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Cardiopulmonary > Pulmonary Conditions > Flashcards

Pulmonary Conditions Flashcards

1
Q

A - Primary Prevention - Definition

A

Don’t have the disease but we want to prevent it

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2
Q

B - Deconditioning

A

Healthy but deconditoned and need exercise.

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3
Q

C - Airway Clearance Dysfunction

A

Every pulmonary condition with secretion

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4
Q

D - Pump Dysfunction

A

Anything to so with the heart

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5
Q

E - Ventilation Dysfunction - Failure

A

Movement of air

Example: Inability to use intercostals to breath

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6
Q

F - Respiratory Failure

A

Diiffusion of gases

Example: Loss of surface area of aveoli = decreased diffusion

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7
Q

G - Neonate

A

Babies/NICU. Postgraduate

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8
Q

H - Lymphatic System

A

Lymphatics

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9
Q

Chronic Bronchitis Defintion

A
  • Inflammation of the mucous membranes lining the bronchial tubesthat leads to the production cough of sputum (mixture of saliva & mucus)
    – Chronic inflammation leads to swelling & hypersecretion of mucus

Type of COPD

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10
Q

Chronic Bronchitis Criteria

A

Cough must persist for 3 months duration over a 2-year period

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11
Q

Prevalence of Chronic Bronchitis

A
  • Women 2x more likely than men
  • Greater among non-Hispanic whites than non-hispanics blacks
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12
Q

Pathogenesis Chronic Bronchitis

A
  • Smoking (primary reason)/air pollution, infection, and illness all can cause continual irritation and damage to lung tissue, leading to an inflammatory response
  • Excessive mucous production
  • Mucous elimination decreased due to smoking paralyzing cilia
  • Chronic bronchitis cough in morning
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13
Q

Chronic Bronchitis Risk Factors

A
  • Cigarette smoking
    – Females at higher risk than males
  • Exposure to air pollution, dust, or toxic gases
  • Asthma
  • Gastric Reflux
  • Compromised immune system due to illness
  • Family history
    – Lung Disease, Childhood Respiratory Disease, GERD
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14
Q

Clinical Manifestations - Chronic Bronchitis

A
  • Cough with mucus production
    – “smoker’s cough”
  • Exertional Dyspnea
  • Cyanosis (late sign) [Blue bloaters (blue skin tint;retained fluid)]
  • Excess body fluids (peripheral edema; RHF fluid in abdomen adn extremities from back up)
    – Crackles (alveoli have mucus and fluid in them)
  • Fatigue (Due to low levels of O2 as it can’t get inside)
  • Slight fever or chills
  • Low Ventilation-perfusion mismatching
    – Low V/Q ratio = blocked airways
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15
Q

Diagnostic Assessment - Chronic Bronchitis

A
  • Health History - Productive cough
    – lasts at least 3 months & multiple times over the course of 2 years & other chronic diseases have been ruled out
  • Physical examination - ascultate the lungs
  • Pulmonary function test
  • Sputum exam
  • Chest X-Ray
  • Computed tomography (CT scan to look at airways in more detail)
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16
Q

Complications - Chronic Bronchitis

A

Can lead to pneumonia (fluid in lungs)
Low endurance/functional capacity
Difficulty talking or breathing
Lack of mental alertness
Tachycardia
Blue or gray fingernails or lips

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17
Q

Emphysema Definition

A

Abnormal permanent enlargement of the air spaces distal to the terminal bronchioles, with destruction of alveolar walls
– Damage to Elastin that makes up alveolar walls
– Decreased surface area for oxygen exchange
– Causes shortness of breath (Use pursed lip breathing to breath again)

Progressive disease
– eventually have symptoms during rest

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18
Q

Genetic Form of Emphysema

A
  • Alpha 1 antitrypsin deficiency
    – Autosomal recessive disorder – Chromosome #14
  • Symptoms of emphysema and pt never smoked
  • Gene is responsible for inactivation of neutrophil elastase
  • Absence of gene allows for destruction of lung tissue (elastin)
  • Seen more in European ancestors (less in Jewish, Japanese and Blacks)
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19
Q

Emphysema Prevalence

A

3rd leading cause of death in US
4th leading cause of death in the world
Usually diagnosed after the age of 50

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20
Q

Emphysema Pathogenesis

A
  • Inhaled particles induce inflammation
  • Leads to destruction of theelastin protein in the alveoli
    – Inner walls of the alveoliweaken and rupture
    – Creates large air spaces
  • Reduces the surface area of the lungs
    – Results in reduced gas exchange
  • Loss of elasticity causes narrowing or collapse of bronchioles
    – Increased ventilatory dead space
    – Increased residual volume
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21
Q

