Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SMP - APP Part 1 > Lectures 1-2/7-8 - Pulmonary Pathophysiology I-IV > Flashcards

Lectures 1-2/7-8 - Pulmonary Pathophysiology I-IV Flashcards

1
Q

2 types of airways? List parts for each.

A
  1. Upper: nose, pharynx, larynx

2. Lower: trachea, bronchi, lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

2 primary functions of the respiratory system? Describe each.

A
  1. Ventilation: air movement

2. Respiratory: gas exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the respiratory membrane made of?

A
  1. Alveolar wall
  2. Capillary wall
  3. Basement membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

2 types of functional airways? Describe each.

A
  1. Conducting airways: nose to terminal bronchioles (0-16th branching) - no gas exchange
  2. Respiratory airways: respiratory bronchioles to alveolar sacs (17-23rd branching) - gas exchange
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Other name for conducting airways?

A

Anatomical dead space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which airway type is involved in obstructive airway disease?

A

Small conducting airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which airway type has a larger proportion of smooth muscle than the other?

A

Small conducting airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What fraction of TV sits in the anatomical dead space under normal conditions?

A

1/3rd

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which airways are considered small?

A

Those with a luminal diameter <2mm => 4-14th branching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is necessary for air to get into the lungs during inspiration?

A

Chest volume increases and pressure inside the lungs must be lower than atmospheric pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Primary muscles of inspiration?

A
  1. Diaphragm

2. Intercostal muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Primary muscles of expiration?

A

None

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens during expiration?

A

Diaphragm relaxes and lung elastic recoil decreases volume and increases intrathoracic pressure to push air out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is an important factor in removing air from the lungs?

A

Lung elasticity and recoil, which is dependent on elastic elements in lungs and surface tension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the 6 factors controlling ventilation?

A
  1. Voluntary: phrenic nerve (somatic)
  2. CO2
  3. O2
  4. pH
  5. Lung stretch
  6. Pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the accessory muscles of respiration?

A
  1. Intercostal muscles
  2. Chest wall muscles
  3. Abdominal muscles
  4. Neck muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How can one identify respiratory distress by simply observing the patient?

A

Look at accessory muscles of respiration and see if they are being recruited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which nerves carry sensory information from peripheral chemoreceptors to the brain to control respiration?

A

Cranial nerves 9 and 10:

  • Vagus nerve
  • Glossopharyngeal nerve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the alveolar sacs lined with? Why is this important?

A

Small layer of water => creates surface tension, which is reduced by surfactant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

4 ways of examining the respiratory system? Describe each.

A
  1. Inspection: respiratory rate, respiratory distress (can the person talk normally?), even chest inflation, use of accessory muscles, cough, respiratory sounds, deformities of the chest wall, tracheal deviation
  2. Palpation: equal respiratory expansion, tactile fremitus
  3. Percussion: dull sounds vs. hyper-resonance
  4. Auscultation: pathological sounds (wheezes, crackles, ronchi etc), egophony
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Normal RR?

A

12-20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is tactile fremitus?

A

Tremulous vibration of the chest wall during speaking that is palpable on physical examination and indicates increased lung consolidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is pulmonary consolidation?

A

Region of (normally compressible) lung tissue that has filled with liquid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Anterior and posterior surface projections of right superior lobe?

A

Anterior = root of neck to above rib 4

Posterior = root of neck to above rib 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Anterior and posterior surface projections of right inferior lobe?

A

Anterior = top of 4th rib to medial 6th rib

Posterior = top of rib 6 to top of rib 10 medially

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Anterior and posterior surface projections of right middle lobe?

A

Anterior = laterally over rib 6 and 5th and 6th intercostal spaces

Posterior = none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Anterior and posterior surface projections of left superior lobe?

A

Anterior = root of neck to above 4th rib and then inverse C-shape to above rib 6

Posterior = root of neck to above rib 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Anterior and posterior surface projections of left inferior lobe?

A

Anterior = over lateral 6th rib and 5th and 6th intercostal spaces above and below

Posterior = top of rib 6 to top of rib 10 medially

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the forced expiratory volume? Notation? What kind of measure is this?

A

Volume of air exhaled in the first second of maximal expiration maneuver = FEV1

Measure of flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the forced vital capacity? Notation?

A

Total volume of air exhaled during a forced expiration = FVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What % of the FVC does the FEV1 comprise in a normal healthy individual? What will affect this normal number in healthy individuals?

A

FEV1/FVC = 75-80% (or within 10% of the normal expected number)

Factors affecting this number: age, height, race, and gender

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the DLCO?

A

Diffusion capacity of the lungs for CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How many lung volumes are there? Describe each. WHICH ONES ARE DIRECTLY MEASURED via spirometry?

A
  1. ***Tidal volume (TV) = amount of air breathed out/in under normal conditions
  2. ***Inspiratory reserve volume (IRV) = max amount inspired above the tidal volume
  3. ***Expiratory reserve volume (ERV) = max amount expired below the tidal volume
  4. Residual volume (RV) = remaining amount of air left after max expiration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How many lung capacities are there? Describe each. WHICH ONES ARE DIRECTLY MEASURED via spirometry?

