac@on arteries. -Cor pulmonale—RV hypertrophy/dila@on from
airway resistance is increased. -Inhala@on centre inac@ve ader 2 sec. -When PO2 in arterial blood is pulmonary hypertension acributed to primary
-Common cause=cigarece smoking/second-hand smoke. stopping impulse below 100 but above 50 mmHg, disorders of lung parenchyma/pulmonary
-Chronic bronchi@s/emphysema oden coexist (COPD). -Diaphragm and intercostals relax peripheral chemoreceptors are vasculature.
-Dis@nguished from asthma by COPD being irreversible. -Impulses from expiratory centre cause s@mulated. -Acute=dila@on only; chronic=characteris@c RV
abdominal/intercostal muscle contrac@on -Nega@ve feedback responds to (oden RA) hypertrophy.
Pathophysiology (only in forced breathing) increased PCO2, decreased pH Process
-Poor airflow due to lung @ssue breakdown 2) Pneumotaxic Centre (pons) (increased H+), and decreased -Alveolar hypoxia causes increased pulmonary
(emphysema) & small airway disease (bronchioli@s). -Coordinates inhala@on and exhala@on PO2 s@mula@ng increased vascular resistance (PVR) causing pulmonary
-Toxic substance exposure=inflamma@on/epithelial -Sends inhibitory signal to inspiratory centre breathing. hypertension.
injury. -Helps shorten inspira@on @me (more ac@ve, -Acutely—hypoxia causes pulmonary
-Goblet cell metaplasia causes small airway disease more rapid breathing) vasoconstric@on diver@ng blood away from poorly
mucous plugging, inflamma@on, and fibrosis. ven@lated alveoli; acempt to maintain V:Q balance.
-Compensa@on via squamous cell metaplasia (no cilia/ 3) Apneus@c Centre (pon) -Chronic—pulmonary vascular bed structural
goblet cells) due to con@nued cigarece smoke. -Helps coordinate changes (remodelling) induced; muscle hypertrophy
-Smoke inac@vate α1-an@trypsin=elastase breakdown inhala@on and in@mal fibrosis making arteries thicker & less
inhibited and compliant (↑ PVR)
-Limited airflow due to exhala@on. -In COPD, have reduc@on in vasodilator synthesis/
a) loss of elas@city & alveolar acachments in -Sends release & prostacyclin (protect against vascular
emphysema—elas@c recoil reduced & expiratory s@mulatory remodelling).
airway collapse impulses to -RV hypertrophies and dilates due to ↑ PVR.
b) Inflamma@on & scaring narrow small airways. inspiratory for
c) Airways blocked from mucus secre@ons. ac@va@on
-Major blockage due to mucus-secre@ng goblet cells in -Overrides
bronchial mucosa. pneumotaxic
centre.