Emphysema - Risk Factors

A
  • Long term exposure to airborne irritants
    – Tobacco smoke & Secondhand smoke
    – Indoorand outdoor pollution
    – Occupational exposure to chemical fumes
  • Age
    – Symptoms begin between ages 40-60
  • Genetically inherited
    – absence of alpha – 1 – antitrypsin
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22
Q

Emphysema Clinical Manifestations

A
  • Cough/Wheezing (Come on later)
  • Dyspnea - worse with activity (Will have to stop moving to breath)
  • Increased CO2 Retention - “Pink Puffer”
    – Puffer: Pursed-lip breathing
    – Hypercapnia (Higher than normal CO2 levels)
  • Sputum production
  • Barrel Chest (Only way to get air in and out)
    – Over-inflation of lungs
    – Decrease voice transmission tests
    – Hyperresonance with percussion
  • Use of accessory breathing muscles
  • Anxiety/Depression
  • Fatigue
  • Weight loss
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23
Q

Explain Barrel Chest - Emphysema

A

Barrel Chest occurs as a result of compensation due to an inability to get proper amounts of O2 from decreased diffusion as a result of loss of surface area of the aveoli. With emphysema air will get trapped in the air spaces and have an inability to get it out resulting in excess levels of CO2. This results in a hyperinflation of the lungs as our body tries to compensate which doesn’t allow for the diaphram to move properly staying in a pushed down position. In hyperinflation the rib cage is always in a slightly expanded position giving us the appearance of a barreled chest as it is increased in an AP direction. In order to get air that we need to breath, incorporation of our accessory breathing muscles is necessary.

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24
Q

Diagnostic Assessment - Emphysema

A
  • Pulmonary Function Tests (Spirometry-check lung function)
  • Blood Tests: ABG (level of PAO2 and PACO2)
  • Chest X-ray: image of internal tissues
    – CT: shows width of airways in lungs and thickness of airway walls
  • Sputum culture: determine if infection is present
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25
Q

Spirometry - Emphysema Diagnostic

A

FEV1/FVC – less than 70% predicted
FEV1 – less than 80% predicted

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26
Q

Complications - Emphysema

A
  • Progressive decrease in functional capacity
    – Dyspnea, weakness loss of function
  • Pneumonia
    – Infection of alveoli and bronchioles, filled with fluid
  • Heart problems
    – Increases pressure of pulmonary arteries
    – Cor pulmonale: Right side heart failure
  • Bullae
    – Large air pocket in the lungs that reduces amount of space available to expand
  • Pneumothorax
    – Rupture of bullae can cause pneumothorax
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27
Q

Cystic Fibrosis Definition

A

A progressivegenetic disease that affects thelungs and digestive system(pancreas and liver); all exocrine glands

Life Expectancy = 37 years; Death most often caused by lung complication

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28
Q

Cystic Fibrosis - Pathogenesis

A
  • Recessive gene mutation.
  • Defective CFTR protein
  • Cl- (Chloride) unable to be released into extracellular matrix
  • Results in thick mucus
  • Each time two CF carriers have a child, the chances are:
    – 25percent (1 in 4) the child will have CF
    – 50 percent (1 in 2) the child will be a carrier but will not have CF
    – 25 percent (1 in 4) the child will not be a carrier and will not have CF
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29
Q

Cystic Fibrosis - Clinical Manifestations

A
  • Salty tasting skin
  • Persistent coughing, extreme amounts of phlegm (impaired mucociliary clearance)
  • Wheezing or shortness of breath
  • Frequent greasy, bulky stools or difficulty with bowel movements
  • Recurring Lung Infections (due to retained mucus)

Cough their entire life even when born. Prone to infection.

Treatment done daily.

30
Q

Cystic Fibrosis Screening - Diagnostic

A
  • Newborn screening (Every newborn) Immunoreactive Trypsinogen (IRT) Test
    – Required by all states
    – Procedure: blood from heel prick placed on Guthrie card and tested for IRT; IRT released bydamagedpancreas
    – (+) possible CF = High IRT
    – Screening only, need Sweat Test
  • Sweat Test (sweat chloride≥ 60mmol/L)
  • Genetic or Carrier Test
  • Clinical evaluation at a CF Foundation center
31
Q

Cystic Fibrosis Complications

A
  • Buildup of mucus
  • Frequent lung infections including pneumonia or bronchitis
  • Poor growth or weight gain
  • Early death

Multisystem problems

32
Q

Asthma - Definition

A
  • Hypersensitivity of airways - potential to trigger anexaggerated immune response
  • Symptoms occur when non-specificstimulitrigger a response by the bronchial tubes resulting in:
    – Bronchioles becoming restricted due tobronchospasms,inflammation, and hypersecretion of mucous
  • Asthma is a type of reversible COPD condition
    – Known as an “episodic” obstructive lung disorder

Leading chronic disease in children.