A
  1. Total lung capacity (TLC) = sum of all lung volumes = TV + IRV + ERV + RV
  2. ***Vital capacity (VC) = largest breath you can take = TV + IRV + ERV
  3. ***Inspiratory capacity (IC) = maximal inspiratory volume = IRV + TV
  4. Functional residual capacity (FRC) = amount of air left after residual expiration = ERV + RV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What 4 arterial blood gas values measure functioning of the respiratory system? What are normal values for each?

A
  1. pH (normal = 7.35 – 7.45)
  2. PaO2 (normal = 75-100 mmHg)
  3. PaCO2 (normal = 35-45 mmHg)
  4. HCO3- (normal = 22-26 mEq/L)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What % of atmospheric air is O2? Notation? Does this vary with altitude?

A

Fraction of Inspired Oxygen = FiO2 = 21%

NOPE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

2 types of lung diseases?

A
  1. Restrictive

2. Obstructive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe restrictive lung disease.

A

Decreased compliance of lung tissue leading to difficulty in lung expansion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is lung compliance?

A

Amount of pressure required to bring a certain volume change = ΔV/ΔP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How are PFT/arterial blood gas values affected by restrictive lung disease?

A
  1. Decreased TLC
  2. Decreased FVC
  3. Normal FEV1/FVC ratio
  4. Possible decreased DLCO
  5. V/Q mismatch
  6. Hypoxemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Difference between hypoxia and hypoxemia?

A

Hypoxia = low CaO2

Hypoxemia = low PaO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

2 types of restrictive lung diseases? Describe each.

A
  1. Extrinsic: chest wall restriction

2. Intrinsic: lung tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

2 types of causes for extrinsic restrictive lung disease? Provide examples for each.

A
  1. Neuromuscular: Guillain-Barre, myasthenia gravis, polio, muscular dystrophy
  2. Non-muscular: chest wall deformity, obesity, pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

3 causes for intrinsic restrictive lung disease?

A
  1. Toxin exposure: airway irritants, drugs, radiation
  2. Systemic disease
  3. Unknown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is intrinsic restrictive lung disease often accompanied by?

A

Decreased diffusion capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Describe the pathophysiology of intrinsic restrictive lung disease.

A

Chronic inflammation => excessive fibrous connective tissue (aka scarring) in the lungs => stiffening of lung and decreased compliance = pulmonary fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is pectus excavatum? What is it an example of?

A

Congenital chest wall deformity in which several ribs and the sternum grow abnormally, producing a concave, or caved-in, appearance in the anterior chest wall

Example of non-muscular extrinsic restrictive lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is idiopathic pulmonary fibrosis? How common is it? Who is affected by it?

A

Progressive and chronic inflammation of lung tissue with unknown cause in which inflammation precedes fibrosis with over activation of immune cells in the lungs

Affects adults over 40 with median survival of 2-4 years (progresses fast), rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is idiopathic pulmonary fibrosis histologically linked to?

A
  1. Overproduction and disorganization of collagen and ECM = fibrosis
  2. Destruction of pulmonary structure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Clinical presentation of idiopathic pulmonary fibrosis?

A
  1. Symptoms of worsening dyspnea
  2. Restrictive pattern on PFTs
  3. Characteristic findings on imaging: honeycomb lung and reduced lung volume
  4. Characteristic findings on lung biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Treatments for idiopathic pulmonary fibrosis?

A
  1. Supportive care: vaccination, oxygen, pulmonary rehab
  2. Inclusion in clinical trials, steroids and other immunosuppressive therapy may slow progression
  3. Lung transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is pneumoconiosis?

A

Inhalation of inorganic dust causing intrinsic restrictive lung disease

  1. Coal => black lung
  2. Silica (ore processing) => silicosis
  3. Asbestos (farm workers, households) => asbestosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What toxin exposure is also linked to lung cancer?

A

Asbestos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Is pulmonary fibrosis reversible?

A

NOPE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is hypersensitivity pneumonitis?

A

Allergic alveolitis (inflammatory response) to a number of organic agents including dusts, grains, animal feces, molds, avian antigen causing intrinsic restrictive lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

3 examples of hypersensitivity pneumonitis?

A
  1. Molds/dust from coffee beans, tea plants, grapes, cheese, potatoes => farmer’s lung
  2. Pigeon breeders
  3. Air ventilation and water-contaminants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How to diagnose intrinsic restrictive lung disease due to exposure?

A
  1. History of exposure to substance (> 10 yrs) - occupational history is important
  2. Keep in mind patients may be asymptomatic despite findings on exam/imaging/PFTs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

4 symptoms of intrinsic restrictive lung disease due to exposure?

A
  1. Dyspnea
  2. Cough
  3. Fatigue
  4. Weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How to treat intrinsic restrictive lung disease due to exposure?

A
  1. Avoid exposure to stop progression

2. Supportive care, corticosteroids to inhibit the immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How to diagnose intrinsic restrictive lung disease due to systemic disorders?

A
  1. Involvement of other organs
  2. Antibody titers
  3. Other disease specific features
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How to treat intrinsic restrictive lung disease due to systemic disorders?

A
  1. Specific disease treatment

2. Steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Example of a systemic disease that causes intrinsic restrictive lung disease?

A

Sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is sarcoidosis? What is it caused by? What patients get it?

