End of Pulmonary at Home Flashcards
1
Q
Define Functional Residual Capacity (FRC)
A
The volume of air in the lungs at the end of a normal passive expiration
2
Q
Functional Residual Capacity: Equation
A
FRC = ERV + RV
3
Q
What is a normal value for FRC?
A
2200 mL
4
Q
Define Vital Capacity (VC)
A
The maximum volume of air that can be moved out during a single breath following a maximal inspiration
5
Q
How would you test a person’s VC?
A
Have patient maximally inspire, then maximally expire.
Max possible volume change
6
Q
Vital Capacity: Equation
A
VC = IRV + TV + ERV
7
Q
Normal value for vital capacity
A
4500 mL
8
Q
Define Total Lung Capacity (TLC)
A
TLC = VC + RV
9
Q
What is a normal value for TLC?
A
- 5700 mL for males
- 4200 mL for females
10
Q
Name the three pulmonary function tests
A
- Spirometry Test
- Forced Expiration (PFT)
- Peak Expiratory Flow Rate
11
Q
What does the spirometry test measure?
A
VOLUME
12
Q
What does forced expiration / PFT measure?
A
Challenge test
13
Q
What does peak expiratory flow rate?
A
Challenge test
14
Q
What changes occur in the lungs with Obstructive Lung Diseases? (4)
A
- Airway narrowing
- Normal airway collapse happens more readily upon maximal expiration
- Problems with expiratory efforts / expansion of residual volume
- Residual volume takes up a larger percentage of total lung capacity
15
Q
What changes occur in the lungs with Restrictive Lung Diseases? (5)
A
- Elasticity / compliance of lungs changes
- Problems with inspiration
- Inspiratory measures are reduced
- Total Lung Capacity decreases
- Vital capacity decreases
16
Q
What stays the same with Obstructive Lung Diseases? (1)
A
- Total lung capacity stays the same
17
Q
What stays the same with Restrictive Lung Diseases? (3)
A
- Residual volume stays the same
- FEC usually not affected
- FEV usually not affected
18
Q
What is an example of a restrictive lung disease?
A
Pulmonary Fibrosis
19
Q
What is an example of an obstructive lung disease?
A
Asthma
20
Q
Define pulmonary fibrosis
A
The development of excess fibrous connective tissue in the lungs (lung scarring)
21
Q
Common causes of pumonary fibrosis (3)
A
- Idiopathic
- Pollutants
- Disorders involving chronic inflammation of CT or collagen
- Certain medications
- Repeated infection
- Genetic
- Radiation therapy to chest
- Certain hypersensitivities
22
Q
3 examples of disorders that can cause pulmonary fibrosis
A
- Scleroderma
- Systemic lupus of erythamatosus
- Rheumatoid arthritis
- Nervous tissue disorders, muscle disorders (of inspiratory muscles)
23
Q
Define Asthma
A
Chronic inflammatory disorder
24
Q
Most common type of asthma
A
Atopic asthma
25
Mechanism of Type 1 Hypersensitivity
-IgE antibodies activate mast cells --> Trigger acute inflammation
26
What occurs with secondary exposures? (asthma)
Mast cell degraunlation --> acute inflammation, resulting in vascular and cellular responses.
27
Vascular responses that occur in asthma
- Vasodilation, increased permeability: Narrow the airway, increase mucus production, thicken airway walls
28
Cellular responses that occur in asthma
- Chemotaxic factors release reactive oxygen species and vasoactive mediators --> BRONCHOSPASM
- Autonomic regulation of smooth muscle is also affected, resulting in further bronchiospasm --> Airway narrowing, difficulty breathing
29
What causes atopic asthma?
Some irritant or allergin
30
Onset and prevalence of atopic asthma
* Onset is often in very young children
| * Rate: On the rise in the last 10-20 years.
31
Key features that distinguish asthma from bronchitis, emphysema (2)
* Bronchospasm
| * Reversible narrowing
32
Asthma ultimately leads to...