33
Q

Pathogenesis - Asthma

A
  • Allergens and irritants interact withcells in the tissues of thebronchial tubes
  • Type I hypersensitivity results in anexaggerated immune reaction
  • Consists of: inflammation, intermittent bronchialobstruction, bronchial hyperreactivity,mucus hypersecretion, and smooth musclehyperplasia
34
Q

Risk Factors - Asthma

A
  • All ages
  • Presence of allergies
  • Family Hx
  • Frequent respiratory infections
  • Exposure to tobacco before or after birth
  • Black ethnicity
  • Raised in a low-income environment
35
Q

Asthma - Clinical Manifestations

A
  • Wheezing
  • Chest Tightness
  • Dyspnea
  • Coughing

Symptoms can be exacerbated by: Exercise, inhaling cold & dry air, environmental factors like dust, pollen, or pollutants

36
Q

Diagnostic - Asthma

A
  • Patient reports:
    – History of coughing, wheezing
    – Symptoms worse at night, withexercise, allergens or otherfactors
  • Reversible obstruction
    – Spirometry - reversible of FEV1
    – Expose to triggers ormedications (Methacholine) to see ifobstruction is reversible
  • Determine severity
    – Intermediate
    – Mild
    – Moderate
    – Severe

Becomes emergency when bradycardic (low HR) and hypotensive, with confusion (When body fails to bring O2 back up it goes into failure resulting in these symptoms)

37
Q

Complications - Asthma

A

Pneumonia (mucus build up in lungs)
Collapsed Lung
Respiratory failure

Both a ventilatory and respiratory. Ventilatory due to air not getting in; respiratory due to fluid in lungs.

38
Q

Bronchiectasis Definition

A
  • Inflammation of bronichole, walls get weakened, walls pop out and become puss pockets.
  • Permanent dialation of bronchi or bronchioles
  • Morning breath x800. Due to putrifying tissue/puss in bronchioles they can’t get out. Walls get weak and can burst open.
39
Q

Bronchiolitis Obliterans (Popcorn lung)

A

Bronchioles damaged and inflamedcausing scarring that blocks the airways and/or
Lung plugged with granulation tissue

40
Q

Bronchiectasis Prevalence

A

Symptoms develop middle age (typically over 60 year old)

41
Q

Bronchiolitis Obliterans - Lung Transplant

A

With lung transplant:
prevalence 50% and mortality rate 40%

42
Q

Bronchiectasis - Pathogenesis

A
  • Mucus plugging and infections cause this condition resulting in:
    – Destruction of muscles/elastic supporting tissue by cycle of infections and inflammation
43
Q

Bronchiolitis Obliterans - Pathogenesis

A
  • Caused by inhalingchemicals (diacetyl)
  • Associated with respiratory infections
  • Associated with graft-versus-host disease following a lung or bone marrow transplant
44
Q

Bronchiectasis - Risk Factors

A
  • Repeated respiratory tract infections
  • Retained secretions
  • Damage to bronchial walls
  • Smoking
  • Exposure to chemicals
  • Lung transplant
  • Work environment
45
Q

Bronchiolitis Obliterans - Risk Factors

A
  • Lung transplantation
  • Chemical diacetyl has been removed from popcorn process
46
Q

Bronchiestasis - clinical manifestations

A
  • Chronic productive cough (wheezing)
  • Copious amounts of sputum
  • Dyspnea
  • Fever due to pulmonary infections (bad breath)
  • Reduced exercise tolerance
47
Q

Bronchiolitis Obliterans - Clinical Manifestations

A
  • Persistentoccurrence of symptoms (dry cough, shortness ofbreath, and/or wheezing)
  • Symptoms may begin 2-8 weeks after exposure and slowlyprogresses for weeks to months
48
Q

Bronchiectasis - Diagnostic

A
  • Pulmonary Function Tests (lung volumes)
    – Results depend on extent of disease present
  • Auscultation Findings
    – Crackles / Wheezing over involved lobes
    – Dullness to percussion
    – Decreased or absent breath sounds with mucus retention
    – Shallow breaths to avoid triggering coughing episodes
49
Q

Bronchiolitis Obliterans - Diagnostic

A
  • Persistence and characteristics of symptoms
  • Pulmonary Function Tests
50
Q

Bronchiectasis - Complications

A
  • Decreased exercise tolerance
  • Hemoptysis (life-threatening)
    – Blood in sputum from erosive airway damage (highly vascular)
  • Will need to be on cough suppressors or additional oxygen to manage symptoms, as there is no cure
  • May be on long term steroids (To help reduce inflammation)
51
Q

Types of Restrictive Lung Disease

A
  1. Pulmonary (IPF, Pneumonconiosis and Sarcoidosis)
  2. Maturational (Aging)
  3. Neuromusculoskeletal (SCI, ALS, GB, Dystrophy)
  4. Musculoskeletal (scoliosis)
  5. Connective Tissue (RA, Lupuss)
  6. Immunologic
52
Q

