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Block 9 Week 3 > Obstructive Lung Diseases- Baker 1 > Flashcards

Obstructive Lung Diseases- Baker 1 Flashcards

1
Q

1: What is FVC?
2: What is FEV?
3: What is PEF?
4: What is FEF?
5: What is TLC
6: What is RV?
7: What is DLCO?

A

1: Total amount of air exhaled during the forced expiration
2: Amount of air expired per second
3: How fast air is coming out
4: Measures airflow halfway through an exhale
5: Measures amount of air in your lungs after you inhale as deeply as possible
6: Amount of air left in your lungs after complex exhalation
7: Measures the ability of the lungs to transfer gas from inhaled air to RBCs in pulmonary capillaries

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2
Q

What does the spirometry test show in obstructive pulmonary disease?

A
  • decreased FEV1
  • decreased FEV1/FVC ratio
  • decreased FEF 25-75
  • normal to increased TLC
  • Increased RV
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3
Q

What will a flow-volume loop look like with an obstruction?

A

decreased expiration showing scooped out pattern

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4
Q

What are the 2 components of COPD?

What are 2 other obstructive pulmonary diseases?

A
  • emphysema and chronic bronchitis
  • asthma
  • bronchiectasis
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5
Q

What is the biggest risk factor of obstructive pulmonary disease?
What is the prevalence?
What percent of smokers develop COPD?

A
  • Smoking
  • 6.2% total (5.2% male and 7.2% female)
  • 10-15% of smokers develop COPD
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6
Q

Who is more likely to get COPD, females or males?

A

females :(

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7
Q

Is COPD killing more or less people as of late?

A

more people :(

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8
Q

What is the trend of tobacco use?

A

less people are using them now

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9
Q

Where is COPD most common?

A

in the south eastern states

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10
Q

Where do most people die of COPD?

A

mid east states and montana and wyoming

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11
Q

Whats happening for the rates of women with COPD?

A

its been increasing since 200 and is now more common in females than males

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12
Q

What are the top 4 causes of death?

What is a risk factor for all of these?

A
  1. heart problems
  2. Cancer
  3. COPD, asthma
  4. Cerebrovascular

Cigarette smoking

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13
Q

How is emphysema defined, clincally or anatomically?

A

anatomically

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14
Q

What is emphysema?

Is there fibrosis in this disorder?

A

the irreversible enlargement of airspaces distal to the terminal bronchioles
-no, there is airspace wall destruction without fibrosis

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15
Q

What are the four types of emphysema?

A
  • Centriacinar
  • Panacinar
  • Paraseptal
  • Irregular
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16
Q

What is the most common type of emphysema?

A

Centriacinar but a lot are a combo of this

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17
Q

What is the type of emphysema seen with smokers? What is it?

A

centriacinar

-damage of the bronciole which results in damage and loss of the alveolar/bronchiole septum.

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18
Q

What is panacinar emphysema?

A

get destruction of the alveolar septum which results in large and fused alveoli

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19
Q

What is this:
initial sparring of the distal acinus. (Involved later)
affects upper lobes/apical segments

A

Centriacinar emphysema

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20
Q

What is this:

associated with chronic bronchitis and smoking (walls with black pigment)

A

centriacinar emphysema

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21
Q

If you see dilated alveoli with destroyed alevolar septum, what are you looking at?

A

emphysema

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22
Q

What is this:
less common
-airspace enlargement from respiratory bronchiole to alveoli (no sparring)
-effects lower lobes/ anterior margins

A

Panacinar Emphysema

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23
Q

What type of emphysema is most severe at lung bases?

What is this emphysema associated with?

A

Panacinar emphysema

-alpha 1 anti-trypsin deficiency

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24
Q

What is the pathogenesis of emphysema?

A

Irritant (such as tobacco)-> ROS-> reduced capacity of antioxidants-> inflammation w/ more neutrophils-> increase elastase + alpha 1 antitrypsin deficiency -> emphysema

Note elastic in lungs is what makes you expire and elastase will destroy this and alpha 1 anti-trypsin will decrease elastase, so without this you will get emphysema

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25
Q

How can you get alpha 1 antitrypsin deficiency that results in emphysema?