A

Systemic disease with unknown cause characterized by noncaseating granuloma (immune cell collection) formation, with the healing of granulomatous tissue leading to fibrotic changes

Onset < 40 yo, more common in women, AA race

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Where is sarcoidosis found in the body?

A

Can be found in all tissue but very common in lungs and lymph nodes (90%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

X-ray presentation of sarcoidosis?

A

Bilateral hilar adenopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Describe the progression of sarcoidosis.

A

Unpredictable course:

  1. Can regress on its own
  2. Some require therapy including immunosuppressive agents (~ 70%) but fully recover
  3. Can become chronic and lead to pulmonary fibrosis and death (~10-15%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Who gets sarcoidosis?

A

Black women before 40 yo is most common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What causes granulomas to form?

A

Antigen that the body cannot break down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Other than in sarcoidosis, in what other disease are granulomas seen?

A

Tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the antigen that the body is attacking in sarcoidosis?

A

Unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Describe obstructive lung disease.

A

Airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How are PFT/arterial blood gas values affected by obstructive lung disease?

A
  1. Decreased FEV1
  2. Decreased FEV1/FVC ratio
  3. Possible elevated RV and TLC due to gas trapping
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

2 types of obstructive lung diseases?

A
  1. Asthma

2. COPD: chronic bronchitis + emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Describe asthma.

A

Reversible airway obstruction (usually expiratory), inflammation and hyper-responsiveness to allergens due to a complex, abnormal, and exaggerated inflammatory response with many immune cells and mediators involved

Inflammation leads to smooth muscle constriction, increased airway edema, and thickened mucus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Which airways are preferentially affected in asthma?

A

Small airways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What are some triggers for asthma attacks?

A
  1. Viral respiratory infections: RSV, rhinovirus
  2. Allergens: dust, pets, cockroaches, molds, occupational etc.
  3. Others: cold air, exercise, irritant exposure (e.g. smoking)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the pathogenesis of asthma? What to note?

A
  1. Immediate phase reaction: over activation of TH2 => IgE production by plasma cells to specific allergens => degranulation of mast cells which release histamine, prostaglandins, and leukotrienes => bronchoconstriction and mucus production/inflammation
  2. Late phase reaction: recruitment of other immune cells (especially eosinophils) => vasoconstriction and epithelial damage

Note: other triggers can cause airway inflammation through non-IgE mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Effect of leukotrienes on the lungs?

A

Bronchoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Clinical presentation of asthma?

A
  1. History: episodes of dyspnea, chest tightness, coughing, increased respiration rate (tachypnea), wheezing
  2. Exam: wheezing and poor-air movement on auscultation, accessory muscle use, tachypnea
  3. Blood gas: hypoxemia and respiratory alkalosis due to hyperventilation, can progress to acidosis as obstruction worsens
  4. PFTs: obstruction may not be seen between episodes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is cough variant asthma?

A

Presents as cough only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is exercise variant asthma?

A

Induced only with exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is status asthmaticus?

A

Prolonged asthma exacerbation unresponsive to therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Asthma risk factors?

A
  1. Genetic
  2. Concurrent atopy, food allergies => predilection to develop IgE response to allergens
  3. Prematurity
  4. Lack of exercise
  5. Exposure: early exposure to allergens, pollution, smoking, viral infection
  6. “Hygiene hypothesis”: early exposure to antibiotics, “cleaner” households, C-section delivery, declined infection exposure (especially parasites), declined outdoor play time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is atopy?

A
  1. Asthma
  2. Allergic rhinitis
  3. Eczema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What 7 factors are used to grade asthma severity?

A
  1. Symptoms
  2. Nightime awakenings
  3. Short-term acting beta-agonist use for symptom control
  4. Interference with normal activity
  5. Lung function
  6. Need for corticosteroids
  7. History of intubation, hospitalization
86
Q

5 asthma therapies?

A
  1. Avoidance of triggers
  2. Short and long acting beta-agonist (to activate sympathetic NS response): dilation of smooth muscle in the bronchi
  3. Inhaled and oral corticosteroids: reduce bronchial inflammation
  4. Leukotriene antagonists: inhibit steps in inflammatory pathway
  5. Immune modulating antibodies block IgE
87
Q

2 types of asthma therapies?

A
  1. Acute therapy

2. Maintenance therapy

88
Q

What is aspirin sensitive asthma?

A

Some patients’ asthma will be triggered by aspirin, because it inhibits the synthesis of thromboxanes/prostaglandins from arachidonic acid leading to the increased synthesis of leukotrienes causing bronchoconstriction

89
Q

How to determine what asthma treatment is appropriate?

A

Step-wise approach

90
Q

Why are long-acting beta agonists never used alone to treat asthma?

A

Because they increase the risk of death from asthma, maybe because they desensitize airways to beta-agonists so they are given with inhaled corticosteroids, which decreases the risk

91
Q

Describe the 5 steps of managing an acute asthma exacerbation.

A
  1. Short-acting beta agonists (SABA) (inhaled or nebulizer) and Ipratropium (anti cholinergic)
  2. Supplemental oxygen
  3. Systemic steroids (glucocorticoids)
  4. Systemic beta agonist (epinephrine)
  5. Intubation and mechanical ventilation
92
Q

When an asthma patient stops wheezing, does it mean he is getting better?

