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Block 9 Week 3 Meg > Baker/Parks: Obstructive Lung Disease > Flashcards

Baker/Parks: Obstructive Lung Disease Flashcards

1
Q

Air that moves into lung with each quiet inspiration

A

tidal volume

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2
Q

Air that can still be breathed in after normal inspiration

A

inspiratory reserve volume

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3
Q

Air that can still be breathed out after normal expiration

A

expiratory reserve volume

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4
Q

Air in lung after maximal expiration; can’t be measured on spirometry

A

residual volume

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5
Q

Volume of gas present in the lungs after maximal inspiration

A

total lung capacity

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6
Q

What is FVC?

A

forced vital capacity - the volume of air that you can forcefully blow out after full expiration

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7
Q

What is FEV1?

A

the volume of air that can forcibly be blown out in one second, after full inspiration

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8
Q

What are three parameters of lung capacity/function that cannot be directly measured with spirometry?

A

total lung capacity (need to know residual volume)
residual volume
DLCO: the ability of the lungs to transfer gas from inhaled air to RBCs in pulmonary capillaries

**need to use body plethysmography to obtain these values

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9
Q

What happens to the following in obstructive pulmonary disease?

FEV1
FEV1/FVC
TLC
RV

A

FEV1 decreases
FEV1/FVC decreases
TLC is normal or INCREASES (due to air being trapped)
increased residual volume

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10
Q

Describe a flow-volume loop and what is shows

A

Flow volume loops map volume on the x axis, and flow on the y axis. Expiration is in the upper quadrant, and inspiration is in the lower quadrant. Expiration should show a rapid initial flow rate, followed by a decrease in flow rate as more volume is exhaled. Inspiration should be a relatively rounded curve

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11
Q

What is the biggest risk factor for COPD? Is it more prevalent in males or females? Do all smokers get COPD?

A

smoking!
more prevalent in females
NO, only 10-15% of smokers get COPD

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12
Q

What is happening to age-adjusted death rates for people with COPD?

A

they are increasing :(

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13
Q

In 2000, what was one noteable change in COPD death rates?

A

In 2000, more women than men were dying of COPD!

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14
Q

Irreversible enlargement of the airspaces distal to the terminal bronchioles
Airspace wall destruction without fibrosis

A

Emphysema

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15
Q

What are the two types of emphysema we should be aware of, and how are they different?

A

centriacinar: more common, associated with smoking, involves upper lobes, initially spares the distal acinus, associated with chronic bronchitis
panacinar: less common, associated with alpha1 antitrypsin deficiency, involves lower lobes, airspace enlargement from respiratory bronchiole to alveoli (no sparring)

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16
Q

Describe two contributing factors to the pathogenesis of emphysema

A
  1. elastase vs alpha1 antitrypsin imbalance: increasing elastase activity released from neutrophils causes loss of elastic lung fibers, decreased recoil, and an increase in lung compliance. Usu alpha1 antitrypsin helps balance this out
  2. ROS vs antioxidant imbalance: ROS from tobacco overwhelms antioxidant ability of body
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17
Q

If you have two copies of PiM (Proteinase inhibitor) gene, what will you present like? If you have two copies of PiZ, what will you present like? If you are heterozygous?

A

PiM x 2 copies = Normal
PiZ x 2 copies = Panacinar Emphysema
PiM + PiZ = Typically has reduced levels of α1AT, but asymptomatic
However, add smoking and risk increases significantly

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18
Q

What are two mechanisms that can help explain how airspace enlargement leads to obstructive physiology?

A
  1. loss of elastic recoil: can’t squeeze air out of lungs
  2. small airway inflammation: goblet cell metaplasia increases mucous, inflammatory cells infiltrate, smooth muscle hypertrophy & peribronchial fibrosis
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19
Q

Persistent cough with sputum production for at least three months in at least two consecutive years.

A

Chronic bronchitis

**this differs from emphysema, bc it is defined clinically vs anatomically

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20
Q

Describe why tobacco smoke can lead to chronic bronchitis

A

inhale tobacco –> deploy inflammatory cells –> hypertrophy of submucosal glands in the trachea/bronchi –> hypersecretion of mucous in large airways –> small airway obstruction

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21
Q

What are some histological findings in chronic bronchitis?

A

goblet cell hyperplasia
mucous gland hyperplasia
lots of mucous!!!

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22
Q

How does emphysema present clinically?

A

starts with dyspnea
+/- cough
weight loss
barrel-chested, pronlonged expiratory phase
sitting forward, hunched over, pursed lip breathing

**pink puffers

23
Q

Why do patients with emphysema breathe through pursed lips?

A

exhaling through pursed lips increases airway pressure and prevents airway collapse while breathing

24
Q

How does chronic bronchitis present clinically?

A

persistent cough cough cough with sputum production; starts with productive cough and then proceeds to dyspnea on exertion, hypoxemia, mild cyanosis, hypercapnea

**blue bloaters

25
Q

T/F: There is a period of time in the progression of COPD where lung function is reduced, but the patient is not yet symptomatic.

A

True

**symptoms might not become present until lung function greatly decreases

26
Q

It is important to avoid (blank) of COPD, which is often what puts these patients in the hospital

A

exacerbation

27
Q

GOLD definition of COPD: A common preventable and treatable disease, is characterized by persistent (blank) limitation that is usually progressive and associated with an enhanced chronic (blank) in the airways and the lung to noxious particles or gases.
(blank) and comorbidities contribute to the overall severity in individual patients.