A

due to the increase ROOS can lead to oxidative inactivation of it
OR
you can have a congenital deficiency

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26
Q

A1 antitrypsin is a proteinase inhibitor (destroys the protein elastase) and the gene for this is found on the locus of chromosome (blank)

A

14

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27
Q

What is the normal config for a1-antitrypsin?

A

PiM X 2 copies=PiMM

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28
Q

What is the panacinar emphysema config for a1-antitrypsin?

A

PiZ X 2copies=PiZZ (2 messed up copies of the gene)

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29
Q

What happens if you are heterozygote for a1-antritrypsin deficiency (PiM +PiZ=PiMZ)?

A

Typically have reduced levels of alpha1AT but asymptomatic

HOWEVER, add smoking and risk increases significantly

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30
Q

Why do people with emphysema use accessory respiratory muscle for inspirations and expirations?

A

Serine elastase breaksdown the elastin in the alveoli-> destruction of the alveoli->lose elasticity of the lungs (ie. Loss of elastic recoil of the lungs) ->must use accessory respiratory muscles for inspirations and expirations.

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31
Q

What does emphysema look like?

Why is emphysema super scary when you get blebs (sacs full of air, like a ballon)?

A
  • Diffuse alveolar destruction with blebs

- this can pop and you can get a pneumothorax

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32
Q

How does airspace enlargment lead to obstructive physiology?

A
  • 2 mechanisms
    1: loss of elastic recoil
    2: small airway inflammation
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33
Q

What is the result of small airway inflammation?

A
  1. goblet cell metaplasia->mucous plugging
  2. inflammatory cell infiltration
  3. smooth muscle hypertrophy and peribronchial fibrosis
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34
Q

What is this:
Defined Clinically:
Persistent cough with sputum production for at least three months in at least two consecutive years.

A

Chronic Bronchitis

35
Q

What is this:
Defined Anatomically:
Irreversible enlargement of the airspaces distal to the terminal bronchioles
Airspace wall destruction without fibrosis

A

Emphysema

36
Q

What are the inflammatory cells that react to an irritant in chronic bronchitis?
What are the proteases?
What glands are affected by this and how?
What happens to the large airways?
What happens to the small airways?

A
  • neutrophils, macrophages, lymphocyts
  • proteases (neutrophil elastase, cathepsin, matrix metalloproteinase)
  • hypertrophy of submucosal glands in the trachea and bronchi
  • hypersecretion of mucous in the large airways
  • small airway obstruction due to increased goblet cells of the small airways (small bronchi and bronchioles). Excessive mucous production
37
Q

If you smoke what happens to your mucous glands?

A

you get mucous gland hyperplasia

38
Q

The main morphologic finding in chronic bronchitis is an increased (blank) apparatus. The bronchial submucosa is greatly (blank) by hyperplastic submucosal glands that compose well over 50% of the thickness of the bronchial wall.

A

bronchial mucus secreting

expanded

39
Q

What are the clinical features of emphysema?

Can you treat this?

A
  • Starts with dyspnea (progressive with slow decline in function)
  • cough
  • weight loss
  • barrel-chested with prolonged expiratory phase
  • sitting forward, hunched over, pursed lip breathing

-not really

40
Q

What are the clinical features of chronic bronchitis?

A

-persistent cought with sputum production for at least 3 months in at least 2 consecutive years (first symptoms)
-productive cough alone for many years, then
*dyspnea
*hypercapnea
*hypoxemia
*mild cyanosis
(often overlapping symptoms with emphysema)

41
Q

Whats scary about COPD?

A

the presymptomatic phase is really long and by the time symptoms show you already have lost huge amounts of lung function therefore you should always test heavy smokers with spirometry

42
Q

What is this:
preventable and treatable disease state characterized by airflow limitation that is not fully reversible.The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking.

A

2004 ATS/ERS definition of COPD

43
Q

Does COPD have systemic consequences?

A

yes

44
Q

What is this:
A common preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases.
Exacerbations and comorbidities contribute to the overall severity in individual patients.

