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respiratory disorders 2.docx

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School
Department
Health Science
Course
HLSC 2461U
Professor
Otto Sanchez
Semester
N/A

Description
Respiratory Disorders 2 Respiratory Distress Syndrome of the Newborn  some infants are born with this and could go into respiratory failure very quickly (premature)  this is related to surfactant What is Surfactant?  a very thin layer of liquid compounds that is covering all the cells in the alveolar cavity  produced by type 2 alveolar cells which have laminar inclusion bodies which secrete it  composed of molecules that decrease surface tension  produced around week 28 of gestation (born before this = no surfactant)  at week 24, laminar bodies are present along with type 2 pneumocytes or in the cuboidal epithelium What Does it Do?  if cells do not have surfactant, it induces surface tension that tends to close the alveoli  surface tension exerts forces that tend to close the alveoli in the absence of surfactant  there is now a tendency for atelectasis (collapse)  when surfactant is present, it decreases surface tension and allows the alveoli to open  closer look at it  you see the immature lungs, the atelectasis, and that ultimately ends in respiratory failure  respiratory failure is caused by the inadequate alveoli ventilation which will induce respiratory acidosis  there will be changes in the pulmonary arteries: increased pulmonary vascular resistance, it will produce a R to L shunt (PDA!!) because the pressures in the pulmonary arteries and the right chambers of the heart will be increased and that will not allow for the closing of the ductus arteriosis and the foramen ovale Pneumonia  infection of the lungs  acute inflammation inside the alveoli and the alveolar walls  lots of neutrophils/acute inflammatory proteins in the alveoli  in the interstitial space you will see neutrophils and alveolar infiltration, interstitial infiltration  there are many causes and it’s not a single disease but many presentations  there are four types of pneumonia that are infectious and the fifth is related to chemicals (bile from aspiration = aspiration pneumonia), doesn’t burn, pH damages the cells, airways and lungs  there are many types of bacteria that can cause pneumonia: Streptococcus (most common) Influenza Measles (immunosuppressed people) RSV (northern/aboriginal) Mycoplasma (happens with AIDS) Pneumocytosis Carinii is a hallmark for people with AIDS Chlamidya (not sexually transmitted) Types of Pneumonia Lobar Pneumonia: affects the whole lobe, no gas exchange whatsoever! Broncho-Pneumonia: affecting the bronchial segments, more localized, good gas exchange Events During Streptococcal Pneumonia  inhaling streptococcus, virus attaches to alveolar macrophages and the inflammatory response is initiated (acute), produce alveolar infiltration, red hepatisation occurs (lung is full of inflammatory cells so it looks like the liver because it’s so red)  objective of inflammation is to heal and remove Complications of Pneumonia Pleural Effusion: inflammatory process can produce exudate that will spill into pleural cavity Lung Abscess: inflammation may destroy the tissues forming a hole called an abscess which is full of neutrophils, bacteria, etc, may be drained by a surgeon Empyema: when pleural effusion is infectious, causes infection in the pleural cavity that can cause scarring, etc Tuberculosis  another type of lung infection which is in fact a type of pneumonia!  bacteria in TB is called mycobacterium  common in people with aids (called typical mycobacterium)  usually rod-shaped bacilli  acid fast stain is needed to see them  macrophages cannot digest these bacteria so they phagocytoze them  they cannot be destroyed  macrophages produce cytokines which induces more and more inflammatory complexes, they end up forming a structure that basically isolates that inflammatory process from the rest of the lungs  production of a fibrous cuff  a round structure full of mycobacteria, macrophages, and lymphocytes which is called a granuloma  what happens in TB is that the mycobacteria end up forming granulomas in the lugs which is what distinguishes TB How does mycobacterium interact with the lungs?  left hand side from the top; inhaled mycobacteria, alveoli, type 2 macrophages capture them, try to eat them but macrophages cannot eat them (can’t digest), produce cytokines to attract more macrophages, eventually form this structure that isolates the inflammatory process from the rest of the lungs (called a granuloma), mycobacterium end up forming a granuloma in the lungs
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