A

Not necessarily because it could mean the airflow is so low you can no longer hear wheezing

93
Q

Do most COPD patients have both emphysema and chronic bronchitis?

A

Most patients have some element of both (with one predominating)

94
Q

Risk factors for COPD?

A
  1. Smoking (80% of COPD patients)

2. Lung irritant exposure

95
Q

4 symptoms of COPD?

A
  1. Progressive dyspnea
  2. Cough
  3. Wheezing
  4. Weight loss
96
Q

How to diagnose COPD?

A
  1. PFT (reduced DLCO in emphysema) - helpful to stage the disease
  2. Hyperinflation on imaging (due to expiratory obstruction causing gas trapping)
  3. History when other causes ruled out
97
Q

Describe chronic bronchitis?

A

Airway obstruction with:

  1. Chronic cough
  2. Bronchial inflammation
  3. Production of thick mucus
98
Q

Pathophysiology of chronic bronchitis?

A

Chronic exposure to irritants leads to mucus hypersecretion and increase in mucus producing cells over time =>

  1. Persistent inflammation increases bronchospasm response
  2. Excess mucus impedes ciliary function and increases infection risk, triggering episodic exacerbations
99
Q

Smoking DIRECT effect on the lungs?

A

Directly inhibits ciliary function and mucus clearance

100
Q

Clinical presentation of chronic bronchitis?

A
  1. Chronic, productive cough and later dyspnea
  2. Increased respiratory infections
  3. Obstruction on PFTs with gas trapping as disease progresses
  4. Hypoxemia leading to digital clubbing, cyanosis, and cardiac manifestations
  5. Decreased respiratory drive leads to hypoventilation and increase CO2 retention => chronic hypercapnia => reset of respiratory centers => ventilation more sensitive to O2 status
101
Q

Which disease has more gas trapping: chronic bronchitis or emphysema?

A

Emphysema

102
Q

Why do we call chronic bronchitis patients “blue bloaters”?

A
  1. Cyanotic due to hypoxemia
  2. Fluid retention due to alveolar hypoxia => pulmonary vasoconstriction => pulmonary HT => low CO => decreased circulating BV => RAAS activation
103
Q

Are emphysema patients blue bloaters like chronic bronchitis patients? Explain.

A

NOPE, because they can compensate for the hypoxemia

104
Q

What is digital clubbing?

A

Angled finger beds

105
Q

Why do chronic bronchitis patients have cardiac manifestations?

A

Because their hypoxia can cause pulmonary HT

106
Q

What is emphysema?

A

Enlargement and destruction of alveolar units in lung without major fibrosis with loss of elastic tissue in lungs => dysfunctional recoil + ineffective expiration:

  • Destruction of capillary-alveoli interface leads to diffusion abnormalities (decreased DLCO)
  • Alveoli hyperinflation leads to air spaces in the pleura and lungs
  • Increase in lung compliance => increased work of breathing => dyspnea, cachexia, pursed-lip breathing and accessory muscle use
107
Q

2 types of emphysema? Describe each. What do they have in common?

A
  1. Primary: genetic alpha I anti-trypsin deficiency
  2. Secondary: exposure to smoking, pollutants

Similar disease progression

108
Q

Why is emphysema an obstructive lung disease?

A

Because the loss of recoil causes a functional obstruction for air to be expired

109
Q

What is the role of alpha I anti-trypsin protein?

A

Responsible for inhibiting specific protein breakdown (elastin)

110
Q

Why does an alpha I anti-trypsin deficiency lead to emphysema?

A

Increased elastase activity => tissue architecture disruption + liver damage/renal/GI disease

111
Q

How does smoking affect emphysema type 1 patients?

A

increases risk and severity

112
Q

Profile of patients with emphysema type 1? What to note?

A

Patients with emphysema under 45 yo, non-smokers and with a family history

Note: very rare

113
Q

How does smoking cause emphysema?

A
  1. Smoking increases neutrophils in lungs and stimulate release of elastase granules
  2. Free radicals both in neutrophils and smoking contaminants inhibit alpha-1 anti trypsin
114
Q

Clinical presentation of severe air-trapping in emphysema patients?

A

Barrel chest = increased AP diameter + hyper-resonant sounds

115
Q

Main difference between chronic bronchitis and emphysema?

A

Emphysema comes with diffusion capacity decrease

116
Q

2 histological classes of emphysema? Describe each. Which is most common?

A
  1. Panacinar emphysema:
    - Entire acinar unit involved
    - Lower lung lobes
    - Alpha 1 antitrypsin deficiency, older smokers
  2. ***Centriacinar emphysema:
    - Respiratory bronchioles and alveolar ducts
    - Upper lung lobes
    - Smokers
117
Q

Why do we call emphysema patients “pink puffers”?

A
  1. Pink: relatively well oxygenated blood until late stage because they have a matched V:Q defect (decreased ventilation due to increase in lung compliance and decreased perfusion due to destruction of capillary beds)
  2. Puffer: air-trapping and hyperventilation to compensate for V:Q defect
118
Q

PFT values for emphysema?

