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Flashcards in Pathoma COPD Deck (47)
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1

COPD conditions involve what general principle?

Can't get air out of the lungs

2

If we can't get air out of the lung, what spirometry value is affected?

FVC. FVC is decreased.

FEV1 is also decreased and it is important to note that FEV1 goes down far more than FVC

3

FVC?

Forced Vital Capacity - The amount of your maximum expiration. Inhale maximally and then exhale as much as you can

4

FEV1?

Amount of air expired in 1 second maximally.

5

Relationship between FEV1 and FVC with airway obstruction

Decrease your FEV1:FVC ratio because FEV1 is more affected

6

What value increases with airway obstruction?

TLC is increased. Air trapped in lung because you can't get rid of it

7

TLC?

Total lung capacity - total amount of air that can be in the lung

8

Chronic Bronchitis is defined exactly in what ways

Chronic productive cost lasting at least 3 months over a minimum of 2 years.

9

Patient complaint related to chronic bronchitis?

"Coughing up buckets of mucus"

10

Cause of chronic bronchitis?

Smoking

11

What are the layers of the lungs we should know of?

What is in them?

Lumen which is laden with pseudostratified ciliated epithelium sitting on a basement membrane. Below this is the Lamina Propria, which has large blood vessels which help keep the air warm.

Below this is the submucosa has glands. Serous glands support by humidifying the air. Mucinous glands make mucous fluid and secretes up to trap loose particles and things.

Cartilage below all of this

12

Mucinous glands take up ____% of the wall

40%

13

What do we see in smokers as far as the submucosa?

Hyperplasia of mucinous glands that are trying to lubricate the drying lung. Hyperplasia can lead to cancers, etc.

14

What is the Reid index

Measure of wall thickness in regards to the mucinous glands

15

In smokers, mucinous glands take up ____% of the entire wall

More than 50%

16

If Reid index is >50%, what do we know?

Hyperplastic mucous glands in the respiratory wall which will lead to coughing (to get the fluid out) and obstruction (as the mucous settles lower)

Classic for chronic bronchitis

17

Clinical features of Chronic Bronchitis?

Productive cough, cyanosis, increased PaCO2 and decreased PaO2.

Increased risk of infection and cor pulmonale

18

Emphysema

Destruction of alveolar air sacs, leading to obstruction for getting air out for 2 reasons

1. Elastic recoil of airsacs is diminished
2. Reduced thickness of tubes leads to faster acceleration out of the lung. Now without the elastic recoil, the walls of the bronchioles have nothing holding them open, so BOOM, the walls go up with the air and close, causing an obstruction

19

What really causes emphysema?

Imbalance of proteases and antiproteases.

At the base of the lungs, we have alveolar macrophages which eat up bad proteins, the very few that make it, when we breathe in, and will cause a little inflammation.

This leads to protease creation, which can damage the lung. THe lung makes antiproteases, particularly the alpha 1 anti-trypsin (A1AT) that takes care of the proteases.

Normally the proteases and antiproteases are in balance. In Emphysema, the ratio favors proteases.

20

The protease/antiprotease problems we see in emphysema patient arise from two diseases most commonly, each having a different specific effect on the ratio with the same outcome. Discuss them.

1. Smokers - Have a ton of inflammation down in the alveolar sacs, meaning A LOT of protease activity. Balance shifts and the antiproteases can't keep up.

2. A1AT deficiency - Less antiprotease leading to proteases taking over

21

Centriacinar emphysema

Hitting the central portion of the acinus.

We see this in our smokers for type 1 emphysema, the type caused by smoking

22

What is the acinus?

The functional unit of the lung, the terminal bronchiole leading into the alveolar air sac

23

What is panacinar emphysema?

Full acinus emphysema which we see in A1AT emphysema

24

Centracinar emphysema, caused by smoking, affects which lobe the most?

Upper

25

What other condition do we see with A1AT deficiency?

Liver Cirrhosis - Liver is still making the A1AT but it is struggling to fold it. These buildups of these messed up proteins can cause the cirrhosis by piling up in the Endoplasmic Reticulum of liver cells

26

A1AT gene comes in multiple alleles. What are they?

PiM = normal allele

PiZ = most common clinically relevant mutation - Leads to the misfolding

27

PiMZ (heterozygotes) present how?

Uusually asymptomatic with decreased circulating llevels of A1AT.

Significant risk for emphysema with smoking

28

PiZZ (homozygous) presents how?

Panacinar emphysema with cirrhosis

29

Clinical features of emphysema

1. Dyspnea and cough with minimal sputum
2. Prolonged expiration with pursed lips (pink puffer)
3. Weight loss
4. Increased AP diameter (barrel-chest)

30

Late complications of emphysema?

Hypoxemia
Cor pulmonale

31

What is asthma?

Reversible airway bronchoconstriction

32

Asthma most often due to what?

Allergic reaction with Type I hypersentitivity

33

Presentation of asthma

Allergic rhinits
Eczema
Family history of atopy

34

Pathogenesis of Asthma

1. Allergens induce TH2 phenotype in CD4+ T cells of genetically suceptible individuals

2. TH2 cells secrete IL-4, IL-5, and IL-10

35

IL-4 does what?

Allows plasma cell to switch to IgE, which mediates allergic reactions

36

IL-5?

Calls in eosinophils

37

IL-10?

Inhibits TH1 and boosts TH2

38

Re-exposure to allergen involved with asthma?

IgE-mediated activation of mast cells (early phase) which dump preformed histamine granules

Inflammation perpetuates bronchoconstriction via leukotriene prooduction (vaso constriction and bronchoconstriction)

This response, overactivity, causes bronchoconstriction to happen more rapidly = asthma

39

Presentation of asthma

SOB, wheezing
Productive cough
Curschmann spirals admixed with Charcot-Leyden crystals (derived from eosinophils)

Severe unrelenting attack can result in status asthmaticus and death (msot extreme asthma)

40

Exercise and viral infection can cause asthma. What drug is none to cause asthma?

Aspirin (called asthma intolerant asthma)

41

Bronchiectasis

Dilatation of the bronchioles and bronchi (loss of tone leads to obstruction, too big of a space to move up out of the lungs)

42

Causes of bronchiectasis

Due to necrotizing inflammation with damage to airway walls (lots of inflammation leads to being overrun by it!)

43

Common diseases that can cause bronchiectasis

1. Cystic fibrosis
2. Kartagener Syndrome
3. Tumor or foreign body
4. Necrotizing infection
5. Allergic bronchopulmonary aspergillosis

44

What is allergic bronchopulmonary aspergillosis? Who gets it?

What does it lead to?

Allergic reaction to aspergillis seen in two types of patients

1. asthma
2. CF patients

Leads to bronchiectasis!

45

Clinical features of Bronchiectasis?

Cough, dyspnea, foul smelling sputum

46

Complications of bronchiectasis?

Complications include hypoxemia with cor pulmonale and secondary amyloidosis

47

Amyloidosis

Deposition of misfolded protein. In bronchiectasis we see a deposition of AA misfolded protein (secondary amyloidosis)