Lecture 9: Pulmonary Pathology & Pharmacology part 3 Flashcards
(38 cards)
Which pulmonary disorder is termed “blue bloater” and is characterized by a recurrent, productive cough?
1) Cystic fibrosis
2) Sleep apnea
3) Emphysema
4) Chronic Bronchitits
4
KNOW: resistrctive lung diseases keep your lungs from expanding
* think putting a gait belt around your rib cage and trying to breath in
Scoleosis / BMI can cause this
Reduced chest wall movement and lung volume
Restrictive lung disease
What would a pulmonary test show for someone w/ resitrictive lung disease
Decreased total lung capacity
The graph would look entirely normal but just be significantly smaller
* because you’re not getting enough air in
* but what you are getting in, you’re also getting out
Clinical manifestation for resitrictive lung disease (6)
1) Rapid, shallow respiratory (because they can’t get a full inhale to get that O2 (leads to shallow breathing because you can’t fully expand)
2) Chronic tacypnea (smaller breaths = need more)
3) Exertional –> Dyspnea at rest
* Starts by being out of breath w/ exertion that leads to dyspnea at rest
4) Decreased chest wall movement
5) Increase use of accessory muscles
* Because the normal inspiratory muscles are enough
6) Clubbing
* Rounded nail beds
Causes of restrictive lung disease
1) Scoliosis
2) Obesity
3) Pleural effusion
4) Lobectomy/pneumonectomy
5) Malignant tumors
6) Rib fractures
7) Ascites
8) Pleurisy
9) Often occurs w/ neuromuscular disorders - think geonbrae, cerebral palsy, SCI (depending on the level, it could keep your abs from contracting = not able to cough anymore)
Normally these have more to do with things outside the lungs
PT interventiosn for RLD
* Exerse testing
* Airway clearance techniques
* Cough activation techniques
* Turning and positioning
* Manual therapy
* Flexibility exercises
Why may neuromuscular disease be the cause of RLD?
Decreased muscle tone, or inability to activate the muscle
Interstitial lung disease; ongoing epithelial dmage –> inflammatory process and scaring (so lungs are fibrotic)
* What is the pathogensis
Pulmonary fibrosis
KNOW: 2/3 of cause / risk factors unknown
1/3 - TB, CF, systemic sclerosis, and acute respiratory distress syndrome
Pathogensis:
* Fibroblast proliferation (increase in fibrosis)
* Abnormal wound healing response - have the inflammation, fibroblasts are laid down ontop and that just keeps going - inflamamtion is never stopped
Clinical manigestation of pulmonary fibrosis (3)
1) Progressive dyspnea (dysonea)
2) Nonproductive cough (dry cough)
3) Decreased total lung capcity, FVC and FEV1 (decreased TLC)
* So our ratio will also be decreased (makes sense)
What two drugs are used for pulmonary fibrosis?
Pirfenidone (antifibrotic)
nintedanib (kinase inhibitor) - decreases inflammatory process
KNOW: Also do pulmonary rehab
* Exercise capicity, breathing techniques improve peripheral musculature function
If it is severe enough and have enough scarring - a lung transplant
* 5 year survivial rate = 44% (on medication and body can reject medication)
Systemic sclerosis lung disease: (you have all the below w/ this)
* Explain scleroderma
* Clinical manifestation (1)
* Drugs (2)
Scleroderma: Disorder of collagen
* typically causes increased webbing in hands, resistricted in ROM because skin gets thick and hard
* will cause resistrictive lung disease because skin will get harder and thick –> typically this disease will have been there a while before you get significant pulmonary involvement (usually have for 7 years B4 pulmonary symptoms)
Clinical manigestations:
* severe dyspnea
Drug therapy:
* Corticosteriods
* Immunosuppressants (because its an auto immune disease)
Again, this is not a pulmonary disease, but at some point in its progression it starts to affect the lungs and keeps them from getting air in
Chest wall trauma or lung disease: Blunt ches truma
Rib fracture or flail chest
* what happens w/ flail chest?
Management?
flial chest: those ribs essentially go opposite what the breathing pattern is
* inspiartion = goes in
* expiration = goes out
Management:
* Postural drainage - because theres inflamamtion, so theres going to be a fluid buildup - you can’t really drain it by doing other therapy techniques
* Manual therapy - okay, but not best 0 have to be careful not to pump a lung with that fractured rib
* Airwar clearance
* Semi fowler postion (HOB elevated)
* Splinting
External resistrive lung disease
* the lung is normal
* so i guess inspiration it blocks the expanding of the lung
* leads to fluid overload
Environmental and occupation disease (again fall under restrictive lung diseases)
Whar is pneumoconiosis:
* risk factors?
* Clinical manigestations?