A
  1. Decreased DLCO
  2. Increased RV
  3. Increased TLC
  4. Decreased VC
119
Q

What does cachexia mean?

A

Severe weight loss

120
Q

Are blood gases normal or abnormal in emphysema patients?

A

Normal at rest because of compensatory hyperventilation

121
Q

What are bullae?

A

Empty spaces filled with air in the lungs in emphysema patients

122
Q

Effect of emphysema on diaphragm?

A

Flattened diaphragmatic borders due to hyperinflation

123
Q

How to clinically manage COPD? 10 interventions.

A
  1. Avoidance of pollutant exposure (stop smoking)
  2. Vaccination to prevent infections
  3. Pulmonary rehabilitation: helps patients use their lungs efficiently
  4. Bronchodilators
  5. Anticholinergics
  6. Inhaled and oral steroids
  7. Expectorants: help clear mucus from airways (make cough more “productive”)
  8. Antibiotics
  9. Supplemental oxygen to avoid pulmonary HT and cardiac manifestations BUT be careful with respiratory drive and smokers!
  10. Lung volume reduction surgery
124
Q

When an emphysema patient stops smoking, will function be re-gained?

A

NOPE - it’ll just stop disease progression

125
Q

3 pulmonary vascular diseases?

A
  1. Pulmonary embolism and infarction
  2. Pulmonary HT
  3. Pulmonary edema
126
Q

What does pulmonary HT lead to in the final stages?

A

Cor pulmonale = RIGHT ventricular heart dysfunction (dilation, hypertrophy) due to the back up of fluid/pressure into the right side of the heart causing increased work

127
Q

What is pulmonary edema?

A

Fluid in alveoli

128
Q

2 types of pulmonary edemas? Describe each. How to tell difference between the 2?

A
  1. Cardiogenic: caused by elevation of capillary hydrostatic pressure from left heart dysfunction
  2. Non-cardiogenic: normal cardiac function, usually from lung injury and increased capillary permeability (e.g. ARDS, high altitude, neurogenic, narcotics, PE)

To tell the difference: right-heart catheterization to measure pulmonary artery wedge pressure to see if the LAP is elevated => if it is: cardiogenic

OR BNP, ECG, X-ray (enlarged cardiac size, septal lines, edema distribution), echo (valvular function and size of cardiac chambers)

129
Q

What is the difference between pulmonary edema and pleural effusion?

A

Pulmonary edema: fluid in alveoli

Pleural effusion: fluid in pleural space

130
Q

What causes ARDS most commonly?

A

Sepsis = systemic inflammatory response in the presence of a known or suspected infectious agent

131
Q

What are 3 causes of left heart dysfunction?

A
  1. Valvular dysfunction
  2. Reduction in left ventricular contractility
  3. Dilated cardiomyopathy
132
Q

Equation to measure net movement of fluids across the alveolar-capillary interface?

A

Jv = Kf . [Pc-Pi - σ.(πc-πi)]

Pc is the capillary hydrostatic pressure
Pi is the interstitial hydrostatic pressure
πc is the capillary oncotic pressure
πi is the interstitial oncotic pressure
Kf is the filtration coefficient – a proportionality constant
σ is the reflection coefficient

133
Q

Describe the pathophysiology of cardiogenic pulmonary edema?

A

Increase in capillary hydrostatic pressure => increase in fluid movement from capillary to alveoli

134
Q

Describe the pathophysiology of non-cardiogenic pulmonary edema?

A

Damage to interface between capillary and alveoli => wider gaps => increase in Kf => allows fluid and proteins to enter the alveoli

135
Q

How is pulmonary capillary hydrostatic pressure affected in non-cardiogenic pulmonary edema?

A

It is not affected

136
Q

Clinical presentation of pulmonary edema? Is it the same for both types? Implication?

A
  1. Dyspnea
  2. Tachypnea
  3. Hypoxemia
  4. Cough (with fluid)
  5. Crackles and other abnormal sounds
  6. JVD: jugular venous distention

Similar presentation between different ideologies, history should focus on primary insult

137
Q

Can patients have both types of pulmonary edema?

A

In some complicated situations, YUP

138
Q

What is a BNP test?

A

Chemical released by heart during heart failure (ANP) so would be elevated in cardiogenic pulmonary edema

139
Q

What is the most common cause of non-cardiogenic pulmonary edema?

A

ARDS = acute respiratory distress syndrome

140
Q

What is ARDS?

A

Acute respiratory failure from acute lung injury and inflammation causing diffuse alveolar damage (injury of alveolar capillary membrane) =>

  1. Increased alveolar capillary permeability => non-cardiogenic edema
  2. Prevents normal gas exchange => hypoxemia
  3. Fluid increases surface tension => increase in alveolar collapse => decreases compliance
  4. Hypoxic vasoconstriction, lung element destruction => increases pulmonary artery pressure
141
Q

Why is ARDS called an acute restrictive lung disease?

A

Because of the decreased compliance caused by the alveolar-capillary membrane damage leading to fluid and increased surface tension

142
Q

What group of diseases is ARDS the most severe of?

A

Most severe spectrum of ALI = acute lung injury

143
Q

What is the role of the immune system in ARDS?

A

Lung injury => activation of inflammatory pathways => neutrophil recruitment + release of chemicals => further promote lung inflammation and damage

144
Q

What are the 4 stages of ARDS? Describe each.