Idiopathic Pulmonary Fibrosis

A
  • Progressive lung disease characterized by abuild-up of scar tissue (lung compliance is decreased)
    – restricting gas exchange
    – lung expansion limited
    – Volume of air (in/out) is decreased

Lose expansion of lungs due to scarring

53
Q

Idiopathic Pulmonary Fibrosis Life Span

A
  • Median survival estimated at 2–5 years from the time of diagnosis
  • Survival is not good without a lung transplant
54
Q

Idiopathic pulmonary fibrosis pathogenesis

A
  • Unkown cause
  • Genetics: 20% have a family member with the condition
  • Environmental: chemical, particles or allergens
  • Smoking: 75% current or previous smokers
  • Dysfunction of inflammatory system
55
Q

Idiopathic pulmonary fibrosis - Clinical manifestations

A
  • Dyspnea
  • Persistent dry or hacking cough
  • Fatigue
  • Unexplained weight loss
  • Aching muscles and joints
  • Clubbing of digits (hypoexmia)
56
Q

IPF Major Diagnostic Criteria

A
  • Exclusion of other known causes interstitiallung disease
  • Abnormal pulmonary function test
57
Q

IPF Minor Diagnostic Criteria

A
  • > 50 years old
  • Insidious onset of otherwiseunexplained dyspnea on exertion
  • Duration of sx > 3 months
  • Inspiratory crackles
58
Q

IPF Complications

A
  • 40,000 annual deaths – respiratory failure (80%)
  • No specific treatment other than lung transplant
  • Prognosis is highly variable – most 3-5 years
  • Lung cancer, pulmonary emboli,pneumonia, pulmonary HTN
59
Q

Pneumoconiosis Defintion

A

a disease of the lungs due to inhalation of dust, characterized by inflammation, coughing, and fibrosis

Miner’s

60
Q

Sarcoidosis Defintion

A

the growth of tiny collections of inflammatory cells (granulomas) in different parts of your body (multisystem)— most commonly the lungs, heart, lymph nodes, eyes and skin.

80% of cases go away; 20% fatal

61
Q

Pneumoconiosis

A

Prolonged exposure to irritants from inhalation

62
Q

Sarcoidosis Pathogenesis

A
  • Doctors unsure of exact cause
  • Believe immune system response to an unknown substance
  • Most likely something inhaled
63
Q

Pneumoconiosis - Risk Factors

A
  • Those in contact with harmful dusts
  • Plumbers, roofers, coal miners, textile workers
64
Q

Sarcoidosis Risk Factors

A
  • Higher likelihood of development:
    – African and Scandinavian descent
    – Women
    – Between age 20-40
    – Exposure to dusty or moldy environments
65
Q

Pneumoconiosis - Clinical Manifestations

A

May be asymptomatic
Cough (black sputum if coal dust)
Dyspnea and chest tightness
Often results in scarring of the lungs (hypoxia)
Progressive weight loss

66
Q

Sarcoidosis - Clinical Manifestations

A
  • Fatigue, dyspnea, nonproductive cough, pain, reduced exercisecapacity, malaise, fever, skin lesions, weight loss, weakness, and erythema nodosum
  • Variable depending on organ system involvement
  • Physical activity canimprove exercise capacity, increase muscle strength, and reduce fatigue.
67
Q

Diagnosis - Pneumoconiosis

A
  • History, including possible exposure
  • Pulmonary function tests (small lung volumes)
  • Chest X-ray
68
Q

Sarcoidosis - Diagnostic

A
  • May be difficult to diagnose
  • Physical exam to check for skin lesions and listen to heart/lungs
  • Chest X-ray and other diagnostic tests to look for complications
69
Q

Pneumoconiosis Complications

A
  • Progressive respiratory failure
  • Lung Cancer
  • TB
  • Autoimmune disease
  • Heart failure from pressure in the lungs

Think low functioning

70
Q

Sarcoidosis Complications

A
  • Lungs: difficulty breathing from lung scarring
  • Eyes: blindness from inflammation
  • Kidneys: kidney failure from impaired ability to handle calcium
  • Heart: irregular heart rhythms and other problems from granulomas. Can result in death
  • Nervous System: granulomas can form in brain and spinal cord. Inflammation around nerves can cause paralysis of that nerve function.
71
Q

Obstructive Conditions

A
  • Chronic Bronchitis
  • Emphysema
  • Asthma
  • Cystic Fibrosis
  • Bronchiectasis and Bronchiolitis Obliterans

90% of PT practice is obstructive

72
Q

Restricitve Conditions

A

Idiopathic Pulmonary Fibrosis
Pneumoconiosis and Sarcoidosis (Back dust; Miner’s Lung)

Cardiopulmonary (21 decks)

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