Lecture 9: Pulmonary Pathology & Pharmacology part 3 Flashcards

1
Q

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

A

4

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2
Q

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

A
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3
Q

Reduced chest wall movement and lung volume

A

Restrictive lung disease

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4
Q

What would a pulmonary test show for someone w/ resitrictive lung disease

A

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

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5
Q

Clinical manifestation for resitrictive lung disease (6)

A

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

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6
Q

Causes of restrictive lung disease

A

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

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7
Q

PT interventiosn for RLD
* Exerse testing
* Airway clearance techniques
* Cough activation techniques
* Turning and positioning
* Manual therapy
* Flexibility exercises

A
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8
Q

Why may neuromuscular disease be the cause of RLD?

A

Decreased muscle tone, or inability to activate the muscle

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9
Q

Interstitial lung disease; ongoing epithelial dmage –> inflammatory process and scaring (so lungs are fibrotic)
* What is the pathogensis

A

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

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10
Q

Clinical manigestation of pulmonary fibrosis (3)

A

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)

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11
Q

What two drugs are used for pulmonary fibrosis?

A

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)

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12
Q

Systemic sclerosis lung disease: (you have all the below w/ this)
* Explain scleroderma
* Clinical manifestation (1)
* Drugs (2)

A

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

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13
Q

Chest wall trauma or lung disease: Blunt ches truma

Rib fracture or flail chest
* what happens w/ flail chest?

Management?

A

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

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14
Q

Environmental and occupation disease (again fall under restrictive lung diseases)

Whar is pneumoconiosis:
* risk factors?
* Clinical manigestations?

A

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

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15
Q

Environmental and occupational diseases (mostly restrictive)
* Asbestosis
* Occupational astham
* Byssinosis
* Coal workers pneumoconiosis (black lung disease)
* COPD
* Hypersensitivity pneumonitits
* Interstatial lung disease
* Mesothelioma
* silicosis

A
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16
Q

What causes hypersensitivity pneumonitits?

A

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

17
Q

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

A
18
Q

Loss of lung volume caused by inadequate expansion of the airspaces, usually collapse
* reabsorption
* Comrpression
* contraction

A

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

19
Q

Excessive fluid accumulation in the lungs
* common causes
* Clinical manifestations

A

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

20
Q

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

A
21
Q

Systemic disease of unknown cause, causing diffuse granulomas
* what does it primarily affect
* where else can it occur?
* Clinical manifestations (3)

A

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.

22
Q
A
23
Q

Malignancy of the epithelium of the respiratory tract
* two types
* Risk factors
* Where does it metastasis typically

A

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

23
Q

When is a pulmonary embolism

A

Loding of a blood clot in a pulmonary artery

23
Q

Clinical manigestations of pulmonary edema?

A

Cardiac arrest
Dyspnea
Pleuritic chest pain (pleural cavity BF is blocked) - sharp and localized
Cough
tachypnea

24
Q

Risk factors of pulmonary embolism?

A

DVT
* this can dislodge and become an embolism

25
Q

Treatment for pulmonary embolism

A

Treatment: anticoagulants, filter in vena cava

we do want movement. This happened likely because they’ve been at rest so long

26
Q

Pulmonary arterial hypertension

A

High blood pressure in pulmonary VEINs - 25 mmHg or greater

Risk factors:
Increase age
genetics
abestos
parasitic infection
down syndrome Or PE
Cocaine or amphetamine use
Smoking
Some chemo agents
Maternal use of SSRIs
CKC
weight loss drugs
clotting disorders
hep B/C
female
thyroid disease
may occur in patients with sclerodema

Clinical manifestation
* Cardiorespriatory symptoms inclide fatigue, weakness, chest dicomfort or pain, syncope, peripheral edema, abdominal distention, unexplained SOB, and exercise perforamnce impairment

27
Q

Pulmonary heart disease; failure of the right ventricle
* Risk factors
* Frequent cause of death in
* Oathogensis
* Clinical Manifestations

A

Cor Pulmonale - RV dilates and causes backflow causing R sided HF

Risk: adult male smokers, pulmonary vascular disease, respiratory disease (emphysema and chronic bronchitits), mechanical ventilation

Frequent cause of death in COPD

Pathogensis: RV lining hypertrophy due to prolonged overload, ventricle dilation, reduced CO, hypotension and shock

Clinical Manigestation: CO falls with EX< ECG, signs of systemic congestion

28
Q

Collagen vascular disease: more commonly reffered to as diffuse connective tissue diseases
* general dryness and lack of airway secretions cause the major problems of hoarseness, cough, and bronchitits in Sjogren syndrome (affects all glands in body), and intersitital lung dises

Ankylosing sponylitits
Dermatomyositits
Polyarteritits nodosa
Polymyositis
Psoriatic arthritits
RA
Scleroderma
Systemic lupus erythematosus

Autoimmune disease

A
29
Q
A
30
Q

Accumulation of air or gas in the pleural cavity, with collapsed lung
* Risk factors
* spontaneous
* traumatic
* latrogenic
* tension

A

Pneumothorax

Risk factors: tall, thin body habitus, male, smoking

Spontaneous pneumothorax - opening in the lung lining and it gets trapped inside

Traumatic pneumothorax - getting stabed etc..
* Open pneumothorax

Latrogenic pneumothorax - because of some medical intervention

Tension pneumothorax - because of fibrosis or some other condition

In the bicture the very black space is the air because the lung has collapsed

31
Q

Spontaneous pneumpthorax occurs when there is an opening on the surface of the lung and air leaks into the pleural cavity
* usually from blebs or bulla (those bubbles in the pizza)
* E cigarrette or vaping associated lung injury

A
32
Q

Inflammation of the pleura caused by viral or bacterial infection, injury or tumor
* clinical manigestation
* Pathogensis

A

Pleurisy - lungs cant expand as they need to which is why its restrictive

clinical manifestion: sudden sharp chest pain, coughing, sneezing, movement associated with deep inspriaration, fever, chills, and tachypnea, pleural rub
* because theres an infection

Pathogensis: wet, dry, or diaphram pleurisy

33
Q

Accumulation of fluid in between the partietal and visceral pleura (so different layers than before because theres 3 layers total)
* Pathogensis
* Clinical manigestations

A

Pleural effusion

Pathogenesis: Fluid and blood migrate through the capillaris, and inflammation occurs; malignant pleuritits

Clinical manigesations:
* Dyspnea on exertion, progressively worse

34
Q

An accumulation of pus that occurs occasionally as a complication of pleurisy or some other respiratory disease, usually pneumonia (actaully an infection)
* Symptoms
* How is it treated

A

Pleural Empyema

Symptoms:
* Dyspnea (can’t expand all the way)
* Coughing (because of the fluid buildup / dryness)
* Ipsilatearl pleural chest or shoulder pain
* Malaise, fever (because of the infection)

Condition is treated with intercostal chest tube drainage, rest, and sedative cough mixtures

pus accumulates in the plueral space often after infection or pneumonia

35
Q

May follow inflammation (espeically from asbestos), hemorrhagic effusion, and infection of the pleurae
* It can present as localized plaques or diffuse

Treatment?

A

Pleural fibrosis

Corticosteriods may decrease incidence byt do not reverse disease
* can’t fix that scarring

36
Q

Which of the following classifies as a parechymal disorder?

1) Sarcoidosis
2) Atelectasis
3) Pleural effusion
4) Cor Pulmonale

A

2

she said this was a bad question