A
  1. Exudative: diffuse alveolar damage (DAD), edema, hyaline membrane (necrotic cell debris, fibrin)
  2. Proliferative: edema resolves, cellular proliferation and collagen deposition
  3. Fibrotic: fibrotic changes and loss of lung architecture
  4. Resolution: surviving patients regain lung function, weeks to months with possible lung impairment
145
Q

How acute is ARDS?

A

Literally happens in one day

146
Q

Mortality rate for ARDS? What does it depend on? What to note?

A

Very high because systemic insult: 40% even with treatment

Depends on cause, severity and co-morbidities

Note: many patients die from primary illness, multi-organ failure, shock etc. rather than respiratory failure

147
Q

What are the criteria to diagnose SIRS? What does it stand for?

A

SIRS: systemic inflammatory response syndrome (in response to sepsis)

2 or more of the following:

  1. Body temp deregulation
  2. High HR
  3. High RR
  4. WBC count
148
Q

11 possible causes of ARDS? Most common?

A
  1. Aspiration pneumonia: aspiration of gastric content into lungs
  2. Pneumonia
  3. Multi-organ trauma (lung contusion)
  4. Burns
  5. Near drowning
  6. Inhalation of toxic irritants, smoke
  7. Drugs/alcohol overdose
  8. Pancreatitis
  9. Multiple blood transfusion, transfusion-related acute lung injury
  10. Emboli
  11. Sepsis***
149
Q

Why is it hard to treat ARDS patients?

A

Causative processes may be simultaneously causing systemic vasodilation (shock) and multi-organ dysfunction (MODS)/failure

150
Q

What does MODS stand for?

A

Multi-organ dysfunction syndrome

151
Q

Clinical presentation of ARDS?

A
  1. Acute onset dyspnea and hypoxia 24-48 hours after injury or infection => shortness of breath, hypoxemia, tachycardia, tachypnea, accessory muscle use etc.
  2. Bilateral infiltrates
  3. PaO2/FiO2 ratio decreased indicating poor transfer of oxygen to blood and refractory to oxygen supplementation
152
Q

3 criteria to diagnose ARDS?

A
  1. Timing: within 1 week of a known clinical insult or new or worsening respiratory symptoms
  2. Chest imaging: bilateral opacities that are not fully explained by effusions, lung collapse, or nodules
  3. Origin of edema: respiratory failure not fully explained by cardiac failure or fluid overload
153
Q

How is ARDS graded?

A

By oxygenation measure (PaO2/FiO2)

154
Q

ARDS treatment?

A
  1. Identification and treatment of underlying cause
  2. Supportive care: sedation, fluid monitoring, prevention of DVT and GI bleed, treatment of nosocomial infections etc.
  3. Mechanical ventilation with high FIO2
155
Q

How to improve ARDS outcomes? 2 interventions

A
  1. Protective ventilation

2. Fluid management

156
Q

What are some common complications of mechanical ventilation of ARDS patients?

A
  1. VALI = ventilator-associated lung injury
  2. Nosocomial infection
  3. DVT
  4. Stress GI ulceration
157
Q

What are the 5 mechanisms of VALI?

A
  1. Barotrauma = increased positive pressure
  2. Volutrauma = over-distention of alveoli by high TV
  3. Mechanical shear stress = cyclic closing and reopening of alveoli
  4. Biotrauma = inflammatory mediators released by shear stress
  5. O2-toxicity = due to toxic oxygen radicals
158
Q

What are the concepts of protective ventilation?

A
  1. Avoid VALI mechanisms
  2. Plateau pressures <=30 cm H2O
  3. TV of 6 mL/kg predicted body weight
  4. Keep alveoli open by PEEP
  5. Try spontaneous breathing early
159
Q

Normal PEEP?

A

0 cm H2O

160
Q

Definition of pulmonary HT?

A

Pulmonary artery mean pressure above 25 mmHg (normal 8-20 mm Hg)

161
Q

3 pathophysiologies/causes of pulmonary HT? Which 2 are reversible?

A
  1. ***Imbalance between vasodilation and vasoconstriction
  2. ***Hypertrophy of smooth muscle in pulmonary arteries => luminal narrowing and increased pressure
  3. Arterial atherosclerosis: remodeling of arteries with fibrotic tissue
162
Q

5 groups of causes for pulmonary HT?

A
  1. PAH
  2. Left heart dysfunction
  3. Lung disease/chronic hypoxemia
  4. Pulmonary vasculature occluded by clots
  5. Multifactorial
163
Q

Secondary effect of pulmonary HT?

A

Right heart hypertrophy

164
Q

Describe PAH causing pulmonary HT. What does it stand for?

A

Pulmonary Arterial HT

Disease localized to the pulmonary arterioles due to:

  1. Idiopathic (rare)
  2. Familial
  3. Persistent pulmonary HT of the newborn
165
Q

What is PAH associated with?

A
  1. Collagen vascular disease
  2. Congenital systemic to pulmonary shunts
  3. Portal HT
  4. HIV
  5. Drugs/toxins
  6. Significant venous or capillary involvement (e.g. pulmonary veno-occlusive disease, pulmonary capillary haemangiomatosis)
166
Q

Describe left heart dysfunction causing pulmonary HT. Diagnostic measure?