Pneumonconiosis: Group of disorders due to inhalation of particles of industrial substances
* decreased because were more careful now
risk factors:
* Occupational inhalnts
* asbestos
clinical manigestation:
* Same as chronic bronchitits and COPD
Environmental and occupational diseases (mostly restrictive)
* Asbestosis
* Occupational astham
* Byssinosis
* Coal workers pneumoconiosis (black lung disease)
* COPD
* Hypersensitivity pneumonitits
* Interstatial lung disease
* Mesothelioma
* silicosis
What causes hypersensitivity pneumonitits?
Exposure to organic dusts may result in hypersensitivity pneumonitis, also called extrinsic allergic alveolitis
Regardless of the specific antigen involved in the pathogensis of hypersensitivity pneumonitits, the pathologic alterations in the lung are similar
* rxn at the alveioli level
* normally some alergic response (autoimmune(
A combination of immune complex-mediated and T cell mediated hypersensitivity reactions occurs, although the exact mechanism of these processes is still unknown
Noxious gases, fumes, and smoke inhalation
Exposure to toxic gases and fumes is an increasing problem in modern industrial societies
Most common mechanism on unjury is local irritation, the specific type and extent depdening on the type and concentration of gas and the duration of exposure
Chemical pneumonitis can result from exposure to toxic gumes
Smoke inhalation injury produces direct mucosal injury
Loss of lung volume caused by inadequate expansion of the airspaces, usually collapse
* reabsorption
* Comrpression
* contraction
Atelectasis
You have a decreased ventilation perfusion ratio and hypoxia because these airspaces have collapsed - its harder to force air in to then expand
* harder to blow air into balloon initially
Nenatal atelectasis (sarfactant) or acquired atelectasis
Part of lung of full lung
Reabsorption atelectasis (obstructive/absorptive)
* there is a blockacage somewhere and the air cannot get to the alveoli - they collapse because the pressure to maintain it open isnt there
Compression atelectasis: fliod in the pleural cavity
* if fluid builds up between visceral and partietal layers, then you’re going to compress the lungs, and they alveoli arent able to fill so they end up collapsing
Contraction atelectasis: Due to fibrosis
* scaring that doesnt let lung expand and deflate
the black is air spaces
Excessive fluid accumulation in the lungs
* common causes
* Clinical manifestations
Pulmonary edema
Commin in: anything that causes fluid overload
* heart failure
* liver cirrhosis: scaring in liver that causes inflamtory process, and you’re not getting rid of it properly
* lymphatic disease: retaining certain fluids
* and acute lung injury / acute respiratory distress syndrome
Fluid overload: filling pressure to the left side of the heart increases, and fluid accumulates in the pulmonary vasculature
Easrly stages: Restless, anxiety (hypoxia), common cold, or asymptomatic
Dyspnea on exertion, cough, crackles, orthopnea
RR increases, wheezing, frothy sputum, hypoxia, unresposive, mechanical ventilation
Acute lung injury and acute respiratory distress syndrome
* can happen due to any trauma (football player developed this in ICU)
Acute respriatory failure after systemic or pulmonary insult
Syndrome, not disease, and usually a fatal complication unless treated immeditaley
Clinical manifestations
* Increased respriatory rate
* Shallow rapid braething, pulmonary edema, atelectasis, crackles, dyspnea, hyperventilation
Systemic disease of unknown cause, causing diffuse granulomas
* what does it primarily affect
* where else can it occur?
* Clinical manifestations (3)
Sacroidosis
Primarily affects lungs and lymphatic tissue
Occurs on any organ
Clinical manigestations:
* Dyspnea
* Dry cough
* This leads to pulmonary fibrosis
cluster of immune cells, called granulomas, form through various organs, espically the lings. The diffuse refers to the fact that these granulomas are spread across large areas ratjer than bing confiend in one spot
A granuloma is a small area of inflammation that forms when the immune system tries to wall off substances it perceives as forien but cannot eliminate, such as bacteria, dust, or other irritants.
In sarcoidosis, the body forms granuloms even without a clear infection or foreign substance, leading to widespread inflammation and potential damage to the affected organs
when granulomas are diffuse, they can interfere with normal organ function, especially in the lungs, where they can lead to breathing difficulities and reduced lung caapacity. In some carses sarcoidosis can also affect the skin, eyes, heart or other organs.
Malignancy of the epithelium of the respiratory tract
* two types
* Risk factors
* Where does it metastasis typically
Lung cancer
Types:
* Small cell lung cancer (oat cell)
* Non-small cell lung cancer: squamous cell (epidermal, adenocarcinoma, large cell (anaplastic)
Leading cause of cancer in the US
Risk factors:
* Smoking
* Occupational exposure (think like coal mining)
* nutrition
* genetic factors
* COPD
* Emphysema
Metastasis: adrenal glands, brain, bone, liver before symptoms
When is a pulmonary embolism
Loding of a blood clot in a pulmonary artery