A

airflow; inflammatory response; exacerbations

28
Q

While suspected clinically, (blank) must be used to make the diagnosis of COPD

A

spirometry

**need a FEV1/FVC of less than 0.70

29
Q

What value for FEV1/FVC is diagnostic for COPD?

A

less than 0.7

30
Q

T/F: It is not worth it to stop smoking if you have already smoked until age 45-65

A

False, you will have decreased rates of disability and death if you stop smoking, even at a later age

31
Q

a common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, [often reversible] airflow obstruction, bronchial hyperresponsiveness, and an underlying inflammation.

A

asthma

32
Q

What is a defining characteristic of asthma?

A

it is reversible!

33
Q

What is the peak age for asthma to occur? Do you grow out of it? Does it progress?

A

peak age is 3yo
usu decreases in adolescence and then returns in adulthood
**it is not usually progressive, meaning that if it starts out mild, it will be mild for life. If it starts out severe, probably severe for life

34
Q

How does acute asthma present?

A 
cough
wheezing
dyspnea
tachypnea
hypoxemia
mucus plugging

**typically lasts hours unless treated

35
Q

This type of asthma has persistent symptoms lasting from days to weeks
Can result in such severe obstruction that it leads to cyanosis and even death

A

Status asthmaticus

36
Q

What will you see histologically in the sputum in asthma? Two important things

A 
Curschmann spiral (shed epithelium forms mucus plugs)
Charcot-Leyden crystals (formed from breakdown of eosinophils in sputum)
37
Q

What will you see in the blood in a patient with asthma?

A

peripheral blood eosinophilia

**usu associated with an allergen

38
Q

What are the two major types of asthma?

A

atopic: most common, classic type I hypersensitivity reaction, usu have positive skin tests to allergens and a positive family history

non-atopic: less common, associated with hyper-irritability of the bronchial tree, usu have negative allergen tests and no family history, typically more severe and persistent symptoms

39
Q

What happens early in the asthma response? Like within the first 30 minutes

A

So, it is a type 1 hypersensitivity reaction driven by IL4, IL5 and IL13, which leads to tissue inflammation, production of IgE, and mast cell degranulation.

All of these leads to bronchoconstriction, increased mucous, vasodilation, and increased vascular permeability

40
Q

What happens late in the asthma response? Like within 2-24 hours…

A

Increased infiltration of inflammatory cells
Continued airway constriction and epithelial destruction

**this is why this reactions take awhile to resolve

41
Q

What does the TH2 helper T cell secrete in the asthma reaction?

A

IL4, IL5, IL13

42
Q

What types of remodeling might you see histologically with asthma?

A

goblet cell hyperplasia (increased mucous)
smooth muscle hypertrophy (increased bronchoconstriction)
smaller lumen

43
Q

Non-atopic asthma is often associated with Samter’s triad. What’s Samter’s triad?

A

asthma
nasal polyps
aspirin-hypersensitivity

44
Q

What can trigger an asthma attack?

A 
allergens
viral infections
meds
exercise
cold air
laughing
strong smells
food
air pollution
hormones (premenstrual worsening, hypo/hyperthyroidism)
45
Q

Asthma is initially suspected clinically, and then is confirmed by spirometry. What happens to FEV1 and FEV1/FVC?

A

they both decrease

46
Q

What spirometry criteria must be met for asthma to be considered reversible?

A

greater than 12% increase in FEV1 and 200mL improvement in FEV1 after inhaling a beta-2 agonist

47
Q

What can be used to test for asthma?

A

methacholine challenge - administer methacholine which reduces FEV1 by 20%

48
Q

T/F: The severity of asthma is usually symptom mediated. For example, night time awakening from asthma is indicative of more severe asthma. Also, decreased lung function is indicative of more severe cases.

A

True

49
Q

Contrast asthma to COPD

A

Asthma: reversible, COPD: irreversible

Asthma: younger age of onset, COPD: older age of onset

Asthma: less likely to be smokers

Asthma: intermittent, variable symptoms, COPD: chronic productive cough, persistent dyspnea

50
Q

Permanent dilation of the bronchi and bronchioles
Caused by destruction of the muscle and elastic tissue
Associated with necrotizing infections

A

Bronchiectasis

**acute/chronic inflammation in walls of bronchi
destruction of epithelium
ulcerations
fibrosis
multiple positive cultures
51
Q

How does an obstruction lead to bronchiectasis (permanent dilation of the bronchi/bronchioles)?

A

an obstruction, like thick mucous, a tumor, or a foreign body prevents secretions and bacteria from being cleared. So, bacterial build up and lead to infection and inflammation and destruction of the smooth muscle, leading to permanent dilation of the bronchi

52
Q

What might you see grossly in bronchiectasis?

A

lower lobe predominance
may be localized
dilated airways with cystic appearing mucopurulent secretions

53
Q

Bronchiectasis can be associated with these conditions…

A

CF (impaired mucociliary clearance leads to obstruction, increase in bacteria, inflammation, etc)
necrotizing pneumonia due to bacteria, viruses, or fungi
bronchial obstruction

54
Q

How will patients with bronchiectasis present?

A

coughing, with foul-smelling (sometimes bloody) sputum
frequent cough in the morning
orthopnea
occasional severe hemoptysis

Block 9 Week 3 Meg (10 decks)

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