A

Increase in pressure in pulmonary vasculature needed to maintain forward driving force against dysfunctional left heart:

  • Left atrial or ventricular heart disease
  • Left sided valvular heart disease

Diagnostic measure = elevated pulmonary capillary wedge pressure

167
Q

Describe lung disease/chronic hypoxemia causing pulmonary HT.

A
  1. Chronic hypoxia => decreases endothelial nitric oxide synthase => less NO (vasodilator) => increase in arachadonic acid pathways and endothelin release => increases smooth muscle calcium concentration
  2. Lung diseases: COPD and interstitial lung disease
168
Q

Why are COPD patients more likely to get pulmonary HT than emphysema patients? What to note?

A

Because COPD patients cannot compensate for hypoxemia, and emphysema patients can

Note: late emphysema can lead to pulmonary HT via alveolar/vascular bed destruction, hyperinflation and increased intra-alveolar pressure

169
Q

Effect of short-term hypoxia on the lungs?

A

Short term hypoxia => vasoconstriction to limit blood flow to poorly oxygenated lung

170
Q

What happens to the lungs after persistent pulmonary HT? What is this called?

A

Irreversible changes and replacement of blood vessel tissue with collagen = onion skinning in histology

171
Q

Clinical presentation of pulmonary HT? What to note?

A
  1. Fatigue
  2. Chest pain
  3. Dyspnea
  4. Tachypnea
  5. Cough
  6. Peripheral edema
  7. Various heart murmurs

Note: may be masked by primary disease

172
Q

How to make a pulmonary HT diagnosis?

A
  1. ECG indicates right ventricular hypertrophy
  2. Enlarged right heart border and pulmonary vasculature on X-ray/echo
  3. Definitive diagnosis by right heart catheterization and measurement of pulmonary artery pressure
173
Q

What is pulmonary HT treatment based on? Explain.

A

Treatment based on grouping classification:

  1. Control of causative disorder (i.e. diuretics, anti-hypertensives for heart failure, anti-coagulants for chronic thrombi)
  2. PH directed therapy: endothelin blockers, NO agonists, prostacyclin analogs
  3. Lung transplantation for idiopathic PAH
  4. COPD with PH: long term O2 therapy, but not all patients respond, especially if long term remodeling
174
Q

What is the most common cause of cor pulmonale?

A

COPD

175
Q

What % of COPD patients have cor pulmonale? In which patients is it more likely?

A

20-30%

More likely in patients with more severe airway obstruction and disease progression

176
Q

Core pulmonale treatment?

A
  1. Treat the pulmonary HT

2. CV support

177
Q

Other name for cor pulmonale?

A

Pulmonary heart disease

178
Q

What is persistent pulmonary HT of the newborn (PPHN)? Why is it called that?

A

Called persistent because fetal circulation has NORMAL pulmonary HT due to elevated pulmonary vascular resistance (PVR) to keep blood out of the fetal lungs => fetal lungs have low oxygen tension, are fluid-filled, their balance of vasodilators/vasoconstrictors is in favor of vasoconstriction, and there are 2 bypass shunts (FO and DA)

In PPHN, there is a persistent elevated PVR causing a right to left shunt (either through FO or DA) and hypoxic respiratory failure

179
Q

What are the 2 vascular transitions at birth under normal conditions?

A
  1. Rise is SVR due to the removal of the placental circulation (low resistance system) and sympathetic effects from the stress of birth
  2. Decrease in PVR due to expansion and oxygenation of lung tissue, removal of fluid from fetal lungs, vasodilatory factors favored and remodeling of blood vessels to favor vasodilation, and bypass shunts close
180
Q

What are 6 potential causes of the elevated neonatal PVR in PPHN?

A
  1. Vasoconstriction: imbalance of vasoactive substances causing constriction with normal lung architecture (acute problems) => asphyxia, pneumonia sepsis (due to Group B strep), meconium aspiration, respiratory distress syndrome
  2. Remodeling of vasculature: smooth muscle proliferation, collagen deposition (chronic problems) => diaphragmatic hernia, chronic intrauterine hypoxia, antenatal ductal closure
  3. Decreased lung size: decreased number of pulmonary vessels cannot accommodate right heart CO => diaphragmatic hernia, intrathoracic space occupying lesions, or chronic oligohydramnios due to renal dysfunction
  4. Intravascular obstruction: hyperviscosity or polycythermia
  5. Idiopathic
  6. Maternal medication use: NSAIDs and SSRIs
181
Q

3 causes of hypoxic respiratory failure in PPHN?

A
  1. Right to left shunt
  2. High PVR so poor lung perfusion
  3. Original cause of PPHN
182
Q

Why can meconium aspiration cause PPHN?

A
  1. Promotes inflammation
  2. Inhibits surfactant

=> vasoconstriction

183
Q

Why can NSAIDs cause PPHN?

A

Because they are COX inhibitors, which cause DA to close prematurely => increase blood flow to fetal lungs during development => shear stress => vasoconstriction

184
Q

Most common cause of PPHN?

A

Meconium aspiration

185
Q

Clinical presentation of PPHN?