Permanent structural damage of the airways, scarring
33
Worst times for asthma exacerbation (2)
- Late at night
| - Early in the morning
34
What is an important tool for assessing risk of asthma exacerbation / attack
Peak Expiratory Flow Rate
35
Two types of asthma treatment and function of each:
1) Control Drug: Designed to REDUCE chronic inflammation
| 2) Rescue drug: Attempts to reverse an acute attack
36
Control drug: Class of drug
Long-acting beta agonists
37
Rescue drug: Class of drug (2)
Beta agonists, bronchodilators
38
Overuse of bronchodilators: What can occur? (3)
o Betadilators may start being produced in lower amounts
o Receptor Down-regulation: Beta agonist being used too frequently → stops working. Cells stop producing the same levels of receptors.
o Extreme form: When bronchodilator is not present, by default, the airway is restricted by default.
39
4 types of obstructive lung diseaes
- Asthma
- Bronchitis
- Emphysema
- COPD
40
What is the distinguishing feature of chronic bronchitis?
Excess mucus buildup?
41
What are two affects of excess mucus buildup of chronic bronchitis
* Causes cilliary dysfunction
| * Promotes bacterial colonization, further inflammation
42
Bronchitis: Cause
Introduction of inhaled irritant
| Most commonly cigarettes
43
Physiological changes in chronic bronchitis (7)
* Inflammation of epithelium
* Vasodilation, increased permeability
* Invasion of inflammatory cells and cytokines
* Edema
* Hyper-secretion of mucus
* Ciliary malfunction: Inability to clear mucus.
* Mucus becomes thicker, home for bacterial colonization → Respiratory infection → More inflammation
44
Clinical manifestations of bronchitis (5)
* Edema and mucus buildup → Airway narrowing → Expiratory air trapping
* Difficulty breathing
* Coughing
* Decreased oxygenation / buildup of CO2 possible
* Eventual progression to fibrosis
45
What does bronchitis lead to?
Emphysema
46
In a nutshell - what is emphysema?
Breakdown of lung tissue itself
47
Emphysema (def)
Abnormal permanent enlargement of gas exchange airways accompanied by destruction of alveolar walls
48
In emphysema, nature of the airway narrowing involves _______
Tissue loss.
Breakdown of lung tissue and Alveolar sacs.
49
The functional narrowing of emphysema results in:
Inter-dependence of alveolar sacks and airways are lost
50
Pathogenesis of primary emphysema
Result of an inherited deficiency in the enzyme α-1 anti-trypsin
51
Prevalence of Primary Emphysema
1-2% of all emphysemas
52
Role of trypsin
Breaks down all protein
53
Role of anti-trypsin
Balances out the losses of protein breakdown
54
What happens as a result of anti-trypsin?
An increase in protease activity and a breakdown of the elastin in the CT of the lungs?
55
Cause of primary inflammation (2)
- Can be inherited
| - Can result from chronic inflammation
56
What causes secondary emphysema?
Chronic bronchitis from smoking (leading cause)
57
What does COPD stand for?
Chronic Obstructive Pulmonary Disease
58
Define COPD
Lung changes consistent with chronic bronchitis or emphysema
59
Clinical manifestations of emphysema all relate to...
Chronic hypertachypnea – chronically high CO2
60
What occurs as a result of the high CO2 in COPD?
The central chemoreceptors adapt and stop responding to CO2 -- therefore the burden relies on peripheral chemoreceptors
61
Why is it problematic for the body to rely on the peripheral chemoreceptors to trigger breathing?
Blood PO2 has to get pretty low for peripheral chemorecptors to respond.
Normal = 100; trigger = 60.
O2sat is at ~92% at this point.
62
What is the optimal oxygen level for a COPD patient?
Why?
92%
PARADOXICALLY, over-oxygenating a COPD patient is going to be very bad for them, because it will turn off their trigger to breathe.
63
Why is 92% a precarious place to be for O2 sat?
Because of the dissociation curve.
o Living on the cliff of the curve, which means that small drops in their PO2 are going to create much longer drops in their O2 sat than with people who have a higher O2 sat.
64
What is the most effective method of exhalation for a COPD patient?
Pursed lip / slow exhalation