A

GOLD definition of COPD

45
Q

While COPD may be suspected clinically, (blank) must be used to make the diagnosis. With a value of (blank)

A

spirometry

post-bronchodialtor FEV1/FVC <.70

46
Q

Smoking causes (reversible/irreversible) damage

A

Irreversible

47
Q

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

A

Asthma

48
Q

What is the prevalence of asthma?

A

300 million worldwide
1 in 11 children (2x male)
1 in 12 adults (males=females)

49
Q

Asthma can present at any age but peak is (blank) years of age.
How do children typically present?
Is it progressive?

A

3

  • children usually grow out of it, and it decreases in adolescents, some have it return in adulthood
  • not usually progressive (i.e mild at presentation then mild for life, severe at presentation then severe for life)
50
Q

What is the presentation of acute asthma exacerbation?

How long oes it last?

A
  • chest tightness
  • wheezing
  • dyspnea
  • cough +/- sputum production

Several hours unless untreated but can sometimes turn into status asthmaticus

51
Q

What is status asthmaticus?

A
  • persistent symptoms lasting for days to weeks

- can result in such severe obstruction as to lead to severe cyanosis and even DEATH

52
Q

What do you see histologically in asthma?

A

Blood: Peripheral blood eosinophilia
Sputum: Curschmann spirals and Charcot-Leyden crystals

53
Q

What are these:

whorls of shed epithelium forming spiral shaped mucous plugs

A

Curschmann spirals

54
Q

What are these:
They are indicative of a disease involving eosinophilic inflammation or proliferation, such as is found in allergic reactions and parasitic infections.

A

Charcot-Leyden crystals

55
Q

What are the two types of asthma?

What is the most common and what causes it?

A

Atopic and non-atopic

Atopic-> immediate (type I) hypersensitivity reaction

56
Q

What does the skin test and fam history look like for atopic asthma?

A

Positive skin test or RAST

-Pos. fam history

57
Q

What causes non-atopic asthma?

What does the skin test and fam history look like? Is it more or less severe than atopic?

A
  • hyperirritability of the bronchial tree
  • negative allergen test
  • neg family history (usually)
  • more severe with more persistent symptoms
58
Q

In atopic asthma. what is the early phase composed of and how long does it last?

A

Early (5-30 minutes)

  • IL-4, IL-5, IL-13
  • Bronchoconstriction
  • INCREASED MUCOUS
  • Vasodilation
  • Increased vascular permeability
59
Q

What are the (TH2 stimulate cytokine release) cytokines released in the early phase of atopic asthma? What does this release cause?

What do the mast cells release in atopic asthma?

A

IL-4, IL-5, IL-12

  • Tissue inflammation
  • IgE production
  • Mast cells release granule contents

LT, C4, D4, E4

60
Q

What happens in the last phase of atopic asthma and when does it start and how long does it last?

A

Increased inflammatory cells

  • Eos, Basophils, Neutrophils, lymphs,
  • “Major basic protein”
  • Continued airway constriction, epithelial destruction

-Late (hour 2-24 hrs)
w/out additional exposure can last for days

61
Q

How do you treat atopic asthma?

A

w/ corticosteroids and bronchodilators

-if dont respond to tx, use monoclonal antibodies to cytokines

62
Q

Why is it so hard to breath with asthma?

A

you get goblet cell hyperplasia creating mucus and you get smooth muscle hyperplasia and hypertrophy in asthma. So they can SUPER bronchoconstrict

63
Q

When do you typically get intrinsic (non-atopic) asthma?

What is a common finding with this?

What is the cause?

A

Adult onset

Samter’s Triad
-Nasal polyps, asthma, aspririn sensitivity

-Local production of IgE

64
Q

What are the triggers for asthma?

A 
Allergens
Viral Infections
Medications
-ASA, beta blockers
Exercise
Cold Air
Laughing
Weather Changes
Strong smells (perfume)
Food (maybe)
Air Pollution
Occupational Exposures
Hormonal factors
-Premenstrual worsening
-Hypo and hyperthyroidism
65
Q

How do you diagnose asthma?
What will the spirometry testing show?
Is it irreversible or reversible?