A
  1. Cyanosis

2. Fluctuating hypoxemia: frequent desaturation and large changes in PaO2

186
Q

In what infants do we see PPHN?

A

Term or post-term infants

187
Q

How to make a PPHN diagnosis? Which method is most significant? 3 methods.

A
  1. ***Echo confirmation of R->L shunt
  2. Need to confirm normal cardiac anatomy to exclude heart disease
  3. Pulmonary artery pressure can be estimated - this alone is not a diagnosis!
188
Q

Treatmens for PPHN?

A

SUPPORTIVE CARE:

  1. Oxygen: FIO2 100% to promote vasodilation of pulmonary vessels
  2. Sedation to prevent agitation, which is associated with O2 drop
  3. Ventilator support to remove CO2, as respiratory acidosis promotes vasoconstriction
  4. Fluid and BP support, Hb optimization

INTERVENTIONS:

  1. Surfactant
  2. Inhaled NO and other vasodilators
  3. ECMO: extracorporeal membrane oxygenation
189
Q

How to assess the need for ECMO?

A

Oxygenation index = Mean airway pressure in cm of water × FIO2 × 100/PaO2 [in mm Hg]

A high OI indicates need for ECMO

190
Q

What is ECMO?

A

Oxygenation and removal of CO2 wastes outside the body, for long-term use (days)

191
Q

Outcome of PPHN treatments?

A

High proportion of surviving infants have future disabilities (delay, motor etc)

192
Q

What is pulmonary embolism?

A

Occlusion of pulmonary vasculature by embolism from origin outside of lung

Can be blood (thrombus), fat, air, bone

193
Q

Most common cause of PE?

A

Thrombus from deep venous thrombosis (blood clot in the deep veins - DVT) of lower limbs

194
Q

2 types of PE?

A
  1. Acutely occurring

2. Chronic (small PEs over time)

195
Q

Risk factors for DVTs? What is this called?

A

Virchow’s Triad:

  1. Venous stasis: prolonged immobility
  2. Hypercoagulation: cancer, pregnancy, estrogen contraceptives, congenital thrombophilia, systemic diseases (lupus, autoimmune), smoking
  3. Vascular endothelial injury: surgery, IV line, medication
196
Q

Risk factors for PE?

A

Same ones as for DVTs = Virchow’s Triad

197
Q

Describe the pathogenesis of PE.

A
  1. V/Q mismatch due to increase in dead space => hypoxemia due to
    - Impaired gas exchange
    - Inflammatory response induced by the embolus that furthers vasoconstriction and diminishes surfactant secretion => atelectasis
  2. Increased PVR causing:
    - Reduced CO and hypotension
    - Pulmonary HT
    - Right heart dysfunction, especially with severe vascular obstruction
198
Q

Clinical presentation of PE? What to note?

A
  1. Dyspnea (acute onset)
  2. Pleuritic chest pain
  3. Tachypnea
  4. Tachycardia
  5. Anxiety
  6. Can present in shock or sudden death
  7. Presence of symptomatic DVT (swollen, erythematous, tender calf) but not always identifiable

NOTE: may be asymptomatic

199
Q

How to make a PE diagnosis? Which method is most significant?

A
  1. Chest x-ray (non-specific)
  2. ECG
  3. Elevated D-dimer: sign of clot degradation, only helpful if negative because many things can cause it to be elevated
  4. ***CT-PA = pulmonary angiography or V/Q scan
200
Q

Treatment for PE?

A
  1. Anti-coagulation therapy: acute and out-patient
  2. Thrombolytic therapy for severe PE
  3. Prevention of risk factors
  4. IVC filter for embolism removal to prevent further clots
201
Q

What is a pulmonary angiography? What will it show if a patient has PE?

A

CT scan with contrast to visualize pulmonary arteries

PE would appear as saddle embolism if the clot is very large and blocks the pulmonary trunk

202
Q

What is a V/Q scan?

A

Uses radionucleotides:

  1. Inhalation for V
  2. IV injection for Q
203
Q

Risk of thrombolytic therapy?

A

Bleeding

204
Q

How does anti-coagulation therapy work?

A

Targets the blood coagulation cascade with specific drugs like warfarin, coumadin, or heparin to increase the INR to 2.5 seconds

205
Q

What is the INR?

A

International Normalized Ratio => measure of how long it takes the blood clotting cascade to be activated compared to normal: prothrombin time

206
Q

Length of anti-coagulation therapy?

A

3 months and then re-assess using D-dimer

207
Q

What is the pulmonary acinus?

A

All branches past the terminal bronchioles

208
Q

Why does hypoxia cause high RBC count?

A

Hypoxia signal on kidneys => signal to bone marrow to produce more RBCs to improve O2 delivery

209
Q

2 symptoms of right heart dysfunction?

A
  1. Distended neck veins

2. Enlarged tender liver

210
Q

2 symptoms of hypercapnia?

A
  1. Somnolence

2. Personality changes

211
Q

How to tell if the DA is patent in PPHN?

A

Preductal vs postductal PaO2: if the difference is of >20 mmHg, or 10% saturation then it is patent:

  • Measure PaO2 in right radial artery vs umbilical artery
  • Measure O2 sat in right thumb vs toes

SMP - APP Part 1 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions