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Respiratory - COPD (*COPD
Chronic Obstructive Pulmonary Disease
mix of…
Respiratory - COPD
*COPD
Chronic Obstructive Pulmonary Disease
- mix of emphysema = barrel chest
- chronic bronchitis / b
PathoPhys of COPD
- main inflammatory cells are macrophages, CD8 T cells and neutrophils
--> neutrophils release protease to cause inflammation oft he alveoli
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COPD Complications / Sequalae
- Oxygen induce hypercapnia and respiratory depression
Oxygen induced hypercapnia / respiratory depression in COPD
- CO2 normally controls medullary centre repiratory drive
--> CO2 more than O2
- COPD patient though have tolerance for high CO2 levels so don't stimulate their drive
- they are used to being hypoxic
--> giving O2 to them at too high a level shocks their body
--> hypoventilation and respiratory depression
Peripheral vs Central Chemoreceptors for Respiratory Centre
- central = CNS = CO2 levels (senses hypercapnea = high CO2)
--> BB barrier only allows CO2
--> CO2 then dissolves into bicarba nd H+ ion
--> H+ ions are then sensed by central chemoreceptors
- peripheral = PO2 sensing hypoxia
- relays through the glossopharyngeal nerve = CN 9
Blood Brain Barrier and CO2 levels
- BB barrier doesn't allow H+ ions to cross
- but it does allow CO2
- 1 more item...
Peripheral Chemoreceptors
- carotid sinus baroreceptors and chemoreceptors
--> glossopharyngeal = CN 9 afferent, Vagus efferent
- aortic arch baroreceptors and chemoreceptors
--> BOTH Vagus afferent and efferent
- peripheral = PO2 sensing hypoxia
- 1 more item...
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V/Q mismatch is the most common cause of COPD O2 induced hypercapnea
- V/Q mismatch presents just as normal hypoxia = lethargy and confusion
- reactive O2 species which is also a cause of COPD O2 hypercap
--> presents witch more acute chest pains, etc. related to the inflammation and damage from the oxygen species
Clinical Cases
Clinical Case
- 3 more items...
COPD caused secondary polycythemia
- due to chronic hypoxia in COPD, the juxtaglomerular cells in the renal cortex and medulla release EPO
--> they are constantly trying to increase the O2 in the blood due to hypoxia of tissues
--> leads to polycythemia = increased hematocrit
- note that polycythemia can be categorized in two ways, primary vs secondary (COPD here) and also true polycythemia or relative polycythemia
Notes:
- note that hypoxemia on COPD comes from the 2 things that cause it = emphysema air trapping and poor diffusion at A-a
- and bronchitis (+ emphysema also)
--> cause mucus plugging + destroyed alveoli
-->cause air trapping
COPD *Exacerbations
- most are caused by the major viruses and bacteria in elderly
--> rhinovirus, influenza, parainfluenza
bacteria = Hib, strep pneumo, and Morexella
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*Chronic Bronchitis
- can be either from COPD
--> directly caused by smoking
- inflammation from other processes?
*Emhphysema
- can be either from COPD
--> directly caused by smoking
--> upper lobes of lungs
- lower lobes of lungs = Alpha-antitrypsin deficiency
--> Alpha antitrypsin made in the liver
--> stops elastin trypsin from breaking down elastin
*Alpha1-antritrypsin deficiency = AAT
- alpha1-antitrypsin made in the liver
--> stops elastin trypsin from breaking down elastin
- A - A - T = ALWAYS AVOID TOBACCO
--> AAT is accelerated by tobacco smoke
--> even second hand smoke
--> most important for AAT people to stay away from smoke
*Elastin in the acini of lungs
- elastin uses non-polar residues and interlinking desmosomes to give lung alveoli stretch
Notes:
- note that elastin gets its rubber like properties from its crosslinking / desmosomes
--> also from nonpolar AA's
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*Acinar vs Panacinar Emphysema
- acinar emphysema = in the bronchioles
--> smoke damage emphysema
--> think of the smoke affecting the bcronchioles mainly on its way in
--> activates macrophages and recruitment of neutrophils to fight the toxins in the bronchioles
- PANacinar emphysema = in the bronchioles
--> from AAT deficiency
--> think of the alveolar macrophages creating damage directly in the alveoli
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Clinical Cases
COPD Case
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Notes:
- note that bronchiectasis and bronchitis of COPD are not the same thing
- bronchitis and COPD are cause primarily by smoking and bronchiectasis is often idiopathic and independent of smoking, although people with COPD can get it
- for questions like this, you need to find the illness they have --> here it is COPD
- COPD is ALWAYS caused by smoking --> this is a behavioural cause
- COPD bronchitis presents with 4 main things
--> thickened bronchial walls
--> lymphocytic infiltrates due to the metaplasia and tobacco toxins always present
--> squamous cell metaplasia in the bronchi
--> more goblet cells making mucus --> think of drinking mucus out of a goblet gross
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*ABGs of COPD
- chronic high CO2 retention
- hypoxemia
- bicarb high due to metabolic compensation for respiratory acidosis
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*Reid index and severity of COPD
- normal Reid index = 0.4
- Reid index measures the ratio of the submucosal bronchial glands = secrete mucus / to the entire submucosa + lamina propria (= everything between the basement membrane epithelial layer and cartilage layer)
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Determine of Lower RTI first
- clinical judgement + sputum
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