A

Clinically (symptoms/signs of variable and intermitttent airway obstruction)

  • decreased FEV1, FEV1/FVC, PEF
  • reversible
66
Q

What defines the reversibility found in asthma?

A

> 12% AND 200mL improvement in FEV1 15 minutes post-inhaled beta-2 agonist

must do a pre and post bronchodilator test*

67
Q

How can you diagnose asthma if you have a difficult case?

A

-Methacholine challenge
PC20 = concentration of methacholine reduces FEV1 by 20%
-Exercise

68
Q

If you have nightime awakenings of asthma what does this indicate?

What is your lung function like with mild asthma?

How do you treat asthma?

A
  • severe cases
  • can be normal or impaired
  • stages of clinical severity have different tx’s
69
Q 
What is this:
An airflow obstruction
Reversible
Less likely to be smokers
Intermitttent, more variable symptoms
A

asthma

70
Q

What is this:

  • an airflow obstruction
  • not fully reversible
  • older age of onset
  • chronic productive cough with persistent dyspnea
  • inconsistent response to drugs
A

COPD

71
Q

What is this:
a PERMANENT dilation of the bronchi and bronchioles.

What is it caused by?

What kind of infection is it associated with?

A
  • Bronchiectasis
  • caused by destruction of the muscle and elastic tissue
  • necrotizing infection
72
Q

What is the pathogenesis of bronchiectasis?

A
  • Bronchiectasis is a severe bronchitis that lasts a long time.
  • You get an obstruction, then bacteria and secretins get trapped in your lungs which will result in recurrent infections and inflammation.
  • This will destroy normal wall and you get dilated airway that results in pools of mucus.
73
Q

Bronchiectasis is in commonly in the (blank) lobe.

The saccular dilations and grape-like clusters are filled with (blank) which are signs of severe bronchiectasis

A

lower

pools of mucus

74
Q

What lobe does bronchiectasis affect the most? Is it diffuse or localized?
What do they airways look like?

A

Lower lobe and in veritcal airways

diffuse but can be localized if due to a local issue like a tumore

dilated and cystic appearing with mucopurlent secretions

75
Q

What are the associated conditions with bronchiectasis?

A

-CF
-Primary ciliary dyskinesia (Kartagener syndrome)
-Necrotizing pneumonia
(bacteria, viruses, fungi)
-Bronchial obstruction (foreign body, tumor, mucous impaction)
-Other (RA, SLE, IBD, post-transplant)

76
Q

What bacteria causes necrotizing pnemonia?
What viruses?
What fungi?

A

Necrotizing pneumonia

  • Bacteria (TB, S. aureus, H. influ, pseudomonas)
  • Viruses (adenovirus, influenza, HIV)
  • Fungi (Aspergillus)
77
Q

Explain pathogensis of bronchiectasis

A

Infection-> inflammation -> necrosis of epithelial cells, SM cells and elastic tissue-> fibrosis and dilation and impaired mucociliary clearance

78
Q

What are the infections that can lead to bronchiectasis?

A

Immunodeficiencies:

  • TB
  • S. aureus
  • H. flu
  • Pseudomonas
79
Q

What are causes of the inflammation seen in brochiectasis?

A

toxic inhalations
aspiration
ABPA
IBD, RA, SLE

80
Q

What are causes of impaired mucociliary clearance found in bronchiectasis?

A

CF

Kartageners

81
Q

What are the clinical features of bronchiectasis?

A

Cough, Cough, Cough

  • foul smelling, sometimes bloody sputum that is frequent in the morning (position changes=drainage)
  • obstructive disease resulting in dyspnea and cyanosis
  • Occasional severe hemoptysis (life threatening)
82
Q

How do you treat bronchiectasis?

A

Chronic antibiotics, prophylactic doxycycline

83
Q

What will you see if you looked at a lung with bronchiectasis?

A
  • Acute and chronic inflammation in walls of bronchi(oles)
  • Desquamation of epithelium
  • Ulcerations
  • Fibrosis
  • Multiple positive cultures

Block 9 Week 3 (6 decks)

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